Parkinson's Disease: Assessment & Treatment Considerations PDF

PARKINSON’S DISEASE ASSESSMENT AND TREATMENT LECTURE 2.1 Neurology CONSIDERATIONS PARKINSON DISEASE (PD) Usually idiopathic Substantia nigra degeneration causes dopamine deficiency in striatum  motor symptoms Dopaminergic therapy relieves motor symptoms ...

PARKINSON’S DISEASE ASSESSMENT AND TREATMENT LECTURE 2.1 Neurology CONSIDERATIONS PARKINSON DISEASE (PD) Usually idiopathic Substantia nigra degeneration causes dopamine deficiency in striatum  motor symptoms Dopaminergic therapy relieves motor symptoms PARKINSON DISEASE: COMMON EARLY COMPLAINTS Resting tremor Writing smaller; harder to do buttons Slowness, “weakness”, limb not working well Stiff or achy limb Stoop, shuffle-walk, “dragging” leg(s) Trouble getting out of chairs or turning in bed Low or soft voice Non-motor: anosmia, dream enactment, constipation, anxiety, depression, “passiveness” PD: MEDS FOR MOTOR SYMPTOMS L-dopa (with carbidopa) is most effective and usually best tolerated Dopamine agonists (ropinirole, pramipexole) Others have only modest benefits (MAO-B inhibitors, anticholinergics, amantadine) EARLY PD: WHEN TO START MEDS? Drugs are symptomatic, not neuroprotective or neurotoxic Level of patient function is best guide Response to dopaminergic therapy (especially l-dopa) is the best available “test” for PD ** Remember the value of exercise! ** WHICH TREATMENT TO START? L-dopa most effective for motor symptoms in general (bradykinesia, tremor, gait changes) Family physicians can start levodopa !! Dopamine agonists cause more non-motor side effects, and are best avoided in patients above 70 TREATMENT PEARLS IN EARLY PD Fear not L-dopa. “Delaying L-dopa” is of no benefit long-term. Treat more for symptoms and function, and less for how the patient “looks”. Generics are fine. Allow adequate dose and time to work before concluding “failure” or “not PD”. Resting tremor may be medication refractory in some patients; don’t conclude “not PD”. LEVODOPA Most effective overall for motor symptoms A fine option for initial therapy of PD By mid to late disease it is almost always needed Non-motor side effects include nausea, orthostasis, sleepiness, hallucinations; but not as much as other PD drugs Motor side effect: dyskinesias  CARBIDOPA/ LEVODOPA DOSING Commonest preparation is regular 25/100mg. Try 1 pill  1.5 pills  2 pills. With meals reduces nausea. 2 weeks between steps to appreciate effect. No response? At least 900mg/ d to say “not PD”. Some patients need more frequent dosing Typical daily l-dopa dose range: 300mg to 1500mg DOPAMINE AGONISTS (ROPINIROLE, PRAMIPEXOLE, ROTIGOTINE) Can be monotherapy in early disease; need l-dopa in mid to late disease Can add to l-dopa to reduce OFF time Frequent side effects! Nausea, sleep attacks, hypotension, compulsive behaviors, LE edema  More prone than l-dopa to causing hallucinations and confusion. Caution in older or demented patients!  MID TO LATE PD: A TRICKY BUSINESS More motor complications including dyskinesias and ON- OFF fluctuations More drug-resistant motor symptoms (e.g. impaired balance with falls) More nonmotor symptoms (especially dementia and hallucinations) More medications, so more side effects Managing these complexities requires experience. “MOTOR COMPLICATIONS” AS PD PROGRESSES Fluctuations. Medication wears off before next dose. OFF periods worse as disease progresses. Dyskinesias (usually at the peak of ON). Need larger and/or more frequent med doses, or combinations of drugs. Deep brain stimulation an option for some patients with medically refractory motor complications. SOME MOTOR SYMPTOMS MAY NOT RESPOND TO MED ADJUSTMENTS Postural instability and falls Freezing of gait Fatigue Dysarthria, dysphagia Some tremor (!) MANAGEMENT Surgical -Stereotactic thalamotomy- temporary improvement of symptoms. Beep Brain Stimulation Physiotherapy -Reduces rigidity & corrects abnormal posture. Speech therapy -Dysarthria/dysphonia. Neuropsychiatric NON-MOTOR SYMPTOMS Psychiatric (depression, anxiety) Autonomic (blood pressure, genitourinary, GI) Sleep (REM behavior disorder, insomnia, hypersomnia, sleep apnea) Fatigue Cognitive (psychosis, dementia) 15 WHY NON-MOTOR SYMPTOMS? PD affects many parts of the nervous system Earliest involvement is in gut nerve plexus, lower brainstem, and olfactory bulb Pathology moves up the brainstem, also to serotonergic, noradrenergic, and cholinergic nuclei Non-motor symptoms (e.g. anosmia, constipation, dream enactment) often predate motor symptoms 16  DEPRESSION AND ANXIETY It’s not just because of the stress of the diagnosis Motor symptoms and wearing off can interact with mood and anxiety levels Can misinterpret “poker face” as depression. Ask the patient! SSRI’s can work; avoid benzodiazepines 17 DEPRESSION AND ANXIETY: OTHER CONSIDERATIONS Consider support services / psychotherapy for patients and caregivers Geriatric psychiatrists usually have better expertise in this population 18 FATIGUE “Tired”, “Wiped out”, “No energy” Is it: Sleepiness? Wearing off? Motor? Mood? Isolated fatigue can be disabling No established treatment, though anti- depressants and stimulants have been tried Encourage light exercise, hobbies, etc We badly need better treatments for this 19  HALLUCINATIONS & DEMENTIA IN PD Complicate many longstanding PD cases Hallucinations are usually visual Main contributors are disease progression (brain pathologic changes), age, and meds Older patients much more at risk Marker for increased morbidity, mortality, and institutionalization HALLUCINATIONS AND DEMENTIA IN PD Assess medical state; B12, TSH Simplify med regimen. Prioritize eliminating anticholinergics and dopamine agonists. Reduce L-dopa last. Rivastigmine (cholinesterase inhibitor) FDA approved in PD dementia Antipsychotics (off label, black-box warning!): quetiapine and clozapine least likely to worsen parkinsonism ASSESSMENT https://www.youtube.com/watch?v=cxHpFWKIfGw (18.45 secs) EXERCISES Focus on ROM, gait, balance, antirigidity, ADLs Leg strength – use equipment, resistive bands Balance/sway – foam pads, retropulsion tests Strengthen trunk muscles for respiration and posture Weight shifting Exercises for transfers EXERCISES Stretching exercises essential  Posterior direction: reaching backwards, walking backwards  Extension exercised  Throwing/kicking a ball  Push-ups;  PROM PNF Respiration exercises Relaxation exercises – Yoga, Tai Chi  Energy Conservation BALANCE TRAINING & HIGH-INTENSITY RESISTANCE TRAINING PD patients have dyssynchrony of leg muscles during movement initiation  Reduced peak torque production in knee extension, flexion, and ankle dorsiflexion LE weakness impairs postural responses to challenged balance High intensity resistance training of knee extensors, flexors, ankle plantarflexors – Nautilus Cycle ergometer TREADMILL TRAINING Many studies conducted and treadmill training shown to be effective in gait training At initial sessions, all patients could walk without freezing phenomenon at higher treadmill speeds Improvement in gait speed and number of steps Effects lasted 4 months! TREADMILL TRAINING Possible that body-weight supported treadmill training induces implicit motor learning by enhancing alternative brain networks Has potential to enhance gait rhythmicity Progressive and intensive treadmill training can minimize impairments in gait, reduce fall risk and ↑ quality of life Positive Aspects of treadmill training:  Rhythmicity  Weight-support  Aerobic training  External pacemaker