Parkinson’s Disease

Parkinson’s Disease

·        Bradykinesia, tremour (70% of cases) and rigidity (unilateral onset) but no early difficulty with gait 

·        Also lack of arm swing (usually only one side at outset), lack of facial expression, paucity of movement. 30% become demented (either due to Alzheimer‟s or widespread Lewy bodies). Also postural hypotension

·        Gradual progression and prolonged course

·        Pathology:

o   Gross: Pallor of substantia nigra 

o   Micro: ¯ in melanin-containing dopaminergic neurones with secondary reactive gliosis. Lewy Bodies may be present in remaining neurones (eosinophilic intracytoplasmic inclusions).

·        Treatment: 

o   L-Dopa ® dyskinesias, and on-off effects after 3 – 5 years. The mainstay of treatment. Give minimum dose to control symptoms, not necessarily signs

o   Carbidopa: prevents peripheral conversion of L=Dopa

o   For younger patients, begin with a dopamine agonist (bromocriptine, pergolide)

o   Selegiline, a MAOB inhibitor delays the time needed for the subsequent introduction of L-Dopa

o   Anticholinergics: stop ACh induced hyper-reactivity: but dry mouth, urinary retention, blurred vision

·        Other causes of Parkinsonism.  Parkinson Disease is a disease of exclusion:

o   Drug induced parkinsonism eg phenothiazines including antiemetics (eg Maxolon)

o   Multisystem atrophy: also have cerebellar ataxia, eye movement disorder, autonomic dysfunction and pyramidal signs

o   Huntington‟s Disease: early presentation may mimic Parkinson‟s, rather than a movement disorder with chorea, myoclonus and dystonia

o   Wilson‟s Disease: consider in younger patients. Behaviour disturbance, dystonia, flapping tremour. Rare but treatable

o   Diffuse Lewy Body Dementia: Males 2:1. All demented eventually. Most have rigidity, bradykinesia but tremour uncommon. Usually begins with cognitive impairment.