Table 2.

Distinctive features of CHANTER syndrome, selected differential diagnoses, and similar cases

Etiology	Clinical presentation	Injury/imaging pattern	Other notes
Syndromes
CHANTER	Acute ↓LOC	Bilateral cbel + hippocampi +/− BN	Risk of obstructive HCP
Acute ischemic stroke	Focal neurologic deficits	DWI+ in a vascular distribution	+/− Evidence of vascular occlusion
HASL (“chasing the dragon”) [4, 12, 13]	Strength or movement abnormalities, ataxia; frequently subacute	Predominantly white matter; unlikely DWI+
PRES [2, 14]	Variable; +/− headache, vision changes, AMS, seizure	Predominantly white matter	Specific provoking factors
Anoxic injury [8, 23–25]	↓LOC	Cerebral cortex +/− cbel, hippocampi, BN	Not typically associated with obstructive HCP
Carbon monoxide (CO) [15, 16, 20, 21]	Headache, AMS	Globus pallidus + BN > cbel + brainstem	Clinical exposure
Cyanide (CN) [17]	Headache, agitation, seizures	BN +/− hippocampi; cbel spared	Clinical exposure
Mercury (Hg) [18]	Acute: systemic symptoms; chronic: personality changes, erethism	Punctate lesions or degeneration without acute edema or DWI+	Clinical exposure
Similar cases
Small/Barash et al. [9, 10]	Memory impairment	Hippocampal DWI+
Bhattacharyya et al. [11]	Various	Hippocampal and other DWI+ areas
Pediatric opiate overdoses [26–31]	↓LOC	+/− Cerebellar edema	Limited examples with MRI to show potential other areas of injury

AMS altered mental status, BN basal nuclei, cbel cerebellum, CHANTER Cerebellar Hippocampal And basal Nuclei Transient Edema with Restricted diffusion, DWI+ hyperintensity on diffusion-weighted imaging, HASL heroin-associated spongiform leukoencephalopathy, HCP hydrocephalus, LOC level of consciousness, PRES posterior reversible encephalopathy syndrome, +/− with or without, > more frequently than