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CHANGES
IN BEHAVIOR Jeffrey Victoroff, MD
Associate Professor of Clinical Neurology USC Keck School of Medicine Redondo Beach, CA Michael Herbst, MD Les Kelley Family Health Center Santa Monica, CA Rosabel Young, MD Assistant Professor and Director, Movement
Disorders Program King-Drew Medical Center Los Angeles, CA Part I: The 15 Minute Neurobehavioral Evaluation
It is 3:30 on Friday
afternoon. The front desk buzzes your nurse, announcing
the arrival - without an appointment - of a 35-year-old woman accompanying
her 83-year-old father. Four
other patients are waiting for examining rooms.
You are with a four-year-old girl whose asthma is worsening. "What's the problem?" you
overhear your nurse ask the receptionist, her tone conveying the slightest
hint of skepticism. "Oh,"
she says. "I see, "
she says. "For how long?"
she asks. She sighs. Hearing that sigh, you know you're going to
be seeing them
This section will attempt to outline the 15 minute neurobehavior
assessment. Today's pace of practice has accelerated from
the epoch of luxurious 45-minute health promotion discussions to an
unsettling "Beat the Clock" of frenetic juggling of priorities,
hoping, in that circus act, not to drop any patient's ball. A high proportion of primary care visits involve
behavioral problems, requiring us to quickly and confidently distinguish
between medical/neurological causes and primary psychiatric conditions.
So it is essential that we devise realistic strategies for
walking into the examining room in total ignorance of the diagnosis
and walking out 15 minutes later with a plan. Naturally, we need flexibility. Some things simply demand more time, perhaps
not as much for diagnosis as for negotiating the exchange of human
information in ways that strengthen the bond between healer and patient. But the burden, increasingly and perhaps absurdly,
is now on primary care physicians to attempt to offer an attending's
experienced care with an intern's time schedule. Hence, we will be practical. Since
the pleasure in practice is often proportional to the sense of mastery,
we hope this plan for rapid neurobehavioral evaluation will make that
Friday afternoon a better day, granting the reward of confidence in
our practical approach.
We will organize the Neurobehavior Evaluation in ways that
aid triage, by following the conventional sequence of history, examination,
and laboratory evaluation. However,
we recognize that there is actually a continuous evolution of diagnostic
hypotheses, a solution to a jigsaw puzzle of biological cause and
behavioral effect with every interlocking piece contributing to the
next step in the strategy, rather than a linear observation of clinical
facts. Given this, we will
present the Neurobehavior Evaluation as a series of decisions that
progressively narrow the focus of etiology and intervention.
This chapter will focus on the following issues for adults:
• Delirium (confusional state) • Dementia • Discrete problems of thinking (eg, amnesia, aphasia, apraxia)
• Psychiatric syndromes having identifiable neurobehavioral/medical
causes (Table
1).
Coma, persistent vegetative state, sleep
disorders, and pediatric neurobehavioral disorders are considered
elsewhere in this volume. Table
1: Adult Neurobehavioral Syndromes
Delirium
(a.k.a. Confusional state) =
altered mental status in an apparently awake or somewhat lethargic
person (but not sleeping or comatose), usually acute or subacute in
onset, with impairment in level of responsiveness or attentiveness
to the environment. Example: hepatic encephalopathy. Key
points: Awake or lethargic Acute
or subacute Impaired
attention
Dementia = acquired impairment in cognition sufficient
to interfere with the conduct of waking life, not due to impaired
arousal, usually with subacute or chronic presentation, usually impairing
multiple aspects of thinking. Example:
dementia of the Alzheimer type. Key
points: Impacts on awake
activities Subacute
or chronic Intact
attention
Discrete
problems of thinking Amnesia = impaired learning Aphasia = impaired language Agnosia
= impaired
recognition of sensory stimuli Apraxia
= impaired
functional motor skills with intact strength and coordination Executive
function impairment
= eg, altered planning, self-monitoring, idea analysis, or idea generation
Psychiatric
syndromes having identifiable neurobehavioral/medical causes Depression
Mania Psychosis Anxiety You enter the room. The elderly man sits, slightly slumped in a
vinyl chair. He looks up slowly
when you enter, not quite making eye contact.
We adopt the "every picture tells a
story" stance in neurobehavioral assessment (Figure 1). From the first
glance, you already know that this man has enough lower extremity
motor function to make it to the examining room, and enough interactiveness
with his daughter to be guided there with neither the support of a
wheelchair nor the swaddling of restraints.
This already favors a fairly well functioning spinal cord and
brainstem for both motor processes and arousal and decreases the odds
of a large stroke, subarachnoid hemorrhage (SAH), or meningitis.
You know he has enough intact peripheral sensory organ function
and enough intact transfer of sensation to sensory cortex to note
your entry into the room, so it's likely that much of the visual pathway
from eye to occipital lobe is working.
You know that the sensory information of your coming, by parallel
processing, has also successfully reached his brainstem arousal system
and parts of the limbic/emotional response system that provide motivation
to respond to your presence. You know that there is working give-and-take
of electrochemical discourse between these systems and the frontal
cortex that is necessary to organize a motor response to your entrance. And you know that this man can manage the transfer
of commands from prefrontal cortex (for planning) to primary motor
cortex (for doing) and from motor cortex passing all the way down
to anterior motor horn cells to activate a symphony of muscle contraction
to lift his head to give you that half-glance.
So you know that at least some of the cortical-to-cortical
connections and the long cortex-to-spinal cord connections work fine.
And, if you happened to notice that his eyes moved together,
roughly in your direction, then you know that the cortical eyefields
can still send signals to the brainstem, which can still coordinate
the third and sixth cranial nerves for purposeful conjugate gaze.
In a second, you already know a lot about this man's brain.
But he does not observe the niceties of social
intercourse. Is he lethargic?
Deaf? Depressed?
Assuming that his vital signs are reasonably reassuring, the
second step after the first glance is history.
What are the priorities? Tables 2A, 2B, and 2C outline key elements
of our assessment, suggesting a few high priority items in the history
and examination. The rapid
neurobehavioral assessment is a matter of triage; not a lock-step
progression, but a hierarchical test of the acuity of the condition
ruling out emergency, then urgency, then more benign or chronic states.
As in pediatrics, our history taking now becomes a delicate
balancing of information you may get from the caregiver, who can be
an ally with varying sophistication and agendas, and from the patient,
whose very responses to historical questions instantly become part
of the exam.
Key Elements Of The Rapid Neurobehavioral
Evaluation
Table
2A. History of the Present
Illness and Past Medical History
History
of Present Illness How much? How quickly? What's changed?
Items of special concern: H
Headache? I
Incontinence? S
Sleep disturbance?
I
Irritability? S
Sensory change, including
numbness, or special senses such as vision
and hearing?
M
Motor changes
such as slowing or tremor? A
Appetite loss? D
Delusions? D
Depression?
Past
Medical History Items of special concern:
1. Lifetime mental health interventions
2. Lifetime drug/alcohol history, especially anticonvulsants
or psychotropics
3. Lifetime traumatic brain injury, stroke, TIA, MI, tumor,
renal or kidney disease Table
2B. Examination
Mental status vital signs: responsiveness,
orientation, agitation Aphasia screen:
1. Say "dog"
2. "What part of my shoe is this?" 3,4,5.
"Please raise your right hand.
Okay, put your left hand on your right shoulder. Good, now first put your right hand on your
left knee, then your left hand on your right ear."
6. "What's the difference between a car and a boat?"
Working memory and mental control
1. Recall "tuna, Paris, strength" after 3-5 minutes
2. Months backwards
Self-reported mood, delusions, hallucinations Features of the physical and elementary
neurological examination of special relevance to the assessment of
behavior
Table
2C. Decisions in the Laboratory
Evaluation
Electrolytes (any major change can cause delirium; low
sodium particularly lowers the seizure threshold) Blood
count (eg,
megaloblastic anemia hints at B12 deficiency; hematocrit <24 may
contribute to delirium) Liver
function tests
(eg, for hepatic encephalophathy) Ca,
Ph, Mg (deficits
lower the seizure threshold; parathyroid disease produces dementia) Thyroid
function tests
(to rule out the most common endocrine dementia) B12 (to rule out subacute combined degeneration) Serum
VDRL (helps
rule out neurosyphilis; positives generally require CSF exam) EKG (cardiac dysfunction may compromise brain
perfusion or hint at metabolic disorders) Neuroimaging (rule out eg strokes, tumors, hydrocephalus) Lumbar
puncture (in
acute delirium to r/o infection or subarachnoid blood; in dementia
usually only when syphilis serology is +) EEG (when seizures, metabolic encephalopathy,
herpes, or Creutzfeldt-Jakob are suspected)
The Chief Complaint And History Of Present
Illness
"What seems to be the problem?" you
might say. The answers come
from the daughter. The patient
doesn't look up. That in itself
is quite telling.
Key
points: How much? How long? What's changed? These are the three questions you want immediate
answers to in assessing altered mental status (AMS). While we present them in a certain order, there
is no strict sequence to getting this information; it's really a matter
of assembling a gestalt.
How
Much Has Behavior Changed? Has the patient gone from a vigorous, sociable
retirement to a tragically contracted, nearly "vegetative"
state? From a sensory deprived
developmentally delayed nearly mute resident of a group home to a
not-feeding-himself sensory deprived developmentally delayed nearly
mute resident of a group home? The
magnitude of the shift from baseline in the overall interactiveness
and independence level is the first cue to acuity.
However, it tells us less about brain locale than we might
wish. The first scenario from retirement to catastrophe
suggests a global dysfunction that is sometimes assumed to be due
to diffuse or multifocal brain injury.
But this picture of profound "global" decline might
be produced by even a modest interruption in the millimeter-range
brainstem arousal systems - such as that caused by systemic infection,
a slower than expected metabolism of digoxin or metoclopramide, or
a tiny critically-placed stroke (eg, in brainstem or thalamus).
The second scenario is more the house-of-cards
effect, where, in a patient whose behavior depends on a tenuous balance
of marginally functioning systems, even a slight shift in one system
may produce marked decline. Another
example might be an emphysematous patient with mild CHF who has just
dropped his PO2 from 65 to 55. Perhaps
the most important thing about "How much" is that it hints
a bit at the plan. Large amplitude
changes are much more likely to warrant prompt work-up, but even a
slight drop in independence may compel dramatic rearrangement in the
caregiving duties.
How
Long Has This Problem Taken to Develop? Has the patient been dwindling for three
years? Or is this a case of,
"He was good when he went to bed last night, but this morning
we found..." Rapid onset is usually assumed to imply some sudden
physiological shift, such as acute infection, toxic ingestion, stroke,
subarachnoid hemorrhage (SAH), or seizure.
And, very roughly speaking, the more rapid the change, the
more urgent the need for diagnosis and intervention.
This is particularly true now that we can provide improved
intervention during the first several hours after a "brain attack"
(acute nonhemorrhagic stroke), and many brain attacks present only
with behavioral symptoms. However,
neurological conditions are notoriously susceptible to threshold effects,
so that even a chronic problem may present acutely. For example, a slow growing brain tumor may
be symptomless until the edema reaches a critical threshold, then
numbness, weakness, or lethargy can appear in minutes.
Again, the main advantage of knowing "how long" is
a matter of the urgency of the plan: Stat labs?
Scan? Hospitalize? All of these may be appropriate in acute confusional
states of unknown cause. On
the other hand, if vital signs are benign and the level of consciousness
has been the same for three weeks, urgent laboratory tests and hospitalization
are less likely to be required this Friday evening. Table 3 lists conditions
organized in terms of rapidity of onset. Table
3: Rate of behavioral change and causes*
In
rough order of frequency. Note
that some conditions span different rates of onset, but are more likely
to appear in one category than in another
Very
Rapid onset, seconds to minutes
Acute intoxication
TIA, stroke
Syncope
Seizure Subarachnoid hemorrhage
Epidural hematoma
Critical decompensation of mass (herniation, hemorrhage)
Panic attack
Intermittent explosive disorder (episodic dyscontrol)
Rapid
onset, hours to days
Toxic/metabolic encephalopathies, including withdrawals Bacterial or viral infection
Stroke
Subdural hematoma
Increased intracranial pressure
Subacute
onset, days to 1 month
Toxic/metabolic encephalopathies Brain tumor HIV-associated syndromes (eg, AIDs-dementia
complex, CNS lymphoma, CNS
Fungal meningitis
Tuberculous meningitis
Carcinomatous meningitis
Increased intracranial pressure Subdural hematoma
Neuroleptic malignant syndrome
Major depressive episode
Post-partum depression
Stroke
Insidious
onset, months to years Neurodegenerative diseases (eg, Alzheimer's, Parkinson's)
Cerebrovascular dementia
Toxic/metabolic encephalopathies Brain tumor
HIV-associated syndromes
Neurosyphilis
Normal Pressure Hydrocephalus
Subdural hematoma
Major depressive episode, Dysthymia
Fluctuating
course
TIAs
Seizures
Syncope
Cardiac arrhythmias, esp. intermittent atrial fibrillation
Dementia with Lewy bodies
Neurocyticercosis
As rapidly as we would like to narrow our
focus on the acute versus chronic, we shouldn't be misled by two types
of chronological confounds. First,
and most frequent, is the "false acute" history. Especially in dementias, it is common for a
family member to suddenly notice a behavior change that has really
been developing for years but suddenly becomes obvious because a minor
illness has robbed the patient's tenuous cognitive reserve. This has sometimes been called a beclouded dementia, but the essential idea is simply that a new mental
or physical stress brings out the previously hidden symptoms of dementia
in a patient who has been getting by on the edge of normal functioning. For instance, a person with mild Alzheimer's
disease or hypothyroidism may not have exhibited obvious dementia
until they get the flu, or their CHF decompensates, or they are given
an antihistamine or anticholinergic agent.
The same thing can happen when a novel life challenge pushes
the patient beyond their reserve: "He was perfectly fine,"
you are told, "until we took him to that new symphony hall for
his birthday, and he just got all turned around in the parking garage."
A visiting relative, a trip to Las Vegas, a driver's license
renewal exam, any such novelty may stress a brain that functions well
in a routine life, uncovering a chronic cognitive impairment.
Second, there is the less frequent "false chronic"
history, when family members suggest that the new problem is long-term,
since today's condition doesn't seem much different from the last
year. This is most common among those with prior behavior problems in
whom change is harder to detect - a developmentally delayed child
or adult who becomes subtly toxic on their anticonvulsant, or a schizophrenic
who develops a tumor-induced aphasia in the last three weeks about
whom it's remarked, "Oh, he's always said things that were hard
to follow."
What's
Changed? Note, even though we will eventually address
the CNS locale, this is not the neurology attending's medical-student-tormenting
question, "Where's the lesion?" This is the simple question, "What's different?"
The following questions may facilitate a focused review of
systems, recalled with the useful mnemonic: THIS IS MADD! (see Table 2A).
The advantage of reviewing these issues
is self-evident; we are searching for the bounds of the problem, and
any hint we can get of etiology or localization.
For instance, asking about recent trauma, even if it was assumed
to spare the head ("Well, he did get into the fender bender two
months ago.") may actually uncover previously unsuspected traumatic
brain injury. Headaches that
have increased in frequency or severity from the patient's formerly
infrequent and mild headaches might hint at hydrocephalus, a space-occupying
lesion, escalating hypertension, or metabolic disorders such as hypoglycemic
episodes. Poor sleep not only occurs in many mood and
thought disorders, but may hint at sleep apnea, a frequently missed
cause of otherwise unexplained mildly impaired cognition, especially
in middle-aged men.
The daughter's answer, "Yes,
he's really slowed down," may not seem to help in identifying
the problem, but it actually can be quite useful because this is not the usual answer in a hemispheric stroke or tumor, which would
be a little more likely to produce a hemiparesis the daughter would
note, and it is more consistent
with diffuse or multifocal processes such as toxic, metabolic, infectious,
or neurodegenerative disorders. Unfortunately,
general slowness might also be due to increased intracranial pressure
that diffuses the effect of a focal mass, or due to focal disorders
of the basal ganglia producing a Parkinson's-like slowing (bradykinesia).
Of course, the answer, "You know, he keeps falling to
the left," or any such hint of asymmetry leads to the "Ah
hah!" that rapidly focuses our inquiry on focal processes such
as stroke or mass lesion or trauma. However, we must also beware of the phenomenon
of "red-herring localization": a diabetic may experience
a drop in glucose level - a systemic problem - and present with right-sided
weakness and aphasia because of some unpredictable asymmetric reserve
capacity of his cortical neurons.
A hyperlipidemic patient with mild basilar artery stenosis,
altogether neurologically asymptomatic until today, may have a visual
hallucination. This may occur because one visual field is
briefly blinded due to global cerebral hypoperfusion that disproportionately
affects the area served by the stenotic vessel, but it's actually
caused by transient cardiac arrhythmia - best treated as a heart more
than brain problem.
So, the first goal is simply to get an accurate fix on "what
about this man's behavior inspired this Friday clinic visit?" The net result of the How much? How long? and What? Questions might simply be: "A 35-year-old woman states that her 83-year-old
father is "just different", really slowed down, and has
been for a month." Such
a seemingly indeterminate characterization is potentially loaded with
diagnostic information. Some
conclusions are obvious: It's less likely to be SAH because we don't
hear about sudden change or head pain.
It's less likely to be a bacterial or viral meningitis, which
are also usually more precipitous. However, despite the "one month"
history, we must still consider problems that you'd ordinarily expect
to cause a sudden change - such as a stroke or traumatic brain injury
- but escape detection because they've also impaired the patient's
ability to complain. "He never said anything," an informant
accurately reports about a history of head trauma, because after standing
up under the open kitchen cabinet door and bumping his or her head
three months ago, the patient shrugged it off as just another of life's
little traumas as their subdural hematoma was forming due to the increased
bleeding tendency caused by the Coumadin they take for their atrial
fibrillation, and today the resulting amnesia prevents their even
recalling the trauma. "No, he/she hasn't complained of weakness
or numbness," the informant accurately reports because the patient's
stroke two weeks ago not only damaged the right frontal lobe causing
a mild left hemiparesis, but also the right parietal cortex, causing
Anosognosia - denial of their own hemiparesis.
Obviously, still open to consideration in this case are toxic
or metabolic disorders, systemic infections, chronic CNS infections,
or neurodegenerative diseases.
The present history, of course, could be considerably elaborated
if we are rigorous and go into recent travel, exposures to others
with illness, exposure to chemicals, nutritional changes, etc.
But, in the parsimony of our 15 minute assessment, the most
commonly missed pertinent parts of the history and the two general
medical questions we must really ask are, 1) "Any infectious
symptoms (UTI's or URI's)?",
2) "What drugs or medicines has he been taking?"
This last question has probably yielded more specific neurobehavioral
diagnoses than any, and notoriously uncovers iatrogenic disorders. Stimulants, depressants, drugs with CNS toxicities,
and illicit drugs including alcohol account for 35 to 60% of cases
of new-onset confusional syndromes.
Table 4 lists some drug causes of altered
mental status (AMS). In addition,
particularly in cases of suspected dementia, we may need to work a
little to establish the onset. "I understand your Dad has been different
for the last month. But, in
the last few years, was he just the same fellow as he was twenty years
ago?" "Pretty much," she answers,
"although he hasn't been gardening so much in the last few years."
This change in activities might be due to arthritis, weather,
or a myriad of other reasons, but such an innocuous answer might also
be the first hint we get that the present illness may actually have
been long in coming on. We might proceed to ask a very open-ended question
that sometimes gets to the depth of the problem: "What worries you most about this?" She ponders a moment. "He's just...not my Dad." Absently, she drags her sleeve across her eye.
There is obviously no exact formula, no turn of phrase or tone
of voice that will reliably elicit key answers, and every family physician
will creatively find their own way.
But answers such as this, vague as they may seem, can alert
us. This is not a minor matter;
the daughter senses that Mr. Johnson is in serious trouble.
Table
4: Drug Causes of Altered Mental Status
Sedative
hypnotics and opioid analgesics
such as benzodiazepines, neuroleptics (eg, haloperidol (Haldol®),
prochlorperazine (Compazine®), metoclopramide (Reglan®), promethazine
(Phenergan®), meperidine (Demerol®), pentazocine (Talwin®), other
opiates
Antihistamines, particularly diphenhydramine (Benadryl®)
Anticholinergic
agents such
as benztropine mesylate (Cogentin®), trihexphenidyl (Artane®), and
tricyclic antidepressants
Histamine
blockers, especially
cimetidine (Tagamet®)
Cardiovascular
agents, including
beta blockers, amiodarone (Cordarone®), calcium channel blockers,
digitalis preparations, doxazosin, disopyramide phosphate (Norpace®), methyldopate HCl (Aldomet®). Selective
serotonin reuptake inhibitors (SSRIs)
such as fluoxetine (Prozac®), sertraline (Zoloft®), paroxetine (Paxil®)
Anti-inflammatory
drugs such
as corticosteroids and nonsteroidal anti-inflammatories (including
aspirin)
Drugs with stimulant or sympathomimetic properties |
