Benign intracranial hypertension: causes, symptoms, diagnosis, treatment

Benign intracranial hypertension (idiopathic intracranial hypertension, pseudotumor cerebri) is characterized by increased intracranial pressure without signs of a space-occupying lesion or hydrocephalus; the composition of the CSF is unchanged.

This pathology is more common in women of childbearing age. The prevalence is 1/100,000 among women with normal body weight and 20/100,000 among obese women. Intracranial pressure is significantly increased (>250 mm H2O); the exact cause is unknown, headache is presumably due to obstruction of cerebral venous outflow.

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What causes benign intracranial hypertension?

In patients with space-occupying lesions of the brain, intracranial hypertension is common. The causes of benign intracranial hypertension are not fully known. A link with long-term use of oral contraceptives has been noted.

There is a disruption of the processes of production and reabsorption of cerebrospinal fluid with phenomena of edema and swelling of the brain, which are both intracellular and intercellular in nature. A disruption of the normal functioning of the blood-brain barrier also plays a role.

Causes of development of intracranial hypertension syndrome:

• the presence of additional intracranial volume caused by a tumor;
• disruption of the cerebrospinal fluid outflow pathways with the development of occlusive hydrocephalus;
• the presence of peritumoral cerebral edema.

The first two causes are the responsibility of the neurosurgeon. The neuroanesthesiologist can only influence the third cause.

Symptoms

Characterized by almost daily generalized headache of variable intensity, sometimes accompanied by nausea. Short-term attacks of blurred vision and diplopia are possible, caused by unilateral or bilateral paresis of the sixth pair of cranial nerves. Loss of visual fields begins from the periphery and is unnoticeable for the patient in the early stages. Later, there is a concentric narrowing of all visual fields, loss of central vision with the possibility of developing complete blindness. Neuroendocrine pathology, as a rule, includes cerebral obesity and irregular menstrual cycle. Most often observed in women aged 20-40.

Diagnostics

A preliminary diagnosis of benign intracranial hypertension is made based on the clinical picture of the disease, the final diagnosis is based on MRI data, preferably with magnetic resonance venography, and lumbar puncture showing increased intracranial pressure at the beginning of the manipulation and normal CSF composition. In rare cases, certain drugs and diseases can cause a clinical picture similar to idiopathic intracranial hypertension.

EEG, CT, and angiography data do not determine pathology. The ventricular system is usually normal; less frequently, some enlargement of the cerebral ventricles is noted.

First of all, it is necessary to exclude a tumor process in the brain.

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Treatment

Benign intracranial hypertension usually resolves spontaneously after stopping oral contraceptives. If the disease develops without taking such contraceptives, its course is also extremely dynamic and can resolve spontaneously. In severe cases, dehydration therapy is performed using glycerol, veroshpiron, vascular therapy is indicated. Drugs such as stugeron, theonikol, cavinton are used. Drugs that improve venous outflow are recommended - troxevasin, glivenol.

Treatment is aimed at reducing intracranial pressure and alleviating symptoms with repeated lumbar punctures and taking diuretics (acetazolamide 250 mg 4 times a day orally). Headache is relieved by taking NSAIDs or antimigraine drugs. Obese patients are recommended to reduce body weight. In case of progressive vision loss against the background of repeated lumbar punctures and drug therapy, decompression (fenestration) of the optic nerve sheaths or lumboperitoneal shunting is indicated.

Intracranial hypertension is treated with drugs from several groups, each of which has both advantages and disadvantages.

The following hypertonic solutions may be indicated in the development of intracranial hypertension

Mannitol, 20% solution, intravenous 400 ml, single dose or Sodium chloride, 7.5% solution, intravenous 200 ml, single dose.

However, it should be remembered that, firstly, the dehydrating effect of hypertonic solutions is realized mainly through dehydration of intact brain matter, and secondly, after the end of the drug’s action, the so-called “rebound phenomenon” can be observed (an increase in intracranial pressure values to values even exceeding the initial ones).

The therapeutic effect of saluretics (furosemide) in such a condition as intracranial hypertension is less pronounced than that of hypertonic solutions. However, their use is justified in combination with osmotic diuretics, since it reduces the risk of developing the "rebound phenomenon":

Furosemide IV 20-60 mg, once (then the frequency of administration is determined by clinical appropriateness). Dexamethasone is the drug of choice in the treatment of peritumoral cerebral edema: Dexamethasone IV 12-24 mg/day, once (then the frequency of administration is determined by clinical appropriateness). However, its use in the treatment of intracranial hypertension in victims with severe TBI and ischemic strokes is not effective.

Acute intracranial hypertension that develops during neurosurgical intervention is effectively treated with barbiturates and the creation of short-term severe hyperventilation:

Thiopental sodium intravenously bolus 350 mg, once, then, if necessary, several times intravenously bolus in a total dose of up to 1.5 g.

In order to monitor the effectiveness of conservative therapy, regular ophthalmological examinations with mandatory perimetry are carried out, since checking visual acuity alone is not sufficient to prevent irreversible loss of visual functions.