Chapter 15 STROKE

Susan B. O’Sullivan, PT, EdD

■ EXAMINATION
The three basic components of a comprehensive physical therapy examination include patient/client
history, systems review, and tests and measures. he selection of examination procedures will vary based
on a number of factors including patient’s age, location and severity of stroke, stage of recovery, data
from initial screenings, phase of rehabilitation, and home/community/work situation, as well as other
factors.
The purposes of the examination are to
• Determine the diagnosis and classification within a specific practice pattern.
• Monitor recovery from stroke.
• Identify patients who are most likely to benefit from rehabilitation services and the most appropriate
choice of a care setting.
• Develop a specific POC, including anticipated goals, expected outcomes, prognosis, and
interventions.
• Monitor progress toward projected goals and outcomes through periodic reevaluation.
• Determine if referral to another practitioner is indicated.
• Plan for discharge.
The comprehensive examination provides the main source of information for clinical decision
making. Examination findings should be coordinated with those of the rehabilitation team in order to
arrive at an integrated POC. Box 15.3 presents Elements of the Examination of the Patient with Stroke41
and possible impairments. Many of these examination procedures, tests, and measures are discussed in
earlier chapters (see Chapters 2 through 9). This section discusses relevant aspects of the examination,
including tests and measures and diagnosis-specific instruments developed for the patient with stroke.
The therapist must differentiate between those impairments that are a direct consequence of the stroke
and those that are indirect or secondary, resulting from sequelae or complications that originate from
other systems. Aspects of functional performance, including activity limitations and restrictions in
participation, are equally important to ascertain.
Data obtained through interview with the patient/family and review of the medical record should
include information on general demographics, medical/surgical history, social and employment history,
family history, living environment, general health status and risk factors, and social and health habits.
Coexisting health problems and medications should also be identified. The older patient with stroke
typically has a history of a number of cardiovascular and other co-morbidities. Data obtained from the
history will help further focus the systems review and in-depth examination.
Cranial Nerve Integrity
 The therapist should examine for facial sensation (CN V), facial movements (CNs V and VII), and
labyrinthine/auditory function (CN VIII). he presence of swallowing difficulties and drooling
necessitates an examination of the motor nuclei of the lower brainstem cranial nerves (CNs IX, X, and
XII) affecting the muscles of the face, tongue, larynx, and pharynx. his includes determination of motor
function of the lips, mouth, tongue, palate, pharynx, and larynx. he gag reflex should be examined
because hypoactivity may lead to aspiration into the airway. Adequacy of cough mechanisms should
also be carefully examined. The therapist needs to be able to recognize the presence of swallowing
difficulties and initiate prompt referral.
The visual system should be carefully investigated, including tests for visual field defects (CN II,
optic radiation, visual cortex), acuity (CN II), pupillary reflexes (CNs II and III), and extraocular
movements (CNs III, IV, and VI). Ocular motility disturbances may be present with brainstem strokes,
such as diplopia, oscillopsia, visual distortions, or paralysis of conjugate gaze. Visual field defects
(homonymous hemianopsia) need to be differentiated from visual neglect, a perceptual deficit
characterized by an inattention to or neglect of visual stimuli presented on the involved side. The patient
with pure hemianopsia is typically aware of the deficit and may spontaneously compensate by moving
the eyes or head toward the side of deficit; the patient with visual neglect will be unaware (inattentive)
of the deficit (see Chapter 29). The use of prescriptive eyeglasses should be determined before any
testing; the therapist should ensure that eyeglasses are worn and clean.
Sensation
Deficits in somatic sensations (touch, temperature, pain, and proprioception) are common after
stroke. The type and extent of impairment are related to the location and size of the vascular lesion.
Specific localized areas of dysfunction are common with cortical lesions, whereas diffuse involvement
throughout one side of the body suggests deeper lesions involving the thalamus and adjacent structures.
Impairment in touch sensation (64% to 94%), proprioception (17% to 52%), vibration (44%), and loss of
pinprick sensation (35% to 71%) have been reported. Sensory loss has also been reported in the
ipsilateral, less affected limbs though to a lesser extent (12% to 25%). Symptoms of crossed anesthesia
(ipsilateral facial impairments with contralateral trunk and limb involvement) typify brainstem lesions.
Disturbances in cortical sensory modalities (two-point discrimination, stereognosis, kinesthesia,
graphesthesia) are also found. Profound sensory impairments will negatively affect motor performance,
motor learning, and rehabilitation outcomes and contribute to unilateral neglect and learned nonuse of
limbs. Sensory impairment is also associated with pressure sores, abrasions, and shoulder pain and
subluxation.
Central post-stroke pain (CPSP) is defined as pain arising as a direct consequence of a lesion or
disease affecting the central somatosensory system and occurs in about 10% of strokes.62 It can result
from lesions at any level of the somatosensory pathways including the medulla, thalamus, and cortex.
The thalamus is thought to play an important part in the underlying pathophysiology of central pain.
CPSP can be severe and persistent (described as “burning,” “aching”), spontaneous and intermittent
(described as “lacerating” or “shooting” pain), or evoked by mechanical (stroking the skin, pressure) or
thermal (heat or cold) stimuli. Symptoms may be focal, affecting the hand/arm or foot/leg, or in severe
cases affect half the body. Development of pain is typically within the first few months after stroke
though onset may be delayed for many months. Spontaneous recovery is rare and chronic suffering
common. The debilitating nature of CPSP frequently limits participation in rehabilitation programs and
outcomes.
A sensory examination should include testing of superficial sensations (e.g., touch, pressure, sharp or
dull discrimination, temperature) and deep sensations (proprioception, kinesthesia, vibration). Combined
(cortical) sensations such as stereognosis, tactile localization, two-point discrimination, and texture
recognition should also be examined once the integrity of the superficial sensations of touch and
pressure is established. Sensory testing procedures are described in detail in Chapter 3, Examination of
Sensory Function. The quality of sensory impairments experienced can range from mild altered
perception to marked changes in sensory thresholds, delayed perceptions, uncertainty of responses,
altered time for sensory adaptation, and sensory persistence. Impairments may be evident in one
sensory modality and not in others. Differences can also be expected between upper and lower
hemiplegic extremities, depending on lesion location. Comparisons with the intact side should be
viewed with caution because impairments may exist in the supposedly “normal” extremities due to aging
and co-morbidities. Sensory testing may be difficult or need to be deferred owing to cognitive or
communication deficits.
Flexibility and Joint Integrity
An examination of joint flexibility should include passive ROM using a goniometer, joint
hypermobility/hypomobility, and soft-tissue changes (swelling, inflammation, or restriction). The
shoulder and wrist should be examined closely because joint malalignment problems are common.
Edema of the wrist often produces malaligned carpal bones with resulting impingement during wrist
extension. Problems with spasticity may result in inconsistent ROM findings, because fluctuations in
tone may occur from one testing session to the next. Thus, tonal abnormalities should be noted at the
time of examination. Active ROM (AROM) may be limited or impossible for the patient in early or
middle recovery in the presence of paresis, spasticity, or obligatory synergies that can preclude isolated
voluntary movements. ROM limitations and developing contractures should be carefully documented.
Contractures can develop anywhere but are particularly apparent in the paretic limbs. As contractures
progress, edema and pain may develop and further restrict mobility. In the UE, limitations in the
shoulder motions of flexion, abduction, and external rotation are common. Contractures are likely in the
elbow flexors, wrist and finger flexors, and forearm pronators. In the LE, plantarflexion contractures are
common.
Motor Function
 Stages of Motor Recovery
Initially, flaccid paralysis is present (stage 1). This is replaced by the development of spasticity,
hyperreflexia, and mass patterns of movement, termed obligatory synergies, all characteristics of upper
motor neuron syndrome. Muscles involved in obligatory synergy patterns are strongly linked in a highly
stereotyped, abnormal pattern; isolated joint movements outside the obligatory pattern are not possible.
During stage 2 (early synergy), facilitatory stimuli will elicit synergies with minimal voluntary
movement. As recovery progresses, spasticity is marked with full strong obligatory synergies (stage 3).
Synergy influence begins to decline in stage 4 as some isolated out-of-synergy joint movements emerge.
During stage 5, relative independence of synergy, spasticity continues to wane and isolated joint
movements become more apparent, and during stage 6 patterns of movement are near normal. his
general pattern of recovery was initially described by Twitchell and Brunnstrom and confirmed by
additional investigators (Box 15.4). Several important points merit consideration. An overall pattern of
motor recovery exists though individual recovery is highly variable. Some patients experience mild
involvement with early full recovery whereas other patients demonstrate severe involvement with
incomplete recovery.
Tone
Flaccidity (hypotonicity) is present immediately after stroke and is due primarily to the effects of
cerebral shock. It is generally short-lived, lasting a few days or weeks. Flaccidity may persist in a small
number of patients with lesions restricted to the primary motor cortex or cerebellum. Spasticity
(hypertonicity) emerges in about 90% of cases and occurs on the side of the body opposite the lesion.
Spasticity in upper motor neuron syndrome occurs predominantly in antigravity muscles (see Chapter 5,
Table 5.3). In the patient with stroke, UE spasticity is frequently strong in scapular retractors; shoulder
adductors, depressors, and internal rotators; elbow flexors and forearm pronators; and wrist and finger
flexors. In the neck and trunk, spasticity may cause increased lateral flexion to the hemiplegic side. In
the LE, spasticity is often strong in the pelvic retractors, hip adductors and internal rotators, hip and knee
extensors, plantarflexors and supinators, and toe flexors. Spasticity results in tight (stiff) muscles that
restrict volitional movement. Posturing of the limbs (e.g., a tightly fisted hand with the elbow flexed and
held tightly against the chest or a stiff extended knee with a plantarflexed foot) is common with
moderate to severe spasticity. Spastic posturing can lead to development of painful spasms (similar to
muscle cramping), degenerative changes, and fixed contractures. The automatic adjustment of postural
muscles that occurs normally in preparation for and during a movement task is also impaired. Thus,
patients with stroke may lack the ability to adjust and stabilize proximal limbs and trunk appropriately
during movement, with resulting postural abnormalities, balance impairments, and increased risk for
falls.
An examination of tone is essential. Passive motion testing can be used to determine the presence of
hypotonicity or spasticity. Severity of spasticity can be graded on the basis of resistance to passive
stretch using the Modified Ashworth Scale (MAS) (see Chapter 5, Table 5.4). The position of the
affected limbs at rest (resting postures) and during voluntary movements should be observed for tonal
influences.
Reflexes
Reflexes are altered and also vary according to the stage of recovery. Initially, stroke results in
hyporeflexia with flaccidity. When spasticity and synergies emerge, hyperreflexia is seen. Deep tendon
reflexes are hyperactive and patients may demonstrate clonus, claspknife response, and a positive
Babinski, all consistent findings of upper motor neuron syndrome (see Chapter 5, Table 5.5).
Tonic reflexes may appear in a readily identifiable form similar to that seen in other types of
neurological insult (e.g., traumatic brain injury [TBI], cerebral palsy [CP]). Thus, movement of the head
or position of the body may elicit an obligatory change in resting tone or movement of the extremities.
he most commonly seen is the asymmetrical tonic neck reflex (ATNR) in which head rotation causes
elbow extension of the UE on the jaw side with elbow flexion of the opposite skull limb (see Chapter 5,
Table 5.7).
Associated reactions are also typically present in patients with stroke who exhibit strong spasticity
and obligatory synergies. These consist of unintentional movements of the hemiparetic limb caused by
voluntary action of another limb or by other stimuli such as yawning, sneezing, or coughing. For
example, the patient vigorously contracts the elbow flexors of the stronger UE; the hemiparetic elbow
also flexes. Or the patient flexes the hip to lift the hemiparetic LE in sitting; the hemiparetic UE also
flexes. Associated reactions can limit functional performance, especially in the UE. An examination of
stretch reflexes and pathological reflexes (e.g., Babinski, tonic reflex acti vity, associated reactions)
should be performed (see Chapter 5, Table 5.7).
Voluntary Movements
Abnormal and highly stereotyped obligatory synergies emerge with spasticity following stroke. Thus,
the patient is unable to perform an isolated movement of a single limb segment without producing
movements in the remainder of the limb. For example, efforts to flex the elbow also result in shoulder
flexion, abduction, and external rotation. The patient is severely limited in the ability to adapt
movements to varying task or environmental demands. Obligatory synergies can appear reflexively
during very early recovery, or as voluntary movements. As recovery progresses they become stronger
and are linked to the presence and severity of spasticity. Two distinct abnormal synergy patterns have
been described for each extremity: a flexion synergy and an extension synergy (Table 15.6). An
inspection of the synergy components reveals that certain muscles are not usually involved in either the
flexion or extension synergy. These muscles include the (1) latissimus dorsi, (2) teres major, (3) serratus
anterior, (4) finger extensors, and (5) ankle evertors. These muscles, therefore, are generally difficult to
activate while the patient is exhibiting these patterns. Obligatory synergies are often incompatible with
normal ADL and functional mobility skills. For example, the patient with a strong LE extensor synergy
will have difficulty walking owing to foot plantarflexion and inversion with hip and knee extension and
adduction (scissoring gait pattern). As recovery progresses, spasticity and obligatory synergies begin to
disappear and more normal synergies with isolated joint control become possible.
Voluntary movement patterns should be examined for synergy influence. he therapist bases the
examination of synergy dominance on knowledge of the typical components of the synergies. It is
possible for one limb to vary significantly from the other (e.g., the UE may demonstrate more
synergistic dominance than the LE). Synergistic dominance versus isolated joint control may also vary
within a limb (e.g., the shoulder may demonstrate more isolated control than the wrist and hand). During
later recovery, voluntary movements demonstrate isolated joint control and appear more normal in the
absence of spasticity and synergy restrictions. See discussion of the Fugl-Meyer Assessment of Physical
Performance later in this section.
Coordination
Proprioceptive losses can result in sensory ataxia. Strokes affecting the cerebellum typically produce
cerebellar ataxia (e.g., lateral medullary syndrome, basilar artery syndrome, pontine syndromes) and
motor weakness. The resulting problems with timing and sequencing of muscles can significantly impair
function and limit adaptability to changing task and environmental demands. Basal ganglia involvement
(posterior cerebral artery syndrome) may lead to slowed movements (bradykinesia) or involuntary
movements (choreoathetosis, hemiballismus).
Coordination tests can be used to examine control. The therapist focuses on elements of speed/rate
control, steadiness, response orientation, and reaction and movement times. Fine motor control and
dexterity should be examined using writing, dressing, and feeding tasks (see Chapter 6, Examination of
Coordination and Balance). Although more significant impairments can be expected on the hemiparetic
side, it is important to remember that subtle deficits can occur on the less involved side. hus, it is
important to examine both unilateral and bilateral movements, including symmetrical, asymmetrical, and
unrelated movements. Performance may vary as the patient moves from supine to sitting to standing
positions with the resultant increased postural demands and greater degrees of freedom.
Motor Programming
Motor praxis is the ability to plan and execute coordinated movement. Lesions of the premotor
frontal cortex of either hemisphere, left inferior parietal lobe, and corpus callosum can produce apraxia.
Apraxia is more evident with left hemisphere damage than right and is commonly seen with aphasia.
The patient demonstrates difficulty planning and executing purposeful movements that cannot be
accounted for by any other reason (i.e., impaired strength, coordination, sensation, tone, cognitive
function, communication, or uncooperativeness). There are two main types of apraxia. Ideational apraxia
is an inability of the patient to produce movement either on command or automatically and represents a
complete breakdown in the conceptualization of the task. The patient has no idea how to do the
movement and thus cannot formulate the required motor programs. With ideomotor apraxia the patient
is unable to produce a movement on command but is able to move automatically. Thus, the patient can
perform habitual tasks when not commanded to do so and often perseverates, repeating the activity over
and over. Significant information on apraxia will be gained by close collaboration with the occupational
therapist. The reader is referred to Chapter 27 for a more complete discussion of these deficits and their
management.
Muscle Strength
Paresis is found in 80% to 90% of all patients after stroke and is a major factor in impaired motor
function, activity limitation, and disability. Patients are unable to generate the force necessary for
initiating and controlling movement. he degree of primary weakness is related to the location and size of
the brain injury and varies from a complete inability to achieve any contraction (hemiplegia) to
hemiparesis with measurable impairments in force production. Deficits on the contralateral side
typically include hemiparesis (opposite UE and LE). Owing to the high incidence of MCA strokes, the
UE is frequently more affected than the LE. About 20% of individuals with MCA strokes fail to regain
any functional use of the affected UE. Typically, distal muscles exhibit greater strength deficits than
proximal. his can be explained by the greater facilitation of distal muscles than proximal by the
corticospinal system. Mild weakness also occurs on the ipsilateral, “supposedly normal” side. This can
be explained by the fact that only 75% to 90% of the corticospinal fibers cross in the medulla to the
contralateral side. he remainder are transmitted to the spinal cord ipsilaterally in the anterior or ventral
corticospinal tract. Once in the spinal cord some of these fibers cross while the rest remain uncrossed,
thereby explaining bilateral weakness. The amount of weakness experienced by the patient may also
vary according to the extent and level of inactivity (disuse atrophy) and the specific functional tasks
attempted. Thus, a patient may appear stronger in some tasks than others.
Post-stroke weakness is associated with a number of changes in both the muscle and the motor unit.
Changes occur in muscle composition, including atrophy of muscle fibers. here is a selective loss of type
II fast-twitch fibers with subsequent increase in the percentage of type I fibers (a finding also reported in
the elderly). This selective loss of type II fibers results in slowed force production, difficulty with
initiation and production of rapid, high-force movements, and rapid onset of fatigue. The number of
functioning motor units and discharge firing rates also decrease. his is explained by the presence of
transsynaptic degeneration of alpha motor neurons that occurs with loss of corticospinal innervation.
Abnormal recruitment of motor units with altered timing occurs. Thus, patients demonstrate inefficient
patterns of muscle activation and higher levels of co-contraction. his opposing muscle activation can
contribute to muscle weakness and incoordination. These impairments in force production and
coordination have been reported in both paretic and less affected UEs after stroke.79,80 Patients
demonstrate increased effort and fatigability with frequent complaints of feelings of weakness.
Denervation potentials on electromyography (EMG) are common, also the result of denervation changes
in the corticospinal tracts. Overall reaction times are increased, a finding also reported in the less
affected extremities and for the elderly in general. Movement times are prolonged, a timing abnormality
that contributes to impairment of coordinated motor sequences.
Although an examination of strength is necessary, the traditional manual muscle test (MMT) poses
problems of validity in the presence of strong spasticity, reflex, and synergy dominance. he patient who
is not able to isolate specific movements should not be examined using MMT. In this situation, an
estimation of strength can be made from observation of active movements during functional activities
(functional strength testing). The patient’s self-report can also yield important indicators of weakness
and fatigue. The patient in later recovery with improving motor control and isolated movement can be
examined using traditional MMT or handheld dynamometry. Use of a computerized isokinetic
dynamometer can reveal important objective data regarding forces generated, peak torque, time to peak
torque, and total work normalized to body weight. See Chapter 4, Musculoskeletal Examination.
Postural Control and Balance
Postural control and balance are disturbed following stroke with impairments in alignment, stability,
symmetry, and dynamic balance common. Common postural alignment deviations following stroke are
presented in Table 15.7.
Balance impairments may exist when reacting to a destabilizing external force (reactive postural
control) and/or during self-initiated movements (proactive or anticipatory postural control). Thus, the
patient may be unable to maintain stable balance in sitting or standing or to move in the posture without
loss of balance. Disruptions of central sensorimotor processing contribute to an inability to recruit
effective postural strategies and adapt postural movements to changing task and environmental
demands. Patients with stroke typically demonstrate uneven weight distribution and increased postural
sway in standing (a finding characteristic of the elderly in general). Delays in the onset of motor activity,
abnormal timing and sequencing of muscle activity, and abnormal co-contraction result in
disorganization of normal postural synergies. For example, proximal muscles are typically activated in
advance of distal muscles or, in some patients, very late (a finding also found in many elderly).
Compensatory responses typically include excessive hip and knee movements. Corrective responses to
perturbations or destabilizing forces are inadequate and result in loss of balance and frequent falls.
Patients with hemiplegia typically fall in the direction of weakness.
Static and dynamic balance control should be examined in sitting and standing. he patient’s ability to
maintain a stable position (steadiness) and position (symmetry) within the base of support (BOS) is
determined. Dynamic stability control can be examined by having the patient move within a given
posture (weight shift) or reach within his or her limits of stability (LOS). The patient should be
encouraged to shift weight in all directions, especially to the more involved side where greater
impairments are expected. Functional tasks that utilize moving from one posture to another (e.g.,
supineto-sit, sit-to-stand) can also be used to examine dynamic postural control.
 Performance-based tests can be used to examine postural control and balance following stroke. hese
tests have been examined for reliability and/or validity and are reviewed in Chapter 6.
• The Berg Balance Scale (BBS)
• The Performance-Oriented Mobility Assessment (POMA, Tinetti)
• The Functional Reach Test (RT) and the Multidirectional Reach Test (MDRT)
• The Timed Up and Go Test (TUG)
• The Clinical Test for Sensory Interaction in Balance (CTSIB)
Stroke-specific tests of postural control and balance include the following:
• The Postural Assessment Scale for Stroke Patients (PASS) was developed to examine the postural
abilities of patients with acute stroke. It includes 12 items that examine sitting and standing without
support, standing on the paretic LE, and changing posture (supine–to–affected side, supine–to–
unaffected side, supine-to-sitting, sitting-to-standing, and standing picking a pencil off the floor). It is
scored using an ordinal scale with descriptors ranging from cannot perform to perform with little help, to
perform without help. It demonstrates good construct validity and high interrater and intrarater reliability
(0.88 and 0.72, respectively).
• The Trunk Impairment Scale was developed to evaluate motor impairment of the trunk after stroke.
It includes 3 items of static control, 10 items of dynamic balance control, and 4 items of coordination. he
items are tested in the sitting position (edge of bed or treatment table) without back or arm support. Each
item is performed three times with the highest score accepted. Scores range from a minimum of 0
(unable) to a maximum of 23.
• The Function in Sitting Test (FIST) was developed by expert consensus as a test for sitting balance
deficits in adults after acute stroke. It includes 14 items that examine static and dynamic balance
function. Static sitting (steady state) is examined by having the patient sit with eyes open and eyes
closed. Reactive challenges are introduced using sternal nudges (anterior, posterior, and lateral).
Dynamic, anticipatory (proactive) challenges are introduced using body segment motions (head turns,
lifting foot up on the least involved side, turning and picking an object up placed behind the patient,
forward and lateral reach, picking an object up off the floor), and scooting movements (posterior,
anterior, lateral). Eleven items examine anterior/posterior control and three items examine
lateral/rotational control. Scoring is based on a 5-point ordinal scale that includes the following: No
Balance (0/4), Poor (1/4), Fair (2/4), Good (3/4) to Normal (4/4). Specific descriptive criteria are given
for each grade for static and dynamic control. Maximum score is 56 (similar to the BBS). Initial
reliability and validity of the FIST has been demonstrated; however, additional testing is indicated.
Ipsilateral Pushing
Ipsilateral pushing (also known as pusher syndrome or contraversive pushing) is an unusual motor
behavior characterized by active pushing with the stronger extremities toward the hemiparetic side with
a lateral postural imbalance. The end result is a tendency to fall toward the hemiparetic side. Ipsilateral
pushing occurs in about 10% of patients with acute stroke and results from stroke affecting the
posterolateral thalamus. The result is an altered perception of the body’s orientation in relation to
gravity. Karnath et al found that patients experienced a misperception of subjective postural vertical
position, perceiving their body as vertical when it was actually tilted about 20° toward the hemiparetic
side. They also found that the visual and vestibular input for orientation perception to vertical remained
intact as patients were able to align their bodies with the help of visual cues and conscious strategies. No
significant association between ipsilateral pushing and hemineglect, anosognosia, aphasia, or apraxia has
been found.
Functional skills are significantly impaired for patients with ipsilateral pushing. During sitting, the
push results in a strong lateral lean toward the weaker side; when sitting in a wheelchair, this often
thrusts the patient over onto the wheelchair arm. In standing, a strong push creates an unstable situation
with a high risk of falls because the hemiparetic LE typically cannot support the body weight. The
patient shows no fear even when active pushing leads to instability and strongly resists any attempts to
passively correct posture to midline, symmetrical weight-bearing. This pattern is totally opposite the
expected postural deficiency seen in most patients after stroke, that is, increased weight-bearing to the
stronger side to compensate for deficits on the hemiparetic side. Patients also typically demonstrate
severe problems in transfers and gait. During transfers to the less involved side, the patient demonstrates
increased pushback away from that side.
During walking, the patient typically exhibits inadequate extension of the hemiparetic LE with
inability to transfer weight toward the less involved LE. During swing, strong scissoring (adduction) of
the more involved LE is typically evident. he use of a cane during ambulation is problematic because
patients use the cane to increase push to the hemiplegic side. Pedersen et al demonstrated that patients
with ipsilateral pushing behavior have poorer rehabilitation outcomes with longer hospital stays and
prolonged recovery times. They also had significantly lower functional scores on admission and
discharge with increased levels of dependence at discharge. However, with training, the brain can
compensate well. he syndrome is rarely still evident at 6 months.
Examination of the patient with ipsilateral pushing should include a focus on several criteria of
behavior, including the following: (1) spontaneous body posture with tilting toward the more paretic
side, (2) an increase of pushing force by the less involved extremities evidenced by increased abduction
and extension, and (3) resistance to passive correction of the posture. Broetz and Karnath94 developed
the Clinical Assessment Scale for Contraversive Pushing (SCP), which scores each of these three criteria
in both sitting and standing. A subjective rating scale is used. he scores for each criteria range from 0 to
1. Because the criteria are examined in both sitting and standing, the maximum for each is 2 with a
maximum possible overall score of 6. Patients are diagnosed with pushing behaviors if all three criteria
are present and a score of 1 or more exists in each of the three criteria. Functional examination will
reveal consistent difficulties with transfers to the less affected side, and difficulties with independent
sitting, standing, and walking.