PHYS 261 West Coast University Parkinsons Disease Physiology Lab Presentation Speech

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DISCUSSION OUTLINE
Definition; Parkinson’s disease (PD) Is defined as the tremulous motion, with lessened muscular
power, in parts not in action and even when supported , with a propensity to bend the trunk forward,
and to pass from a walking to running pace: the senses and intellects being uninjured.
1.
History
i.
In western medical literature it was described by the physician Galen as shaking
palsy in 175 AD
ii.
In 1817 a detailed medical essay was published on subject by London doctor James
Parkinson
iii.
Jean Martin Charcot was the first to truly recognize the importance of
Dr.
Parkinson’s work and renamed the disease which was formerly named paralysis agitans
(shaking palsy) after him
iv.
Famous personalities known to have the disease, Mohammed Ali, Pope paul
2.
Natural History
i.
Begins between 40 and 70 years of age
ii.
peak age onset at the sixth decade
iii.
Infrequent before 30 years of age
iv.
More common in men than women
v.
Trauma, emotional upset, overwork, exposure to cold, rigid personality, etc are
suggested to be the predisposing factors to the disease but none of them have evidence.
vi.
Disease observed in all countries and all races.
3.
Parkinsonism and Parkinson’s disease Idiopathic
i.
Parkinsonism is a clinical syndrome characterized primarily by bradykinesia with
associated increased tone (rigidity), tremor loss of postural reflexes. There are many
causes but the most common is Parkinson’s disease
ii.
When parkinsonism features are present in a person with established etiology it is
called Parkinson disease.
4. Etiology
i.
Drugs and toxins i.e Antipsychotic drugs, Haldol (older and typical),
Lithium, metoclopramide, prochlorperazine, Tetrabenazine, manganese.
ii.
Other degenerative diseases e.g Dementia, progressive supranuclear palsy,
multiple system atrophy, Alzheimer’s disease, corticobasal degeneration.
iii.
Genetics, Genetic abnormalities resulting in protein misfolding and
accumulation and mitochondrial dysfuction are found to be responsible for
PD. Genetic Diseases i.e Huntington’s disease, Fragile X tremor ataxia
syndrome, dopa responsive dystonia, spinocerebellar ataxias, wilson’s
disease
iv.
Arteriosclerosis
v.
Encephalitis infection in response to brain trauma, tumors, hydrocephalus,
or ischaemia
5. Pathophysiology
i.
Antiphysotic drugs, Encephalitis and other cause > affects the the
substansia nigra > destruction of dopamine producing neurons with in the
basal ganglia > reduces the amount of available stratial dopamine
(inhibitory effects)> there is increase in acetylcholine (excitatory effects)
>Excitatory activity of Ach is inadequately balanced > Difficulty in
controlling and initiating voluntary movements.
6. Clinical Manifestations.
i.
In the beginning stages, mild tremors, slight limp, decreased arm swing
ii.
Later, shuffling gait, propulsive gait with arms flexed, loss of postural
reflexes
iii.
Slight change in speech pattern
iv.
Tremors i.e affects handwriting, non-intentional, present at rest but usually
not sleeping.
v.
Rigidity i.e Increased resistance to passive motion, when the limbs are
moved through their range of motion. Muscles feel stiff and required
increased effort to move.
vi.
Bradykinesia (akinesia) i.e slowness of active movement, Difficulty in
initiating movement
vii.
Postural Instability i.e changes in gait, tendency to walk forward on the toes
with small shuffling gait.
viii.
Facial appearance i.e Expressionless, eyes store straight ahead.
ix.
Speech problem i.e low volume, slurred speech, Monotone, difficulty with
starting with the speech.
x.
Visual Problems i.e Blurred Vision, impaired upward gaze.
xi.
Autonomic disturbances
xii.
Cognitive / behavioral i.e Depression, slowed responsiveness, Memory
deficit, Dementia
7. Pharmacological Management.
i.
Anti- cholinergic
ii.
Antihistamines
iii.
Dopaminergic
iv.
Dopamine agonists
v.
Mao Inhibitors
8. Surgical treatment
i.
Thalamotomy
ii.
Pallidotomy
iii.
Fetal tissue transplantation (no cases resulted in complete reversal of
symptoms)
iv.
Transplantation of genetically engineering cell lines or vector mediated
gene transfection.
v.
Deep Brain stimulation.
9. Diagnosis
i.
No specific test exists to diagnose Parkinson’s disease
ii.
Your doctor may suggest a specific single-photon emission computerized
tomography SPECT scan called a dopamine transporter (DAT) scan
iii.
Although this can help support the suspicion that you have Parkinson’s
disease, it is your symptoms and neurologic examination that ultimately
determine the correct diagnosis
iv.
imaging tests — such as MRI, CT, ultrasound of the brain, and PET scans
— may also be used to help rule out other disorders. Imaging tests aren’t
particularly helpful for diagnosing Parkinson’s disease.
10. Covid-19 effects on Parkinson’s disease.
i.
There are concerns around the increased vulnerability of patients living with
a chronic disease, and this also includes neurological conditions like
Parkinson’s disease (PD)
ii.
PD is more common in the elderly, and PD can compromise the respiratory
system, as reflected among others by the increased risk of pneumonia that
is present in patients with advanced PD.
iii.
The pathophysiology of PD puts patients at increased risk of chronic stress,
and a further worsening of this may well be one of various hidden sorrows
of the COVID-19 pandemic.
11. Alternative treatment.
i.
Supportive therapies can help ease some of the symptoms and
complications of Parkinson’s disease, such as pain, fatigue and depression.
When performed in combination with your treatments, these therapies
might improve your quality of life
ii.
Massage. Massage therapy can reduce muscle tension and promote
relaxation
iii.
Tai chi. An ancient form of Chinese exercise, tai chi employs slow, flowing
motions that may improve flexibility, balance and muscle strength.
iv.
Yoga. In yoga, gentle stretching movements and poses may increase your
flexibility and balance.
v.
Alexander technique. This technique — which focuses on muscle posture,
balance and thinking about how you use muscles — may reduce muscle
tension and pain.
vi.
Meditation and pet therapy.
References
Wirdefeldt, K., Adami, H., Cole, P. et al. Epidemiology and etiology of
Parkinson’s disease: a review of the evidence. Eur J Epidemiol 26, 1 (2011).
https://doi.org/10.1007/s10654-011-9581-6
https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/diagnosistreatment/drc-20376062
https://www.michaeljfox.org/news/ask-md-coronavirus-and-parkinsons
Lewis, S. M., Dirksen, S. R., Heitkemper, M. M., Bucher, L., & Harding, M.
(2014). Medical-surgical nursing: Assessment and management of clinical
problems. St. Louis, MO: Elsevier/Mosby.

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