Etiology of the Splenium Lesion
Vascular, infectious, toxic, autoimmune, metabolic, and neoplastic causes should all be investigated. However, we can easily rule out vascular causes because the lesion is midline and would require the unlikelihood that both posterior cerebral arteries are affected. Although similar lesions have been associated with influenza A infection, this would be unlikely given the normal cerebrospinal fluid findings. A neoplastic etiology is certainly possible but is ruled out by MRS. Autoimmune processes, such as acute disseminated encephalomyelitis or multiple sclerosis, are less likely given the appearance of only 1 lesion, which leaves toxic and metabolic processes remaining.
High on the list of possible toxic or metabolic etiologies is Marchiafava-Bignami disease. Signal changes in the splenium were first described in Italian red wine drinkers but have been documented in cases of malnutrition and extrapontine myelinolysis. The clinical features include impaired consciousness, symptoms of interhemispheric disconnection, dysarthria, and neuropsychiatric disorders. These processes are thought to result from osmotic damage, manifesting as edema on MRI.
The neurologist conducts a neurocognitive evaluation to further evaluate the patient's deficits. Although this examination is not standardized for the hearing impaired, in this case it reveals significant impairment that, given this patient's history of good academic performance, cannot be explained only on the basis of hearing deficit. She demonstrates difficulty learning new visual and verbal information and some slowness in executive functions. Finally, although she perceives the input and has good immediate recall, her delayed recall is impaired.
Given these deficits, where would you localize the lesion?
Right frontal lobe
Left parietal lobe
Right temporal lobe
Left temporal lobe
Bilateral temporal lobes
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