Other causes of Parkinsonism
Drug-induced Parkinsonism
Drugs that block dopamine receptors and dopamine transmission can cause secondary drug-induced parkinsonism (DIP). The decrease in dopamine causes a denervation of the D1 and D2 receptors in the nigrostriatal pathway.
The dopamine antagonists that can cause DIP are:
- Antipsychotics such as fluphenazine, haloperidol, paliperidone, and risperidone
- Dopaminergic anti-emetics – such as metoclopramide, domperidone, and prochlorperazine
- Sodium valproate
The main difference in the presentation of DIP vs PD is the symmetrical and generalised tremor, rigidity and bradykinesia seen in DIP.
The most ideal treatment is to stop the causative drug. For psychiatric conditions, this might not be possible. In this case, the treatment for DIP is as follows:
- First line – anticholinergics – benztropine and trihexyphenidyl.
- Second line – amantadine.
Vascular Parkinsonism
Vascular parkinsonism (VP) is due to microangiopathy and lacunar infarcts affecting the basal ganglia, thalamus or the putaminal-pallido outflow.
Patients with VP present with:
- Parkinsonian-ataxic wide-based gait
- Dysphagia
- Dysarthria
- Hypertonia, brisk reflexes, and extensor plantar reflexes
MRI head can show white matter and periventricular hyperdensities.
The treatment for VP is levodopa for parkinsonism and antiplatelets for secondary prevention.
Chronic Traumatic Encephalopathy
Chronic traumatic encephalopathy (CTE) occurs as a result of repetitive head trauma, usually from repetitive subconcussive blows and repetitive concussions. It commonly affects professional athletes in contact sports but also ex-soldiers and domestic violence victims. This trauma causes accumulation of tau and periventricular astrocytic tangles.
Much later in life, those affected develop CTE, which presents as a mixture of parkinsonism and dementia. Unfortunately, CTE can only be definitively diagnosed at post-mortem. There is currently no specific treatment for CTE. However, preventing head trauma with protective equipment and treating traumatic brain injury well might help prevent CTE.
Toxin-induced Parkinsonism
Toxin-induced parkinsonism (TIP) is caused by prolonged exposure to certain toxins that damage dopaminergic neurons. This presents as cogwheel rigidity, bradykinesia and falling when walking backwards.
Causative toxins are:
- Manganese
- Copper
- Mercury
- MPTP – by-product of incorrectly made synthetic heroin
Wilson’s Disease
Wilson’s disease (WD) is an autosomal recessive disorder of copper metabolism from a lack of caeruloplasmin. Caeruloplasmin is the transporter protein of copper and removes excess copper. WD causes an accumulation of copper, especially in the liver and CNS.
The symptoms of WD are:
- Kayser–Fleischer rings
- Liver failure and coagulopathy
- Haemolytic anaemia – result of copper accumulation
- Parkinsonism
The following tests can aid diagnosis of WD:
- Deranged liver function tests
- Low caeruloplasmin levels
- Liver biopsy – raised copper concentration
- Genetic testing
The treatment of WD, including copper chelating medicines, is:
- D-penicillamine –– prevents and repairs the effects of copper overload.
- Trientine
- Zinc acetate – stops copper gut absorption.
- Low copper diet
These treatments can reverse the toxin-induced Parkinsonism seen in WD.
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