Week 8: Parkinsons Flashcards

1
Q

Diagnosis is based on clinical presentation. Classical signs of pD are:

A
  • tremor
  • bradykineasia
  • muscle rigidity
  • postural instability
  • resting/ unilateral
  • slowness of movement
  • Cog wheel
  • gait & balance
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2
Q

Explain the pathology of parkinsons

A

 Neuronal cell death in the substantia nigra pars
compacta
 By diagnosis 60-70% of Dopamine producing
cells have died
 This loss continues in spite of treatment
 With further loss, there is further reduction in
Dopamine levels and associated progression of symptoms

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3
Q

Describe the link between alpha Synuclein, Lewybodies & Parkinsons

A

 Deposition of a protein called alpha synuclein
 Agragates abnormally & forms clumps /Lewy
body
 Damages nerve cell - possibly why the cells die
 Increased interest in Alpha Synuclein based therapies to prevent its formation
 Very promising research- eg.antibodies
directed towards this unwanted protein

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4
Q

What is the Braak Theory?

A
  • the earliest sign of parkinsons are found in the enteric NS, the medulla in particular, olfactory bulk (smell)
  • under theory parkinsons only progresses to substantial nigra and cortex over yrs
  • been pushed aside why? evidence that the non-motor symptoms like loss of sense of smell, hyposmia, sleep disorders + constipation may come after motor features of the disease by several years.
  • So researchers are increasingly focused on non-motor symptoms to detect PD as early as possible to look for ways to stop it.
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5
Q

Goals of Parkinsons treatment is to?

A

Regain balance of dopamine and acetylcholine.
Deficit of Dopamine results in
bradykinesia & muscle rigidity.

Imbalance of Acetylcholine
results in tremor

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6
Q

Timing of medication

slide 22-24

A

 Levodopa has a very short half life – hence has to be taken regularly
 Timing is highly significant for steady plasma DA levels-to provide optimum relief of symptoms.
 Correct timing of medication may dictate how mobile and safe the person with PD is or how well they can communicate/other
 Levodopa should never be stopped abruptly

 Response to drugs is variable
 Individual regimes need to be devised
 The regime must achieve optimum balance between benefits & side effects
 Levodopa best taken before meals (levodopa an amino acid & hence
competes with other dietary amino acids
 Delayed gastric emptying- affects absorption of medications

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7
Q

What are some side effects of Therapy

A

End of Dose Failure - with progression of condition
On/ Off Phenomenon- unable to function
Dyskineasia- Involuntary movements
Dystonia- abnormal posturing

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8
Q

What is dystonia

A

 Manifestation of underlying disease
 Involuntary muscle contractions which
produce abnormal sustained posturing
 Can affect any part of the body eg. feet, toes, neck
 Mostly occurs in the “off ” state but can occur as a peak dose effect
 Can be distressing & painful – report to neurologist as medication adjustment may reduce distress. Stretching / Botox

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9
Q

Long term complications of Parkinsons medication

Dyskinesia

A
  • Writhing, wriggling involuntary movement
  • can affect any part of the body- e.g. head, trunk, limbs and vary in severity- mild, moderate, sever.
  • usually occur at peak dose, end dose or both (biphasic)
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10
Q

What are the motor change that occur in PD and why?

A

The basal ganglia require dopamine to plan & control well learnt automatic movements & complex skills
-people with PD have BG dysfunction resulting in impaired initiation, quality & control of automatic movements.

Motor changes:
-short shuffling gait/ reduced or absent arm swing
 Akinesia (Absence or poverty of movement)
 Freezing (motor block)
 Problems turning – increases falls risk (difficulty turning / rolling over in bed)
 Festination (running, difficulty stopping)
•Reduced pincer grip (hands feel clumsy) •Problems dual tasking (eg.walking & talking)
•Balance problems (Loss of postural •reflexes) Falls
•Reduced “scanning” of environment – • reduced neck movement

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11
Q

Tell me what happens in a freezing episode

A
  • sudden inability to move, as if feet stuck to the floor.
  • can last a few moments to 15-20 mins or more
  • usually occurs in confined spaces
  • can occur in the ‘on’ or ‘off’ state document the time this occurs. This will assist the prescribing doctor when adjusting medications.
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12
Q

What are strategies to enhance movement for patients

A
  • rehearse in mind before starting
  • reduce distractions
  • use visual cues to trigger a movement
  • use auditory cues e.g. Say out loud ‘left right or one two’
  • use physical cues e.g. Rock from side to side or tap on your leg saying ‘one two’
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13
Q

What are destination

A
  • Sudden episoe of an involuntary increase of the stepping rate (hastening) together with a minimisation of step length
  • use cues to help regulate i.e. ‘heel-toe’
  • arange living enviro to mae it easier to move around + reduce persons chances of falling
  • try and avoid cluttering small spaces as it can increase ‘freezing’ spaces.
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14
Q

What is the Etiology of dye-autonomia in PD

A
  • In PD, Lewy body pathology has been identified in both central and peripheral autonomic systems
  • this results in abnormal activation of the parasympathetic & sympathetic systems producing constipation, delayed gastric emptying, urinary retention, erectile dysfunction, orthostasis & heat and cold intolerance.
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15
Q

Orthostatic Hypotensions in PD (form of low blood pressure causing dizziness)
Management

A
  • no swift changes of position- stand up slowly
  • eliminate or reduce antihypertensive meds if possible
  • Have PD medications reviewed
  • increase dietary salt and fluid
  • compression stockings
  • Avoid/ reduce caffein and alcohol
  • avoid excessive increase in body temp (bath, sauna)
  • eat frequent small meals
  • elevate head of bed by 30deg-40
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16
Q

What are the causes of Constipation in PD

A
  • Colonic dysmotility + anorectal dysfunction
  • Lewybody pathology within the myenteric plexus of the colon > slowed transit time and occasionally megacolon, intestinal pseudo obstruction and volvulus
  • combination of disordered contraction & relaxation of the muscles of defecation > excessive straining, pain, sense of incomplete evacuation
  • Faecal incontinence (losse stool) in PD sometimes due to overflow around faecal impaction -x-ray.

Additional factors:

  • medications
  • lack of dietary fibre
  • inadequate fluid intake
  • lack of exercise
  • aging
  • other co-morbidities.
17
Q

Other issues in PD patients?

A

Swallowing- drooling, fatigue during meals, difficulty taking medications 9chi=oking),

Nutrition- prevent dehydration, weight loss due to swallow problems and reduced fine motor skill, nutritional supplements.

Communication:
Reduced facial expression, Soft voice, reduced eye blink (staring), bradyphrenia (slowness in thinking)

18
Q

Pain in parkinsons

A
  • experienced by 70-80% of people with PD
  • most unrecognised & under treated NMS
  • mentioned by James P in his original essay
  • peripheral mechanical pain
  • central neurological pain


 Areas of brain thought to influence pain perception are affected in Parkinson’s
 PWP may have less ability to modulate the heightened sense of pain within the pain matrix
Painmanagement: dopaminergic therapy
 Treat depression as can augment the subjective feeling of pain
 Gabapentin for neuropathic types of pain
 Atypical Neuroleptics for oral/genital pain

19
Q

Explain Peripheral mechanical pain

A

 Dystonic – painful dystonic spasms
associated with “off”+ biphasic states
Affects hands, toes, feet - inversion, curling, extension, flexion. Dystonic pain can also involve the neck or jaw
 Muscoskeletal /rheumatic- rigidity, hypokinesia - aching, cramping, arthraltic
 Neuritic/radicular - pain in region of a nerve root
 Akathitic discomfort- sense of restlessness, need
to move, intolerance of remaining still
 Skin biopsies have revealed alpha synuclein path in peripheral nerves of PWP (but not MSA,PSP or CBD)

20
Q

Explain Central Pain

A


 Burning, stabbing, tingling, formication (like insects crawling on skin)
 Similar to neuropathic pain
 Not always on side most affected + can involve the face, head, epigastrium, abdomen, pelvis, rectum & genitalia
 Oral pain syndrome “burning mouth”
 Tend to occur in “off” periods but not abolished by levodopa or motor nerve blocks

21
Q

What are the Neuropsychiatric changes in Parkinsons

51

A
 Anxiety
 Depression
 Sleep-disturbance  Hallucinations
 Paranoia
 Dementia
Medicationsideeffect ImpulseControldisorder Gambling / Shopping / Hypersexual