Parkinsons Flashcards
What are the basal ganglia for?
- Essential for correct processing of readiness potential – in terms of initiation
- Striatum – Cuadate Nucleus – Putamen
- Globus Pallidus
- Important connections with substantia nigra and subthalamic nucleus
What is Parkinsons disease?
- Neurodegenerative disease
* Destruction of Dopaminergic neurones of the substrantia nigra (that connect to the striatum)
What are the symptoms?
• Bradykinesia • Rigidity • Tremor Insidious onset Resting tremor Stiffness / Slowness of movement Difficulty getting out of a chair Difficulty rolling over in bed Clumsiness Frequent Falls Smaller hand writing Mental Slowness Insomnia • Cranial Nerves: impairment of upward gaze, Repeated taps on forehead causes reflex blinking without fatigue, tremulous eyelids • Psychiatric – Depression – Dementia – Cognitiveproblems • Mask like face • Decreased blinking • Drool • Greasy skin / seborrhoeic dermatitis is common
What are the causes?
– Pesticides, wood pulp
– Genetic susceptibility • Alpha-synuclein (Ch4)
• Neuropleptic therapy
• MPTP toxin (illicit drug contamination)
• Post encephalitis
• Repeated Head Injury
• Juvenile Autosmomal Recessive Parkinsons (Parkin Gene Ch6)
• Sporadic
• Unknown
• ?Environmental
Who develops it?
- 1-2% of 60 year olds
* 20 in 100,000 • Mean age of onset is 57 years old.
What are the cardinal signs of Parkinsons?
• Tremor
• Rigidity
– Lead pipe rigidity • Extensors & flexors
– Cog-wheel rigidity • Sinkinesis
– Normal power and reflexes
• Gait – Simian, Shuffling, small stepped – Reducded arm swing – Falls easily
What happens?
• The flailing limbs is due to medication.
• Difficulty in initiating voluntary movements.
• Requireintenseconcentrationtoinitiate
movement.
• Loose associated movements (arm swing / emotion).
There’s 80% ganglia degeneration before symptoms start.
What’s the pathology?
Pathology – Reduced melanin pigmentation in the SN.
• Macro – (dopamine is a precursor to melanin)
• Micro
– Degeneration of dopaminergic neurones from the SN to the CN & Putamen (Striatum)
What happens normally in the brain and what happens in Parkinson’s?
- The pallidum is spontaneously active
- Various nuclei inhibit the pallidum to allow controlled movement
- Dopamine facilitates the release (of pallidum) from inhibition
- No Dopamine = no inhibition of the striatum = poverty of motion – Greater exertion in effort for a given movement
- Treatment brings excess / uncontrolled dopamine – Dyskinesia
- Pharmacology is gross and cannot reproduce the subtle sophistication of physiology.
What are the treatments?
• Levadopa
Treatments
• Dopa Decarboxylase Inhibitor – Prevents peripheral use of Levadopa – Can’t cross Blood Brain Barrier
• Ecstasy • Deep Brain Stimulation
What are the treatment complications?
• Psychoticsymptoms
– Pyschotics treated with dopamine depletion develop PD.
– Long term PD treatment = psychotic behaviour – Nausea & Vomiting – Confusion – Visual Hallucinations
– Drug Infectivity – End of Dose Dyskinesia / Dopa induced dyskinesia – On and Off Syndrome
How can treatment complications be managed?
- Small doses, more frequently
- Selegiline
- Dopamergic agonists – Potentiate the effects
- Apomorphine Infusion • Drug Holidays
How does Parkinson’s relate to dentistry?
• Dry Mouth
– Regular review, saliva replacement, fluoride
• Cant brush their teeth
• Bruxism / Tooth wear
• Drooling • Lack of control of musculature
• Dentures wont fit – Inhalation risk
• Adrenaline