Systemic dizziness arises from what. What is the difference between systemic and non-systemic dizziness and their treatment. Often used against circling

Feeling of imaginary rotation and / or translational movements of the patient in various planes, less often - the illusion of displacement of a stationary environment in any plane. In clinical practice, the term "dizziness" is interpreted much more broadly, therefore, it includes conditions and sensations caused by impaired receipt of sensory information (visual, proprioceptive, vestibular, etc.), its processing. The main manifestation of dizziness is difficulty in orientation in space. Dizziness can have a variety of causes. The task of diagnosis is to identify the etiology of dizziness, which in the future allows you to determine the most effective tactics for its treatment.

ICD-10

R42 Dizziness and instability

General information

Feeling of imaginary rotation and / or translational movements of the patient in various planes, less often - the illusion of displacement of a stationary environment in any plane. In clinical practice, the term "dizziness" is interpreted much more broadly, therefore, it includes conditions and sensations caused by impaired receipt of sensory information (visual, proprioceptive, vestibular, etc.), its processing. The main manifestation of dizziness is difficulty in orientation in space.

Etiology and pathogenesis of dizziness

Ensuring balance is possible with the integration of the activities of the vestibular, proprioceptive, visual and tactile systems, which are closely related to the cerebral cortex and subcortical formations. Histamine, acting on histamine receptors, plays a crucial role in the transmission of information from the receptors of the semicircular canals. Cholinergic transmission has a modulating effect on histaminergic neurotransmission. Thanks to acetylcholine, it is possible to transfer information from receptors to the lateral vestibular nuclei and the central parts of the vestibular analyzer. It has been proven that vestibulo-vegetative reflexes function due to the interaction of cholin- and histaminergic systems, and histamine- and glutamatergic pathways provide vestibular afferentation to the medial nucleus.

Classification of dizziness

Allocate systemic (vestibular) and non-systemic dizziness. Non-systemic dizziness includes psychogenic dizziness, pre-syncope, imbalance. In some cases, the term "physiological dizziness" may be used. Physiological dizziness is caused by excessive irritation of the vestibular apparatus and occurs as a result of prolonged rotation, a sharp change in speed, and observation of moving objects. It is part of the motion sickness syndrome.

Systemic dizziness is pathogenetically associated with a direct lesion of the vestibular analyzer. Depending on the level of its defeat, central or peripheral systemic dizziness is distinguished. The central one is caused by damage to the semicircular canals, vestibular ganglia and nerves, the peripheral one is caused by damage to the vestibular nuclei of the brain stem and cerebellum. Within the framework of systemic vertigo, there are: proprioceptive (sensation of passive movement of one's own body in space) and tactile or tactile (sensation of swaying on the waves, lifting or falling of the body, unsteadiness of the soil, moving support under the feet).

Non-systemic dizziness is characterized by a feeling of instability, difficulty maintaining a certain posture. It is based on the mismatch of the activity of vestibular, proprioceptive, visual sensitivity, which occurs at various levels of the nervous system.

The clinical picture of dizziness

• Systemic dizziness

Systemic dizziness is observed in 35-50% of patients complaining of feeling dizzy. The occurrence of systemic dizziness is often due to damage to the peripheral part of the vestibular analyzer due to toxic, degenerative and traumatic processes, much less often - acute ischemia these formations. Damage to the structures of the brain located above (subcortical structures, brain stem, cerebral cortex and white matter of the brain) most often occurs in connection with vascular pathology, degenerative and traumatic diseases. The most common causes of systemic vertigo are vestibular neuronitis , Meniere's disease, benign paroxysmal positional vertigo, neuroma VIII pairs of CHN. To determine the nature of the disease already at the first examination of the patient, an adequate assessment of the anamnesis and the results of the clinical examination is necessary.

• Non-systemic dizziness

Balance imbalance can be caused by dysfunction of the vestibular analyzer of various origins. One of the most important distinguishing features is the deterioration of the patient's condition with loss of control of vision (closed eyes). Other causes of imbalance can be damage to the cerebellum, subcortical nuclei, brain stem, multisensory deficit, as well as the use of certain drugs (phenothiazine derivatives, benzodiazepines). In such cases, dizziness is accompanied by impaired concentration, increased drowsiness ( hypersomnia). The severity of these manifestations decreases with a decrease in the dose of the drug.

Pre-syncope - a feeling of dizziness, ringing in the ears, "blackouts in the eyes", lightheadedness, loss of balance. Psychogenic dizziness is one of the most common symptoms panic attacks and is one of the most frequent complaints made by patients suffering from psychogenic disorders ( hysteria , hypochondriacal syndrome , neurasthenia , depressive states). Differs in firmness and the expressed emotional coloring.

Diagnosis and differential diagnosis

To diagnose dizziness neurologist it is necessary first of all to confirm the very fact of dizziness, since patients often put a different meaning into the concept of “dizziness” (headache, blurred vision, etc.). To do this, in the process of differential diagnosis between dizziness and complaints of a different nature, one should not prompt the patient to one or another term or offer them to choose from. It is much more correct to hear from him a detailed description of the existing complaints and sensations.

Much attention should be paid to the neurological examination of the patient (state of CN, identification of nystagmus, coordinating tests, detection of neurological deficit). However, even a full examination does not always make it possible to determine the diagnosis; for this, observation of the patient in dynamics. In such cases, information about previous intoxications, autoimmune and inflammatory diseases may be useful. A patient with dizziness may need a consultation otoneurologist , vestibulologist and examination of the cervical spine: vestibulometry, stabilography , rotation tests and etc.

Treatment of dizziness

The choice of tactics for the treatment of dizziness is based on the cause of the disease and the mechanisms of its development. In any case, therapy should be aimed at relieving the patient of discomfort and associated neurological disorders. Therapy of disorders of cerebral circulation involves the control of blood pressure, the appointment of antiplatelet agents, nootropics, venotonics, vasodilators and, if necessary, antiepileptic drugs. Treatment of Meniere's disease involves the appointment of diuretics, limiting the intake of table salt, and in the absence of the desired effect and ongoing bouts of dizziness, they decide on surgical intervention. Treatment of vestibular neuronitis may require the use of antiviral drugs. Since the use of drugs that inhibit the activity of the vestibular analyzer in BPPV is considered inappropriate, the main method of treating benign paroxysmal positional vertigo is the repositioning of aggregates that irritate the vestibular analyzer according to J.M. Epley.

As a symptomatic treatment of dizziness, vestibulolitics (betahistine) are used. The effectiveness of antihistamines (promethazine, meclozine) has been proven in the case of a predominant lesion of the vestibular analyzer. Of great importance in the treatment of non-systemic dizziness is non-drug therapy. With its help, it is possible to restore coordination of movements and improve gait. Therapy of psychogenic dizziness should be carried out in conjunction with psychotherapist (psychiatrist), as in some cases it may be necessary to prescribe anxiolytics, antidepressants and anticonvulsants.

Prognosis for dizziness

It is known that an attack of dizziness is often accompanied by a feeling of fear, but dizziness, as a condition, is not life-threatening. Therefore, in the case of timely diagnosis of the disease that caused dizziness, as well as its adequate therapy, in most cases the prognosis is favorable.

G dizziness is one of the symptoms most commonly encountered in medical practice. Among the reasons for visiting doctors of all specialties, it is 2-5%.

The cause of dizziness is an imbalance of sensory information coming from the main afferent systems that provide spatial orientation - vestibular, visual and proprioceptive. Violations of the central processing of information and the efferent link of the motor act are also of great importance. In addition, the pathology of the musculoskeletal system plays a certain role.

In most cases dizziness is based on one of the following conditions : peripheral vestibular disorders, multiple sensory impairment, psychogenic causes, circulatory disorders in the brain stem, other diseases of the central nervous system, cardiovascular diseases. A combination of several reasons is possible.

As "dizziness", patients can describe a wide variety of sensations, so the primary diagnostic task is to clarify the nature of the patient's complaints. They can generally be classified into one of four clinical types of vertigo.

Systemic or vestibular vertigo - a sensation of rotation, falling, tilting or rocking of one's own body or surrounding objects. Often accompanied by nausea, vomiting, hyperhidrosis, impaired hearing and balance, as well as oscillopsia (the illusion of fast small-amplitude oscillations of surrounding objects). Systemic vertigo is characteristic of lesions of the vestibular system, both peripheral and central.

Pre-fainting state . Patients note a feeling of lightheadedness, impending loss of consciousness, "lightness" in the head. Often combined with pallor of the skin, palpitations, fear, darkening of the eyes, nausea, increased sweating. The most common causes are heart disease and orthostatic hypotension.

In some cases, by "dizziness" patients mean imbalance . There is instability, unsteadiness when walking, a "drunk" gait. A combination with paresis, sensitivity disorders, discoordination and oscillopsia is characteristic. Symptoms due to imbalance are noted when standing and walking and are absent when sitting and lying down.

For psychogenic dizziness , observed, in particular, in the framework of anxiety, conversion disorders or depression, characterized by hard-to-describe sensations that do not correspond to previous types of dizziness. Patients may complain of "fog", "heaviness" in the head, a feeling of intoxication, lightheadedness. It should be noted that similar vague symptoms may occur in the early stages or in the atypical course of organic diseases.

Along with the clinical type of dizziness, its course, the presence of provoking factors and concomitant symptoms are of diagnostic importance. A single episode of systemic dizziness is most often caused by a stem or cerebellar stroke. Repeated attacks of dizziness can develop both for no apparent reason, and in connection with certain provoking factors. Spontaneous attacks of dizziness, not provoked by sudden movements of the head, as a rule, serve as a manifestation of arrhythmias, transient ischemic attacks (TIA) in the vertebrobasilar basin, Meniere's disease, or epileptic seizures. Recurrent attacks of vertigo, in which provoking factors (changes in body position, head turns) are identified, are most often caused by benign paroxysmal positional vertigo (BPPV) or syncope, in particular, orthostatic.

Systemic dizziness

The most common cause of systemic vertigo is BPPV. The disease usually develops after middle ear infections, traumatic brain injury, or otologic surgery. Short-term (no more than 1 min) attacks of systemic dizziness that occur when the body position changes are characteristic. In the pathogenesis of BPPV, cupulolithiasis plays a leading role - the formation of a clot of calcium carbonate crystals in the cavity of the semicircular tubule, which leads to an increase in the sensitivity of the receptors of the semicircular tubules. Test for positional vertigo Nilena-Barani . From a sitting position, the patient quickly lies on his back, while his head should be thrown back by 45 ° and turned to the side by 45 °. The position is maintained for 30-40 seconds. The test is repeated with the head position in the midline and when turning in the opposite direction. The development of positional vertigo and nystagmus confirms the diagnosis. Isolated positional nystagmus also testifies in favor of DPPG - when the eyeballs are fixed in the middle position, the nystagmus is vertically rotatory, with a fast phase directed upwards and towards the underlying ear. When looking in the direction of the underlying ear, the fast phase of nystagmus is directed in the same direction, the nystagmus is horizontal-rotary, when looking in the opposite direction, it is vertical, beating upwards. A latent period (30-40 seconds) between the start of the test and the onset of nystagmus is characteristic. The extinction of nystagmus during the repetition of the test is characteristic. Positional nystagmus is observed intermittently, more often during an exacerbation. BPPV must be differentiated from central positional vertigo and nystagmus, the most common causes of which include spinocerebellar degeneration, brainstem tumors, Arnold-Chiari anomaly, and multiple sclerosis. Central positional nystagmus does not have a latent period, its duration exceeds 1 min, the direction of nystagmus may vary, often the nystagmus is vertical and does not fade with repeated examination. For the treatment of BPPV, exercises are used to move calcium carbonate crystals from the semicircular tubule into the cavity of the elliptical sac. It is also effective to repeatedly provoke dizziness, which leads to its gradual regression due to central compensation.

The combination of systemic dizziness with focal neurological symptoms is characteristic of circulatory disorders in the vertebrobasilar system, as well as tumors of the cerebellopontine angle and posterior cranial fossa. With vertebrobasilar insufficiency, dizziness usually develops suddenly and persists for several minutes, often accompanied by nausea and vomiting. As a rule, it is combined with other symptoms of ischemia in the vertebrobasilar basin. Early stages of vertebrobasilar insufficiency may present with episodes of isolated systemic vertigo. Longer episodes of isolated systemic vertigo are indicative of other disorders, in particular peripheral vestibular disorders. Along with systemic dizziness, TIAs and strokes in the vertebrobasilar basin can also be manifested by imbalance.

Systemic dizziness, nausea and vomiting are the earliest symptoms of ischemia in the basin of the anterior inferior cerebellar artery , leading to the development of a heart attack of the caudal tegmentum of the pons (lateral inferior pons syndrome, Gasperini's syndrome). Similar symptoms are observed in cerebellar infarction. Such symptoms require a differential diagnosis with peripheral vestibular disorders. With damage to the cerebellum, in contrast to damage to the labyrinth, the fast component of nystagmus is directed towards the focus. Its direction varies depending on the direction of gaze, but nystagmus is most pronounced when looking towards the lesion. Fixing the gaze on any object does not affect nystagmus and dizziness. In addition, there is discoordination in the limbs, which is absent in the defeat of the labyrinth.

Acute systemic vertigo, either alone or in combination with suddenly developed deafness, is characteristic of labyrinth infarction . Deafness caused by labyrinth infarction is usually irreversible, while the severity of vestibular disorders gradually decreases. Perhaps a combination of infarction of the labyrinth and the trunk.

Systemic vertigo is a cardinal symptom of peripheral vestibular disorders . The most important sign that allows differentiating peripheral vestibular disorders from central ones is nystagmus - most often horizontal, directed to the side opposite to the lesion and aggravated when looking in the same direction. In contrast to the central lesion, gaze fixation reduces nystagmus and vertigo.

Acute development of systemic dizziness in combination with nausea and vomiting is characteristic of viral neurolabyrinthitis (vestibular neuronitis, vestibular neuritis). Symptoms usually regress within a few days, in severe cases - after 1-2 weeks. As a rule, symptoms develop 1-2 weeks after a respiratory infection.

Meniere's disease manifested by repeated episodes of severe systemic dizziness, accompanied by hearing loss, a feeling of fullness and noise in the ear, nausea and vomiting. In a few minutes, dizziness reaches a maximum and gradually, over several hours, disappears. Hearing impairment in the early stages of the disease regresses completely, and then becomes irreversible. Within a few days after the attack of Meniere's disease, imbalances may be noted. The first attacks of the disease can be manifested by isolated systemic dizziness. Audiometry is performed to confirm the diagnosis. Hearing loss is more than 10 dB at two different frequencies. The cause of Meniere's disease is recurrent edema of the labyrinth, which develops as a result of a rupture of the membrane separating the endolymph from the perilymph.

Treatment

Treatment of systemic dizziness is largely determined by its cause, in addition, symptomatic therapy plays an important role. Specific treatment for systemic vertigo is known only for a limited range of diseases. Dizziness in the framework of vertebrobasilar insufficiency requires an appointment antiplatelet agents (acetylsalicylic acid 75-330 mg / day, ticlopidine 500 mg / day), and with an increase in symptoms - anticoagulants. With viral neurolabyrinthitis, symptomatic therapy is carried out. The effectiveness of antiviral drugs and glucocorticoids has not been proven.

Treatment of attacks of Meniere's disease is symptomatic. Most effective betahistine . For prevention, a low-salt diet and diuretics are prescribed.

For symptomatic treatment of systemic vertigo, vestibulolytic agents are used that act on vestibular receptors or on central vestibular structures, mainly vestibular nuclei. The first ones are antihistamines : meclozine is prescribed 12.5-25 mg orally 4 times a day, promethazine - 25-50 mg orally, intramuscularly or rectally 4-6 times a day. Have a central vestibulolytic effect benzodiazepines : oxazepam - 10-15 mg orally 4 times a day, diazepam - 5-10 mg orally, intramuscularly or intravenously 4-6 times a day. Also used is a histamine receptor stimulant betahistine - 8-16 mg orally 2-3 times a day, calcium antagonists (cinnarizine 25-50 mg orally or intramuscularly 4 times a day, flunarizine 10 mg per day in the afternoon).

An effective remedy for the treatment of dizziness is a combination drug Phezam containing 400 mg of piracetam and 25 mg of cinnarizine. The action of the drug is complex, including vasoactive and metabolic effects. The combination of two components in the preparation leads to an increase in their therapeutic effect without increasing toxicity. In addition, Phezam was noted to be more effective and tolerable compared to the separate administration of its components.

In a number of double-blind, placebo-controlled studies, Phezam has been shown to be highly effective in systemic vertigo caused by both central and peripheral vestibular disorders. The drug also reduced the severity of dizziness in the pre-syncope state. Phezam is effective in patients with chronic cerebrovascular insufficiency, in whom a significant improvement in cognitive functions was noted during treatment. The drug is prescribed 2 capsules 3 times a day for 3-6 weeks.

For relief of nausea and vomiting prescribe prochlorperazine 5-10 mg orally or intramuscularly 4 times a day, 25 mg rectally once a day or metoclopramide - 5-50 mg orally, intramuscularly or intravenously 4-6 times a day. Thiethylperazine has a central vestibulolytic and antiemetic effect. Assign 6.5 mg orally, rectally, s / c, / m or / in 1-3 times a day. A combination of antihistamines and benzodiazepines is effective. To reduce the sedative effect of vestibulolytic agents, the appointment of methylphenidate hydrochloride 5 mg orally 2 times a day (in the morning) is recommended. Vestibulolytic agents should be prescribed only for acute systemic vertigo. Their reception should be as short as possible, since long-term use slows down the process of central defect compensation.

The main principle of rehabilitation for peripheral vestibular disorders is stimulation of central compensation by repeated stimulation of vestibular receptors. It is necessary to start rehabilitation as early as possible. With damage to the central vestibular structures, rehabilitation is much less effective.

imbalance

One of the causes of imbalance is chronic vestibular dysfunction. Characterized by an increase in symptoms in the dark, when it is impossible to compensate for the defect with the help of vision. Often there is oscillopsia, possibly a combination with hearing loss. The most common cause of chronic bilateral labyrinth damage is the use of ototoxic drugs. The aggravation of imbalance in the dark is also characteristic of disorders of deep sensitivity. The most pronounced imbalances develop in cerebellar disorders. Visual control does not affect the severity of symptoms. With damage to the flocculonodular parts of the cerebellum, oscillopsia is often noted, as well as nystagmus, depending on the direction of gaze. Disorders of cervical proprioception also serve as one of the mechanisms of imbalance. The causes of imbalance caused by changes in the efferent link of the motor act include multiple subcortical infarctions, normotensive hydrocephalus, Parkinson's disease, chronic subdural hematoma, tumors of the frontal lobes, as well as a number of drugs - anticonvulsants (difenin, phenobarbital, finlepsin), benzodiazepines, antipsychotics ( phenothiazines, haloperidol), lithium preparations. Balance imbalance is a characteristic symptom of tumors of the cerebellopontine angle, temporal bone, and posterior cranial fossa. Systemic dizziness is much less common in this pathology. In the vast majority of cases, concomitant neurological symptoms are detected. In addition, one of the causes of imbalance, observed mainly in the elderly, is multiple sensory impairment - a combination of mild disorders of several sensory functions. Violations of the central integration of sensory information play a certain role in its development.

Psychogenic dizziness

Psychogenic dizziness is most common in agoraphobia, depression and panic attacks, and also, usually in the form of pre-syncope, is a manifestation of hyperventilation syndrome. With dizziness of an organic nature, it is also possible to develop restrictive behavior, in particular, secondary agoraphobia or reactive depression. In some cases, both a combination of episodes of organic and psychogenic dizziness, and the development of dizziness of mixed genesis are observed. Treatment is determined by the nature of the underlying disorder. Psychotherapy is of great importance. It is necessary to explain to the patient the essence of his disorders, since often an additional psycho-traumatic factor is the belief that there is a life-threatening disease.

References can be found at http://www.site

Piracetam + Cinnarizine -

Phezam (trade name)

(Balkanpharma)

Robert B. Daroff

Dizziness is a fairly common and often distressing symptom. Patients use this term to describe a variety of sensations (eg, lightness in the head, weakness, whirling, lightness of thought), although some of them do not fit this definition at all, such as blurred vision, blindness, headache, tingling, "walking on cotton legs, etc. Moreover, some patients with gait disorders will describe their difficulties as dizziness. It is necessary to carefully take a history to determine exactly which of the patients who tell the doctor that they are dizzy is actually experiencing this condition.

After excluding sensations such as blurred vision, dizziness can be either a feeling of weakness (similar to the sensations preceding fainting), or systemic dizziness (an illusory sensation of movement of surrounding objects or the body). In other cases, none of these definitions gives an accurate description of the patient's symptoms, and only when spasticity, parkinsonism, or another cause of gait disturbance is detected on neurological examination do the main sources of complaints become clear. For clinical purposes, dizziness is divided into four categories: syncope; systemic dizziness; various mixed sensations from the head and gait disturbances.

Fainting state. Fainting (syncope) is called loss of consciousness due to ischemia of the brain stem (see Chapter 12). Before the development of true syncope, prodromal signs (feeling of weakness) are often noted, reflecting ischemia in a degree not sufficient for loss of consciousness. The sequence of symptoms is fairly uniform and includes an increasing feeling of lightness in the head, partial or complete loss of vision, and heaviness in the legs, increasing to postural unsteadiness. Symptoms increase until loss of consciousness occurs or ischemia is eliminated, for example, the patient is placed in a horizontal position. True systemic vertigo almost never develops during presyncope.

The causes of fainting are described in Chap. 12 and include decreased cardiac output of various etiologies, postural (orthostatic) hypotension, and syncope-like conditions such as vertebrobasilar insufficiency and epileptic seizures.

Systemic dizziness. Systemic vertigo is the apparent movement of surrounding objects or one's own body. Most often, it is manifested by a sensation of rapid rotation around its axis, as a rule, due to damage to the vestibular analyzer. The peripheral part of the vestibular analyzer, located in the bony labyrinth of the inner ear, consists on each side of three semicircular canals and the otolith apparatus (elliptical and spherical sacs). The semicircular canals convert angular acceleration, while the otolithic apparatus converts rectilinear acceleration and static gravitational forces, which provide a sense of head position in space. From the peripheral section, information is transmitted through the VIII pair of cranial nerves to the vestibular nuclei of the brain stem. The main projections from the vestibular nuclei go to the nuclei of the III, IV and VI cranial nerves, the spinal cord, the cerebral cortex and the cerebellum. The vestibulo-ocular reflex serves to maintain constancy of vision during head movements and depends on direct projections from the vestibular nuclei to the nucleus of the VI cranial nerve (abducens) in the bridge and through the medial longitudinal bundle to the nuclei of the III (oculomotor) and IV (trochlear) cranial nerves in the midbrain . These projections are responsible for nystagmus (repetitive movements of the eyeballs), which is an almost indispensable component of the disorder of vestibular functions. Vestibulospinal pathways help maintain a stable position of the body in space. Connections with the cerebral cortex through the thalamus provide awareness of body position and head movements. Vestibular nerves and nuclei are associated with formations of the cerebellum (mainly with a patch and a knot), which modulate the vestibulo-ocular reflex.

The vestibular analyzer is one of the three sensory systems responsible for spatial orientation and body position; the other two include the visual analyzer (from the retina to the occipital cortex) and the somatosensory system, which transmits information from the periphery from skin, joint and muscle receptors. These three stabilizing systems overlap each other sufficiently to compensate for the deficiency (partial or complete) of any of them. Dizziness can be the result of either physiological arousal or a pathological disturbance in the activity of any of these three systems.

Physiological dizziness. It develops in cases where there is a discrepancy between the three above-mentioned systems or the vestibular apparatus is subjected to unusual loads to which it has never been adapted, for example, with seasickness. The discrepancy between sensory systems explains the appearance of sensations of motion sickness when driving in a car, high-altitude dizziness, visual dizziness, most often occurring while watching movies with chase scenes, in the latter case, the visual sensation of the movement of surrounding objects is not accompanied by the corresponding vestibular and somatosensory motor signals. Another example of physiological dizziness is space sickness caused by the active movement of the head in zero gravity.

Pathological dizziness. Occurs as a result of damage to the visual, somatosensory or vestibular analyzers. Dizziness due to visual impairment occurs when wearing new or incorrectly selected glasses or when double vision occurs due to a sudden paresis of the muscles of the eyeball, in any case, as a result of the compensatory activity of the central nervous system, dizziness quickly stops. Somatosensory vertigo, which is more common in combination with other types of vertigo, usually occurs in the case of peripheral neuropathy with a decrease in the amount of sensitive information necessary to turn on the central compensatory mechanisms in cases where there is a violation of the activity of the vestibular or visual analyzers.

Most often, pathological dizziness develops as a result of a disorder of vestibular functions. Vertigo is often accompanied by nausea, clonic nystagmus, postural instability, and ataxia when walking.

Labyrinth defeat. Lesions of the labyrinth lead to the development of dizziness, giving the impression of rotation or linear movement of surrounding objects or one's own body, directed in the direction opposite to the lesion. The fast phase of nystagmus is also directed in the opposite direction to the focus, but there is a tendency to fall in the direction of the lesion.

In the case of a direct immobile position of the head, the peripheral parts of the vestibular analyzer generate resting tonic potentials with a frequency that is the same on both sides. With any rotational acceleration, due to the semicircular canals, there is an increase in potentials on the one hand and a compensatory weakening on the other. These changes in the activity of the potentials are transmitted to the cerebral cortex, where they are added to the information from the visual and somatosensory analyzers, and the corresponding conscious sensation of rotational movement is developed. After the cessation of prolonged rotation, the peripheral sections still continue to respond to inhibition for some time. A decrease in potentials below the resting level is noted on the side with an initial increase in activity and a corresponding increase on the other side. There is a sensation of rotation in the opposite direction. Since there was no true movement of the head, this apparent sensation must be considered vertigo. Dizziness is caused by any lesion of the peripheral part of the vestibular analyzer, which changes the frequency of potentials, leading to an unequal flow of signals to the brain stem and, ultimately, to the cerebral cortex. The symptom can be explained both in the form of inadequate interpretation by the cerebral cortex of pathological signals from the brain stem, and in the form of information about the movement of the head in space. Transient failure leads to short-term symptoms. With persistent unilateral damage, the central compensatory mechanisms eventually reduce the manifestations of dizziness. Since compensation depends on the plasticity of the connections between the vestibular nuclei and the cerebellum, in patients with damage to the brainstem and cerebellum, the compensatory ability is reduced and the symptoms may remain unchanged for an unlimited time. In the case of severe persistent bilateral lesions, recovery will always be incomplete, despite the fact that the cerebellar connections are preserved; patients with such lesions will feel dizzy constantly.

Acute unilateral damage to the labyrinth occurs with infectious diseases, trauma, ischemia and poisoning with drugs or alcohol. Often it is not possible to establish the etiology of the pathological process and the term acute labyrinth or, preferably, acute peripheral vestibulopathy is used to describe it. It is impossible to make a prediction about the further condition of the patient with the first attacks of dizziness.

Schwannomas that affect the vestibular nerve (acoustic neuroma) progress slowly and result in such a gradual decline in labyrinth function that central compensatory mechanisms usually prevent or minimize dizziness. The most common manifestations are hearing loss and tinnitus. Since dizziness can occur suddenly with damage to the brainstem or cerebellum, accompanying objective and subjective signs will help to differentiate them from lesions of the labyrinth (Table 14.1). Sometimes, with acute lesions of the vestibulo-cerebellar tract, dizziness may occur as the only symptom, which makes it difficult to distinguish it from labyrinthopathy.

Repeated unilateral dysfunctions of the labyrinth in combination with objective and subjective signs of cochlear damage (progressive hearing loss and sensation of tinnitus) usually occur with Meniere's disease. If hearing symptoms are absent, the term vestibular neuronitis is used to refer to recurrent dizziness as the only symptom. Transient ischemic attacks in the posterior medulla (vertebrobasilar insufficiency) almost never produce repeated attacks of vertigo without concomitant motor and sensory disorders, cerebellar dysfunction, or signs of cranial nerve damage.

Table 14.1. Differential diagnosis of peripheral and central vertigo

* In Meniere's disease, the direction of the fast phase changes.

Positional vertigo is aggravated by lying on your side. Benign paroxysmal positional vertigo (BPPV) is especially common. Although these disorders may be the result of traumatic brain injury, in most cases, provoking factors are not detected. The dizziness usually goes away on its own within a few weeks or months. Dizziness and accompanying nystagmus have a characteristic latent period, recurrence and end, which distinguishes them from the less common central positional vertigo (CPG) (Table 14.2) that occurs with lesions of the fourth ventricle region.

Positional vertigo should be distinguished from the installation. The latter is caused by the movement of the head in space rather than its position, and is an integral feature of all vestibulopathies, central and peripheral. Since dizziness is aggravated by sudden movements, patients try to keep their head still.

Vestibular epilepsy, dizziness associated with the presence of epileptic activity in the temporal lobe, is rare and almost always closely associated with other manifestations of epilepsy.

Psychogenic vertigo, usually combined with agoraphobia (fear of large open spaces, crowds of people), is inherent in patients who are so "failed" after an attack of dizziness that they cannot leave their home for a long time. Despite the inconvenience, most patients with dizziness of organic origin strive for vigorous activity. Vertigo should be accompanied by nystagmus. In the absence of nystagmus during an attack, dizziness is most likely psychogenic in nature.

Examination of patients with pathological vestibular vertigo. The nature of the examination is determined by the possible etiology of the disease. If there is suspicion of a central origin of dizziness (see Table 14.1), a computed tomography of the head is indicated. Particular attention should be paid to the formations of the posterior cranial fossa. Such an examination is rarely informative in the case of repeated isolated dizziness with no neurological symptoms at the time of examination. BPPV does not require further testing once the diagnosis has been made (see Table 14.2).

Table 14.2. Benign paroxysmal positional vertigo (BPPV) and central positional vertigo (CPV)

a - the time between the establishment of the position of the head and the appearance of symptoms; b - disappearance of symptoms while maintaining the adopted position; c - reduction of symptoms during repeated studies; d - the probability of reproducing symptoms during the examination.

Vestibular tests are used for the purpose of differential diagnosis of dizziness of organic and psychogenic etiology; establishing the localization of the lesion; conducting differential diagnosis of dizziness of peripheral and central origin. The standard test is electronystagmography (ENG) with irritation of the eardrums with warm and cold water (or air) and a comparison of the frequency of the slow phases of the resulting nystagmus on the right and left. Decreased speed on either side indicates hypofunction (“channel paresis”). The condition in which nystagmus cannot be induced by the action of ice water is defined as the “death of the labyrinth”. In some clinics, physicians are able to quantify various elements of the vestibulo-ocular reflex using computerized swivel chairs and accurately record the movements of the eyeballs.

In acute dizziness, bed rest should be prescribed, as well as drugs that suppress vestibular activity, such as antihistamines [meclicin (Meclizine), dimenhydrinate, diprazine], centrally acting anticholinergics (scopolamine) drugs, tranquilizers with a GABAergic effect (diazepam). In cases where vertigo persists for more than a few days, most authors recommend walking in order to bring about the beneficial effects of the central compensatory mechanisms, despite the fact that this may cause some temporary inconvenience to the patient. Chronic dizziness of labyrinthine origin can be treated with a course of systematic exercises that stimulate compensatory mechanisms.

Preventive measures taken to prevent recurrent attacks of dizziness have varying degrees of effectiveness. In these cases, antihistamines are usually used. In Meniere's disease, a salt-restricted diet combined with diuretics is recommended. With rare persistent (from 4 to 6 weeks) BPPV, a clear improvement, usually within 7-10 days, is noted after performing a special set of exercises.

There are many surgical treatments for all forms of persistent chronic and recurrent vertigo, but they are rarely necessary.

Mixed sensations in the head. This definition is used to characterize non-systemic vertigo that is not syncope or true vertigo. In cases where cerebral ischemia or vestibular disorders are of minor severity, there is a slight decrease in blood pressure or mild vestibular instability, sensations may occur other than obvious lightheadedness or dizziness, which could be correctly characterized using provocative tests. Other causes of this type of dizziness may be hyperventilation syndrome, hypoglycemia, and somatic manifestations of clinical depression. Neurological examination of such patients does not reveal any changes.

Gait disorders. In some cases, people with gait disorders complain of dizziness, despite the absence of systemic dizziness or other pathological sensations from the head. The causes of such complaints may be peripheral neuropathy, myelopathy, spasticity, parkinsonian rigidity, cerebellar ataxia. In these cases, the term vertigo is used to describe impaired mobility. There may be a feeling of lightness in the head, especially in the case of impaired sensitivity in the lower extremities, and weakening of vision; this condition is defined as dizziness due to multiple sensory disorders, and it occurs in elderly people who complain of dizziness only during walking. Motor and sensory disturbances due to neuropathy or myelopathy, or visual impairment due to cataracts or retinal degeneration, place an increased burden on the vestibular analyzer. A less accurate but more comforting term is benign fragility of aging.

Examination of patients with complaints of dizziness. The most important diagnostic tool is a carefully taken history, aimed at establishing the true meaning of the term "dizziness" in each case. Is this state of fainting? Is it accompanied by a sensation of whirling? If this is confirmed, and the neurological examination does not reveal pathological disorders, then appropriate examinations should be undertaken to identify possible causes of cerebral ischemia or damage to the vestibular analyzer.

Provocative tests are used to identify the source of dizziness. Such procedures reproduce signs of cerebral ischemia or vestibular insufficiency. These reasons are confirmed if dizziness occurs with orthostatic hypotension. Then a Valsalva test is performed, which reduces cerebral blood flow and provokes symptoms of cerebral ischemia.

The simplest provocative test is a quick rotation on a special swivel seat followed by a sudden stop of movement. This procedure always causes dizziness, which the patient can compare with his feelings. Intense provoked systemic vertigo may not look like spontaneous symptoms, but soon after the test, when the vertigo subsides, it is followed by a feeling of lightness in the head, which can be identified by the patient as the kind of vertigo that he feels. In such cases, a patient with an initial diagnosis of mixed head sensations is diagnosed with vestibulopathy.

Caloric tests are another way to provoke dizziness. The eardrum is irritated with cold water until dizziness occurs; then this sensation is compared with the patient's complaints. Since visual fixation suppresses the caloric reaction, before conducting a provocative caloric test (as opposed to a diagnostic quantitative thermal test with ENG), you should ask the patient to close his eyes or put on special glasses that interfere with fixing the gaze (Frenzel lenses). Patients with signs of positional dizziness should perform appropriate tests (see Table 14.2). Like provocative caloric tests, positional tests are more sensitive if gaze fixation is eliminated.

The last provocative test, requiring the use of Frenzel lenses, is vigorous shaking of the head in the supine position for 10 s. If nystagmus developed after shaking was stopped, then even in the absence of dizziness, this indicates a violation of vestibular functions. The test can then be repeated in an upright position. If, using provocative tests, it was established that dizziness is vestibular in nature, the above assessment of vestibular dizziness is carried out.

In many anxiety patients, the cause of dizziness is hyperventilation; however, they may not feel tingling in their hands and face. Patients with dizziness of unknown etiology and lack of neurological. symptomatology, a two-minute forced hyperventilation is indicated. Symptoms of depression (which the patient states are secondary to dizziness) indicate to the physician that depression is more often the cause than the effect of dizziness.

Injuries to the central nervous system can cause sensations of dizziness of all kinds. Therefore, a neurologic examination is always necessary, even if the history and provocation findings suggest a cardiac, peripheral vestibular, or psychogenic origin for the symptoms. Any changes detected on neurological examination should prompt physicians to conduct appropriate diagnostic tests.

Bibliography

Baloh R.W. Dizziness, Hearing Loss and Tinnitus: The Essentials of Neurology. -

Philadelphia: Davis, 1984. Brandt T., Daroff R. B. The multisensory physiological and pathological vertigo

syndromes. - Ann. Neurol., 1980, 7, 195. Hinchcliffe F.R. Hearing and Balance in the Elderly. - New York: Churchill

Livingstone, 1983, sect. II, 227-488. Leigh R. /., Zee D.S. The neurology of Eye Movements. - Philadelphia: Davis,

1984, Chaps 2 and 9. Oosterveld W.I. Vertigo - Current concepts in management. -Drugs, 1985,

Patients come to the polyclinic with a wide variety of complaints and symptoms, and among them, dizziness is the third most common reason for seeking medical help after headache and back pain. More than 80 diseases and pathological conditions have been described in which dizziness occurs, in 20% of cases there is a combination of several causes. That is why the outpatient service remains leading in this direction. Dizziness can be accompanied by various symptoms, vary in severity, duration, etc. All these parameters have their own diagnostic value and determine the treatment tactics and prognosis of the disease. In this guide, we have tried to structure and outline the main causes of dizziness, clinical and instrumental methods of high diagnostic value. Separately analyzed errors in the management of patients at the stage of the clinic. We hope that our book will help district physicians, general practitioners and neurologists in their daily work with this category of patients.

A series: Doctor of the highest category

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The following excerpt from the book Vertigo (A. L. Vertkin, 2017) provided by our book partner - the company LitRes.

Non-systemic dizziness

In the practice of the therapist, this type of dizziness is more common. It is also called non-vestibular or pseudo-vertigo.

The following provisions are characteristic of non-systemic dizziness:

✓ lack of connection with the defeat of the vestibular system;

✓ no hearing loss;

✓ negative vestibular tests;

✓ As a rule, nausea and vomiting are not observed.

NB! The main distinguishing feature of non-systemic vertigo is the absence of a sense of rotation.

To predisposing factors non-systemic dizziness include:

✓ arterial hypotension (usually orthostatic);

✓ asthenic conditions after acute infectious or somatic diseases;

✓ conditions associated with violations of the volume and quality of blood (anemia, acute blood loss, hypoproteinemia, hypovolemia, dehydration);

✓ cardiac arrhythmias (bradycardia, ventricular arrhythmias, tachycardia, atrial fibrillation, etc.);

✓ mechanical obstruction of venous return (for example, during pregnancy, tumors) and blood flow in the aorta (aortic stenosis), etc.;

✓ metabolic and hormonal disorders.

There are three types of non-systemic dizziness:

✓ lipothymic (pre-syncope) states associated with malnutrition of the visual analyzer, vestibular apparatus or proprioceptive mechanism;

✓ instability, manifested by imbalance and due to the mismatch of the activity of vestibular, proprioceptive and visual sensitivity at various levels of the nervous system;

✓ psychogenic dizziness.

Each type of non-systemic dizziness has its own clinical features.

So, swoon manifested by blurred consciousness, a feeling of "woolness" of the legs / body, ringing in the ears, the appearance of "flies" before the eyes, a decrease in blood pressure, a weak pulse, sweating, pallor, narrowing of the visual fields. There is a premonition of an imminent fall and loss of consciousness, which often ends in fainting.

There are many reasons for causing lipothymic conditions. Lipothymia can also be physiological in nature and occur in healthy people. An example of this is the "syndrome of Turgenev young ladies" described in the literature in honor of the typical heroines of the works of I. S. Turgenev, who often fainted according to the plots of the writer's novels.

Pathological dizziness in the structure of syncope is of two types: neurogenic and somatogenic. This division is fundamentally important, since the therapeutic tactics are fundamentally different.

Neurogenic syncope: vasodepressor (vasovagal, vasodepressor syncope), provoked by various stressful influences (expectation of pain, type of blood, fear, stuffiness, etc.); psychogenic, hyperventilatory, carotid, cough, nocturic, hypoglycemic and orthostatic syncope.

Somatogenic syncope occurs in the following pathological conditions:

✓ asthenia after infections, against the background of anemia;

✓ fever and heat stroke;

✓ hypotension and accompanying asthenia;

✓ pregnancy;

✓ hypoglycemia (for example, with an overdose of insulin and other hypoglycemic agents in patients with diabetes mellitus or insulinoma);

✓ cardiac pathology (ventricular arrhythmias, tachycardia, fibrillation, with "low cardiac output syndrome", namely, with obstructed aortic blood flow with aortic stenosis, etc.);

✓ atherosclerotic vascular lesions (stenosis of the carotid and vertebral arteries);

✓ in the structure of brainstem ischemia, for example, in transient ischemic attack;

✓ Unterharnscheidt's syndrome (attacks of loss of consciousness when turning the head or in a certain position);

✓ drop attacks (attacks of sudden sharp weakness in the legs, which are not accompanied by loss of consciousness).

It should be remembered that lipothymic conditions do not necessarily pass into syncope. It depends on the speed and degree of the fall in blood pressure, since this type of dizziness in the vast majority of cases is associated with orthostatic hypotension, which accompanies many diseases.

In addition, dizziness accompanies orthostatic hypotension in the structure of peripheral autonomic failure ( postural hypotension), which may be of primary or secondary (somatogenic) origin.

Primary peripheral autonomic failure is a neurological pathology (idiopathic orthostatic hypotension, Shy-Drager syndrome, multiple system atrophy), which has a progressive chronic course.

Secondary peripheral autonomic failure has an acute course and develops against the background of amyloidosis, diabetes mellitus, alcoholism, chronic renal failure, porphyria, bronchial carcinoma, Addison's disease, the use of ganglionic blockers, tranquilizers, antihypertensive drugs and dopaminometics (nakom, madopar, dopaminergic receptor agonists), etc.

Non-systemic dizziness in menopausal women is combined with somatic manifestations (headaches, paresthesias, sweating, tachycardia, dyspepsia, flatulence, thermoregulatory disorders) and mental disorders, such as causeless anxiety, irritability, sleep disturbances and fatigue.

Unsteadiness and a feeling of dizziness also occur as a result of an imbalance associated with damage to the parts of the nervous system that provide spatial coordination. Swinging, staggering, stumbling, sensations of "like they were pushed" are characteristic.

Balance disorders can be caused by damage to the cerebellum, subcortical nuclei, brain stem. In the elderly, multisensory deficits may be a common cause of this type of vertigo. Congenital anomalies in the development of the brain (Arnold-Chiari syndrome), injuries of the cervical spine can cause dizziness. Other causes of balance and gait disturbance (dysbasia) may be paretic, ataxic, hyperkinetic, akinetic, apraxis or postural disorders.

Thus, dizziness in violation of balance and coordination can be due to the following reasons:

✓ deep sensitivity disorders ( sensitive ataxia) with damage to the conductors of deep sensitivity in the spinal cord (funicular myelosis, neurosyphilis) or in peripheral nerves (polyneuropathy). A hallmark of sensitive ataxia is increased impairment with loss of visual control (eyes closed and in the dark);

✓ cerebellar ataxia, developing as a result of damage to the cerebellum or its connections (with multiple sclerosis, cerebellar, spinocerebellar degenerations, volumetric processes, etc.). Visual control does not affect the severity of cerebellar ataxia. In addition, when performing coordinating tests, in contrast to vestibular ataxia, intentional trembling appears;

✓ extrapyramidal disorders (hyperkinesis in Huntington's chorea, cerebral palsy, torsion dystonia and other diseases, as well as Parkinson's disease and parkinsonism syndrome);

✓ hemiparesis due to cerebral strokes and other organic diseases of the brain. A feeling of dizziness can occur in some people who put on glasses or contact lenses for the first time, especially when they are unsuccessfully fitted. As a possible cause of dizziness, astigmatism, cataracts, and even oculomotor disorders are described, which leads to a violation of the projection of objects on the retina and the “drawing up” of an incorrect picture in the brain.

Psychogenic(psychophysiological) dizziness can manifest itself after strong emotional experiences or due to severe fatigue. At the same time, a person feels ambiguity in the head and a feeling of instability. In other cases, it occurs in a specific situation (for example, when visiting a store, traveling by public transport, crossing a bridge, in an empty room, or at a concert) and is included in the structure of the phobic syndrome:

✓ acrophobia(Fear of heights);

End of introductory segment.