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

Linda Nichols
Linda Nichols
 e 
Jane Alty
Jane Alty
   | 01 giu 2024
Australasian Journal of Neuroscience's Cover Image
INFORMAZIONI SU QUESTO ARTICOLO
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Pubblicato online: 01 giu 2024
Pagine: 49 - 63
DOI: https://doi.org/10.21307/ajon-2024-006
© 2024 Dr. Linda Nichols et al., published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

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 disorders Other conditions
Parkinson’s disease Vascular parkinsonism
Progressive Supranuclear Palsy Functional neurological disorder
Multisystem Atrophy Hyperthyroidism
Corticobasal Syndrome Benzodiazepine withdrawal
Dementia with Lewy bodies Infective and autoimmune encephalitis

Differentiating features of Parkinson’s disease and DIP

Feature Parkinson’s Disease Drug Induced Parkinsonism (DIP)
Age of Onset Sixth decade (but 20% are <50 years old) Variable
Sex More common in males Uncertain
Onset Chronic Acute or subacute
Symptom Onset Unilateral or asymmetric Bilateral and symmetric
Akathisia Absent Present
Bradykinesia Present Present
Tremor Rest tremor occurs in 70% Usually absent or a postural tremor
Rigidity Progressive and may be marked Usually mild
Response to Levodopa Good Poor
Response to stopping D2 blocking drug Slight non-sustained improvement then progressive parkinsonism Good with complete reversal of parkinsonism
DaTscan/VMAT scan Abnormal: Reduced uptake of pre-synaptic markers Normal

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 Antipsychotics Chlorpromazine, Prochlorperazine, Promethazine, Fluphenazine, Haloperidol, Primozide, Sulpiride
Atypical Antipsychotics Olanzapine, Risperidone, Ziprasidone, Aripiparazole, Clozapine, Quetiapine
Anti-emetics Metoclopramide, Domperidone, Itopride
Dopamine Depleters Reserpine, Tetrabenazine
Calcium-Channel Blockers Flunarizine, Cinnarizine
Pharmaceutical Agents Less Frequently Associated with DIP
Mood Stabilizers Lithium Carbonate
Antiepileptics Valproic acid, Phenytoin, Levetiracetam
Anti-hypertensives Diltiazem
Antidepressants Paroxetine, Sertraline, Fluoxetine
Antiarrhythmics Amiodarone, Procaine
Statins Lovastatin
Immunosuppressants Ciclosporin, Tacrolimus
Antivirals Acyclovir, Vidarabine
Antibacterials Sulfamethoxazole, Trimethoprim
Antifungals Amphotericin B
eISSN:
2208-6781
Lingua:
Inglese
Frequenza di pubblicazione:
2 volte all'anno
Argomenti della rivista:
Medicine, Basic Medical Science, other
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