Neuroleptic-induced parkinsonism is associated with olfactory dysfunction

Krüger, Stephanie; Haehner, Antje; Thiem, Claudia; Hummel, Thomas

doi:10.1007/s00415-008-0993-5

Cited by 34 publications

(26 citation statements)

References 38 publications

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“…The findings of present study suggest that smell deficits in DIP patients are more related to PD-like neurodegeneration rather than to a simple functional D2 receptor blockade, as hypothesized by Krueger et al [14]. Neurodegeneration in PD involves not only the dopaminergic nigrostriatal neurons, but also additional extrastriatal domains, potentially contributing to the spectrum of nonmotor symptoms [5].…”

Section: Discussionsupporting

confidence: 63%

“…Krueger et al [14] used the Sniffin' Sticks test to investigate olfactory function in depressed patients treated with neuroleptic (NL) drugs and developing DIP (n = 15), depressed patients treated with neuroleptics but without DIP (no-DIP patients; n = 44), and depressed neuroleptic-naïve controls (no-NL patients; n = 20). The 15 patients with DIP had significantly lower olfactory scores than the no-DIP patients and the no-NL patients.…”

Section: Discussionmentioning

confidence: 99%

“…Current evidence suggests some olfactory impairment in depressed DIP patients, which was attributed to the functional blockade of D2 receptors rather than to dysfunction of the nigrostriatal system [14]. Another study showed an olfactory function similar to that of control subjects, even if the only DIP patient with reduced smell capacity had decreased iodine-131-meta-iodo-benzyl-guanidine (MIBG) cardiac uptake (a marker of neurodegeneration in PD) [15].…”

Section: Introductionmentioning

confidence: 99%

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The status of olfactory function and the striatal dopaminergic system in drug-induced parkinsonism

et al. 2010

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Olfactory impairment has been reported in drug-induced parkinsonism (DIP), but the relationship between dopaminergic dysfunction and smell deficits in DIP patients has not been characterized. To this end, we studied 16 DIP patients and 13 patients affected by Parkinson's disease (PD) using the "Sniffin' Sticks" test and [(123)I] FP-CIT SPECT (single-photon emission computed tomography). DIP patients were divided based on normal (n = 9) and abnormal (n = 7) putamen dopamine transporter binding. Nineteen healthy age- and sex-matched subjects served as controls of smell function. Patients with DIP and pathological putamen uptake had abnormal olfactory function. In this group of patients, olfactory TDI scores (odor threshold, discrimination and identification) correlated significantly with putamen uptake values, as observed in PD patients. By contrast, DIP patients with normal putamen uptake showed odor functions-with the exception of the threshold subtest-similar to control subjects. In this group of patients, no significant correlation was observed between olfactory TDI scores and putamen uptake values. The results of our study suggest that the presence of smell deficits in DIP patients might be more associated with dopaminergic loss rather than with a drug-mediated dopamine receptor blockade. These preliminary results might have prognostic and therapeutic implications, as abnormalities in these individuals may be suggestive of an underlying PD-like neurodegenerative process.

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The status of olfactory function and the striatal dopaminergic system in drug-induced parkinsonism

et al. 2010

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“…Considered from the “flip-side” perspective, the neuroleptic drugs used to treat psychosis dampen down dopamine signaling and, as a consequence, tend to foster symptoms of Parkinsonism, as well as obesity, in some vulnerable individuals [132, 133]. There is also a close relationship between psychotic disorders and a host of addictions such as to cigarette smoking, alcoholism, and opiate abuse [134–136].…”

Section: The Modern Food Environmentmentioning

confidence: 99%

From Passive Overeating to “Food Addiction”: A Spectrum of Compulsion and Severity

2013

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A psychobiological dimension of eating behaviour is proposed, which is anchored at the low end by energy intake that is relatively well matched to energy output and is reflected by a stable body mass index (BMI) in the healthy range. Further along the continuum are increasing degrees of overeating (and BMI) characterized by more severe and more compulsive ingestive behaviours. In light of the many similarities between chronic binge eating and drug abuse, several authorities have adopted the perspective that an apparent dependence on highly palatable food—accompanied by emotional and social distress—can be best conceptualized as an addiction disorder. Therefore, this review also considers the overlapping symptoms and characteristics of binge eating disorder (BED) and models of food addiction, both in preclinical animal studies and in human research. It also presents this work in the context of the modern and “toxic” food environment and therein the ubiquitous triggers for over-consumption. We complete the review by providing evidence that what we have come to call “food addiction” may simply be a more acute and pathologically dense form of BED.

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“…Olfactory function is reported to be normal in drug induced parkinsonism in some studies38 but not in others,39 whereas olfactory dysfunction is common in Parkinson’s disease.…”

Section: Managementmentioning

confidence: 99%

Drug induced parkinsonism: a common cause of parkinsonism in older people

Thanvi

Treadwell

2009

Postgraduate Medical Journal

125

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Drug induced parkinsonism is the second most common cause of parkinsonism in older people after idiopathic Parkinson's disease (PD). Risk factors for developing drug induced parkinsonism include: older age; female gender; dose and duration of treatment; type of agent used; cognitive impairment; acquired immunodeficiency syndrome (AIDS); tardive dyskinesia; and pre-existing extrapyramidal disorder. In most patients parkinsonism is reversible upon stopping the offending drug, though it may take several months to resolve fully and in some patients it may even persist. In this case, one needs to consider the possibility of PD which has been unmasked by the offending drug, and treatment with dopaminergic agents may be warranted. Drug induced parkinsonism adversely affects the quality of life in older patients and is potentially reversible, highlighting the importance of early recognition of this condition. This article discusses the drugs implicated, as well as the epidemiology, pathophysiology, clinical features, and management of drug induced parkinsonism.

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Neuroleptic-induced parkinsonism is associated with olfactory dysfunction

Cited by 34 publications

References 38 publications

The status of olfactory function and the striatal dopaminergic system in drug-induced parkinsonism

The status of olfactory function and the striatal dopaminergic system in drug-induced parkinsonism

From Passive Overeating to “Food Addiction”: A Spectrum of Compulsion and Severity

Drug induced parkinsonism: a common cause of parkinsonism in older people

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