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 483 patients admitted to the emergency room because of syncope were reviewed. Thirty seven patients (7.7%) were found to suffer from transient ischemic attack- (TIA) related syncope. This group is the subject of this report. Of these patients, 28 (76%) were men (mean age 71 years). Seven patients reported previous syncopal episodes. Past history revealed a high rate of ischemic heart disease (70%) and hypertension (68%). Concurrent neurologic symptoms, which led to the diagnosis of TIA-related syncope, included mainly vertebrobasilar symptoms: vertigo (in 55% of the patients), ataxia (46%), parasthesia (41%). Two patients most probably were presenting bilateral carotid artery disease. Various diagnostic tests (including electroencephalography, computed tomography, sonography, and cerebral angiography) were used to exclude other causes of syncope. During follow-up (mean 14.5 months) four patients (11%) had an additional episode of TIA and in three of them syncope reappeared. One patient had a complete stroke. We conclude that TIA is a much more frequent explanation for syncope than has been previously argued. These patients tend to be elderly males with high incidence of ischemic heart disease and hypertension. The concurrent neurologic symptoms, leading to the diagnosis, represent mainly vertebrobasilar territory ischemia.
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PMID:Transient ischemic attack-related syncope. 204 43

Acute autonomic and sensory neuropathy (AASN), one subtype of acute pandysautonomia, in which dorsal root ganglia and autonomic ganglia are involved is uncommon. Little is so far known on central nervous system involvement in AASN. In the present paper we described a rare case of AASN associated with the central nervous system manifestations such as galactorrhea-amenorrhea syndrome and intractable anorexia. A 30-year-old woman rapidly developed burning pain and numbness in her arms and legs as well as orthostatic syncope. She had severe anorexia and no no menstruation from onset. On physical examination, she was emaciated. There was marked orthostatic hypotension with tachycardia. Skin was dry. Moderate galactorrhea was detected. Neurological examination showed prominent paresthesia and dullness of superficial sensation, predominantly to pinprick and thermal stimuli, segmentally over the neck, occipital scalp, and extremities. Deep sensation was intact. She had no weakness or ataxia. Deep tendon reflexes were almost normal. NCV and SEP were normal, while EEG was abnormal. Sural nerve biopsy demonstrated axonal degeneration with the loss of myelinated, predominantly in small-caliber fibers, and unmyelinated fibers. The levels of HVA and MHPG in CSF were decreased. The autonomic nervous function tests revealed postganglionic dysfunction. alpha-adrenergic system was predominantly impaired, while beta-adrenergic system was relatively preserved. The endocrinological studies demonstrated mild or moderate elevation of PRL basal value and hyper-response of PRL and LH for TRH and LH-RH loading test, which suggested disorder of the hypothalamo-hypophysial system. Cranial MRI showed moderate dilatation of the 3rd ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute autonomic and sensory neuropathy associated with galactorrhea-amenorrhea syndrome and intractable anorexia]. 255 96

The clinical effectiveness of flecainide acetate was evaluated in 36 patients (29 male and 7 female, average age 56 years) in whom therapy with previous antiarrhythmic agents had failed. All patients had documented ventricular tachycardia on Holter electrocardiographic recording and 31 of 36 (86%) had had syncope or required cardiopulmonary resuscitation, or both. Angiographic findings demonstrated significant coronary artery disease in 22 (61%) and primary left ventricular dysfunction in 14 (39%), with a left ventricular ejection of 0.39 +/- 0.4. Patients were treated with an average flecainide dose of 302 +/- 76 mg/day. The follow-up time was 101 +/- 156 days. Thirty-two of 36 patients (89%) had complete elimination of ventricular tachycardia from Holter monitoring and only 2 patients had flecainide discontinued because of noncardiac side effects (numbness, blurred vision and ataxia). However, the drug was subsequently discontinued in 5 patients because of cardiac side effects (proarrhythmic effect in 2, sinus bradycardia in 1, complete atrioventricular block in 1 and new left bundle branch block in 1) and 10 patients died during flecainide therapy (1 with cerebral stroke, 3 with congestive heart failure and 6 with incessant ventricular tachycardia). A comparison of the general cardiac features of those who died with those who did not revealed a significantly lower ejection fraction (0.24 +/- 0.1 vs 0.45 +/- 0.1, p less than 0.05) and a significantly higher flecainide dose (350 +/- 85 versus 276 +/- 59 mg/day, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of flecainide acetate in the management of patients at high risk of sudden cardiac death. 669 14

Herniation of the hindbrain occurs when the lowest parts of the cerebellum and sometimes part of the medulla are moved downwards through the foramen magnum, a pressure difference acting across the foramen magnum moulding the tissues into a plug. It is suggested that the clinical course in both adults and babies with spina bifida may be explained by the hindbrain hernia acting as a valve.The term 'Chiari Type I deformity' is commonly used for an abnormality in which the tonsils and lowermost parts of the cerebellar hemispheres are prolapsed through a normal foramen magnum. Acute herniation may occur as a result of space-occupying lesions. Chronic herniation may be morphologically identical although it tends to be more severe. Sometimes it will produce few symptoms which often may be delayed so that the original causative lesion may not be apparent. Causes include bone softening, tumour, or previous meningitis. Birth injury is probably the commonest cause of the deformity, which presents clinically in adults.In infants with severe forms of spina bifida a hindbrain herniation is present. This abnormality may be called 'Chiari Type II deformity' or Arnold-Chiari deformity and is an intra-uterine abnormality in which the fourth ventricle and medulla are grotesquely herniated before they are properly developed and the foramen magnum is enlarged.The commonest clinical presentation of Chiari Type I deformity is syringomyelia, which is usually not diagnosed until adult life. Other presentations include syringobulbia, headache, oscillopsia, attacks of giddiness, lower cranial nerve palsies, and ataxia. Particularly characteristic are cough headache and cough syncope. Syringomyelia and syringobulbia in particular may be irreversible by the time they are diagnosed. Nevertheless, surgical decompression may be successful in relieving symptoms of headache, cough syncope, and long-tract compression; most cases of syringomyelia show some improvement and in others progression of the disease is arrested. Operative techniques for hindbrain herniation are discussed.Chiari Type II deformity is probably responsible for the progression of hydrocephalus after birth in the majority of babies with spina bifida. Measurement of pressure in the cerebrospinal fluid above and below the foramen magnum shows that intermittent pressure difference is commonly present at times of neurological deterioration. Surgical decompression of the hernia in adults allows correction of the valvular effect, which may be monitored by pressure measurements. In babies the associated hydrocephalus is usually so gross that it requires separate treatment, but pressure monitoring may be of value in assessing the state of the disease.
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PMID:Chronic herniation of the hindbrain. 701 51

A man with a subclinical cobalamin deficiency developed syncope, vertigo, paresthesias, and ataxia after two exposures to nitrous oxide anesthesia. Patients with unrecognized cobalamin deficiency may be particularly susceptible to brief exposures to nitrous oxide, which inactivates the cobalamin-dependent enzyme methionine synthase and may cause a myeloneuropathy. Clinicians should consider this entity when confronted with patients with neuropathic symptoms after surgical or dental procedures.
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PMID:'Anesthesia paresthetica': nitrous oxide-induced cobalamin deficiency. 764 61

Chiari malformation, also called Arnold-Chiari deformities, are rare hindbrain herniations that may present in children or adults. The most common symptoms include headache, syncope, disordered eye movement, sensory loss, weakness, and cerebellar features such as ataxia. Dysphagia occurs in 5-15% of patients, although only a few reports describe dysphagia as the only presenting symptom. We report a case of a 27-year-old woman who presented with a three-year history of dysphagia, chest pain, and weight loss. Esophageal manometrics revealed markedly disordered esophageal motility and gastroesophageal reflux. Her symptoms failed to respond to high doses of omeprazole, prokinetics, and eventually surgical fundoplication. The subsequent onset of neurological symptoms led to the diagnosis of Chiari type I malformation. Following posterior craniotomy with decompression, her dysphagia and chest discomfort completely resolved. Repeat esophageal manometrics revealed complete resolution of prior abnormalities.
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PMID:Esophageal dysphagia as the sole symptom in type I Chiari malformation. 861 24

Aging is a physiological process that shares many behavioral, biochemical and neuroendocrine phenomena with the pathophysiological situation of unresolved stress, as well as with a pharmacologically induced syndrome resulting from chronic benzodiazepine (BZ) consumption. Behavioral findings include symptoms such as drowsiness, ataxia, fatigue, confusion, weakness, dizziness, vertigo, syncope, reversible dementia, depression, impairment of intellectual, psychomotor and sexual function, agitation, auditory and visual hallucinations, paranoid ideation, panic, delirium, depersonalization, sleepwalking, aggressivity, orthostatic hypotension, and insomnia. Neuroendocrine findings include: central depletion of noradrenaline (NA), dopamine, adrenaline (AD), and serotonin (5-HT); reduction in the ratio of circulating NA/AD as well as platelet 5-HT and increase of AD, plasma free 5-HT and cortisol. These disturbances together with the increased platelet aggregability observed in the three groups are typical of unresolved-stress situations. Immunological findings include significant reduction of peripheral T lymphocytes (CD3, CD4, CD8) and the CD4/CD8 ratio, CD16 and gamma-delta cells. On the other hand, the three groups (elderly subjects, subjects faced with unresolved stress, and BZ consumers) show increase of the CD57 lymphocyte subset as well as natural killer cytotoxicity. Alterations of several biological markers have also been found, specifically in the oral glucose tolerance test, the intramuscular clonidine test, and the supine/orthostasis/exercise test. From a clinical point of view, the three groups appear to be more susceptible to the appearance and progression of many acute and chronic diseases (infectious and malignant diseases). As a result, chronic consumption of BZs should be avoided in both the elderly and subjects in unresolved-stress situations.
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PMID:Benzodiazepines: tolerability in elderly patients. 884 97

A 37-year-old woman with a 5-year history of multiple sclerosis is reported. She began having recurrent syncope even in the sitting position; other neurological features included hiccup, faciooro-lingual flushing and clumsiness of the hands. She had alternating Horner's syndrome, mild hypoalgesia of the right face, exaggerated deep tendon reflexes of the upper extremities, decreased deep sensation and ataxia of the upper extremities, and incomplete transverse myelopathy with a T4 sensory level. Head-up tilt testing confirmed orthostatic hypotension with relative preservation of the heart rate increase. Magnetic resonance imaging indicated abnormal intensities in the paramedian tegmentum and base of the medulla, which may have been additionally responsible for orthostatic hypotension. Steroid pulse therapy and L-threo-3,4-dihydroxyphenylserine caused regression of brainstem signs and reduced syncopal attacks.
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PMID:Orthostatic hypotension in a case with multiple sclerosis. 923 62

Extracranial-intracranial (EC-IC) bypass grafting procedures were specially designed for treatment of bilateral internal carotid artery occlusion. When performed in an expeditious manner, EC-IC bypass procedures have produced effective and durable results, despite the recent disfavor given to this procedure. This communication reports a 68-year-old white man who developed generalized cerebral ischemia manifested as confusion, incoherence, disorientation, ataxia, and numerous episodes of syncope daily. A cerebral angiogram revealed bilateral external carotid arteries and left solitary vertebral artery critical stenosis. Transcranial Doppler study demonstrated reduction of cerebral and vertebral-basilar perfusion. However, the patient's EC-IC bypass graft had remained patent since 1985. The patient's recurrent symptoms of global ischemia and syncope resolved after carotid endarterectomy, vein patch external carotid artery, and vertebral-to-common carotid artery transposition. This report reiterates the value of the EC-IC bypass procedure and presents the surgical management of symptomatic external carotid and vertebral artery stenosis in patients after EC-IC bypass procedures.
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PMID:Revascularization of cerebral ischemia after previous bilateral extracranial-intracranial bypass procedures. 947 4

This study examined the efficacy of glycerol and water hyperhydration (1 h before exercise) on tolerance and cardiovascular strain during uncompensable exercise-heat stress. The approach was to determine whether 1-h preexercise hyperhydration (29.1 ml H2O/kg lean body mass with or without 1.2 g/kg lean body mass of glycerol) provided a physiological advantage over euhydration. Eight heat-acclimated men completed three trials (control euhydration before exercise, and glycerol and water hyperhydrations) consisting of treadmill exercise-heat stress (ratio of evaporative heat loss required to maximal capacity of climate = 416). During exercise ( approximately 55% maximal O2 uptake), there was no difference between glycerol and water hyperhydration methods for increasing (P < 0.05) total body water. Glycerol hyperhydration endurance time (33. 8 +/- 3.0 min) was longer (P < 0.05) than for control (29.5 +/- 3.5 min), but was not different (P > 0.05) from that of water hyperhydration (31.3 +/- 3.1 min). Hyperhydration did not alter (P > 0.05) core temperature, whole body sweating rate, cardiac output, blood pressure, total peripheral resistance, or core temperature tolerance. Exhaustion from heat strain occurred at similar core and skin temperatures and heart rates in each trial. Symptoms at exhaustion included syncope and ataxia, fatigue, dyspnea, and muscle cramps (n = 11, 10, 2, and 1 cases, respectively). We conclude that 1-h preexercise glycerol hyperhydration provides no meaningful physiological advantage over water hyperhydration and that hyperhydration per se only provides the advantage (over euhydration) of delaying hypohydration during uncompensble exercise-heat stress.
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PMID:Hyperhydration: tolerance and cardiovascular effects during uncompensable exercise-heat stress. 960 77


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