Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 24-year-old female was admitted to our hospital on Aug. 20 in 1986 because of blurred vision and right pupillary dilatation. She had sometimes noticed headache later than 1976, and blurred vision without headache several times a year later than 1983. She had been told her right pupil dilated when she had complained of blurred vision. Neurological examination revealed abnormal findings as follows; diminished sense of smell in the right side, anisocoria (R 8 mm, L 5 mm), bilateral hippus, hypesthesioalgesia in her right face, left trunk and left arm. The pupils were round and contracted promptly to light. Accommodation reflex and ciliospinal reflexes were normal. Neither blepharoptosis nor external ocular muscle paresis were observed. Deep tendon reflexes were normal. Planter responses were flexor. There was no meningeal irritative sign. No abnormal findings were obtained in blood and urine, chest X-p, brain enhanced CT scan, EEG, and cerebral angiography except for slight degree of anemia. Serum TPHA was negative. However, the cell count of cerebrospinal fluid (CSF) was 18/mm3 (Ly 100%) and decreased to 9/mm3 (Ly 100%) in nine days. Protein content and glucose level of CSF were normal. Pupils were not constricted by 0.125% pilocarpine instillation. Loss of smell and sensory disturbance disappeared within three days and her pupils became isocoric by five days after admission. The patients of episodic unilateral mydriasis without apparent cause had relatively same clinical features as "unilateral springing pupil" proposed by Hallett et al. (1970). Except for mydriasis, they had no abnormal findings of neurological and laboratory examinations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Recurrent episodic unilateral mydriasis with pleocytosis in the cerebrospinal fluid--a case report]. 259 48

Cerebral symptoms were registered in a multicenter study including 64 patients with severe hypertension, diastolic blood pressure (DBP) greater than or equal to 135 mmHg, and more or less pronounced hypertensive encephalopathy. The symptoms were: headache (70%), dizziness (35%), consciousness disturbances (28%), nausea (27%), paresis (23%), blurred vision (22%), paraesthesia (21%) and vomiting (14%). None had convulsions or coma. Initial treatment was furosemide i.v., and if DBP was greater than or equal to 125 mmHg after one hour, patients were randomized to treatment with either i.v. diazoxide (bolus injections of 75-150 mg) or i.m. dihydralazine (bolus injections of 6-12.5 mg). A gradual fall in blood pressure (BP) was obtained in all three groups. Along with BP reduction a substantial regression of neurological symptoms was registered. After 5 hours only minor cerebral symptoms were present without significant difference between diazoxide and dihydralazine. None developed cerebral complications. The study failed to show a significant correlation between BP reduction and regression of neurological symptoms graded semiquantitatively. Reduction of BP by titration using small repeated bolus injections is recommended, but oral treatment should be considered in the patients who are able to ingest peroral medication in spite of neurological symptoms.
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PMID:Reversibility of cerebral symptoms in severe hypertension in relation to acute antihypertensive therapy. Danish Multicenter Study. 353 94

The doll's eye reflex represents the vestibulo-ocular reflex (VOR) elicited by high-acceleration head rotation. After complete unilateral vestibular lesions, the ipsilateral, horizontal doll's eye reflex is replaced by a series of "catch-up" saccades. These cause permanent symptoms of blurred vision and dizziness during ipsilateral turns. We compared normal controls and patients with complete surgical lesions or canal paresis of up to 9 years duration via electronystagmography (ENG) to determine the usefulness of the doll's eye test as a diagnostic test for complete vestibular lesions. This test was found to be more sensitive in diagnosis of such lesions than head-shaking nystagmus, rotatory directional preponderance, and spontaneous nystagmus. It is also useful to document VOR function in patients in whom caloric irrigation is contraindicated.
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PMID:Functional loss of the horizontal doll's eye reflex following unilateral vestibular lesions. 816 88

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74

Movement disorders following midbrain haemorrhage are infrequently encountered in rehabilitation, and are uncommonly corrected by pharmacologic means. This report describes a 20 year-old male with a prior history of cocaine abuse who presented with a 4 day history of dysarthria and blurred vision following methamphetamine abuse. Physical examination demonstrated hypertension, left facial hemispasm, bilateral upward gaze paresis and ataxic gait. Magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) showed multifocal parenchymal haematomas in the mesencephalic tegmentum, subcortical left front region and right anterior thalamus consistent with cavernous angiomas. The patient was transferred to rehabilitation on hospital day 5. The following day, he developed choreoathetoid movements, dystonia, and aphasia, secondary to an extension of the midbrain haemorrhage. Cogentin was initiated with slight improvement in choreoathetoid movements. The patient began intensive multidisciplinary rehabilitation therapy but after 18 days of therapy, the patient remained totally dependent in activities of daily living (ADLs), transfers, mobility and was unable to communicate in any manner. A trial of Sinemet was initiated, with resultant steady improvement in functional ability over the next month. By discharge, the patient was independent in ADLs and ambulation. By 9 months post discharge follow-up, the patient was fully independent with normal cognition, and had self tapered all medications without ill effect. Dopamine agonist trials of appropriate duration appear indicated in cases of movement disorder (paucity or excess) following midbrain lesions.
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PMID:Pharmacologic management of movement disorder after midbrain haemorrhage. 965 26

Subacute disseminated histoplasmosis is an uncommon entity. Typical neuro-ophthalmologic manifestations are usually secondary to histoplasmomas or encephalitis. A 45-year-old man noted blurred vision while receiving empiric antituberculosis therapy for fever and diffuse granulomatous disease of unknown origin. Vertical-gaze palsy, right horizontal-gaze paresis, and mild right optic neuropathy were found on neuro-ophthalmologic examination. Further questioning revealed a history of frequent contact with fighting cocks from South America. Magnetic resonance images were consistent with multiple hemorrhagic infarcts, areas of inflammation, or both, and cerebral angiography showed changes consistent with vasculitis. A previously obtained biopsy specimen from the duodenum was restained and found to be positive for fungal elements. Serum antigen titers for Histoplasma capsulatum demonstrated evidence of active infection. This case is a rare example of a supranuclear ocular motility disturbance and optic neuropathy secondary to an occlusive vascular process in a patient with subacute disseminated histoplasmosis.
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PMID:Disseminated histoplasmosis causing reversible gaze palsy and optic neuropathy. 1038 Jan 38

In the last 10 years, wound botulism has increasingly been reported and nearly all of these new cases have occurred in injecting-drug abusers. After absorption into the bloodstream, botulinum toxin binds irreversibly to the presynaptic nerve endings, where it inhibits the release of acetylcholine. Diplopia, blurred vision, dysarthria, dysphagia, respiratory failure and paresis of the limbs are common symptoms of this intoxication. Surprisingly and despite the well-known blocking action of the botulinum toxin on the autonomic nerve system, little attention has been paid to changes in the lower urinary tract following acute botulinum toxin poisoning. Here we report a case of bladder paralysis following wound botulism. Early diagnosis and adequate management of bladder paralysis following botulism is mandatory to avoid urologic complications. Accordingly, the prognosis is usually favorable and the bladder recovery complete.
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PMID:Transient paralysis of the bladder due to wound botulism. 1146 47

This report describes a 16-year old female patient who presented with acute paresis in both lower limbs, acute urinary retention, blurred vision and arthritis. The patient was diagnosed as having systemic lupus erythematosus with myelitis and bilateral abducent nerves palsy. The administration of steroids resulted in marked improvement in her neurological symptoms.
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PMID:A case of neuropsychiatric lupus with myelopathy successfully treated with corticosteroids. 1528

We report a case of severe dysphagia in a 29-yr-old woman with cerebral palsy after she was injected with botulinum toxin B to her lower limbs and lumbar paraspinal muscles. Four days after the treatment, she developed difficulty swallowing, more severe for solid foods than for liquids, accompanied by dry mouth, blurred vision, and voice hoarseness. Fifteen days after the injection, with worsening of her dysphagia, she was hospitalized. A laryngoscopic evaluation revealed bilateral vocal cord paresis, and a modified barium swallow test demonstrated delayed oral initiation, upper airway penetration, and no reflexive cough. In the following days, she improved spontaneously and was discharged 12 days later when she re-acquired the ability to swallow solid foods. Her symptoms resolved completely only 75 days after the injection. Although dysphagia is a common side effect of botulinum injection in the neck, to our knowledge, this is the first reported case of severe dysphagia after injection in a distant anatomic site.
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PMID:Severe Dysphagia after botulinum toxin B injection to the lower limbs and lumbar paraspinal muscles. 1703 94

Many medicines, mainly with neurological purpose, interfere with the oculomotricity. The biochemistry of the oculomotor systems and thus, the mechanisms of action of these drug interferences are not completely clarified. Most medicines impair the eye movements at the level of their fine adjustment by feed-back loops implying the cerebellum. Quite often, the interferences remain asymptomatic, restricted to a saccadic pursuit, hypometric saccades or an end-point nystagmus. Sometimes however, symptoms of dizziness or oscillopsia appear, due to loss of the vestibulo-ocular reflexes efficiency. A diplopia or a blurred vision by double outline could be suggestive of an ocular motor paresis or a loss of the binocular fusion due to drugs action.
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PMID:[Oculomotor anomalies from medications]. 1771 42


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