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).
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 brainstem (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 (Table 5.2). Increased tonic contraction of muscles is seen at rest, evidenced by abnormal typical resting postures. When movements are attempted, the result is action-induced abnormal movement patterns (stereotyped movement synergies or spastic dystonia). Additional signs include associated reactions, 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.14,15,16
Table 5.2Positive and Negative Features of Upper Motor Neuron Syndrome ||Download (.pdf) Table 5.2 Positive and Negative Features of Upper Motor Neuron Syndrome
|Negative Features ||Positive Features |
|Paresis and paralysis ||Spasticity |
|Loss of dexterity ||Stereotyped movement synergies; spastic dystonia |
|Fatigue ||Spasms (flexor, extensor/adductor) |
| ||Spastic co-contraction |
| ||Extensor plantar response (Babinskisign) |
| ||Clonus |
| ||Exaggerated deep tendon reflexes (DTR) |
| ||Associated reactions |
| ||Disturbances in movement efficiency and speed; mass movements |
Rigidity is a hypertonic state characterized by constant resistance throughout ROM that is independent of the velocity of movement (lead-pipe rigidity). It is associated with lesions of the basal ganglia system (extrapyramidal syndromes) 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. Patients demonstrate stiffness, inflexibility, and significant functional limitation. Cogwheel rigidity refers to a hypertonic state with superimposed ratchet-like jerkiness and is commonly seen in upper extremity movements (e.g., wrist or elbow flexion and extension) in patients with Parkinson's disease. It may represent the presence of tremor superimposed on rigidity. 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 legs 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 wrist and fingers flexed. The legs are held in stiff extension with plantarflexion. Decorticate rigidity is indicative of a corticospinal tract lesion at the level of diencephalon (above the superior colliculus), whereas decerebrate rigidity indicates a corticospinal lesion in the brainstem 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 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, for hours, or permanently. 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 arm).17
Hypotonia and flaccidity are the terms used to define decreased 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 classic UMN signs.
An examination of tone consists of (1) initial observation of resting posture and palpation, (2) passive motion testing, and (3) active motion testing. Variability of tone is common. For example, patients with spasticity can vary in their 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 arriving at a determination of 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 upper extremity is typically held fixed against the body with the shoulder adducted, elbow flexed, forearm supinated with wrist/fingers flexed. In the supine position, the lower extremities are typically held in extension, adduction with plantarflexion, and inversion (Table 5.3).18 Limbs that appear floppy and lifeless (e.g., a lower extremity [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.
Table 5.3Typical Patterns of Spasticity in Upper Motor Neuron Syndrome ||Download (.pdf) Table 5.3 Typical Patterns of Spasticity in Upper Motor Neuron Syndrome
|Upper Limbs ||Actions ||Muscles Affected |
|Scapula ||Retraction, downward rotation ||Rhomboids |
|Shoulder ||Adduction and internal rotation, depression ||Pectoralis major, latissimus dorsi, teres major, subscapularis |
|Elbow ||Flexion ||Biceps, brachialis, brachioradialis |
|Forearm ||Pronation ||Pronator teres, Pronator quadratus |
|Wrist ||Flexion, adduction ||Flexor carpi radialis |
|Hand ||Finger flexion, clenched fist thumb, adducted in palm ||Flexor digitorum profundus/sublimis, adductor pollicis brevis, flexor pollicis brevis |
|Pelvis ||Retraction (hip hiking) ||Quadratus lumborum |
|Hip || |
Adductor magnus, gracilis
|Knee ||Extension ||Quadriceps |
|Foot and ankle || |
(tarsometatarsal extension, metatarsophalangeal flexion)
(tarso-and metatarsophalangeal flexion)
Long toe flexors
Extensor hallucis longus
|Hip and knee (prolonged sitting posture) || |
Rectus femoris, pectineus
|Trunk ||Lateral flexion with concavity Rotation ||Rotators Internal/external obliques |
|Posture forward (prolonged sitting posture) || |
Excessive forward flexion
Rectus abdominis, external obliques
The form and intensity of spasticity may vary greatly, depending on the CNS lesion site and extent of damage. The degree of spasticity can fluctuate within each individual (i.e., due to body position, level of excitation, sensory stimulation, and voluntary effort). Spasticity predominates in antigravity muscles (i.e., the flexors of the upper extremity and the extensors of the lower extremity). If left untreated, spasticity can result in movement deficiencies, subsequent contractures, degenerative joint changes, and deformity.
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. Some older adults may find it difficult to relax; 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%.15 In the patient with rigidity, resistance is constant and not responsive to increasing the velocity of passive motion.
Clonus, a phasic stretch response, 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. The presence of a clasp-knife response should also be noted. 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 always indicative of neurological dysfunction.
A subjective determination of the degree of tone can be made. Therapists need to be familiar with the wide range of normal and abnormal tonal responses to develop an appropriate frame of reference to grade tone. For documentation in the medical record, tone is typically graded on a 0 to 4+ scale:
|0 ||No response (flaccidity) |
|1+ ||Decreased response (hypotonia) |
|2+ ||Normal response |
|3+ ||Exaggerated response (mild to moderate hypertonia) |
|4+ ||Sustained response (severe hypertonia) |
The Modified Ashworth Scale (MAS) is a clinical scale used to assess muscle spasticity that is in commonly used in many rehabilitation facilities and spasticity clinics (Table 5.4). The original Ashworth Scale (AS), a 4-point ordinal scale, was developed as a simple clinical tool to test the efficacy of an antispastic drug in patients with MS.19 Bohannon and Smith20 modified the instrument scale by adding an additional 1+ grade to increase the sensitivity of the instrument, making it a 5-point scale. In both versions, the examiner uses passive motion to evaluate resistance to passive motion due to spasticity. The MAS has been shown to have moderate to good intrarater reliability but only poor to moderate interrater reliability.21,22,23,24,25,26 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). Agreement on the MAS middle scores (1, 1+, and 2) is the most problematic. Training should be considered to improve interrater reliability between examiners. See Box 5.1 Evidence Summary on the reliability of the Modified Ashworth Scale as a clinical tool for assessing spasticity.
Table 5.4Modified Ashworth Scale for Grading Spasticity ||Download (.pdf) Table 5.4 Modified Ashworth Scale for Grading Spasticity
|Grade ||Description |
|0 ||No increase in muscle tone. |
|1 ||Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the ROM when the affected part(s) is moved in flexion or extension. |
|1+ ||Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM. |
|2 ||More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved. |
|3 ||Considerable increase in muscle tone, passive movement difficult. |
|4 ||Affected part(s) rigid in flexion or extension. |
Box 5.1 Evidence Summary Reliability of Measurements Obtained With the Modified Ashworth Scale (MAS)
|Reference ||Subjects ||Design/Interventions ||Results ||Comments |
|Ghotbi et al (2011)21 ||Tested 23 subjects with LE spasticity and stroke or MS (14 w; 9 m) ||Test-retest study of intrarater reliability; MAS scores obtained by one senior PT using standardized test positions; testing 2 days apart; three LE muscles assessed ||Kappa (k) value for overall agreement was very good (weighted k = 0.87); mod. for hip adductors, good for knee extension, and very good for PF). ||Intrarater reliability with patients with LE spasticity was very good. Reliability for ankle PF was significantly higher than that for hip adductors. |
|Craven and Morris (2010)22 ||Tested 20 subjects with chronic SCI (C5-T10, ASIA A-D, > 12 mo) ||Test-retest study of intrarater and interrater reliability; MAS scores obtained by two blinded raters; ratings taken at same time of day, weekly for 5 weeks, using standardized positions; six LE muscles assessed ||Intrarater reliability was substantial to high (0.6 < k < 1.0) for rater A; poor to fair for rater B (k < 0.4); interrater reliability was poor-to-moderate for all muscle groups (k < 0.6). ||Intrarater reliability with patients with LE spasticity was very good; showed poor to mod. interrater and modest intersession reliability. Differences existed in abilities of raters. An alternative measure for quantifying spasticity was recommended. |
|Ansari et al (2008)23 ||Tested 30 subjects with UE and LE muscle spasticity ||Test-retest study of intrarater and interrater reliability; MAS scores obtained by two experienced PTs; examined 1 week apart; random order of muscles tested using both UE and LE muscles. ||Interrater reliability was mod. (k = 0.514); intrarater reliability also mod. (k = 0.590). Agreement between UE and LE was similar. Agreement on UE distal wrist flexor was significantly higher between rater than proximal shoulder adduction. ||Interrater and intrarater reliability was mod. Limbs had no effect on reliability. Researchers question validity of measurements. |
|Mehrholz et al (2005)24 ||Tested 30 subjects with severe TBI and impaired consciousness ||Test-retest study of intrarater and interrater reliability; MAS scores obtained by four experienced PTs; examined over 2 consecutive days; random order of muscles tested using both UE and LE muscles. ||Intrarater reliability was mod. to good (k = 0.47-0.62); interrater reliability was poor to mod. (k = 0.16-0.42) ||Interrater reliability is limited. Both intrarater and interrater reliability were significantly higher with the Modified Tardieu Scale compared to the MAS. Researchers question the use of MAS as the gold standard for assessing spasticity. |
|Blackburn et al (2002)25 ||Tested 20 subjects 2 weeks post-stroke; 20 subjects 12 weeks post-stroke ||Test-retest study of intrarater and interrater reliability; MAS scores obtained by experienced PTs; testing performed 1 hour apart; testing repeated 1 week later; three LE muscles tested. ||Interrater reliability for 2 raters was poor, correlation was .062 (P = .461); intrarater reliability was .567 (P < .001) ||Intrarater reliability was mod. for a single examiner; interrater reliability between examiners was poor. Most agreement at grade of 0; poor agreement on grades of 1, 1+, and 2. Researchers question the use of the MAS |
|Pandyan et al (1999)26 ||Seven reliability studies identified; four using MAS, two using AS, one using both ||Systematic review of the literature of studies on MAS ||Intrarater reliability was superior to interrater reliability. || |
Confusion exists on the characteristics and limitations of MAS and AS.
AS scale is an ordinal measure of resistance to PM.
MAS is a nominal measure of resistance to PM; ambiguity exists between 1 and 1+ grades.
Training should be considered to improve reliability between examiners.
|Bohannon and Smith (1987)20 ||Tested 30 subjects (1 MS; 5 TBI; 24 CVA) ||Test-retest study of interrater reliability; MAS scores obtained by two senior PTs using standardized test positions; testing several minutes apart; elbow flexor muscles assessed ||Interrater agreement was 86.7%, Kendall's tau correlation of .847 (P < .001) ||Interrater reliability of a manual test of elbow flexor spasticity was good. |
In the lower limbs, spasticity can be examined using the pendulum test. The patient is positioned in supine with knees flexed over the end of a table. The examiner passively extends the knee fully against gravity and then allows the leg to drop and swing like a pendulum. A normal and hypotonic limb will swing freely for several oscillations. In patients with quadriceps or hamstring spasticity, the leg is resistant to full extension and when dropped swings for only a few repetitions. It quickly returns to the initial dependent starting position. The pendulum test can be quantified using an isokinetic dynamometer, an electrogoniometer, or computerized video equipment with high test–retest reliability.27,28
Tonic stretch reflexes can be accurately measured using electromyography (EMG). Response to stretch can be documented for various velocities of stretch and spastic co-contraction can be quantified (see EMG section later in this chapter). A myotonometer is a handheld computerized electronic device developed by Leonard and co-workers that can be used to measure muscle tone. It provides quantitative measurements of force and displacement of muscle tissue and is able to detect small changes in both extremity and postural tone.29,30
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.
A reflex is an involuntary, predictable, and specific response to a stimulus 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. In the medical record, reflexes are graded on a 0 to 4+ scale:
|0 ||Absent, no response |
|1+ ||Slight reflex, present but depressed, low normal |
|2+ ||Normal, typical reflex |
|3+ ||Brisk reflex, possibly but not necessarily abnormal |
|4+ ||Very brisk reflex, abnormal, clonus |
Table 5.5 presents an overview of the examination of DTRs.
Table 5.5Examination of Deep Tendon Reflexes ||Download (.pdf) Table 5.5 Examination of Deep Tendon Reflexes
|Myostatic Reflexes (Stretch) ||Stimulus ||Response |
|Jaw (CN V) ||Patient is sitting, with jaw relaxed and slightly open. Place finger on top of chin; tap downward on top of finger in a direction that causes the jaw to open. ||Jaw rebounds and closes |
|Biceps Musculocutaneous nerve (C5, C6) ||Patient is sitting with arm flexed and supported. Place thumb over the biceps tendon in the cubital fossa, stretching it slightly. Tap thumb or directly on tendon. ||Slight contraction of elbow flexors |
|Brachioradialis (supinator) Radial nerve (C5,C6) ||Patient is sitting with arm flexed onto the abdomen. Place finger on the radial tuberosity and tap finger with hammer. ||Slight contraction of elbow flexors, slight wrist extension or radial deviation |
|Triceps Radial nerve (C6,C7) ||Patient is sitting with arm supported in abduction, elbow flexed. Palpate triceps tendon just above olecranon. Tap directly on tendon. ||Slight contraction of elbow extensors |
|Finger flexors Median nerve (C6-T1) ||Hold hand in neutral position. Place finger across palmar surface of distal phalanges of four fingers and tap. ||Slight contraction of finger flexors |
|Hamstrings Tibial branch, sciatic nerve (L5,SI,S2) ||Patient is prone with knee semiflexed and supported. Palpate tendon at the knee. Tap on finger or directly on tendon. ||Slight contraction of knee flexors |
|Quadriceps (patellar, knee jerk) Femoral nerve (L2, L3, L4) ||Patient is sitting with knee flexed, foot unsupported. Tap tendon of quadriceps muscle between the patella and tibial tuberosity. ||Slight contraction of knee extensors |
|Achilles (ankle jerk) Tibial (S1-S2) ||Patient is prone with foot over the end of the plinth or sitting with knee flexed and foot held in slight dorsiflexion. Tap tendon just above its insertion on the calcaneus. Maintaining slight tension on the gastrocnemius-soleus group improves the response. ||Slight contraction of plantarflexors |
If DTRs are difficult to elicit, responses can be enhanced by specific reinforcement maneuvers. In the Jendrassik maneuver, the patient hooks together the fingers of the hands 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 dorsiflexion (upgoing) of the big toe, with fanning of the lateral four toes. It is indicative of a corticospinal (UMN) lesion. The Chaddock's reflex (or sign) is elicited by stroking around the lateral ankle and up the lateral dorsal aspect of the foot. It also produces extension dorsiflexion 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 quadrant 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 with in patients with obesity or abdominal surgeries. Table 5.6 presents an overview of the examination of superficial cutaneous reflexes.
Table 5.6Examination of Superficial Cutaneous Reflexes ||Download (.pdf) Table 5.6 Examination of Superficial Cutaneous Reflexes
|Superficial Reflexes (Cutaneous) ||Stimulus ||Response |
|Plantar (SI, S2) || |
With blunt object (key or wooden end of applicator stick), stroke the lateral aspect of the sole, moving from the heel to the ball of the foot, curving medially across the ball of the foot.
Alternate stimuli for plantar (for sensitive feet):
Normal response is flexion (plantarflexion) of the great toe, and sometimes the other toes (negative Babinski sign).
Abnormal response, termed a positive Babinski sign, is extension (dorsiflexion) of the great toe with fanning of the four other toes (indicates UMN lesions). Same as for plantar.
|Abdominal reflexes ||Position patient in supine, relaxed. Make brisk, light stroke over each quadrant of the abdominals from the periphery to the umbilicus. ||Localized contraction under the stimulus, causing the umbilicus to move toward the stimulus. |
|Above umbilicus = T8-T10 || ||Masked by obesity. |
|Below umbilicus = T10-T12 || ||Can be absent in both UMN and LMN disorders. |
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+ scale:31,32
|0+ ||Absent |
|1+ ||Tone change: slight, transient with no movement of the extremities |
|2+ ||Visible movement of extremities |
|3+ ||Exaggerated, full movement of extremities |
|4+ ||Obligatory and sustained movement, lasting for more than 30 seconds |
Table 5.7 presents an overview of the examination of primitive and tonic reflexes.
Table 5.7Examination of Primitive and Tonic Reflexes ||Download (.pdf) Table 5.7 Examination of Primitive and Tonic Reflexes
|Primitive/Spinal Reflexes ||Stimulus ||Response |
|Flexor withdrawal ||Noxious stimulus (pinprick) to sole of foot. Tested in supine or sitting position. || |
Toes extend, foot dorsiflexes, entire LE flexes uncontrollably.
Onset: 28 weeks of gestation. Integrated: 1-2 months.
|Crossed extension ||Noxious stimulus to ball of foot of LE fixed in extension; tested in supine position. ||Opposite LE flexes, then adducts and extends. Onset: 28 weeks of gestation. Integrated: 1-2 months. |
|Traction ||Grasp forearm and pull up from supine into sitting position. ||Grasp and total flexion of the UE. Onset: 28 weeks of gestation. Integrated: 2-5 months. |
|Moro ||Sudden change in position of head in relation to trunk; drop patient backward from sitting position. || |
Extension, abduction of UEs, hand opening, and crying followed by flexion, adduction of arms across chest.
Onset: 28 weeks of gestation. Integrated: 5-6 months.
|Startle ||Sudden loud or harsh noise. || |
Sudden extension or abduction of UEs, crying.
|Grasp ||Maintained pressure to palm of hand (palmar grasp) or to ball of foot under toes (plantar grasp). ||Maintained flexion of fingers or toes. Onset: palmar, birth; plantar, 28 weeks of gestation. Integrated: palmer, 4-6 months; plantar, 9 months. |
|Tonic/Brainstem Reflexes ||Stimulus ||Response |
|Asymmetrical tonic neck(ATNR) ||Rotation of the head to one side. ||Flexion of skull limbs, extension of the jaw limbs, "bow and arrow" or "fencing" posture. Onset: birth. Integrated: 4-6 months. |
|Symmetrical tonic neck(STNR) ||Flexion or extension of the head. ||With head flexion: flexion of UEs, extension of LEs; with head extension: extension of UEs, flexion of LEs. Onset: 4-6 months. Integrated: 8-12 months. |
|Symmetrical tonic labyrinthine (TLRor STLR) ||Prone or supine position. ||With prone position: increased flexor tone/flexion of all limbs; with supine: increased extensor tone/extension of all limbs. Onset: birth. Integrated: 6 months. |
|Positive supporting ||Contact to the ball of the foot in upright standing position. ||Rigid extension (co-contraction) of the LEs. Onset: birth. Integrated: 6 months. |
|Associated reactions ||Resisted voluntary movement in any part of the body. ||Involuntary movement in a resting extremity. Onset: birth-3 months. Integrated: 8-9 years. |
Documentation of Reflex Integrity
Documentation of reflex abnormalities should include a determination of (1) specific reflexes tested, (2) the degree of abnormality observed, (3) associated signs (e.g., UMN syndrome), and (4) factors that modify reflexes. Of great importance is a description of the effects of abnormal reflex behavior on active movements, posture, and function.
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, and 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, brainstem, 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 genicu-late 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.
Table 5.8Examination of Cranial Nerve Integrity ||Download (.pdf) Table 5.8 Examination of Cranial Nerve Integrity
|Cranial Nerve ||Function ||Test ||Possible Abnormal Findings |
|I Olfactory ||Smell ||Test sense of smell on each side (close off other nostril): use common, nonirritating odors. ||Anosmia (inability to detect smells), seen with frontal lobe lesions |
|II Optic ||Vision ||Test visual acuity. Central: Snellen eye chart; test each eye separately (covering other eye); test at distance of 20 ft. Test peripheral vision (visual fields) by confrontation. || |
Blindness, myopia (impaired far vision), presbyopia (impaired near vision)
Field defects: homonymous hemianopsia
|II,III Optic and oculomotor ||Pupillary reflexes ||Test pupillary reactions (constriction) by shining light in eye light; if abnormal, test near reaction. Examine pupillary size/shape. || |
Absence of pupillary constriction
Anisocoria (unequal pupils) Horner's syndrome, CN III paralysis
|III, IV, VI Oculomotor, trochlear, and abducens ||Extraocular movements ||Test saccadic (patient is asked to look in each direction) and pursuit eye movements (patient follows moving finger). ||Strabismus (eye deviates from normal conjugate position) Impaired eye movements Double vision |
|III ||Medial, superior, and inferior rectus: inferior oblique; turns eye up, down, in. Elevates eyelid. ||Observe position of eye. Test eye movements. || |
Strabismus: eye pulled outward by CN VI
Eye cannot look upward, downward, inward movements. May see ptosis, pupillary dilation.
|IV ||Superior oblique: turns eye down when adducted. ||Test eye movements. ||Eye cannot look down when eye is adducted. |
|VI ||Lateral rectus: turns eye out. ||Observe position of eye. Test eye movements. ||Esotropia (eye pulled inward) Eye cannot lookout. |
|V Trigeminal Ophthalmic, maxillary, mandibular divisions || |
Sensory: cornea Motor: muscles of mastication
Test pain, light touch sensations: forehead, cheeks, jaw (eyes closed). Test corneal reflex: touch lightly with wisp of cotton.
Palpate temporal and masseter muscles.
Observe spontaneous movements. Have patient clench teeth, hold against resistance.
Loss of facial sensations, numbness with CN V lesion Trigger area with trigeminal neuralgia Loss of corneal reflex ipsilaterally (blinking in response to corneal touch)
Weakness, wasting of muscles When opened, deviation of jaw to ipsilateral side
|VII Facial || |
Taste to anterior two thirds of tongue
Test motor function facial muscles. Raise eyebrows, frown. Show teeth, smile. Close eyes tightly. Puff out both cheeks.
Apply saline solution and sugar solution using a cotton swab.
|Paralysis: Inability to close eye, Drooping corner of mouth, Difficulty with speech articulation Unilateral LMN: Bell's palsy (PNI) Bilateral LMN: Guillain-Barré Unilateral UMN: stroke Incorrectly identifies solution. |
|VIII Vestibulocochlear (acoustic) || |
Test balance: vestibulospinal function (VSR).
Test eye-head coordination: vestibular ocular reflex (VOR).
Test auditory acuity. Test for lateralization (Weber test): place vibrating tuning fork on top of head, mid-position; check if sound heard in one ear, or equally in both.
Compare air and bone conduction (Rinne test): place vibrating tuning fork on mastoid bone, then close to ear canal; sound heard longer through air than bone.
Vertigo, dysequilibrium Gaze instability with head rotations, nystagmus (constant, involuntary cyclical movement of the eyeball)
Deafness, impaired hearing, tinnitus Unilateral conductive loss: sound lateralized to impaired ear Sensorineural loss: sound heard in good ear
Conductive loss: sound heard through bone is equal to or longer than air Sensorineural loss: sound heard longer through air
|IX Glossopharyngeal ||Sensory to posterior one third of tongue, pharynx, middle ear ||Apply saline solution and sugar solution. Not typically tested ||Incorrectly identifies solution. |
|IX, X Glossopharyngeal and vagus || |
Palatal, pharynx control
Listen to voice quality. Examine for difficulty in swallowing glass of water.
Have patient say "ah"; observe motion of soft palate (elevates) and position of uvula (remains midline). Stimulate back of throat lightly on each side.
|Dysphonia: hoarseness denotes vocal cord weakness; nasal quality denotes palatal weakness. Dysphagia Paralysis: palate fails to elevate (lesion of CN X); asymmetrical elevation with unilateral paralysis Absent reflex: lesion of CN IX; possibly CN X |
|XI Spinal accessory || |
Motor function: Trapezius muscle
Examine bulk, strength. Shrug both shoulders upward against resistance.
Turn head to each side against resistance.
|LMN: atrophy, fasciculations, ipsilateral weakness Inability to shrug ipsilateral shoulder; shoulder droops Inability to turn head to opposite side UMN: weakness of ipsilateral sternocleidomastoid and contralateral trapezius |
|XII Hypoglossal ||Tongue movements || |
Listen to patient's articulation.
Examine resting position of tongue.
Examine tongue movements: ask patient to protrude tongue, move side-to-side.
|Dysarthria (seen with lesions of CNXorCNXII, alsoV,VII) Atrophy or fasciculations of tongue (LMN, ALS) Impaired movements, deviation to weak side UMN lesion: tongue deviates away from side of cortical lesion |
Documentation of Cranial Nerve Integrity
Documentation of an examination of CN integrity should include a determination of (1) specific cranial nerves tested, (2) 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.
Atrophy, the loss of muscle bulk (wasting), occurs as a result of the loss of functional mobility (disuse atrophy), 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.33 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 or decreased or absent DTRs, fasciculations, weak or absent voluntary movements). Distribution is limited to a segmental or focal pattern (nerve root).
Examination of Muscle Bulk
During the examination, 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.
Muscle performance is "the capacity of a muscle or a group of muscles to generate forces."4, p. 688 Muscle strength is "the muscle force exerted by a muscle or a group of muscles to overcome a resistance under a specific set of circumstances."4, p. 688 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 "work produced per unit of time or the product of strength and speed."4, p. 688 Muscle performance depends on a number of interrelated factors, including length–tension characteristics, viscoelasticity, velocity, and metabolic adequacy (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, as well as the muscle fibers.
Patients with impairments in motor control 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 spasticity and hyperactive reflexes. 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.34,35,36 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.37,38 Impairments in grip strength impairments are observed, including an exaggeration of grip force, altered times to achieve grip, and difficulty maintaining grip.39 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.40,41,42 Strength losses are typically greater in the distal extremity than proximal. Strength losses have also been found on the "supposedly normal" extremities.43,44,45 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). 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.46,47 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 stereotypic 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 using the following criteria:
Muscles with visible movement that are unable to overcome gravity and move throughout the ROM receive a poor grade.
Muscles that are able to move against gravity throughout the range but can take no additional resistance receive a fair grade.
Muscles that can move against gravity throughout the range and against some resistance (moderate resistance) receive a good grade.
Muscles that can move throughout the range and against strong resistance receive a grade of normal.
The reader will recognize obvious similarities to the standard MMT grading system. However, in this case muscle performance involves groups of muscles moving during specific functional tasks and not during isolated joint movements with standardized protocols.
If MMT is to be used, therapists should utilize standardized positions whenever possible. If a modified position is required (e.g., the patient lacks full 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.
Handheld dynamometers are small portable devices that measure mechanical force; they have been incorporated clinically into MMT procedures. The therapist reads the exact amount of force applied to the muscle during tests for good and normal grades instead of estimating the amount of resistance. High intratester and intertester reliability scores have been reported. Limitations in their use include difficulty in stabilizing both the limb and device, controlling the rate of muscle tension development, and applying sufficient force for a break test. These may be influential factors in reports that indicate the portable dynamometer is less reliable for testing LE muscle groups.48,49,50,51
The use of an isokinetic dynamometer allows the therapist to monitor many important parameters of motor control. It allows examination of a muscle's ability to generate force throughout the range, peak torques, and ability to generate torques at changing velocities. 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. This information is especially important for an understanding of functional performance.52
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.53,54
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 also 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 is "the ability to sustain forces repeatedly or to generate forces over a period of time."4, p. 688 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, amyotrophic lateral sclerosis (ALS), Duchenne muscular dystrophy, and Guillain-Barré syndrome.55,56 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).
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."57, 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 (DOMS) is prolonged in patients with overwork weakness, peaking between 1 and 5 days after activity.
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, defined as "that level of exercise that cannot be sustained indefinitely."58, p. 691 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. One example is the Modified Fatigue Impact Scale (MFIS), an instrument initially developed to assess quality-of-life problems related to fatigue in patients with MS. It includes questions on the cognitive and social domains, as well as physical performance (see Chapter 16, Multiple Sclerosis, Appendix 16.B).59
The examination then proceeds with specific performance-based testing. As this is likely to be fatiguing to the patient, performance testing should be limited to those key functional activities identified in the earlier interview or questionnaire. The therapist should carefully document the patient's level of fatigue during performance testing, including level of independence, modified independence (device required), or level of assistance required (minimal, moderate, or maximal). 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.60 During performance testing, perceived level of fatigue can be documented using the Borg Scale for Rating of Perceived Exertion.61 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). The therapist is then able to differentiate between peripheral factors and central factors contributing to fatigue.
Examination of muscle fatigue can also include both volitional and electrically elicited fatigue tests using an isokinetic dynamometer. This equipment permits quantification of torque outputs. Patients are asked to perform repetitive, submaximal isokinetic contractions. A drop-off of peak torque by 50% can be used as an index of fatigue.62 Electrically induced fatigue tests can also be used to examine muscle performance and may provide a more reliable measure in individuals with low motivation or who have a disorder of central drive (e.g., stroke). The muscle is stimulated with groups of electrical pulses (pulse trains) and percentage of decline in force production is measured.63,64 Timed performance on functional tasks (e.g., timed self-care tasks, time to walk a particular distance, 6-minute walk test) also provides objective and reproducible measures of muscular endurance.
Documentation of muscle endurance 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) frequency and effectiveness of rest attempts; (4) compensatory strategies adopted and effectiveness; and (5) 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 Movement Patterns
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 (see Chapter 6, Examination of Coordination and Balance). 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 Synergistic Patterns
Synergistic organization of movement may be disturbed with pathology of the CNS. Lesions of the corticospinal tracts (e.g., stroke) can produce 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, Table 15.5). Abnormal synergies are highly predictable and characteristic of middle stages of recovery from stroke.65,66,67
The examination of abnormal synergies 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. As CNS recovery progresses, the synergy patterns become less dominant, and reemerge only under conditions of stress or fatigue. Lessening of synergy dominance and emergence of selective movement control are evidence of sequential recovery in patients with stroke.64,65,66 The Fugl-Meyer Post-Stroke Assessment of Physical Performance provides an objective and quantifiable measure of obligatory synergistic dominance and recovery after stroke68 (see Chapter 15, Stroke, Appendix 15.A).
Documentation of abnormal synergies should include a determination of (1) what abnormal synergies are present; (2) the overall strength of the synergies present; (3) the strongest components in each synergy; (4) the influence of other UMN signs on synergies; (5) what variations in movement from the typical synergies are possible, if any; and (6) the effect of obligatory synergies on function (basic activities of daily living [BADL], functional mobility skills).
Table 5.9 presents a summary of the differential diagnosis summary comparing UMN and LMN syndromes. Table 5.10 presents a summary of the differential diagnosis summary comparing the major types of CNS disorders by location of lesion/motor control disorders.
Table 5.9Differential Diagnosis: Comparison of Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) Syndromes ||Download (.pdf) Table 5.9 Differential Diagnosis: Comparison of Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) Syndromes
| ||UMN Lesion ||LMN Lesion |
|Location of lesion, structures involved ||Central nervous system cortex, brainstem, corticospinal tracts, spinal cord || |
Cranial nerve nuclei/nerves
Spinal cord: anterior horn cell, spinal roots Peripheral nerve
|Diagnosis/pathology ||Stroke, traumatic brain injury, spinal cord injury || |
Peripheral nerve injury
|Tone ||Increased: hypertonia Velocity dependent ||Decreased or absent: hypotonia, flaccidity Not velocity dependent |
|Reflexes || |
Increased: hyperreflexia, clonus
Exaggerated cutaneous and autonomie reflexes,+Babinski
|Decreased or absent: hyporeflexia Cutaneous reflexes decreased or absent |
|Involuntary movements ||Muscle spasms: flexor or extensor ||With denervation: fasciculations |
|Strength || |
Weakness or paralysis: ipsilateral (stroke) or bilateral (SCI)
Corticospinal: contralateral if above decussation in medulla; ipsilateral if below Distribution: never focal
Ipsilateral weakness or paralysis
Limited distribution: segmentai or focal pattern, root-innervated pattern
|Muscle bulk ||Disuse atrophy: variable, widespread distribution, especially of antigravity muscles ||Neurogenic atrophy: rapid, focal distribution, severe wasting |
|Voluntary movements ||Impaired or absent: dyssynergic patterns, obligatory mass synergies ||Weak or absent if nerve interrupted |
Table 5.10Differential Diagnosis: Comparison of Major Types of Central Nervous System Disorders ||Download (.pdf) Table 5.10 Differential Diagnosis: Comparison of Major Types of Central Nervous System Disorders
|Location of Lesion ||Cerebral Cortex Corticospinal Tracts ||Basal Ganglia ||Cerebellum ||Spinal Cord |
|Diagnosis/pathology ||Stroke ||Parkinson's disease ||Tumor, stroke ||Trauma, tumor, vascular insult: complete, incomplete SCI |
|Sensation ||Impaired or absent: depends on lesion location; contralateral sensory loss ||Not affected ||Not affected ||Impaired or absent below the level of lesion |
|Tone || |
Hypertonia/spasticity velocity-dependent; clasp-knife
Initial flaccidity: cerebral shock
Lead-pipe rigidity: increased, uniform resistance
Cogwheel rigidity: increased, ratchet-like resistance
|Normal or may be decreased || |
Hypertonia/spasticity below the level of the lesion
Initial flaccidity: spinal shock
|Reflexes ||Hyperreflexia ||Normal or maybe decreased ||Normal or may be decreased ||Hyperreflexia |
|Strength ||Contralateral weakness or paralysis: hemiplegia or hemiparesis Disuse weakness in chronic stage ||Disuse weakness in chronic stage ||Normal or weak: asthenia ||Impaired or absent below the level of the lesion: paraplegia or paraparesis; tetraplegia or tetraparesis |
|Muscle bulk ||Normal during acute stage; disuse atrophy in chronic stage ||Normal or disuse atrophy ||Normal ||Disuse atrophy |
|Involuntary movements ||Spasms ||Resting tremor ||None ||Spasms |
|Voluntary movements ||Dyssynergic: abnormal timing, co-activation, fatigability ||Bradykinesia: slowness of movement Akinesia: absence of movement ||Ataxia: intention tremor dysdiadochokinesia dysmetria dyssynergia nystagmus ||Above level of lesion: intact (normal) Below level of lesion: impaired or absent |
|Postural control ||Impaired or absent, depends on lesion location Impaired balance ||Impaired: stooped (flexed) Impaired balance ||Impaired: truncal ataxia Impaired balance ||Impaired below level of lesion Impaired balance |
|Gait ||Impaired: gait deficits due to abnormal weakness, synergies, spasticity, timing deficits ||Impaired: shuffling, festinating gait ||Impaired: ataxic gait deficits, wide-based, unsteady ||Impaired or absent: depends on level of lesion |
Activity-based Task Analysis
Examination at the functional level focuses on observation and classification of functional abilities and the identification of activity limitations. Performance-based instruments yield important information about function and levels of independence or dependence (supervision, assistance, assistive devices). Numerous instruments are available with quantitative scoring systems (e.g., the FIM). See Chapter 8, Examination of Function, for a thorough discussion of performance-based measures.
Activity-based 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 performance demonstrated. It 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. A determination of how the environment affects performance must also be made. 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. 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. In addition, the patient is highly distractible with poor attention demonstrated in the busy clinic environment. 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 to provide a guide for qualitative task analysis.
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 (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: rolling, bridging, scooting in bed, moving from supine-to-sit and sit-to-supine
Transfers: moving from sit-to-stand and stand-to-sit, transfers from one surface to another (e.g., bed-to-wheelchair and back, on and off a toilet, to and from a car seat), and moving from floor-to-standing
Walking and stair climbing
Control can also be examined in other postures including prone-on-elbows, quadruped (hands and knees), kneeling, and half-kneeling. It is important to note that there is considerable variability in motor performance of FMS across the life span.69,70,71,72,73 Changes are influenced by such factors as changing body dimensions, age, health, and level of physical activity. Thus, the activities of rolling over and sitting up may vary considerably between two adults of different size, age, or health.
Box 5.2 Functional Task Analysis Worksheet
Task analysis begins with an appreciation of normal movements. An examination and evaluation of the patient's task performance is completed and a comparison of the differences is made. Critical skills include accurate observation, recognition and interpretation of movement deficiencies, determination of how underlying impairments relate to the movement deficiencies observed, and determination of what needs be altered and how. The following questions can be used as a guide for qualitative functional task analysis.
A. What are the normal requirements of the functional task being observed?
What is the overall movement sequence (motor plan)?
What are the initial conditions required? Starting position and initial alignment?
How and where is the movement initiated?
How is the movement executed?
What are the musculoskeletal components required for successful completion of the task?
What are the motor control strategies required for successful completion of the task?
What are the requirements for timing, force, and direction of movements?
What are the requirements for balance?
How is the movement terminated?
What are the environmental constraints that must be considered?
What are the motor learning factors that must be considered?
B. How successful is the patient's overall movement in terms of outcome?
Was the overall movement sequence completed?
What components of the patient's movements are normal? Almost normal?
What components of the patient's movements are abnormal?
What components of the patient's movements are missing? Delayed?
If abnormal, are the movements compensatory and functional? Noncompensatory and nonfunctional?
What are the underlying impairments that constrain or impair the movements?
Do the movement errors increase over time? Is fatigue a constraining factor?
Is this a transitional mobility activity? Are the requirements met?
Is this a stability level activity? Are the requirements met for static and dynamic control?
Is this a skill level activity? Are the requirements met?
Are balance requirements met? Is patient safety evident throughout the task?
What environmental factors constrained or impaired the movements?
Can the patient adapt to changing task and environmental demands?
What difficulties do you expect this patient will have with other functional tasks?
What difficulties do you expect this patient will have in other environments?
How successful were the motor learning strategies?
Adapted from A Compendium for Teaching Professional Level Neurologic Content, Neurology Section, American Physical
Tasks can also be grouped according to the actions and type and nature of motor control (neuromotor processes) required during performance of the task. These include (1) transitional mobility, (2) stability (static postural control), (3) dynamic postural control (controlled mobility), and (4) skill. Difficulty varies according to the degree of postural and movement control required. Thus, those tasks with increased degrees of freedom and attentional demands such as standing and walking are more difficult than prone or supine tasks with limited body segments to control.
Transitional mobility is the ability to move from one position to another independently and safely (e.g., rolling, supine-to-sit, sit-to-stand, transfers). Common characteristics of normal mobility include the ability to initiate movement, control movement, and terminate movement while maintaining postural control. Deficits in mobility range from failure to initiate or sustain movements to poorly controlled movement to failure to successfully terminate the movement. At the very lowest level, the impaired patient is only able to roll partially over to side lying and exhibits poor ability to sustain movements. At the highest end, the patient is asked to stand up and walk across the room. The impaired patient exhibits difficulty standing up (may require several attempts) but once up is able to walk with only a few abnormal gait characteristics. Key elements the therapist should observe and document include (1) the ability to initiate movements; (2) strategies utilized and overall control of movement; (3) the ability to terminate movement; (4) the level and type of assistance required (manual cues, verbal cues, guided movements); and (5) environmental constraints that influenced performance.
Stability (static postural control) is the ability to maintain postural stability and orientation with the center of mass (COM) over the base of support (BOS) and the body at rest. For example, the patient demonstrates stability in sitting or standing if he or she is able to maintain the posture with minimum sway, no loss of balance, and no handhold. Key elements the therapist should observe and document include (1) the BOS; (2) the position and stability of the COM within the BOS; (3) the degree of postural sway; (4) the degree of stabilization from UEs or LEs (e.g., handhold, hooked legs); (5) the number of episodes and direction of loss of balance (LOB) and fall safety risk; (6) the level and type of assistance required (manual cues, verbal cues, guided movements); and (7) environmental constraints that influenced performance.
Dynamic postural control (dynamic balance, or controlled mobility) is the ability to maintain postural stability (a stable, nonmoving BOS, COM within the BOS) while parts of the body are in motion. Thus, an individual is able to weight shift or rock back and forth or side to side in a posture (e.g., in sitting or standing) without losing control. The adjustment of postural control while performing a secondary task with a limb freed from weight-bearing is also evidence of dynamic postural control (sometimes called static-dynamic control). The initial weight shift and redistributed weight-bearing places increased demands for stability on the support segments while the dynamic limb challenges control. For example, a patient with TBI is positioned in quadruped and demonstrates difficulty when asked to lift either an upper or lower limb, or lift the opposite upper and lower limbs together. In sitting, the patient with stroke is unable to reach forward and toward the affected side with the less affected limb without losing balance and falling over. In standing, the patient with cerebellar ataxia is unable to step forward, backward, or out to the side without losing balance. Key elements the therapist should observe and document include (1) the degree of postural stability maintained by the weight-bearing segments; (2) the range and degree of control of the dynamically moving segments; (3) the level and type of assistance required (e.g., verbal cues, manual cues, guided movements); and (4) environmental constraints that influenced performance.
Skill is the ability to consistently perform coordinated movement sequences for the purposes of attaining an action goal. Skilled behaviors allow for purposeful investigation and interaction with the physical and social environment (e.g., manipulation or transport). Skills are learned, and are the direct result of practice and experience with actions organized in advance of movement using a motor plan. Skilled movements are variable and not constrained by one set movement pattern but rather are organized by the action goal and the environment. Thus, a skilled individual is able to adapt movements easily to changes in task demands and the environments in which they occur. For example, control of walking is evident in the clinic as well as in home and community environments. Skills can be performed using consistent or variable movements. Regulatory conditions can vary from a stationary environment to motion in the environment.74
Motor skills can be further categorized. Kicking a ball is an example of a discrete skill, with a recognizable beginning and end. Walking is a continuous skill (no recognizable beginning and end), and playing a piano represents a serial skill (a series of discrete actions put together). A movement skill performed in a stable, nonchanging environment is called a closed motor skill, and a movement skill performed in a variable, changing environment is called an open motor skill.1 A skilled individual is also able to perform a simultaneous secondary task while moving (dual task control). For example, the patient with stroke is able to stand or walk while holding or manipulating an object (e.g., bouncing a ball), talking, or performing a cognitive task (counting backwards by 3's from 100). Table 5.11 provides a summary of categories of motor skills.
Table 5.11Categories of Motor Skills ||Download (.pdf) Table 5.11 Categories of Motor Skills
|Categories ||Characteristics ||Examples ||Impairments |
|Transitional mobility ||Ability to move from one posture to another; BOS and/or COM is changing ||Rolling; supine-to-sit; sit-to-stand; transfers ||Failure to initiate or sustain movements through the range; poorly controlled movements |
|Static postural control (stability, static equilibrium, or static balance) ||Ability to maintain postural stability and orientation with the COM over the BOS with the body not in motion; BOS is fixed ||Holding in antigravity postures: prone-on-elbows, quadruped, sitting, kneeling, half-kneeling, modified plantigrade, or standing ||Failure to maintain a steady posture; excessive postural sway; wide BOS; high guard arm position or handhold; loss of balance (COM exceeds BOS) |
|Dynamic postural control (controlled mobility, dynamic equilibrium, or dynamic balance) ||Ability to maintain postural stability and orientation with the COM over the BOS while parts of the body are in motion; BOS is fixed ||Weight shifting; UE reaching in any of the above antigravity postures; LE stepping in modified plantigrade or standing ||Failure to maintain or control posture during dynamic trunk or extremity movements; loss of balance |
|Skill ||Ability to consistently perform coordinated UE and LE movement sequences for the purposes of investigation and interaction with the physical and social environment; during locomotion, COM is in motion and BOS is changing || |
UE skills: Grasp and manipulation
LE skills: Bipedal locomotion
|Poorly coordinated movements; lack of precision, control, consistency, and economy of effort |
During functional task analysis, key elements the therapist should observe and document include (1) the ability to organize and control movements; (2) economy of effort; (3) the success of attaining an action-goal (outcome); (4) ability to easily and successfully adapt a task; (5) ability to easily and successfully adapt to changing environments; and (6) verbal cues and assistance, if any, required. Box 5.2 provides a Functional Task Analysis Worksheet.
The qualitative analysis of motor skills can be enhanced by the use of videography. 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). Depending on equipment capabilities, videotapes can be viewed repeatedly at different speeds to determine control during different tasks and at different body segments. 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. Verbal descriptions of the performance during each trial can be edited directly onto a videotape or documented in a written summary.75