Parkinson’s disease: What it is, how to manage and 10 ways to prevent it.

Parkinson’s Disease is an age-related chronic, progressive neurodegenerative disorder that primarily affects movement is the progressive loss of dopaminergic neurons in the substantia nigra pars compacta (midbrain). which is responsible for controlling movement and coordination. This condition is best known for how it affects muscle control, balance and movement, it can also cause a wide range of other effects on your senses, thinking ability, mental health and more..This leads to:

  • Formation of Lewy bodies, abnormal intracellular aggregates made of the protein alpha-synuclein, which are toxic to neurons.
  • Dopamine depletion in the striatum, a key component of the basal ganglia, which regulates voluntary motor control.
Parkinson's disease
Parkinson’s disease

Major Pathological Processes:

pathology
Pathology
  1. Mitochondrial dysfunction – Impaired complex I of ETC.
  2. Oxidative stress – Excess ROS damage neuronal membranes.
  3. Neuroinflammation – Microglial activation exacerbates neuronal loss.
  4. Protein aggregation – Due to dysfunctional autophagy and lysosomal path

What is the difference between Parkinson’s disease vs. parkinsonism?

“Parkinsonism” is an umbrella term that describes Parkinson’s disease and conditions with similar symptoms. It can refer not only to Parkinson’s disease but also to other conditions like multiple system atrophy or corticobasal degeneration.

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Parkinson’s disease
Definition
A specific neurodegenerative disease caused primarily by dopamine deficiency in the substantia nigra.

Cause
Idiopathic (unknown exact cause), often linked to loss of dopaminergic neurons and Lewy body formation.

Underlying Pathology
Alpha-synuclein aggregation (Lewy bodies), dopamine neuron loss in substantia nigra.

Motor Symptoms
Classic triad: Resting tremor, bradykinesia, rigidity (initially asymmetric).

Response to Levodopa
Typically shows good improvement, especially early in disease.

Disease Progression
Slowly progressive, over many years.

Non-Motor Symptoms
Present (e.g., loss of smell, depression, REM sleep behavior disorder).

Examples
Idiopathic Parkinson’s Disease (only one type).

Neuroimaging
DaTscan: Decreased dopamine transporter uptake.

Treatment
Levodopa, dopamine agonists, MAO-B inhibitors, DBS in later stages.

Prognosis
Generally better, long-term management possible.

Parkinsonism (Parkinsonian Syndromes)

Definition
A broad clinical syndrome with signs similar to PD (e.g., tremor, rigidity), but can have many different causes.

Cause
Can be due to: <ul><li>Other neurodegenerative diseases (atypical Parkinsonism)</li><li>Medications (drug-induced)</li><li>Stroke, trauma, toxins</li></ul>

Underlying Pathology
Depends on cause: <ul><li>No Lewy bodies in drug-induced forms</li><li>Different proteinopathies in atypical types (e.g., tau in PSP)</li></ul>

Motor Symptoms
Similar motor signs, but often: <ul><li>More symmetric</li><li>More rapid progression</li><li>Less tremor</li></ul>

Response to Levodopa
Poor or minimal response in most forms of secondary or atypical Parkinsonism.

Disease Progression
Often faster progression (especially atypical forms like PSP or MSA).

Non-Motor Symptoms
May be less common or more rapidly developing cognitive/neurological issues.

Examples
Includes:
🔹 Atypical Parkinsonism (e.g., PSP, MSA, CBD)
🔹 Drug-induced Parkinsonism
🔹 Vascular Parkinsonism
🔹 Toxin-induced (e.g., manganese poisoning)

Neuroimaging
In drug-induced: Normal DaTscan
In atypical: Abnormal patterns (e.g., atrophy in MSA, PSP).

Treatment
Focuses on treating the underlying cause (e.g., stopping offending drug), supportive therapy

Prognosis
Often poorer prognosis, especially in neurodegenerative atypical syndromes.

Motor and Non-Motor Symptoms – In Depth

Motor Symptoms Explained in Detail

SymptomDescription
Resting TremorTypically “pill-rolling” movement in fingers. Disappears with intentional movement.
BradykinesiaSlowness in initiating and executing movements. Major cause of disability.
Rigidity“Lead-pipe” or “cogwheel” stiffness felt during passive movement. Can be painful.
Postural InstabilityImpaired reflexes, leading to frequent falls. Appears in later stages.
Gait FreezingSudden inability to move feet, especially when turning or approaching doorways.

Non-Motor Symptoms – Often Underdiagnosed but Critical

DomainSymptom
CognitiveMemory loss, slow thinking (bradyphrenia), executive dysfunction, Parkinson’s dementia.
PsychiatricDepression, anxiety, hallucinations (especially with medications), apathy.
AutonomicOrthostatic hypotension, constipation, urinary dysfunction, erectile dysfunction.
SensoryPain (central pain, muscle pain), loss of smell, visual disturbances.
SleepREM sleep behavior disorder (acting out dreams), insomnia, excessive daytime sleepiness.

Braak Staging of Parkinson’s Disease (Neuropathological)

StageRegion AffectedSymptoms
1-2Medulla, olfactory bulbEarly non-motor (constipation, anosmia)
3-4Midbrain (substantia nigra)Classic motor signs appear
5-6Cortex (temporal, frontal)Cognitive and behavioral symptoms
parkinsons symptoms

Hoehn and Yahr Clinical Staging

  • Stage 1: Unilateral symptoms only.
  • Stage 2: Bilateral symptoms, balance intact.
  • Stage 3: Postural instability, independent.
  • Stage 4: Severely disabling, needs assistance.
  • Stage 5: Wheelchair/bedridden

Causes

The cause of Parkinson’s disease is unknown, but several factors seem to play a role, including:

  • Genes. Specific genetic changes are linked to Parkinson’s disease.
  • Environmental factors. Exposure to certain toxins or other environmental factors may increase the risk of later Parkinson’s disease.
  • The presence of Lewy bodies. Clumps of proteins in the brain are associated with Parkinson’s disease. 
  • Alpha-synuclein found within Lewy bodies. Alpha-synuclein is a protein found in all Lewy bodies.
  • Altered mitochondria. Mitochondria are powerhouse compartments inside cells that create most of the body’s energy.

Diagnosis

A. Clinical Diagnosis (Based on MDS-UPDRS Criteria)

  • Bradykinesia + at least one of tremor/rigidity/postural instability
  • Absence of red flags (e.g., early falls, gaze palsy)

B. Imaging

  • MRI: Normal or subtle nigral degeneration
  • DaTscan (Ioflupane SPECT): Shows dopamine transporter deficit
  • PET scan: Decreased uptake of [18F] DOPA

C. Other Biomarkers (Emerging)

  • Alpha-synuclein in CSF, skin biopsy, or salivary glands
  • Urine dopamine metabolites
  • Blood neurofilament light chain (NfL)

Pharmacological Management

Drug ClassExamplesKey Notes
Levodopa/CarbidopaSinemetMost effective, but long-term use causes dyskinesias
Dopamine AgonistsPramipexole, RopiniroleUse in younger patients, risk of hallucinations
MAO-B InhibitorsRasagiline, SelegilineMild effect, delays Levodopa use
COMT InhibitorsEntacapone, TolcaponeReduces Levodopa wearing-off
AmantadineReduces dyskinesias
AnticholinergicsTrihexyphenidylUseful for tremor, avoided in elderl

Multidisciplinary Rehabilitation

DisciplineRole
PhysiotherapyGait, balance, fall prevention, mobility
Speech TherapyVoice therapy (LSVT LOUD), swallowing support
Occupational TherapyActivities of daily living (ADLs), home safety
NeuropsychologyCognitive training, mood stabilization
DieticianHigh-fiber, protein-spaced meals to improve Levodopa absorption
PHYSIOTHERAPY MANAGEMENT IN PARKINSON’S DISEASE
physiotherapy in parkinsons
Parkinsons physiotherapy management
Early Stage Parkinson’s (Hoehn & Yahr Stage I–II)

Focus: Prevention, education, promoting activity

Treatment Plan:

Home safety education: Ergonomics and fall prevention advice.

Postural training: Encourage upright posture to prevent stooping.

Flexibility exercises: Focus on neck, trunk, hips, and shoulders.

Aerobic exercises: Brisk walking, cycling, swimming (3–5x/week).

Breathing exercises: To maintain chest expansion and reduce rigidity.

Middle Stage (Stage III–IV)

Focus: Improve balance, manage gait problems, reduce fall risk

Key Physiotherapy Techniques:

A. Gait Training

  • Cueing strategies:
    • Auditory: Use of metronome or rhythmic beats to enhance walking pace.
    • Visual: Floor markings, laser lights for freezing episodes.
  • Treadmill training (with or without body weight support)
  • High-amplitude movement training: Use of LSVT BIG (see below)
  • Practice turns, dual-task walking, and obstacle navigation

B. Balance Training

  • Static and dynamic balance exercises on firm and unstable surfaces.
  • Tai Chi, balance boards, stepping over objects.
  • Training in response to perturbations.

C. Strength Training

2–3 sessions/week

Resistance bands, light weights

Emphasis on extensor muscles (hip, trunk, shoulders)

Advanced Stage (Stage IV–V)

Focus: Prevent complications, maximize comfort and caregiver support

Interventions:

  • Bed mobility and transfers training
  • Passive ROM (Range of Motion) exercises to prevent contractures
  • Respiratory physiotherapy – deep breathing, incentive spirometry
  • Seating and wheelchair positioning
  • Education to caregivers: Transfers, safety, skin care

10 Preventive Strategies for Parkinson’s Disease

1. Engage in Regular Physical Exercise

2. Adopt an Antioxidant-Rich Diet

3. Drink Caffeine in Moderation

4. Avoid Exposure to Environmental Toxins

5. Manage and Review Medications

6. Protect and Support Gut Health

7. Manage Chronic Stress and Mental Health

8. Prioritize Quality Sleep

9. Genetic Counseling (for At-Risk Families)

10. Stay Mentally and Socially Active

Public Health & Epidemiology

  • Affects >10 million globally; ~1 million in India
  • Prevalence increases with age: ~1% over age 60
  • Men > Women (1.5:1 ratio)
  • Cost burden includes medications, care support, and productivity loss

📈 Global Trends (2023–2025)

  • Projected 30–40% rise by 2030 due to population aging
  • Parkinson’s now fastest-growing neurological disorder worldwide (Lancet Neurology)

Research and Innovations (2024–2025)

A. Emerging Drug Classes

  • GLP-1 receptor agonists (Exenatide)
  • Kinase inhibitors (LRRK2 blockers)
  • Anti-alpha-synuclein monoclonal antibodies (Prasinezumab, Cinpanemab)

B. Gene Therapy Trials

  • AADC gene via AAV vector – enhances dopamine synthesis
  • GBA gene therapy in genetic PD

C. Cell-based Therapies

  • Induced pluripotent stem cells (iPSC) derived dopaminergic neurons

D. Microbiome–Parkinson’s Axis

  • Dysbiosis may drive early PD symptoms
  • Probiotic and fecal transplant therapies under exploration

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