Leila Bagherzadeh

Essential tremor (ET) is one of the most prevalent adult‐onset movement disorders, which significantly impairs quality of life. So far, there are few therapeutic options with limited efficacy. This study investigated the therapeutic potential of baricitinib, a selective JAK1/2 inhibitor, in the harmaline‐induced model of ET. Male Swiss mice were randomly assigned to five groups ( n = 8): control, harmaline, and harmaline plus baricitinib at 10, 20, or 50 mg/kg doses. ET was induced using harmaline (10 mg/kg, i.p.). Baricitinib was administered orally daily for 14 days. Assessments included behavioral tests and cerebellar gene expression analysis of inflammatory markers (TNF‐α, IL‐6, NF‐κB), neurotrophic factors (BDNF), ET‐related targets (Lingo‐1, NMDA receptor), and histopathological evaluation. Baricitinib reduced harmaline‐induced tremor severity. The drug also significantly ameliorated anxiety‐like behaviors in elevated plus maze and open field tests, while reducing depressive‐like behavior in the tail suspension test. Passive avoidance outcomes changed in a direction suggestive of improved retention; however, the high‐dose findings should be interpreted cautiously because 50 mg/kg was associated with motor coordination impairment. Molecular analyses revealed baricitinib completely normalized cerebellar pro‐inflammatory cytokines TNF‐α and IL‐6 and suppressed NF‐κB expression. The drug restored BDNF levels and reduced Lingo‐1 expression. Histopathological examination also suggested reduced Purkinje cell degeneration, with 20 and 50 mg/kg doses reducing Purkinje cell degeneration to control levels. Baricitinib reduced tremor and affective behaviors in a harmaline‐induced ET model, though gait abnormalities persisted. Cognitive benefits at lower doses were observed, with cautious interpretation required for the high dose due to motor effects. Molecular and histological analyses supported anti‐inflammatory and neuroprotective effects, indicating selective benefits via neuroinflammatory modulation.

Purpose: Ulnar neuropathy (UN) is the second most common focal neuropathy in the upper extremities. Electrodiagnostic studies (EDx), including nerve conduction study (NCS) and electromyography (EMG), are reliable tools for the diagnosis of ulnar neuropathy. We aimed to retrospectively analyze the medical records of patients diagnosed with ulnar neuropathy in a seven-year period and report our findings. Patients and methods: In this retrospective study, documents of the patients whose ulnar nerve injury was confirmed through electrodiagnostic study in two departments of Physical Medicine and Rehabilitation were collected and demographic data, subjective complaints of the patient, the cause, and electrodiagnostic findings were extracted from each patient’s file. The following points were specifically evaluated in the electrodiagnostic records; type of injury, location, accompanying injuries, sensory nerve action potentials (SNAP) of the fifth finger, SNAP of dorsal ulnar cutaneous nerve (DUCN), compound muscle action potential (CMAP) of abductor digiti minimi (ADM) muscle, nerve conduction velocity (NCV) across elbow, patterns of muscle involvement, and the severity of insult. Results: Out of 441 records, 305 (69.2%) were male and 68.1% were non-traumatic. Based on our clinical criteria, the intensity of the injury was mild in most cases. The elbow and forearm were the most involved regions in non-traumatic and traumatic cases respectively. Across elbow nerve conduction velocity showed decreased velocity in 71% of records. In non-traumatic cases, the most affected muscle was ADM (97%) and then FDI (85%). Conclusion: In focal entrapments such as ulnar neuropathy, electrodiagnostic findings are very helpful in assessing location, severity, and type of injury. If a consensus is achieved for the diagnosis of UN, even retrospective studies can become valuable sources for studying UN.

Carpal tunnel syndrome is the most common peripheral entrapment neuropathy, for which conservative treatments are the first measures taken. However, these measures are not usually sufficient. Recently major attention has been drawn to platelet-rich plasma for its possible effects on axon regeneration and neurological recovery. Although few studies have evaluated the effects of this treatment in carpal tunnel syndrome, further investigation is required to reach concrete conclusion. In this randomized controlled trial, women referring to the physical medicine and rehabilitation clinic at Shahid Modarres Hospital during 2016 with a diagnosis of mild and moderate idiopathic carpal tunnel syndrome were chosen. They were randomly assigned to two groups: (i) a control group using only a wrist splint, and (ii) a platelet-rich plasma group that received wrist splints along with a single local injection of platelet-rich plasma. The outcome measures were assessed via Visual Analogue Scale, the Boston Carpal Tunnel Syndrome Questionnaire and electrophysiological findings including the peak latency of sensory nerve action potential and the onset latency of the compound muscle action potential. A total of 41 women were included (20 wrists as control group) and (21 wrists as platelet-rich plasma group). Before treatment there were no significant differences between the two groups except for the median peak latency of sensory nerve action potential which was significantly higher among the patients in the platelet-rich plasma group (p = 0.03). All the measured variables significantly decreased in both groups after 10 weeks of treatment except for the median onset latency of the compound muscle action potential (p = 0.472). Finally, the changes in neither of the evaluated outcome measures were found to significantly differ between the two groups, even when the analyses were adjusted for age of the patients. The findings of this study showed that in a relatively short period of time after treatment, a single injection of platelet-rich plasma in the wrist does not significantly add to the effects of conservative treatment with wrist splints, in regards to the women pain and symptom severity, functional status and electrophysiological parameters. The trial has been retrospectively registered with an ID: IRCT2017041513442N13 (Date of registration: 2017–06-19).