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Generalized seizure in a 30-year-old man with presumed intracranial hemorrhage: a case report
S McFarlane1, C Doty, S Zehtabchi
1Department of Emergency Medicine, Kings County Hospital Center and State University of New York, Health Science Center at Brooklyn, Brooklyn, NY 11203, USA.
Insights
Hypoparathyroidism can cause hypocalcemic seizures and basal ganglia calcifications. Prompt diagnosis and management are crucial, especially in emergency settings, to avoid misdiagnosis of intracranial hemorrhages.
Area of Science:
- Neurology
- Endocrinology
- Emergency Medicine
Background:
- Recurrent generalized tonic-clonic seizures can be a symptom of underlying metabolic disorders.
- Hypocalcemia, a common electrolyte imbalance, can precipitate neurological symptoms including seizures.
Observation:
- A 30-year-old male presented with seizures, found to be hypocalcemic.
- Initial CT scans suggested intracranial hemorrhages, leading to transfer for neurosurgical evaluation.
- Further clinical and biochemical assessments confirmed hypoparathyroidism with hypocalcemic seizures and basal ganglia calcifications.
Findings:
- Hypoparathyroidism was the underlying cause of the patient's seizures and hypocalcemia.
- Basal ganglia calcifications were identified as a consequence of chronic hypocalcemia.
- The case highlights potential diagnostic pitfalls in emergency settings.
Implications:
- Recognizing hypoparathyroidism is critical for appropriate management of seizures.
- Early biochemical evaluation can prevent misdiagnosis and unnecessary interventions.
- This case underscores the importance of considering metabolic causes for neurological emergencies.
Abstract:
A 30-year-old man presented to the emergency department of another institution with recurrent episodes of generalized tonic-clonic seizures. He was found to be hypocalcemic and was treated with an intravenous infusion of calcium followed by Dilantin. A computed tomography scan of the head was obtained, and the patient was transferred to our institution for neurosurgical evaluation and possible intervention of what was thought to be bilateral intracranial hemorrhages. After further evaluation at our institution, the diagnoses of hypoparathyroidism associated with hypocalcemic seizures and basal ganglia calcifications were established on both clinical and biochemical grounds. This case report discusses the clinical presentation, pathogenesis, diagnostic work-up, and management of hypoparathyroidism and associated seizures, highlighting the possible diagnostic and therapeutic pitfalls that are most pertinent to the emergency physician.