by Juan P. Recagno Cepeda
The contents of the skull have three components that maintain normal intracranial pressure and these are nervous tissue, cerebrospinal fluid (CSF) and blood. When by some circumstance this balance is broken, the pressure is altered; when it rises, it is referred to as intracranial hypersensitivity, which can occur due to normal, trivial and transitory causes; But when it acquires significance, due to its magnitude and its persistence, it conditions the intracranial hypertension syndrome, which is one of the most frequent reasons for neurological death. Intracranial hypotension, which is one of the most frequent reasons for neurological death. Intracranial hypotension is less common and of much less clinical significance: we are not talking about it.
The three intracranial components mentioned allow an exchange in their proportions; by increasing brain mass, blood circulation decreases and CSF shifts
Towards the marrow, also decreasing its production and increasing its reabsorption. If it is the blood that increases within the skull, CSF is fundamentally displaced since the brain only allows a limited degree of compression, and something similar occurs when the behavior of the CSF is enlarged.
When the process is of sufficient magnitude or acts acutely, without giving time for a reconditioning of the intracranial content, the syndrome of intracranial hypertension appears, the diagnosis of which can be presumed by the clinical picture and by some special tests. The certainty, however, will be given by the direct control of intracranial pressure, which normally should not exceed 200 ml H2O and which is determined:
a) by lumbar puncture, when the CSF pathways are not obstructed (and that in practice should never be done because it is formally contraindicated), or b) measuring it directly in the lateral ventricles through the fontanelles or a trephine hole, by ventricular puncture; or c) by implanting a special sensor on the brain surface that directly marks the pressure figure, and which is the method most used today in the clinic to control these conditions.
There are four causes that can cause this syndrome: 1) cerebral edema, 2) circulation disorders 3) intracranial occupying mass, and 4) obstruction in the venous drainage.
1. Brain edema. It is the most frequent cause, not only as an isolated condition, but also as a complication of other processes such as intracranial expansions. Edema is the increase in tissue fluid and two fundamental types are described: a) vasogenic, due to rupture of the capillary blood-brain barrier and exudation of blood plasma into the extravascular interstitial space, and b) cytotoxic, where due to a deficit in the supply of 02 the intraneuronal sodium pump is disturbed, incorporating fluid and swelling. The first is the typical edema of the white matter and the other of the gray matter. In addition, the following are described: c) interstitial edema, which is produced by periventricular extracellular imbibition, in which the CSF filters through the ependyma and fills the nearby spaces, in cases of high-pressure hydrocephalus; here there is no neuronal injury or breakdown of the barrier. Adams places among these, likewise, d) the edema produced by electrolytic alterations, as in hypernatremia, and e) the ischemic or mixed, which is seen in cerebrovascular accidents and which is a cytotoxic edema to which vascular injury is added with the consequent vasogenic edema. In encephalitis, in some poisonings (by lead in children) and in Reye's syndrome there is edema of multiple mechanisms.
2. Disorders of CSF circulation . 5e are due to the obstruction of their circulation paths anywhere along their path with an increase in pressure above the interruption and dilation of the cavities. The most common cause is brain tumors. There are congenital or inflammatory conditions that cause stenosis of the aqueduct of Silvio. Likewise, inflammatory or hemorrhagic processes originate, due to organized exudates, obstructions at the base of the skull.
3. Expansive intracranial lesions . Due to the same mass they occupy, they produce intracranial hypertension. Slow-growing benign tumors allow reconditioning of the brain that makes the onset of intracranial hypertension very late; On the other hand, the more acute processes, such as intracerebral hemorrhage, an abscess or a very malignant gliomatous tumor, condition a rapidly evolving and progressive syndrome. Any other expansive process: parasitic river. inflammatory, post-traumatic (such as chronic hematomas) finally leads to the syndrome by this basic mechanism, to which is added the presence of edema.
There is a possibility that the process - especially if it is tumorous - obliterates some of the narrow portions of the CSF pathways and adds an obstructive factor. The inflammatory processes of the meninges, which cause a great hyperproduction of CSF, the extended hemorrhages (although they are not clearly expansive) and the ependymal papillomas can be included in this mechanism.
4. Obstruction of the venous drainage . The pathological increase in cerebral blood content can be caused by a difficulty in venous return, as in some syndromes that have elevated intrathoracic pressure, or in venous obstructions due to thrombophlebitis, or more frequently in those derived from cerebral hernias, severe complication of intracranial hypertension that considerably aggravates the initial picture, by adding a new factor.
Cerebral hernias are movements of the brain or of any of its parts through the endocranial anatomical orifices, motivated by an increase in their volume, of any etiology. The intracranial cavity is subdivided into several compartments by a series of dural partitions (falx cerebri, tentorium, etc.). When in one of them there is an expansive process that increases the pressure, the portion located there tends to come out through the natural orifices of the compartment that contains it, squeezing the structures that pass through said orifice and causing the pertinent symptoms. There are several types of hernia, but the most important are: a) the tentorial, which can be unilateral or bilateral, depending on whether the process is of a hemisphere or of the brain as a whole, as occurs in large generalized edema. It gives symptoms corresponding to the III pair, which passes to that level, and to the brainstem; at the level of the midbrain, ipsilateral palpebral ptosis will appear and later hemiparesis, usually contralateral, and b) the tonsillar cerebellar, in which the organ tends to exit through the foramen magnum and compresses the medulla oblongata.
Symptoms and signs
This syndrome has a classic triad that should always be remembered: 1) headaches, 2) vomiting, and 3) papilledema.
1. Headaches . By meningeal or vascular compression, gravitational, progressive, disabling, permanent or predominantly morning, generalized or localized, which usually calms with vomiting and increases with exercise and effort.
2. Vomiting . Explosive or gushing, unexpected or preceded by nausea, often misinterpreted in children, and produced by compression of the floor of the fourth ventricle.
3. Papilledema . In the examination with the ophthalmoscope, it begins with venous congestion and then the edges of the optic disc are erased, after loss of the physiological excavation; subsequently the papilla tends to rise above the plane of the retina and the vessels must bend to reach it. There is an early increase in the size of the blind spot in the visual field. If the process continues, hemorrhages and exudates may appear and eventually the papilla turns pale and ends in secondary atrophy with diffuse edges and poor or no vision. When its cause is solved in a timely manner, it regresses in about six weeks. This sign can appear fairly quickly, but is generally considered late and today a brain tumor must be diagnosed before the onset of papilledema.
4. There may be false signs of localization, such as some generalized seizures, paresis of the sixth pair with convergent strabismus, decreased consciousness of variable degree, and general signs such as arterial hypertension.
Benign intracranial hypertension, or cerebral pseudomotor, is a picture of non-precise etiology that consists of intracranial hypertension without added neurological signs and with normal complementary tests. However, some causes are known, such as postmastoiditis obstruction of the lateral sinus, toxic processes due to vitamin deficiency A, administration of corticosteroids and some antibiotics; the cause is generally ignored, and external or internal decompression relieves and cures the patient.
Anamnesis . The following should be taken into account: a) the picture should be suspected in the event of any unexpected, progressive and fundamentally disabling headache; in a chronic headache, warn about any change in their usual characteristics. Remember the classic saying: headache subsides when papilloedema starts; b) in children suspect it before any vomiting in a stream without a clear cause; in adults when vomiting relieves headache, especially if it is morning; c) papilledema causes delayed vision loss and it is very rare for this symptom to initiate intracranial hypertension, and d) the other symptoms are quite nonspecific, but in the event of a seizure, mental deterioration, or sixth nerve paralysis, it is necessary to carry out complementary tests to clarify the diagnosis.
Eye fundus . It is a routine examination in neurology, and its modifications will alert about the diagnosis.
Skull X-rays . They are also routine examinations that allow to visualize chronic signs of hypertension (in children, separation of sutures; in adults, decalcification of the base), deviation of normal calcified structures (such as the pineal), localized vascular alterations. Currently it is used less, due to the widespread use of computed axial tomography.
Routine analysis . They can add very little: a high erythrocyte sedimentation rate in metatasis, some special antigen in certain tumors. The LCR, on the other hand, can reveal modifications; in tumors, hyperalbuminorrhea not too high and nonspecific.
Electroencephalogram . It is a routine neurological examination that in generalized intracranial hypertension shows diffuse flattening with slight slowing down of brain waves, and in localized processes focal signs characterized almost always in delta wave tumors, which are high amplitude and low frequency.
Proven exams . Those that use air or iodized substances are now practically in disuse, due to the incorporation of the current most improved, useful and innocuous study methods. Cerebral arteriography or panarteriography are used in intracranial hypertension as a complementary study in certain brain tumors, the vascularization of which may be important to determine for diagnostic purposes or surgical strategy.
Computed axial tomography and nuclear magnetic resonance . They are relatively recent diagnostic imaging methods, which by different mechanisms study the constitution of the brain substance and allow the visualization and localization of expansive processes of all kinds with great precision.
Radioisotopes . These studies are currently confined to cases of Hakim syndrome or normal pressure hydrocephalus.