Hemiplegia
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Hemiplegia

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Hemiplegia Hemiplegia Presentation Transcript

  • Hemiplegia By Dr. Osman Sadig Bukhari
    • 1- lecture at 8:30
    • 2- No student is allowed to attend za lecture
    • after 8:45 & is considered as absen
    • - Hemiplegia :
    • Complete loss of power or weakness on
    • one side of za body
    • - Hemiparesis:
    • Incomplete loss of power or weakness on
    • one side of za body
    • Hemiplegia & hemiparesis are most commonly due to stroke i.e. CVA .
    View slide
  •   View slide
  •  
    • Stroke is:
    • - is za 3 rd commonest cause of death and
    • disability in za developed world
    • - mortality from stroke is 20-30% in the
    • 1 st month & 60% of survivors are dependant.
    • - prevalence is2- 5 /1000/year & it is rising because of the aging population.
    • - male > females
    • Risk factors for hemiplegia
    • 1- Non modifiable factors
    • - age - gender
    • - race - hereditary
    • 2- Modifiable factors
    • - Arterial HT - Cardiac diseases
    • - DM - Cigarette smoking
    • - Hyperlipidaemia - Thrombocythemia
    • - Polycythemia - Physical inactivity
    • - Obesity - OCPs
    • - High alcohol intake - Trauma
    • - Peripheral vascular disease
    • Stroke is:
    • uncommon before 40years except with:
    • - trauma
    • - cardiac diseases e.g RHD
    • - congenital vascular abn
    • - inflammatory arteritis
    • - vascular disease
    • - SS anaemia
    • Hemiplegia is either due to: 1- Thromboembolic infarction (ischemic) (80%): thrombosis/embolism
    • 2- Haemorrhage (15%):
    • intracerebral/ subarachnoid
    • 3- Dissection of carotid & vertebral arteries
    • 4- Cortical venous or dural venous sinus thromb
    • 5- Subdural & extradural bleeding
    • Site of stroke
    • - internal capsule - brainstem
    • - cerebral cortex - basal ganglia
    • - cerebellum
    • Mechanism of stroke:
    • 1- Cerebral infarction (Ischemic)
    • - thrombosis at za site of atheroma
    • - embolism to a cerebral artery from
    • - extracranial vessels
    • - heart
    • * cerebral oedema may complicate infarction
    • and impair blood supply & cause further
    • damage
    • 2- Cerebral haemorrhage
    • - subarachnoid haemorrhage
    • - ruptured beri aneurysm
    • - ruptured AVM
    • - intracerebral haemorrhage
    • - rupture of perforating vessels weakened
    • by HT or atheromatous degeneration
    • ( micro aneurysm= 0.8-1.0 mm)
    • - rupture of aneurysms or AVM
    • * SAH arterial spasm & cerebral infarction
    • * ICH may extend to subarachnoid space.
    • * Disability from stroke depends on the
    • site & extent of damage
    • * Cerebellar hage can be fatal if there is
    • compression of brain stem.
    • Clinical classification of stroke
    • 1 - Transient ischemic attack (TIA): sudden
    • loss of focal neurological fn lasting < 24hrs. 2- Completed stroke : loss of focal neurological fn with symptoms lasting > 24hrs.
    • - Major stroke
    • - Minor stroke ( recovery in 1-2Ws), RIND.
    • 3- Evolving stroke (stroke –in-evolution )
    • symptoms worsening gradually or in
    • stepwise fashion over hrs or days or Ws involving adjacent motor or sensory sites within za distribution of a major cerebral artery (DD= tumour, SDH).
    • Disorders causing stroke comprises:
    • 1- Thromboembolic disease (infarction)
    • - atherosclerosis
    • - arteriosclerosis (HT, degenerative)
    • - embolism (20%)
    • - arteritis (syph, TA, PAN, SLE)
    • - dissection (spontaneous, traumatic)
    • - Vasospasm (migraine, SAH, angiogr)
    • - hyper viscosity (PRV)
    • - anti phospholipid syndrome
    • - SS disease - hypotension - OCPs
    • 2- Haemorrhage( intracerebral in 50% & 50% SAH
    • - rupture of a vessel or micro aneurysm in HT
    • - AVM
    • - Beri aneurysms
    • - Degenerative aneurysms
    • - HT arteriolar aneurysms
    • - Mycotic aneurysms
    • - Anticoagulants, thrombolytic therapy
    • - Bleeding disorders (ITP, DIC, haemophilia)
    • - Alcohol, cocaine, amphetamine.
    • - Sub dural or extra dural bleeding
    • Clinical features of stroke
    • Depends on za site & extent & involves a combination of features that may include:
    • - hemiparesis - loss of speech
    • - hemianaethesia
    • - The clinical onset is often rapid and reaches max within few hours - Unilateral weakness +/- dysphasia is the commonest presentation.
    • - Hypotonia, depressed reflexes and extensor reflex occur initially, followed later by hypertonia, hyper reflexia & extensor planter
    • response
    • - There may be impaired consciousness because of brain oedema (+/- papilloedema).
    • - With severe strokes flaccid paralysis is
    • accompanied by HA, vomiting, seizures
    • gaze paresis, impaired consciousness +/- papilloedema 2ndry to cerebral oedema - - Ataxia & hemisensory loss occur with deeply
    • seated lacunar infarcts.
    • - Monoparesis or dysphasia occur wz cortical lesions - Hemianaethesia & visual fields defects
    • - With brain stem lesions C/f depends on the structures involved. The cardinal feature is ipsilateral nuclear signs and contralateral pyramidal and S/T tract lesions signs ( crossed ). Coma may occur due to damage to reticular activating system.
    • - Recovery from stroke takes days, weeks or
    • months.
    • ** In cerebral hage there is profound hemiplegia
    • from the start
    • ** The onset in cerebral emboli is abrupt with
    • clear predisposing factor
    • ** In cerebral thrombosis there is usually no
    • coma
    • ** In HT encephalopathy the BP is very high
    • ** Always consider head injury & intra cranial
    • bleeding in pts with hemiplegia.
    • Differential diag of acute stroke
    • 1- cerebral tumours
    • 2- subdural haematoma
    • 3- cerebral abscess, cysts
    • 4- Todd's paralysis
    • 5- demyelinating disorders
    • 6- hypoglycemia
    • 7- encephalitis
    • 8- hysterical conversion
    • - eye lids firmly shut, pt resisting opening
    • - normal corneal reflex
    • - normal caloric response is diagnostic.
    • Investigation of stroke
    • 1- Investigations to confirm the diagnosis
    • Is it ischemic or haemorrhagicgic?? - CT brain - MRI
    • - MRA - L puncture.
    • * Exclusion of hage is important if any form of
    • anti thrombotic therapy is contemplated.
  • Rt cerebral haemorrhage
  • Rt cerebral infarction
  • Subdural haematoma
    • 2- Investigations to establish za underlying
    • disease and the possibility of a treatable
    • cause :
    • a/ embolism from the heart b/ embolism from large arteries c/ temporal arteritis d/surgical treatable hage. - ECG - CXR - Echo Doppler US - Carotid angiography
    • 3- Investigations to identify risk factors :
    • CBC, blood sugar, lipid profile, serology
    • for syphilis, clotting studies, serology for
    • collagen diseases, blood cultures for
    • SBE is suspected, sickling test, tests for
    • thrombophilia (protein C & S, anti thrombin 3)
    • Management of Hemiplegia
    • The aim is :-
    • 1- To minimize brain damage
    • 2- To reduce disability through rehabilitation
    • 3- To prevent complications
    • 4- To treat za underlying cause .
    • 5-To prevent za recurrence of stroke
    • 6- To refer pts wz SAH to neurosurgery .
    • ** To admit or not depends on za clinical
    • state & facilities at home ( TIAs & min
    • stroke at home)
    • No specific treatment is available for most pts with stroke, so their immediate management is supportive with General measures :
    • - ABC
    • - nursing care
    • - fluid balance & nutrition= NG feeding and
    • hydration. TR of infections.
    • - urinary cath if not continent
    • - physiotherapy, occupational, speech
    • and psychotherapy.
    • Med treatment:
    • 1- Anti hypertensives not given at the
    • start unless very high (> 180/110)
    • as some pts show reactive increase in BP.
    • It is gradually lowered after za 1 st week
    • 2- Anti platelets reduce za incidence of
    • stroke by 25% e.g. aspirin 75-300mg
    • dipyridamol 75 tds, clopidogrel
    • 3 - Anti coagulants only if there is a
    • source of emboli & avoided in za 1 st
    • 2Ws following infarction. It may be
    • used in evolving stroke, but C/I in
    • intra cranial hage & cerebral tumours
    • which should be rouled out by CT
    • 4- Thrombolysis (tpA) in USA given within
    • 3 hours of cerebral infarction.
    • 5- Manitol 200ml 20% & dexamethazone
    • reduce mortality in pts with brain oedema
    • 2ndry to severe stroke (dilating pupils,
    • increasing BP & reduced PR= Cushing’s
    • sign).
    • 6- Baclofe n (GABA antagonist) for spasticity
    • Surgical treatment:
    • 1- carotid endarterectomy in TIAs and
    • minor stroke when stenosis is > 70%. It
    • reduces incidence of stroke by 75%.
    • Avoided over in pts 65 years.
    • 2 - surgical evacuation of haematoma if
    • accessible & if pat continue to deteriorate e.g cerebellar hage to prevent brainstem compression.
    • Rehabilitation:
    • - identify risk factors & treat
    • - TR 2ndry depression
    • Secondary prevention of stroke
    • 1- control of cardiovascular risk factors
    • 2- control of HT
    • 3- long term anti platelet therapy unless the
    • stroke was hagic
    • 4- Pts with atrial fibrillation should be considered
    • for anti coagulation & if there is a major
    • CI should receive anti platelets
    • Primary prevention of stroke
    • 1- control of HT
    • 2- control of DM
    • 3- stopping of smoking
    • 4- lowering of lipid levels
    • 5- anti coagulation in atrial fibrillation if no CI
    • 6- reducing Hb in polycythemia vera
    • 7- diagnosis & surgical TR of carotid atheroma
    • Complications of acute stroke
    • - pneumonia - dehydration
    • - hyponatraemia - hypoxaemia
    • - hypoglycemia - DVT
    • - seizures - subluxation of joints
    • - frozen shoulder - pressure sores
    • - UTI - constipation
    • Prognosis:
    • - 25% die as a direct result of stroke.
    • More in hagic stroke.
    • - 50-75% who survive stroke achieve functional
    • independency in 3Ms
    • - poor outcome in pts wz deep coma and
    • dense hemiplegia
    • - mortality during za 1 st month is about 40-50%
    • from extension of za cerebral damage, aspirat
    • pneumonia & DVT wz pulmonary embolism.
    • - recurrent stroke occur in 5-10%/ year
    • - patient may die of cardiovascular disease.