Neuropsychiatric presentation of multiple sclerosis.

Abstract

Ms. A was a 54-year-old woman who first came to an outpatient c linic because she had stopped taking her thyroxine. She was crying, appeared depressed, and reported that God had “told her” to stop taking her medications. She reported no history of psychiatric illness, substance abuse, seizures, traumatic brain injury, or exposure to poisons or toxins. Eight days later, at the psychiatry emergency care center, she was seen with pressured speech, tangentiality, disorganization, grandiose delusions (reporting receiving messages from God), labile affect, and difficulty paying attention. Collateral sources indicated that she had been hearing “God’s voice” for the last year. The voices had instructed her to leave her successful 20-year career to become an evangelist. No clinically obvious cognitive deficits were observed. Ms. A was admitted to the inpatient psychiatry unit with a preliminary diagnosis of bipolar disorder (manic episode) and was given divalproex sodium and risperidone. Initially, Ms. A appeared to respond to the mood stabilizer and antipsychotic medication. However, over the ensuing hospitalization, she had significant vacillations in affect (crying, screaming, and euphoria) and thought processes (incoherence, tangentiality, and loosening of associations) despite reported medication adherence. Of particular concern were her poor cognitive function and judgment. Although she had a high premorbid level of functioning, at the hospital, she was unable to understand medication regimens and showed little understanding of her medical condition. A concurrent medical workup was initiated to explain her symptoms. Neurology consultants performed complete physical and neurological examinations. The only abnormal finding was uniformly reduced reflexes bilaterally in the upper and lower extremities. Measures of Ms. A’s electrolyte levels and blood counts were within normal limits, as were results of a urinalysis and measures of B12, folic acid, protime and international normalized ratio, partial thromboplastine time, and liver function. The results of the following tests were negative: rapid plasma reagin, microhemagglutination-Treponema pallidum, hepatitis B and C, HIV, antinuclear antibody, rheumatoid factor, erythrocyte sedimentation rate, a urine drug screen, and a pregnancy test. Ms. A’s initial thyroid function tests revealed a slightly elevated level of thyroid stimulating hormone (6.98 μU/ml) but normal levels of free T3 and T4. A computed tomography imaging of Ms. A’s head was remarkable for reduced white matter in the parietal lobes. Subsequent magnetic resonance imaging (MRI) of the brain revealed diffuse and multifocal high signal intensity lesions in the brain parenchyma, mainly in the deep white matter of the cerebral hemispheres. These were best seen on fluid-attenuated inversion recovery images. White matter abnormalities, atrophy, and focal lesions in the remaining white matter of the cerebral hemispheres also were present (Figure 1). The lesions were suggestive of demyelinating disease, although none was enhanced with gadolinium contrast; i.e., the lesions were unlikely to be active. A single photon emission computed tomography scan identified mildly reduced perfusion to the frontal and parietal lobes bilaterally, with normal blood flow in the remainder of the brain (Figure 1).