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1 : Parkinson Disease Ramesh Sangwan B.Pharm-3rd year
2 : What is Parkinson’s? Parkinson’s is a neurodegenerative disease. Movement is normally controlled by dopamine, a chemical that carries signals between the nerves in the brain. When cells that normally produce dopamine die, the symptoms of Parkinson’s appear.
3 : Outline Parkinson’s is a neurodegenerative disease that impairs motor movement due to the loss of dopaminergic neurons in the substantia nigra. It occurs mainly in people over the age of 60. This neurodegeneration may be a result of a genetic predisposition, or by environmental factors such as toxins and drugs that increase the oxidative stress of dopaminergic neurons Symptoms result when dopamine levels are reduced by about 90% The main symptoms are MIST – Muscle rigidity, Impaired balance, Slowness and Stiffness and Tremor There is no cure. Treatment for Parkinson’s disease targets the alleviation of symptoms only Non-pharmacological therapy includes physical, occupational and speech therapy Pharmacological therapy includes dopamine agonists, MOA-B inhibitors, dopamine replacement therapy, COMT inhibitors, amantadine, anticholinergics and surgery.
4 : Main Symptoms - MIST M – muscle rigidity I – impaired balance S – slowness and stiffness T - tremor
5 : Other Motor Symptoms Soft speech Problems with handwriting (small) Reduced facial expression Shuffling when walking Muscle pain Stooped posture Difficulty turning in bed Lack of facial expression Slowed activity of daily living
6 : Other Non-motor Symptoms Constipation Sleep disturbances Fatigue Bladder urgency and frequency Dizziness on standing Depression: feeling sad, having less energy Memory problems Increase sweating Low voice volume Diminished sence of smell
7 : Progression of Parkinson’s Currently, there is no cure Progresses at different rates for each person Medication will need to be adjusted as symptoms change Other non-motor symptoms may appear such as depression, difficulty swallowing, sexual problems, or cognitive changes May progress more quickly in people who are older when symptoms begin May progress more slowly when the main symptom is tremor Parkinson’s is not a mental disease, although 30% of people with Parkinson’s will eventually develop dementia
8 : Incidence and Risk Factors Affects 100 000 Canadians – both men and women, from all ethnic backgrounds Not only found in older people – it can affect people as young as 30 or 40, although average age of onset is 60 Genetic predisposition Environmental factors (toxins)
9 : Pathophysiology Results from the loss of dopaminergic neurons of the basal ganglia Specifically affects the pathway going from the substantia nigra to the striatum As with most brain tissue, the neurons atrophy with age If this loss of neurons becomes too great to reduce dopamine levels by about 90% then Parkinson’s symptoms result
10 : Pathophysiology Movement disorders arise from this disfunctioning of the nigrostriatal pathway Normally input from the substantia nigra to the striatum can promote movement, both by the excitation of a direct pathway and inhibition of an indirect pathway In Parkinson’s patients loss of dopaminergic neurons in this pathway, resulting in increased difficulty initiating movements The movement pathway involved is related to those movements guided by internal cues and movements guided by external cues are unaffected AKA STRIATUM
11 : Drug-induced Parkinsonism The use of dopamine 2 receptor antagonists in the treatment of psychotic disorders, such as schizophrenia, can result in some serious side effects When these drugs block D2 receptors in the nigrostriatal pathway, disorders of movement resembling Parkinson’s disease can result These side effects are known as extrapyramidal symptoms (EPS)
12 : Chemical Model of Parkinson’s There are many hypotheses for the cause of Parkinson’s disease, the most notable being environmental factors such as exposure to toxins A model has been developed for use in monkeys using the chemical MPTP (1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine) MPTP, a contaminant in synthetically made heroin, was first discovered in drug addicts that showed Parkinson’s symptoms MPTP is metabolized by monoamine oxidase, which is highly concentrated in dopaminergic neurons, to MPP+ MPP+ concentrates in substantia nigra neurons by binding to neuromelanin and causes cell toxicity by disrupting the electron transport chain in mitochondria As a result, exposure to MPTP leads to Parkinson’s disease and can be used in animal models to study the disease
13 : Mechanisms for Neuronal Degeneration Many hypotheses as to the biochemical mechanisms that lead to neuronal cell death occurring in Parkinson’s disease Role of mitochondrial dysfunction and oxidative stress in contributing to neuronal cell death in the substantia nigra Inhibitors of Complex I of the mitochondrial electron transport chain have been shown to reproduce the pathological features of the disease Mis-folding and abnormal degradation of proteins within the cell has also been associated with increased dopaminergic neuronal death Increased levels of the enzyme monoamine oxidase (MAO) results in increased generation of H2O2 which cause oxidative damage to mitochondria in the neuron Increased levels of ferrous iron, which facilitates the conversion of H2O2 to reactive and damaging hydroxyl radicals, were observed in dopaminergic neurons of Parkinson’s patients
14 : Treatment Options Non-pharmacologic – education, exercise, nutrition, support Physical therapy helps mobility, flexibility and balance Occupational therapy helps with daily activities Speech therapy helps with voice control Exercise helps muscles and joints and improves overall health and well-being Drug therapy is only for symptom management, there is no drug that can cure but slow the progression of the disease.
15 : Treatment Options MAO type B inhibitors: prevents dopamine metabolism within the brain Usually first drug of choice if disease in early stages May be neuroprotective Dopamine agonists: directly stimulate dopamine receptors. Also an initial drug of choice if the patient is functionally young Dopamine replacement therapy: Levodopa immediate precursor to dopamine, converted to dopamine in brain When more symptom relief is required Effect wears off over time Patients can develop motor fluctuations (levodopa induced dyskinesias)
16 : Treatment Options COMT (catechol-O-methyltransferase) inhibitors: used in conjunction with levodopa Reduces motor fluctuations caused by levodopa Amantadine: Used with levodopa, for antidyskinesia effect, MOA unknown Anticholinergics: blocks acetylcholine effects (i.e. tremor) that are increased in the absence of dopamine Surgery: deep brain stimulation of the subthalamic nucleus for severe disabling dyskinesias.
17 : Special Thanks To- Dhirender kaushik (Guide line) Dr. Manoj Kumar (co-guide line) Rishi dev Yadav (Computer help)
18 : Thank you for Attention Jai Hind Jai Bharat Goodby

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