2. Introduction
• Parkinson’s disease (PD) is a complex progressive neurodegenerative
disease characterized by tremor, rigidity, and bradykinesia, with postural
instability appearing in some patients as the disease progresses.
• It was first described by James Parkinson in 1817 and further
characterized by Jean-Martin Charcot, and our knowledge of PD is
continuing to expand.
• PD is the second most common neurodegenerative disease after
Alzheimer’s disease (AD), with a prevalence of approximately 0.5–1%
among those 65–69 years of age, rising to 1–3% among persons 80 years
of age and older.
3. Risk Factors Associated With PD
• Elevated cholesterol
• Environmental toxins
• Head trauma
• High caloric intake
• Increased body mass index
• Inflammation associated with activation of microglia
• Methcathinone (manganese content)
• Methamphetamine/amphetamine abuse
• Mitochondrial dysfunction
• Nitric oxide toxicity
• Oxidative stress
4. Symptoms PD
• Symptoms include resting tremor, bradykinesia, gait, speech difficulties, hypophonia,
muscle dystrophy, postural deformities and instability. Pain, stiffness or numbness in
limbs, bradykinesia, tremors, a decline in facial expressions, and hypophonia are motor
symptoms seen in the early stages of this disease’s onset.
• Late-stage motor features may include motor fluctuations, dyskinesia, gait freezing, and
falling. Initial diagnosis may be made based on evaluation of clinical features of patient
history and examination.
6. General Cause PD
The Commoner causes of parkinsonism:
• Drug-induced parkinsonism
• Multisystem atrophy
• Progressive supranuclear palsy
• Normal-pressure hydrocephalus
• Multiple lacunar strokes
• Cortico basal degeneration
• Dementia with lewy bodies
7. Pathogenesis of Parkinson’s disease
A number of mechanisms have been implicated in PD pathogenesis, with α-
synuclein aggregation central to the development of the disease. Multiple
other processes are thought to be involved, with several studies suggesting
that abnormal protein clearance, mitochondrial dysfunction, and
neuroinflammation play a role in the onset and progression of PD. However,
the relationship between these pathways remains unclear.
• α-synuclein misfolding and aggregation
• Mitochondrial dysfunction
• Dysfunctional protein clearance systems
• Ubiquitin-proteasome system
• Autophagy- lysosome system
• Neuroinflammation
8. Diagnosis
The signs and symptoms of hypothyroidism can include one or more of the
following
• Fatigue
• Weight gain from fluid retention
• Dry skin and cold intolerance
• Yellow skin
• Coarseness or loss of hair
• Hoarseness
• Goiter
• Reflex delay, relaxation phase
• Ataxia
• Constipation
9. Treatment Approaches
• Treatments can vary from drugs, surgeries, therapy, or a combination
of different treatments. They must also be adjusted throughout the
course of the disease, as some common treatments, such as L-DOPA
lose effectiveness over time. Treatment of PD using available drugs
has positive symptomatic effects; however, there are no disease-
modifying or neuroprotective therapies available to slow the
progression of the disease.
10. Treatment
• Dopaminergic Medications: Dopamine agonists taken orally or through injection.
• MAOIs, inhibitors and antagonists: Inhibit breakdown of levodopa and dopamine
through oral drugs.
• Anticholinergics: Reduce acetylcholine activity at choline receptors through oral
drugs.
• Neurotrophic Factors: Small natural proteins, specifically glial cell line-derived
neurotrophic factor .
• Nanomedicine:Modification of existing drugs to improve delivery method.
11. Treatment
• Surgical Treatments: Can have high effectiveness with long-term results.
• Ablative Surgery: Incision into the global pallidus, thalamus, or subthalamic nucleus either
bilaterally or unilaterally.
• Deep Brain Stimulation: Implant that stimulates the basal ganglia through high frequency
electrical stimulation.
• Transplantation and Gene Therapy: Transplantation of stem cells into the striatum, insertion
of non-disease and disease modifying transgenes.
• Physical Therapy: Addresses mobility and motor-related symptoms through physical
training.
12. Treatment
• Occupational Therapy: Help patients maintain work, leisure, and self-care activities
for as long as possible.
• Speech Therapy: Improves speech through voice exercises.
• Cognitive Behavioral Therapy: Management of a symptom through behavioral
training methods.
13. Conclusion
• PD is a chronic, progressive neurodegenerative disease characterized by
both motor and nonmotor features. Striatal dopamine depletion has been
identified as the major cause of the disorder’s motor symptoms and
bradykinesia. Nonmotor symptoms include sleep disorders, depression, and
cognitive changes. The differential diagnosis of PD should include a
comprehensive history and physical examination.
• The primary goal in the management of PD is to treat the symptomatic
motor and nonmotor features of the disorder, with the objective of
improving the patient’s overall quality of life. Therapies that slow the
progression of the disease or provide a neuroprotective effect have not been
identified.
