Implications of median sensory study to the thumb and deltoid/biceps motor unit recruitment on identifying C6 root avulsion in upper neonatal brachial plexus palsy.

INTRODUCTION/AIMS: Anatomic representation suggests that a median sensory nerve conduction study recording the thumb (median D1 NCS) may effectively assess upper neonatal brachial plexus palsy (NBPP). We sought to determine the feasibility of technique, establish reference data, and assess its ability to: (a) identify focal upper plexus lesions; and (b) identify C6 root avulsion. In a secondary analysis, we explored the association between absence/presence of motor unit action potentials (MUAPs) during needle electromyography (EMG) of the deltoid and biceps brachii muscles and C6 avulsion status. METHODS: A retrospective chart review was performed of surgical patients with severe upper NBPP who ultimately underwent surgical reconstruction (between 2017 and 2020). Median D1 sensory nerve action potential (SNAP) amplitude ranges were determined in affected and contralateral limbs and analyzed by C6 root avulsion status. Also, presence/absence of MUAPs during EMG of the deltoid and biceps brachii was compared between C6 avulsion patients and controls. RESULTS: Thirty-eight patients were included in our analysis. A median D1 NCS study was readily performed, showing a contralateral limb mean amplitude of 27.42 µV (range, 3.8-54.7 µV). Most patients had a low ipsilateral median D1 SNAP amplitude, regardless of C6 avulsion status. Detectable MUAPs in either deltoid or biceps brachii on EMG were atypical in C6 root avulsion. DISCUSSION: The median D1 NCS identifies upper NBPP, but does not distinguish C6 avulsions from post-ganglionic lesions, likely due to the frequent co-occurrence of post-ganglionic axonal disruption. The presence of MUAPs on deltoid/biceps brachii EMG suggests C6 avulsion is unlikely.

Brain Amygdala Volume Increases in Veterans and Active-Duty Military Personnel With Combat-Related Posttraumatic Stress Disorder and Mild Traumatic Brain Injury.

OBJECTIVE: To identify amygdalar volumetric differences associated with posttraumatic stress disorder (PTSD) in individuals with comorbid mild traumatic brain injury (mTBI) compared with those with mTBI-only and to examine the effects of intracranial volume (ICV) on amygdala volumetric measures. SETTING: Marine Corps Base and VA Healthcare System. PARTICIPANTS: A cohort of veterans and active-duty military personnel with combat-related mTBI (N = 89). DESIGN: Twenty-nine participants were identified with comorbid PTSD and mTBI. The remaining 60 formed the mTBI-only control group. Structural images of brains were obtained with a 1.5-T MRI scanner using a T1-weighted 3D-IR-FSPGR pulse sequence. Automatic segmentation was performed in Freesurfer. MAIN MEASURES: Amygdala volumes with/without normalizations to ICV. RESULTS: The comorbid mTBI/PTSD group had significantly larger amygdala volumes, when normalized to ICV, compared with the mTBI-only group. The right and left amygdala volumes after normalization to ICV were 0.122% ± 0.012% and 0.118% ± 0.011%, respectively, in the comorbid group compared with 0.115% ± 0.012% and 0.112% ± 0.009%, respectively, in the mTBI-only group (corrected P < .05). CONCLUSIONS: The ICV normalization analysis performed here may resolve previous literature discrepancies. This is an intriguing structural finding, given the role of the amygdala in the challenging neuroemotive symptoms witnessed in casualties of combat-related mTBI and PTSD.

Glutathione-dependent reductive stress triggers mitochondrial oxidation and cytotoxicity.

To investigate the effects of the predominant nonprotein thiol, glutathione (GSH), on redox homeostasis, we employed complementary pharmacological and genetic strategies to determine the consequences of both loss- and gain-of-function GSH content in vitro. We monitored the redox events in the cytosol and mitochondria using reduction-oxidation sensitive green fluorescent protein (roGFP) probes and the level of reduced/oxidized thioredoxins (Trxs). Either H(2)O(2) or the Trx reductase inhibitor 1-chloro-2,4-dinitrobenzene (DNCB), in embryonic rat heart (H9c2) cells, evoked 8 or 50 mV more oxidizing glutathione redox potential, E(hc) (GSSG/2GSH), respectively. In contrast, N-acetyl-L-cysteine (NAC) treatment in H9c2 cells, or overexpression of either the glutamate cysteine ligase (GCL) catalytic subunit (GCLC) or GCL modifier subunit (GCLM) in human embryonic kidney 293 T (HEK293T) cells, led to 3- to 4-fold increase of GSH and caused 7 or 12 mV more reducing E(hc), respectively. This condition paradoxically increased the level of mitochondrial oxidation, as demonstrated by redox shifts in mitochondrial roGFP and Trx2. Lastly, either NAC treatment (EC(50) 4 mM) or either GCLC or GCLM overexpression exhibited increased cytotoxicity and the susceptibility to the more reducing milieu was achieved at decreased levels of ROS. Taken together, our findings reveal a novel mechanism by which GSH-dependent reductive stress triggers mitochondrial oxidation and cytotoxicity.