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Program Written Summary
Audio-Digest Neurology
Volume 03, Issue 07
April 7, 2012

Parkinson disease – Herbert C. Sier, MD
Recognition, prevention, and management of delirium – Adnan Arseven, MD

From Geriatrics For The Primary Care Clinician, Sponsored By Northwestern University Feinberg School Of Medicine, Division Of Geriatrics And Office Of Continuing Medical Education
Digital Media $24.99
Audio CD $27.99

The following is an abstracted summary, not a verbatim transcript, of the lectures/discussions on this audio program.

Neurology Program Info  Accreditation InfoCultural & Linguistic Competency Resources

Focus on Geriatrics

From Geriatrics for the Primary Care Clinician, sponsored by Northwestern University Feinberg School of Medicine, Division of Geriatrics and Office of Continuing Medical Education

Educational Objectives

The goal of this program is to improve the diagnosis and management of Parkinson disease (PD) and delirium. After hearing and assimilating this program, the clinician will be better able to:

1. Diagnose traditional PD and differentiate it from Lewy body dementia, secondary parkinsonism, normal pressure hydrocephalus, and essential tremor.

2. Identify patients with atypical or parkinsonian plus syndromes.

3. Appropriately treat patients with PD and PD dementia and manage associated psychoses, mood and sleep disorders, and autonomic dysfunction.

4. Screen for, diagnose, and manage delirium among hospitalized patients.

5. Implement effective interventions to prevent the development of delirium.

Faculty Disclosure

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, the faculty and the planning committee reported nothing to disclose. In their lectures, Drs. Sier and Arseven present information related to the off-label or investigational use of a product, therapy, or device.

Parkinson Disease

Herbert C. Sier, MD, Assistant Professor of Medicine–Geriatrics, Northwestern University Feinberg School of Medicine, Chicago, IL

Background: mean age at onset of traditional Parkinson disease (PD) 60 to 70 yr of age (75%) but may occur at 30 to 40 yr of age

Pathology: caused primarily by decreased dopamine; 60% to 80% loss required before motor symptoms appear; degeneration occurs primarily in area of basal ganglia; involves striatum (ie, putamen and caudate), globus pallidus interna and externa, subthalamic nucleus, and substantia nigra; Lewy bodies (intraneuronal cytoplasmic inclusions) seen in PD and Lewy body dementia (LBD)

Nondopaminergic pathology: neuronal degeneration occurs in cholinergic neurons in nucleus basalis of Meynert, norepinephrine neurons in area of locus caeruleus, serotonin neurons in raphe nuclei of brainstem, and neurons of olfactory system, cerebral hemispheres, spinal cord, and peripheral and autonomic systems

Symptoms: preclinical — loss of smell, constipation, and rapid eye movement behavior disorder (RBD) appear several years before motor symptoms; motor symptoms — rigidity, bradykinesia, tremor, and resting tremor; autonomic symptoms — orthostatic hypotension, urinary and sexual dysfunction, and paradoxical sweating; gastrointestinal symptoms — dysphagia, constipation, and drooling (caused by inability to swallow); sensory symptoms — pain (eg, from rigidity, dystonic movement, or arthritis exacerbated by abnormal postures and movements), olfactory disturbance, and blurring of vision; general — fatigue, loss of weight, mood disorders, and gait dysfunction

Diagnosis: traditional PD — requires presence of 2 of 3 motor signs (ie, tremor, rigidity, or akinesia), postural instability, plus response to levodopa and exclusion of other diagnoses or causes; tests of blood or cerebrospinal fluid and brain imaging not specific; tremor — usually resting or pill-rolling, possibly postural; not always present

Differential diagnosis: includes LBD and secondary PD caused by medications (eg, neuroleptic agents, antipsychotics, selective serotonin reuptake inhibitors [SSRIs], valproic acid, amiodarone) and strokes (eg, lacunar infarctions in basal ganglia or small vessels in subcortical structure); presentation — vascular PD presents more often with rigidity (usually in lower body or legs, causing gait dysfunction); drug-induced PD often presents symmetrically (sometimes with tremor and bradykinesia); traditional PD begins asymmetrically in hand or arm, goes to ipsilateral leg, then crosses to other side; other secondary forms — caused by head trauma, toxins (eg, carbon monoxide), metabolic disorders (eg, Wilson disease), neoplasms, and infection (eg, human immunodeficiency virus or neurosyphilis); normal pressure hydrocephalus (NPH) — presents with dementia, gait disorder, and incontinence; essential tremor — action tremor

Atypical or parkinsonism plus syndromes: multisystem atrophy (MSA) — classified according to whether findings predominantly parkinsonian or cerebellar; presents earlier with profound orthostatic hypotension, gait ataxia, and spasticity; presents symmetrically with rapid progression and poorer response to dopamine; often presents between 50 to 60 yr of age; progressive supranuclear palsy — patients have rigidity in axial skeleton and frequent falls; usually begins in sixth or seventh decade; dementia involves more t pathology than a-synuclein pathology; corticobasal degeneration — also involves t pathology; amyloid plaques and abnormally phosphorylated t protein also seen in Alzheimer disease (AD); begins in sixth to seventh decade; presents with asymmetric rigidity, alien limb phenomenon, myoclonus, dystonic and postural instability, and (later) primary progressive aphasia, dementia or frontotemporal dementia

Diagnostic testing: includes neurologic examination, complete blood count (CBC), and comprehensive chemistry panel; use computed tomography (CT) or magnetic resonance imaging (MRI) of brain to exclude other diagnoses; positron emission tomography (PET) currently under investigation for use in PD; single photon emission computed tomography (SPECT) uses ligands targeting dopamine presynaptic transporter to differentiate PD from essential tremor

Treatment: levodopa — gold standard for traditional PD; combination of carbidopa and levodopa used (carbidopa prevents peripheral decarboxylation of levodopa and reduces nausea, vomiting, and orthostatic hypotension); within 5 yr, 50% of patients develop motor fluctuations, slower onset of action (“on” effect), and medication wears off sooner (“off” effect), with increasing bradykinesia and dyskinesias (usually choreiform [ie, purposeless], or dystonic or myoclonic movements); direct dopamine agonists — usually prescribed for patients ,60 yr of age; levodopa required as illness progresses; produce more cognitive side effects, swelling of legs, and impulse control disorder (ICD); monoamine oxidase (MAO)-B inhibitors — (eg, selegiline, rasagiline) used in early disease; possibly neuroprotective; help some motor symptoms; later in disease, they help lessen “off” period; amantadine — possible to use in early disease but causes confusion in elderly and requires renal dosing; in later stage, only medication that helps dyskinesias; catechol O-methyl-transferase (COMT) inhibitors — (eg, entacapone) help increase half-life of levodopa by preventing its peripheral metabolism

Dementia: PD dementia develops $1 yr after motor symptoms; LBD defined as dementia that occurs before, during, or ,1 yr after motor symptoms; presentation of both includes impaired attention, executive dysfunction, and visuospatial problems; language function not as impaired as in AD; short term memory deficit involves retrieval; LBs seen in cortical and subcortical regions (many in amygdala and hippocampus); aggravated by hyponatremia, dehydration, sedatives, anxiolytics, antiparkinson medications, colds, and urinary tract infections; LBDcore features include fluctuations in thinking and variable level of alertness, early visual hallucinations, paranoid delusions, stiffness, bradykinesia, and postural instability; psychosis common and aggravated by antiparkinson medications

Treatment: dopaminergic therapy can improve alertness and visuospatial attention but worsens cognition; cholinesterase inhibitors — rivastigmine approved; studies showed efficacy for donepezil (Aricept) and galantamine; conflicting evidence reported for efficacy of memantine (used off-label)

Management of psychosis: identify cause, eg, infection, metabolic problems, non-PD medications; reduce PD medications by stepwise elimination of anticholinergics, amantadine, MAO-B inhibitors, COMT inhibitors, and dopamine agonists; consider adding cholinesterase inhibitor or atypical neuroleptics; literature supports use of clozapine (Clozaril, FazaClo), but 1% to 2% of patients develop agranulocytosis (monitor CBC); fewer supportive data reported for quetiapine (Seroquel); olanzapine, risperidone (Risperdal), and aripiprazole (Abilify) can worsen symptoms of PD

Mood disorders: depression, anxiety, panic disorder, and generalized anxiety disorder common; if caused by wearing off of dopamine medication, increase dopamine; depression — consider dopamine agonists (eg, pramipexole), SSRIs, mirtazapine, trazodone, nortriptyline, or electroconvulsive therapy; anxiety — treat with SSRIs or lorazepam; apathy — may use methylphenidate or modafinil (anecdotal reports of efficacy)

Impulse control disorder: primarily associated with direct dopamine agonists; commonly presents with gambling, hypersexuality, or shopping; reduce drug

Sleep disorders: initiation and maintenance — restless legs syndrome (also associated with iron deficiency and chronic renal failure) and periodic limb movements of sleep treated with dopaminergic medication (eg, pramipexole, carbidopa/levodopa); sleep apnea common; increase dose of dopaminergic agent for nighttime stiffness but decrease nighttime dose for dyskinesias at night; avoid short-acting sedatives; may use quetiapine; parasomnias — dopaminergic agents can cause vivid dreams and hallucinations; clonazepam helpful for RBD; dopaminergic agents may improve RBD but can induce nightmares; excessive daytime sleepiness — reduce or eliminate sedating medications, use lowest dose of dopaminergic agent, rule out medical issues (eg, hypothyroidism, depression), and consider sleep study or modafinil

Orthostatic hypotension: try liberal use of salt, elevation of head of bed, and frequent small low-carbohydrate meals; may need to use a-agonist, eg, midodrine, fludrocortisone (Florinef), but with caution because of potential for hypokalemia and edema; may need to decrease dopaminergic agents

Autonomic dysfunction: sexual dysfunction — prescribe cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase agents; pain — consider increasing dopaminergic agents if pain due to stiffness; urinary incontinence — treat overactive bladder with anticholinergic medication (may worsen confusion); consider prostatic cause in older men; constipation — caused by Lewy bodies involving myenteric plexus; treat with bowel regimen, dietary changes, and exercise (may add laxative); hypersalivation — injection of botulinum toxin into parotid or submandibular glands effective; may use glycopyrrolate (anticholinergic); botulinum toxin also effective for excessive focal sweating

Deep brain stimulation: do not use in confused elderly patients to avoid increasing confusion

Experimental treatments: continuous infusions of levodopa and dopamine tested in Europe; in United States, administration slow-release of levodopa gel into jejunum via percutaneous endoscopic gastrostomy (PEG) tube and gastrojejunostomy being studied; shown effective in reducing on-off phenomena and dyskinesias

Recognition, Prevention, and Management of Delirium

Adnan Arseven, MD, Assistant Professor of Medicine–Geriatrics, Northwestern University Feinberg School of Medicine, Chicago, IL

Definition of delirium: acute decline in attention and cognition with fluctuating course; Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria — disturbance of consciousness and attention; acute and fluctuating course; changes in cognition and/or perception which cannot be explained by other illnesses, eg, dementia; caused by medical condition or toxicity or withdrawal of drug

Epidemiology among patients .70 yr of age: ≈25% have dementia during hospital stay; among outpatients, only 12% to 40% with dementia recognized by primary care physician; delirium occurs in ≈33% in acute care (≈50% admitted with delirium, and ≈50% become delirious in hospital) and ≈85% to 90% in intensive care; ≈65% of patients with dementia at baseline become delirious in hospital; prevalence of delirium 20% to 60% in nursing homes

Rehabilitation: ≈25% of patients $65 yr of age in rehabilitation delirious at admission; only ≈33% recover from delirium during stay; recovery — study found ≈50% of patients recovered within 2 wk, but ≈50% remained delirious at 6 mo

Diagnostic steps: cognitive screening complemented by attention test; Confusion Assessment Method (CAM) useful; tests to assess attention include reciting days of week or months of year backwards and digit span test; CAM criteria — diagnosis of delirium requires acute onset with fluctuating course and inattention plus disorganized thinking or altered level of consciousness; diagnosis of dementia requires progressive, chronic cognitive impairment documented by testing; history of gradual decline over time with sudden recent change suggests baseline dementia with delirium; differentiating features of dementia — include insidious onset, normal attention (unless severe), normal consciousness, and normal speech (although empty of content); assume symptoms due to delirium until proven otherwise, because they may represent only manifestation of life-threatening illness

Etiology of delirium: medical causes — hypoxemia, sepsis, electrolyte imbalance, ischemic disease, medications, metabolic problems, or infections; delirium always has multiple causes; predisposing (risk) factors — vision impairment, severe illness, dementia, and high ratio of serum urea nitrogen (BUN) to creatinine; precipitating factors — physical restraint, malnutrition, addition of .3 new medications, restraint of patients with bladder catheters, or iatrogenic events; combinations of predisposing and precipitating factors can increase risk for delirium by ≈26-fold

Evaluation: perform physical examination, review of medications, and laboratory testing; neuroimaging seldom needed

Drug classes associated with delirium: anticholinergics (worst), benzodiazepines, and opioids

Prevention: best strategy when risk factors present because once delirium occurs, difficult to change course; studies on intervention — Yale trial of nonpharmacologic interventions for patients with various risk factors found ≈5% reduction of absolute risk among entire study population (17% reduction among patients with baseline dementia); treatment of 7 patients needed to prevent 1 case of delirium; second trial found 18% reduction of absolute risk among patients with hip fractures after interventions to prevent delirium

Management: must be multidisciplinary; address precipitating factors; correct medications or sensory impairment; provide full supportive care, including feeding; prevent complications; medications — review and minimize or stop as many medications as possible; sleep protocol — use of 5-min back rub, warm drink, and relaxing music decreased need for sleep medication from 54% to 34%; do not awaken patient during night for interventions, eg, blood drawing; avoid complications — hide intravenous lines and catheters and remove as soon as possible; avoid oversedation to prevent constipation, aspiration, and falls; agitation — ask family or staff member to stay with patient if feasible; if patient dangerous to self or others, haloperidol drug of choice (never use benzodiazepines unless withdrawal from alcohol or benzodiazepine documented); haloperidol may also cause delirium; use small repeated doses, just sufficient to calm patient, ie, 0.5 to 1.0 mg every 30 to 45 min, #3.5 mg total (higher doses cause extrapyramidal side effects); if patient has PD or LBD, use quetiapine to avoid exacerbating stiffness; taper off in 2 to 3 days; may use antipsychotic medications at bedtime to improve sleep if necessary; monitor for prolongation of QT interval; among benzodiazepines, lorazepam drug of choice; eliminate restraints

Suggested Reading

Aarsland D et al: Depression in Parkinson disease — epidemiology, mechanisms, and management. Nat Rev Neurol 8:35, 2011; Ahlskog JE: Cheaper, simpler, and better: tips for treating seniors with Parkinson disease. Mayo Clin Proc 86:1211, 2011; Allen J, Alexander E: Prevention, recognition, and management of delirium in the intensive care unit. AACN Adv Crit Care 23:5, 2012; Bernal-Pacheco O et al: Nonmotor manifestations in Parkinson disease. Neurologist 18:1, 2012; Blonder LX, Slevin JT: Emotional dysfunction in Parkinson’s disease. Behav Neurol 24:201, 2011; Boot BP et al: Probable rapid eye movement sleep behavior disorder increases risk for mild cognitive impairment and Parkinson disease: a population-based study. Ann Neurol 71:49, 2012; Flaherty JH, Little MO: Matching the environment to patients with delirium: lessons learned from the delirium room, a restraint-free environment for older hospitalized adults with delirium. J Am Geriatr Soc 59 (Suppl 2):S295, 2011; Garcia Ruiz PJ et al: Initial motor symptoms of Parkinson disease. Neurologist 17 (Suppl 1):S18, 2011; Ha AD et al: The prevalence of symptomatic orthostatic hypotension in patients with Parkinson’s disease and atypical parkinsonism. Parkinsonism Relat Disord 17:625, 2011; Iranzo de Riquer A et al: Sleep disorders in Parkinson disease. Neurologist 17 (Suppl 1):S38, 2011; Krenk L et al: Delirium after fast-track hip and knee arthroplasty. Br J Anaesth Jan 24, 2012 [Epub ahead of print]; Liepelt-Scarfone I et al: Co-occurrence of parkinsonism and dementia in clinical practice: relevant differential diagnoses. Z Gerontol Geriatr 45:23, 2012; Neufeld KJ et al: The Johns Hopkins Delirium Consortium: a model for collaborating across disciplines and departments for delirium prevention and treatment. J Am Geriatr Soc 59 (Suppl 2):S244, 2011; Quinlan N, Rudolph JL: Postoperative delirium and functional decline after noncardiac surgery. J Am Geriatr Soc 59 (Suppl 2):S301, 2011; Rudolph JL et al: Validation of a medical record-based delirium risk assessment. J Am Geriatr Soc 59 (Suppl 2):S289, 2011; Siderowf A et al: Impaired olfaction and other prodromal features in the Parkinson At-risk Syndrome study. Mov Disord Jan 11, 2012 [Epub ahead of print]; Van de Berg WD et al: Patterns of alpha-synuclein pathology in incidental cases and clinical subtypes of Parkinson’s disease. Parkinsonism Relat Disord 18 (Suppl 1): S28, 2012; Willis AW et al: Predictors of survival in patients with Parkinson disease. Arch Neurol Jan 2, 2012 [Epub ahead of print].

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