Descriptive Psychopathology: The Signs and Symptoms of ...

81 Chapter 3: The brain and psychopathologyexample, are lost. Finally, although the clinicopathological neurologic literatureoffers the clearest picture of the neurobiology of delusions, sample sizes are smalland the form of the delusions studied are also not commonly detailed.One theme throughout the clinicopathological literature, however, is that primarydelusions are associated with lesions or dysfunction in the non-dominantcerebral hemisphere. MacDonald Critchley’s patients with parietal lobe diseaseand delusions cited above demonstrate the association. Many case studies usingdifferent strategies (EEG, functional imaging, and lesion localization) haveconfirmed the correlation, 164 particularly for misidentification delusions. 165For example, in 35 reported cases with imaging findings, 20 had right-sidedand 15 bilateral lesions. Twenty-one were in the frontal and 13 in the temporallobe. 166 In a study of 55 patients with Alzheimer’s disease, Lee et al. (2004)reported bilateral abnormalities associated with delusional misidentification. 167A right-sided brain lesion or dysfunction is a common factor for manydelusions of misidentification to develop. 168 In Capgras and Fregoli syndromes(delusions of impostors and false identification, respectively), poor facial recognition(temporal–parietal), an inability in self-assessment (frontal) and symptomrecognition (anosagnosia) characterize the process, the patient unable to properlymatch a facial misperception with facial memory. 169The process by which a lesion in the non-dominant prefrontal or posterior–inferior parietal cortex elicits a delusion is unknown. Several psychologicaltheories are offered to explain persecutory delusions, but these do not considerthe clinicopathological findings implicating the right hemisphere, focusinginstead on fragmented views of putative psychological processes in schizophrenia.170 The conclusions of these studies are not warranted. For example, thetheory of attentional bias to threat and hypervigilance as the cause of persecutorydelusions is unsatisfactory, as hypervigilance could just as readily be the result ofa persecutory delusion rather than its cause. 171 The idea that attribution biaselicits persecutory delusions fails for the same reason. The hypothesis is based onstudies that report schizophrenic patients with persecutory delusions and patientswith delusional disorder excessively attribute hypothetical positive events tointernal self-generated influences (“its due to me”) and hypothetical negativeevents to external causes (“its due to them”). Patients with other kinds ofdelusional content are reported to not show such attribution bias. 172 But thepersecutory delusional state could just as well account for the attribution ratherthan the other way around. Another theory states that deluded patients morereadily jump to conclusions than do non-deluded patients. 173 This idea fits thelong-accepted notion that arbitrary thinking is the basis for delusions of anycontent and does not advance the understanding of delusional pathophysiology.Finally, “the theory of the mind” concept invokes the idea that humans naturally