Evaluation of Motor Control

1. The Graded Wolf Motor Function Test (GWMFT) is a new assessment developed to measure functional gains after a hemiparetic event from cerebrovascular accident or traumatic brain injury.⁷² This test was based on the Wolf Motor Function Test.⁹ It is called “Graded” because there are two levels of difficulty for each task: level A is more advanced, and level B is easier (Figure 19-3). Gorman³⁸ investigated the interreliability and intrareliability of the GWMFT with a sample of eight physical therapist investigators and three subjects. Intrarater and interrater reliability was .935 on the timing scores. Intrarater reliability was .897 and interrater reliability was .879 on the functional ability scores. This is a very useful test that can be used on a wide variety of clients with hemiparesis with varying degrees of motor recovery. More research is needed to confirm the validity and reliability of this test.

    In the aforementioned case study, Juan’s mean functional ability score was 5.5 (see Figure 19-3). He performed the test items slowly, with effort and lack of precision.

2. The Wolf Motor Function Test (WMFT) has been used to quantify the motor abilities of chronic clients from a population with high upper extremity function following CVA or traumatic brain injury. It has an interrater reliability range of .95 to .97.⁹

3. The Functional Test for the Hemiplegic/Paretic Upper Extremity¹⁰³ assesses the client’s ability to use the involved arm for purposeful tasks. This test provides objective documentation of functional improvement and includes tasks ranging from those that involve basic stabilization to more difficult tasks requiring fine manipulation and proximal stabilization. Examples include holding a pouch, stabilizing a jar, wringing a rag, hooking and zipping a zipper, folding a sheet, and putting in a light bulb overhead.¹⁰³

4. The Fugl-Meyer⁵⁵ assessment is based on the natural progression of neurologic recovery after CVA. Low scores on the Fugl-Meyer have been closely correlated with the presence of severe spasticity. Fugl-Meyer and associates developed a quantitative assessment of motor function following stroke by measuring such parameters as range of motion (ROM), pain, sensation, and balance. Scores on the Fugl-Meyer assessment correlate with ADL performance.⁵⁵

5. The Arm Motor Ability Test (AMAT)⁵⁸ is a functional assessment of upper extremity function. Cutting meat, making a sandwich, opening a jar, and putting on a T-shirt are some of the tasks included in this test. This test has high interrater and test-retest reliability.⁵⁸

6. The Motricity Index (MI)²¹ is a valid and reliable test of motor impairment that can be performed quickly. The test assesses pinching a cube with the index finger and thumb, as well as elbow flexion, shoulder abduction, ankle dorsiflexion, knee extension, and hip flexion.²¹

7. The Assessment of Motor and Process Skills (AMPS)⁷ is a standardized test that assesses motor and process skills in IADLs. The test was created by occupational therapists. Although this test is not diagnosis specific, it has been widely used with clients who have had a CVA. Occupational therapy practitioners are eligible to become certified in the use of this test upon completion of a 5-day training course.⁷

1. Effective coactivation (stabilization) at axial and proximal joints

2. Ability to move against gravity and resistance

3. Ability to maintain the position of the limb if it is placed passively by the examiner and then released

4. Balanced tone between agonistic and antagonistic muscles

5. Ease of ability to shift from stability to mobility and to reverse as needed

6. Ability to use muscles in groups or selectively with normal timing and coordination

7. Resilience or slight resistance in response to passive movement

Flaccidity

Flaccidity refers to the absence of tone. The client will have absent deep tendon reflexes. Active movement is absent as well. Flaccidity can result from spinal or cerebral shock immediately after a spinal or cerebral insult. In traumatic upper motor neuron lesions of cerebral or spinal origin, flaccidity usually is present initially and then changes to hypertonicity within a few weeks.⁶³

Flaccidity also can result from lower motor neuron dysfunction, such as peripheral nerve injury or disruption of the reflex arc at the alpha motor neuron level. The muscles feel soft and offer no resistance to passive movement. If the flaccid limb is moved passively, it will feel heavy. If moved to a given position and released, the limb will drop because the muscles are unable to resist the pull of gravity.⁹⁶

Hypotonus

Hypotonus is considered by many to be a decrease in normal muscle tone (i.e., low tone). Deep tendon reflexes are diminished or absent. Van der Meche and Van der Gijn¹⁰⁰ suggested that hypotonus could be an erroneous clinical concept. They performed electromyography (EMG) analysis on the quadriceps muscles in “hypotonic” clients (e.g., peripheral neuropathy, cerebral infarction, other diagnoses) and in relaxed normal subjects in a lower leg free-fall test. They concluded in their study that if a client’s limb feels hypotonic or flaccid, this is the result of weakness, not of long-latency stretch reflexes.¹⁰⁰

Hypertonus

Hypertonus is increased muscle tone. Hypertonicity can occur when a lesion is present in the premotor cortex, the basal ganglia, or descending pathways. Damage to upper motor neuron systems increases stimulation of the lower motor neurons, with resultant increased alpha motor activity. Any neurologic condition that changes the upper motor neuron pathways that directly or indirectly facilitate alpha motor neuron activity may result in hypertonicity. Other spinal or brainstem reflexes may become hyperactive, which leads to hypertonus patterns such as the flexor withdrawal or the re-emergence of tonic neck reflexes.⁶³

Hypertonicity often occurs in a synergistic neuromuscular pattern, particularly when seen after CVA or traumatic brain injury. Synergies are defined as patterned movement characterized by co-contraction of flexors and extensors. A typical synergy seen in the upper extremity after CVA or traumatic brain injury is a flexion synergy.⁶² In contrast, an extension synergy is seen in the lower extremity.

The energy cost in moving against hypertonicity is considerable. It takes a great deal of effort for clients with moderate to severe hypertonicity to move against this drawing force. Antagonist power may be insufficient to overcome the spastic agonist muscle groups. Even clients with mild hypertonicity report frustration during functional activities. Loss of reciprocal inhibition is noted between spastic agonists and antagonists. Clients are unable to rapidly turn off their muscles. The client with an upper motor neuron lesion will have dysfunction in spatial and temporal timing of movement. This makes his/her movements very uncoordinated.¹⁰⁴ This frustration, coupled with the fatigue, decreased dexterity, and paresis associated with UMNS, can influence therapy participation.⁸⁰ Furthermore, the architecture of hypertonic muscles changes over time. The muscles lose their ability to lengthen and shorten because of viscoelastic changes that result from the hypertonia.^18,54

The abnormal timing of Juan’s distal upper extremity muscles, particularly between the finger flexors and extensors, impaired his coordination so much that he could not play the keyboard with his left hand.

Hypertonicity can increase as a result of painful or noxious stimuli. These stimuli often can be reduced with good medical care. Stimuli that can increase tone include pressure sores, ingrown toenails, tight elastic straps on a urine collection leg bag, tight clothing, an obstructed catheter, urinary tract infection, constipation, and fecal impaction.^29,51 Other triggering factors include fear, anxiety, environmental temperature extremes, heterotopic ossification, and sensory overload. These factors are true for both cerebral and spinal hypertonicity; however, they are more pronounced in spinal hypertonia. Therapeutic intervention should be designed to reduce, eliminate, or cope with these extrinsic factors.

Clients with hypertonicity often have difficulty initiating movement, especially rapid movement.⁵⁴ Although hypertonic muscles appear to be able to take a lot of resistance, they do not function as normal, strong muscles do. Through the mechanism of reciprocal inhibition, hypertonic muscles inhibit the activity of their antagonists and thus can mask potentially good or normal function of antagonists.^83,97 Four types of hypertonia are described in the following paragraphs.

Spasticity

Much controversy in recent years has surrounded the difference between spasticity and hypertonia. Lance’s⁵⁹ definition of spasticity is still accepted by many physicians and therapists. He defined spasticity as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex as one component of the upper motor neuron syndrome.”⁵⁹

Little and Massagli^62,63 believe that pure spasticity is a subset of hypertonia. It is possible that Lance’s definition does not adequately distinguish between the presence of phasic and tonic stretch reflexes, which present different clinical scenarios. This chapter attempts to clarify the differences using current physiatry literature.

Spasticity has three characteristics:

One of the main systems affected when spasticity is present is the pyramidal system, which consists of the corticospinal and corticobulbar tracts. The corticospinal tract controls goal-directed, voluntary movement by influencing the lower motor neuron. The corticobulbar tract influences the voluntary action of the cranial nerves.¹⁸

Therapists often confuse hypertonia with spasticity. These two conditions are similar because both pull the limb into a unilateral direction.

Hypertonia is different from spasticity in two ways:

Rigidity

Rigidity is a simultaneous increase in muscle tone of agonist and antagonist muscles (i.e., muscles on both sides of the joint). Both groups of muscles contract steadily, leading to increased resistance to passive movement in any direction and throughout the ROM. Rigidity signals involvement of the extrapyramidal pathways in the circuitry of the basal ganglia, diencephalon, and brainstem. It occurs in isolated forms in disorders such as Parkinson’s disease, traumatic brain injury, some degenerative diseases, encephalitis, and tumors,²⁵ and after poisoning from certain toxins and carbon monoxide. Rigidity also is seen in conjunction with spasticity in those with stroke and traumatic brain injury. Rigidity is not velocity dependent.⁹⁶

Rigidity is evaluated during muscle tone evaluation (see Figure 19-4). Four types of rigidity are commonly seen:

Both lead pipe and cogwheel rigidity can occur in Parkinson’s disease. In lead pipe rigidity, constant resistance is felt throughout the ROM when the part is moved slowly and passively in any direction. This rigidity feels similar to the feeling of bending solder or a lead pipe, thus its name. In cogwheel rigidity, a rhythmic give in resistance occurs throughout the ROM, much like the feeling of turning a cogwheel. It is thought that cogwheel rigidity is lead pipe rigidity with concomitant tremor, which results in the ratchety pattern.⁷⁰ Deep tendon reflexes are normal or are only mildly increased in Parkinson’s rigidity.

Decerebrate and decorticate rigidity can occur after severe traumatic brain injury with diffuse cerebral damage or anoxia. These abnormal postures occur immediately after injury and can last a few days or weeks if recovery occurs, or can persist indefinitely if there is little or no recovery.

Decerebrate rigidity results from lesions in the bilateral hemispheres of the diencephalon and midbrain. It appears as rigid extension posturing of all limbs and the neck. Bilateral cortical lesions can result in decorticate rigidity, which appears as flexion hypertonus in the upper extremities and as extension tone in the lower extremities. Supine positioning increases the abnormal tone, and with either type of rigidity it may be extremely difficult to position clients in a sitting position.⁶³

Guidelines for Muscle Tone Assessment

The following steps describe correct procedures for assessing muscle tone.

It is helpful to rate spasticity and hypertonia with the client in the same position, preferably at the same time of day, to enhance reliability, because body and head position influence cerebral hypertonus. The client’s upper extremity muscle tone usually is evaluated with the client sitting on a mat table when possible. Remember that the client’s trunk posture (e.g., the seated client bearing weight symmetrically vs. slumped or leaning to one side) will affect the results of the tone evaluation. Tone fluctuates from hour to hour and from day to day because of intrinsic and extrinsic factors that influence it. This fluctuation makes accurate measurement difficult, particularly for cerebral hypertonia. Rating tone is still worthwhile, especially in the managed care environment, in which objective measures of progress are needed to justify the continuation of therapy.

Grasp the client’s limb proximal and distal to the joint to be tested and move the joint slowly through its range to determine the free and easy ROM available. Note the presence and location of pain. If there is no active movement and if the limb feels heavy, record that the limb is flaccid or “0” in strength. If the limb has some active movement and no evidence of increased tone, the affected muscle or muscle group may be labeled “paretic” instead of “hypotonic.” The paretic antagonist muscle can then be graded in strength (usually the strength grade will fall between 1 and 4−). Grading the paretic antagonist muscles provides more objective clinical information than merely labeling the muscles as hypotonic. Strength grading antagonists can help the occupational therapist to triage phenol block and botulinum toxin type A or B injection candidates who have the potential to improve function; for example, a client with an elbow extension strength grade of 2− (in the presence of elbow flexor tone) would be a better block candidate than a client with a triceps strength grade of 0.

Juan did not have sufficient strength in his supinators (4−/5) or in his finger extensors (extrinsic 3−/5, intrinsic 2−/5) to counteract the pull of moderate finger flexor and pronator hypertonia.

Hold the limb on the lateral aspects to avoid giving tactile stimulation to the muscle belly of the muscle being tested.

Clinical assessment of spasticity involves holding the client’s limb as just described and moving it rapidly through its full range while the client is relaxed. Label the tone “mild,” “moderate,” or “severe.” (Refer to tone rating scales defined in the next section.)

Clinical assessment of rigidity and hypertonia involves moving the limb slowly during the range, noting the location of first tone or resistance to movement in degrees and labeling it “mild,” “moderate,” or “severe.” Some physicians find goniometric measuring of the location of the first tone helpful before and after long-acting nerve block. Others find documentation of the limb’s resting position helpful before and after injection.⁶⁵

Record findings for various muscle groups or movements.

Manual Rating Scales for Spasticity and Hypertonicity

Mechanical and Computer Rating Systems for Spasticity and Hypertonicity

Mechanically determined parameters of assessing hypertonia may be more reliable than the aforementioned manual methods. McCrea and coworkers⁶⁷ concluded that using a linear spring damper model to assess the hypertonic elbow was reliable and valid. This model is not widely used in clinical practice, nor even in research practice, because of time constraints and difficulty accessing certain muscle groups (e.g., it is easier to set up and measure elbow hypertonia than hip hypertonia in a mechanical tone rating device).

Leonard and associates investigated the construct validity of the Myotonometer (Neurogenic Technologies, Inc., Missoula, Mont), a newly developed computerized, electronic device with a probe (that looks similar to an ultrasound transducer) that is placed on top of the skin over the muscle belly. Measurements were taken over the biceps brachii at rest and during maximum voluntary muscle contraction. They revealed a significant difference between affected and unaffected extremities in subjects with upper motor neuron spasticity. The authors concluded that the Myotonometer could provide objective data about the tone reduction efficacy of various tone reducing procedures.⁶¹

Clearly, more research is needed in the areas of manual, mechanical, and computer rating systems for assessment of hypertonia. Sehgal and McGuire summed up the controversy over hypertonia/spasticity rating scales quite well: “A uniformly acceptable, reliable and practical measure of spasticity continues to elude the clinician.”⁸⁸

Range-of-Motion Assessment in Evaluation of Tone

Passive ROM (PROM) assessment supplements and often correlates with tone assessment. For example, if a client with acute CVA (1 month after onset) has a wrist ROM measurement of 20 degrees extension (normal, 70 degrees), and if orthopedic causes (e.g., arthritis, fixed contracture) have been ruled out, the therapist should assess the tone in the wrist flexors and the extrinsic finger flexors. Hypertonicity of any of these muscles can prohibit full wrist extension. Assessment of PROM can reveal possible signs of joint changes (e.g., subluxation, dislocation, contracture) that have occurred from chronic hypertonus, such as proximal interphalangeal joints (PIPs) that measure −45 to 125 degrees instead of 0 to 100 degrees. Some physicians find PROM measurements useful in documenting the location of the first tone, or resting position, before and after Botox¹² or Myobloc⁷³ injections.

Juan had only 20 degrees of active supination. His passive range of motion was not limited. He has a soft tissue limitation of active supination as the result of paresis of the supinator and hypertonicity of the pronators; 20 degrees of supination is not enough to orient his hand palm up to hold coins.

Other Considerations in Tone Assessment

Changes in bone or other peripheral structures can lead to ROM limitations. For example, the presence of heterotopic ossification can limit joint ROM. Heterotopic ossification is the formation of new bone in soft tissue or joints, which can lead to joint ankylosis. Heterotopic ossification can occur in individuals with traumatic brain injury and spinal cord injury, along with severe spasticity, or with other types of severe injuries.^11,53,102 Conversely, the presence of fixed contractures may be incorrectly labeled as hypertonus. Physiatrists and other physician specialists can aid in the diagnosis of contractures with the use of diagnostic short-term nerve blocks, EMG, and/or X-rays.⁸³

Incidentally, Juan had no passive range-of-motion deficits, so he did not have contractures.

Assessing Movement and Control

Along with the assessment of muscle tone previously described, the occupational therapist performs an assessment of upper extremity movement and control. The therapist identifies where and how much the client’s motor control is dominated by synergies, and where selective, isolated movement is present. The degree to which abnormal tone interferes with selective control is identified. Also, identifying in which direction of movement hypertonicity occurs and how it affects function helps in determining the need for intervention.

Manual muscle testing usually is not appropriate for clients who exhibit moderate to severe hypertonicity or rigidity, because the relative tone and strength of the muscles are not normal, and movement is not voluntary or selective. Tone and strength are influenced by the position of the head and body in space, as well as by abnormal contraction, deficits in tactile and proprioceptive sensation, and impaired reciprocal inhibition.¹⁰⁴ However, if hypertonia is mild and selective movements are possible, it is helpful to grade the strength of the antagonists to measure progress objectively.⁸³

Position change, spinal reflexes, the reticular formation, and supraspinal reflexes influence muscle tone and motor control. Because the level and distribution of muscle tone change as the position of the head in space and of the head in relation to the body changes, tone cannot be assessed in isolation from postural mechanisms, motor function, synergies present, task specificity, and other factors related to motor control.⁴⁸

Sensation

The following sensibility tests are recommended for clients with damage to the central nervous system: static two-point discrimination, kinesthesia, proprioception, pain, and light touch using the Semmes-Weinstein monofilament test.⁵ The therapist can assess light touch more accurately with the Semmes-Weinstein monofilaments because they provide better pressure control than a cotton ball. (Chapter 23 discusses procedures for administration of these sensory tests.)

Medical Assessment of Muscle Tone

Physiatrists, orthopedic surgeons, and neurologists are some of the physicians who may specialize in assessment of muscle tone. They may use static or dynamic surface or percutaneous (needle) EMG. Multiple channels are used in dynamic EMG to evaluate the hypertonicity of many contributing muscles.⁶² EMG helps the physician determine abnormal, excessive electrical activity in muscles. EMG can help physiatrists and neurologists plan and implement short- and long-acting nerve blocks to treat hypertonia. Clients who have local muscle wasting, flaccidity, numbness, or unexplained paresis should undergo EMG assessment to rule out peripheral neuropathy.¹⁰²

Righting Reactions

Righting reactions direct the head to an upright position. Righting reactions help one assume a position. Automatic reactions maintain and restore the normal position of the head in space and the normal relationship of the head to the trunk, as well as the normal alignment of the trunk and limbs. Without effective righting reactions, the client will have difficulty getting up from the floor, getting out of bed, sitting up, and kneeling.⁹²

Equilibrium Reactions

Equilibrium reactions help one sustain or keep a position. They are the “first line of defense against falling.”⁸⁷ Equilibrium reactions, which are elicited by stimulation of the labyrinths within the inner ear, are used to maintain and regain balance in all activities. These reactions ensure sufficient postural alignment when the body’s center of gravity is altered by a change in the supporting surface.⁵² Without equilibrium reactions, the client will have difficulty maintaining and recovering balance in all positions and activities.

Protective Reactions

Protective reactions are the second line of defense against falling if the equilibrium reactions cannot correct a balance perturbation. They consist of protective extension of the arms and hands, which is used to protect the head and face when one is falling. Stepping and hopping are examples of lower extremity protective reactions. Without protective reactions, the client may fall or may be reluctant to bear weight on the affected side during normal bilateral activities.⁸⁷

Primitive Reflexes

The dominance of primitive reflex movement patterns can interfere with the client’s occupational performance. Difficulties that may be encountered are described in the following paragraphs. Observation of these motor behaviors is a way of evaluating for the presence of primitive reflexes.

Trunk Control Assessment

Collin and Wade²¹ designed a quick and easily administered test of trunk control that is valid and reliable in clients with a diagnosis of CVA. It involves four timed tests: (1) rolling to the weak side, (2) rolling to the sound side, (3) moving from supine to sitting, and (4) sitting on the side of the bed with feet off the floor for 30 seconds.²¹

To accurately assess trunk control, the therapist must evaluate strength and control in the following muscle groups: trunk flexors, extensors, lateral flexors, and rotators. The client should be sitting upright on a mat table with the feet supported for all tests. Again, the client should not be left unattended on the mat table until the therapist determines that the client has adequate trunk control and sitting balance. The procedures described in the following sections are condensed from Gillen’s Stroke Rehabilitation: A Function-Based Approach.³⁶

Cerebellar Disorders

Cerebellar dysfunction can cause incoordination that may affect any body region and cause a variety of clinical symptoms. For example, the client may have postural difficulties that include slouching or leaning positions (caused by bilateral lesions) or spinal curvature (caused by unilateral lesions) and wide-based standing. Eye movements, both voluntary and reflexive, may be affected, as well as the resting position of the eye. The following are common signs of cerebellar dysfunction that the therapist may encounter.⁹⁸

Extrapyramidal Disorders

Extrapyramidal disorders are characterized by hypokinesia or hyperkinesia. Parkinson’s disease is characterized by hypokinesia (bradykinesia), cogwheel and lead pipe rigidity, a decrease in or loss of postural mechanisms, and a resting, pill-rolling tremor.²⁷

Parkinson’s plus is the name given to a group of movement disorders that have signs of Parkinson’s disease with concomitant neurologic deficits. Progressive supranuclear palsy (PSP) is one such disease.⁵⁰ Clients affected with PSP have “loss of vertical ocular gaze, rigidity of the neck and trunk muscles, dementia, and parkinsonian signs,”⁴⁹ usually in the absence of tremor. Life expectancy is shorter than in Parkinson’s disease. Death often occurs within 6 to 10 years.⁴⁹

Medical Assessment of Coordination

Incoordination consists of errors in rate, rhythm, range, direction, and force of movement.³⁵ Therefore, observation is an important element of the clinical examination. The neurologic examination for incoordination may include the nose-finger-nose test, the finger-nose test, the heel-knee test, the knee pat (pronation-supination) test, hand pat and foot pat tests, finger wiggling, and drawing a spiral. Such tests can reveal dysmetria, dyssynergia, adiadochokinesis, tremors, and ataxia. Usually the neurologist or the physiatrist performs these examinations. Magnetic resonance imaging and computed tomography scans also may be ordered. Tremors are frequency rated with EMG, which helps the physician accurately diagnose tremor type.⁴⁹

Occupational Therapy Assessment of Coordination

Selected activities and specific performance tests can reveal the effects of incoordination on function. The occupational therapist can observe for coordination difficulties during ADL assessment. The therapist can prepare simulated tasks that require coordinated muscle function, such as writing, opening containers, tossing and catching a bean bag or ball, or playing a board game.⁹⁰ The therapist should observe for irregularity in the rate of movement and for sudden, corrective movements in an attempt to compensate for incoordination. Movement during the performance of various activities may appear irregular and jerky and may overreach the mark. The following general guidelines and questions can be used when evaluating incoordination:

Numerous standardized tests of motor function and manual dexterity are available and can be administered to evaluate coordination. These tests include the Purdue Pegboard,⁸⁴ the Minnesota Rate of Manipulation Test,⁷¹ the Pennsylvania Bimanual Work Sample,⁷⁹ the Crawford Small Parts Dexterity Test,²² the Jebsen-Taylor Hand Function Test,⁵¹ and the 9-Hole Peg Test.⁶⁴ Standardized functional assessments for CVA (e.g., the GWMFT) mentioned earlier in this chapter may be useful for measuring the efficacy of occupational therapy intervention for impaired coordination.⁷²

Intervention for Hypertonicity and Spasticity

Hypertonicity is only one part of the UMNS. It is very important to treat other performance deficits of the UMNS such as paresis, fatigue, and decreased dexterity. These deficits can impede function to a greater extent than hypertonia.¹⁴

Before treating hypertonus, the therapist and the physician need to closely evaluate the function of the tone. Hypertonicity can have beneficial effects, such as aiding in standing and transfers, maintaining muscle bulk, and preventing deep vein thrombosis, osteoporosis, and edema. Intervention is necessary when spasticity interferes with ADLs, gait, sleep, or wheelchair positioning, or when it causes severe pain and limits hygiene (e.g., the client is unable to wash hand or axilla) or leads to contractures or decubitus ulcers. Hypertonicity or spasticity may be treated with conservative therapeutic interventions, pharmacologic agents, or surgery.⁸³

Treatment of Rigidity

Decerebrate and decorticate rigidity can wax and wane. When rigidity is waning, it is recommended that the client be transferred to a wheelchair or a reclining chair because rigidity decreases in sitting. Rigidity is worse during episodes of agitation.⁵⁷ Parkinson’s rigidity responds temporarily to heat, massage, stretching, and ROM exercises. Rocking back and forth before standing can aid in the transition.⁶² See Chapter 35 for a discussion of Parkinson’s disease and additional treatment strategies for rigidity.

Treatment of Flaccidity

Flaccidity stemming from upper motor neuron dysfunction (e.g., recovering from spinal or cerebral shock resulting from acute CNS insult) is treated with facilitation techniques such as weight bearing, high-frequency vibration, tapping, quick stretch, bed positioning with weight on the flaccid side most of the time, and functional neuromuscular electrical stimulation. Splinting of the hand and wrist may be indicated for support. Therapists should closely supervise splinting because contractures can result from excessive splint wear. Passive ROM exercises also are indicated. The arm can be passively positioned as normally as possible during ADL tasks to provide sensory and proprioceptive feedback. When the client is eating, have him or her place his or her arm on the dining room table, resting on top of a piece of Dycem.²⁹ Client and family education on proper positioning and joint protection is important to prevent overlengthening of soft tissues and trauma (e.g., having his or her arm fall off of the lap and bump the wheel of the wheelchair).⁸³

Treatment of Incoordination

Treatment of incoordination is difficult. Activities graded on the basis of motor learning and control may be helpful for attaining proximal stability and then mobility. Therapy directed toward the modulation of reflexes and abnormal synergy patterns and the enhancement of postural control mechanisms, such as the righting and equilibrium reactions, can help to improve coordination. Weight bearing, joint approximation, placing and holding techniques, and fixed points of stability (having the client stabilize his elbow or wrist on the tabletop) can be helpful.

It is critical that the therapist encourage the client to use his or her vision to help direct upper extremity movements. The therapist should begin with small ranges of movement and gradually increase them as the client progresses. Initially, work is done in the plane and direction of movement that are easiest for the client, then work progresses toward more difficult areas. Some of the involuntary movements of cerebellar or extrapyramidal origin, particularly primary movement disorders, are difficult to manage or change. Therapists have greater influence over movement disorders that are associated with traumatic brain injury and stroke.

Methods and devices to compensate for incoordination may be necessary to make BADLs and IADLs safer, more possible, and more satisfying. Obtaining a thorough occupational profile is necessary to make appropriate activity and equipment choices and to determine adaptive strategies that the client can carry over to the home environment. The physician may employ pharmacologic agents or surgical intervention in an effort to dampen tremors or other involuntary movement patterns.⁷⁰

Surgical Intervention for Movement Disorders

Neurosurgical intervention for movement disorders may include stereotactic thalatomy for ballismus, chorea (Huntington’s), Parkinson’s disease, essential tremor, and athetosis. Surgical treatment for dystonia may include rhizotomy, neurectomy, cryothalotomy, or ITB implantation.⁴⁹ Deep brain stimulation has been effective in tremor reduction in essential tremor and Parkinson’s disease.^70,93

Because of the current managed care system, occupational therapists are receiving more referrals than ever before from primary care physicians. Occupational therapists who have a basic knowledge of medical and surgical options in ameliorating motor control problems can play a triage role in suggesting referral to physician specialists.

Review Questions

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