Orris

Complete notes on parkinsonism

Reading File
Parkinsonism covers a lot of ground, so I'll give you the map and a short overview first. Then you can pick one area to cover in depth.

Topic breakdown

  1. Definition and classification (Parkinson disease, atypical parkinsonism, secondary parkinsonism)
  2. Epidemiology, etiology and risk factors (genetics, environment)
  3. Pathophysiology (basal ganglia circuits, dopamine loss, alpha-synuclein, Lewy bodies)
  4. Clinical features, motor (bradykinesia, rigidity, tremor, postural instability, gait)
  5. Clinical features, non-motor (autonomic, sleep, cognitive, psychiatric, sensory)
  6. Diagnosis (UK Brain Bank and MDS criteria, DaTscan, MRI, levodopa challenge)
  7. Atypical parkinsonism (MSA, PSP, CBD, DLB) and red flags
  8. Secondary parkinsonism (drug-induced, vascular, toxic, post-encephalitic, NPH)
  9. Differential diagnosis (essential tremor, dystonic tremor, and others)
  10. Pharmacological management (levodopa, dopamine agonists, MAO-B and COMT inhibitors, amantadine, anticholinergics)
  11. Motor complications (wearing-off, dyskinesias, on-off phenomena) and how to manage them
  12. Surgical and advanced therapies (DBS, apomorphine, levodopa-carbidopa intestinal gel, focused ultrasound)
  13. Management of non-motor symptoms, and rehabilitation and supportive care
  14. Prognosis, staging (Hoehn and Yahr) and complications

Brief overview

Parkinsonism is a clinical syndrome of bradykinesia plus at least one of rest tremor (4-6 Hz, pill-rolling), rigidity (lead-pipe or cogwheel) or postural instability. Bradykinesia is essential for the diagnosis. Parkinson disease is the most common cause, accounting for about 80% of cases. The rest are atypical parkinsonian disorders (MSA, PSP, CBD, DLB) and secondary causes. The commonest secondary causes are dopamine-blocking drugs such as antipsychotics, metoclopramide and prochlorperazine. Others include vascular lesions, toxins, normal pressure hydrocephalus and structural lesions.
In Parkinson disease, dopaminergic neurons of the substantia nigra pars compacta degenerate. Motor signs appear after roughly 50-60% of neurons are lost, and striatal dopamine is reduced by about 80%. Alpha-synuclein aggregates into Lewy bodies, and pathology may spread in a caudal to rostral pattern (Braak staging). This loss disrupts the basal ganglia circuits: the direct pathway is underactive and the indirect pathway is overactive. The result is excess inhibition of the thalamus and motor cortex.
Non-motor features often come first or dominate the course. These include hyposmia, REM sleep behaviour disorder, constipation, depression, orthostatic hypotension and later dementia.
Diagnosis is clinical. DaTscan helps in uncertain cases. Early falls, poor levodopa response, early dysautonomia, vertical gaze palsy or cerebellar signs point to an atypical syndrome.
Levodopa with a decarboxylase inhibitor is the most effective treatment. Long-term use leads to wearing-off and dyskinesias. For these, options include adding COMT or MAO-B inhibitors, using dopamine agonists, deep brain stimulation or infusion therapies.
Asking for Preferences

Which topic would you like in full detail first?

This is a shared conversation. Sign in to Orris to start your own chat.