This document discusses medical therapies for Parkinson's disease. It begins by describing the pathophysiology of Parkinson's, noting that dopamine neuron loss in the substantia nigra leads to neuronal imbalance and motor symptoms. The document then reviews various pharmacological treatments including levodopa, dopamine agonists, NMDA receptor antagonists, MAO-B inhibitors, and COMT inhibitors. For each class of drug, it discusses chemistry, mechanisms of action, pharmacokinetics, indications, adverse effects, drug interactions and contraindications. Surgical therapies are also briefly mentioned.
the presentation on anti parkinson drug contain their classification of drugs, mechanism of action. uses of drugs, side effect, causes, symptoms, additional symptoms, physiology, pathophysiology
A brief overview on Neuroleptic Malignant Syndrome presented for the PGs and the faculty of Dept. of Medicine, Govt. Medical College Kannur, Kerala, India
the presentation on anti parkinson drug contain their classification of drugs, mechanism of action. uses of drugs, side effect, causes, symptoms, additional symptoms, physiology, pathophysiology
A brief overview on Neuroleptic Malignant Syndrome presented for the PGs and the faculty of Dept. of Medicine, Govt. Medical College Kannur, Kerala, India
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
3. Pathophysiology
• Basal ganglia
• Modulates motor function
• Parts of the Basal ganglia include
• Striatum
• Globus pallidus
• Substantia nigra
• Subthalamic nucleus
• Thalamus
• Interacts with motor cortex
3
4. • The striatium receives excitatory input from the cortex
• Mediated by the excitatory neurotransmitter, glutamate
• The striatum also receives inhibitory input from inhibitory neurons
mediated by GABA
• Dopamine neurons from the substantia nigra project to both of these
exicitatory and inhibitory neurons
4
5. • In PD Dopaminergic neurons that project from the substantia nigra to
the striatum die
• The loss of the striatal dopamine neurons produces an imbalance in
striatum
• The overall consequence is reduction in the thalamic-cortical pathway
• Which leads to suppression of the motor cortex
5
8. CORTEX
Striatum
Globus pallidus
Substantia
nigra, pars
compacta
Thalamus
Subthalamic
Nucleus
Substantia nigra,
pars reticulate
GLutamate
GABA
Dopamine
Ach Direct
Pathway
↓ activity
Indirect
Pathway
Neuronal imbalance in this brain region and
alterations of striatal outflow pathways (called
direct pathway and indirect pathway)
The direct pathway of the striatum to the
substantia nigra pars compacta becomes less
active
The indirect pathway (striatum to
globus pallidus to subthalamic
nucleus to substantia nigra pars
reticulate increase in activity
The consequence is an enhanced activation of the
par reticulate neurons which exert an overall
reduction of the thalamic-cortical pathway
8
10. Pharmacological management Parkinson's
disease
• Medications restore dopaminergic activity → reduce symptoms,
improve quality of life
• Therapeutic options:
• Levodopa (increases dopamine supply)
• Dopamine agonists (increase activation of D2 and D3 receptors)
• N-methyl-D-aspartate (NMDA) receptor antagonists
• Monoamine oxidase(MAO) type B inhibitors
• Catechol O-methyltransferase (COMT) inhibitors
• Anticholinergics
10
11. COMT: catechol O-methyltransferase
3-MT: 3-Methoxytyramine
3-OMD: 3-O-methyldopa
DOPAC: 3,4-dihydroxy-phenylacetic
acid
L-DOPA: levodopa
MAO-B: monoamine oxidase type B
11
12. Levodopa
• Structure:
• Amino acid precursor of dopamine
• Levo rotatory stereoisomer of dopa (L-dopa)
• Mechanism of action:
• Levodopa crosses (BBB ); dopamine itself cannot cross the BBB .
• Converted to dopamine in the brain , even if the dopaminergic neurons are dying.
• Protected in the plasma from decarboxylation by concomitant administration of
carbidopa
• In the brain parenchyma, levodopa is decarboxylated to dopamine .
• Dopamine supply is restored → stimulates dopaminergic receptors
12
13. Pharmacokinetics
• Absorption:
• Absorbed in 30–60 minutes, increased with high-fat/high-protein meals
• Oral preparations include carbidopa to prevent decarboxylation in the plasma.
• Distribution:
• Crosses the BBB
• Peak plasma concentration: 20–30 minutes
• Half-life: 30 minutes to 4 hours
• Metabolism: in the brain parenchyma → metabolized into dopamine
• Excretion: urine
13
14. Adverse effects
• Nausea ,dizziness, headache, somnolence
• Arrhythmias:
• Ventricular extrasystole
• Atrial fibrillation
• Orthostatic hypotension
• Neuroleptic malignant syndrome(NMS)–like symptoms can be seen
with the sudden withdrawal of levodopa:
• Hyperthermia, confusion, muscle rigidity, diaphoresis, tachycardia
14
15. Drug–drug interactions
• Dopamine antagonists may reduce therapeutic effects.
• Pyridoxine increases extracerebral metabolism → decreased bioavailability
Contraindications
• Pre existing neuropathy
• Combination with (MAOIs) → hypertensive crisis
• Requires 14 day washout period between either drug (MAOI or levodopa–
carbidopa)
15
16. Dopamine Agonists
Chemistry and pharmacodynamics
• Dopamine agonists:
• Greater affinity for D2 and D3 receptors
• Inhibit anterior pituitary prolactin secretion
• Drugs include-Bromocriptine, Pramipexole, Ropinirole, Rotigotine
(transdermal patch), apomorphine
• Mechanism of action:
• Bind to dopamine receptors directly on the postsynaptic terminal
• The D2, D3, and D4 receptors couple to the Gi/o family of G proteins,
and dopamine agonists inhibit adenylyl cyclase and thus cAMP synthesis.
16
17. Pharmacokinetics
• Absorption:
• Absorbed quickly, with peak plasma concentration in 30 minutes to 6 hours
• Available in immediate-acting or extended-release forms
• Distribution:
• Crosses the BBB
• Half-life: 5–12 hours
• Metabolism: hepatic cytochrome P450system (CYP1A2 and CYP3A4)
• Excretion: renal and fecal
17
18. Indications
• Mild to moderate symptoms of PD
non-Parkinson indications for dopamine agonists:
• Pramipexole, ropinirole, and rotigotine: restless legs syndrome
• Bromocriptine: Hyperprolactinemia due to prolactin-
secreting pituitary adenoma and Acromegaly
18
19. Adverse effects
• Sleep attacks, particularly with pramipexole and ropinirole
• Nausea/vomiting, Dizziness, Orthostatic hypotension, Headache,
Cardiac arrhythmia, Dyskinesias
• Long-term use may cause:
• Choreiform and dystonic movements
• Psychiatric symptoms: Mania or depression, Hallucinations/psychosis,
Delusions
19
20. Drug–drug interactions
• MAOIs ,Dopamine antagonists (1st- and 2nd-generation antipsychotics)
• Other drugs that are metabolized by cytochrome P450 enzymes
Contraindications
• History of psychotic illness
• Severe cardiovascular disease
• Postpartum or breastfeeding
• Type 1 diabetes
• Sleep disorder
• Alcohol use
20
21. Amantadine (N-methyl-D-aspartate
Antagonist)
Chemistry and pharmacodynamics
• Structure: synthetic tricyclic amine
• Mechanism of action:
• Antagonist of the NMDA-type glutamate receptor → antidyskinetic effect
• May influence synthesis, release, or reuptake of dopamine
• Antagonizes the effects of adenosine at adenosine alpha-2-adrenergic
(A2A) receptors
21
22. Pharmacokinetics
• Absorption: oral
• Distribution:
• Cross the BBB
• Onset of action: within 48 hours
• Peak plasma concentration: 2–12 hours, depending on the dosage form
• Half-life: 9–31 hours
• Metabolism: conjugation, other unknown mechanisms
• Excretion: urine (up to 90% unchanged)
Indications
• Originally used as a treatment for influenza A
• Recommended for mild Parkinsonian symptoms, specifically dyskinesia and rigidity:
• May be used in combination with other agents
• Therapeutic effect lasts only 1st few weeks.
22
23. • Adverse effects- restlessness, depression, suicidal ideation, somnolence,
insomnia, agitation, hallucinations/psychosis.
Drug–drug interactions
• Clozapine: may cause severe constipation or ileus
• Trimethoprim: may increase amantadine levels and risk of psychosis
• Bupropion: may increase risk of adverse CNS effects
Contraindications
• Pregnancy and breastfeeding
• End-stage renal disease
23
24. Monoamine Oxidase (MAO) Inhibitors
Chemistry and pharmacodynamics
• Classified as:
• Irreversible inhibitors: selegiline and rasagiline
• Reversible inhibitors: safinamide
• Mechanism of action:
• Types of MAO:
• Type A metabolizes norepinephrine, serotonin, and dopamine (used for depression).
• Type B metabolizes dopamine selectively (used for PD).
• In the brain parenchyma, MAO type B (MAO-B) is selectively inhibited →
increased intracerebral concentration of dopamine
24
25. Pharmacokinetics
• Absorption: oral or transdermal
• Distribution:
• Crosses the BBB
• Peak plasma concentration: 1–3 hours, depending on the agent
• Onset of action: 2–3 weeks
• Half-life: 3–26 hours, depending on the agent
• Metabolism: hepatic (substrate of CYP1A2, CYP2D6, and other
CYP450 enzymes
• Excretion: renal and fecal, in different proportions, depending on the agent
25
26. Indications
• Recommended as an adjunct therapy for individuals with PD
• taking levodopa–carbidopa who exhibit a deterioration in response to it.
• Transdermal form has also been used in individuals with major depressive
disorder.
Adverse effects
• Drug–food interactions can lead to a hypertensive crisis:
• Avoid foods with high tyramine levels
• Xerostomia
• NauseaDiarrhea or constipation
• Drowsiness or insomnia
• Dizziness
26
27. Drug–drug interactions and
contraindications
• drugs that use the cytochrome P450 enzymesfor metabolism interact with MAO-
B inhibitors:
• CYP2B6 substrates NSAIDs: naproxen
• beta-blockers (bisoprolol) → additive hypotension
• Antidepressant bupropion → increased risk of hypertension
• Opioid pain medications
• Risk of serotonin syndrome with:
• SSRIs- fluoxetine, paroxetine
• SNRIs- duloxetine
• TCAs-amitriptyline
• Triptans
• Symptoms include altered mental status, autonomic instability, tremors, myoclonus, and
seizures
27
29. Catechol O-methyltransferase (COMT)
Inhibitors
Chemistry and pharmacodynamics
• Structure: parent compound is 3-nitrobenzene-1,2-diol, also called
nitrocatechol.
• Drug names:Entacapone,tolcapone, opicapone
• Mechanism of action:
• COMT peripherally metabolizes levodopa into 3-O-methyldopa.
• COMT is selectively inhibited → increased bioavailability of levodopa →
prolonged action of levodopa
• Clearance of levodopa is also decreased → greater bioavailability
29
34. General Approach to Treatment
• Initial therapy added when sxs become bothersome
• MAO-B inhibitors for mild sxs for some patients
• Levodopa or dopamine agonists are typical 1st line therapy
• Levodopa provides better motor control than dopamine agonists
• Adjunctive therapy
• If on Dopamine agonist add levodopa
• If on levodopa (800-1000mg/day) add next agent based on patient’s
characteristics
• Watch for symptoms of excess dopamine and decrease levodopa as necessary
34
36. Changes in motor response associated with chronic levodopa treatment. Levodopa-induced
motor complications. Schematic illustration of the gradual shortening of the duration of a beneficial
motor response to levodopa (wearing off) and the appearance of dyskinesias complicating “on” time.
PD, Parkinson’s disease
36
37. • “wearing off”
• Occur when last dose of
Carbidopa/levodopa stops working
• Add dopamine agonist
• Add COMT
• Increase frequency/dose of levodopa
• “on-off”
• Fluctuation of response to drug
• Periods of improved symptoms
alternating with poor symptom control
• Add COMT
• Examine protein intake as protein
decrease absoprtion of levodopa
• Dyskinesias with levodopa/carbidopa
• Remove selegiline
• Decrease levodopa dose
• Add amantadine
• Hallucinations/psychosis
• D/c/reduce dose of PD medication
• Add antipsychotic with least amount of
dopamine antagonism
• Quetiapine or clozapine
37
39. Management of nonmotor symptoms in Parkinson disease
• Depression
• Apathy
• Anxiety
• Cognitive impairment
• Psychosis
• Insomnia and other sleep disorders
• Daytime sleepiness
• Fatigue
• Dysphagia
• Autonomic dysfunction-
Constipation, Sialorrhea,
Rhinorrhea, Sexual dysfunction,
Orthostatic hypotension
39
40. Depression
• most common psychiatric disturbance and associated with suicidal
ideation and thoughts of death are common.
• Treatment — Patients with depression should be offered
antidepressants , CBT, or both
• AAN reviewed six small, RCT of pharmacologic treatment for
depression in patients with PD.
• SNRI or SSRI can be prescribed because of less adverse events than
TCA
40
41. Safety considerations with SSRI use
• QT prolongation
• Exacerbation of motor symptoms – induce or worsen dystonia,
akathisia, tremor.
• Exacerbation of comorbid sleep disorders – worsens RLS and rapid
eye movement sleep behavior disorder (RBD).
• Serotonin syndrome-uncommon but serious adverse event on
combination of MAO B inhibitor with antidepressant.
41
42. ANXIETY
• occur alone, or with depression.
• may be a symptom of wearing off of dopaminergic medication
• SSRIs such as citalopam, sertraline and SNRIs such as venlafaxine, mirtazapine
• Psychotherapy is also an option
• cannabinoids like nabilone is under trial
42
43. PSYCHOSIS
• characterized mainly by visual hallucinations and delusions
• dopamine agonists are the important cause of psychosis.
• Also triggered by infection, delirium, dementia.
• Treatment includes PD medication adjustments.
pharmacologic treatment include
• Pimavanserin-. 34 mg daily
• Quetiapine-12.5 mg to100 mg
• Clozapine-12.5 mg to 50 mg
43
45. FATIGUE
• Excessive daytime sleepiness (EDS) and depression are most common
and the most treatable identifiable causes
• empiric treatment amantadine and stimulants such
as methylphenidate and pemoline, are options.
45
46. DYSPHAGIA
• All phases of swallow are impacted due to abnormalities in both
striated and smooth muscle function, ineffective tongue movements,
delayed swallow responses, and weak cough-expectoration response.
• contributes to sialorrhea and increases risk of aspiration and
pneumonia.
46
47. Constipation
• related to autonomic dysfunction and slowed colonic transit time
• patient education, behavior modification and dietary changes and laxative
therapy.
• Polyethylene glycol , Probiotics.
• Lubiprostone, a locally acting chloride channel activator .
• alpha-synuclein deposited in the enteric nervous system, and therapies
targeting gut pathologic alpha-synuclein are under investigation
• ENT-01 (squalamine phosphate) is an oral steroid-polyamine conjugate that
displaces alpha-synuclein from enteric nerve cell membranes in preclinical
models.
47
48. Sialorrhea
• Due to reduced oro motor control and autonomic dysfunction
• anticholinergic medications- glycopyrrolate, atropine, hyoscine,
sublingual ipratropium
48
49. Sexual dysfunction
• Range from underactivity to hypersexuality
• Hypersexuality occur more in younger men and patients treated with
dopamine agonist therapy or DBS
• Erectile dysfunction may benefit from treatment
with sildenafil , tadalafil and vardenafil .
49
50. Orthostatic hypotension —
• Caused by disease itself or the PD medications including levodopa,
dopamine agonists, and (MAO B) inhibitors
50
54. Nonpharmacologic management of Parkinson disease
• Education
• Social prescribing- promote social engagement and lifestyle modifications
• EXERCISE AND PHYSICAL THERAPY- improve balance, flexibility, and strength.
Brisk walks, tai chi, swimming, and water aerobic exercises may be useful
• SPEECH and OCCUPATIONAL THERAPY
• Nutrition – high-fiber diet, adequate hydration, and regular exercise and MIND
diet may be associated with a lower risk of cognitive impairment.
Nutt JG, Carter JH. Dietary issues in the treatment of Parkinson's disease. In: Therapy of
Parkinson's Disease, Koller WC, Paulson G (Eds), Marcel Dekker, New York 1990. p.531.
Metcalfe-Roach A, Yu AC, Golz E, et al. MIND and Mediterranean Diets Associated with
Later Onset of Parkinson's Disease. Mov Disord 2021; 36:977. 54
56. Immunosuppressant
Azathioprine ISRCTN14616801,
EudraCT-2018-
003089-14 (AZA-PD)
2 Early PD MDS-UPDRS part III
Statin
Simvastatin NCT02787590,
ISRCTN16108482,
EudraCT-2015-
000148-40,
PDSTAT2015
2 PD with wearing-off
phenomenon
MDS-UPDRS part III
Lovastatin NCT03242499,
NCTRC201702
2 Early PD MDS-UPDRS part III
Mitochondrial enhancer
Ursodeoxycholic
acid
NCT03840005, STH1
8493,
EudraCT-2018-
001887-46 (UP
study)
2 Early PD Number of adverse
treatment reactions
Number of serious
adverse events
Number of patients
completing the
study
Murakami H, Shiraishi T, Umehara T, Omoto S, Iguchi Y. Recent Advances in Drug Therapy for Parkinson's
Disease. Intern Med. 2023 Jan 1;62(1):33-42. doi: 10.2169/internalmedicine.8940-21. Epub 2022 Feb 1. PMID:
35110492; PMCID: PMC9876715.
56
57. SUMMARY AND RECOMMENDATIONS
• When to initiate therapy – Treatment should generally begin when motor
symptoms are affecting function and quality of life.
• Preferred therapy for most patients –levodopa has superior effects on motor
function, activities of daily life, and quality of life and is often the best tolerated,
especially in older adults.
• Alternatives in select patients- DA, MAO B inhibitor, or amantadine is a
reasonable alternative. significant tremor despite levodopa may benefit from
add-on therapy with amantadine or an anticholinergic.
57