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Medicine 2 - Fourth Year BHMS

Contents

Medicine 2 - Fourth Year BHMS

Contents

CoursesBHMSMedicine 2 - Fourth Year BHMSParkinsonism

Parkinsonism

Content

Parkinsonism

1. Definition

Parkinsonism is a syndrome of movement disorder marked by resting tremor, muscular rigidity, slowness of voluntary movement (bradykinesia) and impaired postural balance. It represents the clinical picture that may arise from several different pathological processes affecting the basal ganglia.

2. Synonyms (if any)

  • Parkinson’s disease – the most common idiopathic form of parkinsonism.
  • Secondary parkinsonism – used when the picture is produced by an identifiable cause such as drugs or vascular lesions.

3. Causes / Etiology

  • Idiopathic (primary) Parkinson’s disease – no definite cause; presumed loss of dopaminergic neurons in the substantia nigra. Most cases are sporadic.
  • Genetic factors – mutations in SNCA, PARK2, LRRK2, PINK1, DJ‑1 may predispose; often seen in early‑onset families. Family history is a clue.
  • Environmental toxins – chronic exposure to pesticides (e.g., paraquat), herbicides, heavy metals (manganese, lead) increases risk. Occupational history is important.
  • Drug‑induced (secondary) parkinsonism – antipsychotics, metoclopramide, some anti‑emetics block dopamine receptors. Symptoms may improve on withdrawal.
  • Vascular parkinsonism – multiple small infarcts in the basal ganglia region produce a parkinsonian picture, usually with gait disturbance. Often seen in elderly hypertensives.
  • Post‑traumatic or metabolic – head injury, Wilson’s disease, carbon monoxide poisoning can damage the nigro‑striatal pathway. Look for associated systemic signs.

4. Types / Classification

TypeDefinitionTypical CausesMain Clinical FeaturesTypical Duration / CourseAcute‑vs‑Chronic Notes
Idiopathic Parkinson’s disease (IPD)Classic Parkinson’s disease without identifiable external causeDegeneration of dopaminergic neurons (unknown trigger)Resting tremor, cogwheel rigidity, bradykinesia, shuffling gaitSlowly progressive over years; motor signs appear graduallyChronic; no sudden onset
Drug‑induced parkinsonismParkinsonian signs produced by dopamine‑blocking drugsAntipsychotics, anti‑emetics, calcium‑channel blockersSymmetrical rigidity, mild tremor, often early onset after drug startMay appear within weeks to months of exposure; may improve after stopping drugCan be acute (days‑weeks) if drug started abruptly
Vascular parkinsonismParkinsonism due to multiple small cerebrovascular lesionsHypertensive small‑vessel disease, lacunar infarctsPredominant gait disturbance, lower‑limb rigidity, less tremorInsidious but may have step‑wise worsening after each infarctChronic, step‑wise progression
Atypical (secondary) parkinsonismParkinsonian picture associated with other neuro‑degenerative disordersMultiple system atrophy, progressive supranuclear palsy, corticobasal degenerationEarly autonomic failure, early falls, poor levodopa responseRapid progression (months‑few years)Chronic, often more aggressive than IPD

5. Pathophysiology / Pathology

  1. Loss of dopaminergic neurons in the pars compacta of the substantia nigra pars reticulata → ↓ dopamine in the striatum.
  2. Imbalance of basal ganglia circuits – reduced inhibitory output from the direct pathway and excess activity of the indirect pathway → increased inhibition of thalamic motor nuclei.
  3. Resulting motor output – slowed initiation of movement, rigidity, and tremor at rest.
  4. Lewy bodies – eosinophilic intraneuronal inclusions composed of α‑synuclein appear in surviving neurons; they are a pathological hallmark of idiopathic PD.
  5. Non‑dopaminergic involvement – degeneration of serotonergic, noradrenergic and cholinergic systems contributes to non‑motor symptoms.
    The cascade explains why dopamine replacement improves motor signs but does not fully reverse non‑motor features.

6. Clinical Features

  • General motor signs – resting “pill‑rolling” tremor, cogwheel rigidity, bradykinesia, reduced arm swing, shuffling gait, festination, postural instability (late).
  • Specific motor signs – micrographia, masked facies, hypophonia, drooling, difficulty with fine tasks.
  • Non‑motor features – depression, anxiety, sleep disturbances (REM behavior disorder), constipation, urinary urgency, hyposmia, cognitive decline.
  • Acute features (drug‑induced) – sudden onset of rigidity and tremor shortly after drug exposure; often symmetrical.
  • Chronic features (idiopathic) – gradual worsening over years; tremor may be the first sign.
    Recognition of non‑motor signs aids early diagnosis.

7. Complications

  • Motor complications – wearing‑off phenomenon, motor fluctuations, dyskinesias (especially after long‑term levodopa). Require dose adjustment.
  • Falls and fractures – due to postural instability and gait freezing; major cause of morbidity. Fall‑prevention strategies are essential.
  • Neuropsychiatric problems – hallucinations, psychosis, severe depression, dementia in later stages. May need antipsychotic therapy with caution.
  • Autonomic dysfunction – orthostatic hypotension, constipation, urinary retention; can lead to dehydration or infections. Hydration and bowel programs help.

8. Investigations / Diagnosis

  • Clinical examination – UPDRS (Unified Parkinson’s Disease Rating Scale) or MDS‑UPDRS to grade severity.
  • Neuroimaging – MRI brain to exclude structural lesions; DaT‑SPECT (DAT scan) shows reduced dopamine transporter uptake in idiopathic PD. Helps differentiate from essential tremor.
  • Laboratory tests – CBC, liver & renal function, thyroid profile, serum ceruloplasmin (to rule out Wilson’s disease) when atypical features present.
  • Response to levodopa trial – marked improvement (>30 % in motor score) supports diagnosis of idiopathic PD. A practical bedside test.

9. Differential Diagnosis

  1. Essential tremor – action tremor, improves with alcohol, absent rigidity; no bradykinesia. Tremor is postural, not resting.
  2. Multiple system atrophy (MSA) – early autonomic failure, cerebellar signs, poor levodopa response. Rapid progression distinguishes it.
  3. Progressive supranuclear palsy (PSP) – vertical gaze palsy, early falls, axial rigidity; levodopa response minimal. Eye movement abnormality is key.
  4. Drug‑induced parkinsonism – history of dopamine‑blocking agents, symmetrical signs, rapid onset; improves after drug withdrawal. Temporal relation to medication is decisive.

10. Management / Treatment

General management –

  • Encourage regular physiotherapy to maintain flexibility and gait training.
  • Occupational therapy for activities of daily living; speech therapy for dysarthria and swallowing.
  • Education of patient and caregivers about fall safety and medication timing.

Modern medicine treatment –

  • Levodopa + carbidopa – most effective for motor symptoms; start low, titrate slowly.
  • Dopamine agonists (pramipexole, ropinirole, rotigotine) – useful in younger patients to delay levodopa use.
  • MAO‑B inhibitors (selegiline, rasagiline) – modest symptomatic benefit, neuroprotective potential.
  • COMT inhibitor (entacapone) – prolongs levodopa effect, reduces wearing‑off.
  • Anticholinergics (trihexyphenidyl) – help tremor in younger patients, but limited by side effects.
  • Amantadine – reduces dyskinesias and mild motor symptoms.

Diet and lifestyle advice –

  • High‑protein meals should be spaced away from levodopa dose (protein interferes with absorption).
  • Adequate fluid intake and fiber to prevent constipation.
  • Regular aerobic exercise (walking, cycling) improves mobility and mood.
  • Avoid alcohol excess and sedatives that may worsen balance.

11. Homeopathic Therapeutics (7 remedies, each with 8 bullet points)

1. Causticum

  • Causation – prolonged exposure to cold, damp environments.
  • Characteristic symptoms – marked rigidity, tremor, weakness of limbs.
  • Modalities – worse from cold, dampness; better from warmth and gentle motion.
  • Mental state – anxious, feeling of impending doom, fear of death.
  • Thirst & appetite – increased thirst, appetite often reduced.
  • Discharges – scanty, may have dry skin.
  • Physical generals – muscular wasting, cold extremities.
  • Suitable constitution – persons with a history of exposure to cold, damp weather, often farmers.
  • How it helps – reputed to restore muscular tone and reduce rigidity by acting on the nervous system.

2. Mercurius

  • Causation – exposure to mercury or other heavy metals, chronic infections.
  • Characteristic symptoms – tremor, shaking, excessive salivation, weakness.
  • Modalities – worse from cold, better from warmth and rest.
  • Mental state – irritability, restlessness, fear of being ill.
  • Thirst & appetite – thirst increased, appetite variable, often loss of appetite.
  • Discharges – profuse watery salivation, sometimes metallic taste.
  • Physical generals – trembling of hands, swollen glands.
  • Suitable constitution – individuals with metallic taste, who are overly sensitive to cold.
  • How it helps – thought to detoxify heavy‑metal load and calm nervous excitability.

3. Zincum metallicum

  • Causation – zinc deficiency or excess, chronic stress.
  • Characteristic symptoms – fine tremor, weakness of fingers, clumsiness.
  • Modalities – worse from mental strain, better from rest and cool air.
  • Mental state – anxiety, fear of losing control, indecisiveness.
  • Thirst & appetite – thirst normal, appetite may be poor.
  • Discharges – none specific, occasional dry cough.
  • Physical generals – brittle nails, hair loss, skin eruptions.
  • Suitable constitution – students, office workers under mental pressure.
  • How it helps – supplies essential trace element, improves neuromuscular coordination.

4. Gelsemium sempervirens

  • Causation – over‑exertion, emotional exhaustion.
  • Characteristic symptoms – trembling of limbs, heaviness, sluggish movements.
  • Modalities – worse from mental effort, better from lying down.
  • Mental state – anticipatory anxiety, feeling of impending failure.
  • Thirst & appetite – decreased thirst, appetite often reduced.
  • Discharges – dry mouth, occasional nasal discharge.
  • Physical generals – weak pulse, cold extremities.
  • Suitable constitution – persons with performance anxiety, exam stress.
  • How it helps – calms the nervous system, reduces tremor caused by stress.

5. Physostigma alkaloide

  • Causation – prolonged use of dopamine‑blocking drugs, toxic exposure.
  • Characteristic symptoms – rigidity, tremor, occasional convulsions.
  • Modalities – worse after taking offending drug, better after withdrawal.
  • Mental state – confusion, delirium, fear of loss of control.
  • Thirst & appetite – thirst normal, appetite may be poor.
  • Discharges – may have excessive sweating.
  • Physical generals – hyperreflexia, occasional muscle twitching.
  • Suitable constitution – patients on long‑term antipsychotics or anti‑emetics.
  • How it helps – assists in restoring normal neurotransmission after drug‑induced blockade.

6. Cuprum metallicum

  • Causation – copper imbalance (deficiency or excess), occupational exposure.
  • Characteristic symptoms – tremor, weakness, metallic taste.
  • Modalities – worse from heat, better from cool fresh air.
  • Mental state – irritability, feeling of being misunderstood.
  • Thirst & appetite – thirst normal, appetite may be diminished.
  • Discharges – occasional metallic saliva, loose stools.
  • Physical generals – hair loss, skin discoloration, joint pains.
  • Suitable constitution – metal workers, people with dietary copper excess.
  • How it helps – normalises copper metabolism, which influences dopaminergic pathways.

7. Silicea

  • Causation – chronic illness, prolonged stress, exposure to silica dust.
  • Characteristic symptoms – fine tremor, muscle weakness, delayed healing.
  • Modalities – worse from cold, better from warm dry environment.
  • Mental state – timidity, lack of confidence, fear of criticism.
  • Thirst & appetite – increased thirst, appetite moderate.
  • Discharges – scanty urine, occasional nasal discharge.
  • Physical generals – brittle nails, thin hair, poor skin texture.
  • Suitable constitution – individuals with long‑standing fatigue, workers in construction.
  • How it helps – strengthens connective tissue and nervous resilience, reducing tremor.

8. Natrum muriaticum (optional if eight are needed)

  • Causation – emotional suppression, grief, excessive salt intake.
  • Characteristic symptoms – tremor that improves with distraction, rigidity in the neck.
  • Modalities – worse from warm drinks, better from cool fresh air.
  • Mental state – melancholy, feeling of being misunderstood, craving solitude.
  • Thirst & appetite – thirst for salty foods, appetite reduced.
  • Discharges – dry mucous membranes.
  • Physical generals – dry skin, brittle hair.
  • Suitable constitution – persons with a history of unexpressed grief, often students.
  • How it helps – releases emotional tension that may aggravate motor symptoms.

12. Prognosis

  • The disease is progressive; life expectancy is near normal but quality of life declines with motor and non‑motor complications.
  • Early onset (<50 y) often leads to a longer disease course with higher risk of dyskinesias; late onset may progress faster but with fewer medication‑induced problems.
  • Good response to levodopa and adherence to physiotherapy improve functional outcome. Prognosis is therefore variable and depends on age, severity at presentation and treatment compliance.

13. Prevention

  • No definitive primary prevention, but avoidance of known risk factors (pesticide exposure, chronic heavy‑metal contact) reduces incidence.
  • Regular physical activity and a diet rich in antioxidants (fruits, vegetables) may delay onset or slow progression. Early lifestyle modification is the practical preventive measure.

14. Diet

  • Recommended foods – fresh fruits, vegetables, whole grains, lean protein (fish, poultry), omega‑3 fatty acids, adequate water. These support neuronal health and prevent constipation.
  • Foods to avoid – excessive protein meals taken with levodopa, high‑fat fried foods, alcohol excess, caffeine in large amounts (may worsen tremor). They interfere with drug absorption or exacerbate symptoms.