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Cerebrovascular Accident (CVA)
Reported by: Lalin Fe P. EvangelistaPT Intern 2012UPH-DJGTMU
1
Table of Contents
Anatomy
Definition
Epidemiology
Classification
Clinical key
Risk Factors
Pathophysiology
Types
Medical Management
Rehabilitation Management
Fundamental Anatomy
Arteries of the brain>Internal Carotid Artery
2
-Opthalmic Artery, Post. Communicating artery, choroidal artery, ACA, MCA>Vertebral Artery
-ascends in the neck by passing through upper 6 cervical vertebrae, at level of pons it unite to form basilar artery
Branches: meningeal branches, ant. Spinal artery, posterior spinal artery, PICA, medullary arteries
>Basilar Artery- at the upper border of pons, it divides into two PCA
Branches: pontine arteries, labyrinthine artery, AICA, SCA, PCA
Notes to Specific brain areas:>corpus striatum and internal capsule are supplied mainly by medial and lateral striate central branches of MCA>thalamus- supplied by branches of PCA, basilar and PCA>midbrain- PCA, superior cerebellar and basilar arteries>pons- supplied by basilar, anterior, inferior and superior cerebellar arteries, basilar arteries.>medulla oblongata- ant. And post spinal arteries>cerebellum- superior cerebellar, AICA, PICA
“Christy Often Stays Frying For Ian Jay Howard”(memonics)
Blood Supply of the Brain
3
Anterior circulation
controls most motor, activity, sensation, thought, speech, and emotion
supplied by the carotid arteries
Hallmark:
◦ Aphasia & monocular blindness
Posterior circulation
supplies the brainstem and the cerebellum, controlling the automatic parts of brain function and coordination
supplied by the vertebrobasilar arteries
Hallmark:
CN affectation
Neurological Deficit by the artery involved:
MCA- UE>LE, aphasia, visual agnosia
4
ACA- LE>UE, apraxia, urinary incontinence, impaired judgement/ insight
PCA- visual agnosia, alexia, memory impairments
Neurological deficit by laterality:
(L) optimist
aphasia
Alexia without agraphia
Visual agnosia
(R) pessimist
Auditory agnosia
Music and art d/o
Judgement
Poor retention of new tasks
Gait problem
CEREBROVASCULAR ACCIDENT
Definition
sudden loss of neurological function caused by an interruption of blood flow to the brain (Sullivan)
A sudden onset of focal neurological deficits caused by a vascular lesion to the brain (Payton)
5
Rapidly developing clinical signs of a focal or global disturbance of cerebral function presumed to be of vascular origin and lasting for more than 24 hrs ( WHO)
Other Names:
◦ Stroke
◦ Apoplexy
◦ Cerebrovascular Occlusion
“Stroke”
◦ Is clinical term implying a vascular pathogenesis
“Stroke is a non-traumatic brain injury caused by failure of transport of oxygen due to occlusion or rupture of cerebral vessel.”
Epidemiology
3rd leading cause of death
◦ after heart disease and cancer
most common:
a. serious neurologic disorder in the United States
comprise half of all patients admitted to hospital for a neurologic disease
b. cause of chronic disability among adults in the United States
6
age related
◦ uncommon before age 50
◦ Incidence doubles each decade after age 55
Gender:
◦ more common in men
Race:
◦ African american 2x > Whites > Asians
Mortality rate:
◦ hemorrhagic stroke account for the largest number of deaths
Most common cause of disability
>65 y/o
Classifications of Stroke
1. Duration and severity of neurological signs
◦ TIA, RIND etc.
2. Etiology
◦ ischemia vs. hemorrhage
3. Specific location of vascular injury
◦ MCA, ACA, PCA etc.
4. Management categories
◦ dependent on early acute care management
◦ Initial management is an indicator for the progress of the px
7
◦ ex: Management for TIA is different from the management of mild stroke
Temporal Classification of Stroke
1. TIA
◦ signs of focal neurological deficits lasting for a few a minutes to several hours but do not last > for 24 hrs.
◦ A.K.A mini stroke
2. RIND (Reversible Ischemic Neurological Deficit)
◦ focal brain ischemia in which the neurological deficits may resolve spontaneously (generally within 3 weeks)
i.e. as brain swelling or clot formation subsides, thus lessening neurological deficit
◦ this term is no longer used
8
3. RNI (Residual Neurological Impairment)
◦ neurological impairments that persist longer than 3 weeks and may lead to permanent disability
◦ the patient presents with fixed deficits
due to cellular death and/or cerebral infarction
◦ can present in 3 forms:
1. stable
the neurological deficit is permanent and will not improve or deteriorate
Completed stroke
2. improving
return of previously lost neurological function over several days to weeks
3. progressing
the neurological status continues to deteriorate following the initial onset of focal deficits
may see a stabilization period, followed by further progression
Stroke in evolution
9
Temporal Classification of Stroke
TIA- neurological deficits persist less than 24 hrs
RIND- greater than 24 hrs but is resolved within 1 week
Stroke in evolution- hallmark is increasing neurological deficit after 1 week
Cresendo- series of sudden neurological deficit 1week up to 3 mos.
Completed- stable neurolic deficit persistent throughout life
TIA
episodes of a temporary reduction in perfusion to a focal region of the brain
causes a short-lived/ temporary disturbance of function
symptoms vary depending on the CNS anatomy involved, and may include:
◦ numbness of the hand, arm, or one side of the face or tongue
◦ weakness or paralysis of a limb
◦ slurred speech
onset is rapid
no neurological deficit remains after the attack
10
may be the only warning of an impending stroke
one episode in a lifetime to > 20 in one day
Factors that may cause TIA:
1. occlusive episodes
2. emboli
3. reduction of cerebral perfusion
arrhythmia (irregular breathing)
↓ CO
Hypotension
over medication with anti-HTN drugs
Subclavian Steal Syndrome
caused by excessive aerobic exercise of upper limb
due to obstruction of subclavian artery before the origin of cerebral artery
blood flow to vertebral artery goes in the subclavian artery
4. Cerebrovascular spasm
Etiological Classification of Stroke
1. Ischemic Stroke
◦ caused by a decreased blood supply to the brain
11
◦ result of a thrombus, embolus, or conditions that produce low systemic perfusion pressures
Maybe 2° to cardiac failure or significant blood loss with resulting systemic hypotension
◦ deprives the brain of needed oxygen and glucose, disrupts cellular metabolism, and leads to injury and death of tissues
2. Hemorrhagic Stroke
◦ Caused by large amounts of blood within a closed cranial cavity
◦ abnormal bleeding into the extravascular areas of the brain
Due to a rupture of a cerebral vessel or trauma
◦ Has a very sudden onset
◦ Closely linked to chronic hypertension
Classification of Ischemic StrokeThrombotic
Most common type of stroke
Accounts for ~40% of all stroke
Has a gradual onset
12
Occurs commonly at night during sleep or during periods of inactivity
due to development of a clot within the large cerebral arteries or their branches in
◦ with large infarctions, edema may be severe enough to cause brain displacement, herniation, and death
Embolic
Accounts for 30% of all stroke
Has an abrupt onset
may arise from thrombi in the heart, or on heart valves or the large extracranial arteries
occlusion occurs in small cortical vessels
◦ Commonly in the middle cerebral artery
large vessel occlusions do occur
◦ may involve the carotid or vertebrobasilar circulation (rarely)
commonly affect the elderly
represent an important cause of stroke in younger adults
Cortical deficit is the hallmark of embolic stroke & includes:
◦ Seizures
◦ Aphasia ( dominant hemisphere)
◦ Neglect (non dominant hemisphere)
emboli may consist of:
13
◦ fat (from fractured long bones)
◦ air (in decompression sickness)
◦ venous clot that passes through a patent foramen ovale with shunt (paradoxical embolus)
Causes of cerebral embolism:
1. Cardiac
Atrial fibrillation, other arrhythmias
recent MI
rheumatic heart disease (eg, mitral stenosis)
cardiomyopathy
Bacterial endocarditis
Valve prosthesis
Nonbacterial valve vegetations
Atrial myxoma
2. Large artery
Atherosclerosis of aorta and carotid arteries
3. Paradoxical
Peripheral venous embolism with R-to-L cardiac shunt
Lacunar
constitute ~20% of all strokes
14
May be gradual or sudden in onset
Affect small, deep penetrating branches of the large vessels which perfuse the subcortical structures
◦ i.e. lenticulostriate arteries (MCA)
Lacunae
◦ small, circumscribed lesions
◦ <1.5 cm in diameter
◦ seen in the putamen, pons, thalamus, caudate, and internal capsule
More commonly seen in patients with hypertension and diabetes
Pathology is due to microatheroma with progressive vessel wall thickening and fibrinoid necrosis, microembolism, or rarely arteritis
Hallmark: pure motor or pure sensory stroke
(-) involvement of higher cortical function (language, praxis, nondominant hemisphere syndrome, vision)
Classification of Hemorrhagic Stroke Intracerebral hemorrhage
Has an abrupt onset
Linked to chronic hypertension
Occurs due to rupture of microaneurysms (Charcot-Bouchard aneurysms)
◦ “false” aneurysms due to arterial wall dilations 2˚ to HTN
15
> 1/3 occur in normotensives
commonly occurs at the site of small, deep, penetrating arteries
◦ weakened by atherosclerosis producing an aneurysm
◦ Locations include the putamen, thalamus, pons, cerebellum, and cerebrum
◦ Frequently extends to ventricular subarachnoid space
Symptoms:
◦ Sudden onset of headache and/or LOC
◦ Vomiting at onset in 22–44%.
◦ Seizures occur in 10% of cases (first few days after onset)
◦ Nuchal rigidity is common
Subarachnoid hemorrhage
affects large blood vessels
Results from from rupture of an arterial aneurysm at the base of the brain with bleeding into the subarachnoid space
◦ saccular or berry aneurysm
Arterial dilations found at bifurcations of larger arteries at the base of the brain
90–95% of saccular aneurysms occur on the anterior part of the Circle of Willis
Rupture occurs usually when patient is active rather than during sleep (eg, straining, coitus)
16
Peak age for rupture is between 5th & 6th decade
usually asymptomatic prior to rupture
Clinical key for diagnosis of hemorrhagic stroke:
◦ Increase in intracranial pressure
◦ headache
◦ Vomiting
◦ Decrease level of consciousness
Patient may be lethargic or comatose
17
18
Cause %
Large vessel occlusion/infarction 32
Embolism 32
Small vessel occlusion, lacunar 18
Intracerebral hemorrhage 11
Subarachnoid hemorrhage 7
Pathophysiology
Atherosclerosis, cerebral edema, bleeding
19
↓
Interruption/restricted supply of blood flow going to the brain
↓
Oxgen and/or nutrient deprivation
↓
cell damage
↓
impaired neurologic function
Sites of Predilection (of atherosclerotic plaque)
include bifurcations,constrictions, dilation, or angulations of arteries
The most common sites for lesions to occur are at the:
1. origin of the common carotid artery
2. transition of common carotid into the middle cerebral artery
3. at the main bifurcation of the middle cerebral artery
4. junction of the vertebral arteries with the basilar artery
Risk Factors:Non-modifiable (Biological indicators)
1. Age
20
◦ the 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
2. Sex
◦ male > female
◦ Acc. To Sullivan:
Women has higher risk because they tend to live longer
3. Race
◦ African Americans 2 > whites > Asians
4. Family history of stroke
Risk Factors:Modifiable
1. Hypertension (A)
◦ the most important modifiable risk factor
21
◦ Especially for subjects with BP levels higher than 160/95 mm Hg
◦ increases the risk of thrombotic, lacunar, and hemorrhagic stroke and increases the likelihood of subarachnoid hemorrhage
2. History of TIA/prior stroke (S)
◦ ~ 5% of patients with TIA will develop a completed stroke within 1 month if untreated
◦ ~ 14% of patients with TIA will develop a completed stroke within 1 year
3. Heart disease (A)
◦ Ischemic/ hypertensive
◦ Congestive heart failure (CHF) and coronary artery disease (CAD) increase risk by twofold
◦ Valvular heart disease and arrhythmias increase risk of embolic stroke
◦ Atrial fibrillation is an independent risk factor
increased risk of stroke 5x
4. Diabetes (A)
◦ Independent risk factor
◦ increases the risk b y twofold
◦ Unfortunately, good blood sugar control has not been shown to alter the risk of stroke
5. Cigarette smoking (A)
◦ risk of ischemic stroke in smokers is about double that of nonsmokers
22
6. Hyperlipidemia (A)
◦ Elevated low-density lipoprotein (LDL) cholesterol is an important risk factor for ischemic heart disease
◦ small additional risk, mainly for individuals younger than age of 55
◦ 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)
6. Carotid stenosis (and carotid bruit)
◦ risk of stroke decreases with carotid endarterectomy (CEA) on selected symptomatic patients (> 70% stenosis)
7. ETOH abuse/cocaine use
◦ < 2 drinks/day relative risk 0.51
◦ > 7 drinks/day relative risk 2.96 (Sacco, 1999)
8. High-dose estrogens (birth control pills)
◦ considerable increased risk when linked with cigarette smoking
9. Systemic diseases associated with hypercoagulable states (A)
◦ Result to generalized reduction of cerebral blood flow
Elevated RBC count
Elevated hematocrit
Elevated fibrinogen
are higher in individuals who smoke and have a high-cholesterol diet
23
Protein S and C deficiencies
Sickle-cell anemia
Cancer
10. Migraine headaches
11. Sleep apnea
12. Patent foramen ovale (PFO)
Note: Obesity/sedentary life style have no clear relationship with increased risk of stroke
Other risk factors
Geographical location:
◦ higher risk of stroke in the southeastern United States than in other areas
the so-called “stroke belt” states
Socioeconomic factors
◦ some evidence that strokes are more common in people with low income than among more affluent people
24
Signs of Focal/ Neurological deficits
changes in the level of consciousness
sensory impairment
◦ on the side of the body opposite to the side of the lesion
motor impairment
◦ on the side of the body opposite to the side of the lesion
◦ Hemiparesis or hemiplegia
cognitive impairment
perceptual impairment
language impairment
◦ aphasia, dysarthria
Note: to be classified as stroke, the above signs of focal deficits must be present for at least 24 hrs.
25
Determinants of Severity of Neurological deficits
Location of brain injury
Extent of brain injury
Amount of collateral blood flow
Early acute care management
◦ important indicator for the progress of the patient
26
DIFFERENTIAL DIAGNOSIS (according to De lisa)
Symptoms seldom due to CVA
◦ Vertigo alone, Dizziness
◦ Dysarthria alone
◦ Dysphagia alone
◦ Displopia alone
◦ Headache
◦ Tremor
◦ Confusion
◦ Memory loss
◦ Delirium
◦ Coma
◦ Syncope (loss of consciousness)
◦ Incontinence (Inability to control excretory function)
◦ Tinnitus (Ringing of ear)
Condition Most Frequency Mistaken
◦ Seizures
◦ Cerebral tremor
◦ Subdural hematoma
◦ Cerebral Abscess
◦ Peripheral neuropathy
◦ Multiple Sclerosis
◦ Encephalitis
◦ Psychogenic
◦ Migraine
27
ACA Syndrome
supplies the medial aspect of the cerebral hemisphere (frontal and parietal lobes) and subcortical structures, including:
◦ basal ganglia (anterior internal capsule, inferior caudate nucleus),
◦ anterior fornix
◦ anterior four fifths of the corpus callosum
Occlusion proximal to anterior communicating results in minimal deficit
◦ Because it allows perfusion on either side
Lesions distal to AcomA produce more significant deficits
◦ Contralateral weakness and sensory loss, affecting mainly distal contralateral leg
◦ Mild or no involvement of upper extremity
◦ Head and eyes may be deviated toward side of lesion acutely (frontal gaze)
◦ Urinary incontinence with contralateral grasp reflex and paratonic rigidity may be present
◦ May produce transcortical motor aphasia if left side is affected ((loss of power to comprehend written or spoken words; patient can repeat)
◦ Gait apraxia (if corpus callosum is affected)
If both anterior cerebral territories are affected, profound mental symptoms may result (akinetic mutism)
28
MCA SyndromeSuperior division
supplies rolandic and prerolandic areas
Most common cause of occlusion is an embolus
S/sx:
1. Sensory and motor deficits on contralateral face and arm > leg
2. Head and eyes deviated toward side of infarct (frontal gaze)
3. Muscle tone usually decreased initially and gradually increases over days or weeks to spasticity
4. With left side lesion (dominant hemisphere)
- global aphasia initially, then turns into Broca’s aphasia (motor speech disorder)
5. Right side lesion (nondominant hemisphere)
- deficits on spatial perception, hemineglect, constructional apraxia, dressing apraxia
MCA SyndromeInferior division
blood supply to the lateral temporal and inferior parietal lobes
Left side lesion
29
◦ Wernicke’s aphasia
Right side lesion
◦ left visual neglect
PCA Syndrome
supplies the corresponding occipital lobe and medial and inferior temporal lobe
also supplies the upper brainstem, midbrain, and posterior diencephalon, including most of the thalamus
Occlusion proximal to the posterior communicating artery results in minimal
◦ deficits owing to the collateral blood supply from the posterior communicating artery
S/sx:
1. Occlusion of thalamic branches
- may produce hemianesthesia (contralateral sensory loss) or central post-stroke (thalamic) pain
2. Occipital infarction
◦ homonymous hemianopsia, visual agnosia, prosopagnosia, or, if bilateral, cortical blindness (Anton syndrome), alexia (inability to read)
3. Temporal lobe ischemia
30
◦ amnesia (memory loss)
4. Cerebral peduncle
◦ Contralateral hemiplegia
5. Brainstem
◦ Affectation of CN3 (oculomotor palsy) & CN4 (vertical gaze palsy)
◦ Weber syndrome
Vertebrobasilar Syndrome
Vertebral arteries supply:
cerebellum (via posterior inferior cerebellar arteries)
medulla (via the medullary arteries)
Basilar artery supplies:
pons (via pontine arteries)
the internal ear (via labyrinthine arteries)
cerebellum (via the anterior inferior and superior cerebellar arteries)
31
Occlusions of the vertebrobasilar system can produce a wide variety of symptoms with both ipsilateral and contralateral sign
Cerebellar and cranial nerve abnormalities also are present
There is absence of cortical signs (such as aphasias or cognitive deficits) that are
may present with any combination of the following signs/symptoms:
◦ Vertigo
◦ Nystagmus
◦ Abnormalities of motor function often bilaterally
◦ Ipsilateral cranial nerve dysfunction
◦ Crossed signs: motor or sensory deficit on ipsilateral side of face and contralateral
◦ side of body; ataxia, dysphagia, dysarthria
32
Weber Syndrome (Base of Midbrain)
Obstruction of interpeduncular branches of posterior cerebral artery or posterior choroidal artery or both
S/Sx:
◦ Ipsilateral CN3 paralysis
◦ Contralateral hemiplegia
◦ contralateral Parkinson signs
◦ contralateral dystaxia (mild degree of ataxia)
Benedikt Syndrome (Red Nucleus/Tegmentum of Midbrain)
• Obstruction of interpeduncular branches of basilar or posterior cerebral artery, or both
S/Sx:
◦ Ipsilateral CNIII nerve paralysis with mydriasis
◦ contralateral hypesthesia (medial lemniscus)
◦ hyperkinesia (ataxia, tremor, chorea, athetosis) due to damage to red nucleus
Locked-in syndrome (LIS)
occurs with basilar artery occlusion
33
thrombosis and bilateral infarction of the ventral pons
is a catastrophic event with sudden onset
S/Sx:
acute hemiparesis rapidly progressing to tetraplegia
lower bulbar paralysis (CN V through XII)
Initially the patient is dysarthric and dysphonic but rapidly
progresses to mutism (anarthria)
preserved consciousness and sensation
◦ The patient cannot move or speak but remains alert and oriented
Horizontal eye movements are impaired
vertical eye movements and blinking remain intact
◦ Communication can be established via these eye movements
Millard-Gubler Syndrome (Base of Pons)
Obstruction of circumferential branches of basilar artery
S/Sx:
Ipsilateral abducens (CN6) and facial (CN7) palsies
Contralateral hemiplegia, analgesia, hypoesthesia
◦ Extension to medial lemniscus = Raymond-Foville Syndrome (with gaze palsy to side of lesion)
34
Lateral Medullary (Wallenberg) Syndrome
A.K.A PICA syndrome, and vertebral artery syndrome
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
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
35
◦ Vertigo; nausea and vomiting
◦ Hiccups
◦ Nystagmus, diplopia
Note: No facial or extremity muscle weakness seen in this syndrome
ICA Syndrome
supplies both ACA & MCA
Ocular infarction
◦ Transient monocular blindness (amaurosis fugax)
embolic occlusion of retinal branch of opthalmic artery
occurs prior to onset of stroke in approximately 25% of cases of ICA occlusion.
Cerebral infarction
◦ variable presentation with complete ICA occlusion
◦ from no symptoms (if good collateral circulation exists) to severe, massive infarction in ACA and MCA distributions
◦ Patients will present with contralateral motor and/or sensory symptoms
◦ significant edema
◦ will lead to coma & eventually death
◦ (+) uncal herniation
36
Gerstmann syndrome
37
Anatomy: cerebral hemisphere—dominant parietal lobe
Artery: middle cerebral artery
Symptoms:
Agraphia
◦ acalculia
◦
◦ Finger agnosia
◦ Right and left disorientation
Anton syndrome
Anatomy: cerebral hemispheres—bilateral occipital lobes
Artery: posterior cerebral artery (bilateral basilar artery)
Symptoms: visual loss—bilateral
◦ Unawareness or denial of blindness
Weber syndrome
• Anatomy: midbrain–base
38
• Artery: posterior ocerebral artery (penetrating branches t midbrain)
• Symptoms: contralateral hemiparesis
• Ipsilateral lateral gaze weakness
Dejerine–Roussy syndrome
• Anatomy: thalamus
• Artery: posterior cerebral artery—penetrating branches to thalamus
• Symptoms: hemisensory loss—all modalities
• Hemi-body pain
Medical ManagementGoals
1. improve cerebral perfusion, re-establish circulation & O2
◦ O2 via mask or nasal cannula
◦ coma – assisted ventilation, suctioning, intubation
39
2. maintain adequate BP
3. maintain sufficient CO by meds
4. restoring fluid & electrolyte balances
5. maintain blood – glucose level within (N) range
6. control seizures/ infection (common in ICA syndrome)
7. control ICP & herniation using anti – edema agents
◦ if surgery – ventriculostomy (drain & monitor ICP)
8. maintain bladder fxn. by catheterization
9. maintain jt. integrity
◦ coma, complete bed rest, paralysis - PROM
10. maintain skin integrity – turning every 2 hrs.
◦ WC Pº relief should be done every 15 – 20 mins. or 10 – 15 mins.
Pharmacological Management
1. anti-coagulant therapy
◦ inhibits clotting factors
◦ Indicated for:
1. embolic strokes
Not given for lacunar strokes and completed strokes
2. also prevent DVT and pulmonary embolism
◦ Heparin (through IV route) – given for stroke in evolution
40
◦ Coumadin (Warfarin)- given orally; for short term
2. anti-platelet therapy – Aspirin (ASA), Aspirin/Dipyridamole (Aggrenox), Clopidogrel (Plavix)
◦ indicated to reduce the risk of subsequent attacks after an initial TIA or other event indicating risk of future ischemic stroke
Patients with non-cardioembolic ischemic stroke or TIA (for thrombotic, embolic, & lacunar stroke only)
Patients who are at risk of recurrent stroke and other cardiovascular events
◦ Given orally (The daily dose given is 100 mg)
◦ beneficial as secondary stroke prevention of presumed arterial origin
◦ improves cerebral perfusion
↓ platelet aggregation
◦ long – term, low dose = ↓ risk of recurrence of stroke
◦ high dose = given to px with independent risk factor (Atrial fib)
3. anti-HTN agents
◦ indicated for acute stroke (especially hemorrhagic)
if acute myocardial infarction, aortic dissection, severe CHF or hypertensive encephalopathy are present
41
◦ Diuretics, Beta blockers, ACE inhibitor , Ca channel blockers
4. anti- spasticity drugs
◦ Diazepam/ Benzodiazepine (BNz) vs. baclofen & dantrolene sodium
Tests & Measures(Laboratory Tests)
Complete blood count (CBC)
platelet count
prothrombin time (PT) and partial thromboplastin time (PTT)
electrolytes, calcium, glucose, blood urea nitrogen (BUN) creatinine
chest x-ray
electrocardiogram (EKG)
sedimentation rate
Lipid profile
thyroid profile
In selected cases, antithrombin III, protein C and protein S
42
Tests & Measures(Imaging Studies)
1. Non contrast CT Scan
◦ evaluates presence of blood (cerebral hemorrhage or hemorrhagic infarction)
especially when thrombolysis is being considered
◦ CT studies are often normal during the first few hours after brain infarction
2. MRI Scan
◦ More sensitive than CT scan in detecting ischemic infarcts (including small lacunes)
◦ Can detect edema due to ischemia within a few hours of onset of infarct
3. Carotid Doppler/ultrasound
◦ can be useful in screening the extracranial internal carotid arteries for significant stenosis
43
4. Magnetic resonance angiography (MRA)
◦ may be used to evaluate the carotid circulation, the vertebral-basilar system, the circle of Willis, and the anterior, middle, and posterior cerebral arteries and their major branches
◦ Tends to overestimate the degree of stenosis compared with contrast angiography
◦ 5. Contrast cerebral angiography
◦ provides the most detailed and reliable information on the presence of carotid and intracranial disease
◦ In experienced hands, complications should result in less than 1% morbidity and mortality
44
Factors influencing functional outcomes
45
Good functional outcome
◦ Hemiparesis
◦ no sensory loss (or pure motor stroke)
◦ Absence of significant associated disease like DM, HPN, MI etc.
◦ Young age
◦ signs of motor recovery of the hand by 4 weeks (full or good recovery of hand function)
Fair functional Outcome
◦ (+) hemiplegia w/ moderate spasticity
◦ (+) expressive aphasia
◦ (+) intermittent incontinence at night
◦ Mild sensory loss
Poor functional Outcome
◦ Advanced age (old) 60 above
◦ Presence of global aphasia
◦ Continuing urinary and bowel incontinence
◦ Severe sensory loss
◦ No measurable grasp strength by 4 weeks
◦ Severe proximal spasticity
◦ Prolonged “flaccidity” period
◦ Complete arm paralysis at onset (poor prognosis of recovery of useful hand function)
46
◦ Late return of proprioceptive facilitation (tapping) response > 9 days
◦ Late return of proximal traction response (shoulder flexors/adductors) > 13 days
OTHER RISK FACTORS FOR DISABILITY AFTER STROKE
Global aphasia
Severe neglect
Sensory and visual deficits
Impaired cognition
Delay in medical care
47
Delay in rehabilitation
Bilateral lesions
Previous stroke
Previous functional disability
Diabetes mellitus
Cardiac disease
Electrocardiograph abnormalities
Negative Factors for Return to Work After a Stroke
Low score on Barthel index at time of rehabilitation discharge
Prolonged rehabilitation length of stay
Aphasia
Prior alcohol abuse
ImpairmentsI. Sensory
impaired but rarely absent on the hemiplegic side
48
Type and extent of impairment is related to the location and size of the vascular lesion
distribution of sensory loss
◦ face-UE-LE-pattern
◦ cortical lesions
localized areas of dysfunction
Involves complicated sensory processing such as two-point discrimination, accurate localisation of perceptions, stereognosis, and graphesthesia
◦ subcortical lesion
diffuse involvement throughout one side of the (e.g. history of significant numbness or sensory loss)
involving the thalamus and adjacent structures
◦ brainstem lesion
crossed anesthesia
ipsilateral facial impairment, contralateral arm & LE lesion
thalamic pain
◦ constant, severe burning pain with intermittent sharp pain exaggerated response to specific stimulus
◦ usually in the contralateral half of the body
◦ stimulus: touch, pain (pin prick), Pº, light (bright), sounds, Tº (hot or cold)
◦ prevents the patient from actively participating in rehabilitation
49
II. Motor
1. Weakness or paralysis
2. tone alteration
Flaccidity
present immediately after stroke due to cerebral shock
short – lived tone (last for few days or wks.)
occur to px with 1º motor cortex & cerebellar type of lesion (PCA)
Spastic stage
occurs in antigravity ms.
UE: scapular retractors, shoulder adductors, depressors & IR, elbow flexors, forearm pronators, wrist & finger flexors
LE: pelvic retractors, hip adductors, IR & extensors, knee extensors, ankle plantarflexors & supinators, toe flexors
Trunk/ neck: lateral flexors of hemiplegic side2. tone
3. Abnormal Synergy
emerge with spasticity
can be elicited by: reflex, associated reaction, minimal voluntary mov’t.
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III. Abnormal reflexes
Occurs during recovery when spasticity and synergies are strong
ATNR
if persists, may cause difficulty in rolling & midline hand play
to promote midline hand play & promote self – feeding, place px in sidelying postn.
STNR
if persist, may cause difficulty in assuming quadruped position
Moro
tested last coz it will result to crying
Tonic labyrinthine reflex
Tonic lumbar reflex
Rot. of trunk to one side : result in flex. of the UE and LE and vice versa
Galant
stroke lumbar area on the ®, lateral flexion to the ®
Associated rxn
◦ Consist of ab(N) automatic response of the involved limb, resulting from acton occurring in some part of the
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body by voluntary or reflex stimulation (yawning, sneezing, or coughing)
◦ SOUQUE’S PHENOMENON
Elevation of the hemi. arm above the horizontal plane may elicit an extension and abd. response of the fingers
◦ RAIMESTE’S PHENOMENON
Resistance to add. R abduction produce a like response in the opposite Limb
◦ HOMOLATERAL LIMB SYNKINESIS
Flex of the arm elicits flex. of the leg on the hemi. side.
IV. Posture & Balance
altered coordination
◦ Result from cerebellar or basal ganglia involvement & proprioceptive losses or weakness
◦ sensory ataxia (with PCA lesion involving basal ganglia)
◦ Motor ataxia (with cerebellar lesion)
◦ apraxia (basal ganglia lesion or cerebellar lesion)
Ipsilateral Pushing/ Pusher’s syndrome/ Controversive Syndrome
◦ unusual motor behavior characterized by active pushing of the stronger ms. esp. towards the weak side
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◦ Results to listing towards the affected side
◦ results to fall
◦ caused by severe misperception of body orientation in relation to gravity
◦ Has a poor prognosis
Typical arm posture
Cortical thumb
V. Visual
Homonymous hemianopsia
◦ lesion in the optic radiation in the internal capsule (if the MCA is affected) or the 1º Visual cortex (if PCA is affected)
Monocular blindness
Visual neglect (visual inattention)
◦ ® Hemispheric lesion = visuospatial neglect
Forced gazed deviations
◦ Hemispheric lesion
the px’s eye deviate away from hemiplegic side
◦ Brainstem lesion
px’s eye deviate towards the hemiplegic side
VI. Speech, Language & Swallowing
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Aphasia
◦ an acquired communication disorder caused by brain damage
◦ characterized by an impairment of language comprehension, formulation, and use
Dysarthria
◦ motor speech disorders caused by lesions in parts of the central or peripheral nervous system that mediate speech production
◦ lesion can be located in the primary motor cortex in the frontal lobe, the primary sensory cortex in the parietal lobe, or the cerebellum
Dysphagia
◦ Difficulty in swallowing
◦ CN 9 & 10
VII. Perception
Due to lesion of the parietal lobe of the non-dominant hemisphere
1. Spatial relations disorder
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a difficulty in perceiving the relationship between the self and two or more objects in the environment
Pt. may not be able to judge distance, size, position, rate of movement, or the relation of parts to the whole
figure–ground discrimination, form discrimination, spatial relations, position in space
Pt. may consistently bump the W/C into the door frame and seem unable to get through the doorway
2. Body image / Body scheme disorder
◦ Body Image – Visual and mental memory of the body parts
◦ Body Scheme – Perception of precise location and relationship of body parts.
◦ Simultagnosia or Autopagnosia
impairment of body scheme
Lack of awareness of the body structure and relation of body parts on one’s self or on other
Lesion site is the dominant parietal lobe or post. Temporal lobe
3. Topographic Disorientation
◦ Difficulty n understanding and remembering the relation of one place to another
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◦ Lesion site : occipital- parietal lobe of the non dominant hemisphere
4. Agnosia
◦ inability to recognize incoming information despite intact sensory capacities
◦ can include visual object agnosia, auditory agnosia or tactile agnosia
5. Unilateral Neglect
Pt. are unaware of what happens on the hemi. side.
Inability to register and integrate stimuli and perceptions from one side of the body and the environment
Lesion on (R) nondominant hemisphere parietal lobe.
6. Apraxia
◦ Disorder of vol. learned mov’t.
◦ Inability to perform purposeful mov’t in the absence of paralysis/ impaired sensation
◦ Ideomotor Apraxia
Ref. to breakdown bet. concept or performance
Pt. is able to carry out habitual tasks automatically and describe how they are done but is unable to perform a task upon command and is unable to imitate gesture
Lesion : Dominant supramarginal gyrus.
◦ Ideational Apraxia
Failure in the conceptualization of the task.
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Inability to perform a purposeful motor act bec. pt. can’t understand the overall concept of act, can’t retain the idea of the task and can’t formulate the motor pattern required.
Lesion : dominant parietal lobe
◦ Constructional Apraxia
Inability to prod. 2 or 3 dimensional forms by drawing constructing, or arranging blocks or obj. spontaneously or upon command.
Lesion : either hemisphere.
◦ Dressing Apraxia
Inability to dress one’s self properly owning to a disorder in the body scheme or spatial relationship.
Lesion site : nondominant occipital lobe.
VIII. Cognition
Attention disorder
Memory disorder
Perseveration
◦ continued repetition of words, thoughts, or acts not related to current context
◦ lesions in the premotor and/or prefrontal cortex
lack of abstract thinking, impaired organization and sequencing (executive functions)
Dementia
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delirium
IX. Emotional Status
pseudobulbar affect (PBA)
◦ also known as emotional lability or emotional dysregulation syndrome
◦ emotional outbursts of uncontrolled or exaggerated
◦ laughing or crying that are inconsistent with mood
Depression
◦ Seen with lesions in the left frontal lobe (acute stage) and with
◦ lesions in the right parietal lobes (subacute stage)
◦ Occurs between 6 mos – 2 years post CVA
Apathy
Euphoria
X. Bladder & Bowel
Urinary incontinence
◦ Common during acute phase
◦ may be caused by CNS damage, UTI, impaired ability to transfer to toilet or impaired mobility, confusion, communication disorder/aphasia, and cognitive perceptual deficits that result in lack of awareness of bladder fullness
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◦ Persistent incontinence is associated with a poor long-term prognosis for functional recovery
◦ Treatments
◦ – Treat possible underlying causes (eg, UTI)
◦ – Regulation of fluid intake
◦ – Transfer and dressing-skill training
◦ – Patient and family education
◦ – Medications (if no improvement with conservative measures)
◦ – Timed bladder-emptying program
◦ – Remove indwelling catheter and perform postvoid residuals (PVRs)
◦ – Intermittent catheterization (IC)
Bowel incontinence
◦ 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
Constipation
◦ Management:
adequate fluid intake/hydration
modify diet (eg, increase in dietary fiber)
bowel management (stool softeners, stool stimulants, suppositories
allow commode/ bathroom privileges
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Physical activity is also helpful to improve these problems
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Rehab Management
Should begin early in the acute stage when the patients condition is stable
Includes:
1. Traditional therapy
◦ positioning, ROM exercises, strengthening, mobilization, compensatory techniques, endurance training (eg, aerobics)
2. PNF (by Knott & Voss)
3. NDT’s (Bobath)
4. Brunnstrom’s movement therapy
5. Rood’s tech.
6. Motor relearning (Carr and Shepard Approach)
7. FES, ES
Bobath
◦ Stage 1- Flaccidity
◦ Stage 2- Spasticity
◦ Stage 3- Relative Recovery
PNF
Indicated for patients with orthooedic and neurologic condition
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Can be use to assist problem with strength
(recite components)
BS, BA, BRCD,BRSD
BOBATH
Principle: to inhibit spasticity and facilitate (N) movement
Sequence:
◦ Normalization of tone
◦ Selective movement
◦ Practice using functional movement
BRUNNSTOM
Long duration of flaccidity and severe spasticity are poor prognosis
Mirroring reflex
ATNR
UE flexor synergy elbow flexion and supination, sh adduction *first to appear and last to disappear
Isolation and combination
Factors that might influence the timing of rehabilitation effect include:
1. Medical stability
2. motivation
3. Patient endurance
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4. stage of recovery
5. ability to learn
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