The present article reviewed the pharmacologic therapies of traumatic brain injury (TBI), including current and potential treatments. Pharmacologic therapies are an essential part of TBI care, and several agents have well-established effects in TBI care. In the acute phase, tranexamic acid, antiepileptics, hyperosmolar agents, and anesthetics are the mainstay of pharmacotherapy, which have proven efficacies. In the post-acute phase, SSRIs, SNRIs, antipsychotics, zolpidem and amantadine, as well as other drugs, have been used to manage neuropsychological problems, while muscle relaxants and botulinum toxin have been used to manage spasticity. In addition, increasing numbers of pre-clinical and clinical studies of pharmaceutical agents, including potential neuroprotective nutrients and natural therapies, are being carried out. In the present article, we classify the treatments into established and potential agents based on the level of clinical evidence and standard of practice. It is expected that many of the potential medicines under investigation will eventually be accepted as standard practice in the care of TBI patients.

Objective: The present study investigates the peripheral neuropathy in Primary Sjögren's syndrome (pSS) using the nerve excitability test to further elucidate how peripheral nerves are affected by the autoantibodies.Methods: Each patient received clinical evaluation, examination for anti‐SSA/Ro and anti‐SSB/La antibodies titer, paired motor and sensory nerve excitability test, thermal quantitative sensory test (QST), and nerve conduction study (NCS).Results: A total of 40 pSS patients wasenrolled. Motor axonal study of the pSS with positive anti‐SSA/Ro or anti‐SSB/La antibodies (n = 28) was found to have increased stimulus for 50% compound muscle action potential (CMAP) (P < 0.05), increased rheobase (P < 0.01), increased minimum I/V slope (P < 0.01) and hyperpolarizing I/V slope (P < 0.05), increased relative refractory period (RRP, P < 0.001), decreased accommodation of threshold electrotonus toward depolarizing current (P < 0.05), and increased accommodation toward hyperpolarizing current (P < 0.05). Seronegative pSS (n = 10) showed much less prominent motor axonal changes, showing only increased minimum I/V slope (P < 0.05). Sensory axonal study in seropositive pSS patients is found to have increased stimulus for 50% sensory nerve action potential (SNAP) (P < 0.01), decreased latency (P < 0.01), increased RRP (P < 0.01), and increased subexcitability (P < 0.05). Seronegative pSS patients have shown no significant sensory axonal changes. Thermal QST showed more prominent abnormalities in seronegative pSS compared to seropositive pSS.Interpretation: Anti‐SSA/Ro and anti‐SSB/La autoantibodies might cause dysfunction in nodal and internodal region of the axon and small nerve fibers; meanwhile, autoreactive antibodies in seronegative pSS mainly affect small nerve fibers. Thus, the underlying pathophysiology for the two types of pSS is different.

Aims/Introduction: To elucidate whether axonal changes arise in the prediabetic state and to find a biomarker for early detection of neurophysiological changes.Materials and Methods: We enrolled asymptomatic diabetes patients, as well as prediabetic and normoglycemic individuals to test sensory nerve excitability, and we analyzed those findings and their correlation with clinical profiles.Results: In nerve excitability tests, superexcitability in the recovery cycle showed increasing changes in the normoglycemic, prediabetes and diabetes cohorts (−19.09 ± 4.56% in normoglycemia, −22.39 ± 3.16% in prediabetes and −23.71 ± 5.15% in diabetes, P = 0.002). Relatively prolonged distal sensory latency was observed in the median nerve (3.12 ± 0.29 ms in normoglycemia, 3.23 ± 0.38 ms in prediabetes and 3.45 ± 0.43 ms in diabetes, P = 0.019). Superexcitability was positively correlated with fasting plasma glucose (r = 0.291, P = 0.009) and glycated hemoglobin (r = 0.331, P = 0.003) in all participants.Conclusions: Sensory superexcitability and latencies are the most sensitive parameters for detecting preclinical physiological dysfunction in prediabetes. In addition, changes in favor of superexcitability were positively correlated with glycated hemoglobin for all participants. These results suggest that early axonal changes start in the prediabetic stage, and that the monitoring strategy for polyneuropathy should start as early as prediabetes.

To investigate nerve excitability changes in patients with fibromyalgia and the correlation with clinical severity. We enrolled 20 subjects with fibromyalgia and 22 sex and age-matched healthy subjects to receive nerve excitability test and nerve conduction study to evaluate the peripheral axonal function. In the fibromyalgia cohort, the sensory axonal excitability test revealed increased superexcitability (%) (P = 0.029) compared to healthy control. Correlational study showed a negative correlation between increased subexcitability (%) (r = -0.534, P = 0.022) with fibromyalgia impact questionnaire (FIQ) score. Computer modeling confirmed that the sensory axon excitability pattern we observed in fibromyalgia cohort was best explained by increased Barrett-Barrett conductance, which was thought to be attributed to paranodal fast K+ channel dysfunction. The present study revealed that paranodal sensory K+ conductance was altered in patients with fibromyalgia. The altered conductance indicated dysfunction of paranodal fast K+ channels, which is known to be associated with the generation of pain.

The present study proposes a cognitive prosthesis device for face memory impairment as a proof-of-concept for the domain-specific cognitive prosthesis. Healthy subjects (n = 6) and a patient with poor face memory were enrolled. An acquaintance face recognition test with and without the use of cognitive prosthesis for face memory impairment, face recognition tests, quality of life, neuropsychological assessments, and machine learning performance of the cognitive prosthesis were followed-up throughout four weeks of real-world device use by the patient. The healthy subjects had an accuracy of 92.38 ± 4.41% and reaction time of 1.27 ± 0.12 s in the initial attempt of the acquaintance face recognition test, which changed to 80.48 ± 6.23% (p = 0.06) and 2.11 ± 0.20 s (p < 0.01) with prosthesis use. The patient had an accuracy of 74.29% and a reaction time of 6.65 s, which improved to 94.29% and 3.28 s with prosthesis use. After four weeks, the patient’s unassisted accuracy and reaction time improved to 100% and 1.23 s. Functional MRI study revealed activation of the left superior temporal lobe during face recognition task without prosthesis use and activation of the right precentral motor area with prosthesis use. The prosthesis could improve the patient’s performance by bypassing the brain area inefficient for facial recognition and employing the area more efficiently for the cognitive task.

Spinal endoscopy procedure is commonly used in the diagnosis and treatment of various health problems and is effective. Bleeding is one of the most common complications of spinal endoscopy procedures. Blood vision obstruction (BVO), that is, obstruction of the endoscopic camera lens caused by the accumulation of blood in the surgical field, is a serious problem in endoscopic procedures. This study presents what we believe to be a new approach to addressing BVO with external multispectral imaging. The study was completed using a BVO simulation model, and the results reveal that this technology can be used to effectively overcome BVO and provide clear images of the anatomy, enabling more effective diagnosis and treatment. This technique may enable improvement of the outcomes of endoscopic procedures and could have far-reaching implications in the field of endoscopy.