Idiopathic intracranial hypertension. Intracranial hypertension: what it is, how to recognize it and why it is dangerous. Congenital pathologies and developmental anomalies as a cause of ICH

Intracranial hypertension is increased pressure in the cranium. Intracranial pressure (ICP) is the force with which intracerebral fluid presses on the brain.

Its increase is usually due to an increase in the volume of contents of the cranial cavity (blood, cerebrospinal fluid, tissue fluid, foreign tissue). ICP may periodically increase or decrease due to changing conditions environment and the body’s need to adapt to them. If its high values ​​persist for a long time, intracranial hypertension syndrome is diagnosed.

The causes of the syndrome are different, most often these are congenital and acquired pathologies. Intracranial hypertension in children and adults develops with hypertension, cerebral edema, tumors, traumatic brain injuries, encephalitis, meningitis, hydrocephalus, hemorrhagic strokes, heart failure, hematomas, abscesses.

What it is?

Intracranial hypertension is a pathological condition in which pressure increases inside the skull. That is, in essence, this is nothing more than increased intracranial pressure.

Basic Concepts

Intracranial pressure is the difference between pressure in the cranial cavity and atmospheric pressure. Normally, this figure in adults ranges from 5 to 15 mmHg. The pathophysiology of intracranial pressure follows the Monroe-Kelly doctrine.

This concept is based on the dynamic balance of three components:

1. Brain;
2. Cerebrospinal fluid;
3. Blood.

A change in the pressure level of one of the components should lead to a compensatory transformation of the others. This mainly occurs due to the properties of blood and cerebrospinal fluid to maintain a constant acid-base balance, that is, to act as buffer systems. In addition, brain tissue and blood vessels have sufficient elasticity, which is an additional option for maintaining such a balance. Due to such protective mechanisms, normal pressure inside the skull is maintained.

If any reasons cause a breakdown in regulation (the so-called pressure conflict), intracranial hypertension(VCHG).

In the absence of a focal cause for the development of the syndrome (for example, with moderate overproduction of cerebrospinal fluid or with slight venous discirculation), benign intracranial hypertension is formed. Only this diagnosis is present in international classification diseases ICD 10 (code G93.2). There is also a slightly different concept - “idiopathic intracranial hypertension”. In this condition, the etiology of the syndrome cannot be established.

Reasons for development

Most often, increased intracranial pressure occurs due to impaired circulation of cerebrospinal fluid (CSF). This is possible when its production increases, its outflow is disrupted, and its absorption deteriorates. Circulatory disorders cause poor flow of arterial blood and its stagnation in the venous section, which increases the total volume of blood in the cranial cavity and also leads to increased intracranial pressure.

In general, the most common causes of intracranial hypertension may be:

• tumors of the cranial cavity, including metastases of tumors of other localizations;
• inflammatory processes (encephalitis, meningitis, abscess);
• congenital anomalies of the structure of the brain, blood vessels, the skull itself (infection of the cerebrospinal fluid outflow tract, Arnold-Chiari anomaly, and so on);
• traumatic brain injuries (concussions, bruises, intracranial hematomas, birth injuries and so on);
• spicy and chronic disorders cerebral circulation(stroke, thrombosis of the dural sinuses);
• diseases of other organs that lead to difficulty in the outflow of venous blood from the cranial cavity (heart defects, obstructive pulmonary diseases, neoplasms of the neck and mediastinum, and others);
• poisoning and metabolic disorders (poisoning with alcohol, lead, carbon monoxide, its own metabolites, for example in liver cirrhosis, hyponatremia, and so on).

This, of course, is not all possible situations leading to the development of intracranial hypertension. Separately, I would like to say about the existence of so-called benign intracranial hypertension, when an increase in intracranial pressure occurs seemingly without cause.

Symptoms

The formation of clinical hypertension syndrome and the nature of its manifestations depend on the localization of the pathological process, its prevalence and speed of development.

Intracranial hypertension syndrome manifests itself with the following symptoms in adults:

1. Headache of increased frequency or severity (increasing headache), sometimes awakening from sleep, often forced positioning of the head, nausea, and repeated vomiting. It can be complicated by coughing, a painful urge to urinate and defecate, and actions similar to the Valsalva maneuver. Possible disturbances of consciousness and convulsive seizures. With prolonged existence, visual impairment occurs.
2. History may include trauma, ischemia, meningitis, cerebrospinal fluid shunt, lead intoxication or metabolic disorder (Reye's syndrome, diabetic ketoacidosis). Newborns with cerebral ventricular hemorrhage or meningomyelocele are predisposed to intracranial hydrocephalus. Children with blue heart disease are predisposed to an abscess, and children with sickle cell disease may have a stroke leading to intracranial hypertension.

Objective signs of intracranial hypertension are disc swelling optic nerve, increased cerebrospinal fluid pressure, increased osmotic pressure of the extremities, typical x-ray changes in the bones of the skull. It should be borne in mind that these signs do not appear immediately, but after a long time (except for increased cerebrospinal fluid pressure).

There are also signs such as:

• loss of appetite, nausea, vomiting, headache, drowsiness;
• inattention, decreased ability to awaken;
• papilledema, upward gaze paresis;
• increased tone, positive Babinski reflex;

With a significant increase in intracranial pressure, disturbances of consciousness are possible, seizures, visceral-vegetative changes. With dislocation and herniation of brain stem structures, bradycardia and respiratory failure occur, the reaction of the pupils to light decreases or disappears, and systemic arterial pressure.

Intracranial hypertension in children

There are two types of pathology in children:

1. The syndrome slowly increases in the first months of life, when the fontanelles are not closed.
2. The disease develops rapidly in children after a year, when the sutures and fontanelles have closed.

In children under one year of age, due to open cranial sutures and fontanelles, symptoms are usually mild. Compensation occurs due to the opening of the sutures and fontanelles and an increase in the volume of the head.

The first type of pathology is characterized by the following symptoms:

• vomiting occurs several times a day;
• the baby sleeps little;
• diverge cranial sutures;
• the child cries often and for a long time without reason;
• the fontanelles swell, the pulsation in them cannot be heard;
• veins are clearly visible under the skin;
• children are developmentally delayed and later begin to hold their head up and sit;
• the skull is large for its age;
• the bones of the skull are formed disproportionately, the forehead protrudes unnaturally;
• when a child looks down, between the iris and upper eyelid a white stripe of the white of the eyeball is visible.

Each of these signs individually does not indicate increased pressure inside the skull, but the presence of at least two of them is a reason to examine the child.

When the fontanelles and cranial sutures close, the manifestations of intracranial hypertension become pronounced. At this time, the child develops the following symptoms:

• constant vomiting;
• anxiety;
• convulsions;
• loss of consciousness.

In this case, you must definitely call an ambulance.

The syndrome can also develop at an older age. In children over two years of age, the disease manifests itself as follows:

• the functions of the sense organs are impaired due to the accumulation of cerebrospinal fluid;
• vomiting occurs;
• in the morning when waking up, bursting headaches appear that put pressure on the eyes;
• when rising, the pain weakens or recedes due to the outflow of cerebrospinal fluid;
• the child is stunted and overweight.

Increased ICP in children leads to disturbances in brain development, so it is important to detect the pathology as early as possible.

Benign intracranial hypertension (BIH)

This is one of the types of ICP, which can be attributed to a temporary phenomenon that is caused by a number of unfavorable factors. The condition of benign intracranial hypertension is reversible and does not pose a serious danger, since in this case the compression of the brain does not occur due to the influence of any foreign body.

The following factors can cause ADHD:

1. Hyperparathyroidism;
2. Disruptions in the menstrual cycle;
3. Discontinuation of certain medications;
4. Hypovitaminosis;
5. Obesity;
6. Pregnancy;
7. Overdose of vitamin A, etc.

Benign intracranial hypertension is associated with impaired absorption or outflow of cerebrospinal fluid. Patients complain of headaches that get worse with movement, and sometimes even with sneezing or coughing. The main difference between the disease and classic cerebral hypertension is that the patient does not show any signs of depression of consciousness, and the condition itself does not have any consequences and does not require special treatment.

Complications

The brain is a vulnerable organ. Prolonged compression leads to atrophy nerve tissue, which means they suffer mental development, ability to move, autonomic disorders occur.

If you do not contact a specialist in time, compression will occur. The brain may be forced into the foramen magnum or into the notch of the tentorium cerebellum. This compresses the medulla oblongata, where the centers of respiration and circulation are located. This will lead to the death of a person. Pressing into the notch of the tentorium is accompanied by constant drowsiness, yawning, breathing becomes deep and rapid, the pupils are noticeably constricted. Wedging of the hippocampal hook occurs, a symptom of which is dilation of the pupil or the absence of a light reaction on the side of the damage. An increase in pressure will lead to dilation of the second pupil, disruption of the breathing rhythm and coma.

High intracranial pressure is always accompanied by loss of vision due to compression of the optic nerve.

Diagnostics

For diagnosis, the pressure inside the skull is measured by inserting a needle attached to a pressure gauge into the spinal canal or into the fluid cavities of the skull.

For staging, a number of signs are taken into account:

1. It is determined by poor outflow of venous blood from the skull area.
2. According to MRI (magnetic resonance imaging) and CT (computed tomography).
3. Judged by the degree of rarefaction of the edges of the ventricles of the brain and the expansion of liquid cavities.
4. According to the degree of dilation and blood filling of the veins of the eyeball.
5. According to ultrasound data of cerebral vessels.
6. According to the results of the encephalogram.
7. If the ophthalmic veins are clearly visible and heavily filled with blood (red eyes), then we can indirectly say that there is an increase in pressure inside the skull.

In practice, in most cases, for a more accurate diagnosis and the degree of development of the disease, differentiation of the symptoms of clinical manifestations of hypertension is used in combination with the results of a hardware study of the brain.

Treatment of intracranial hypertension

What is the treatment for increased intracranial pressure in adults? If it is benign hypertension, the neurologist prescribes diuretics. As a rule, this alone is enough to alleviate the patient’s condition. However this traditional treatment is not always acceptable for the patient and cannot always be carried out by him. You can’t “sit” on diuretics during working hours. Therefore, special exercises can be performed to reduce intracranial pressure.

Also very helpful for intracranial hypertension is a special drinking regimen, a gentle diet, manual therapy, physiotherapeutic procedures and acupuncture. In some cases, the patient manages even without drug treatment. Signs of the disease may disappear within the first week from the start of treatment.

A slightly different treatment is used for cranial hypertension caused by some other disease. But before treating the consequences of these diseases, it is necessary to eliminate their cause. For example, if a person has developed a tumor that creates pressure in the skull, the patient must first get rid of this tumor, and then deal with the consequences of its development. If it is meningitis, then there is no point in treating with diuretics without simultaneously combating the inflammatory process.

In very severe cases (for example, cerebrospinal fluid block after neurosurgical operations or congenital cerebrospinal fluid block), surgical treatment is used. For example, a technology has been developed to implant tubes (shunts) to drain excess cerebrospinal fluid.

PS: Dehydration of the body (vomiting, diarrhea, large blood losses), chronic stress, vegetative-vascular dystonia, depression, neurosis, diseases accompanied by circulatory disorders in the vessels of the brain (for example, ischemia, encephalopathy, cervical osteochondrosis) lead to a decrease in intracranial pressure (hypotension). ).

Bottom line

Thus, intracranial hypertension is a pathological condition that can occur under the most various diseases brain and more. It requires mandatory treatment. Otherwise, a wide variety of outcomes are possible (including complete blindness and even death).

The earlier it is diagnosed this pathology, the better results can be achieved with less effort. Therefore, you should not delay visiting a doctor if you suspect increased intracranial pressure.

Every person experiences a headache sooner or later. A fairly common cause of frequent pain is intracranial hypertension. Increased intracranial pressure may result from an increase in the volume of cerebrospinal fluid, blood, or interstitial fluid in the brain. The pathology is dangerous and requires timely treatment.

The term "intracranial hypertension" is used primarily by doctors. People far from medicine are more accustomed to calling the disorder “high intracranial pressure.”

Increased pressure in the skull may be due to:

• an increase in the volume of cerebrospinal fluid (cerebrospinal fluid);
• cerebral hemorrhages;
• formation of tumors;
• cerebrovascular accident.

Intracranial pressure (ICP) is an important indicator for every person. Intracranial hypertension syndrome is a dangerous neurological pathology that can lead to serious consequences.

Intracranial hypertension according to ICD-10 is designated as G93.2 when it comes to benign pathology.

Intracranial hypertension can be either a congenital or acquired disease. Children encounter this pathology no less often than adults. No person is immune from intracranial hypertension, so it is important to be able to recognize specific symptoms and consult a doctor in a timely manner. If you suspect increased intracranial pressure, you should first visit a neurologist and undergo all examinations.

Causes of high intracranial pressure

The main reason for the development of intracranial hypertension is a change in the amount of cerebrospinal fluid or impaired circulation of cerebrospinal fluid. Such disorders may be associated with traumatic brain injuries, spinal injuries, and neurological pathologies.

Poor circulation of cerebrospinal fluid leads to increased intracranial pressure

The second most common cause of this type of hypertension is circulatory disorders. Intracranial hypertension may occur due to venous blood stagnation. Impaired blood flow to the brain with subsequent stagnation of blood in the venous region leads to an increase in the total volume of circulating blood in the skull. The result is a slowly growing headache and the development of a number of neurological disorders.

In the case of brain tumors, the volume and density of brain tissue increases, which also leads to increased pressure inside the skull.

All these pathological processes are a consequence:

• severe traumatic brain injury;
• cerebrovascular accidents;
• neoplasms in the skull;
• inflammation of the meninges;
• severe intoxication.

Quite often, the cause of the development of intracranial hypertension is cranial trauma, indirect signs of which the patient may not immediately detect. In this case, due to the injury, the normal circulation of cerebrospinal fluid is disrupted and intracranial pressure gradually increases. Concussions as a result of an accident or a strong blow, severe blows to the head, bruises of the skull and hematomas can lead to the development of this dangerous pathology.

Intracranial injuries sustained during an accident may not be noticed at first and manifest themselves later as increased blood pressure.

Cerebrovascular accident leading to the development of ICH (intracranial hypertension) in adult patients is caused by a stroke. The cause may also be thrombosis of the meninges.

Malignant and benign neoplasms lead to an increase in the amount of brain tissue, which can also result in increased pressure inside the skull. ICH is often diagnosed when cancer has metastasized to the brain.

Inflammatory pathologies affecting the brain develop in people regardless of age. Meningitis, meningoencephalitis, encephalitis and brain abscess all lead to an increase in the volume of cerebrospinal fluid and increased intracranial pressure.

Neurological disorders that provoke changes in the circulation of cerebrospinal fluid or venous stagnation may be the result of severe alcohol intoxication, heavy metal or carbon monoxide poisoning.

Separately, there is an increase in intracranial pressure in people with pathologies of cardio-vascular system. Congenital defects heart disease and severe disorders of the cardiovascular system can lead to impaired blood circulation in the brain, resulting in increased intracranial pressure.

Pathologies of the cardiovascular system affect the normal functioning of the brain

Congenital pathologies and developmental anomalies as a cause of ICH

ICH can be either a congenital or acquired pathology. No one is immune from this disorder; increased intracranial pressure is equally common in people of different age groups. While in adult patients the cause is often injuries or acquired pathologies, in children the disorder is most often congenital.

Causes of ICH in children:

• damage to the skull during passage through the birth canal;
• intrauterine hypoxia;
• severe prematurity;
• abnormalities in the structure of the skull;
• hydrocephalus.

Infections suffered by a woman during pregnancy can also cause increased intracranial pressure. A special place is occupied by neuroinfections, which in infants manifest themselves with a whole neurological symptom complex, including increased intracranial pressure.

Idiopathic and chronic ICH

According to the nature of the course and the reasons for its development, intracranial hypertension is divided into two types - chronic and idiopathic.

Chronic intracranial hypertension is called ICH with clearly identified causes, characteristic symptoms and course. It can be triggered by traumatic brain injury, birth trauma, inflammation of the meninges, or cancer.

Idiopathic is called ICH, the causes of which cannot be reliably determined. In this case, factors provoking the development of the disease may be various pathologies, only indirectly related to the head or spinal cord or circulatory system.

Idiopathic or benign intracranial hypertension is diagnosed mainly in women over the age of 20 years. Doctors associate the risks of developing this form of intracranial hypertension with the presence of excess weight, hormonal and metabolic disorders, since the vast majority of patients are obese young women with menstrual disorders.

Presumably, idiopathic intracranial hypertension is a secondary symptom of the following pathologies:

• systemic lupus erythematosus;
• Cushing's syndrome;
• vitamin D deficiency;
• hyperthyroidism;
• Iron-deficiency anemia;
• severe renal failure.

Also, idiopathic ICH can be a consequence of long-term therapy with corticosteroids and tetracyclines.

Symptoms of pathology

Having understood what ICH is in adults and children, you should be able to promptly recognize the symptoms of intracranial hypertension in order to seek medical help in time.

With intracranial hypertension, symptoms depend on how much intracranial pressure has increased.

The main symptom of the disease is headache. Moderate intracranial hypertension is characterized by intermittent rather than constant headaches. In severe forms of the disorder, the headache is generalized, spreading to the entire head, and pain is observed daily.

Headache – main symptom intracranial hypertension

In addition to headaches, intracranial hypertension is characterized by the following symptoms:

• nausea with vomiting;
• prostration;
• decreased performance;
• irritability and nervousness;
• noise and ringing in the ears;
• memory impairment;
• impaired concentration;
• decreased clarity of vision.

Indirect signs of intracranial hypertension are weight loss, the appearance of bruises under the eyes, decreased libido, and less commonly, seizures.

With increased intracranial pressure, signs of vegetative-vascular dystonia may be observed. This symptom complex has more than 100 specific signs, including angina, shortness of breath, blurred vision and tinnitus.

Patients with ICH suddenly notice increased sensitivity to weather conditions, and peak headaches may occur at the time of a sharp increase in atmospheric pressure.

Headache with ICH worsens at night and immediately after sleep. This is due to an increase in the volume of brain fluid in the supine position. During the day, the headache spreads throughout the skull, the intensity of the pain syndrome may change. Quite often, simple analgesics do not have the expected therapeutic effect in ICH.

In adult patients, intracranial hypertension may be accompanied by sudden surges in blood pressure. During the day, your health may change several times. Patients often complain of bouts of disorientation, fainting, fluttering before the eyes and a feeling of their own heartbeat.

The symptoms of benign hypertension are somewhat different from the chronic form of the disease. If, with chronic ICH, the patient constantly suffers from headaches, intensifying at night, the pain syndrome with benign intracranial hypertension subsides at rest and intensifies with movement. The peak of headaches occurs during heavy physical activity.

The main feature of chronic intracranial hypertension is a disturbance of consciousness, a change in character, and a deterioration in the cognitive functions of the brain. With benign ICH, such symptoms are completely absent; the disorder is manifested only by a headache, which intensifies during exercise.

Diagnosis of the disease

If you suspect intracranial hypertension, you should consult a neurologist. First, the doctor will conduct a questioning, check reflexes and examine the patient. To confirm the diagnosis, it is necessary to undergo several hardware tests. First of all, Doppler ultrasound of intracanal vessels is prescribed to exclude cerebral circulatory disorders.

Signs of intracranial hypertension are clearly visible using MRI - magnetic resonance imaging. This examination is the most informative. To exclude inflammatory pathologies, the patient must undergo a general and biochemical blood test. To exclude injuries to the skull and the development of ICH due to injuries, radiography of the skull and cervical spine spine.

Intracranial pressure is measured by lumbar puncture. This is a traumatic and unsafe procedure, during which a burr hole is made in the skull, so it is prescribed only in particularly severe cases. Usually, hardware tests are sufficient to make a diagnosis. To determine the composition of the cerebrospinal fluid, a study of cerebrospinal fluid may be prescribed. Material for analysis is taken by performing a lumbar puncture.

When intracranial pressure increases, an important diagnostic step is to exclude autoimmune pathologies, for example, lupus erythematosus, which can cause the development of idiopathic or benign ICH.

MRI is an informative and non-traumatic diagnostic method

Treatment of ICH

For intracranial hypertension, treatment depends on the cause of the disorder. Treatment of intracranial hypertension and ICP in adults begins with differential diagnosis to identify the exact causes of the disease.

If the cause is tumor neoplasms, the patient is advised surgical intervention. Removal of the tumor quickly normalizes intracranial pressure by reducing the amount of brain fluid, therefore additional medications ICP is not required to normalize. However, this is only true for benign neoplasms, since malignant pathologies cannot always be removed surgically.

With internal hematomas, blood flows into the skull, which leads to increased pressure. If an MRI reveals such a disorder, a minimally invasive operation is performed to remove the leaked blood. The result is rapid normalization of intracranial pressure.

Inflammatory diseases of the meninges are treated with antibacterial drugs. Medicines are administered by drip or injection into the subarachnoid space. When performing such a puncture, a small part of the cerebrospinal fluid is removed for further analysis, and a small wound is formed at the puncture site. Removing part of the cerebrospinal fluid helps to instantly reduce intracranial pressure to normal values.

Treatment of benign ICH

For intracanal pathology such as benign intracranial hypertension, specific treatment is not carried out; it is enough to identify and eliminate the cause, which may be autoimmune or hormonal disorders. In overweight women, intracranial pressure gradually decreases as they lose weight, and headaches go away.

Benign intracranial hypertension often develops during pregnancy. In this case, no treatment is prescribed; the pressure will return to normal after childbirth, as the amount of fluid in the brain tissue and throughout the body decreases.

There is no specific therapy aimed at reducing intracranial pressure. ICH is treated by eliminating the cause that caused an increase in the amount of cerebrospinal fluid and an increase in intracranial pressure. Diuretics can be used to reduce the amount of circulating fluid. The following drugs are prescribed:

• Furosemide;
• Lasix;
• Diacarb;
• Acetazolamide.

The drugs are taken in short three-day courses, with a break of two days. Exact dosage selected by the doctor individually for each patient. During pregnancy, your doctor may prescribe a diet and a reduction in the amount of fluid you take to reduce intracranial pressure.

Taking diuretics allows you to remove excess fluid from the body and lower blood pressure. At the same time, the rate of cerebrospinal fluid production decreases, which means intracranial pressure gradually drops. This is only true if the cause of intracranial hypertension is an increase in the volume of cerebrospinal or cerebral fluid, but not trauma, hematoma or tumor.

For benign ICH, fluid intake should be reduced to one and a half liters per day. This applies not only to ordinary drinking water, but also any liquid dishes, including juices and soups. At the same time, a diet is prescribed and physiotherapy leading to a decrease in intracranial pressure.

Adult patients may be prescribed physiotherapeutic treatment methods - magnetic therapy or electrophoresis of the cervical-collar area. It is advisable to use such methods when the symptoms of ICH are moderate.

It is important to get rid of excess water in the body

Surgical methods

Increased intracranial pressure is dangerous condition which may progress. If conservative treatment does not bring the expected result, they resort to surgical methods, the purpose of which is to reduce the production of cerebrospinal fluid. For this purpose shunting is used.

The shunt is inserted into the cerebrospinal fluid space through an opening. The other end of the artificial vessel is brought into abdominal cavity. Through this tube, excess cerebrospinal fluid is constantly drained into the abdominal cavity, thereby reducing intracranial pressure.

Bypass surgery is rarely used, as the procedure is associated with a number of risks. Indications for bypass surgery:

• constant increase in intracranial pressure;
• high risk of complications;
• hydrocephalus;
• ineffectiveness of other methods to reduce ICP.

Shunting refers to emergency measures, which are used for lack of alternatives.

Possible complications of ICH

VCH is dangerous pathology, which requires timely diagnosis and treatment. Otherwise, chronic ICH can lead to complications, some of which are incompatible with life.

One of the most likely complications with high intracranial pressure is compression of the optic disc with subsequent atrophy, which leads to complete and irreversible loss of vision.

High intracranial pressure can lead to the development of a cerebral stroke. This complication can be fatal. Severe intracranial hypertension leads to damage to brain tissue, which leads to disruption of nervous activity and can threaten the death of the patient.

In especially severe cases, the disease leads to the development of hydrocephalus. High pressure of the cerebrospinal fluid on the brain leads to loss of vision, respiratory failure, deterioration of cardiac activity, development seizures. There are cases where intracranial hypertension became the impetus for the development of epilepsy.

The prognosis depends on how early treatment is started. With uncomplicated intracranial hypertension, even with timely measures taken, no one is immune from negative consequences. Possible development mental disorders, changes in speech, paralysis. Among the neurological disorders that are observed with intracranial hypertension are impaired reflex activity, short-term paresis, and local impairment of skin sensitivity. If the cerebellum is affected due to high pressure, problems with coordination of movements may develop.

With benign ICH, the prognosis is favorable. Timely contact with a neurologist, diuretic therapy and treatment of the cause of increased intracranial pressure can get rid of headaches without negative consequences. In other cases, the prognosis depends on the timeliness of therapy and which areas of the brain are damaged due to ICH.

Symptoms of intracranial hypertension (including unilateral or bilateral papilledema).
. With lumbar puncture, an increase in intracranial pressure above 200 mm H2O is determined.
. Absence of focal neurological symptoms (except for paresis of the VI pair of cranial nerves).
. Absence of deformation, displacement or obstruction of the ventricular system, or other brain pathology according to magnetic resonance imaging, with the exception of signs of increased cerebrospinal fluid pressure.
. Despite high level intracranial pressure, the patient’s consciousness is usually preserved.
. There are no other causes of increased intracranial pressure.
The syndrome of idiopathic intracranial hypertension was first mentioned in 1897 by Quincke. The term “pseudotumor cerebri” was proposed in 1914 by Warrington. Foley in 1955 introduced the name “benign intracranial hypertension” into practice, but Bucheit in 1969 objected to the concept of “benign”, emphasizing that for visual functions the outcome of this syndrome may be “non-benign”. He proposed the name “idiopathic” or “secondary” intracranial hypertension, depending on whether the pathological condition with which it is associated is known.
Etiology and pathogenesis
The reason for the development of pseudotumor cerebri remains unclear, but the occurrence of this syndrome associated with a number of different pathological conditions, and the list continues to grow. Among them, the most frequently mentioned are: obesity, pregnancy, disorder menstrual cycle, eclampsia, hypoparathyroidism, Addison's disease, scurvy, diabetic ketoacidosis, heavy metal poisoning (lead, arsenic), intake medicines(vitamin A, tetracyclines, nitrofuran, nalidixic acid, oral contraceptives, long-term corticosteroid therapy or its withdrawal, psychotropic drugs), some infectious diseases, parasitic infections (torulosis, trepanosomiasis), chronic uremia, leukemia, anemia (usually iron deficiency), hemophilia, idiopathic thrombocytopenic purpura, systemic lupus erythematosus, sarcoidosis, syphilis, Paget's disease, Whipple's disease, Guillain-Barre syndrome, etc. In these cases, hypertension is regarded as secondary, since the elimination of these pathological factors contributes to its resolution. However, in at least half of the cases, this condition cannot be associated with other diseases, and it is regarded as idiopathic.
Clinic
This pathology occurs in all age groups (most often in 30-40 years); in women - approximately 8 times more often than in men (1 case per 100,000 of the general population and 19 cases per 100,000 overweight young women).
The most common symptom in patients with pseudotumor cerebri is headache of varying intensity, occurring in 90% of cases (according to Johnson, Paterson and Weisberg 1974). As a rule, such a headache is generalized, most severe in the morning, and worsens with the Valsalva maneuver, coughing or sneezing (due to increased pressure in the intracranial veins). Visual impairment, according to various sources, occurs in 35-70% of cases. Symptoms of visual impairment are similar to those of any other type of intracranial hypertension. As a rule, they precede headaches and include attacks of short-term blurred vision, loss of visual fields and horizontal diplopia.
An objective examination may reveal unilateral or bilateral paresis of the VI pair of cranial nerves and an afferent pupillary defect. Ophthalmoscopy reveals bilateral or unilateral papilledema. varying degrees severity, which over time in 10-26% of cases leads to an irreversible decrease in vision as a result of damage to nerve fibers.
Visual field defects to varying degrees of severity occur in at least half of patients with pseudotumor cerebri; most often at the initial stage they represent a narrowing of the isopters in the inferior nasal quadrant. Subsequently, a generalized narrowing of all isopters occurs, loss of central vision or loss of visual fields along the horizontal meridian.
A neurological examination reveals signs of increased intracranial pressure in the absence of focal neurological symptoms (with the exception of unilateral or bilateral paresis of the VI pair of cranial nerves).
In many cases, pseudotumor cerebri resolves on its own, but recurs in 40% of cases. Possible transition to chronic form, which requires dynamic monitoring of patients. For at least two years after diagnosis, such patients should also be observed by a neurologist with repeated MRI of the brain to completely exclude occult tumors.
The consequences of even self-resolving pseudotumor cerebri can be catastrophic for visual function, ranging from moderate narrowing of visual fields to almost complete blindness. Optic nerve atrophy (preventable with timely treatment) develops in the absence of a clear correlation with the duration of the course, severity clinical picture and relapse rate.
Research methods
Magnetic resonance imaging (MRI) of the brain
According to Brodsky M.C. and Vaphiades M. (1998), intracranial hypertension leads to a number of changes detected using MRI, which suggest the presence of pseudotumor cerebri in the patient. In this case, a prerequisite is the absence of signs of a volumetric process or expansion of the ventricular system.
1) Flattening of the posterior pole of the sclera was noted in 80% of cases. Emergence of this characteristic associated with the transmission of increased cerebrospinal fluid pressure in the subarachnoid space of the optic nerve to the pliable sclera. Atta H.R. and Byrne S.F. (1988) found a similar flattening of the sclera also on B-scans.
2) An empty (or partially empty) sella turcica in such patients occurs in 70% of cases (George A.E., 1989). The frequency of occurrence of this sign varied from 10% when analyzing plain X-rays to 94% when assessing third-generation computed tomograms.
3) An increase in the contrast of the prelaminar part of the optic nerve occurs in 50% of patients. The increase in contrast of the edematous disc is analogous to the increase in fluorescence of the optic disc during fluorescein angiography: the cause in both cases is diffuse sweating of the contrast agent from the prelaminar capillaries due to pronounced venous stagnation (Brodsky V., Glasier CV, 1995; Manfre L., Lagalla R. , Mangiameli A. 1995).
4) Expansion of the perineural subarachnoid space in patients with pseudotumor cerebri, most pronounced in the anterior parts, and to a lesser extent at the posterior pole of the orbit, was found in 45% of cases. With the expansion of the perineural subarachnoid space, the optic nerve itself appears to be narrowed with a small, but statistically significant increase the average diameter of its shells. In some cases, axial magnetic resonance imaging showed the so-called “string sign”: a string-thin optic nerve surrounded by an expanded subarachnoid space, enclosed in a normal-sized dura mater.
5) Vertical tortuosity of the orbital part of the optic nerve was noted in 40% of patients.
6) Intraocular protrusion of the prelaminar part of the optic nerve was noted in 30% of cases.
Ultrasonography
orbital part of the optic nerve
Using ultrasound methods, it is possible to detect the accumulation of excess cerebrospinal fluid in the perineural subarachnoid space.
With an A-scan, in this case, one can detect an expanded subarachnoid space in the form of an area of ​​very low reflectivity, and with a B-scan, a transparent signal around the optic nerve parenchyma in the form of a crescent or circle - a “doughnut symptom”, as well as flattening of the posterior pole of the sclera.
To confirm the presence of excess fluid in the perineural subarachnoid space, use the 30° test developed by Ossoing et al. for A-scan. The 30° test technique is as follows: the diameter of the optic nerve is measured in the anterior and posterior sections while fixing the patient's gaze straight ahead. Then the fixation point is shifted by 30 (or more towards the sensor and the measurements are repeated. In the presence of excess fluid in the perineural subarachnoid space, the dimensions compared to the original ones will decrease by at least 10% (up to 25-30%). In this case, between measurements intervals of a few minutes should be observed.
Using A-scan it is also possible to measure cross section the optic nerve with its membranes and assessment of their reflectivity. The width of the optic nerve with its sheaths, according to Gans and Byrne (1987), normally ranges from 2.2 to 3.3 mm (average 2.5 mm).
Transcranial Dopplerography
Transcranial Dopplerography makes it possible to detect an increase in systolic blood flow velocity with a decrease in diastolic velocity, which leads to an increase in the pulsation index without significant changes in the average velocity indicators in main vessels brain and is an indirect sign of intracranial hypertension.
Patient examination scheme
with suspected pseudotumor cerebri
n MRI of the brain
n Examination by a neurologist
n Examination by a neurosurgeon, lumbar puncture
n Examination by a neuro-ophthalmologist
n Perimetry according to Goldman or computer perimetry (Humphrey) test 30 - 2.
n Photographing the optic disc.
n Ultrasound examination (B-scan and A-scan with measuring the diameter of the sheaths of the orbital part of the optic nerve and performing a 30° test).
Treatment of patients with pseudotumor cerebri
Indications for treatment of patients with pseudotumor cerebri are:
1) persistent and intense headaches.
2) signs of optical neuropathy.
The treatment method is to eliminate the provoking factor (if it is known), combat excess weight, drug therapy, and in the absence positive effect- various surgical interventions.
Conservative therapy
1. Limiting salt and water.
2. Diuretics:
a) furosemide: start with a dose of 160 mg per day (adults), assess effectiveness according to clinical manifestations and the condition of the fundus (but not the level of cerebrospinal fluid pressure), if there is no effect, increase the dose to 320 mg per day;
b) acetazolamide 125-250 mg every 8-12 hours (or long-acting Diamox Sequels® 500 mg).
3. If ineffective, add dexamethasone to treatment at a dose of 12 mg per day.
Liu and Glazer (1994) suggest methylprednisolone 250 mg intravenously 4 times daily for 5 days followed by oral tapering, in combination with acetazolamide and ranitidine.
The absence of a positive effect from conservative therapy within 2 months from the start of treatment is an indication for surgical intervention.
Surgery
Repeated lumbar punctures
Repeated lumbar punctures are performed until remission is obtained (in 25% of cases, remission is achieved after the first lumbar puncture), taking up to 30 ml of cerebrospinal fluid. Punctures are performed every other day until the pressure reaches a level of 200 mm H2O, then once a week.
Bypass operations
Currently, most neurosurgeons prefer lumboperitoneal shunting, first used for this pathology by Vander Ark et al. in 1972. Using this method, pressure is reduced in the entire subarachnoid space of the brain and secondarily in the associated perineural subarachnoid space in the absence of pronounced adhesions there.
If the presence of arachnoiditis does not allow the use of the lumbar subarachnoid space for shunting, ventriculoperitoneal shunting is used (which can also be difficult, since often the ventricles with this pathology are narrowed or slit-like). Complications of bypass surgery include infection, blockage of the shunt, or overfunctioning of the shunt, leading to increased headaches and dizziness.
Optic nerve sheath decompression
IN last years There is increasing evidence that decompression of the optic nerve itself is effective in preventing irreversible loss of visual function.
According to Tse et al. (1988), Corbett et al., Kellen and Burde et al., decompression of the optic nerve should be performed before the onset of visual acuity loss. Since a sign of incipient damage to the optic nerve is a concentric narrowing of the visual fields while maintaining normal visual acuity, surgical intervention is indicated when the narrowing of the visual fields progresses.
Corbett (1983) notes that in the absence of stabilization of the process (decrease in visual acuity, increase in existing visual field defects or the appearance of new ones, increase in afferent pupillary defect), decompression should be performed without waiting for vision to decrease to any specific level. Expansion of the blind spot or transient blurred vision in the absence of visual field defects in themselves are not an indication for surgical intervention.
The purpose of the operation is to restore visual functions lost as a result of edema of the optic disc or to stabilize the process by reducing the pressure of cerebrospinal fluid in the subarachnoid space of the orbital part of the optic nerve, which leads to the reverse development of edema.
Decompression (fenestration of the sheath) of the optic nerve was first proposed by De Wecker in 1872 as a method surgical treatment neuroretinitis. However, this operation was practically not used until 1969, when Hoyt and Newton, simultaneously with Davidson and Smith, again proposed it as a method of surgical treatment of chronic congestive optic disc. However, over the next 19 years, only about 60 cases of surgical decompression of the optic nerve sheath were described in the literature.
This operation became widely accepted only in 1988, after Sergott, Savino, Bosley and Ramocki, simultaneously with Brourman and Spoor, Corbett, Nerad, Tse and Anderson published a series of successful results of surgical decompression of the optic nerve sheath in patients with idiopathic intracranial hypertension.
Currently, surgical decompression of the optic nerve sheaths is the method of choice in the treatment of patients with visual impairment due to chronic papilledema in conditions such as pseudotumor cerebri and dural sinus thrombosis. Both medial and lateral approaches with various modifications are used.
The effect of optic nerve sheath decompression on cerebral liquor dynamics
Kaye et al. in 1981, they monitored intracranial pressure in a patient with pseudotumor cerebri before and after bilateral optic nerve decompression and did not find a statistically significant decrease, despite a decrease in disc edema. The authors concluded that the improvement in the condition of the optic nerve head did not result from a decrease in intracranial pressure as a whole, but as a result of an isolated decrease in cerebrospinal fluid pressure within its membranes.
The small volume of cerebrospinal fluid flowing through the fistula from the perineural subarachnoid space is sufficient to decompress the optic nerve sheath itself, but this amount may not be enough to decompress the entire subarachnoid space.
Management of patients with pseudotumor cerebri
Patients with pseudotumor cerebri require constant dynamic monitoring both at the stage conservative treatment, before making a decision about surgery, and in the postoperative period.
Corbett et al. discharged their patients the next day after surgery. Then all patients were examined a week after surgery, then monthly until visual functions stabilized. Subsequently, examinations were carried out every 3-6 months.
Early signs of reverse development of optic disc edema in some cases appeared on days 1-3 and were the appearance of clearer outlines of the temporal half of the disc. A small area of ​​the nasal half of the disc often remained swollen for a longer period of time.
As a criterion for the effectiveness of the decompression performed, Lee S.Y. et al. proposed to also evaluate the caliber of the retinal veins. According to their data, the venous caliber decreases significantly after surgery and continues to decrease for an average of 3.2 months, not only in the operated eye, but also in the other eye. This once again confirms that the mechanism of action of the operation is the slow filtration of fluid through a surgically formed fistula in the optic nerve sheath.

Symptoms of Increased Intracranial Pressure - Treatment: Medicines, Diet, Surgical Techniques - Complications of Increased Intracranial Pressure

Idiopathic Intracranial Hypertension – Increased Intracranial Pressure

Intracranial hypertension syndrome is increased intracranial pressure due to a number of potential causes, such as disruption of the flow of cerebrospinal fluid (hydrocephalus), infection, obstruction of blood flow, or brain tumors.

Not so long ago, before the introduction into medical practice CT and MRI scans and brain tumors were diagnosed based on a neurological examination. One of the common combinations was a combination of chronic headache and signs of papilledema on fundus examination.
In English-language literature this syndrome is called false brain tumor , since these signs are present, but the tumor is not. Syndrome idiopathic intracranial hypertension is caused by an increase in brain volume due to the accumulation of fluid in its tissues. The reason for this phenomenon is unknown. An increase in volume leads to an increase in intracranial pressure.

The reason for visiting a doctor for this disease is usually chronic headache and transient visual disturbances.

Symptoms of Intracranial Hypertension

Headache

Headache is universal with intracranial hypertension. The nature of the headache and its intensity are very individual. Headache is often present at night. At the same time, the presence of night pain is not necessary. The pain can be either local or involve the entire head.

The intensity of the headache varies from mild to moderate, only occasionally it can be intense. The nature of the pain can be pulsating, bursting, or described by patients as a feeling of a hoop around the head. Often present increased sensitivity to the light.

The main quality of headache with intracranial hypertension is its persistence. Although, even this quality is not very universal.

The presence of unexplained chronic headache is only suspicious but not sufficient to make this diagnosis. Depression, chronic lack of sleep for any reason, and sleep apnea cause identical headaches.

Short term visual impairment

Episodes of short-term vision loss, as if the television screen had momentarily switched off, "sparks in the fields of vision" or short-term visual disturbances such as the feeling of looking through a cloudy glass, are not uncommon.
They are often triggered by changes in head or body position (especially bending or standing) and last from seconds to minutes. Short-term visual impairment can occur in one or both eyes.

All these visual symptoms– the phenomenon is temporary and they do not pose any danger in themselves. However, the main potential complication of intracranial hypertension is loss of some portion of peripheral vision.
In exceptional cases, with a strong increase in intracranial pressure, a serious decrease in visual acuity may occur, even to the point of blindness.

Long-term visual impairment is a potentially irreversible process that requires urgent intervention.

Normally, we do not notice the so-called “blind spot,” which is formed by a small “blind” area of ​​the retina at the exit of the optic nerve. Swelling of the optic nerves can make the blind spot more prominent, resulting in a sensation of movement in the periphery of the visual field.

Double vision

Double vision is another common early symptom intracranial hypertension. An increase in brain volume compresses the nerves supplying the extraocular muscles. The result is double vision. Double vision should disappear when either eye is closed.

Most often, the VI nerve is damaged on both sides, each of which diverts the eye towards the temple on its side. In this case, the doubling is horizontal, i.e. The images are side by side. Since the eyes turn toward the nose, double vision increases when looking into the distance.

Massive swelling of the optic nerves can lead to retinal edema. In this case, distortion of the shape of objects occurs (metamorphopsia). For this reason, sometimes a sensation of “double vision” is created even in one eye. Papilledema should be visible on fundus examination.

Other Symptoms

Pulsatile tinnitus also often occurs with intracranial hypertension.

Causes of Idiopathic Intracranial Hypertension

Idiopathic intracranial hypertension is called in cases where no explanation for the increase in intracranial pressure can be found. The very word “idiopathic” actually means the absence of a known cause. Additional volume is created by increasing the volume of the brain itself, which retains fluid in its tissues. Why is unknown.

There are some risk factors that contribute to the development of intracranial hypertension, but they are not necessary for the development of the disease. Here are some of them: iron deficiency, pregnancy, thyroid disease, chronic renal failure.
Medicines such as tetracyclines, vitamin A overdose, corticosteroids, hormonal contraceptives, sulfonamides, Tamoxifen, Cyclosporine and some others can cause increased intracranial pressure.

In most cases, however, we are talking about idiopathic intracranial hypertension, in which there is no cause.

Although there is no known cause, the syndrome idiopathic intracranial hypertension occurs in young women who are significantly overweight in the overwhelming percentage of cases.

Diagnosis of Intracranial Hypertension

Ophthalmological Examination

The cardinal finding in the fundus with increased intracranial pressure is swelling of the optic nerves on both sides. The absence of this casts doubt on the diagnosis of intracranial hypertension.
Visual field testing may reveal an enlarged blind spot and a wide variety of visual field defects.
Oculomotor problems, if present, are most often limited to insufficient eye abduction towards the temple on both sides.

Neurological Examination

Neurological examination is normal except for the ocular abnormalities described above. The presence of additional findings on neurological examination requires the exclusion of other causes of increased intracranial pressure.

Brain MRI

MRI examination in idiopathic intracranial hypertension is normal in most cases. The purpose of MRI is to rule out tumors, infections, and hydrocephalus. Sometimes an MRI should be done with contrast.

There are no findings that would either exclude or confirm idiopathic intracranial hypertension. Some anatomical features, which in themselves are insignificant, can indirectly confirm the fact of increased intracranial pressure.
These include sella turcica syndrome, flattening of the eyeballs, fluid around the optic nerves, brain ventricles that are narrow for age, or narrowing of the venous sinuses. All of them may be present in healthy people and absent in idiopathic intracranial hypertension.

Venous sinus thrombosis can cause symptoms similar to idiopathic intracranial hypertension. MR Venography or CT scan of the head with contrast will help with this diagnosis.

Spinal Tap

If intracranial hypertension is suspected, a spinal puncture is done for only one purpose - to measure the pressure of the cerebrospinal fluid. All other laboratory parameters in the idiopathic form should be normal. If not, then the cause of the symptoms is different.

Fluid pressure greater than 250 mmH2O in adults and >280 mmH2O in children is considered elevated.

The technique of spinal puncture plays a fundamental role. In order to measure pressure, it should be done while the patient is lying horizontally on his side. Incorrect technique can lead to artificially inflated results. Cerebrospinal fluid pressure is constantly changing. U fat people Blood pressure is usually higher even in normal conditions. Spinal tap is useful for diagnosing intracranial hypertension. However, this diagnosis is not made solely on the basis of elevated blood pressure in the absence of other typical symptoms of intracranial hypertension.

Treatment of Idiopathic Intracranial Hypertension

Weight loss

The fact that losing body weight reduces swelling of the optic nerves is a known fact proven by numerous studies. Although this method is effective, swelling of the optic nerve subsides slowly. There is a correlation between the degree of weight loss and its therapeutic effect. On average, a loss of at least 6% of body weight is required to relieve significant optic nerve swelling.

Weight loss is a mandatory, but not the only necessary component of treatment. Despite the reduction in optic nerve swelling, diet alone is not enough to improve the prognosis for loss of normal vision. A combination of diet and medications is required to improve prognosis.

Drug Treatment

Treatment of idiopathic intracranial hypertension is aimed at reducing intracranial pressure.
Acetazolamide (Diacarb) is the most commonly used. It is a carbonic anhydrase inhibitor with mild diuretic activity. It reduces intracranial pressure by reducing the amount of cerebrospinal fluid produced.

Research shows that acetazolamide can not only reduce papilledema, but also, over time, in combination with weight loss, reduce peripheral vision defects.

The dose of Acetazoloamide has to be used quite high. The initial dose is usually 1 gram per day, divided into two doses. If necessary, the dose can be increased to 4 grams per day if tolerated.

The most common side effect is numbness and a pins and needles sensation (often severe), which is most often experienced in the upper half of the body. Fatigue and intestinal disturbances are less common. Long-term use may lead to kidney stones and elevated liver enzymes in blood tests.

Acetazolamide belongs to the sulfonamides group, but its structure is very different from antimicrobials. Therefore, an allergy to sulfonamides does not necessarily mean an allergy to Acetazolamide.

Some doctors are trying to use one of the antiepileptic drugs, Topiramate (Topamah), instead of Diacarb. The logic is that Topiramate is also a carbonic anhydrase inhibitor. In addition, long-term use of Topiramate often leads to weight loss. His side effects similar to Diacarb, but Topiramate is much less well tolerated.

Corticosteroids may temporarily reduce symptoms of intracranial hypertension. However, they increase weight and themselves can cause an increase in intracranial pressure.

Therapeutic Spinal Tap

In emergency cases, with a sharp drop in vision, a spinal puncture is performed, not for diagnostic purposes, but therapeutic purpose. As a result of drainage of cerebrospinal fluid, the symptoms of intracranial hypertension are reduced, but temporarily.

Considering that about 500 ml of cerebrospinal fluid is produced per day, intracranial pressure very quickly rises to its previous level. However, this procedure buys a little time to prescribe other types of treatment.

Surgical Methods for the Treatment of Intracranial Hypertension

Surgical treatment is indicated for severe forms of the disease and in cases where there is no effect of conservative treatment, as well as when there is a threat of vision loss.

Decompression ( Fenestration) Optic Nerve Sheath

The main goal of the procedure is to prevent vision loss. Headache by itself is not a sufficient indication.

During this procedure, several incisions are made in the dura mater surrounding the optic nerves. Thus, drainage of the cerebrospinal fluid relieves pressure on the optic nerves. This procedure is not very simple and is performed under general anesthesia.

Fenestration of the optic nerve sheaths on only one side in some cases can solve the problem on opposite side. The initially good effect may not last long. In about a third of cases, vision begins to deteriorate again after 3 to 5 years.

Cerebrospinal Fluid Shunt

There are several variations of shunting for idiopathic intracranial hypertension. The idea behind a shunt is to permanently drain the cerebrospinal fluid.

Any of the shunts is a tube with a built-in valve that regulates the outflow depending on the pressure level. One end of the tube is placed either in the ventricle of the brain or inside the spinal canal in the lumbar region. The other end of the tube drains the cerebrospinal fluid into pleural cavity(chest), peritoneal cavity (stomach) or atrium (one of the chambers of the heart).

Each drainage option has pros and cons.
With intracranial hypertension, the ventricles of the brain are very small and difficult to enter.
For this reason, lumboperitoneal shunting (back to abdomen) for idiopathic intracranial hypertension is used more often.
The problem is that the lumboperitoneal shunt (back - stomach) gets clogged twice as often as the ventriculoperitoneal shunt (head - stomach).

The initial effect of the bypass is simply magnificent. Improvement is observed in 95%. However, after 3 years the numbers drop by half.

Another problem is shunt dysfunction, which occurs in about 75% within 2 years. So, it is necessary to make frequent revisions of the shunt.

The information on the site is provided for educational purposes only. Please do not self-medicate! Final diagnosis your health problems remains the prerogative of medical professionals. The material on the site will only help you become familiar with potential methods for diagnosing and treating neurological diseases and increase the productivity of your communication with doctors. The information on the site is updated whenever possible to take into account recent changes in the approach to the diagnosis and treatment of neurological diseases. However, the author of the articles does not guarantee immediate updates of information as it becomes available. I would be grateful if you could share your thoughts: [email protected]
Content copyright 2018. . All rights reserved.
By Andre Strizhak, M.D. Bayview Neurology P.C., 2626 East 14th Street, Ste 204, Brooklyn, NY 11235, USA

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