Stroke Rehabilitation: Michael R. Yochelson, Andrew Cullen Dennison, SR., and Amy L. Kolarova
Stroke Rehabilitation: Michael R. Yochelson, Andrew Cullen Dennison, SR., and Amy L. Kolarova
Stroke Rehabilitation
M I C H A E L R . YO CHELS O N, A ND REW CU LLE N D ENNISO N, SR. ,
A N D A M Y L . KO LAR OVA
954
CHAPTER 44 Stroke Rehabilitation 955
Premotor Motor
area cortex
Knee
Angular gyrus
Hip
Trunk
Shoulder
Elbow
Wrist
Hand
Fingers
Thumb Parietal
Neck
Brow
Eyelid
Face Caudate
Lips nucleus
Jaw
Tongue
Pharynx Internal capsule
Frontal
Thalamus
Occipital
Lentiform
nucleus
Temporal Broca
area
Wernicke area
Primary
A Broca area auditory cortex
Arcuate
fasciculus
Hip Wernicke
Trunk
Shoulder Knee area
Elbow Ankle
Wrist
Hand Caudate
Fingers
Neck nucleus Geniculocalcarine
Brow tracts
Eyelid Toe Thalamus
Face
Lips
Lentiform Visual
Jaw C cortex
Tongue
nucleus
Pharynx
B
• Fig. 44.1(A–C) Surface anatomy of the cerebral cortex. (From https://netterimages.com/cerebrum-lateral-
views-labeled-anatomy-atlas-5e-physiology-frank-h-netter-5274.html.)
and tract run along the inferior aspect of the frontal lobe bilat- inferior to the occipital lobe is the cerebellum. The primary
erally near the interhemispheric fissure. The most anterior por- visual cortex is located in the occipital lobe.
tion is the frontal pole. • The insular cortex is covered laterally by a lip of the frontal
• The parietal lobe is separated from the frontal lobe by the cen- cortex anterior and parietal cortex posteriorly.
tral sulcus anteriorly but has no clear demarcation from the • Subcortical refers to several areas including the caudate nucleus
temporal lobes inferolaterally. The demarcation for the occipi- and putamen (striatum), globus pallidus, subthalamic nucleus,
tal lobe is at the parieto-occipital sulcus. Directly posterior to and substantia nigra. The caudate and putamen are separated
the central sulcus lies the postcentral gyrus/sulcus (primary by the internal capsule. The putamen forms the lateral portion,
somatosensory cortex). fusing with the head of the caudate anteriorly and ventrally.
• The temporal lobe has no clear demarcation from the pari- Just medial to the putamen is the globus pallidus, which has
etal or occipital lobes; it lies inferior to the frontal lobe, internal and external segments. The thalamus sits nearby, sepa-
separated by the Sylvian fissure. The most anterior portion rated from the lentiform nucleus by the posterior limb of the
is the temporal pole. The primary auditory cortex is located internal capsule. The substantia nigra is just dorsal to the cere-
near the Sylvian fissure in the superior medial portion of the bral peduncles and is separated from the globus pallidus by the
temporal lobe. internal capsule.
• The occipital lobe has no clear demarcation from the temporal • The brainstem is divided into the midbrain, pons, and medulla.
lobe. The parieto-occipital sulcus separates it from the parietal The midbrain connects the pons and cerebellum to the thal-
lobe. The most posterior portion is the occipital pole. Directly amus and cerebral hemispheres. It contains the cerebral
956 SECTION 4 Issues in Specific Diagnoses
Anterior peduncles as well as the aqueduct between the third and fourth
communicating ventricles. The pons links information from the medulla to the
artery
higher cortical areas of the cortex and is also connected to the
Recurrent artery
of Heubner
cerebellum through the middle cerebellar peduncle; it includes
A2 segment
the pontine reticular formation as well as centers for respira-
Anterior cerebral
artery A1 segment tion. The medulla contains the crossing of tracts relaying infor-
mation between the cortex and spinal cord. It contains centers
Middle for respiration as well as vasomotor and cardiac function and
cerebral M1 segment the mechanisms for cough, gag, and swallowing.
artery
Internal • The cerebellum consists of a midline vermis and two cerebel-
Anterior carotid lar hemispheres. The largest fissure is called the primary fissure
choroidal artery
artery and separates the cerebellum into anterior and posterior lobes.
Posterior
P2 segment The posterolateral fissure separates the posterior lobe from the
communicating flocculonodular lobe. The tonsils are at midline, and laterally
artery there are three cerebellar peduncles: the superior (which is the
P1 segment
Posterior cerebral most medial), the middle (which is the most lateral) and the
artery Basilar inferior (which is the most inferior).14,40,107␣
artery
Vascular Anatomy
The circle of Willis (see Fig. 44.2) is supplied by the right and
• Fig. 44.2Territories of the cerebral arteries. (From https://netterimages. left ICAs anteriorly and the basilar artery posteriorly. Prior to
com/color-illustration-of-territories-of-the-cerebral-arteries-labeled-jones- the bifurcation of the MCA and ACA, the ICA gives off the
1e-neurology-neurosciences-frank-h-netter-6951.html.)
Anterior
cerebral
artery
Posterior cerebral
A Middle cerebral artery B artery
M4
M3 M2 M1 Lateral
lenticulostriate Middle cerebral
C arteries artery
• Fig. 44.3 (A–C) Circle of Willis. (From https://www.netterimages.com/cerebral-arterial-circle-willis-labeled-
anatomy-atlas-5e-general-anatomy-frank-h-netter-4694.html.)
CHAPTER 44 Stroke Rehabilitation 957
TABLE
44.1
Cerebellar Stroke Syndromes
Rostral cerebellar syndrome Subthalamic region, thalamus, occipitotemporal Coma ± tetraplegia, ipsilateral dysmetria, Horner
lobes, lateral tegmental area of upper pons syndrome, contralateral pain/temp deficit,
cranial nerve IV palsy, dysarthria, headache,
dizziness, emesis, delayed coma
Medial cerebellar syndrome Lateral area of the lower pons Ipsilateral cranial nerve V, VII, VIII, Horner syndrome,
dysmetria, contralateral pain/temp deficit
Caudal cerebellar syndrome Dorsolateral medullary area Vertigo, headache, emesis, ataxia, delayed coma
Modified from Zorowitz RD: Stroke syndromes: infratentorial. In Stein J, Harvey RL, Winstein CJ, et al, editors: Stroke recovery and rehabilitation, ed 2, New York, 2015, Demos Medical Publishing.
TABLE
44.2
Major Artery Clinical Syndromes
Artery Deficits
L MCA S R face/arm weakness, Broca/nonfluent aphasia, ± sensory loss
L MCA I Fluent/Wernicke aphasia, R visual field deficit. R face/arm ± sensory loss; motor findings absent; confused; mild R weakness
L MCA D R pure motor hemiparesis, larger infarcts may produce cortical deficits
L MCA stem Combination of all above with R hemiplegia/anesthesia, R homonymous hemianopia and global aphasia; L gaze preference
R MCA S L face/arm weakness, L hemineglect to a variable extent, ± sensory loss
R MCA I Profound L hemineglect; L visual field and somatosensory deficits but hard to test due to neglect; mild L weakness may be present; R gaze
R MCA D L pure motor hemiparesis, larger infarct can include cortical and neglect
R MCA stem Combination of above with L hemi, L homonymous hemi, and profound L neglect with R gaze preference
L ACA R leg weakness with sensory loss, grasp reflex, frontal lobe behaviors, transcortical aphasia ± larger may cause R hemi with lower
extremity > upper extremity relatively
R ACA L leg weakness with sensory loss, grasp reflex, frontal behaviors, L hemineglect; larger infarcts may cause full L hemi
L PCA R homonymous hemianopia; extension to the splenium of the corpus callosum can cause alexia w/o agraphia; larger infarcts with thala-
mus and IC may cause aphasia, R hemisensory loss, and R hemiparesis
R PCA L homonymous hemianopia; larger infarcts with thalamus and IC may cause L hemisensory loss and L hemiparesis
ACA, Anterior cerebral artery; D, deep; I, inferior; IC, internal capsule; L, left; MCA, middle cerebral artery; PCA, posterior cerebral artery; R, right; S, superior.
Modified from Blumenfeld H: Neuroanatomy through clinical cases, ed 2, Sunderland, 2010, Sinauer Associates.
TABLE
44.3
Common Lacunar Syndromes
IC, Internal capsule; MCA, middle cerebral artery; PCA, posterior cerebral artery; VPL, ventral posterolateral nucleus.
Modified from Blumenfeld H: Neuroanatomy through clinical cases, ed 2, Sunderland, 2010, Sinauer Associates.
958 SECTION 4 Issues in Specific Diagnoses
TABLE
44.4
Common Brainstem Syndromes
Lateral medulla Wallenberg syndrome Vertebral > PICA CN XII, vestibular, and trigeminal Ipsilateral ataxia, vertigo, nystagmus,
nuclei, cerebellar peduncle, nausea, face decreased pain and
spinothalamic tract, sympa- temperature, Horner syndrome and
thetic tract, nucleus ambiguus decreased taste. Contralateral body
and solitarius decreased pain/temp, hoarseness,
dysphagia
Pons
Medial pons 1. Dysarthric hemipa- Paramedian branches of 1. Corticospinal/corticobulbar tract 1. Contralateral face/arm/leg weak-
basis resis the basilar and vertebral 2. Above + pons nuclei and ponto- ness, dysarthria
2. Ataxic hemiparesis cerebellar tract 2. All the above plus contralateral
ataxia
Medial pons 1. Millard-Gubler Branches of basilar, 1. Corticospinal/corticobulbar tract 1. Contralateral face/arm/leg weakness
basis/teg- syndrome ventral, and dorsal 2. Corticospinal/corticobulbar tract 2. Contralateral face/arm/leg weakness
mentum 2. Foville syndrome territories plus facial colliculus plus dysarthria with ipsilateral face
weakness/gaze
Lateral caudal AICA syndrome AICA Middle cerebellar peduncle, Ipsilateral ataxia, facial decrease in pain/
pons vestibular, trigeminal nuclei, temp, Horner syndrome, contralateral
spinothalamic, and sympathetic body decrease in pain/temp, vertigo,
tracts nystagmus
Dorsolateral SCA syndrome SCA Superior cerebellar peduncle, Ipsilateral ataxia plus possible AICA inclu-
rostral pons lateral structures sions
Bilateral pons Locked-in syndrome Basilar artery Bilateral corticospinal/corticobulbar/ Tetraplegia, facial palsy with sparing
pontine, reticular formation of eye blinking, bilateral horizontal
gaze palsy
Midbrain
Midbrain basis Weber syndrome PCA, basilar CN III, cerebral peduncle Ipsilateral third nerve palsy and contra-
lateral hemiparesis
Midbrain teg- Claude syndrome PCA, basilar CN III, superior cerebral peduncle, Ipsilateral third nerve palsy, contralat-
mentum red nucleus eral ataxia, rubral tremor
Midbrain Benedikt syndrome PCA, basilar All of the above plus substantia Ipsilateral third nerve palsy, contralateral
basis and nigra ± ML and ST tract hemiparesis, ataxia, tremor and
tegmentum involuntary movements
Dorsal rostral Parinaud syndrome PCA, basilar Rostral interstitial MLF Multiple oculomotor abnormalities
midbrain include upgaze palsy, tonic down-
ward gaze (“setting sun”), vertical
nystagmus, bilateral ptosis
Rostral Top of the basilar PCA, basilar Rostral midbrain, thalami, pos- Parinaud + abulia, hypersomnolence,
midbrain syndrome terior temporal and occipital memory impairment
lobes
AICA, Anteroinferior cerebellar artery; ML, medial lemniscus; MLF, medial longitudinal fasciculus; PCA, posterior cerebral artery; PICA, posteroinferior cerebellar artery; SCA, superior cerebellar artery;
ST, spinothalamic tract.
Modified from Blumenfeld H: Neuroanatomy through clinical cases, ed 2, Sunderland, 2010, Sinauer Associates.
CHAPTER 44 Stroke Rehabilitation 959
ophthalmic, anterior choroidal, and PComm arteries. From the (rtPA) alteplase.27,51 There is very clear decrement in benefit and
ACA arise the anterior communicating artery, recurrent artery of increased risk of complications as time from onset elapses. The
Heubner, and the pericallosal and medial lenticulostriate arter- benefit of rtPA clearly outweighs the risk in the first 3 hours. The
ies. The MCA provides the lateral lenticulostriate, branching into benefit-to-risk ratio worsens over the next 90 minutes, but the risk
the superior (S), inferior (I), and deep (D) branches bilaterally for severe complications, primarily intracranial hemorrhage (ICH),
(MCA S, MCA I, and MCA D). The basilar artery bifurcates into still remains relatively low. Between 4.5 and 6 hours, however, the
the posterior cerebral artery (PCA), with the circle being com- risk of ICH increases, and the benefit decreases to the point that
pleted by the anastomoses of the PComm arteries with the PCA rtPA is no longer recommended beyond the 4.5-hour window. Of
bilaterally. The major vascular anatomy of the brain is shown in note, there are multiple contraindications to the administration of
Fig. 44.3. The vertebral arteries provide the majority of the blood rtPA, one of which is prior stroke or serious head trauma within the
supply to the brainstem structures and merge into the basilar preceding 3 months. Therefore this would rarely be appropriate for
artery, which provides the pontine and medullary branches. The a patient who experiences a recurrent stroke during his or her inpa-
posteroinferior cerebellar artery (PICA) supplies the medulla as tient rehabilitation period.37 A cardiac evaluation should include
well as portions of the spinothalamic tract. The anteroinferior an electrocardiogram (ECG), troponin, and chest x-ray. However,
cerebellar artery (AICA) supplies the pons, the facial and spinal these should not delay administration of the rtPA. Unlike intrave-
trigeminal nucleus and tract, as well as the inferior and middle nous rtPA, intraarterial thrombolytics can be given up to 6 hours
cerebellar peduncles and spinothalamic tract. Blood supply for after stroke onset.
the cerebellum is provided by three branches of the vertebral and In the inpatient rehabilitation setting, a stroke patient with
basilar arteries. The PICA supplies the lateral medulla, inferior a new or worsening neurologic deficit should be evaluated with
half of the cerebellum, and inferior vermis. The AICA supplies the noncontrast CT to make sure that there has not been hemor-
inferolateral pons, middle cerebellar peduncle, and ventral ante- rhagic conversion. Given the increased risk of seizures poststroke
rior strip of cerebellum between the PICA and superior cerebellar (approximately 10% incidence),12,42 an electroencephalogram
artery (SCA) territories. The SCA supplies the upper lateral pons, (EEG) is indicated if the neuroimaging does not indicate a new
superior cerebellar peduncle, and most of the superior half of the stroke or bleed.
cerebellar hemisphere.14,107␣ Mechanical thrombolysis expands the treatment window
of acute stroke up to 24 hours.22,39,86,92 However, it is lim-
Initial Workup/Management ited to large-vessel thrombotic strokes typically affecting the
carotid or MCA territory. These techniques can also be used
This section refers primarily to those patients being evaluated for in patients who have already received intravenous rtPA.76 It
a first stroke (or a recurrence greater than 3 months following a is possible that these interventions could be used in some-
previous stroke). Many of the principles in this section apply even one who has more recently had a stroke; however, the stud-
during a recurrence in the first 30 days, which is the period dur- ies typically required a prestroke Rankin score of 0 to 1, so it
ing which the patient is at highest risk for recurrence. However, remains unclear whether it would be appropriate for patients
certain contraindications, particularly related to anticoagulation, who are still in inpatient rehabilitation, as they would have
in the setting of acute stroke are also discussed. a higher Rankin score. The DAWN and DEFUSE 3 studies
Just as the general population should be able to recognize the demonstrate benefit of mechanical thrombolysis up to 24 and
warning signs of stroke, so should the nurses and other clinicians 16 hours, respectively, after stroke onset, allowing these treat-
caring for patients who are in the time window for increased risk of ments to be used for “wakeup” strokes.5,76,77 Previously, treat-
recurrence. Symptoms include the acute onset of focal neurologic ment in this population was extremely limited, because if you
symptoms (e.g., weakness, dizziness, or slurred speech), mental sta- could not determine the exact onset of symptoms, the patient
tus changes, or sudden severe headaches. Initiation of an emergency would be ineligible for treatment with intravenous rtPA and
response process is paramount as time is of the essence. Standard usually also ineligible for intraarterial thrombolysis.
protocols—including assessment, obtaining intravenous access, Hypertension is more commonly seen than hypotension. “Per-
administration of oxygen and appropriate fluids, and management missive hypertension” is reasonable, but significant elevations,
of hypotension and hypoglycemia—should be followed. The emer- particularly if a fibrinolytic therapy is being used, should be cor-
gency department should be ready to receive a stroke patient and rected. Overcorrection must be avoided, as arterial hypotension
have the physician assessment, including the National Institutes of is associated with a worse outcome. If the patient received fibri-
Health Stroke Scale (NIHSS), completed within minutes of arrival, nolytic therapy, blood pressures should be maintained below 185
and also a noncontrast computed tomography (CT) image of the mm Hg systolic and 110 mm Hg diastolic. If no fibrinolytic ther-
head within 20 minutes of arrival. A noncontrast magnetic reso- apy was used, the blood pressure may be allowed to go to 220 mm
nance imaging (MRI) scan of the brain using diffusion-weighted Hg systolic and 120 mm Hg diastolic. If the blood pressure must
imaging (DWI) is more sensitive than CT to ischemia, particularly be managed, an appropriate goal is a decrease of 15% gradually
in the posterior fossa and brainstem, but is often not feasible because over 24 hours. For patients with hypertensive lacunar infarcts and
of access or time constraints.51 Evaluation should include a thor- those with diabetes, it is recommended that their systolic blood
ough history to exclude stroke mimics such as seizure, migraine, and pressure is maintained below 130 mm Hg.11,57 Although there
conversion disorder. These mimics must be considered in patients is no clearly defined goal for blood pressure control poststroke, a
who are being evaluated for recurrent strokes as well as for primary Cochrane review by Zonneveld et al. did find a trend for “inten-
stroke.94 Seizures in particular should be considered if the new neu- sive blood pressure lowering in reducing the risk for recurrent
rologic deficit correlates with the same territory as the initial stroke. stroke and major vascular events.”106 In addition to blood pressure
If it is determined that the patient has suffered an ischemic stroke control, the patient’s oxygen saturation should be maintained at
and completes the workup within 4.5 hours of onset, he or she is a 94% or higher. Hypovolemia should be rapidly treated and main-
candidate for intravenous recombinant tissue plasminogen activator tenance intravenous fluids should be run.
960 SECTION 4 Issues in Specific Diagnoses
Hyperglycemia should also be treated, as it has been associ- of their stroke should continue this—the reason being that, in a
ated with worse outcomes. Very tight control is inadvisable, as the small randomized trial, it was noted that those who discontin-
patient could become hypoglycemic, particularly in the postacute ued had greater odds of death or dependency at 3 months post-
period when he or she may have a lower caloric intake than usual stroke.13,51 Although this does not necessarily imply that starting
and is increasing physical activity during therapy. A goal of 140 to a patient on a statin poststroke will provide neuroprotection, it is
180 mg/dL in the acute period is reasonable.51 recommended to continue the statin in those patients who had
Anticoagulation is often necessary for the treatment of already been taking it.␣
venothrombosis, atrial fibrillation, or other cardiac issues. It is
important that it not be started within 24 hours of the use of Complications of Stroke
intravenous rtPA. There is no indication for emergent anticoagu-
lation in the face of acute stroke or neurologic worsening. The risk Guidelines for the management of adult stroke rehabilitation and
of ICH is increased, and an improved outcome has not been dem- recovery have been published by the American Heart Associa-
onstrated. It has not been shown to reduce the risk of stroke recur- tion (AHA) and the American Stroke Association (ASA) and have
rence even in the face of a cardioembolic stroke.51 Dabigatran has been endorsed by the American Academy of Physical Medicine
been approved for the prevention of stroke associated with atrial and Rehabilitation and the American Society of Neurorehabilita-
fibrillation, but the timing of its initiation poststroke has not been tion.105 These guidelines will be referenced in the discussion of
established. both the prevention and management of complications as well
Antiplatelet agents should be used to reduce the risk of stroke as the rehabilitation treatment of stroke in this chapter, exten-
and stroke recurrence.24 Aspirin may be initiated at 325 mg sively referring to levels of evidence as noted in Fig. 44.4. Note
within 24 to 48 hours of onset of symptoms. If clopidogrel is that unless otherwise noted, all references to levels of evidence
being used as the antiplatelet agent, initiating treatment with the using the Level A–C/Class I–III system are in reference to the
maintenance dose of 75 mg/day will delay platelet inhibition by 2016 AHA/ASA Guidelines for Adult Stroke Rehabilitation and
approximately 5 days. Therefore either a loading dose of clopido- Recovery.
grel should be used or it should be started in conjunction with 325 In order to provide excellent stroke rehabilitation, it is critical
mg of aspirin.51 The European Stroke Prevention Study 2 (ESPS- for the rehabilitationist to be able to prevent, identify, and cor-
2) demonstrated that the combination of dipyridamole 200 mg rectly treat the common complications that follow stroke. Overall,
and aspirin 25 mg twice a day also reduces the risk of recurrent complications are frequent and are seen in up to 85% of stroke
stroke. Thus options for antiplatelet treatment to reduce risk for patients during hospitalization (Table 44.5).59
stroke recurrence should include aspirin alone, aspirin with dipyr- An autopsy study101 looking at cause of death in a sample of
idamole, or clopidogrel. The aspirin/dipyridamole may be less well 409 stroke patients identified different likely diagnoses at different
tolerated due to side effects of gastrointestinal (GI) symptoms and times out from stroke. The study evaluated 82 of the 95 patients
headaches. For any patient with a stroke severe enough to warrant who died within the first 3 months. Direct effects of stroke were
inpatient rehabilitation, the combination of aspirin and clopido- the most common cause of death in the first week (90%), pulmo-
grel is not recommended, as it has shown no benefit over mono- nary embolism (PE) most common in the second to fourth weeks
therapy in two studies and may increase the risk of bleeding in (30%), and bronchopneumonia in the second to third months
patients with prior stroke.33,45,53 In the POINT study, Johnston (27%). Of the 61 of 128 patients who died after 3 months, cardiac
et al. suggest that patients with mild ischemic stroke (NIHSS ≤3) disease was the most common cause (37%). Overall, death was
or high-risk transient ischemic attack (TIA) (ABCD2 ≥4) may due to causes other than stroke in 59% of ischemic stroke patients
benefit from a combination of clopidogrel and aspirin. Those and 24% of hemorrhagic stroke patients. These data point to the
treated with the combination therapy from day 2 through 90 importance of effective and mindful treatment in the rehabilita-
poststroke had a lower rate of stroke recurrence, major myocardial tion environment in relation to venous thromboembolism (VTE),
infarction, and death; however, the combination group did have prevention of pulmonary complications, and appropriate medi-
an increased risk of major hemorrhage.53 Currently there are no cations and lifestyle adjustments to decrease the rate of cardiac
clear guidelines on the best antiplatelet regimen for a patient who disease after discharge.
has had a stroke while taking aspirin.45
There is a great deal of interest in neuroprotective agents, Neurologic Complications
several of which have shown efficacy in animal studies. To date
there is very limited evidence of effective neuroprotection in Hemorrhagic Conversion
human studies. This may be due to differences between the study Hemorrhagic conversion is relatively common after ischemic
animals and humans or, in some cases, may just be a timing stroke even when current acute stroke interventions such as fibri-
issue. In the case of animal studies, the timing of administra- nolysis or mechanical thrombectomy have not been received;
tion of a neuroprotective agent can be hyperacute, whereas in previous studies have noted an incidence of 40.6% after cerebral
human studies, a delay in administration may render a treat- embolism79 and 43% in cerebral infarction.50 Okada et al. noted
ment ineffective. Intravenous magnesium has been studied and that bleeding risk was much higher in moderate- to large-size
has not shown benefit when given within 12 hours with the infarcts (50%) compared with small infarcts (2.9%) and that
possible exception of a moderate effect in lacunar strokes.72,91 bleeding risk increased with age. However, only the more severe
Statins have been felt to have a neuroprotective benefit due to parenchymal hematoma type 2 (PH2) within the Fiorelli classi-
their direct influence on endothelial function, reduction of oxi- fication (Table 44.6)35 was shown to be a significant predictor of
dative stress, antiinflammatory properties, influence on plaque neurologic deterioration and 3-month mortality. The PH2 clas-
stability, and other properties. Although neuroprotection has sification includes hemorrhagic conversion with a homogeneous
not been clearly established, patients taking a statin at the time hyperdensity occupying more than 30% of the infarct zone,
CHAPTER 44 Stroke Rehabilitation 961
Suggested phrases for Should is reasonable may/might be considered COR III: COR III:
writing recommendations is recommended can be useful/effective/ may/might be reasonable No Benefit Harm
is indicated beneficial usefulness/effectiveness is is not potentially
is useful/effective/ is probably recommended unknown/unclear/uncertain recommended harmful
beneficial or indicated or not well established
is not indicated causes harm
should not be associated with
Comparative treatment/strategy A is treatment/strategy A is probably excess morbidity/
performed/
effectiveness recommended/indicated in recommended/indicated in mortality
administered/
phrases† preference to treatment B preference to treatment B
other should not be
treatment A should be it is reasonable to choose performed/
is not useful/
chosen over treatment B treatment A over treatment B administered/
beneficial/
effective other
• Fig. 44.4 Classification of recommendations and level of evidence. (From Winstein CJ, Stein J, Arena R,
et al: Guidelines for Adult Stroke Rehabilitation and Recovery: A Guideline for Healthcare Professionals
From the American Heart Association/American Stroke Association, Stroke 47[6]:e100, 2016.)
significant mass effect, or any homogenous hyperdensity located period. The most important risk factor to target for secondary
beyond the borders of the infarct zone. The presence of either stroke prevention is hypertension.30,57 In most cases antihyper-
hemorrhagic infarction type 1 (HI1), hemorrhagic infarction tensives should be restarted 24 hours poststroke in any patient
type 2 (HI2), or parenchymal hematoma type 1 (PH1) was not who was taking them prior to the stroke.57 Erdur et al. in their
shown to be associated with early neurologic decline or 3-month study of 5106 patients reported on the risk of stroke recurrence
mortality. The incidence of hemorrhagic transformation follow- during the period of acute inpatient hospitalization. The overall
ing intervention for acute stroke is complicated and beyond the risk in their study was less than 1%, but the patients at highest
scope of this chapter.93␣ risk for recurrence were those with a history of TIA, high-grade
symptomatic carotid stenosis, or stroke secondary to another
Repeat Stroke determined etiology (e.g., giant cell arteritis, cervical arterial
Because of more aggressive medical treatment specifically to dissection). Pneumonia poststroke was also associated with an
reduce secondary strokes, the rate of recurrence of stroke after increased risk of recurrence, and aphasia was associated with a
ischemic stroke and/or TIAs has dropped to about 3% to 4% decreased risk. There was no difference in the medical manage-
per year.67 The rate of recurrence is highest in the first 30 ment of those with and without recurrence.32 When a recur-
days following the initial stroke/TIA. Approximately half of rence of stroke is suspected during an inpatient rehabilitation
all strokes that recur within 90 days occur within the first 2 stay, the patient should be evaluated by CT to rule out hemor-
weeks, thus highlighting the importance of aggressive measures rhagic transformation and make sure that no acute neurosurgi-
and close monitoring during the acute inpatient rehabilitation cal intervention or management of intracranial hypertension is
962 SECTION 4 Issues in Specific Diagnoses
syndrome (CRPS) with compression of the metacarpophalangeal be provided to patients and caregivers to target environmental
joints and evaluation for skin and autonomic changes may be modification (IIaB). Participation in exercise programs with
helpful in identifying etiology.96 In certain cases, electrodiagnostic a goal to reduce falls is recommended (IB), and Tai Chi is a
evaluation can be beneficial should peripheral nerve or nerve root potentially effective intervention to decrease the risk of falls
injury be suspected. In terms of prevention, patients and families (IIbB).105 One small study demonstrated an increased risk for
should be trained on positioning and appropriate range of motion hip fractures due to falls in chronic elderly stroke patients defi-
(IC). The strongest evidence recommends botulinum toxin for cient in vitamin D, suggesting a benefit to supplementation.90␣
hypertonic muscles contributing to shoulder pain (IIaA), neuro-
pathic pain medications in those with signs consistent with neuro- Depression/Psychiatric Issues
pathic pain (e.g. allodynia and dysesthesia) (IIaA), and the use of
supportive devices and slings to limit forces leading to subluxation Guidelines strongly promote standardized assessments of mood,
and thus also potentially decreasing pain (IIaC). Less convincing education with a focus on adjustment, and the careful use of anti-
evidence also exists to support neuromuscular electrical stimula- depressants in those with poststroke depression (IB). However,
tion (NMES) (IIbA), acupuncture (IIbB), suprascapular nerve there is no clear recommendation of a particular antidepressant
block (IIbB), and subacromial/glenohumeral joint steroid injec- class in this population despite the fact that selective serotonin
tion (IIbB).105 Although previous work on NMES for subluxation reuptake inhibitors (SSRIs) are generally well tolerated (IIIA). The
has shown improvement in subluxation but a lack of significant use of SSRIs or dextromethorphan/quinidine is recommended
improvement in pain and function,60 new implantable devices26 for the treatment of pseudobulbar affect after stroke (IIaA). In
may be more useful than peripheral surface stimulation in decreas- addition to behavioral health professional consultation (IIaC),
ing pain, and these are beginning to be used. Should CRPS exist, education, counseling, and support (IIbB), a consistent exercise
a course of oral steroids, bisphosphonates, visual imagery includ- program of at least 4 weeks may be helpful for poststroke depres-
ing mirror visual feedback, and stellate ganglion blocks may all be sion (IIbB).105␣
considered.18 Finally, there is an option of surgical tenotomy of
shoulder internal rotators in cases of severely restricted shoulder Rehabilitation: Treatment of Stroke Sequelae
range of motion (IIbC). Overhead pulley exercises are particu-
larly not recommended (IIIC).105 Finally, in the case of adhesive For the initial inpatient hospitalization, the guidelines recom-
capsulitis, hydraulic distension with or without steroid has been mend that early rehabilitation for hospitalized stroke patients
used with promising but mixed results.20 Both fluoroscopic and should be “provided in environments with organized, interprofes-
ultrasound-guided techniques have been used successfully.7␣ sional stroke care” (IA) but that “very early mobilization within
24 hours of stroke can reduce the odds of a favorable outcome at
Contractures 3 months and is not recommended” (IIIA). In terms of provision
of rehabilitation after the initial hospitalization, guidelines suggest
Contractures may frequently develop after stroke and can restrict that stroke patients who are “candidates for postacute rehabilita-
eventual function and cause potential pain and skin breakdown. tion receive organized, coordinated, and interprofessional care”
Resting the hand and wearing wrist orthoses as well as regular (IA) and that those who “qualify for and have access to an IRF
stretching or serial casting may be helpful for reducing elbow and [inpatient rehabilitation facility] should receive care at an IRF
wrist contractures (IIbC). Surgical release of elbow flexor muscles rather than a SNF [skilled nursing facility]” (IB).105
can be considered for elbow pain and contractures (IIbB). Ankle
splints may also be helpful for preventing ankle plantarflexion Functional Assessment
contractures (IIbC). Care must be taken with splinting to avoid
skin breakdown. Guidelines recommend positioning the hemiple- Although a strong recommendation exists to obtain a formal
gic shoulder in the maximum external rotation tolerated for 30 assessment of functional status in both the acute hospitalization
minutes a day (IIaB).105␣ and subsequent levels of care (IB), the exact nature of the assess-
ment is less certain. Standardized measures of motor impairment,
upper extremity function, balance, and mobility are all generally
Skin Ulcers thought to be possibly useful (IIbC). It is also likely that serial
Appropriate skin management requires regular assessments with assessment with standardized measures could help to determine
use of standardized measures such as the Braden scale (IC). progress (IIbC). The communication evaluation should include
Regular interventions—including nutritional assessment, skin a range of interview, observation, and both standardized and
hygiene maintenance, turning and weight-shift schedules, and the nonstandardized measures with a goal of identifying strengths
appropriate use of pressure-relieving mattresses and wheelchair and weaknesses and developing compensatory strategies (IB). All
cushions—are also recommended, along with ongoing family stroke patients should receive a cognitive screening (IB), and those
education (IC).105␣ with deficits should receive more detailed testing (IIaC). Assess-
ment should also include sensory impairments in touch, vision,
and hearing (IIaB).105␣
Falls
Falls are a critical issue after stroke and require both a for- Cognition/Aphasia/Speech
mal fall prevention program during inpatient rehabilitation
(IA) as well as continued screening in the outpatient environ- The strongest recommendation for nondrug interventions appears
ment using an established measure such as the Berg Balance to be the use of enriched environments (IA), including the use of
Scale61 or the Morse Fall Scale70 (IIaB). Information should technology (such as internet, virtual reality, and music) and other
CHAPTER 44 Stroke Rehabilitation 965
TABLE
44.7
Barthel Index43
Activity Score
Feeding: 0 = unable, 5 = needs help cutting, spreading butter, etc, or requires modified diet, 10 = independent
Bathing: 0 = dependent, 5 = independent (or in shower)
Grooming: 0 = needs to help with personal care, 5 = independent face/hair/teeth/shaving (implements provided)
Dressing: 0 = dependent, 5 = needs help but can do about half unaided, 10 = independent (including buttons, zips, laces, etc.)
Bowels: 0 = incontinent (or needs to be given enemas), 5 = occasional accident, 10 = continent
Bladder: 0 = incontinent or catheterized and unable to manage alone, 5 = occasional accident, 10 = continent
Toilet Use: 0 = dependent, 5 = needs some help but can do something alone, 10 = independent (on and off, dressing, wiping)
Transfers (bed to chair and back): 0 = unable, no sitting balance, 5 = major help (one or two people, physical), can sit, 10 = minor help (verbal or
physical), 15 = independent
Mobility (on level surfaces): 0 = immobile or <50 yards, 5 = wheelchair independent, including corners, >50 yards, 10 = walks with help of one
person (verbal or physical) >50 yards, 15 = independent (but may use any aid; for example, stick) >50 yards
Stairs: 0 = unable, 5 = needs help (verbal, physical, carrying aid), 10 = independent
Total: (0–100)
968 SECTION 4 Issues in Specific Diagnoses
TABLE
44.9
Glasgow Outcome Scale (GOS)52 and Glasgow Outcome Scale–Extended (GOS–E)104
GOS GOS–E
1. Death Patient has sustained severe injury or has died without recovery of con- 1. Dead
sciousness.
2. Persistent Patient has sustained severe damage with prolonged state of unresponsive- 2. Vegetative state
vegetative state ness and a lack of higher mental functions/condition of unawareness with
only reflex responses but with periods of spontaneous eye opening.
3. Severe disability Patient has sustained severe injury with permanent need for help with activi-
ties of daily living.
Patient is dependent for daily support due to mental or physical disability— 3. Low severe disability
usually a combination of both. Patient cannot be left alone for more than
8 h at home.
Patient is dependent for daily support due to mental or physical disability— 4. Upper severe disability
usually a combination of both. Patient cannot be left alone for more than
8 h at home.
4. Moderate Patient does not need assistance in everyday life; employment is possible
disability but may require special equipment.
Patient has some disability such as aphasia, hemiparesis, or epilepsy and/ 5. Low moderate disability
or deficits of memory or personality but is capable of self-care. Patient is
independent at home but dependent outside. Patient is not able to return
to work even with special arrangements.
Patient has some disability—such as aphasia, hemiparesis, or epilepsy— 6. Upper moderate disability
and/or deficits of memory or personality but is capable of self-care.
Patient is independent at home but dependent outside. Patient is able to
return to work with special arrangements.
5. Low disability Patient has sustained light damage with minor neurologic and psychological
deficits.
Patient is able to resume normal life with the capacity to work even if prein- 7. Low good recovery
jury status has not been achieved. Some patients have minor neurologic
or psychological deficits. These deficits are disabling.
Patient is able to resume normal life with the capacity to work even if prein- 8. Upper good recovery
jury status has not been achieved. Some patients have minor neurologic
or psychological deficits. These deficits are not disabling.
Many factors are correlated with poorer outcome after isch- in certain situations may be reasonably encouraged to continue
emic stroke, such as lesion volume and age, though neither is to engage in attempts to regain function under the appropriate
highly specific and both are dependent on other factors.102␣ circumstances.63 However, at the same time it is important to
note that there is a general trend of decreased quality of life and
Time Frames for Recovery less functional independence based on a Barthel score greater
than 95 during the 5 years after stroke that is independent of
For ischemic stroke, the Copenhagen Stroke Study provides age, stroke severity, and other predictors of decline.28,29␣
guidance on time frames for duration of recovery, with mildly
impaired patients requiring on average 2 months, moderately Recovery Thresholds/Individual Impairments
impaired patients requiring 3 months, severely impaired patients
requiring 4 months, and the most severely impaired patients Regardless of intensity of rehabilitation and therapeutic inter-
requiring 5 months.54,55 Later studies have shown potential ventions, impairments and limitations are common after an
recovery even further out with severely impaired patients with ischemic cerebrovascular accident (CVA). The Framingham
Hankey et al. showing the median time to recovery in the Study demonstrated a range of issues after first-time ischemic
18.5% of severe patients who achieved independence (an MRS CVA at evaluation 6 months out from initial hospitalization:
score of <3) in their study to be to be 18 months.46 This fur- 26.2% with a BI below 60, 30.8% unable to walk unassisted,
ther reinforces the need to take into account stroke severity in 22.2% with bladder incontinence, 35.3% with depression, and
determining times frames of recovery in stroke (Figs. 44.7 and 25.9% institutionalized. Of note, the likelihood of a BI below
44.8). Notably, discoveries in the reversal of learned non-use 60 was dependent on age, including 16.7% of those aged 65 to
and the potential of massed practice within the CIMT model 74, 25.5% of those aged 75 to 84, and 45% of those aged 85 to
have altered opinions on time frames of recovery, and patients 94 years.56
CHAPTER 44 Stroke Rehabilitation 969
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
0-3 points 4-6 points 7-10 points 11-15 points 16-22 points 23+ points
n = 170 n = 409 n = 323 n = 205 n = 103 n = 059
• Fig. 44.5 Effect of baseline National Institutes of Health Stroke Scale score on outcome at 7 days. (From
Adams HP Jr., Davis PH, Leira EC, et al: Baseline NIH Stroke Scale score strongly predicts outcome after
stroke: a report of the Trial of Org 10172 in Acute Stroke Treatment [TOAST], Neurology 53[1]:127, 1999.)
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
0-3 points 4-6 points 7-10 points 11-15 points 16-22 points 23+ points
n = 170 n = 409 n = 323 n = 205 n = 103 n = 059
• Fig. 44.6 Effect of baseline National Institutes of Health Stroke Scale score on outcome at 3 months.
(From Adams HP., Jr., Davis PH, Leira EC, et al: Baseline NIH Stroke Scale score strongly predicts out-
come after stroke: a report of the Trial of Org 10172 in Acute Stroke Treatment [TOAST], Neurology
53[1]:128, 1999.)
In terms of individual impairment and disability, despite the Dysphagia is common in stroke patients, with up to 20%
heterogeneity of stroke presentation and outcome, there are data of patients in one study being shown by modified barium swal-
to guide expectations on time frames for improvement. low to be proven aspirators.95 However, despite this incidence, a
Aphasia recovery, similarly to motor recovery, is dependent relatively smaller percentage requires the eventual placement of a
upon initial impairment, but one study suggests time to stationary percutaneous gastrojejunostomy feeding tube, with only 5.7% of
language function following stroke to be 2 weeks for mild aphasia, this same sample of stroke patients receiving a tube. Notably, risk
6 weeks for moderate aphasia, and 10 weeks for severe aphasia.81 of tube placement is much higher (19.3%) in brainstem stroke
970 SECTION 4 Issues in Specific Diagnoses
100
In terms of predicting ambulation, sitting balance combined
with ability to recruit the hemiparetic leg is a predictive marker
for independent ambulation at 6 months. Of those who are able
80 to maintain sitting balance and recruit activation in the hemi-
paretic leg within 72 hours from stroke, 98% were independent
60 in ambulation at 6 months, whereas patients unable to main-
%
tain sitting balance or activate the hemiparetic leg within 72
hours had a 27% chance of independent ambulation. Those still
40
unable to maintain sitting balance and recruit the hemiparetic
All leg by day 9 had only a 10% likelihood of independent ambula-
20 Mild
Moderate
tion at 6 months.100
Severe Regarding visuospatial neglect, one study demonstrated
Very severe
0 that 31.5% of a group of 27 patients with evidence of visuospa-
0 1/7 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18>18
tial neglect had continued evidence of neglect at 3 months.19
Weeks From Stroke Onset
Hier et al. demonstrated a relatively more rapid recovery from
left neglect, prosopagnosia, anosognosia than for hemianopia,
• Fig. 44.7Time course of recovery (peak to best neurologic outcome). hemiparesis, motor impersistence and extinction.49 The recov-
(From Jorgensen HS, Nakayama H, Raaschou HO, et al: Outcome and ery from homonymous hemianopia (HH) appears to be depen-
time course of recovery in stroke. Part II: time course of recovery. The dent upon severity of impairment with a recovery of 17% and
Copenhagen Stroke Study, Arch Phys Med Rehabil 76[5]:408, 1995.) 72% of patients with full HH and partial HH at 1 month,
respectively.44␣