With an annual incidence of more than 600,000 cases, thromboembolic stroke is the third leading cause of death in the United States after heart disease and cancer (Kochanek et al., 2004). The number of stroke survivors has increased to 4.5 million adults nationally as the management of acute stroke continues to improve (AHA, 2002). Psychiatric syndromes are common complications of stroke and are associated with psychologic distress, increased impairment, poor rehabilitation outcomes, and excess morbidity. The purpose of this chapter is to describe clinically important poststroke psychiatric disorders and suggest appropriate treatment. Cognitive deficits are the most common psychiatric complication of stroke and affect nearly all stroke survivors. The type of cognitive disturbance depends on the location of the brain injury. Left hemisphere strokes frequently cause aphasia. Right hemisphere strokes cause substantial (but often underrecognized) cognitive impairments such as diminished insight, decreased attention, impaired spatial reasoning, and neglect syndromes. Furthermore, depending on the location of a stroke, other functions such as motivation, memory, judgment, and impulse control may also be affected. A large stroke or a series of small strokes affecting both hemispheres may lead to the global cognitive impairment of dementia. When a series of strokes is involved, the cognitive decline develops in a stepwise manner. This vascular dementia or multi-infarct dementia may be difficult to distinguish from Alzheimer’s disease. Autopsy studies of patients diagnosed with vascular dementia have often demonstrated the presence of Alzheimer’s disease pathology. As many as 25% of all dementia cases are attributable to a combined neuropathology of Alzheimer’s disease and multiple infarcts (Massoud et al., 1999). In addition to strategies such as speech and language therapy, physical and occupational therapy, and cognitive rehabilitation, pharmacologic treatment may improve cognitive deficits in some stroke patients. The parallels between vascular dementia and Alzheimer’s disease, as well as the evidence that reduced cholinergic function may play a role in both (Gottfries et al., 1994) have encouraged the use of acetylcholinesterase inhibitors (eg, donepezil) in vascular dementia. These drugs have shown modest benefits in such patients (Roman et al., 2005), and their use is described in Chapter 20.