Central vestibular syndromes: causes, symptoms, diagnosis, treatment

Central vestibular syndromes occur when neurons and conduction pathways of the vestibular analyzer are damaged, starting from the vestibular nuclei and ending with the cortical zones of this analyzer, as well as when similar damage occurs to structures of the brain adjacent to the central vestibular structures. Central vestibular syndromes are characterized by the erasure of vestibular symptoms proper, losing the signs of directionality (vectoriality) characteristic of peripheral damage; this syndrome is accompanied by many signs of impairment of other specific functions of the central nervous system, including other sense organs. This circumstance causes polymorphism of the clinical picture of central vestibular syndromes, which can combine signs of vestibular dysfunction proper with alternating brainstem and cerebellar syndromes, with signs of damage to the pyramidal, extrapyramidal and limbic-reticular systems, etc. All central vestibular syndromes are divided into brainstem, or subtentorial, and supra-brainstem, or supratentorial. Information about these syndromes is an important part of otoneurology and is extremely necessary in the differential diagnosis of peripheral and central lesions of the vestibular system.

Subtentorial vestibular syndromes. Signs of brainstem damage are determined by the level of damage. The brainstem includes the cerebral peduncles, pons, and medulla oblongata. Damage to these structures causes alternating syndromes characterized by dysfunction of the cranial nerves on the side of the lesion and central paralysis of the limbs or conduction disorders on the opposite side. Subtentorial vestibular syndromes are based on bulbar alternating syndromes: Avellis syndrome (damage to the nuclei of the glossopharyngeal and vagus nerves and the adjacent pyramidal and sensory tracts); Babinski-Nageotte syndrome (infarction or hemorrhage of the inferior cerebellar peduncle; cerebellar hemiataxia, nystagmus, miosis, enophthalmos, ptosis, etc.); Wallenberg-Zakharchenko syndrome (thrombosis of the inferior posterior cerebellar artery; extensive infarctions and necrosis in the corresponding half of the medulla oblongata with damage to the vestibular nuclei and nuclei of the vagus, trigeminal and glossopharyngeal nerves; dissociated sensory disturbances, vomiting, dizziness, spontaneous nystagmus, lateropulsion towards the lesion; Bernard-Horner syndrome (lesion of C7-Th1; triad of symptoms - ptosis, miosis, enophthalmos; occurs with syringobulbia and syringomyelia, tumors, tumors of the brainstem and spinal cord; Jackson syndrome (thrombosis of the vertebral artery, circulatory disorder in the upper parts of the medulla oblongata; damage to the nucleus of the hypoglossal nerve on the side of the lesion, central paralysis of the limbs on the opposite side), etc.

Signs of cerebellar damage are caused by damage to both its tissue and neighboring anatomical structures. These signs include:

• impaired coordination of limb movements (unilateral impairment of proportionality and rhythm of movements, for example, adiadochokinesia of the upper limbs;
• cerebellar paresis (decreased force of muscle contraction on the affected side);
• hyperkinesis (ataxic tremor, which intensifies with voluntary targeted movements of the upper limbs, and myoclonus, characterized by rapid twitching of individual muscle groups or muscles that occur in the limbs, neck, and swallowing muscles;
• cerebellar ataxia (impaired statics and gait);
• cerebellar muscle tone disorders (spontaneous movement of the upper limb with closed eyes on the affected side);
• asynergy (impaired symmetry of movements of both limbs);
• speech disorders (bradilalia and scanned speech).

Supratentorial vestibular syndromes. These syndromes are distinguished by significant polymorphism, manifesting both by specific "direct" signs and associative symptoms mediated through the thalamic system.

Opticostriatal vestibular syndromes. Many authors admit that the nuclei of the opticostriatal system are the second vestibular center, since some pathological conditions of this system also cause signs of vestibular dysfunction. For example, in Parkinson's disease, chorea and other processes developing in the extrapyramidal system, many authors have described spontaneous pathological vestibular symptoms indicating the involvement of the vestibular system in the pathological process. However, these symptoms are vague and not systematized. Most often, vestibular dysfunction manifests itself as non-systemic dizziness, experimental vestibular tests are normal, however, during the caloric test, along with the usual nystagmus with closed eyes, an involuntary deviation of the head towards the MC of nystagmus occurs, lasting exactly as long as the culmination phase of nystagmus lasts.

Cortical vestibular syndrome. It is generally accepted that the cortical projections of the vestibular apparatus are located in the temporal lobes of the brain, but central pathological vestibular reactions cause damage not only to the temporal lobes, but to all the others. This is explained by the fact that the vestibular apparatus probably has its projections in all parts of the cerebral cortex. Other explanations are based on the existence of interlobar connections and the influence of the cortical pathological focus on the nuclei of the optic-striatal system.

In tumors of the temporal lobe and often in lesions of other lobes, spontaneous nystagmus is observed, less often horizontal, more often circular and positional. In the Romberg pose, patients usually deviate to the healthy side in tumors of the temporal lobe and to the diseased side in tumors of the parietal lobe. As a rule, provocative vestibular tests are normal or indicate some hyperreactivity of the vestibular analyzer. Spontaneous nystagmus is usually absent. Dizziness, if it occurs, is of an indefinite nature and rather resembles a peculiar aura, sometimes observed before an epileptic seizure.

Vestibular disorders in intracranial hypertensive syndrome. Intracranial hypertensive syndrome occurs when the circulation of cerebrospinal fluid is impaired due to obstruction of the cerebrospinal fluid pathways. It manifests itself with the following characteristic signs: headache; nausea and vomiting, more often in the morning and when changing the position of the head; congestion of the optic discs is revealed, sometimes with visual impairment. Vestibular symptoms appear more often with tumors in the posterior cranial fossa than with volumetric supratentorial processes, and systemic dizziness, horizontal or multiple spontaneous nystagmus, and positional nystagmus occur. Patients tolerate provocative tests with difficulty due to the occurrence of Meniere-like syndrome during their implementation. If a caloric test is successful, then pronounced interlabyrinthine asymmetry is revealed in the direction with a predominance of nystagmus to the healthy side.

Central auditory syndromes. These syndromes occur when the conduction pathways and auditory nuclei are damaged in any part of them. The resulting hearing impairments progress along with the underlying pathological process and are distinguished by the fact that the higher the localization of this process, the less "tonal" hearing suffers and the more "speech" hearing suffers, while the noise immunity of the sound analyzer is sharply reduced. G. Greiner et al. (1952) classify tonal threshold audiograms in central auditory syndromes into three types:

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

Central auditory syndromes are characterized by bilateral impairment of auditory function, loss of musical hearing, and absence of FUNG. With cortical lesions of auditory zones, auditory hallucinations and speech perception disorders often occur.

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