Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042571 (vertigo)
 7,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-year-old Italian woman developed migraine-like headaches with increasing frequency 5 years after menopause. The simultaneous onset of severe bilateral uveitis, neurological signs such as vertigo, hearing loss, small sensomotor hemisyndrome, cognitive brain dysfunction and lymphocyte liquor pleocytosis confirmed the diagnosis of Vogt-Koyanagi-Harada syndrome, a rare disease of probably autoimmune origin with destruction of pigment containing neuroepithelium. Other vasculitic diseases, especially those of infectious or rheumatologic origin, were excluded. Systemic corticoid treatment suppressed the activity of the illness but on dose reduction relapses occurred. Additional immunosuppressive medication prevented uveitic relapses and made it possible to reduce the corticoid dose.
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PMID:[Rare form of uveitis with neurological symptoms: the Vogt-Koyanagi-Harada uveomeningoencephalitic syndrome]. 154 80

Hypoglycaemia is possibly the most frequent metabolic emergency, in that insulin-induced hypoglycaemia is a common side-effect of treatment of a common disease. The symptoms are partly sympathetic and related to the release of catecholamines. These symptoms include sweating, tremor, palpitations, sensation of hunger, restlessness and anxiety. Other symptoms are caused by an insufficient supply of glucose to the brain, resulting in neuroglucopenia with symptoms like blurred vision, weakness, slurred speech, vertigo and difficulties in concentration. Symptom recognition is the primary and most effective defence against cerebral dysfunction which is the ultimate consequence of hypoglycaemia. Even in insulin-treated diabetic patients symptom failure might occur. Patients who experience severe episodes of hypoglycaemia do not constitute a special subgroup of patients. However, near-normalization of blood glucose levels have resulted in an increase in the incidence of severe hypoglycaemia. Moreover, the threshold for hormonal counter-regulatory responses in adrenaline, growth hormone and cortisol is lowered after a period of strict metabolic control in insulin-dependent diabetic patients. The glucose level at which the patients become subjectively aware of hypoglycaemia is correspondingly reduced. Other reasons for hypoglycaemia to occur are oral hypoglycaemic agents, especially sulfonylureas which may be potentiated by other drugs. Prolonged hypoglycaemia may be seen after first-order sulfonylureas, and may indicate glucose infusion as treatment. Next to insulin and sulfonylurea, ethanol is the most common cause of hypoglycaemia. In non-diabetics, hypoglycaemia will typically develop 6-24 h after a moderate or heavy intake of ethanol by a person who has had an insufficient intake of food for 1 or 2 days. Insulin-producing tumours, insulinomas and non-islet cell tumours may also be reasons for hypoglycaemia in non-diabetics. Treatment of mild episodes of hypoglycaemia is intake of fast-absorbing carbohydrates. Severe episodes can be treated with either i.v. dextrose or glucagon injected i.m. or i.v. The glycaemic response and recovery of a normal level of consciousness is 1-2 min slower after glucagon than after glucose.
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PMID:Endocrine emergencies. Hypoglycaemia. 173 95

Neurological signs and symptoms were recorded from 156 air and saturation divers and 100 controls. Fifty one (33%) of the divers had had symptoms from the central nervous system during decompression. Also, 22 (14%) had been unconscious while diving. In total 79 (51%) had had decompression sickness (DCS). Twelve (8%) of the divers and no controls had had specific neurological symptoms (vision disturbances, vertigo, reduced skin sensitivity) in non-diving situations, and six (4%) of the divers (no controls) had had episodes of cerebral dysfunction (seizures, transient cerebral ischaemia, transient amnesia). The divers had significantly more general symptoms from the nervous system and more abnormal neurological findings than the controls. The most prominent symptoms were difficulties in concentration and problems with long and short term memory. The most prominent abnormal findings in the divers were compatible with dysfunction in the distal spinal cord or nerve roots, and polyneuropathy. The general neurological symptoms and findings were independently significantly correlated with diving exposure, prevalence of DCS, and age.
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PMID:Influence of occupational diving upon the nervous system: an epidemiological study. 217 31

A group of 23 professional divers was investigated before and after dives to 300 and 350 metres of sea water. 12 divers were also studied during the actual dive. All divers presented neurological symptoms and signs during compression. Intention tremor, ataxia, motor weakness, sensory symptoms, vertigo, nausea and reduced memory were the most prominent features of the High Pressure Nervous Syndrome (HPNS). There were considerable individual differences. Neuropsychological and neurophysiological investigations performed after one dive showed no significant changes in any of the divers, while there was a clear-cut impairment in a group of 6 divers who had performed 2 dives 3 months apart. These changes indicate that there may be pressure-induced brain dysfunction which persists for a transient post-dive period. Loss of short-term memory is a prominent part of this dysfunction. Transitory neurological signs indicating focal cerebral dysfunction were found immediately post-dive in 4 divers, presumably reflecting the unmasking of pre-existing subclinical minimal CNS lesions.
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PMID:Central nervous dysfunction associated with deep-sea diving. 397 49

A 29-year-old man developed vertigo, diplopia, confusion and spasticity. Brain biopsy revealed multifocal microinfarcts. Bilateral hearing loss and retinal microangiopathy were also noted. Deficits were stable years after onset. Repeated neuropsychological testing was suggestive of diffuse cerebral dysfunction, with likely prominent involvement of reciprocal diencephalic-cortical projections.
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PMID:Susac's syndrome: neuropsychological characteristics in a young man. 871 93

Mild traumatic brain injury (TBI) is common but accurate diagnosis and defining criteria for mild TBI and its clinical consequences have been problematic. Mild TBI causes transient neurophysiologic brain dysfunction, sometimes with structural axonal and neuronal damage. Biomarkers, such as newer imaging technologies and protein markers, are promising indicators of brain injury but are not ready for clinical use. Diagnosis relies on clinical criteria regarding depth and duration of impaired consciousness and amnesia. These criteria are particularly difficult to confirm at the least severe end of the mild TBI continuum, especially when relying on subjective, retrospective accounts. The postconcussive syndrome is a controversial concept because of varying criteria, inconsistent symptom clusters and the evidence that similar symptom profiles occur with other disorders, and even in a proportion of healthy individuals. The clinical consequences of mild TBI can be conceptualized as two multidimensional disorders: (1) a constellation of acute symptoms that might be termed early phase post-traumatic disorder (e.g., headache, dizziness, imbalance, fatigue, sleep disruption, impaired cognition), that typically resolve in days to weeks and are largely related to brain trauma and concomitant injuries; (2) a later set of symptoms, a late phase post-traumatic disorder, evolving out of the early phase in a minority of patients, with a more prolonged (months to years), sometimes worsening set of somatic, emotional, and cognitive symptoms. The later phase disorder is highly influenced by a variety of psychosocial factors and has little specificity for brain injury, although a history of multiple concussions seems to increase the risk of more severe and longer duration symptoms. Effective early phase management may prevent or limit the later phase disorder and should include education about symptoms and expectations for recovery, as well as recommendations for activity modifications. Later phase treatment should be informed by thoughtful differential diagnosis and the multiplicity of premorbid and comorbid conditions that may influence symptoms. Treatment should incorporate a hierarchical, sequential approach to symptom management, prioritizing problems with significant functional impact and effective, available interventions (e.g., headache, depression, anxiety, insomnia, vertigo).
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PMID:Mild traumatic brain injury. 2570 14

"Cutis Marmorata" skin symptoms after diving, most frequently in the form of an itching or painful cutaneous red-bluish discoloration are commonly regarded as a mild form of decompression sickness (DCS), and treated with oxygen inhalation without reverting to hyperbaric recompression treatment. It has been observed that the occurrence of Cutis Marmorata is frequently associated with the presence of a Patent Foramen Ovale (PFO) of the heart, and indeed, with a properly executed contrast echocardiographic technique, these patients have an almost 100% prevalence of PFO. Only occasionally, Cutis Marmorata is accompanied by other symptoms of DCS. These symptoms usually are in the form of visual distortions, vertigo, or mild, vague but generalized cerebral dysfunction (such as abnormal fatigue, clumsiness, concentration problems). The pathogenesis of these other manifestations is clearly emboligenic, and we hypothesize that Cutis Marmorata is also a manifestation of gas bubbles embolizing the brain stem: the site of autonomic nervous system regulation of skin blood vessel dilation and constriction. The consequences of this hypothesis are that Cutis Marmorata skin decompression sickness should no longer be considered a mild, innocuous form but rather a serious, neurological form and treated accordingly.
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PMID:Cutis Marmorata skin decompression sickness is a manifestation of brainstem bubble embolization, not of local skin bubbles. 2643 31