Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the light of three case histories, other personal observations and the literature, the clinical and electroencephalographical differences between absences in the limited sense and continuous LENNOX petit-mal state are described and the problems of the latter discussed. As a rule, petit-mal state is diagnosed as such in young people or adults, and practically never before the 10th year of life. In about two thirds of cases, its clinical symptomatology consists of a twilight condition lasting some hours to a few days, coupled with inertia and apathy. The remaining third of the patients usually experience milder disturbances, e.g. in the form of concentration difficulties, tiredness, and (more rarely) severe forms including lethargy. The EEG correlate of a petit-mal state is made up of continuous bilaterally synchronous, frontally marked (less frequently with exclusively frontal localization), usually irregular spike waves or poly-spike waves, which frequently occur in only rudimentary forms and register a frequency of 2 1/2-4 c/sec. For the treatment of petit-mal state, benzodiazepines and in particular clonazepam (Rivotril) (1-2 mg i.v.) are recommended. During the interval condition the same therapy as with an absence epilepsy, e.g. succinimides or dipropylacetate (Depakine) is administered. Anti-grand-mal remedies, especially hydantoins, may trigger petit-mal status.
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PMID:[The petit-mal-status]. 1 55

In 11 patients with complex partial epileptic seizures stuporous states were observed during treatment with valproate (VPA) (2 cases), with VPA and phenobarbitone (PB) (4 cases), or with VPA, PB and a third anti-epileptic drug (5 cases). Based on 3 characteristic cases, an attempt is made to define the role of VPA, the nature of the stuporous states, and the origin of digestive disorders which often herald the onset of behavioural disorders. Several clinical studies have suggested the direct responsibility of VPA even if the adverse effects are potentiated by many other anti-epileptic drugs. Stuporous states are not due to VPA overdose and do not depend on the mode of administration. No correlation has been found between electroclinical signs and plasma or CSF levels of the different anti-epileptic drugs. Reported data and the present cases suggest a paradoxical epileptogenic role for VPA on complex partial seizures: there exists a close similarity of electroclinical findings between spontaneous epileptic seizures and stuporous states during DPA treatment. Digestive disorders appear to result from a central mechanism and not from digestive tract intolerance. In some cases, it is likely that partial seizures with digestive symptoms and signs do occur.
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PMID:[Stuporous states during treatment with sodium valproate. Pathogenetic hypotheses]. 679 80

This study was conducted to determine whether Depakene could be substituted for Depakote, which would represent a significant financial savings, without sacrificing symptom control or drug tolerance. Over an 8-week period of intensive monitoring, we changed 77 patients from Depakote to Depakene. Results showed no change in seizure control, no adverse upper gastrointestinal side effect, no weight change, no sleep disturbance, no change in aberrant behavior, and no change in appetite. Patients were less less lethargic on Depakene than on Depakote. However, there was some increase in diarrhea, of uncertain cause. Some changes in psychiatric symptoms were also noted. Overall, this drug change was well-tolerated.
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PMID:Effects on individuals with mental retardation of changing Depakote to Depakene. 798 19

Depakote-induced hepatotoxicity has been well established as an adverse effect, and periodic monitoring of drug level is often required. Depakote-induced hepatotoxicity mostly occurs at supratherapeutic drug level. Rarely, an idiosyncratic response is triggered, and hepatotoxicity can occur at the therapeutic drug level mostly in chronic users. Here, we describe a rare case of idiosyncratic depakote-induced hepatotoxicity. A 25-year-old female with non-insulin-dependent diabetes mellitus, hypothyroidism, seizure disorder, and Dandy Walker Syndrome presented with an unwitnessed seizure and altered mental status. The patient's medication list included zonisamide, depakote, and synthroid. She was noted to be lethargic, disoriented, nonverbal, but awake. An arterial blood gas examination showed severe anion gap metabolic acidosis. Blood work was consistent with hepatitis, hyperammonemia, thrombocytopenia, and coagulopathy. The Depakote level was therapeutic. Head computed tomography and liver ultrasound results were not significant. After ruling out all other causes and seeing improvement of parameters after the drug was discontinued, idiosyncratic depakote toxicity was diagnosed. Based on the patient's rapid improvement; idiosyncratic valproate toxicity was confirmed. This case signifies the importance of recognizing, diagnosing, and treating depakote toxicity in chronic users who have no other explanation for their symptomatology.
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PMID:Thinking beyond the obvious: hepatotoxicity secondary to idiosyncratic depakote toxicity. 2124 13