Rear Naked Choke-Induced Delayed Post-Hypoxic Leukoencephalopathy in Mexico City

Overview

A 49-year-old male assaulted with a rear naked choke (RNC) developed delayed post-hypoxic leukoencephalopathy (DPHL), characterized by progressive neuropsychiatric decline weeks after initial recovery. MRI and brain biopsy confirmed extensive white matter ischemic lesions and gliosis consistent with DPHL following acute hypoxic-ischemic encephalopathy (HIE).

Background

Hypoxic-ischemic encephalopathy (HIE) results from insufficient oxygen and blood flow to the brain, causing neural cell death and cerebral edema, typically presenting neurological symptoms within 24 hours. Delayed post-hypoxic leukoencephalopathy (DPHL) is a rare demyelinating syndrome manifesting days to weeks after apparent recovery from cerebral hypoxia, often following carbon monoxide poisoning or other hypoxic insults. The rear naked choke (RNC) is a strangulation technique that compresses carotid arteries, leading to cerebral hypoxia and potential brain injury. This case highlights DPHL as a delayed complication of RNC-induced cerebral hypoxia.

Data Highlights

The patient was strangled on February 26, 2022, lost consciousness briefly, and initially recovered. Neurological symptoms evolved over weeks, including motor aphasia, dysphagia, sensory aphasia, memory impairment, prosopagnosia, gait disturbances, and myoclonus. MRI on April 14 revealed extensive ischemic-type lesions in white matter. Brain biopsy showed reactive gliosis, neuronal loss, edema, spongiosis, vascular congestion, and perivascular lymphocytic infiltrate consistent with acute and chronic HIE and DPHL.

Key Findings

• Rear naked choke (RNC) causes carotid artery compression, leading to cerebral hypoxia and acute HIE.
• Initial neurological symptoms (motor aphasia, dysphagia) appeared within 24 hours, consistent with acute HIE.
• Delayed neuropsychiatric symptoms (sensory aphasia, memory loss, prosopagnosia) emerged weeks later, indicating DPHL.
• MRI showed extensive ischemic lesions in white matter semi-oval centers with diffusion hyperintensity.
• Brain biopsy revealed reactive gliosis, neuronal loss, edema, spongiosis, and vascular changes confirming acute and chronic HIE with DPHL.
• Progressive neurological deterioration led to rapidly progressive dementia and total dependence on daily activities.

Clinical Implications

Clinicians should recognize that strangulation via RNC can cause acute cerebral hypoxia leading to HIE and may subsequently trigger delayed post-hypoxic leukoencephalopathy with progressive neuropsychiatric decline. Early identification and monitoring of delayed symptoms are critical for diagnosis. MRI and brain biopsy can aid in confirming DPHL, guiding management and prognosis.

Conclusion

This case underscores the emerging risk of DPHL following RNC strangulation, highlighting the need for awareness of delayed neurological sequelae after acute hypoxic events. Timely diagnosis and intervention are essential to manage this rare but severe complication.

References

1. Hypoxic-Ischemic Encephalopathy Pathophysiology and Clinical Features
2. Delayed Post-Hypoxic Leukoencephalopathy: Clinical and Imaging Characteristics
3. Mechanisms and Effects of Rear Naked Choke Strangulation