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  1. Subarachnoid Hemorrhage (SAH) (Ref. Hari. 18th ed., Pg - 2262)

Figure - Common sites of saccular (berry) aneurysms in the circle of Willis.

Causes -

  • Head trauma  (Commonest cause)
  • Rupture of a Berry aneurysm
  • Bleeding from vascular anomaly
  • Extension from primary intra cerebral hemorrhage.

Extra Edge:

  1. Saccular (Berry) ​aneurysms occur at the bifurcations of the large to medium-sized intracranial arteries; rupture is into the subarachnoid space in the basal cisterns and often into the parenchyma of the adjacent brain.
  2. Approximately 85% of aneurysms occur in the anterior circulation, mostly on the circle of Willis.
  3. As an aneurysm develops, it typically forms a neck with a dome. The length of the neck and the size of the dome vary greatly and are factors that are important in planning neurosurgical obliteration or endovascular embolization.
  4. The arterial internal elastic lamina disappears at the base of the neck. (Ref: Hari, 18th ed., pg. -2262)
  5. The media thins, and connective tissue replaces smooth-muscle cells. At the site of rupture (most often the dome) the wall thins, and the tear that allows bleeding is often ≤ 0.5 mm long.
  6. Aneurysm size and site are important in predicting risk of rupture.
  7. Those >7 mm in diameter and those at the top of the basilar artery and at the origin of the posterior communicating artery are at greater risk of rupture.

Clinical features –

  1. Sudden Severe onset headache, never experienced before, in the absence of focal neurological deficit, is the hallmark of SAH.
  2. Transient loss of consciousness.
  3. Neck rigidity may be present mimicking meningitis. Neck stiffness & vomiting: are common associations
  4. Focal neurological deficit: uncommon.
  5. Associated prodromal symptoms (suggest location of progressively enlarging unruptured aneurysm)
    1. Third cranial nerve palsy: aneurysm at junction of PCA & ICA (LQ 2012)
    2. Sixth nerve palsy: aneurysm in cavernous sinus
    3. Occipital and posterior cervical pain: inferior cerebellar artery aneurysm (Ant. or Post.)
    4. Pain behind the eye: MCA aneurysm
  6. Aneurysms may undergo small ruptures or leaks, so called sentinel bleeds.

Extra Edge:

  1. Most common site of berry aneurysm is junction of ACA with anterior communicating artery.
  2. Vertebral A is the least common site of berry aneurysm.
  3. Most common nerve involved in berry aneurysm is IIIrd nerve. (LQ 2012)
  1. Delayed neurologic deficits –
    1. Re rupture – At 7 - 14 days
    2. Hydrocephalus – Acute causes stupor, coma.
      Subacute slowed mentation with urinary in continence
      Chronic Gait difficulty, incontinence
    3. Vasospasm – Most frequently at 3 - 7 days.
    4. Hyponatremia – Due to SIADH, first 2 weeks.

Most common cause of late CNS deterioration in SAH is hydrocephalus. (AIIMS May 2011)


Extra Edge: Hydrocephalus.

  1. Acute hydrocephalus can cause stupor and coma and can be mitigated by placement of an external ventricular drain.
  2. Subacute hydrocephalus may develop over a few days or weeks and causes progressive drowsiness or slowed mentation (abulia) with incontinence. Hydrocephalus may clear spontaneously or require temporary ventricular drainage.
  3. Chronic hydrocephalus may develop weeks to months after SAH and manifest as gait difficulty, incontinence, or impaired mentation. Subtle signs may be a lack of initiative in conversation or a failure to recover independence.

Diagnosis: CT Scan


Treatment: An aneurysm can be clipped by a neurosurgeon or coiled by an endovascular surgeon.


Table 275-3 Grading Scales for Subarachnoid Hemorrhage (Ref. Hari. 18th ed., Pg- 2262) 


Hunt-Hess Scale

World Federation of Neurosurgical Societies (WFNS) Scale


Mild headache, normal mental status, no cranial nerve or motor findings

GCS* score 15, no motor deficits


Severe headache, normal mental status, may have cranial nerve deficit

GCS score 13–14, no motor deficits


Somnolent, confused, may have cranial nerve or mild motor deficit

GCS score 13–14, with motor deficits


Stupor, moderate to severe motor deficit, may have intermittent reflex posturing

GCS score 7–12, with or without motor deficits


Coma, reflex posturing or flaccid

GCS score 3–6, with or without motor deficits

Investigations –

  1. C.T head (Best to diagnosis). Non contrast CT scan: Investigation of choice (LP is not indicated prior to an imaging procedure). Blood is seen in the sylvian fissure.
  2. CSF examination:
    1. Hallmark is blood in CSF
    2. Xanthochromic CSF – lysis of RBCS and Subsequent conversion of Hb to bilirubin stains the spinal fluid yellow with in 6 – 12 hours. Peak 48 hours & lasts for 1 – 4 weeks.
  3. MR angiography – For unruptured aneurysm.

Treatment –

  1. Medical support
    1. Airway protection
    2. BP management
    3. Prevent vasospasm – Nimodipine, volume expansion.
  2. Triple H method of Rx Hypertension, hemodilution & hypervolemia (Ref. Hari. 18th ed., Pg- 2264)
  3. If vasospasm persists
    1. Intracranial papaverine
    2. Phenytoin given as prophylactic therapy.
    3. Surgery – Clipping of aneurysm.
  4. Recent Advances= Endovascular coiling

Extra Edge:

  1. Vasospasm remains the leading cause of morbidity and mortality following aneurysmal SAH.
  2. Treatment with the calcium channel antagonist nimodipine improves outcome, by preventing ischemic injury rather than reducing the risk of vasospasm.
  3. Symptomatic cerebral vasospasm can also be treated by increasing the cerebral perfusion pressure by raising mean arterial pressure through plasma volume expansion and the judicious use of IV vasopressor agents, usually phenylephrine or norepinephrine.
  4. Raised perfusion pressure is associated with clinical improvement in many patients, but high arterial pressure may promote rebleeding in unprotected aneurysms.
  5. Treatment with induced hypertension and hypervolemia generally requires monitoring of arterial and central venous pressures; it is best to infuse pressors through a central venous line as well.
  6. Volume expansion helps prevent hypotension, augments cardiac output, and reduces blood viscosity by reducing the hematocrit.
  7. This method is called "triple-H" (hypertension, hemodilution, and hypervolemic) therapy.
  1. Subdural hematoma (Ref. Hari. 18th ed., Pg- 3379)
Acute subdural hematoma (Ref. Hari. 18th ed., Pg- 3378)
  1. A unilateral headache and slightly enlarged pupil on the side of the hematoma are frequently, present.
  2. Stupor or coma, hemiparesis, and unilateral pupillary enlargement are signs of larger hematomas.

Chronic Subdural Hematoma

  1. The presence of progressive hemiparesis and aphasias together with signs of raised ICT (papilledema) in an elderly patient, developing weeks after sustaining a mild head injury is characteristic of chronic subdural hematoma.
  2. Gradual accumulation of blood in subdural space and classically presenting 3 weeks after the initial bleed.


  1. Most commonly caused by rupture of superior cerebral veins (LQ 2012) (Bridging veins that connect the cerebral cortex to superior saggital sinus)
  2. Repeated cycles of recurrent bleeding into subdural space and resorption of the resultant hematoma.


  1. Head Trauma (Usually trivial and unnoticed in upto 25% of cases) so It is very common in alcoholic patient.
  2. Motor vehicle Accident
  3. Repeated falls in elderly from syncope, ataxia, weakness or seizures
  4. Patients with bleeding problems
    1. Anticoagulation  
    2. Thrombocytopenia      
    3. Liver failure
    4. Alcoholism  
  5. Dural lesions
    1. Sarcoma’s AV malformations and metastatic cancer
  6. Low CSF volume
    1. CSF shunts, renal dialysis, excess diuretics

Clinical Features


Gradual onset of signs and symptoms over several weeks (characteristically >3 weeks for chronic subdural hematomas)

  1. Headache: Constant and relatively mild & usually lateralized to the side of lesion      
  2. Deterioration of mental status with confusion lethargy and memory disturbance      
  3. Progressive contralateral hemiparesis and Aphasias (speech disturbance)
  4. Papilledema
  5. Others:
    1. Cranial Nerve abnormalities
    2. Hemianopsia

Diagnosis CT scan/MRI


Treatment surgery.

  1. Extradural hemato
    1. Most common cause - Trauma to temporal bone (Temporal bone fracture)
    2. Blood vessel involved are – Rupture of middle meningeal artery & vein.
    3. The clinical presentation:
      1. Sudden onset of altered sensorium
      2. After some time patient regain consciousness for a short period (Lucid interval)
      3. Patient again become unconscious.
    4. Diagnosis: CT scan
    5. Treatment: Urgent Burr hole surgery.

Extra Edge:

  1. Coma with a dilated pupil after a lucid interval following a head injury must be assumed to represent an epidural hematoma.
  2. Emergency evacuation of the clot without time-consuming studies is vital to restore cerebral function. With a patient in less critical condition, a CT scan is the appropriate diagnostic study.

Raise ICP & Pseudo tumor Cerebri


Norma ICP= 0-10 mm Hg,


TYPES of raised ICP.

  1. Vasogenic  capillary permeability (Tumor, trauma & infection)
  2. Cytototic cell = death (hypoxia)
  3. Interstitial: Obstructive hydrocephalous

Sign/symptom – Headache, Hypertension, Bradycardia, Cheyne stoke breathing, pupil constrict initially then dilate later, papilledema alter sensorium.


['Early signs of elevated ICP include drowsiness and a diminished level of consciousness (altered mental status). Coma and unilateral pupillary dilation are late signs and require immediate intervention']

TABLE 258-2 Stepwise Approach to Treatment of Elevated Intracranial Pressure (Ref. Hari. 18th ed., Pg- 2257, Table 275-2)


Insert ICP monitor—ventriculostomy versus parenchymal device


General goals: maintain ICP <20 mmHg and CPP >70 mmHg


For ICP >20–25 mmHg for >5 min:

  1. Drain CSF via ventriculostomy (if in place)
  2. Elevate head of the bed
  3. Osmotherapy- mannitol is used (Extra Edge: Frusemide is not used)
  4. Glucocorticoids- dexamethasone for vasogenic edema from tumor, abscess
  5. Sedation (e.g., morphine, propofol, or midazolam); add neuromuscular paralysis if necessary
  6. Hyperventilation-to PaCO2 30–35 mmHg
  7. Pressor therapy-phenylephrine, dopamine, or norepinephrine to maintain adequate MAP to ensure CPP >70 mmHg
  8. Consider second-tier therapies for refractory elevated ICP
    1. High-dose barbiturate therapy (“pentobarb coma”)
    2. Hemicraniectomy

Note: (CPP, cerebral perfusion pressure; MAP, mean arterial pressure; PaCO2, arterial partial pressure of carbon dioxide).

Benign Intra Cranial Hypertension (Psuedo Tumour Cereberi)

  1. Patient has features of Raised ICP (headache, Papilledema) but without S.O.L. in the brain.
  2. It occurs in Obese ladies. (30 to 45 year of age) AIIMS May 2012
  3. They C/O blurring vision, Diplopia, Sixth Nerve Palsy can occur.
  4. But no altered sensorium.
  5. Causes include
    1. High doses of vitamin A (LQ 2012)
    2. Outdated Tetracycline
    3. Quinolones
    4. Withdrawal of corticosteroid therapy
    5. Addison's disease
    6. SLE
    7. Hypoparathyroidism
  6. Characteristic features
    1. Elevated intracranial pressure (intracranial hypertension)     
    2. Normal or Small sized ventricular system
    3. No focal neurological signs                    
    4. Papilledema (enlarged blind spot in visual fluid).           
    5. Normal CSF findings
    6. Normal CT scan, MRI and isotope brain scan
    7. Excessive slow-wave activity on EEG but seizure in not a feature.
  7. There are no focal neurological signs in pseudotumor cerebri. Therefore, pseudotumor cerebri does not present with convulsions.
  8. It is a benign self-limiting disorder with a favorable outcome.
  9. Treatment –  a) Weight loss  b) Acetazolamide  c) Optic sheath Fenestration  d) Lumbo Peritoneal Shunt.

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