Chapter 5: Examination of Motor Function: Motor Control and Motor Learning

Motor control evolves from a complex set of neural, physical, and behavioral processes that govern posture and movement. Some movements have a genetic basis and emerge through processes of normal growth and development. Examples of these include the largely reactive reflex patterns that predominate during much of early life and in some patients with brain damage. Other movements, termed motor skills, are learned through interaction and exploration of the environment. Practice and feedback are important variables in defining motor learning and motor skill development. Sensory information about movement is used to guide and shape the development of motor programs. A motor program is defined as “an abstract representation that, when initiated, results in the production of a coordinated movement sequence.”^{1, p. 497} Examples include the complex neural circuitry in the spinal cord known as central pattern generators that control locomotion and gait.

Higher-level motor programs can be viewed as abstract rules or code for coordinated actions that are stored (generalized motor programs [GMPs]). GMPs contain information about the order of events, the timing of events (temporal structure), the overall force of contractions, and the muscle(s) or limb(s) used in the movements. Sensory feedback from the responding limbs, as well as from the environment, modifies the resulting movements. A motor plan (complex motor program) is an idea or plan for purposeful movement that is made up of several component motor programs. Motor memory (procedural memory) involves the recall of motor programs or subroutines and includes information on (1) initial movement conditions; (2) sensory parameters (how the movement felt, looked, and sounded); (3) specific movement performance parameters (knowledge of performance); and (4) outcome of the movement (knowledge of results).

The cooperative actions of multiple systems allow for accommodation of movement to match the specific demands of the task and the environment. This is defined by systems theory, a distributed model of motor control. The central concept is that many systems interact to produce coordinated movement, not just the nervous system. For example, mechanical factors of the musculoskeletal system (body mass, inertia, and gravity) contribute to the overall quality of the movement produced. Cognition (attention, memory, learning, judgment, and decision making) and perception (interpretation of sensation) are also critical. Impairments in any of these interacting systems can significantly alter the quality of the movement produced and the level of function achieved.² Another concept is that units of the central nervous system (CNS) are organized around specific task demands (termed task systems). The entire CNS may be necessary for complex tasks, whereas only small portions may be needed for simple tasks. Command levels vary depending on the specific task executed. Thus, the highest level of command may not be required in the execution of some simple movements.^2,3 Lateral pathways are involved in voluntary movements of distal musculature and are under direct cortical control (i.e., corticospinal and rubrospinal tracts). Ventromedial pathways are involved in control of posture and locomotion and are under brain stem control (i.e., vestibulospinal tracts, tectospinal tract, and pontine and medullary reticulospinal tracts). The neurons of the ventral horn of the spinal cord are the final common pathway to engage the peripheral muscles for function.

Motor skills are acquired and modified by actions of the CNS through processes of motor learning. Motor learning is defined as “a set of internal processes associated with practice or experience leading to relatively permanent changes in the capability for skilled behavior.”^{1, p. 497} The CNS organizes and integrates vast amounts of sensory information. Feedback is response-produced information received during or after the movement and is used to monitor output for corrective actions. Feedforward, the sending of signals in advance of movement to ready the sensorimotor systems, allows for anticipatory adjustments in postural activity. Processing of information by the CNS is both serial and parallel, leading to the production of coordinated movement. Coordination is the ability to execute smooth, accurate, and controlled motor responses. Coordinative structures (synergies) are the functionally linked muscles that are constrained by the nervous system to act cooperatively to produce an intended movement.¹

Recovery is the reacquisition of the ability to perform movement in the same manner as it was performed prior to injury (i.e., same body segments). Function is restored in neural tissue that was initially lost after injury. Task performance is similar to that used by nondisabled individuals. Compensation refers to the performance of movement in a new manner. Alternative movements can result from (1) the adaptation of remaining motor elements or (2) substitution of movements using different motor elements or body segments. Neural tissue acquires a new function, and tasks are accomplished using alternate muscles or limbs. For example, the patient with stroke dresses using the less involved upper extremity (UE). A determination needs to be made as to whether the movements demonstrate recovery or compensation. If compensatory movements are present, are they of sufficient quality and efficiency to permit return of function?⁴

Neural plasticity refers to the adaptive capacity of the CNS to change and repair itself. The brain changes in both structure and function as it encodes experiences and learns new behaviors (i.e., experience-dependent neural plasticity). Learning involves both short-term changes (e.g., increases in the strength of synaptic connections) and long-term changes (e.g., changes in genes, neurons, and neuronal networks within specific brain regions).⁵ As learning progresses, there is a shift from short-term to long-term processes. Motor (procedural) memory allows for continued access of this information for repeat performance or modification of existing patterns of movement. Thus the patient with brain damage (e.g., traumatic brain injury [TBI], stroke) can progress and improve in motor function with an effective rehabilitation plan of care. The therapist needs to ensure the examination accurately identifies all elements of the patient’s motor function. Box 5.1 summarizes terminology related to motor control. See additional discussion in Chapter 10, Strategies to Improve Motor Function.

Damage to the CNS interferes with motor function processes. Lesions affecting areas of the CNS can produce specific, recognizable deficits that are relatively consistent among patients (e.g., patients with upper motor neuron syndrome). Individual differences in neural plasticity, recovery, and functional outcomes can be expected. In conditions with widespread damage to the CNS (e.g., TBI) the resultant problems in motor function are numerous, complex, and difficult to delineate. An accurate picture of the scope of deficits may not be readily apparent on initial examination. A process of reexamination over time will generally yield an understanding of the patient’s performance capabilities and deficits. The comprehensive examination focuses on delineation of impairments, activity limitations, and participation restrictions. Those impairments that directly affect motor function should be clearly identified. Goals, expected outcomes, and a plan of care (POC) can then be effectively developed.

This chapter will review essential components of examination, factors that may constrain the motor function examination (preliminary examinations), and elements of the motor function examination (with the exception of the examination of coordination and balance, which is discussed in Chapter 6, Examination of Coordination and Balance). Required elements of motor learning and examination are also discussed. Finally, instrumentation systems and general methodology used to perform an electromyography (EMG) and nerve conduction velocity (NCV) examination are discussed along with the characteristics of normal and abnormal EMG and NCV findings.

The examination of motor function involves three components: (1) patient history, (2) a review of relevant systems, and (3) specific tests and measures that allow formulation of the diagnosis, prognosis, and POC.⁶

Patient History

During the patient/client history, information is gathered on (1) general demographics, (2) social history, (3) employment/work (job/school/play), (4) living environment, (5) general health status, (6) social/health habits, (7) family history, (8) medical/surgical history, (9) current condition(s)/chief complaint(s), (10) functional status and activity level, (11) medications, and (12) other clinical tests. Information is obtained from the patient and other interested persons (e.g., family members, significant others, and caregivers). If the patient is unable to communicate accurate and meaningful information, as is frequently the case with injury to the brain, data must be gathered from other sources (e.g., family members, caregivers). A review of the medical record can be used to verify and triangulate data obtained from personal communications. Often, the medical record of a patient with pronounced deficits in motor function (e.g., the patient with TBI) contains a large amount of data that can be unwieldy and difficult to sort through. The therapist can benefit from the application of a framework to identify and classify problems. The International Classification of Functioning, Disability and Health (ICF) model⁷ focuses on impairments, activity limitations, and participation restrictions, and provides a useful framework. It is discussed fully in Chapter 1, Clinical Decision Making.

Systems Review

A systems review serves the purpose of a screening examination; that is, a brief or limited examination of body systems. The physical therapist can then use this information to identify potential problems that will require more extensive testing. For example, screening examinations for posture and tone may reveal significant impairments. More detailed tests and measures are then required to delineate the exact nature of the problems uncovered. Sometimes screening examinations reveal problems in communication and/or cognition that preclude further testing. For example, a patient with stroke and severe communication and cognitive impairments will be unable to follow directions and cooperate with many individual tests of physical function. The therapist will document this in the medical record as unable to test at the present time due to severe communication/cognitive deficits.

Tests and Measures

Therapists should select standardized methods and instruments with established validity and reliability whenever possible, consistent with the American Physical Therapy Association’s (APTA) goal of evidence-based practice.⁶ Examination of motor function is a multifaceted process that typically requires a number of different tests and measures. Information should be obtained about specific impairments (i.e., body functions and structure) and their impact on movement and function (i.e., activity limitations and participation restrictions). Instruments can be general (providing an overall measure of health) or specific (providing condition-specific, body-region specific, or individual-specific data). Instruments can be self-report or performance-based with a focus on qualitative or quantitative aspects of movement.⁶ Many different instruments focusing on motor function are discussed in later chapters in this text. The Rehabilitation Measures Database developed by the Rehabilitation Institute of Chicago, Center for Rehabilitation Outcomes Research (www.rehabmeasures.org), provides a valuable source of information on specific tests and measures, as does the Academy of Neurologic Physical Therapy EDGE Task-force Outcome Measures (www.neuropt.org).

Qualitative assessment of motor function requires insights and understanding of patterns of normal movement or postures. The therapist uses inductive reasoning processes (formulating generalizations from specific observations). The experienced therapist or expert clinician is far more efficient in reaching decisions about qualitative performance than the novice therapist. Quantitative instruments use objective measurement as a way of examining performance. Documentation requirements imposed by the health care system and third-party payers increasingly emphasize objective instruments as evidence of the need for, as well as the effectiveness, of services. However, many aspects of motor function are not easily measured, especially in the patient with neurological insult or injury. For example, motor learning is not directly measurable but rather is inferred from measures of performance, retention, generalizability, and adaptability. Thus, these constructs are used to infer changes in the CNS that occur with learning. The therapist must be sensitive to the nature of the variables being examined and identify appropriate measures that provide a meaningful analysis of patient function. It is not likely that any one measure will provide all of the data needed for the examination of motor function.

Reexamination is performed to determine if goals and outcomes are being met and if the patient is benefiting from the POC. If goals and expected outcomes are not being met, modifications in the POC are needed. The patient who has reached a plateau and does not show continued progress over time should be considered for discharge. Many patients with deficits in motor function typically undergo multiple episodes of rehabilitation as recovery occurs (e.g., TBI or stroke). Patients with chronic progressive conditions (e.g., Parkinson’s disease, multiple sclerosis) also typically experience multiple episodes of rehabilitation when deterioration with loss of function occurs.

Patients who sustain brain damage either through trauma or disease may present with a number of cognitive, emotional, perceptual, or communication deficits that can significantly affect how they experience the environment and interact with others. Impairments in sensation and sensory integrity can also profoundly influence a patient’s movement responses. It is important to understand how the examination of motor function can be influenced by these factors. Using tests and directions that confuse a patient during an examination or are clearly beyond the capabilities of the patient will only yield inaccurate information about a patient’s movements.

Consciousness and Arousal

Examination of consciousness and arousal is important in determining the degree to which an individual is able to respond. The ascending reticular activating system includes core neurons in the brain stem, the locus coeruleus, and raphe nuclei that synapse directly on the thalamus, cortex, and other brain regions. It functions to arouse and awaken the brain and control sleep–wake cycles. High levels of activity are associated with extreme excitement (high arousal), whereas lesions in the brain stem are associated with sleep and coma. The descending reticular activating system is composed of the pontine and medullary reticulospinal tracts. The pontine (medial) reticulospinal tract enhances spinal cord antigravity reflexes and extensor tone of lower limbs. The medullary (lateral) reticulospinal tract has the opposite effect, reducing antigravity control.⁸

Five different levels of consciousness have been identified. Consciousness refers to a state of arousal accompanied by awareness of one’s environment. A conscious patient is awake, alert, and oriented to his or her surroundings. Lethargy refers to altered consciousness in which a person’s level of arousal is diminished. The lethargic patient appears drowsy but when questioned can open the eyes and respond briefly. The patient easily falls asleep if not continually stimulated and does not fully appreciate the environment. Attempts to communicate with the patient are difficult, owing to deficits in maintaining focus. The therapist should speak in a loud voice while calling the patient’s name. Questions should be simple and directed toward the individual (e.g., How are you feeling?).

Obtunded state refers to diminished arousal and awareness. The obtunded patient is difficult to arouse from sleeping and once aroused, appears confused. Attempts to interact with the patient are generally nonproductive. The patient responds slowly and demonstrates little interest in or awareness of the environment. The therapist should shake the patient gently as if awakening someone from sleep and again use simple questions. Stupor refers to a state of altered mental status and responsiveness to one’s environment. The patient can be aroused only with vigorous or unpleasant stimuli (e.g., painful stimuli such as flexion of the great toe, sharp pressure or pinch, or rolling a pencil across the nail bed). The patient demonstrates little in the way of voluntary verbal or motor responses. Mass movement responses may be observed in response to painful stimuli or loud noises. The unconscious patient is said to be in a coma and cannot be aroused. The eyes remain closed and there are no sleep–wake cycles. The patient does not respond to repeated painful stimuli and may be ventilator dependent. Reflex reactions may or may not be seen, depending on the location of the lesion(s) within the CNS.⁹

Clinically, the patient can progress from one level of consciousness to another. For example, with an intracranial bleed, the swelling and mass effect compresses the brain, resulting in decreasing levels of consciousness. The patient progresses from consciousness, to lethargy, to stupor, and finally to coma. If medical interventions are successful, recovery is evidenced by a reverse progression. True coma is generally time limited. Patients emerge into a minimally conscious (vegetative) state, characterized by return of irregular sleep–wake cycles and normalization of the so-called vegetative functions—respiration, digestion, and blood pressure control. The patient may be aroused but remains unaware of his or her environment. There is no purposeful attention or cognitive responsiveness. The term persistent vegetative state is used to describe individuals who remain in a vegetative state 1 year or longer after TBI and 3 months or more for anoxic brain injury. This state is caused by severe brain injury.

The Glasgow Coma Scale (GCS) is a gold standard instrument used to document level of consciousness in acute brain injury. Three areas of function are examined: eye opening, best motor response, and verbal response. Total GCS scores range from a low of 3 to a high of 15. A total score of 8 or less is indicative of severe brain injury and coma, a score between 9 and 12 is indicative of moderate brain injury, and a score between 13 and 15 is indicative of mild brain injury.¹⁰ The Rancho Los Amigos Levels of Cognitive Function is widely used in rehabilitation facilities to examine the return of the person with brain injury from coma (Level I, no response) to consciousness (Level VIII, purposeful–appropriate). Different levels of behavioral function are described (e.g., confused states, automatic states).¹¹ See Chapter 19, Traumatic Brain Injury, for a complete discussion of both these instruments.

Examination of the pupillary size and reaction can also reveal important information about the unconscious patient. Pupils that are bilaterally small may be indicative of damage to the sympathetic pathways in the hypothalamus or metabolic encephalopathy. Pinpoint pupils are suggestive of a hemorrhagic pontine lesion or narcotic overdose (e.g., morphine, heroin). Pupils that are fixed in mid-position and slightly dilated are suggestive of midbrain damage, whereas large bilaterally fixed and dilated pupils suggest severe anoxia or drug toxicity (e.g., tricyclic antidepressants). If only one pupil is fixed and dilated, temporal lobe herniation with compression of the oculomotor nerve and midbrain is likely.⁸

Whereas an appropriate level of arousal allows for optimal motor performance, very low or high levels of arousal can cause deterioration in motor performance. This is referred to as the inverted-U principle (Yerkes–Dodson law).^12,13 Patients at either end of the arousal continuum (either very high or very low) may not respond at all or may respond in an unpredictable manner. This phenomenon may explain the reactions of patients with brain damage who are labile and lack homeostatic controls for normal function. Under conditions of severe stress, performance can become severely disrupted.

Therapists need to examine autonomic nervous system (ANS) responses. The actions of the ANS are typically widespread with multiple systems engaged. The ANS has two main divisions: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS) (Table 5.1). The SNS allows actions to be initiated to protect the individual during conditions of stress (the alarm system). Motor systems become engaged in carrying out defensive commands, producing fight or flight responses (e.g., the aroused patient with TBI may hit or bite). The PNS is activated continuously to maintain homeostasis. It shuts down when the SNS is activated and works to restore homeostasis afterward.

Critical components for baseline examination include (1) a representative sampling of ANS responses, including heart rate (HR), blood pressure (BP), respiratory rate (RR), pupil dilation, and sweating; (2) a determination of patient reactivity, including the degree and rate of response to stimulation; and (3) a determination of physiological stressors (e.g., environmental factors). Careful monitoring during a motor performance examination assists in defining homeostatic stability. Specific guidelines for the examination of vital functions can be found in Chapter 2, Examination of Vital Signs.

Autonomic dysregulation is characteristic of certain diseases and conditions and can be seen in patients with TBI, Parkinson’s disease, multiple sclerosis (MS), and spinal cord injury (SCI) (particularly injury above T5). Examination of baseline ANS parameters should, therefore, precede other elements of the motor examination in the patient suspected of autonomic instability. Ongoing monitoring is also critical to ensuring that accurate data are collected and to safeguard the patient.

Cognition

A screening examination of cognitive abilities should include orientation, attention, memory, and executive or higher-order cognition (e.g., calculating abilities, abstract thinking, constructional ability). Abnormalities can occur with neurological disease (e.g., frontal lobe disease, TBI) or psychiatric illness (e.g., panic attacks, depression following stroke). Impaired cognitive function deficits can range from orientation and memory deficits to poor judgment; distractibility; and difficulties in information processing, abstract reasoning, and learning, to name just a few. Patients with deficits across many or all areas of cognitive function demonstrate diffuse or multifocal pathology (e.g., Alzheimer’s disease, chronic brain syndrome). Patients with deficits in only one or a few areas of testing typically demonstrate focal deficits (e.g., stroke).¹⁴ The physical therapist may be one of the first professionals to interact with the patient and should be able to screen for cognitive deficits and initiate appropriate referrals. Consultation with an occupational therapist or neuropsychologist is necessary to obtain an accurate picture of these deficits and to help structure the examination of motor function. The reader is referred to Chapter 27, Cognitive and Perceptual Dysfunction.

Orientation

Orientation is the ability to comprehend and to adjust oneself with regard to time, location, and identity of persons. It is examined with respect to (1) time (What day/month/season/year is it? What is the time of day?); (2) place (Where are you? What city/state are we in? What is the name of this place?); and (3) person (What is your name? How old are you? Where were you born? What is the name of your wife/husband?). The therapist records the accuracy of the patient’s responses. Findings are documented in the medical record as follows: Patient is alert and oriented ×3 (time, person, place) or ×2 (person, place), depending on the domains correctly identified. An additional domain that can be examined is circumstance (What happened to you? What kind of a place is this? Why do people come here?). To answer these last questions correctly, the individual must be able to take in, store, and recall new information. This may be severely disrupted in the patient with TBI. Disorientation is also common in the patient with delirium or advanced dementia.

Attention

Attention is the directing of consciousness to a person, thing, perception, or thought. It is dependent on the capacity of the brain to process information from the environment or from long-term memory. An individual with intact selective attention is able to screen and process relevant sensory information about both the task and the environment while screening out irrelevant information. The complexity and familiarity of the task determine the degree of attention required. If new or complex information is presented, concentration and effort are increased. Patients who are inattentive will have difficulty concentrating. Attention deficits are typically seen in individuals with delirium, brain injury, dementia, mental retardation, or performance anxiety.

Selective attention can be examined by asking the patient to attend to a particular task. For example, the therapist asks the patient to repeat a short list of numbers forward or backward (digit span test). The therapist documents the number of digits the patients is able to recall. Normally individuals can recall seven forward and five backward numbers. For patients with communication impairments, the therapist can read a list of items while the patient is asked to identify or signal each time a particular item is mentioned. Sustained attention (or vigilance) is examined by determining how long the patient is able to maintain attention on a particular task (time on task). Alternating attention (attention flexibility) is examined by requesting the patient to alternate back and forth between two different tasks (e.g., add the first two pairs of numbers, then subtract the next two pairs of numbers). Requesting the patient to perform two tasks simultaneously is used to determine divided attention. For example, the patient talks while walking (Talks While Walking Test), or walks while locating an object placed to the side (simulated grocery shopping). Documentation should include the specific component of attention examined, timed responses of slowness or hesitation in the response (latency), the duration and frequency of episodes of inattention, the environmental conditions that contribute to or hinder attention abilities, and the amount of required redirection (verbal cueing) to the task.

Memory

Memory is the process of registration, retention, and recall of past experience, knowledge, and ideas. Declarative (explicit) memory involves the conscious recollection of facts, past events, experiences, and places. Motor (procedural or implicit) memory involves recall of movements or motor information and storage of motor programs, subroutines, or schema as well as perceptual and cognitive skills. Patients with brain injury and deficits in the medial temporal lobe areas and hippocampus demonstrate profound deficits in declarative memory while they may retain elements of motor memory, which is more broadly distributed in the CNS motor areas (striatum, cerebellum, premotor cortex).

The length of time required from initial acquisition into memory also distinguishes types of memory. Immediate memory (immediate recall) refers to the immediate registration and recall of information after an interval of a few seconds (e.g., “Repeat these three items after me”). Short-term memory (STM) (recent memory) refers to the capability to remember current, day-to-day events (e.g., what was eaten for breakfast, the date), learn new material, and retrieve material after an interval of minutes, hours, or days. Long-term memory (LTM) (remote memory) refers to the recall of facts or events that occurred years before (e.g., birthdays, anniversary, historic facts). It includes items an individual would be expected to know.

A simple test for memory involves presenting a short list of words of unrelated objects (e.g., pony, coin, pencil) and asking the patient to repeat those words immediately after presentation (immediate recall) and again 5 minutes after presentation (STM). LTM can be determined by having the patient recall events or persons from his or her past (Where were you born? Where did you go to school? Where do/did you work?). The patient’s fund of general knowledge can also be examined (Who is the president? Who was president during World War II?). The questions selected should represent sensitivity to the cultural and educational background of the patient. It is important to consider that memory may be influenced by attention, motivation, rehearsal, fatigue, and other factors. The Mini-Mental Status Examination (MMSE) provides a valid and reliable quick screen of cognitive function.¹⁵

Patients with amnesia experience partial or total, permanent or transient loss of memory. Anterograde amnesia (post-traumatic amnesia) refers to the inability to learn new material acquired after a brain insult. Retrograde amnesia refers to the inability to remember previous learning acquired before the occurrence of a brain insult. Patients with delirium (acute confusional state) typically demonstrate impairments in immediate memory and STM along with confusion, agitation, disorientation, and usually illusions or hallucinations. Patients with dementia demonstrate broad-based memory and learning impairments. Significant memory deficits are also seen in patients with diffuse encephalopathies, bilateral temporal lesions, and Korsakoff’s psychosis (thiamine deficiency). Certain drugs can improve memory (e.g., CNS stimulates, cholinergic agents), whereas other drugs can degrade memory (e.g., benzodiazepines, anticholinergic drugs).

Patients who demonstrate difficulty in retrieving information will often relate that the information is on the “tip of their tongue” (the tip of the tongue phenomenon). Various different strategies can be used to facilitate recall of information (e.g., prompting, rehearsal, and repetition). If attention and memory are impaired, instructions during the examination should be kept simple and brief (one-level commands vs. two- or three-level commands). The therapist should structure or choose an environment in which distractions are reduced (i.e., a closed environment) to ensure maximum performance during the examination. Demonstration and positive feedback can assist the patient to understand what is expected and can be used to motivate and improve performance. Use of any memory-enhancing strategies during an examination should be carefully documented in the patient’s record. It is also important to remember that diffuse declarative memory deficits can persist while procedural memory for well-learned motor tasks can be retained (e.g., the patient with brain injury remembers how to pedal a bicycle). Documentation should include delineation of declarative versus procedural memory deficits.

Executive Functions

Executive functions (higher cognitive functions) include abstract thinking, problem-solving, judgment, reasoning, and so forth. They represent advanced cognitive function and are dependent on the presence and interaction of basic cognitive functions (i.e., attention, memory, language). The patient with brain injury may demonstrate an inability to manipulate information, initiate and terminate activities, recognize errors, problem-solve, and think abstractly. Insight (the ability to understand either oneself or an external situation) and judgment (the ability to form an opinion, reach a decision, or plan an action after analyzing a problem and comparing choices) are also affected by brain injury.¹⁴ The presence of any of these deficits can significantly impact the examination of motor function, as well as learning and performance. Referral to an occupational therapist and/or neuropsychologist is indicated for comprehensive examination and evaluation (see Chapter 27, Cognitive and Perceptual Dysfunction). Recognition and understanding of these deficits can improve the validity of the motor function examination and the effectiveness of the rehabilitation POC. Collaboration and consistency of team members is paramount in order to reduce potential frustrations and inappropriate expectations.

Communication

The patient’s grasp of information and ability to communicate should be ascertained. The physical therapist should listen carefully to spontaneous speech during the initial examination sessions. The patient’s understanding of spoken language can be determined using simple tests. Word comprehension can be determined by varying the difficulty of commands, from one- to two- or three-stage commands (e.g., Point to your nose; Point to your right hand and lift your left hand). Repetition and naming can be tested (Repeat after me; name the parts of a watch). Problems with articulation (dysarthria) are evidenced by speech errors, such as difficulties with timing, vocal quality, pitch, volume, and breath control. Problems of fluency, word flow without pauses or breaks, should be noted. Speech that flows smoothly but contains errors, neologisms (nonsense words), misuse of words, and circumlocutions (word substitution) is indicative of fluent aphasia (e.g., Wernicke’s aphasia, sensory or receptive aphasia). The patient typically demonstrates deficits in auditory comprehension with well-articulated speech marked by word substitutions.

Speech that is slow and hesitant with limited vocabulary and impaired syntax is indicative of nonfluent aphasia (e.g., Broca’s aphasia). Articulation is labored and word-finding difficulties are apparent. In some settings, especially the acute hospital setting, the physical therapist may be the first to become aware of communication deficits. Referral to a speech language pathologist is indicated for comprehensive examination and evaluation (see Chapter 28, Neurogenic Disorders of Speech and Language). Recognition and understanding of these deficits can improve the validity of the motor function examination and the effectiveness of the POC. This may include simplifying instructions, using written instructions, or using alternative forms of communication such as gestures, pantomime, or communication boards. A common error is to assume that the patient understands the task at hand when he or she really has no idea what is expected. To ensure accuracy of testing, frequent checks for comprehension should be performed throughout the examination. For example, the use of message discrepancies (saying one thing and gesturing another) can be used to test the patient’s level of understanding.

Sensory Integrity and Integration

Sensory information is a critical component of motor function. It provides the necessary feedback for determination of initial position before a movement, error detection during the movement, and movement outcomes necessary to shape further learning. A closed-loop system of motor control is defined as “a control system that employs feedback, a reference of correctness, computation of error, and subsequent correction in order to maintain a desired state.”^{1, p. 462} A variety of feedback sources are used to monitor movement, including visual, vestibular, proprioceptive, and tactile inputs. The term somatosensation (or somatosensory inputs) is sometimes used to refer to sensory information received from the skin and musculoskeletal systems. The CNS analyzes all available movement information, determines error, and institutes appropriate corrective actions as necessary. Thus, a thorough sensory examination of each of these systems is an important first step in the examination of motor function. See Chapter 3, Examination of Sensory Function, for a complete discussion of this topic. The primary role of closed-loop systems in motor control appears to be the monitoring of constant states such as posture and balance, and the control of slow movements, or those requiring a high degree of precision or accuracy.

Feedback information is also essential during learning of new motor skills. Patients who have deficits in any movement-monitoring sensory system may be able to compensate with other sensory systems. For example, the patient with major proprioceptive losses can use vision as an error-correcting system to maintain a stable posture. When vision is also impaired (e.g. the patient with diabetic neuropathy and retinopathy), however, postural instability becomes readily apparent. Significant sensory losses and inadequate compensatory shifts to other sensory systems may result in severely disordered movement responses. The patient with proprioceptive losses and severe visual disturbances such as diplopia (commonly seen in the patient with MS) may be unable to maintain a stable posture. An accurate examination, therefore, requires that the therapist not only look at each individual sensory system but also at the overall sensory interaction and integration and the adequacy of compensatory adjustments. Postural tasks, balance, slow (ramp) movements, tracking tasks, or new motor tasks provide the ideal challenge in which to test feedback control mechanisms and closed-loop processes. See discussion in Chapter 6, Examination of Coordination and Balance.

An open-loop system of motor control is a “control system with preprogrammed instructions to a set of an effectors; it does not use feedback information and error-detection processes.”^{1, p. 497} Movements emerge from learned motor schema that contain “a rule, concept, or relationship formed on the basis of experience.”^{1, p. 499} Rapid and skilled movement sequences or well-learned movements can thus be completed without the benefit of sensory feedback. In reality, most movements have elements of both closed- and open-loop control processes (hybrid control system).

Tone

Tone is defined as the resistance of muscle to passive elongation or stretch. It represents a state of slight residual contraction in normally innervated, resting muscle, or steady-state contraction. Tone is influenced by a number of factors, including (1) physical inertia, (2) intrinsic mechanical-elastic stiffness of muscle and connective tissues, and (3) spinal reflex muscle contraction (tonic stretch reflexes). It excludes resistance to passive stretch from fixed soft tissue contracture. Because muscles rarely work in isolation, the term postural tone is preferred by some clinicians to describe a pattern of muscular tension that exists throughout the body and affects groups of muscles. Tonal abnormalities are categorized as hypertonia (increased above normal resting levels), hypotonia (decreased below normal resting levels), or dystonia (impaired or disordered tonicity).

Hypertonia

Spasticity

Spasticity is a motor disorder characterized by a velocity-dependent increase in muscle tone with increased resistance to stretch; the larger and quicker the stretch, the stronger the resistance of the spastic muscle. During rapid movement, initial high resistance (spastic catch) may be followed by a sudden inhibition or letting go of the limb (relaxation) in response to a stretch stimulus, termed clasp-knife response. Chronic spasticity is associated with contracture, abnormal posturing and deformity, functional limitations, and disability.

Spasticity arises from injury to descending motor pathways from the cortex (pyramidal tracts) or brain stem (medial and lateral vestibulospinal tracts, dorsal reticulospinal tract), producing disinhibition of spinal reflexes with hyperactive tonic stretch reflexes or a failure of reciprocal inhibition. The result is hyperexcitability of the alpha motor neuron pool. It occurs as part of upper motor neuron (UMN) syndrome. See Table 5.2 for a review of both the negative and positive features of UMN syndrome. Typical patterns of spasticity that influence both resting posture and movement are seen in UMN syndrome (Table 5.3). In addition, the patient with UMN syndrome will also typically present with spasms, spastic co-contraction, associated reactions, clonus, and the Babinski sign. Associated reactions are defined as involuntary movements resulting from activity occurring in other parts of the body (e.g., sneezing, yawning, squeezing the hand). Clonus is characterized by cyclical, spasmodic alternation of muscular contraction and relaxation in response to sustained stretch of a spastic muscle. Clonus is common in the plantarflexors but may also occur in other areas of the body such as the jaw or wrist. The Babinski sign is dorsiflexion of the great toe with fanning of the other toes on stimulation of the lateral sole of the foot.^16-18

Rigidity

Rigidity is a hypertonic state characterized by stiffness and resistance to movement that is independent of the velocity of movement. It is associated with lesions of the basal ganglia and is seen in Parkinson’s disease. Rigidity is the result of excessive supraspinal drive (upper motor neuron facilitation) acting on alpha motor neurons; spinal reflex mechanisms are typically normal. Leadpipe rigidity refers to a constant increase in muscular tone and stiffness of affected muscles. Cogwheel rigidity refers to the coexistence of rigidity with tremor producing stiffness and a ratchet-like jerkiness when a body part is manipulated. It is commonly seen in UE movements (e.g., wrist or elbow flexion and extension). Tremor, bradykinesia, and loss of postural stability are also associated motor deficits in patients with Parkinson’s disease.

Decorticate and Decerebrate Rigidity

Severe brain injury can result in coma with decorticate or decerebrate rigidity. Decorticate rigidity refers to sustained contraction and posturing of the upper limbs in flexion and the lower limbs in extension. The elbows, wrists, and fingers are held in flexion with shoulders adducted tightly to the sides while the lower extremities (LEs) are held in extension, internal rotation, and plantarflexion. Decerebrate rigidity (abnormal extensor response) refers to sustained contraction and posturing of the trunk and limbs in a position of full extension. The elbows are extended with shoulders adducted, forearms pronated, and wrists and fingers flexed. The LEs are held in stiff extension with plantarflexion. Decorticate rigidity is indicative of a corticospinal tract lesion at the level of the diencephalon (above the superior colliculus), whereas decerebrate rigidity indicates a corticospinal lesion in the brain stem between the superior colliculus and vestibular nucleus. Opisthotonus is characterized by strong and sustained contraction of the extensor muscles of the neck and trunk, resulting in a rigid, hyperextended posture. Extensor muscles of the proximal limbs may also be involved. These postures are considered exaggerated and severe forms of spasticity.

Dystonia

Dystonia is a prolonged involuntary movement disorder characterized by twisting or writhing repetitive movements and increased muscular tone. Dystonic posturing refers to sustained abnormal postures caused by co-contraction of muscles that may last for several minutes or hours, or may be permanent. Dystonia results from a CNS lesion commonly in the basal ganglia and can be inherited (primary idiopathic dystonia), associated with neurodegenerative disorders (Wilson’s disease, Parkinson’s disease on excessive L-dopa therapy), or metabolic disorders (amino acid or lipid disorders). Dystonia can affect only one part of the body (focal dystonia) as seen in spasmodic torticollis (wry neck) or isolated writer’s cramp. Segmental dystonia affects two or more adjacent areas (e.g., torticollis and dystonic posturing of the UE).¹⁷

Hypotonia

Hypotonia and flaccidity are terms used to define abnormally low tone or absent muscular tone. Resistance to passive movement is diminished, stretch reflexes are dampened or absent, and limbs are easily moved (floppy). Hyperextensibility of joints is common. Lower motor neuron (LMN) syndrome results from lesions that affect the anterior horn cell and peripheral nerve (e.g., peripheral neuropathy, cauda equina lesion, radiculopathy). It produces symptoms of decreased or absent tone, decreased or absent reflexes, paresis, muscle fasciculations and fibrillations with denervation, and neurogenic atrophy. Mild decreases in tone along with asthenia (weakness) can also be seen in cerebellar lesions. Acute UMN lesions (e.g., hemiplegia, tetraplegia, paraplegia) can produce temporary hypotonia, termed spinal shock or cerebral shock, depending on the location of the lesion. The duration of CNS depression and hypotonia that occurs with shock is highly variable, lasting days or weeks. It is typically followed by the development of spasticity and UMN signs.

Examination of Tone

An examination of tone consists of (1) initial observation of resting posture, (2) passive motion testing, and (3) active motion testing. Variability of tone is common. For example, spasticity can vary in presentation from morning to afternoon, day to day, or even hour to hour, depending on a number of factors, including (1) volitional effort and movement, (2) anxiety and pain, (3) position and interaction of tonic reflexes, (4) medications, (5) general health, (6) ambient temperature, and (7) state of CNS arousal or alertness. In addition, urinary bladder status (full or empty), fever and infection, and metabolic and/or electrolyte imbalance can also influence tone. The therapist should therefore consider the impact of each of these factors in determining tone. Repeat (serial) testing and a consistent approach to examination is necessary to improve the accuracy and reliability of test results.¹⁷

Initial observation of the patient can reveal abnormal posturing of the limbs or body. Careful inspection should be made regarding the position of the limbs, trunk, and head. With spasticity, posturing in fixed, antigravity positions is common; for example, a spastic UE is typically held fixed against the body with the shoulder adducted, elbow flexed, forearm supinated with wrist/fingers flexed. In the supine position, the LEs are typically held in extension, adduction with plantarflexion, and inversion (see Table 5.3).¹⁹ Limbs that appear floppy and lifeless (e.g., LE rolled out to the side in external rotation) may indicate hypotonicity. Palpation of the muscle belly may yield additional information about the resting state of muscle. Consistency, firmness, and turgor should all be examined. Hypotonic muscles will feel soft and flabby, whereas hypertonic muscles will feel taut and harder than normal.

Passive motion testing reveals information about the responsiveness of muscles to stretch. Because these responses should be examined in the absence of voluntary control, the patient is instructed to relax, letting the therapist support and move the limb. During a passive motion test, the therapist should maintain firm and constant manual contact, moving the limb in all motions. When tone is normal, the limb moves easily and the therapist is able to alter direction and speed without feeling abnormal resistance. The limb is responsive and feels light. Hypertonic limbs generally feel stiff and resistant to movement, whereas flaccid limbs feel heavy and unresponsive. Many older individuals may find it difficult to relax during passive movements (termed paratonia); their stiffness should not be mistaken for hypertonicity. Varying the speed of movement is an important determinant of spasticity. In a spastic limb, resistance may be near normal when the limb is moved at a slow velocity. Faster movements intensify the resistance to passive motion. It is also important to remember that muscle stiffness with spasticity will offer the greatest resistance during the first stretch and that with each successive stretch resistance can be reduced by as much as 20% to 60%.¹⁷ In the patient with rigidity, resistance is constant and not responsive to increasing the velocity of passive motion.

Clonus, spasmodic alteration of antagonistic muscle contractions, is examined using a quick stretch stimulus that is then maintained. For example, ankle clonus is tested by sudden dorsiflexion of the foot and maintaining the foot in dorsiflexion. Clasp-knife phenomenon, increased muscle resistance to passive movement followed by a sudden release of the muscle, is examined by passive motion testing. All limbs and body segments are examined, with particular attention given to those identified as problematic in the initial observation. Comparisons should be made between upper and lower limbs and right and left extremities. Asymmetrical tonal abnormalities are typically indicative of neurological dysfunction.

Modified Ashworth Scale

The Modified Ashworth Scale (MAS) is the gold standard used to assess muscle spasticity in patients with lesions of the CNS and is commonly used in many rehabilitation facilities (Table 5.4). The original Ashworth Scale (AS), a 5-point ordinal scale, was developed as a simple clinical tool to test the efficacy of an antispastic drug in patients with MS.²⁰ Bohannon and Smith²¹ modified the instrument scale by adding an additional 1+ grade to increase the sensitivity of the instrument, making it a 6-point scale. In both versions, the examiner uses passive motion to assess resistance to passive motion due to spasticity. There is a lack of operational definitions as to how fast to move the limb. Thus the MAS measures muscle tone at one, unspecified velocity, which can result in variation in overall reliability. For example, the MAS has been shown to have moderate to good intrarater reliability but only poor to moderate interrater reliability. Reliability has also been shown to vary with the muscles being tested.²² Limitations with use of the scale include (1) inability to detect small changes, (2) inability to distinguish between soft tissue viscoelastic and neural changes, and (3) problems with psychometric properties (unequal distances of scores). The lower MAS ratings of 1, 1+, and 2 are most problematic. Training is suggested to improve interrater reliability between examiners.^23-29

Tardieu/Modified Tardieu Scale

The Tardieu Scale for assessing spasticity is a performance-based test of the quality of muscle tone during three different velocities: slow-velocity stretch (V1, as slow as possible), the speed of the limb falling under gravity (V2), and fast-velocity stretch (V3, moving as fast as possible).^30,31 The quality of muscle reaction is measured using an ordinal scale (0–5), where 0 is no spasticity, 4 is severe spasticity, and 5 is joint immobility. The Modified Tardieu Scale uses an additional measurement of joint angles. One goniometric measurement (R1) is taken at the onset of resistance (catch or clonus) to quick stretch (V3). The second measurement (R2) is taken at the full PROM, taken at very slow speed (V1). The difference between the two measures, R2–R1, represents the velocity-dependent tone component of the muscle. Intrarater reliability is adequate to excellent and varies with muscles tested and training.^32,33 For example, in patients with severe brain injury, reliability ranged from 0.64 to 0.87.³³ Interrater reliabilities are lower and also vary with training.^34-36

Documentation of Tone Abnormalities

Documentation of tone abnormalities should include a determination of the specific body segments demonstrating abnormal tone, the type of abnormality present (e.g., spasticity, rigidity), whether the changes are symmetrical or asymmetrical, resting postures and associated signs (e.g., UMN syndrome), and factors that modify (increase or diminish) tone. It is important to remember that measurement of tone in one position does not mean that tone will be the same in other positions or during functional activities. A change in position such as sitting up or standing up can substantially alter the requirements for postural tone. Of great importance is a description of the effects of tone on active movements, posture, and function.

Reflex Integrity

Deep Tendon Reflexes

A reflex is an involuntary, predictable, and specific response to a stimulus that is dependent on an intact reflex arc (sensory receptor, afferent neurons, efferent neurons, and responding muscles or gland). The deep tendon reflex (DTR) results from stimulation of the stretch-sensitive IA afferents of the neuromuscular spindle, producing muscle contraction via a monosynaptic pathway. DTRs are tested by tapping sharply over the muscle tendon with a standard reflex hammer or with the tips of the therapist’s fingers. To ensure adequate response, the muscle is positioned in midrange and the patient is instructed to relax. Stimulation can result in observable movement of the joint (brisk or strong responses). Weak responses may be evident only with palpation (slight or sluggish responses with little or no joint movement). The quality and magnitude of responses should be carefully documented. Reflexes are graded on a 0 to 5+ scale:

Table 5.5 presents an overview of the examination of DTRs.

If DTRs are difficult to elicit, responses can be enhanced by specific reinforcement maneuvers. In the Jendrassik maneuver, the patient hooks the fingers of both hands together and strongly pulls them apart. While this pressure is maintained, LE reflexes are tested. Maneuvers that can be used to reinforce responses in the upper extremities (UEs) include squeezing the knees together, clenching the teeth, or making a fist with the contralateral extremity. The use of any reinforcing maneuvers to elicit responses in patients with hyporeflexia should be carefully documented.

DTRs are increased in UMN syndrome (e.g., stroke) and decreased in LMN syndrome (e.g., peripheral neuropathy, nerve root compression), cerebellar syndrome, and muscle disease. Reflex spread (the extension of the response beyond the muscle normally expected to contract) is indicative of UMN syndrome. Because each DTR arises from specific spinal segments, an absent reflex can be used to identify the level of a spinal lesion (e.g., radiculopathy).

Superficial Cutaneous Reflexes

Superficial cutaneous reflexes are elicited with a light stroke applied to the skin. The expected response is brief contraction of muscles innervated by the same spinal segments receiving the afferent inputs from the cutaneous receptors. A stimulus that is strong may produce irradiation of cutaneous signals with activation of protective withdrawal reflexes. Cutaneous reflexes include the plantar reflex, confirming toe signs (Chaddock), and abdominal reflexes. The plantar reflex (S1, S2) is tested by applying a stroking stimulus on the sole of the foot along the lateral border and up across the ball of the foot. A normal response consists of flexion of the big toe; sometimes the other toes will demonstrate a downgoing (flexion) response or no response at all. An abnormal response (positive Babinski sign) consists of extension (up-going) of the big toe, with fanning of the lateral four toes. It is indicative of a corticospinal (UMN) lesion. The Chaddock’s sign is elicited by stroking around the lateral ankle and up the lateral dorsal aspect of the foot. It also produces extension of the big toe and is considered a confirmatory toe sign. The abdominal reflex is elicited with brisk, light strokes over the skin of the abdominal muscles. A localized contraction under the stimulus is produced, with a resultant deviation of the umbilicus toward the area stimulated. Each of the four quadrants should be tested in a diagonal direction. Umbilical deviation in a superior/lateral direction indicates integrity of spinal segments T8 to T9. Umbilical deviation in an inferior/lateral direction indicates integrity of spinal segments T10 to T12. Loss of response is abnormal and indicative of pathology (e.g., thoracic spinal cord injury). Asymmetry from side to side is highly significant with respect to neurological disease. Abdominal reflexes may be absent in patients with obesity or abdominal surgeries. Table 5.6 presents an overview of the examination of superficial cutaneous reflexes.

Primitive and Tonic Reflexes

Primitive and tonic reflexes are present during infancy as a stage in normal development and become integrated by the CNS at an early age. Once integrated, these reflexes are not generally recognizable in adults in their pure form. They may continue, however, as adaptive fragments of behavior, underlying normal motor control. Persistent reflexes (sometimes termed obligatory reflexes) beyond the expected age of development or appearing in adult patients following brain injury are always indicative of neurological involvement. Patients who exhibit these reflexes typically present with extensive brain damage (e.g., stroke, TBI) and other UMN signs.

Reflexes important to examine in the patient suspected of abnormal reflex activity include flexor withdrawal, traction, grasp, tonic neck, tonic labyrinthine, positive support, and associated reactions. Flexor withdrawal reflex is generally the simplest to observe and is judged by appearance of an overt movement response. Tonic neck reflexes, on the other hand, bias the musculature and may not be visible through overt movement responses. In fact, movement is rarely produced but rather posture is typically influenced through tonal adjustments. Thus, the term tuning reflexes is an appropriate description of their function. Abnormal postures should be examined for their reflex dependence (e.g., the patient with brain injury exhibits excessive extensor tone in supine but not in side-lying). To obtain an accurate examination, the therapist must be concerned with several factors. The patient must be positioned appropriately to allow for the expected response. An adequate test stimulus is essential, including both an adequate magnitude and duration of stimulation. Keen observation skills are needed to detect what may be subtle movement changes and abnormal responses. Palpation skills can assist in identifying tonal changes not readily apparent to the eye. Primitive and tonic reflexes are graded using a 0 to 4+ scale³⁷:

Table 5.7 presents an overview of the examination of primitive and tonic reflexes.

Documentation of Reflex Integrity

Documentation of reflex abnormalities should include a determination of (1) specific reflexes tested; (2) findings, including degree of abnormality found (specific deficits); (3) associated signs (e.g., UMN syndrome); and (4) factors that influence or modify reflexes. Of great importance is a description of the effects of abnormal reflex behavior on active movements, posture, and function.

Cranial Nerve Integrity

There are 12 pairs of cranial nerves (CNs), all distributed to the head and neck with the exception of CN X (vagus), which is distributed to the thorax and abdomen. CNs I, II, and VIII are purely sensory and carry the special senses of smell, vision, hearing, and equilibrium. Cranial nerves III, IV, and VI are purely motor and control pupillary constriction and eye movements. Cranial nerves XI and XII are also purely motor, innervating the sternocleidomastoid, trapezius, and tongue muscles. Cranial nerves V, VII, IX, and X are mixed, containing both motor and sensory fibers. Motor functions include chewing (V), facial expression (VII), swallowing (IX, X), and vocal sounds (X). Sensations are carried from the face and head (V, VII, IX), alimentary tract, heart, vessels, lungs (IX, X), and tongue, mouth, and palate (VII, IX, X). Parasympathetic secretomotor fibers (ANS) are carried by CN III for control of smooth muscles in the eyeball, VII for control of salivary and lacrimal glands, IX to the parotid salivary gland, and X to the heart, lungs, and most of the digestive system.

An examination of CN function should be performed with suspected lesions of the brain, brain stem, and cervical spine. Deficits in olfactory function (CN I) should be suspected with lesions of the nasal cavity and anterior/inferior cerebrum. Lesions of the optic pathways (optic nerve [CN II], optic chiasma, optic tract, lateral geniculate body, superior colliculus) and visual cortex may produce visual deficits. Midbrain (mesencephalic) lesions may result in deficits of CNs III and IV (oculomotor, trochlear). Pontine lesions may involve several CNs, including V (ophthalmic, maxillary, and mandibular branches) and VI (abducens). Nuclei of CNs VII (facial) and VIII (vestibular and cochlear branches) are located at the junction of the pons and medulla. Lesions affecting the medulla may involve CNs IX (glossopharyngeal), X (vagus), XI (spinal accessory), and XII (hypoglossal). The spinal root of XI is found in the upper five cervical segments. The CNs, their function, clinical tests, and possible abnormal findings are presented in Table 5.8.

Documentation of Cranial Nerve Integrity

Documentation of an examination of CN integrity should include a determination of (1) specific cranial nerves tested; (2) findings, including the degree of abnormality observed (specific deficits); and (3) the effects of abnormal cranial nerve integrity on function. The patient’s perceptions of loss of function should also be identified.

Musculoskeletal Integrity

Examination of the musculoskeletal system is essential and should occur early in the examination of motor function. Important elements include joint integrity and mobility, as well as muscle performance, including strength, power, endurance, and length. See discussion in Chapter 6, Musculoskeletal Examination.

Postural Alignment, Joint Integrity, and Mobility

Joint limitations restrict the normal coordinated action of muscles and alter the biomechanical alignment of body segments and posture. Long-standing immobilization results in contracture (a fixed resistance resulting from fibrosis of tissues surrounding a joint) and restricted movement. The resultant compensatory movement patterns are frequently dysfunctional, producing additional stresses and strains on the musculoskeletal system. They are also more energy costly and can significantly limit motor and functional performance. For example, shortening of the gastrocnemius muscles results in a toe-walking gait pattern; tightness of the hip adductors results in a scissoring gait pattern. Changes in alignment secondary to muscle tightness alter postural control. For example, in standing, anterior pelvic tilting and flexion of the hips and knees are typically the result of hip flexor tightness. In sitting, posterior pelvic tilting is associated with kyphosis and forward head position and is typically the result of hamstring tightness. Abnormalities in alignment that alter the center of mass (COM) within the base of support (BOS) place increased demands on the postural control system. For example, the patient with chronic stroke will demonstrate altered postural alignment in standing with more weight distributed over the less affected limb and away from the more affected limb. This patient also typically demonstrates a more forward leaning posture with greater anterior pelvic tilt, resulting in limitations in balance and postural control.³⁸

Muscle Atrophy

Atrophy, the loss of muscle bulk (wasting), occurs when functional mobility is lost (disuse atrophy) and from LMN disease (neurogenic atrophy) or protein–calorie malnutrition. Disuse atrophy is evident after periods of inactivity, developing in weeks or months. It is generally widespread and affects antigravity muscles to a greater extent. Strength can be negatively influenced by disuse atrophy. The lack of resistive load on muscle reduces the overall number of sarcomeres and results in diminished capacity of muscle for developing torque (contractile strength). It also results in reduced passive tension of muscle with loss of joint stability and increased risk for postural abnormality.³⁹ Neurogenic atrophy accompanies LMN injury (e.g., peripheral nerve injury, spinal root injury) and occurs rapidly, generally within 2 to 3 weeks. Atrophy is also accompanied by other signs of LMN injury (e.g., decreased or absent tone, decreased or absent DTRs, fasciculations, weak or absent voluntary movements). Distribution is limited to a segmental or focal pattern (nerve root).

Examination of Muscle Atrophy

During the examination of muscle atrophy, the therapist should visually inspect the muscle symmetry and shapes, comparing and contrasting their size and contour. Muscles that look flat or concave are indicative of atrophy. Comparisons should be made between and within limbs. Is the atrophy unilateral or bilateral? Are multiple limbs involved? Is the atrophy more proximal, or distal, or both? Limb girth measurements can be used to compare a limb undergoing neurogenic atrophy with the corresponding normal limb. Palpation at rest and during muscle contraction is used to determine muscle tension. Girth measurements or volumetric displacement measures (e.g., hands or feet) can be used to confirm visual inspection findings.

Strength and Power

Muscle performance is the capacity of muscle(s) to generate forces while muscle strength is the force exerted by muscle(s) to overcome a resistance.⁶ Isotonic contractions involve active shortening of muscles, and eccentric contractions involve active lengthening of muscles. Isometric contractions produce high levels of tension for holding contractions without overt movement. Muscle power is defined as the work produced per unit of time or the product of strength and speed.⁶ Muscle performance depends on a number of interrelated factors, including length–tension characteristics, viscoelasticity, velocity, and metabolic adequacy (i.e., fuel storage and delivery). Of equal importance are the integrated actions of the CNS (neuromuscular control factors) acting on motor units, including (1) the number of motor units recruited, (2) the type of motor units recruited, and (3) the discharge rate and continuing modulation of motor units. The CNS controls the recruitment order and timing of muscles. Synergistic movements and postural adjustments are also dependent on the integrity of the peripheral nerves and on the muscle fibers.

Patients with impairments in motor function and neurological injury pose unique challenges for the examination of muscle performance. Weakness is the inability to generate sufficient levels of force and can vary from paresis (partial weakness) to plegia (absence of muscle strength). Weakness is seen in patients with UMN syndrome, along with other UMN signs (e.g., spasticity, hyperreflexia). Patients may present with hemiplegia (one-sided paralysis), paraplegia (LE paralysis), or tetraplegia (quadriplegia). Weakness also appears in patients with LMN lesions.

Patients with stroke demonstrate significant changes in muscle performance, including altered recruitment patterns, abnormal times to achieve force, and decreased motor unit firing rates.⁴⁰ They also demonstrate up to a 50% decrease in motor units of affected extremities within 2 months after insult with greater losses of Type II (fast twitch) fibers.⁴¹ Muscle performance in patients with stroke is influenced by the presence of other UMN impairments, including spasticity, disordered synergistic activity/mass patterns of movements, abnormal muscle co-contraction, and/or profound sensory deficit.^42-44 Strength losses are typically greater in the distal extremity than the proximal. Strength losses have also been found on the “supposedly normal” extremities.^45,46 The bilateral effects of an ipsilateral cortical lesion is evidence of the small percentage (estimated 10%) of corticospinal tract fibers that remain uncrossed. Possible other unidentified factors may also exist. This information has prompted use of terms such as less involved or less affected in place of more traditional terms such as unaffected, uninvolved, sound, normal, or good side. This also casts doubt as to the validity of using the contralateral uninvolved side as a reference for normal muscle strength in patients with hemiplegia.

In patients with peripheral sensorimotor neuropathy (e.g., chronic diabetic neuropathy) or acute motor neuropathy (e.g., Guillain-Barré), strength losses are typically greater in distal segments (i.e., foot and ankle) than proximal with involvement of more proximal segments as the disease progresses. In neuropathy, the progression is slow (months or years), whereas in Guillain-Barré the progression is rapid (days or weeks) and more complete, involving not just the proximal LEs but also the trunk, UEs, and in some cases the lower CN nerves. Patients with primary muscle disease (e.g., myopathies) typically experience proximal weakness, whereas patients with myasthenia gravis experience decremental strength losses. Thus, the first contraction of a muscle may start out strong and then each succeeding contraction gets weaker and weaker.

Examination of Muscle Strength and Power

The clinical examination of muscle strength and power utilizes standardized methods and protocols (e.g., manual muscle testing [MMT], handheld dynamometers, instrumented isokinetic systems). See Chapter 4, Musculoskeletal Examination, for a thorough discussion of this topic. Analysis of muscle timing, including amplitude, duration, waveform, and frequency can be obtained using EMG (see later section in this chapter on EMG examination). Activity analysis of functional performance also yields important data about muscle performance.

Strength testing measures (MMT) were originally developed to examine motor function in patients with polio (an LMN disease). There are validity issues when used in the clinical examination of patients with UMN lesions.^47,48 Strength testing using standardized protocols may be inappropriate for some patients with UMN syndrome. Appropriate criteria are therefore critical in determining whether the standards of validity and reliability of MMT are met. First and foremost, the therapist must consider the patient’s movement capabilities. Individual isolated joint movements, mandated by standardized MMT procedures and isokinetic protocols, may not be possible in the presence of UMN lesion where stereotypical abnormal movement patterns (obligatory synergies) are present. The presence of abnormal co-activation, spasticity, and abnormal posturing may preclude the patient’s ability to perform isolated joint movements. These barriers to normal movement are termed active restraint. The prescribed test positions may also be precluded by the presence of abnormal reflex activity (e.g., supine testing influenced by presence of the tonic labyrinthine reflex). Muscle and soft tissue changes in viscoelasticity (e.g., contracture) offer a form of passive restraint and may also preclude the use of standardized testing. In these instances, the decision should be made not to use standardized MMT procedures. An estimation of strength can be made from observations of active movements during performance of functional activities. For example, shallow knee bends or sit-to-stand transfers can be used to examine the strength of hip extensors and knee extensors. Standing heel-rises or toe-rises can be used to examine the strength of foot–ankle muscles (dorsiflexors, plantarflexors). Documentation should clearly indicate that UMN involvement precluded use of standardized MMT procedures. Estimates of strength can be made based on observations during active functional movements. Inability to move or support the body against gravity should receive a poor grade. The ability to move the body against gravity should receive a fair grade, while the ability to move the body against gravity and resistance should receive a good grade. When using functional tasks, it is important to remember that muscle performance is graded using the synergistic actions of muscles acting together and not the isolated actions of individual muscles as required in the MMT.

If MMT is used, therapists should utilize standardized positions whenever possible. If a modified position is required (e.g., the patient lacks full range of motion [ROM] or adequate stabilization), it should be carefully documented. Substitutions (muscle actions that compensate for specific muscle weakness) should be identified, eliminated whenever possible, and carefully documented. For example, the patient with SCI typically presents with common muscle substitutions (e.g., wrist extensors are used to close the fingers using tenodesis grasp). Knowledge of common substitutions is very helpful when working with this patient group.

Isokinetic testing is an important part of a comprehensive examination of patients with disorders of motor function. It allows the therapist to monitor many important parameters of motor function, including a muscle’s ability to generate force throughout the range, peak torques, and ability to generate torques at changing velocities (velocity-spectrum testing). Rate of tension development (time to peak torque) and shape of the torque curve can also be determined. Concentric, isometric, and eccentric contractions and reciprocal agonist/antagonist relationships can be analyzed. Testing results yield important information for understanding functional performance.^49-52 Validity and reliability of isokinetic testing is well established.^53-57

Patients with stroke typically demonstrate a variety of deficits when tested with an isokinetic dynamometer, including (1) decreased torque overall in the more affected limb when compared to the less affected limb; (2) decreased torque with increasing movement speeds; (3) decreased limb excursion; (4) extended times to peak torque development and the duration time peak torque is held; and (5) increased time intervals between reciprocal contractions. For example, many patients with stroke are unable to develop tension above 70° to 80° per second. When this value is compared to the speed needed for normal walking (100° per second), reasons for gait difficulties become readily apparent. Normative data, when available, can provide an appropriate reference for evaluating and interpreting patient data.^59,60

Documentation of Strength and Power

Documentation of strength and power changes should include a determination of the specific muscles and body segments tested and tests used; the type and degree of changes present (e.g., paresis, paralysis); whether the changes are symmetrical or asymmetrical, distal or proximal; presence of associated signs (e.g., UMN or LMN); presence of atrophy; and factors that modify muscle performance. A description of the effects of muscle weakness on active movements, posture, and function should be included. When examining functional performance, it is important to remember that strength estimates taken in one position do not necessarily generalize to other positions (e.g., ability to move while supporting full body weight in upright standing).

Muscle Endurance and Fatigue

Muscle endurance allows the muscle to sustain forces or to generate forces repeatedly over time.⁶ An examination of muscle endurance is important in determining functional capacity. Fatigue is an overwhelming sustained sense of exhaustion and decreased capacity for physical and mental work at the usual level. Fatigue can be the result of excessive activity caused by an accumulation of metabolic waste products (e.g., lactic acid); malnutrition (i.e., deficiency of nutrients); cardiorespiratory disturbances (i.e., inadequate oxygen and nutrients to the tissues); emotional stress; and other factors. Although fatigue is protective and serves a useful function in guarding against overwork and injury, it is a serious problem for some individuals. For example, patients with postpolio syndrome or chronic fatigue syndrome may experience significant restrictions in their functional activities and work as a result of debilitating fatigue. Other groups of individuals who may also experience significant limitations as a result of fatigue include those with MS, Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Duchenne muscular dystrophy, and Guillain-Barré syndrome. Additional factors that can influence fatigue include health status, environmental context (e.g., stressful environment), and temperature (e.g., heat stress in the patient with MS).⁶¹

Exhaustion is defined as the limit of endurance, beyond which no further performance is possible. Most patients can report with great accuracy the point at which exhaustion is reached. Of concern with some patients is overwork weakness (injury), defined as “a prolonged decrease in absolute strength and endurance due to excessive activity of partially denervated muscle.”^{62, p. 22} For example, patients with postpolio syndrome may experience weakness following strenuous activity that is not recovered with ordinary rest. They report having to spend the entire next day or two in bed following an exhaustive exercise session. It is therefore important to document the type, length, and effectiveness of rest attempts. Delayed onset muscle soreness is prolonged in patients with overwork weakness, peaking between 1 and 5 days after activity.

Examination of Fatigue

An examination of fatigue begins with the initial interview. The patient is asked to identify those activities that are fatiguing, the frequency and severity of fatigue episodes, and the circumstances surrounding the onset of fatigue. It is important to identify the fatigue threshold, which is that level of exercise that cannot be sustained.⁶³ In most cases, the onset of fatigue is gradual, not abrupt, and dependent on the intensity and duration of the activity attempted. Precipitating activities should be identified within the context of habitual daily activity. The patient is asked to identify any solutions used to overcome debilitating fatigue and how successful they are.

Self-assessment questionnaires are particularly useful for the patient with significant fatigue. The Modified Fatigue Impact Scale (MFIS) is an instrument initially developed to assess quality-of-life problems related to fatigue in patients with MS. The scale has 21 items that focus on three areas of function. It uses a 5-point Likert scale, with 0 = Never to 4 = Almost always. The total score is 0 to 84, with subscales for physical (0–36), cognitive (0–40), and psychosocial (0–8) functioning.^64,65 It has excellent test-retest reliability (ICC = 0.85) when used with patients with MS.⁶⁶ The Fatigue Severity Scale is a 9-item questionnaire with questions that focus on the severity of fatigue and how it interferes with activity levels and lifestyle. The items are scored on a 7-point scale, with 1 = strongly disagree and 7= strongly agree. It has been used with multiple populations, including those with MS, PD, and post-polio syndrome, and has been shown to be a good screening tool in PD.^67-71

The examination can then proceed with specific performance-based testing. As this is likely to be fatiguing to the patient, performance testing should focus on those key functional activities important to the patient’s daily life that were identified in the earlier interview or questionnaire. The therapist should carefully document the patient’s reported level of fatigue during performance testing. The level of independence, modified independence (device required), or level of assistance required (minimal, moderate, or maximal) should also be documented. The grading criteria for the Functional Independence Measure (FIM) provides a useful scoring key, and the functional activities tested (e.g., transfers, locomotion) are basic to independent living.⁷² During performance testing, perceived level of fatigue can also be documented using the Borg Scale for Rating of Perceived Exertion.⁷³ In order to better determine the level of muscle fatigue, the therapist should ask the patient to identify two separate scores, one for the level of muscular fatigue and one for the level of central fatigue (breathlessness). Timed performance on functional tasks (e.g., timed self-care tasks, time to walk, 6-minute walk test) also provides objective and reproducible measures of levels of muscle fatigue.

Documentation

Documentation of muscle endurance and fatigue should include a determination of (1) activities that result in debilitating fatigue, including onset, duration, and recovery; (2) level of assistance or assistive devices required; (3) the time on task; (4) the frequency and effectiveness of rest attempts; (5) any compensatory strategies adopted and their effectiveness; and (6) perceived impact on quality of life. Results of specific questionnaires and tests are documented. Social and environmental stressors should also be described along with the patient’s emotional/psychological responses (e.g., degree of depression or anxiety).

Voluntary Movements

Synergies are functionally linked muscles that are constrained by the CNS to act cooperatively to produce an intended motor action. They are used to simplify control, reduce or constrain the degrees of freedom, and initiate coordinated patterns of movement. Degrees of freedom refers to the number of separate independent dimensions of movement that must be controlled by engaging these cooperative units of muscle action.¹ Synergistic movements are defined by precise spatial and temporal organization that requires a high degree of coordination involving control of speed, distance, direction, rhythm, and levels of muscle tension. In individuals with normal motor control, voluntary movement patterns are functional, task specific, and highly variable, depending on the task purpose and environment. The CNS controls patterns of (1) single-limb and multiple-limb movements, (2) bilateral (bimanual) symmetrical and asymmetrical movements, (3) reciprocal movements, and (4) patterns of proximal stabilization and postural support. Movements are also appropriately timed with events in the environment (coincident timing).

Abnormal Patterns of Movement

Organization of movement is typically disturbed with pathology of the CNS. Lesions of the cerebellum produce significant deficits in coordination (i.e., dyssynergia, dysmetria, dysdiadochokinesia, tremor, dysarthria, gait ataxia), tone (i.e., hypotonia), and strength (i.e., asthenia). Lesions of the basal ganglia produce significant deficits in tone and movement (i.e., rigidity, tremor, akinesia, bradykinesia, dystonia, chorea, hemiballismus). See Chapter 6, Examination of Coordination and Balance, for a complete discussion.

Lesions of the corticospinal tracts (e.g., stroke, TBI) can produce atypical movement patterns or abnormal obligatory synergies, defined as movements that are primitive and highly stereotyped. Voluntary movements are limited with loss of ability to adapt movements to changing demands. Selective movement control (isolated joint movements) is severely disordered or disappears completely. Patients with stroke typically demonstrate obligatory flexion and extension synergies (see Chapter 15, Stroke). Abnormal synergies are highly predictable and characteristic of the middle stages of recovery from stroke.^74,75

The examination of obligatory synergistic patterns is both qualitative and quantitative. The therapist observes whether voluntary movement can be initiated, whether it can be completed, and how the movement is carried out. If movement is stereotypic and obligatory, what muscle groups are linked together? How strong are the linkages between muscle groups? Are there linkages between upper and lower limbs or one side to another (associated reactions)? Are the movements influenced by other components of UMN syndrome, such as primitive reflexes, spasticity, paresis, or position? For example, does elbow, wrist, and finger flexion always occur when shoulder flexion is initiated? Is head turning used to initiate or reinforce UE flexion (asymmetric tonic neck reflex [ATNR])? Therapists also need to identify when these patterns occur, under what circumstances, and what variations are possible. In patients with brain lesions, lessening of abnormal synergy dominance and emergence of selective movement control are evidence of recovery. Disability-specific measures such as the Fugl-Meyer Post-Stroke Assessment of Physical Performance have been developed to provide an objective and quantifiable measure of obligatory synergies and recovery after stroke⁷⁶ (see Chapter 15, Stroke). Many of the available standardized tests and measures to assess abnormal movement patterns and control are discussed in later chapters. For example, tests and measures used to assess voluntary movement control include Motor Assessment Scale,⁷⁷ Rivermead Mobility Index,⁷⁸ Wolf Motor Function Test,⁷⁹ Motor Activity Log,⁸⁰ Arm Motor Ability Test.⁸¹

Abnormal Postural Patterns

Postural patterns and control of the trunk are also typically disturbed in patients with brain lesions. Primary impairments seen in patients with stroke or TBI (i.e., changes in strength, tone, muscle activation and timing, and sensation) all contribute to disordered postural control. The therapist needs to closely examine the patient’s postural patterns and movement control during changes in position that require greater and greater levels of control. For example, the patient is asked to move from supine to side-lying to sitting and finally to standing. Disordered postural control and loss of balance typically becomes evident as the patient moves into the higher postures characterized by a reduced base of support (BOS) and higher center of gravity (COG) (e.g., moving from sitting to standing). Examples of the standardized tests and measures used to assess postural control include the Trunk Control Test,⁸² Trunk Impairment Scale,⁸³ Function in Sitting Test,⁸⁴ and the Postural Assessment Scale for Stroke Patients.⁸⁵

Documentation

Documentation of abnormal movements should include a determination of (1) what abnormal movements are present and where; (2) what is the nature of the abnormal movement pattern (e.g., obligatory synergies); (3) what are the elements or components; (4) what influences the abnormal movements (e.g., spasticity and hyperreflexia coexist with obligatory synergies); (5) what variations or adaptive movements are possible, if any; and (6) what is the effect of abnormal movements on function.

Table 5.9 presents a summary of the differential diagnosis summary comparing UMN and LMN syndromes. Table 5.10 compares the major types of CNS disorders by location of lesion/motor control disorders.

Task analysis is the process of breaking a specific activity down into its component parts to understand and evaluate the demands of the task and the underlying characteristics of the performance demonstrated. Task organization refers to how the components of the task are interdependent. Tasks can demonstrate low organization in which the task components are relatively independent (e.g., dressing). High organization refers to task components that are highly interrelated (e.g., walking). The process begins with an understanding of normal movements and normal kinesiology associated with the task. The therapist examines and evaluates the patient’s performance and analyzes the differences compared to “typical” or expected performance. Critical skills in this process include accurate observation and recognition of barriers or obstacles to moving in the correct pattern. Interpretations are made about the nature of the motor performance and the possible links between documented impairments and performance difficulties. For example, the patient who is unable to transfer from bed to wheelchair may lack postural trunk support (stability), adequate LE extensor control (strength), and ability to maintain control while moving from one surface to the other (dynamic control). Or the patient with acute stroke sits up from supine using the less affected UE for support and propulsion. The more affected extremities lag behind, not well integrated into the movement pattern. The final sitting position is asymmetrical with most of the weight borne on the less affected side and the more affected UE held in an abnormally flexed and adducted position. A determination of how the environment affects performance must also be made. For example, the patient with TBI is highly distractible with poor attention in the busy clinic environment, resulting in an inability to complete a transfer task. It is important to document these qualitative findings, as they provide valuable information necessary for developing an effective POC to improve motor function. The term activity demands refers to the requirements imbedded in each step of the activity. The term environmental demands (constraints) refers to the physical characteristics of the environment or features required for successful performance of movement (regulatory conditions). Questions posed in Box 5.2 can be used as a guide for movement/task analysis.

Functional Tasks

Tasks are commonly grouped into functional categories. Activities of daily living (ADL) refer to those daily living skills necessary for an adult to manage life. Basic ADL (BADL) include grooming skills (e.g., oral hygiene, showering or bathing, dressing), toilet hygiene, feeding, and personal device care. Instrumental ADL (IADL) include money management, functional communication and socialization, functional and community mobility, and health maintenance. Functional mobility skills (FMS) refer to those skills involved in bed mobility transfers, walking, and stair climbing.^86-90 See Chapter 8, Examination of Function, for a complete discussion.

Motor Skills

Motor skills can be categorized by different classification schemes.⁹¹ One widely used classification scheme in physical therapy categorizes tasks by either mobility or stability functions. Mobility tasks require the individual to move the body from one posture to another in a controlled manner. Both the base of support (BOS) and center of mass (COM) are moving. Stability (static postural control) tasks require the individual to maintain posture in a stable, unchanging position with the COM over the BOS. Stability can be further divided into static versus dynamic postural control. During dynamic postural control, stability is adjusted and maintained while parts of the body (UE or LE) are moving. See Table 5.11 for characteristics, examples of movement tasks, and potential impairments.

During the examination of tasks requiring mobility, key elements the therapist should observe and document include:

• The ability to initiate movements.

• Strategies utilized and overall control of movement.

• The ability to terminate movement.

• The level and type of assistance required (e.g., manual cues, verbal cues, guided movements).

• Environmental constraints that may influence performance.

During examination of tasks requiring static postural control, key elements the therapist should observe and document include:

• The position and stability of the BOS.

• The position and stability of the COM within the BOS.

• The length of time the posture can be maintained.

• Postural steadiness (degree of postural sway and direction of instability).

• The number of episodes and direction of loss of balance (LOB) and fall safety risk.

• The degree of added stabilization required from UEs or LEs (e.g., handhold, hooked legs).

• The level and type of assistance required (manual, verbal).

• Environmental constraints that may influence performance.

During examination of tasks requiring dynamic postural control, key elements the therapist should observe and document include:

• The ability of the patient to modify the BOS to accommodate changing COM during extremity movements.

• The degree of postural stability maintained by the weight-bearing segments using above stability criteria.

• The range and degree of control of extremity movements.

• Environmental constraints that may influence performance.

Documentation

During an analysis of motor skills, key elements the therapist should observe and document include (1) the type of skill being demonstrated; (2) the ability to organize and control movements; (3) the overall quality, efficiency, and economy of movement; (4) the success in attaining the action-goal (outcome); (5) the ability to easily and successfully adapt to changing task demands; (6) the ability to easily and successfully adapt to changing environmental demands; and (7) verbal cues and assistance, if any, required.

The qualitative analysis of motor skills can be enhanced by filming patient performance. Patient responses are recorded, providing a permanent record of motor performance that allows the therapist the opportunity to compare responses over time. Recordings made at 3 or 6 weeks of recovery can be compared easily without reliance on the therapist’s memory or written notes. Accuracy of observations can be improved. A therapist who is closely involved in assisting or guarding during performance may not be attentive enough to observe all movement parameters (e.g., when assisting the patient with TBI with severe ataxia). Films can be viewed on a computer repeatedly at different speeds to determine control during different tasks and at different body segments. Two visuals can also be viewed side by side (simultaneously) for comparison. For example, a patient’s performance in a task such as sitting up from supine can be observed first at regular speeds, then at slow-motion speeds. Stop-action or freezing a frame can be used to isolate a problematic point in the movement sequence. This may be helpful, particularly for the inexperienced therapist, in improving both the quality and reliability of observations. Repeat trials on a functional performance test may needlessly tire the patient while yielding a decrease in performance. Sequential recordings over the course of rehabilitation provide visual documentation of patient progress and can be an important motivational and educational tool in therapy for use with the patient and family.

Reliability of recordings for intersession comparisons can be improved by the following measures. Placement of equipment should be planned in advance to achieve the best location and should be consistently placed over subsequent sessions. Use of a tripod can improve the stability of the recording. Using the voice-over function, verbal descriptions of the performance during each trial can be added to the visuals and can be documented in a written summary.⁹² Examples of recorded case studies accompanying this text can be viewed online at http://davisplus.fadavis.com.

Motor learning is a complex process that requires spatial, temporal, and hierarchical organization within the CNS, leading to relatively permanent changes in the capability for motor skill.¹ As mentioned earlier, changes in the CNS are not directly observable, but rather are inferred from improvement in performance as a result of practice or experience. Individual differences in learning are expected and influence both the rate and degree of learning possible. Motor learning abilities among individuals vary across three main foundational categories of abilities: cognitive abilities, perceptual speed ability, and psychomotor ability.⁹³ Differences occur as a result of both genetics and experience. The therapist should be sensitive to such factors as alertness, anxiety, memory, speed of processing information, speed and accuracy of movements, and uniqueness of the setting. In addition, recovering patients may vary in their learning potential according to the pathology present, the number and type of impairments, recovery potential and general health status, and comorbidities. Although most skills can be learned through practice or experience, the therapist should be sensitive to the patient’s underlying capabilities (abilities) that support certain skills. For example, some patients with SCI may not be able to learn to manage curbs using “wheelies” because of the difficulty of the task, their residual abilities, and their general health status.

Stages of Motor Learning

Fitts and Posner⁹⁴ described three main stages in learning a motor skill: (1) the cognitive stage, (2) the associative stage, and (3) the autonomous stage of learning. Their model provides a useful framework for examining and developing strategies to improve motor learning and is used in this chapter as well as in Chapter 10, Strategies to Improve Motor Function. A three-stage process was later supported by the work of Anderson.^95,96 It is important to remember that these stages are not fixed or discrete but rather are overlapping.¹

In the early cognitive stage, the learner develops an understanding of task. During practice, cognitive mapping allows the learner to assess abilities and task demands, identify relevant and important stimuli, and develop an initial movement strategy (motor program) based on explicit memory of prior movement experiences. The learner performs initial practice of the task, retaining some strategies while discarding others in order to develop an initial movement strategy. During successive practice trials, the learner modifies and refines the movements. During this stage, there is considerable cognitive activity and each movement requires a high degree of conscious attention and thought. Most learners are highly dependent on the use of visual feedback to shape movements. Performance is initially inconsistent, with large gains occurring as the patient progresses to the next stage. The basic “What to do?” decision is answered.

The second and middle stage is the associated stage of motor learning. During this stage, the learner practices and refines the motor patterns, making subtle adjustments. Spatial and temporal organization increases while errors and extraneous movements decrease. Performance becomes more consistent and cognitive activity decreases. The learner is less dependent on visual feedback while use of proprioceptive feedback increases. Thus, the learner begins to learn the “feel” of the movement. This stage can persist, depending on the learner and the level of practice. The “How to do?” decision is answered.

The third and final stage is the autonomous phase of motor learning. The learner continues to practice and refine motor patterns. The spatial and temporal components of movement become highly organized over time with extensive periods of practice (e.g., weeks, months or years). Performance is at a very high level (e.g., skilled gymnast). At this stage of learning, movements are largely error-free and automatic with only a minimal level of cognitive monitoring and attention. The learner is now free to concentrate on other things such as a secondary task (dual-task performance) or on other aspects of the environment (e.g., sports competition). The “How to succeed?” decision has been answered.

Patients with brain injury admitted to active rehabilitation often have to relearn basic motor skills using entirely different motor control mechanisms and strategies. Activities and movements that were easily done before now become unfamiliar and challenging. These patients can persist in the cognitive learning stage for some time before they develop the idea of a movement skill. Impairments in motor control can influence performance and learning during the associated stage, which can also be prolonged. Many times patients are discharged from rehabilitation before the skills become refined and learning completed. Many patients fail to reach the third stage of learning evidenced by highly skilled performance.

Measures of Motor Learning

Performance Observations

Traditionally, changes in performance during practice have been used to assess motor learning. However, it is possible to improve performance during the initial practice session (acquisition phase) while not retaining the skill. For example, the patient with stroke demonstrates improved sitting posture and balance at the end of a therapy session but on return the next day continues to demonstrate prior poor sitting posture and loss of balance. This is indicative of temporary changes associated with practice versus true motor learning (retained motor skills), which may only become evident with repeat practice sessions. In addition, factors such as fatigue, anxiety, poor motivation, boredom, or drugs can cause performance to deteriorate during practice while learning may still be occurring. For example, the patient with MS who is fatigued and stressed performs very poorly during scheduled treatment but returns after the weekend rested and calm and is able to perform the task with ease.

Performance is best used as a measure of motor learning during a retention test or a transfer test (discussed later in this section). Table 5.12 presents some possible measures of motor performance. For example, an individual recovering from stroke is able to demonstrate functional independence in transfers after a series of training sessions. Improvement in functional scores (e.g., FIM scores) documents changes in the level of assistance needed. Qualitative changes in performance compared to the criterion skill can also be used to document motor learning. Thus, the movement is performed with improved motor control, indicative of changes in spatial and temporal organization. Error scores can be used to document accuracy of movement. Therefore, therapists can report the number and type of errors (constant, variable) that occur within a given practice session and across practice attempts. A decrease in the frequency of error provides indirect evidence of improvements in learning. One common measurement problem in skill learning is the speed–accuracy trade-off. Typically, initial practice sessions are characterized by slowed performance in order to improve movement accuracy. As learning progresses, performance speed is increased once accuracy demands are satisfied. The therapist documents the time it takes to complete the activity along with the number of errors. Reduced effort and concentration are indicative of improved performance and should be documented. A high degree of cognitive monitoring is necessary in early learning (cognitive stage). In contrast, performance across the associative and autonomous stages of motor learning is characterized by a reduced level of cognitive monitoring and increased automaticity.⁹³ As learning progresses, performance is increasingly characterized by consistency and accuracy. Thus, the acquired skills are observed for variability within and across practice sessions, which can be expected to decrease.

Performance plateaus, defined as a leveling off of performance after a period of steady improvement, characterize normal practice and can be expected. During plateaus, learning may still be going on, whereas performance is not changing. Problems can also occur with the measurement instruments selected. Failure to demonstrate improved performance can be the result of ceiling effects, defined as a high level of performance in which further improvement cannot be detected owing to limitations in the performance measure. Conversely, floor effects are a low level of performance in which further decreases cannot be detected by limitations in the performance measure. They can affect a determination of negative learning.

Retention Tests

Reliable inferences about motor learning can be made through the use of retention tests and transfer tests. Retention refers to the ability of the learner to demonstrate the skill over time and after a period of no practice (retention interval). A retention test is defined as “a performance test administered after a retention interval for the purposes of assessing learning.”^{1, p. 499} Retention intervals can be of varying lengths. For example, a patient who is seen only once a week in an outpatient clinic is asked to demonstrate a skill practiced the previous week. Performance after the retention interval is compared to performance on the initial practice session. A difference score can be determined and documented—that is, the difference in performance scores from the end of the original acquisition phase and the beginning of the retention phase. Performance may show a slight initial decrease but should return to original performance levels within relatively few practice trials after the retention interval if learning has occurred (termed warm-up decrement). It is important not to provide any verbal cueing or knowledge of results during the retention trial. This same patient may have been given a home exercise program (HEP) that includes daily practice of the desired skill. If, on return to the clinic some weeks later, performance of the desired skill has not been maintained or has deteriorated, the therapist might reasonably conclude that the patient has not been diligent with the HEP and learning has not been retained.

Transfer Tests

Transfer of learning refers to the gain (or loss) in the capability for performance in one task as a result of practice or experience on some other task.^{1, p. 465} Learning obtained from the criterion task enhances (positive transfer) or detracts from (negative transfer) learning on other tasks. For example, the patient with stroke practices feeding skills using the less affected UE. The feeding task is then practiced using the more affected UE. During a transfer test, the therapist observes and documents the effectiveness of task performance on the second task (e.g., number and frequency of practice trials, time, effort) and compares it with the performance on the first criterion task. Transfer of learning is greatest when tasks have similar stimuli and similar responses.

Adaptation of Motor Skills

Adaptation of motor skills refers to the ability to modify (adapt) how movements are performed in response to changing task and environmental demands.¹ Adaptation of skills (transfer of skills) refers to the ability of the individual to apply a learned motor skill to the learning of other similar or related skills. For example, individuals who learn to transfer from wheelchair to platform mat can apply that learning to other variations of transfers (e.g., wheelchair to car, wheelchair to bathtub). The therapist observes and documents how successful the patient was in learning the variation of the skill (i.e., number of practice trials, time, and effort required to perform these new types of transfers). These parameters are typically reduced from that required to learn the initial skill.

Adaptation of context (changing environmental demands) is also an important measure of learning. This is the adaptability required to perform a learned motor skill in altered environmental situations. Thus, an individual who has learned a skill (e.g., walking with a cane in the physical therapy clinic) should be able to apply that learning to new and variable environments (e.g., walking at home, outdoors, or on a busy street). The therapist observes and documents how successful the patient is in performing the skill in the new and varied environments. The patient who is able to perform the skill in only one type of environment—for example, the patient with TBI who is only able to function within a tightly controlled, clinic environment (closed environment)—demonstrates limited and largely nonfunctional skills in other more open environments. This patient is not likely to return home independent in the community environment and will likely require placement in an more structured, assisted living setting.

Problem-Solving Skills

The patient who is able to engage in active introspection and self-evaluation of performance and reach decisions independently about how to improve performance demonstrates an important element of learning. Some physical therapists overemphasize guided movements and errorless practice. Although this may be important for safety reasons, lack of exposure to performance errors may preclude the patient from developing capabilities for self-evaluation. In an era of fiscal responsibility and limitations on the amount of physical therapy sessions allowed, many patients are able to learn only the very basic skills while in active rehabilitation. Much of the necessary learning of functional skills occurs after discharge and during outpatient episodes of care. The therapist cannot possibly structure practice sessions to meet all of the functional challenges the patient may face. The acquisition of independent problem-solving/decision making skills ensures that the final goal of rehabilitation—independent function—can be achieved. The therapist needs to promote, observe, and document this very important function, including the patient’s self-perceptions of how effective the decisions reached are.

Motivation

Motivational factors include personal sense of self-determination (i.e., choice and collaboration), self-efficacy (i.e., confidence in one’s capabilities), and focused attention. They are important factors in ensuring active participation, learning, and retention of motor skills.⁹⁷ Highly motivated individuals devote greater effort to learning a task and are willing to devote more focused time to practice. Individuals who are not motivated to learn are not engaged and limit their effort and practice. Therapists need to explore with the patient their own perceptions about their disability or injury, their personal goals, their feelings about competence, and perceptions for success in achieving their goals. Equally important is an assessment of the patient’s understanding of the relevance of the learning activity or skill to their daily life. A rehabilitation POC that focuses on involved decision making, active participation, and self-direction is critical in ensuring that the patient will be able to continue practice once discharged and retain learned motor skills. Self-determination and self-management are key elements in ensuring success in real-world environments. Assessment of these factors should be an ongoing process throughout the rehabilitation episode of care. It is important to remember that the patient will experience a number of motivational “ups and downs.” The therapist who accurately identifies and reacts to these changes can provide effective intervention, including encouragement and positive reinforcement. Continuing documentation of the patient’s motivational and emotional status is key.

Memory and Learning Styles

Learning is the acquisition of knowledge or ability. In declarative (explicit) learning, individuals acquire specific knowledge about the world they live in through conscious processes (i.e., attention, awareness, memorization). Procedural (implicit or motor) memory refers to the acquisition or modification of movement.² During rehabilitation, patients are called upon to use both types of learning. For example, declarative memory is used to learn the sequence of events in a transfer while procedural memory is used to perform the motor skill. Individuals vary in their learning style, defined as their characteristic mode of acquiring, processing, and storing knowledge. Learning styles differ according to a number of factors, including personality characteristics, reasoning styles (inductive or deductive), and initiative (active or passive). Some individuals utilize an analytical/objective learning style. They process information in a step-by-step order and learn best with factual information and structure. Other individuals are more intuitive/global learners. They tend to process information all at once and learn best when information is personalized and presented within the context of practical, real-life examples. They may have difficulty in ordering steps and comprehending details. Some individuals rely heavily on visual processing and demonstration to learn a task. Others depend more on auditory processing, talking themselves through a task. Individual characteristics and preferences are best determined by talking with the patient and family, using careful listening and observation skills. The medical record may also provide information concerning relevant premorbid history (e.g., educational level, occupation, interests). A thorough understanding of each of these factors allows the therapist to appropriately structure the learning environment and therapist–patient interactions.

In the evaluation of muscle performance and motor control, we are concerned with the integrity of both central and peripheral mechanisms. The assessment of electrophysiological properties of nerve and muscle provides essential information to understand and assist in the diagnosis of neuromuscular disease or trauma, identify the location of a lesion within the PNS, and establish reasonable prognosis or rate of healing or decay. In order to appreciate deficiencies in peripheral neuromuscular function, clinicians must have a basic understanding of the anatomy and physiology of the nerve and muscle cells. Requirements for peripheral motor response include the successful ability to create an action potential at the lower motor neuron, transmit that signal down the motor neuron and across the neuromuscular junction and result in subsequent muscle contraction. There is a potential for failure in each of these “phases” of neuromuscular transmission due to pathology. Such disorders can result in weakness or lack of motor coordination in movement, resulting in disruption to feedback and motor control mechanisms. These conditions may be related to disorders or disease processes affecting the peripheral nerve (sensory and motor), muscle, or the neuromuscular junction.^98,99

Electrodiagnosis (EDX) of muscle and nerve is a specialization applied to evaluate the scope of a neuromuscular disorder through assessment of muscle and nerve activity using EMG and NCS. EMG assesses muscle function at rest and during activity, and NCS determines the speed and strength with which a peripheral motor or sensory nerve conducts an impulse. Together, data from EMG and NCS tests assist with establishing goals and expected outcomes for patients with musculoskeletal and neuromuscular disorders. Practitioners providing EDX should have thorough knowledge of anatomy and physiology of muscle and nerve, the biophysical understanding of the instruments used to collect signals, and an understanding of the pathophysiology of nerve and muscle disorders. EDX is only part of a complete patient examination, which will include a thorough understanding of the patient’s history and clinical findings. For example, the therapist would also examine muscle strength, pain, reflexes, fatigue, sensory function, and the presence of atrophy, as well as functional abilities and special tests related to the suspected condition. The findings from the clinical examination will suggest which muscles and/or nerves will be tested with EMG and NCS. EDX findings are not diagnostic in isolation and must be considered in relation to other clinical findings and findings from other physical therapy, medical, and physiological tests and measurements.⁹⁹

Neuromuscular Transmission, Injury, and Repair

Neuromuscular Transmission

Nerve cells (neurons) communicate with one another and to other organs, such as muscle and sensory organs, in order to transmit signals that allow motor and sensory function. Neurons are small in diameter, usually much smaller than a hair, and can be as long as the distance from your back to the tip of your toe! A motor unit is composed of one anterior horn cell, one axon, its neuromuscular junction, and all the muscle fibers innervated by that axon (Fig. 5.1). The cell body or nucleus of the neuron is the location of many protein particles and organelles that provide critical neuron function to keep the cell alive and allow repair. Without communication with the cell body, a peripheral nerve will die. This process is called Wallerian degeneration. Dendrites are proximal terminals that receive input from other cells. The axons project away from the cell bodies and carry electrical signals toward targeted organs such as muscles.

Nerves are comprised of groups of neurons that can provide sensory, motor, or autonomic signals to and from other nerves and transmitting organs. Peripheral nerves (Fig 5.2) are typically surrounded by myelin, which is made of water, fat, and protein and provides electrical insulation to the neurons; this allows for neurons to conduct impulses at increased speed. The main cell of myelin in the peripheral nervous system is called the Schwann cell, and spaces between the cells are called the nodes of Ranvier. Nerves are like coated cables that are comprised of bundles of neurons. Each bundle is called a fascicle, and the nerve trunk is a collection of fascicles. Connective tissue structures assist in the organization and protection of neurons and are known as the endoneurium, perineurium, and epineurium. The endoneurium surrounds individual axons and provides a conduit for nerves to grow and travel. Perineurium envelopes the fascicles and epineurium surrounds the entire nerve trunk.¹⁰⁰

The Neuromuscular Junction

The neuromuscular junction (NMJ) (Fig. 5.3) is the location of electrical transmission from the nerve to the muscle cell and is comprised of three distinct parts. The synaptic terminal is the end bulb of the lower motor neuron. Within the synaptic terminal are large numbers of synaptic vesicles that contain acetylcholine (ACH), which is a substance necessary for electrical neurotransmission. The motor end plate is the part of the muscle cell in closest proximity to the synaptic terminal, where there is a high concentration of post-synaptic terminals. These terminals are arranged in folds of muscle membrane and increase the area to which ACH can bind. The space between the synaptic terminal and motor end plate is known as the synaptic cleft.¹⁰⁰

The Muscle Cell

Striated skeletal muscle cell is comprised of bundles of elongated myofibrils (actin and myosin) surrounded by a cellular membrane known as the sarcolemma. The sarcolemma is enveloped in capillaries, t-tubules, nuclei, and sarcoplasmic reticulum, which collectively comprise the muscle fiber. Muscle fibers are covered in a connective tissue matrix known as endomysium and are bundled similarly to peripheral nerve in a cable-like fashion of fascicles. The connective tissue surrounding individual fascicles is known as perimysium. The epimysium surrounds the total bundle of many fascicles. These connective tissue structures continue beyond the contractile structures of the muscle cell as the tendons, which then attach onto the bone¹⁰⁰ (see Fig 5.3).

The Action Potential

When descending/ascending electrical input reaches an axon, there is a disruption in the resting membrane potential, which is a balance of sodium and potassium concentrations within and outside the cell. Resting membrane potential is variable, from –90 to –70 mV. When descending electrical input reaches the lower motor neuron, voltage-gated sodium channels open and there is an exchange where sodium can rush into the cell in an attempt to balance the concentrations of these ions. Smaller positively charged potassium ions are subsequently forced out the cell, and the resting membrane polarity becomes more positive. If the electrical potential reaches a threshold for depolarization (approximately 20 mV), an action potential is created and an impulse travels down the axon. The speed and success of the action potential conduction is dependent on the thickness of the axon and the presence of myelin. Action potentials travel down the myelinated axons through saltatory conduction, in which the action potential jumps from one node of Ranvier to the next, where there are high concentrations of sodium/potassium channels.¹⁰⁰ When myelin or axon thickness is disrupted in certain pathologies, the ability of the axon to transmit at normal speeds and strengths can be affected and can lead to abnormal motor or sensory function. When nerve injury affects myelin, it is considered demyelination, and when there is Wallerian degeneration of the axon, it is considered axonal loss. Collectively, injury or disease to the nerve itself is called neuropathy and can occur in individual nerves, isolated areas, or more widespread throughout the peripheral nerves.⁹⁹

Neuromuscular Transmission

When the nerve action potential reaches the terminal axon, calcium channels open and acetylcholine (ACH) is released into the NMJ. ACH binds to ACH receptors on the motor end plate, and an action potential is generated; this causes the release of calcium ions and finally triggers contraction of the muscle cell. Certain disease processes affecting the release of calcium at the presynaptic terminal or binding of ACH at the post-synaptic terminal can diminish neuromuscular transmission and subsequently impair muscle function. A condition affecting neuromuscular transmission would be considered a neuromuscular junction disorder.¹⁰⁰

Muscle Contraction

During muscle contraction, proteins and structural cells slide over one another to create a shortening of the muscle. Calcium released from the “sarcoplasmic reticulum” at the motor end plate opens binding sites on actin filaments, which bind to myosin. Myosin heads undergo a pivoting action to shorten the cell and then detaches when adenosine triphosphate (ATP) binds to the myosin.¹⁰⁰ The muscle cell is secured to the extracellular matrix through a series of protein molecules, including dystrophin, which allows for mechanical stability and provides a reasonable anchor for contraction. In certain disease or inflammatory processes, such as the muscular dystrophies or myositis, the muscle cell loses structural integrity and leads to poor muscle performance. This destructive muscle condition leads to variability of muscle fiber size and infiltration of fibrous connective tissue. This is considered a myopathy.

Nerve Injury and Repair

Nerve injury is generally characterized by demyelination or axon loss and can be partial or complete. Demyelination can result from inflammation, immune disorders, genetic predisposition, or exposure to toxic chemicals and/or mechanical forces such as compression or shearing. Disturbance of the myelin can reduce myelin thickness or invagination that leads to a widening of the nodes of Ranvier with sodium channel redistribution. This can occur focally, segmentally, or uniformly along a nerve. When this occurs, saltatory conduction is altered and results in slowing, altered shapes of nerve potentials and/or blocking of nerve transmission altogether (conduction block).⁹⁹

When an axon loses continuity with its cell body, Wallerian degeneration occurs. Also known as axon loss, this process begins immediately with one or two nodes of Ranvier dying back and with progressive degeneration distally along the neuron. This degenerative process typically requires 5 to 7 days to complete in motor neurons and 7 to 10 days in sensory neurons. As long as the cell body has continuity with its terminal nerve branch, the branch will remain alive. For example, if an upper motor neuron is damaged due to stroke, the lower motor neuron (whose cell body lies within the anterior horn of the spinal cord) remains intact, as does the remainder of the lower motor neuron. Even though the patient cannot fire the nerve because of the central damage in the brain, the lower motor neuron remains alive and can carry information normally. Similarly, imagine a patient with cervical radiculopathy who has weakness and sensory changes in a specific nerve root distribution. There may be weakness and Wallerian degeneration involving the lower motor neuron but not in the sensory neurons because the primary sensory neuron cell bodies reside in the dorsal root ganglia, which are distal to the typical site of nerve root compression in cervical radiculopathy. Injury to nerve proximal to the dorsal root ganglia is often called a preganglionic lesion. This is a very important concept in understanding EDX, evaluating data, and formulating a reasonable diagnostic impression.⁹⁹

In an attempt to organize nerve structure and progression of injury, an early publication by Seddon¹⁰¹ proposed classifications of nerve injury, which was later expanded by Sunderland¹⁰² to highlight involvement of the connective tissue support system of the axon. Seddon’s classification of nerve injury by neuropraxia, axonotmesis, and neurotmesis and Sunderland’s first- to fifth-degree injury classification have become common methods of describing nerve damage (Fig 5.4). It is important to recognize that neuropraxia and first-degree injury involve demyelination and more specifically conduction block. Axonotmesis/neurotmesis and second- to fifth-degree injury involve axon loss with gradual loss of supportive connective tissue elements in the nerve. Ability of a nerve to recover is largely dependent on the preservation of a regenerating neuron’s connective tissue support structure, specifically preservation of the endoneurium. In axonotmesis and second-degree injuries, the endoneurium remains intact and serves as a conduit for the regenerating axon, which improves the likelihood of nerve recovery. In contrast, with neurotmesis or third- to fifth-degree injuries, the endoneurium, perineurium, or epineurium is lost, and no conduit exists for neuron regeneration.

Nerve healing occurs through either remyelination or reinnervation by way of axonal sprouting or axonal regeneration (Fig 5.5). In remyelination and with optimal conditions of nutrition, removal or control of disease, and/or cessation of compression, Schwann cells produce new myelin, and action potential speeds and strengths will improve and can even return to normal. Reinnervation due to collateral axon sprouting requires the presence of uninjured axons within the injured nerve bundle. Similar to surviving branches on a tree that has been pruned, uninjured neurons will sprout new branches to reinnervate the target organs of the injured neurons. Earliest collateral sprouts require 6 to 8 weeks to be documented. It is generally agreed that a nerve will require about 20% to 25% of uninjured axons to achieve recovery without residual functional weakness. This occurs from collateral axon sprouting, as each terminal neuron branch can grow up to five collateral sprouts. This means that a peripheral nerve can lose quite a large percentage of axons and still recover well. Reinnervation owing to axonal regeneration is a slower process, and under optimal conditions, the injured nerve bulb can regenerate along an intact endoneurium at a rate of about 1 mm per day, or 1 inch (25.4 mm) per month. Age, other disease processes, and distance to the target organ significantly influence a neuron’s successful regeneration. EDX can assist in identifying nerve injury through localization, determining the extent of injury and involvement of myelin versus axon loss, and assessing reinnervation by way of collateral axon sprouting versus axon regeneration.⁹⁹

Concepts of Electrodiagnosis

Both EMG and NCS recordings are made using biomedical equipment that can record and store evoked potential data elicited from the stimulation of nerves and electrical activity from within the muscle (Fig 5.6A). Electrodes are placed on, in, or near muscle or nerve to record bioelectric charges. Recordings are transported to an amplifier for signal processing. Following amplification, the equipment filters ambient noise that would otherwise distort the intended bioelectric charges, and the digitized analog signal is displayed on an oscilloscope for analysis. Audio amplification with speakers also permits acoustic monitoring of these nerve and muscle potentials.

A stimulator is used in NCS and is electronically synchronized with the oscilloscope to fire the nerve. Intensity of the stimulator is dependent upon the voltage, amperage, and pulse duration of the stimulus.

There are three types of electrodes used for recordings. A ground electrode serves as a zero voltage reference and reduces extraneous electrical noise and interference. The recording electrode (pickup electrode) records the intended potential and extraneous signals, and the reference electrode records extraneous signals and different aspects of the intended potential.

In NCS, small surface electrodes are usually used to record the evoked potential from the test muscle or directly from the nerve under study. NCS recordings can also be made using intramuscular or subcutaneous needles. The recording electrode is placed over the belly of the test muscle and a reference electrode is taped over the tendon of the muscle (see Fig 5.6B).

For EMG, the most common types of needle electrodes are bipolar and monopolar. A bipolar electrode is a hypodermic needle, through which a single wire made of platinum or silver is threaded. The cannula shaft and wire are insulated from each other, and only their tips are exposed. The wire and the needle cannula act as recording and reference electrodes, and the difference in potential between them is recorded in volts. A monopolar needle electrode is composed of a single fine needle, insulated except at the tip. A second surface electrode placed on the skin near the site of insertion serves as the reference electrode. These electrodes are generally less painful than bipolar electrodes because they are smaller in diameter and do not have a cutting edge (see Fig. 5.6C).

Bioelectric potentials travel through body fluids in all directions, not just in the direction of the recording electrode. Fibrous tissue, fat, and blood vessels act as insulators in this process. Therefore, the actual pattern of the flow of electrical activity is not predictable. The signals that do reach the electrode are transmitted to an amplifier. The activity produced by all the individual fibers of nerve or muscle at any one time is summated, reaching the electrode almost simultaneously. Electrodes only record potentials they pick up, without differentiating their origin. Therefore, if two motor units contract at the same time, from the same or adjacent muscles, the activity from fibers of both units will be summated and recorded as one large potential.

The size and shape of the evoked potentials can be affected by several variables. The proximity of the electrodes to the nerve and muscle that are firing will affect the amplitude and duration of the recorded potential. Targets that are farther away will contribute less to the recorded potential. The number and size of the muscle fibers or neurons will influence the evoked potential size. Finally, the distance between the fibers will affect the output, because if the fibers are very spread out, less of their total activity is likely to reach the electrodes.

In addition to these variables, many excess signals, or artifacts, can be recorded and processed simultaneously with the EMG signal. An artifact is any unwanted electrical activity that arises outside of the tissues being examined. These artifacts can be of sufficient voltage to distort the output signal markedly, such as those coming from other electrical equipment or fluorescent lights. Electromyographers will usually observe the output signal on an oscilloscope or computer screen to monitor artifacts, then employ troubleshooting techniques to minimize unwanted noise.

The EMG Examination

EMG is the recording of the electrical activity of muscle while at rest and during motor unit activation. Data are visualized on an oscilloscope with audio feedback that allows the examiner to distinguish between normal and abnormal activity.

Insertional Activity

Initially, the patient is asked to relax the muscle to be examined during insertion of the needle electrode. Insertion into a contracting muscle is uncomfortable but tolerable. At this time, the electromyographer will observe a spontaneous burst of potentials, called insertional activity, which is possibly caused by the needle breaking through muscle fiber membranes. This normally lasts less than 300 milliseconds (msec).¹⁰³ Insertional activity can be described as normal, reduced, absent or increased (Fig 5.7). Increased insertional activity is representative of muscle membrane instability and is frequently seen in nerve injury or muscle degeneration. Reduced insertional activities generally represent chronic neuropathy or myopathy in which there has been significant atrophy of muscle and/or infiltration of fat and connective tissue within the muscle. Decreased insertional activity implies non-viable muscle tissue, and the examiner may feel increased resistance when advancing the needle. The needle electrode will be moved to different areas and depths of each muscle. This is necessary because of the small area from which a needle electrode will pick up electrical activity and because the effects of pathology may vary within a single muscle. Up to 25 different points within a single muscle may be examined by moving and redirecting the needle electrode.

Resting Activity

Following cessation of insertional activity, a normal relaxed muscle will exhibit electrical silence, which is the absence of electrical potentials. Observation of silence in the relaxed state is an important part of the EMG examination. Potentials arising spontaneously during this period can be seen in normal muscle if the needle electrode is close to a neuromuscular junction. Miniature end plate potentials are thought to represent small releases of ACH at a NMJ that are not sufficient to propagate a muscle fiber action potential, and end plate spikes/end plate potentials represent sufficient release of ACH at the NMJ to cause depolarization of individual muscle fibers. End plate potentials are irregular in their firing rates and are often uncomfortable to the patient when encountered.⁹⁹ They are not indicative of pathology and are seen frequently in normal muscle. When encountered, it is important to confirm what they are and then move the needle away from the painful area (Fig. 5.8A,B).

There are several characteristic potentials observed during the relaxed state that are considered abnormal. Fibrillation potentials are believed to arise from spontaneous depolarization of a single muscle fiber. They are not visible through the skin. Fibrillation potentials are biphasic spikes and are indicative of muscle membrane instability. They are seen in neuropathic disorders, such as peripheral nerve lesions, anterior horn cell disease, radiculopathies, and polyneuropathies with axonal degeneration (see Fig 5.8C). They are also found in muscle degenerative conditions such as muscular dystrophy, dermatomyositis, polymyositis, and less frequently in myasthenia gravis. Their sound is a high-pitched click, which has been likened to the sound of rain falling on a roof or rhythmic wrinkling tissue paper. Positive sharp waves have been observed in denervated muscle at rest, often accompanied by fibrillation potentials, and they, too, are reported in primary muscle disease, especially muscular dystrophy and polymyositis. The waves are typically biphasic, with a sharp initial positive deflection (below baseline) followed by a slow negative phase. The negative phase is of much lower amplitude than the positive phase and of much longer duration, sometimes up to 100 msec. The peak-to-peak amplitude may be variable, with voltages from 50 microvolts (uV) to 2 millivolts (mV). The sound has been described as a dull thud (see Fig. 5.8D). While morphology (shape) is different in positive sharp waves and fibrillations, it is thought that they represent the same phenomena of spontaneous discharge of a muscle fiber but look differently due to the orientation of the needle electrode with respect to the discharging muscle fiber.⁹⁹ In fact, it is common to see a fibrillation or positive sharp wave morph from one to the other during the examination. Fibrillations and positive sharp waves can be observed in EMG within a week, particularly in proximal muscles, but require up to 3 weeks following axon loss injury to become more widespread.

Complex repetitive discharges may be seen with lesions of the anterior horn cell and peripheral nerves and with myopathies. The discharge is characterized by an extended train of potentials with the same or nearly the same waveform. The feature that distinguishes these discharges from other spontaneous potentials is their regular and repetitive waveform. The frequency usually ranges from 5 to 100 impulses per second. Myotonic discharges are repetitive potentials that increase and decrease in amplitude in a waxing and waning fashion. They are found in myotonic disorders such as myotonic dystrophy, as well as other myopathies. The sound is highly characteristic and sounds like a dive-bomber. High-frequency discharges are probably triggered by movement of the needle electrode within unstable muscle fibers or by volitional activity.⁹⁹

Fasciculations are spontaneous motor unit action potentials (MUAPs) seen with irritation or degeneration of the anterior horn cell, chronic peripheral nerve lesions, nerve root compression, and muscle spasms or cramps. They are believed to represent the involuntary asynchronous firing of motor units. Their sound has been described as a low-pitched thump. Fasciculations are often visible through the skin and can be seen as a small twitch. They are not by themselves a definitive abnormal finding, as they are often seen in normal individuals, particularly in muscles of the calves, eyes, hands, and feet.¹⁰⁴ Myokymia also represents spontaneous bursts of motor unit firing that is more uniform and can fire fast at rates from 2 Hz to 60 Hz.⁹⁹ Like fasciculations, myokymic potentials are not by themselves indicative of pathology and may be seen in normal or fatigued muscle.

Motor Unit Morphology and Recruitment

After observing the muscle at rest, the patient is asked to contract the muscle minimally. When a muscle is contracted to produce force, a single axon conducts an impulse to all its muscle fibers, causing them to depolarize at relatively the same time. This depolarization produces electrical activity that is manifested as a MUAP and can be recorded and displayed graphically. A MUAP is actually the summation of electrical potentials from all the fibers of that unit close enough to the electrodes to be recorded. The amplitude (voltage) is affected by the number of fibers involved or by the motor unit territory. The duration and shape are functions of the distance of the fibers from the recording electrodes, the more distant fibers contributing to terminal phases of the potential. Because of these variables, each motor unit will have a distinctive shape and vary in amplitude and number of phases, where a phase represents a section of a potential crossing above or below the baseline. MUAPs are examined with respect to morphology (amplitude, duration, shape) and frequency of firing. These parameters are the essential characteristics that distinguish normal from abnormal potentials. Initially, a type I MUAP is recruited at approximately 5 Hz. As resistance is increased, that first MUAP increases frequency until it reaches approximately 10 Hz, when another type I MUAP is recruited. The pattern of increasing frequency and addition of more MUAPs continues until type II MUAPs are recruited. Typically, only one to three MUAPs can visibly be assessed qualitatively at any given time for morphology and frequency. Gradually increasing the force of contraction will allow the electromyographer to observe the pattern of recruitment in the muscle but not qualitatively assess morphology. With greater effort, the increased numbers of potentials are summated and can no longer be recognized, but an overall interference pattern can be estimated. The characteristics of the MUAP will change when there is damage to either the nerve or muscle. EMG equipment has improved over the years and most models have features to provide quantitative MUAP analysis that can improve the objective assessment of MUAP characteristics. In normal muscle, the peak-to-peak amplitude of typical MUAP may range from 150 microvolts uV to 5 millivolts mV. The duration of the potential is a measure of time from onset to cessation of the electrical potential, typically from 2 to 14 msec¹⁰⁵ (Fig 5.9A). The typical shape of a MUAP is biphasic or triphasic and generally not displaying greater than four phases.

Polyphasic potentials, which are MUAPs having five or more phases, are generally considered abnormal when seen in large numbers (see Fig 5.9B). It is normal to observe small numbers of polyphasic potentials; however, when polyphasic potentials represent approximately 20% or more of a muscle’s output, it may be an abnormal finding. However, caution is warranted in identifying pathology based solely on the presence of polyphasic MUAPs, as some authors have reported their appearance in greater than 30% of normal subjects.⁹⁹ Polyphasic potentials may also be seen during degeneration and after regeneration of a peripheral nerve. Polyphasic potentials with longer than normal durations are considered a sign of motor neuropathy and may be a result of the asynchronous firing of muscle fibers within a MUAP that is undergoing reinnervation owing to collateral sprouting. This phenomenon is probably due to the difference in the length of the terminal branches and maturity of myelin in the sprouting axons extending to each muscle fiber. As some muscle fibers become reinnervated by collateral sprouts, they will generate action potentials along with the other muscle fibers within that motor unit. The result is a normal amplitude MUAP with larger number of phases and longer duration than a normal motor unit.

Following axonal degeneration, collateral sprouts mature. Successfully reinnervated muscle fibers typically demonstrate larger than normal amplitude MUAP, also known as a Giant MUAP (see Fig 5.9C). Generally, MUAPs exceeding 5 mV are considered larger than normal. These potentials may be seen in post-polio syndrome and other neuropathic conditions such as chronic radiculopathy or focal nerve entrapments like carpal tunnel syndrome.^106-108

In a complete axon loss nerve injury, reinnervation can occur due to axonal regeneration. Recall that the presence of an endoneurial tube is critical for successful axonal regeneration. As the first regenerating axons reach their intended muscle fibers, the potential will look very similar to a fibrillation potential, and as more terminal branches reach muscle fibers, the MUAP will be small in amplitude and highly polyphasic. Early MUAPs representing axonal regeneration have been termed nascent motor units. As these MUAPs mature, the number of phases will decrease and the morphology and duration will become more normal.

In primary muscle disease (myopathies), polyphasic potentials are seen but are generally of smaller amplitude than normal motor units and are typically of shorter duration. These multiphasic changes occur because of a decrease in the number of active muscle fibers within the individual motor units due to pathology. Although the entire unit will fire during voluntary contraction, fewer fibers are available in each unit to contribute to the total voltage and the duration of the potential. The result is a MUAP of lower than normal amplitude and potentially shorter duration (see Fig. 5.9D).

Firing frequencies of any given MUAP are generally less than 12 Hz to 15 Hz if only one to three MUAPs are isolated on an oscilloscope. In a condition of motor axon loss where there are less available MUAPs for recruitment to produce force, firing frequencies may be seen in excess of 15 Hz and can be accompanied by a less than full interference pattern. The MUAP morphological changes consisting of long duration polyphasia or larger than normal amplitudes with overall reduced and fast firing frequencies is consistent with neuropathic recruitment (see Fig 5.9C). Conversely and as discussed in primary muscle generation, motor unit morphology can show MUAPs with shorter duration and low amplitude polyphasia. The total availability of motor units remains normal, so overall interference patterns will be normal; however, muscle degeneration will result in less viable muscle tissue producing resistance to demanded force during the EMG. The resulting interference pattern will occur sooner than anticipated and is considered early recruitment. The combination of MUAP morphology changes consisting of low amplitude, short-duration polyphasia with early recruitment is consistent with myopathic recruitment (see Fig 5.9D).

Nerve Conduction Studies

Nerve conduction studies (NCS) involve direct stimulation to initiate an impulse in motor or sensory nerves. The conduction time is measured by recording the evoked potential either from the muscle innervated by the motor nerve or from the sensory nerve itself. NCS can be tested on any peripheral nerve that is superficial enough to be stimulated through the skin at two different points. The most commonly tested motor nerves are the ulnar, median, fibular (peroneal), tibial, radial, femoral, and sciatic nerves. Commonly tested sensory nerves include the median, ulnar, radial, sural, and superficial fibular nerves, but this is not at all a comprehensive list of available nerves to examine. Complete guidelines for performing NCS tests are available in comprehensive references.^{99,103,105,109,110}

Motor Nerve Conduction Studies

Because a peripheral nerve trunk houses both sensory and motor fibers, recording potentials directly from a peripheral nerve makes monitoring of purely sensory or motor nerves impossible. Therefore, to isolate the potentials conducted by motor axons of a mixed nerve, the evoked potential is recorded from a distal muscle innervated by the nerve under study. Although the stimulation of the nerve will evoke sensory and motor impulses, only the motor fibers contribute to the contraction of the muscle. For example, to test the ulnar nerve, the test muscle is typically the abductor digiti minimi. Other examples are the following: for the median nerve, the abductor pollicis brevis; for the fibular nerve, the extensor digitorum brevis; and for the tibial nerve, the abductor hallucis. Of course, motor evoked potentials can be recorded from any muscle if its target nerve can be stimulated and a recording electrode can be properly placed on or within the muscle.

For the purposes of illustration, the test procedure for the motor NCV of the median nerve will be described (Fig. 5.10). The technique is basically the same for all nerves, except for the sites of stimulation and placement of the electrodes. For this example, the recording electrode is taped over the abductor pollicis brevis. The stimulating electrode is placed over the median nerve at multiple sites, including the palm, wrist, elbow, and axilla, and a recording is made at each site. At the moment the stimulus is produced, the stimulus artifact is seen at the left of the oscilloscope screen. A trigger mechanism controls this and it will, therefore, always appear in the same spot on the screen, facilitating consistent measurements. This spike is purely mechanical and does not represent any muscle activity. The stimulus intensity starts out low and is slowly increased until the evoked potential is clearly observed. When the stimulating electrode is properly placed over the nerve, all muscles innervated distal to that point will contract and the patient will see and feel the hand jump. The intensity is then increased until the evoked response no longer increases in size. At that time, the intensity is increased further to be sure that the stimulus is supramaximal. Because the intensity must be sufficient to reach the threshold of all motor fibers in the nerve, a supramaximal stimulus is required. It is also essential that the stimulator be properly placed over the nerve trunk so that the stimulus reaches all the motor axons.

As in the EMG signal, the potentials seen on the screen represent the electrical activity detected by the recording electrode. The signal will represent the difference in electrical potential between the recording and reference electrodes. When the supramaximal stimulus is applied to the median nerve at the wrist, all the axons in the nerve will depolarize and begin conducting an impulse, transmitting the signal across the motor end plate, initiating depolarization of the muscle fibers. During these events, the recording electrodes do not record a difference in potential because no activity is taking place beneath the electrodes. When the muscle fibers begin to depolarize, the electrical potentials are transmitted to the electrodes, and a deflection is seen on the oscilloscope. This is the evoked potential, which is called the M wave. The M wave is also referred to as the motor action potential (MAP) or compound motor action potential (CMAP). The CMAP represents the summated activity of all motor units in the muscle that responded to stimulation of the nerve trunk. The amplitude of this potential is, therefore, a function of the total voltage produced by the contracting motor units. The initial deflection of the CMAP is the negative portion of the wave, above the baseline. Conduction parameters of interest include latency, nerve conduction velocity, amplitude, and morphology.^99,103

Calculation of Motor Nerve Conduction Velocity

The point at which the CMAP leaves the baseline indicates the time elapsed from the initial propagation of the nerve impulse to the depolarization of the muscle fibers beneath the electrodes. This is called the response latency. The latency is measured in milliseconds from the stimulus artifact to the onset of the CMAP. This time alone is not a valid measurement of nerve conduction because it incorporates time related to other events besides pure nerve conduction—namely, transmission across the NMJ and generation of the muscle action potential. Therefore, these extraneous factors must be eliminated from the calculation of the motor NCV, so that the measurement reflects only the speed of conduction within the nerve trunk.

To account for these distal variables, the nerve is stimulated at a second, more proximal point. This will produce a response similar to that seen with distal stimulation. The stimulus artifact will appear in the same spot on the screen, but the CMAP will originate in a different place because the time for the impulses to reach the muscle would, obviously, be longer. Subtraction of the distal latency from the proximal latency will determine the conduction time for the nerve trunk segment between the two points of stimulation. Nerve conduction velocity (NCV) is determined by dividing the distance between the two points of stimulation (measured along the surface) by the difference between the two latencies (velocity = distance/time).

NCV is always expressed in meters per second (m/s), although distance is usually measured in centimeters and latencies in milliseconds. These units must be converted during calculation. To compute the motor NCV, the latencies are determined for each stimulation site along the nerve by measuring the time from the stimulus artifact to the initial CMAP deflection. The segment conduction time is calculated by taking the difference between latencies of adjacent stimulation sites. Conduction distance is then determined by measuring the length of the nerve between the two points of stimulation. For example in Figure 5.11:

• Wrist latency: 3.1 msec

• Elbow latency: 6.7 msec

• Conduction distance: 220 mm or 22 cm

• CV = 220 mm / (6.7 msec – 3.1 msec) = 220 mm/3.6 msec = 61 m/s

Interpretation of the motor NCV is made in relation to normal values, which are usually expressed as mean values, standard deviations, and ranges. Many investigators in different laboratories have determined normal values.¹¹⁰ Even so, average values seem to be fairly consistent. The motor NCV for the UE has a fairly wide range, with values reported from 50 to 70 m/s. The average normal value is about 60 m/s. For the LE, the average value is about 50 m/s. Distal latencies and average normal amplitudes of CMAPs are also available in such tables, but these must be viewed with caution, because technique, electrode setup, instrumentation, and patient size can affect these values. Age and temperature can also influence NCS measurements, decreasing after age 35 and with lower temperature.⁹⁸ The reader is referred to more comprehensive discussions for complete details about techniques for studying various nerves and for tables of normal values.^105,109,110

It is important to note that the value calculated as the conduction velocity is actually a reflection of the speed of the fastest axons in the nerve. Although all axons are stimulated at the same point in time, and supposedly fire at the same time, their conduction rates vary with their size. Not all motor units will contract at the same time; some receive their nerve impulse later than others. Therefore, the initial CMAP deflection represents the contraction of the motor unit, or units, with the fastest conduction velocity. The curved shape of the CMAP is reflective of the progressively slower axons reaching their motor units at a later time. Figure 5.12A demonstrates slower than normal wrist to palm conduction velocity and slower wrist to abductor pollicis latency in a patient with carpal tunnel syndrome.

The CMAP can also provide useful information about the integrity of the nerve or muscle. The shape and configuration of the CMAP should be examined along the course of the nerve tested and changes duly noted. Temporal dispersion is a phenomenon representing asynchronous recording of muscle fibers contributing to the CMAP due to varying speeds of individual motor neurons. While increasing the length of a segment will accentuate some disparity among neuron speed, demyelinating conditions often cause significant temporal dispersion in CMAPs.^99,103 Figure 5.12B demonstrates temporal dispersion in the tibial motor CMAP of a patient with diabetes-related peripheral polyneuropathy. Notice that the distal latency and leg velocity measures fall just outside of normal limits, but the CMAP morphology is longer in duration with smaller amplitude when comparing the knee to ankle CMAPs.

In instances of partial neuropraxia or conduction block, distal CMAP amplitude is normal, but stimulation proximal to the lesion is comparatively reduced without significant temporal dispersion. Figure 5.12C shows slowing with partial conduction block of just over 30% occurring at or just distal to the medial epicondyle in the ulnar motor NCS of a patient with cubital tunnel syndrome. To identify a conduction block, stimulation must occur distally and proximally to the nerve lesion. However, there are scenarios where this is not possible. For example, in assessing a brachial plexus disorder, difficulty may be experienced stimulating the axillary nerve distal to the clavicle. In contrast, stimulating the radial nerve is generally easily accessible both distally and proximally. This is an important concept, particularly when recognizing the improved prognostic implications of a neuropathy demonstrating conduction block as opposed to axon loss.

In motor axon loss, the CMAP distal to the lesion is expected to reflect lower than normal CMAP amplitude. Figure 5.12D depicts the motor NCS in a patient with severe carpal tunnel syndrome. In addition to slowed latency from wrist to the abductor pollicis brevis and slowed NCV from wrist to palm, the amplitude of the CMAP is well below the lower limit of normal. These parameters reflect the summated voltage over time produced by all the contracting motor units within the test muscle. Therefore, as this muscle is partially denervated, fewer motor units are contracting after nerve stimulation. This will cause the CMAP amplitude to decrease. Temporal dispersion may accentuate, depending on the conduction velocity of the intact units. Similar changes may also be evident in myopathic conditions, in which all motor units are intact but fewer fibers of variable size are available in each motor unit.

The shape of the CMAP can also be variable. Deviation from a smooth curve need not be abnormal, and it is often useful to compare the proximal and distal CMAPs with each other as well as with the contralateral side if indicated. They should be similar. In abnormal conditions, changes in shape may be the result of a significant slowing of conduction in some axons, repetitive firing, or asynchronous firing of axons after a single stimulus. Anatomic variations in innervation of muscle can also influence distal to proximal CMAP morphology, so it is important that EDX providers have a thorough understanding of neuromuscular anatomy and physiology.

Sensory Nerve Conduction Studies

Sensory neurons demonstrate the same physiological properties as motor neurons, and NCV can be measured in a similar way. However, some differences in technique are necessary to differentiate between sensory and motor axons. Although sensory fibers can be tested using orthodromic conduction (physiological direction) or antidromic conduction (opposite to normal conduction), antidromic measurements appear to be more common. For the same reason that motor axons are examined by recording over muscle, sensory axons are either stimulated or recorded from digital sensory nerves. This minimizes the activity of the motor axons from the recorded potentials.

The stimulating electrode used for sensory NCS tests is typically provided by ring, surface, or needle electrodes placed around the base of the digit innervated by the nerve, directly over or subcutaneously near the anatomic location of the nerve. Again, a comprehensive understanding of surface anatomy is paramount. Sensory potentials for the median and ulnar nerves can be recorded antidromically by stimulating at the wrist, elbow, and upper arm. Typically the sensory study of these nerves is limited to stimulation at the wrist. Other sensory nerves can be studied in the UEs and include the superficial radial, medial antebrachial cutaneous, lateral antebrachial cutaneous, and the dorsal cutaneous branch of the ulnar nerve. In the LEs, the sensory nerves most commonly studied are the sural nerve and the superficial fibular (peroneal) nerves. Other nerves that have been studied include the lateral femoral cutaneous, saphenous, and deep fibular (peroneal). Sensory evoked potentials are also called sensory nerve action potentials (SNAPs). Like motor nerve conduction, the sensory conduction parameters of interest include latency, amplitude, NCV, and morphology. Normal sensory NCV ranges between 40 and 75 m/s. Amplitude, measured with surface electrodes, are variable and can range from 2 uV to 120 uV, and duration should be short, generally less than 2 msec. Sensory evoked potentials are usually sharp, not rounded like the CMAP. Sensory NCVs are slightly faster than motor NCVs because of the uniformly larger diameter of sensory nerves contributing to the SNAP.^99,103 Figure 5.13A depicts normal antidromic sensory NCS of a median nerve to digit III. In this figure, latency is measured to the negative peak of the potential and SNAP amplitude from baseline to negative peak. Figure 5.13B depicts abnormal sensory NCS from the median nerve of a patient with mild carpal tunnel syndrome.

H Reflex

The H reflex is a useful diagnostic measure for radiculopathy and peripheral neuropathy. Its most common application is in testing the integrity of the sensory and motor monosynaptic pathways of S1 nerve roots via the tibial nerve and to a lesser extent at C6–C7 and L3–4 via the median or femoral nerves.¹¹¹ In traditional testing, a submaximal stimulus is applied to the tibial nerve at the popliteal fossa, and a motor response is recorded from the medial portion of the soleus muscle. The action potentials travel along the IA afferent neurons toward the spinal cord, synapsing onto interneurons at the level of the spinal cord, then alpha motor neurons within the anterior horn. The consequent activation of the motor neuron leads to an impulse traveling peripherally to the soleus muscle, resulting in a muscle contraction. Because the stimulus causes impulses to travel both distally and proximally within a mixed motor and sensory neuron, the latency of this response comprises a measure of the integrity of both sensory and motor fibers (Fig. 5.14A).

An average tibial H reflex latency is around 30 msec but is affected by limb length, age, and temperature.¹¹² A slowed latency with otherwise normal distal NCS parameters is indicative of abnormal proximal function, often from a herniated disc or other nerve root impingement. Because of more proximal involvement, the peripheral motor and sensory NCS would not be affected. This latency may also identify nerve root compression before obvious EMG changes occur.

The F wave

F waves are a form of NCS test that allows for study of proximal nerve segments that would otherwise be inaccessible to routine nerve conduction studies. F wave abnormalities can be an indicator of peripheral nerve pathology or demyelination. The F wave ratio compares the conduction in the proximal half of the total pathway with the distal and may be used to determine the site of conduction slowing—for example, to distinguish a root lesion from a distal generalized neuropathy.¹¹³ The F wave is elicited by the supramaximal stimulus of a peripheral nerve at a distal site, leading to propagation of impulses in both directions. While the orthodromic impulse travels to the distal muscle, the antidromic response travels to the anterior horn cell, depolarizing the axon hillock, leading to depolarization of dendrites, which in turn depolarizes the axon hillock once again, generating an orthodromic volley back to the muscle. No synapse is involved, so the F wave is not considered a reflex, but rather a measure of motor neuron conduction (see Fig 5.14B).

The F wave has some merit to assist other nerve conduction and EMG measures and is most helpful in the diagnosis of conditions where the most proximal portion of the axon is involved, such as Guillain-Barré syndrome, thoracic outlet syndrome, brachial plexus injuries, and radiculopathies with more than one nerve root involved.¹⁰⁵ The latency of the F wave is generally about 30 seconds in the upper limb and less than 60 seconds in the lower limb and is influenced by age and limb length. Only a small percent of motor neurons actually participate in the F response.⁹⁹ Because it is an inconsistent response, it must be calculated on the basis of at least 10 successive trials.¹⁰³

Repetitive Nerve Stimulation

Repetitive nerve stimulation (RNS) is a technique used to evaluate for suspected NMJ disorders. RNS requires technical proficiency, attention to electrode placement, immobilization of the limb, and temperature control.^114-117 A baseline CMAP is recorded from a target muscle (preferably one that is clinically weak). Then a protocol of repetitive supramaximal stimulations is delivered in a train of 5 to 10 CMAPs at a low rate of stimulus frequency, around 2 Hz to 5 Hz. Comparisons of amplitude are made typically between the first and fourth or first and fifth CMAPs. If there is an amplitude decrement greater than 10%, it is considered abnormal. Following the first train of stimuli, a protocol series of exercise and periods of rest are performed between trains of stimuli. If there is decrement at low rates of stimulation, either fast RNS (20–50 Hz) or brief isometric contraction (to mimic tetany) is performed followed by another train of stimuli. In NMJ disorders, the response to slow and fast RNS can help determine pre- versus post-synaptic NMJ disorders (Fig. 5.15)

Disorders of Peripheral Nerve

Electrophysiological findings usually correlate with clinical signs in patients with neuropathic or myopathic involvement. As discussed, lesions of peripheral nerve fall into two categories, demyelination and axonal loss. Lesions involving peripheral nerve can occur focally, diffusely, segmentally or along a specific nerve root distribution. They can also involve motor nerves sparing sensory nerves or sensory nerve sparing motor nerves. A skilled electrodiagnostician should have the capabilities to perform and interpret findings from the EMG and NCS in order to concisely convey an impression of the neurophysiological state of a patient’s condition.

In focal neuropathy, NCS tests can detect evidence of degeneration and slowing of fibers across the site of compression but may be normal above and below that site. For example, patients with carpal tunnel syndrome may have abnormal motor and sensory NCS findings across the wrist with normal findings in the median nerve proximal to the carpal tunnel and in other nerves of the same limb. EMG abnormalities of increased insertion, fibrillations, and positive sharp waves may be noted in the thenar muscles but not in proximal median innervated muscles or other muscles of the same limb. Recruitment in the thenar muscles may show reduced interference pattern with fast-firing, long-duration polyphasic and/or larger than normal amplitude MUAPs.

Radiculopathy may involve sensory and motor abnormalities on clinical examination, but generally, the motor and sensory NCS is fairly normal unless motor axon loss is severe, at which point low amplitude CMAPs may be evident. SNAP amplitudes are generally preserved, despite the patient complaining of altered sensation, as most nerve root compression due to radiculopathy occurs proximal to the dorsal root ganglia and the cell body is in continuity with the distal axon. This is considered a preganglionic lesion and is an important distinguishing EDX characteristic in radiculopathy. H reflexes or F waves could be absent or delayed in the nerves supplied by the involvement spinal root level. EMG may show evidence of neuropathy with insertion, rest, and volitional testing in the distribution of the radiculopathy with sparing of muscles supplied by other nerve root levels.

Plexopathy refers to neuropathy involving components of the brachial, cervical, lumbar, or lumbosacral plexuses. It can be related to a number of different causes, including trauma, immune-mediated inflammation, birth-related injury, tumors, surgical complications, and unknown etiology (idiopathic). Plexopathy can occur in isolated trunks, divisions, or cords with or without extension of the injury distal into the terminal nerve branches. Isolated lesions involving a single trunk, division, or cord is rare. Slowed NCV across the plexus can be recognized. SNAP amplitudes with EMG changes in the distribution of the plexus components involved are the most sensitive indicators of sensory and motor axon loss in plexopathy.^118,119 Sparing of EMG changes in the paraspinal muscles helps rule out nerve root pathology.

Polyneuropathy affects multiple nerves and typically results in sensory changes, distal weakness, and hyporeflexia. It can be related to medical conditions, such as diabetes, alcoholism, or renal disease, as well as secondary complications related to cancer and its treatments.^99,103 These conditions manifest as axonal damage and/or demyelination and sensory and/or motor nerve involvement. Polyneuropathy can occur diffusely, segmentally, or peripherally. While EMG/NCS findings are not specific to a single diagnosis, the pattern of involvement can assist with narrowing the cause of the polyneuropathy.¹²⁰

Motor Neuron Disorders

Motor neuron disorders typically involve degeneration of the anterior horn cell, such as in poliomyelitis, or diseases that involve both UMNs and LMNs, such as ALS. Abnormal resting potentials are classically seen with these disorders, as well as reduced recruitment, allowing single motor unit potentials to be visible even with an interference pattern. CMAPs may be reduced in amplitude. Motor NCV can be slightly slowed, depending on the distribution of degeneration and propensity for larger, faster fibers to undergo loss earlier in the disease. EMG will show neuropathic patterns with normal sensory NCS findings.

Myopathies

In myopathy, such as the muscular dystrophies and inflammatory myopathies (e.g., myositis, polymyositis, dermatomyositis), the motor unit remains intact, but degeneration of muscle fibers is evident. Motor latencies and NCVs should be normal, although the CMAP amplitudes can be reduced in more weak and involved muscles. Sensory NCS will also be normal. In early stages, EMG will show prolonged insertion activity, fibrillations, and positive sharp waves at rest and often complex repetitive discharges. Recruitment will show full interference patterns with minimal recruitment (early recruitment) with motor unit morphology demonstrating short-duration, low-amplitude polyphasic potentials with voluntary activity. In advanced stages, insertional activity becomes reduced with increased resistance to needle advancement with little electrical activity due to fibrosis of muscle tissue.

Neuromuscular Junction Disorders

In NMJ disorders, such as botulism toxicity, myasthenia gravis (MG), and Lambert-Eaton myasthenic syndrome (LEMS), there is a disturbance of neuromuscular transmission occurring at the NMJ at either the pre- or post-synaptic terminals. EDX abnormalities are most commonly seen using repetitive nerve stimulation and with observed CMAP changes to brief exercise. In post-synaptic NMJ disorders such as MG, baseline CMAPs are generally normal with no change following brief contraction. In slow RNS of 2 Hz to 5 Hz, a decrement may be seen.¹¹⁶ With fast RNS of 20 Hz to 30 Hz, decrements persist or do not change. In LEMS, baseline CMAPs are generally low with significant improvement following brief exercise. Slow RNS shows decrement, but fast RNS demonstrates significant increase in CMAP amplitude.¹¹⁵ Sensory NCS and EMG is generally normal in NMJ disorders, although there may be some MUAP amplitude variability. In LEMS, one could expect reduced recruitment.¹¹⁴

Assessing Severity and Estimating Prognosis in Neuropathy

Seddon and Sunderland offer a reasonable concept of nerve injury classification and lay the foundation for the progression of nerve injury from demyelination to axon loss.^101,102 Table 5.13 illustrates a proposed alternative classification of injury-predicted recovery.^99,121,122 It identifies severity of nerve injury from very mild to complete. Characteristics of the EDX in both the EMG and NCS can assist in determining if an injury involves predominantly myelin, axons, or both. Typically, more mild cases of neuropathy involve myelin and are characterized by slowing of motor/sensory latencies and NCV with possible conduction block. Nerve injury is considered more severe as axonal loss occurs. Axonal loss is recognized in the NCS as decrements in SNAP and CMAP amplitudes, and in the EMG with abnormal resting potentials, reduced recruitment, and motor unit morphological changes representing evidence of collateral axonal sprouting. Preservation of motor axons is essential for muscle function and is therefore a critical characteristic of interest. When there is significant loss of motor axons, the timing required for healing can be protracted with the possibility of residual deficit that can be influenced by age, other illnesses, and distance from the injury to the target muscles.

Evaluation refers to the clinical judgments therapists make based on the data gathered from the examination. Numerous factors influence the judgments therapists make when working with patients with impairments of motor function, including complexity and understanding of the nervous system, clinical findings, psychosocial considerations, and overall physical function and health. Therapists evaluate data in terms of severity of problems (impairments, activity limitations, participation restrictions) and level of recovery or chronicity. Therapists must also consider the consequences of failure to intervene appropriately when the patient is at risk for additional impairments or prolonged activity limitation. Potential discharge placement and resources also influence evaluation of the data and development of the POC. There is a clear need for the therapist to focus on those problems that directly affect function and can be successfully remediated.

The physical therapy diagnosis is determined from evaluation of examination findings and is based on the results of both qualitative and quantitative assessments. Level of impairments, activity limitations, and participation restrictions are identified. Information is used to determine the diagnosis, which describes the impact of the condition on function at the level of the movement system and the whole person. It serves to direct the physical therapy intervention.⁶ See discussion in Chapter 1, Clinical Decision Making. The therapist must also consider the results of an examination of skills in motor learning and problem-solving, motivation and emotional status, and learning styles. Typically the patient with brain insult or injury demonstrates profound deficits in motor function. Novice therapists can gain understanding and insights into the complex examination and practice issues facing therapists who work with these patients from experienced, senior therapists.

Examination of motor function is a challenging process that requires the physical therapist to accurately determine and categorize findings. An understanding of normal motor control and motor learning is essential to this process. Determining the causative factors responsible for abnormal movement patterns and behaviors is based on comparison of expected or normal responses (norm-referenced behaviors) with the patient’s abnormal ones. This can best be achieved by a systematic and thorough approach to examination. Emphasis should be on the use of valid, reliable, and responsive measurement tools. The assessment of electrophysiological properties of nerve and muscle provides essential information to understand neuromuscular disease or trauma, the location of a lesion in the PNS, and prognosis or rate of healing or decay.

Examination of systems yields valuable information about the integrity of individual components (e.g., neuromuscular, musculoskeletal, cognitive). It is important to recall that normal motor control and motor learning is achieved through the integrated action of the CNS. The therapist must therefore also focus on integrated function evidenced through an examination at the functional level. Success in rehabilitation is also dependent on our ability to understand the motivation and learning abilities of the patient and potential training strategies important for cognitive engagement and practice. Our theoretical understanding of the CNS, motor control, and motor learning processes is both incomplete and imperfect. Therapists must, therefore, be constantly aware of the changing knowledge base in neuroscience and in neurological rehabilitation to incorporate new ideas into their examination and intervention plan.

Note: The authors gratefully acknowledge the contributions of Mark Brooks, PT, DSc, ECS, OCS to this chapter.

Questions for Review

1. Differentiate between recovery of function and compensation.

2. Describe the examination of consciousness and arousal. How can the levels of consciousness and arousal influence the motor function examination?

3. Differentiate between selective attention and alternating attention. How should each be examined?

4. Differentiate between spasticity and rigidity. How should each be examined?

5. Describe the examination of a hyperactive patellar deep tendon reflex. What scores are used to document an increased DTR?

6. A patient with stroke exhibits abnormal control of eye muscles and is unable to move the eyes smoothly in all directions. Cranial nerve testing should include which nerves and tests?

7. What are the issues of validity for using manual muscle testing as part of the examination of a patient with UMN syndrome (stroke) who exhibits strong spasticity and strong obligatory synergies?

8. A patient with multiple sclerosis reports fatigue as the number one symptom that impairs functional independence in the home environment. How should this patient’s fatigue be examined and documented?

9. Define stability. How should it be examined?

10. Differentiate between the use of performance observations and retention tests in providing evidence of motor learning.

11. Differentiate EMG from NCS and how each can be utilized to assess nerve and muscle integrity.

12. Differentiate EMG from NCS and how each can be utilized to assess nerve and muscle integrity.

13. Describe how the EMG and NCS can estimate severity of nerve injury and prognosis for recovery.

14. What is a fibrillation potential on EMG? What is it indicative of?

15. How is nerve conduction velocity calculated?

The patient is a 17-year-old female who is 6 months post–motor vehicle accident (MVA). At the time of admission to the hospital, she was comatose and decerebrate. CT scan revealed intracranial bleeding into the right occipital horn. She received a tracheostomy and a gastrostomy. Two months post-MVA, she was transferred to a long-term care facility specializing in TBI.

On initial admission she was able to open her eyes to verbal and tactile stimuli but was unable to visually track. She withdrew her upper and lower extremities in response to stimulation but was not able to move them on command. She was alert but confused, and was unable to carry on a conversation. ROM was within normal limits (WNL) except for right elbow flexion (20° to 100°) and right knee flexion (10° to 110°). She demonstrated increased tone in her left upper extremity (LUE), 3 on Modified Ashworth Scale, 4 on MAS in her right upper extremity (RUE), and 4 in both lower extremities (BLEs). She exhibited 4+ bilateral ankle clonus. She was unable to sit unsupported. During supported sitting in the wheelchair, her head and trunk control was poor, with persistent posturing to the left side.

She is now 6 months post-MVA and is currently being examined for transfer to active rehabilitation status.

PHYSICAL THERAPY EXAMINATION FINDINGS

Consciousness/Arousal

• Fully awake; responds appropriately to varying stimuli.

• Oriented to person; some confusion with orientation to place and time.

• Can become agitated with minimal stimulation, especially when tired.

Cognition/Behavior

• Demonstrates difficulty with concentration and attention.

• Able to follow simple instructions (one-level commands) but occasionally forgets what is asked of her.

• Reaction time is slowed as the number of choices is increased.

• Easily forgets what she is doing.

Sensory Integrity

• Aware of sensory input (pinprick, vibration, light touch) to all extremities.

• Unable to discern common objects placed in either hand for stereognosis discrimination.

Joint Integrity and Mobility

• RLE: plantarflexion contracture (40° to 50°); flexion contractures at the hip (10° to 120°) and knee (10° to 120°).

• RUE: flexor contracture at the elbow (10° to 110°).

• Full passive ROM in the LUE and LLE.

Tone

• Increased bilaterally (R > L).

• On Modified Ashworth Scale: RUE and RLE 3; LUE and LLE 2.

Reflex Integrity

• Hyperactive, 3+ DTRs RUE, RLE.

• 3+ bilateral ankle clonus.

Cranial Nerve Integrity

• Dysphagia and dysphonia are present.

Muscle Performance

• Strength is decreased in the RUE, RLE, and trunk (unable to test with MMT).

• She is unable to sustain R knee extension during standing.

Voluntary Movement Patterns

• RUE moves in partial range, obligatory mass flexor synergy pattern only.

• RLE moves in flexor and extensor synergy patterns with no variation.

• LUE and LLE demonstrate full voluntary control with isolated joint movements. Coordination is decreased. Unable to reach directly to an object that is held out to her and demonstrates foot placement problems with the LLE in sitting or in standing.

• Demonstrates problems with coordinating limb and trunk movements.

Postural Control and Balance

• Demonstrates good head control in all positions.

• Sitting: can sit independently for up to 5 minutes. Demonstrates difficulty in maintaining weight equally on both buttocks. Tends to list to the right side while placing weight primarily on her left buttock. Able to reach to the left and forward; demonstrates loss of balance (LOB) with minimal reaching to right.

• Standing: able to stand in parallel bars with minimal assistance of 1 (Min A x 1) for up to 2 minutes. Has to be reminded to place weight on RLE. Tends to lose her balance easily if she moves quickly; associated with brief episodes of dizziness and vertigo.

Functional Mobility Skills

• Rolling: requires supervision and occasional Min A × 1 with rolling to the right; she requires maximal assist (Max A x 1) when rolling to the left.

• Supine-to-sit: able to come to sitting by rolling to the L side and pushing up with her LUE; requires Min A × 1.

• Transfers: able to perform stand pivot transfers with Min A × 1.

• Gait: does not initiate ambulation on her own. Can ambulate the length of the parallel bars (2 m or 6 ft) with maximal assistance of two persons. Requires posterior splint to stabilize R knee.

• Propels wheelchair by using the LUE and both feet for pushing; requires supervision for safety.

Motor Learning

• Demonstrates profound deficits in short-term memory; unable to remember new information presented during therapy. Her memory for events and learning that occurred before the MVA is good.

GUIDING QUESTIONS

Based on your evaluation of the data presented in the case history and the physical therapy examination, answer the following questions:

1. How has this patient’s level of consciousness/arousal changed from admission to the long-term care facility to the current evaluation? How might this influence the examination of motor function?

2. Develop a physical therapy problem list. Categorize the patient’s problems in terms of (1) direct impairments, (2) indirect impairments, and (3) functional limitations.

3. Prioritize the problems in terms of this patient’s needs for the POC.

4. Determine the physical therapy diagnosis for this patient.