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PubMed1998

Fatalities from black powder percussion handguns.

Three suicides and one homicide from black powder muzzle loading handguns are reported and the muzzle velocities of two weapons are recorded. The fatal head shots caused wide wound tracts traversing the brains and intracerebral haemorrhages remote from the tract were present in every case. The skulls showed considerable fractures which were pronounced in the cases of contact shots but were also present when the range of fire was 5 m. These extensive injuries from soft lead spheres with muzzle velocities of only approximately 200 m/s are attributed to the expansion of the spheres. The regularly occurring deformation resulted in 13-16 mm calibre missiles in the cases of .44 spheres. The special features of black powder such as incomplete and slow combustion resulted in intense soot deposits in the vicinity of the entrance wound and in long ranges the gunshot residues travelled. In contact shots, large pocket-like underminings even in deeper tissue layers, abundant soot along the trajectory and skin burns were observed.

Adult↗
PubMed1996

Acute and prolonged alterations in brain free magnesium following fluid percussion-induced brain trauma in rats.

Several studies have reported declines in brain total and free magnesium concentration after a traumatic insult to the CNS. Although the evidence suggests that this magnesium decline is associated with eventual neurologic outcome after trauma, the duration of free magnesium decline and its impact on related bioenergetic variables are relatively unknown. The present study has therefore used phosphorus magnetic resonance spectroscopy to determine the length of time that free magnesium remains suppressed after traumatic brain injury in rats. Immediately after the traumatic event, brain intracellular free magnesium declined to < 60% of preinjury values and remained significantly depressed (50 +/- 8%; p < 0.001) for 5 days before recovering to preinjury levels by day 8. Cytosolic phosphorylation ratio and mitochondrial oxidative capacity also significantly decreased (p = 0.008) and increased (p = 0.002), respectively, after trauma. However, unlike the time of maximum magnesium change, the maximum changes in these bioenergetic variables occurred at 16-24 h after trauma and thereafter remained stable until after the magnesium had recovered. We conclude that free magnesium decline after trauma precedes changes in bioenergetic variables. Furthermore, therapies targeted at reestablishing magnesium homeostasis after trauma may require administration over a 1-week period.

Animals↗
PubMed1995

Neuropathological changes produced by non-penetrating percussive captive bolt stunning of cattle.

A blunt, non-missile head injury inflicted by a non-penetrating captive bolt pistol in cattle at slaughter resulted in immediate loss of consciousness, a depressed fracture of the frontal bone and widespread subarachnoid haemorrhage, particularly beneath the impact site, in the temporal and frontal lobes, and around the brainstem. There was also invariably petechial haemorrhage in the basal ganglia and thalamus. The large concussive force applied to the cranium by the stunner was probably responsible for rendering the animal insensible and the vascular damage produced by this force and the sudden ventrocaudal acceleration of the brain after impact. These findings supported the use of this mode of stunning, followed by exsanguination, as an acceptable form of slaughter of cattle in abattoirs.

Journal Article↗
PubMed2005

Percussion pacing in a three-year-old girl with complete heart block during cardiac catheterization.

Complete heart block frequently requires emergency pacing to restore systemic perfusion. We report the case of a 3-yr-old girl undergoing interventional atrial septal defect closure who suffered from transient complete heart block with circulatory arrest. Transthoracic mechanical pacing for more than 3 min provided temporary support, sustaining an adequate cardiac output until sinus rhythm resumed.

Cardiac Catheterization↗
PubMed2006

NAAG peptidase inhibitor increases dialysate NAAG and reduces glutamate, aspartate and GABA levels in the dorsal hippocampus following fluid percussion injury in the rat.

Traumatic brain injury (TBI) produces a rapid and excessive elevation in extracellular glutamate that induces excitotoxic brain cell death. The peptide neurotransmitter N-acetylaspartylglutamate (NAAG) is reported to suppress neurotransmitter release through selective activation of presynaptic group II metabotropic glutamate receptors. Therefore, strategies to elevate levels of NAAG following brain injury could reduce excessive glutamate release associated with TBI. We hypothesized that the NAAG peptidase inhibitor, ZJ-43 would elevate extracellular NAAG levels and reduce extracellular levels of amino acid neurotransmitters following TBI by a group II metabotropic glutamate receptor (mGluR)-mediated mechanism. Dialysate levels of NAAG, glutamate, aspartate and GABA from the dorsal hippocampus were elevated after TBI as measured by in vivo microdialysis. Dialysate levels of NAAG were higher and remained elevated in the ZJ-43 treated group (50 mg/kg, i.p.) compared with control. ZJ-43 treatment also reduced the rise of dialysate glutamate, aspartate, and GABA levels. Co-administration of the group II mGluR antagonist, LY341495 (1 mg/kg, i.p.) partially blocked the effects of ZJ-43 on dialysate glutamate and GABA, suggesting that NAAG effects are mediated through mGluR activation. The results are consistent with the hypothesis that inhibition of NAAG peptidase may reduce excitotoxic events associated with TBI.

Animals↗
PubMed2026

Multi-centre randomised controlled feasibility trial with embedded process evaluation of a samba percussion intervention for people living with Parkinson's disease: a protocol for the Sparky Samba trial.

INTRODUCTION: Parkinson's disease (PD) is the second most common neurodegenerative disorder, its principal symptom being deterioration of motor function. Current treatment options are limited to symptom management but there is evidence that physical activity can provide motor benefits. More recently there is evidence to suggest that rhythmic auditory stimulation may improve gait and balance in PD. Sparky Samba is a community initiative in South Wales, UK, founded by a person living with PD. Sessions incorporate the following samba rhythms from a trained facilitator and are held weekly in a community setting. METHODS: The Sparky Samba trial is a multi-site, non-blinded, randomised controlled feasibility trial of Sparky Samba compared with activity as usual. A total of 60 people with PD will be randomised 1:1 to take part in a local Sparky Samba group for 12 weeks or continue their normal activities for the same length of time. The primary outcome is feasibility defined by recruitment, retention, data completeness and intervention adherence. Secondary outcomes relating to motor function, cognition, well-being and self-efficacy will also be assessed at baseline and at 12 weeks. Additionally, we will conduct a process evaluation to understand contextual mechanisms surrounding Sparky Samba. This will be achieved through qualitative interviews and structured participant questionnaires following individual trial completion and through structured questionnaires with intervention delivery staff, supplemented with qualitative interviews. ANALYSIS: Feasibility outcomes will be assessed according to pre-defined criteria. For secondary outcomes, means and standard deviations (or medians and IQRs) will be calculated by arm, alongside 95% CIs for change from baseline to 12-week follow-up. Qualitative data will be subject to thematic analysis using NVivo software. ETHICS AND DISSEMINATION: This study received a favourable ethical opinion from the North of Scotland Research Ethics Committee in April 2025 (REC reference 25/NS/0037). Study results will be disseminated through the peer-review literature, the ISRCTN registry and directly to participants, which will be facilitated by the study's public and patient involvement steering group. TRIAL REGISTRATION NUMBER: ISRCTN11861663.

Humans↗