Memory Impairment
Konrad C. Nau
Memory is the cognitive domain that gives us the ability to store and retrieve information. Up to 80% of community dwelling elderly report subjective memory defects.
Approach
A. Screening tools must be used. Significant memory and other cognitive deficits and depression can exist in patients with fully intact doctor’s office social skills (1).
B. Dementias are ruled in if memory and other progressive cognitive defects are found (Chapter 4.4)
C. Red flags that signal delirium include acute onset (<1 to 2 weeks), fluctuating levels of alertness, and new urinary incontinence. Medication side effects, serious systemic illness, or intracranial catastrophes are common (2).
History
A. Presentation. Dementia patients are brought in by relatives about memory problems; whereas, depressed and age-associated memory impairment (AAMI) patients come in on their own to complain (3).
B. Chronology. Determine if the onset is gradual as in Alzheimer’s disease (AD) or abrupt as in multi-infarct dementia (MID), subdural hematoma (SH), Creutzfeld–Jakob disease (CJD); and steady (AD) or stepwise (MID) deterioration. Check for history of past strokes (MID); head trauma (AD, SH); medication; sexually transmitted diseases; human immunodeficiency virus (HIV) risk; alcohol use; heavy metal exposure; past depression; and many “I don’t know” answers (depression).
C. Family reports of change in the patient’s judgment and executive functioning indicate other nonmemory cognitive problems (dementia) or visual hallucinations, as in Lewy body dementia (LBD).
D. Family history. Inquire about a possible familial tendency for Huntington’s disease (HD), AD, Parkinson’s disease with dementia (PDWD), Pick’s disease (PD), or alcoholism.
Physical examination (PE)
A. Normal physical findings are reported in most patients with AD, AAMI, and depression.
B. Specific abnormalities that help classify dementias include resting tremor (LBD, PDWD), myoclonus (CJD, LBD), glabellar reflex (AD), palmomental reflex (AD, PD), cogwheel rigidity (LBD, PDWD), stooped shuffling gait (LBD, PDWD), asterixis (alcoholism), chorea (HD), focal motor or sensory deficits (MID), asymmetric reflexes (MID, CJD), apraxic gait-wide based, feet stuck to floor or magnetic (normal pressure hydrocephalus, NPH), diffuse muscle wasting early in clinical course (CJD, HIV, dementia), and gaze paresis especially downward (progressive supranuclear palsy, PSNP).
Testing
A. Tests useful in clinical practice are presented in Table 4.1.
B. Clinical laboratory tests can rule out treatable dementias. Check complete blood count, electrolytes, calcium, phosphorous, magnesium, glucose, blood urea nitrogen, creatinine, liver and thyroid function tests, vitamin B12 level, and syphilis test (VDRL). If indicated, test for HIV and heavy metals.
C. Cerebral spinal fluid (CSF) examination is indicated in patients with early onset dementia, metastatic cancer, reactive VDRL, fever, or rapidly progressive dementia. If NPH is suspected, the withdrawal of 30 ml CSF with subsequent clinical improvement may predict therapeutic ventriculoperitoneal shunt success.
D. Diagnostic imaging is indicated in all except perhaps longstanding end-stage dementia. Magnetic resonance imaging is most sensitive but computerized tomography (CT) will suffice to rule out subdural hematoma, central nervous system (CNS) tumor, hydrocephalus, cerebral atrophy, and infarction. Positron emission tomography scans promise to be most specific.
E. Electroencephalogram usually reveals nonspecific slowing, except in CJD (diagnostic high voltage bursts).
Diagnostic assessment
A. AAMI (benign forgetfulness) is a nonprogressive memory problem with recalling people’s names and relatively minor recent events in those aged more than 65 years. Other cognitive domains are intact and this does not appear to predict future acquired dementias.
B. Depression causes a pseudodementia that can be diagnosed using the Mini-Mental Status Examination (MMSE) (score >23) and the Geriatric Depression Scale Short Form (score >4).
C. AD is the leading cause of dementia (127/100,000 population). Gradual onset of a progressive memory impairment along with at least two other cognitive defects that impair social or occupational function, a normal PE and laboratory determinations, and some cerebral atrophy on CT make a probable AD diagnosis. This is substantiated on postmortem examination 85% of the time (Chapter 4.4).
D. LBD is the second leading cause of dementia with a fluctuating course, parkinsonian features, early visual hallucinations, and myoclonus developing within 1 year of the dementia. Patients with LBD are exquisitely sensitive to the extrapyramidal side effects of traditional major tranquilizers and have a two- to threefold increased mortality if on these (4).
E. MID is the third leading dementia type with its stepwise or abrupt history and focal sensor-motor defects.
F. PDWD occurs in 30/100,000 population and develops in up to one-third of Parkinson’s disease patients.
G. NPH is suspected with the triad of dementia, urinary incontinence, and an apraxic gait.
H. PSNP is a Parkinson-plus condition with paresis of downward, then later upward and horizontal gaze.
I. HD occurs in 5 to 10/100,000 population with chorea, prominent behavioral problems, dementia, and high suicide rates; onset occurs in individuals in the third and fourth decade of life. It has autosomal dominant heritance on chromosome 4.
J. CJD is a rare (1/1,000,000 population), viral prion CNS infection with rapid progression of dementia, wasting, and myoclonic jerks. Death occurs within 6 to 9 months in these patients aged 40 to 50 years.
K. HIV dementia is rare in the absence of symptoms of systemic infection. Use CSF to rule out CNS infections.
L. PD is rare with psychiatric disorders, blindness, and language defects (compared with more memory defects in AD) (5).
References
1. Gallo JJ, Reichel W, Andersen L. Handbook of geriatric assessment. Rockville, MD: Aspen Publishers, Inc., 1988:11–64.
2. Goldmacher DJ, Whitehouse PJ. Evaluation of dementia. N Engl J Med 1996;
335:330–336.
3. Robbins LJ. Dementia, delirium and depression: approach to the confused elderly patient. In: Geriatric medicine for the FP audio CME lectures and workshops. Kansas City, MO: American Academy of Family Physicians, 1997:9–36.
4. Lapalio LR, Sakala SS. Distinguishing Lewy body dementia. Hosp Prac 1998;
33:93–108.
5. Neary D, Snowden JS. Classification of the dementias. London: Churchill Livingstone, 1998:717–725.
Pictures
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Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
Other Book Chapters Related to Cognitive impairment
Read excerpts from these other book chapters related to Cognitive impairment:
Medical Books Excerpts
- DELIRIUM
- "Algorithmic Diagnosis of Symptoms and Signs" (2003)
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- DEMENTIA
- "Algorithmic Diagnosis of Symptoms and Signs" (2003)
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- Delirium
- "In A Page: Pediatric Signs and Symptoms" (2007)
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- DELIRIUM
- "Differential Diagnosis in Primary Care" (2007)
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- Dementia*
- "A Pocket Manual of Differential Diagnosis" (1999)
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- Delirium
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
- Dementia
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
- Memory Impairment
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
- DELIRIUM
- "Differential Diagnosis in Primary Care" (2007)
- [ read ]
Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.
More About Causes of Cognitive impairment
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Dementia (Field Guide to Bedside Diagnosis)
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