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Query: UMLS:C0042571 (vertigo)
 7,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Positional and positioning vertigo and nystagmus syndromes can be attributed to either peripheral or central vestibular dysfunction. The most common form is benign paroxysmal positioning vertigo which is caused by cupulolithiasis into the posterior semicircular canal. Other labyrinthine manifestations such as positional alcohol nystagmus, positional nystagmus with macroglobulinaemia and "heavy water" or glycerol ingestion occur because of a specific gravity differential between the cupula and the endolymph (buoyancy mechanism). Neurovascular compression of the vestibular nerve may be a causative factor for "disabling positional vertigo" which is an insufficiently described entity. Hesitation is highly justifiable since retromastoid craniectomy for microvascular decompression is the recommended management. Central positional vertigo is either induced by head movements which result in a transient ischaemia of the ponto-medullary brainstem, or by a change in head position relative to the gravitational vector. The latter is comprised of at least three forms: positional downbeat nystagmus (nodulus), positional nystagmus without concurrent vertigo, and positional vertigo with nystagmus. The site of the lesion is always near the fourth ventricle and the vestibular nuclei. The most probable explanation for the positional response is a vestibular tone imbalance caused by disinhibition of the vestibular reflexes on perception, eye, head and body position.
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PMID:Positional and positioning vertigo and nystagmus. 143 92

Excluding vascular involvement, vertigo due to a central vestibular syndrome reflects a median or paramedian lesion of the brain stem or the cerebellum. Recurrent attacks of vertigo usually occur with peripheral lesions. Persistent acute vertigo with peripheral destruction can reveal ischemia of the brain stem. Central positional vertigo is rare and has symptomatology that is different from that of benign positional vertigo. Persistent instability has a symptomatology that is more difficult to analyse and is usually associated with a central vestibular syndrome when it is organic. Diagnosis of a central vestibular syndrome is based on detection of well-defined clinical or electronystagmographic signs of which abnormal nystagmus is primordial. Some of them such as inferior vertical nystagmus or dissociated nystagmus can localise the site. MRI has become the diagnostic procedure which is best adapted for identifying the most frequent aetiologies such as tumors, congenital malformations and multiple sclerosis.
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PMID:[Vertigo in non-vascular diseases of the central nervous system]. 817 98

The history usually provides the key information for distinguishing between peripheral and central causes of vertigo. Probably the only central lesion that could masquerade as a peripheral vestibular lesion is cerebellar infarction because vertigo and severe imbalance may be the only presenting features. MRI is indicated in any patient with acute vertigo and profound imbalance suspected to be the result of cerebellar infarct or hemorrhage. Patients with chronic recurrent attacks of vertigo often have normal examination results, including normal vestibular function in between attacks. The duration of attacks is most helpful in distinguishing between central and peripheral causes; vertigo associated with vertebrobasilar insufficiency typically lasts minutes, whereas peripheral inner ear causes of recurrent vertigo typically last hours. Positional vertigo nearly always is a benign condition that can be cured easily at the bedside, but in rare cases it can be a symptom of a central lesion, particularly one near the fourth ventricle. Central positional nystagmus is nearly always purely vertical (either upbeating or downbeating), and there are usually associated neurologic findings.
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PMID:Differentiating between peripheral and central causes of vertigo. 967 15