In 2008, a 70-year-old man was admitted in the Department of Psychiatry in Strasbourg after a suicide attempt; he had tried to stab himself with a knife. Psychotic features associated with depression were characterized by thoughts of worthlessness, delusional guilt, feelings of helplessness, and hopelessness. Depressive symptoms alternated within a few hours with hypomania, which manifested as mild euphoria associated with pressured speech and psychomotor agitation. His blood pressure was 170/100 mmHg. The patient was disoriented in time and space, without identifiable focal neurological symptoms.
The patient had no personal or familial history of previous psychiatric disorder, but past record of hypertension, ischemic heart disease with angioplasty (in 2002), and aortic valve replacement (2007).
Oral olanzapine treatment was started at a dosage of 7.5 mg per day. The MR scan done the next day showed multiple white-matter T2 hyperintensities, some of which were recent, according to the diffusion-weighted images. Psychiatric symptoms regressed rapidly. Two weeks later, the patient presented with an acute manic agitation associated with mystical delusions and visual hallucinations concomitant to a bout of hypertension (210/110 mmHg). Increasing the antipsychotic dosage had no effect. The electroencephalogram (EEG) showed no sign of epilepsy. The MRI scan excluded a reversible posterior leukoencephalopathy syndrome, but showed new T2 hyperintensities in the periventricular white matter with increased diffusion-weighted signal, supporting recent ischemic damage. The angioMR provided no evidence of an arterial clot (Figure 1). Two days later, the clinical picture was completed by a livedo reticularis on the back and the buttocks (Figure 2). Antiphospholipid antibodies were slightly increased (× 1.5 increase in IgM anti-beta 2 glycoprotein 1 and IGM anticardiolipid), but returned to normal 6 weeks later. At this age, and considering their low level, antiphospholipid antibodies do not significantly increase the vascular risk.4 The diagnosis of Sneddon syndrome without antiphospholipid antibody was finally adopted. We could not identify an embolic cause, although it remains the best hypothesis, considering the background.
FIGURE 1.MRI Scan Shows New T2 Hyperintensities in the Periventricular White Matter With Increased Diffusion-Weighted Signal
FIGURE 2.Livedo Reticularis on the Back and Buttocks