Acquired Hydrocephalus and Increased Intracranial Tension

It is caused by subarachnoid hemorrhage, Basal meningitis and Neoplasms obstructing the aqueduct. The basal foramina may be obstructed in meningitis and subarachnoid hemorrhage. The skull is not enlarged if hydrocephalus occurs after closure of the fontanelles. Rise of intracranial tension leads to radiological features such as resorption of the cliniod processes and thining of the skull vault giving rise to a 'silver beaten' appearance.

Increased intracranial Tension
Persistent increase in tension of CSF above 120 mm CSF (or water) in the recumbent posture constitutes raised intracranial tension (ICT). The normal contents of the cranium are the nervous tissue, cicrculating blood and CSF. Rise in intracranial tension may result from increase in the contents of the cranium. E.g, clots, tumors, abscesses or edema of the brain or due to obstruction to the flow of CSF into the subarachnoid space to be absorbed by the arachnoid granulations. Some degree of compensation is possible to normalize the intracranial tension in health and disease. These mechanisms include:
1. displacement of CSF from the cranium and
2. drainage of blood by the emissary veins.

When rise of intracranial tension proceeds, these compensatory mechanisms are overcome. Rise in intracranial tension leads to disturbances of hypothalamic vasomotor regulatory mechanisms. These lead to the development of bradycardia and systolic hypertension (Cushing's vasomotor phenomena). Further rise in tension results in displacement of the brain. If the rise in tension is caused by a unilateral lesion in the brain, the ipsilateral hemisphere is pushed to the opposite side under the falx cerebri-subfalcine herniation. The medial part of the temporal lobe is pushed down through the tentorial hiatus-transtentorial herniation. This gives rise to paralysis of the third nerve. Pressure of the ipsilateral cerebral peduncles gives rise to contralateral hemiparesis. Contre-coup pressure on the opposite cerebral peduncle by the free margin or the tentorium cerebelli gives rise to hemiparesis of the ipsilateral side as well. As the tension increases further, both the pupils dilate, both the cerebral peduncles are compressed and the picture is one of decerebrate rigidity. Opistotonic seizures may develop. When the intracranial tension reaches that of arterial blood pressure, cerebral blood flow is considerably diminished. Medullary centres are dp[ressed. The cerebellar tonsils herniated down the foramen magnum compressing the medulla and this leads to respiratory paralysis and death. Lesions in the posterior cranial fossa give rise to ICT earlier than supratentorial lesions.

Clinical features
Headache: Early symptom is headache, which is dull initially and it tends to worsen in the mornings. Later it becomes persistent and assumes a bursting character. Sharp rise in intracranial tension caused by coughing, straining at stools or stooping forwards gives rise to aggravation of the headache. Later the headache may become so severe and constant that the patient may not even complain of it unless specifically asked for.

Vomiting: Stimulation of mid-line structures in the medulla (Vomiting center) gives rise to effortless and projectile vomiting. In projectile vomiting nausea is usually absent.

Loss of vision: As the ICT rises, vision deteriorates. Defects in the visual fields, diplopia, and total blindness may follow. Fundus-copy shows papilledema and later on, optic atrophy.

Mental changes: These include apathy, abnormal behavior and lack of attention to personal details. With further rise in ICT the patient may become comatose.

Seizures: These may be the presenting symptom in many. These may be generalized motor, focal, complex, sensory or psychomotor in type.

Focal neurological deficits: These depend upon the location of the primary lesion. These may take the form of irritative phenomena like focal seizures, paralysis or disturbance of higher functions.

Hypothalamic disturbances: Endocrine disturbances develop in longstanding cases whereas the rise in ICT is gradual and prolonged. These may result in disturbances of the hypothalamus, pituitary or both. Symptoms include amenorrhea, precocious puberty, obesity, gigantism, somnolence, and hyperphagia.
In children, constipation is frequent and this results from the fear to defecate since the act of defecation causes rapid worsening of the headache.

Common causes of raised ICT
1. Space occupying lesions: Tumors, abscess, granulomas, cysts
2. Inflammation: Meningitis, encephalitis, cerebral edema
3. Vascular accidents: Cerebral and subarachnoid hemorrhage, thromboembolic episodes giving rise to cerebral edema, cerebral venous thrombosis.
4. Obstruction to flow of CSF
5. Miscellaneous causes: Systemic hypertension, especially malignant hypertension; chronic respiratory failure, water, intoxication.

Investigation: Apart from general investigations to exclude systemic disorders, specific investigations include radiological studies, electroencephalography, CT scanning, isotope studies, and CSF examination. It is to be remembered that lumbar puncture is a risky procedure in the presence of raised ICT and this should not be performed without neurological assistance.

General measures
Osmotic agents: Administration of mannitol 20% solution 300 ml as a intravenous drip within 30 minutes, helps to draw fluid from the brain and transfer it to the vascular compartment. This leads to a temporary fall in ICT. Other hyperosmotic solutions such as 50% sucrose (50 ml) and 20% Urea (200 ml) also act on the same principle but they are less efficient. Dexamethasone in a dose of 8-12 mb given intramuscularly every 6 hours also serves to lower ICT.

Specific management: Treatment of the cause relieves the raised ICT also. Surgical measures may be required in many cases.