PD is a progressive movement disorder, but it is only one cause of the broader set of symptoms known as Parkinsonism. Parkinsonism is a clinical syndrome defined by a characteristic combination of motor difficulties stemming from multiple underlying diseases. These conditions share the outward appearance of PD, making initial diagnosis challenging. Understanding these “Parkinson’s-like” diseases is important because their causes, progression, and responses to treatment are often vastly different from classic PD.
The Defining Motor Symptoms of Parkinsonism
The clinical definition of Parkinsonism rests on four core motor symptoms, though not all must be present for a diagnosis. Slowness of movement, known as bradykinesia, is the most fundamental feature and must be present for the syndrome to be identified. Bradykinesia manifests as reduced speed and amplitude of movement, leading to difficulties with repetitive tasks like buttoning a shirt or walking.
Rigidity is a stiffness or inflexibility of the muscles of the trunk and limbs. This resistance to movement leads to a decreased range of motion and often contributes to a stooped posture. Many people also experience a resting tremor, which is a rhythmic, involuntary shaking that appears when the limb is relaxed and often lessens during intentional movement.
Postural instability, or difficulty maintaining balance, is the fourth component of the syndrome. This symptom often leads to an increased risk of falls as the condition progresses. The specific combination, severity, and presence of other non-motor issues ultimately distinguish Parkinson’s disease from its many mimics.
The Major Neurodegenerative Mimics
A group of progressive brain disorders, often called Atypical Parkinsonian Syndromes or “Parkinson’s Plus” diseases, closely resemble PD but progress more rapidly and are less responsive to standard levodopa medication.
Multiple System Atrophy (MSA) is characterized by early and severe autonomic failure. This dysfunction of the nervous system controls involuntary actions and often presents as orthostatic hypotension, a significant drop in blood pressure upon standing that leads to dizziness or fainting. MSA also causes early urinary and bowel issues, as well as problems with coordination or ataxia.
Progressive Supranuclear Palsy (PSP) is primarily a tauopathy, marked by the accumulation of tau protein in the brain. The distinguishing feature is vertical gaze palsy, the inability to move the eyes vertically, especially downwards. This issue, combined with early and unexplained falls due to severe postural instability and axial rigidity, makes PSP distinct. Falls often occur within the first year, significantly sooner than typically seen in PD.
Corticobasal Syndrome (CBS) often presents with an extreme asymmetry of symptoms. Patients frequently exhibit severe stiffness and apraxia, which is the inability to perform familiar, purposeful movements despite having the physical strength. A unique sign is the “alien limb phenomenon,” where a limb seems to act on its own, performing involuntary movements that the person does not control.
Lewy Body Dementia (LBD) is closely related to PD because both involve abnormal alpha-synuclein protein deposits, called Lewy bodies, in the brain. LBD is characterized by prominent cognitive fluctuations, where a person’s alertness and attention can change dramatically over hours or days. Recurrent, detailed visual hallucinations are also a hallmark feature that typically appears early in the disease course.
Parkinsonism Stemming from External Factors
Not all forms of Parkinsonism are caused by neurodegenerative diseases; some are secondary, resulting from an external cause or structural damage.
Drug-Induced Parkinsonism (DIP) is the second most common cause of Parkinsonism after PD. This condition occurs when certain medications, most notably antipsychotics and some anti-nausea drugs, block dopamine receptors in the brain, mimicking the loss of dopamine seen in PD.
The symptoms of DIP, including tremor, stiffness, and slowness, usually develop within days to months of starting the offending medication. DIP often presents with bilateral and symmetrical symptoms and is typically reversible once the problematic drug is discontinued. Unlike true PD, the brain’s dopaminergic system remains largely intact, even if symptoms persist for several months after stopping the medication.
Vascular Parkinsonism (VP) is caused by small strokes or multiple lacunar infarcts in the brain’s subcortical regions that control movement. This structural damage leads to symptoms often concentrated in the lower body, sometimes called “lower-body Parkinsonism.” Patients with VP commonly experience prominent gait freezing, shuffling steps, and early balance problems, while a resting tremor is often absent. The onset of VP can be sudden, correlating with a stroke event, or gradual due to the accumulation of small vessel damage.
How Clinicians Differentiate the Disorders
The initial distinction between Parkinson’s disease and its mimics relies heavily on a detailed clinical history and physical examination that notes “red flag” symptoms. A significant factor is the patient’s response to levodopa, the primary medication for PD. Patients with PD typically show a robust and sustained improvement in motor symptoms, whereas the atypical syndromes generally exhibit a poor or transient response.
The early onset of certain non-motor features also suggests an alternative diagnosis. For example, the appearance of severe dementia or visual hallucinations early in the disease course points toward Lewy Body Dementia. Profound autonomic dysfunction, such as early urinary incontinence or severe drops in blood pressure, is a strong indicator of Multiple System Atrophy.
Imaging techniques like the DaTscan use a radiotracer to visualize dopamine transporters in the brain, confirming a dopamine deficiency. An abnormal DaTscan helps differentiate a Parkinsonian syndrome from conditions like essential tremor or Drug-Induced Parkinsonism, which do not involve the loss of dopamine-producing neurons. However, the scan cannot distinguish between PD and neurodegenerative mimics like MSA or PSP, as all these conditions involve the loss of those same neurons.
The overall rate of disease progression provides a final piece of evidence, as the atypical Parkinsonian syndromes usually progress much faster than classic PD. Ultimately, diagnosis requires a careful synthesis of motor symptoms, specific non-motor symptoms, speed of decline, and response to levodopa therapy.