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Introduction
The assignment for this chapter is to describe a clinical evaluation of mental
status. Several assumptions constrain this evaluation: 1) It should have transparent
clinical validity; 2) It cannot require equipment that is not readily available in the office
or at the bedside, and it must be informative in the time restrictions of a clinical schedule;
3) It should not pirate tests from neuropsychological that might be more informative if
they were embedded in a full neuropsychological evaluation; 4) It should be broadly
useful across the adult age span.
Most reviews of mental status are organized around separable cognitive domains
such as language, memory, attention, executive functions, etc. (Weintraub, Mesulam
1985) Each domain is defined and the tests that probe various aspects of that domain are
described. This approach comprehensively surveys all tests, but for several reasons it is
not optimally organized for actual clinical purposes: 1) it assumes that the cognitive
domains are cleanly distinguishable at the clinical level, but they are not; 2) it presumes
that all tests are useful in all settings; 3) it leaves a novice practitioner uninformed by
clinical probabilities. Experienced clinicians will surmount these limitations, but then
experienced clinicians have no need for this chapter. How can novices be guided to a
useful, practical assessment?
One approach might be to declare the clinical cognitive assessment to be
unproductive and abandon all efforts. Judging by the number of neurological assessments
that begin with the second cranial nerve, even when the patient’s complaints are
cognitive, many neurologists have apparently been trained in this school. A complaint of
cognitive difficulties leads directly to magnetic resonance imaging (MRI), an
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electroencephalogram, and a neuropsychology referral. Imaging may determine an
etiology, for example that memory complaints are secondary to a large frontal glioma,
thus leading directly to medical treatment. But what to do if the imaging does not provide
a diagnosis? Are those MRI paraventricular T2 hyperintensities responsible for or
sufficient to explain the elderly patient’s memory complaints? Another limitation placed
upon neurologists who choose to abandon the clinical cognitive exam is the inability to
make suggestions about treatment or rehabilitation or to judge the appropriateness of
treatments suggested by others, such as Occupational Therapists, Speech Pathologists, or
Neuropsychologists.
Neuropsychological testing has many advantages over clinical assessment.
Neuropsychological instruments are mostly psychometrically proven; validity, reliability
and practice effects have been demonstrated. Age, gender, educational, and cultural
confounds are mostly established. They are supported by a rich literature detailing
patterns of impairment most consistent with various types and locations of brain
dysfunction and even with specific diagnoses. Quantitative measurement allows better
definition of severity and better tracking of change over time or with treatment. A
competently performed neuropsychological evaluation is infinitely preferable to a casual
clinical examination.
Some of the power of neuropsychological tests derives from their sensitivity, but
their weakness is their poor specificity, often even in aggregate, when the diagnosis is
difficult. Can neuropsychological tests alone distinguish between the mild dementia
patterns of Parkinson’s disease and vascular dementia (Jacobs, Marder, Coté et al. 1995)
or between mild cognitive impairments in multiple sclerosis(Rao 1986) ((Callanan,
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Logsdail, Ron et al. 1989) and depression? Can they clarify the reason for failure to return
to work of a patient, apparently well recovered from aphasia following stroke, depressed
about residual weakness of the dominant hand? The typical neuropsychological
assessment incorporates quantified versions of the elementary examination - tapping
speed, grip strength, cancellation tests, stereognosis, etc. - and of emotional and
personality state - Beck Depression Inventory (Beck, Ward, Mendelson et al. 1961),
MMPI (Dahlstrom, Welsh, Dahlstrom 1975), etc. When integrated into the cognitive
assessment, specificity of diagnosis in some situations may be increased, but differential
diagnosis remains a weakness of neuropsychological testing.
Neuropsychological testing also has substantial logistical limitations. It cannot be
applied in many clinical settings such as the emergency department (ED), the ICU, or, in
the United States, in the managed care, single visit approved consultation.
Neuropsychologists can confuse cooperation for motivation. The tests require a motivated
patient for interpretation, so patients who are depressed, anxious, sleep deprived, irritable,
resistive or in pain may cooperate but underperform. It may require hours of effort and
days of delay for results. In the US reports often run to many, single-spaced pages filled
with boilerplate as though to discourage physicians from even attempting to read them
sufficiently to understand the reasoning behind the conclusions. It is expensive.
Both the clinical evaluation and the neuropsychological assessment, like the
medical student’s physical examination, is at risk of treating the patient as an unknown on
whom all tests must be undertaken. In most clinical settings, the patient is anything but an
unknown. Patients arrive at the ED, the hospital, the clinic, or the office with significantly
constrained diagnostic possibilities:
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A 74 year old man accompanied by his wife and daughter who complains of his 1
year history of worsening forgetfulness.
An 81 year old woman arrives in the ED via ambulance from home with new
onset “confusion”.
A 46 year old woman is referred by her primary physician because she continues
to complains of memory loss several months after a minor CHI with brief LOC;
numerous neurologic studies have been normal.
A 68 year old man with a 5 year history of treated Parkinson’s disease has been
having episodes of nocturnal confusion and difficulties with paying his bills for a few
weeks.
A 79 year old man is admitted directly from his physician’s office with new onset
right hemiparesis and altered mental state.
A 22 year old man who suffered a severe traumatic brain injury 2 weeks earlier is
now alert but agitated and demanding to be discharged.
A 38 year old woman with a 15 year history of chronically progressive multiple
sclerosis has begun neglecting her house and young children.
Although it may be useful for any of the above scenarios, there is no single mental
status examination that is appropriate for all of those cases. Furthermore,
neuropsychological assessment should not be essential for any of them. Thus, the goal of
this chapter is to parse Behavioral Neurology into a few specific clinical situations that
can illuminate the utility of clinical assessment.
Beyond diagnosis, the clinical mental status examination may have other valuable
roles. It may suggest the most fruitful investigations. It may pinpoint the deficits that most
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require intervention or at least explanation to the family. It may inform decisions about
rehabilitation potential or pharmacological treatment. It will allow characterization of
deficits sufficiently well that follow up evaluation can distinguish between improvement
and decline. The clinical evaluation should produce an overall definition of the patient’s
deficits that allows easy communication with other physicians and medical staff.
“Moderately severe dementia, probable Alzheimer’s Disease” carries important
management implications to everyone in contact with the patient. The PCP will get
another family member to confirm medication compliance, the OT in the outpatient clinic
will accelerate the driving assessment, family members will meet to establish a plan for
closer supervision, etc.
Throughout the text to follow, the reader will find hypothetical clinical situations
meant to clarify the use of the history or the examination tool being considered.
Clinical History
The first step in mental status examination is the history. The presenting
complaint will prune the examination tree dramatically. If the patient is on the medical
service and abruptly becomes confused that day, possible diagnoses are limited. A plan
for the mental status examination may be to attack only attention, memory, and language,
at least until talking to the patient is sufficient to reveal his left spatial neglect when the
examination plan will shift to spatial and perceptual tasks.
Consider how much of the mental status examination is embedded in eliciting a
history. Attention: Is wakefulness maintained? Is the patient following your questions?
Are the content and structure of responses organized? Is a train of thought being
maintained? Is he distractible, perseverative or repetitive? Language: In relating the
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history is language well constructed and grammatical? Are there word finding lapses,
circumlocutions or paraphasias? Does he comprehend questions? Are answers fully
elaborated and organized? Are there confabulations or delusions? Memory: In responding
to questions can the patient recall salient features of his illness, his current circumstances
or his past history? Psychomotor: As the history proceeds what can be observed of motor
function such as restlessness, postural abnormalities, asymmetries of movement or
bradykinesia? Affect and behavior: In responding does the patient’s voice carry affect?
Do facial expressions and bodily postures correspond to the expressed emotion? Do
movement and expression convey a mood disorder or anxiety? Is behavior during the
interview appropriate? Is he intrusive, rude, indifferent, or suspicious? How is he dressed
(in the office anyway)? Does he behave maturely? Are there unexpected behaviors?
As the history unfolds the diagnosis may already be clear. The patient’s nephew
states that he is concerned about his aunt’s gradually decreasing memory. She reports no
problems except that her belongings are being misplaced. In the interview, it is apparent
that she does not know her recent medical history or her medications. In responding she is
clearly anomic and circumlocutory. Her movements, posture, affect and comportment are
normal. She almost certainly has Alzheimer’s disease although focal atrophy or structural
lesion of the left temporal lobe are not impossible. The examination to distinguish
between these alternatives should be clear: 1) search for right lateralized visual field,
motor, or sensory deficits that support a focal lesion; 2) probe recall of recent events
because patients with focal temporal lesions - but not patients with Alzheimer’s disease may be quite aware of events although aphasic in describing them; 3) probe praxis and
visuoperceptual functions that are more likely to be intact in frontotemporal dementia
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than Alzheimer’s disease. If the diagnosis is not clear after the interview, the history at
least will have powerfully constrained the subsequent examination.
Clinical settings of the mental status examination:
Acute confusional state (ACS):
The patient has an abrupt change in alertness, awareness or attention. This may
occur outside of observation, such as someone living alone, found by another, so that the
actual onset is unknown. It may occur under close supervision, such as post operative
delirium emerging in recovery. It may occur without known underlying potential cause, or
it may be in a patient already known to have predisposing risk, such as chronic liver
disease, alcoholism, Alzheimer’s disease or use of centrally active medications. In any
case, the patient will usually have no overt systemic signs (fever, diaphoresis, etc) and no
focal neurological signs coincident with the onset of confusion (hemiparesis, neglect,
etc.) which would have generated a different initial premise about the patient’s
fundamental problem. The patient will often have had a negative CT before mental status
has been carefully assessed.
ACS is a medical problem, not specifically a cognitive one. The assessment
requires medical evaluation - review of history, medication use (including over the
counter, herbal and alternative medications), medical examination, neurological
examination and various laboratory studies. During medical evaluation, cognitive
assessment of confusion in different contexts will have quite different rationales. In
patients with a known cause (delerium tremons, toxic states, metabolic encephalopathies,
viral encephalitis, etc.) the main role of assessment will be to establish severity of
confusion so that effects of treatment or detection of worsening can be established. In
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patients without a known cause, assessment may carry an additional role of attempting to
determine the etiology, perhaps through detection of idiosyncrasies characteristic of
specific causes.
Consider confusional states to be disorders of attention, much as aphasias are
disorders of language. The steps in assessment are: 1) determine that the symptoms are
truly due to impaired attention and not actually due to aphasia; 2) assess the arousal state
underlying attentional impairments; 3) determine if the patient has hallucinations and if
she is delusional or paranoid; 4) obtain some markers of severity that can be reliably used
to follow clinical progress.
Establishing an attentional impairment: The only likely diagnostic error is
mistaking an acute Wernicke’s aphasia without other neurological signs for confusion.
The pressured abnormal language with unreliable response to requests may suggest
delirium, particularly if the patient is not a native speaker of the examiner’s language.
Patients with very acute Wernicke’s aphasia may not reliably respond to nonverbal
communication cues. Evidence for a primary language disorder will emerge in
conversation with the patient. Frankly paraphasic speech, in particular phonemically
derived paraphasias, is not characteristic of ACS. Content may be deranged in ACS, but
the elements of language are preserved. Failure to respond appropriately to very simple
questions about personal information is more suggestive of aphasia. In ACS except at the
extremes of arousal, those questions generally produce some appropriate, albeit not
always correct, responses. Unlike patients with ACS, patients with Wernicke’s aphasia
commonly appear normal when not being examined. In Wernicke’s aphasia, arousal is
normal, and simple pragmatic actions such as locating a bathroom are often normal.
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Patients with acute global aphasia without hemiparesis may present as an acute
change in mental status. The absence of verbal response to any question or command
despite normal arousal should suggest a primary language disorder.
Level of arousal: Depending upon cause and chronicity patients in ACS may be
underaroused - sleepy to lethargic to stuporous but responsive - or normally aroused - or
overaroused - pressured to agitated to delirious. Underarousal suggests sedative
medication overdose, intracranial disease, post ictal state or one of the more gradual
metabolic causes. Overarousal suggests stimulant medication or drug withdrawal states.
Hallucinations and delusions: Most patients with hallucinations will not
spontaneously complain of them. That the patient is hallucinating may be apparent from
observation: sudden shift in spatial attention to an area where you see or hear nothing,
movements into space that appear to have no stimulus, responses to unasked questions, or
statements to no particular visible audience. When directly asked, some patients are able
to acknowledge hallucinations or describe visual or auditory content that you can infer
represent hallucinations. Visual hallucinations are much more common than auditory or
tactile in ACS. Visual hallucinations are particularly prominent in delerium tremons
(DTs), Lewy Body Disease or drug toxic Parkinson’s disease patients, some psychoactive
drug overdoses or in elderly patients with eye disease.
Delusional states and paranoia frequently develop in ACS whether due to specific
neurochemical or neuroanatomical features or simply as manifestations of severely
disordered reasoning. Confabulated delusions are common with acute frontal lesions
(Fischer, Alexander, D'Esposito et al. 1995). An occupational delusion represents the
patient’s belief that he is involved in some aspect of his routine employment. Patients
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with acute frontal lesions and patients emerging from traumatic coma seem particularly
prone to occupational delirium.
Paranoid delusions are common in ACS, particularly DTs, but also in acute
confusion superimposed on Parkinson’s disease (Klatka, Louis, Schiffer 1996), Lewy
Body disease (McKeith, Fairbairn, Bothwell et al. 1994) or Alzheimer’s disease (Mega,
Cummings, Fiorello et al. 1996). The exact basis for emergence of paranoid delusions is
not known. The importance of recognition of paranoid delusions is that they are often
extremely distressing and may lead to escalating agitation unless treated.
Assessment of ACS: The goals of clinical evaluation are to quantify severity, at
least approximately, to facilitate reassessment of what may be a rapidly changing
situation, and to probe for any unexpected, possibly diagnostic, deficits. Evaluation will
focus on attention and memory, sustained attention, concentration and simple learning.
Depending upon the patient’s ability to cooperate there may be quite little to assess.
Tasks: Immediate memory can be probed with digit span forward (dsf). Sustained
attention (working memory) can be assessed with digit span backwards (dsb) or a variety
of mental control tasks depending upon severity. Note two important features of these
tests. First, they are cognitively trivial, that is, they require only attention, and no or
minimal cognitive computation. Second, they are dependent upon normal language, so for
patients with even mild aphasia they are probably uninterpretable. Counting backwards
from 20 may be the easiest. Reciting the months in reverse order is slightly more difficult.
Serial subtractions, such by 3’s from 60 is yet more demanding. For mildly confused
patients who can do the tasks, comparing the time for twenty backwards by 1’s and 60
backwards by 3’s can be useful because both require 20 responses and the differences in
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times and errors are due to the extra load of serial subtractions. It is usually worth at least
attempting all levels to track upward or downward course. For mild ACS testing verbal
fluency - naming as many examples of any category, such as animals, in 60 seconds - may
be a useful probe of sustained attention.
Testing orientation is self-explanatory, but it should also include probes for
awareness of illness and deficits. To test learning the examiner has choices. If the patient
is disoriented, the examiner can reorient, rehearse and repeat correct orienting
information with the patient, then retest orientation in a few moments. If the patient is
oriented, the examiner can have the patient learn and rehearse a short (less than the dsf)
list of familiar words or a few facts about his circumstances and test for recall in a few
minutes. In either case, inquiry about the current illness may reveal memory loss for a
definable time prior to the onset.
If during testing there is any suggestion of left visual field neglect, more specific
tests of neglect should be used. Cancellation of lines on a page may be the most sensitive
ad hoc test for neglect (McGlinchey-Berroth, Bullis, Milberg et al. 1996).
Structure of assessment: This will depend upon the overall severity. When
appropriate, placing the examination tasks within the interview and a period of calm
conversation works best. He may never realize that he was tested. Begin with open ended
probes about illness. Sliding into gentle orientation questions might follow. If disoriented,
reorient. If oriented, ask him to learn a few facts about his current situation, such as the
exact location, your name, or his illness and also a few common words. Spend a few
moments inquiring about awareness of specific deficits, such as, “Is your memory
working right?” Recheck orientation and learning. If recall is poor, indicate your concern
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and the necessity to probe a little more. In less than five minutes, you should be able to
check orientation, to do dsf, to have him learn a short list of words, to do dsb, to do
mental control tasks, to recheck orientation and awareness, to recall the word list and
observe for hemineglect or test word list generation.
Reporting your findings: In a brief note, you can summarize level of arousal,
responsiveness, dsf (attention), dsb, mental control in seconds and errors and perhaps
word list generation (all sustained attention), orientation, learning, awareness,
hallucinations, delusions, language content and neglect.
Gradual mental decline or memory loss in the older patient with a normal
neurological examination:
The patient has a history of months to years of gradual decline. There is no history
of stroke at onset or of focal neurological disease. What are the diagnostic possibilities?
They are probably limited to a few metabolic disorders such as hypothyroidism or
hypercalcemia that the referring physician may have already eliminated, to frontal or
anterior temporal structural lesions (tumor or stroke) or subdural hematomas without
evident neurological abnormalities that may also have been eliminated by neuroimaging,
to depression, to Alzheimer’s disease, or to frontotemporal dementia.
Simply taking the history is likely to point to the pertinent examination. Does
observation suggest extrapyramidal disease? Is the patient disheveled, minimally
responsive, unconcerned, unselfcensored, concrete or confabulatory? You will focus on
executive tasks. Is he anomic, paraphasic, or unable to understand your requests? You
will focus on language tasks. Is she uncertain of her own history? You will focus on
memory. Is she sad, self deprecatory or tearful? You will focus on mood. Does he show
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some combination of deficits? You will disperse your focus. In each case, all domains
will be sampled.
The examination will include: orientation, immediate memory, language - at least
naming and repetition, limb praxis, verbal memory, drawing tests and executive
functions.
Structure of assessment: Begin with unthreatening memory probes. Does he know
how he came to be referred to you? Ask a few orientation questions, including knowledge
of your name. If disoriented, reorient. Ask about current events and prominent
personalities. Shift to language tasks: naming common objects and parts of objects. Do a
few repetition tasks. Embed dsf and dsb at the end of the repetition.
Depending on the findings to this point, the examination can take several paths. If
naming was impaired, it is necessary to switch to comprehension tasks, such as having
the patient point to the objects in response to spoken name, a subpart name or a functional
description. If this is impaired, more detailed comprehension testing is necessary (see
section on aphasia assessment). If naming is demonstrably affected, verbal memory drills
are unlikely to be meaningful.
If naming and repetition are good, return to verbal memory with list learning. You
will have to judge appropriate difficulty, i.e., span or supraspan length as determined by
the dsf. Rehearse the list until it can be repeated or until 5 trials if it is apparent that it
cannot be learned. Warn the patient that you will ask for this list again in a few minutes.
Present a few stimuli for reading aloud. If previously impaired, reinquire about
orientation.
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Turn to a few simple executive tasks. Verbal fluency can be tested with a semantic
category (animals, foods, brands of automobiles, etc.) Normal performance is at least 12.
If normal, test with a letter category, such as “b’ or “f” without allowing proper names.
(Patients with significant confrontation naming impairment should be spared this task.)
The timing is usually right to ask the patient to recall the word list. Errors may be no
recall or extraneous recalls, often from the verbal fluency tasks just performed. You can
return to other executive tasks such as similarities or proverb explanation or the more
difficult mental control tasks. An easy bedside task for mental flexibility and monitoring
is a coin switch game. Manipulating a coin behind your back, bring your fists forward and
ask the patient to guess the hand holding the coin. Open your hands to show the location,
then move your hands behind your back and repeat. The coin’s location can be
manipulated by any pattern (alternating, always left, always right, two consecutive lefts
followed by two consecutive rights, etc.) If the patient detects the pattern and gets six
consecutive correct locations, switch to another pattern without warning and determine if
he can follow the shift.
Test limb praxis (see section on aphasia). After praxis tests, the transition to
pencil tasks, beginning with writing, will appear seamless. Have the patient write a
sentence to dictation. Deficient recall of the dictated sentence, impaired spelling, and
various motor control problems (micrographia, perseveration, or awkward letter
construction) may be noted. Then move to spatial tasks with a pencil: drawing from
memory a few common objects, then copying a complex nonrepresentational figure.
Errors in configuration and detail placement and in execution, such as overdrawing,
spatial inattention, closing in on the target, etc. are all noted.
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Assessment of mood requires direct inquiries about emotion and associated
symptoms such as sleep patterns and appetite.
At the conclusion, elicit the patient’s opinion about his performance. If he
underreports difficulties and errors, probe about specific impairments to determine the
depth of poor awareness.
This examination should allow categorization of deficits. When deficits are
limited to language a left perisylvian lesion, primary progressive aphasia or semantic
dementia are suggested. Memory impairment with accompanying praxis, spatial or
language deficits suggests Alzheimer’s disease. Preponderant executive dysfunction
implies frontal lesion, hydrocephalus or FLD or possibly depression if associated with
affective disturbance. Significant depression substantially blunts attention and motivation
and produces cognitive impairments. It may be impossible to have confidence in the
significance of cognitive impairments when testing a patent who is depressed, particularly
an elderly depressed patient.
A standard screen of cognition, such as the Mini Mental State Examination
(Folstein, Folstein, McHugh 1975), may be a useful conclusion to testing, specifying
severity and simplifying reassessments. Neuroimaging will resolve structural versus
degenerative uncertainties and may even show a pattern of focal atrophy characteristic of
one of the degenerative possibilities.
Cognitive impairment in patients with known degenerative neurologic
disease:
The presenting questions might be: 1) Is the decline consistent with the underlying
disease? 2) Is the decline unlike (worse than?) that anticipated with the underlying
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disease? 3) If so, is the primary diagnosis correct? 4) If it is correct, is the unexpected
cognitive change due to a coincident problem?
Prototypical examples of this category include a patient with treated Parkinson’s
disease who begins to show functionally limiting cognitive impairments or a patient with
documented Alzheimer’s disease who suddenly becomes agitated and paranoid. The
history may have already suggested the answer to the mental status change: subacute
worsening occurring after a medication increase, numerous falls, disrupted sleep
secondary to nocturia, etc. If not, the elementary examination may suggest the answer to
the cognitive change: severe standing hypotension, new subtle left hemiparesis, etc. Thus,
a mental status examination may follow other diagnostic efforts that have constrained the
goals of the examination.
The mental state evaluation in this context will take one of three directions:
1) Is there evidence of a superimposed ACS, a potentially transient impairment
due to a specific factor such as medication or sleep disorder? The tests will follow the
path suggested previously for ACS.
2) Are the mental changes simply compatible with progression of the underlying
disorder? Testing this question requires some knowledge of the natural history of the
degenerative diseases: DAT (Stern, Richards, Sano et al. 1993; Green 1995), Parkinson’s
Disease (Stern, Richards, Sano et al. 1993), Huntington’s Disease (de Boo, Tibben,
Lanser et al. 1997), progressive supranuclear palsy (PSP) (Golbe, Davis, Schoenberg et
al. 1988), corticobasal degeneration (CBD) (Litvan, Agid, Goetz et al. 1997), Lewy Body
disease (LBD) (McKeith, Galasko, Kosaka et al. 1996), and frontotemporal dementia
(FTD) (Gregory 1999) (Hodges, Patterson, Ward et al. 1999). At a minimum in DAT,
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Parkinson’s disease, Huntington’s disease, PSP and FTD progression of executive
impairments is entirely expected. In LBD progressive confusion with hallucinations is
common. In Huntington’s disease worsening memory is expected. In CBD progression of
limb apraxia and spatial deficits would be anticipated. In FTD increasing apathy,
amotivational behavior and environmental dependency behaviors are common.
3) Has there been a shift in the qualitative nature of the deficits? There is a large
(30-40%) overlap of Alzheimer’s disease and Parkinson’s disease (Stern, Richards, Sano
et al. 1993). The Parkinson’s disease patient with cognitive decline should be reevaluated
with language and praxis tasks. In the absence of any drug induced ACS, confrontation
naming, repetition, bedside comprehension and representational limb praxis should be
essentially normal in Parkinson’s disease. Overt anomia, paraphasias, word
comprehension deficits or limb apraxia would be important clues to Alzheimer’s disease.
Apraxia is a clue to reconsider CBD a disorder with many extrapyramidal features
(Litvan, Agid, Goetz et al. 1997). Chronic ACS with hallucinations in the absence of
major medication changes might now suggest LBD (McKeith, Galasko, Kosaka et al.
1996).
There is a considerable pathological overlap between PSP, CBD, and
frontotemporal dementia (Feany, Mattiace, Dickson 1996; Kertesz, Munoz 1998). Even
an unequivocal presentation as one can evolve into a confusing mixture. In each,
assessment for the allegedly characteristic features of the others is required. Sustained
attention, executive functions, limb praxis, naming and generative language (verbal
fluency and narrative discourse) must be assessed.
Cognitive deficits during recovery from severe traumatic brain injury (TBI):
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Severe TBI can produce two different pathologies with different primary patterns
of cognitive impairment. Focal cortical contusions (FCC) produce signs that are
characteristic of the local damage of the contusion: aphasia after left lateral temporal,
visual neglect after right parietal, etc. The most common sites of FCC are anterior and
inferior frontal and temporal, not including the hippocampus (Adams, Scott, Parker et al.
1980). The acute manifestations of these frontal and temporal FCC are similar to ACS.
The same clinical tests are appropriate.
Diffuse axonal injury (DAI) produces loss of consciousness (LOC) (Adams,
Graham, Murray et al. 1982) and initial clinical assessments are restricted to reliable
measures of arousal. It is customary to use the Glasgow Coma Score (GCS) (Teasdale,
Jennett 1974) until more detailed evaluation of cognition is possible, usually at
improvement to GCS 12-13. As patients emerge from coma the preeminent problem is an
ACS that may be quite prolonged. The measures suggested for ACS are appropriate. If a
more reliable metric is preferred, the Galveston Orientation Amnesia Test is a readily
applied simple bedside tool (Levin, O'Donnell, Grossman 1979). Because of its powerful
correlation with eventual outcome, post traumatic amnesia (PTA) should be clearly
defined (Ellenberg, Levin, Saydjari 1996). PTA is the duration of confusion. It is over
when some day-to-day memory is established. Evidence may be incidental such as
recollection of a therapist’s or nurse’s name or explicitly remembering visitors from the
previous day or a particular medical test. It can be demonstrated by simple tasks of
delayed recall or overnight recall of a short word list or set of names.
As confusion clears patients are generally left impaired in all tasks that require
sustained attention or working memory for complex mental operations. Thus, naming
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normalizes, but verbal fluency lags. Recall of remote crystallized knowledge (personal
data, overlearned historical facts) and of simple orientation normalizes, but supraspan
explicit learning lags. Clinical assessment will gradually shift to more and more
demanding tasks as the patient recovers. The time course of this shift in assessment
strategies is a reflection of injury severity. In mild cases (see below) the shift may move
from GCS to complex tasks in hours. In very severe cases it may require weeks and
months.
Many patients have both FCC and DAI. In the presence of both frontal FCC and
severe DAI it may be quite difficult to distinguish the relative contributions of the two to
executive impairment during recovery. For most clinical purposes crisp distinction
between them may not matter. The goals of assessment are to establish disability level
and target rehabilitation interventions. How the patient comes to be forgetful, distractible
and inflexible may be less important than defining appropriate care and compensation. It
is generally believed that FCC recover over weeks to months as with many other focal
destructive lesions but that DAI may recover over a much longer time span so
demonstrating deficits after injury may have substantially different prognostic
implications depending upon the dominant pathology, FCC or DAI (Katz, Alexdander
1994).
Evaluation of the residual deficits of severe DAI and frontal FCC is much more
satisfactorily accomplished with neuropsychological testing than with clinical. The
clinical setting does not provide sufficiently complex tools. The various executive tasks
described below (see frontal) will certainly identify major impairments, but they can be
essentially normal in patients who have disabling limitations in problem solving, response
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inhibition, mental flexibility and real life tasks such as budgeting, shopping, and
employment.
An additional obstacle to unambiguous determination of deficits in severe
traumatic brain injury is correction for premorbid capacities. Residual deficits after severe
traumatic brain injury often predominantly affect complex behaviors such as planning and
accurate monitoring or self assessment of performance (Stuss 1987). Achieving skill in
the complex, context varying arenas of mature behavior is often poorly accomplished
even by people with no history or evidence of brain injury. There are few psychometric
norms for strategy application in completion of the multiple sequential and sometimes
simultaneous activities of real life. How can testing distinguish between premorbid
developmental limitations and post injury loss of ability? It cannot, particularly at the
considerably constrained clinical level. Simply telling a person the expected performance
or outcome of a test and its likely duration provides vastly more structure than many of
the conditional activities of life. The act of constraining a test so that it may be reliable
can cost it validity as a predictor of real time behavior. There are no clinical tests that
surmount this problem.
Many partly and even completely recovered patients with severe traumatic brain
injury develop mood and behavioral disorders (Grant, Alves 1987). Some of these are
surely reactive adjustments to injury, incapacity and the psychosocial consequences of
prolonged disability. The prominent damage to frontal systems with traumatic brain
injury, however, means that many behavioral and mood regulation deficits will be
intrinsically neurologically based. Whatever the mechanism, depression, low frustration
tolerance, anxiety and impulsiveness will also have an effect on cognition. Is the patient
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depressed by his injury and prolonged recovery and because of depression unable to
motivate a full effort in testing? Or is a frontal injury blunting persistence on the tasks
giving the appearance of poor motivation, in turn causing depression because of repeated,
and to the patient incomprehensible, negative reports about his poor motivation? Any
number of similar unresolvable questions will arise during clinical assessment of a late
traumatic brain injury patient. There is no bedside test to answer these questions. Clinical
intuition is a very insensitive tool, but it may be the only one available. Neuroimaging
may be useful if it reveals a lesion of such magnitude that lesion effects are likely to have
overwhelmed reactive effects. Neuropsychological testing can illuminate the facets of this
problem with more systematic and sensitive probes, but even well performed
Neuropsychological assessment may not resolve these problems.
Mild traumatic brain injury (MTBI):
MTBI is defined as a traumatic brain injury due to direct trauma or to inertial
force (deceleration) sufficient to produce transient LOC or alteration of consciousness.
The neuropathology of MTBI is DAI. As noted above, DAI severity is correlated with
length of coma and duration of PTA. Thus, the clinical limits of mild traumatic brain
injury are: 1) initial GCS 13-15; 2) duration of coma < 30 minutes; 3) PTA < 24 hours; 4)
no focal lesion or CT or MRI. MTBI is usually synonymous with concussion. There is no
compelling scientific evidence that clinically significant DAI occurs when there us head
trauma or deceleration that does not produce at least brief LOC and PTA. At present, the
explanation for cognitive impairments in patients with head trauma or whiplash but no
LOC or PTA does not lie in clinical Neurology.
21
The mental state examination of a patient emerging from MTBI is identical to that
for severe traumatic brain injury, but the emergence is so rapid that only in the first hours
or days will clinical evaluation be revealing. The core residual deficits are in attention and
memory (Gronwall, Wrightson 1974; Stuss, Ely, Hugenholtz et al. 1985; Stuss, Stethem,
Hugenholtz et al. 1989). Tests that are useful will be difficult mental control measures
and challenging learning tasks.
Structure of testing: It is essential to determine duration of PTA. If the
examination is occurring in the ER as PTA is clearing, the exam may consist of little
more than reorienting until the patient remains oriented and noting the time. If the exam
is occurring days or weeks later, the history will have to focus on minute by minute and
hour by hour recollection probes until PTA is at least approximately determined. What
can the patient recall? Being in the car at the scene? The arrival of the ambulance?
Talking to police at the scene? Boarding the ambulance? Triage in the ER? Initial
examinations? A head CT? Other tests or treatments? Admission to the hospital or
discharge form the ER?
To begin the assessment, tell the patient that you will be testing concentration and
memory and that the duration of the testing will be brief - to encourage effort. Begin with
supraspan list learning; remind the patient that he will be asked the list again. Test
immediate attention with dsf. This is usually very resistant to MTBI and significant
difficulty suggests an additional problem in motivation, perhaps secondary to pain or
mood. Then test sustained attention with dsb and mental control, in which abnormalities
may be found although again these tasks are relatively resistant except in the first few
days. For intelligent, largely recovered patients you may wish to adopt an ad hoc mental
22
control task that has higher complexity: serial subtraction alternating four and seven from
a random number such as 114 or alternating counting forwards by threes with reciting the
alphabet in reverse order. Such an extemporaneous task will, of course, have no real
validity, but may still give some clinical insight.
Ask the patient to describe one or two current events in as much detail as
possible. Afterwards ask him to recall the word list. Use multiple choice probes for
recognition of items not recalled. Warn the patient that you are switching to a different
type of memory and assess verbal fluency, at least letter based if not both letter and
semantic. Switch to problem solving, either coin switch or a multistep mental calculation,
estimated to be within her preinjury capacities. If purchasing a Starbucks doppio for
$1.69 and a chocolate croissant for $1.59 with a $5.00 bill, you receive $1.56 in change;
what was the sales tax?
The natural history of cognitive deficits after MTBI in case-controlled,
prospective studies is very well described (Gronwall, Wrightson 1974; Levin, Mattis,
Ruff et al. 1987; Hugenholtz, Stuss, Stethem et al. 1988). Recovery of processing speed,
rapid processing inhibition, sustained attention and efficient learning requires
approximately 4-12 weeks for the modal patient younger than 50 with brief LOC, PTA of
20-40 minutes and no FCC. Note that this is longer than customarily allowed. As age or
injury severity measures rise, time to recovery increases. There is, at present, no
compelling neurological explanation for cognitive complaints or even for findings that
persist for months or years. This sweeping generalization may be invalidated with future
research. Even now, it is tempered in patients with more severe, although still mild,
traumatic brain injury, for older patients, and for patients who have had multiple MTBIs,
23
particularly if separated only by weeks. For the modal patient, lasting cognitive deficits
appear to be caused primarily by comorbid psychological factors - depression, anxiety,
and somatic complaints, either clearly related to injury or contributing to a somatoform
disorder (Dikmen, McLean, Armsden 1986; Schoenhuber, Gentilini 1988; Alexander
1997). Thus, the mental state examination in these late patients must include a diligent
probe of mood, pain severity and anxiety or stress factors. Borrowing one of the short
psychiatric interviews or mood inventories may be most appropriate for the office or
clinic (Beck, Ward, Mendelson et al. 1961). If impairments are prolonged, patients should
undergo MRI to eliminate the possibility of FCC undetected by the acute CT.
Neuropsychological testing can utilize a variety of tasks of processing speed, reaction
time, sustained attention and memory that may clarify the diagnosis in these patients, but
there is little evidence that the tasks have adequate specificity to distinguish
unambiguously brain injury from the common differential and simultaneous processes
being considered in these patients - depression, anxiety, pain or sleep disorder.
Throughout the examination the goal is to supply some texture to the patient’s
complaints of poor memory and concentration. The bedside tests will provide definition
to severity and to variability. If patients have excellent knowledge of events in previous
days despite their complaints that their memories have been very poor, it is an indication
that despite their claims, they are quite capable of learning. Patients often provide
excruciating details of examples of their poor memory, telling every little step and detail
of how they misplace things. In testing you may demonstrate poor sustained attention or
sensitivity to interference even when straightforward list learning and recall of events is
excellent. You may discover that the patient has flat learning of a list, little increase in
24
number recalled from trial to trial. He may also have poor verbal fluency. This
combination suggests that there may be limited ability to generate mental effort. Could it
be because of pain, sleep disorder, depression? Remind yourself of the PTA duration, his
age, the time since injury, other medical history and medications.
Mental status examination in patients with known focal lesions:
Many patients seen in the hospital or clinic are known to have a specific brain
injury - stroke, tumor, encephalitis, etc. The mental state examination may not be critical
for diagnosis, but there maybe other motivations for a thorough cognitive assessment: to
identify progression, to document effects of treatment, to direct rehabilitation or
vocational efforts, to clarify to the patient or to the family the nature of disabilities, or to
establish mental competence. The evaluations outlined below will also define anatomical
diagnoses in cases for whom the etiology is unknown.
Left brain injury:
The unique issues of left brain injury are aphasia, apraxia and verbal learning
inpairments.
Aphasia evaluation: Taking, or attempting to take, a history may be all the
evaluation required. For patients with Wernicke’s aphasia with pressured, neologistic
output and no meaningful responses to rudimentary personal questions or simple requests,
a formal language evaluation will add little. For any aphasic patient who appears to
understand little or nothing from the interview, comprehension testing may only be a
search for some fragmentary category of understanding and a brief probe of written
comprehension looking for unexpected relative preservation. In patients who present no
propositional output during the interview, the evaluation may be limited to probes for any
25
category of cue or context that allows some meaningful production and to assessment of
writing, brief unless some preservation of capacity is promptly noted.
Clinical assessment is performed along several dimensions.
1. Fluency: The first dimension is the structural property of language output. Ask
the patient open-ended questions and evaluate the best responses. Judge phrase length:
Are complete responses five, seven, or more words? Judge grammatical form: Are there
complete sentences, complex structures such as compound sentences and dependent
clauses? Fluent language is produced in lengthy and grammatical units, at least for the
best utterances detected in the exam. Nonfluent language is truncated and grammatically
incorrect (agrammatic) or at least grossly simplified. Either may be anomic or paraphasic;
it is only the phrase and sentence length and structure that are being evaluated. Speech
qualities may be normal or abnormal, but speech properties are irrelevant to fluency
decisions.
There are three common errors in fluency judgments. Patients with terse,
unelaborated language will be considered nonfluent even though the abbreviated best
responses show complex grammar, and no responses are actually agrammatic. These
patients usually have frontal lesions and will have a diagnosis of transcortical motor
aphasia (TCMA). A second common error involves patients with severe phonemic
paraphasia but good monitoring of output. Such patients will be called nonfluent because
no lengthy utterances occur. These patients attempt to correct all phonemic errors or
anticipate and block production of any phonemic errors to the point that most utterances
are cut short. The examiner will hear something like, “I had a tro …, a tro …, a ….”
When pressed to speak through the errors, the utterance emerges as, “I had a toke, well,
26
not exactly but a sto …, one of those wings with the bain.” These patients usually have
discrete inferior parietal lesions and a diagnosis of conduction aphasia. The third common
error in fluency judgments involves patients who produce no meaningful output but do
produce lengthy strings of minimally varying, repetitive utterances with considerable
sentential inflection (Poeck, de Bleser, von Keyserlingk 1984). The repetitive utterances
may be words, usually very restricted and carrying no meaning (verbal stereotypy), or
nonwords (nonverbal stereotypies), but based on the inflectional variability across a
lengthy speech production, a sense of sentence structure is produced. These patients are
incorrectly called jargon aphasia when they are a variation on nonfluency. No lengthy
sentences of propositional intent and varying lexical and syntactic structure are heard.
2. Lexical semantics of spontaneous output: Whatever the fluency judgment, if
there are any spontaneous utterances, the examiner should evaluate the errors in word
retrieval and word form.
Retrieval: Word finding deficits may be manifested as hesitation before
production, block at production when the entire utterance stops, use of nonspecific
substitutions (“it”, “doing”, etc.), circumlocution (describing or speaking around the
unretrieved word) or perseveration (repetition of previously used words in an incorrect
context). There is no localizing value to anomia or to the type of errors.
Form: Phonemic paraphasias are substitutions (often sounding like omissions) of
discrete, linguistically meaningful portions of a word. Thus, stroke becomes “shoke” or
“roke” or “shope”. Phonemic paraphasias are most frequent after posterior perisylvian
lesions. Semantic paraphasias are substitutions of entire words for target words. These
may be supraordinate terms, such as “food” for carrots, or empty nonspecific filler words
27
such as “thing” for nouns and “going” or “doing” for verbs. For some categories of
words, such as numbers and family members, there is often a substitution within the
category. Semantic paraphasias may be seen after lesions virtually anywhere in the left
lateral convexity or subcortical structures, but the inferior/middle temporal lobe may be
most specific.
3. Comprehension: To assess comprehension accurately takes some time and
determination. The approach is identical for auditory and written testing. At the bedside
there are a few easy approaches.
Word comprehension: Place four to six common objects on the table. Indicate
them all. Ask the patient to show you the items as they are named. If that is successful,
ask her to show you the parts of the objects as you name them (egs., frames, eraser,
lenses, crystal, teeth, etc.) Ask her to indicate the object that matches a functional
description (eg., “the one used to improve vision.”) The same approach can be taken to
comprehension of the names of body parts, colors or any category of concrete stimulus.
Using the same array of objects, assess auditory span and comprehension of actions. Span
is assessed by asking the patient to point to progressively longer strings of objects in
array. Comprehension of action depends upon understanding verbs, serial order, and
prepositions. Examples would be, “Turn the key over”, “Place the watch on top of the
comb”, etc.
Some patients appear to grope to understand as though they were deaf. These
patients perform much better when speech is slowed. Other patients will repeat words
correctly but appear to grope for meaning. The former are sometimes called “word deaf”
(Auerbach, Allard, Naeser et al. 1982) and the latter “word meaning deaf” [Alexannder,
28
1989 #42].The former are impaired at language specific sound recognition; the latter at
semantic knowledge or access. The former are likely to have lesions in superior temporal
gyrus; the latter in inferior/middle temporal lobe. Many patients have both components,
even though they appear intuitively to be mutually exclusive.
4. Repetition: At this point, the patient can be classified along two dimensions:
fluency and comprehension. Next assess repetition. A patient with mild aphasia with rare
paraphasias is likely to have good repetition so the evaluation can begin with a few
complex targets as a screen. Patients with severely restricted stereotypic output are
unlikely to repeat and a few simple targets may suffice to convince you. For other
patients, repetition may clarify the nature of the language substitutions that pass by
rapidly in spontaneous speech. The hierarchy of stimuli passes from single, short,
substantive words (examples: “cat”, “book”, etc.) to short sentences consisting of only
substantive words (examples: “dogs chase cats”) to phonologically complex words and
phrases (examples: “Presbyterian preacher”) to short functor heavy sentences (example:
“he did it”) to complex natural sentences (example: “Traffic is at a standstill on the
Central Artery”) to pronouncable pseudowords (examples: “dop”, “plage”, etc.) There are
four easily recognized error patterns: 1) phonemic paraphasias, particularly on
phonologically complex targets; 2) semantic substitutions, often on functor words, so that
“he did it” becomes “she was it”; 3) perseverations at any level from sounds
(example:“dogs dase dats”) to words within stimuli (example: dogs … dog cats”) to
words across stimuli; 4) auditory span failures seen in any stimulus that exceeds span
(example: “Traffic is … … the Artery.”)
29
The use of repetition, although it is no way entirely independent of comprehension
or natural output, creates a third variable for aphasia classification, and thus eight aphasia
types. Those with impaired repetition are Broca’s, Wernicke’s, conduction, and global.
Those with preserved repetition are the transcortical aphasias.
5. Naming: Using the same stimuli as comprehension testing allows modest
control of word frequency in comparison of comprehension and naming. If objects are
named, request the names of parts of the objects, usually lower frequency words. The
examiner has on him/herself an abundance of targets: jacket to lapel, sleeve, cuff, lining,
flap, boutonniere, etc. Naming body parts, colors or any other category can use the same
approach of moving from more familiar to less familiar words.
6. Writing: Testing written language at the bedside can be quite laborious. Most
aphasic patients write worse that they speak, perhaps because narrative writing is so
rarely practiced by most adults. Unlike speaking, errors remain in front of the patient, and
many aphasic patients either become stuck attempting to correct output or will not
persevere once errors appear. In principle, the same strategies for spoken output can be
used for written, but in practice, the goals may be more modest. For severe aphasic
patients, the examination goal may only be to determine if the patient can produce any
language elements or if they can do more word production with writing than with speech.
Test written naming (same objects as spoken naming) and writing to dictation.
Some patients can make no consistently recognizable letters, called apraxic agraphia.
When this occurs in a patient with minimal aphasia who is using his preferred right hand,
lesions will almost always be in the left superior parietal lobule (Alexander, Fischer, Friedman
30
1992). In aphasic patients writing with the nonpreferred left hand, there are several
possible anatomical bases.
Assuming that legible letters can be produced, the same error analysis as for
speech applies: grammaticality, structure, word finding and paraphasias. Classes of
impairments may be similar as well. Some patients cannot write functor words in
isolation and substitute related words for substantive words, similar to the spoken output
in Broca’s aphasia. Others make phonological errors and cannot spell pronounceable
pseudowords, similar to repetition deficits in conduction aphasia. Note that there is not
perfect correspondence between these grossly similar patterns and that some patients have
different patterns in spoken and written output. Similarities highlight fundamental
language processes that are independent of the output avenue.
7. Reading: Clinical assessment of reading comprehension was outlined above
under comprehension. Unless the examiner carries ready-made stimuli, assessment of
reading is also very time consuming. Most patients have reading comprehension roughly
comparable to auditory comprehension and oral reading roughly comparable to repetition.
In most aphasic patients assessment of reading may be little more that a probe for
comparability using the same stimuli as for all other parts of the examination but now
reading the names aloud and matching to objects. In some aphasic patients the evaluation
may be limited to probes for any sign of preferentially spared reading comprehension.
Many severe aphasic patients simply read all stimuli aloud, or attempt to, not
understanding that they are to do something to indicate comprehension. Giving them a
multiple choice task of selecting their own names or hometown from a short list may
establish set for comprehension.
31
Determination of error types follows that described for repetition, naming and
writing. There may be nonresponses, semantic substitutions (paralexias), often suggesting
some “deep” recognition of the word’s meaning, such as “baby” for “diaper”, or of the
word’s role as a part of speech, such as “with” for “in”, phonological substitutions
suggesting production problems at a sublexical level after word recognition, and
perseverations within and across words or stimulus sets. If pure “word deafness” (see
above) represents inadequate registration and discrimination of phonic (sound) elements
in speech without any necessary language impairment, so-called “pure alexia” is its
parallel in the written domain: inadequate registration and discrimination of letters and
words without any overt language (Farah, Wallace 1991). In both cases, once the
stimulus is clearly determined, comprehension is prompt. Thus, in both cases once the
patient can repeat - or read aloud - the target, there is no comprehension problem. The
clinical assessment for “pure alexia” can be restricted to patients with left occipital
lesions.
If there is reading impairment without writing impairment or if a patient is known
to have a left occipital lesion, the examiner should specify object and color naming
performance. Some of these patients will have difficulty naming objects presented
visually but not by description or to palpation (optic aphasia or visual anomia) (Beauvois
1982). Some may have naming deficits for colors out of proportion to other categories.
Have these patients read aloud (perhaps more appropriately considered naming) single
letters, letter strings and then words of increasing length. Some patients cannot read aloud
or match to spoken letter name any letter (agnosic alexia). For less impaired patients,
responses will be slow. Words will be read letter by letter, just like the meaningless letter
32
strings, and only if the letters are read off without error will the patient recognize the
word (Patterson, Kay 1982). It is as though he is spelling the word to himself. The longer
the word, the longer the latency will be for reading. Frequency and part of speech are not
very relevant to success. The final test is to spell aloud words that he could not read. If
comprehension is prompt, you have proven that the impairment is in visual access to
word meaning. The opposite profile can be seen with superior temporal/ supramarginal
gyrus lesions. For these patients, auditory span is inadequate to keep a letter string in
mind so patients cannot recognize words spelled aloud, but visual word recognition is
normal, whether the word is read aloud correctly or with phonological (output) errors.
Some patients with lesions at the temporoparietoocciptal junction can have some
elements of all of these disorders. Discrete and restricted deficits may be more accessible
to remediation than the complex, multidimensional deficits that many patients show.
Praxis: Praxis is the capacity to demonstrate learned motor behaviors. Testing
praxis has very modest clinical goals, but there are a few interesting and important
dimensions to testing:
1) Part of body: Establishing a practiced motor behavior requires experience with
the behavior. There are some brain structures that may be recruited for all types of motor
learning, perhaps the cerebellum and basal ganglia. For movements predominantly
involving the legs and the trunk, such as dancing, bicycling, etc, those may be the primary
regions. For movements of the arms and hands, particularly lateralized movements of the
preferred hand, such as writing, brushing, chopping, beckoning, etc., cortical areas in the
parietal lobe of the dominant hemisphere are essential (Kertesz, Ferro 1984; Alexander,
Baker, Naeser et al. 1992). In this context, the dominant hemisphere refers to the
33
hemisphere responsible for motor learning. This will usually be the left hemisphere
although there is unpredictable variation, especially in left handers. For nonverbal
movements of the face, mouth, tongue, and larynx, which are bilaterally integrated, such
as blowing, coughing, sucking, etc. the dominant (usually left) lower perirolandic motorsensory cortex is critical (Tognola, Vignolo 1980; Alexander, Baker, Naeser et al. 1992).
Thus, learned movements of different body parts must be independently assessed.
The tested movements must be purposeful and acquired, i.e., learned through motor
experience.
Limb movements: a) no object required: make a fist, point, wave, salute, beckon,
etc.; b) object required but pretending: hammer, paint, shave, brush teeth, throw, etc.
Buccofacial movements: a) no object required: show teeth, protrude tongue,
cough, etc.; b) object required but pretending: suck a straw, lick a spoon, blow out a
match, etc.
If impaired when pretending or if symptoms suggest trouble with actually using
objects for either limb or buccofacial movements, test them with the real objects in real
context.
Whole body movements: There is rarely any clinical purpose to testing these stand up, step backwards, dance, tee up a golf ball, etc. - because there are so many
patients who are too limited motorically for results to be interpretable. This class of
movements to command is relatively resistant to brain injury (Alexander, Baker, Naeser
et al. 1992), thus demonstrating the preservation of whole body movements to verbal
command may be a useful way to prove that severely aphasic patients can “understand”
requests.
34
2) Modality of eliciting movement: In clinical examinations, it is customary to ask
patients to do these movements. Significant aphasia complicates interpretation of deficits.
An alternative method of evoking movement is to demonstrate the movement and request
imitation. This circumvents language impairment although some patients may have
trouble with gesture comprehension (Rothi, Heilman, Watson 1985). Verbal requests and
imitation may differ markedly in the naturalness of the eventual gesture. We wave when
waved at, and salute when saluted, but most gestures are usually neither requested nor
imitated. In particular, movements requiring an object are rarely pretended in the absence
of the object. Thus, there are two more levels of evoking movement. The object can be
provided in the absence of any context: a straw to suck but no milk shake, a hammer to
wield but no table to build. This setting presumably makes comprehension of the request
absolutely clear, but the context of movement remains very unreal. The object can,
finally, be provided in the natural context of its use: a straw to drink a soda, a hammer to
hang a picture hook, etc.
Impairments can be seen up and down these ladders of context, body part by body
part. A reasonable strategy for testing is to select 4-6 buccofacial tasks and 4-6 limb tasks
for which there is certainty about normal performance characteristics. Use the same tasks
for every patient. Request movement after broadly indicating the part of the body that is
being tested. After doing tasks to request, ask patient to imitate movements that were
incorrectly done to request alone. If movements are normal at this point, there is no
specific ideomotor apraxia. If patients have known left parietal lesions, if history suggests
trouble with object use, or if Occupational Therapists report difficulty using objects, test
patients with a few common objects. Using real objects in real space is much more
35
spatially constrained than pretending to use them loosely in unspecified space. Thus, there
may be a double dissociation between ideomotor apraxia and ideational apraxia, and each
should be tested if clinical history is appropriate (De Renzi 1989).
Error types in praxis can be differentiated and point to a variety of possible brain
impairments: 1) failure to understand the request with either no response or
demonstration of a correctly performed movement, but not the requested one, generally
rapidly circumvented by gesture; 2) undifferentiated movements or vocalizations (for
buccofacial movements) whatever the eliciting stimulus; 3) generally the requested
movement but with spatial or temporal imprecisions, including failure to allow for the
size of the pretended object, for example sawing with side of the hand; 4) perseveration
from previous movements.
The clinical importance of this examination is limited: 1) it can be an avenue to
demonstrate islands of preserved comprehension in aphasia; 2) it indicates difficulty with
following motor requests that may be mistaken for poor comprehension; 3) it clarifies
patients ability to use implements safely (good ideational praxis despite poor ideomotor
praxis) or unsafely (good ideomotor praxis despite poor ideational praxis).
Localization of deficits in praxis is moderately reliable. Buccofacial apraxia is
usually associated with lesions in the language dominant hemisphere, usually left,
centered in the lower perirolandic region (Tognola, Vignolo 1980) (Alexander, Baker,
Naeser et al. 1992). Small lesions may only cause dysarthria and paresis of contralateral
lower facial muscles. Larger lesions produce buccofacial apraxia. Large lesions of left
putamen, anterior limb internal capsule, and frontal periventricular white matter may also
produce transient facial apraxia.
36
Limb ideomotor apraxia is associated with lesions of left parietal lobe (De Renzi
1989)or of extensive deep central white matter (Kertesz, Ferro 1984). Persistent
ideomotor apraxia may require very extensive parietal injury or else very significant
damage to the white matter connections of parietal and frontal association cortices. The
latter lesion usually causes right hemiparesis so praxis can only be tested in the left hand.
Ideomotor apraxia limited to the left hand can occur with large lesions of the body of the
corpus callosum, presumably through a similar mechanism of disrupting interactions
between dominant parietal lobe and the nondominant frontal region directing movement
of the left hand.
Ideomotor apraxia is usually associated with extensive damage to the left parietal
lobe, inferior and superior cortical regions and dorsal white matter pathways(De Renzi,
Lucchelli 1988).
Right brain injury:
Clinical assessment of patients with right brain lesions explores several functions.
Most deficits characteristic of right brain injury have less anatomic specificity than the
common patterns of language or praxis impairment, but clinical probes can define the
important deficits.
Attention: Many right brain lesions impair attention, at least sustained attention,
without impairing arousal. As language function is normal the same tasks described for
“Acute Confusional State” and traumatic brain injury can be utilized: digit span forward,
backward and various mental control tasks. Motor impersistence is the inability to
maintain postures and various positions without prompts. When seen with focal lesions, it
is most reliably associated with right frontal damage (Kertesz, Nicholson, Cancelliere et
37
al. 1985). Patients can be led to hold several simple postures simultaneously: eyes closed,
tongue protruded and right arm elevated. With motor impersistence either adding a new
position causes a previous one to be lost, i.e., protruding the tongue causes the eyes to
open. or once all positions are reached, one by one, they are lost within seconds. In severe
cases the patients cannot even do simple, single postures such as holding their breath.
Ability to do this task appears to rely on sustained attention.
Affect: Loss of affective vocal inflections and of spontaneous facial expressions
frequently occurs after damage to right ventrolateral frontal lobe, lower motor cortex and
their connecting and descending pathways (Gorelick, Ross 1987). While several clinical
tests for affective expression have been suggested, none is sufficiently validated or
reliable to be worth implementing. If the interview suggests flattening of emotional
properties in voice, the examiner can probe by asking the patient to repeat a sentence in
an angry voice or a sad voice. Loss of singing ability often accompanies this affective
prosody impairment, and inability to produce a familiar melody may support a diagnosis
of prosodic impairment (Ross, Edmondson, Seibert et al. 1987).
There is ample evidence that the right hemisphere also extracts affective intent in
communication from the auditory signal (temporal) (Tucker, Watson, Heilman 1977)and
from the visual cues such as facial expression (occipital) (Borod, Koff, Perlman et al.
1986). Reliable and sensitive tasks to demonstrate such deficits have not been devised.
Configurational visuospatial capacity: The right brain is not, as is sometimes said,
dominant for visuospatial function or for spatial attention (De Renzi 1997). The right
brain contributes configurational, low spatial frequency manipulations to
visuoconstructive and perceptual operations. The left brain contributes featural, high
38
spatial frequency capacities. Thus, the characteristic errors of right brain brain damaged
patients are failure to detect or utilize global configurations. Drawing and copying tend to
produce segmented structures in which individual elements of a figure are scattered in
poor overall spatial relationships.
The characteristic error of left brain damaged patients is impoverished placement
of internal details despite good specification of boundary configurations. The overall
appearance of drawings by left brain damaged patients is better than that of right brain
damaged patients, so the right brain has the reputation for visuospatial dominance. Both
hemispheres play important and complementary roles in visuoperceptual and constructive
functions.
The other characteristic of right brain damage visuospatial function is hemispatial
neglect. The striking asymmetry in severity of lateralized neglect comparing left damage
to right damage, has led to theories about right brain dominance for spatial attention. It
appears again, however, that the hemispheres play different roles in attention (Rafal 1997;
Marshall, Halligan 19994). The right brain attends to global, configurational aspects and
the left brain attends to local, featural aspects. Each hemisphere also preferentially orients
to contralateral space. Left brain injury allows orientation to the left but preserved large
scale visual analysis in the right brain continually orients across the entire visual world or
at least any stimulus, thus mitigating right neglect. Right brain injury, however, allows
orientation to the right, but the preserved small scale attentional and featural capacities of
the left brain reinforces attentional focus on any stimulus in the right field, failing to
mitigate, and probably reinforcing, left neglect.
39
Whatever the mechanism, neglect may be seen in drawing from memory, copying.
oral reading, adding columns of figures, search tasks, line bisection, and even in mental
imagery. Search tasks, such as cancellation of short lines scattered on a page, and
bisection tasks, particularly of relatively long horizontal lines, appear to operate
somewhat independently. Both should be tested and neglect may be observed in drawing
and other tasks as well.
Other abnormalities of spatial function seen after right brain injury include
topographical disorientation (Hublet, Demeurisse 1992; Aguirre, D'Esposito 1997) and
dressing apraxia. Both are associated with superior parietal injury, and both appear to
represent an inability to form a mental representation of the body’s position in space.
Thus, relative directions, movement pathways to an out of sight target (an arm hole or a
destination over the horizon), and simply orienting the body to other elements in nearby
space (clothing or hallways) are all impaired. There are no good clinical probes of these
capacities. If history or examination or imaging or Nursing or Occupational Therapy
assessments suggest that they are present, there is no short cut. You must watch the
patient find the way in an environment known to her and watch her dress with clothing
that has not been laid out manikin-like already oriented to the body.
Patients with severe neglect may fail to dress the left body or to navigate into left
space, but these are not equivalent to dressing apraxia and topographical disorientation.
Some patients with large lesions in the right parietal and central regions may have all of
these problems simultaneously.
The final perceptual function that is lateralized to the right brain and that might be
probed in clinical testing is facial recognition. Recognition of familiar faces can be
40
accomplished through large scale, configurational match to visual memory or by
discrimination of one (or more) uniquely identifying small scale features. Considerable
evidence indicates, in keeping with the recurring assertion of this section, that the right
brain, in this case particularly the right inferior occipitotemporal region, is faster and
more accurate using configurational capacity than the left inferior occipitotemporal region
using a featural detection capacity (De Renzi, Perani, Carlesimo 1994). Patients with
right inferior occipitotemporal lesions may have prosopagnosia although it improves and
may clear as the left brain gradually unravels identities with feature strategies. Bilateral
inferior occipitotemporal lesions produce permanent prosopagnosia (Damasio, Damasio,
Van Hoesen 1982). Prosopagnosia is often associated with topographical agnosia which
is a loss of ability to remember navigation courses or recognize environmental markers
(Landis, Cummings, Benson et al. 1986).
There is no easy clinical test for these problems because a large set of photographs
of historically prominent or personally significant people would be required. When
clinically important, a quick assessment can be performed by gathering several drivers’
licenses, covering the names and asking the patient to identify family members from the
pictures. Am alternative is to page through a newspaper or magazine and ask the patient
to identify prominent people pictured there. Similar perceptual skills are required for, and
thus similar clinical deficits can be demonstrated, in distinguishing makes of automobiles,
breeds of terriers, styles of furniture, etc., if the patient had good visual knowledge of any
such domains prior to injury. Depending upon time constraints and the examiner’s
ingenuity, an idiosyncratic perceptual skill of this sort might be explored.
Frontal lobe disorders:
41
The previous sections described assessment of frontal functions in several specific
clinical contexts: behavioral and cognitive deficits after severe MTBI, language fluency
after left frontal lesions, and sustained attention, spatial attention and affective prosody
after right brain, including frontal, injuries. Other commonly impaired functions with
frontal disease are partly extensions of those impairments and partly more complex
behavioral problems.
Left dorsolateral frontal injury produces TCMA - truncated and unelaborated but
fundamentally grammatical output with normal repetition and generally intact
comprehension (Freedman, Alexander, Naeser 1984). With recovery of TCMA or as a
primary manifestation of frontal polar injury patients may have entirely normal
conversational and responsive language but impairments in most aspects of generative,
effortful language organization (Costello, Warrington 1989; Robinson, Blair, Cipolotti
1998). The medical history will be sparse and details omitted. The examiner will have to
constantly pull at the history for it to emerge. On examination the ability to perform a
wide variety of generative tasks maybe abnormal: 1) word list generation, either semantic
or letter based; 2) sentence generation from a given verb; 3) story generation, particularly
producing detailed narratives; 4) complex verbal learning requiring some strategic effort,
such as learning a supraspan word list.
Right dorsolateral frontal injury impairs sustained attention. Narrating a familiar
story, the patient may fail to organize a coherent line, lose track of the intended narrative
or even confabulate elements based on idiosyncratic associations from story elements to
unrelated facts (Novoa, Ardila 1987). On word list generation and supraspan word list
learning patients with right frontal lesions maybe particularly likely to perseverate,
42
confabulate and lose track of the task, asking for repetition of instructions, producing
completely irrelevant material or commenting on their performances.
Patients with frontal lesions of either hemisphere have trouble regulating
responsiveness. They may be apathetic and slow to respond to a situation. They may be
unable to identify any motive for responding. They may respond impulsively despite the
examiner’s attempts to control responses. They may be unable to suppress practiced
responses to familiar situations and contexts, i.e., they are stimulus bound and
environmentally dependent, so seeing a stapler on your desk, they may pick it up and look
for papers to staple together (Lhermitte, Pillon, Serdaru 1986). They may be unable to
organize a complex action plan that requires staged recruitment of several cognitive or
motor systems. A task as mundane as going to the movies may have too many elements of
action for them to complete - checking times, computing travel time, checking prices and
available money, etc.
If, in a very simplistic way, the left temporooccipital region “knows” how to
recognize building materials and summon the correct names, and the left parietal lobe
“knows” how to hammer and saw, and the left temporal lobe “knows” how to read
purchase orders, and the right temporoccipital region “knows” how to read a blueprint,
and the right parietal lobe “knows” how to rotate the plan on to the building lot, the
frontal lobes are still required to build the deck.
There is no good clinical task to probe this organizational, planning capacity.
Customary clinical probes include asking patients to describe how they would carry out
some relatively complex daily operation, such as prepare an omelet, repair a flat tire, or
obtain a mortgage. Impulsive responsiveness can be assessed with a simple go/no go task
43
although the specificity and sensitivity of these types of clinical tests are unknown: “If I
tap once, you tap twice. If I tap twice, don’t tap at all.” Monitoring responses can be
probed with the coin switch task described earlier. Much of the “examination” is in the
history and in observation of the patient’s response behaviors, comportment and
appearance during the interview.
The clinical settings in which these frontal assessments will be important are
numerous, and the purposes of the assessments will vary somewhat with setting:
1) disorders expected to improve, typically large focal lesions such as strokes,
traumatic contusions, or benign tumor resections; the goals will be to clarify impairment
so that decisions about rehabilitation referral, independent living, or vocational
placements can be most clear and so that a clear baseline is established for following
change, including the effects of treatments;
2) disorders expected to worsen, such as malignant tumors or frontal lobe
dementia; the goals are to establish sensitive measures of change so that decline can be
detected without waiting for paralysis, incontinence or mutism;
3) patients with lacunar strokes or posssible vascular dementia; the early
manifestations of vascular dementia, with or without clinically overt multiple strokes, are
in this “frontal” domain, presumably due to damage to frontal or to subcortical circuits,
either through the striatum or the cerebellum, returning through the thalamus (Fukuda,
Kobayashi, Okada et al. 1990; Corbett, Bennett, Kos 1994). These circuits are essential
for regulating cognition. Even brief assessment of learning efficiency (supraspan list
learning), sustained attention and generative language can reveal surprising limitations in
patients with “pure motor” stroke who appear superficially cognitively intact;
44
4) patients with multiple sclerosis and possible cognitive decline; the common
manifestations of cognitive decline in multiple sclerosis are also”frontal” (Callanan,
Logsdail, Ron et al. 1989), presumably reflecting loss of frontal-posterior bidirectional
pathways in the corona radiata as well as the frontal thalamic circuitry. Patients with
chronic progressive multiple sclerosis often become quite impaired in behavior and
planning, including blunted motivation and concern as paraventricular white matter
change accumulates. The same tasks suggested above for vascular dementia should be
sensitive to early changes in multiple sclerosis (Rao 1986).
Clinical assessment in these domains should probably always be supplemented
with more precise neuropsychological instruments. Two notes of warning about
neuropsychological assessment of “frontal” functions must be sounded. First, although
the sensitivity of neuropsychological “executive” tasks is higher than the clinical tasks,
the specificity remains low. Some novel, but relatively unvalidated, tasks appear to have
more transparent relationship to the impairments that limit patients with frontal lesions.
“Multiple tasks”, multiple “errands”(Shallice, Burgess 1991), and cognitive estimation
(Shallice, Evans 1978) all demand considerable executive capacity, and may speak to
real life functional deficits better than the usual sorting and response inhibition tests used
in standard neuropsychological assessment. Second, there is no single test of frontal lobe
function. Even the classic neuropsychological tests have quite different results in patients
with lesions in different frontal regions.
Memory:
In the previous sections some clinical settings that require memory assessment
were reviewed: older patients with gradual cognitive decline, recovering traumatic injury
45
and patients with frontal systems disease. Patients with injury to medial temporal,
posterior fornical, medial thalamic and septal regions also frequently have memory
impairments. Different disorders present different arrays of clinical questions. The core
evaluations of memory will generally be the same: immediate memory, current memory,
new learning and recall of remote memories.
Immediate memory is tested with digit span forward to establish span. Current
memory is tested with inquiries about orientation, the nature of the presenting illness or
the reason for evaluation and about current and relatively recent personalities and events.
Verbal new learning, is easily assessed with list learning. In the most direct
approach simply present a 10 word list, repeated until learned or 5 trials. After a five
minute filled delayed interval ask for the list. Give clues to any omitted words.
Complexity is added by presenting a second list of 10 words immediately after the last
presentation of the first list. Then, after a 5 minute delay, ask for recall of just the first
list. After 20 minutes perform a recognition task, asking the patient to identify only words
from the first list out of a 30 word list including both of the earlier lists plus 10 new
words. This is too complex to perform ad lib, but materials are easily prepared and kept in
the desk or bag. Much more material is available for analysis beyond the direct measure
of recall: 1) efficiency - learning list #1 over multiple trials; 2) proactive interference comparison of the second list to the first presentation of the first list; 3) monitoring appearance of words from the second list on the recall task; 4) source memory - clear
separation of two lists during recognition.
For patients with obviously severe amnesia who are disoriented, verbal learning
may consist of reorienting them and re-inquiring after a brief delay. Recall that patients
46
with any noteworthy anomia cannot be expected to do these more demanding recall tasks.
If a patient cannot “recall” a name on a direct confrontation naming task, he is unlikely to
“recall” it from a mental trace recently experienced.
Current events and personalities serve as markers for learning in the days and
weeks prior to evaluation. It is useful when there is an event that no person with intact
memory could fail to know, such as the O.J. Simpson trial, the Monica Lewinsky story,
the death of John Kennedy, Jr., the Egypt Air crash etc. Otherwise probe for prominent
personalities (politicians, entertainers, sports stars, etc.) and their recent activities, for the
outcome of sporting events, for any recent weather or natural disasters, acknowledging
that people have different interests and inclinations to keep informed about different
topics. A clinically intuitive, and potentially very fallible, allowance must be made for
education, age, culture and gender effects on this knowledge.
Nonverbal new learning has two components: visuoperceptual and spatial. Both
are awkward to test in the clinic or at the bedside, although a quick screen of the former is
manageable. Whatever complex, unlabelable stimulus is used for drawing to copy can be
used as a visual learning and recall stimulus. Tell the patient that she will be asked to
draw the figure from memory in a few minutes, proceed with other testing, and after a 5
minute interval ask for its reproduction. As patients with aphasia cannot be expected to
recall words that they cannot produce to confrontation, a patient with severe visuospatial
impairment who cannot copy a figure should not be expected to produce it from memory.
If the initial copy is abnormal, the examiner can guide the patient to a complete
production with cues and then probe for recall. Testing spatial new learning is essentially
impossible as a clinical task.
47
For remote memory there is substantial controversy regarding its neural
representations. At least four prototypes of remote memories have been proposed: 1)
autobiographical - emotionally textured, personal experiential memories; 2) personal
semantics - context free, repeated personal facts, such as birth date, education address,
etc.; 3) historical knowledge, personally experienced, such as political events during
one’s lifetime of which one was aware as they happened; 4) public events not personally
attended to.
Clinical probes for the first type are necessarily imprecise as the memories
themselves are idiosyncratic. Patients who confabulate are often producing a recollection
with at least the skeleton of real experience but warped in its associations and placement
in time. Most disorders producing amnesia, which is failure of anterograde memory produce a graded loss of remote memory (Squire, Alvarez 1995). With purely
hippocampal injury the epoch of remote loss may be short (days to weeks), and it may
shrink as, and if, anterograde amnesia clears. With more extensive injury to
parahippocampal structures or to frontal structures, including thalamus, remote memory
loss may be very extensive.
The clinical evaluation can usually only give a hint of the specifics of this loss.
Patients with little or no remote amnesia are easily identified by their recall of events
immediately preceding their illness. (Note that loss of memory from the onset of illness to
the time of assessment is not retrograde or remote amnesia. It is anterograde amnesia
during a pre-evaluation epoch.) To track more extensive remote amnesia, the examiner
must simply probe slowly backwards. If a patient’s personal history is known, events such
as death of a family member, recent job loss or move, etc. in that domain can be explored.
48
It is often true that only the historical domain is accessible: prominent public events of
recent and more remote times. Politics, sports, climate, entertainment and any other area
that a particular patient might be informed about is appropriate. When retrograde amnesia
is difficult to time but has clinical or functional importance (for instance, can the patient
recall why he changed his will two years ago?), formal neuropsychology has some
reasonably straightforward evaluations of past memory (Kopelman, Wilson, Baddeley
1989).
Semantic memory refers to the associational network of “things” known by the
brain independently of any recollection of how they are known. It includes the domain of
words for which the term “semantic” memory seems most fitting, but it also includes vast
and intersecting domains of perception, of procedures, of space, of function, of behavior,
and perhaps of emotion. Seeing an ocelot in the wild for the first time, you are likely to
know without pause and without knowing the animal’s name that it is a member of a
group of solitary, furred, mammalian hunters that does not include foxes, hounds, weasels
or dolphins but does include your prized Burmese. You know how your house in the
suburbs is part of a domain that includes igloos and urban tenements and usually excludes
caves, but with a slight juggling of the category’s sense, would include caves but might
exclude tenements and apartments. You know that a hammer and a saw belong to a
domain that a rock does not, but that a hammer and a rock belong to another domain,
defined by functional properties, that a saw does not.
Needless to say, there is no easy clinical probe for semantic memory. Patients
with a variety of posterior lesions will have deficits in semantic domains. Right inferior
occipitotemporal lesions appear to damage knowledge of faces and perceptually related
49
visual knowledge (De Renzi, Perani, Carlesimo 1994). Left inferior lateral temporal
lesions appear to damage knowledge of so-called natural perceptual categories: animals,
insects, flowers, etc. Left posterior parietooccipital lesions appear to damage knowledge
of functionally related groups; tools, body parts, etc. (Warrington 1975). Left superior
parietooccipital lesions appear to damage knowledge of spatially specific functional use
of tools (De Renzi, Lucchelli 1988). Right inferomedial occipitotemporal lesions appear
to damage knowledge of exocentric space (as examples, where Dallas is located on the
map or how north is related to south) (Landis, Cummings, Benson et al. 1986). When
patients have damage to an area with high probability of such a deficit, the examiner
should create an ad hoc probe for loss of knowledge. Any suggestion of such a loss is
justification for a more systematic probe by Neuropsychology.
Conclusion:
Without writing a book on Behavioral Neurology, no additional specifics about
the mental state examination can be addressed. Recall the assignment for this introductory
chapter:
1) Clinical validity: Always be certain that you are testing what you think that you
are testing. Patients with aphasia, confusion and frontal systems injuries may all fail many
tests designed to assess memory because they fail to understand, to attend or to care.
2) Clinical practicality: At most, the tests described here require that the examiner
approach the patient dressed, with a few common objects in the pockets, speaking a
common language with the patient, carrying a pencil and a few sheets of paper, and
prepared with some stimuli in mind or written out on a sheet. It is suitable for the office,
the clinic, the bedside or the Emergency Department.
50
3) Clinical separation from formal Neuropsychology: While a certain amount of
pirating of the strategies used in formal testing is inevitable, most of those strategies are
hardly the patentable province of Neuropsychology. Sustained attention, list learning and
executive tasks probably threaten the greatest overlap, but especially if the exact stimuli
differ, practice effects seem unlikely in patients impaired in those domains.
4) Clinical applicability: The procedures are appropriate for any adult from
adolescence to senescence. The context requires minimal or no adjustment because of age
or gender. Literacy, education and culture will constrain content of testing.
There is no reason for a clinician - physician or psychologist - to be ill prepared
for a meaningful assessment of cognition for purposes of diagnosis, prognosis, treatment,
and rehabilitation management of disability. Well performed neuropsychological testing,
alert to issues of differential diagnosis, can add precision to the clinical test and assess
some areas of cognition that are opaque to clinical evaluation, such as spatial memory,
high level executive function and remote memory. The physician who has performed a
well-organized clinical mental state examination will extract much more information
from a subsequent complete neuropsychological assessment.
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