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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A shipyard worker was poisoned by hydrogen sulfide (H2S), and rescued after 15-20 min. He regained consciousness after 2 days. Three days later his condition deteriorated, and he was more or less comatose for a month. When he woke up, he was amnesic, nearly blind, had reduced hearing, and had a moderate spastic tetraparesis and ataxia. Two months after the accident, he had greatly improved. Audiograms showed hearing loss with maximum at 2000 Hz and significantly poorer speech discrimination. EEG showed generalized dysrhythmia. At follow-up 5 years later he had not been able to resume his work, and had slight motor, memory and visual symptoms. CT and MRI showed slight cerebral atrophy. EEG and evoked responses were normal.
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PMID:Delayed neuropsychiatric sequelae after acute hydrogen sulfide poisoning: affection of motor function, memory, vision and hearing. 177 8

Nontraumatic intracerebellar hemorrhage is rare during childhood. We report such a case due to rupture of arteriovenous malformation, in which surgery was able to bring about satisfactory recovery from deep coma without spontaneous respiration. This case shows that operative treatment should not be abandoned even though neurological deficits are very serious. This 6-year-old boy suddenly complained of headache while playing in a nursery and became restless. Because of deterioration of consciousness level followed by loss of respiration, he was transferred from a local physician to our clinic 4 hours after the onset. Computerized tomography scan disclosed a hematoma in the cerebellar hemisphere. Emergency suboccipital craniectomy was carried out 1 hour later. Immediately after operation, respiration was restored. Vertebral arteriography was performed 1 month after the operation, when the patient had recovered but could barely communicate with his family. The study revealed a small arteriovenous malformation supplied by the anterior inferior cerebellar artery. The malformation was removed 3 months after admission. The postoperative course was uneventful and the patient attended a primary school without neurological deficits except for slight ataxia 6 months after the onset.
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PMID:[A case of intracerebellar hemorrhage in infancy]. 189 25

An open-label, dose-escalation study was conducted to determine doses of lorazepam required to induce anterograde amnesia and sedation in children without producing excessive toxicity. Oncology patients 4 to 17 years of age undergoing lumbar puncture or bone marrow aspiration were eligible; a patient could be entered in the study for a second procedure at a different lorazepam dose. A single oral dose of lorazepam was administered 45-60 minutes before the procedure. Starting with 0.02 mg/kg, the same dose was given to three patients; if no dose-limiting effects occurred, dose was increased by 0.01 mg/kg. Before the procedure the patient was shown a toy that he or she was later asked to identify. Immediately after the procedure (usually 60-75 minutes after the lorazepam dose), sedation was assessed on a scale of 0 (alert) to 4 (coma), and the clinician performing the procedure was asked to subjectively evaluate sedation. Patients were rated for amnesia 24 hours after the procedure; a scale of 0 (recalls procedure and toy without prompting) to 4 (recalls nothing since procedure) was used. Twenty patients received 28 doses of lorazepam. The study was terminated when two patients who received 0.10 mg/kg had excessive ataxia. Sedation was subjectively considered adequate for 24 of the procedures. Sedation and amnesia scores were not well correlated with increased dose. Amnesia occurred in some patients with doses as low as 0.03 mg/kg. In children undergoing lumbar puncture or bone marrow aspiration, premedication with oral lorazepam 0.02-0.09 mg/kg generally produced adequate sedation for the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determination of sedative and amnestic doses of lorazepam in children. 193 19

During 1984-1989, 19 Bedouin children, 4-8 years old, were hospitalized because of henbane plant (Hyoscyamus reticulatus) poisoning. There were 14 cases in the autumn, 3 in the spring and 2 in the summer. The most prominent signs were altered state of consciousness (including deep coma in 3) and flushed dry, warm skin in all. Pupils were dilated in 18 of the 19 and restlessness and hallucinations were present in 17. Less common were vomiting, increased tendon reflexes, convulsions, involuntary movements, ataxia, hypertension, hyperpyrexia and tachycardia. Therapy included intravenous physostigmine in 7 and sedatives (diazepam and triclofos) in 6. All were free of symptoms within 24 hours of admission. Henbane may grow as an annual or biennial. Renewed growth of leaf rosettes occurs before the first rains and they attract attention in the fields. The parts of the plant eaten by most of the children were the roots, which are easily mistaken for the edible roots of other plants. The main alkaloids in henbane are atropine (hyoscyamine) and scopolamine (hyoscine) which explains the clinical picture of mixed stimulation and depression of the brain. Educational measures should be undertaken to prevent poisoning of Bedouin children by eating such plants.
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PMID:[Henbane (Hyoscyamus reticulatus) poisoning in children in the Negev]. 195 6

Out of 604 Gambian children admitted with falciparum malaria to one hospital between September and December, 1988, 308 had cerebral malaria and 203 were severely anaemic (haemoglobin less than 60 g/l). 14% of those with cerebral malaria died, as did 7.8% of those with severe anaemia. 32 (12%) of children surviving cerebral malaria had residual neurological deficit. 69 other children were admitted with clinical features strongly suggestive of cerebral malaria but with negative blood films; 16 of these died and 3 had residual neurological deficits. The commonest sequelae of cerebral malaria were hemiplegia (23 cases), cortical blindness (11), aphasia (9), and ataxia (6). Factors predisposing to sequelae included prolonged coma, protracted convulsions, severe anaemia, and a biphasic clinical course characterised by recovery of consciousness followed by recurrent convulsions and coma. At follow up 1-6 months later over half these children had made a full recovery, but a quarter were left with a major residual neurological deficit. Cerebral malaria in childhood may be an important cause of neurological handicap in the tropics.
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PMID:Neurological sequelae of cerebral malaria in children. 197 27

We analysed two of our own and 21 patients described in the literature with listeria brainstem encephalitis. The disease was characterised by a prodromal state with fever, nausea and headache followed by severe brainstem dysfunction with multiple cranial nerve palsies, ataxia, respiratory insufficiency and coma. The diagnosis was established by isolation of Listeria monocytogenes from CSF and/or serum. Serological tests are without diagnostic evidence. Cerebrospinal fluid examination may not initially point to a bacterial infection. Computed tomography and magnetic resonance imaging technique might supply evidence of brainstem involvement and contribute to an early diagnosis. There is a high percentage of lethal outcome without early antibiotic therapy.
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PMID:Listeria brainstem encephalitis: two own cases and literature review. 201 6

Acute mountain sickness is a pathologic reaction as a result of bad adaptation to high altitudes (greater than 2.500 meters). The main symptoms are headache, nausea, vomits, and insomnia. When severe it can produce oliguria, retinal hemorrhage, ataxia and sometimes coma. Its etiology is not well known. It is considered that the first producer factor of the disease is tissular hypoxia secondary to low partial oxygen pressure existing in areas of high sea level. The treatment consists of descent and the use of dexametasone and acetazolamide.
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PMID:[Acute mountain sickness]. 210 53

Pharmacological interest in the tripeptide thyrotropin-releasing hormone (TRH) is due to the multiple effects it produces. In fact, apart from taking part in regulating the activity of the hypothalamo-pituitary-thyroid axis, TRH produces various neuropharmacological effects which indicate a biological role that is probably more important than that of a releasing hormone. Trials performed in animals have shown, for example, the dose-dependent capacity of TRH to induce analgesia, probably by interacting with the opioid peptide system. Motor activity is affected by TRH. In fact this tripeptide elicits an increase in spontaneous motor and explorative activities by interacting with the dopaminergic neurotransmitter system at the nucleus accumbens level. The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. A most interesting property of TRH is that of counteracting the neurological deficit due to experimental lesion of the spinal cord particularly with regard to spasticity and ataxia. Electrophysiological trials have shown that TRH depolarizes the motoneurons in frog spinal cord thereby increasing the monosynaptic reflex. Furthermore, TRH has recently been shown to have a trophic effect on cultures of rat fetus spinal cord. On this basis TRH has been used successfully for the treatment of amyotropic lateral sclerosis (Charcot's syndrome) and spinocerebellar degeneration. Further support for this therapeutic strategy is given by the demonstration that deafferentiation of rat spinal cord produces an increased density of TRH spinal receptors. Recent studies have also given encouraging results on the possible therapeutic use of TRH for the treatment of Alzheimer's disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pharmacologic profile of protirelin tartrate]. 212 84

Thirty-one children aged 3 to 15 years were followed for 5 to 11 years after suffering severe closed head trauma which caused coma for 1 week or more (median duration of coma 3 weeks). One patient remained in a persistent vegetative state until his death 9 years later. The other 30 recovered consciousness and were discharged. All suffered diminution of their abilities, and 24 of them had major permanent disability. The most common motor disabilities were pure spastic hemiparesis (seven cases), basal ganglia syndromes (four cases), ataxia (three cases), and a combination of hemiparesis and ataxia (five cases). Of the 30 patients, 26 regained independent ambulation, seven were epileptic, and 14 were dysarthric in various degrees. Only 10 had the cognitive ability to profit from the normal educational system, and none had attempted postsecondary education. Social problems were common. The worst outcomes were associated with intracranial bleeding and/or brain contusion seen on computerized tomography (CT) scans at the acute stage; the best were associated with normal CT scans. The degree of residual disability in these children seems no less than that of adults with trauma of similar severity.
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PMID:Long-term follow-up review of 31 children with severe closed head trauma. 214 3

Thallium, a rodenticide, has been shown to produce several neurological symptoms including motor weakness, ataxia, tremor, convulsion, coma and death. The present study was designed to evaluate the effects of acute or subacute exposure to thallium on several neurochemical biomarkers in rat brain. In the acute study, adult male CD rats were treated with 0 or 20 mg thallium/kg intraperitoneally (ip) and sacrificed 2, 6, or 24 hr after exposure. In the subacute study, animals were treated with 0 or 5 mg thallium/kg ip daily for 10 days and sacrificed 24 hr after the last dose. Acute injections of thallium produced in the frontal cortex significant increases in glutamine concentration after 6 hr and in taurine after 6 and 24 hr. In hippocampus, significant decreases in aspartic acid and taurine concentrations were found after 6 hr. Subacute exposure to thallium produced significant increases of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and serotonin (5-HT) in amygdala and increases in 5-HT concentration in hypothalamus. DA or muscarinic cholinergic (MCh) receptor binding did not show any significant alterations in caudate nucleus or frontal cortex after acute or subacute exposure to thallium. However, when membranes prepared from control caudate nuclei were incubated with thallium (1-100 microM) in vitro, we observed a dose-dependent decrease in DA and MCh receptor binding. These data suggest that the neurotoxicity produced by thallium exposure may be associated with changes in the concentrations of amino acids and other neurotransmitters in various regions of the rat brain.
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PMID:Thallium intoxication produces neurochemical alterations in rat brain. 217 76


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