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Dementia/Delirium 2017. Denise Kresevic RN Ph. D, APN-BC FAAN Louis Stokes Cleveland VAMC University Hospitals Case Medical Center. Am I mostly normal ?. Grocery list- left at home Enter a room and cant remember Just cant remember names
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Dementia/Delirium2017 Denise Kresevic RN Ph. D, APN-BC FAAN Louis Stokes Cleveland VAMC University Hospitals Case Medical Center
Am I mostly normal ? • Grocery list- left at home • Enter a room and cant remember • Just cant remember names • Cant remember NPI #, OAARS # and all computer passwords
Normal/ Abnormal Normal Abnormal Consistent bad choices Occasional missed payment Miss season/year Much difficulty with conversation Often loses things cant retrace steps, blames others • Occasional bad decision • Loss of ability to do $ • Miss date/day • Occasional problem with words • Lose things occasionally
What does dementia look like in everyday life? • Can’t remember familiar recipes • Lose things around the house • Get lost in or going to familiar places • Forget to pay bills or forget to mail bills • Difficulty balancing checkbook • Miss appointments / forget to take medication • Usually don’t recognize there’s a problem • May become paranoid, people taking things
What does dementia look like in everyday life? • Decreased interest in activity or life – Apathy • Increasingly confused as it becomes dark • Hygiene / grooming may become worse • Irritable, with reminders from family • Sleep disturbance • Forget to eat or drink adequately • Language problems (ex: Not native English) • Cooking accidents / inability to fix things • Personality Changes / Behavioral Changes
Dementia • - a syndrome characterized by progressive decline in multiple areas of cognitive function, which eventually produces significant deficits in ability self-care and social and occupational performance.
Consequences • Patients with dementia have difficulty: • identifying changes in health status • describing symptoms of comorbid conditions • asking clearly for pain relief • comprehending instructions • following directions for self care and safety • They are more vulnerable to stress when making transitions in care • Payments for care for 2012 are estimated to be: $200 Billion 0000_NICHE Program Development
Theories of Etiology Amyloid Cascade Hypothesis • Amyloid Precursor Protein Error – produces plaques (genetic abnormality on Chromosome 21) • Studies suggest that about 25 percent of adults with Down syndrome over age 35 have symptoms of Alzheimer’s disease ; most over age 50 will develop AD 1. Plaques – toxic peptides Amyloid Beta – 40, 42, 43 (Aβ) extracellular 2. Aβ - 42 oligomers form / interfere with synaptic functioning 3. Plaques cause inflammation (microglia, astrocytes cytokines / free radicals 4. Plaques induce tangles causes Abnormal Tau Phosphorylation Microtubles convert to tangles within the neuron - intracellular 5. Cholinergic Neuronal dysfunction / loss spreads Apo-E – defect in the protein that binds to amyloid to remove it Dysfunction of Glutamate • Excitotoxicity • Follows in the later stages
Dementia Characteristics • Impairs cognition -- primarily memory – but also language, insight, judgment, ability to plan • Affects ability to care for self, including managing own care • Causes behavioral and psychological problems • Creates strain for family caregivers 3
Medical History: Risk Factors • Cardiac / Vascular HTN (what’s bad for the heart is bad for the brain) • Cerebrovascular, TBI falls • Diabetes • Parkinson’s, Multiple Sclerosis (neurodegenerative) • Family History of Dementia (AD, ) • Alcohol / Substance Abuse – Chronic • Smoking / Obesity • Low Folate / High Homocysteine
Dementia in DSM-V- • Memory Impairment (ability to learn new or recall previously learned info is impaired) • Cognitive Disturbance a) Aphasia (language disturbance) b) Apraxia (impaired ability to carry out motor activities despite intact motor function) c) Agnosia (failure to recognize or identify objects despite intact sensory function) d) Disturbance in Executive Functioning: Driving • Both cause significant impairment in social or occupational functioning
Types of Dementia • Alzheimer’s Type • Vascular Dementia • Lewy Body Dementia • Frontotemporal Dementia Dr. Alois Alzheimer • Alcohol/Substance-Induced Dementia • Parkinson’s Dementia • Huntington’s Dementia • HIV induced Dementia • Dementia due to Creutzfeldt-Jakob Disease • Dementia due to Head Trauma
Alzheimer’s Disease 0000_NICHE Program Development
The Real World • Miss S. 72 years old has been followed for primary care HTN OA for several years • Retired teacher (was forced to retire) ex-nun • Vague history of anxiety • Lives with her sister for last 30 years • Comes to the office today at the insistence of her sister who is “very concerned” about her memory
Subjective Data • Forgets names, words, appointments, looses keys • HTN –Lisinopril 20 mg daily HCTZ BP 140/90 • Multi vitamin, Vitamin D 2000 U daily • No alcohol or tobacco • Negative CP DOE dizziness edema • OA Tylenal 650mg 1-2 times a day • Weight stable • Watches salt
More history for Miss S. • How long (several months maybe longer) • No urinary symptoms • Still driving – no tickets accidents – a few weeks ago took a “wrong turn” coming home from the movies • Able to balance check book ok • No other over the counter meds • No recent falls/trauma
Dementia History/Work-Up • Medical History • Family History • Onset / Progression of Symptoms • Areas of Dysfunction • Behavioral Manifestations • Affect or Personality Changes • Medication Review / Reconciliation, Consider other causes for the patient’s symptoms before making conclusions
Medication Reconciliation • Anti-Cholinergic Load • Bladder Agents • TCA (pain, mood, sleep) • SSRI’s, Antipsychotics • Sleep Aids • Anti-histamines, hypnotics • Old supply Ativan • Benzodiazepines • May have been on for 20 years • Pain Medications • Narcotics
Cognitive Screening ? • MMSE (Folstein) – no longer public domain • MoCA (adjusts for education) • Clock Drawing Test • Trails Test A & B • Verbal Fluency • Geriatric Depression Scale • Mini-Cog
Screening Tools 23 1/6/2020 2:24:57 PM 0000_NICHE Program Development
Cognitive Screening • MMSE (Folstein) – no longer public domain • MoCA (adjusts for education) • Clock Drawing Test • Trails Test A & B • Verbal Fluency • Geriatric Depression Scale • Mini-Cog
Clock Drawing Test (part of Mini Coag) • CDT – draw the face of a clock, put all the numbers in, then make it read 11:10 • 4 point scoring method • Circle • All 12 numbers present • Numbers in correct position • Hands in correct position • 10 point scoring method
Mini Mental Status Exam • MMSE max score = 30 / education based Normal score: 24/30 or higher (most say < 26/30 = impaired) Educational and Age Norms • Orientation • Recall (3 item) • Calculation • Sentence Construction • Pentagon
Montreal Cognitive Assessment • MoCA < 26/30 = Mild Cognitive Impairment • 5 item recall • Sentence recall • Found to be more sensitive in detecting mild impairment in general population and in those with Parkinson’s Disease (NIH study) • Journal of the American Geriatric Society (2009), Feb (2), 304-308 • www.mocatest.org
Depression • Single question-no • Geriatric Depression scale < 5 ( 2/15 wnl) • Likes to stay home, worries about bad things
Miss S. Physical Assessment • Apical, postural BP slight elevation • Hearing/vision ok • Motor, ok gait, Romberg, no drift • Minicog, abnormal clock/recall 1/3
Dementia Work-Up • Labwork: CBC, CMP, TSH, B-12, Folate, RPR, Homocysteine, drug levels /VDRL • Neuro-Imaging: CT of Head, MRI of Brain, PET scan • Cognitive Testing – per Psychologist, Neuropsychologist, Occupational Therapist / Speech Therapist • Cognitive Screening
Dementia Work-Up • Labwork: CBC, CMP, TSH, B-12, Folate, RPR, Homocysteine, drug levels • Neuro-Imaging: CTof Head, MRI of Brain, PET scan • Cognitive Testing – per Psychologist, Neuropsychologist, Occupational Therapist / Speech Therapist • Cognitive Screening/depresson screen
Vascular DementiaDiagnosis • No widely accepted neuropathological criteria established • Onset of cognitive decline may be sudden or progressive • Found in Pt’s with Stroke, Chronic HTN, Micro-Vascular Disease, Arteriosclerosis, amputations, CABG, other bypass procedures, DVT’s,SDH, Emboli, coagproblems • May be Focal Deficits: based on location of lesion • Presents of abnormal vascular anatomy on CT of Head or MRI • Occupational Exposure: Repeated TBI (new concern) • Vascular Depression: Common • Sertraline most researched for treatment
Vascular Dementia • May result from genetic diseases, endocarditis (infection of a heart valve). • Or due to amyloid angiopathy (a process in which amyloid protein builds up in the brain's blood vessels, sometimes causing hemorrhagic or "bleeding" strokes) Adapted from slideshow found at: http://www.emedicinehealth.com/slideshow_dementia/article_em.htm University Hospitals Harrington Heart and Vascular Institute
Vascular Dementia • Second most common type of dementia. • Can be result of one infarct (usually on left hemisphere) or in hippocampus. • Or several smaller infarcts. • Conditions that cause hypoperfusion (HF) may contribute to vascular dementia. Adapted from slideshow found at: http://www.emedicinehealth.com/slideshow_dementia/article_em.htm
Imaging • Discussion/rationale for patient/family • $ • MRI-non contrast no gadolinium • No contra indications • r/o mass, hydrocephalus, old stokes, small vessel disease • Pet (research)?
Plan for Miss. S. • Labs (no VDRL) • Stop Ativan (was taking 1-2 week) • Continue BP Tylenol current meds • Sleep hygiene • Education overview of MCI Dementia • Wants to think about MRI, • RTC 1 month
Dementia with Lewy BodiesDiagnosis • Cognitive changes with Parkinson features • Other signs of Autonomic Dysfunction • Syncope / falls • Unexplained loss of consciousness • Other psychotic symptoms – delusions/non-visual hallucinations
Dementia with Lewy BodiesDiagnosis • Core Features (2 are needed for dx) • Fluctuating cognition • Recurrent Visual Hallucinations – people/animals • Spontaneous signs of Parkinsonism • Suggestive Features • REM sleep behavior disorder • SEVERE NEUROLEPTIC SENSITIVITY • PET imaging decreased metabolism
Parkinson’s Dementia ETIOLOGY Abnormal protein: Accumulates inside neurons of the substantianigra. This accumulation is called "alpha-synuclein" first described by a Professor Lewy Lewy Body:Proteins are also found in the brain's neurons outside the deep brain structures, in the "thinking" parts of the brain in Parkinson's Disease Dementia and in Lewy body dementia.
Frontotemporal DementiaDiagnosis • Strong evidence of familial link • 5 genes identified • Effect younger population • Onset b/ 51-63yr • Can be Rapid Progression • Does not effect Cholinergic system, has effect on serotonergic system • Tau - toxic protein pathology
Frontotemporal DementiaDiagnosis PET Scan – Imaging most sensitive FTD
Frontal-temporal Dementia • Abnormal tau proteins accumulate inside brain cells causing cell decline. • The brain atrophies in the frontal and temporal regions. • This type of dementia occurs at ages 40 – 65 yrs. and typically has a genetic factor. Adapted from slideshow found at: http://www.emedicinehealth.com/slideshow_dementia/article_em.htm
Frontotemporal DementiaDiagnosis Insidious onset / gradual progression May present with depression, apathy, aggression, personality changes, language deficits and disinhibition Decline in social inter-personal conduct Impairment in regulation of personal conduct (sexual inappropriateness) Progressive Language Impairment Emotional blunting Loss of insight
Frontotemporal Lobe DementiaTreatment MOST DIFFICULT TO TREAT No FDA approved medications Target symptom management Trazadone/Nefazadone – some evidence of improved behaviors (start Trazadone 25 TID) SSRI’s – some efficacy with irritability, anxiety, disinhibition Mood Stabilizers – can be helpful
Medications for Alzheimer’s Type Dementia • Acetylcholinesterase Inhibitors (AchI’s) Donepezil (Aricept) all stages Indicated: All stages of Alzheimer’s Dementia • Initiate 5 mg daily x 4 wk; then increase 10 mg • Renal impairment leave at 5 mg daily • New Dose = 23 mg daily (sustained release) for Mod-Sev Stages (should be on 10 mg daily for at least 3 months first) • ½ life 70 hr; steady state in 15 days • Wt loss ,night mares, bradycardia
Medications for Alzheimer’s Type Dementia Acetylcholinesterase Inhibitors • Rivastigmine (Exelon) –mild mod • Indicated for Parkinson’s Dementia • Indicate mod-sev Alzheimer’s Dementia • 1.5mg BID x 1 mo; 3mg BID x 1 mo; 4.5 mg BID x 1 mo; 6 mg BID (with largest meals of the day) • Patch 4.6mg/24hr & 9.5 mg/24hr ( less GI) • No known CYP450 enzyme interactions • No recommended hepatic / renal dosing
Medications for Alzheimer’s Type Dementia • Acetylcholinesterase Inhibitors • Galantamine (Razadyne) (formally Reminyl) (mild mod) • Indicated: mod-sev Alzheimer’s Dementia • 4mg BID x 1 mo; 8 mg BID x 1 mo; 12 mg BID ER formulation – 8,16,24mg daily ( q 4 wk) • Do not exceed 16 mg/day with hepatic/renal impairment • Metabolized by CYP 450 enzymes 2D6, 3A4 • Caution: Tagamet, Nizoral, EES, Paxil, NSAID’s, Anti-Cholinergic agents