Influence of increased intracranial pressure on the nervous system

June 12, 2018 23:30 | Neurology
A special group is represented by patients with elevated intracranial pressure. They often show signs of insufficiency of hepato-renal and cardiovascular apparatus. Increased intracranial pressure can develop slowly, but often occurs quickly with malignant hypertension. Signs of his headaches, vomiting, bradycardia, total weight loss. In the future, there may be meningeal symptoms. All these phenomena, combined with changes in the bottom of the eye, create a picture of pseudotumor. However, there are cases when a significant increase in intracranial pressure occurs without clinical symptoms.

Changes in the bottom of the eye are the earliest and frequent sign of increased intracranial pressure. The detection of these changes in malignant hypertension is of great diagnostic and prognostic significance. Changes at the bottom of the eye are of two types: 1) neuroretinitis, as in renal patients;2) stasis with the widening of the veins and various variations in the edema of the papilla of the optic nerve, beginning with a latent pericapillary stasis without exudate to a sharp expansion of vessels with a large exudate and radial foci of hemorrhages. In some cases, a combination of neuroretinitis with edema of the papilla of the optic nerve is observed. The described changes can occur in the early stages, when the lesions of the kidneys and the heart are insignificant.


In most patients of this group, changes at the bottom of the eye are combined with an increase in the pressure of the cerebrospinal fluid( up to 200-500 mm of the water column) and sometimes with protein-cell dissociation in it. Differential diagnosis with a brain tumor in these patients can be very difficult, as illustrated by the following observation.

Patient B., 29 years old, had no pain in the past. In June, headaches appeared, a month later, vision decreased, first on the left eye, and then on the right eye. The oculist was diagnosed with a stagnant nipple, and the patient 23.X was placed in the Neurosurgical Institute with a diagnosis of a brain tumor. This diagnosis was rejected and the patient was transferred to a hospital named after SP Botkin.

Mucous lips, facial skin, ears are cyanotic. The border of the heart is slightly enlarged to the left, its diameter is 11.5 cm, the vascular bundle is 4 cm. Pulse is 100 beats per minute. Accent of the second tone on the aorta. Arterial pressure 175/130 mm of mercury. Lungs are normal Liver and spleen are not probed. From the side of the nervous system, except for a hint of Babinsky's symptom on the left, there are no organic symptoms. The borders of the nipples of the optic nerves are more shaded on the left. The veins are enlarged, their lumen is uneven, in the region of the yellow patch on the left, the atrophic focus is the trace of the former hemorrhage. At the bottom of both eyes there are fresh hemorrhages. The visual acuity of both eyes is 0,09.In the urine, the protein is 0.45%.in the rest there are no abnormalities. In adrenaline, 0.17 mg, creatinine 2.2%, sugar and chlorine are normal. Wasserman's reaction is negative. Cerebrospinal fluid: pressure 290 mm of water column, protein 0.39%, cytosis 0.

Written out in a month with significant improvement.

Further observation of the patient confirmed the correctness of the diagnosis of hypertension .

Increased intracranial pressure in patients with hypertension is not directly related to increased blood pressure, as in the vast majority of cases with high blood pressure it remains normal. In some patients, the increase in intracranial pressure is due to the increase in venous pressure, which occurs when the compensation of cardiac activity is impaired.

AI Zlatoverov, Alazhzhanin and Tyurel tend to recognize venous hypertension as the main cause of increased intracranial pressure, but Blashko's studies showed that in many patients with high intracranial pressure, venous pressure remained normal. Apparently, a significant role in this is played by toxic factors, a violation of the metabolism of chlorides and water. At present, it is impossible to clarify the role of each of these factors separately. Clinical observations show that azotemia does not in itself cause an increase in intracranial pressure. Apparently, the delay of chlorides is much more important.

Zaum observed a woman of 28 years with severe headaches, changes in the bottom of the eye and high intracranial pressure with moderate azotemia. Under the influence of the chlorohydride diet, she suddenly decreased intracranial pressure and significantly improved the picture of the bottom of the eye. Thus, azotemia, without causing an increase in intracranial pressure, is often a sign of kidney damage, which causes a violation of the metabolism of chlorides and water. Therapeutic measures( regimen, diet, cardiac agents) sometimes sharply reduce intracranial pressure and thereby confirm the role of toxic factors in its increase. In some patients after appropriate therapy, diuresis increases, chloremia and azotemia disappear, intracranial pressure drops to normal, while arterial and venous pressure remains at the same level.

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