Psychotic disorders due to stroke are rare. They are classified according to the predominant symptom, with prominent hallucinations or with delusions. Delusions are of two main types: delusional misiden-tification syndromes and delusional ideation. This can be observed in patients with Wernicke's aphasia
and severe comprehension defect. Kumral and Ozturk  found that delusions started 0-3 days after stroke, and the predominant types were mixed, perse-cutory, jealousy and suspicion. Delusional ideation was transient, with a mean duration of 13 days. The prevalence of psychosis and of delusional ideation (1-5%) in stroke survivors is also low. It is predominantly associated with right hemispheric strokes. There is no association between delusion type and infarct site.
The delusional misidentification syndromes include Capgras syndrome, where the patient believes a familiar person is not the real person but has been replaced by a similar one; Fregoli syndrome, where the patient believes it is the same person but with different features; and intermetamorphosis, where the familiar person has been transformed into another one. Somatoparaphrenia is associated with hemiassomatognosia and denial of hemiplegia. In spatial delirium the patient believes he/she is in a different place than the actual one, even in the face of compelling counter-evidence. Spatial delirium can have three grades of severity or stages of evolution: (1) confabulatory mislocation: "I am not in hospital X but in hospital Y"; (2) reduplication: "I am not in the real hospital X but in an identical building"; (3) chimeric assimilation: "I am not in the real hospital X but in my house which was transformed into a hospital". Spatial delirium is in some cases associated with delirium, neglect, memory or visuo-spatial disturbances and is seen predominantly after right-hemispheric lesions.
Hallucinations in stroke patients are predominantly visual and can be due to: (1) sensory deprivation: poor vision (Charles Bonnet syndrome), darkness, deafness . . .; (2) delirium and substance withdrawal (alcohol, drugs); (3) rostral brainstem and thalamic lesions (peduncular hallucinosis) (subcortical hallucinations); (4) partial occipital lesions ("release" hallucinations) (cortical hallucinations). Functional imagery studies showed that in subjects with visual hallucinations there was activation of the ventral extrastriate visual cortex and that the type of hallucinations reflected the functional specialization of the activated region.
In rostral brainstem and thalamic strokes, hallucinations are vivid, complex, visual, naturalist and scenic. Less frequently they are auditory or combined. They appear during the day or night, and last for minutes. Patients have variable insight and reactive behavior, but sometimes there is a strong emotional reaction of anxiety and fear. Peduncular hallucinosis can recur in a stereotyped manner over weeks. In posterior cerebral artery infarcts, hallucinations are more common after partial occipital lesions. Hallucinations are complex, colored, stereotyped, featuring animal or human figures. They are apparent in the abnormal visual field. They appear in general with a delay of days after the vascular event. The phenomenology of hallucinations does not always reflect the localization of the lesion, because the damaged area may serve as the focus of an abnormally activated neuronal network. Visual hallucinations can be associated with seizures and the EEG may show epilepti-form activity. Visual hallucinations usually resolve spontaneously, but are resistant to treatment.
Auditory hallucinations are much rarer than visual hallucinations and have been reported following right temporal and left dorsomedial thalamic strokes. These auditory hallucinations are transient .
Psychotic disorders due to stroke are rare. Most frequent are visual hallucinations related to rostral brainstem, thalamic and partial occipital lesions.
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