Mechanism of Delayed Convulsion in Fish: The Actions of Norepinephrine in Spinal Cord

Cranial spiking (CS) is among the most popular slaughtering methods for delaying the rigor mortis progress of fish muscles. However, it may cause a convulsion (subsequently referred to as delayed convulsion), which undermines the meat quality and taste. This study aimed to elucidate the mechanism underlying the delayed convulsion and examine its influence on ATP consumption. Ten carps, nine tilapias, ten rainbow trouts, two ayus, three greenling, thirty-five red seabreams, two striped jack and two stone flounders underwent CS around the medulla oblongata area, which induced different delayed convulsion profiles specific to each species. To investigate the norepinephrine (NE) actions related to delayed convulsion, 27 red seabreams, a representative fish species that exhibits delayed convulsion, were treated with a monoamine-depleting agent, reserpine, or with a monoamine oxidase inhibitor, pargyline, two hours before CS. Spinal cord destruction (SCD) was employed to completely prevent spinal cord functions of the fish in another group. Compared with the control group (CS only), the reserpine, pargyline, and SCD groups showed significantly inhibited delayed convulsion and ATP consumption. This suggests that delayed convulsion is the main ATP-consuming response. Our findings suggest that delayed clonic convulsion in red seabreams is associated with the rapid decrease in spinal cord NE levels, which triggered the rebound motor neuron hyperactivity.

Are Predator Smell (TMT)-Induced Behavioral Alterations in Rats Able to Inhibit Seizures?

We aimed to evaluate the chemical and behavioral effects of 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) after olfactory exposure and to verify their influence in the expression of acute audiogenic seizures in the Wistar Audiogenic Rat (WAR) strain. PROTOCOL 1: TMT gas chromatography was applied to define odor saturation in a chamber to different concentrations, time required for saturation and desaturation, and if saturation was homogeneous. Also, male Adult Wistar rats were exposed to saline (SAL) or to different TMT concentrations and their behaviors were evaluated (neuroethology). PROTOCOL 2: Male adult WARs were exposed for 15 s to SAL or TMT, followed by sound stimulation for 1 min or until tonic–clonic convulsion. Behavioral analysis included latencies (wild running and tonic–clonic convulsion), seizure severity indexes, and neuroethology. Gas chromatography established a saturation homogeneous to different concentrations of TMT, indicating that saturation and desaturation occurred in 30 min. TMT triggered fear-like or aversion-like reactions associated with reduction in motor activity and in grooming behavior, in the 2 highest concentrations. Pure TMT presented anticonvulsant properties, such as less-severe seizure phenotype, as well as a decrease in tonic–clonic convulsion expression. TMT elicited fear-like or aversion-like behaviors in Wistar and WAR and can be utilized in a quantifiable and controllable way. Our results suggested possible antagonism between “fear-related” or “aversion-related” and “seizure-related” networks.

Neurologist, 30 years’ experience, New Zealand

This chapter describes how a neurologist treated a patient who had been treated for epilepsy for fifteen-years. The patient gave a seizure description that was superficially like that of a tonic-clonic convulsion, but with what would now be recognized as clear indicators of a psychogenic seizure diagnosis. After inquiring about potential causes, the neurologist found out that the patient had a history of sexual abuse. The patient’s reaction to the diagnosis was initially one of skepticism, but this quickly turned to anger. After a lot of resistance, he agreed to withdraw his anticonvulsants and this was arranged under the supervision of his general practitioner. The patient then came back to see the neurologist for a follow-up visit. By this time, he was off his anticonvulsants and his seizures had stopped. This experience prompted the neurologist to start doing research into psychogenic seizures.

Disease Profile of Seizure in Children

This study was done in the Departmen tof Paediatrics, Rajshahi Medical College Hospital, Rajshahi to final out the disease profile of children Hospitalised with seizure presentation. From 01/01/14 to 31/12/14 period a total of 12,560 children in the age group 6 months to 12 years were admitted in the Paediatric department. Among these 656 (5.2%) children were admitted due to convulsion. 62.8% were male and 37.2% female, 53% febrile and 47% a febrile, 59% were less than 5 years. Generalized tonic clonic convulsion (GTC) was the most common seizure type (72.8%). Febrile convulsion, seizure disorder, meningitis and encephalitis were common causes of convulsion.TAJ 2012; 25: 35-37

Intradural spinal neurocysticercosis: case illustration

Introduction: Neurocysticercosis (NCC) is a common parasitic infection of the central nervous system caused by the larvae of the Taenia solium. Spinal cord involvement is very uncommon. Clinical case: A female patient with a history of NCC presented with chronic and recurrent headache associated with motor and sensory deficit, which develops tonic-clonic convulsion, with spatial disorientation. She also had intracranial hypertension syndrome, meningitis syndrome, and pyramidal sygns suggestive of spinal NCC. Conclusions: Neurocysticercosis usually occurs in developing countries and should be considered as a differential diagnosis of neurological diseases. Early diagnosis and treatment are mandatory, as well as education to the community to primary prevention.

Anticonvulsant effect of nifedipine, dizepam and in combination on pentylenetetrazol induced experimental models of epilepsy on albino rats

Background: In many patients, the presently available antiepileptic drugs such as phenobarbital, phenytoin, benzodiazepines, sodium valproate, etc., are unable to control seizures efficiently and the problem of adverse effects has also not been circumvented completely and approximately 30% of the patients continue to have seizures with current antiepileptic drugs therapy. Hence, search should continue to develop newer, more effective, and safer neuro-protective agents for treatment of epilepsy. Aim of the study was to investigate the activity of nifedipine, the dihydropyridine calcium channel blocker, diazepam, the benzodiazepine anti- convulsant of established efficacy and their combinations against rat models of pentylenetetrazol (PTZ) induced convulsions. Method: Wister albino rats of either sex, weighing between 150-220gm were used. Rats were divided into 10 groups, in each group n=6 total N=60.Methods: PTZ was administration 30 min after test drug administration. Intraperitoneal injection of PTZ at the dose of 80mg/Kg body weight were administered to the rats to produce chemically-induced seizure. The effect of nifedipine and diazepam were assessed on such seizure model. The onset and duration of clonic convulsion were recorded.Results: The onset time of PTZ-induced clonic convulsion was significantly prolonged with the Nifedipine in the doses of 4mg and 8mg per Kg. in comparison to nifedipine in dose of 2mg per Kg. The interesting observation was that while Diazepam in 1mg/Kg. dose significantly (P<0.05) prolonged the onset time, there was significant decrease (P <0.001) in the onset time of PTZ-induced clonic convulsion with diazepam in doses of 2 and 4mg per Kg. in comparison to Diazepam 1mg per Kg. But the combination of diazepam 2.5 mg and Nifedipine 2.6mg and 5.3mg exhibited significant prolongation of the onset time. Diazepam 1 and 2mg per Kg was found to be equally effective in reduction of convulsion time, while 4mg dose showed more reduction of convulsion time. The combination of diazepam and nifedipine showed no better reduction in the convulsion time and also valproic acid in doses of 135mg. Kg.Conclusions: Nifedipine (3-5mg/Kg) and diazepam (2.5mg/Kg.) combination delayed the onset of convulsion. Diazepam 2mg / Kg. alone was effective in reduction of duration of convulsion. The combination dose having 2.6mg of nifedipine showed comparable protection with valproic acid 135mg per Kg. while the combination having 5.3mg of nifedipine showed significantly better protection.