Wound syndrome: causes, symptoms, diagnosis

Intracranial pressure is the pressure in the cranial cavity and the ventricles of the brain, in the formation of which the membranes of the brain, cerebrospinal fluid, brain tissue, intracellular and extracellular fluid, and blood circulating through the cerebral vessels participate. In the horizontal position, the intracranial pressure is, on average, 150 mm of water column. A persistent increase in the pressure in the cranial cavity above the normal values (above 200 mmHg) indicates the development of intracranial hypertension and is most often observed as a result of cerebral edema, increased intracranial contents, intracranial hemorrhages, and disorders of liquor circulation, provided that the compensatory mechanisms maintenance of cerebral perfusion pressure. Intracranial hypertension can lead to the dislocation of various parts of the brain and wedging syndromes.

The most common causes of intracranial hypertension are: increased tissue volume (tumor, abscess), increased blood volume (hypercapnia, hypoxia, venous sinus occlusion), cytotoxic edema (ischemia, brain tumor, hyperosmolar condition, inflammation), interstitial edema ( hydrocephalus with transpedymal flow cerebrospinal fluid).

Causes of the wedge syndrome

I. Intracranial voluminous formations

1. Tumors (primary and metastatic)
2. Hematomas (intracerebral, subdural, epidural)
3. Abscesses
4. Granulomas
5. Parasitic diseases of the nervous system

II. Hydrocephalus

III. Intracranial infections

1. Meningitis
2. Encephalitis

IV. Edema of the brain

1. Ischemic
2. Toxic
3. Radiation
4. With hydration

V. Craniocerebral trauma

VI. Vascular acute disorders (ischemia, hemorrhage, hypertensive crisis, vascular spasm)

VII. Anomalies in the development of the brain and spinal cord

VIII Venous hypertension

1. Occlusion of the superior or lateral sinus
2. Occlusion of the internal jugular vein
3. Obesity
4. Obstruction of the superior vena cava
5. Obstructive lung disease
6. Arteriovenous shunt

IX. Parainfection and autoimmune disorders

1. Guillain-Barre syndrome
2. Infections (poliomyelitis, acute lymphocytic choriomeningitis, mononucleosis, HIV infection, Lyme disease)
3. Chorea
4. Systemic lupus erythematosus
5. Allergies and post-vaccination reactions

X. Metabolic disorders

1. Uremia
2. Diabetes
3. Anemia
4. Hypercapnia

XI. Endocrinopathies

1. Hyaparathyroidism
2. Adison's disease
3. Cushing's Disease
4. Thyrotoxicosis
5. Menarche, pregnancy

XII. Nutritive disorders (hypervitaminosis A, hypovitaminosis A)

XIII. Idiopathic intracranial hypertension

XIV. Intoxications (including medicinal) (phenothiazines, lithium, diphenine, indomethacin, tetracycline, sinemet, corticosteroids, etc.).

I. Intracranial voluminous formations

Intracranial volumetric formations (tumors, hematomas, abscesses, granulomas, some parasitic diseases) is one of the frequent causes of increased intracranial pressure. Clinical manifestations depend on the mechanism of increasing intracranial pressure and the rate of its development; processes that impede the outflow of cerebrospinal fluid (tumors, adhesions) can lead to a paroxysmal increase in intracranial pressure and are manifested by occlusal hydrocephalic syndrome. Typical symptoms: intense constant headache, nausea, vomiting, stagnant nipples of optic nerves in ophthalmoscopy, autonomic disorders in the form of violation of the frequency and rhythm of breathing, heart rate and blood pressure. With acute increase (craniocerebral trauma, tumors, brain edema) intracranial pressure, a dislocation of the brain and infringement of some of its parts (most often in the field of the tentorial and large occipital orifice) is possible with the appearance of stem symptoms, violation of cardiovascular activity and breathing up to its stop.

Causes of obstructive (non-communicating) hydrocephalus: stenosis of the Sylvian aqueduct; malformation of Arnold - Chiari (with or without myelodysplasia); the Dandy-Walker malformation (Dandy-Walker); atresia of the Monroe orifice; anomalies of the bones of the base of the skull; volumetric formations (tumors, cysts); inflammatory ventriculitis (infection, hemorrhages, chemical irrigation, cyst rupture).

Causes of communicating hydrocephalus: Arnold-Chiari malformation or Dandy-Walker malformation syndrome (without blockage of the liquor-conducting pathways); benign cysts; inflammation of the mild cerebral membrane (viral and bacterial infections, subarachnoid hemorrhage in vascular malformations or trauma, including surgical, medicinal arachnoiditis); carcinomatous meningitis.

Diagnostic criteria of hydrocephalus

Ventriculomegaly with signs of increased intracranial pressure (headache, vomiting, drowsiness, changes in muscle tone). The main paraclinic methods of confirming and evaluating intracranial hypertension: ophthalmoscopy, measurement of CSF pressure, CT or MRI, as a rule, easily detect processes that limit space in the cranial cavity, developmental abnormalities, signs of intracranial hypertension. For the same purposes, echoencephalography, angiography, and radiography of the skull are also used.

Other causes of intracranial hypertension: brain edema (ischemic, toxic, radiation damage to the nervous system, excessive hydration); venous hypertension (occlusion of the superior or lateral sinus, sinus thrombosis, unilateral or bilateral occlusion of the internal jugular vein, obstruction of the superior vena cava, arterio-venous malformation, obesity, obstructive pulmonary disease); acute vascular disorders (ischemia, hemorrhage, hypertensive crisis, vascular spasm); parainfection and immunological disorders (Guillain-Barre syndrome, such as poliomyelitis, lymphocytic choriomeningitis, mononucleosis, HIV infection, Lyme disease, Sydenham's chorea, systemic lupus erythematosus, post-vaccination reactions); metabolic disorders (uremia, diabetic coma, iron deficiency anemia, hypercapnia); endocrinopathy (hypoparathyroidism, Adison's disease, Cushing's disease, thyrotoxicosis, menarche, pregnancy); nutritional disorders (hypervitaminosis A, hypovitaminosis A); intraspinal tumors (rarely).

The cause of intracranial hypertension can be idiopathic intracranial hypertension (benign intracranial hypertension, Pseudotumor cerebri).

Diagnostic criteria for idiopathic intracranial hypertension:

• Increased pressure of spinal fluid (> 200 mm of water column in patients without obesity and> 250 mm of water column in obese patients).
• Normal neurological status with the exception of paralysis of the VI cranial nerve (n. Abducens).
• The normal composition of the liquor.
• Absence of intracerebral volumetric formations.
• Bilateral edema of the nipple of the optic nerve. Rarely may there be an increase in CSF pressure without edema of the nipple of the optic nerve.

Typical complaints of these patients: daily headaches (often pulsating), visual disorders; possible changes in the fields of vision. The majority of patients are obese women. "Pseudotumor" can coexist with obstructive sleep apnea.

Along with idiopathic intracranial hypertension, secondary "pseudotumor" occurs as a consequence of disturbance of venous blood flow and venous hypertension (chronic ear diseases, craniocerebral trauma, meningioma, heart failure, chronic lung diseases contribute to the violation of venous circulation). Compression of the cavernous sinus (an empty Turkish saddle, pituitary adenoma) may be the cause of a secondary "pseudotumor". Contribute to the disease hypoparathyroidism, adrenal insufficiency, estrogen imbalance.

Differential diagnosis with diseases that may resemble "pseudotumor": sinus thrombosis, infectious lesions of the nervous system, malignant neoplasms. With "pseudotumor" may also coexist tension headaches, migraines, abusus headaches - pain and depression. For diagnosis of benign intracranial hypertension, lumbar puncture is important with the measurement of CSF pressure, neuroimaging and ophthalmoscopy.

Finally, intoxications can sometimes lead to the development of intracranial hypertension (phenothiazines, lithium, diphenine, indomethacin, tetracycline, sinemet, corticosteroids, gonadotropins, lithium, nitroglycerin, vitamin A, and herbicides, pesticides and some other substances).

Complications of intracranial hypertension are manifested by the syndromes of infringement (wedging, herniation) of certain parts of the brain. Intracranial hypertension, when it increases in conditions of stiffness of the bones of the skull, can lead to a shift in parts of the brain from their normal location and cause compression of some areas of the brain tissue. Such a shift is more often observed under the sickle-shaped process (falx), near the edge of the tentorial incision and in the large occipital foramen. Lumbar function in such cases can cause dangerous wedging and death of the patient.

The lateral displacement of the brain under a large sickle-shaped process leads to the infringement of one cingular gyrus under the falx, which can be observed if one of the hemispheres increases in volume. The main manifestations are the compression of the internal cerebral vein and the anterior cerebral artery, which causes an even greater increase in intracranial pressure due to a decrease in venous outflow and the development of a cerebral infarction.

Displacements under the cerebellar nasal can be one-sided and two-sided and are manifested by compression of the midbrain (the so-called secondary cerebral sinus syndrome).

One-sided transcendental wedge develops when the increased temporal lobe leads to the protrusion of the hippocampal hook into the tentorial incision. This picture often accompanies and infringement under falksom. Consciousness usually decreases before infringement and continues to worsen as the compression of the brainstem increases. Direct pressure on the oculomotor nerve causes ipsilateral expansion of the pupil (prolapse of parasymatic innervation of the pupil). Sometimes the contralateral pupil also widens, since the dislocation of the entire brainstem results in compression of the opposite oculomotor nerve at the edge of the clipping of the hint. Contralateral homonymous hemianopsia develops (but it can not be detected in a patient unconscious) due to compression of the ipsilateral posterior cerebral artery. With further compression of the middle brain, both pupils become enlarged and fixed, breathing becomes irregular, blood pressure rises, the pulse shrinks, decerebrate convulsions develop, and death may occur due to cardio-respiratory collapse.

Two-sided (central) transcendental wedging is usually due to generalized cerebral edema. Both hemispheres tend to move downward: both the diencephalon and the middle brain are displaced caudally through the tentorial aperture. Clinical manifestations consist of impaired consciousness, narrowing and then dilating pupils; broken view up (elements of the quadruple syndrome); irregular breathing is observed, thermoregulation is disrupted, decerebriation or decortication convulsions and death develop.

An increase in pressure in the posterior cranial fossa can cause the cerebellum to move upward and its infringement at the edge of the tentorial tenderloin, or lead to the displacement of the cerebellum down (more often) and infringement of its tonsils in the large occipital orifice. Displacement upward leads to compression of the midbrain (paresis of the gaze upward, dilated or fixed pupils, irregular breathing).

Displacement of the cerebellum down causes compression of the medulla oblongata (there are no disorders of consciousness or come secondarily, there are pains in the occipital region, a paresis of the gaze upward, and paralysis of caudal cranial nerves with dysarthria and swallowing disorder); weakness in the arms or legs with symptoms of the defeat of the pyramidal tract and a violation of the sensitivity of different modalities below the head ( big occipital foramen syndrome). One of the earliest manifestations of cerebellar herniation in the large occipital foramen is the rigidity of the neck muscles or the inclination of the head in order to lower the pressure in the region of the foramen magnum. Breathing stops suddenly.

[1], [2], [3], [4], [5],

Variants and symptoms of the wedge syndrome

The wedge of the medial surface of the cerebral hemisphere under the sickle-shaped process (a semilunar wedge)

At the same time, part of the cingulate gyrus is displaced into a free slit, formed from below by a corpus callosum, from above - by the free edge of a sickle-shaped process. As a consequence, squeezing of small arterial vessels feeding the indicated area of the brain, ipsilateral foci of the anterior cerebral artery, as well as a large vein of the brain, occurs. The reason for dislocation of this kind is the presence of a voluminous pathological process in the frontal, parietal, and rarely - in the temporal lobe. Most often, the dysfunction of the cingulate gyrus has no pronounced clinical manifestations.

Temporal Tentorial Injection

Asymmetric displacement of the medial structures of the temporal lobe (the para-hippocampal gyrus and its hook) into the Binta gap between the edge of the incision of the cerebellum nest and the brain stem. It arises as the next stage of the development of a dislocation syndrome in tumors of hemispheric localization. It is accompanied by compression of the oculomotor nerve, displacement of the posterior cerebral artery, and by pressing the tentorial aperture of the midbrain to the opposite edge. In this case, the ipsilateral pupil first narrows, then gradually expands to a fixed mydriasis, the eye deviates to the outside and ptosis forms. Later there is a gradual dilatation of the pupil on the opposite side and a disturbance of consciousness. Disorders of the motor sphere are formed according to the type of the central tetraparesis and then tetraparesis. There is an alternating Weber syndrome. Occlusal hydrocephalus is formed. Possible occurrence of decerebrate rigidity.

Cerebral-Tentorial Injection

It does not occur often, with a marked increase in pressure in the posterior cranial fossa (in particular, in tumors of the cerebellum) and is characterized by the displacement of the cerebellum tissue through a gap in the aperture of the tentorial opening in the middle cranial fossa. Compression is the upper legs of the cerebellum, the upper cerebral sail, the plate of the midbrain, sometimes the brain drain and the cistern of the subarachnoid space of the middle cranial fossa on the side of the wedge. Clinically, this is manifested by the onset of coma, paralysis of the eyesight, narrowing of the fixed pupils with conserved lateral oculocephalic reflexes, signs of occlusive hydrocephalus.

[6], [7], [8], [9], [10], [11], [12]

Inflammation of the tonsils of the cerebellum into a cervical dural funnel

Inflammation of the tonsils of the cerebellum into a cervical dural funnel often occurs with volumetric processes in the subtentorial space. At the same time, the cerebellar tonsils move in the caudal direction and they are wedged between the edge of the large occipital foramen and the medulla oblongata, which inevitably leads to the ischemia of the cerebellum, impaired breathing, regulation of cardiac activity and, as a consequence, death of the patient.