Cerebellar, hippocampal, and basal nuclei transient edema with restricted diffusion (CHANTER) syndrome
Presentation
Polysubstance user who was found with lethargy, confusion, and left arm weakness. Glucose was 48 mg/dL. There was no immediate neurologic improvement after IV dextrose and intranasal naloxone. Noncontrast CT of the head, CT angiography of the head and neck, and CT perfusion showed no hemorrhage, large territorial infarction, large vessel occlusion, or perfusion abnormality.
Patient Data
Abnormal bilateral restricted diffusion and T2 hyperintensity consistent with cytotoxic edema involving the hippocampi diffusely, areas of the cerebellar cortex, and less conspicuously the globi pallidi.
Case Discussion
The imaging findings were suggestive of cerebellar, hippocampal, and basal nuclei transient edema with restricted diffusion (CHANTER) syndrome. Collateral history indicated recent self-medication with illicitly obtained opioids after a left shoulder injury. Neurologic re-examination showed antegrade and retrograde amnesia and improvement in left arm weakness. Initial laboratory evaluation showed elevations of serum creatine kinase, troponin T, and alanine and aspartate transaminase, suggestive of a multiorgan hypoxic injury. Toxicology was positive for ethanol, cocaine, cannabinoids, fentanyl, and norfentanyl, but negative for oxycodone and 6-monoacetylmorphine.
The case met proposed criteria for opioid-associated amnestic syndrome 1. The additional involvement of the cerebellum and (subtly) the globi pallidi were consistent with CHANTER syndrome, which may be considered a variant of opioid-associated amnestic syndrome 1,2. In this case, the degree of cerebellar and basal ganglia involvement was mild and posed no risk for complications that can occur in CHANTER syndrome such as obstructive hydrocephalus from cerebellar swelling. Both syndromes are likely opioid-specific toxidromes exacerbated by hypoxia. As in this case, the combination of fentanyl and cocaine has been implicated repeatedly in other case reports.
The other parts of the current case presentation was explained by opioid overdose-related cardiorespiratory depression resulting in multiorgan hypoxia, and the transient focal neurologic deficit (arm weakness) may have represented post-ictal Todd paralysis or limitation by pain and rhabdomyolysis.
Follow-up brain MRI two months after presentation showed complete resolution of the T2 and DWI abnormalities involving the hippocampi, cerebellum, and globi pallidi. The patient's memory improved to near normal, with only occasional lapses in episodic memory.
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