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Cerebral amyloid angiopathy presenting with neuropsychiatric symptoms

A 74 year-old man with a past medical history of hypertension presented to the emergency department with a several-day history of confusion associated with auditory and visual hallucinations. He had no past psychiatric history. He was provisionally diagnosed with delirium, but no cause could be found on screening blood tests, urinalysis, chest x-ray or CT brain. The episode resolved spontaneously with supportive inpatient care. Six weeks later he developed a major depressive episode with psychotic features, which was treated to remission with venlafaxine and olanzapine. He remained free of psychiatric symptoms over the next 12 months, but complained of deteriorating memory and demonstrated deficits of both recent memory and verbal fluency on cognitive testing. An MRI was obtained and demonstrated multiple punctate regions of signal loss on T2*-weighted gradientrecalled echo (GRE) sequences (Figure 1(a) and (b)). The lesions were noted to be located peripherally, largely sparing the basal ganglia, and were not visible on conventional T1or T2-weighted sequences (Figure 1(c) and (d)). These findings are typical of cerebral amyloid angiopathy (CAA). Areas of high T2 (Figure 1(d)) and low T1 (Figure 1(c)) white matter signal were also seen, suggesting chronic small vessel ischaemic change. Hypertensive encephalopathy was considered as a differential diagnosis, but CAA was favoured on account of the peripheral distribution of lesions and relative sparing of the basal ganglia, thalamus and cerebellum. CAA is a neurovascular disorder characterised by the deposition and accumulation of beta-amyloid in smaller cerebral arterial vessels. The sporadic forms mostly affect older patients, though rarer hereditary variants occur in younger individuals. Lobar intracerebral haemorrhage is a common presentation, but microhaemorrhages and demyelination may also present with focal neurological deficits, seizures and cognitive impairment. In addition, CAA has been associated with neuropsychiatric symptoms including personality change, depression, and delirium (Gahr et al., 2013). Although a definitive diagnosis of CAA can only be made by postmortem examination of the brain, a probable clinical diagnosis can be made with imaging support (Knudsen et al., 2001). GRE and, if available,