Bedside Examination
Bedside Examination
Bedside Examination
Howard R. Kessler
The Bedside
Neuropsychological
Examination
76
Howard R. Kessler
the practitioner both guidelines and a clinical template for performing such an examination at the bedside.
I. DISORDERS OF COMMON
REFERRAL POPULATIONS
Patients possessing a number of different conditions may be
referred for bedside assessment, each presenting unique barriers
to the evaluation. These conditions include the following.
A. Stroke
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between delirium and dementia, or between dementia and depression. A variety of systemic diseases, such as brittle hypertension, diabetes, and heart disease, can cause progressive neurological decline, owing to vascular insufficiency. Patients receiving
chemotherapy or cranial irradiation can also experience cognitive decline as treatment side effects (see review by AndersonHanley, Sherman, Riggs, Agocha, & Compas, 2003). Because the
genesis of the disorder is often a crucial diagnostic marker, the
clinician may need to go to great lengths to acquire accurate
historical information from family members. In the case of the
differential diagnosis of dementia, this may not prove to be
entirely helpful. For example, the traditional literature on the
differential diagnosis of vascular versus Alzheimer's type dementia depended heavily on the "stepwise" decline observed in vascular (or what was previously called multi-infarct) dementia,
compared with the gradual decline noted in Alzheimer's disease.
However, the newer nomenclature involving "vascular" dementia recognizes the fact that decline can be more gradual, because
of chronic vascular insufficiency, which provokes a more gradual course of small vessel ischemic disease, mimicking the course
seen in cases of Alzheimer's. This renders it more difficult to
identify discrete episodes of onset of cognitive impairment. Depression can also be either a complicating or a clarifying factor
in the diagnosis of vascular dementia. On the one hand, patients
with depression clearly can appear to suffer from a dementia,
despite the fact that their cognitive impairment is functionally
determined. On the other hand, however, is the fact that depression is often an early symptom in cases of vascular dementia.
This differential diagnosis thus requires an interpretation of
qualitative aspects of performance. Both groups may manifest
similar overall levels of performance on tests of attention, memory, and executive function. However, the patient with vascular
dementia will be more likely to manifest pathognomic signs
such as perseveration or confabulation.
D. Delirium
Delirious patients may demonstrate a fluctuating level of consciousness, as well as fluctuating levels of orientation and cognitive capacity. These patients often need to be examined across
a number of days, and at various times of the day, for an accurate
diagnostic impression to be obtained. This may necessitate the
addition to the test battery of a very brief, repeatable measure
that may be sensitive to such fluctuating levels of cognition and
awareness. Further complicating the diagnosis is the fact that
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Howard R. Kessler
the variability in cognitive functioning that characterizes delirium can often mask the presence of other underlying disease
states, such as dementia. The presence of an etiology provoking
delirium can often be ascertained by reviewing the medical
record for evidence of electrolyte imbalance or medications that
might provoke cognitive side effects. Further, the delirious patient will be more likely than, for example, patients with progressive dementia to have some degree of awareness that something
is amiss.
E. Postsurgical Deficits
Patients may demonstrate acute neuropsychological deficits immediately after invasive, nonneurological surgery. A determination needs to be made as to whether changes in cognitive function are due to the effects of anesthesia, medications (especially
narcotics), or an intraoperative or postoperative event such as
stroke during or after coronary artery bypass graft (CABG). This
may be an extremely difficult differential diagnosis because of
the acuity of these patients, and there is also a high false-positive
rate of diagnosis. For example, although CABG may result in
stroke, the vast majority of patients demonstrating acute cognitive deficits after such surgery spontaneously remit. The timing
of the evaluation is thus crucial in such cases, and it would be
prudent to wait at least 24 hours before performing comprehensive neuropsychological testing while monitoring the patient's
level of consciousness in the interim.
F. Systemic Illness
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Howard R. Kessler
occupying tumors. Most commonly, however, EEC-noted abnormalities are such things as "slowing of the background
rhythm" or "diffuse bifrontal slowing." Such findings often possess little diagnostic value to the clinician, nor are they of localizing value to the neurologist. They are often found in Alzheimer's
disease and in delirium and are not useful in rendering differential diagnoses between such conditions. Furthermore, approximately 50% of healthy people have abnormal EEGs, so there
can be a high false-positive rate. Alternatively, there might be
a high false-negative rate when using EEG in cases of seizure
disorder, in that the EEG is not a useful measure unless the
patient is actively convulsive during the administration of the
procedure, showing what is commonly referred to in the report
as clinical correlation.
CT scanning, though progressing in its utility, nonetheless
remains relatively insensitive to disorders affecting subcortical
white matter, for example, vascular insufficiency. Similarly,
most CT scanning techniques remain insensitive to the effects
of concussion. CT scans are useful in identifying the presence of
space-occupying lesions (e.g., tumors) or cerebral hemorrhages.
MRI scans are more sensitive to white matter disease. T2-weighted images are sensitive to the chronic effects of ischemic demyelination (small vessel occlusive disease), whereas Flair and gadolinium-enhanced scans are sensitive to active white matter
disease, for example, as seen in active multiple sclerosis. When
reading the interpretations of MRI or CT findings, it is important
to note whether the pathology observed represents abnormality
or simply normal variation. For example, cortical atrophy is
global and nonlocalizing, and can often be noted to be "appropriate for age." Similar statements may be found in the interpretation of white matter lesions. It is important to be able to
correlate the MRI or CT abnormalities with clinical findings as
well. For example, white matter changes, noted on MRI T2
weighted images, are not uncommon in normal aging. Such
findings, in the absence of objective cognitive impairment,
should not be used to infer the presence of neurological disease.
Furthermore, one pitfall in MRI administration and interpretation is that the examination is often geared toward the referral
questions. Hence, an abnormality related to, say, multiple sclerosis, may not be revealed if the referral question is one of
concussion or headache.
D. Medications
It is particularly important to account for the effects of a variety
of psychoactive medications on test performance. This is
81
particularly crucial in testing elderly patients, in whom polypharmacy can present a hindrance to test performance and
interpretation. It is also important to look at interactions between drugs and their side effects, within the context of a particular patient's medical condition. For example, patients with
hepatic disease may experience heightened side effects of neuroleptics (such as Haldol) because they are metabolized by the
liver. Similarly, because benzodiazepines are metabolized by the
kidneys, they may provoke increased side effects in patients
with renal disease or those undergoing renal dialysis. Anticholinergics, such as amitryptiline (which is often used as a sleep
aid or for pain), may have heightened side effects in patients
experiencing cardiovascular or cerebrovascular disease, hence
provoking increased sedation or memory impairment. Similar
findings might be noted in patients taking beta-blockers. This
is because both classes of medication may inhibit vascular flow.
Side effects found in commonly prescribed medications can be
found in Table 5.1 (excerpted from Ellsworth, Witt, Dugdale,
& Oliver, 2003).
III. CONDUCTING THE BEDSIDE EXAMINATION
A. Background History and Clinical Interview
The interview and history taking should be a standard part of
the bedside assessment. Formats for history taking can be found
in many sources and are not reviewed in depth here. (One
of the best sources is Strub & Black's [1993] The Mental Status
Examination in Neurology.) In the case of the bedside assessment,
certain background factors are particularly critical and often
require that a reliable informant (other than the patient) be
identified to provide corroborating information. These factors
include the following:
1. GENESIS OF THE DISORDER
A number of questions need to be asked to ascertain information regarding both the onset and progression of a given
disorder. For example, was the onset rapid or progressive? Was
the onset associated with some medical, psychosocial, or environmental event or stressor? Has the downward progression
been relatively linear, or has it occurred in a relatively stepwise
or variable fashion? Does the disorder represent a qualitative
change in the patient's functioning or an exacerbation of a
preexisting condition?
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2. SELF-CARE
Has the patient been compliant in taking his or her medications? If hypertension or diabetes is present, how stable or brittle
has the condition been? If the patient suffers from diabetes,
how often has the patient tested his or her blood glucose levels?
Has the patient conformed to dietary restrictions? How cognitively and physically active and stimulated was the patient prior
to hospital admission? Has there been risk of inadvertent selfharm at home (e.g., from falls or burns)?
3. PRIOR CNS INSULTS
Mild traumatic brain injury (TBI) often goes unnoticed and
is rarely found in the patient's medical record. Many physicians,
in fact, generally do not address the issue in the standard history.
It is important to question the patient regarding the history of
such events. It is crucial to look for evidence of not only incidents accompanied by loss of consciousness and anterograde
or retrograde amnesia but also more subtle events accompanied
by some "alteration" in consciousness. Because whiplash injury
can present with cognitive impairment, the history of such episodes must also be ascertained. Additional questions should be
posited, looking for a history of things such as near-drowning
episodes or a history of toxic exposure. Has the patient experienced episodes of brief interruptions in consciousness (e.g.,
fugue, or frank loss of consciousness), which may indicate some
ongoing or episodic process, such as cerebrovascular disease or
seizures? Is there a history of excessive alcohol, drug, or tobacco
use, which may contribute to or provoke neurological disease?
The literature on alcohol and drug effects on cognition is fairly
specific with regard to the effects of various agents. It is important to be aware of the reversibility or permanence of cognitive
impairment provoked by these substances. It is also important
to note that withdrawal from some substances may provoke
temporary alterations in cognition.
4. INSIGHT, SELF-AWARENESS, AND CONCERN
During the course of the clinical interview, it is important
to determine the patient's level of awareness of his or her medical state and insight into cognitive and physical limitations.
Lack of awareness alone is not necessarily pathognomic of cognitive decline. For example, it is not unusual for a patient to be
unaware of medical subtleties because the condition has not
been explained adequately to him or her. Poor awareness, in
combination with neuropsychological deficits, is, however,
helpful in neuropsychological diagnosis. For example, some
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Because of the acuity of the patient's medical status, the principles of bedside assessment differ from those used in less acute
88
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General
Cognitive
SpeechLanguage
AttentionMemory
Specific tests
Cognistat/Neurobehavioral Cognitive
Status Examination or Brief
Neuropsychological Cognitive
Examination or Kaplan-Baycrest
Neurocognitive Assessment or Repeatable
Battery for the Assessment of
Neuropsychological Status
WAIS-III Short Form (individual subtests or
Satz-Mogel)
Boston Naming Test
Writing-spelling sample (BDAE CookieTheft, WAB Kite, writing to dictation)
Reading sample (Gray Oral Reading
paragraphs, WRAT-3 Reading short form)
Comprehension (complex ideational
material)
Brief screening of repetition and ability to
follow commands (e.g., Token Test short
form) if any of the above language skills are
impaired
Language-mediated abilities (Benton
Left-Right Orientation, WAB Praxis,
Kinsbourne-Warrington finger gnosis or
HRNB Finger Localization)
Stroop Neuropsychological Screening Test
Paced Auditory Serial Addition Test (PASAT)
Spatial Span (WMS-III)
Visual Search tasks, if evidence of hemiinattention (letter cancellation)
Verbal list learning (Buschke Verbal Selective
Reminding, Hopkins Verbal Learning, with
delayed recall and recognition)
Figural recall (design recall, such as Complex
Figure or WMS-III designs, with delayed
recall and recognition)
Narrative recall (administer if list learning is
impaired; Babcock-Levy, WMS-III Logical
Memory, with delayed recall and
recognition)
Visual recognition (administer if figural recall
is impaired; CVMT)
Recognition Memory Test (Warrington, if
recall impaired)
Three Words/Three Shapes (Mesulam) for
lower functioning patients
(Continued)
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Specific tests
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101
Leach, L., Kaplan, E., Rewilak, D., Richards, B., & Proulx, G. B.
(2000). Kaplan Baycrest Neurocognitive Assessment. San Antonio, TX: Psychological Corporation.
Mattis, S., Jurica, P. J., & Leitten, C. L. (2001). Dementia Rating
Scale2 (DRS-2). San Antonio, TX: Psychological Corporation.
Randolph, C. (1998). Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). San Antonio, TX: Psychological Corporation.
Stern, R. A., & White, T. (2003). Neuropsychological Assessment
Battery (NAB). Lutz, FL: Psychological Assessment Resources.
Tonkonogy, J. M. (n.d.). Brief'Neuropsychological Cognitive Examination. Los Angeles: Western Psychological Services.