Parkinsonism describes neurological disorders with movement problems resembling Parkinson’s disease, including tremors, muscle stiffness, and slowed movements. Secondary parkinsonism is a specific type caused by an identifiable external factor or another medical condition, rather than a primary neurodegenerative process.
Key Characteristics of Secondary Parkinsonism
Secondary parkinsonism presents with symptoms like tremors, slow movement (bradykinesia), and limb or trunk stiffness. Symptoms often begin symmetrically, affecting both sides of the body equally. Progression can be more rapid or abrupt than in idiopathic Parkinson’s disease. Other neurological signs may include early balance problems, cognitive changes, and eye movement abnormalities. Tremors may be less pronounced or differ from the resting tremor seen in Parkinson’s disease.
Common Causes of Secondary Parkinsonism
Secondary parkinsonism arises from various identifiable factors.
Medication-Induced Parkinsonism
Certain drugs, particularly antipsychotics and anti-nausea medications, can block dopamine receptors in the brain, interfering with dopamine pathways and leading to parkinsonian symptoms. Examples include haloperidol, chlorpromazine, and metoclopramide, which reduce dopamine’s activity in the basal ganglia. Some calcium channel blockers, antidepressants, and anticonvulsants can also induce these symptoms.
Vascular Parkinsonism
Vascular issues are another cause, known as vascular parkinsonism. This occurs when blood flow to brain areas controlling movement is disrupted, often due to small strokes (lacunar infarctions). Conditions like high blood pressure, diabetes, and smoking increase the risk of these cerebrovascular events. Damage from strokes can affect regions like the basal ganglia, leading to symptoms often affecting the lower body, causing gait and balance problems.
Toxin Exposure
Exposure to certain toxins can also lead to secondary parkinsonism. Chemicals like manganese, often from occupational exposure, accumulate in brain regions such as the globus pallidus and striatum, causing neuronal degeneration. Carbon monoxide poisoning can result in delayed encephalopathy and parkinsonism due to brain hypoxia. MPTP, a contaminant in some illicit drugs, specifically damages dopamine-producing neurons in the substantia nigra, closely mimicking Parkinson’s disease.
Other Neurological Conditions
Normal pressure hydrocephalus (NPH), where cerebrospinal fluid accumulates in the brain’s ventricles, can cause gait disturbances, cognitive decline, and urinary problems resembling parkinsonism. Brain tumors, especially those affecting the basal ganglia, can also induce parkinsonian symptoms. Metabolic disorders, such as vitamin B12 deficiency or hypothyroidism, may also present with similar symptoms.
Distinguishing Secondary Parkinsonism from Parkinson’s Disease
Distinguishing secondary parkinsonism from Parkinson’s disease (PD) is important for diagnosis. A primary distinction lies in their origins: secondary parkinsonism has an identifiable external cause (e.g., medication, vascular events, toxins), while PD is largely idiopathic, involving progressive degeneration of dopamine-producing neurons.
Symptom symmetry often provides a clue; secondary parkinsonism commonly presents with symptoms affecting both sides of the body equally from the outset. In contrast, PD typically begins with asymmetrical symptoms, more pronounced on one side. Response to levodopa, a common PD medication, also differs; individuals with secondary parkinsonism often show little to no improvement, unlike those with PD who typically respond well.
Symptom progression can also vary. Secondary parkinsonism may have a more rapid onset or progression, and symptoms might stabilize or improve if the cause is treated. This is generally not the case for the neurodegenerative progression of PD. Associated features like early, prominent balance issues leading to falls, early cognitive decline (dementia within one year of motor symptom onset), or a lack of the characteristic resting tremor, suggest secondary parkinsonism or atypical parkinsonian syndromes.
Diagnosis and Management
Diagnosing secondary parkinsonism begins with a comprehensive medical history, including a detailed review of medications, as drug-induced parkinsonism is common. A thorough neurological examination assesses movement, reflexes, and coordination, helping identify symptom patterns and other neurological signs.
Imaging studies, such as MRI of the brain, are frequently used to identify structural abnormalities like vascular lesions, brain tumors, or normal pressure hydrocephalus. While MRI cannot diagnose Parkinson’s disease, it helps rule out or identify other causes of parkinsonism. A dopamine transporter scan (DaTscan) can further aid differentiation; an abnormal DaTscan suggests dopamine neuron loss (seen in Parkinson’s disease), while a normal DaTscan often points to drug-induced or vascular parkinsonism.
Management focuses on addressing the underlying cause. For medication-induced parkinsonism, discontinuing the offending drug or switching to an alternative is the first step, often leading to symptom reduction or resolution over weeks to months.
For vascular parkinsonism, managing risk factors like high blood pressure and diabetes is important to prevent further strokes. If a brain tumor is present, surgical removal may improve symptoms. For normal pressure hydrocephalus, surgical shunt placement can alleviate symptoms. If the underlying cause cannot be fully eliminated, symptomatic treatments, including medications or physical therapy, can manage movement difficulties.