Parkinsons Flashcards

1
Q

What are the basal ganglia for?

A
  • 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
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2
Q

What is Parkinsons disease?

A
  • Neurodegenerative disease

* Destruction of Dopaminergic neurones of the substrantia nigra (that connect to the striatum)

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3
Q

What are the symptoms?

A
• 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
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4
Q

What are the causes?

A

– 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

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5
Q

Who develops it?

A
  • 1-2% of 60 year olds

* 20 in 100,000 • Mean age of onset is 57 years old.

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6
Q

What are the cardinal signs of Parkinsons?

A

• 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

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7
Q

What happens?

A

• 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.

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8
Q

What’s the pathology?

A

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)

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9
Q

What happens normally in the brain and what happens in Parkinson’s?

A
  • 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.
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10
Q

What are the treatments?

A

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

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11
Q

What are the treatment complications?

A

• 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

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12
Q

How can treatment complications be managed?

A
  • Small doses, more frequently
  • Selegiline
  • Dopamergic agonists – Potentiate the effects
  • Apomorphine Infusion • Drug Holidays
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13
Q

How does Parkinson’s relate to dentistry?

A

• 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

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