SUN-576 - Basal Ganglia Calcifications Presenting as Refractory Glycemic-Attributed Neurocognitive Symptoms in a Patient with Long-Standing Type 2 Diabetes

Neurologic and cognitive symptoms are common in patients with long-standing diabetes and are frequently attributed to dysglycemia, hypoglycemia, or glucose variability. This assumption often drives escalation of insulin therapy, even when symptoms persist outside of documented glycemic excursions. Diagnostic anchoring may delay recognition of alternative etiologies and increase the risk of iatrogenic hypoglycemia. Fahr disease, characterized by idiopathic bilateral intracranial calcifications involving the basal ganglia and cerebellum, can present with neurocognitive dysfunction, gait disturbance, and seizure-like activity, symptoms that closely overlap with those commonly ascribed to glucose abnormalities.

A 46-year-old man with long-standing type 2 diabetes mellitus presented to the emergency department for hypoglycemia in the setting of marked blood glucose variability. He reported worsening confusion over two weeks that persisted even when glucose values were within target range. His wife described a longer history of progressive neurologic symptoms, including dizziness, ataxia, confusion, and intermittent seizure-like movements, which had consistently been attributed to glycemic irregularity.
In response to presumed glycemic causality, insulin therapy had been intensified, resulting in increased hypoglycemic episodes without improvement in neurologic symptoms. Given persistence of symptoms despite glucose optimization, neuroimaging was pursued. Non-contrast CT of the head demonstrated dense, bilateral, symmetric calcifications of the basal ganglia and cerebellum. Additional imaging revealed advanced calcific atherosclerosis of the internal carotid and vertebral arteries with stenosis disproportionate to age. The clinical and radiographic findings were most consistent with Fahr disease.

This case highlights a common endocrine diagnostic pitfall in which neurologic symptoms are attributed to dysglycemia without reassessment when symptoms persist despite glycemic correction. In this patient, continued insulin escalation increased hypoglycemia risk while obscuring a non-glycemic neurologic etiology. Recognition of Fahr disease reframed symptom interpretation and prevented further inappropriate intensification of diabetes therapy.

It is essential to maintain a high index of suspicion for non-glycemic causes of neurologic dysfunction in patients with diabetes when symptoms persist despite glucose optimization. Early diagnostic reassessment can prevent iatrogenic hypoglycemia and inappropriate diabetes management, as illustrated by this case of Fahr disease presenting as refractory glycemic-attributed neurocognitive symptoms.

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