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)

Kava is an extract from the Piper methysticum Forst. f. plant that has social and spiritual importance in Pacific islands societies. Herbal remedies that contain kava are used for the psychiatric treatment of anxiety and insomnia. Laboratory studies have found only subtle, if any, changes on cognitive or motor functions from the acute effects of consuming small clinical doses of kava products. Intoxication from recreational doses of kava has not been studied. The performance of individuals intoxicated from drinking kava (n=11) was compared with a control group (n=17) using saccade and cognitive tests. On average, intoxicated individuals had consumed 205 g of kava powder each (approximately 150 times clinical doses) in a group session that went for 14.4 h and ended 8 h prior to testing. Intoxicated kava drinkers showed ataxia, tremors, sedation, blepharospasm and elevated liver enzymes (GGT and ALP), together with saccadic dysmetria, saccadic slowing and reduced accuracy performing a visual search task that only became evident as the task complexity increased. Kava intoxication is characterized by specific abnormalities of movement coordination and visual attention but normal performance of complex cognitive functions. Saccade abnormalities suggest disruption of cerebellar and GABAergic functions.
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PMID:Saccade and cognitive impairment associated with kava intoxication. 1453 34

The goal of this study was to design a prolonged release system of the hypnotic agent zolpidem (ZP) useful for the treatment of insomnia. In this work, ZP alone or in the presence of HP-beta-CD was encapsulated in microparticles constituted by poly(DL-lactide) (PDLLA) and poly(DL-lactide-co-glycolide) (PLGA) and the drug release from these systems was evaluated. ZP alone-loaded microparticles were prepared by the classical O/W emulsion-solvent evaporation method. Conversely, ZP/HP-beta-CD containing microparticles were prepared by the W/O/W emulsion-solvent evaporation method following two different procedures (i.e. A and B). Following procedure A, the previously produced ZP/HP-beta-CD solid complex was added to the water phase of primary emulsion. In the procedure B, HP-beta-CD was added to the aqueous phase and ZP to the organic phase. The resulting microparticles were characterized about morphology, size, encapsulation efficiency and release rates. FT-IR, X-ray, and DSC results suggest the drug is in an essentially amorphous state within the microparticles. The release profiles of ZP from microparticles were in general biphasic, being characterized by an initial burst effect and a subsequent slow ZP release. It resulted that co-encapsulating ZP with or without HP-beta-CD in PDLLA and PLGA the drug release from the corresponding microparticles was protracted. Moreover, in a preliminary pharmacological screening, the ataxic activity in rats was investigated and it was found that intragastric administration of the ZP/HP-beta-CD/PLGA microparticles prepared according to procedure B produced the same ataxic induction time as the one induced by the currently used formulation Stilnox. Interestingly moreover, there was a longer ataxic lasting and a lower intensity of ataxia produced by the ZP/HP-beta-CD/PLGA-B-formulation already after 60 min following the administration. However, a need for further pharmacokinetic and pharmacodynamic studies resulted to fully evaluate the utility of this last formulation for the sustained delivery of ZP.
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PMID:Encapsulation and release of the hypnotic agent zolpidem from biodegradable polymer microparticles containing hydroxypropyl-beta-cyclodextrin. 1464 76

We describe the clinical and genetic characteristics of the 85 definite or probable human prion diseases cases died between January 1993 and December 2002 in Catalonia (an autonomous community of Spain, 6 million population). Seventy-three (86%) cases were sporadic Creutzfeld-Jakob diseases (sCJD) (49 definite, 24 probable), with a median age at onset of 66 years. The clinical presentation was dementia in 29 cases, ataxia in 14 and visual symptoms in five. The median survival was 3 months. The 14-3-3 assay was positive in 93% cases, 62% presented periodic sharp wave complexes (PSWC) in EEG but only 18% the typical signs on MRI. Forty-eight sCJD were studied for codon 129 PRNP polymorphism: 69% were methionine/methionine (M/M), 14.5% valine/valine (V/V) and 16.5% M/V. Six out of seven V/V cases did not present PSWC and in two survival was longer than 20 months. Eleven cases (13%) were genetic: five familial fatal insomnia and six familial CJD (fCJD). Up to four (67%) fCJD lacked family history of disease, two presented seizures early at onset and one neurosensorial deafness. The only iatrogenic case was related to a dura mater graft. No case of variant CJD was registered. The study confirms in our population the consistent pattern reported worldwide on human prion diseases. Atypical features were seen more frequently in sporadic 129 V/V CJD and fCJD cases.
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PMID:Clinical and genetic features of human prion diseases in Catalonia: 1993-2002. 1546 48

The term Morvan's disease, first coined in 1890, is still in use, although the generic term neuromyotonia--which is not exempt from criticism--has largely superseded it. Symptoms and signs are variable, ranging from benign painful fasciculations, pseudomyotonic cases, rigid forms, cases in which central nervous system features are also present (with, in addition to nerve hyperexcitability, agitation, confusion, delirium, insomnia, hyperhidrosis and tachycardia). A distal peripheral motor nerve is the origin of nerve hyperexcitability. There is growing evidence that autoimmunity is involved in the pathogenesis of many cases. Antibodies to voltage-gated potassium channels are detected in the serum of many patients with peripheral nerve hyperexcitability. Other cases are probably genetic. Inherited disorders are related to episodic dominant ataxia type 1, with the same mutation of a gene coding for potassium channel subunit Kv 1-1. Many inappropriate or non specific names are used to refer to peripheral nerve hyperexcitability. Isaacs syndrome, voltage-gated potassium channelopathy, or Morvan's syndrome are suggested.
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PMID:[From Morvan's disease to potassium channelopathies]. 1550 15

The aim of this study was to evaluate the efficacy and tolerability of iron protein succinylate in the treatment of iron-deficiency anemia in pregnancy. One hundred and thirty anemic pregnant women were studied. Inclusion criteria were iron-deficiency type of anemia, and hemoglobin levels below of 11.5, 10.9 and 10.3 g/dl for the three trimesters of pregnancy, respectively. Twenty-five women who presented pregnancy-related complications were excluded during treatment. The remaining 105 were treated with 1600-mg iron protein succinylate per os daily for a period of four months. A group of anemia-related clinical signs and symptoms, and hematological parameters were recorded at the beginning of treatment, as well as two and four months later. They included epidermis and mucosal paleness, skin and nail lesions, glossitis, heart pulse, sickness, anorexia, apathy, ataxia, polypnea, insomnia, nervousness, paresthesias and other neurological symptoms; the hematological parameters included Hgb, hct, RBCs, WBCs, MCV, MCH, MCHC, PLTs, serum Fe and ferritin. Possible side or adverse effects were considered during treatment. The majority of symptoms and signs of anemia were gradually improved. There was a statistically significant increase in the means of Hgb, hct, WBCs, MCV, MCH, PLTs and serum ferritin (p < 0.05). Anemia was effectively treated in 100/105 (95.2%) women, but not in five patients (4.8%) who displayed poor compliance to the therapeutic protocol. There were transient and mild side-effects in seven (6.6%) treated women, namely diarrhea, epigastralgia, vomiting, and nausea, which however, did not necessitate discontinuation of the therapeutic protocol. Iron protein succinylate is an effective and well tolerated treatment of iron-deficiency anemia in pregnancy.
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PMID:The efficacy and tolerability of iron protein succinylate in the treatment of iron-deficiency anemia in pregnancy. 1610 96

Fatal Familial Insomnia (FFI) is characterized by loss of sleep, oneiric stupor with autonomic/motor hyperactivity and somato-motor abnormalities (pyramidal signs, myoclonus, dysarthria/dysphagia, ataxia). Positon emission tomography (PET) disclosed thalamic hypometabolism and milder involvement of the cortex; neuropathology severe neuronal loss in the thalamic nuclei variably affecting the caudate, gyrus cinguli and fronto-temporal cortices. Genetic analysis disclosed a mutation in the PRNP gene and FFI was transmitted to experimental animals, thus classifying FFI within the prion diseases. Rare Sporadic Fatal Insomnia (SFI) cases occur without PRNP mutation but with features similar to FFI. FFI represents a model disease for the study of sleep-wake regulation: (I) the profound thalamic hypometabolism/atrophy associated with lack of sleep spindles and delta sleep implicate the thalamus in the origin of slow wave sleep (SWS); (II) loss of SWS is associated with marked autonomic and motor hyperactivity; termed 'agrypnia excitata', this association has been proposed as a useful clinical concept representative of thalamo-limbic dysfunction; (III) lack of SWS occurs with substantial preservation of stage 1 NREM sleep, implying that the latter has mechanisms different from SWS and unaffected by thalamic atrophy; accordingly, conflating stage 1 NREM with SWS into NREM sleep is inappropriate.
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PMID:Fatal familial insomnia: a model disease in sleep physiopathology. 1610 94

Effective, pharmacologic approaches to the treatment of cerebellar ataxia are lacking or inadequate. We recently reported preliminary evidence that tandospirone citrate (tandospirone), a 5-HT1A agonist, improved cerebellar ataxia in patients with Machado-Joseph disease (MJD). In the course of that study, we found that such treatment also alleviated the pain associated with cold sensations in the legs, insomnia, anorexia, and depression, all of which are thought to be mediated through activation of the 5-HT1A receptor. In this paper, we reviewed the few published clinical trials that involved the use of 5-HT1A receptor agonists for the treatment of cerebellar ataxia, and discussed the current theories regarding their mechanism of action. Cortical cerebellar atrophy (CCA) was reported, in a double-blind study, to be amenable to treatment with tandospirone. Other types of spinocerebellar degeneration (SCD) i.e., olivopontocerebellar atrophy (OPCA) and Machado-Joseph disease (MJD) have also been reported to respond to the drug, but these have been small studies. Responsive patients exhibited only mild ataxia. The doses of 5-HT1A agonists that have been used successfully ranged from 12.5 mg/day to 60 mg/day (or 1 mg/kg), and were well tolerated by most patients.
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PMID:Treatment of cerebellar ataxia with 5-HT1A agonist. 1614 54

Western medicine was introduced to Taiwan in 1865 when Dr. James L. Maxwell, a missionary doctor of the English Presbyterian Church, established a hospital in nowadays Tainan. The period of the missionary medicine lasted for over 30 years until Japanese took over. During this period, however, official records of diseases in Taiwan that were based on Western medicine were scanty or not available. Fortunately, port surgeons stationing respectively in Tamsui and Kelung in the north and in Takow and Taiwan-fu in the south reported semi-annually diseases seen in the ports, foreign communities and missionary hospitals that they volunteered to work. The diseases reported by port surgeons were either cases or summary of cases with classification and statistics. Their medical reports covered from 1871 to 1900. The data show that neurological diseases and/or disorders in the late 19th century Taiwan were uncommon, comprising only 2-3% of total diseases. The data further show that common neurological diseases were leprosy, opium smoking, syphilitic dementia (GPI), paralysis, hysteria, neuralgia, epilepsy, mania, sciatica, meningitis and ataxia. Stroke was uncommon while Parkinson's disease and Alzheimer's disease were not mentioned, indicating that neurological diseases related to old age and neurodegeneration were not yet a threat to health. Similarly, headache, insomnia, anxiety and depression, hallmark of functional disorders of the modern society, were also not mentioned, suggesting that these disorders were indeed rare or did not cause sufficient concern for patients to seek help from doctors of Western medicine.
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PMID:[Neurological diseases in late 19th century Taiwan--medical reports of the Chinese Imperial Maritime Customs]. 1642 51

Zolpidem and zaleplon are used for the treatment of insomnia. The objective of this study was to compare the patterns of zolpidem and zaleplon exposures reported to Texas poison control centers during 1998-2004. There were 5842 total reported zolpidem exposures, of which 2918 (50%) were isolated exposures, and 467 total reported zaleplon exposures, of which 201 (43%) were isolated exposures. Zolpidem patients were 62% male and 67% adult. Zaleplon patients were 67% male and 34% adult. The exposure was intentional in 62% of zolpidem and 58% of zaleplon exposures. The exposure occurred at the patient's own residence in 94% of zolpidem and 97% of zaleplon exposures. Management occurred outside of a health care facility for 29% of zolpidem and 32% of zaleplon exposures. The medical outcome involved no symptoms due to exposure for 29% of zolpidem and 44% of zaleplon exposures, a statistically significant difference. Although many of the most frequently reported adverse clinical effects for the two drugs were similar (drowsiness, slurred speech, hallucinations, ataxia, tachycardia, dizziness, confusion, vomiting), the proportion of exposures with a given adverse clinical effect was generally lower for zaleplon. Thus, although zolpidem and zaleplon exposures were generally similar with respect to patient gender and age, exposure reason and site, and management site, zaleplon exposures were less likely to result in minor medical outcomes or manifest as adverse clinical effects.
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PMID:Comparison of zolpidem and zaleplon exposures in Texas, 1998-2004. 1695 7

In the serum and cerebrospinal fluid of a patient with recurrent acute episodes of respiratory crises, autonomic symptoms and total insomnia (agrypnia), we identified a novel anti-neural complement fixing antibody directed against GABA(B) receptor (GABA(B)R). Patient purified IgG recognized a band of approximately 110 kDa on protein extracts of mouse cerebellum, cortex and brainstem and immunolabelled cultured Chinese hamster ovary (CHO) cells, transfected with human GABA(B)R1 and rat GABA(B)R2 receptors. Western blot analysis of transfected CHO homogenates showed the same band using both patient purified IgG and anti-GABA(B)R1 antibody. In order to verify the pathogenic role of these purified antibodies, we injected patient IgG intrathecally into cisterna magna of C57BL/6 mice pre-implanted with EEG electrodes and we observed severe ataxia followed by breathing depression and total suppression of slow wave sleep, as evidenced by EEG recording, in a dose-dependent manner. Immunohistochemistry on brain sections of mice injected with patient IgG showed the simultaneous presence of bound human IgG and C5b-9 deposits on Purkinje cells and cerebellar granular layer. After incubation with anti-GABA(B)R antibody, a marked reduction of receptor immunostaining was found with relative sparing of neuronal architecture. In conclusion we recognized an anti-neuronal autoantibody directed against GABA(B)R that is associated with autoimmune agrypnia and we showed that our patient purified IgG was able to induce in mice experimental autoimmune agrypnia characterized by a complex neurological syndrome affecting several CNS functions.
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PMID:A human anti-neuronal autoantibody against GABA B receptor induces experimental autoimmune agrypnia. 1733 94


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