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Cerebrovascular Disease
 

Cerebrovascular Disease

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    Cerebrovascular Disease Cerebrovascular Disease Presentation Transcript

    • Cerebrovascular disease & Strokes Dr. Osman Sadig Bukhari
      • Stroke is:
      • - is za 3 rd commonest cause of death
      • - 2/1000/year
      • - male > females
      • - uncommon before 40years except with:
      • - trauma
      • - cardiac diseases e.g RHD
      • - congenital vascular abn
      • - inflammatory arteritis
      • - vascular disease
      • - SS anaemia
      • Cerebral circulation
      • Cerebral vascular diseases comprise:
      • 1- Thromboembolic infarction ( thrombosis and
      • embolism)
      • 2- Intracerebral haemorrhage (ICH)
      • 3- Subarachnoid haemorrhage (SAH)
      • 4- Extradural hage & subdural haematoma
      • 5- Cortical venous & dural venous sinus thromb
    •  
    •  
      • Stroke is either due to:
      • 1- Infarction (ischemic) (80-85%)
      • - thrombosis
      • - embolism
      • 2- Haemorrhage (15-20%):
      • - intracerebral
      • - subarachnoid
      • 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- Completed stroke
      • focal neurological episodes with sympto
      • lasting > 24hrs.
      • - Major stroke
      • - Minor stroke ( recovery in 1-2Ws)
      • 2- Evolving stroke
      • symptoms worsening gradually or in
      • stepwise fashion over hrs or days
      • ( DD= tumour, SDH)
      • 3- Transient ischemic attack (TIA)
      • symptoms lasting < 24hrs.
      • 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 50%
      • - sub arachnoid 50%
      • - AVM
      • - Beri aneurysms
      • - Degenerative aneurysms
      • - HT arteriolar aneurysms
      • - Mycotic aneurysms
      • - Anticoagulants, thrombolytic therapy
      • - Bleeding disorders (ITP, DIC, haemop
      • - Alcohol, cocaine, amphetamine)
      • Risk factors for stroke
      • 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
      • Transient ischemic attacks TIA
      • Definition : focal neurological symptoms
      • (due to cerebral ischemia) wz symptoms
      • lasting < 24hrs.
      • Causes :
      • - emboli or PL material from extracranial
      • arteries
      • - cardiac emboli
      • - severe stenosis of a major artery +
      • haemdynamic disturbance ( e.g V/basilar
      • - small infarcts, hage, brainstem tumours and SDH can cause TIA
      • Clinical features:
      • Carotid system Vertebrobasilar syst
      • - amaurosis fugax - diplopia, vertigo, vomiting
      • - aphasia -dysphagia, dysarthria
      • - hemiparesis - facial numb & weakness
      • - hemisensory loss - ataxia, nystagmus
      • - hemianopic visual - hemisensory loss
      • loss - hemianopic visual
      • loss
      • - transient global
      • amnesia & confusion
      • - tetraparesis, coma, and
      • cortical blindness.
      + evidence of underlying disease
      • * TIAs may herald completed stroke and
      • 25% of pts wz completed stroke recall
      • previous TIA
      • * TIAs require to investigate za underlying
      • cause & prevent to reduce za completed
      • stroke
      • * 40% of pts wz TIAs suffer completed
      • stroke in 5 years.
      • * 25% of pts wz TIAs die from stroke or
      • coronary heart disease.
      • * management of TIAs
      • - identify risk factors & correct
      • - antiplatelets reduce za risk of stroke
      • by 25%.
      • - anticoagulants for definite cardiac
      • source of thromboembolism.
      • - carotid endarterectomy reduce za risk
      • of stroke by 75%.
      • Clinical features of stroke
      • Depends on za site & extent
      • 1- Acute focal neurological deficit :
      • - Hemiparesis +/- dysphasia is the
      • commonest presentation. Weakness 1 st
      • and recovery takes place over days, Ws
      • or months.
      • - Hypotonia, depressed reflexes and
      • extensor reflex occur initially, followed
      • later by hypertonia & hyper reflexia.
      • - Monoparesis or dysphasia occur wz cortical
      • lesions
      • - Hemianaethesia & visual fields defects
      • - With brain stem lesions C/f depends on
      • the structures involved and leads to
      • coma due to damage to reticular
      • activating system. The cardinal feature
      • is ipsilateral nuclear signs and
      • contralateral signs of pyramidal & S/T
      • tract lesions signs ( crossed ).
      • - 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.
      • 2- Dementia :
      • gradual decline in intellectual fn, sp
      • in ischemic strokes, with or without
      • sensorimotor limb deficit or gait disord
      • 3- SAH:
      • - HA. Neck stiffness & vomiting
      • - with or without focal neurological defi
      • 4- Diseases of cerebral circulation
      • ** General med ex wz PR & rhythm, BP,
      • peripheral vessels, carotid bruits, heart
      • ex & complete neurological ex leads to
      • correct diagnosis.
      • 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
      • Investigation of stroke
      • 1- Investigations to confirm the diagnosis
      • ( ? Ischemic, ? Hagic)= CT brain, MRI,
      • and L puncture.
      • 2-Investigations to establish za underlying
      • disease = ECG, Echo, CXR, MRA, 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 stroke
      • The aim is :-
      • 1- To minimize brain damage
      • 2- To reduce disability through rehabilitati
      • 3- Tom 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)
      • ** General measures:
      • - ABC
      • - nursing care
      • - fluid balance & nutrition
      • - urinary cath if not continent
      • - physiotherapy, occupational, speech
      • and psychotherapy
      • ** Specific therapy:
      • 1- Med treatment
      • - 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
      • - Anti platelets reduce za incidence of
      • stroke by 25% e.g. aspirin 75-300mg
      • dipyridamol 75 tds, clopidogrel
      • - 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
      • - Thrombolysis (tpA) in USA given
      • within 3hrs.
      • - Manitol 200ml 20% & dexamethazone
      • reduce mortality in pts with brain oedema
      • 2ndry to severe stroke.
      • - Baclofe n (GABA antagonist) for spasticity
      • 2- Surgical treatment
      • - carotid endarterectomy in TIAs and
      • minor stroke when stenosis is > 70%
      • reduce incidence of stroke by 75%.
      • Avoided over 65 years.
      • - surgical evacuation of haematoma if
      • accessible & if pat continue to deteriorate e.g cerebellar hage to prevent brainstem compression.
      • 3- Rehabilitation
      • - identify risk factors & treat
      • - TR 2ndry depression
      • Prognosis
      • - 25% die as a direct result of stroke.
      • More in hagic stroke.
      • - 50-75% who survive stroke achieve fnal
      • independency in 3Ms
      • - poor outcome in pts wz deep coma and
      • dense hemiplegia
      • - recurrent stroke in5-10%/ year
      • - patient may die of cardiovascular dis.
      • Complications of acute stroke
      • - pneumonia - dehydration
      • - hyponatraemia - hypoxaemia
      • - hypoglycemia - DVT
      • - seizures - subluxation of joints
      • - frozen shoulder - pressure sores
      • - UTI - constipation
      • Lateral medullary syndrome
      • - due to occlusion of PICA or vertebral art.
      • - there is ipsilateral ataxia, nystagmus,
      • facial numbness, palatal palsy, diplopia
      • (6 th CN) & Horners
      • - contralateral S/T signs. Hemiparesis rare
      • - often vertigo.
      • Weber syndrome
      • - ipsilateral 3 rd cranial N palsy
      • - contralateral pyramidal
      • Pontine hage
      • - impaired consciousness
      • - hyperpyrexia
      • - pinpoint pupils
      • - paresis
      • Visual cortical infarcts
      • - cortical blindness
      • - hemianopia
      • Lacunar infarcts
      • - <1.5 cm
      • - commonly HT
      • - pure motor, sensory or cerebellar
      • Multi infarct dementia
      • - stepwise gradual intellectual loss
      • - pseudobulbar palsy
      • - Parkinsonian gait.
      • Water shed infarcts
      • - multiple infarcts at border zones betwee
      • areas supplied by cerebral arteries
      • following prolonged periods of cerebral
      • ischemia
      • - cortical blindness
      • - amnesia
      • - intellectual impairment.
      • Cerebellar hage
      • - headache is severe & occipital
      • - brainstem symptoms may occur e.g
      • diplopia, vertigo wz rapid deterioration of
      • conswciousness
      • - may cause acute hydrocephalus
      • - immediate surgical evacuation of haemat
      • Subarachnoid hage (SAH)
      • - 10% of strokes
      • - Causes :
      • - Berry aneurysm 70%
      • - AVM 10%
      • - rare causes
      • - extension of I/C hage - anticoagul
      • - rupture of atheromatous vessel
      • - bleeding disorders - brain tumou
      • - acute bact meningitis - arteritis SLE
      • - spinal AVM - co arcitation of Ao
      • - APKD - Marfan’s
      • Berry aneurysm:
      • - post & ant communicating arteries
      • - middle cerebral art
      • - basilar, PICA, retinal & intra cavernous
      • carotid art
      • - bleeds
      • - pressure on surrounding structures e.g.
      • 3 rd CN
      • AVM:
      • - developmental anomaly within za brain
      • - SAH
      • - focal neurological deficits & epilepsy.
      • Clinical features :
      • - occurs during exertion high Bp
      • - sudden severe occipital headache
      • - neck stiffness & +ve Kerning sign
      • - fever & vomiting
      • - photophobia & irritability
      • - consciousness may be lost & seizures
      • may develop
      • - sub hyaloid hage & papilloededema
      • - focal neurological signs (ischemia from
      • arterial spasm & bleeding into brain
      • - CT diagnostic
      • - LP if CT is –ve (hagic)
      • - look for bruits over head & eyes
      • - DD= meningitis, migraine, meningism, C malar
      • Complications :
      • - hydrocephalus due to obstruction of
      • subarachnoid space by clots.
      • - intra cranial arterial spasm & neurological deficits
      • Management:
      • - Immediate : bed rest, control of HT,
      • dexamethazone if brain oedema
      • - Specific: refer to neurosurgical unit as
      • soon as diag is proven.? Angiography,
      • clipping of za neck of aneurysm
      • micro embolization, focal R/T & surgery for AVM
      • Prognosis:
      • -50% early mortality
      • - 10-20% die from rebleeding within 2Ws
      • - comatosed pts & those wz severe
      • neurological deficit carry bad prognosis.
      • Cerebral venous thrombosis
      • - Uncommon
      • - Causes patchy hagic ischemia & ICP
      • - predisposing factors
      • - dehydration - hypotension
      • - polythycemia - pregnancy
      • - Anti phospholipid syndrome - OCP
      • - Severe intercurrent infection
      • - Para nasal sinusitis - Facial skin infection
      • - Otitis media - mastoiditis
      • - meningitis -Subdural embyema
      • - Fracture skull - penetrating head inury
      • 1- Cortical venous thrombosis
      • - fever
      • - focal cerebral dysfunction:
      • - epilepsy - hemiparesis
      • - dysarthria
      • 2- Cerebral venous sinus thrombosis
      • Depends on za sinus involved
      • a- cavernous sinus: Often bilateral
      • - pt very ill, headache, ptosis,
      • proptosis, ophthalmoplegia, fever
      • papilloedema, sensation ophth V
      • b- Superior sagittal sinus:
      • headache, seizures, papilloedema,
      • +/- advancing motor & sensory def
      • c- Transverse sinus:
      • hemiparesis, seizures, & papilloedem
      • spreading to jugular foramen
      • X1, X, X11 palsies.
      • Investigations
      • - CT, MRA to detect occluded v or sinus
      • - CSF under pressure
      • Treatment
      • - broad spectrum antibiotics
      • - drain infected site ( sinus, middle ear)
      • - dexamethazone for brain oedema
      • - anticoagulants early on may limit the
      • spread of thrombosis.
      • Chronic subdural haematoma (SDH)
      • - affects elderly & alcoholics even with
      • minor head trauma
      • - fluctuating headache, drowsiness and
      • confusion
      • - focal signs: hemiparesis, hemisensory
      • loss
      • - seizures, papilloedma, stupor & coma
      • - fatal if untreated
      • - conservative TR hoping that spontaneous
      • stopping of bleeding, otherwise burr hole.
      • Extradural hage
      • - due to tearing of middle meningeal art
      • following linear skull vault fracture.
      • - brief loss of consciousness (concussion)
      • followed by lucid interval of recovery
      • - with progressive hemiparesis, stupor and
      • rapid transtentorial coning with ipsilat
      • dilated pupil followed by dilatation of
      • of za other, quadriparesis & death if
      • untreated.
      • - prompt CT & MRI if suspected & urgent
      • neurosurgery.