title: Apathy following stroke.
abstract: OBJECTIVE
  We will review the available evidence on the frequency, clinical correlates, mechanism, and treatment of apathy following stroke.
  
  
  METHODS
  We have explored relevant databases (that is, PubMed, MEDLINE, and PsycINFO) using the following key words and their combinations: apathy, motivation, abulia, stroke, cerebrovascular disease, basal ganglia, prefrontal cortex, anterior cerebral infarction, and thalamus.
  
  
  RESULTS
  The frequency of apathy following stroke has been consistently estimated between 20% and 25%. It appears to be associated with the presence of cognitive impairment, a chronic course characterized by progressive functional decline, and with disruption of neural networks connecting the anterior cingulate gyrus, the dorsomedial frontal cortex, and the frontal pole with the ventral aspects of the caudate nucleus, the anterior and ventral globus pallidus, and the dorsomedian and intralaminar thalamic nuclei. Published treatment studies have been mostly limited to anecdotal case reports, generally using dopamine agonists or stimulant medications. Cholinesterase inhibitors and nefiracetam may significantly reduce apathetic symptoms. However, their efficacy was examined in relatively small clinical trials that require replication.
  
  
  CONCLUSIONS
  Apathy is a frequent neuropsychiatric complication of stroke that, although often associated with depression and cognitive impairment, may occur independently of both. Its presence has been consistently associated with greater functional decline. However, there is no conclusive evidence about which is the best treatment for this condition.
authors.affiliation: Department of Psychiatry, The University of Iowa, Iowa City, 52242, USA. ricardo-jorge@uiowa.edu <ricardo-jorge@uiowa.edu>
authors.forename: Ricardo E
authors.initials: RE
authors.lastname: Jorge
authors.forename: Sergio E
authors.initials: SE
authors.lastname: Starkstein
authors.forename: Robert G
authors.initials: RG
authors.lastname: Robinson
mesh_terms: D000342:Affective Symptoms / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology / Q000523:psychology; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D001931:Brain Mapping; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use; D003072:Cognition Disorders / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology / Q000523:psychology; D003866:Depressive Disorder / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology / Q000523:psychology; D004292:Dominance, Cerebral / Q000502:physiology; D006801:Humans; D009042:Motivation / Q000502:physiology; D009415:Nerve Net / Q000187:drug effects / Q000503:physiopathology; D018697:Nootropic Agents / Q000627:therapeutic use; D011760:Pyrrolidinones / Q000627:therapeutic use; D020521:Stroke / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology / Q000523:psychology*
chemical_list: D002800:Cholinesterase Inhibitors; D018697:Nootropic Agents; D011760:Pyrrolidinones; C058876:nefiracetam