Neuroglycopenia

Neuroglycopenia is a medical condition characterized by insufficient glucose delivery to the brain, resulting in impaired brain function. The brain depends heavily on glucose for energy, so a drop in plasma glucose can rapidly disrupt neuronal activity. The term is commonly used to describe the neuroglycemic manifestations of hypoglycemia, especially when glucose levels fall low enough to produce central nervous system symptoms.

Causes commonly include acute hypoglycemia in people with diabetes treated with insulin or other glucose-lowering agents, during prolonged fasting, or in critical illness with impaired glucose production. Less common contributors can include severe liver disease, adrenal insufficiency, or insulin-secreting tumors. The severity and duration of low glucose influence the onset and intensity of neuroglycopenic symptoms.

Clinical features are primarily neuroglycemic and may include confusion, slowed thinking, difficulty speaking, dizziness, weakness, and visual disturbances. As glucose falls further, somnolence, seizures, or loss of consciousness can occur. Autonomic symptoms such as sweating or tremor may appear earlier, but neuroglycopenia emphasizes CNS deficits.

Diagnosis relies on documenting low plasma glucose levels at the time of neurologic symptoms and excluding alternative causes of altered mental status. In diabetes care, this is often confirmed during a hypoglycemic episode.

Management requires prompt reversal of hypoglycemia: fast-acting carbohydrates if the patient is conscious, or intravenous dextrose or intramuscular glucagon if conscious intake is not possible. After stabilization, clinicians assess the cause and adjust therapy to prevent recurrence. Prognosis is generally favorable with rapid treatment, though prolonged episodes can lead to neuronal injury or cognitive impairment.