Response inhibition − or the ability to withhold a suboptimal response − relies on the efficacy of fronto-striatal networks, and is impaired in neuropsychiatric disorders including addiction. Cortical paired associative stimulation (cPAS) is a form of transcranial magnetic stimulation (TMS) which can strengthen neuronal connections via spike-timing-dependent plasticity mechanisms. Here, we used cPAS targeting the fronto-striatal inhibitory network to modulate performance on a response inhibition measure in chronic alcohol use.

Fifty-five participants (20 patients with a formal alcohol use disorder (AUD) diagnosis (26–74 years, 6[30%] females) and 20 matched healthy controls (HCs) (27–73 years, 6[30%] females) within a larger sample of 35 HCs (23–84 years, 11[31.4%] females) underwent two randomized sessions of cPAS 1-week apart: right inferior frontal cortex stimulation preceding right presupplementary motor area stimulation by either 4 ms (excitation condition) or 100 ms (control condition), and were subsequently administered the Stop Signal Task (SST) in both sessions.

HCs showed decreased stop signal reaction time in the excitation condition (t(19) = −3.01, p = 0.007, [CIs]:−35.6 to −6.42); this facilitatory effect was not observed for AUD (F(1,31) = 9.57, p = 0.004, CIs: −68.64 to −14.11). Individually, rates of SST improvement were substantially higher for healthy (72%) relative to AUD (13.6%) groups (OR: 2.33, p = 0.006, CIs:−3.34 to −0.55).

In line with previous findings, cPAS improved response inhibition in healthy adults by strengthening the fronto-striatal network through putative long-term potentiation-like plasticity mechanisms. Furthermore, we identified a possible marker of impaired cortical excitability, and, thus, diminished capacity for cPAS-induced neuroplasticity in AUD with direct implications to a disorder-relevant cognitive process.

Exposure to cold temperature is a serious but often neglected problem in prehospital care. It not only is an uncomfortable, subjective experience, but it also can cause severe disturbances in vital functions, gradually leading to hypothermia.

The aim of this study was to examine healthy subjects'physiological and subjective reactions to cold exposure (30 minutes at -5°C in the a climatic chamber) while they were lying in a protective covering.

Healthy volunteers (n = 20) participated in the experiment, which consisted of a 10-minute stabilization period of vital functions at room temperature (23°C), 30 minutes of cold exposure (-5°C), and a 30-minute recovery period at room temperature. Subjects lay supinely in protective covering during the entire experiment. Skin temperatures, oxygen saturation, pulse rates, pulse wave amplitude in the middle finger, and surface electromyography (EMG) activity of the major pectoral muscle were recorded continuously during the test. Before and immediately after the cold exposure, tympanic membrane temperatures were measured. In addition, subjects were asked to estimate cold using a standard scale.

During the cold exposure, the decrease in tympanic membrane temperature was not significant.The pulse wave amplitude in the finger decreased sharply upon entering the cold chamber. Skin temperatures, especially of the fingers and toes, decreased during the cold exposure.There were no clear signs of shivering in electromyographic recordings. Subjective cold feelings followed decreasing skin temperatures. Skin temperatures did not return quickly. Even 30 minutes after the exposure, all the skin temperatures still had not returnedto normal levels.However, subjective cold feeling was relieved immediately.

Cold exposure provoked immediate protective vasoconstriction in the peripheral compartment, which caused linear decreases of local skin temperatures. This probably was triggered from the unprotected face and upper respiratory areas.