Authors: Lewis,
Steven L.
Steven L.
Title: Field
Guide to the Neurologic Examination, 1st Edition
Guide to the Neurologic Examination, 1st Edition
Copyright ©2004 Lippincott Williams &
Wilkins
Wilkins
> Table of Contents > Section 3 –
Neurologic Examination in Common Clinical Scenarios >Chapter 43 –
Examination of the Patient With Altered Mental Status
Neurologic Examination in Common Clinical Scenarios >Chapter 43 –
Examination of the Patient With Altered Mental Status
Chapter 43
Examination of the Patient With Altered Mental Status
GOAL
The main goal of the history and examination of the patient with an
alteration in mental status is to look for evidence of whether the patient’s
symptoms represent a diffuse encephalopathic process, a dementing illness, or a
symptom of focal brain dysfunction.
alteration in mental status is to look for evidence of whether the patient’s
symptoms represent a diffuse encephalopathic process, a dementing illness, or a
symptom of focal brain dysfunction.
PATHOPHYSIOLOGY OF ALTERED MENTAL STATUS
Mental status can be affected by disorders that affect the level of
consciousness (alertness) or disorders that affect cognitive function (see Chapter 5, Approach to the Mental Status Examination).
consciousness (alertness) or disorders that affect cognitive function (see Chapter 5, Approach to the Mental Status Examination).
Disorders of Level of
Consciousness
Consciousness
The pathophysiology of changes in consciousness severe enough to
cause coma are discussed in Chapter 42, Examination of the
Comatose Patient. All of the same processes and mechanisms, either focal or
diffuse, that can cause coma can also present as lesser degrees of altered
consciousness. One common cause of disordered consciousness, manifested as an
acute confusional state, is a toxic-metabolic
encephalopathy, the neurologists’ term for delirium; this represents the
severe altered mental status that can occur in the setting of a systemic illness
or as a result of many metabolic or toxic disorders.
cause coma are discussed in Chapter 42, Examination of the
Comatose Patient. All of the same processes and mechanisms, either focal or
diffuse, that can cause coma can also present as lesser degrees of altered
consciousness. One common cause of disordered consciousness, manifested as an
acute confusional state, is a toxic-metabolic
encephalopathy, the neurologists’ term for delirium; this represents the
severe altered mental status that can occur in the setting of a systemic illness
or as a result of many metabolic or toxic disorders.
Disorders of Cognition
Dementias are neurologic illnesses that impair function in memory
and at least one other aspect of cognitive function, such as judgment,
personality, visualspatial ability, language, and abstract thinking. Causes of
dementia include, among others, degenerative illnesses (e.g., Alzheimer’s
disease, frontotemporal dementia, and Lewy body dementia), multiinfarct
dementia, and Creutzfeldt-Jakob disease. Dementing illnesses, for the most part,
affect cognitive function without impairing the level of consciousness.
Cognitive function can also be affected by any focal neurologic process
affecting cognitively important cortical regions.
and at least one other aspect of cognitive function, such as judgment,
personality, visualspatial ability, language, and abstract thinking. Causes of
dementia include, among others, degenerative illnesses (e.g., Alzheimer’s
disease, frontotemporal dementia, and Lewy body dementia), multiinfarct
dementia, and Creutzfeldt-Jakob disease. Dementing illnesses, for the most part,
affect cognitive function without impairing the level of consciousness.
Cognitive function can also be affected by any focal neurologic process
affecting cognitively important cortical regions.
TAKING THE HISTORY OF A PATIENT WITH AN ALTERED MENTAL
STATUS
STATUS
Depending on the severity of the illness, patients with an
alteration in consciousness or cognition may or may not be able to provide much
history or have insight into their dysfunction. In most cases, details of the
history need to be obtained from family members (see Chapter
42, Examination of the Comatose Patient).
alteration in consciousness or cognition may or may not be able to provide much
history or have insight into their dysfunction. In most cases, details of the
history need to be obtained from family members (see Chapter
42, Examination of the Comatose Patient).
Ask about the time course of the change in mental status. An
acute onset of altered mental status over seconds suggests an acute focal
process, such as stroke affecting cognitive regions. A subacute onset over
hours or days would be expected in most toxic-metabolic encephalopathies or
many
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structural processes. A chronic and
progressive course over months or years would be expected in dementing
illnesses (although Creutzfeldt-Jakob disease would be more rapid, and
vascular dementia should have a step-wise course).
Ask about the details of the dysfunction. Lethargy or agitation
(or both) would be expected in delirium; hallucinations (especially visual)
may also be present. Patients with dementias usually present with recent
memory impairment as their most prominent symptom or may have personality and
behavioral changes, but they rarely have impairment in their level of
consciousness, at least not early in their course.
Ask about the presence of new systemic symptoms that would
suggest toxic-metabolic dysfunction in the acutely confused patient or focal
neurologic symptoms that might suggest a focal process.
Look for any medications the patient may be taking that might be
causing central nervous system side effects.
Ask about symptoms of depression, such as changes in mood,
appetite, and sleep, that might suggest the presence of a
pseudodementia.
HOW TO EXAMINE THE PATIENT WITH ALTERED MENTAL STATUS
In the patient with acutely or subacutely altered mental status,
approach your general assessment as described in Chapter
42, Examination of the Comatose Patient. Fever would suggest the
possibility of meningitis, encephalitis, or sepsis (systemic infection is a
common cause of toxic-metabolic encephalopathy).
Assess the patient’s level of consciousness by observation. In
the absence of other significant focal neurologic signs (see below), any
impairment in alertness suggests the possibility of a diffuse
(toxic-metabolic) encephalopathic process.
Chapters 5, 6, and
7 describe the details of the mental status examination,
which should be attempted in all patients with any alteration in mental
status. In particular, assess the patient’s orientation, language,
concentration, and memory.
In the patient with an acute onset of confusion, always consider
the possibility that the patient might have Wernicke’s aphasia (see Chapter 6, Language Testing); listen carefully for any
paraphasic errors and neologisms.
In those patients in whom a detailed motor and sensory
examination may not be possible because of confusion, look for gross
asymmetries in motor function, including testing for drift, to assess for
evidence of focal brain dysfunction. Also, look for obvious reflex asymmetry
or a Babinski sign.
A helpful examination finding in many patients with
toxic-metabolic encephalopathies is asterixis. Asterixis consists of brief,
often subtle, downward flapping or jerking of the extended hands due to lapses
in muscle tone. Asterixis is seen in many toxic-metabolic encephalopathic
processes but is particularly common in hepatic and uremic encephalopathies.
Perform the following to test for asterixis:
Ask your patient to hold his or her arms extended, directly in
front of him or her.
Have the patient dorsiflex his or her wrists so that the hands
are straight up, “like you are stopping traffic.”
Observe the patient for at least a few seconds as he or she
tries to maintain the hands in this position. Look for any subtle lapses in
tone (asterixis), manifested as brief downward jerks of the hands at the
wrists.
In some patients with severe toxic-metabolic encephalopathies,
especially those of hepatic or uremic origin, diffuse myoclonus (see Chapter 46, Examination of the Patient with a Movement
Disorder) may also be observed and can be a prominent clinical finding.
Myoclonic jerks of the extremities can also be seen in Creutzfeldt-Jakob
disease.
In patients with dementia, the Folstein Mini-Mental State
Examination (MMSE), a standardized battery of various cognitive tasks, is
often used to assess global cognitive function (see Chapter
5, Approach to the Mental Status Examination); the MMSE score can be
followed serially over subsequent visits to assess for change in the patient’s
cognition as an adjunct to the interval history. Another advantage of using
the MMSE is that it allows you to remember to test most of the important
cognitive tasks (always report each incorrect item and not just the absolute
score out of the total of 30 points). Although the score on the MMSE
correlates with severity of cognitive dysfunction, the absolute score is not
diagnostic of any particular cause of dementia or any other cause of
encephalopathy.
Gait examination can provide clues to the cause of dementing
illnesses. A parkinsonian gait (see Chapter 39,
Examination of Gait) would suggest the possibility of Lewy body dementia. Gait
disorders, however, particularly apraxia of gait (described in Chapter 39, Examination of Gait), may be seen late in the
course of any severe chronic dementia as a sign of frontal lobe dysfunction.
Patients with the syndrome of normal pressure hydrocephalus would be
particularly likely to manifest an apraxia of gait as an early
finding.
Gegenhalten rigidity (described in Chapter
27, Examination of Tone) can be seen late in the course of any severe
chronic dementia, but it is a nonspecific sign. Other classic frontal release
signs, such as the glabellar reflex (continual blinking when the patient’s
mid-forehead is repeatedly tapped), the grasp reflex (flexion of the patient’s
fingers and grasping of the patient’s hand when lightly brushed by the
examiner’s hand), and the palmomental reflex (twitch of the patient’s
ipsilateral chin when the patient’s palm is lightly scratched by a blunt
object) are also nonspecific, are of doubtful efficacy in neurologic
assessment of any patient, and can be
skipped.
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