Parkinson s Disease. Graham A. Glass, MD. Assistant Professor of Neurology University of California San Francisco
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1 Parkinson s Disease Graham A. Glass, MD Assistant Professor of Neurology University of California San Francisco San Francisco VA Medical Center Parkinson s Disease Research, Education and Clinical Center (PADRECC)
2 History of PD First described by James Parkinson, English physician & geologist, in 1817 Called paralysis agitans by Marshall Hall in 1841
3 Epidemiology of PD Mean age of onset: 60 years Prevalence increases with increasing age 1/1,000 in middle-age 50/1,000 in the elderly Third most common neurodegenerative disease Men & women roughly equally affected Minority of cases strongly familial???
4 Pathology of PD
5 Staging of brain pathology related to sporadic Parkinson s disease Heiko Braak, a, Kelly Del Tredicia, Udo Rüba, Rob A. I. de Vosb, Ernst N. H. Jansen Steurb and Eva Braaka, Neurobiology of Aging. v. 24. no p DM- dorsal motor CO coeruleus SN substantia nigra MC- motor cortex HC high order sensory areas and prefrontal fields FC- 1 st order sensory assoc areas, motor planning
6 Cardinal Clinical Features of PD Definition: an idiopathic, relentlessly progressive neurological disorder manifested by: Bradykinesia/akinesia Tremor Rigidity +/- Postural instability
7 Bradykinesia
8 Tremor
9 Rigidity
10 Postural Instability
11 Parkinson s as a Multi-system Disease Langston, 2006
12 Multiple Sites of Neurodegeneration SNc ->Dopamine red Locus Ceruleus ->Norepinephrine green Raphe N. Amygdala->Serotonin orange Acetylcholine - blue Lang & Lozano (1998)
13
14 Earliest Signs & Symptoms of PD
15 Excessive Fatigue in Parkinson s 33-58% of Parkinson Patients complain of extreme fatigue 1/3 of PD patients consider fatigue to be the most disabling symptom May precede diagnosis. May worsen as PD progresses May or may not relate to depression You sometimes have to bring this problem to the attention of your doctor!!
16 Dream Enactment Behavior
17 Autonomic Changes in PD
18 Dysautonomia Erectile dysfunction (men) Neurogenic bladder Constipation Orthostatic hypotension Testing: autonomic reflex screen, sweat test, anal sphincter EMG, urodynamics
19 Cognitive Changes in PD
20 Prevalence of depression Data from: Birrer, RB, Vemuri, SP. depression in later life:
21 Medications for Parkinsonism Dopaminergic L-dopa (Sinemet IR/CR,Parcopa) COMT inhibitors (Tasmar, Comtan) Dopamine agonists (Bromocriptine, Permax, Mirapex, Requip, Apokyn,rotigatine) MAO-B inhibitors (Selegiline, Rasagiline) Anticholinergic (Artane, Cogentin) Amantadine
22 Mechanism of Action DOPAC HVA Selegiline rasagiline 3-MT MAO-B MAO-B COMT tyrosine TH l-dopa AADC DA Amantadine DA 3-OMD l-dopa COMT Tolcapone Entacapone Pergolide Bromocriptine Pramipexole Ropinirole
23 Dopamine Agonists May delay the need for Sinemet (CALM-PD) Slower titration and typically less robust than Sinemet Not associated with dyskinesias alone as much as with levodopa Not metabolized or effected by protein intake Considered treatment of choice for young onset patients (young??)
24 DA s: Common Adverse Effects Nausea, Vomiting Dizziness, postural hypotension Lower extremity edema Drowsiness and somnolence, sleep attacks Compulsive Behaviors Confusion, hallucinations, paranoia, sleep disturbances Pulmonary and retroperitoneal fibrosis; pleural effusion and pleural thickening Raynaud s phenomena, valvular disease(more common with ergots).
25 Sinemet Most effective Rx for majority of symptoms First developed in the late 1960s, rapidly became the drug of choice for PD Large neutral amino acid, requires active transport across the gut-blood and blood-brain barriers Rapid peripheral decarboxylation to dopamine without a (L-aromatic-Amino- acid decarboxylase inhibitor) >75 mg/day carbidopa Side effects: nausea, postural hypotension, sedation, neuropsychiatric effects
26 Sinemet Formulations Onset Duration Immediate Release min 2-4 hours 10/100, 25/100, 25/250 Controlled Release min 3-6 hours 25/100, 50/200 Liquid levodopa (dissolved tablets) min
27 COMT Inhibition Periphery CNS MAO-B carbidop a dopamine AADC dopamine COMT L-dopa L-dopa COMT entacapone/ tolcapone? 3-OMD COMT 3-OMD tolcapone BBB
28 Entacapone (Comtan) Dosage: 200 mg w/each Sinemet Studies: Increased on time by 24% per dose, decreased levodopa 16% (Rinne et al., 1996). Increased on time by 1 hr/day by home diaries, decreased Levodopa 12%. (Parkinson s Study Group, 1997). Approved in 1998 for use in motor fluctuations. Side effects: Diarrhea (3%), dopaminergic symptoms, discolored urine
29 Tolcapone (Tasmar) First COMT-inhibitor licensed in the U.S. 100mg TID or 200mg TID Studies: Increased on time 21% in pt with wearing off, and significant reduction in LD dosage. ( Bass et al, 1997). Increased on time from 2.1 to 2.5 hrs/day in fluctuating pts, reduced LD dosage from 23% to 29%. (Adler et al, 1998). Side effects: Diarrhea, OH, dyskinesia, confusion Acute fulminant hepatic necrosis 3/60,000+ patients FDA warning prevents use unless alternative therapy unsuccessful Liver monitoring q2 wks for one year and less frequently thereafter
30 In June 2003, the FDA approved Stalevo for the treatment of pts with idiopathic Parkinson's disease who experience signs and symptoms of end-of-dose 'wearing off'. Stalevo
31 MAO-B Inhibitors Selegiline (Eldepryl, Zelapar) and rasagiline (Azilect) Well tolerated and once daily dosing Azilect cost is $7.43 per pill vs <$0.50 for selegiline Neuroprotection (DATATOP, TEMPO, ADIAGO)?
32 Anticholinergics Dopaminergic depletion- cholinergic overactivity Initially used in the 1950 s Effective mainly for tremor and rigidity Common agents (Start low, go slow) Trihexyphenidyl (Artane): 2-15 mg/day Benztropine (Cogentin): 1-8 mg/day Side effects: Dry mouth, sedation, delirium, confusion, hallucinations, constipation, urinary retention
33 Amantadine (Symmetrel) Antiviral agent: PD benefit found accidentally Improves: tremor, bradykinesia, rigidity and dyskinesias Exact mechanism unknown; possibly:» Enhancing release of stored dopamine» Inhibiting presynaptic reuptake of catecholamines» Dopamine receptor blockade» NMDA receptor blockade Side effects- autonomic, blurred vision, psychiatric 100 mg tab, total mg/day
34 L-DOPA Narrowing Therapeutic Window with Time dyskinesia therapeutic window bradykinesia off state years
35 Super on On Off
36 Super on On Off
37 PD Treatment Continuum Agonists Mild Levodopa Etc. Severe Surgery
38 Dyskinesia
39
40 Principles for Management of Wearing off and on-off Phenomena Deliver more dopamine medication in a constant state to the brain Increase total dosage of PD meds Increase frequency of dosage Add Controlled Release L-dopa Add COMT- inhibitor Add Dopamine agonist Add Apomorphine
41 Principles of Management of Dyskinesias Decrease fluctuations of Levodopa blood levels Add DA agonist and reduce Levodopa Add Amantadine Surgery????
42 Surgical Treatment of PD Deep brain stimulation Thalamic (Vim) DBS Pallidal (GPi) DBS Subthalamic (STN) DBS
43 Candidates for DBS Idiopathic Parkinson s Disease Disabling motor symptoms, despite optimized medical regime Disability is relative Questions to ask» Percent time on, off, dyskinetic» Activities that are impossible or difficult» Adverse effects of PD medications
44 Candidates for DBS Optimized pharmacotherapy Immediate release levodopa dosed in appropriate amounts at appropriate intervals for the patient s ADL Use of COMT- inhibitor Use of Dopamine agonist Amantadine for dyskinesias +/- other ancillary drugs
45 Candidates for DBS Continued response (even brief) to levodopa Document off-med and on-med exam: > 30% improvement in UPDRS III score desired Levodopa response predicts response to DBS Absence of significant dementia or depression Formal neurocognitive testing desirable; Mattis DRS within SD of age adjusted norm Absence of uncontrolled hypertension or bleeding diathesis Still ambulatory when on Realistic expectations; acceptable risk/benefit ratio
46 Clinical effects of DBS in PD Improvement seen in: Improved rigidity, bradykinesia, and tremor Increased on time Decreased motor fluctuations Decreased dyskinesias Possible reduction in PD meds Possible improvement in freezing if occurring as an off state symptom
47 STN DBS for PD Pre-Op: Off Meds Post-Op: Off Meds, Bilateral STN DBS
48 Post DBS
49
50 UCSF/ SFVA Movement Disorders Team Movement Disorders Neurology William J. Marks, Jr, MD Jill L.Ostrem, MD Graham A. Glass, MD Gail Kang, MD Chad Christine, MD Michael Aminoff, MD Robert Edwards, MD Ken Nakamura, MD Functional Neurosurgeons Philip Starr, MD, PhD Paul Larson, MD Neuropsychologists Randall Cockshott, PhD Johannes Rothlind, PhD Nursing/Coordinators Susan Heath, RN, MS Elaine Lanier, RN, MS Monica Volz, RN, MS Robin Taylor, NP Jamie Grace Program support Lori Anzaldo Guiomar Scheid Diane Hollander Jason Funk Fellows Rima Ash, MD Nick Galifianakis,MD Lauren Schrock, MD
51
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