The relationship between lesion location and neuropsychiatric sequelae in stroke patients has been extensively studied. Emotional disorders associated with right hemisphere stroke include depression, anxiety, anger, and/or mania. Pharmacotherapy, electroconvulsive therapy, and/or psychotherapy are common treatments for these disorders. This article reviews the clinical presentations of seven right hemisphere stroke patients. The treatment rationale and course of treatment are described for two of these patients. The aims of this paper are to explore the appropriateness of various assessment tools and treatment modalities for stroke patients as well as to demonstrate the techniques of psychotherapy as applied to the two cases featured in this article. Specific factors that may significantly influence treatment outcome, such as lesion location and degree of cognitive impairment, are considered.

Depression and apathy are the two most frequent behavioral complications of stroke. This article reviews the prevalence of these conditions in poststroke patients, as well as their clinical correlates, longitudinal course, and possible mediators. A number of controlled clinical trials of the efficacy of various drugs in the treatment of poststroke depression are also reviewed.

Brain ischemia is a process of delayed neuronal cell death, not an instantaneous event. The concept of neuroprotection is based on this principle. Diminished cerebral blood flow initiates a series of events (the “ischemic cascade”) that lead to cell destruction. This ischemic cascade is akin to a spreading epidemic starting from a hypothesized core of ischemia and radiating outward. If intervention occurs early, the process may be halted.

Interventions have been directed toward salvaging the ischemic penumbra. Hypothermia decreases the size of the ischemic insult in both anecdotal clinical and laboratory reports. In addition, a wide variety of agents have been shown to reduce infant volume in animal models. Pharmacologic interventions that involve thrombolysis, calcium channel blockade, and cell membrane receptor antagonism have been studied and have been found to be beneficial in animal cortical stroke models. Human trials of neuroprotective therapies have been disappointing. Other than thrombolytics, no agents, have shown an unequivocal benefit. The future of neuroprotection will require a logical extension of what has been learned in the laboratory and previous human trials. A sensible approach to the use of multiple-agent cocktails used in combination with thrombolytics is likely to offer the highest chance for benefit.

Psychopharmacology is rapidly becoming an adjuvant treatment to traditional rehabilitation strategies for patients with stroke or brain injury because it helps to facilitate recovery in a time-efficient manner. Norepinephrine, dopamine, acetylcholine, and serotonin appear to play important roles in recovery from stroke or brain injury. Animal models have shown that blockade of these neurotransmitters inhibits recovery, whereas recovery is promoted by drugs that promote norepinephrine, dopamine, acetylcholine, and serotonin activity. Preliminary evidence from human trials supports these finding. Further study is needed, but expanded use of pharmacologic agents for stroke and brain-injured patients appears imminent.

Despite advances in the treatment of acute cerebral infarction, the most effective method of reducing stroke morbidity and mortality is the identification and modification of stroke risk factors. Modifiable stroke risk factors include hypertension, atrial fibrillation, hypercholesterolemia, cigarette smoking, hyperhomocystinemia, and carotid stenosis. Improved identification of individuals at increased stroke risk due to these factors can reduce individual risk and the cost to society of the consequences of stroke.