CEREBROVASCULAR DISEASES ????? Jie Ming Shen, M.D., Ph.D. Department of Neurology Ruijin Hospital, SSMU

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CEREBROVASCULAR DISEASES ????? Jie Ming Shen,
M.D., Ph.D. Department of Neurology Ruijin
Hospital, SSMU
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ANATOMY
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CEREBROCIRCULATION

• CBF 800-1200ml/?
• 15-20 of cardiac output
• Brain weight 2-3 of body weight
• O2 72 L/d
• Glucose 150 g/d

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Blood supply to the brain

• Internal carotid Arteries
• Vertebral Arteries

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Internal carotid A.

• Ophthalmic A.
• Posterior communication A.
• Anterior chloroidal A.
• Anterior cerevral A.
• Middle cerebral A.

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Vertebrobasilar A.

• Vertebral A.
• Posterior spinal A.
• Anterior spinal A.
• Medulla A.
• Posterior inferior cerebellar A.

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Basilar A.

• Anterior inferior cerebellar A.
• Pontine A.
• Internal auditoryA.
• Superior cerebellar A.
• Posterior cerebral A.

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Circle of Willis

• R. Internal carotid A.
• Anterior communication A.
• L. Internal carotid A.
• Internal carotid A.
• Posterior communication A.
• Posterior cerebral A.

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Causes of cerebrovascular disease

• Vessel wall (angiopathy)
• Blood constituent and blood rheology
• Hemodynamic changes
• Others

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Risk factors

• age
• family history of stroke
• hypo- or hypertension
• cardiac disease
• diabetes mellitus

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Risk factors

• hyperlipemia
• cigarette smoking and alcohol consumption
• obesity
• dietary aspects salt, saturated fatty acid
• oral contraceptive

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TRANSIENT ISCHEMIC ATTACK(TIA)
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CLINICAL MANIFESTATION

• Cause Atherosclerosis
• Pathogenesis
• Micro-emboli
• Hemodynamic changes
• Extracranial mechanical arterial compression
• Others steal syndrome, vasospasm, altered
  coagulability

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CLINICAL MANIFESTATION

• Age and sex 50-70 y-o, M gt F
• Onset abrupt
• duration minutes to hours, but lt 24
  hours
• recurrent

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CLINICAL MANIFESTATION

• Symptoms
• Internal carotid artery system
• contralateral hemiparesis or monoparesis,
  hemisensory disturbances, aphasia with lesion in
  the dominant hemisphere, ipsilateral monocular
  disturbance, i.e. amaurosis.

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CLINICAL MANIFESTATION

• Symptoms
• Vertebrobasilar artery system
• dizziness, vertigo, diplopia, ataxia , dysphagia,
  drop attack.
• Limbic system (hippocampal gyrus or vault)
  transient global amnesia.

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PHYSIOLOGICAL EXAMINATION

• Palpation arteriopalmus ?
• Auscultation bruit in carotid
• bifurcation area supraclavicular regions
• Retinal examinationbright plaques

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LAB. EXAMINATION

• EKG and UCG heart diseases
• Blood rheology blood viscosity ?
• X-ray cervical spondylopathy
• CT normal
• CAG arteriosclerotic plaque
• stenosis

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DIAGNOSIS

• Medical history
• Etiological signs

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DIFFERENTIAL DIAGNOSIS

• 1. Epilepsy (partial seizures)
• 2. Meniere disease

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TREATMENT

• Etiological treatment
• Pharmacologic treatment
• Surgical treatment

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Pharmacologic treatment

• Vasodilation and blood dilution
• Low molecular dextran
• Platelet antiaggregants
• Aspirin 50-300 mg/d
• Ticlopidine 0.25 g/d

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Pharmacologic treatment

• Anticoagulants
• Heparin (inhibit thrombin generation or action)
• Warfarin

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Pharmacologic treatment

• Calcium channel blockers
• Nimodipine 40 mg t.i.d
• Sibeline 5-10 mg q.n.
• Chinese medicine
• Radix salviae miltiorrhize

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Surgical treatment

• Carotid endarterectomy
• Extracranial intracranial bypass surgery

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PROGNOSIS

• One-third complete infarction
• One-third continue to have TIAs
• One-third ceasing attacks

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CEREBRAL THROMBOSIS ?????
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ETIOLOGY PATHOGENESIS

• Cause
• Atherosclerosis and /or hypertension
• Arteritis
• Others vascular malformation, erythrocythemia,
  high coagulate state

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ETIOLOGY PATHOGENESIS

• Pathogenesis
• 1. Thrombosis
• hypertension, hyperlipidemia, cigarette smoke ?
  endothelial injury of large to medium-sized
  arteries ? thromlus ? thrombosis
  ?
• BP?, cerebral flow ?,
  blood viscosity ?
• 2. Thrombo-embolism
• fragment of thrombus ? distal artery

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PATHOLOGY

• Site
• arterial branch points or opposite arterial
  bifurcations.
• lt 6 hours reversible

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PATHOLOGY

• Pale infarcts
• 8-48 hours - necrosis stage
• 2-3 days (7-14 d)- softening stage
• 3-4 weeks or more - restoration stage

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PATHOLOGY

• Red infarcts (hemorrhagic infarction)
• brain infarct punctate hemorrhages, large
  collection of blood

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CLINICAL TYPES

• Symptomatic types
• Complete stroke
• Progressing stroke
• 3) RIND (reversible ischemic neurologic deficit)

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CLINICAL TYPES

• Neurological imaging types
• Massive infarct
• Cerebral watershed infarction
• Hemorrhagic infarct
• Multiple infarct

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CLINICAL TYPES

• Lacunar infarct territory lt1.5 cm
• penetrating arteries or arterioles lt 200 um

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CLINICAL MANIFESTATION

• 50-60 y-o persons
• arteriosclerosis, hypertension, diabetes mellitus
  
• under quiet condition
• Previous history of TIA

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CLINICAL MANIFESTATION

• progression in several hours, or 1-3 days
• consciousness

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CLINICAL MANIFESTATION

• Internal carotid artery
• OA ipsilateral blindness
• Motor contralateral hemiparalysis
• Sensory contralateral hemianesthesia
• Dominant hemispheric lesions aphasia

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CLINICAL MANIFESTATION

• Middle cerebral artery
• Main trunk
• contralateral Hemiplegia
• contralateral hemianesthesia
• hemianopia
• aphasia with the dominant hemispheric lesions
• Deep penetrating branch contralateral
  hemiparalysis

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CLINICAL MANIFESTATION

• Anterior cerebral artery
• contralateral sensory and motor deficit of the
  low limb, urinary incontinence
• Bilateral ACA disorders of behavior.

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CLINICAL MANIFESTATION

• Posterior cerebral artery
• contralateral hemianopia, cerebral blindness,
  aphasia, alexia, apraxia, agraphia.
• Deep penetrating branch thalamus syndrome,
  extrapyramidal symptom.

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CLINICAL MANIFESTATION

• Vertebrobasilar arteries
• dizziness, vertigo, nystagmus, diplopia, ataxia,
  dyslalia, dysphagia, ataxia, crossed paralysis

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CLINICAL MANIFESTATION

• Weber's syndrome
• Ipisilateral oculomotor nerv.
• Contralateral plegia

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CLINICAL MANIFESTATION

• Posterior inferior cerebellar artery
• (Wallenberg's syndrome )
• vertigo
• nystagmus
• ipsilateral Horner's syndrome
• ipsilateral ataxia
• crossed impaired sensation
• bulbar paralysis

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LAB. EXAMINATION

• CT lt 6 hours normal
• 24-48 hours hypodensity in the distribution
  of artery
• MRI
• TCD
• rCBF
• Lumbar puncture normal

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DIAGNOSIS

• elderly persons
• prodromal symptoms of TIA
• onset under a quiet condition
• progressive evolution
• neurologic deficit symptoms and signs
• laboratory examination

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DIFFERENTIAL DIAGNOSIS

• ICH
• cerebral embolism
• space occupying

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TREATMENT

• MANAGEMENT IN THE ACUTE PHASE
• 1. General management
• 2. Control of hypertension
• 3. Thrombolytic and defibrinogenating
• 4. Anticoagulants
• 5. Blood dilution

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TREATMENT

• MANAGEMENT IN THE ACUTE PHASE
• 6. Cerebral vasodilators
• 7. Therapy for cerebral edema
• 8. Platelet antiaggregants
• 9. Calcium channel blockers
• 10.Cerebral metabolics

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TREATMENT

• General management
• Control of hypertension

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REHABILITATION
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CEREBRAL EMBOLISM???
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ETIOLOGY PATHOLOGY

• Cause
• 1. Cardiac origin
• 2. Noncardiac origin
• 3. Undetermined origin

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Pathology

• Embolus ? vessel ? spasm ? infarct(red, pale or
  mixed).

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CLINICAL MANIFESTATION

• 1. onset most rapidly, the full-flown picture
  evolves with several seconds or a minute.
• 2. complete stroke.

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CLINICAL MANIFESTATION

• 3. transient disturbance of consciousness.
• 4. neurologic picture related to the
  angioanatomic territory.
• 5. vasospasm - epilepsy
• 6. embolus-original disease

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LABORATORY EXAMINATION

• CSF normal
• CT,MRI
• EKG,UCG,
• X-ray of chest

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DIAGNOSIS

• 1. Sudden onset of hemiplegia
• 2. Transient disturbance of consciousness with
  seizes
• 3. Embolism in the other part of the body.
• 4. Medical history of the embolus-original
  disease

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DIFFERENTIAL DIAGNOSIS

• Cerebral thrombosis
• Cerebral hemorrhage

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TREATMENT

• 1. Treatment for the cerebral lesion same as
  that of cerebral thrombosis
• Contraindication hemorrhagic infarction show on
  CT, red blood cess in CSF, SUE
• Fat embolism heparin,hydrocortisone, 5 SB
• 2.Treatment for the primary disease

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INTRACEREBRAL HEMORRHAGE???
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ETIOLOGY PATHOLOGY

• Cause hypertension and arteriosclerosis
• Others

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Pathology

• Hematoma ? cerebral edema, ? intracranial
  hypertension ? midline structure shift ?
  herniation ? death.
• clot ? semiliquid red-brown mass ? cavity.

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CLINICAL MANIFESTATION

• 1. over 50-60 y-o persons with hypertension
• 2. physical exertion
• 3. sudden onset
• 4. headache, nausea, vomiting
• 5. disturbance of consciousness

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Neurovascular symptoms

• 1. basal ganglia
• contralateral hemiplegia, hemianesthesia,
  hemianopia

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Neurovascular symptoms

• 2. lobe / subcortical white matter
• 1) hemianopia, tetartanopia, aphagia, behavioral
  abnormality
• 2) hemiplegia, hemianesthesia

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Neurovascular symptoms

• 3. pontine hemorrhage
• crossed paralysis (Weber's syndrome,
  Millard-Gubler's syndrome)
• massive coma, flaccid quadriplegia, decerebrate
  rigidity, central hyperthermia
• 4. cerebellar hemorrhage
• dizziness, vomiting, ataxia, nystagmus, ?
  tonsillar hernia ? death

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Neurovascular symptoms

• 5. ventricle hemorrhage
• massive coma, vomiting, needle-like pupils,
  flaccid quadriplegia, hyperthermia, - decerebral
  rigidity -death

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LABORATORY EXAMINATION

• CT
• homogeneous region of increased density
• mass effect

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LABORATORY EXAMINATION

• LP increased pressure, grossly bloody CSF
• CAG
• DSA

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DIAGNOSIS DIFFERENTIAL DIAGNOSIS

• DIAGNOSIS
• 1. Over 50 y-o patient with hypertension
• 2. Onset precipitated by exertion
• 3. Intracranial hypertension
• 4. Signs of neurological deficit

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DIAGNOSIS DIFFERENTIAL DIAGNOSIS

• DIFFERENTIAL DIAGNOSIS
• 1. Systemic coma
• 2. Traumatic hematoma
• 3. Cerebral infarction, SAH

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TREATMENT

• 1. Nursing care
• 2.Treatment of cerebral edema
• 20 mannitol 125-250 ml q. 6-8 h.
• 10 glycerin 500 ml q.d. /b.i.d.
• 3. Control hypertension
• 4. Surgical removal of the clot (evacuation,
  aspiration)

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REHABILITATION
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SUBARACHNOID HEMORRHAGE???????
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AETIOLOGY PATHOLOGY

• Cause Aneurysm, vascular malformation,
  hypertensive atherosclerosis, etc.

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CLINICAL MANIFESTATION

• 1. Age Adolescents
• arteriovenous malformation
• Adults aneurysm
• Elders atherosclerosis
• 2.Onset abrupt and usually evoked by some
  exertion

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CLINICAL MANIFESTATION

• 3. Symptoms sever headache, nausea, vomiting,
  loss of
• consciousness
• seizure
• some psychic symptoms

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CLINICAL MANIFESTATION

• 5. Signs
• 1) Meningeal irritation
• 2) Oculomotor nerve palsy.
• 3) Secondary paresis and sensory disturbance
• 4) Subhyloid hemorrhages
• 5) Etiological signs

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WORK-UP

• CT diffuse blood throughout the subarachnoid
  space
• Lumbar puncture - diagnostic test
• CAG and DSA

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DIAGNOSIS DIFFERENTIAL DIAGNOSIS

• DIAGNOSIS
• 1. Abrupt sever headache, vomiting
• 2. Meningeal irritation signs
• 3. Subhyaloid hemorrhage
• 4. CT and CSF

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DIFFERENTIAL DIAGNOSIS

• DIFFERENTIAL DIAGNOSIS
• 1) Meningitis
• 2) Secondary SAH due to hypertensive cerebral
  hemorrhage

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TREATMENT

• 1. bedrest for at least 4-6 weeks.
• 2. Mild sedation, stool softeners, anticonvulsive
  medications.
• 3. Antifibrinolitic agents PAMBA, EACA.
• 4. Stool softeners, control of hypertension.
• 5. Prevention of vasospasm

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TREATMENT

• 6. Surgical treatment