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1.
Cureus ; 16(5): e61318, 2024 May.
Artigo em Inglês | MEDLINE | ID: mdl-38813074

RESUMO

This study details the development of severe post-partum hypothyroidism exacerbating psychogenic non-epileptiform seizures (PNES) and culminating in myxedema coma. A 29-year-old female with a history of anxiety, attention-deficit/hyperactivity disorder (ADHD), and post-partum depression presented with confusion, aphasia, and severe bilateral leg cramping five months following vaginal delivery. Initial laboratory tests indicated elevated creatine kinase (CK) levels, suggestive of non-traumatic rhabdomyolysis. Subsequent seizure-like episodes and the absence of epileptiform activity on the electroencephalogram (EEG) raised suspicions of PNES. Further investigation upon readmittance to the hospital revealed a thyroid-stimulating hormone (TSH) level of 216 mIU/L (range: 0.4-4.0 mIU/L), free thyroxine (T4) level of 0.2 ng/dL (range: 0.8-1.8 ng/dL), and a CK level of 2083 U/L (range in females: 30-150 U/L), indicating severe hypothyroidism with myopathy. Reintroducing levothyroxine (Synthroid), which was previously discontinued during pregnancy, rapidly resolved her symptoms, supporting suspicions that her non-epileptic seizures and myopathy were both caused by her underlying severe post-partum hypothyroidism. She was maintained on levothyroxine with only one seizure-like episode following hospital discharge. This case illustrates the importance of a thorough endocrine assessment in patients with neuropsychiatric presentations, particularly in the peripartum period. It highlights the potential for severe thyroid dysfunction to manifest as PNES, emphasizing the complexity of diagnosing and managing such cases. The findings advocate for a multidisciplinary approach to evaluating post-partum females with neurological and psychiatric symptoms and provide evidence for the link between thyroid disorders and PNES, advocating for a nuanced approach in similar clinical scenarios.

2.
eNeurologicalSci ; 34: 100488, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38089428

RESUMO

Central hypoventilation syndrome (CHS) is a rare condition resulting from damage to the respiratory centers in the central nervous system (CNS). It can be congenital or acquired and can cause hypoventilation, inadequate gas exchange, and respiratory failure, often during sleep but sometimes even while awake. CHS can lead to respiratory failure and life-threatening complications if not identified promptly. In this report, we present a rare case of a patient with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), who developed CHS likely due to an opportunistic infection by cytomegalovirus (CMV) and varicella zoster virus (VZV), manifesting as a lesion in the medullary respiratory nuclei. After treatment with ganciclovir, the patient showed clinical improvement, and his medullary lesion resolved.

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