Differential effects of clonazepam on declarative memory formation and face recognition.

Benzodiazepines are commonly used drugs to treat anxiety in crime witnesses. These increase GABA inhibitory effects, which impairs aversive memory encoding and consolidation. Eyewitness memory is essential in justice. However, memory is malleable leading to false memories that could cause a selection of an innocent in a lineup. Here, we studied whether a low dose of Clonazepam impairs memory encoding as well as consolidation of faces and narrative of the event. We performed two experiments using a double-blind and between subject design (N = 216). Day 1: subjects watched a crime video and received Clonazepam 0.25 mg (CLZ group) or placebo (PLC group) before (Exp. 1) or after the video (Exp. 2) to assess the effect on encoding and consolidation. One week later, the memory was assessed using a present and absent target lineup and asking for a free recall. Regarding encoding, we found that in the CLZ group memory was impaired in the free recall task, while no differences were found for recognition memory. Regarding consolidation, we did not observe memory measures that were affected by this dose of benzodiazepines. The results suggest that while some aspects of eyewitness memory could be modulated even with low doses of benzodiazepine, others could not be affected. More studies should be performed with higher doses of CLZ similar to those administered in real life. These results are relevant in the judicial field to assess the reliability of the eyewitness elections under the effects of this drug.

Association of oxamniquine praziquantel and clonazepam in experimental Schistosomiasis mansoni

The antischistosomal activity of clonazepam, when administered alone or in association with oxamniquine and praziquantel, was experimentally evaluated in mice infected with Schistosoma mansoni. The animals were treated 45 days post-infection with a single dose, by oral route, according to three treatment schedules: clonazepam 25 mg/kg and sacrificed 15 min, 1h or 4 h after treatment; clonazepam 1.0, 2.5 or 10.0 mg/kg and sacrificed 15 days post-treatment or with the dose of 10 mg/kg in association with oxamniquine 50 mg/kg or praziquantel 200 mg/kg, single dose, orally, every schedule with a control group. The efficacy of the drugs in vivo was assessed by means of worm counts and their distribution in mesentery and liver, mortality and oogram changes. In the chemotherapeutic schedules used, clonazepam did not present antischistosomal activity and the result of the association of this drug with oxamniquine or praziquantel was not significantly different from the one obtained when these two last drugs were administered alone. In the in vitro experiments, the worms exposed to 0.6 mg/mL clonazepam remained motionless throughout the 8-day-period of observation, without egg-laying, whereas the worms of the control group showed normal movements, egg-laying and hatching of miracidia on the last day of observation. The results obtained in the present study confirm the action of clonazepam on S. mansoni adult worm, in vitro, causing total paralysis of males and females. However, no additive or synergistic effects were observed when clonazepam were used in association with oxamniquine or praziquantel.

Palatal myoclonus: report of two cases

We describe two cases of palatal myoclonus (PM), one essential and another secondary to a stroke. Case 1: a 64 years old female who developed clicking sounds in both ears after a stroke and three years later on noticed a progressive involuntary movement of the throat associated with rhythmic contractions of the soft palate, muscles of tongue and throat. MRI showed an ischemic area in brainstem. The patient had a partial response to the use of sumatriptan 6 mg subcutaneously. Case 2: a 66 years old female who began with ear clicking at left ear that worsed slowly associated with tinnitus and arrhythmic movements of soft palate and an audible click at left ear. Brain MRI was normal; audiometry showed bilateral neurosensory loss. She was prescribed clonazepan 1 mg daily with complete recovery. Primary and secondary palatal myoclonus share the same clinical features but probably have different pathophysiological underlying mechanisms

Trastorno conductual del sueño REM en dos casos documentados con polisomnogragía / REM sleep behavior disorder: report of two cases

We report a 69 years old male with a parkinsonian syndrome and a 50 years old female without neurological problems who showed violent behavior during REM sleep. Polysomnography showed that both had tonic or phasic muscular activity during REM sleep and a REM sleep behavior disorder was diagnosed. Clonazepam was used in both, with good clinical response. This condition is frequently unrecognized and confused with nightmares, nocturnal delirium or other parasomnias

Clonazepan in social phobia

Fundamento - A farmacoterapia da fobia social ainda näo está bem estudada. Mais ensaios clínicos com o clonazepam, dentre outros medicamentos, säo necessários. Método - Quarenta pacientes sofrendo de fobia social (DSM-III-R) foram tratados com clonazepam durante 16 semanas. As avaliaçöes compreenderam: Impressöes Clínicas Globais, Escala de Liebowitz para Fobia social, Escala de Hamilton para Ansiedade, Escala de Hamilton para Depressäo, Escalas de Sheehan para Incapacitaçäo, Inventário de Personalidade de Willoughby, Escala de Evitaçäo Social e o SCL-90. Resultados - A dose diária média foi de 4,8 mg. Em todos os instrumentos de avaliaçäo diferenças estatisticamentes significativas demostraram melhora acentuada em 86, 8 por cento dos casos. Efeitos indesejáveis foram frequentes, principalmente transtornos cognitivos e sexuais. Somente dois droupouts ocorreram devido a efeitos colaterais sexuais. Na fase de retirada do medicamento (semanas 17 a 24) manifestaçöes de abstinência/rebote foram frequentes. Conclusöes - O clonazepam é muito eficaz no tratamento da fobia social. Em um caso particular o clínico deve avaliar a relaçäo risco-benefício. Outras opçöes, como a moclobemida, devem também, ser consideradas

Efectos de medicamentos benzodiazepínicos y antihistamínicos en las arritmias post-infarto experimentales / Effects of bonzodiazepines and antihistamines in experimental post-infaction arrhythmias

En el infarto agudo del miocardio, las arritmias ventriculares son las que producen con mayor frecuencia la muerte. Nuestro objetivo fue establecer si algunos medicamentos antihistamínicos y benzodiazepínicos reducen la pruducción de tales arritmias en el infarto experimental del perro. Con este fin se disecó la arteria coronaria descendente anterior izquierda y se ligó doblemente. A una serie de diez perros, una hora antes de aplicarles la ligadura, se les administró por vía intravenosa (I.V.) solución salina isotónica, formando el grupo control. Además se integraron otros cinco grupos experimentales, a cad auno de los cuales se les administró por vía I.V. antes de la ligadura, uno de los siguientes fármacos: lidocaína (2 mg/kg de peso corporal, n=16), clonazepam (20 mcg/kg, n=16), flunitrazepam (30 mcg/kg, n=11) y astemizol) 1 mg/kg, n=16). Registros control de frecuencia cardiaca, presión arterial y ECG se tomaron 10 minutos antes de la ligadura y cada 5 minutos durante 90 minutos después de practicarse la ligadura. La tasa de protección contra el desarrollo de fibrilación ventricular para cada grupo fue: control 20 por ciento, lidocaína 81.25 por ciento, clonazepam 50 por ciento, flunitrazepan 76 por ciento, terfenadina 54,6 por ciento, y astemizol 75 por ciento. De estos resultados concluimos que la lidocaína, una benzodiazepina del tipo del flunitrazapam y un antihistamínico como el astemizol, reducen en mayor proporción la incidencia de arritmias ventriculares inducidas por el infarto experimental en el perro