Extensive pallidal and white matter injury following cocaine overdose

Excerpt

Sir: A 46-year-old man with a history of heroin and cannabis addiction treated with methadone and diazepam was admitted after an acute “binge” of cocaine. He had been found by the mobile emergency unit with a Glasgow Coma Scale (GCS) of 3, respiratory rate 12/min, pulse rate 124/min, arterial pressure 80/60 mmHg, and oxygen saturation (SpO₂) 90%. He was immediately intubated and mechanically ventilated with FIO₂ 0.5. Inhalation pneumonia was further diagnosed. Blood glucose was 107 mg/dl. Arterial blood gas analysis revealed: pH 7.31, pO₂ 93 mmHg, pCO₂ 46 mmHg, total bicarbonate 23 mmol/l, HbCO 1%. No clinical or electrophysiological sign of seizure was present. Toxicological screening confirmed the presence of methadone in urine, and of metabolites of cocaine in blood and urine samples. The GCS improved to 7 by the second day. The patient did not present hypotension or hypoxia during ICU stay. An initial brain magnetic resonance imaging (MRI) was performed on day 7, which showed abnormally elevated signal intensity within both pallidi, and at a very lesser degree within the splenium of the corpus callosum on the fluid-attenuated inversion recovery (FLAIR) images (Fig. 1, left). Both areas disclosed strong hyperintensity on diffusion-weighted images due to drastic reduction in apparent diffusion coefficient reflecting cytotoxic edema. A point-resolved spectroscopy monovoxel proton spectrum obtained with a short echo time at 30 ms from central gray nuclei well demonstrated increased peaks of glutamine-glutamate at 2.1–2.2 ppm and at 3.7–3.9 ppm, reflecting intense excitotoxic activity (Fig. 1, middle). Follow-up MRI performed 3 weeks later revealed pallidal damage to liquefaction necrosis together with the appearance of extensive supratentorial white matter changes (Fig. 1, right). At 2-month clinical follow-up the patient suffered mainly from akinetic mutism and mixed extrapyramidal and pyramidal spasticity.

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