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What caused this 37-year-old man to suddenly lose his sight? And why did he wait 3 days before presenting to the emergency department? That's what Juliane Hiesgen, Dr med, and Jacques Badenhorst, MBChB, of the University of Pretoria in South Africa, tried to determine in a recently published case in .

At the initial consultation, Hiesgen and Badenhorst learned that the patient had waited to seek care because he believed his blindness was a temporary reaction due to his recent binge of alcohol and stimulant use.

The patient explained that he had been using alcohol and methamphetamines for 3 nights in a row before he lost his sight; however, he had not consumed any home-brewed alcohol or any methanol-containing spirits. He noted that he usually did not take recreational drugs. There was no open fire or other source of carbon monoxide at his home.

The patient had significant vision impairment; he could only detect very bright light, and his pupils were dilated and unresponsive. A fundoscopic examination was performed, with no notable findings.

The patient did not have any other symptoms, and neurological findings were normal. He underwent a CT scan of the brain, which showed bilateral basal ganglia hypodensities.

Routine blood work and cerebrospinal fluid analysis returned normal results, and arterial blood gas analysis showed no indication of metabolic acidosis. Aside from being positive for methamphetamines, urinalysis screening did not detect evidence of any other substance misuse.

The patient's vision improved gradually over the next few days, to the extent that he could recognize shapes and, eventually, objects. However, he continued to be unable to identify the color red on color testing.

The patient was scheduled for an MRI of his brain 3 weeks after his admission. This revealed that the basal ganglia abnormalities that affected both lentiform nuclei had persisted. MRI showed a hyperintense signal of the external capsules and posterior internal capsules, "forming the prongs of the fork," Hiesgen and Badenhorst explained. "The stem of the fork is formed by the confluence of the edematous internal and external capsules at the posterior putamen," findings that reflect the radiological pattern that the lentiform fork sign is known for.

Additional susceptibility-weighted imaging revealed bilateral areas of hypointense signal within the posterior putamina suggestive of hemorrhage, and T1-weighted gadolinium-enhanced imaging showed rim enhancement of the hemorrhagic areas suggestive of necrosis.

Nevertheless, "the patient did not have any clinical features of encephalopathy or movement disorder at presentation and follow-up over 3 months," the authors wrote. They considered his visual symptoms to be "highly suggestive of a toxic optic neuropathy with acute, painless, bilateral onset of anterior optic pathway pathology, dyschromatopsia, and gradual improvement during recovery."

Discussion

While methamphetamine use has been associated with extensive basal ganglia lesions, the lentiform fork sign most commonly occurs in the setting of uremic encephalopathy and metabolic acidosis. In addition, the lentiform fork sign has been noted in the context of intoxications, particularly methanol, and genetic .

In rare cases, it has been reported to not involve acidosis, Hiesgen and Badenhorst noted, such as atypical .

Resolution of the lentiform fork sign has been observed after 3 to 6 months, according to anecdotal reports of consecutive MRI studies, but only in the setting of vasogenic edema. has been associated with ocular damage, especially corneal ulcers, crystalline retinopathy, and retinal artery occlusion. Still, temporary vision loss as noted in this case is a rare manifestation.

"This case demonstrates that basal ganglia edema with the lentiform fork sign on MRI may occur secondary to alcohol and methamphetamine intoxication, emphasizing that alternative causes besides uremia may result in this characteristic imaging finding," Hiesgen and Badenhorst concluded.

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