Gene/Protein Disease Symptom Drug Enzyme Compound
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Anorectics and bulimics often complain sleep onset insomnia and disrupted sleep. During awakenings bulimics can have binges. Conversely, eating disorders can be a clinical expression of a concomitantly occurring sleep disorder. Two clinical entities have been recently described: the Night Eating Syndrome (NES) and the Sleep Related Eating Disorders. The main goal of this literature review was to better characterize the relationships between eating disorders and sleep disturbances. No specific EEG sleep pattern emerges in anorectic and bulimic patients. However, all studies include several methodological limitations: a few number of patients, heterogeneous patient groups, various diagnostic criteria. The results of studies evaluating the impact of depression on sleep EEG in eating disorder patients are also subject to controversy. The only study examining the relationship between sleep EEG and morphological alterations in anorectics and normal weight bulimics shows that patients with enlarged cerebrospinal fluid spaces spent more time in slow wave sleep and that the duration of rapid eye movement (REM) sleep was reduced. The ventricular brain ratio was negatively correlated with REM sleep. The Night Eating Syndrome consists in insomnia, binge eating and morning anorexia. Other criteria are proposed to characterize the NES: more than 50% of the daily energy intake is consumed after the last evening meal, awakenings at least once a night, repetition of the provisional criteria for more than 3 months, subjects do not meet criteria for bulimia nervosa or binge eating disorder. Patients have no amnesia nor alteration of alertness, and no other sleep disorder. There is no modification of sleep EEG except sleep maintenance. The prevalence of the NES is 1.5% in the general population. Some neuroendocrine disturbances have been found in the NES. The delimitation with eating disorders is not yet clearly established. If it shares the compulsive features with eating disorders, particularly the "Binge Eating Disorder", and occurs during full awakenings, the night eating syndrome may be recognized as a specific eating disorder. The sleep related eating syndrome is also characterized by compulsive binge eating during awakenings. But in this case, night eating is linked with a reduced consciousness and sleep disorders, mainly somnambulism. Patients never experience hunger, abdominal pain, nausea or hypoglycemia. Night-eating takes place invariant across weekdays, weekend and vacations. Patients consumed high caloric foods and fluids but never alcohol and purging does not occur. Diurnal bulimia is frequently associated with the sleep-related eating disorder. In conclusion, the sleep related eating disorder seems rather be a clinical subtype of sleep disorders whereas the NES could be considered as an eating disorder.
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PMID:[Correlation between eating disorders and sleep disturbances]. 1176 Jun 92

Zolpidem is a sedative and hypnotic drug belonging to imidazopyridine family. Zolpidem facilitates GABAA function more selectively than benzodiazepines, and produces a selective hypnotic effect. In comparison with benzodiazepines this mechanism could be reduce liability to induce dependence. Recently, some cases of zolpidem abuse and dependence have been published. The Authors report 2 cases of addiction to high dose of zolpidem and compare them with others described in the literature. Both patients had been reknown drug addicts before their first prescription of zolpidem and a borderline personality disorder was diagnosed. The patients rapidly developed over consumption and dependence of the molecule, when taking doses as high as 240 and 400 mg daily. To get zolpidem, one patient falsifies prescriptions. They don't suffer from the sedative effects while searching for anxiolytic and stimulating effects. They were also dysarthric, confused, high energy for mental and physical activity. The cases of zolpidem abuse and dependence in the literature describe these symptoms and others such as losing sense of orientation in time and space, amnesia and visual hallucinations. The most typical withdrawal symptom is high levels of anxiety. Moreover, one patient presents an epileptic seizure whereas the other display a severe psychiatric complication such a psychosis. In the literature, withdrawal was accompanied by confusion, suicidal ideas, nausea, vomiting, sweat, tremors, tachycardia and insomnia rebound. The epileptic seizures are described but acute psychosis complication is rare. Pharmacological hypotheses are described. The effects of zolpidem on GABAA receptor gene expression are consistent with the reduced tolerance liability of this drug as well as with other ability to induce both physical dependence and withdrawal syndrome. Through the review of the literature, the Authors noted that 50% of the cases of dependence on zolpidem are drug addicts, therefore concluding that drug addicts are more likely to become dependent on zolpidem.
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PMID:[Dependence on zolpidem: a report of two cases]. 1510 18

The explosive RDX (hexogen, cyclonite) is usually used for the production of C-4 explosive. The rare occurrence of accidental and intentional RDX intoxications has been reported during manufacturing process or in wartime. In this article, the authors report 5 cases of accidental oral RDX poisoning. On admission, observed signs and symptoms included repetitive generalized tonic-clonic convulsions, postictal coma, lethargy, confusion, hyperreflexia, postictal amnesia, nausea, vomiting, abdominal tenderness, sinusal tachycardia, dysrhythmia with frequent ventricular premature beats, generalized muscle spasms, and myoclonus. Leukocytosis, mild anemia, methemoglobinemia, elevated levels of blood glucose, serum aspartate transaminase, alanine transaminase, lactic dehydrogenase, creatine phosphokinase, amilase, hypokalemia, metabolic acidosis, proteinuria, glucosuria, and myoglobinuria were also noted. Plasma RDX concentrations were 268 to 969 ng/mL at 3 hours of ingestion. For management, supportive and symptomatic measures were taken. Whole-bowel irrigation might have been an effective therapeutic procedure due to probable slow gastrointestinal absorption of RDX. Three patients who developed severe metabolic acidosis underwent urgent hemodialysis. All patients were discharged 7 to 21 days after admission without any sequelae. Plasma RDX levels were strongly correlated with the clinical and laboratory manifestations. The available toxicological data on this rare accidental poisoning are reviewed in light of the literature.
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PMID:Accidental oral poisoning caused by RDX (cyclonite): a report of 5 cases. 1518 66

The management of depression in subjects aged over 65 is based on the isolated or combined use of antidepressant chemotherapy, psychotherapy and electroconvulsive therapy. Electroconvulsive therapy, under general anaesthesia and use of curare, consists in producing a generalised seizure using a short, pulsed, electrical current administered via the transcranial route. There is renewed interest in electroconvulsive therapy with the development of specific rules and conditions for its use, together with the recruitment of depressed patients resistant to classical treatments in hospital settings. The efficacy of electroconvulsive therapy has been demonstrated in the elderly. The immediate side effects, related to the electrical stimulation and the seizure, such as headaches, nausea, confusion, and transient amnesia, regress within a few minutes or hours after the session. The limits of electroconvulsive therapy are the high risk of relapse on suspension of the sessions, relapse basically related to the severity of the depression. Consolidation electroconvulsive therapy provides new hope for better control of such relapses.
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PMID:[Utility of electroconvulsive therapy for severe depression in subjects aged over 65]. 1590 82

A thirty-two-year-old woman who had been diagnosed MELAS with 3243A > G mutation presented headache, nausea, decreased bilateral visual acuity, and topographical disturbance on January 1 in 2002. Although brain CT showed no fresh lesion, recurrence of stroke-like episode was considered. Immediately, she was treated with ubiquinone (210 mg/day, p.o.) and tocopherol nicotinate (300 mg/day, p.o.). She became confused on the fifth day. Diffusion weighted- and T2 weighted-MRI revealed appearance of hyperintense lesion at the right occipital lobe. We started edaravone infusion (30 mg, twice a day, div.) for two weeks with informed consent from her family. On 13th day her consciousness was improved. Edema and signal intensity of the lesion were decreased on MRI with minimal spread to the parietal lobe. She discharged on the 30th day with marked visual field loss, hemispatial neglect, and topographical amnesia. MRI after four months showed remarkable atrophy of the right occipital region. In our department, five stroke-like episodes including this case were treated with ubuiquinone and tocopherol nicotinate. This regimen was effective in prevention of progressive spread of lesions only in two episodes. Edaravone is radical scavenger used in acute cerebral infarction. Progressive spread into the neighboring regions is one of characteristics of MELAS, although its precise mechanisms are not well known. Oxidative stress induced by released free radicals through mitochondrial dysfunction might be one of factors and edaravone would make an effect through blockage of the free radicals. Edaravone could not rescue neurons in the initial lesion. Although more numbers of cases are needed to establish the effect of edaravone on MELAS, it could minimize the neurological deficits after stroke-like episode of MELAS.
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PMID:[A case of stroke-like episode of MELAS of which progressive spread would be prevented by edaravone]. 1602 65

General anesthesia, at a minimum, provides amnesia and unresponsiveness. Although anesthetics have many modulatory effects on neuronal ionophore protein complexes, it is not clear that the resulting electrophysiologic changes are the sole mechanisms of clinical anesthetic action. Cells respond to environmental changes in several ways, including alterations in DNA transcription leading to changes in the cell's proteins. We sought to expose the changes in global genomic expression, seeking potential targets involved in the processes of anesthetic-induced amnesia, and persistent long-term side effects of general anesthesia, including nausea and postoperative cognitive decline. Using Affymetrix GeneChips, we surveyed changes in expression across the entire expressed genome of Sprague-Dawley rat (n = 10 baseline, n = 6 isoflurane) basolateral amygdala 6 h after exposure to 15 min of 2% (1.4 MAC) isoflurane. Isoflurane administration was associated with altered expression in 269 unique genes possessing functional annotation. Affected genes were related to DNA transcription, protein synthesis, metabolism, signaling cascades, cytoskeletal structural proteins, and neural-specific proteins, among others. Even brief exposure to isoflurane leads to widespread changes in the genetic control in the amygdala 6 h after exposure. Gene expression is a dynamic process that may explain some long-term effects of anesthesia and that has the potential to modulate some of those effects using specific molecular therapeutics.
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PMID:Isoflurane modulates genomic expression in rat amygdala. 1745

We reported a case of X-linked lymphoproliferative syndrome (XLP) with multiple nodular lesions in the brain and lungs. A 21-year-old man was admitted because of one month history of low grade fever, headache, nausea, and amnesia. He developed agammaglobulinemia following Epstein-Barr virus infection at 3-year-old, and thereafter was administered 7.5g of immunoglobulin every 3 weeks with a diagnosis of XLP. Physical examination was unremarkable on admission. Neurological examination revealed disorientation of time, and bilateral gaze-evoked nystagmus. Neuropsychological tests demonstrated impairment of recent memory and calculation. Pleocytosis (83/microl) and increase of protein (1269 mg/dl) and IgG (141 mg/dl) in the CSF were observed. Brain MRI showed multiple nodular lesions with high intense signal on T2-weighted images and Gd-DTPA enhancement on T1-weighted images. Chest CT showed multiple nodular lesions in the bilateral lungs. The needle lung biopsy was performed, which showed infiltration of lymphocytes around the vessels. An immunohistochemical study showed that the infiltrating cells were mainly CD8 positive T lymphocytes. B lymphocyte and plasma cells were not seen. The histological findings excluded intravascular malignant lymphoma and lymphomatoid granulomatosis. Therefore we diagnosed lymphoid vasculitis. The patient developed pancytopenia caused by hemophagocytic syndrome 48 days after admission and was treated with 1 g of methylprednisolone per day for 3 days and a tapered dose of steroid (500 mg to 125 mg of methylprednisolone and 60 mg to 10mg of predonisolone) for 21 days, which resulted in the improvement of clinical features (hemophagocytic syndrome and central nervous system symptoms) and the abnormal CSF findings. The multple nodular lesions in the brain and the lungs shrank 1 month after treatment and disappeared 11 months later. There are few reports concerning lymphoid vasculitis with XLP, and no effective treatment has been described. Our case suggests that steroid therapy may be useful for the treatment of lymphoid vasculitis in XLP.
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PMID:[Case of X-linked lymphoproliferative syndrome (XLP) with multiple nodular lesions in the brain]. 1676 91

A concussion is defined as a complex pathophysiologic process affecting the brain that is induced by traumatic biomechanical forces. Concussions are caused by a direct or indirect blow that leads to a graded set of syndromes characterized by functional rather than structural disturbances to the brain. Concussions are characterized by a wide variety of presenting symptoms, including loss of consciousness, amnesia, confusion, headache, and nausea. Concussions occur in patients participating in all levels of athletic activities, with most occurring in younger athletes. The evaluation of a patient with a concussion should include assessment of the airway, breathing, circulation, level of consciousness, orientation, memory, concentration, and neurologic function. Multiple grading scales and return to play guidelines have been published to assist the clinician in the treatment of patients with concussions. Diagnostic and treatment concerns include spinal cord injury, intracranial pathology, second impact syndrome, and long-term impairment of cognitive function. Computerized neuropsychologic testing is a new tool in the treatment of concussions. These tests measure memory, new learning, attention, and reaction time and should be used as an adjunct to other tools for clinical decision making. Published guidelines will assist in treatment decisions; however, it should be kept in mind that all concussions are unique injuries.
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PMID:Concussions in adolescent athletes. 1695 3

Concussions remain one of the most troublesome injuries sports physicians face. Studies suggest recovery takes hours to weeks, but at what point is the concussed brain no longer at increased risk for reinjury is unknown. Physicians must be alert to the symptoms of concussion and be familiar with the available tools to assess neurocognitive dysfunction. Prospectively validated signs and symptoms include amnesia, loss of consciousness, headache, dizziness, blurred vision, attention deficit, memory, postural instability, and nausea. A player with any signs or symptoms of a concussion should not be allowed to return to the current game or practice and should be monitored closely for deterioration of symptoms. Return-to-play should be individually based and proceed in a step-wise manner. The ongoing risk-benefit analysis of return-to-play must currently be based on experience, corollary data from traumatic brain injuries in animals and humans, and limited prospective data with sports-related concussions.
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PMID:Sideline management of sport-related concussions. 1713 69

The factors affecting outcome were analyzed in 1,064 patients, 621 males and 443 females aged 10 to 104 years (mean 46 +/- 23 years), with mild head injury (Glasgow Coma Scale [GCS] score > or =14) but no neurological signs presenting within 6 hours after injury. Intracranial lesion was found in 4.7% (50/1,064), and 0.66% (7/1,064) required surgical treatment. The Japan Coma Scale (JCS) and GCS assessments were well correlated (r = 0.797). Multivariate analysis revealed significant correlations between computed tomography (CT) abnormality and age > or =60 years, male sex, JCS score > or =1, alcohol consumption, headache, nausea/vomiting, and transient loss of consciousness (LOC)/amnesia. Univariate analysis revealed that pedestrian in a motor vehicle accident, falling from height, and mechanisms of injuries except blows were correlated to intracranial injury. No significant correlations were found between craniofacial soft tissue injury and intracranial injury. Patients with occipital impact, nonfrontal impact, or skull fracture were more likely have intracranial lesions. Bleeding tendency was not correlated with CT abnormality. The following indications were proposed for CT: JCS score >0, presence of accessory symptoms (headache, nausea/vomiting, LOC/amnesia), and age > or =60 years. These criteria would reduce the frequency of CT by 29% (309/1,064). Applying these indications to subsequent patients with GCS scores 14-15, 114 of 168 patients required CT, and intracranial lesions were found in 13. Two refused CT. Fifty-four of the 168 patients did not need CT according to the indications, but 38 of the 54 patients actually underwent CT because of social reasons (n = 21) or patient request (n = 17). These indications for CT including JCS may be useful in the management of patients with mild head injury.
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PMID:Indications for computed tomography in patients with mild head injury. 1765 14


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