ArticleCureus2025
Basal Ganglia Calcification With Treatment-Resistant Hypocalcaemia and Persistent Psychosis in an 18-Year-Old: A Case Report.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basal ganglia calcification (BGC) in young adults represents a pathological finding requiring systematic investigation, contrasting with incidental age-related calcification in elderly populations. We report an 18-year-old male patient who presented to the emergency department with a first episode of generalized tonic-clonic seizure with subsequent imaging revealing extensive bilateral BGC involving the basal ganglia, thalami, and cerebellum. His inpatient stay was complicated by treatment-resistant hypocalcaemia. A retrospective review revealed that hypocalcaemia had been documented eight months prior to this presentation. The patient had been suffering from new-onset psychotic symptoms beginning 12 months prior, which were poorly responsive to multiple antipsychotics and had initially been managed as primary functional psychosis. This presentation suggested that the neurological, psychiatric, and metabolic presentations are organically interlinked. Comprehensive screening for autoimmune encephalitis and infectious aetiologies was negative, with genetic testing for pseudohypoparathyroidism currently ongoing. Pseudohypoparathyroidism emerges as the leading hypothesis based on treatment-resistant hypocalcaemia, elevated parathyroid hormone (PTH) levels, and extensive calcification. The temporal sequence, psychosis (12 months) → documented hypocalcaemia (eight months) → seizure, suggests that long-standing calcium dysregulation and progressive BGC may have contributed to the psychiatric presentation, ultimately manifesting as seizure. This case demonstrates that investigating treatment-resistant psychiatric symptoms for organic causes and recognizing BGC in young patients as pathological red flags may facilitate earlier diagnosis before acute neurological complications.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.