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Introduction to Common CNS Disorders:

Introduction to Common CNS Disorders III - PD UNIT 3 PR 6 th edition: Chapter 18, p807-828 (Parkinson’s Disease)

Epidemiology:

Epidemiology > 2% of population > 65yrs 1million Americans are living with PD 50-60 000 new cases diagnosed each year in the US Incidence dramatically increases with age : 10 new cases/ 100 000 under 50yrs and 300 new cases / 100 000 ages 80-99yrs Incidence will increase with aging population Average onset 50 – 60 yrs *, 10% < 40yrs III - PD

Etiology:

Etiology Chronic, progressive neurodegenerative disease 80% idiopathic??? Insecticides (older onset) Genetic factors (younger onset) Acceleration of aging process 20% Non-idiopathic “Secondary Parkinsonism” Head trauma Drugs (MPTP) Infection - encephalitis etc III - PD

Awakenings: influenza epidemic causing encephalitis pts “frozen” for 30yrs:

Awakenings: influenza epidemic causing encephalitis pts “frozen” for 30yrs Robin Williams and Robert DeNiro

Pathophysiology – the basal ganglia:

Pathophysiology – the basal ganglia Striatum = caudate & putamen Globus Pallidus Subthalamic Substantia Nigra (* pars compacta and reticularis) III - PD

Pathophysiology:

Pathophysiology BG facilitates and inhibits movement via direct (+ve) and indirect (-ve) pathways respectively III - PD

Pathophysiology:

Pathophysiology 60% of the substantia nigra (pc) dopamine producing neurons die before motor symptoms emerge Dopamine acts on the striatum Decreased dopamine leads to: Overactivity of the inhibitory pathways (indirect) results in akinesias , bradykinesis and postural instability Overactivity of facilitory pathways (direct) leads to rigidity and tremor III - PD Depigmentation

4 Cardinal Features of PD (DIRECT impairments):

4 Cardinal Features of PD (DIRECT impairments) T remor R igidity leadpipe cogwheel masked face Bradykinesia / A kinesia akinesia aka: freezing episodes Triggers: narrow spaces, change in surfaces, turns 4. P ostural Instability ( pull test) “T.R.A.P” III - PD

PowerPoint Presentation:

+ ve (i.e. the patient failed the test) Pull test 3 or more steps is positive 1-2 is considered normal Note the asymmetrical tremor (present on the right but absent on the left) Advanced PD: Absence of a postural strategy Note that the tremor is present bilaterally with advanced disease

10 early warning signs of PD:

10 early warning signs of PD 1: Tremor 2: Micrographia 3: Loss of Smell 4: Trouble sleeping 5: Trouble walking (shuffling/reduced arm swing) 6: Constipation 7: Soft Voice 8: Dizziness (postural) 9: Kypohosis 10: Masked face/reduced blinking

DIRECT IMPAIRMENTS:

DIRECT IMPAIRMENTS Autonomic /cardiovascular dysfunction B &B, sex dysfxn Orthostatic hypofunction Dementia (20-40%) Depression Muscle weakness Insufficient neural activation Extensors > flexors Contributes to the “ stooped” kyphotic posture III - PD

INDIRECT IMPAIRMENTS:

INDIRECT IMPAIRMENTS Postural: Stooped/ kypohtic (indirect-composite) Contractures: Gait disturbances (VIDEO ) See box 18.2, p816: Festinating gait (p813) Dysphagia and drooling Hypokinetic dysarthria, hypophonia Cardiovascular decline Micrographia III - PD PD gait “off” meds f/b “on” meds, note the short “freezing” of gait that occurs during turns

2 Clinical Subgroups:

2 Clinical Subgroups Postural instability, gait disturbances (freezing) Bradykinesia (akinesia) Debilitating Rapid progression Impaired Cognition/dementia (late onset; >65yrs) Less bradykinesia and postural instability Less debilitating Slow progression Earlier onset (<65yrs) PIGD (30%) Tremor (70%) III - PD

Disease progression & Stages, Table 18.1, p 817:

Disease progression & Stages, Table 18.1, p 817 Hoehn & Yahr Stages: I – unilateral II – bilateral involvement, or midline involvement (no postural instability) III – postural instability (aka: poor balance and falls, + ve pull test) present but still independent IV – all symptoms present, needs assistance to stand/walk V – w/c or bed bound III - PD

Medical Management:

Medical Management Brain imaging and blood work normal Clinical diagnosis 2/4 cardinal symptoms ( TRAP ) present and asymmetrical R/o other neurodegenerative diseases +ve response to levodopa New test: proteins in salivary glands III - PD

Pharmacological Management p817-818 Levadopa (L-dopa):

Pharmacological Management p817-818 Levadopa (L-dopa) L – dopa is a dopamine precursor Given with carbidopa to inhibit metabolism Low protein diet required Treats bradykinesia and rigidity > instability and tremor Sinemet loses full effect after 4-6 yrs End-dose deterioration (“wearing off” state) On-off phenomenon ( unpredictable fluctuations) Common side effects: dyskinesia , visual hallucinations, hypotension, nausea to name a few III - PD sinemet

Pharmacological Management:

Pharmacological Management Dopamine Agonists Mirapex, Requip – stimulate postsynaptic dopamine receptors Permits a lower dose of levodopa ( sinemet ) Anticholingergics Artane : tremor and dystonia Monoamine Oxidase B Inhibitors (MAO-B inhibitors) Azilect : inhibits the enzyme that degrades dopamine Permits a lower dose of levodopa ( sinemet )

Drug induced dyskinesia:

Drug induced dyskinesia

Deep Brain Stimulator (DBS):

Deep Brain Stimulator (DBS) III - PD “Brain pacemaker” STN ( subthalamic n.) stimulation to control rigidity/tremor Chronic stimulation for rigidity Intermittent for tremor Becomes less effective over time Not useful for postural reflexes, gait disturbances, or speech Lowers amount of levodopa needed

FYI::

FYI: Removal/ lesioning of the thalamus or pallidum Irreversible/permanent Largely replaced by DBS Fetal cell transplantation Not practiced in the USA