Psychosis in a Patient With Silent Vascular Brain Lesions

A 69-year-old white man was transferred from the intensive care unit, where he was being treated for possible delirium tremens, to the psychiatric unit, for persistent depressive and psychotic symptoms. He had a longstanding history of alcohol use. He also had type 2 diabetes mellitus, dyslipidemia, and coronary artery disease, and had an implantable cardioverter defibrillator. During his index presentation, the patient endorsed delusions that his wife was having an affair with a neighbor and had persecutory delusions regarding this person. His depressive symptoms included sad mood, loss of interest, easy fatigability, trouble staying asleep, and decreased energy. The psychotic symptoms had started about 3 years ago, whereas the depressive symptoms had been present for the past 3 months. The patient scored 18/30 on the Montreal Cognitive Assessment, with impairment in visuospatial/executive skills, attention, verbal fluency, and delayed recall.³ He scored 11/18 on the Frontal Assessment Battery, with impairment in conceptualization, lexical fluency, programming, and inhibitory (Go/No-Go) domains.⁴ His blood counts, electrolytes, renal function tests, TSH, B₁₂, and folic acid were normal. Urine analysis and urine drug screen were non-contributory. Neurologic examination was unremarkable. Abnormal laboratory parameters included fasting glucose (128 mg/dl), alanine aminotransferase (82 units/liter), and aspartate aminotransferase (81 units/liter). Head CT scan showed an area of encephalomalacia (1.3 cm x 2.2 cm) in the anterior and lateral aspect of the right frontal lobe. There were scattered low-attenuation foci in the external capsule bilaterally, left more than right. The head CT results did not differ from another study done about 3 years ago (done after the patient had a fall), but neither the patient nor his family were aware of the results of the previous head CT. However, the family did corroborate the onset of the patient's psychotic symptoms approximately to the time of the first head CT study. Although the patient was started on quetiapine for psychotic symptoms at that time, the late-onset psychotic symptoms were not correlated with the head CT findings. The patient and his family denied that the patient was ever treated for stroke or had any overt neurological symptoms in the past. The patient was diagnosed with Vascular Dementia with Delusions and Depressed Mood, and Alcohol Dependence, according to DSM-IV-TR criteria. During his present admission, the patient was treated with sertraline (150 mg/day) and quetiapine (100 mg/day), with improvement in both depressive and psychotic symptoms. He did not consent to a trial of donepezil.

A silent cerebral infarction can present with one of the four psychiatric symptom clusters: affective, paranoid delusional, confusional state, and changes in mood with behavioral disturbance.⁵ However, without a high index of suspicion, these silent vascular brain lesions are like1y to be missed in patients presenting with prototypical psychiatric syndromes. In our patient, besides the vascular brain changes, chronic alcohol use, comorbid depression, and, possibly, vascular dementia itself may have contributed to the presentation. Right-side brain lesions are more common in patients who develop psychosis after stroke.^6–8 The role of frontal lobe deficits in this patient also deserves mention. Delusions in patients with dementia are associated with frontal lobe changes,⁹ and patients with psychotic depression demonstrate fronto-temporal atrophy and also do poorly on frontal-lobe tests, as compared with nonpsychotic patients.¹⁰ Thus, clinicians should explore for underlying silent vascular brain lesions, especially in older patients with psychosis and frontal lobe/executive function deficits. Whereas vascular depression and mania have operational definitions, more research is needed on “vascular psychosis” in this respect.^11,12 It would be interesting to elucidate whether vascular psychosis is an independent entity or exists on a continuum comprising vascular depression and vascular dementia, considering a report of the progression of vascular depression to vascular dementia in a patient with silent vascular brain lesions.¹³