Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The records of 21 horses with rabies were reviewed. Results of fluorescent antibody testing for rabies antigen in brain tissue were positive in each case. According to the histories, 5 of the horses had been vaccinated for rabies between 4 to 24 months prior to the onset of the clinical signs. Bite wounds were not observed on any of the horses, and exposure to a suspected rabid animal was witnessed in only 5 cases. Clinical signs of disease at the time of initial examination included ataxia and paresis of the hindquarters (9/21, 43%), lameness (5/21, 24%), recumbency (3/21, 14%), pharyngeal paralysis (2/21, 10%), and colic (2/21, 10%). The major clinical signs observed over the course of hospitalization included recumbency (21/21; 100%), hyperesthesia (17/21; 81%), loss of tail and anal sphincter tone (12/21; 57%), fever (11/21; 52%), and ataxia and paresis of the hindquarters (11/21; 52%). Mean survival time after the onset of clinical signs was 4.47 days (range, 1 to 7 days). Supportive treatment, given to 9 horses, had no effect on survival time and did not correlate with the detection of negri bodies at necropsy. Cerebrospinal fluid (CSF) was obtained from 6 horses and was determined to be abnormal in 5. The most common abnormality was a slightly high total cell count (5/6), with a predominance of lymphocytes (4/6). The CSF total protein concentration was high in only 2 horses. At necropsy, there was gross evidence of diffuse brain edema, meningeal congestion, and focal areas of hemorrhage in 5 horses (24%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rabies in horses: 21 cases (1970-1990). 160 22

Optimal techniques for the preoperative assessment and intraoperative management of the petrous carotid artery remain undefined. While purposeful "avoidance" of this structure may result in partial tumor removal, limited exposure of the petrous carotid artery may lead to inadvertent injury with life-threatening neurovascular sequelae. Twenty-five cases are reported in which surgical manipulation of the petrous carotid artery was necessary to accomplish total tumor removal or gain operative exposure to the skull base. A standard diagnostic radiographic assessment consisted of high-resolution computed tomography, magnetic resonance imaging, and a 4-vessel angiography. Preoperative balloon occlusion of the involved internal carotid artery was performed in four patients. Surgical approaches used in this series were broadly classified as: infratemporal-anterolateral (14), pterional-infratemporal (6), or pterional-anterolateral (5). Intraoperative management of the carotid artery consisted of total decompression in 19 cases, decompression with mobilization in four patients, and resection in two instances. Major neurovascular complications included one stroke and death caused by arterial occlusion, one stroke and death caused by arterial spasm, one stroke caused by brain edema, and one death related to a postoperative carotid hemorrhage. Other nonvascular complications included brain swelling, cranial nerve palsies, dysphagia, ataxia, cerebrospinal fluid fistulae, flap necrosis with wound infection, and pneumocephalus. Invasive and noninvasive methods are outlined for the preoperative assessment of the petrous carotid in cases of advanced skull base disease and intraoperative management options are detailed.
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PMID:The perioperative management of the petrous carotid artery in contemporary surgery of the skull base. 211 30

We examined the effect of dilazep dihydrochloride (dilazep) on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats (SHRs). Ataxia and loss of the righting reflex were noted in some SHR after 4 hr occlusion of the bilateral common carotid arteries; and 11 of 15 animals died within 72 hr after reperfusion. One hour after reperfusion, the cerebral water content increased significantly. The chemiluminescence value in the brain homogenate increased slightly during occlusion; and following reperfusion, there was a transient but marked further increase, indicating the acceleration of lipid peroxidation that resulted from free radical reactions. The i.v. infusion of dilazep (0.3-3 mg/kg/hr for 4 hr) during occlusion dose-dependently reduced the appearances of neurological symptoms and mortality during occlusion and after reperfusion. The increase in cerebral water content and chemiluminescence value were clearly prevented by dilazep (3 mg/kg/hr). It is concluded that dilazep possesses the ability to prevent the appearances of neurological symptoms and brain edema induced by ischemia and reperfusion. The suppression of lipid peroxidation may be involved in the mechanism of the preventive effect of dilazep on cerebral injury.
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PMID:[Effect of dilazep dihydrochloride on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats]. 235 33

The lethality of Poa huecu, a plant toxic to cattle and sheep, was followed by injection of chromatographic fractions in mice. The lethal aqueous extract was administered i.p. to Rockland mice of either sex and produced motor incoordination, transient ataxia, rough hair coat, tremors and muscle contractions and, occasionally, blindness. Doses greater than 1.5 g/kg mouse were always lethal. Fractionation of this lethal extract included dialysis, column chromatography on Sephadex G-25 and fractional precipitation with ethanol. Precipitates obtained with 70% and 85% ethanol were further purified on a DEAE-cellulose column. Eight fractions were obtained, each was injected into mice. Only fractions 3-6 were toxic. Fraction 3 produced slight hepatosis and hyperemia in the liver and gliosis in the brain. None of the other tissues exhibited histological lesions. Fractions 4 and 5 caused death of all animals within 30 min to 4 hr after injection. Polyacrylamide gel electrophoresis and acid hydrolysis showed that fractions 4 and 5 contained a glycoprotein of nearly the same mol. wt (67,000-94,000). Microscopic pathology in the mice treated with the lethal glycoprotein of fraction 4 included hyperemia in the kidneys, megakaryocytes in the spleen, slight hepatosis and focal coagulative necrosis with nuclear pyknosis and karyonexis in the liver, gliosis, intracellular brain edema with axon degeneration and swollen astrocytes in the brain. These brain injuries may relate to the motor incoordination of cattle that causes a delayed righting reflex. The major monosaccharides of the lethal glycoprotein are glucose and mannose, while rhamnose, arabinose, xylose and galactose are present in low percentages. Proline and the acidic amino acids (glutamic and aspartic acids) are the most abundant in the peptidic residue.
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PMID:The lethal principle of Poa huecu (coiron blanco): a plant indigenous to Argentina. 262 69

We report our experience with and long-term results of 37 patients with tentorial meningiomas who underwent surgery between 1972 and 1993. The average age was 43 years, and the mean duration of symptoms was 36 months. Headache (83.8%) and extremity or gait ataxia (35.1%) were the most common complaints. On neurological examination, signs of elevated intracranial pressure and cerebellar deficits (51.4%) were the most common findings, followed by third nerve involvement (35.1%). Computed tomography, angiography, and, in recent years, magnetic resonance imaging were used as diagnostic tools and for planning the surgical procedure. According to the primary site of attachment, the tentorial meningiomas were divided into three subgroups: medial, lateral, and falcotentorial. The lateral and medial tumors, with mainly supratentorial development, were approached from above by using a temporal, temporooccipital, or parietooccipital craniotomy. For tumors developing mainly in the posterior cranial fossa, suboccipital craniectomy was performed. In six patients who showed medial tentorial and petrous apex attachment, a combined subtemporal transpetrosal and retromastoid approach was performed. In 31 patients, the tumors were totally removed, and, in 6 patients, only subtotal excision could be done. Seven patients had postoperative complications, but only one of them died of severe brain edema. Our mortality rate was 2.7%. In this article, appropriate preoperative studies, surgical techniques, and surgical results are discussed.
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PMID:Tentorial meningiomas. 770 67

Two cases of neurocysticercosis from Maharaj Nakorn Chiang Mai Hospital were reported with autopsy and surgical findings. The autopsy case was a 14-year-old girl who had a single cyst at the cisterna ambiens of the pineal region, causing hydrocephalus and severe brain edema accompanied with increased intracranial pressure and psychiatric problems but no definite localizing signs. The surgical case was a 35-year-old man with symptoms of increased intracranial pressure, localizing signs of ataxia of the left lower extremity and hearing loss in the right ear. Computed brain tomography showed a posterior fossa cyst with obstructive hydrocephalus. The cyst and the tissues from CP angle region were removed and sent to the Department of Pathology. Histopathologic appearance of both cases showed cysticercosis.
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PMID:Cysticercosis in the posterior cranial fossa. 774 77

A 25-year-old woman suffered from hyperemesis gravidarum when she was seven weeks pregnant. Since her vomiting continued, she received intravenous dextrose and electrolytes without thiamine in a hospital. One month later, she developed gait disturbance, followed by confusion and dysarthria. On admission to our department, she was confusional and had ataxic dysarthria. Spontaneous and gaze evoked nystagmus was present. Limb coordination was bilaterally ataxic. Based on her clinical course and symptoms, she was diagnosed as having Wernicke's encephalopathy. From the admission day, intravenous infusion of vitamin B1 (600 mg/day) was started. A few days later, her consciousness and limb ataxia began to improve. However, truncal ataxia and polyneuropathy became evident. Eight weeks after onset, she developed Korsakoff's psychosis such as anterograde and retrograde amnesia, disorientation and confabulation. We administered large amounts of corticosteroid (methylprednisolone 500 mg/day) in order to reduce brain edema or stabilize the impaired blood-brain barrier. Soon after, her psychosis began to improve gradually. She recovered remarkably from the psychosis, but she was left with persistent nystagmus, mild ataxic gait and polyneuropathy. The present case suggests that corticosteroid may have the beneficial effect on Wernicke-Korsakoff syndrome.
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PMID:[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]. 795 22

The mouse is considered to be insensitive and the hen sensitive to clinical expression of organophosphorus-induced delayed neuropathy (OPIDN) which is associated with inhibition of neuropathy target esterase (NTE). This species difference is reevaluated with two optimized inhibitors of hen brain NTE by examining them for potential neurotoxic effects in mice. 2-Octyl-4H-1,3,2-benzodioxaphosphorin 2-oxide (OBDPO) and ethyl octylphosphonofluoridate (EOPF) inhibit mouse brain NTE in vitro by 50% at 0.12 and 0.02 nM and induce neurotoxic signs in mice at 10 and 5 mg/kg, respectively. The action of these compounds in both l- and 6-month-old mice, sometimes after early transient cholinergic signs, involves ataxia, paralysis, and death in 1 to 3 days and is accordingly referred to as subacute neurotoxicity. The neurotoxic signs are associated with brain edema and severe vacuolation in the grey matter of the brain and spinal cord, particularly the neuropile. Subacute neurotoxic signs are always associated with at least 80% inhibition of brain NTE activity 16-24 hr after treatment. Acetylcholinesterase and butyrylcholinesterase are much less sensitive than NTE to inhibition by OBDPO and EOPF both in vitro and in vivo. Selected carbamates, thiocarbamates, phosphinates, and sulfanyl fluorides are prophylactic agents and dipentyl 2,2-dichlorovinyl phosphate is a promoter for OBDPO-induced subacute neurotoxicity. Although this type of neurotoxicity in mice is similar to OPIDN in the correlation with NTE inhibition and the prophylactic action of reversible NTE inhibitors, it differs from OPIDN in the delay time prior to onset, the sensitivity of both young and old animals, and the high incidence of fatality. A full neuropathological study is desirable to further characterize this subacute neurotoxicity.
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PMID:Subacute neurotoxicity induced in mice by potent organophosphorus neuropathy target esterase inhibitors. 868 3

The human immunodeficiency virus type 1 (HIV-1) Tat protein is a key pathogenic factor in a variety of acquired immune deficiency syndrome (AIDS)-associated disorders. A number of studies have documented the neurotoxic property of Tat protein, and Tat has therefore been proposed to contribute to AIDS-associated neurological diseases. Nevertheless, the bulk of these studies are performed in in vitro neuronal cultures without taking into account the intricate cell-cell interaction in the brain, or by injection of recombinant Tat protein into the brain, which may cause secondary stress or damage to the brain. To gain a better understanding of the roles of Tat protein in HIV-1 neuropathogenesis, we attempted to establish a transgenic mouse model in which Tat expression was regulated by both the astrocyte-specific glial fibrillary acidic protein promoter and a doxycycline (Dox)-inducible promoter. In the present study, we characterized the phenotypic and neuropathogenic features of these mice. Both in vitro and in vivo assays confirmed that Tat expression occurred exclusively in astrocytes and was Dox-dependent. Tat expression in the brain caused failure to thrive, hunched gesture, tremor, ataxia, and slow cognitive and motor movement, seizures, and premature death. Neuropathologies of these mice were characterized by breakdown of cerebellum and cortex, brain edema, astrocytosis, degeneration of neuronal dendrites, neuronal apoptosis, and increased infiltration of activated monocytes and T lymphocytes. These results together demonstrate that Tat expression in the absence of HIV-1 infection is sufficient to cause neuropathologies similar to most of those noted in the brain of AIDS patients, and provide the first evidence in the context of a whole organism to support a critical role of Tat protein in HIV-1 neuropathogenesis. More importantly, our data suggest that the Dox inducible, brain-targeted Tat transgenic mice offer an in vivo model for delineating the molecular mechanisms of Tat neurotoxicity and for developing therapeutic strategies for treating HIV-associated neurological disorders.
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PMID:Neuropathologies in transgenic mice expressing human immunodeficiency virus type 1 Tat protein under the regulation of the astrocyte-specific glial fibrillary acidic protein promoter and doxycycline. 1270 54

An 11-year-old male was admitted because of frequent vomiting and truncal ataxia which had lasted for over one week. He had clear consciousness but slowly-progressive mild headache and ataxic gait. Cranial CT revealed a 4 cm hematoma in the right cerebellar hemisphere. Angiography showed a 2 x 2 cm nidus of a pial arteriovenous malformation (AVM) in the right hemisphere fed from the right posterior inferior cerebellar artery and draining into the inferior hemispheric vein. We performed a surgical resection of the AVM after decompression therapy to counteract the brain edema. He recovered completely without any neurological deficits. This case suggests that cerebellar hemorrhage caused by AVM should be considered as a possible diagnosis when mild symptoms of headache and ataxia proceed gradually.
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PMID:A juvenile case of cerebellar arteriovenous malformation (AVM) with gradual onset of headache and ataxia. 1277 82


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