A review of pathologic nystagmus.
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From a group of 101 children, eleven (10.9 p.c. ranging in age from 4--12) reported transient visual disturbances such as blurred vision, grey vision or photopsias immediately after a light head trauma. As to the origin of these impediments all evidence points to the occipital areas. Oculopupillary defects or pathological nystagmus phenomena were in no case associated. The frequency of pathological EEG recording over the occipital area was statistically significant (chi-quadrat = 4.27; p less than or equal to 0.05). The pathogenetic mechanism may be explained by means of a local oedematous reaction.
Clade 2.3.4.4b highly pathogenic avian influenza viruses (HPAIVs) continue to circulate widely in East Asia and undergo frequent reassortment in wild birds. Raptors are regarded as spillover hosts that may be exposed through predation or scavenging, yet integrated clinicopathologic and genomic investigations in cinereous vultures remain limited. Here, we describe a fatal H5N1 HPAIV infection in a cinereous vulture (Aegypius monachus) found in South Korea on January 17, 2026. On presentation, the cinereous vulture showed severe neurologic dysfunction, including inability to stand, right-sided head tilt with pathologic nystagmus, reduced oculocephalic and palpebral reflexes, and intermittent bilateral leg tremors. The cinereous vulture died within 2 days after rescue, and a complete necropsy was performed. Hematologic and biochemical testing revealed marked heterophil predominance, severe lymphopenia, mild monocytosis, and globulin values near the upper end of the reference interval. An oropharyngeal swab tested positive for influenza A virus, and a virus isolate, designated A/Cinereous_Vulture/Korea/26-JBN47/2026(H5N1), was recovered in embryonated chicken eggs. Histopathology showed nonsuppurative encephalitis and necrotizing myocarditis, and influenza A nucleoprotein was detected immunohistochemically in neurons and cardiomyocytes. Tissue real-time RT-PCR showed the lowest cycle threshold value in the brain. Whole-genome sequencing demonstrated that 26-JBN47 belonged to clade 2.3.4.4b and contained a polybasic HA cleavage site (PLREKRRKR/GLF). Segment-level phylogenetic analysis revealed a reassortant genome constellation comprising a maintained H5N1 backbone in HA, NA, and M; low PAIV (LPAIV)-associated but H5N1-incorporated PA and NP segments; flyway-associated PB2 and NS segments; and a PB1 segment phylogenetically linked to regional LPAIV lineages. Molecular marker analysis identified multiple substitutions previously reported to be associated with receptor-binding properties, polymerase-related fitness, virulence, and host-response modulation, whereas canonical PB2 mammalian-adaptive markers were absent. These findings show that 26-JBN47 was a reassortant clade 2.3.4.4b H5N1 HPAIV associated with systemic disease and clinicopathological findings consistent with neurotropic and cardiotropic infection in a cinereous vulture. They also support the potential value of scavenging raptors as sentinels of local or regional HPAIV circulation involving reassortant viruses in East Asia.
120 subjects were selected from a large number of healthy persons on the grounds of their medical history and preexaminations including audiogram, which excluded the possibility of previous cochelo-vestibular illness. These 120 healthy persons were examined by means of electronystagmography. We were searching for spontaneous and positional nystagmus in 5 positions with open eyes in darkness and with closed eyes. 50% proved to have a horizontal and 82% a vertical spontaneous nystagmus in at least 1 position. The sex had no influence on the frequency and there was no difference in results under smokers and non-smokers. There was the same frequency of nystagmus directed to right and left. We conclude that there is a physiological horizontal spontaneous nystagmus of low intensity if fixation is completedly excluded. In our opinion it is not possible to determine a certain level of intensity above which a spontaneous nystagmus is pathological as the intensity of nystagmus is essentially dependent upon non-vestibular elements.
Thirty patients with simple or ophthalmic migraine had an otoneurological examination. 13% complained of vertigo during attacks of migraine, 17% of giddiness and 6.7% of tinnitus. The usual tests for equilibrium were normal. On electronystagmographical examination 17% of the patients showed only pathological spontaneous nystagmus, 33% only disturbances of caloric response and 7% a combination of both. Audiological testing was normal. The incidence of vestibular disturbances, particularly sensitivity differences of the labyrinths, was significantly greater in the group of patients with migraine than in a control group of 30 healthy persons (P less than or equal to 0.025). On the average, the sensitivity differences, in terms of duration of reactive nystagmus, were greater for these than for the healthy persons (P less than or equal to 0.01). Patients with vestibular disturbances did not show a greater frequency of pathological EEG readings than patients with normal vestibular function. Some hypotheses concerning the pathogenesis of vestibular symptoms as found in migrainous patients are mentioned.
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The present paper is based on an exact analysis of the neurootological findings in 30 cases of multiple sclerosis (MS). Ms-diagnosis was verified using Schumacher's criteria and cerebro-spinal fluid findings. Central vestibular disorders were found in most of the cases. From our observation it may be assumed that the brainstem is an early site of involvement causing imbalance which can only be verified by an accurate neuro-otological evaluation. The most important pathological findings are the following: central spontaneous nystagmus, gaze-deviation nystagmus, positional nystagmus, disinhibition of induced (caloric and galvanic) nystagmus, delay of the reversal phenomenon of galvanic nystagmus,dysrhythmia as well as distorted optokinetic nystagmus. An extensive neuro-otological investigation is of clinical importance with respect to detecting cases of MS at an early stage of this disease.
Multiple sclerosis is a disease of the central nervous system whose clinical manifestations include animportant group of ocular pathologies, e.g., unilateral retrobulbar neuritis, uveitis, decreased visual function, nystagmus, internuclear ophthalmoplegia, diplopia, optic papillitis and Marcus Gunn pupil. Additionally, it is not generally appreciated that bitemporal hemianopia, usually associated with tumors of the optic chiasm, may also result from multiple sclerosis. Since most of a patient's life is spent in the remission phase of the disease, it is important for the practitioner to recognize the ocular findings present during this period. Additionally, studies have shown that such patients lead longer and more productive lives than most practitioners realize, and often have prolonged periods of remission. While the onset of the disease may present with ocular symptoms, such as loss of vision or diplopia, the patients tend to recover and retain relatively good function for many years.
The effect of Diazepam (Valium), Dimenhydrinate (Vomex A, Novomina, Epha Retard), Sulpirid (Dogmatil) and Placebo has been investigated in regard to the intensity of pathological vestibular spontaneous nystagmus by application of the double blind method on 50 patients with peripheral vestibular (n = 37) and central vestibular (n = 12) diseases, as well as on a case of spontaneous nystagmus of undefined origin. Since by acute vestibular disease the intensity of spontaneous nystagmus is generally closely related to the severity of vertigo, the influence on a pathological spontaneous nystagmus by antivertiginosa seems to be a dependable criterium in the evaluation of their effectiveness. Dimenhydrinate (2 mg/kg KG) and Sulpirid (2.86 mg/kg KG) led to a statistically significant reduction, however not in the case of Diazepam and Placebo. Nevertheless, the effectiveness of Dimenhydrinate and Sulpirid is not definitely predictable in individual cases: in 2 out of 10 patients the preparations were without effect. Characteristics and areas of indication of Dimenhydrinate and Sulpirid are described in greater detail.
In 111 patients with a chronic otitis media and symptoms of dizziness the positional reactions were examined. Among 75 patients, who underwent operations later on, a fistula of the labyrinth was preoperatively expected in 25 patients according to a positive fistula pressure sign or a pathological fistula positional reaction. A positive fistula positional sign shows a contralateral beating transitory nystagmus in the head hanging position, while after rapid sit up the nystagmus is starting to beat into the ipsilateral direction. A labyrinthine fistula was operatively confirmed in 15 patients out of 25 suspicious cases. In these 15 cases both the fistula and the positional test were positive in 9 cases. 3 had a positive fistula pressure test and 3 a positive fistula positional sign. In 50 patients with negative fistula reactions only one fistula was observed during operation. These data underline the importance of both pressure and positional reactions in the prediction of labyrinthine fistulas.
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The vertical vergences are rather weak physiological conjugate movements of the eyes. When the ocular axes approach each other or deviate, a vertical convergence or divergence occurs. These reflex movements are evoked either by visual stimuli (fusional vergence) or by labyrinthine stimuli. In pathological situations vertical vergences may become evident in permanent or alternating hyperphorias, in the strabismus occurring in the Hertwig-Magendie syndrome, in see-saw nystagmus and in labyrinthine lesions (such as Meniere's disease, after labyrinthectomy and after section of the VIIIth nerve).
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We wanted to ascertain whether a physiological horizontal vestibular spontaneous nystagmus is existent, or whether the spontaneous and positional nystagmus seen in clinically healthy persons in the electronystagmogram -- when fixation had been excluded completely -- was always the result of earlier damages to the vestibular system (Jatho). For this purpose we tried to detect a spontaneous and positional nystagmus in 102 healthy persons from 6 age groups (17 each) between 11 and 70 years of age. When the ENG was registered with open eyes in darkness, 63 out of the 102 test persons had a horizontal spontaneous or positional nystagmus, however, under the Frenzel glasses there was a nystagmus in only 2 out of these test persons. With open eyes in darkness, the frequency and intensity was the same in all age groups. With this, we believe to have proved that a physiological horizontal vestibular nystagmus does exist. We share Kornhuber's opinion that the examination with the Frenzel glasses in a dark room, together with the head shaking test and positional test, at the present time represents the best method for differentiating between physiological and pathological spontaneous nystagmus.
25 patients suffering from vertigo due to peripheral-vestibular disorders resistant to medical treatment underwent neurectomy of the vestibular nerve. Präoperatively 24 showed a pathological result in the neurotological examination. In 83% of the cases an abnormal caloric reaction could be seen in the frequency-calorigram, which graphically represents the caloric test. The postoperative objective vestibular results always correlated with the subjective feeling of vertigo. We could see a decrease and finally a disappearance of the horizontal unidirectional spontaneous nystagmus. It is of value to examine the gaze nystagmus in none directions of gaze. In the positiogram, a quantitative scheme of the positional test, one could recongize a decrease of the nystagmus intensity in the follow-up examination. The same was found by testing the vestibulo-spinal reactions. Although the neurectomy of the vestibular nerve involves a serious operation it is nevertheless the first choice of treatment. 96% of the cases are free from vertigo. Postoperative there is a very low complication quota.
The disorders of ocular motility seen in association with brainstem or cerebellar disorders may point to rather specific anatomical or pathological correlations. Pontine gaze palsy reflects involvement of the pontine paramedian reticular formation. Internuclear ophthalmoplegia signifies a lesion in the medial longitudinal fasciculus. Skew deviation may result from a lesion anywhere in the posterior fossa. Ocular bobbing typically results from a pontine lesion. The Sylvian aqueduct syndrome is characteristic of involvement in the upper midbrain-pretectal region, usually a pinealoma. Cerebellar lesions may be manifested by gaze paresis, skew deviation, disturbances of saccadic or smooth pursuit movements, ocular myoclonus, or several characteristic forms of nystagmus. Familiarity with these disorders may be of great help to the physician dealing with a patient with a possible posterior fossa lesion.
Report on a sudden peripheral vestibular upset 8 days after a serologically evidenced herpes simplex infection. Reference to the significance of virological-serological examinations in any cases of acute vestibular upset, sudden deafness and peripheral facial palsy. Discussion of etiology, pathology and probable localization of this affection, about which medical literature does not contain any relevant observations made in connection with herpes simplex infection. Electronystagmographic control of the course of the disease, demonstrating the complete restitution of the vestibular organ. Thus, justified assumption of rather a peripheral vestibular lesion.
The Argentine hemorrhagic fever (AHF) is an infectious disease, endemo-epidemical, of viral etiology, produced by the Junin virus and limited to the Buenos Aires Province, South of Córdoba, East of La Pampa, and South of Santa Fe. It generally assails rural workers at harvest-time, especially during corn-harvest. The incubation period of the disease does not exceed 12 days. A feverish syndrome with asthenia, adynamia, myalgias, migraine, photophobia, epigastralgia etc., appear. The patient has a facial erythema, petechias on the skin, enantema on the palate, conjunctive micropolyadenopaty injection. The laboratory shows a low erytro, leukopenia with aneosinophilia, thrombopenia and a urine with albuminuria and virous cells. After the fourth day, hemorrhage and a neurological case appears. The laboratory tends to normalize and cast appears in the urine. The most striking neurological signs are the following: muscular hypotonia, proprioceptive hyporreflexia or arreflexia, marinesco reflex, shakings, difficulty to stand and walk, oscillations in consciousness level, and ocular disturbances. The cytochemical test of the C.L. Rachis in the usual ways of the AHF is within its normal characteristics; on the other hand there are modifications in the nervous cases: the total proteins are nearly always increased and the cells augmented with a great predominance of mononuclear cells. The electroencephalogrammes were always abnormal, varying from a brief disorganization up to a diffusive and permanent slowness. The half of which additionally presented paroxisms generalized by slow waves. The pathological anatomy over the central nervous system makes us think that the lesion would not primitively neuronal but that the action of the virus would be indirectly done through the capillar wall. This capillar lesion is produced by multiple focuses. The neuronal destruction with necrosis by microinfarcts is minimum. The symptoms and neurological signs are present in 10% of the clinical cases; the death-rate in the nervous clinical cases having reached 50% of them. The premature treatment allows the death-rate to diminish and the cases that survive have not many after effects.