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Behavioural pharmacology
Published in Adam Doble, Ian L Martin, David Nutt, Calming the Brain: Benzodiazepines and related drugs from laboratory to clinic, 2020
Adam Doble, Ian L Martin, David Nutt
This phenomenon seems to be a general property of convulsant and proconvulsant agents (Racine, 1978) so it may be related to some general epileptogenic mechanism in the brain rather than a change in the set-point of the benzodiazepine receptor efficacy spectrum. However, the finding that this treatmentalso leads to a loss of efficacy for diazepam (Schneider and Stephens, 1988) would argue in favour of a mechanism involving a change in the receptor set-point. This last phenomenon is not really benzodiazepine tolerance (’false tolerance’ may be a more appropriate term), since the challenge drug has a different pharmacological activity to the drug used for the chronic treatment.
Toward a Theory of Infra-Low Frequency Neurofeedback
Published in Hanno W. Kirk, Restoring the Brain, 2020
The context out of which brain instabilities arise tends to be one of neuronal hyper-excitability. The roots of this concept also go back to Freud, who as early as 1894 referred to the “sum of excitation,” which he saw as relevant to psychopathologies such as hysteria and hallucinatory psychoses. As we now conceptualize the issue, there is a cellular (synaptic or other membrane) aspect to hyper-excitability, one that is typically addressed by anti-epileptic drugs, and there is a network aspect. The ILF training impinges on the network aspect in first instance, and over time appears to also affect the setpoints of excitability at the cellular level. That proposition is testified to by the observation that often levels of anti-convulsants can be reduced or even eliminated through the course of neurofeedback training.
Pharmacological interventions
Published in Ilana B. Crome, Richard Williams, Roger Bloor, Xenofon Sgouros, Substance Misuse and Young People, 2019
Young people who have a confirmed history of epilepsy require cautious rates of reduction during their treatment for benzodiazepine dependence that is informed by ongoing monitoring. A review of any currently prescribed anti-convulsant medication should be organised, with advice from a specialist if required.
The state-of-the-art pharmacotherapeutic options for the treatment of chronic non-cancer pain
Published in Expert Opinion on Pharmacotherapy, 2022
Ryan S. D’Souza, Brendan Langford, Rachel E. Wilson, Yeng F. Her, Justin Schappell, Jennifer S. Eller, Timothy C. Evans, Jonathan M. Hagedorn
The most commonly reported side effects of anti-convulsant agents include somnolence, dizziness, difficulty with concentration, and nausea [55]. Black box warning for serious rashes such as Steven-Johnson Syndrome (SJS) or Toxic epidermal necrolysis (TEN) have been placed for carbamazepine and lamotrigine. Even though phenytoin, levetiracetam, and gabapentin do not have a black box warning for dermatologic rash, there is a small risk for SJS/TEN [55]. Phenytoin carries a black box warning for severe hypotension and cardiac arrhythmia with its intravenous formulation [55]. Hyponatremia is a side effect unique to carbamazepine and oxcarbazepine, and warrants close monitoring with interval laboratory workup. Metabolic acidosis is associated with topiramate and zonisamide use due to its carbonic anhydrase inhibition property. Lastly, development of withdrawal symptoms is associated with discontinuation of any anti-convulsant medication [55].
Oral glutamine supplementation increases seizure severity in a rodent model of mesial temporal lobe epilepsy
Published in Nutritional Neuroscience, 2022
Roni Dhaher, Eric C. Chen, Edgar Perez, Amedeo Rapuano, Mani Ratnesh S. Sandhu, Shaun E. Gruenbaum, Ketaki Deshpande, Feng Dai, Hitten P. Zaveri, Tore Eid
The pro-convulsant effect of glutamine on the seizures can be explained by several mechanisms. Firstly, in the event that the excess glutamine enters the brain, as has been previously established [16], some of the amino acid may be converted to glutamate and ammonia via the phosphate-activated glutaminase reaction [16], and if glutamate and ammonia are allowed to accumulate, mitochondrial damage, seizures, and neuron loss could occur [17]. Even though the net flux of glutamine normally is directed from the brain to the blood [18], because of the established role of glutamate in epilepsy [6], testing the brain glutamate/ammonia accumulation hypothesis is necessary. It is also possible that the elevated extracellular glutamine may be converted to neurotransmitter GABA by glutamate decarboxylase (GAD) containing, inhibitory neurons. However, considering the fact that the number of excitatory neurons are nine times higher than inhibitory neurons [19] and 90% of all axon terminals release glutamate [20], it is most likely that the net effect of the enhanced neurotransmitter synthesis is increased excitatory transmission.
Carbamazepine and levetiracetam-loaded PLGA nanoparticles prepared by nanoprecipitation method: in vitro and in vivo studies
Published in Drug Development and Industrial Pharmacy, 2020
Busra Kandilli, Afife Busra Ugur Kaplan, Meltem Cetin, Numan Taspinar, Muhammed Sait Ertugrul, Ismail Cagri Aydin, Ahmet Hacimuftuoglu
The solution of PTZ in physiological saline (0.9% NaCl) (35 mg/kg) was administered intraperitoneally (i.p.) to rats three times a week (01:00 p.m.–05:00 p.m.; Monday, Wednesday, and Friday; total 27 times) until to generate chemical kindling in rats [29]. After each PTZ-injection, severity of seizures in rats was evaluated by observing for 30 min. The convulsant response was classified according to the stages (stages 0–5) defined by Fischer and Kittner [30]. As a result, the rats that exhibited at least five seizures of stage 3–5 were selected for further experimentation. Later, the kindled rats were randomly divided into seven groups. Later, CBZ, LEV, CBZ + LEV, B-PLGA-NPs, and CBZ + LEV-PLGA-NPs (equivalent to 30 mg/kg of CBZ) were dispersed/dissolved in 0.9% of NaCl solution containing 1% Tween 80 (0.9% NaCl–1% Tween 80). The prepared suspensions/solutions were administered i.p. five times in total with one day break between 01:00 p.m. and 05:00 p.m. to the groups according to Table 1. Thirty minutes after drug application, the solution of PTZ (35 mg/kg) was administered i.p. to the groups and the animals were placed in Plexiglass cages separately were observed for 30 min and seizure behavior was scored to determine anticonvulsant action of pure drugs/their combination/CBZ + LEV-loaded NPs.