Cerebrovascular Disease/Accidents (CVA’s) (Stroke)

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Cerebrovascular Disease/Accidents (CVA’s) (Stroke)

Common acute nonconvulsive focal neurological clinical syndrome due to ischaemia or haemorrhage – not necessarily a diagnosis, but a symptom of an underlying aetiologic diagnosis. Occurs when oxygen supply to brain is suddenly stopped  upper motor neuron death  focal and/or global signs of disturbed neurological function. Major cause of death and disability.

Risk factors:
Age (2/3rd >65yrs; strongest risk factor; >80yrs, 30x greater risk); male (30-80% greater risk; no greater risk in those that are younger); cigarette smoking (2-4x greater risk; risk declines after stoping smoking); hypertension (4x greater risk; risk almost double with each 7.5mmHg increase in diastolic pressure; increases risk for severity of atheroma); diabetes mellitus (2x greater risk; not known if good glycaemic control decreases risk); dyslipidaemia (decreased HDL and increased LDL are significant risk factors); obesity (link is likely to be confounded by its relationship to hypertension, diabetes, dyslipidaemia, etc); sedentary lifestyle/lack of physical exercise; alcohol consumption (relationship may be U shaped and not linear; modest consumption may be protective); oral contraceptives; polycythemia; atrial fibrillation (5x greater risk; clot can form in left atrium and embolise to brain); family history; history of prior stroke or transient ischaemic attack; elevated homocysteine levels (inborn error complicated by arterial and venous thrombosis)

• Transient ischaemic attack (see below)
• evolving stroke (an ischaemic or haemorrhagic stroke that worsens in a step wise fashion while under observation)
• completed stroke (an ischaemic or haemorrhagic stroke that has caused its maximum deficit)

Ischaemic strokes – thrombotic brain infarct (45-65%); embolic brain infarct (10-20%)
Haemorrhagic strokes – intracerebral haemorrhage (5-15%); subarachnoid haemorrhage (5-10%)
Unknown, combined, other strokes – up to 10%

Unusual types/causes:
trauma (arterial trauma; eg penetrating neck injury)
arterial dissection
connective tissue diseases (eg SLE – inflammatory reaction in arterial wall; giant cell arteritis; antiphospholipid syndrome)
congenital arterial anomalies
migraine (Migrainous stroke is a well defined syndrome)
haematological disorders (eg polycythemia – increased thrombotic tendency; disseminated intravascular coagulation)
stroke associated with MI (cerebral and cardiac atheroma usually present in same patient)

Reduction in blood supply (usually atherosclerotic in origin or from clot)  direct damage to tissue and changes in osmotic pressures that lead to cerebral oedema; intracellular pH drops and lactic acid levels increase in absence of aerobic metabolism; neurons dies within minute of oxygen deprivation; cellular damage  clinical manifested as neurological features.

Intracerebral haemorrhage (see later)

Clinical features:
70% present with hemiparesis, 20% with aphasia; abrupt onset

The clinical features of ischaemic strokes usually depend on which artery is involved. Classical syndromes of clinical features are ascribed to the involvement of specific arteries, but in isolation that appear only infrequently clinically, with a significant amount of overlap with the final clinical picture also be related to the extent of the occlusion:
a) Middle cerebral artery (MCA):
Most common pattern; extent of clinical signs will depend on collateral circulation and site of occlusion; usually embolic. Contralateral hemiparesis and hemisensory loss (usually severe) – mainly face and arms; eyes deviate to side of infarct; feet and legs less affected than arms; aphasia if dominant hemisphere is affected; may later develop confusional states (if left hemisphere) or depressive states (if right hemisphere)

b) Anterior cerebral artery:
Collateral circulation is often adequate, so less common; face not normally involved; eyes deviate towards side of lesion; hemiplegia, motor and sensory deficits of contralateral limb (sensory loss affects leg more that arm). If paracentral lobe  mainly leg and foot affected with hemiparesis and hemisensory loss. If frontal and parietal lobe  inability to correctly identify objects; apathy and personality changes

c) Posterior cerebral artery:
Contralateral homonymous hemianopsia; hemisensory loss; thalamic pain visual agnosia; impairment of memory

d) Internal carotid artery:
Contralateral hemiparesis and hemisensory loss; partial loss of sight; half have history of TIA’s – tend to have variable signs of the above three arteries (depends on location and severity)

e) Vertebrobasilar artery:
Imbalance, vertigo, vomiting, nystagmus; lack of co-ordination; ipsilateral pain and temperature sensory loss on face and contralateral loss in rest of body; ipsilateral ataxia; Horner’s syndrome,

d) Lacunar stroke:
Common in those with hypertension; due to occlusion of small arterioles or single deep perforating artery  small deep cystic infarcts (lacunar infarcts). 4 common clinical types – a motor hemiparesis stroke (pure motor stroke); a hemisensory stroke; a dysarthria and arm involvement; and an ataxia with crural paresis (there are other less common types)

Haemorrhagic stokes:
Sudden severe ‘explosive’ headache with loss of consciousness; grand mal seizure; severe confusional state (often fluctuating); bradycardia.

Limb synergy patterns:
These are patterns of mass movement of the limbs that occur after injury to the cerebral voluntary movement system (not just in CVA’s) – limb assumes a flexion or extension synergy pattern:
Lower extremity flexion synergy pattern  pelvic protraction, pelvic depression, hip flexion, hip abduction, hip external rotation, knee flexion, ankle dorsiflexion, foot inversion, toe and hallux dorsiflexion.
Lower extremity extension synergy pattern  pelvic retraction, pelvic elevation, hip extension, hip adduction, hip internal rotation, knee extension, ankle plantarflexion, foot inversion toe and hallux plantarflexion

Acute – medical emergency - stabilise patient, protect airway; assessment by CT or MRI to determine if ischaemic or haemorrhagic ( possible neurosurgical correction of subdural haematoma); IV tissue plasminogen activator (tPA) – improves outcomes if given within 3-6 hours of acute ischaemic stroke; control blood pressure; adequate oxygen; followed by early mobilisation, adequate hydration, bowel program, prevent pressure sores, prevention of emboli, reduction of oedema
Post-acute – rehabilitation therapy (physiotherapy, occupational therapy, speech therapy), social services, evaluate for depression, management of risk factors; pharmacological (aspirin)

Stroke rehabilitation units lead to better outcomes (however resources need to be used judiciously – ie reasonable benefit expected).

Prevention – control of hypertension and cessation of smoking are considered the two most important preventative factors; lowering cholesterol decreases risk; aspirin, ticlopidine, clopidogrel or dipyridamole (antiplatelet therapy) can help; carotid endarterectomy for those with severe carotid stenosis; warfarin in those with atrial fibrillation;

Post stroke outcomes:
Prognosis – 20% die in hospital (higher if older age or haemorrhagic stroke). Up to 30% regain normal ambulation

Other residual features:
• in first month after stroke, death can occur from stroke, pneumonia, cardiac disease or from pulmonary embolism
• can affect cognitive and learning abilities (eg ‘post stroke dementia’ can persist after initial acute illness)
• DVT can occur in up to 75% of CVA survivors
• up to 50% are left with dysphagia
• up to 30% have bowel dysfunction
• 60-70% have shoulder pain (poorly understood; usually a subluxation, adhesive capsulitis, neuropathies, impingement syndromes, tendinopathy; important that flaccid arm is supported and carers need to use methods to avoid traction injuries; range of passive movements needs to be maintained)
• falls and fractures (eg up to 40% fall during in-patient rehabilitation)
• aphasia (if left hemisphere affected)
• up to 70% develop a post stroke depression; many also have low mood and anxiety problems; boredom is often a problem
• dependency on other for daily living activities (will vary depending on extent and level of recovery but includes, for example, bowel function, grooming feeding, dressing, bathing, etc)

Recovery of motor function usually follows a predictable course following stroke induced hemiplegia. However, it is difficult to predict an individual’s outcome early after stroke onset.

Pattern is most consistent when middle cerebral artery is involved:
initially muscles are flaccid, followed by return of reflexes and development if spasticity
lower extremity function recovers sooner and most completely, followed by upper limb and hand
tone usually returns before voluntary movement
control over proximal limb before distal limb
spasticity decreases as voluntary control increases
mass movement or synergy patterns of movements occur before recovery to isolated co-ordinated movements
motor recovery usually plateaus around 3-4 months

Brunnstromm (1970) stages of motor recovery in those with hemiplegia:
Stage 1 – flaccidity; phasic stretch reflexes absent; no volitional or reflex-induced active movement
Stage 2 – spasticity, resistance to passive movement; basic limb synergy patterns; associated reactions; movement patterns stimulated reflexively; minimal voluntary movement
Stage 3 – marked spasticity; semivoluntary; volitional movement of involved limbs, resulting in synergy; usually flexion in arm and extension in leg
Stage 4 – spasticity reduced; synergy patterns still predominant; some complex movements deviating from synergy
Stage 5 – spasticity declines more, but still present with rapid movements; more difficult movement patterns deviating from synergy; voluntary isolated environmentally specific movements predominate
Stage 6 – spasticity disappearing; co-ordination improves to near normal; individual joint movements possible; still some abnormal movement and faulty timing during complex actions
Stage 7 – restoration of normal variety of rapid complex movements patterns with normal timing, co-ordination, strength and endurance

Post-stroke pain syndrome/Thalamic pain/Dejerine-Roussy Syndrome:
Occurs in <5% of CVA survivors; results in severe pain that is often resistant to treatment; pain is usually as described as "burning" or "freezing"; often have sensory disturbances – especially temperature; have exaggerated reaction to external cutaneous stimulus (hyperpathia); only 50% have had a thalamic stroke; pathophysiology probably involves lesions of the spinothalamic pathways with disinhibition and excitation of NMDA receptors in the thalamus.Psychosocial factors: High incidence of depression; less satisfaction with life (correlate with functional deficit); inability of many to return to work; problem with access to transport; lack of community support may be a problemInvolvement of the foot: 3 hemiplegic movement patterns that influence control and alignment of the foot (ref to Physical Therapy of the Foot): 1. Characterised by severe loss of motor control. Weight is born largely by unaffected leg  centre of gravity shifted toward that leg. Affected side has flexed knee, plantarflexed ankle, weight is born by forefoot, midtarsal and subtalar joints pronate; poor toe clearance during swing; muscle contractures.2. Characterised by an incomplete pattern of motor function recovery, an inability to sequence muscle firing and the presence hypertonicity. Affected side tends to have a genu recurvatum (but retraining may have corrected this); forefoot makes initial contact during stance; lack of ankle dorsiflexion and early forefoot contact  midtarsal joint collapse and subtalar joint pronation; claw toes due to extensor substitution; elevates pelvis to initiate swing  toe clearance; during swing foot supinates and adducts during to firing of anterior and posterior tibial muscles3. Characterised by an abnormality of muscle co-activation, an inability to selectively fire the appropriate initiation patterns and the inability to stop firing patterns once they are activated. Do not have control of agonist and antagonist muscles. Ankle is plantarflexed and rearfoot is supinated during swing  lateral border contacts ground first – if rigid  foot remains inverted. If flexible  midtarsal joint collapses; claw toes develop.Problems of foot: Weakness of some muscle groups and spasticity of others; loss of mobility due to foot pathology; joint hypermobility and poor alignment due to proximal influences; oedema is common; muscle contractures; lack of ankle dorsiflexion  compensatory changes at midtarsal and subtalar joints; midtarsal joint collapse; clawing of toes; skin hyperkeratosis as a result of mechanical changes – fifth metatarsal head and styloid process are most common (hyperkeratotic lesions can also develop from pressure of orthoses); may have poorly localised pain/discomfort in foot and leg that is of central origin. Swelling with pitting oedema (sometimes pain) is common in paralysed leg  may further limit movement. Swelling may be due to gravity in dependant limb, lack of contraction of muscle, DVT, cardiac failure, hypoalbuminuria or reflex sympathetic dystrophy. Feeling of coldness is limb occurs in some (arm more frequent than leg) Ankle-foot orthoses are usually used to improve the gait of those with hemiparetic gait  increased stability, increased toe clearance, increased speed and normalised heel strike duration; however an inappropriate AFO can make walking more difficultPodiatric management: • good understanding of disease process and its psychosocial implications • Good alignment of foot and ankle is important goal of therapy  good base of support for more proximal motor control • Hyperkeratotic lesions and ulcers  debridement (toe crests/props often needed for digital deformity) • education and advice (eg footwear; social contact; limb elevation for oedema) • Jordan et al (1998) found that 74% of consecutive patients in a stroke rehabilitation unit had one or more ‘podiatric’ problems that had the potential to adversely affect the stroke rehabilitation program.

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