• RESEARCH 4 BUSINESS 2016, Ljubljana, 5 and 6 of May 2016

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    Present, past, and future in patients with migraine, sildenafil low cost epilepsy, temporal lobe hemorrhage, and brain tumors. There is no synthesis across methods and technologies used, the diagnoses of the patients studied, and important clinical features such as chronicity. Stimulation of temporal–limbic areas184 in epileptic patients elicits these hallucinations. Olfactory hallucinations are also seen in patients with schizophrenia, depressive illness, and eating disorder.226 Delusions237 There are no systematic studies assessing brain structural and functional neuroimaging in persons with delusions, and the meager findings are inconsistent.

    The brain areas responsible for olfaction and touch may also be involved.205 Olfactory hallucinations have been reported 80 Section 1. Many studies do not differentiate between delusions and hallucinations, and lump them together as “psychotic features”.218 The only consistent finding is that delusional patients have disturbances in frontal–temporal–limbic networks.159 This is neurologically consistent with the delineated phases of delusions (see Chapter 10), but non-specific as many forms of psychopathology are associated with dysfunction in these brain regions.

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    A. L., & Lewis, D. Hemispheric differences in layer III pyramidal neurons of the anterior language area.

    Archives of Neurology, 50, 531–545. Anatomical specialization of the anterior motor speech area.

  • The central serotoninergic deficiency may be implicated in cognitive processes sildenafil low cost. The decrease was greater in the hippocampus and frontal cortex. Cortical Lesions Alterations of neurons in the cerebral cortex (i.e., diffuse Lewy body inclusions and AD-like histological changes) probably occur in most PD dementia cases, suggesting that intrinsic cortical pathology may account for some of the cognitive deficits and behavioral features. It seems, however, that, like the noradrenergic deficiency, the serotoninergic deficit is more likely to be implicated in depressive states in patients with PD. Examples include loss of neurons both in the basal ganglia, as suggested by the dysfunction of various peptidergic and amino acid–containing neurons and in the brainstem, where cell loss in the pedunculopontine tegmental nucleus has been Parkinson’s Disease and Dementia 533 found in some patients.

    Dysfunction of other neuronal circuitry also may be implicated directly or indirectly in the genesis of cognitive symptomatology in PD, in addition to massive involvement of the nigrostriatal dopaminergic pathway and partial degeneration of the long ascending subcorticocortical systems. 4-HIAA (8-hydroxyindoleacetic acid) concentrations in the CSF are lower in depressed patients with PD than in the others (Mayeux, Stern, Cote, & Williams, 1985), and imipramine-like drugs, which are inhibitors of serotonin uptake, have significant antidepressant activity in patients with PD. No difference between patients with and without dementia was observed.

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    CRF has been shown to be increased during withdrawal from chronic administration of other major drugs of abuse, including cocaine, ethanol, and cannabinoids (Baldwin et al., 1987. NAChR mRNA has been located in neurons throughout the rat amygdala, including the central nucleus of the amygdala (Wada et al., 1989), indicating potential functional nAChRs within these areas.

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    NIDA Research Monograph, vol. H.