Levodopa treatment Levodopa, also known as L-DOPA, is the precursor to several catecholamines, specifically of dopamine, epinephrine and norepinephrine. It is clinically used to treat Parkinson's disease and dopamine-responsive dystonia. Clinical studies have shown that the use of levodopa can lead to visual hallucinations and<unk> s. In most patients,<unk> s were more salient than hallucinations. With prolonged use of levodopa, the<unk> s occupy almost all of a patient's attention. In experimental studies, when the concentration of levodopa decreases, the number of reported<unk> s decreases as well. It has been concluded that<unk> s related to antiparkinsonian medications are one of the leading causes of<unk>  syndrome. Traumatic brain injury Injury to the right frontal and left temporo-parietal areas can cause<unk>  syndrome. Research by Feinberg, et al. has shown that significant deficits in executive and memory functions follow shortly after damage in the right frontal or left temporoparietal areas. Tests performed on patients that have suffered from a brain injury revealed that basic attention ability and visuomotor processing speed are typically normal. However, these patients made many errors when they were called to participate in detailed attention tasks. Selective attention tests involving auditory targets were also performed, and brain-injured patients had many errors; this meant that they were deficient in their response regulation and inhibition. The most profound finding in Feinberg et al.'s paper is that performance tests on the retrieval process of memory was significantly damaged in brain-injured patients. They found, however, that these patients chose incorrect answers that were related semantically (i.e., chose vegetable instead of fruit). More importantly, tests of visual memory showed that there was a severe inability in visual recollection. Overall, brain-injured patients were severely impaired in many executive functions such as self-monitoring, mental flexibility, and social reasoning.<unk>  syndrome is an illusion of positive doubles where there is an over-familiarity with the environment. This over-familiarity may have four causes: * impaired self monitoring — passive acceptance of inaccurate conclusions * faulty filtering — tendency to select salient associations rather than a relevant one * mnemonic association from routine thoughts * perseveration — unable to come up with an alternate hypothesis Thus, executive dysfunction appears to be necessary to identify one as having<unk> 's syndrome. Fusiform gyrus Current research has shown that lesions in the right temporal lobe and the fusiform gyrus may contribute to DMSs. MRIs of patients exemplifying<unk>  symptoms have shown parahippocampal and hippocampal damage in the anterior fusiform gyrus, as well as the middle and inferior of the right temporal gyri. The inferior and medial of the right temporal gyri are the storage locations for long-term memory in retrieving information on visual recognition, specifically of faces; thus, damage to these intricate connections could be one of the leading factors in face misidentification disorders. Recently, a face-specific area in the fusiform gyrus has been discovered and is close to the anterior fusiform gyrus. MRI studies performed by Hudson, et al. have shown lesions in the anterior fusiform gyrus, which is close to the face specific area (ventral fusiform cortex), may also be associated with<unk>  syndrome and other DMSs. Such damage may cause disruption in long-term visual memory and lead to improper associations of human faces. On another note, our brains interpret visual scenes in two pathways: one is via the Parietal lobe-occipital dorsal pathway (visual spatial material is analyzed here), and the other is via the temporal-occipital ventral pathway (recognizes objects and faces). Thus, lesions in either structures or disruption of delicate connections may produce DMSs. Abnormal P300<unk> al misidentification syndrome is thought to occur due to a dissociation between identification and recognition processes. The integration of information for further processing is referred to as working memory (WM). The P300 (P stands for positive voltage potential and the 300 for the 300-millisecond poststimulus) is an index of WM and is used during a WM test in DMS patients. In comparison to normal patients, DMS patients generally exhibit an attenuated amplitude of P300 at many abductions. These patients also exhibit prolonged latencies of P300 at all abductions. These implications suggest that DMSs are accompanied by abnormal WM, specifically affecting the prefrontal cortex (both outside and inside). Past studies have shown correlations between DMS and damages to the right-hemispheric function, which has an array of functions (insight, 3D shapes, art awareness, imagination, left-hand control, music awareness, etc.). In recent years, the P300 auditory component, which forms in response to a detection task that occurs a short time after a stimulus, has acquired a great deal of recognition. The P300 component is an index of mental activity in that its amplitude increases highly with increased stimuli. This P300 component is correlated with updating the working memory to what is expected in the environment. Other findings enhance the belief that defects in the working memory are associated with DMS. Papageorgio et al.'s paper, psychological evidence for altered information processing in<unk> al misidentification syndromes, hypothesized that electrophysiological brain activity in the working memory and P300 component can help identify the mechanisms of DMS. Thus, they concentrated on P300 released during a working memory test in DMS patients. Papageorgio et al. also found that DMS patients had a lower P300 amplitude in the right hemisphere compared to the control group (non-DMS patients). From this result, the researchers implied that shorter P300 amplitudes are highly correlated with gray matter abnormalities; this finding is consistent with the DMS patients' characteristics and the presence of gray-matter deterioration. DMS patients were also found to have prolonged P300 lag, and their memory performance was lower than the control groups. The researchers were, thus, able to imply that DMS patients have trouble in focusing their resources to a stimulus; this was hypothesized to be caused by the neurodegeneration of the right hemisphere. Overall, other research studies have also provided evidence in the correlation of DMS and gray-matter degeneration of the right frontal region, which controls attentional resources. This research is important, because it can help determine the mechanisms of DMS, which can then help conjure a more effective target drug and/or treatment plan for those suffering from DMS.
Fregoli delusion
Cotard delusion
Capgras delusion
Visual hallucinations in psychosis
Gemütlose psychopathy
Monothematic delusion
Unitary psychosis
Peduncular hallucinosis