Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical symptoms of 32 stutterers--schoolchildren of 14-year average age were evaluated according to the questionnaire containing 45 complaints of tetanic syndrome. We found headache, fatigue, anxiety, paresthesias and hypothermia of limbs in 30 per cent of this group. More than 80 per cent of the patients had positive Chvostek sign and 60 per cent had positive ischemic and hyperventilation tests.
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PMID:Tetanic syndrome questionnaire in stutterers. 183 77

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Ipsilateral carotid and vertebral vasomotor phenomena are marked components of a unilateral cluster headache crisis. Investigation of lateralisation at the height of a crisis has shown that Doppler findings supplement Heick's observation of the reversible opening of both intra and extracranial arteriovenous shunts. This observation is in line with personal thermographic evidence and that of Lance indicating local hypothermia, and with Wolff's demonstration of dilatation and congestion associated with the superficial temporal artery. Personal dynamographic findings now point to a local extra-intracranial artery pressure gradient as the cause of the peripheral component of lateralisation in cluster headache.
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PMID:[Lateralization phenomena and headache]. 638 23

The case reported here concerns a 40-year-old woman who has suffered from severe migraine without aura since she was 23. The patient has been taking 1-3 suppositories of Virdex (2 mg of ergotamine tartrate, 250 mg of aminophenazone, caffeine) every day for the past three years. In addition to headache, the onset of short, sporadic cramps in the limbs together with paresthesia, hyposthenia, hypothermia and skin pallor with a slight increase in diastolic pressure, made hospital treatment necessary. Instrumental investigation through a stress test on a moving carpet, doppler, echo-doppler and digitalized angiography of the arterial vessels of the lower limbs shows the presence of bilateral impairment attributable to the chronic intake of ergotamine.
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PMID:Vascular injuries in ergotamine abuse: a case report. 831 18

Sudden bleeding in the advanced stage of pregnancy is usually caused by abruptio placentae. Pre-eclampsia may develop rapidly into eclampsia and should lead to immediate hospitalization of the patient. A pregnant woman suffering from high blood pressure, headaches and epigastric pains, might be developing the life threatening HELLP syndrome. Sudden labour at term, either at home or in the ambulance, does not usually involve major complications. Hypothermia of the newborn baby should be avoided by drying it and placing it at the mother's breast. The umbilical chord is cut at the obstetrical department.
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PMID:[Emergency obstetrics]. 832 52

Traumatic subacute subdural hematoma is a condition in which the major symptoms affecting prognosis most appear in the subacute stage after head trauma, while traumatic acute subdural hematoma is treated conservatively when the symptoms are mild. The cause of the major symptoms occurring in the subacute stage is mostly expansion of the subdural hematoma volume. The authors report a case of traumatic subacute subdural hematoma in which the cause of the major symptoms was cerebral hemispheric edema instead of expansion of the subdural hematoma volume. To our knowledge, only one similar case to the present case has been previously reported. A 44-year-old female fell from the stairs on July 21, 1995 and was suffering from headache. On July 23, she was admitted to our hospital because of generalized convulsion. On admission, she was drowsy but showed no convulsion. Head CT showed an acute subdural hematoma on the right side with a slight midline shift and no other abnormalities. She was treated conservatively because of the mildness of the symptoms and two days later became alert with no symptoms. Thereafter she only complained of occasional headache which was controlled with medicine. On August 3, she suddenly fell into coma. Head CT showed severe cerebral hemispheric edema on the right side without change of the subdural hematoma size. Emergency cerebral angiography showed no definitive abnormalities such as occlusion of the arteries or of the venous sinuses. Craniotomy associated with external decompression was performed. The hematoma was composed of red-brown jelly accompanied with some liquid component and had a thin black-brown outer membrane. While removing the hematoma, bleeding from a vein on the cerebral surface around the sylvian fissure was observed and this location was suspected to be the sources of the bleeding point. Postoperatively, she received steroid and barbiturate therapy associated with moderate hypothermia under hyperventilation. She tolerated this treatment well and left the hospital, on September 26, 1995 with only diplopia during downward gaze. Although the mechanisms of the cerebral hemispheric edema occurring in the subacute stage was unclear, a failure in the cerebral venous circulation arising from compression to the bridging veins, which may be hypoplastic, by the subdural hematoma was suspected to have been the cause.
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PMID:[A case of traumatic subacute subdural hematoma presenting symptoms arising from cerebral hemispheric edema]. 962 56

We described herein a case of the fulminant form of acute disseminated encephalomyelitis (ADEM) that developed after mycoplasma pneumonia. A 28-year-old man who presented with fever, headache, and writing difficulty was admitted to our hospital in August 1997. He developed hernia on the 3rd hospital day. Surgical decompression and intravenous prednisolone failed to halt his progressive deterioration. We introduced systemic hypothermia and he has shown marked recovery; despite having Broca's type aphasia, he could comprehend spoken language and communicate with others by gesture. Head MRI demonstrated diffuse high signals over the white matter on fluid attenuated inversion recovery (FLAIR) images, which suggested extensive demyelination. The clinical course, imaging studies and presence of polymorphonuclear dominant leucocytosis in the blood and CSF in the patient are somewhat similar to findings in acute hemorrhagic leukoencephalitis, however, the result of a brain biopsy was inconclusive. The fulminant form of ADEM is usually fatal. Treatments such as corticosteroids, intravenous immunoglobulin, and surgical decompression have been performed to improve the prognosis. Our case results indicate that hypothermia, which suppresses both brain edema and immune response, may be included in the repertoire of treatment for the fulminant form of ADEM.
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PMID:Fulminant form of acute disseminated encephalomyelitis: successful treatment with hypothermia. 1042 55

Episodic spontaneous hypothermia is an infrequent disorder, with unknown pathogenic mechanisms. A systemic cause or underlying brain lesion has not been found for the disease. We report four new patients, 3-9 years old, with episodic hypothermia lower than 35 degrees C, marked facial pallor, and absent shivering. The episodes could last a few hours or four days, and recurred once a week or every 2-3 months. Two patients also demonstrated bradycardia, mild hypertension, and somnolence during the events; in one of them, profuse sweating was also a feature, and all four presented with either headache, a periodic childhood syndrome, or both (recurrent abdominal pain, cyclic vomiting, or vertigo). Three patients reported a family history of migraine. Neurologic examination, endocrine function, and imaging studies were normal. Migraine prophylactic therapy was of moderate efficacy. Spontaneous resolution was observed in one patient. The clinical characteristics of the syndrome allow for its inclusion as a childhood periodic syndrome related to migraine.
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PMID:Episodic spontaneous hypothermia: a periodic childhood syndrome. 1284 86

Arachidonylethanolamide (anandamide, AEA) is believed to be the endogenous ligand of the cannabinoid CB(1) and CB(2) receptors. CB(1) receptors have been found localized on fibers in the spinal trigeminal tract and spinal trigeminal nucleus caudalis. Known behavioral effects of anandamide are antinociception, catalepsy, hypothermia, and depression of motor activity, similar to Delta(9)-tetrahydocannanbinol, the psychoactive constituent of cannabis. It may be a possible therapeutic target for migraine. In this study, we looked at the possible role of the CB(1) receptor in the trigeminovascular system, using intravital microscopy to study the effects of anandamide against various vasodilator agents. Anandamide was able to inhibit dural blood vessel dilation brought about by electrical stimulation by 50%, calcitonin gene-related peptide (CGRP) by 30%, capsaicin by 45%, and nitric oxide by 40%. CGRP(8-37) was also able to attenuate nitric oxide (NO)-induced dilation by 50%. The anandamide inhibition was reversed by the CB(1) receptor antagonist AM251. Anandamide also reduced the blood pressure changes caused by CGRP injection, this effect was not reversed by AM251. It would seem that anandamide acts both presynaptically, to prevent CGRP release from trigeminal sensory fibers, and postsynaptically to inhibit the CGRP-induced NO release in the smooth muscle of dural arteries. CB(1) receptors seem to be involved in the NO/CGRP relationship that exists in causing headache and dural blood vessel dilation. It also seems that some of the blood pressure changes caused by anandamide are mediated by a noncannabinoid receptor, as AM251 was unable to reverse these effects. It can be suggested that anandamide is tonically released to play some form of modulatory role in the trigeminovascular system.
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PMID:Anandamide is able to inhibit trigeminal neurons using an in vivo model of trigeminovascular-mediated nociception. 1471 91

Delayed cerebral ischemia as a result of cerebral vasospasm is the most common cause of death and disability after aneurysmal subarachnoid hemorrhage (SAH). It leads to death or permanent neurologic deficits in over 17-40% of SAH patients. The initial and main symptom of cerebral vasospasm is diffuse headache and may be accompanied with a slight increase in discomfort from neck stiffness and fever. The clinical diagnosis of cerebral vasospasm is made when the patient experiences an altered level of consciousness or a new focal neurologic deficit. There has been a great progress in identifying the patients at risk, putative mechanisms, and possible treatment options for cerebral vasospasm. However, the problem is by no means solved, mainly due to a limited understanding of the pathologic mechanisms of this complex disease. The iatrogenic factors that can increase the risk of cerebral vasospasm include prolongation of the subarachnoid clot by antifibrinolytic drugs, hypotension, inappropriate treatment of hyponatremia, hypovolemia, hyperthermia and increased intracranial pressure. Nimodipine has been shown to improve neurologic outcome and decrease the incidence of cerebral vasospasm. Triple H therapy is a treatment designed to augment cerebral blood flow for patient with cerebral vasospasm. Hypervolemic hypertension is induced with intravenous volume expansion with crystalloid or colloid to increase cardiac output and raise blood pressure. However, small randomized trials showed no clear benefit. Recently, balloon and chemical angioplasty with superselective intra-arterial injection of vasodilators has emerged as the primary intervention for treating medically refractory ischemia from cerebral vasospasm and in many centers is being used as a first-line treatment or even prophylactically. In addition, promising new treatments for cerebral vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia; however, all still need further clinical trials. Newly recognized mediators of cerebral vasospasm after SAH include endothelium-derived mediators, vascular smooth-muscle-derived mediators, proinflammatory mediators involved in blood-brain barrier disruption, cytokines and adhesion molecules, stress-induced gene activation, and platelet-derived growth factors. Moreover, observations in the laboratory have, in many circumstances, matched those of reported small series. Larger, prospective, randomized trials are needed to verify several hypotheses of molecular pathophysiology and clinical treatment regimens.
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PMID:Treatment of cerebral vasospasm after subarachnoid hemorrhage--a review. 1567 31


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