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Flashcards in Parkinsons Deck (13)
1

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

2

What is Parkinsons disease?

• Neurodegenerative disease
• Destruction of Dopaminergic neurones of the substrantia nigra (that connect to the striatum)

3

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

4

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

5

Who develops it?

• 1-2% of 60 year olds
• 20 in 100,000 • Mean age of onset is 57 years old.

6

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

7

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.

8

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)

9

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.

10

What are the treatments?

• Levadopa
Treatments
• Dopa Decarboxylase Inhibitor – Prevents peripheral use of Levadopa – Can’t cross Blood Brain Barrier
• Ecstasy • Deep Brain Stimulation

11

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

12

How can treatment complications be managed?

• Small doses, more frequently
• Selegiline
• Dopamergic agonists – Potentiate the effects
• Apomorphine Infusion • Drug Holidays

13

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