CEREBRALVASCULAR DISEASE

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CEREBRALVASCULAR DISEASE

• Dr. LU, QINCHI
• DEPARTMENT OF NEUROLOGY
• REN JI HOSPITAL
• SHANGHAI JIAO TONG UNIVERSITY
• SCHOOL OF MEDICINE
• Tel [phone]
• Email qinchilu_at_hotmail.com

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Cerebral vascular Disease

• Definition of term
• The term cerebrovascular disease designates any
  abnormality of the brain resulting from a
  pathologic process of the blood vessels. Sudden
  loss of neurological function is the hallmark of
  cerebrovascular disease.
• Cerebrovascular disease is the third most common
  cause of death and the most common disabling
  neurologic disorder in western civilized
  countries where an increasing proportion of
  people survive to old age. Shanghai is entering
  the aging society
• Its incidence increases with age and is somewhat
  higher in men than in women.

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Risk factors for stroke

• Systolic or diastolic hypertension
• Diabetics
• Hypercholesterolemia
• Heart disease (afib)
• Cigarette smoking
• Heavy alcohol consumption
• High homocystine
• Oral contraceptive use

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The major types of cerebrovascular disease

• Cerebral ischaemia and infarction
• Transient Ischemic Attacks
• Atherosclerotic thrombosis
• Lacunes
• Embolism
• Hemorrhage
• Hypertensive hemorrhage
• Ruptured aneurysms and vascular malformations
• Other

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I?Cerebral ischaemia and infarction

• Anatomy and pathology
• The principal pathological process under
  consideration here is the occlusion of arteries
  supplying the brain. The two internal carotid
  arteries and the basilar artery form the Circle
  of Willis at the base of the brain, which acts as
  an efficient anatomotic device in the event of
  occlusion of arteries proximal to it.

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• Anatomy and pathology
• Occlusion leads to sudden severe ischaemia in the
  area of brain tissue supplied by the occluded
  artery, and recovery depends upon rapid lysis or
  fragmentation of the occluding materialReversal
  of neurological function within minutes or hours
  gives rise to the clinical picture of a
  transient ischaemic attack.

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• Anatomy and pathology
• When the neurological deficit lasts longer than
  24 hours, it may be called a reversible ischaemic
  neurological deficit ( RIND ) if it recovers
  completely in a few days,or a completed stroke
  if there is a persistent deficit.Sometimes
  recovery is very slow and incomplete.

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Neurological symptoms and signs

• The loss of function that the patient notices,
  and which may be apparent on examination,
  entirely depends on the area of brain tissue
  involved in the ischaemic process.

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Neurological symptoms and signs

• The following suggest middle cerebral territory
• DysphasiaDyslexia, dysgraphia,
  dyscalculiaLoss of use of contralateral face
  and armLoss of feeling in contralateral face
  and arm.

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Neurological symptoms and signs

• The following suggests anterior cerebral
  territoryLoss of use and/ or feeling in the
  contralateral leg.
• The following suggests posterior cerebral
  territoryDevelopment of a contralateral
  homonymous hemianopia.

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Neurological symptoms and signs

• The following suggests a deep-seated lesion
  affecting the internal capsule which is supplied
  by small perforating branches of the middle and
  posterior cerebral arteries close to their
  originsComplete loss of motor and sensory
  function throughout the whole of the
  contralateral side of the body with a homonymous
  hemianopia.

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Neurological symptoms and signs

• The following suggests ophthalmic artery
  territory (the ophthalmic artery arises from the
  internal carotid artery just below the Circle of
  Willis)Monocular loss of vision.

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Neurological symptoms and signs

• The following suggest vertebro-basilar
  territorydouble vision( 3,4,6)facial
  numbness(5)facial weakness(7)vertigo
  (8)dysphagia (9, 10)dysarthria ( 9, 10,
  12)ataxiadrop attacksmotor or sensory loss
  in both arms or legs.

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1. Transient Ischemic Attacks(TIA)

• Definition of term
• Current opinion holds that TIAs are brief,
  reversible episodes of focal, nonconvulsive
  ischaemic neurologic disturbance, Consensus has
  been that their duration should be less than 24
  h.

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Clinical picture

• Transient Ischaemic Attacks can reflect the
  involvement of any cerebral artery. The loss of
  function entirely depends on the influenced
  artery.It may last a few seconds or up to 12
  to 24 h, Most of them last 2 to 15 min.There are
  only a few attacks or several hundred.Between
  attacks, the neurologic examination may disclose
  no abnormalities.A stroke may occur after
  numerous attacks have occurred over a period of
  weeks or months.

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Differential diagnosis of TIAs

• Transient episodes, indistinguishable from TIAs,
  are known to occur in patients with
  Seizure,Migraine,Transient global amnesia,and
  occasionally in patients with multiple sclerosis,
  meningioma, glioblastoma ,metastatic brain tumors
  situated in or near the cortex ,and even with
  subdural hematoma.

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2. Cerebral thrombosis

• Most cerebrovascular disease can be attributed to
  atheroscleroses and chronic hypertension until
  ways are found to prevent or control them,
  vascular disease of the brain will continue to be
  a major cause of morbidity.

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Pathogenesis

• Pathogenesis of Ischemic neuronal death
• Ischemia
• ?
• Excitatory amino acid receptors
• ?
• Borderzone or penumbra ?
• Programmed cell death

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Clinical picture

• In general, evolution of the clinical phenomena
  in relation to cerebral thrombosis is more
  variable than that of embolism and hemorrhage.
  The loss of function that the patient notices,
  and which may be apparent on examination,
  entirely depends on the area of brain tissue
  involved in the ischaemic process.(above)

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Clinical picture

• In more than half of patients, the main part of
  the stroke is preceded by minor signs or one or
  more transient attacks of focal neurologic
  dysfunction. The final stroke may be preceded by
  one or two attacks or a hundred or more brief
  TIAs, and stroke may follow the onset of the
  attacks by hours, weeks, or, rarely, months.
• The most occurrence of the thrombotic stroke is
  during sleep.The patient awakens paralyzed.
  Either during the night or in the morning.
• Unaware of any difficulty, he may arise and fall
  helplessly to the floor with the first step.

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Clinical picture

• Associated symptoms
• Seizures accompany the onset of stroke in a small
  number of cases (10-50) in other instances,
  they follow the stroke by weeks to years. The
  presence of seizures does not definitively
  distinguish embolic from thrombotic strokes, but
  seizure at the onset of stroke may be more
  common with embolus.

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Clinical picture

• Associated symptoms
• Headache occurs in about 25 of patients with
  ischaemic stroke, possibly because of the acute
  dilation of collateral vessels.

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Laboratory Findings

• CT Scan or MRI A CT scan or MRI should be
  obtained routinely to distinguish between
  infarction and hemorrhage as the cause of stroke,
  to exclude other lesions (eg, tumor, abscess)
  that can mimic stroke, and to localize the
  lesion. CT is usually preferred for initial
  diagnosis because it is widely available and
  rapid and can readily make the critical
  distinction between ischaemia and hemorrhage.
• Lumbar Puncture This should be performed in
  selected cases to exclude subarachnoid
  hemorrhage.

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Laboratory Findings

• Cerebral Angiography Intra-arterial angiography
  is used to identify operable extracranial carotid
  lesions in patients with anterior circulation
  TIAs who are good surgical candidates. It also
  can be used for intra-arterial thrombolysis (
  r-tPA)
• Magnetic resonance angiography (MRA) may detect
  stenosis of large cerebral arteries, aneurysms,
  and other vascular lesion, but its sensitivity is
  generally inferior to that of conventional
  angiography.

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Differential Diagnosis

• Vascular disorders are mistaken for ischaemic
  stroke include intracerebral hemorrhage, subdural
  or epidural hematoma , and subarachnoid
  hemorrhage from rupture of an aneurysm or
  vascular malformation. These condition can often
  be distinguished by a history of trauma or of
  excruciating headache at onset, a more marked
  depression of consciousness, or by the presence
  of neck stiffness on examination. They can be
  excluded by CT scan or MRI.

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Differential Diagnosis

• Differential Diagnosis Other structural brain
  lesion such as tumor or abscess can also produce
  focal cerebral symptoms of acute onset. Brain
  abscess is suggested by concurrent fever, and
  both abscess and tumor can usually be diagnosed
  by CT scan or MRI. Metabolic disturbances,
  particularly hypoglycemia and hyperosmolar
  nonketotic hyperglycemia, may present in stroke
  like fashion. The serum glucose level should
  therefore be determined in all patients with
  apparent stroke.

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Treatment of Cerebral Thrombosis and Transient
Ischemic Attacks

• The current treatment of it may be divided into
  four parts
• Management in the acute phase
• Measures to restore the circulation and arrest
  the pathologic process
• 1. Thrombolytic agents ( t-PA only for
  completed stroke,w/in 36hrs ) 2.Anticoagulant
  drugs ( Heparin, LMWH warfarin)
• 3. Antiplatelet drugs ( Aspirin or
  Clopidogrel, Dipyridamole or Ticlopidine )
• 4.Difibrase
• 5. Neuroprotective agents barbiturates,
  opioid antagonist naloxone,Manitol

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Treatment

• Treatment of cerebral edema and raised
  intracranial pressure
• Acute surgical revascularization
• Surgery for symptomatic carotid stenosis
• Carotid endarterectomy, intralumenal stents,
  extracranial-intracranial bypass
• Physical therapy and rehabilitation
• Measures to prevent further strokes and
  progression of vascular disease.

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Treatment

• Since the primary objective in the treatment of
  atherothrombotic disease is prevention ,
  efforts to control the risk factors must
  continue.
• Aspirin
• Hypotensive agents
• Oversedation should be avoided
• Systemic hypotension, severe anemia should be
  treated promptly
• Particular care should be taken to maintain the
  systemic blood pressure, oxygenation and
  intracranial blood flow during surgical
  procedures, especially in elderly patient.

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Course and Prognosis

• When the patient is seen early in the cerebral
  thrombosis, it is difficult to give an accurate
  prognosis.
• As for the eventual or long-term prognosis of the
  neurologic deficit , there are many
  possibilities.
• It must be mentioned that having had one
  thrombotic stroke, the patient is at risk in the
  ensuing months and years of having a stroke at
  the same or another site, especially if there is
  hypertension or diabetes mellitus.

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3.Embolic infarction

• This is one of the most common cause of stroke.
  In most cases of cerebral embolism, the embolic
  material consists of a fragment that has broken
  away from a thrombus within the heart. Embolism
  due to fat, tumor cells, fibrocartilage, amniotic
  fluid, or air is a rare occurrence and seldom
  enters into the differential diagnosis of
  stroke.

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Clinical Picture

• Of all strokes, those due to cerebral embolism
  develop most rapidly.The embolus strikes at any
  time of the day or night. Getting up to go to the
  bathroom is a time of danger.The neurologic
  picture will depend on the artery involved and
  the site of obstruction.

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Clinical Picture

• It is important to repeat that an embolus may
  produce a severe neurologic deficit that is only
  temporary symptoms disappear as the embolus
  fragments. In other words , embolism is a common
  cause of a single evanescent stroke that may
  reasonably be called a prolonged TIA. Also as
  already pointed out, several emboli can give rise
  to two or three transient attacks of differing
  pattern or , rarely , of almost identical
  pattern.

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Causes of cerebral embolism

• Cardiac originNoncardiac originUndetermined
  origin

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Laboratory Findings

• Not infrequently the first sign of myocardial
  infarction is the occurrence of embolism
  therefore it is advisable that an ECG and
  echocardiogram be obtained in all patients with
  stroke of uncertain origin.Prolonged study of
  heart rhythm with Holter monitoring should be
  undertaken.

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Laboratory Findings

• In some 30 percent of cases, cerebral embolism
  produces a hemorrhagic infarction. CT scanning or
  MRI may be helpful in showing the more intense
  hemorrhagic infarcts, particularly if the scan is
  repeated on the second or third day.

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Course and prognosis

• Most patients survive the initial insult, and in
  many the neurologic deficit may recede relatively
  rapidly, as indicated above. The eventual
  prognosis is determined by the occurrence of
  further emboli and the gravity of the underlying
  illness- cardiac failure myocardial infarction,
  bacterial endocarditis and so on.

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Treatment and prevention

• Three phases of therapy General medical
  management in the acute phase,Measures directed
  to restoring the circulationPhysical therapy and
  rehabilitationThese are much the same as
  described above the prevention of
  atherothrombotic infarction.

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4. Lacunar infarct

• As one might surmise, small penetrating branches
  of the cerebral arteries may become occluded, and
  the resulting infarcts may be so small or so
  situated as to cause no symptoms whatever. As the
  softened tissue is removed, it leaves a small
  cavity, or lacune.

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Lacunar infarct

• In our clinical and pathologic material, there
  has always been a strong correlation of the
  lacunar state with a combination of hypertension
  and atherosclerosis and, to a lesser degree, with
  diabetes.In all the cases of lacunar infarction,
  the diagnosis depends essentially on the
  occurrence of the certain unique stroke syndromes
  of limited proportions.

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Lacunar infarct

• As mentioned above, CT scanning is less reliable
  than MRI in demonstrating the lacunes. The EEG
  may be helpful in a negative sense in the case
  of lacunes in the pons or the internal capsule,
  there is a notable discrepancy between the
  unilateral paralysis or sensory loss and the
  negligible electrical changes over the affected
  hemisphere.

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Lacunar infarct

• Recognition of lacunar stroke is important
• Future lacunar stroke can be reduced by
• treating HTN
• Anticoagulation is not indicated ( No
  evidence)
• Aspirin is also of uncertanty

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II. Intracranial Hemorrhage

• This is the common, well-known spontaneous
  brain hemorrhage. It is due predominantly to
  chronic hypertension and degenerative changes in
  cerebral arteries.Hemorrhage may interfere with
  cerebral function through a variety of
  mechanisms, including destruction or compression
  of brain tissue and compression of vascular
  structures, leading to secondary ischaemia and
  edema.

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Intracranial Hemorrhage

• Intracranial hemorrhage is classified by its
  location as intracerebral, subarachnoid,
  subdural, or epidural, all of which- except
  subdural hemorrhage- are usually caused by
  arterial bleeding.

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Intracranial Hemorrhage

• The bleeding occurs within brain tissue, and
  rupture of arteries lying in the subarachnoid
  space is practically unknown apart from
  aneurysms. The extravasation forms a roughly
  circular or oval mass that disrupts the tissue
  and grows in volume as the bleeding continues .
  Adjacent brain tissue is distorted and
  compressed. If the hemorrhage is large, midline
  structures are displaced to the opposite side and
  reticular activating and respiratory centers are
  compromised, leading to coma and death.

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1. Intracerebral HemorrhageOf all the
cerebrovascular diseases, brain hemorrhage is the
most dramatic.It has been given its own name,
apoplexy.
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Clinical Picture

• With smaller hemorrhages, the clinical picture
  conforms more closely to the usual temporal
  profile of a stroke, i.e, an abrupt onset of
  symptoms that evolve gradually and steadily over
  minutes, hours, or a day or two, depending on the
  size of the ruptured artery and the speed of
  bleeding.
• Headache and vomiting are cardinal features.Very
  small hemorrhages in silent regions of the
  brain may escape clinical detection.

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Clinical Picture

• Clinical features vary with the site of
  hemorrhage.
• Deep cerebral hemorrhage The two most common
  sites of hypertensive hemorrhage are the putamen
  and the thalamus, which are separated by the
  posterior limb of the internal capsule. This
  segment of the internal capsule is traversed by
  descending motor fibers and ascending sensory
  fibers, including the optic radiations.

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Clinical Picture

• Lobar hemorrhage Hypertensive hemorrhages also
  occur in subcortical white matter underlying the
  frontal, parietal, temporal, and occipital lobes.
  Symptoms and signs vary according to the
  location.

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Clinical Picture

• Pontine hemorrhage With bleeding into the pons,
  coma occurs within seconds to minutes and usually
  leads to death within 48 hours. Ocular findings
  typically include pinpoint pupils. Horizontal eye
  movements are absent or impaired, but vertical
  eye movements may be preserved.
• Cerebellar hemorrhage The distinctive symptoms
  of cerebellar hemorrhage (headache, dizziness,
  vomiting, and the inability to stand or walk)
  begin suddenly, within minutes after onset of
  bleeding.

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Laboratory Findings

• Among laboratory methods for the diagnosis of
  intracerebral hemorrhage, the CT scan occupies
  the foremost position. In CT scans, fresh blood
  is visualized as a white mass as soon as it is
  shed. The mass effect and the surrounding
  extruded serum and edema are hypodense.
• By MRI, either in T1-or-T2 weighted images, the
  hemorrhage is not easily visible in the 2 or 3
  days after bleeding.

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Laboratory Findings

• In general, lumbar puncture is ill advised, for
  it may precipitate or aggravate an impending
  shift of central structures and herniation. The
  white cell count in the peripheral blood may rise
  transiently to 15,000 per cubic millimeter, a
  higher figure than in thrombosis.

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Differential Diagnosis

• Putaminal, thalamic, and lobar hypertensive
  hemorrhages may be difficult to distinguish from
  cerebral infarctions. To some extent, the
  presence of severe headache, nausea and vomiting,
  and impairment of consciousness are useful clues
  that a hemorrhage may have occurred the CT scan
  identifies the underlying disorder definitively.
• CT scan or MRI is the most useful diagnostic
  procedure, since hematomas can be quickly and
  accurately localized.

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Treatment

• The management of patients with large
  intracerebral hemorrhages and coma includes the
  maintenance of adequate ventilation, use of
  controlled hyperventilation to a Pco2 of 25 to 30
  mmHg, monitoring of intracranial pressure (ICP)
  in some cases and its control by the use of
  tissue-dehydrating agents such as mannitol
  (osmolality kept at 295 to 305 mosmol/L and Na at
  145 to 150 meq), and limiting intravenous
  infusions to normal saline.

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Treatment

• Rapid reduction in blood pressure, in the hope of
  reducing further bleeding , is not recommended,
  since it risks compromising cerebral perfusion in
  cases of raised intracranial pressure. On the
  other hand, sustained mean blood pressure of
  greater than 110mmHg may exaggerate cerebral
  edema and risk extension of the clot. It is at
  approximately this level of acute hypertension
  that the use of beta-blocking drugs(esmolol,
  labetalol) or angiotensin-converting enzyme
  inhibitory drugs is recommended.

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Treatment

• In contrast to cerebral hemorrhage, the surgical
  evacuation of cerebellar hematomas is a generally
  accepted treatment and is a more urgent matter
  because of the proximity of the mass to brainstem
  and the risk of abrupt progression to coma and
  respiratory failure.

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Course and Prognosis

• The immediate prognosis for large and medium-size
  cerebral clots is grave some 30 to 35 percent of
  patients die in 1 to 30 days.
• Either the hemorrhage extends into the
  ventricular system or intracranial pressure is
  elevated to levels that preclude normal perfusion
  of the brain.
• Sometimes the hemorrhage itself seeps into vital
  centers such as the hypothalamus or midbrain.

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Course and Prognosis

• A volume of 30 ml or less, calculated from the CT
  scan, predicted a generally favorable outcome.
• In patients with clots of 60 ml or larger and an
  initial Glasgow Coma Scale score of 8 or less,
  the mortality was 90 percent. As remarked
  earlier, it is the location of the clinical
  effects.

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2.Spontaneous Subarachnoid Hemorrhage

• This is the fourth most frequent cerebrovascular
  disorder following atherothrombosis, embolism,
  and primary intracerebral hemorrhage. Saccular
  aneurysms are also called berry aneurysms
  actually they take the form of small, thin-walled
  blisters protruding from arteries of the circle
  of Willis or its major branches. Their rupture
  causes a flooding of the subarachnoid space with
  blood under high pressure.
• Aneurysms are multiple in 20 percent of patients

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Spontaneous Subarachnoid Hemorrhage

• In childhood , rupture of saccular aneurysms is
  rare, and they are seldom found at routine
  postmortem examination beyond childhood, they
  gradually increase in frequency to reach their
  peak incidence between 35 and 65 years of age.
• Approximately 90 to 95 percent of saccular
  aneurysms lie on the anterior part of the circle
  of Willis.

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Clinical picture

• Prior to rupture, saccular aneurysms are usually
  asymptomatic. Exceptionally, if sufficiently
  large to compress pain-sensitive structures, they
  may cause localized cranial pain.
• The presence of a partial oculomotor palsy with
  dilated pupil may be indicative of an aneurysm of
  the posterior communicating-- internal carotid
  junction.
• With rupture of the aneurysm, blood under high
  pressure is forced into the subarachnoid
  space(where the circle of Willis lies).

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Clinical picture

• Rupture of the aneurysm usually occurs while the
  patient is active rather than during sleep , and
  in some instances sexual intercourse, straining
  at stool, lifting heavy objects, or other
  sustaining exertion precipitates the ictus. In
  patients who survive the initial rupture, the
  most feared complication is rerupture, an event
  that may occur at any time from minutes up to 2
  or 3 weeks later.
• In less severe cases, consciousness, if lost ,
  may be regained within a few minutes or hours,
  but a residual of drowsiness, confusion, and
  amnesia accompanied by severe headache and stiff
  neck persists for several days.

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Clinical picture

• Since the hemorrhage is confined to the
  subarachnoid space, there are few or no focal
  neurologic signs.
• AVM is another most common cause for SAH
• Convulsive seizures, usually brief and
  generalized.

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Clinical picture

• Vasospasm Delayed hemiplegia or other focal
  deficit usually appears 3 to 12 days after
  rupture and rarely before or after this period.
  These delayed accidents and the focal narrowing
  of a large artery or arteries, seen on
  angiography, are refered to as vasospasm.
• Hydrocephalus If a large amount of blood
  ruptures into the ventricular system or floods
  the basal subarachnoid space, The patient then
  may become confused or unconscious as a result of
  acute hydrocephalus. A subacute hydrocephalus due
  to blockage of the CSF pathways by blood may
  appear after 2 to 4 weeks.

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Laboratory Findings

• A CT scan will detect blood locally or diffusely
  in the subarachnoid spaces or within the brain or
  ventricular system in more than 90 percent of
  cases and in practically all cases in which the
  hemorrhage has been severe enough to cause
  momentary or persistent loss of consciousness.
• In all other cases a lumbar puncture should be
  undertaken when the clinical features suggest a
  subarachnoid hemorrhage. Usually the CSF is
  grossly bloody within 30 min of the hemorrhage,
  with RBC counts up to 1 million per cubic
  millimeter or even higher.

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Laboratory Findings

• Carotid and vertebral angiography is the only
  certain means of demonstrating an aneurysm and
  does so in some 85 percent of patients in whom
  the correct diagnosis of spontaneous subarachnoid
  hemorrhage is made on clinical grounds.
• MRI and MRA detect most aneurysms of the basal
  vessels but are as yet of insufficient
  sensitivity to replace conventional angiography.
  Even when MRA or CT angiography demonstrates
  the aneurysm, the surgeon usually requires the
  kind of anatomic definition that can only be
  obtained by conventional angiography.

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Establish the diagnosis

• If there is a typical history, marked neck
  stiffness and no focal neurological deficit,
  lumbar puncture is still the best way to make the
  diagnosis, revealing uniformly blood-stained CSF.

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Establish the diagnosis

• If the history is typical with marked neck
  stiffness, but the patient remains in coma or
  shows a marked focal neurological deficit, a CT
  scan is a safer way to establish the diagnosis
  (revealing blood in the subarachnoid space),since
  lumbar puncture may lead to worse condition in
  this group of patients (whose coma or focal
  neurological deficit may indicate the presence of
  an associated intracerebral blood clot).

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Treatment

• This is influenced by the neurologic and general
  medical state of the patient as well as by the
  location and morphology of the aneurysm.
• The general medical management in the acute stage
  includes the following , in all or part
• bed rest
• fluid administration to maintain above-normal
  circulating volume and central venous pressure
• use of elastic stockings and stool softeners
• administration of beta-blockers
• calcium channel blockers

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Treatment

• intravenous nitroprusside
• or other medication to reduce greatly elevated
  blood pressure and then maintain systolic blood
  pressure at 150 mmHg or less
• and pain-relieving medication for headache ( this
  alone will often reduce the hypertension ).
• The prevention of systemic venous thrombosis is
  critical, usually accomplished by the use of
  cyclically inflated whole-leg compression boots.

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Treatment

• The use of anticonvulsants is controversial many
  neurosurgeons administer them early, with a view
  of preventing a seizure-induced risk of
  rebleeding.
• Calcium channel blockers are being used
  extensively to reduce the incidence of stroke
  from vasospasm. Nimodipine 50 mg, administered
  intravenus, is currently favored.

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Treatment

• Notable advances in the techniques for the
  obliteration of aneurysms, particularly the
  operating microscope, and the management of
  circulatory volume have significantly improved
  the outcome of patients with ruptured aneurysms.
• Both the risk of rerupture of the aneurysm and
  some of the secondary problems that arise because
  of the massive amount of blood in the
  subarachnoid space can be obviated by early
  obliteration of the aneurysm.

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Treatment

• lumbar puncture is carried out for diagnostic
  purposes if the CT scan is inconclusive
  thereafter this procedure is performed only for
  the relief of intractable headache, to detect
  recurrence of bleeding, or to measure the
  intracranial pressure prior to surgery.

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Treatment

• Advice from specialist neurosurgical units should
  be sought. Patients who have withstood their
  first bleed well are submitted to carotid and
  vertebral angiography within a few days to
  establish whether or not an operable aneurysm is
  present. Patients who do not recover from their
  first bleed well, patients with inoperable
  aneurysms should be nursed in bed for a few weeks
  and then mobilized over a further few weeks,
  being encouraged to return to full normal
  activities at about 3-4 months.
• Prevent re-bleeding

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Rehabilition

• Since the incidence of significant damage to the
  brain is high in patients surviving subarachnoid
  haemorrhage, many will not be able to return to
  normal activities.
• They will need support from relatives, nurses,
  physiotherapists, speech therapists, occupational
  therapists, social workers and specialist units
  in rehabilitation.

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Course and prognosis

• Patients with the typical clinical picture of
  spontaneous subarachnoid hemorrhage in whom an
  aneurysm or arteriorvenous malformation cannot be
  demonstrated angiographically have a distinctly
  better prognosis than those in whom the lesion
  is visualized.
• Vasospasm and rebleeding were the leasing
  causes of morbidity and mortality in addition to
  the initial bleed. In respect to rebleeding ,
  Aoyagi and Hayakawa found that this occurred
  within 2 weeks in 20 percent of patients, with a
  peak incidence in the 24 h after the initial
  bleed.

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• THANKS!