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Lamotrigine, a widely utilized broad-spectrum anticonvulsant, is commonly prescribed for epilepsy management and bipolar mood disorders. Despite its extensive clinical usage, instances of lamotrigine overdose are underreported. Here, we present a case involving acute encephalopathy and seizure onset following an intentional lamotrigine overdose. This case underscores the importance of recognizing the potential clinical manifestations of lamotrigine toxicity, such as encephalopathy and seizures, emphasizing the necessity for vigilant management of patients receiving this medication.

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Background: Brown adipose tissue (BAT) plays a role in modulating energy expenditure. People with obesity have been shown to have reduced activation of BAT. Agents such as ß-agonists, capsinoids, thyroid hormone, sildenafil, caffeine, or cold exposure may lead to activation of BAT in humans, potentially modulating metabolism to promote weight loss. Methods: We systematically searched electronic databases for clinical trials testing the effect of these agents and cold exposure on energy expenditure/thermogenesis and the extent to which they may impact weight loss in adults. Results: A total of 695 studies from PubMed, Web of Science, and Medline electronic databases were identified. After the removal of duplicates and further evaluation, 47 clinical trials were analyzed. We observed significant heterogeneity in the duration of interventions and the metrics utilized to estimate thermogenesis/energy expenditure. Changes observed in energy expenditure do not correlate with major weight changes with different interventions commonly known to stimulate thermogenesis. Even though cold exposure appears to consistently activate BAT and induce thermogenesis, studies are small, and it appears to be an unlikely sustainable therapy to combat obesity. Most studies were small and potential risks associated with known side effects of some agents such as ß-agonists (tachycardia), sibutramine (hypertension, tachycardia), thyroid hormone (arrhythmias) cannot be fully evaluated from these small trials. Conclusion: Though the impact of BAT activation and associated increases in energy expenditure on clinically meaningful weight loss is a topic of great interest, further data is needed to determine long-term feasibility and efficacy.

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Background: Drooling related to bulbar weakness and dysfunction is a common concern in patients with neuromuscular disease. While there are numerous medications to manage sialorrhea, they are often limited by side effects and lack of efficacy. Botulinum toxin has shown to benefit ALS patients in a few studies, but there is scant data on the benefit in other neuromuscular conditions. Objective: To assess the effectiveness of Botulinum toxin in reducing sialorrhea in patients with various neuromuscular disease. Design/Methods: 25 patients (19M, 6F; 54.36 ± 17.09 yr) with documented neuromuscular illness and concern for drooling was followed for 6 weeks after Botulinum toxin injection. These patients had one of the following diagnoses: Duchenne muscular dystrophy (3), myotonic dystrophy (3), oculopharyngeal muscular dystrophy (1), inclusion body myositis (2), primary lateral sclerosis (1), amyotrophic lateral sclerosis (9), spinal muscular atrophy type 2 and 3 (2), spinal-bulbar muscular atrophy (2), and Becker's muscular dystrophy (2). A subjective drooling scale (1: markedly worse, 5: markedly better) and drooling thickness score (0=normal, 100=thick) was calculated on these patients prior to the injection and 4 and 6 weeks after the injection. Botulinum toxin 20-30 units were injected into bilateral parotid gland (70% of the dose) and submandibular gland (30% of the dose). Results: The drooling thickness score at before the injection was 75.2 ± 10.46. At 4 and 6 weeks, average scores reduced to 47.2 ± 6.14 and 18.8 ± 5.26, respectively (p < 0.05). The average pre injection perception about drooling was 3.0 (p < 0.05). The average change in perception was +0.84 and +1.28 at 4 and 6 weeks, respectively, (p < 0.05) implying significant improvement. There were no reported adverse effects. Conclusion: This study provides preliminary evidence for the use of botulinum toxin for refractory sialorrhea for a variety of neuromuscular conditions.

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We present a young 21-year-old male with drug-resistant epilepsy who developed vagus nerve stimulator (VNS)-induced severe obstructive sleep apnea (OSA). Severe OSA resolved after the VNS was turned off.

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Stiff person syndrome (SPS), with a prevalence of one to two per million, is an extremely rare neurological condition that is characterized by axial muscle stiffness and rigidity along with intermittent painful muscle spasms. It is often associated with psychiatric co-morbidities such as anxiety and depression. The pathophysiology, although poorly understood, is widely believed to be autoimmune in nature due to the association of anti-glutamic acid decarboxylase-65 (anti-GAD 65) antibodies with this condition. There is also a paraneoplastic variant that is more commonly associated with anti-ampiphysin antibodies. It occurs most commonly in patients with breast cancer followed by colon cancer. Most of the practising neurologists encounter just one or two cases of SPS in their entire careers, hence this condition remains underdiagnosed, leading to significant disability and distress to the patient. In this case report we describe a postmenopausal female who presented initially with symptoms of vertigo and dizziness and was hospitalized multiple times before the diagnosis was reached. Through this article, we attempt to increase awareness about this condition among practising physicians so as to increase the likelihood of earlier diagnosis and treatment.