BLOOD SUPPLY OF BRAIN

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BLOOD SUPPLY OF BRAIN
CEREBRO-VASCULAR DISEASE STROKE
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• CEREBRO-VASCULAR DISEASE STROKE
• Stroke is the second commonest cause of death in
  developed countries.
• Hypertension is the most treatable risk factor.
• Thromboembolic infarction (80), cerebral and
  cerebellar haemorrhage (10) and subarachnoid
  haemorrhage (about 5) are the major
  cerebrovascular problems.
• DEFINITIONS
• Stroke is defined as the clinical syndrome of
  rapid onset of cerebral deficit (usually focal)
  lasting more than 24 hours or leading to death,
  with no apparent cause other than a vascular one.
  
• Completed stroke means the deficit has become
  maximal, usually within 6 hours.
• Stroke-in-evolution describes progression during
  the first 24 hours.
• Minor stroke. Patients recover without
  significant deficit, usually within a week.
• Transient ischemic attack (TIA). This means a
  focal deficit, such as a weak limb, aphasia or
  loss of vision lasting from a few seconds to 24
  hours. There is complete recovery. The attack is
  usually sudden.
• PATHOPHYSIOLOGY COMPLETE STROKE
• One of three mechanisms is usual
• arterial embolism from a distant site
• arterial thrombosis
• haemorrhage into the brain (intracerebral or
  subarachnoid).
• Less commonly

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TRANSIENT ISCHEMIC ATTACKS (TIAs)

• RISK FACTORS OF CEREBRAL HAEMORRHAGEa
• Hypertension
• Bleeding disorders
• Pre-existing cerebral aneurysm
• Anticoagulant and antiplatelet drug therapy
• TRANSIENT ISCHEMIC ATTACKS (TIAs)
• Symptoms
• TIAs cause sudden loss of function, usually
  within seconds, and last for minutes or hours
  (but by definition lt24 hours). The site is often
  suggested by the type of attack.

Features of transient ischemic
attacks Anterior circulation
Posterior circulation Carotid system
Vertebrobasilar system Amaurosis fugax
Diplopia, vertigo, vomiting Aphasia
Choking and
dysarthria Hemiparesis
Ataxia Hemisensory loss
Hemisensory loss Hemianopic visual loss
Hemianopic visual loss 
Transient global amnesia 

Tetraparesis
Loss of consciousness (rare)

• Clinical findings in TIA
• It is unusual to witness an attack.
• Consciousness is usually preserved in TIA.
• There may be clinical evidence of a source of
  embolus, such as carotid arterial bruit
  (stenosis), atrial fibrillation or other
  dysrhythmia, valvular heart disease/endocarditis,
  recent myocardial infarction or difference
  between right and left brachial BP.
• Un underlying condition may be evident
• atheroma
• hypertension
• postural hypotension
• bradycardia or low cardiac output
• diabetes mellitus
• rarely, arteritis, polycythaemia
• antiphospholipid syndrome
• Differential diagnosis
• Mass lesion
• Focal epilepsy
• A focal prodrome of migraine
• Prognosis Prospective studies show that 5 years
  after a single thromboembolic TIA

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BRAIN STEM INFARCTION

• TYPICAL STROKE SYNDROMES Cerebral infarction
• Clinical features
• The most common stroke is caused by infarction in
  the internal capsule following thromboembolism in
  a middle cerebral artery branch. A similar
  picture is caused by internal carotid occlusion.
• Limb weakness on the opposite side to the infarct
  develops over seconds, minutes or hours.
• There is a contralateral hemiplegia or
  hemiparesis with facial weakness.
• Aphasia is usual when the dominant hemisphere is
  affected.
• Weak limbs are at first flaccid and areflexic.
• Headache is unusual. Consciousness is usually
  preserved.
• After a variable interval, usually several days,
  reflexes return, becoming exaggerated. An
  extensor plantar response appears.

CLINICAL PICTURE STRUCTURE
INVOLVED Hemiparesis or tetraparesis
Corticospinal tracts Sensory loss
Medial lemniscus and spinothalamic
tracts Diplopia
Oculomotor system Facial numbness
Fifth nerve nuclei Facial weakness (LMN)
Seventh nerve nucleus Nystagmus, vertigo
Vestibular connections Dysphagia, dysarthria
Ninth and tenth nerve nuclei Dysarthria,
ataxia, hiccups Brainstem and cerebellar
connections Horner's syndrome
Sympathetic fibres Altered consciousness
Reticular formation This causes complex signs
depending on the relationship of the infarct to
cranial nerve nuclei, long tracts and brainstem
connections

• The lateral medullary syndrome
• The lateral medullary syndrome, also called
  posterior inferior cerebellar artery (PICA)
  thrombosis, or Wallenberg's syndrome, is a common
  example of brain-stem infarction presenting as
  acute vertigo with cerebellar and other signs. It
  follows thrombo-embolism in the PICA or its
  branches, vertebral artery thrombo-embolism or
  dissection. The clinical picture depends on the
  precise structure damaged.
• Clinical picture of PICA occlusion
• Ipsilateral
• Facial numbness 5th
• Diplopia 6th
• Nystagmus
• Ataxia (cerebellar)
• Horners syndrome
• 9th and 10th nerve lesion
• Contralateral
• Spinothalamic sensory loss
• Hemiplegia (mild, unusual)
• Lacunar infarction
• Lacunes are small (lt1.5 cm3) infarcts seen on MRI
  or at autopsy. Hypertension is commonly present.
  Minor strokes (e.g. pure motor stroke, pure
  sensory stroke, sudden unilateral ataxia and
  sudden dysarthria with a clumsy hand) are
  syndromes caused typically by single lacunar
  infarcts. Lacunar infarction is also often
  symptomless.
• Hypertensive encephalopathy

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• Multi-infarct dementia (vascular dementia)
• Multiple lacunes or larger infarcts cause
  generalized intellectual loss seen with advanced
  cerebrovascular disease. The condition tends to
  occur with a stepwise progression over months or
  years with each subsequent infarct. There is
  eventually dementia, pseudobulbar palsy and a
  shuffling gait with small steps (parkinsonism).
  Binswanger's disease is an imaging term
  describing low attenuation in cerebral white
  matter, with dementia, TIAs and stroke episodes
  in hypertensive patients.
• Acute stroke immediate care, and thrombolysis
• Paramedics and members of the public are
  encouraged to make the diagnosis of stroke on a
  simple history and examination
• FAST
• Face sudden weakness of the face
• Arm sudden weakness of one or both arms
• Speech difficulty speaking, slurred speech
• Time the sooner treatment can be started, the
  better.
• Dedicated units with multidisciplinary, organized
  teams deliver higher standards of care than a
  general hospital ward
• Investigations
• The purpose of investigations in both stroke and
• TIA is
• to confirm clinical diagnosis
• to distinguish between haemorrhage and
  thromboembolic infarction
• to look for underlying causes of disease and to
  direct therapy, either medical or surgical

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• Immediate management
• Admit to multidisciplinary hospital stroke unit
  if possible.
• General medical measures
• Care of the unconscious patient, Oxygen by mask,
  Assessment of swallowing, Check BP and look for
  source of emboli.
• Immediate brain imaging is essential.
• Cerebral infarction If CT shows infarction,
  give aspirin (300 mg/day initially) antiplatelet
  therapy if no contraindications, give alteplase
  thrombolysis, which must be started within 3
  hours (aim for 90 min) of stroke informed
  consent is essential.
• Cerebral haemorrhage If CT shows haemorrhage, do
  not give any therapy that may interfere with
  clotting. Neurosurgery may be required.
• Further management
• Appropriate drugs for hypertension, heart
  disease, diabetes, other medical conditions
• Other antiplatelet agents, e.g. dipyridamole
• Question of endarterectomy
• Question of anticoagulation
• Speech therapy, dysphagia care, physiotherapy,
  occupational therapy
• Specific neurological issues, e.g. epilepsy,
  pain, incontinence
• Preparations for future care
• Long term management

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Internal carotid artery aneurysm

• Etiology
• Intracerebral haemorrhage causes around 10 of
  strokes.
• Haemorrhage is usually massive, often fatal and
  occurs in chronic hypertension and at
  well-defined sites - basal ganglia, pons,
  cerebellum and subcortical white matter.
• Recognition
• At the bedside, there is no entirely reliable way
  of distinguishing between intracerebral
  haemorrhage and thromboembolic infarction. Both
  produce stroke. Intracerebral haemorrhage,
  however, tends to be dramatic with severe
  headache. It is more likely to lead to coma than
  thromboembolic stroke.
• Brain haemorrhage is seen on CT imaging
  immediately - as intracerebral, intraventricular,
  or subarachnoid blood. MR imaging may not
  identify an acute haemorrhage correctly in the
  first few hours. Thereafter T2 weighted MR is
  very reliable.
• Managing hemorrhagic stroke
• The principles are those for cerebral infarction.
  The immediate prognosis is less good.
• Antiplatelet drugs and, of course, anticoagulants
  are contraindicated.
• Control of hypertension is vital.
• Urgent neurosurgical clot evacuation is sometimes
  considered when there is deepening coma and
  coning (particularly in cerebellar haemorrhage).
  
• The outlook is usually poor.
• Cerebellar hemorrhage
• There is headache and rapid reduction of
  consciousness with signs of brainstem origin
  (e.g. nystagmus, ocular palsies).
• Gaze deviates towards the haemorrhage.

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• Investigations
• CT imaging is the initial investigation of
  choice. Subarachnoid or intraventricular blood is
  usually seen.
• Lumbar puncture is not necessary if SAH is
  confirmed by CT, but should be performed if doubt
  remains. The CSF becomes yellow (xanthochromic)
  several hours after SAH. Visual inspection of the
  supernatant CSF is usually sufficiently reliable
  for diagnosis, but there is a move to use
  spectrophotometry to estimate bilirubin released
  from lysed cells to define with certainty SAH in
  doubtful cases.
• MR angiography is usually performed in all
  potentially fit for surgery, i.e. generally below
  65 years and not in coma. In some cases, no
  aneurysm is found despite a definite SAH.

A-V malformation

• Complications
• Blood in the subarachnoid space can lead to
  obstruction of CSF flow and hydrocephalus. This
  can be asymptomatic but may cause deteriorating
  consciousness after SAH. Diagnosis is by CT.
  Shunting may be required.
• Severe arterial spasm (visible on cerebral
  angiography and a cause of coma or stroke)
  sometimes complicates SAH. It is a poor
  prognostic sign.
• Management
• Immediate treatment of SAH is bed rest and
  supportive measures.
• Hypertension should be controlled.
• Dexamethasone to reduce cerebral oedema and to
  stabilize the blood-brain barrier.
• Nimodipine, a calcium-channel blocking agent,
  reduces mortality.
• When angiography demonstrates aneurysm, a direct
  neurosurgical approach to clip the neck of the
  aneurysm is carried out.
• Invasive radiological techniques, such as
  inserting a fine wire coil into an aneurysm are
  also used.
• Direct surgery, microembolism and focal
  radiotherapy ('gamma knife') are used in AVM.
• Subdural hematoma
• SDH means accumulation of blood in the subdural
  space following rupture of a vein. It usually
  follows a head injury, which may be trivial. The
  interval between injury and symptoms may be days,
  weeks or months. Chronic, unsuspected or
  spontaneous SDH is common in the elderly and in
  alcohol abuse.
• Headache, drowsiness and confusion are common
  symptoms are indolent and often fluctuate. Focal
  deficits such as hemiparesis or sensory loss
  develop. Epilepsy occasionally occurs. Stupor,
  coma and coning may follow, but there is a
  tendency for SDH to resolve spontaneously.
• Extradural hemorrhage
• This follows a linear skull vault fracture
  tearing a branch of the middle meningeal artery.
  Blood accumulates rapidly over minutes/hours in
  the extradural space. The most characteristic
  picture is of a head injury with a brief duration
  of unconsciousness followed by a lucid interval
  of recovery. The patient then develops a
  progressive hemiparesis and stupor, and rapid
  transtentorial coning, with first an ipsilateral
  dilated pupil, followed by bilateral fixed
  dilated pupils, tetraplegia and respiratory
  arrest.