Insomnia, fatal

Creutzfeldt-Jakob disease (CJD) New variant CJD Gerstmann-Straussler-Scheinker disease Fatal familial insomnia Kuru Prion protein Extracellular deposits... 

Human prion disease models have also been developed in mice [154,155]. Crossing the species barrier into an experimentally accessible animal system, the prions responsible for Creutzfeldt Jakob disease, new variant CJD, Gerstmann-Straussler-Scheinker disease, and fatal familial insomnia produce a reproducible time-dependent neuronal degeneration leading to death. 

The prion diseases are a closely related group of neuro-degenerative conditions which affect both humans and animals. They have previously been described as the subacute spongiform encephalopathies, slow virus diseases and transmissible dementias, and include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and the human prion diseases, Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker disease (GSS), fatal familial insomnia (FFI) and kuru. Prion diseases are... 

COPI coat protein FFI fatal familial insomnia... 

Citalopram (Celexa) [Antidepressant/SSRI] WARNING Closely monitor for worsening depression or emergence of suicidality, particularly in pts <24 y Uses Depression Action SSRI Dose Initial 20 mg/d, may t to 40 mg/d X in elderly hqjatic/renal insuff Caution [C, +/-] Hx of mania, Szs pts at risk for suicide Contra MAOI or w/in 14 d of MAOI use Disp Tabs, cap, soln SE Somnolence, insomnia, anxiety, xerostomia, diaphoresis, sexual dysfxn Notes May cause X Na /SIADH Interactions t Effects W/ azole antifungals, cimetidine, Li, macrolides, EtOH t effects OF BBs, carbamazepine, CNS drugs, warfarin X effects W/ carbamaz ine X effects OF phenytoin may cause fatal Rxn W/ MAOIs EMS Use caution w/ CNS depressants, may need a reduced dose concurrent EtOH... 

Peg Interferon Alfa 2b (PEG-Intron) [Antiviral/ Immunomodulator] WARNING Can cause or aggravate fatal or life-threatening neuropsychiatric, autoimmune, ischemic, and infectious disord s. Monitor pts closely Uses Rx Hep C Action Immune modulation Dose 1 mcg/kg/wk SQ 1.5 mcg/kg/wk combined w/ ribavirin Caution [C, X if used w/ ribavirin /-] w/ Hx psychiatric Contra Autoimmune H, decompensated Uvct Dz, hemoglobinopathy Disp Vials 50, 80, 120, 150 mcg/0.5 mL Redipen 50, 80,120,150 mcg/5 mL reconstitute w/ 0.7 mL w/ sterile water SE D ession, insomnia, suicidal behavior, GI upset, neutropenia, thrombocytopenia, alopecia, pruritus Interactions t Myelosuppression W/ antineoplastics t effects OF doxorubicin, theophylline t neurotox W7 vinblastine EMS See Peg Interf on Alfa-2a may cause flu-like Sxs... 

Hydrogen sulfide is a highly toxic and flammable gas. A 5-minute exposure to 1,000 ppm concentration in air can be fatal to humans (Patnaik, P. 1999. A Comprehensive Guide to the Hazardous Properties of Chemical Substances, 2nd ed. New York John Wiley). The symptoms are headache, nausea, nervousness, cough, eye irritation, and insomnia. High doses can produce unconsciousness and respiratory paralysis. 

Abacavir is associated with side effects such as anorexia, nausea, vomiting, malaise, headache, and insomnia. A potentially fatal hypersensitivity reaction develops in approximately 5% of patients, usually early in the course of treatment. Fever and rash are the most common symptoms of this reaction malaise, respiratory symptoms, and gastrointestinal complaints may also occur. Resistance to abacavir may be associated with resistance to zidovudine, didanosine, and lamivudine. 

Prion diseases have attracted immense attention over the past decade, prompted, in part, by the outbreak of mad cow disease in the United Kingdom. The most common prion disease is sporadic Creutzfeldt-Jakob disease (CJD). Clinically, CJD is characterized by a rapidly progressive dementia accompanied variably by early-onset seizures, insomnia, disordered movements, and psychiatric disturbances the disease is uniformly fatal. Histochemically, the principal pathological feature of prion disease is the abnormal accumulation of an amyloid-like material composed of prion protein (PrP), which is encoded by a single gene on the short arm of chromosome 20. 

Phenobarbital, mephobarbital and metarbital are the only oral anticonvulsants which are effective at sub-hypnotic levels. Many barbiturates are classified as Schedule II, III, or IV due to their high potential for overdose and dependence. Abrupt withdrawal may cause seizures, restlessness, trembling, and insomnia and may be fatal. Phenobarbital is used as an anticonvulsant for the treatment of epilepsy and in some combination medications for the relief of irritable bowel syndrome. 

An overdosage of local anesthetics can produce dose-dependent central nervous system (CNS) side effects such as insomnia, visual and auditory disturbances, nystagmus, shivering, tonic-clonic convulsions, and finally fatal CNS depression. The initial CNS excitation and convulsions may be brought under control by diazepam or thiopental. 

Note Benzodiazepines have only a limited capacity to produce profound and potentially fatal CNS depression. Although coma may be produced at very high doses, benzodiazepines cannot induce a state of surgical anesthesia by themselves and are virtually incapable of causing fatal respiratory depression or cardiovascular collapse unless other CNS depressants also are present. Because of this measure of safety, benzodiazepines have substantially replaced older agents for the treatment of insomnia or anxiety. 

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