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)

Selective embolization of the internal carotid artery bifurcation (ICA bifurcation) was performed in monkeys (Macaca mulatta) to study acute regional cerebral ischemia in the middle cerebral artery (MCA) territory with minimum surgical intervention in the neck under sedated conditions. The anthropomorphic similarity in angio-anatomy of the carotid system of monkeys and the use of silastic spheres, as artificial emboli, of the critical diameter of 1.2 to 1.4 mm resulted in the overall success rate of 87% in localizing the site of embolization to the ICA bifurcation, producing ischemia in the whole middle cerebral artery territory. All the animals with ICA-bifurcation embolization had contralateral deep motor weakness and conjugate eye deviation with nystagmus toward the site of embolization. Simultaneous EEG recording showed flattening of the basic background activities over the affected MCA area and cerebral arteriograms showed definite retrograde filling of the proximally occluded MCA. Clinical recovery was observed in a few animals within two to five hours of embolization. Gross ischemic swelling in the affected MCA territory, particularly in the gray matter, became obvious in six of eight animals which were exposed to four to five hours of ischemia. The angio-anatomical study of the carotid system of this experimental animal as a background for this MCA stroke model confirmed the previous observations of other investigators that the extremely abundant leptomeningeal anastomoses would be one of the major factors leading to the variability in the clinicopathological pictures seen in the models of proximal MCA occlusion. In addition, the pre-parenchymal anastomoses in the base of brain between the medial striate arteries from the proximal anterior cerebral (ACA) and lateral lenticulostriate arteries from the MCA were observed and described as a possible functional collateral to the basal ganglia in case of proximal MCA occlusion.
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PMID:Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 1: Angio-anatomy and description of an experimental model with selective embolization of the internal carotid artery bifurcation. 40 41

Basilar migraine has been studied by Bickerstaff who considers that there is a vasoconstriction in the basilar territory resulting in transient ischemia with the corresponding neurological symptoms including vertigo, and followed by the vasodilatation causing the headache. Three cases, treated in neurology, have had an audiovestibular investigation with an E.N.G. and an audiogram and are described herein. Nystagmus and hearing loss have been observed in one of these cases and it is suggested that the internal auditory artery participates in the basilar migrainous processes. The diagnosis of basilar migraine is impossible to prove and the investigation is very limited. Finally it is the evolution of the patient which helps in establishing the diagnosis of basilar migraine.
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PMID:[Basilar migraine]. 61 47

We reported a patient with brainstem infarction who presented paralytic pontine exotropia (PPE) in acute phase and non-paralytic pontine exotropia (NPPE) during the recovery phase. On March 10, 1991, a 60-year-old man was brought to our hospital with chief complaints of double vision and right hemiparesis. The ocular position of the left eye on forward gaze was fixed at the midline, while the right eye was abducted, and skew deviation was observed. On leftward gaze, neither eye could pass the midline, and on rightward gaze the right eye was abducted and monocular nystagmus was noted in the abducted right eye, which indicated paralytic pontine exotropia. T2-weighted MRI showed high signal intensity lesions in the left paramedian portion of the mid-pontine tegmentum beneath the fourth ventricle, and in the midline of the pontine base extending to the left side. The next day, similar disturbance of ocular movement was seen on rightward gaze, but the limitation of leftward gaze had improved and NPPE was noted to have developed. On the third day, there was no abduction of the right eye on forward gaze, but left MLF syndrome was still present. Seven days later, the disturbances of ocular movement disappeared. The lesion was considered to be due to partial impairment of the left paramedian pontine reticular formation in addition to the MLF. PPE caused by ischemia due to the perforating arteries of the brainstem, different from that due to basilar artery occlusion may recover after progression through NPPE and MLF syndromes. Hence, one-and-a-half syndrome, PPE, NPPE, and MLF syndromes are considered to be analogous to one another.
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PMID:[A case of brainstem infarction presenting with paralytic pontine exotropia and non-paralytic pontine exotropia]. 181 90

A 38-year-old woman developed intermittent oscillopsia occurring every 45 to 90 minutes and lasting 20 to 40 seconds. She had a right-beating jerk nystagmus during these episodes. At other times, her neurologic examination was normal, and no nystagmus could be elicited. The nystagmus resolved when her classic migraine headaches were controlled with medical therapy. This intermittent unidirectional nystagmus may represent dormant periodic alternating nystagmus or another type of dormant nystagmus appearing intermittently due to episodic migrainous brainstem ischemia.
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PMID:Intermittent unidirectional nystagmus. 236 28

Three men developed acute esotropia, stupor, and impaired upward gaze. Vestibulo-ocular stimulation showed that the adducted eye remained immobile while the fellow eye responded normally. The alteration of consciousness, the long-tract neurologic signs, and the esotropia quickly resolved. Upgaze paresis and brief bursts of convergence-retraction nystagmus were the major residual signs. Imaging techniques demonstrated lesions of the contralateral posterior thalamus in each patient. Several mechanisms are proposed to explain the acute esotropia. Impairment of monocular projections in the contralateral posterior thalamus could disinhibit neurons in the oculomotor complex, or ischemia of inputs to neurons involved with vergence control in the midbrain could result in tonic activation of the medial rectus. The clinical and radiographic findings are consistent with infarction in the territory of penetrating branches of the basilar-communicating (mesencephalic) artery. Embolism to the top of the basilar artery is presumed to be the precipitating event.
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PMID:Acute thalamic esotropia. 1117 22

A broad range of neuro-ophthalmologic signs occurs with the rostral basilar artery syndrome (RBAS) and transient ischemia or infarction of the midbrain, thalamus, hypothalamus, paramedian diencephalon, and posterior temporal and occipital lobes. The pattern of affected neuroanatomic regions results in diverse patterns of interrelated functional disabilities in the areas of vertical gaze, nystagmus, oculomotor function, pupillary reactivity, visual fields, color vision, and visual illusions. With increasing recognition of more clinically benign forms of RBAS, it has become apparent that the vascular syndrome is often improperly diagnosed and may be associated with remediable occult medical disorders. To facilitate the acquisition of accurate diagnostic and therapeutic information, neuro-ophthalmologic signs were prospectively assessed in 61 patients with RBAS. The clinicoanatomic correlates of these diverse ocular manifestations are presented.
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PMID:The neuro-ophthalmologic spectrum of the rostral basilar artery syndrome. 341 27

Benign paroxysmal vertigo of childhood is a vestibular disorder characterized by multiple sudden brief episodes of true vertigo with nystagmus usually beginning after the age of 4. The diagnosis is based on the characteristic history, because the otologic and neurologic examinations, electronystagmogram, audiogram, and electroencephalogram are usually normal. The etiology of the disorder remains unknown, although a vascular disturbance of the posterior circulation with ischemia of the labyrinth or vestibular nuclei is most commonly postulated. A review of the literature and five new cases are used to acquaint otolaryngologists with this entity, review the characteristic clinical history, discuss differential diagnosis, and emphasize the usual clinical course.
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PMID:Benign paroxysmal vertigo of childhood. 349 65

We report two cases of non periodic alternating nystagmus, one of vascular origin (ischemia of the vertebrobasilar territory) and a second of traumatic origin (whiplash injury) with otoneurological signs, typical of lesions in posterior cranial fossa and in particular of vestibulum-cerebellum and brainstem: gaze paretic nystagmus, rebound nystagmus, saccadic dysmetria, vestibular hyperreflexia and impaired visual suppression test. In one case it was possible to give baclofen therapy, which yielded positive results. Suspension of drug administration resulted in the worsening of clinical signs. The mechanism of action of the drug will be discussed.
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PMID:Aperiodic alternating nystagmus: report of two cases and treatment by baclofen. 375 19

Both ictal nystagmus and cortical blindness may occur transiently in acute cerebral disorders and therefore escape clinical detection, particularly in confused, agitated patients. The following case report describes a young woman with chronic myelogenous leukemia who became progressively ill following bone marrow transplantation. During the course of her illness, acute ictal nystagmus developed from focal right occipital ischemia; postictally she remained cortically blind with possible visual hallucinations for 48 hours.
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PMID:Cortical blindness following ictal nystagmus. 397 48

Adenosine diphosphate (ADP) injection into a unilateral vertebral artery in rabbits decreased per-rotational nystagmus; the nystagmus beating toward the injected side was predominantly suppressed. This influence became obvious when the animal's blood pressure was low. Field potentials were recorded in the vestibular nuclei upon electric stimulation of the vestibular labyrinth. ADP administration into the vertebral artery also suppressed the amplitude of vestibular evoked potentials (VEPs). Effects of ADP upon the vestibulo-ocular reflex and VEP were considered to be due to regional ischemia induced by the microemboli, which consisted of platelet aggregation.
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PMID:Effects of adenosine diphosphate administration on the vestibulo-oculomotor reflex of rabbits. 612 15


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