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Identifying and Managing Drug Induced Parkinsonism: The Role of Neuroscience Nurses Cover

Identifying and Managing Drug Induced Parkinsonism: The Role of Neuroscience Nurses

By: Linda Nichols and  Jane Alty  
Open Access
|Jun 2024

Figures & Tables

Figure 1:

A schematic of dopaminergic neurons in the striatum.
A schematic of dopaminergic neurons in the striatum.

Figure 2.

DaTscan (FP-CIT SPECT): the images demonstrate the density of pre-synaptic dopaminergic neurons in the striatum. In the healthy state and in drug-induced parkinsonism, there is no loss of pre-synaptic dopaminergic neurons, and the striatum is a normal ‘comma’ shape. In Parkinson’s disease (and some other degenerative disorders), there is a loss of pre-synaptic dopaminergic neurons in the putamen (white arrow) and the striatum looks like a “full stop” shape. Later in the disease, with further progressive degeneration, the ‘full stop’ shape also disappears.
DaTscan (FP-CIT SPECT): the images demonstrate the density of pre-synaptic dopaminergic neurons in the striatum. In the healthy state and in drug-induced parkinsonism, there is no loss of pre-synaptic dopaminergic neurons, and the striatum is a normal ‘comma’ shape. In Parkinson’s disease (and some other degenerative disorders), there is a loss of pre-synaptic dopaminergic neurons in the putamen (white arrow) and the striatum looks like a “full stop” shape. Later in the disease, with further progressive degeneration, the ‘full stop’ shape also disappears.

Differential diagnoses of DIP

Neurodegenerative disordersOther conditions
Parkinson’s diseaseVascular parkinsonism
Progressive Supranuclear PalsyFunctional neurological disorder
Multisystem AtrophyHyperthyroidism
Corticobasal SyndromeBenzodiazepine withdrawal
Dementia with Lewy bodiesInfective and autoimmune encephalitis

Differentiating features of Parkinson’s disease and DIP

FeatureParkinson’s DiseaseDrug Induced Parkinsonism (DIP)
Age of OnsetSixth decade (but 20% are <50 years old)Variable
SexMore common in malesUncertain
OnsetChronicAcute or subacute
Symptom OnsetUnilateral or asymmetricBilateral and symmetric
AkathisiaAbsentPresent
BradykinesiaPresentPresent
TremorRest tremor occurs in 70%Usually absent or a postural tremor
RigidityProgressive and may be markedUsually mild
Response to LevodopaGoodPoor
Response to stopping D2 blocking drugSlight non-sustained improvement then progressive parkinsonismGood with complete reversal of parkinsonism
DaTscan/VMAT scanAbnormal: Reduced uptake of pre-synaptic markersNormal

Guide to the Diagnostic Approach to Suspected DIP

No previous history of parkinsonism before the prescription of the offending drug.
Review medical history including past and present medications, assessing for potentiation, polypharmacy and potential drug interactions.
Consider possible exposure to toxins or recreational drugs.
Individuals with AIDS have an increased risk of DIP due to loss of neuronal cell bodies.
Consider the individual’s age as Parkinson’s disease is less likely in individuals younger than 50 years.
Review falls in combination with psychotropic administration as medications can lower blood pressure and increase the risk of falls in confused or at-risk patients.
Review the timeframes associated with the onset of symptoms (usually acute or subacute with DIP). DIP has a temporal relationship with new medications and can occur within days of commencing a new drug, although in some cases it may be months prior to the onset of symptoms.
Assess for signs and symptoms that are inconsistent with DIP including unilateral symptoms, significant axial impairment, freezing gait, hyposmia, or tremor.
DIP is generally characterised as bilateral and symmetric parkinsonism.
Response to levodopa is limited in DIP, yet diagnostically useful in Parkinson’s disease.
Consider DaT scan, single proton emission computerized tomography (SPECT) particularly in cases where symptoms have not resolved within six months of ceasing offending drugs.
Consider a comorbid or alternative diagnosis.

Drug classes and pharmaceutical agents associated with DIP

Pharmaceutical Agents Frequently Associated with DIP
Typical AntipsychoticsChlorpromazine, Prochlorperazine, Promethazine, Fluphenazine, Haloperidol, Primozide, Sulpiride
Atypical AntipsychoticsOlanzapine, Risperidone, Ziprasidone, Aripiparazole, Clozapine, Quetiapine
Anti-emeticsMetoclopramide, Domperidone, Itopride
Dopamine DepletersReserpine, Tetrabenazine
Calcium-Channel BlockersFlunarizine, Cinnarizine
Pharmaceutical Agents Less Frequently Associated with DIP
Mood StabilizersLithium Carbonate
AntiepilepticsValproic acid, Phenytoin, Levetiracetam
Anti-hypertensivesDiltiazem
AntidepressantsParoxetine, Sertraline, Fluoxetine
AntiarrhythmicsAmiodarone, Procaine
StatinsLovastatin
ImmunosuppressantsCiclosporin, Tacrolimus
AntiviralsAcyclovir, Vidarabine
AntibacterialsSulfamethoxazole, Trimethoprim
AntifungalsAmphotericin B
DOI: https://doi.org/10.21307/ajon-2024-006 | Journal eISSN: 2208-6781 | Journal ISSN: 1032-335X
Language: English
Page range: 49 - 63
Published on: Jun 1, 2024
In partnership with: Paradigm Publishing Services
Publication frequency: 2 issues per year

© 2024 Linda Nichols, Jane Alty, published by Australasian Neuroscience Nurses Association
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.