Secondary parkinsonism encompasses a group of disorders presenting with symptoms that mimic Parkinson’s disease, such as tremors and slowed movement. Unlike idiopathic Parkinson’s disease, where the origin is unknown, secondary parkinsonism results from identifiable causes. This distinction is important, as management and recovery are linked to the underlying factor affecting the brain’s movement control systems.
Differentiating Symptoms and Presentation
While the signs of secondary parkinsonism resemble Parkinson’s disease, there are subtle differences in presentation. A key distinction is the pattern of symptom onset. Secondary parkinsonism frequently begins symmetrically, affecting both sides of the body simultaneously, whereas idiopathic Parkinson’s starts on one side before gradually progressing to the other. This bilateral start is a clinical clue.
Another differentiating feature is the early emergence of balance problems and falls. People with secondary parkinsonism may experience postural instability early in the course of the condition, a symptom that appears much later in those with idiopathic Parkinson’s. Additionally, the classic resting tremor may be less prominent or entirely absent. Instead, movements are characterized by general slowness, known as bradykinesia, and muscle stiffness.
The clinical picture may also include “atypical” signs. These can include early cognitive changes, dementia, or difficulties with eye movements. The presence of these symptoms helps guide neurologists away from a diagnosis of idiopathic Parkinson’s and toward an investigation for an underlying cause.
Identifiable Causes and Triggers
The causes of secondary parkinsonism interfere with the dopamine pathways responsible for smooth, controlled muscle movement. Understanding these triggers is part of diagnosis and management.
Drug-Induced Parkinsonism
One of the most common forms of secondary parkinsonism is a side effect of certain medications. This occurs when drugs block dopamine receptors in the brain, mimicking the dopamine deficiency seen in Parkinson’s disease. Antipsychotic medications, particularly older ones, are frequent culprits. Certain anti-nausea drugs and some calcium channel blockers can also induce these symptoms. The symptoms usually appear on both sides of the body and may resolve slowly after the offending medication is discontinued.
Vascular Parkinsonism
This form results from cerebrovascular disease, where multiple small strokes damage brain tissue in areas that control movement, such as the basal ganglia. The cumulative effect of these minor strokes, which can go unnoticed individually, disrupts the brain’s motor circuits. Vascular parkinsonism often presents as “lower body parkinsonism,” primarily affecting gait and balance. Individuals may have a shuffling walk and be prone to falls, with less prominent tremor in the upper limbs compared to idiopathic Parkinson’s.
Toxin-Induced Parkinsonism
Exposure to specific environmental or industrial toxins can lead to parkinsonian symptoms by destroying dopamine-producing neurons. Implicated substances include:
- Chronic exposure to manganese, a metal used in welding and steel production.
- Carbon monoxide.
- Cyanide.
- Certain pesticides.
- MPTP, a contaminant found in some illicit drugs that caused severe and permanent parkinsonism.
Other Neurological Conditions
Secondary parkinsonism can also be a feature of other neurological disorders. Normal Pressure Hydrocephalus (NPH) is a condition involving a buildup of cerebrospinal fluid in the brain’s ventricles, which can lead to difficulty walking, cognitive impairment, and urinary incontinence. Brain tumors, particularly those located in or near the basal ganglia, can compress these structures and produce parkinsonian signs. Repeated head trauma, such as that experienced by boxers, can also cause brain damage that manifests with these symptoms.
The Diagnostic Process
Diagnosing secondary parkinsonism is a process of exclusion aimed at identifying an underlying cause. The process begins with a detailed review of the patient’s medical history. A clinician will examine the individual’s current and past medications for any drugs known to induce parkinsonian symptoms and ask about occupational or environmental exposures to potential toxins.
A neurological examination is then performed to assess the specific characteristics of the symptoms. The physician will observe the person’s posture, gait, and movements, looking for signs that point away from idiopathic Parkinson’s. This clinical evaluation helps differentiate the condition from other movement disorders.
Brain imaging helps identify structural causes. A magnetic resonance imaging (MRI) or computed tomography (CT) scan can reveal evidence of strokes, brain tumors, or the enlarged ventricles characteristic of Normal Pressure Hydrocephalus.
In some cases, a specialized imaging test called a dopamine transporter scan (DaTscan) may be used. This scan visualizes the dopamine system in the brain. While it cannot distinguish between different types of parkinsonism, it can help differentiate parkinsonian syndromes from other conditions that cause tremor. A poor response to a trial of levodopa, the primary medication for Parkinson’s disease, is another indicator that the symptoms may stem from a secondary cause.
Treatment Approaches and Prognosis
The management strategy for secondary parkinsonism targets the underlying cause. When possible, removing the trigger is the primary goal. For instance, in cases of drug-induced parkinsonism, discontinuing the responsible medication under a doctor’s guidance can lead to a significant improvement or even complete resolution of symptoms, although this process can take months.
When the cause is not reversible, such as with vascular parkinsonism, treatment focuses on managing symptoms and preventing further damage. Medications like levodopa, which are effective for idiopathic Parkinson’s, often provide limited or no benefit for most types of secondary parkinsonism. This is because the underlying problem is damage to brain cells or receptor blockade, not a simple dopamine deficiency.
Physical, occupational, and speech therapies help manage the condition. Physical therapy can improve balance, mobility, and strength, while occupational therapy can assist with adapting daily activities to maintain independence. Speech therapy can address difficulties with speaking and swallowing.
The prognosis for secondary parkinsonism is variable and directly linked to its cause. Drug-induced parkinsonism often has a favorable outlook if the offending agent can be stopped. In contrast, conditions like vascular parkinsonism may be progressive, although managing cardiovascular risk factors can help slow its advance. For causes like brain tumors, the outcome depends on the success of the tumor treatment itself.