Partial Recovery in Toxic Leukoencephalopathy: Is It Really a Slow Improvement or a Warning Sign?

Abstract

A 55-year-old African American man who was found down by a friend nine hours after being last seen at the same place was brought to the emergency department (ED) with encephalopathy, lactic acidosis, rhabdomyolysis, elevated troponin, acute kidney injury (AKI), and transaminitis. His urine drug screen (UDS) was positive for cocaine. Intravenous (IV) Narcan was given with minimal improvement in mental status. A computed tomography (CT) scan of the head and a CT scan of the cervical spine in the ED showed no acute findings. Due to hypoxia, the patient was eventually intubated. The patient also required a fasciotomy and eventually hyperbaric oxygen (HBO) therapy due to the left lower extremity wound. He was transferred to our facility for further care. Due to incomplete cognitive recovery, as the patient was oriented to self only, further neurological workup, including magnetic resonance imaging (MRI) of the brain, was obtained, which showed bilateral symmetric T2 FLAIR (Fluid attenuated inversion recovery) hyperintensity in the globus pallidus. The patient had slow and gradual deterioration with worsening encephalopathy, akinetic mutism, parkinsonian features, and seizures, which prompted further evaluation from neurology. The patient eventually underwent extensive workup, including a continuous video electroencephalogram (cvEEG), repeat MRI brain with and without contrast, lumbar puncture for cerebrospinal fluid (CSF) analysis, MRI brain with diffusion tensor imaging (DTI), and magnetic resonance spectroscopy (MRS). The patient was treated with multivitamin therapy and coenzyme Q10, but there was no significant benefit. We report a case of cocaine-induced leukoencephalopathy with findings like 'chasing the dragon encephalopathy' with a possible component of delayed post-hypoxic injury with underlying neuroinflammation.

Keywords: chasing the dragon encephalitis; cocaine induced encephalitis; delayed post hypoxic encephalitis; encephalitis; toxic encephalopathy.

Figure 1. Initial MRI brain imaging

Bilateral symmetric globus pallidus signal abnormality: (a) hypointense on T1 (b) hyperintense on FLAIR,  and (c) absence of diffusion restriction on DWI

Figure 2. Follow-up MRI brain imaging

Interval development of extensive and diffuse cerebral white matter (A and D) T2-FLAIR hyperintensity and (B and E) diffusion restriction, symmetrically involving all the lobar white matter without cortical involvement. Hypointense (C and F) T1 images

Figure 3. MR spectroscopy

MR spectroscopy shows an elevated choline peak in (A) normal as well as (B) abnormal regions of interest and a decreased NAA peak in (C) normal and (D) abnormal regions of interest. Absent lactate peak.