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The Distortion of Consciousness
Published in Max R. Bennett, The Idea of Consciousness, 2020
What are the side effects of these antipsychotic drugs, or neuroleptics as they are now called? The most obvious of them are movements characteristic of those with Parkinsonian disorders, such as tremor of the limbs. The suggestion that chlorpromazine and haloperidol are catecholamine receptor molecule blockers was a major breakthrough10. The idea was that the neuroleptics act at synapses by occupying sites, called receptors, on the membrane of neurons opposite nerve terminals which release substances like norepinephrine and dopamine; this action blocks the ability of these catecholamines to bind to the membrane receptors of the neurons during synaptic transmission, and so they are referred to as receptor molecule blockers. Anden and his colleagues finally showed in 1970 that the neuroleptics are dopamine receptor molecule blockers. This observation provided the key to the explanation of why the neuroleptics produce the Parkinsonian syndrome as a side effect to their antipsychotic action. The Parkinsonian condition arises as a consequence of the neuroleptics blocking the dopaminergic projection from the substantia nigra in the midbrain to the basal ganglia (Figure 5.6A and S.6C), a condition that is known to give rise to the Parkinsonian syndrome. Most importantly, the various components of the schizophrenic syndrome enumerated above, such as hallucinations, avolitional changes and negative affect, that point to failure of neural networks in the cingulate cortex, frontal cortex as well as the amygdala and hippocampus, can all be considered to arise as a consequence of the excessive action of dopamine. This transmitter is released from the nerve terminals of the dopaminergic neurons in the ventral tegmentum that end in diese parts of the cortex and hippocampus (Figure 5.6A and S.6B). The action of drugs, such as chlorpromazine and haloperidol, to block the action of dopamine released from the terminals of the ventral tegmentum then alleviates these symptoms of the schizophrenic syndrome. In addition, the ventral striatum of the basal ganglia projects to the cingulate cortex (Figure 5.6A). Excess dopaminergic transmission from the substantia nigra to the basal ganglia (Figure 5.6C) can lead to profound changes in the workings of the neural networks in the cingulate cortex, with all the implications for the pathological release of behavior associated with schizophrenia.
Unmet needs in the diagnosis and treatment of Parkinson’s disease psychosis and dementia-related psychosis
Published in International Journal of Psychiatry in Clinical Practice, 2023
Marwan Sabbagh, Gary W. Small, Stuart H. Isaacson, Yasar Torres-Yaghi, Fernando Pagan, Rajesh Pahwa
In addition, there is a lack of evidence to support the use of quetiapine in the treatment of DRP (Seppi et al., 2019). A systematic review of seven randomised controlled trials on the role of quetiapine in the treatment of psychosis in Parkinson’s disease, Lewy body dementia, or any other neurodegenerative parkinsonian disorders demonstrated that quetiapine did not demonstrate significant efficacy over placebo (Desmarais et al., 2016). In another double-blind, placebo-controlled trial, quetiapine was evaluated for efficacy in the treatment of Alzheimer’s disease. The results showed that quetiapine was possibly safe, and also did not demonstrate efficacy over placebo (Ballard et al., 2005). Adverse effects of quetiapine due to off-target receptor affinity can limit its utility in the elderly with neurodegenerative dementia, including somnolence, constipation, and orthostatic hypotension (AstraZeneca Pharmaceuticals LP, 2003; Xu et al., 2021).
Early recognition and diagnosis of multiple system atrophy: best practice and emerging concepts
Published in Expert Review of Neurotherapeutics, 2021
Luca Marsili, Giulia Giannini, Pietro Cortelli, Carlo Colosimo
Consensus criteria for clinically possible and probable MSA have been developed to assist clinicians with the diagnosis [1]. Despite this set of criteria, its diagnostic accuracy is still relatively low [16–18], and several novel ancillary investigations have been proposed to help in the diagnostic process. A large clinicopathological study on 203 MSA patients documented accuracy of diagnosis during lifetime of 78.8% against neuropathologically established diagnosis (n = 160/203), revealing an alternative pathological diagnosis in the remaining 21.2% (n = 43) patients [19]. The differential diagnosis with PD and other conditions belonging to the group of atypical parkinsonian disorders (APD) (mainly progressive supranuclear palsy – PSP, and corticobasal degeneration, CBD) from one side, and with idiopathic late-onset cerebellar ataxias (ILOCA) from the other side might be difficult, particularly in the early phases of the disease [2]. Regardless of the predominant motor features, MSA clinical spectrum also includes various non-motor symptoms that may precede motor symptoms for several years [20–25].
Smell tests to distinguish Parkinson’s disease from other neurological disorders: a systematic review and meta-analysis
Published in Expert Review of Neurotherapeutics, 2021
Cintia C. G. Alonso, Fernanda G. Silva, Leonardo O. P. Costa, Sandra M. S. F. Freitas
Smell impairments have been reported on a wide range of neurological conditions such as Alzheimer’s disease, dementia with Lewy bodies, multiple system atrophy, and Huntington’s disease [9]. Therefore, it remains to be quantified which tests used to assess olfactory function can distinguish PD when compared to other neurological disorders. We aimed to identify the tests that have been used to assess the olfactory function in PD and to examine the ability of them to distinguish individuals with PD from those with other neurological disorders. Although we expected that most studies would compare PD with other parkinsonian disorders, in order to have a full knowledge of the available findings, restrictions to the smell tests and the neurological disorders during searches were not applied. Hence, in this systematic review, we searched cross-sectional studies that compared the scores obtained in any smell test of individuals with PD and other neurological disorders.