Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An electro-behaviour dissociation was described, at first by animals next about the man, in experiment testing and in the drug addictions. This non concordance appear as lesser if it is be considered not only the sleeping waves but also all the electrical signs of the vigil state: non-existent, fluctuating, limited in topography, behind the stimulation, incomplete or emphasized. In this view we study some pathological states: narcotic and alcoholic addictions, confusion and pre-senile illness. Sometimes it is the abnormal sleep (coma or amazement) which alter the vigil state: absent, decreased, etc. Sometimes the vigilance is "numbed", the behaviour and the recording are those of lethargy. Sometimes also, the drowsiness has insomnia characteristics, associating a deep sleep loss, a reactivity to stimulations at once emphasized and undiscriminated, and "strangeness" insurmontable for the consciousness (perplexity, delusions, nightmare and level anomalies).
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PMID:[Alterations of arousal in some psychopathologic states]. 134 49

Whatever induces general anesthesia, i.e. cerebral arrest, tends to cause respiratory and cardiac arrest also. However, general anesthesia does not necessarily exclude nor block all other mechanisms which can provoke one or more of these three phenomena. Amongst many such more or less equipotent factors are intracranial, intrapleural, intra-abdominal and intratracheal pressures. These mechanical factors occurring but unrecognized in surgical patients cause puzzling complications including, insomnia, coma and unexpected sudden death.
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PMID:Insomnia-coma and auto-electrocution complicating general anesthesia. Incidental factors which also cause cerebral, respiratory and cardiac arrest. 158 8

A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid (CSF) lactic acidosis was reported. A 44-year-old Japanese woman noted tarry stool on July 2, 1988 and was treated with metoclopramide and cimetidine for nausea and vomiting. Hydroxyzine pamoate was also administered for insomnia at 3:10 am and she became comatose with muscle rigidity at 3:40-4:30 am on July 3. Tachycardia and high fever (39.5 degrees C) were evident at 8:00 am on July 4. She was transferred to the Kyushu University Hospital. On admission, serum creatine kinase was elevated to 1640 IU/1; MM fraction was 100%. She was diagnosed as malignant syndrome. Cerebrospinal fluid was normocellular with protein 38 mg/dl and glucose 122 mg/dl. Cerebrospinal fluid lactate increased markedly to 3.43 mmol/l, CSF pH was 7.264, HCO3- 14.4 mEq/l, indicating CSF metabolic acidosis. She became afebrile after the 10th hospital day, and gradually but completely recovered within a month. She was discharged on August 16, 1988. The anti-dopaminergic activity of metoclopramide was considered to be primarily responsible for the development of malignant syndrome in this case. Cerebrospinal fluid lactic acidosis seemed to reflect hyperpyrexia or malignant syndrome induced derangement of the brain metabolism.
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PMID:[A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid lactic acidosis]. 188 79

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

The patient was 56-year-old female, who suffered from ataxia and then fell into coma on the next day after she had moved from the sea level to an altitude of 4,200 m. After she was brought to lower altitude, consciousness recovered within several hours. For about 2 days thereafter, disorientation was observed, and she was diagnosed as AMS (acute mountain sickness). Only insomnia continued in chronic stage. The results of X-ray computed tomography (CT) on 25th day after the onset of the disease revealed no abnormal finding except the slightly increasing uptake of contrast material. Symmetrical low density regions were seen in bilateral basal ganglia after one year, and the globus pallidus lesions were confirmed by magnetic resonance imaging. In the past, cerebral edema has been reported in most cases of AMS, and the neurotic symptoms of AMS have been attributed to cerebral edema, while the essential condition of this disease is not yet elucidated. In the present case, the globus pallidus lesions could be identified through the following-up of the central nervous system by X-ray CT and MRI as the first attempt for the case of AMS. There has been no report of globus pallidus lesions in the cases of AMS. Whereas low oxygen partial pressure is the primary cause of AMS, and it is highly probable that the disorders in globus pallidus as reported in the cases of carbon monoxide poisoning, anesthetic accident, etc. are related to the occurrence of AMS.
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PMID:[A case of acute mountain sickness with bilateral lesion of pallidum]. 222 57

The case of a patient developing hypomagnesemic encephalopathy and coma secondary to intensive treatment for severe cardiac failure, is reported. Following an early improvement of symptoms and signs of cardiac failure, a rapidly developing neurologic disorder appeared. This was characterized by insomnia, agitation, mental derangement and, finally, sopor and I-II degree coma. Serum magnesium concentration was 1.0 mEq/l. Magnesium sulfate iv infusion was followed by a immediate and complete recovery from the neurological disorder. Patients with cardiac failure undergoing prolonged intensive therapy are prone to develop hypomagnesemia. This electrolyte alteration may be responsible for symptoms and signs of central nervous system involvement (metabolic encephalopathy) that need to be differentiated from those of organic origin.
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PMID:[Hypomagnesemic coma in heart failure: description of a case]. 237 57

Practically all drugs administered in large amounts can give rise to neurologic symptoms such as drowsiness, insomnia, confusion, seizures or coma and extrapyramidal disorders. In this study, five classes of agents are reviewed: antipsychotic drugs, drugs for Parkinson's disease, antiepileptic drugs, calcium antagonists and salts of bismuth.
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PMID:[Various encephalopathies caused by drugs]. 256 72

Many therapeutic effects of benzodiazepines are mediated by neuronal high-affinity binding sites, i.e. benzodiazepine receptors (BR), located on GABAA receptors. Recently, endogenous BR ligands have partially been identified which, as agonists, either increase or, as inverse agonists, decrease GABAergic inhibition in the brain. BR antagonists, previously described as intrinsically inactive, induce effects in animals and humans under particular circumstances emphasizing a functional relevance of endogenous BR ligands. Several brain disorders, e.g. anxiety, insomnia, epilepsy, spasticity, alcoholism, coma, dementia, may be associated with a disequilibrium of opposing endogenous BR ligands changing the excitability of neurons implicated in aforementioned diseases. It is proposed that, depending on the relative role endogenous BR ligands play in the pathophysiology of these disorders, BR antagonists might demonstrate a variable efficacy in improving their symptomatology. In fact, such therapy would restore the homeostatic balance among various endogenous BR ligands being disturbed during an illness.
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PMID:Involvement of endogenous benzodiazepine receptor ligands in brain disorders: therapeutic potential for benzodiazepine antagonists? 747 87

Sleep-related disorders are revisited in the light of the physiological modality of NREM sleep expressed by the cyclic alternating pattern (CAP). Owing to its fluctuating properties on vigilance, muscle tone, and vegetative activities, CAP represents a highly favorable condition for the occurrence of interictal generalized and focal lesional EEG discharges, for motor seizures, and for periodic jerks in nocturnal myoclonus. All these manifestations are significantly associated with the components of activation during CAP, i.e., the A phases. On the contrary, the B phases of CAP appear chronologically linked to inhibitory phenomena in epileptic patients and in nocturnal myoclonus. The two phases of CAP seem especially involved in sleep apnea syndrome, where respiration is interrupted during a phase B and restored during a phase A. CAP rate, that measures the effort of the brain to maintain sleep, is increased by all conditions that induce vigilance instability such as noise, clinical insomnia, interictal EEG paroxysms, nocturnal seizures, periodic leg movements, and in certain extreme pathologic conditions such as Creutzfeldt-Jakob disease and stage 2 coma.
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PMID:Clinical applications of cyclic alternating pattern. 824 61

Creutzfeldt-Jakob disease (CJD) is a prion-related subacute encephalopathy producing widespread neuronal degeneration and spongiform pathological changes, especially in the neocortex. Progressive dementia, motor signs and electroencephalographic (EEG) alterations characterize the full stage of the disease. A series of eight 24-hour polygraphic recordings were carried out in the last 3 months of life of a 68-year-old female patient affected by CJD that was confirmed neuropathologically. Genetic classification demonstrated this patient to have a sporadic form of the disease. The polygraphic recordings demonstrated three types of EEG findings, as follows: 1) sustained pseudoperiodic discharges (SPD), characterized by long-lasting diffuse sequences of slow sharp waves or di- or triphasic slow waves recurring at 0.5- to 1.5-second intervals; 2) discontinuous pseudoperiodic discharges (DPD), consisting of runs of pseudoperiodic discharges (PD)(phase A) cyclically replaced at about 1-minute intervals with semi-rhythmic theta-delta activities (phase B); 3) non-rapid eye movement (NREM) sleep-like pattern, with dominant 0.5- to 4-Hz activities, less rhythmic than the EEG of phase B. Only these three EEG patterns occurred spontaneously during the repeated polygraphic sessions. The NREM sleep-like pattern was found only in the first recording, whereas the following polygraphic sessions were occupied exclusively by SPD or by a DPD pattern. SPD was associated with either a relatively high level of vigilance (along the first three recordings) or a state of alert-appearing silent immobility (following the fourth recording). During DPD, the patient was unable to accomplish any voluntary movement and fluctuated between levels of greater arousal (phase A) and lesser arousal (phase B). Just as in stage 2 coma, the fluctuations between phases A and B of DPD were synchronous with phasic modifications of muscle activity and neurovegetative functions. In particular, reinforcement of muscle tone and myoclonic spasms coincided with phase A, whereas heart rate deceleration and respiratory pauses or decrease in flow were synchronous with phase B. As EEG evolved toward the disappearance of DPD and finally to flatness, the phase-locked coordination among arousal, somatic and vegetative activities was progressively impaired and was replaced with an uncontrolled exaggeration of cardiorespiratory activity. The genetic, neuropathological and polysomnographic differences between CJD and another prion disease, fatal familial insomnia, are discussed.
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PMID:Precocious loss of physiological sleep in a case of Creutzfeldt Jakob disease: a serial polygraphic study. 874 91


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