The American College of Physicians (ACP) developed this clinical guideline on pharmacologic treatments for internal medicine physicians and other clinicians caring in outpatient settings for females with menopausal vasomotor symptoms.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by upper and lower motor neuron dysfunction. Electromyography (EMG) is central to its evaluation, but neurogenic abnormalities and fasciculations are not specific to ALS and must be interpreted within the clinical phenotype and disease trajectory. This study reports a 52-year-old man with an approximately eight-year history of intermittent muscle twitching, bilateral upper-limb tremor, muscular tightness and warmth, and asymmetric cutaneous hypersensitivity. An initial electrodiagnostic evaluation raised concern for diffuse motor neuron disease, despite preserved strength, normal gait, absence of muscle wasting, and lack of clear upper motor neuron signs. Extensive evaluation for inflammatory, autoimmune, metabolic, toxic, infectious, paraneoplastic, neuromuscular junction, and peripheral nerve hyperexcitability disorders was unrevealing. Serum creatine kinase was mildly and variably elevated, while aldolase and a comprehensive myositis panel were normal. Brain magnetic resonance imaging (MRI) demonstrated no supportive features of ALS. Sudomotor testing showed reduced electrochemical skin conductance (ESC) in the hands, supporting small-fiber/autonomic dysfunction in the context of prominent sensory symptoms. Repeat EMG, performed after interval follow-up with broad muscle sampling, demonstrated focal neurogenic abnormalities involving bilateral ulnar distributions and left L5-S1 radiculopathy but found no electrophysiological evidence of a neurodegenerative disorder. The patient was treated symptomatically with gabapentin and vitamin E and reported approximately 80% improvement after six weeks. This case highlights the importance of clinicophysiological correlation, disease trajectory, sensory phenomenology, and repeat electrophysiology when an initial EMG suggests motor neuron disease but the longitudinal clinical picture is discordant. It also illustrates how small-fiber dysfunction and focal neurogenic abnormalities may coexist and mimic a progressive motor neuron syndrome.

Despite recent increases in gabapentin misuse among Black Americans who use opioids, there is a dearth of research examining gabapentin misuse among this high-risk group. The current study examines associations between health-related risk factors (e.g., pain and insomnia) and gabapentin misuse among Black adults who use opioids, as well as gender differences in these associations. Data were derived from a mixed-methods study examining opioid misuse among Black adults. The current sample included participants who confirmed lifetime prescription opioid misuse during the study survey (n=758). Stepwise logistic regression analyses, controlling for age, education, and past 30-day depression and anxiety, were used to examine main and interaction effects of pain, insomnia, and gender on odds of gabapentin misuse. Pain was assessed using the Brief Pain Inventory, and insomnia was assessed using the Insomnia Severity Index. Gabapentin misuse, depression, and anxiety were assessed using a modified version of the Addiction Severity Index-Lite. Overall, approximately 16% of participants reported gabapentin misuse in the past 30 days. Analyses showed a significant main effect of age (AOR=1.03, 95% CI [1.01, 1.04]), gender (AOR=5.60, 95% CI[2.44, 12.86]), pain (AOR=2.54, 95%CI [1.24, 5.22]) and insomnia (AOR=2.86, 95%CI [1.24, 6.38]) on odds of gabapentin misuse, and a significant interaction between gender and insomnia (AOR=.36, 95%CI [.13, .95]). Findings highlight a need to address sleep concerns among Black adults who misuse opioids and gabapentin, and for intervention approaches tailored by race and gender.

Orthobunyaviruses are linked to a broad spectrum of neurological disorders. However, the molecular determinants governing bunyavirus neuropathogenesis remain poorly understood, precluding the identification of drugs able to alleviate virus-induced neuronal dysfunctions. Here, we show that the prevalent, yet neglected, orthobunyavirus Ťahyňa virus (TAHV) disrupts neuronal integrity and proteostasis in human cerebral organoids (hCO), significantly decreasing synaptic protein expression and density. Moreover, TAHV-induced synaptic remodeling is associated with perturbed local field potential in organotypic cultures of human post-mortem adult brain explants (OPAB) and higher expression of the metabotropic Glutamate receptor 1 (mGluR1) in mice in the absence of overt neurological disease or neuroinflammation. Using proteome-based network medicine, we identified gabapentin as a therapeutic candidate that restores neurotransmitter receptor levels back to baseline in mice, and prevents TAHV-induced hyperexcitability in OPAB. Together, our data highlights the underappreciated neuropathological potential of a neglected orthobunyavirus, that interferes with neural integrity and neurotransmission, while neuromodulatory interventions may help to preserve cerebral functions.

Perimenopause, the hormonal transition preceding menopause, typically begins in the late 30s to mid-40s and lasts an average of seven years. Its neurobiological effects, including disruptions to serotonin synthesis, dopamine signaling, γ-aminobutyric acid receptor activity, and hypothalamic-pituitary-adrenal axis reactivity, produce a symptom profile nearly identical to primary psychiatric disorders. Women presenting with new or worsening anxiety, depression, insomnia, or cognitive changes during midlife are routinely diagnosed with psychiatric conditions before a hormonal etiology is considered, a pattern with measurable consequences for patients. Perimenopause does not require abnormal laboratory values or menstrual irregularity for a diagnosis to be made. Nurses across various settings encounter perimenopausal women daily. Nurses in any role can recognize the pattern and advocate for hormonal evaluation. Advanced practice RNs, including psychiatric NPs, can integrate perimenopause into the psychiatric intake, conduct structured hormonal assessments, and initiate or coordinate evidence-based treatment. This article aims to equip nurses with the tools to recognize perimenopause, challenge five pervasive clinical misconceptions, conduct a hormonally informed assessment, and support appropriate management in any practice setting.

The patient was a woman in her 20s. In June of a certain year, she experienced cardiopulmonary arrest due to acute epiglottitis and was admitted to the ICU and required mechanical ventilation. From the first day of hospitalization, she exhibited generalized seizures and was diagnosed with acute symptomatic seizures following hypoxic brain injury. Treatment with diazepam and levetiracetam was initiated, leading to symptom resolution. However, around the seventh day of hospitalization, she began experiencing episodic limb muscle hypertonia and fever. Based on diagnostic criteria, she was diagnosed with paroxysmal sympathetic hyperactivity on the 20th day of hospitalization. Although treatment with propranolol, gabapentin, and baclofen was initiated, her symptoms persisted. On the 38th day of hospitalization, morphine hydrochloride and methylprednisolone were administered, resulting in remarkable improvement. The present case shows that accurate diagnosis of paroxysmal sympathetic hyperactivity following hypoxic brain injury, particularly its differentiation from acute symptomatic seizures, is essential for appropriate management.