Neurosychiatric Presentation in Parkinsons Disease (PD)

  • Symptoms of Parkinson's disease have been known and treated since medieval times
  • 1817 in An Essay on the Shaking Palsy by the British physician James Parkinson. (Parkinson's disease was then known as paralysis agitans)
  • The term "Parkinson's disease" was coined by Jean-Martin Charcot.
  • The underlying biochemical changes in the brain were identified in the 1950s: work of Swedish scientist Arvid Carlsson, who won Nobel Prize.
  • L-dopa entered clinical practice in 1967

Causes of Parkinsonism

  • Idiopathic
  • Parkinsonian-plus syndrome: PSP, MSA, CBS
  • Secondary parkinsonism: vascular, drug induced, post-encephalitic
  • Degenerative disorders: Alz, Parkinson-dementia-MND complex
  • Genetic disorder: Wilson’s disease, Huntington Disease

Epidemiology of PD

  • Incidence: 18/100,000
  • Prevalence: 150/100,000
  • In UK: 100,000cases at any time
  • M:F-1.35:1
  • ↑risk of PD: pesticide
  • ↓risk associated with caffeine and cigarette smoking

Pathophysilogy of PD

  • Hallmark of PD presence of Lewy bodies + neuronal cell death in the pars compacta of the substantia nigra(SN)
  • PD does not develop until striatal dopamine levels drop to 20% and SN cell loss exceeds 50%
  • Functional anatomy:  primary motor cortex, supplementary motor area, stratum (putamen, caudate),  globus pallidus, substantia nigra, sub thalamic nucleus(STN), thalamus
  • SN acts as accelerator on the basal ganglia and damage results in slowing
  • STN is brake and damage therefore causes excessive movement

Clinical Features of PD

  • Bradykinesia plus one of other
  • Rigidity
  • Rest Tremor: may be the first symptom(75%),  20% do not develop tremor
  • Postural instability
  • Features supportive of PD > 3: unilateral onset, rest tremors, progressive, good response to L-Dopa
  • Other features: Anosmia (80%), Dystonia, bladder bowel symptoms, postural hypotension, speech disorder, dementia

Differential Diagnosis of PD

  • Essential Tremors
  • Multiple  system atrophy
  • Vascular parkinsonism
  • Dementia with Lewy Bodies

Investigations of PD

  • No diagnostic test
  • 1231-FP-CIT SPECT Scan (Da T scan): ligands bond to dopamine re-uptake transporter protein in the pre-synaptic terminal
  • Exclude Wilson
  • Cognitive assessment
  • MRI

Neuropsychiatric Presentation of PD: Depression

  • Can be reactive  in  nature
  • Shows correlation between the severity
  • A integral relationship to disease progression itself
  • Affects quality of life in 40%. Proportionate relationship to the degree of disability
  • Deficiency of noradrenalin, dopamine and 5-hydroxytryptamine
  • Emotionalism
  • SSRI (Citalopram or sertraline) are first choice, may cause deterioration of PD symptoms
  • Mirtazepine (presynaptic α2 antagonist)
  • ECT

Neuropsychiatric Presentation of PD: Psychosis

  • Occurs in 10-15%
  • Mild illusion, visual hallucination, paranoid delusion
  • Pathophysiology is combination of development of cortical Lewy body dementia and drugs
  • Management:
  • Treat any infection, metabolic derangement
  • Reduce anticholinergic, selegiline, amantadine, DA, levodopa
  • Newer antipsychotic(low dose quetiapine), low dose clozapine(6.25-50mg)

Neuropsychiatric Presentation of PD: Dementia

  • Features of Lewy body dementia: visual hallucination, fluctuating course with lucid intervals, sensitivity to neuroleptics
  • Benefits with cholinesterase inhibitors

Neuropsychiatric Presentation of PD: Sleep disturbance

  • Stiffness and rigidity: consider CR levodopa
  • Bladder disturbance: oxybutynin, tolterodine
  • Restless legs: CR Levodopa or Cabergoline
  • REM sleep behaviour disorder: Clonazepam

Complication of anticholinergic drugs

  • Acute organic reaction
  • Benzhexol: confusion, excitement, agitation, paranoid delusions, hallucination and suicidal ideation
  • Levodopa: confusion, visual hallucination, delusion, illusion
  • Dopamine agonist: Ergot-derived(pergolide, cabergoline), non-ergot derived (Ropinirole, pramipexole): confusion, hallucination, somnolence
  • Hyper sexuality and gambling

Excessive salivation

  • Treated with anticholinergic drugs
  • Hyoscine patch
  • Botulinium injection


  • Especially in doorways: visual, patterned cues across door-way helps
  • Laser cane

Falls and postural instability

Multidisciplinary assessment by physiotherapist and OT to acquire walking aids and make appropriate adaptation.


Some of the pathological defence mechanism: denial, reaction formation, projection, rationalisation, sublimated aggression, neurotic conflicts due to dependency

Surgical treatment of PD

  • DBS: Bilateral stimulation of thalamic (VIM nucleus), STN, Pallidus
  • Stimulation induced depression, adjustment disorder
  • Past history usually predicts outcome post surgically
  • Symptom control is a major predictor of outcome  post surgically
  • Surgery: Posteroventral pallidotomy, thalamotomy (VIM nucleus)