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Neurology         |  Inracerebral Hemorrhage 2005


DX: CT scan of the head.

Typically occurs in

  1. The putamen & adjacent internal capsule. (the most common site)
  2. The thalamus.
  3. The pons.
  4. The cerebellum.

Most hypertensive intracerebral hemorrhages (HIH) develop over a few minutes to 60 min, but some may evolve over 24-38 hrs, esp in anticoagulated pts. Once bleeding stops, it has generally been thought not to start again. Edema in the compressed tissue around the hemorrhage often leads to increasing mass effect, & worsening of the clnical state.

SX: headache & vomiting are hallmarks of acute hemorrhages. Seizures are uncommon but occur in a few instances.

Putamenal hemorrhage SX:

Contraleteral hemiplegia; in mild cases, over 5-30 min, the face sags on one side, speech becomes slurred, the arm & leg gradually weaken, & the eyes deviate away from the side of the hemiparesis. In the worst case, the drowsiness gives way to stupor as signs of upper brainstem compression appear. Coma ensues, accompanied by deep, irregular or intermittent respiration, a dilated & fixed ipsilateral pupil, bilateral Babinski signs, & decerebrate rigidity. Edema formation in the adjacent brain may cause progressive deterioration over 12-72 hrs.

Thalamic hemorrhages SX:

Hemiplegia or hemiparesis. A prominet sensory deficit involving all modalities is usually present. Aphasia, often with preserved verbal repetition, may occur after hemorrhage into the dominant left thalamus, & apractagnosia or mutism occurs in some cases of nondominant hemorrhage. There also may be a transient homonymous visual field defect. Several typical ocular disturbances are deviation of the eyes downward & inward so that they appear to be looking at the pt's nose, unequal pupils with absence of light reaction, skew deviation with the eye opposite the hemorrhage displaced downward & medially, ipsilateral ptosis & miosis (Horner's syndrome), absence of convergence, paralysis of vertical gaze, an assortment of lateral gaze abnormalities (paresis or pseudoparesis of the sixth nerve), & retraction nystagmus.

Pontine hemorrhages SX:

Deep coma with quadriplegia usually occurs over a few minutes. There is often prominent decrebrate rigidity & small (1 mm) pupils that react to light. There is impairment of reflex horizontal eye movements evoked by head turning (Doll's head or oculocephalic maneuver) or by irrigation of the ears with cold water. Hyperpnea, severe acute hypertension, & hyperhidrosis are common. Death usually occurs within a few hours, but there are esceptions where consciousness is retained because the hemorrhage is limited to the tegmentum.

Cerebellar hemorrhages

Sx of repeated vomiting & inability to walk or stand usually develop over several hours.

In mild cases there may be no other neurologic signs; Occipital headache & dizziness or vertigo may be prominent Sx. There is often paresis of conjugate lateral gaze toward the side of the hemorrhage, forced deviation of the eyes to the opposite side, or an ipsilateral sixth nerve palsy. Other less frequent ocular signs include blepharospasm, involuntary closure of one eye, ocular bobbing, & skew deviation. There may be little or no evidence of the usual signs of cerevellar disease, & only a minority of cases show nystagmus or ataxia of the limbs. A mild ipsilateral facial weakness & a diminished corneal reflex are common. Dysarthria & dysphagia may occur. There are no Babinski signs until late in the evolution of the hemorrhage as it expands to the brainstem. As the hours pass, & occasionally with unanticipated suddenness, the pt becomes stuporous, then comatose as a result of brainstem compression, at which point reversal of the syndrome by surgical removal of the clot is seldom successful.

The size & location of the hematoma determine the Rx & prognosis.

Superatentorial hematomas >5cm in largest diameter generally have a poor prognosis, & infratentorial pontine hematomas >3cm are usually fatal.

The occurence of edema in the week after the intracerebral hemorrhage often worsens the prognosis.

Surgical removal of an acute supratentorial clot is controversial, but most surgeons have found it necessary on rare occasions. In stuporous pts who still have reflex eye movements & some pupillary reaction, surgery may prevent temporal love herniation & irreversible brainstem compression.

One important randomized trial has shown a benefit of surgery, though marginal, only in pts in this state.

Lifesaving surgery may onetheless leave major neurologic residue.

In contrast, surgical Rx of acute cerebellar hemorrhage is nearly always recommended because it prevents secondary brainstem compression that is the mechanism of death & it offers an excellent prognosis for recovery. If pts are alert without focal brainstem signs & if the cerebellar hematoma is small, acute surgical removal may not be necessary.

Mannitol & other osmotic agents reduce intracranial pressure that has been raised by the volume of the hematoma & edema.

Glucocorticoids are of uncertain value in curtaining edema from intracerevral hematoma.

Monitoring of the intracranial pressure may help to assess medical therapy.

Both excessive hypotension & hypertension should be avoided.

Toxemia of pregnancy & malignant hypertension associated with acute hemorrhage syould be treated cautiously to avoid excessive or precipitous lowering of the blood pressure.

Lobar Intracerebral Hemorrhage (outside the basal ganglia & thalamus areas)
- appear on CT scan as oval or circular clots in the subcortical white matter.

The most common reason is arteriovenous malformation. Others are due to bleeding deathesis, often associated with anticoagulation, hemorrhages into tumor, & aneurysm of the circle of Willis that bleed into brain substance.

Most pts have focal headachesas pain over the ipsilateral eyes in occipital hemorrhage; pain in ipsilateral ear in temporal hemorrhage; pain over forehead or frontal quarant in frontal hemorrhage; pain over the temple region in parietal hemorrhage. Stiff neck or seizures are uncommon, but more than half the pts vomit or are initially drowsy.

Sx appear suddenly over one to several minutes. Most lobar hemorrhages are small enough to cause a restricted clnical syndrome that simulates an embolus to a vessel supplying one lobe.

Sx of occipital hemorrhage is hemianopsis. Sx of left temporal hemorrhage is aphasia & deliriu; Sx of parietal hemorrhage is thalamic-like hemisensory loss; Sx of frontal hemorrhage is arm weakness.

Large hemorrhages may be associated with stupor or coma if they secondarily compress the lower thalamus midbrain.

In a awake or drowsy pts, surgical evacuation offers little benefit over medical management with fluid restriction & osmotic agents. Stuporous or comatose pts who do not respond rapidly to medical therapy for raised intracranial pressure should generally have the clot evacuated.

REF: HARRISON 13th Ed. 1994,p.2251-2252

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Medical Progress: Spontaneous Intracerebral Hemorrhage
Adnan I. Qureshi, Stanley Tuhrim, Joseph P. Broderick, H. Hunt Batjer, Hideki Hondo, Daniel F. Hanley
The New England Journal of Medicine -- May 10, 2001 -- Vol. 344, No. 19