Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 4 cases of arterio-veinous malformations located within the occipito-cerebello-mesencephalic dihedral (which is this region of the brain including the cistern of Galen and the surrounding formations : the quadrigeminal bodies forwards, the splenium of the corpus callosum upwards, the upper face of the cerebellum and the pedonculus cerebellaris superior below) the authors related their own experience. These 4 cases are detailed from a clinical point of view. Them, a synthetic study is undertaken in which a comparison is done between the literature and the clinical features encountered : headache, sub-archnoid hemorrhage, impairment of consciousness, clinical features such as cranial nerve impairment, nystagmus motor impairment, cerebellar deficit, hydrocephaly. The value of angiography, ventriculography and CAT is discussed. All these patients have been operated upon as far as the authors think that a better chance can thus be offered to them. The choice of the technique is discussed. For one patient, the sub-temporal route was performed ; but it seems worth using the posterior inter-occipital route : this allows a better view on the lesion and an easier treatment of the malformation. These 4 patients suffered post operatively of a visual defect. The control angiography revealed no more arterio-venious malformation in two patients, a mild one in two others.
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PMID:[Arterio-veinous malformations located within the occipito-cerebello-mesencephalic dihedral (author's transl)]. 31 28

Optokinetic nystagmus (OKN) asymmetry in 4 patients with localized lesions of the unilateral visual cortices (2 in the right hemisphere and 2 in the left hemisphere), confirmed at autopsy or by CAT scan, was detected by computer analysis. The ENG recordings showed typical asymmetry of OKP: lower amplitude in the contralateral optokinetic pattern (OKP) than on the side with the visual cortex lesion. Analysis of this asymmetry revealed lower amplitude, remarkably impaired slow-phase velocity, and mildly impaired fast-phase velocity, with a slight difference in number of OKN. The findings suggested that asymmetry of OKP in patients with localized lesions of the unilateral visual cortices is primarily caused by the impaired slow-phase velocity of the contralateral OKN because of a slight change in number of OKN.
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PMID:Analysis of optokinetic nystagmus in patients with localized lesions of unilateral visual cortices. 269 88

Primary amebic meningoencephalitis and granulomatous amebic encephalitis are well recognized clinicopathological entities caused by free-living amebas. Associated arteritis and "mycotic aneurysms" with infiltration of intracranial arteries by lymphocytes, amebic trophozoites and cysts have not been previously reported. A 26-month-old girl had a 3-week history of encephalitis, characterized, initially, by vomiting and low-grade fever. Subsequently, she developed ataxia, generalized weakness, lethargy, and esotropia. The first CSF showed 490 RBC/microliters, 705 WBC/microliters with 90% mononuclears. Her pupils reacted briskly to light. Moderate nuchal rigidity, nystagmus, fixed downward gaze, anisocoria, bilateral 6th nerve palsy, left arm monoparesis and left Babinski were present. CAT scan revealed slight symmetrical dilatation of anterior horns of lateral ventricles and an area of abnormal enhancement above the 3rd ventricle. She died 14 days after admission, 5 weeks after onset of symptoms. The brain showed focal necrotizing encephalopathy, involving thalami, cerebellum, brain stem, and cervical and upper thoracic spinal cord. Numerous free-living amebic trophozoites and cysts were present within a chronic granulomatous encephalitis. There were trombosis of basilar, posterior cerebral, and vertebral arteries with profuse chronic panarteritis, fibrinoid necrosis, and mycotic aneurysms.
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PMID:Granulomatous encephalitis, intracranial arteritis, and mycotic aneurysm due to a free-living ameba. 689 86

A new clinical case of Pontine Reticular Formation (P.R.F.) syndrome is reported and analysed using electro-oculograms. The CAT scan showed a probably metastatic tumour, clearly limited and located in the ventral part of the left tegmentum in the lower pons. The oculomotor disorders were typical of the P.R.F. syndrome and similar to those previously reported in pathological studies. The left P.R.F. damage was clinically evidenced by the loss of all leftward saccades (voluntary saccades and quick phases of nystagmus), including also those situated in the right hemifield of movement. It was noticed that the voluntary return movement driving both eyes from the right lateral position to the midline was remarkably slow and twice slower for the left eye (10 degrees/s) than for the right one (20 degrees/s). The loss of pursuit movements in the left hemifield of movement suggested that the lower part of the left P.R.F. was affected by the lesion. The preservation of normal leftward oculocephalic movements for the right eye indicated that the left abducens nucleus was spared. Lastly, the complete abductive paralysis of the left eye including the oculocephalic movement implied that the left abducens motoneurons passing through the lower part of the P.R.F. were damaged. All these functional and structural correlates are consistent with the location of the lesion given by the CAT scan. They are reviewed in the light of recent experimental and clinico-pathological data. A detailed physiopathological interpretation accounting for the slow voluntary movements, observed in place of the leftward return saccades in the right hemifield of movement, is proposed. The slowness of the movements of both eyes results from lack of phasic excitation of the motoneurons of the agonist muscles and from lack of phasic inhibition of the motoneurons of the antagonist muscles, both mechanisms being suppressed by the lesion which damages the excitatory burst neurons of the left P.R.F. As the tonic cells of the left P.R.F. are also out of action, these slow movements could mainly be controlled by the tonic cells of the right P.R.F. For the left eye, as the root fibres of the left abducens nucleus are damaged, no excitation can occur on the agonist muscle (left lateral rectus) and there is only a voluntary tonic disfacilitation of the motoneurons of the antagonist muscle (left medial rectus). For the right eye, the same mechanism involving the antagonist muscle (right lateral rectus) would be combined with some tonic excitation of the motoneurons of the agonist muscle (right medial rectus), thus accounting for the twice faster velocity of this eye. This tonic excitation reaching the right medial rectus could be mediated either by one of the other afferent neurons of the left abducens nucleus encoding eye position--namely those arising from the vestibular nuclei or from both prepositus hypoglossi nuclei--or by the right ascending tract of Deiters projecting to the right medial rectus motoneurons.
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PMID:[The pontine reticular formation syndrome. Physiopathologic data on voluntary eye movement abnormalities]. 715 38

Optokinetic nystagmus (OKN) was studied by computer analysis in nine patients with lesions on the left unilateral parietal lobe (group A) and in five patients with lesions on the entire left hemisphere (group B), as confirmed by CAT or MRI scans. OKN stimulation and recordings were evaluated based on the optokinetic pattern (OKP). In group A, there was no directional preponderance. However, in group B, the Electronystagmography recordings showed typical asymmetry of OKP. This asymmetry was revealed by a low amplitude and a significantly impaired slow-phase eye velocity of the right OKP. Asymmetry of OKP resulted from the impaired slow-phase eye velocity of the contralateral OKN to the damaged hemisphere because of a slight change in fast-phase eye velocity.
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PMID:Analysis of optokinetic nystagmus in patients with lesions on the left unilateral parietal lobe or the entire left hemisphere. 1167 33