The use of TASER devices in UK policing: an update for clinicians following the recent introduction of the TASER 7.

Taser was introduced into UK policing in 2003 to bridge the operational gap between use of incapacitant sprays and firearms. Use of force reporting in the UK indicates that Taser is relatively safe provided that it is used lawfully. Taser use can result in injuries and has been implicated in a small number of deaths. The latest version of the weapon, the TASER 7, has entered UK policing. The TASER 7 uses a novel probe that has implications for the medical community. A review of Taser medical effects and probe removal for TASER 7 are presented.

An analysis of officer-reported TASER X2™ probe discharge effectiveness in the United Kingdom.

Conducted energy devices (CEDs) are designed to immobilise aggressive individuals through the application of an electrical discharge administered via probes fired at the subject. Although the discharge is intended to disrupt voluntary movement, CEDs have their limitations and several factors are qualitatively understood to adversely influence CED effectiveness. The introduction of the twin-cartridge TASER X2™ into UK policing in 2017 provided a unique opportunity to undertake a quantitative assessment of the factors modulating probe discharge effectiveness based on data reported by police officers firing the device operationally. The overall operational subdual effectiveness of the TASER X2™ was 68.5%. However, several factors were identified that could alter the likelihood of achieving subdual of the subject. The officer-reported data show that probe discharge was highly effective at subduing subjects when both probes had penetrated the skin, least effective when both probes were in clothing and confirmed the reduced effectiveness of narrow probe spreads. The most commonly cited reasons why probe discharge failed to subdue the subject were thick or loose clothing, probe misses and narrow probe spread. These findings, which are likely to generalise to other types of CED, may be used to inform tactics and training to optimise the likelihood of achieving incapacitation when probes are deployed, with benefits for the safety of both the police and the public. The findings may also assist investigations requiring the reconstruction of incidents in which probe discharge has been deployed.

Effects of anticonvulsants on soman-induced epileptiform activity in the guinea-pig in vitro hippocampus.

Seizures arising from acetylcholinesterase inhibition are a feature of organophosphate anticholinesterase intoxication. Although benzodiazepines are effective against these seizures, alternative anticonvulsant drugs may possess greater efficacy and fewer side-effects. We have investigated in the guinea-pig hippocampal slice preparation the ability of a series of anticonvulsants to suppress epileptiform bursting induced by the irreversible organophosphate anticholinesterase, soman (100 nM). Carbamazepine (300 microM), phenytoin (100 microM), topiramate (100-300 microM) and retigabine (1-30 microM) reduced the frequency of bursting but only carbamazepine and phenytoin induced a concurrent reduction in burst duration. Felbamate (100-500 microM) and clomethiazole (100-300 microM) had no effect on burst frequency but decreased burst duration. Clozapine (3-30 microM) reduced the frequency but did not influence burst duration. Levetiracetam (100-300 microM) and gabapentin (100-300 microM) were without effect. These data suggest that several compounds, in particular clomethiazole, clozapine, felbamate, topiramate and retigabine, merit further evaluation as possible treatments for organophosphate poisoning.

Effects of seven drugs of abuse on action potential repolarisation in sheep cardiac Purkinje fibres.

Seven drugs of abuse have been examined for effects on the action potential in sheep isolated cardiac Purkinje fibres. Phencyclidine (5 microM) induced a significant increase (30.7%) in action potential duration at 90% repolarisation (APD(90)). Similarly, 10 microM 3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy') induced a significant increase in APD(90) of 12.1%. Although Delta(9)-tetrahydrocannabinol (0.1 microM) induced a small, but statistically significant, 4.8% increase in APD(90), no effects were observed at 0.01 or 1 microM. Cocaethylene (10 microM) induced a significant shortening of APD(90) (-23.8%). Cocaine (up to 1 microM), (+)-methamphetamine ('Speed'; up to 5 microM), and the heroin metabolite, morphine (up to 5 microM), had no statistically significant effects. The possible significance of these findings is discussed in the context of other recognised cardiac effects of the tested drugs.

A guinea pig hippocampal slice model of organophosphate-induced seizure activity.

Extracellular recording techniques have been used in the guinea pig hippocampal slice preparation to investigate the electrophysiological actions of the organophosphate (OP) anticholinesterase soman. When applied at a concentration of 100 nM, soman induced epileptiform activity in the CA1 region in approximately 75% of slices. This effect was mimicked by the anticholinesterases paraoxon (1 and 3 microM), physostigmine (30 microM), and neostigmine (30 microM), thus providing indirect evidence that the epileptiform response was mediated by elevated acetylcholine levels. Soman-induced bursting was inhibited by the muscarinic receptor antagonists atropine (concentrations tested, 0.1-10 microM), telenzepine (0.03-3 microM), AF-DX116 [11-(2-[(diethylamino)methyl]-1-piperidinyl acetyl)-5,11-dihydro-6H-pyrido 92.b-b) (1,4)-benzodiazepin-6-one] (0.3-300 microM), and biperiden (0.1-10 microM) and by the benzodiazepine anticonvulsants diazepam (3-30 microM) and midazolam (3-30 microM), but it was not inhibited by the nicotinic antagonists mecamylamine (30 microM) and methyllycaconitine (300 nM). In contrast to soman-induced epileptiform activity, bursting induced by the K(+) channel blocker 4-aminopyridine (30 microM), the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (30 nM) or perfusion with low Mg(2+) buffer was insensitive to atropine (10 microM). The ability of muscarinic antagonists and benzodiazepines to inhibit soman-induced epileptiform activity is in accordance with the in vivo pharmacology of soman-induced seizures and suggests that the guinea pig hippocampal slice preparation may provide a useful tool for the evaluation of novel anticonvulsant therapies for the treatment of seizures related to OP poisoning.