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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 6-year period (1970-1975), a total number of 10,730 patients were examined oto-neurologically by the same physician, all of the patients being referred from the neuromedical and neurosurgical departments. Persistent positional nystagmus is in this material the same as central positional nystagmus, because the lesion in all cases was of central origin. Central positional nystagmus was found to be a rare symptom, since it was only demonstrated in 124 patients (1%). Central positional nystagmus was defined as being with no latency, low and irregular frequency, nonfatiguable with no accompanying dizziness, and the patients examined in the following positions: right and left side, supine and with hanging head. In 52 cases (42%) the nystagmus was only demonstrated with hanging head. The diagnoses were dominated by intracranial tumors (34 infra-tentorial, 19 supratentorial). Among other diagnoses encountered were intracranial vascular disease, encephalopathia, epilepsy and multiple sclerosis. 21 patients were children under 15 years of age, and in this group the intracranial tumors, especially the infratentorial, were even more dominant.
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PMID:Positional nystagmus of the persistent type. 57 Jun 91

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 central vestibular system operates to precisely estimate the rotational velocity and gravity orientation using the inherently ambiguous information from peripheral vestibular system. Therefore, any lesions disrupting this function can generate positional nystagmus. Central positional nystagmus (CPN) can be classified into the paroxysmal (transient) and persistent forms. The paroxysmal CPN has the features suggesting a semicircular canal origin regarding the latency, duration, and direction of nystagmus. Patients with paroxysmal CPN commonly show several different types of nystagmus classified according to the provoking positioning. The persistent form of CPN mostly appears as downbeat nystagmus while prone or supine, or apogeotropic or geotropic horizontal nystagmus when the head is turned to either side while supine. CPN may be ascribed to erroneous neural processing within the velocity-storage circuit that functions in estimating angular head velocity, gravity direction, and inertia. Paroxysmal CPN appears to be post-rotatory rebound nystagmus due to lesions involving the cerebellar nodulus and uvula. In contrast, persistent CPN may arise from erroneous gravity estimation. The overlap of lesion location responsible for both paroxysmal and persistent CPN may account for the frequent coexistence of both forms of nystagmus in a single patient.
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PMID:Central positional nystagmus: Characteristics and model-based explanations. 3132 81