ABSTRACT The brachial plexus is a complex somatic nerve plexus that innervates the upper limb. Due to its complex developmental pattern, anatomical variations are relatively common. Awareness of these variations is important for anatomists, radiologists, anesthesiologists, and surgeons. During routine dissection of a 65‐year‐old female cadaver, variations in the formation of the brachial plexus on the right side were observed. In this case, the posterior cord does not receive the posterior division of the lower trunk. The inferior trunk did not divide into anterior and posterior divisions, and the anterior division of the middle trunk instead joined the inferior trunk. In other words, the lateral cord is formed solely by the anterior division of the superior trunk. Accordingly, the lateral root of the median nerve is distinctly narrower than its medial root. It is concluded that these variations from standard anatomic structures may not have affected the function of the upper extremity in this individual. However, awareness of the possible existence of such variations may help surgeons reduce the risk of surgical complications and intraoperative oversights.
ABSTRACT Clozapine is the gold standard, evidence‐based treatment of choice for treatment‐resistant schizophrenia. However, clozapine can induce serious, life‐threatening adverse effects, including neutropenia and agranulocytosis. There is accumulating evidence to suggest that rechallenging with clozapine should be considered in most patients with clozapine‐associated neutropenia (mild to moderate neutropenia) who do not respond to other treatments. Ruling out other causes of coincidental neutropenia is important when the neutropenia occurs after 2 years of treatment on clozapine, as the risk of developing neutropenia becomes negligible after 2 years and becomes nonspecific to clozapine. When our patient developed neutropenia whilst taking clozapine during Covid‐19 infection, she benefitted from Filgrastim [a Granulocyte‐Colony Stimulating Factor (G‐CSF)], which provided symptomatic treatment.
ABSTRACT Acquired hepatocerebral degeneration (AHD) is an uncommon neurological manifestation of chronic liver disease, most often associated with portosystemic shunting. The disorder is characterised by a combination of movement abnormalities, cognitive decline, and psychiatric disturbance. Manganese accumulation within the basal ganglia, secondary to impaired hepatic clearance, is considered the principal mechanism. The clinical overlap with more common neurodegenerative disorders frequently delays diagnosis. We describe a patient who presented with tremor, bradykinesia, and reduced facial expression in the context of compensated cirrhosis, whose neuroimaging findings were consistent with AHD. This case underscores the importance of considering AHD in patients with liver disease presenting with extrapyramidal or cognitive symptoms, as early recognition can alter management and improve outcomes.
ABSTRACT Brain tumors, particularly those involving the frontal and temporal lobes, may initially present with psychiatric manifestations such as mood disturbances, personality changes, cognitive impairment, or behavioral abnormalities. These atypical presentations frequently lead to misdiagnosis as primary psychiatric disorders, resulting in delayed diagnosis and treatment. Diagnostic difficulty is further increased by the overlap between psychiatric and neurological symptom profiles, limited access to early neuroimaging or neuropsychiatric assessment, and persistent clinical stigma. We conducted a narrative review of the literature (1990–2025) using PubMed, Embase, PsycINFO and Web of Science, focusing on adult patients initially diagnosed with psychiatric disorders who were later found to have underlying brain tumors. The reviewed evidence indicates that such misdiagnoses are often associated with delayed recognition of neurological disease, missed therapeutic windows, and increased morbidity. Contributing factors include cognitive bias in clinical reasoning, under‐recognition of subtle neurological signs, and systemic limitations in access to diagnostic imaging. Addressing these challenges requires a high index of suspicion in atypical psychiatric presentations, earlier use of neuroimaging, and a multidisciplinary approach integrating neurology, psychiatry, and neurosurgery. Improved clinical awareness, structured assessment pathways, and patient and caregiver education may further reduce diagnostic delays. Overall, early identification of brain tumors presenting with psychiatric symptoms is essential to improve prognosis, prevent irreversible neurological damage, and optimize functional outcomes.
ABSTRACT A frequent sleep issue called insomnia can lead to a number of disorders, including despair and anxiety. In order to cure insomnia, this study aims to evaluate the sedative effects of PRO in Swiss mice and use an in silico approach to look into the molecular processes at play. In our investigation, five mice were given oral PRO at doses of 2.5 and 10 mg/kg. The vehicle (NC) and diazepam (DZP), which serve as a positive allosteric modulator of the gamma‐aminobutyric acid A (GABA A ) receptor and a control, respectively, were used to measure the effects utilizing parameters including sleep duration and latency. Thiopental sodium (T‐Na) was employed in this instance as a sleep aid. Molecular docking experiments were also used to quantify PRO and DZP's binding capability to the GABA A receptor, which is linked to the sedative effect. The results show that PRO significantly affects mice's sleep patterns. PRO at 2.5 and 10 mg/kg extended sleep duration and reduced sleep latency in comparison to the NC. DZP (3 mg/kg) exhibited the greatest individual effect, even though PRO (10 mg/kg) and DZP combined further enhanced both measures, indicating a synergistic action. In the in silico investigation, PRO showed a significant binding affinity to the GABA A receptor with a docking score of −9.7 kcal/mol. It created several hydrophobic contacts and 11 hydrogen bonds with significant amino acid residues. PRO induces a sedative effect in mice primarily by modulating and activating the GABAergic neurotransmission system. We recommend more clinical research to validate PRO as a trustworthy sedative agent.
