Parkinson's and Multiple Sclerosis
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| cardinal signs of PD | akinesia/hypokinesia, rigidity, tremor, posture/gait abnormalities
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| secondary signs of PD | cognitive dysfunction, autonomic dysfunction, speech disturbances, micrographia, masked facies
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| can start pt on a dopamine agonist or levodopa. what are the primary symptom management advantages of each drug? | levodopa improves motor disability and dopamine agonists lessen motor complications.
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| MAOb inhibitors available for PD | selegiline and rasagiline
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| what problems arise with doses of selegiline greater than 10 mg daily | decrease MAOb selectivity
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| ADEs with selegiline | hallucinations, nausea, orthostatic hypotension, insomnia
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| what is the mechanism for insomnia with selegiline | it is metabolized to amphetamine
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| what drugs should be contraindicated with MAObs and why | tramadol, methadone, dextromethorphan, sympathomimetics, fluoxetine/fluvoxamine, meperidine due to serotonin syndrome risk. also cipro can double the concentration via cyp inhibition
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| purpose of carbidopa in PD | prevents peripheral levodopa conversion to dopamine allowing greater concentrations into the CNS.
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| dietary concerns with carbidopa/levodopa | high protein diets decrease absorption
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| acute adverse effects of Sinemet | GI, hypotension, cardiac arrhythmias, confusion, agitation, hallucinations
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| long term adverse effects of Sinemet | wearing off and on off, dyskinesias (involuntary movements)
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| return of PD symptoms before the next dose of Sinemet. How do you treat this? | wearing off. treat with amantadine.
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| profound unpredictable return of PD sx without respect to dosing interval. How do you treat this? | on-off. treat with entacapone, an MAOb inhibitors, pamipexole, ropinirole, apomorphine
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| typical ratio of carbidopa/levodopa | 25/100 mg
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| direct dopamine agonist options for treatment of PD | bromocriptine, pramipexole, ropinirole, rotigotine
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| ADEs associated with direct dopamine agonists | GI sx. postural hypotension, hallucinations, hypersexuality, compulsive behaviors.
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| contraindications with apomorphine | 5HT3 antagonists (ondansetron, palonosetron etc) and sulfite allergy
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| dosing concerns with apomorphine | poor PO bioavailability due to extensive first pass metabolism. given as a SQ shot.
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| ADEs associated with apomorphine | severe NV requires trt with trimethobenzamide before treatment and for at least 6 weeks during treatment. hypotension, hallucinations, dyskinesias
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| what is the role of anticholinergics in the treatment of PD and what drugs are used | tremor. trihexyphenidyl and benztropine
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| role of amantadine in treatment of PD. and ADEs | antidyskinesia agent. dizziness, insomnia, anxiety, livedo reticularis, nausea, nightmares
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| COMT inhibitor drugs used for PD and ADEs and role in therapy | used to decrease dopamine breakdown to increase levodopa in periphery. tolcapone. tolcapone req consent form due to hepatotoxicity. entacapone ADEs: dyskinesias, N/D-delayed up to 2 weeks, urine discoloration to orange, hallucinations and vivid dreams
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| preferred antipsychotics used in PD related to drug reactions or from disease | clozapine or quetiapine
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| how to treat dyskinesias associated with PD | lower levodopa dose or add amantadine
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| type of MS in which episodes of acute worsening of neurologic function are followed by a varying degree of recovery with a stable course between attacks. | relapsing remitting MS. common at diagnosis
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| type of MS in which initial relapsing remitting disease course is followed by progression with or without occasional relapses, minor remissions and plateaus | secondary progressive. presents in about half of patients after ~10 years.
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| type of MS in which gradual almost continuous worsening occurs with minor fluctuations but no distinct relapses. | primary progressive - ~10% of patients at diagnosis
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| type of MS in which disease is progressive from onset with clear acute relapses with or without recovery with periods between relapses characterized by continuing progression. | progressive-relapsing.of patients at diagnosis
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| how are acute relapses treated in MS | corticosteroids. methylpred IV 1 g QD x 3-5 days or PO prednisone 1250 mg QOD. IV ACTH
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| disease modifying drugs for MS | beta interferons (i.e. avonex, betaseron, extavia, rebif), dimethyl fumarate (Tecfidera), glatiramer acetate (Copaxone), fingolimod (Gilenya), Mitoxantrone (Novantrone), natalizumab (Tysabri), teriflunomide (Aubagio),
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| ADEs associated with beta interferons | injection site reactions, flu like symptoms (usually limited to first couple months), neutralizing antibodies (18-24 months of therapy and may increase relapse rates with pts with high antibody titers but may disappear with continued therapy)
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| ADEs associated with dimethyl fumarate (Tecfidera) | flushing helped with ASA and taking with food, starts 30 min after dose and ends after 30 mins. GI effects peak within first month. lymphocytes decrease by 30% in first year then stabilize
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| ADEs associated with glatiramer acetate (Copaxone) | injection site reactions, flusing, chest tightness, palpitations, anxiety, shortness of breath
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| ADEs associated with fingolimod (Gilenya) | bradycardia requiring monitoring for 6 hours after first dose and after any break over 2 wks in duration. AV conduction delays - first and second degree block, decrease in lymphocytes poss inc in infections. macular edema, resp effects, HTN, inc LFTs
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| ADEs associated with mitoxantrone (Novantrone) | potential for toxicity so only used for pts with rapidly advancing disease resistant to other therapies. cardiotoxicity requiring monitoring with ECG and not related to dose. acute leukemia in 0.8% of pts,
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| ADEs associated with Natalizumab (Tysabri) | hypersensitivity reactions, progressive multifocal leukoencephalopathy. reserved for failed therapies.
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| ADEs for teriflunomide (Aubagio) | liver tox, GI effects, alopecia, rash, infection including neutropenia and lymphopenia, preggers categpory X
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| due to the extremely long half live of terifunomide (Aubagio), what treatments can help to accelerate elimination | activated charcoal and cholestyramine
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| treatment for fatigue associated with MS | rest, assistive devices, cooling strategies, exercise, stress management, amantadine, methylphenidate
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| treatment for spasticity associated with MS | must be centrally acting. first line baclofen or tizanidine. second line dantrolene, diazepam. third line intrathecal baclofen. focal spasticity botox
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| treatment of walking impairment associated with MS |
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