Symptoms of dizziness is largely determined by the level of damage (peripheral or central parts of the vestibular analyzer, other parts of the nervous system) and associated concomitant neurological symptoms. To establish the location of the lesion and its nature, a thorough analysis of the clinical picture, the characteristics of dizziness, and consideration of accompanying symptoms are necessary. Thus, systemic dizziness, which occurs as a result of damage to the vestibular analyzer, in 2/3 of cases can be accompanied by a feeling of tinnitus and autonomic disorders.
Systemic dizziness
Systemic dizziness is observed in 30-50% of all patients who complain of dizziness, and its frequency increases with age. Its causes are varied, the most common of which are Meniere’s disease, neuroma of the VIII pair of cranial nerves, benign paroxysmal positional vertigo, vestibular neuronitis. A correct assessment of anamnestic information and the results of a clinical examination make it possible in 90% of cases to make a correct assumption about the nature of the disease after the first examination of the patient.
Benign paroxysmal positional vertigo
Benign paroxysmal positional vertigo (BPPV) is the most common cause of systemic vertigo. In Western European countries, the prevalence of BPPV in the general population reaches 8% and increases with age. The basis of this disease is cupulolithiasis – the formation of calcium carbonate aggregates in the cavity of the semicircular canals, which have an irritating effect on the receptors of the vestibular analyzer. It is characterized by short-term (up to 1 minute) episodes of intense dizziness that occur when the head position changes (moving to a horizontal position, turning in bed). At the same time, the patient often experiences nausea and other autonomic disorders (hyperhidrosis, bradycardia). Upon examination, horizontal or horizontal-rotatory nystagmus is revealed, the duration of which corresponds to the duration of dizziness. The distinctive features of BPPV are the stereotypical nature of attacks, their clear connection with the position of the head, greater severity in the morning and a decrease in the second half of the day. An important distinguishing feature is the absence of focal neurological deficits, tinnitus and hearing impairment.
Vestibular neuronitis
Vestibular neuronitis is characterized by episodes of acute dizziness lasting from several hours to a day (sometimes more). The disease occurs acutely, much less often – subacutely, usually after a viral or bacterial infection, less often – intoxication. People aged 30-35 years become ill more often. Dizziness is intense, with pronounced autonomic disorders. Characteristic features are preserved hearing and the absence of meningeal and focal neurological symptoms.
Post-traumatic vertigo
Post-traumatic dizziness occurs immediately after a head injury, while meningeal syndrome, as well as focal symptoms of damage to the brain and cranial nerves, may be absent. This clinical picture suggests an acute traumatic injury to the labyrinth itself. Much less often, dizziness occurs a few days after the injury, which presumably may be associated with the formation of serous labyrinthitis. In some patients, head trauma with damage to the vestibular apparatus can lead to the development of cupulolithiasis, manifesting itself as BPPV syndrome. In many patients, the psychogenic component of dizziness is important.
Toxic damage to the vestibular apparatus
Toxic damage to the vestibular apparatus can develop with the use of aminoglycosides, which differ in their ability to accumulate in the endo- and perilymph. It should be noted that if gentamicin more often leads to damage to the vestibular apparatus, then aminoglycosides such as tobramycin and kanamycin more often cause hearing impairment due to damage to the cochlea. The toxic effects of aminoglycosides lead to the development of progressive systemic dizziness in combination with impaired motor coordination. When prescribing drugs from this group, it should be taken into account that they are excreted primarily by the kidneys. The ototoxic effect of aminoglycosides is usually irreversible.
Meniere’s disease
Meniere’s disease is characterized by repeated attacks of intense systemic dizziness, noise, tinnitus, severe autonomic disorders and fluctuating hearing loss. The basis of these manifestations is hydrops – an increase in the volume of endolymph, causing stretching of the walls of the labyrinth canals. The process is often idiopathic in nature, less often develops as a result of an infectious disease or intoxication. The onset occurs at the age of 30-40 years, women are affected somewhat more often. Attacks of dizziness last from several minutes to 24 hours with a frequency from once a year to several times a day. They are often preceded by a feeling of stuffiness in the ear, heaviness, noise in the head, lack of coordination, etc. During an attack, severe imbalances and autonomic disorders are observed. After the end of an attack of systemic dizziness, the patient may experience instability when walking and coordination problems for from several hours to several days. Characteristic is early hearing loss, usually unilateral, progressing over time, but complete hearing loss is not observed. Spontaneous remissions are possible, the duration of which decreases as the disease progresses.
Vertebro-basilar insufficiency
During transient ischemic attacks in the vertebral-basilar system, a reversible dysfunction of the formations of the brain stem, cerebellum and other structures supplied by the branches of the vertebral and basilar arteries occurs. Transient ischemic attacks occur against the background of impaired patency of the vertebral or main arteries, caused primarily by atherosclerotic stenosis, less often by inflammatory diseases (arteritis), vascular aplasia, extravasal compression (for example, with trauma to the cervical spine). An important cause is damage to small-caliber arteries due to arterial hypertension, diabetes mellitus, or a combination of both. Transient ischemic attacks in the vertebrobasilar system can be precursors of stroke with persistent residual effects.
Among the causes of dizziness, cerebrovascular disorders account for 6%. The direct cause of dizziness may be damage to the labyrinth itself due to impaired blood circulation in the vascularization zone a. auditiva, and lesions in the area of the brain stem, cerebellum, and conduction systems of the cerebral hemispheres. The vast majority of patients with vertebrobasilar insufficiency also exhibit other neurological symptoms (damage to the cranial nerves, conduction motor, sensory disorders, visual, static-coordination disorders). Dizziness as the only manifestation of vascular pathology of the brain is observed extremely rarely, although it is possible with acute occlusion of the auditory artery, the anterior inferior cerebellar artery. In such cases, further diagnostic testing is necessary to exclude other causes of dizziness. Episodes of paroxysmal dizziness that occur when changing the position of the head should not be associated with compression of the vertebral arteries by the changed cervical vertebrae: the vast majority of these cases are BPPV.
Volumetric processes
Systemic vertigo can be caused by a tumor of the cerebellopontine angle, brain stem, cerebellum, usually a neuroma of the VIII cranial nerve; less commonly, cholesteatoma, meningioma or metastases are detected in this area. Over a certain period of time, vestibular disorders may be the only clinical manifestation of the disease, preceding hearing disorders, and the systemic nature of dizziness is observed only in half of the cases. In some cases, the cause of dizziness may be tumors of the cerebellum or cerebral hemispheres, causing compression of the frontopontine and temporopontine tracts.
temporal lobe epilepsy
Repeated stereotypical unprovoked episodes of systemic dizziness, accompanied by severe autonomic symptoms (feelings of heat, epigastric pain, nausea, hyperhidrosis and hypersalivation, bradycardia), may be a manifestation of temporal lobe epilepsy. The clinical picture of a seizure may include visual hallucinations and other perceptual disturbances.
Migraine
It is possible to develop dizziness as an aura preceding a migraine attack. Diagnostic difficulties arise if the headache attack itself is absent or occurs in a reduced form.
Evidence has been obtained of a higher incidence of migraine in families with BPPV.
Demyelinating diseases
Dizziness is often observed in patients with demyelinating lesions of the central nervous system, primarily with multiple sclerosis. The characteristic remitting course of the disease, multifocal lesions, and examination results make it possible to recognize the nature of the pathological process. Diagnostic difficulties may arise if dizziness occurs at the onset of the disease, in the absence or moderate severity of other symptoms of damage to the brain stem and cerebellum. Dizziness in patients with demyelinating lesions of the nervous system can be of a mixed nature and characterized by a persistent course.
Encephalitis
Damage to the vestibular analyzer at the level of the brain stem and cerebellum is possible with inflammatory lesions of the brain – encephalitis. A distinctive feature is the single-phase nature of the disease with acute or subacute onset and stabilization or gradual regression of symptoms. Along with vestibular disorders, the patient is also diagnosed with other signs of damage to the nervous system.
Developmental anomalies of the cervical spine and skull base
Dizziness, often of a mixed nature, can occur in patients with developmental anomalies of the cervical spine and base of the skull (platybasia, basilar impression, Arnold-Chiari syndrome), as well as with syringomyelia (syringobulbia). The mechanisms of dizziness in this situation are complex and diverse; often their connection with developmental defects is not obvious and can be mediated by vertebrobasilar insufficiency and vestibular dysfunction.
Unsystematic dizziness
Balance disorders
Balance disorders can be caused by a complex of reasons, including dysfunction of the vestibular analyzer of various origins. An important distinguishing feature is the deterioration of the patient’s condition with his eyes closed, when vision control is lost. With damage to the cerebellum, on the contrary, vision control is not accompanied by a decrease in the severity of ataxia. Balance disturbances are observed in patients with damage to the subcortical nuclei and brain stem (neurodegeneration, intoxication, consequences of traumatic, inflammatory, vascular disease, hydrocephalus). The cause of the disorder may also be a multisensory deficit – a violation of the receipt and processing of impulses from vestibular, visual, and proprioceptive receptors. Balance disturbances are possible with a lack of information, in particular from proprioceptors (polyneuropathy), with damage to the posterior columns of the spinal cord (tabes dorsalis, myelopathy). The resulting ataxia cannot be corrected by vision control. Balance disorders, combined with non-systemic dizziness, often occur during the use of certain medications (benzodiazepines, phenothiazine derivatives, anticonvulsants). Dizziness is usually accompanied by increased drowsiness and impaired concentration, the severity of which decreases with decreasing dosage of drugs.
Presyncope
Non-systemic dizziness within the framework of pre-fainting (lipothymic) states is manifested by a feeling of lightheadedness, instability, loss of balance. “darkening in the eyes”, ringing in the ears. These conditions may precede the development of fainting, but a complete loss of consciousness may not occur. Severe emotional disorders are characteristic – a feeling of restlessness, anxiety, fear or, conversely, depression, powerlessness, and a sharp loss of strength.
Most often, such conditions occur with a decrease in systemic blood pressure (hypersensitivity of the sinus node, vasovagal syncope, orthostatic syncope, paroxysmal disturbances of heart rhythm and conduction). Many antihypertensive drugs, anticonvulsants (carbamazepine), sedatives (benzodiazepines), diuretics, drugs can cause lipotimic states Levodopa. The likelihood of dizziness increases when combining drugs, using them in high doses, in elderly patients, as well as against the background of concomitant somatic pathology. Pre-syncope and fainting conditions can also be caused by disturbances in the biochemical and cytological composition of the blood (hypoglycemia, anemia, hypoproteinemia, dehydration).
Psychogenic dizziness
Psychogenic dizziness is often associated with agoraphobia, neurogenic hyperventilation. Dizziness is one of the most common complaints made by patients with psychogenic disorders (depressive states, hypochondriacal syndrome, hysteria). Dizziness is one of the most common symptoms of panic attacks. A common form of psychogenic disorders of the vestibular apparatus is phobic positional vertigo, which is characterized by a feeling of instability, unsteadiness of the floor underfoot, subjective disturbances in walking and coordination of movements in the limbs in the absence of objective signs of ataxia and satisfactory performance of coordination tests. Psychogenic dizziness is characterized by persistence and expressed emotional overtones. Anxiety disorders can also develop over time in patients with true vestibular vertigo, which can lead to the formation of restrictive behavior in the patient.