It accounts for 12% of total stroke cases in clinical practice.
1.Hypertension with cerebral atherosclerosis-most important cause (90%). Hypertension is associated with Charcot Bouchard micro-aneurysms which ruptures and produces intra-cerebral haemorrhage.
3. Whooping cough.
4.Blood dyscrasias including anticoagulant and thrombolytic therapy
S Ruptured intracerebral aneurysm or angiomata.
6. Haemorrhage in a neoplasm (primary or secondary).
7. Haemorrhage around an infarction.
8. Arterial and venous inflammation including inflammatory vasculopathy from collagenosis and drug abuse.
9. Amyloid vasculopathy.
10. Liver disease.
11. Vascular anomaly, e.g. arteriovenous malformation and cavernous haemangioma.
12. Abuse of drugs and agents, e.g., Alcohol, Amphetamine and Cocaine.
13. Unknown cause
The usual site of haemorrhage is near about the internal capsule in the basal ganglia) Less common sites are pons, thalamus, cerebellum and cerebral white mater. The pathologic basis for haemorrhage is possible rupture of the mocroaneurysm on the perforating vessels (100-30 um in diameter) in hypertensive patients.
Blood then rushes outside, tearing the friable brain substance whereby internal capsule is involved. The effused blood enters the cerebral ventricles or into the subarachnoid space when signs of meningeal irritation may develop, and ultimately death occurs due to paralysis of vital centres. The most vulnerable artery is the perforating branch of middle cerebral artery known as lenticulostriate artery. Due to this vulnerability this artery is called artery of cerebral haemorrhage of Charcot.
Onset is sudden
Age: Above 40 usually
Sex: Common in males.
Mental stresS and strain or sudden emotional upsets are precipitating factors.
Patient complains of sudden headache along with vomiting both of which are due to increased intracranial tension. Consciousness is rapidly lost in about 50% of cases. Rarely symptoms may be minimal or resemble tschaemic stroke when cerebral haemorrhage is localised and involves more peripheral or polar region of hemisphere.
Head is turned towards one side. Gradually decep coma develops. Conjugate deviation of the eyes is present-at first away from the irritative lesion and gradually towards the side of lesion.
Pupils are unequal and in the early stage they react to light but in late stages they are widely dilated and fixed. In pontine haemorrhage both the pupils are pin-pointed. The face is congested and sweating may be present. The angle of the mouth is dropped, the nasolabial furrow is flat and cheek is puffed out on the paralysed side. Movements of limbs are only present on the non-paralysed side. Paralysed side remains motionless but there may be some involuntary movements. Urinary bladder may be full. There may be involuntary evacuation of urine and faeces. Pulse is full and bounding but the rate is slow (due to increased intracranial tension). Thickening of the peripheral arteries may be present. Respiration rate is also slow. Stertorous or Cheyne-Stoke’s breathing may be seen. BP is always high, usually above 200 mm of Hg systolic. Temperature is usually normal but in cases of pontine haemorrhage temperature is raised.
Limbs are flaccid but more so on the paralysed side. Plantar reflex is extensor on the paralysed side to start with but may be so on both sides if the patient is in coma. Abdominal reflexes are lost on both sides and the deep reflexes are either diminished or absent on the paralysed side-though sometimes they may be brisk. Nuchal rigidity is sometimes present. Ophthalmoscopic examination may show retinal arteriosclerosis and sometimes papilloedema due to previous hypertension. Heart may show left ventricular enlargement which is again due to previous hypertension. Lumbar puncture shows frank blood.
In some cases of cerebral haemorrhage, the onset is not so abrupt and stormy but gradual; consciousness is not lost; neurologic deficits are neither progressive nor profound, clinical situation does not show rapid deterioration. This condition is really indistinguishable from cerebral infarction except by lumbar puncture. In ingravescent haemorrhage the clinical signs gradually increase for a period of one week or so. As there is profound coma often it becomes difficult if not impossible to find out the side of hemiplegia which should always be searched is such cases. The following signs will be helpful in determining the side of hemiplegia:
1.Flattening of the nasolabial furrow.
2.Puffing out of cheek with each breath.
3.Loss of corneal reflex.
4.Spontaneous involuntary movement of the limbs.
5. Absence of movement of the limbs after painful stimuli.
6. More flaccidity and inertness of the limbs.
8. Sluggish or brisk deep reflexes.
9. Extensor planter response
The sites for intracerebral haemorrhages with their distinctive clinical features are given below;
1. Internal capsule or putamen-commonest (50%).
2. Different parts of central white matter including frontal lobe, corona radiata etc. which are secondary to capsular haemorrhage.
4. Brain stem.
Capsular or Putamenal Haemorrhage
Here the site of bleeding is near the internal capsules. In presence of huge bleeding profound coma develops very rapidly and the general condition rapidly deteriorates. Flaccid hemiplegia, hemisensory loss (with deeply located lesion) and homonymous hemianopia loss (with deeply loocked lesion) and hemisphere is involved aphasia develops. There may be convulsive seizure. There is conjugate deviation of the eyes towards the side of haemorrhage and opposite to the paralysed limb. All these features may also develop gradually. Features of brain stem compression may develop with coma, bilateral extensor plantar reflex, dilated fixed pupils, irregular respiration and sometimes decerebrate rigidity. When capsular haemorrhage bursts into the lateral ventricle it is difficult to differentiate this condition from pontine haemorrhage. There may be shivering, nausea, vomiting etc. Haemorrhage may produce transtentorial herniation and compression followed by death. In this condition, the signs of pyramidal lesion develop on both sides with rapidly deepening coma, rigid cxtension of the upper limbs and pyrexia.
Secondary affection of frontal lobe, corona radiata, etc from capsular haemorrhage
They may produce clinical features of such lesions though it is very difficult to localise them.
There is either hemiplegia or hemiparesis but hemisensory loss of all types of sensation is more prominent than motor deficit. Consciousness is not lost. Compression of tectum of midbrain may produce drowsiness followed by coma in rapidly fatal cases. Homonymous hemianopia is present though it disappears after sometimes. Due to extension of haemorrhage in the subthalamic area or compression of the posterior commissure there may be paralysis of the upward gaze with forced deviation of the eyes downwards and laterally. This is pathognomonic of bleeding at this site. There may be unequal pupils with poor reaction to light, slight ptosis and absence of convergence resembling oculomotor palsy There may be miosis, ptosis and absence of convergence on the side of haemorrhage with deviation of the eyes downwards and medially on the opposite side resembling 6th nerve palsy. Neck rigidity is prominent, mutism may develop when haemorrhage involves non-dominant thalamus.
When pons is involved there will be deep coma, hyperpyrexia, reversed conjugate ocular deviation or bilateral gaze palsy, bilateral pin-point pupil with reaction to light, decerebrate or decortical rigidity, absence of lateral eye movement on head turning or after aural irrigation with iced water. In haemorrhage into the midbrain and medulla rapid loss of consciousness, quadriplegia, irregular Cheyne-Stoke’s type breathing, decerebrate rigidity and oculomotor palsy may develop.
Initially occipital headache, nausea, vomiting, vertigo, slurred speech, conguate gaze paralysis with diplopia and gaze deviates towards the side, nystagmus and ataxia are present. When suspicion of stroke is strong but hemiplegia conjugate ocular movement are one should suspect cerebellar haemorrhage. Upper motor neurone signs are lacking here but may be present when haemorrhage has pierced its way to compress lateral side of pons.
Acute hydrocephalus may be produced. When the course of the disease is intermediate there will be lateral conjugate gaze palsies to the side of lesion, small reactive pupil, contralateral hemiplegia, peripheral facial weakness, ataxic gait with ataxia of limbs and trunk, Cheyne-Stoke’s breathing, etc. CSF does not show blood.
1. CSF shows increased pressure, colour frank blood, protein level is raised, microscopic examination shows plenty of RBC. However, LP is contraindicated in presence of large haematoma as it may precipitate medullary herniation.
2. Urine may show albumin and sugar due to cerebral lesion.
3. Blood examination, TC, DC, Hb%, Platelet count, BT, CT, Prothrombin time, Partial thromboplastin times, Liver function test, Renal function tests are to be done which may give a clue for haemorrhage.
4. CT scan is particularly helpful for localised small haemorrhage which does not bring blood to CSF. It is not only helpful for diagnosis of haemorrhage but also for assessment of the site and size of haematoma.
It is said to be superior to MRI. If patient’s conditions permits cerebral angiography may also be done.
Patient is usually kept in Intensive Care Unit in a railed cot with head-end slightly raised facilitating venous return from the brain with least movement to the body. All management for a comatose patient should be instituted. Lumbar puncture is to be done only for diagnostic purpose because it may be associated with hazards of tentorial or cerebellar herniation, Surgical removal of the blood clot is not practically possible in each case but can be considered in younger individuals particularly when there is mass effect, incipient tentorial herniation and also in cases of cerebellar haemorrhage.
Antibiotics may sometimes be useful to prevent secondary infection. Nutrition is to be maintained by intravenous or gastric feeding. To reduce intracranial tension Glycerine, Mannitol, Fructose, etc. may be used.
Physiotherapy can be considered in cases where the patient gains consciousness with residual hemiplegia.