Abstract 222: CHANTER Syndrome: A Rare Cause of Encephalopathy
Authors: Kahn M. , Rodriguez W. , Polhemus L. , Arshid M. , Linares G. 
Published: January 2025

CHANTER Syndrome

A Rare Cause of Encephalopathy.

Introduction/Purpose

Cerebellar, Hippocampal, and Basal Nuclei Transient Edema with RestrictedDiffusion (CHANTER) syndrome is a rare diagnosis stemming from its pattern of radiologic findings on MRI. This syndrome is rare and typically occurs in the setting of intoxicant exposure, the most reported being opioids. Patients typically present with a depressed level of consciousness and can present with seizures. Differential diagnoses include hypoxic ischemic encephalopathy (HIE), posterior reversible encephalopathy syndrome (PRES), heroin‐associated spongiform leukoencephalopathy, and opioid‐associated amnestic syndrome (OAA). The most common complication is obstructive hydrocephalus due to cerebellar edema causing crowding of the fourth ventricle. Outcomes range from near‐complete recovery to brain herniation and death.

Materials/Methods

NA

Results

A 38‐year‐old man with a history of polysubstance abuse disorder presented to the emergency department after being found unresponsive in his vehicle by bystanders. Emergency medical services (EMS) noted miosis and administered Narcan, but there was no improvement. On initial examination, the patient was unresponsive and showed no spontaneous movement. He was intubated for airway protection. Significant lab results included a lactic acid level of 10.6 mmol/L, creatinine kinase of 3,600 U/L, blood ethanol of 122 mg/dL, and a urine drug screen positive for cannabis, cocaine, and fentanyl. Continuous EEG revealed generalized slowing without evidence of seizures. An MRI demonstrated confluent areas of restricted diffusion in the bilateral cerebellar hemispheres, scattered small foci of restricted diffusion in the basal ganglia, and symmetric restricted diffusion in the bilateral hippocampi. On the third day of admission, he was extubated. The patient was disoriented in place and time, had inattention, memory impairment, and appendicular ataxia, which improved during his hospital stay. By the time of discharge, he was oriented to self and place but not to time, and had no motor or sensory deficits. After a 12‐day hospital stay, he was discharged to an acute rehabilitation facility. At his three‐month outpatient follow‐up, his overall condition was improving, although he continued to experience significant short‐term memory deficits. A follow‐up brain MRI showed the resolution of the lesions seen on admission.

Conclusion

We present a rare case of CHANTER syndrome secondary to opioid intoxication. Despite the resolution of brain lesions observed on MRI and significant clinical recovery, the patient continued to experience cognitive deficits. Early recognition of this syndrome is crucial, as prompt management appears to lead to more favorable outcomes.

References

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