Recurrent opisthotonus in catatonia: An atypical presentation.

Opisthotonus is known to occur in tetanus, rabies, cerebral malaria, neurosyphilis, acute cerebral injury and other medical conditions. Opisthotonus, so far, has not been reported in any major psychiatric disorder. Authors report a case of recurrent opisthotonus presenting concurrently with other catatonic signs which showed dramatic response to combination of lorazepam and electroconvulsive therapy (ECT). Clinicians should consider the possibility of catatonia in the differential diagnosis of opisthotonus since catatonia can be treated easily with benzodiazepines and ECT.

Differential response to gepirone but not to chlordiazepoxide in malnourished rats subjected to learned helplessness

The learned helplessness (LH) paradigm is characterized by learning deficits resulting from inescapable events. The aims of the present study were to determine if protein-calorie malnutrition (PCM) alters learning deficits induced by LH and if the neurochemical changes induced by malnutrition alter the reactivity to treatment with GABA-ergic and serotonergic drugs during LH. Well-nourished (W) and PCM Wistar rats (61 days old) were exposed or not to inescapable shocks (IS) and treated with gepirone (GEP, 0.0-7.5 mg/kg, intraperitoneally, N = 128) or chlordiazepoxide (0.0-7.5 mg/kg, intraperitoneally, N = 128) 72 h later, 30 min before the test session (30 trials of escape learning). The results showed that rats exposed to IS had higher escape latency than non-exposed rats (12.6 ± 2.2 vs 4.4 ± 0.8 s) and that malnutrition increased learning impairment produced by LH. GEP increased the escape latency of W animals exposed or non-exposed to IS, but did not affect the response of PCM animals, while chlordiazepoxide reduced the escape deficit of both W and PCM rats. The data suggest that PCM animals were more sensitive to the impairment produced by LH and that PCM led to neurochemical changes in the serotonergic system, resulting in hyporeactivity to the anxiogenic effects of GEP in the LH paradigm.

Zumbido pulsátil: tratamento com clonazepan e propranolol / Pulsatile tinnitus: treatment with clonazepam and propranolol

O zumbido pulsátil sincrônico com os batimentos cardíacos é pouco freqüente, sendo de etiologia tanto vascular arterial (malformacões, fístulas artério-venosas) ou venosa (anormalidades do bulbo jugular, tumor glômico jugular ou timpânico). A identificacão precoce da etiologia é essencial para que a terapêutica adequada possa ser instituída. A angioressonância possibilita a identificacão de alteracões vasculares com maior precisão. Relatamos um caso onde, após o diagnóstico de uma alteracão vascular arterial, foi instituído o tratamento com propranolol e clonazepam, com melhora da sintomatologia.

Newer aspects of hepatic encephalopathy.

Recently attempts have been made to standardize terminology in the field of hepatic encephalopathy. We are now facing a new problem. Chronic hepatitis C-induced cirrhosis occurs in an older population; this may change the presentation pattern of hepatic encephalopathy in future. Ammonia has once again become prominent as the leading toxin likely to play a role in the pathogenesis of this syndrome. How ammonia interacts with other proposed mechanisms should be an area of active research. The treatment arena has seen some advances. Unfortunately, the economics of having newer treatments approved in the USA is formidable. Rifaximine, L-ornithine-L-aspartate, sodium benzoate and possibly flumazenil appear to be significant advances. More elective shunt suppression for selected patients will be seen. Liver transplantation remains the only option for truly intractable hepatic encephalopathy.

Neuroprotective agents in acute ischemic stroke.

The concept of neuroprotection relies on the principle that delayed neuronal injury occurs after ischemia. The phenomenon of the "ischemic cascade" has been described, and each step along this cascade provides a target for therapeutic intervention. A wide variety of drugs have been studied in humans. Ten classes of neuroprotective agents have reached phase III efficacy trials but have shown mixed results. They included calcium channel antagonists, NMDA receptor antagonists, lubeluzole, CDP-choline, the free radical scavenger tirilazad and ebselen, enlimomab, GABA agonist clomethiazole, the sodium channel antagonist fosphenytoin, magnesium, glycine site antagonist GV150526 and piracetam. Furthermore, the mechanisms that underlie the development of focal ischemic injury continue to be discovered, opening new therapeutic perspective for neuroprotection that might clinically be applicable in the future.

Midazolam for the treatment of phantom limb pain exacerbation: preliminary reports.

Phantom pain is one of the most difficult intractable pains to manage. The pain may result from the imbalance of self-sustaining neural activity that exceeds the inhibitory control. The management of acute severe exacerbation of phantom pain is extremely difficult. Midazolam acts by potentiation of gamma aminobutyric acid (GABA) and enhance the inhibitory action of glycine receptor at spinal neurons. We describe two preliminary reports of complete pain relief of severe phantom pain exacerbation by intravenous midazolam 3-5 mg.

Double-blind clonazepam vs placebo in panic disorder treatment

OBJECTIVE: To assess the effectiveness of clonazepam, in a fixed dose (2 mg/day), compared with placebo in the treatment of panic disorder patients. METHOD: 24 panic disorder patients with agoraphobia were randomly selected. The diagnosis was obtained using the structured clinical interview for DSM-IV . All twenty-four subjects were randomly assigned to either treatment with clonazepam (2 mg/day) or placebo, during 6 weeks. Efficacy assessments included: change from baseline in the number of panic attacks; CGI scores for panic disorder; Hamilton rating scale for anxiety; and panic associated symptoms scale. RESULTS: At the therapeutic endpoint, only one of 9 placebo patients (11.1 percent) were free of panic attacks, compared with 8 of 13 (61.5 percent) clonazepam patients (Fisher exact test; p=0,031). CONCLUSION: the results provide evidence for the efficacy of clonazepam in panic disorder patients