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quarta-feira, 27 de abril de 2011

STROKE Acidente vascular cerebral (AVC)

STROKE


Autors: Richard Zorowitz, M.D., Edgardo Baerga, M.D., and Sara Cuccurullo, M.D.
INTRODUCTION

DEFINITION OF STROKE

• Sudden focal (sometimes global) neurologic deficit secondary to occlusion or rupture of blood vessels supplying the brain

• Symptoms > 24 hours = stroke

• Symptoms < 24 hours = transient ischemic attack (TIA)

• Reversible ischemic neurologic deficit (RIND) = (this term is no longer used)

EPIDEMIOLOGY

• Stroke, after heart disease and cancer, is the third leading cause of death in the United States.

• The American Heart Association (AHA) estimates 600,000 strokes annually; 500,000 new cases, and 100,000 recurrent cases. (2000 AHA Heart and Stroke Statistical Update)

• Nearly four million stroke survivors in the United States

• 46% decline in cerebral infarcts and hemorrhages from 1950–1954 period to 1975–1979 period (Broderick, 1993)

– Decline attributed to better management of blood pressure (BP), heart disease, decrease in cigarette smoking, etc.

• Incidence increases 17% from 1975–1979 period to 1980–1984 period (attributed to increased use of CT scan)

• There has been no change in the incidence of aneurysmal rupture

• Mortality from strokes has been steadily declining since 1950s

– A sharp decline noted in the 1970s, possibly related to improved diagnosis (Dx) and treatment (Tx) of hypertension (HTN)

– Improved Dx by modern diagnostic imaging tools (CT and MRI), may also have created a statistical decline in calculated mortality as smaller (less severe) strokes were identified (Sacco, 1995).

RISK FACTORS (Stewart, 1999)

Nonmodifiable:

• Age—single most important risk factor for stroke worldwide; after age 55, incidence increases for both males and females

• Risk more than doubles each decade after age 55

• Sex ( male > female)

• Race ( African Americans 2× > whites > Asians)

• Family history (Hx) of stroke

Modifiable (treatable) risk factors:

• Hypertension—probably the most important modifiable risk factor for both ischemic and hemorrhagic stroke; increases risk by sevenfold

• History of TIA/prior stroke (~ 5% of patients with TIA will develop a completed stroke within 1 month if untreated)

• Heart disease (Dz.)

– Congestive heart failure (CHF) and coronary artery disease (CAD): increases risk by twofold
– Valvular heart Dz. and arrhythmias atrial fibrillation (A. Fib.)—increases risk of embolic stroke

A. Fib.: fivefold increase risk (Ryder, 1999)


• Diabetes—twofold increase in risk; unfortunately, good blood sugar control has not been

shown to alter the risk of stroke

• Cigarette smoking

• Carotid stenosis (and carotid bruit); risk of stroke decreases with carotid endarterectomy

(CEA) on selected symptomatic patients (> 70% stenosis)

• ETOH abuse/cocaine use

• High-dose estrogens (birth control pills)—considerable increase in risk when linked to

cigarette smoking

• Systemic diseases associated with hypercoagulable states

– Elevated RBC count, hematocrit, fibrinogen

– Protein S and C deficiency

– Sickle-cell anemia

– Cancer

• Hyperlipidemia—several clinical trials have shown a reduction in stroke with use of

cholesterol reducing agents (~ 30% reduction risk of stroke with use of HMG-CoA reductase

inhibitors)

• Migraine headaches

• Sleep apnea

• Patent Foramen Ovale

[Obesity/sedentary life style (no clear relationship with increased risk of stroke)]



BASIC NEUROANATOMICAL REVIEW OF THE MAJOR VESSELS INVOLVED IN STROKE





 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
ISCHEMIC STROKES


Thrombotic (large artery thrombosis): 35% of all strokes

• Usually occurs during sleep (patient often awakens unaware of deficits)

• May have “stuttering,” intermittent progression of neurologic deficits or be slowly progressive (over 24–48 hours)

• Profound loss of consciousness rare, except when area of infarction is large or when brainstem involved

• Neurologic deficit varies according to cerebral territory affected

• Perfusion failure distal to site of severe stenosis or occlusion of major vessels

• Emboli from incompletely thrombosed artery may precipitate an abrupt deficit. May have embolism from extracranial arteries affected by stenosis or ulcer

Embolic: 30% of all strokes

• Usually occurs during waking hours

• Deficit is immediate

• Seizures may occur at onset of stroke

• Cortical signs more frequent

• Most often embolus plugs one of the branches of the middle cerebral artery. An embolus may cause severe neurologic deficits that are temporary; symptoms resolve as the embolus fragments

• Presence of atrial fibrillation, history of recent myocardial infarction (MI) and occurrence of emboli to other regions of the body support Dx of cerebral embolism

• Suggested by history and by hemorrhagic infarction on CT (seen in 30% of patients withembolism) also by large low-density zone on CT encompassing entire territory of major cerebral artery or its main divisions

• Most commonly due to cardiac source: mural thrombi and platelet aggregates

• Chronic atrial fibrillation is the most common cause. Seen with myocardial infarction, cardiac aneurysm, cardiomyopathy, atrial myxoma, valvular heart disease (rheumatic, bacterial endocarditis, calcific aortic stenosis, mitral valve prolapse), sick sinus syndrome

• 75% of cardiogenic emboli go to brain

Lacunar infarction: 20% of all strokes

Lacunes are small (less than 15 mm) infarcts seen in the putamen, pons, thalamus, caudate, and internal capsule

• Due to occlusive arteriolar or small artery disease (occlusion of deep penetrating branches of large vessels)

• Occlusion occurs in small arteries of 50—200 m in diameter

• Strong correlation with hypertension (up to 81%); also associated with micro-atheroma, microembolism or rarely arteritis

• Onset may be abrupt or gradual; up to 30% develop slowly over or up to 36 hours

• CT shows lesion in about 2/3 of cases (MRI may be more sensitive)

• Relatively pure syndromes often (motor, sensory)—discussed below

• Absence of higher cortical function involvement (language, praxis, non-dominant hemisphere syndrome, vision)

Neuroanatomic Location of Ischemic Stroke (Adams, 1997)

1. Anterior Circulation

INTERNAL CAROTID ARTERY (ICA): (most variable syndrome): Occlusion occurs most frequently in the first part of the ICA immediately beyond the carotid bifurcation. ICA occlusions often asymptomatic ( 30–40% of cases) (Fig. 1–7)

• Ocular infarction: (embolic occlusion of either retinal branch or central retinal artery)

• Transient monocular blindness (amaurosis fugax): the ICA nourishes the optic nerve and retina as well as the brain; transient monocular blindness occurs prior to onset of stroke in approximately 25% of cases of internal carotid occlusion. Central retinal artery ischemia is very rare because of collateral supply

• Cerebral infarction: Presentation of complete ICA occlusion variable, from no symptoms (if good collateral circulation exists) to severe, massive infarction on ACA and MCA distribution.

Failure of distal perfusion of internal carotid artery may involve all or part of the middle cerebral territory and, when the anterior communicating artery is small, the ipsilateral anterior cerebral artery. Contralateral motor and/or sensory symptoms present.


 
MIDDLE CEREBRAL ARTERY (MCA): Occlusion occurs at stem of middle cerebral or at one


of the two divisions of the artery in the sylvian sulcus. (Figure 1–8)

Superior Division

Most common cause of occlusion of superior division of MCA is an embolus (superior division of MCA supplies rolandic and prerolandic areas)

Presentation:

• Sensory and motor deficits on contralateral face and arm > leg

• Head and eyes deviated toward side of infarct

• With left-side lesion (dominant hemisphere)—global aphasia initially, then turns into Broca’s aphasia (motor speech disorder)

• Right side lesion (nondominant hemisphere)—deficits on spatial perception, hemineglect, constructional apraxia, dressing apraxia

• Muscle tone usually decreased initially and gradually increases over days or weeks to spasticity

• Transient loss of consciousness is uncommon

Inferior division (lateral temporal and inferior parietal lobes)

Presentation:

• With lesion on either side—superior quadrantanopia or homonymous hemianopsia

• Left side lesion—Wernicke’s aphasia

• Right side lesion—left visual neglect


ANTERIOR CEREBRAL ARTERY (ACA) (Figure 1–9):


• If occlusion is at the stem of the anterior cerebral artery proximal to its connection with the anterior communicating artery ⇒ it is usually well tolerated because adequate collateral circulation comes from the artery of the opposite side

• If both anterior cerebral arteries arise from one stem ⇒ major disturbances occur with infarction occurring at the medial aspects of both cerebral hemispheres resulting in aphasia, paraplegia, incontinence and frontal lobe/personality dysfunction

• Occlusion of one anterior cerebral artery distal to anterior communicating artery results in:

– Contralateral weakness and sensory loss, affecting mainly distal contralateral leg (foot/leg more affected than thigh)

– Mild or no involvement of upper extremity

– Head and eyes may be deviated toward side of lesion acutely

– Urinary incontinence with contralateral grasp reflex and paratonic rigidity may be present

– May produce transcortical motor aphasia if left side is affected

– Disturbances in gait and stance = gait apraxia


2. Posterior Circulation: Vertebrobasilar Arteries & Posterior Cerebral Arteries


POSTERIOR CEREBRAL ARTERY (PCA):

Occlusion of PCA can produce a variety of clinical effects because both the upper brainstem and the inferior parts of the temporal lobe and the medial parts of the occipital lobe are supplied by it.

Particular area of occlusion varies for PCA because anatomy varies

• 70% of times both PCAs arise from basilar artery; connected to internal carotids through posterior communicating artery

• 20%–25%: one PCA comes from basilar; one PCA comes from ICA

• 5%-–10%: both PCA arise from carotids

Clinical presentation includes:

• Visual field cuts (including cortical blindness when bilateral)

• May have prosopagnosia (can’t read faces)

• palinopsia (abnormal recurring visual imagery)

• alexia (can’t read)

• transcortical sensory aphasia (loss of power to comprehend written or spoken words; patient can repeat)

• Structures supplied by the interpeduncular branches of the PCA include the oculomotor cranial nerve (CN 3) and trochlear (CN 4) nuclei and nerves

• Clinical syndromes caused by the occlusion of these branches include oculomotor palsy with contralateral hemiplegia = Weber’s syndrome (discussed below) and palsies of vertical gaze (trochlear nerve palsy)

VERTEBROBASILAR SYSTEM:

• Vertebral and basilar arteries: supply midbrain, pons, medulla, cerebellum, and posterior and ventral aspects of the cerebral hemispheres (through the PCAs.)

• Vertebral arteries: branches of the subclavian; are the main arteries of the medulla. At the pontomedullary junction, the two vertebral arteries join to form the basilar artery, which supplies branches to the pons and midbrain. Cerebellum is supplied by posterior-inferior cerebellar artery (PICA) from vertebral arteries, and by anterior-inferior cerebellar artery (AICA) and superior cerebellar artery, from basilar artery

• Vertebrobasilar system involvement may present any combination of the following signs/symptoms: vertigo, nystagmus, abnormalities of motor function often bilateral. usually ipsilateral cranial nerve dysfunction

• Crossed signs: motor or sensory deficit on ipsilateral side of face and opposite side of body; ataxia, dysphagia, dysarthria

Important: There is absence of cortical signs (such as aphasias or cognitive deficits) that are characteristic of anterior circulation involvement

Syndromes of the Vertebrobasilar System
 
I. Lateral Medullary (Wallenberg’s) Syndrome


This syndrome is one of the most striking in neurology. It occurs due to occlusion of the

following:

1. vertebral arteries (involved in 8 out of 10 cases)

2. posterior inferior cerebellar artery (PICA)

3. superior lateral medullary artery

4. middle lateral medullary artery

5. inferior lateral medullary artery

• Wallenberg’s syndrome also known as lateral medullary syndrome, PICA syndrome, and vertebral artery syndrome.

Signs and symptoms include the following:

– Ipsilateral side
Horner’s syndrome (ptosis, anhydrosis, and miosis) decrease in pain and temperature sensation on the ipsilateral face cerebellar signs such as ataxia on ipsilateral extremities (patient falls to side of lesion)

– Contralateral side

Decreased pain and temperature on contralateral body

– Dysphagia, dysarthria, hoarseness, paralysis of vocal cord

– Vertigo; nausea and vomiting

– Hiccups

– Nystagmus, diplopia

Note: No facial or extremity muscle weakness seen in this syndrome

II. Benedikt’s Syndrome (Red Nucleus/Tegmentum of Midbrain):

• Obstruction of interpeduncular branches of basilar or posterior cerebral artery or both

• Ipsilateral III nerve paralysis with mydriasis, contralateral hypesthesia (medial lemniscus), contralateral hyperkinesia (ataxia, tremor, chorea, athetosis) due to damage to red nucleus

III. Syndromes of the ParamedianArea (Medial Brainstem):

Paramedian area contains:

• Motor nuclei of CNs

• Cortico-spinal tract

• Medial lemniscus

• Cortico-bulbar tract

Signs/symptoms include:

• contralateral hemiparalysis

• ipsilateral CN paralysis
 

Weber Syndrome


(Base of midbrain): Obstruction of interpeduncular branches of posterior cerebral artery or

posterior choroidal artery or both. Ipsilateral CN 3 cranial nerve paralysis, contralateral

hemiplegia, contralateral Parkinson’s signs, contralateral dystaxia (mild degree of ataxia).

Millard-Gubler Syndrome

(Base of pons): Obstruction of circumferential branches of basilar artery. Ipsilateral facial

(CN 7) and abducens (CN 6) palsy, contralateral hemiplegia, analgesia, hypoesthesia.

• Extension to medial lemniscus = Raymond-Foville’s Syndrome (with gaze palsy to side of lesion)

Medial Medullary Syndrome

Caused by an infarction of the medial medulla due to occlusion (usually atherothrombotic) of penetrating branches of the vertebral arteries (upper medulla) or anterior spinal artery (lower medulla and medullo-cervical junction).

• Rare; ratio of medial medullary infarct to lateral medullary infarct ~ 1–2 : 10

• Typical syndrome:

– Ipsilateral hypoglossal palsy (with deviation toward the side of the lesion)

– Contralateral hemiparesis

– Contralateral lemniscal sensory loss (proprioception and position sense)

IV. Basilar Artery Occlusion Syndrome

Occlusion may arise in several ways:

• atherosclerotic plaque in the basilar artery itself (usually lower third)

• occlusion of both vertebral arteries

• occlusion of one vertebral artery when it is the only one of adequate size

Note:

• Thrombosis usually only obstructs a branch of basilar artery rather than the trunk
• Emboli, if they get through the vertebral arteries, usually lodge in one of the posterior cerebral arteries or at the upper bifurcation of the basilar artery
 
May cause internuclear ophthalmoplegia, conjugate horizontal gaze palsy, ocular bobbing.
Ptosis, nystagmus common but variable. May see palatal myoclonus, coma.

Locked-in syndrome: tetraparesis with patients only able to move eyes vertically or blink; patient remains fully conscious secondary to sparing of the reticular activating system; caused by bilateral lesions of the ventral pons (basilar artery occlusion). Some degree of paresis accompanies nearly all cases of basilar artery occlusion.
HEMORRHAGIC STROKES (see Table 1–1)

15% of all strokes may be secondary to hypertension, ruptured aneurysm, arteriovenous malformation (AVM), blood dyscrasias/bleeding disorders, anticoagulants, bleeding into tumors, angiopathies.

I. Hypertensive Intracerebral Hemorrhage

• Linked to chronic HTN (> one-third occur in normotensives)

• Sudden onset of headache, and/or loss of consciousness

• Vomiting at onset in 22%–44%

• Seizures occur in 10% of cases (first few days after onset)

• Nuchal rigidity common

• Sites: putamen, thalamus, pons, cerebellum; some from white matter

• Frequently extends to ventricular subarachnoid space

• Preceded by formation of “false” aneurysms (microaneurysms) of Charcot & Bouchard = arterial wall dilations 2° to HTN

Locations

1. Putamen: Most common; hemiplegia 2° to compression of adjacent internal capsule.

Vomiting in ~ 50%; headache frequent but not invariable

• Large hemorrhage: Stupor/coma + hemiplegia with deterioration in hours.

• With smaller hemorrhages: Headache (HA) leading to aphasia, hemiplegia, eyes deviate away from paretic limbs

• These symptoms, occurring over few minutes to one-half hour, are strongly suggestive of progressive intracerebral bleeding

2. Thalamus: Hemiplegia by compression of adjacent internal capsule; contralateral sensory deficits; aphasia present with lesions of the dominant side; contralateral hemineglec with involvement on the nondominant side. Ocular disturbances with extension
of hemorrhage into subthalamus


3. Pontine: Deep coma results in a few minutes; total paralysis, small pupils (1 mm) that

react to light; decerebrate rigidity → death occurs in few hours. Patient may survive if

hemorrhage is small (smaller than 1 cm)

4. Cerebellum: Develops over several hours. Coma/loss of consciousness (LOC)

unusual vomiting, occipital HA, vertigo, inability to sit, stand or walk, eyes deviate to

opposite side (ipsilateral CN 6 palsy); dysarthria, dysphagia

5. Lobar hemorrhage: HA and vomiting. A study of 26 patients revealed:

• 11 occipital: Dense homonymous hemianopsia and pain ipsilateral eye

• 7 temporal: Partial hemianopsia/fluent aphasia/pain ear

• 4 frontal: Contralateral hemiplegia (mainly the arm) and frontal headache

• 3 parietal: Hemisensory deficit (contralateral)/anterior temporal HA

II. Subarachnoid Hemorrhage (SAH) (Ruptured Saccular Arterial Aneurysm)

• Saccular aneurysms = Berry aneurysms

• Arterial dilations found at bifurcations of larger arteries at base of brain (circle of Willis or major branches). (Fig. 1–10) 90%–95% of saccular aneurysms occur on the anterior part of the circle of Willis.

Presumed to result from congenital medial and elastica defects vs hemodynamic forces causing focal destruction of internal elastic membrane at bifurcations. (Adams, 1997)

• Multiple in 20% of patients (either unilateral or bilateral)

• Other types of aneurysms: arteriosclerotic, mycotic, dissecting aneurysms, traumatic,neoplastic

• More likely to rupture if 10mm or larger (rupture may occur in smaller aneurysms)

• Rupture occurs usually when patient is active rather than during sleep (e.g., straining, coitus)

• Peak age for rupture = fifth and sixth decade


Clinical Presentation of Saccular Aneurysms/SAH:


Symptoms due to aneurysms; presentation can be either:

1. None, usually asymptomatic prior to rupture. (intracranial aneurysms are common, found during 3%–5% of routine autopsies)

2. Compression of adjacent structures

(e.g., Compression of oculomotor nerve (CN 3) with posterior communicating— internal carotid junction aneurysm or posterior communicating—posterior cerebral artery aneurysm)

Signs of CN 3 involvement:

• Deviation of ipsilateral eye to lateral side (lateral or divergent strabismus) because of  unopposed action of lateral rectus muscle

• Ptosis

• Mydriasis (dilated pupil) and paralysis of accommodation due to interruption of parasympathetic fibers in the CN 3


3. Rupture of aneurysm producing subarachnoid hemorrhage with or without intracerebral

hematoma

• “Sentinel” HA prior to rupture in ~ 50% of patients

• With subarachnoid hemorrhage, blood is irritating to the dura causing severe HA

classically described as “worst headache of my life”

• Sudden, transient loss of consciousness in 20%–45% at onset

• May have CN 3 or CN 6 palsy (from direct pressure from the aneurysm vs. accumulation

of an intracerebral hematoma vs early development of arterial spasm), hemiparesis,

aphasia (dominant hemisphere), memory loss

• Seizures: 4% at onset/25% overall

• Mortality 25% during first 24 hours

• Risk of rebleeding within one month 30%; 2.2% per year during first decade

• Mortality from rebleeding in the early weeks after initial event: 50% to 60%

• Vasospasm: common complication occurring in ~ 25% of cases; caused by the presence

of blood breakdown products (vasoactive amines) on the subarachnoid space,

acting in the adventitia of the arteries. Occurs 3–12 days after rupture (frequently ~

7 days after rupture)

16 STROKE

• Meds: nimodipine, a calcium channel blocker, is useful in the treatment of cerebral

blood vessel spasm after subarachnoid hemorrhage (see Treatment section below)

III. Vascular Malformations/AVMs

• Consists of a tangle of dilated vessels that form an abnormal communication between

the arterial and venous systems: an arteriovenous (AV) fistula

• Congenital lesions originating early in fetal life

• AVM composed of coiled mass of arteries and veins with displacement rather than invasion

of normal brain tissue

• AVMs are usually low-pressure systems; the larger the shunt, the lower the interior

pressure. Thus, with these large dilated vessels there needs to be an occlusion distally to

raise luminal pressures to cause hemorrhage

• Hemorrhage appears to be more common in smaller malformations, which is probably

due to higher resistance and pressure within these lesions

• Patients are believed to have a 40%–50% risk of hemorrhage from AVM in life span

• Natural history of AVMs: bleeding rate per year = 2%–4%

• Rebleeding rate 6% first year post-hemorrhage

• Annual mortality rate: 1% (per year)

• First hemorrhage fatal in ~10% of these patients

• Bleeding commonly occurs between the ages of 20–40 years

Clinical Presentation of AVM Rupture:

• Hemorrhage: Majority of symptomatic patients present with hemorrhage. Cerebral

hemorrhage first clinical manifestation in ~ 50% of cases; may be parenchymal (41%),

subarachnoid (23%), or intraventricular (17%) (Brown et al., 1996)

• Seizures: presenting feature in 30% of cases

• Headaches: presenting complaint in 20% of cases; 10% (overall) with migraine-like

headache



TREATMENT



IMMEDIATE MANAGEMENT (Ferri, 1998; Rosen, 1992; Stewart, 1999)

• Respiratory support/ABCs of critical care

• Airway obstruction can occur with paralysis of throat, tongue, or mouth muscles and

pooling of saliva. Stroke patients with recurrent seizures are at increased risk of airway

obstruction. Aspiration of vomiting is a concern in hemorrhagic strokes (increased association

of vomiting at onset). Breathing abnormalities (central) occasionally seen in patients

with severe strokes

• Control of blood pressure (see following)

• Indications for emergent CT scan

– Because the clinical picture of hemorrhagic and ischemic stroke may overlap, CT scan without contrast is needed in most cases to definitively differentiate between the two

– Determine if patient is a candidate for emergent thrombolytic therapy

– Impaired level of consciousness/coma: If there is acute deterioration of level of consciousness, evaluate for hematoma/acute hydrocephalus; treatment: emergency surgery

– Coagulopathy present (i.e., rule out (R/O) hemorrhage)

– Fever and concern regarding brain ulcers or meningitis

• Seizure management (see below)

• Obtain blood sugar levels immediately

– Hypoglycemia → bolus 50% dextrose

– Hyperglycemia: shown to potentiate severity of brain ischemia in animal studies.

– Insulin if blood sugar > 300 mg/dl

• Control of Intracranial Pressure (ICP) (see below)

• Fever: potentially damaging to the ischemic brain.

– Antipyretics (acetaminophen) should be given early while the source of fever is being ascertained

• Intravenous Fluid: Normal Saline Solution (NSS) or Ringer’s lactate; avoid hypotonic solutions or excessive loading because they may worsen brain edema
• Keep patient NPO if at risk of aspiration

Blood Pressure Management:

Management of blood pressure after acute ischemic and hemorrhagic stroke is controversial.
Many patients have HTN after ischemic or hemorrhagic strokes but few require emergency treatment. Elevations in blood pressure usually resolve without antihypertensive medications during the first few days after stroke. (Biller and Bruno, 1997)
Antihypertensive treatment can lower cerebral perfusion and lead to worsening of stroke.
The response of stroke patients to antihypertensive medications can be exaggerated.
Current treatment recommendations are based on the type of stroke, ischemic vs. Hemorrhagic

• IV labetalol and enalapril are favored antihypertensive agents.


Hemorrhagic Strokes:

Treatment of increased BP during hemorrhagic strokes is controversial. Usual recommendation is to treat at lower levels of blood pressure than for ischemic strokes because of concerns of rebleeding and extension of bleeding.

• Frequent practice is to treat BP if: SBP > 180, DBP > 105

• Agent of choice: IV labetalol (labetalol does not cause cerebral vasodilation, which could worsen increased ICP)

Seizure Management:

• Recurrent seizures: potentially life-threatening complication of stroke (see Stroke Rehabilitation)

• Seizures can substantially worsen elevated ICP

• Benzodiazepines = first-line agents for treating seizures

• IV lorazepam or diazepam
 
• If seizures don’t respond to IV benzodiazepines, treat with long acting anticonvulsants:


Phenytoin – 18 mg/kg

Also fosphenytoin – 17 mg/kg

Phenobarbital – 1000 mg or 20 mg/kg

Intracranial Pressure Management:

• Increased ICP reduces cerebral blood perfusion

• Cerebral perfusion calculated by subtracting ICP from mean arterial pressure (MAP). It

should remain > 60 mm Hg to ensure cerebral blood flow

• Fever, hyperglycemia, hyponatremia, and seizures can worsen cerebral edema by increasing

ICP

Management of ICP:

• Correction of factors exacerbating increased ICP

– Hypercarbia

– Hypoxia

– Hyperthermia

– Acidosis

– Hypotension

– Hypovolemia

• Positional

– Avoid flat, supine position; elevate head of bed 30°

– Avoid head and neck positions compressing jugular veins

• Medical Therapy

– Intubation and hyperventilation: reduction of PaCO2 through hyperventilation is the

most rapid means of lowering ICP. Keep ICP < 20 mmHg

– Hyperventilation should be used with caution because it reduces brain tissue PO2

(PbrO2); hypoxia may lead to ischemia of brain tissue, causing further damage in the

CNS after stroke

– Optimal PaCO2 ~ 25–30 mmHg

– Hyperosmolar therapy with mannitol improves ischemic brain swelling (by diuresis

and intravascular fluid shifts)

– Furosemide/acetazolamide may also be used

– High doses of barbiturates (e.g., thiopental) rapidly lower ICP and suppress electrical

brain activity

• Fluid Restriction

– Avoid glucose solutions; use normal saline; maintain euvolemia

– Replace urinary losses with normal saline in patients receiving mannitol

• Surgical Therapy

– Neurosurgical decompression

THROMBOLYTIC THERAPY

IV tissue – plasminogen activator (t-PA)

First FDA approved Tx for ischemic strokes in selected patients

• In National Institute of Neurologic Disorders (1995) trial, patients given t-PA within three

hours of onset of stroke were 30% more likely to have minimal or no disability at three

months compared to patrents treated with placebo

• There was a tenfold increase in hemorrhage (overall) with t-PAcompared to placebo (6.4%

vs. 0.6%) and in fatal ICH (3% vs. 0.3%)

• However, mortality was higher in placebo group than in t-PA groups; overall mortality:

17% t-PA (including hemorrhage cases) vs. 21% placebo

Inclusion criteria

• Age 18 yrs or older

• Time of onset of symptoms well established to be < three hours before treatment would begin

• Patients with measurable neurologic deficits (moderate to severe stroke symptoms)

• CT negative for blood

Exclusion criteria
 
• Minor stroke symptoms/TIA (symptoms rapidly improving)


• CT positive for blood

• Blood Pressure > 185/100 despite moderate Tx

• Increased PT/PTT

• Decreased PLTs

• Blood Sugar < 50, > 400

• Hx stroke past 3 month

• Hx of ICH, AVM or aneurysm

• Seizure at onset of stroke

Streptokinase

Three recent large randomized trials of streptokinase in stroke suspended because of increase

in hemorrhage and mortality in treatment group

ANTICOAGULANT THERAPY

Heparin

• Frequently used in patients with acute ischemic stroke, but its value is unproven

• There is no unanimity on when heparin should be started, desired level of anticoagulation

or if bolus dose should be given or not

Low molecular-weight heparin

• has more selective antithrombotic action than heparin (may be safer)

• Kay et al. (1995) study reporting improvement in survival and decrease in eventual rate of

dependency (rated by Barthel Index) in patients treated with low molecular-weight heparin

(LMWH) within 48 hours of onset of stroke compared to placebo

Aspirin, warfarin, ticlopidine (Ticlid®), clopidogrel, Plavix® (Creager, 1998)

• All have been shown to decrease the risk of subsequent stroke in patients with TIA.

• Usefulness in Tx of acute stroke unknown

• Anticoagulant therapy with warfarin: Stroke incidence and mortality in patients at high

risk reduced; might be the best option for patients with a history of atrial fibrillation, prior

stroke (or TIA), HTN, diabetes and CHF (Ryder, 1999)

Indications for Anticoagulation (Controversial)

• Stroke in evolution:

Neurologic deficit developing in stepwise progression (over 18 to 24 hours in carotid circulation;

up to 72 hours in vertebrobasilar circulation). IV heparin efficacy unproven as previously

mentioned. Generally, IV heparin given for at least several days to increase PTT to 1.5

to 2.5 times control. Coumadin® may be used for longer period (e.g, 6-month trial)

• Cardiac emboli (best reason to anticoagulate):

– Primarily from nonvalvular atrial fibrillation and mural thrombus from myocardial

infarction (MI)

– Anticoagulation reported to reduce incidence of cerebral emboli in patients with MI by

75%

– Timing of anticoagulation in patients with cardiac emboli controversial; probable risk of

inducing cerebral hemorrhage or hemorrhagic infarction within large infarcts if anticoagulated

in first 24–32 hours

– If neurologic deficit is mild (and CT shows no hemorrhage) may begin anticoagulation

immediately

– If deficit severe (clinically and/or CT), wait 3–5 days before starting anticoagulation

– 15% of cardiogenic emboli lodge in the brain. The most common cause is chronic atrial

fibrillation

• Transient Ischemic Attacks:

– Some studies suggest that a cluster of recent, frequent (“crescendo”) TIAs is an indication

for anticoagulation therapy. Use of anticoagulants (heparin, Coumadin®) in TIA is empirical

– May consider use of Coumadin® when antiplatelet drugs fail to reduce attacks

• Completed Stroke:

– Anticoagulation not considered beneficial after major infarction and usually not of great

value once stroke is fully developed

– Empirically, some will utilize anticoagulation (initially with IV heparin) in setting of

mild infarct to theoretically prevent further progression in same vascular territory

Coumadin® may be continued for several weeks to 3 to 6 months

– Anticoagulation generally not employed for lacunar infarction

CORTICOSTEROIDS:

• No value in ischemic strokes

• Some studies suggest worsening in prognosis of stroke patients due to hyperglycemia

CAROTID ENDARTERECTOMY (CEA)

Symptomatic carotid stenosis

CEA for symptomatic lesions with > 70% stenosis (70%–99%) is effective in reducing the incidence

of ipsilateral hemisphere stroke. (North American Symptomatic Carotid

Endarterectomy Trial Collaborators, 1991), (Endarterectomy for moderate symptomatic

carotid stenosis: Interim results from the MRC European Carotid Surgery Trial, 1996)

(Executive Committee for Asymptomatic Carotid Artherosclerosis Study, 1995)

American Heart Association (AHA) guidelines for CEA (Moore, 1995)

1. CEA is proven beneficial in:

• Symptomatic patients with one or more TIAs (or mild stroke) within the past 6 months

and carotid stenosis ≥ 70%

2. CEA is “Acceptable but not proven”:

• TIAs or mild and moderate strokes within the last 6 months and stenosis 50% to 69%

• Progressive stroke and stenosis ≥ 70%

CEA for Asymptomatic Carotid Stenosis

• Indications—Controversial

• AHA guidelines (Moore, 1995)

“Acceptable but not proven”: in stenosis > 75% by linear diameter (asymptomatic cases)

Note: recent studies present opposing views on indications for surgery in asymptomatic

carotid stenosis



Asymptomatic Carotid Atherosclerosis Study (ACAS) (Executive Committee for the

Asymptomatic Carotid Artherosclerosis Study, 1995) (Young et al., 1996)

• Study showed a significant reduction (53%) in risk of ipsilateral stroke in a five-year

period in asymptomatic patients with > 60% carotid stenosis (and < 3% rate perioperative

morbidity/mortality); risk was 5.1% on patients treated surgically vs. 11.0% in

patients treated medically.

• ACAS study not evaluated for AHA guidelines on 1995

ECST (Endarterectomy for moderate symptomatic carotid stenosis: Interim results from

the MRC European Carotid Surgery Trial, 1996). This 3 year study showed:

• In patients with asymptomatic carotid stenosis < 70%, risk of stroke is low, 2%. In

patients with stenosis > 70%, risk also is low, 5.7%

• Conclusion of study was that CEA is not justified in asymptomatic carotid stenosis



TREATMENT OF SUBARACHNOID HEMORRHAGE (see also Tx of ICP)

• Bed rest in a quiet, dark room with cardiac monitoring (cardiac arrhythmias are common)

• Control of headaches with acetaminophen and codeine

• Mannitol to reduce cerebral edema

• Control of blood pressure—have the patient avoid all forms of straining (give stool softeners

and mild laxatives)

• Early surgery (with clipping of aneurysm) better; reduces risk of rebleeding; does not

prevent vasospasm or cerebral ischemia

• Nimodipine (calcium channel blocker) shown to improve outcome after SAH

(decreased vasospasms). It is useful in the treatment of cerebral blood vessel spasm after

SAH. It decreases the incidence of permanent neurologic damage and death. Therapy

should be initiated within 96 hours of the onset of hemorrhage

TREATMENT OF INTRACRANIAL HEMORRHAGE
 
• Management of increased ICP and blood pressure (see previous)


• Large intracranial or cerebellar hematomas often require surgical intervention

TREATMENT OF ARTERIOVENOUS MALFORMATION (AVM) (Hamilton and Septzler,

1994; Schaller, Scramm, and Haun, 1998)

• Treatment advised in both symptomatic and asymptomatic AVMs

• Surgical excision if size and location feasible (and depending on perioperative risk)

• Embolization

• Proton Beam Therapy (via stereotaxic procedure)

• Small asymptomatic AVMs: radiosurgery/microsurgical resection recommended





STROKE REHABILITATION

INTRODUCTION

The primary goal of stroke rehabilitation is functional enhancement by maximizing the independence,

life style, and dignity of the patient.

This approach implies rehabilitative efforts from a physical, behavioral, cognitive,

social, vocational, adaptive, and re-educational point of view. The multidimensional nature

of stroke and its consequences make coordinated and combined interdisciplinary team care

the most appropriate strategy to treat the stroke patient.

Recovery from impairments

Hemiparesis and motor recovery have been the most studied of all stroke impairments. Up

to 88% of acute stroke patients have hemiparesis

The process of recovery from stroke usually follows a relatively predictable, stereotyped

series of events in patients with stroke-induced hemiplegia. These sequence of events

have been systematically described by several clinical researchers.

Twitchell (1951) published a highly detailed report describing the pattern of motor recovery

following a stroke (pattern most consistent in patients with cerebral infarction in the MCA

distribution)

• His sample included 121 patients, all except three having suffered either thrombosis or

embolism of one of the cerebral vessels

• Immediately following onset of hemiplegia there is total loss of voluntary movement and

loss or decrease of the tendon reflexes

• This is followed (within 48 hours) by increased deep tendon reflexes on the involved side,

and then (within a short time) by increased resistance to passive movement (tone returns

→ spasticity), especially in flexors and adductors in the upper extremity (UE) and extensors

and adductors in the lower extremity (LE)

• As spasticity increased, clonus (in ankle plantar flexors) appeared in 1–38 days post- onset

of hemiplegia

• Recovery of movement:

– 6 to 33 days after the onset of hemiplegia, the first “intentional” movements (shoulder

flexion) appears

– In the UE, a flexor synergy pattern develops (with shoulder, elbow, wrist and finger

flexion) followed by development of an extensor synergy pattern. Voluntary movement

in the lower limb also begins with flexor synergy (also proximal—hip) followed by

extensor synergy pattern

• With increase of voluntary movement, there is a decrease in the spasticity of the muscles

involved

• Tendon reflexes remain increased despite complete recovery of movement

• At onset of hemiplegia, the arm is more involved than the leg, and eventual motor

recovery in the leg occurs earlier, and is more complete, than in the arm

• Most recovery takes place in the first three months and only minor additional recovery

occurs after six months post onset

Predictors of motor recovery:

• Severity of arm weakness at onset:

– With complete arm paralysis at onset, there is a poor prognosis of recovery of useful

hand function (only 9% gain good recovery of hand function)

• Timing of return of hand movement:

– If the patient shows some motor recovery of the hand by four weeks, there is up to 70%

chance of making a full or good recovery

– Poor prognosis with no measurable grasp strength by four weeks

• Poor prognosis associated also with:

– Severe proximal spasticity

– Prolonged “flaccidity” period

– Late return of proprioceptive facilitation (tapping) response > nine days

– Late return of proximal traction response (shoulder flexors/adductors) > 13 days

Brunnstrom (1966, 1970) and Sawner (1992) also described the process of recovery following

stroke-induced hemiplegia. The process was divided into a number of stages:

1. Flaccidity (immediately after the onset)

No “voluntary” movements on the affected side can be initiated

2. Spasticity appears

Basic synergy patterns appear

Minimal voluntary movements may be present

3. Patient gains voluntary control over synergies

Increase in spasticity

4. Some movement patterns out of synergy are mastered (synergy patterns still predominate)

Decrease in spasticity

5. If progress continues, more complex movement combinations are learned as the basic

synergies lose their dominance over motor acts

Further decrease in spasticity

6. Disappearance of spasticity

Ιndividual joint movements become possible and coordination approaches normal

7. Normal function is restored

REHABILITATION METHODS FOR MOTOR DEFICITS: Major theories of rehabilitation

training

Traditional Therapy:

Traditional therapeutic exercise program consists of positioning, ROM exercises, strengthening,

mobilization, compensatory techniques, endurance training (e.g., aerobics).

Traditional approaches for improving motor control and coordination: emphasize need of

repetition of specific movements for learning, the importance of sensation to the control of

movement, and the need to develop basic movements and postures. (Kirsteins, Black,

Schaffer, and Harvey, 1999)

Proprioceptive (or peripheral) Neuromuscular Facilitation (PNF) (Knott and Voss, 1968)

• Uses spiral and diagonal components of movement rather than the traditional movements in cardinal

planes of motion with the goal of facilitating movement patterns that will have more functional

relevance than the traditional technique of strengthening individual group muscles

• Theory of spiral and diagonal movement patterns arose from observation that the body

will use muscle groups synergistically related (e.g., extensors vs. flexors) when performing

a maximal physical activity

• Stimulation of nerve/muscle/sensory receptors to evoke responses through manual

stimuli to increase ease of movement-promotion function

• It uses resistance during the spiral and diagonal movement patterns with the goal of facilitating

“irradiation” of impulses to other parts of the body associated with the primary

movement (through increased membrane potentials of surrounding alpha motoneurons,

rendering them more excitable to additional stimuli and thus affecting the weaker components

of a given part)

• Mass-movement patterns keep Beevor’s axiom: Brain knows nothing of individual muscle

action but only movement

Bobath approach / neurodevelopmental technique (NDT) (Bobath, 1978)

• The goal of NDT is to normalize tone, to inhibit primitive patterns of movement, and to facilitate

automatic, voluntary reactions and subsequent normal movement patterns.

• Based on the concept that pathologic movement patterns (limb synergies and primitive

reflexes) must not be used for training because continuous use of the pathologic pathways

may make it too readily available to use at expense of the normal pathways

• Probably the most commonly used approach

• Suppress abnormal muscle patterns before normal patterns introduced

• Mass synergies avoided, although they may strengthen weak, unresponsive muscles,

because these reinforce abnormally increased tonic reflexes, spasticity

• Abnormal patterns modified at proximal key points of control (e.g., shoulder and pelvic girdle)

• Opposite to Brunnstrom approach (which encourages the use of abnormal movements); see

the following

Brunstrom approach/Movement therapy (Brunnstrom, 1970)

• Uses primitive synergistic patterns in training in attempting to improve motor control through

central facilitation

• Based on concept that damaged CNS regressed to phylogenetically older patterns of

movements (limb synergies and primitive reflexes); thus, synergies, primitive reflexes, and

other abnormal movements are considered normal processes of recovery before normal

patterns of movements are attained

• Patients are taught to use and voluntarily control the motor patterns available to them at

a particular point during their recovery process (e.g., limb synergies)

• Enhances specific synergies through use of cutaneous/proprioceptive stimuli, central

facilitation using Twitchell’s recovery

• Opposite to Bobath (which inhibits abnormal patterns of movement)

Sensorimotor approach/Rood approach (Noll, Bender, and Nelson, 1996)

• Modification of muscle tone and voluntary motor activity using cutaneous sensorimotor

stimulation

• Facilitatory or inhibitory inputs through the use of sensorimotor stimuli, including, quick

stretch, icing, fast brushing, slow stroking, tendon tapping, vibration, and joint compression

to promote contraction of proximal muscles

Motor relearning program/Carr and Shepard approach (Carr et al., 1985)

• Based on cognitive motor relearning theory and influenced by Bobath’s approach

• Goal is for the patient to relearn how to move functionally and how to problem solve

during attempts at new tasks

• Instead of emphasizing repetitive performance of a specific movement for improving skill,

it teaches general strategies for solving motor problems.

• Emphasizes functional training of specific tasks, such as standing and walking, and carryover

of those tasks

Behavioral approaches (Noll, Bender, and Nelson, 1996) include:

• Kinesthetic or positional biofeedback and forced-use exercises

• Electromyographic biofeedback EMGBF: makes patient aware of muscle activity or lack of

it by using external representation (e.g., auditory or visual cues) of internal activity as a

way to assist in the modification of voluntary control

– In addition to trying to modify autonomic function, EMGBF also attempts to modify pain

and motor disturbances by using volitional control and auditory, visual, and sensory clues

– Electrodes placed over agonists/antagonists for facilitation/inhibition

– Accurate sensory information reaches brain through systems unaffected by brain → via

visual and auditory for proprioception

UPPER EXTREMITY MANAGEMENT (Black-Shaffer, Kirsteins, and Harvey, 1999)

• Shoulder pain: 70%–84% of stroke patients with hemiplegia have shoulder pain with

varying degrees of severity

• Of the patients with shoulder pain, the majority (85%) will develop it during the spastic

phase of recovery

• It is generally accepted that the most common causes of hemiplegic shoulder pain are the

shoulder-hand syndrome/reflex sympathetic dystrophy (RSD) and soft-tissue lesions

(including plexus lesions)

Complex Regional Pain Syndrome Type I (CRPS, Type I)/Reflex Sympathetic

Dystrophy (RSD)

• Disorder characterized by sympathetic-maintained pain and related sensory abnormalities,

abnormal blood flow, abnormalities in the motor system, and changes in both superficial

and deep structures with trophic changes

• Has been reported in 12% to 25% of hemiplegic stroke patients

• CRPS Type I = RSD

(CRPS type II = causalgia—pain limited to a peripheral nerve distribution)

• Most common subtype of RSD in stroke is shoulder-hand syndrome

Stages:

• Stage 1—acute: burning pain, diffuse swelling/edema, exquisite tenderness, vasomotor

changes in hand/fingers (with increased nail and hair growth, hyperthermia or

hypothermia, sweating). Lasts three to six months

• Stage 2—dystrophic: pain becomes more intense and spreads proximally, skin/muscle

atrophy, brawny edema, cold insensitivity, brittle nails/nail atrophy, decrease ROM,

mottled skin, early atrophy and osteopenia (late). Lasts three to six months

• Stage 3—atrophic: pain decreases, trophic changes, hand skin pale and cyanotic, with a

smooth, shiny appearance and feels cool and dry, bone demineralization progresses with

muscular weakness/atrophy, contractures/flexion deformities of shoulder/hand,

tapering digits, no vasomotor changes

Pathogenesis

• Multiple theories postulated including:

– Abnormal adrenergic sensitivity develops in injured nociceptors, and circulating or

locally secreted sympathetic neurotransmitters trigger the painful afferent activity

– Cutaneous injury activates nociceptor fibers → central pain-signaling system → pain

– Central sensitization of pain-signaling system

– Low-threshold mechanoreceptor input develops capacity to evoke pain

– With time, efferent sympathetic fibers develop capacity to activate nociceptor fibers



Diagnosis

• X rays—in initial stages, X rays normal; periarticular osteopenia may be seen in later

stages; use is questionable, given that bone mineral density starts to decrease in the paralytic

arm one month after stroke

– Need 30%–50% demineralization for detection

• Bone Scan—30 stroke survivors < 3 months onset, evaluated for CRPS Type I using

triple phase bone scan (Kozin, 1981; Simon and Carlson, 1980; Habert, Eckelman, and

Neuman, 1996)

– Sensitivity ~ 92%

– Specificity ~ 56%

– Positive predictive value (PPV) ~ 58%

– Negative predictive value (NPV) ~ 91% (Holder and Mackinnon, 1984)

– Diffusely increased juxta-articular tracer activity on delayed images is the most sensitive

indicator for RSD (sensitivity 96%, specificity 97%, and PPV 88%)

• EMG—as predictor for RSD (Cheng and Hong, 1995)

– Association between spontaneous activity and eventual development of RSD (vs no

spontaneous activity on EMG)

• Clinical (Wang et al., 1998)

– Clinical diagnosis difficult, presentation fairly incomplete

– Most consistent early diagnostic signs: shoulder pain with ROM (flexion/abduction/

external rotation), absence of pain in elbow and with forearm pronation/

supination; wrist dorsiflexion pain with dorsal edema; pain MCP/PIP flexion with

fusiform PIP edema

– Pain out of proportion to injury and clinical findings

– Shoulder/hand pain preceded by rapid ROM loss

– Tepperman et al. (1984) Greyson and Tepperman (1984)

– Studied 85 consecutive post-CVA hemiplegic patients

– 25% had radionuclide evidence for RSD: positive diagnosis was evident when delayed

image showed increased uptake in wrist, MCP and IP joints

– In this study, the most valuable clinical sign was MCP tenderness to compression with

100% predictive value, sensitivity 85%, and specificity 100%

• Stellate ganglion block

– Alleviation of pain following sympathetic blockade of the stellate ganglion using local

anesthetic: is the gold standard Dx of sympathetically mediated CRPS Type I

Treatment (Arlet and Mazieres, 1997)

• ROM exercises involved joint-pain free within three weeks, most < four to six days with

passive stretch of involved joints

• Corticosteroids (systemic): a large majority of patients respond to systemic steroids instituted

in the acute phase of the disease. Usually prednisone in doses up to 100–200 mg/day

or 1 mg/kg, and tapered over two weeks

– More effective in RSD confirmed by bone scan than on “clinical” RSD with negative

bone scan. Bone scan may be useful not only in establishing the Dx of RSD, but also in

identifying patients likely to respond to oral steroid therapy. In a study, 90% of the

patients. with positive bone scan findings for RSD treated with corticosteroids had good

or excellent response, whereas 64% of the patients, without bone scan abnormalities had

poor or fair response.

– In recent study, 31/34 MCA stroke patients with RSD became pain free by 14 days after

starting methylprednisolone 8 mg PO QID (patients treated for two weeks, followed by

two-week taper)

• Intra-articular injections with corticosteroids

• Analgesics (NSAIDs)

• Tricyclic antidepressants

• Diphosphonates

• Calcitonin

• Anticonvulsants (as Neurontin® or Tegretol®)

• Alpha-adrenergic blockers (clonidine, prazosin)

• Beta-blockers (propranolol and pindolol)

• Calcium channel blockers (nifedipine)

• Topical capsaicin

• TENS

• Contrast baths

• Edema control measures

• Desensitization techniques

• Ultrasound (U/S)

• Sympathetic ganglion blocks (i.e., stellate ganglion) may be diagnostic as well as therapeutic

• Local injections (procaine, corticosteroid)

• Sympathectomy

Shoulder Subluxation

Characterized by the presence of a palpable gap between the acromion and the humeral head

Etiology is unknown, but may be due to changes in the mechanical integrity of the glenohumeral

joint

Pathogenesis: factors that are thought to be related to shoulder subluxation include: angulation

of the glenoid fossa, the influence of the supraspinatus muscle on the humeral head

sitting, the support of the scapula on the rib cage, the contraction of the deltoid and rotator

cuff muscles on the abducted humerus

• A number of recent studies have failed to show any correlation between shoulder subluxation

and pain

• There might be a correlation with between-shoulder pain and decrease in arm external

rotation

• Basmajian Principle: Decreased trapezius tone—the scapula rotates and humeral head subluxates

from glenoid fossa

Treatment

Shoulder slings: use is controversial

Routine use of sling for the subluxed shoulder (or for shoulder pain) is not indicated

• Friedland—sling does not prevent/correct subluxation, not necessary to support painfree

shoulder (Friedland, 1975)

• Hurd—no appreciable difference in shoulder ROM, subluxation, or shoulder pain in

patients wearing slings or not (Hurd et al., 1974)

Pros: May be used when patient ambulates to support extremity (may prevent upper extremity

trauma, which in turn may cause increase pain or predispose to development of RSD)

30 STROKE

Cons: May encourage contractures in shoulder adduction/internal rotation, elbow flexion

(flexor synergy pattern)

Other widely used treatments for shoulder subluxation:

• Functional Electrical Stimulation (FES)

• Armboard, arm trough, lapboard—used in poor upper-extremity recovery, primary

wheelchair users

– Arm board may overcorrect subluxation

• Overhead slings—prevents hand edema (may use foam wedge on armboard)

Prevention:

• Subluxation may be prevented by combining the early reactivation of shoulder musculature

(specifically supraspinatus and post- and mid-deltoid) with the provision of FES or a

passive support of the soft-tissue structures of the glenohumeral joint (e.g., arm trough)

Brachial Plexus/Peripheral Nerve Injury

Etiology: “Traction” neuropathy

Diagnosis:

• Clinical: atypical functional return, segmental muscle atrophy, finger extensor contracture,

delayed onset of spasticity

• Electrodiagnostic studies (EMG)—lower motor neuron findings

Treatment:

• Proper bed positioning to prevent patient from rolling onto his paretic arm, trapping it

behind his back or through the bed rails and place a traction stress on it.

• ROM to prevent contracture while traction avoided

• 45-degree shoulder-abduction sling for nighttime positioning

• Sling for ambulation to prevent traction by gravity

• Armrest in wheelchair as needed

Prognosis—may require 8 to 12 months for reinnervation

Bicipital Tendinitis

• Chronic pain anterolateral shoulder, pain in abduction/external rotation, painful over

bicipital groove

• Positive Yergason test: with arm on side and elbow flexed, external rotation of the arm is

exerted by the examiner (while pulling downward on the elbow) as the patient resists the

movement. If the biceps tendon is unstable on the bicipital groove, it will pop-out and the

patient will experience pain

• Greatest excursion of long head biceps from flexion/internal rotation, to elevation/abduction,

depression/external rotation/extension

• May progress to adhesive capsulitis (frozen shoulder)

Diagnosis may be confirmed with decreased pain after injection of tendon sheath with lidocaine;

bicipital tendinitis may respond to steroid injection of the tendon sheath.

Rotator Cuff Tear, Impingement Syndrome, Adhesive Capsulitis (frozen shoulder):

All are causes of poststroke shoulder pain—see Table 1.7; see Musculoskeletal chapter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Heterotopic Ossification


• Infrequent (in stroke), but may be seen in elbow, shoulder

• Occurs only on extensor side of elbow

• No problems in pronation/supination since proximal radioulnar joint not involved

• Treatment: joint mobilization/ROM, etidronate disodium

Dependent Edema

May be treated with use of compression glove, foam wedge, pneumatic compression, retrograde

massage, arm elevation

OTHER ASPECTS OF STROKE REHABILITATION

Spasticity Management

For a detailed discussion of spasticity, see the Spasticity chapter

Spasticity in stroke:

• Usually seen days to weeks after ischemic strokes

• Usually follows classic upper-extremity flexor and lower-extremity extensor patterns

• Clinical features include velocity-dependent resistance to passive movement of affected

muscles at rest, and posturing in the patterns previously mentioned during ambulation

and with irritative/noxious stimuli

Treatment:

• Noninvasive Tx: stretching program, splints/orthosis, serial casting, electrical stimulation,

local application of cold

• Medications:

– The use of benzodiazepines, baclofen, dantrolene, and the alpha agonists clonidine and

tizanidine, in stroke patients, remains controversial

– These drugs have modest effects on the hypertonicity and posturing associated with

stroke and their side-effects limit their usefulness

• Injection of chemical agents:

– Botulinum toxin: may be particularly useful in control of increased tone in smaller

muscles of the forearm and leg (e.g., brachioradialis, finger, wrist, and thumb flexors, in

the upper extremity, and long and short toe flexors, extensor hallucis injury (EHL), and

ankle invertors in the lower extremity)

– Phenol: may remain the agent of choice for injection of large muscle groups (e.g., hip

adductors and extensors, the pectorals, lats, and biceps)

• Intrathecal baclofen: limited experience of its use in stroke patients; usefulness remains to

be determined in this population

• Surgical procedures:

– Uncommonly used in stroke, probably because of expected decrease in survival and

increase in rate of medical co-morbidities

– May be useful in selected cases when specific goals are pursued (e.g., increase in function,

improve hygiene, decrease in pain)Deep Vein Thrombosis (DVT)

• Common medical complication after stroke; occurring in 20%–75% of untreated stroke survivors

(60%–75% in affected extremity, 25% proximal DVT; PE, 1%–2%)

• Diagnosis: Usually can be made using noninvasive techniques:

– Ultrasonography

– Impedance plethysmography

– Contrast venography reserved for cases with inconclusive results.

– D-dimer assays (a cross-linked fibrin degradation product): may be useful as screening

tool for DVT in stroke patients

• Prophylaxis:

Currently, recommended prophylaxis regimens include:

– Low dose subcutaneous (SQ) heparin/low molecular weight heparin

– Intermittent pneumatic compression (IPC) of the lower extremity (LE) (for patients with

a contraindication to heparin)

– Gradient compression stockings in combination with SQ heparin or IPC

Bladder Dysfunction

• Incidence of urinary incontinence is 50%–70% during the first month after stroke and 15%

after 6 months (similar to general population—incidence ≈ 17%.)

• Incontinence may be caused by CNS damage itself, UTI, impaired ability to transfer to

toilet or impaired mobility, confusion, communication disorder/aphasia, and cognitiveperceptual

deficits that result in lack of awareness of bladder fullness

• Types of voiding disorders: areflexia, uninhibited spastic bladder (with complete/incomplete

emptying), outlet obstruction

• Treatment: implementation of timed bladder-emptying program

– Treat possible underlying causes (e.g., UTI)

– Regulation of fluid intake

– Transfer and dressing-skill training
– Patient and family education


– Medications (if no improvement with conservative measures)

• Remove indwelling catheter—perform postvoid residuals, intermittent catheterization—

perform urodynamics evaluation

Bowel Dysfunction

Patient unable to inhibit urge to defecate → incontinence

• Incidence of bowel incontinence in stroke patients 31%

• Incontinence usually resolves within the first two weeks; persistence may reflect severe

brain damage

• Decrease in bowel continence may be associated with infection resulting in diarrhea,

inability to transfer to toilet or to manage clothing, and communication impairment/

inability to express toileting needs

• Tx: treat underlying causes (e.g., bowel infection, diarrhea), timed-toileting schedule,

training in toilet transfers and communication skills

Impairment of intestinal peristalsis—constipation

• Management: adequate fluid intake/hydration, modify diet (e.g., increase in dietary fiber),

bowel management (stool softeners, stool stimulants, suppositories), allow

commode/bathroom privileges

Dysphagia

Dysphagia (difficulty swallowing), in stroke, has an incidence of 30% to 45% (overall)

• 67% of brainstem strokes

• 28% of all left hemispheric strokes

• 21% of all right hemispheric strokes

• More common in bilateral hemisphere lesions than in unilateral hemisphere lesions

• More common in large-vessel than in small-vessel strokes

Predictors on bed-side swallowing exam of aspiration include:

• Abnormal cough

• Cough after swallow

• Dysphonia

• Dysarthria

• Abnormal gag reflex

• Voice change after swallow (wet voice) (Aronson, 1990)

SWALLOWING

Three phases:

1. Oral

2. Pharyngeal

3. Esophageal













































Important Definitions


• Chin tuck—compensatory technique to provide airway protection by preventing entry of liquid into the larynx (probably by facilitating forward motion of the larynx). Also, chin tuck decreases the space between the base of the tongue and the posterior pharyngeal wall, and so creates increased pharyngeal pressure to move the bolus through the pharyngeal region.

• Aspiration

– Aspiration, by definition, is the penetration of a substance into the laryngeal vestibule and below the vocal folds (true vocal cords) into the trachea
– Aspiration is missed on bedside swallowing evaluations in 40% to 60% of patients (i.e., silent aspiration)

– It can be reliably diagnosed on videofluoroscopic swallowing study (penetration of contrast material below the true vocal cords)

– Using videofluoroscopic swallowing study, aspiration has been found to occur in 40% to 70% of stroke patients.

– Predictors of aspiration on videofluoroscopic swallowing study include:

Delayed initiation of the swallow reflex

Decreased pharyngeal peristalsis

• Aspiration pneumonia

Risk factors for development of pneumonia secondary to aspiration include:

– Decreased level of consciousness

– Tracheostomy

– Emesis

– Reflux

– Nasogastric tube (NGT) feeding

– Dysphagia

– Prolonged pharyngeal transit time

As dysphagia is a frequent and potentially serious (because of aspiration) complication of

stroke, careful bedside swallowing evaluation should be performed in all patients before oral

feeding is started. If a patient is believed to be at high risk of recurrent aspiration after

bedside and/or videofluoroscopic evaluation, he/she should be kept NPO and enterally fed,

initially via NGT, and then via G-tube or J-tube if long-term enteral feeding is required.

• Non-oral feeding:

– Clear contraindication for oral feeding is pulmonary pathology due to aspiration in the presence of documented airway contamination

– NPO also indicated in patients at high risk of aspiration because of reduced alertness, reduced responsiveness to stimulation, absent swallow, absent protective cough, and

difficulty handling secretions, or when there is significant reduction of oral pharyngeal and laryngeal movements

– NPO is disadvantageous in treating dysphagia because swallowing itself is the best treatment

Treatment of dysphagia/prevention of aspiration:

• Changes in posture and head position

• Elevation of the head of the bed

• Feeding in the upright position

• Chin tuck

• Turning the head to the paretic side

• Diet modifications (e.g., thickened fluids, pureed or soft foods in smaller boluses)

Inconclusive evidence of long-term efficacy in dysphagia:

• Thermal stimulation (to sensitize the swallowing reflex)

• Oral/motor exercises (to improve tongue and lip strength, ROM, velocity, and precision,

and vocal-fold adduction)

Other complications of dysphagia include dehydration and malnutrition:

• Malnutrition found in 49% of patients admitted to rehabilitation in recent study and was

associated with a prolonged length of stay and slower rate of functional gains

• Malnourished patients—higher stress reaction, frequency of infection and decubiti

Recovery of dysphagia in stroke:

Few studies available on recovery of dysphagia in stroke:

• Gresham (1990) reports his findings regarding 53 patients in a swallowing program poststroke

– 85% (45/53) on full oral nutrition at discharge

– 17% (9/53) could not drink thin liquids safely

– 8% (4/53) could not adequately maintain cohesive bolus of varied texture

• Gordon (1987)

– 41 of 91 (45%) stroke patients + dysphagia

– 90% hemispheric lesions (17% bilateral)

– Swallowing function regained within 14 days in 86% (of patients who survived unilateral

stroke)

• Logemann (1991)

– Recovery of swallowing function in most brainstem strokes occurs in the first three

weeks poststroke

Nasal speech: hypernasality caused by partial or complete failure of soft palate to close-off

the nasal cavity from the oral cavity or by incomplete closure of the hard palate. Uplifting the

soft palate prevents nasal speech (speech abnormally resonated in the nasal cavities).

APHASIA

• Aphasia is an impairment of the ability to utilize language due to brain damage.

Characterized by paraphasias, word-finding difficulties, and impaired comprehension.
Also common, but not obligatory, features are disturbances in reading and writing, nonverbal constructional and problem-solving difficulty and impairment of gesture

Transcortical mixed aphasia: Lesions in border zone of frontal, parietal, and temporal areas

Characteristics:

• Poor comprehension

• Nonfluent (decrease rate and initiation of speech)

• Preserved repetition (echolalia)

Note: Language areas are anatomically clustered around the sylvian fissure of the dominant hemisphere—left hemisphere in 95% of people.

Paraphasias: Incorrect substitutions of words or part of words

• Literal or phonemic paraphasias: similar sounds (e.g., “sound” for “found”)

• Verbal or semantic paraphasias: word substituted for another from same semantic class (e.g., “fork” for “spoon”)

Recovery Language Deficits/Aphasia Post Stroke:

The greatest amount of improvement in patients with aphasia occurs in the first two to three months after the onset; after six months, there is a significant drop in the rate of recovery.
In the majority of cases of patients with aphasia spontaneous recovery does not seem to occur after a year. However, there are reports of improvements many years after their stroke in patients undergoing therapy.

MEDICAL MANAGEMENT PROBLEMS

Poststroke Depression

• Etiology:

– Organic: May be related to catecholamine depletion through lesion-induced damage to the frontal nonadrenergic, dopaminergic and serotonergic projections (Heilman and Valenstein, 1993)

– Reactive: Grief/psychological responses for physical and personal losses associated with stroke, loss of control that often accompany severe disability, etc.

• Prevalence of depression in stroke patients reported ≈ 40% (25% to 79%); occur in similar proportion in their caregivers. (Flick, 1999)

• Most prevalent six months to two years

• A psychiatric evaluation for DSM-IV criteria and vegetative signs may be a clinically useful diagnostic tool in stroke patients

• There may be higher risk for major depression in left frontal lesions (relationship still controversial)

• Risk factors: prior psychiatric Hx, significant impairment in ADLs, high severity of deficits, female gender, nonfluent aphasia, cognitive impairment, and lack of social supports

• Persistent depression correlates with delayed recovery and poorer outcome

• Treatment: Active Tx should be considered for all patients with significant clinical depression

• Psychosocial interventional program: psychotherapy

• Medications: SSRIs preferred because of fewer side effects (compared to TCAs); methylphenidate has also been shown to be effective in poststroke depression

• SSRIs and TCAs also been shown to be effective in poststroke emotional lability



Sexual Dysfunction

• Well documented that the majority of elderly people continue to enjoy active and satisfying sexual relationships

• No significant changes in sexual interest or desire, but marked decline in behavior in both sexes (after stroke)

• There is a marked decline in sexual activity poststroke

• Fugl-Meyer (1980)—67 patients sexually active prestroke (Fugl-Meyer and Jaaski, 1980)

– 36% remained active poststroke

– 33% men resumed unaltered intercourse

– 43% women resumed unaltered intercourse

– Decreased frequency due to altered sensation, custodial attitudes taken by spouse

Other factors related to decrease in sexual activity poststroke:

Emotional factors—fear, anxiety and guilt; low self esteem; and fear of rejection by partner

Treatment: supportive psychotherapy, counseling.

Seizures

• Can be classified as occurring:

– At stroke onset

– Early after stroke (1–2 weeks)

– Late after stroke (> 2 weeks)

• In prospective study after first time stroke, 27 of 1099 (2.5%) of patients had seizures within 48 hours postictus.

• Seizures associated with older age, confusion, and large parietal or temporal hemorrhages

• Majority of seizures were generalized tonic-clonic

• In-hospital mortality higher in patients with seizures

• Early seizures tend not to recur; these are associated with acute metabolic derangement associated with ischemia or hemorrhage.

• Stroke patients requiring inpatient rehabilitation have higher probability of developing seizures than the general stroke population

• Seizures occurring > 2 weeks after stroke have higher probability of recurrence

• In study with 77 ischemic stroke victims followed two to four years

– 6%–9% develop seizures

– 6/23 (26%) patients with cortical lesions develop seizures

– 1/54 (2%) patients with subcortical lesions develop seizures

• Risk Factors: Cortical lesions, persistent paresis (6/12 = 50%)

• Treatment: choice of anticonvulsant drugs for patients with cerebral injury discussed in the

TBI chapter.



FACTORS THAT PREDICT MORTALITY AND FUNCTIONAL RECOVERY IN STROKE PATIENTS

Mortality Factors

• Mortality of ischemic strokes in the first 30 days ranges from 17%–34%

• Hemorrhagic strokes are more likely to present as severe strokes and with mortality rate

reported to be up to 48%

• Mortality in the first year after stroke 25% to 40%

• The risk of another stroke within the first year 12% to 25%



RISK FACTORS FOR ACUTE STROKE MORTALITY — 30 DAY MORTALITY



• Stroke severity

• Low level of consciousness

• Diabetes mellitus

• Cardiac disease

• Electrocardiograph abnormalities

• Old age

• Delay in medical care

• Elevated blood sugar in non-diabetic

• Brainstem involvement

• Hemorrhagic stroke

• Admission from nursing home



Functional Recovery and Disability Factors

• As stroke mortality has declined in the last few decades, the number of stroke survivors

with impairments and disabilities has increased

• There are 300,000 to 400,000 stroke survivors annually

• 78% to 85% of stroke patients regain ability to walk (with or without assistive device)

• 48% to 58% regain independence with their self-care skills

• 10% to 29% are admitted to nursing homes



RISK FACTORS FOR DISABILITY AFTER STROKE

• Severe stroke (minimal motor recovery at 4 weeks)

• Low level of consciousness

• Diabetes mellitus

• Cardiac disease

• Electrocardiograph abnormalities

• Old age

• Delay in medical care

• Delay in rehabilitation

• Bilateral lesions

• Previous stroke

• Previous functional disability

• Poor sitting balance

• Global aphasia

• Severe neglect

• Sensory and visual deficits

• Impaired cognition

• Incontinence (>1–2 weeks)



Negative Factors of Return to Work (Black-Shaffer and Osberg, 1990)

• Low score on Barthel Index at time of rehabilitation discharge

• Prolonged rehabilitation length of stay

• Aphasia

• Prior alcohol abuse

(Barthel Index is a functional assessment tool that measures independence in ADLs on 0–100 scale)



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