Presentation
GCS3. Suspected drug use.
Patient Data
Diffuse periventricular white matter increased signal on T2-weighted images and FLAIR,
showing diffusion restriction.
Bilateral basal ganglia and cortex appear normal.
Imaging features are in keeping with leukoencephalopathy - likely toxic, given the presentation.
The diffuse periventricular white matter T1 hyperintensity and restricted diffusion identified
previously have evolved further. There is now extensive cystic necrosis in these areas. This is manifest as diffuse high T2 signal and low T1 signal with reversal of the previous restricted diffusion/
The process is limited to the white matter with complete sparing of the overlying cortex.
No evidence of encephalomalacia or atrophy at present.
Minor areas of gliosis are present at the margins of the cystic necrosis bilaterally.
The sparing of the cortex and basal ganglia suggest a toxic etiology rather than hypoxia.
Case Discussion
This is a case of suspected toxic (narcotic) leukoencephalopathy.
The patient had a prolonged ICU and rehab admission with a subsequent acquired brain injury.
A potential differential for the etiology underlying the leukoencephalopathy evident on MRI is a post-hypoxic encephalopathy. There is considerable overlap in the spectrum of the imaging appearance of the two entities. One of the hallmarks of delayed hypoxic encephalopathy is the clinical biphasic pattern of deterioration, which usually has an initial improvement and then neurological decline.
In this case, the patient suffered a neurological insult fairly immediately and had a fluctuating GCS of 3-7 for several days in the ICU, with a spastic quadriparesis, and had only mildly improved with extensive rehab (i.e. there was no real recovery period as in the classic pattern for delayed hypoxic encephalopathy). While it remains relatively difficult to separate whether this case was secondary to the toxic stimulus or a related hypoxic event, the patient was thought to most likely have a toxic leukoencephalopathy.
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