INTRODUCTION
In most patients, the physical examination confirms thoughts formulated during history taking that are often the key to patient evaluation. Time of onset, symptom progression, associated complaints, and exacerbating factors are important historical points to guide appropriate examination and other testing. The neurologic examination does not exist in isolation from the general physical examination or imaging procedures, and it is unusual for the neurologic examination to delineate a problem not already suggested by the patient’s history or general physical examination. Few findings of the neurologic examination are pathognomonic of clinical conditions or are sufficiently specific that examination alone secures the diagnosis. Further complicating the value of the neurologic examination is that the sensitivity and specificity of different examination techniques have not been rigorously investigated, and the degree of interobserver variability is not known. The uncooperative patient or patient with altered mental status presents additional challenges in performing a detailed examination.
The idea of performing a “complete” examination in the ED is impractical, because most frequently, a “complete” examination is neither required nor appropriate. An adequate examination is one that is sufficient for the task at hand. Examination of children follows the same framework as that for adults, but even more information is gathered indirectly by observation. For example, interacting with a child playing with a toy or other object allows the examiner to assess vision, extraocular motion, coordination, and strength as the child reaches for and grasps the toy.1 Traditional neurologic formulation follows a three-tiered approach: (1) Is there a lesion of the nervous system? (2) Where is the lesion? (3) What is the lesion? The examination detailed in this chapter is arbitrarily divided into eight sections with basic and advanced levels described for each section.
ORGANIZATIONAL FRAMEWORK
Organization of the neurologic examination into a framework of subsections is a convenient technique. At the bedside, mentally review the framework as during the examination, and select more detailed tests as needed. Some of the tests grouped in a section assess several aspects of nervous system function, and listing of tests in a particular section is for organizational convenience. For example, visual field testing, although technically a test of higher cortical function, is listed with cranial nerve testing because the examining physician may find it easier to evaluate visual fields during that portion of the examination assessing cranial nerve function. One organizational scheme divides the examination into eight elements:
Mental status testing
Higher cerebral functions
Cranial nerves
Sensory examination
Motor system
Reflexes
Cerebellar testing
Gait and station
MENTAL STATUS TESTING
A mental status examination is part of every patient encounter. The observation may be brief and descriptive, such as, “The patient is awake, alert, and conversant,” or it may be quite detailed. Mental status assesses the emotional and intellectual functioning of the patient. It is important to make some assessment of mental status, because the patient with an abnormal mental status cannot be relied on for an accurate medical history.
Major elements of mental status testing are assessment of appearance, mood, and insight; assessment for thought disorders or abnormal thought content such as hallucinations; and testing of the sensorium. Sensorium is a term for the appropriate awareness and perception of consciousness. Mental status testing is covered more fully in chapter 168, Altered Mental Status and Coma.
One key element in mental status testing is attention and memory assessment. Attention testing is performed with digit repetition. The average adult of normal intelligence should be able to repeat six or seven digits forward and four or five digits backward. Failure to do so may suggest confusion, delirium, or a problem with language perception. Often this represents a problem with attention rather than with memory. Memory is a complex process but is often simply broken into long-term and short-term activities. Long-term memory is recall of events of some months or years ago. Short-term memory is assessed by asking about events of the day or by three-object recall at 5 minutes. State three items in a neutral tone and ask the patient to repeat; reassess at 5 minutes to obtain a gross assessment of short-term memory function. Failure to repeat the items immediately after presentation is likely an indication of an attention problem rather than of a memory problem.
Evaluation by screening tools is described in chapter 168. Other screening tests for depression, substance abuse, and other problems are outside the scope of this chapter.
In general, patients with abnormal mental status, especially attention problems or disorientation, are more likely to have medical problems rather than functional or psychiatric causes. If a patient suffers from significant inattention, it is unlikely that the examiner will truly be able to determine whether the primary problem is one of cognition or attention.
HIGHER CEREBRAL FUNCTIONS
Higher cerebral functions test neurologic tasks that are thought to reside in the cerebral cortex. Language function defines the dominant hemisphere. The majority of the population is right-handed; for 90% of these patients, the left hemisphere is where language functions reside; hence, they are referred to as left-hemisphere dominant. Even in left-handed patients, most will be left-hemisphere dominant for language. Thus, a large cortical stroke affecting the cortex of the dominant hemisphere (the left hemisphere in most patients, whether they are left- or right-hand dominant) likely will affect language functions.
The nondominant hemisphere is concerned with spatial relationships. Often a nondominant hemispheric problem is suspected in the ED when the patient has consistent visual inattention to a care provider approaching from one side (usually the left since most patients are left-hemisphere dominant).
Higher cerebral function pragmatically involves the assessment of language. For a patient with speech that is difficult to understand, a fundamental distinction must be made between dysarthria and a dysphasia (aphasia and dysphasia are often used interchangeably in clinical practice). Dysarthria is a mechanical disorder of speech resulting from difficulty in the production of sound from weakness or incoordination of facial or oral muscles; this may result from a motor system problem (cortical, subcortical, brainstem, cranial nerve, or cerebellar), but it does not represent a disorder of higher cerebral function. Dysphasia is a problem of language resulting from cortical or subcortical damage; the portion of the brain concerned with comprehension, processing, or producing language is impaired.
There are many different types of aphasias, but a simplified scheme is sufficient for assessment. A description of aphasia into fluent, nonfluent, or mixed patterns is adequate for testing in the ED and for communicating with other physicians.
Normal conversation monitoring for correct responses is the common screening examination for a language disorder. If suspicion of a language disorder exists, a series of assessments allows confirmation and categorization of the aphasia.
Test comprehension initially by the ability to follow simple commands. Asking the patient to identify common objects may also be part of the assessment. Use commonly available objects, such as a watch, a pen, or a glass, as a stimulus. Query the patient regarding the names of different parts of the objects. Ask the patient to demonstrate how an object is used. The inability to show how an object is used, assuming hearing and motor functions are intact, may represent an apraxia, defined as the inability to perform a willed act.
In a nonfluent aphasia (a rough synonym is motor or expressive aphasia), the speed of language and the ability to find the correct words may be impaired. A common type of nonfluent motor aphasia is known as Broca’s aphasia. Speech may be halting and slow, with stops between words or word fragments.
In a fluent aphasia (a rough synonym is auditory or receptive aphasia), the quantity of word production is normal or even increased. Sentences may have normal grammatical structure with normal rhythm, and intonation may be clearly articulated. However, language is impaired, and the listener may be struck by peculiarities of conversation that lack appropriate content. Incorrect words may be substituted within sentences that may be sound-alike words or words with similar yet incorrect meanings. A global or mixed aphasia involves elements of fluent and nonfluent aphasias and is the most common type encountered in clinical practice.
Nondominant hemisphere problems may show problems of auditory or visual inattention or sensory inattention.
Testing of mental status and cognitive function requires an appreciation of cultural context and language barriers. Further assessment of comprehension may involve showing the patient a picture (there are some standard stimuli, but almost any magazine photo may be used) and asking for the patient’s interpretation of the picture while noting if the content is correctly described and if the sentence structure and word selection of the descriptions are correct.
Assessing the ability of the patient to repeat a phrase may be a key point in delineating some types of fluent aphasias. Typically, the ability to repeat short words is more impaired than the ability to repeat longer words. A classic test involves the patient repeating the phrase, “No ifs, ands, or buts.” In one type of fluent aphasia, Wernicke’s aphasia, comprehension is impaired, as is repetition.
Paraphasic errors may be further characterized in patients with fluent aphasia. A literal paraphasic error is one in which part of a word is replaced by an incorrect sound. The use of spool when spoon is meant is an example of a literal paraphasic error. At times, the errors may reach the point at which the substitutions are not understandable, and a neologism (a meaningless collection of syllables that takes the place of a word in conversation) is produced. Verbal paraphasic errors involve substitution of one correct word for another; for example, a patient may wish to use spoon in a sentence and substitute fork or even bike; the word is a correct word, but the meaning of the sentence is transformed erroneously.2
A patient aphasic in speaking will also be aphasic in written communication. Writing and drawing simple constructions may be revealing in some patients. A sequence of simple commands such as requesting the patient to draw a circle and then placing numbers like numbers on a clock may reveal constructional errors. A response consistent with dysfunction of the nondominant hemisphere might be numbering half the clock face and stopping or placing all the numbers around one half of the circle.
Impairment of sensory perception on the cortical level may involve the inability to distinguish objects by touch alone. Implied in this testing is that the primary sensory modalities (sharp, light touch, etc.) are intact. In cases of nondominant hemisphere lesions, the ability to identify objects placed in a hand, such as a coin, may be impaired.
Fluent aphasias may so severely impair communication that the patient is thought to be intoxicated or psychotic. Pay attention to the pattern of speaking—this may give the first indication of a language problem, and further constructional or language testing may demonstrate the presence of an aphasia.
CRANIAL NERVES
A survey of the cranial nerves is an integral part of neurologic assessment. Much information may be gathered informally. Look for facial asymmetry (cranial nerve VII) at rest or with movement. Lingual movement (XII) and other facial movements may be inferred during conversation if articulation is good. However, a more formal approach often is used in examination. Most examiners start sequentially with cranial nerve II in testing; cranial nerve I (olfactory) testing has infrequent application in emergency medicine.
Cranial nerve II is the optic nerve active in the afferent function of light and visual perception. The optic nerve head is visible with direct ophthalmoscopy and may be inspected for abnormalities. Common tests for optic nerve function include visual acuity and stimulation for pupillary reactivity. The response to bright light stimulation involves direct and indirect (consensual) pupillary responses. This is a reflex arc, with the afferent limb being cranial nerve II and the efferent limb of the arc being cranial nerve III, which carries the pupilloconstrictors. A bright light directed into one eye should cause a brisk constriction of equal magnitude in both pupils. In the swinging flashlight test, observe the pupils as the light is slowly moved from one pupil to the other. A seemingly paradoxical dilation of one pupil as the light is moved onto that pupil may indicate optic nerve dysfunction of that eye; this is referred to as an afferent pupillary defect (see chapter 241, Eye Emergencies).
Cranial nerves III, IV, and VI are concerned with extraocular eye movements (see chapter 241). Tracing an object through a full-H pattern allows assessment of the different cranial nerves. Cranial nerve VI innervates the lateral rectus muscle, which abducts the globe, moving it laterally away from the midline; this lateral movement will be impaired or lost in the case of cranial nerve VI palsy. In fact, the unopposed adduction movement of medial rectus muscle innervated by cranial nerve III may result in the globe being medially deviated. Cranial nerve III innervates the extraocular muscles that adduct each eye and those that elevate and depress the globe. Impairment of cranial nerve III will reveal several abnormalities of extraocular movement, reflecting weakness in the innervated muscles. A complete paresis of cranial nerve III will show a dilated pupil in a globe deviated downward and outward. An isolated cranial nerve IV weakness may be hard to detect; cranial nerve IV supplies the superior oblique muscle that elevates and intorts the globe.
Cranial nerve III also carries the parasympathetic pupilloconstrictors to the eye; a lesion of cranial nerve III may impair those fibers, resulting in unopposed dilatation (by functioning sympathetic fibers reaching the eye by a circuitous path) and a pupil larger than in the unaffected eye. Ptosis from levator muscle paralysis is another finding of cranial nerve III paresis.