What causes dizziness?

The diagnostic search for complaints of dizziness begins with a thorough analysis of the complaints themselves. Complaining of dizziness, the patient usually means one of three sensations: "true" dizziness, which is recommended to include systemic (rotational, circular) dizziness; a state of "faintness" in the form of a feeling of general weakness, nausea, discomfort, cold sweat, a premonition of an imminent fall and loss of consciousness, and, finally, the third type of dizziness implies sensations that are difficult to describe in words, sometimes arising during the patient's movement due to impaired coordination of movements, body instability, gait disorders of various types, visual and vision disorders, etc.

All three types of completely different sensations are designated by patients with one word - "dizziness", but behind each of them there are different neurological syndromes leading to different series of diseases. The first type of dizziness is called vestibular and is accompanied by a characteristic vestibular symptom complex; the second type of dizziness is typical for lipothymic states and fainting of various origins (non-systemic dizziness); the third type of dizziness is less often the cause of diagnostic difficulties and reflects visual-vestibular, postural, aprakto-ataxic and other similar disorders of ambiguous, often mixed nature. So-called psychogenic dizziness stands apart.

Main causes of dizziness

Systemic (vestibular) dizziness:

1. Benign positional vertigo.
2. Vestibular neuronitis.
3. Meniere's disease.
4. Herpetic lesion of the intermediate nerve.
5. Intoxication.
6. Infarction, aneurysm or brain tumor of various locations (cerebellum, brainstem, cerebral hemispheres).
7. Vertebrobasilar insufficiency.
8. Traumatic brain injury and post-concussion syndrome.
9. Epilepsy.
10. Labyrinthitis or labyrinthine infarction.
11. Multiple sclerosis.
12. Dysgenesis (platybasia, Arnold-Chiari syndrome and other craniovertebral anomalies).
13. Syringobulbia.
14. Other diseases of the brain stem.
15. Constitutionally determined vestibulopathy.
16. Arterial hypertension.
17. Diabetes mellitus.

Non-systemic dizziness in the picture of a lipothymic state:

1. Vasodepressor (vasovagal) syncope.
2. Hyperventilation syncope.
3. Carotid sinus hypersensitivity syndrome.
4. Cough syncope.
5. Nocturic syncope.
6. Hypoglycemic syncope.
7. Orthostatic hypotension of neurogenic (primary peripheral autonomic failure) and somatogenic origin (secondary peripheral autonomic failure).
8. Orthostatic circulatory disorders in diseases of the heart and blood vessels (aortic stenosis, ventricular arrhythmia, tachycardia, fibrillation, etc.).
9. Sympathectomy.
10. Arterial hypertension.
11. Diabetes mellitus.
12. Ischemia in the brainstem region.
13. Anemia, acute blood loss, hypoproteinemia.
14. Dehydration.
15. Pregnancy.

Dizziness of mixed or unspecified nature:

1. Dizziness associated with pathological processes in the neck area (Unterharnscheidt syndrome, platybasia, Arnold-Chiari syndrome, “posterior cervical sympathetic syndrome”, “whiplash” injuries, myofascial pain syndromes of the cervical localization).
2. Dizziness with certain visual impairments and oculomotor disorders (incorrectly selected glasses, astigmatism, cataracts, paresis of the oculomotor nerves, etc.).
3. Drug intoxication (apressin, clonidine, trazicor, visken, aminocaproic acid, lithium, amitriptyline, sonapax, diphenin, phenobarbital, finlepsin, nacom, madopar, parlodel, mirapex, brufen, voltaren, phenibut, insulin, lasix, ephedrine, tavegil, oral contraceptives, mydocalm, atropine, clonazepam, prednisolone and others).
4. Dizziness in migraine sufferers.
5. Dizziness due to impaired coordination, standing and gait (dysbasia of various origins).

Dizziness of psychogenic origin

Systemic (vestibular) dizziness

Systemic vertigo can occur with involvement of the vestibular system at any level, from the inner ear in the pyramid of the temporal bone, vestibular nerve, cerebellopontine angle, brainstem and ending with subcortical structures and the cerebral cortex (in the temporal and parietal lobes).

The final diagnosis of the level of vestibular dysfunction is established on the basis of the vestibular passport indicators and accompanying neurological symptoms.

Any processes affecting vestibular conductors at the peripheral level (from the inner ear and vestibular nerve to the pontocerebellar angle and vestibular nerve nuclei in the brainstem) are usually accompanied not only by a vestibular symptom complex, but also by hearing impairment (Meniere's disease, labyrinth infarction, labyrinthitis, neurinoma of the VIII nerve, etc.), since at this level the vestibular and auditory nerves go together, forming nervus statoacusticus. Thus, the systemic nature of dizziness and hearing loss in one ear in the absence of other neurological signs is a characteristic sign of damage to the peripheral parts of the vestibular system. In addition, with processes of this localization, dizziness often has the character of an acute attack (Meniere's syndrome).

Meniere's syndrome consists of auditory and vestibular components. Auditory components include: noise, ringing in the ear, and hearing loss on the affected side. Vestibular components are: vestibular (systemic) vertigo (visual, less often proprioceptive and tactile), spontaneous nystagmus, vestibular ataxia, and autonomic disorders in the form of nausea, vomiting, and other symptoms. Meniere's disease manifests itself in repeated attacks, each of which can leave behind some residual persistent hearing loss, which increases with repeated attacks and eventually leads to significant hearing loss in one ear.

Benign paroxysmal positional vertigo is a peculiar disease of unclear genesis, which manifests itself in short (from several seconds to several minutes) attacks of dizziness that occur when changing body position. In typical cases, dizziness develops in a strictly defined position of the head, a change in the position of which (the patient turns, for example, to the other side) leads to the cessation of dizziness. The prognosis is favorable. Benign paroxysmal positional vertigo usually goes away on its own within a few months. However, the diagnosis of this syndrome always requires careful exclusion of other possible causes of dizziness.

Vestibular neuronitis is also a disease with an unknown pathogenesis; it often begins after an acute respiratory infection, less often associated with metabolic disorders. The development of symptoms is acute: systemic dizziness, nausea, vomiting, which can last for several days. The prognosis is favorable. The disease completely regresses, although a "tail" of poor health in the form of general weakness, slight instability, a subjective feeling of "lack of balance", especially with sharp turns of the head, is possible. Apart from nystagmus, there are no other neurological symptoms in this syndrome.

Vertigo in processes in the cerebellopontine angle area is combined with symptoms of involvement of other cranial nerves, primarily the roots of the facial and auditory nerves, as well as the intermediate nerve passing between them. Depending on the size of the pathological focus and the direction of the process, lesions of the trigeminal and abducens nerves, disorders of cerebellar functions on the side of the focus, pyramidal signs on the side opposite the focus, and even symptoms of compression of the caudal parts of the brainstem may join in. As the process progresses, symptoms of intracranial hypertension appear (neurinomas, meningiomas, cholesteatomas, tumors of the cerebellum or brainstem, inflammatory processes, herpetic lesions of the intermediate nerve). As a rule, CT or MRI are currently of decisive importance in diagnostics.

Almost any brainstem lesions can be accompanied by dizziness and vestibular-cerebellar ataxia: vertebrobasilar insufficiency, multiple sclerosis, platybasia, syringubulbia, vertebral artery aneurysms, tumors of the fourth ventricle and posterior cranial fossa (including in the picture of Bruns syndrome).

The presence of systemic dizziness against the background of a vascular disease (outside of its exacerbation) in the absence of any other focal neurological symptoms cannot serve as a sufficient basis for diagnosing a transient ischemic attack. It is known that the vestibular system is most sensitive to hypoxic, toxic and other damaging effects, and therefore vestibular reactions easily develop even with relatively light functional loads on this system (for example, vestibular-vegetative disorders in the picture of vegetative dystonia syndrome). Only transient visual and oculomotor disorders, as well as dysarthria or ataxia of a mixed vestibular-cerebellar nature against the background of dizziness (both systemic and non-systemic), less often - other neurological symptoms, indicate ischemia in the brainstem. It is necessary that at least two of the listed symptoms be present in order to presumptively speak of a TIA in the vertebrobasilar vascular pool.

Visual disturbances are manifested by blurred vision, unclear vision of objects, sometimes photopsies and visual field loss. Oculomotor disturbances are often manifested by transient diplopia with mild paresis of the eye muscles. Unsteadiness and staggering when walking and standing are characteristic.

For diagnostics, it is important that certain symptoms of brainstem damage almost always appear simultaneously with or shortly after the onset of dizziness. Episodes of isolated systemic dizziness often serve as a reason for overdiagnosis of vertebrobasilar insufficiency. Such patients require a thorough examination to verify the suspected vascular disease (ultrasound examination of the main arteries, MRI in angiographic mode). Transient ischemic attacks in this vascular pool can also manifest as non-systemic dizziness.

Some forms of nystagmus are never observed with labyrinth lesions and are typical for brainstem lesions: vertical nystagmus, multiple nystagmus, monocular nystagmus, as well as rarer types of nystagmus - convergent and retractor nystagmus).

Pathological processes in the cerebrum or cerebellum (infarctions, aneurysms, tumors) affecting the conductors of the vestibular system may be accompanied by systemic dizziness. Diagnosis is facilitated by identifying accompanying symptoms of damage to the hemispheric and other brain structures (conduction symptoms; signs of damage to the gray subcortical matter; forced head position; intracranial hypertension).

Dizziness may be part of the aura of an epileptic seizure (cortical projections of the vestibular apparatus are located in the temporal region and, partially, in the parietal region). Usually, such patients also have other clinical and electroencephalographic signs of epilepsy.

Arterial hypertension may be accompanied by systemic dizziness with a sharp rise in blood pressure. Diabetes mellitus more often leads to episodes of non-systemic dizziness (in the picture of peripheral autonomic failure).

Constitutionally conditioned vestibulopathy manifests itself mainly in increased sensitivity and intolerance to vestibular loads (swings, dancing, some types of transport, etc.).

Non-systemic dizziness in the picture of lipothymic state

This type of dizziness has nothing in common with systemic dizziness and is manifested by sudden general weakness, a feeling of nausea, "darkening in the eyes", ringing in the ears, a feeling of "the ground floating away", a premonition of loss of consciousness, which often actually happens (fainting). But the lipothymic state does not necessarily turn into fainting, it depends on the speed and degree of the drop in blood pressure. Lipothymic states can often recur, and then the main complaint of the patient will be dizziness.

Causes and differential diagnosis of lipothymic states and fainting (vasodepressor syncope, hyperventilation syncope, GCS syndrome, cough syncope, nocturic, hypoglycemic, orthostatic syncope of various origins, etc.) see the section "Sudden loss of consciousness".

When blood pressure drops against the background of an ongoing cerebrovascular disease, ischemia often develops in the brainstem region, manifested by characteristic brainstem phenomena and non-systemic dizziness. In addition to postural instability when walking and standing, the following may occur:

1. a feeling of displacement of the surrounding environment when turning the head,
2. lipothymic states with a feeling of nausea without focal neurological symptoms,
3. Unterharnscheidt syndrome (attacks of lipothymia followed by loss of consciousness that occur when turning the head or in a certain position of the head),
4. "drop attacks" in the form of attacks of sudden, sharp weakness in the limbs (in the legs), which are not accompanied by loss of consciousness. In typical cases, lipothymia is also not present here. Sometimes these attacks are also provoked by turning the head, especially hyperextension (overextension), but can develop spontaneously.

The attacks develop without warning signs, the patient falls without having time to prepare for the fall ("legs give way") and therefore often gets injured when falling. The attack lasts for several minutes. It is based on a transient defect of postural control. Such patients need a thorough examination to exclude cardiogenic syncope (cardiac arrhythmia), epilepsy and other diseases.

Conditions associated with a decrease in blood volume (anemia, acute blood loss, hypoproteinemia and low plasma volume, dehydration, arterial hypotension) predispose to type II dizziness (i.e. non-systemic dizziness).

For purely pragmatic reasons, it is useful to remember that a common physiological cause of non-systemic dizziness in women is pregnancy, and among the pathological causes is diabetes mellitus.

Dizziness of mixed or unspecified nature

This group of syndromes is clinically heterogeneous and includes a number of diseases that are difficult to classify into the first or second group of diseases mentioned above and accompanied by dizziness. The nature of dizziness here is also ambiguous and not always clearly defined.

Dizziness due to pathological processes in the neck area

In addition to Unterharnscheidt syndrome, which was mentioned above, this includes dizziness in congenital bone pathology (platybasia, Arnold-Chiari syndrome and others), some syndromes of cervical osteochondrosis and spondylosis (for example, dizziness in the picture of the so-called "posterior cervical sympathetic syndrome"). Whiplash-type injuries are usually accompanied by dizziness, sometimes very pronounced, such as with hyperextension trauma. Disturbances of balance, dizziness and some vegetative (local and generalized) complications of myofascial syndromes are described, especially with the cervical localization of the latter.

Some people who put on glasses for the first time, especially if the lenses are poorly chosen, complain of dizziness, the causal connection of which with the condition of the organ of vision may not be recognized by the patient himself. Diseases such as astigmatism, cataracts and even oculomotor disorders have been described as possible causes of dizziness.

Some pharmacological drugs may have dizziness as a side effect, the genesis of which in some cases is unclear. In the practice of a neurologist, such drugs are apressin, clonidine; trazicor, visken; aminocaproic acid; lithium, amitriptyline, sonapax; diphenin, phenobarbital, finlepsin; nacom, madopar, parlodel; brufen, voltaren; phenibut; insulin; lasix; ephedrine; tavegil; oral contraceptives; mydocalm; atropine; clonazepam; prednisolone.

Dizziness is often encountered in patients with migraine. Its genesis is not entirely clear. In some forms of migraine, such as basilar migraine, dizziness is part of the attack and is accompanied by other typical manifestations (ataxia, dysarthria, visual disturbances, etc., up to and including impaired consciousness). In other forms of migraine, dizziness may be in the aura of the attack, precede an attack of cephalgia, develop during a migraine attack (rare), or appear independently of a headache attack, which is much more common.

Disturbances of balance and gait (dysbasia) associated with paretic, ataxic, hyperkinetic, akinetic, apraktic or postural disorders are sometimes perceived and described by patients as conditions resembling dizziness (e.g., dysbasia in multiple sclerosis, parkinsonism, Huntington's chorea, severe generalized essential tremor, normotensive hydrocephalus, torsion dystonia, etc.). Here, the patient sometimes describes disturbances of stability and balance using the word "dizziness" to describe them. However, analysis of the patient's sensations shows in such cases that the patient may not experience dizziness in the literal sense of the word, but there is a decrease in control over his body in the process of its orientation in space.

Dizziness of psychogenic origin

Dizziness in some psychogenic disorders has already been partially mentioned above: in the picture of neurogenic fainting and pre-fainting conditions, with hyperventilation syndrome, etc. A peculiar vestibulopathy, as a rule, accompanies protracted neurotic disorders. But dizziness can occur as the main psychogenic disorder. Thus, the patient may have a gait disorder (dysbasia) in the form of careful, slow movement along the wall due to the fear of falling and a feeling of dizziness as the leading complaint. A thorough analysis of such "dizziness" shows that the patient understands dizziness as a fear of a possible fall, which is not supported by vestibular dysfunction or any other threat of a real fall. Such patients, usually prone to obsessive disorders, have a subjective feeling of instability when standing and walking - the so-called "phobic postural dizziness".

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