Central vestibular syndromes: causes, symptoms, diagnosis, treatment

Central vestibular syndromes occur when neurons and conductive pathways of the vestibular analyzer are affected, starting from the vestibular nuclei and ending with the cortical zones of this analyzer, as well as in the occurrence of similar lesions of brain structures adjacent to the central vestibular structures. Central vestibular syndromes are characterized by the erasure of the vestibular symptoms proper, which lose the attributes of directionality (vectoriality) characteristic for peripheral lesions, this syndrome is accompanied by many signs of disturbance of other specific functions of the central nervous system, including other sensory organs. This circumstance determines the polymorphism of the clinical picture of central vestibular syndromes, in which the signs of actual vestibular dysfunction with alternating stem and cerebellar syndromes, with signs of pyramidal, extrapyramidal and limbic-reticular systems, etc. Can be combined. All central vestibular syndromes are divided into stem, or subtentorial, and supratemoral, or supratentorial. Information about these syndromes form an important part of otoneurology and is extremely necessary for differential diagnosis of peripheral and central lesions of the vestibular system.

Subtentorial vestibular syndromes. The signs of brain stem damage are determined by the level of its lesion. The brain stem includes the legs of the brain, the bridge, the medulla oblongata. When these lesions are affected, there are alternating syndromes characterized by impaired functions of the cranial nerves on the side of the lesion and central paralysis of the extremities or conductor disorders on the opposite side. The basis of subtentorial vestibular syndromes is formed by bulbar alternating syndromes: Avellis syndrome (defeat of the nuclei of the glossopharyngeal and vagus nerves and the pyramidal and sensitive pathways passing by); Babinsky-Najotta syndrome (infarction or hemorrhage of the lower peduncle of the cerebellum, cerebellar hemiataxy, nystagmus, miosis, enophthalmus, ptosis, etc.); Vallenberg-Zakharchenko syndrome (thrombosis of the posterior posterior cerebellar artery, extensive infarctions and necrosis in the corresponding half of the medulla oblongata with lesions of the vestibular nuclei and the nuclei of the vagus, trigeminal and glossopharyngeal nerves, dissociated sensitivity disorders, vomiting, dizziness, spontaneous nystagmus, latency in the direction of the lesion; Bernard-Horner syndrome (C7-Th1 lesion, triad of symptoms - ptosis, miosis, enophthalmus, arises with syringobulbia and syringomyelia, tumors, tumors of the trunk and spinnoga about the brain, Jackson's syndrome (vertebral artery thrombosis, circulatory disorders in the upper parts of the medulla oblongata, defeat of the sublingual nerve nucleus on the side of the lesion, central paralysis of the extremities on the opposite side), etc.

Symptoms of cerebellar involvement are caused by damage to both its tissue and neighboring anatomical formations. These attributes include:

• violation of coordination of limb movements (one-sided violation of proportionality and rhythm of movements, for example adioadochokinesis of the upper limbs;
• cerebellar paresis (reduction of the muscle contraction force on the side of the lesion);
• hyperkinesis (ataxic tremor, amplified for arbitrary target movements of the upper limbs, and myoclonus, characterized by rapid twitching of individual muscle groups or muscles arising in the limbs, neck and swallowing muscles;
• cerebellar ataxia (violation of statics and gait);
• cerebellar muscle tone disorders (spontaneous miss of the upper limb with closed eyes on the side of the lesion);
• asynergia (violation of symmetry of movements of both extremities);
• speech disturbances (bradily and scandalized speech).

Supratentorial vestibular syndromes. These syndromes are distinguished by significant polymorphism, manifested as specific "direct" signs, and associative symptoms mediated through the thalamus system.

Opto-striatal vestibular syndromes. Many authors admit that the nuclei of the optic-striatal system are the second vestibular center, since in some pathological states of this system there are signs of vestibular dysfunction. For example, with Parkinson's disease, chorea and other processes developing in the extrapyramidal system, many authors describe spontaneous pathological vestibular symptoms, indicative of involvement in the pathological process and the vestibular system. However, these symptoms are indistinct and do not have a systematized character. Most often, vestibular dysfunction manifests as non-systemic dizziness, experimental vestibular tests are normal, but with a caloric test, in addition to the usual nystagmus with closed eyes, involuntary deflection of the head towards the MC nystagmus occurs, lasting exactly as long as the culminating phase of the nystagmus continues.

Cortical vestibular syndrome. It is generally believed that the cortical projections of the vestibular apparatus are located in the temporal lobes of the brain, but central pathological vestibular reactions cause lesions not only of temporal lobes, but of all others. The explanation is that, probably, the vestibular apparatus has its projections in all parts of the cerebral cortex. Other explanations are based on the existence of interlobar links and the influence of the cortical pathological focus on the nuclei of the optic-striatal system.

With tumors of the temporal lobe and often with lesions of other lobes, spontaneous nystagmus is observed, rarely horizontal, more often - circular and positional. In the Romberg pose, patients usually deviate to a healthy side with tumors of the temporal lobes and in the diseased side with tumors of the parietal lobe. As a rule, provocative vestibular tests are normal or indicate some hyperreactivity of the vestibular analyzer. Spontaneous nystagmus, as a rule, is absent. Vertigo, if it arises, is vague and resembles, rather, a peculiar aura, sometimes observed before an epileptic fit.

Vestibular disorders with intracranial hypertensive syndrome. Intracranial hypertensive syndrome occurs when the circulation of the cerebrospinal fluid is impaired as a result of the obstruction of the liquorids. It manifests itself with the following characteristic signs: headache; nausea and vomiting, more often in the morning hours and with a change in the position of the head; stagnant discs of the optic nerves, sometimes with visual impairments. Vestibular symptoms appear more frequently in tumors in the posterior cranial fossa than in bulk supratentorial processes, with a systemic dizziness, horizontal or multiple spontaneous nystagmus, and nystagmus of the position. Provocative tests patients are difficult to tolerate because of the occurrence of a lesser-like syndrome in their conduct. If it is possible to carry out a caloric test, then a marked interlabyrinth asymmetry in the direction with prevalence of nystagmus in a healthy direction is revealed.

Central auditory syndromes. These syndromes occur when the pathways and auditory nuclei are damaged in any part of them. The resulting hearing impairments progress together with the main pathological process and are characterized by the feature that the higher the localization of this process, the less the "tonal" and more "speech" hearing suffers, while the noise immunity of the sound analyzer decreases drastically. Tonal threshold audiograms with central auditory syndromes G.Greiner et al. (1952) classifies into three types:

1. the predominant loss of hearing for low frequencies occurs with lesions of the bottom of the IV ventricle;
2. a decrease in the tonal curve for both low and high frequencies with an even sharper decrease in the curve in the region of so-called speech frequencies is characteristic of bulbar lesions of the brainstem;
3. Atypical tonal audiograms of mixed type may indicate both an extramedullary pathological process and an intramedullary disease, for example, with syringobulbia or multiple sclerosis.

Central auditory syndromes are characterized by bilateral violation of auditory function, loss of musical ear, absence of FUNG. Cortical lesions of the auditory zones often cause auditory hallucinations and speech perception disorders.

[1], [2], [3], [4], [5], [6], [7]