Dementia and Alzheimer’s Disease : Recognition and Diagnosis
Non Alzheimer’s Dementia
description
Transcript of Non Alzheimer’s Dementia
Non Alzheimer’s Dementia
Kevin Overbeck, DOAssistant ProfessorUMDNJ –SOM NJISA
Non-Alzheimer’s Dementia
This medical student presentation is offered by the New Jersey Institute for
Successful Aging.
This lecture series is supported by an educational grant from the Donald W. Reynolds Foundation Aging and
Quality of Life program.
Learning Objectives
• Compare and contrast clinical features that distinguish vascular dementia, frontotemporal dementia, and Lewy body dementia
• Differentiate between Alzheimer's disease and all other dementias
Prevalence of Common Dementias
Image Source: Weiss BD. Elder Care: A Resource for Interprofessional providers. http://aging.medicine.arizona.edu Accessed: October 5, 2011.
Evaluation of Memory Loss• HPI (establish timeline and clinical
presenting features)• Detailed MED review• CAM• GDS• MMSE/CDT• Pertinent physical exam findings• LABs (BMP, CBC, LFTs, TSH, B12, Folate)• Brain imaging (CT Scan or MRI [MRI
preferred])• Other considered studies – RPR, UDS,
EtOH level, EEG, CXR, EKG, HIV
Evaluation of Memory LossPatient with Known or
Suspected Memory Loss
CAM
Identify Underlying Cause of Delirium &
Treat GDS
No Delirium
SWEET 16/
MMSE
Treat Depression or
Discuss Options
LabBrain Imaging
Re-evaluate After
TreatmentNo
Action
NormalAbnormal
Equivocal or Inconsistent
with Depression
Consistent with
Depression
Impaired Not Impaired
Vascular Dementia
• Onset of cognitive deficits with a stroke• Abrupt onset of symptoms with stepwise
deterioration• Often neurological exam findings
consistent with a prior stroke• Infarcts on cerebral imaging
Vascular DementiaClinical Feature Value
Abrupt Onset 2Stepwise Detioration 1Fluctuating Course 2Nocturnal Confusion 1Preservation of Personality
1
Depression 1Somatic Complaints 1Emotional Incontinence
1
HTN 1Hx Stroke 2Associated Atherosclerosis
1
Focal Neurological Symptoms
2
Focal Neurological Signs
2
Hachinski Ischemic Index highlights clinical features
Scores > 7 suggest vascular dementia
Also of note: patients with vascular dementia are more likely to have impaired executive function than those with AD
Vascular Dementia
• HTN• DM• Statins• Aspirin
Frontotemporal Lobe Dementia
(FTD)• Atrophy of the frontal and temporal
lobes• Absence of AD pathology• Clinically: personality, behavior &
language problems• Impaired executive function
FTD
• Ages 35-70 years• Rare after age 75• Familial occurrence in ~40% of cases• More rapidly progressive disorder than
AD • Fatal Illness
FTD
• Pick’s disease is a subtype of FTD but was the first described
• Presence of Pick bodies (silver staining intracytoplasmic inclusion bodies)
Note: All FTD is associated with a serotonergic deficit and decreased dopaminergic activity has been described; acetylcholinesterase activity is relatively intact
FTD
• Inappropriate social behavior (conduct)
• <10% have short term memory impairment on testing @ initial presentation
• Poor insight into their condition
• Often mistaken for a psychiatric condition
Clinical Manifestations
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FTD: A CaseA 68 year old male presents to subacute rehabilitation following a fall and subdural hematoma. A diagnosis of FTD was made two years prior to the incident via neuropsychological testing.
Despite much improved mobility and function back to baseline, he was “made” long term care at a local nursing home, due to poor safety awareness (primarily concerns about wandering).
Admission MMSE 21/30 (deficits noted below)/abnormal CDT 2/4– 1/3 short term recall– 1/5 serial sevens– 0/1 pentagon– 8/10 orientation
FTD: A Case“I want to see what I can do about getting out of here?” He would go to report that his wife is taking his money and “she’s trying to divorce me you know.”
Very often a visit from his wife (or a telephone call) was the only thing that could calm him down.
Other behaviors were collecting towels, poor hygiene.
Then… he ate my sandwich.
FTD
• The FDA has not approved any drugs to treat this condition.
• Memantine is presently being studied.
FTD vs AD
Characteristic FTD Alzheimer’s Disease
Age of Onset <70 and even < 65 Usually greater >65Memory Deficits Late EarlyExecutive Function Deficits
Early Late
Behavioral Disturbance
Early Late
Brain Imaging Frontotemporal Atrophy
Diffuse Atrophy
Response to Cholinesterase Inhibitors
None Some
Family Hx ~ 40%
Weiss BD. Elder Care: A Resource for Interprofessional providers. http://aging.medicine.arizona.edu Accessed: October 5, 2011.
Lewy Body Dementia
• DLB is the 3rd most common dementia after AD
• Progressive gradual dementia• Fluctuations in cognitive function• Persistent, well-formed hallucinations• Spontaneous motor features of
parkinsonism
Lewy Body Dementia: A CaseAn 81 year old former PhD psychologist is transferred to assisted living from her independent living home due to significant increased deficits in her functional status – including multiple falls, inability to self-administer medications, a reversal of the sleep-wake cycle, and profound weight loss
– Admission MMSE: 28/30 (+) deficit 3/5 serial sevens
– Admission Weight: 108 lbsDuring the next four weeks there is stabilization of the sleep-wake cycle and weight gain (112 lbs)
Lewy Body Dementia: A Case
During the next year, despite several falls that responded to physical therapy she continues to need considerable more help dressing as well as orientation/cuing (i.e. meals and medication times). Observation from nursing is that she is just “lost” and even ostracized by other residents.
On two separate occasions she reported that she saw a mouse running across the ceiling. It was investigated in earnest but no evidence of mice could be found.
Lewy Body Dementia: A Case
She is transferred to a specialized dementia unit in which her behavior (now observed more closely) is vastly different than other’s with Alzheimer’s dementia.
One year later (+) cogwheel rigidity is noted.
Lewy Body Dementia
• The FDA has not approved any drugs to treat this condition.
Lewy Body Dementia vs. AD
Characteristic Lewy Body Dementia
Alzheimer’s Disease
Age of Onset >65 Usually >65Memory Deficits Late EarlyExecutive Function Deficits
Early Late
Visual Disturbance 2/3’s of Patients Rare (or very late)Brain Imaging Diffuse Atrophy Diffuse AtrophyResponse to Cholinesterase Inhibitors
Not FDA approved
Family Hx Sporadic
Parkinson’s Disease Dementia
• Estimated six-fold increased risk for becoming demented compared with people without the disorder.
• Dementia typically occurs in the last half of the PD clinical course (whereas, in DLB, it’s the presenting feature)
• Executive dysfunction is a hallmark feature
Parkinson’s Disease Dementia
• Rivastigmine (Exelon®) has been approved for use in mild-to-moderate Parkinson’s related dementia.
Normal Pressure Hydrocephalus (NPH)
• “Classic Triad” of symptoms:– Dementia– Gait Disturbance– Urinary Incontinence
• Pathologically enlarged ventricular size• Normal opening pressures on lumbar
puncture• Potentially reversible by the placement
of a ventriculoperitoneal shunt
HIV Associated Dementia• Age is a significant risk factor in HIV-
associated dementia• Clinical Symptoms
– Distractibility/Poor Concentration– Mood Changes/Apathy vs Lability– Gait Dysfunction/Clumsiness– Reduced psychomotor speed
• Absence aphasia, agnosia, & apraxia (until late disease course) helps distinguish from AD
Huntington’s Disease (HD)
• Huntington’s Disease - traced to emigrants (1630) from East Anglican village of Bures, England:
- Dominant inheritance (1 parent with gene) - CAG
- Choreoathetosis starting at 35-45 years of age- Dementia & emotional lability also
Creutzfeldt-Jakob Disease• Rapidly progressive dementia• Pathogenesis: Prions• Typically fatal within 1-2 years after
symptom onset• Motor deficits & seizures often
occur• Not treatable• Potentially transmissible• No clear cut MRI findings
Alcoholic Dementia
• Alcoholic dementia - Cerebellar and corpus callosum atrophy- Affective prosody comprehension decline- Gait problems- Abstract reasoning decline more than
education knowledge