We report the case of a 35-year-old male with a history of chronic, escalating nitrous oxide abuse who presented to the ER with a history of recent onset generalized weakness, altered sensorium, abnormal posturing of the hands, urinary complaints, and decreased balance. Physical examination was notable for pathologically brisk reflexes in all extremities, generalized flexion contracture of the fingers, decreased sensation in a stocking and glove distribution, and a weakly positive Babinski sign. The patient was noted to be a poor historian with decreased attention and concentration though otherwise generally alert and oriented. No discrete sensory level in the chest or trunk was detected, and the overall clinical appearance was felt to be most compatible with a mixed myeloneuropathic pattern of central and peripheral involvement. Laboratory findings were normal and noncontributory. Cervical spine MRI subsequently performed to rule out cord compression, intrinsic spinal cord mass, or demyelinating disease was notable for a long segment of increased T2 signal extending from C2-C3 to C6-C7 localizing to the dorsal columns of the cord in a typical "inverted V" fashion. No associated cord expansion was seen nor was there evidence of extrinsic compression; faint associated contrast enhancement was observed on post-gadolinium images. Further evaluation with nerve conduction velocity and electromyographic testing was deferred. Based on the exam findings, clinical history, and presentation, a diagnosis of nitrous oxide-related myeloneuropathy was made, and treatment with high-dose vitamin B12 supplementation was instituted. Recovery has been slow to date.
Terson syndrome, the presence of intraocular hemorrhage in the setting of acutely elevated intracranial pressure, was historically described in conjunction with acute subarachnoid hemorrhage; however, more recently, it has been associated with a gamut of intracranial pathophysiology ranging from blunt or penetrating injury to neurosurgical procedures. We describe two cases of profound intracranial injury, secondary to ballistic injury, and a ruptured intracranial aneurysm, in which posterior chamber ocular hemorrhage was noted on CT imaging. Though the outcome in such cases, as with ours, is often poor, the findings are germane to clinical care as the presence of Terson syndrome has been noted to be a negative prognostic factor in multiple clinical reviews. Additionally, clinical recovery can be impacted adversely by lasting visual deficits or retinal degradation in the absence of timely ophthalmologic intervention.
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