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Idiopathic Parkinson's Disease, environmental factors - dietary intake…
Idiopathic Parkinson's Disease
Pathology
: state the single most well known and characteristics (hallmark) change in the diease e.g., cell type, cellular change observed, and structures that are affected
degeneration of neurons in the substantia nigra pars compacta
diagnosis:
briefly describe 3 steps/test used to aid diagnosis (purpose of each step/test) e.g., nerve conduction test to measure AP conduction velocity
Evaluates person's response to medications used to treat PD
Macphee & Steward 2012
Clinical Ax may include standard test for olfactory function and REM sleep behaviour disorder
Macphee & Steward 2012
Physician observes current clinical signs, eliminates other neurodegenerative diseases as the cause of those signs/symptoms (no diagnostic test available)
Macphee & Steward 2012
risk factors
: list three examples of well established risk factors
use of beta-blockers and antipyschotics enhance risk of PD
Kalia & Lang
Environmental elements - rural areas, drinking well water, having an agricultural occupation and being exposed to pesticides
Kalia & Lang
genetic factors
clinical manifestations
prodromal signs/sumptoms
: 3 examples
REM sleep behaviour disorder, and fatigue
Kalia & Lang; Macphee & Stewart 2012
depression, anxiety,
constipation
cardinal motor signs/symptoms
: 4 examples
resting tremor (noted initially in the hand on one side and sometimes in the foot) - increase under stress or intense mental activity
muscle rigidity
bradykinesia
shuffling gait
Connolly & Lang 2014
non-motor signs/symptoms
: 3 examples
visual perceptual deficits (spatial perception, contrast sensitivity, colour discrimination, visuospatial problem solving)
Isenkul, 2019
Sleep disturbances, including REM, sleep behaviour disorder, and insomina
Yu, Tan and Wu 2015
cognitive impairments (reduced attention, memory, executive functions)
Dong et al., 2020; Smith et al., 2019
Pathophysiology
Dopaminergic pathophysiology:
list three major abnormalities that occur
death of dopaminergic neurons in the substantia nigra pars compacta
the substantia nigra is located in the basil ganglia - produces dopamine and transports to the dorsal striatum
decreased dopamine leads to deficits in the speed and quality of motor movements, postural stability, cognitive skills, affective expression (impairment of extrapyramida tracts controllinggcomplex body movement
rigidity
bradykinesia
tremors
postural change
presence of lewy bodies - protein abnormally fold and form intracellular inclusions within the cell body and neurons, neuroinflammation is another typical feature of PD
occurs through 6 stages overtime and throughout the CNS beginning with the (stage 1) PNS, olfactory system, medulla and progressing through (stage 2) the pons, spinal cord grey matter, (stage 3) midbrain, basal forebrain, limbic system, (stage 4) thalamus, and temporal cortex
(stage 5-6) affects multiple cortical regions of the brain
Braak et al., 2003
serotonergic loss (happens at a slower pace)
Politis & Niccolini 2015)
Non-dopaminergic pathophysiology
: list one major abnormality that occurs e.g., plasma membrane, cytosol, organelles, nucleus, and/or cell structure of a neuron (include name of type of neuron affected and where in the brain
Neurodegeneration owith lewy bodies can be found in cholinergic neurons of the nucleus basalis of Meynert (NBM), epinephrine neurones of the locus coeruleus (LC), and serotonin neurons of the median raphe,in additon to neurons in the olfactory system, cerebral cortex, spinal cord, and peripheral autonomic nervous system
Olanow, CW, Stocchi, F & Lang, A 2011,
PD progresses beggining as non-dopaminergic neurons of the dorsal motor nucleus of vagus (DMV)
Glial cell pathophysiology
: list one abnormality that occurs e.g., abnormality in the plasma membrane, cytosol, organelles, nucleus and/or cell structure
Activation of astrocytes and microglia -
release of neuroprotective/harmful mediators
microglia - during early stages of PD
during late stages excessive activation leads to release of proinflammatory mediators that accelerate the degeneration of dopaminergic neurons
NA+/K+ -ATPase (pump)- reduced
increases dystonia - involuntary muscle contraction
genetic mutations
: two examples of known genetic mutations e.g., mutattions in GTODD1 and GTODD2 genes
treatment
: name common medication that is used to treat the clinical manifestations ---
briefly describe how mechanism of action of Madopar specfically relates to hallmark pathology/pathophysiology
medication to treat primary motor symptoms
- aim to increase the concentrations and uptake of dopamine include levodopa, dopamine agonists, and monoamine oxidase type B inhibitors
Connolly & Lang 2014; Kalia & Lang 2015
deep brain stimulation may be used to treat PD that is no longer responding well to medications
Yin et al., 2018; Dong et al., 2020
- sends electrical impulses to the subthalamic nucleus, internal globus pallidus/thalamus to reduce tremours :red_cross:
aetiology
(cause): brief description of one current and widely accepted aetiology for idiopathic parkinson's disease ----
relate/link to pathology/pathophysiology
environmental factors - dietary intake, exposure to environment elements, a history of head trauma, and type II diabetes
Camargo Maluf et al., 2019
Asssociation between diet and the risk for PD e.g., exposure to iron sources, intake of too much iron supplement, increased diary consumption (in men) and higher total blood cholesterol levels (in woman)
Kalia & Lang
Kalia and Lang 2015
PET and SPECT scans can be used to assess the density of presynaptic dopaminergic terminals within the striatum
Kalia & Lang
fMRI may be used to examine the executive control network and its functional connections
Dong et al., 2020
:red_cross:
(effectiveness of medications may decrease while side effects increase) - levodopa complications - motor complications, primarily comprised of fluctuations in motor response and involuntary movements of dyskinesias (associated with higher dose)
Olanow, CW, Stocchi, F & Lang, A 2011,
(side effects include depression, slurred speech, tingling in the head and hands and problems with balance)
dopamine replacement effective treatment streategy for PD
Olanow, CW, Stocchi, F & Lang, A 2011,
lewy body relates to both dopaminergic/non-dopaminergic
relates to non-dopaminergic pathophysiology
relates to dopaminergic pathophysiology
depression <<>>
Leentjens, AF 2015, ‘Parkinson disease: Depression - Risk factor or early symptom in Parkinson disease?’, Nature Reviews. Neurology, vol. 11, no. 8, pp. 432–433.
Boscia, F, Begum, G, Pignataro, G, Sirabella, R, Cuomo, O, Casamassa, A, … Annunziato, L 2016, ‘Glial Na+-dependent ion transporters in pathophysiological conditions’, Glia, vol. 64, no. 10, pp. 1677–1697.
Homayoun, H, Stebbins, G, Tilley, B & Goetz, C 2012, ‘Fatigue in Parkinson's Disease (P06.052)’, Neurology, vol. 78, no. Meeting Abstracts 1, pp. P06–P06.052.
dopamine terminal loss in the caudate nucleus and putamen
Identified that reduced glucocerebrosidase (GCase) increase the risk of developing PD even in people without mutations in GBA1 gene. This occurs is prior to α-synuclein accumulation and relates to reduced chaperone-mediated autophagy, increased α-synuclein and decreased ceramide, identifying therapeutic targets
https://www.neura.edu.au/health/parkinsons-disease/extra-information/?gclid=EAIaIQobChMIpa3qrNek-gIVyZlmAh3x5gCsEAAYASABEgI3-vD_BwE