Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Spontaneous and positional nystagmus in healthy persons demonstrated only by electronystagmography: physiological spontaneous nystagmus or "functional scar"? 30 84

Recent papers underline the possible involvement of the central nervous system when an acquired peripheral demyelinating disease occurs and vice-versa. We describe five patients with chronic polyneuropathy and "benign" gammopathy, monoclonal (IgM-K, IgA-k, IgG-k) in three cases and polyclonal (IgG, IgM) in two cases; the monoclonal gammopathies were detected in cases of peripheral nerve disease. Three patients showed tremor and signs of pyramidal system impairment when the peripheral damage had improved or was stable. All cases underwent a longitudinal assessment according to clinical, CSF, EMG-ENG, neuroradiological and pathological criteria. The MRI finding always showed multiple alterations of encephalic white matter. When related to neurophysiological and pathological data supporting a chronic demyelinating neuropathy, such results point to possible encephalic involvement in chronic polyneuropathies due to a pathogenetic mechanism common to both.
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PMID:Evidence of central nervous system involvement in chronic demyelinating neuropathies associated with "benign" gammopathies. 254 77

The clinical features of congenital nystagmus (CN) were studied statistically in 106 cases of CN. The point of the nystagmus at which the patients could best see the targets was detected in some patients. The effects of superior colliculectomy on their visual disturbance and the mechanism will be discussed. The study population comprises 106 patients, 79 males and 27 females, aged from one to 64 (mean 19.4 years). Patients with jerky type classified on ENG were found in 53 cases (50%), pendular type in 39 cases (37%), and mixed type in 14 cases (13%). Patients with jerky type showed significantly good visual acuity (mean 0.69 +/- 0.31, p less than 0.005). They showed significant abnormalities during pregnancy and delivery (p less than 0.01) and had a neutral point (p less than 0.01). Patients with pendular type, on the other hand, showed poor visual acuity (mean 0.26 +/- 0.30) and had significant frequency of family history (p less than 0.05), head tremor (p less than 0.01) and strabismus (p less than 0.01). Thirteen cases (12%) had ocular diseases which involved the retina, cornea and optic nerve. Visual function was elaborated on such parameters of ENG as perception, peak variation and plateau time. Perception, which means the ability to detect the dim flashes during the appearance of the nystagmus, was manifested by pushing a button when patients could detect flashes presented at random on the screen. At the turning point from the quick phase to the slow phase, the detection was executed most successfully. It is thought that in CN, a target is usually gazed upon at a point, changing the direction from the quick phase to the slow phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A study of visual function in congenital nystagmus--mechanism of visual improvement after stereotactic superior colliculectomy]. 319 Sep 32

A quantitative analysis of horizontal head-shaking nystagmus (HSN) was made on 48 patients with unilateral peripheral vestibular disorders in conjunction with stimulus intensity (the number of head-shakes). Each patient underwent three head-shaking tests with 10, 30 and 50 horizontal head-shakes, with a rapidity of about 2 Hz, in random order. HSN was recorded by ENG with the eyes open in a completely dark room, and various components of nystagmus were measured manually. 1. HSN appeared in a biphasic or monophasic pattern. In some patients with biphasic HSN, the 2nd phase disappeared as the stimulus intensity diminished. 2. The maximal slow-phase eye velocity (MSV) of the 1st phase of biphasic HSN was significantly greater than that of monophasic HSN. The tendency to increase in proportion to stimulus intensity was also greater in biphasic than in monophasic HSN. The MSV values of the 2nd phase of biphasic HSN were smaller than in the 1st phase (less than one-third) at all stimulus intensities. 3. The duration and total number of HSN beats were greater in the 2nd phase of biphasic HSN and increased markedly in proportion to stimulus intensity. In contrast, in the 1st phase of biphasic HSN and in monophasic HSN, the values of these nystagmus components were smaller, there was no clear relationship with stimulus intensity, and when the stimulus intensity was high, they were instead significantly smaller in the 1st phase of biphasic HSN than in monophasic nystagmus. 4. As the stimulus intensity rose to a high level, the interval between the 1st and 2nd phases of biphasic HSN (2nd phase latency) shortened, and the 2nd phase tended to appear more quickly after head-shaking. 5. The time constant of the decline in slow-phase eye velocity was nearly constant in both the 1st phase of biphasic HSN and monophasic HSN, regardless of stimulus intensity. It was especially noteworthy that in response to an increase in stimulus intensity, both the MSV in the 1st phase and the duration of the 2nd phase of biphasic HSN increased, while the duration of the 1st phase of biphasic HSN was inversely suppressed by the 2nd phase.
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PMID:[Quantitative analysis of head-shaking nystagmus of peripheral vestibular origin in conjunction with stimulus intensity]. 816 34

A quantitative analysis of horizontal head-shaking nystagmus (HSN) was made on 48 patients with unilateral peripheral vestibular lesions in conjunction with stimulus intensity. Each patient underwent three head-shaking tests with 10, 30 and 50 horizontal head-excursions at a frequency of approximately 2 Hz, and HSN was recorded on ENG with eyes open in total darkness. i) HSN appeared in a biphasic or monophasic pattern. ii) The maximal slow-phase eye velocity (MSV) of the 1st phase (PI) of biphasic HSN increased significantly in proportion to stimulus intensity, and was significantly greater than that of monophasic HSN. iii) The duration of HSN was greater in the 2nd phase (PII) of biphasic HSN than in PI and increased markedly in proportion to stimulus intensity. iv) As the stimulus intensity rose to a high level, the interval between PI and PII (2nd phase latency) shortened, and the PII tended to appear more quickly after head-shaking. It was especially noteworthy that in response to an increase in stimulus intensity, both the MSV in PI and the duration of PII of biphasic HSN increased, but the duration of PI was reversely suppressed by the PII.
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PMID:A quantitative analysis of head-shaking nystagmus of peripheral vestibular origin. 874 24

Vestibular compensation, or neuronal plasticity in the central vestibular system, is quite an important process in patients with acute unilateral peripheral vestibular disease, allowing them to lead a comfortable daily life when medical treatments fail to cure the peripheral vestibular function. Is the residual unilateral vestibular input from damaged vestibular endo-organs a positive or negative factor for the development of dynamic vestibular compensation in the central nervous system? To elucidate the true mechanism of vestibular compensation, we examined the ENG findings and dizziness handicap inventory questionnaire in patients with vestibular neuronitis (VN), sudden deafness with vertigo (SDV), Meniere's disease (MD) and acoustic tumor (AT) during remission of the vertigo attacks. We obtained neuro-otological findings from caloric tests and head shaking after nystagmus using ENG and information on motion-evoked dizziness in daily life using the questionnaire. There were no significant differences in the sex, age or canal paresis % (CP%) among the four groups. The results of the present study showed that dynamic vestibular compensation processes developed progressively in the order of patients with SDV, VN, MD and AT (Kruskal-Wallis : p < 0.05). This finding suggests that processes of dynamic vestibular compensation could be accelerated in patients with fixed vestibular lesions caused by SDV and VN more than in those with fluctuating vestibular functions caused by MD and AT. In patients with fixed vestibular lesions caused by SDV and VN, patients with lower CP% showed dynamic vestibular compensation (i.e. disappearance of head shaking after nystagmus (chi-square: p < 0.05) and motion-evoked dizziness (Mann-Whitney: p < 0.0005)) more rapidly than those with higher CP%. In patients with fluctuating vestibular functions caused by MD and AT, patients with lower CP% did not always develop dynamic vestibular compensation more smoothly than those with higher CP%.
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PMID:[Dynamic vestibular compensation in vestibular peripheral diseases]. 1806 76