The diagnostic search for complaints of dizziness begins with a thorough analysis of the complaints themselves. When 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 “lightheadedness” 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 version of dizziness involves sensations that are difficult to describe in words, sometimes arising during the patient’s movement due to poor coordination of movements and body instability , gait disorders of various types, visual and gaze 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 version of dizziness is characteristic of lipotimic states and fainting of various natures (non-systemic dizziness); The third type of dizziness is less likely to cause diagnostic difficulties and reflects visual-vestibular, postural, apratic-atactic and other similar disorders that have an ambiguous, often mixed nature. The so-called psychogenic dizziness stands apart.

Main causes of dizziness

Systemic (vestibular) dizziness:

  • Benign positional vertigo.
  • Vestibular neuronitis.
  • Meniere’s disease.
  • Herpetic lesion of the intermediate nerve.
  • Intoxication.
  • Heart attack, aneurysm or brain tumor of different localization (cerebellum, brain stem, cerebral hemispheres).
  • Vertebro-basilar insufficiency.
  • Traumatic brain injury and post-commotion syndrome.
  • Epilepsy.
  • Labyrinthitis or infarction of the labyrinth.
  • Multiple sclerosis.
  • Dysgynesia (platybasia, Arnold-Chiari syndrome and other cranio-vertebral anomalies).
  • Syringobulbia.
  • Other diseases of the brain stem.
  • Constitutionally determined vestibulopathy.
  • Arterial hypertension.
  • Diabetes.

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

  • Vasodepressor (vasovagal) syncope.
  • Hyperventilation syncope.
  • Carotid sinus hypersensitivity syndrome.
  • Cough fainting.
  • Nocturic syncope.
  • Hypoglycemic syncope.
  • Orthostatic hypotension of neurogenic (primary peripheral autonomic failure) and somatogenic origin (secondary peripheral autonomic failure).
  • Orthostatic circulatory disorders in diseases of the heart and blood vessels (aortic stenosis, ventricular arrhythmia, tachycardia, fibrillation, etc.).
  • Sympathectomy.
  • Arterial hypertension.
  • Diabetes.
  • Ischemia in the brain stem area.
  • Anemia, acute blood loss, hypoproteinemia.
  • Dehydration.
  • Pregnancy.

Dizziness of mixed or uncertain character:

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

Dizziness of a psychogenic nature

Systemic (vestibular) vertigo

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

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

Any processes that affect the vestibular conductors at the peripheral level (from the inner ear and the vestibular nerve to the cerebellopontine angle and the nuclei of the vestibular nerve in the brain stem), as a rule, are accompanied not only by the vestibular symptom complex, but also by hearing impairment (Meniere’s disease, labyrinthine infarction , labyrinthitis, neuroma of the VIII nerve, etc.), since at this level the vestibular and auditory nerves go together, forming the nervus statoacusticus. Thus, the systemic nature of dizziness and decreased hearing 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, during 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 decreased hearing 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 manifestations. Meniere’s disease is manifested by repeated attacks, each of which can leave behind some residual persistent hearing loss, which increases with repeated attacks and ultimately leads to a pronounced decrease in hearing in one ear.

Benign paroxysmal positional vertigo is a peculiar disease of unknown origin, 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, changing 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 there may be a “tail” of poor health in the form of general weakness, slight instability, and a subjective feeling of “lack of balance,” especially with sudden turns of the head. Apart from nystagmus, there are no other neurological symptoms with this syndrome.

Dizziness during processes in the area of ​​the cerebellopontine angle 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 spread of the process, lesions of the trigeminal and abducens nerves, disorders of cerebellar functions on the side of the lesion, pyramidal signs on the side opposite to the lesion, and even symptoms of compression of the caudal parts of the brain stem may occur. As the process progresses, symptoms of intracranial hypertension appear (neurinomas, menigiomas, cholesteatomas, tumors of the cerebellum or brain stem, inflammatory processes, herpetic lesions of the intermediate nerve). As a rule, CT or MRI currently play a decisive role in diagnosis.

Almost any lesion of the brain stem can be accompanied by dizziness and vestibular-cerebellar ataxia: vertebrobasilar insufficiency, multiple sclerosis, platybasia, syringubulbia, aneurysms of the vertebral artery, 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 (beyond 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 influences and therefore vestibular reactions easily develop even with relatively light functional loads on this system (for example, vestibular-vegetative disorders in the picture of autonomic 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), and less often other neurological symptoms, indicate ischemia in the brain stem. It is necessary to have at least two of the listed symptoms in order to presumably talk about TIA in the vertebrobasilar vascular system.

Visual disturbances are manifested by blurred vision, blurred vision of objects, sometimes photopsia and loss of visual fields. Oculomotor disorders often manifest as transient diplopia with mild paresis of the eye muscles. Characterized by instability and staggering when walking and standing.

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

Some forms of nystagmus are never observed with labyrinthine lesions and are typical of brainstem lesions: vertical nystagmus, multiple nystagmus, monocular nystagmus, as well as rarer types of nystagmus – converging and retractor nystagmus).

Pathological processes in the area of ​​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 concomitant symptoms of damage to hemispheric and other brain structures (conductor symptoms; signs of damage to the gray subcortical matter; forced position of the head; 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). Typically, such patients also exhibit 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 caused vestibulopathy manifests itself mainly in increased sensitivity and intolerance to vestibular stress (swings, dancing, some types of transport, etc.).

Non-systemic dizziness in the picture of a lipothymic state

This type of dizziness has nothing to do with systemic dizziness and is manifested by a sudden onset of general weakness, a feeling of lightheadedness, “darkening in the eyes,” ringing in the ears, a feeling of “floating away of the ground,” a premonition of loss of consciousness, which often actually happens (fainting) . But the lipothymic state does not necessarily lead to fainting, it depends on the speed and extent of the fall in blood pressure. Lipotymic conditions can often recur and then the main complaint of the patient will be dizziness.

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

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

  • a feeling of a shift in the environment when you turn your head,
  • lipothymic states with a feeling of lightheadedness without focal neurological symptoms,
  • Unterharnscheidt syndrome (attacks of lipothymia followed by loss of consciousness that occur when turning the head or in a certain position of the head),
  • “drop attacks” in the form of attacks of sudden severe weakness in the limbs (legs), which are not accompanied by loss of consciousness. In typical cases, there is no lipothymia here either. Sometimes these attacks are also provoked by turning the head, especially hyperextension (hyperextension), but can develop spontaneously.

Attacks develop without warning, the patient falls without having time to prepare for the fall (“legs give way”) and therefore often receives injuries when falling. The attack lasts several minutes. It is based on a transient defect in postural control. Such patients need careful examination to exclude cardiogenic syncope (cardiac arrhythmias), 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 dizziness of the second type (that is, non-systemic dizziness).

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

Dizziness of mixed or vague nature

This group of syndromes is clinically heterogeneous and includes a number of diseases that are difficult to attribute to 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’s syndrome, which was already mentioned above, this includes dizziness due to 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 injuries are usually accompanied by dizziness, sometimes very pronounced, such as with a hyperextension injury. Balance disorders, dizziness and some vegetative (local and generalized) complications of myofascial syndromes, especially when the latter are localized in the cervical region, have been described.

Some people who put on glasses for the first time, especially with poorly chosen lenses, experience complaints of dizziness, the causal connection of which with the state of the organ of vision may not be realized by the patient himself. Diseases such as astigmatism, cataracts, and even oculomotor disorders have been described as a possible cause of dizziness.

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

Dizziness is common in migraine patients. Their genesis is not entirely clear. In some forms of migraine, for example basilar, dizziness is part of the attack and is accompanied by other typical manifestations (ataxia, dysarthria, visual disturbances, etc., including impairment of consciousness). In other forms of migraine, dizziness can be in the aura of an attack, precede an attack of cephalalgia, develop during a migraine attack (rarely) or appear independently of a headache attack, which is much more common.

Balance and gait disturbances (dysbasia) associated with paretic, atactic, hyperkinetic, akinetic, apractic or postural disorders are sometimes perceived and described by patients as conditions resembling vertigo (for example, dysbasia in multiple sclerosis, parkinsonism, Huntington’s chorea, severe generalized essential tremor , normal pressure hydrocephalus, torsion dystonia, etc.). Here, the patient sometimes describes disturbances in stability and balance by using the word “dizziness” to denote them. However, an analysis of the patient’s sensations shows in such cases that the patient may not have 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 a psychogenic nature

Dizziness in some psychogenic disorders has already been partially mentioned above: in the picture of neurogenic fainting and presyncope, with hyperventilation syndrome, etc. A kind of vestibulopathy, as a rule, accompanies protracted neurotic disorders. But dizziness occurs as the main psychogenic disorder. Thus, the patient may have a gait disturbance (dysbasia) in the form of careful slow movement along the wall due to fear of falling and a feeling of dizziness as the leading complaint. A careful analysis of such “dizziness” shows that by dizziness the patient understands the 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”.

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