The Neurological Examination of the Patient
Oculomotor, Trochlear, and Abducens Nerves (Cranial N. III, IV, VI)
THE KEY TO THE ANALYSIS OF SIGNS and symptoms referable to the nervous system is a rigorous neurological examination of the patient. This examination begins with an assessment of the patient’s mental functioning.
Mental Status
Alertness and Attentiveness
A patient’s level of consciousness is defined in terms of responses to stimuli. Rather than simply using terms such as lethargy, obtundation, stupor, and coma, the examiner needs to note the minimal stimulus that elicits a response (eg, voice, shaking the patient, applying pain) and the response (eg, sustained alertness vs. fleeting eye opening with mumbling).
An impaired attention span is usually apparent during history taking. It can be tested more formally by having the patient repeat a series of numbers or count backward from 20. Sequential digit testing is sensitive, but the test is not specific; difficulty may connote impairment of immediate (working) memory.
Inattentiveness so severe that meaningful interaction with the environment is impossible is characteristic of delirium. Such patients are often agitated.
Behavior, Mood, and Thought
Neuropsychiatric abnormalities can be identified in this part of the mental status examination. Affect, the outward expression of mood, may be manifested in clothing, facial expression, amount and type of activity, and stream of conversation. If depression is suspected, the patient should be specifically queried; mood may be more disturbed than affect suggests.
Schizophrenic patients may demonstrate indifference, flattening of affect, or inappropriate mood. They may appear hostile and paranoid. Behavior sometimes suggests hallucinations even when they are denied. Schizophrenic speech may reveal loosening of associations, incoherence, blocking, stereotypy, or distractibility.
Slowing of speech and activity is a manifestation of medial frontal lobe damage (abulia). Lesions of the frontal lobe also produce social disinhibition, inappropriate jocularity, and difficulty sustaining goal-directed behavior.
Orientation and Memory
People aware of their own identity as well as of the basic facts of their surroundings (hospital, home address, city, state; time of day, day of week, month, year) are said to be “oriented to person, place, and time.” Memory impairment secondary to brain injury or a dementing illness is usually greater for recent than remote events; such patients are disoriented to place and time but not to person. Disorientation is neither a sensitive nor a specific marker of amnesia, however.
Memory is clinically categorized as immediate (working), recent, and remote. A sensitive test for recent memory is to have the patient repeat three unrelated words (eg, Chicago, orange, thirty-three) and then repeat them after 5 minutes. If unable to recall the words, the patient is asked to select the words from a list. Amnestic disorders tend to affect recall more than recognition. Long-term memory can be tested by having the patient recall people or events from the past and then verifying the answers.
Conventional testing identifies disturbances of explicit memory (see Chapter 67). Amnestic or dementing illnesses are less likely to affect implicit memory systems such as procedural memory (remembering how to perform a skilled motor act).
Cognitive Abilities
Intellectual skills are assessed in standardized IQ tests, which are subject to educational and cultural bias. Tests include calculation, word similarities, word opposites, and proverb interpretation.
Language Disorders
Aphasia is a disturbance of language unexplained by an impairment of the neural machinery for hearing, vision, or vocalizing (see Chapter 60). Clinical subtypes of aphasia can be identified by assessing six basic components of language: spontaneous speech, speech comprehension, naming, repetition, writing, and reading (Figure B–1).
Figure B-1 A stroke in the left middle cerebral artery (MCA) territory producing contralateral hemiparesis and aphasia.
A. The patient develops sudden right-sided weakness involving face, arm, and leg. Examination reveals left gaze preference and weakness of extensor muscles of the right arm, more pronounced distally than proximally, and to a lesser degree weakness of flexors of the right leg. In the first few days tendon reflexes may be absent at the right triceps, knee, and ankle. A right Babinski reflex is present (arrow). Numbers indicate the strength of the reflex, where 2+ is normal. (See the section on Deep Tendon Reflexes.)
B. In weeks to months the patient may develop tonic flexure posture of the right arm and extensor posture of the right leg. Tendon reflexes on the right will become brisk with a positive Babinski reflex.
C. There is weakness of the right side of the face, characterized by widening of the palpebral fissure because of a lax lower lid, blunting of the right nasolabial fold, and drooping of the right corner of the mouth. There may also be acute weakness of the forehead with decreased furrowing of the brow, but this usually resolves quickly as the upper facial motor neurons receive bilateral supranuclear innervation. The patient has a nonfluent aphasia. Speech is effortful and telegraphic, and the prosody is abnormal. The patient cannot repeat words or phrases and becomes easily frustrated but can follow simple commands.
D. Site of stroke is on the left parieto-frontal region. Note that the left is shown on the right in diagnostic brain scans.
Spontaneous Speech
The patient’s speech may be abnormal in a number of ways. Fluency, the amount of speech produced over time, may be reduced. Prosody, the musical qualities of speech (pitch, accent, rhythm), can also be impaired. In paraphasias incorrect words are substituted for correct ones. Patients with literal (or phonemic) paraphasia use words that phonetically resemble the intended word but contain one or more substituted syllables (eg, “hosicle” instead of “hospital”). Those with verbal (or semantic) paraphasia use real but unintended words (eg, “hotel” instead of “hospital”). In some patients paraphasic errors are simply occasional contaminants of speech; in others, they almost entirely replace it.
Even in the absence of paraphasias the content of aphasic speech may be difficult to grasp. Severely restricted vocabulary may be reflected by logorrheic but empty speech as well as by hesitation before certain words. Paragrammatic speech preserves some semblance of syntax despite such profoundly restricted semantic content. By contrast, agrammatic (or telegram-matic) speech omits relational words (such as prepositions or conjunctions).
Speech Comprehension
Casual conversation with the patient may not reveal abnormalities of speech comprehension, which can be mild, moderate, or severe. Specific testing is required. Assessment of speech comprehension should not depend on the patient’s verbal responses to commands or questions. A wrong answer to a question could signify a paraphasic error rather than failure of comprehension. If a simple or complex command is followed, it can be presumed that the command was understood. However, failure to follow a command could have explanations other than impaired comprehension, for example, paralysis, apraxia, pain, or negativism.
A more reliable method of testing speech comprehension is to ask yes-or-no questions. Even patients with severely restricted speech output can usually indicate affirmative or negative. Both the patient and the examiner must of course know the correct answers. Still another way of testing speech comprehension is to ask the patient to point to objects or body parts.
As with abnormal speech output, semantic and syntactic (relational) comprehension can be dissociated. Syntactic comprehension can be assessed by asking the patient to handle objects. For example, after identifying a comb, a pen, and a key, ask the patient to put the key on top of the comb or the comb between the key and the pen.
Naming
Patients with adequate vision can be shown objects, body parts, colors, or pictures of actions (confrontation naming). A variety of abnormal responses indicate anomia, the loss of the ability to recall or recognize the names of things. Some patients exhibit paraphasias. Some hesitate and grope for the correct word (tip-of-the-tongue phenomenon). Some patients describe rather than name an object. For example, instead of saying “necktie,” the patient says, “It’s what you wear around your neck.”
Repetition
The patient is asked to repeat sentences such as “In the winter the President lives in Washington.” Syntactically complex sentences may be particularly difficult (for example, “If he were to come, I would go out”). Errors most often consist of paraphasic substitutions.
Writing
Testing of writing begins by having patients sign their names. More specific tests of writing include dictated sentences, words, or letters, as well as spontaneous writing; for example, describing what is seen in a room.
Reading
Reading ability is tested by having the patient read aloud simple sentences, words, or letters. Reading comprehension can be tested by having the patient follow written commands that were previously successfully executed as oral commands or by having the patient answer written yes-or-no questions.
Praxis
Praxis refers to performance of a learned motor act. In its broadest sense apraxia refers to impaired motor activity not explained by weakness, incoordination, abnormal tone, bradykinesia, movement disorder, dementia, aphasia, or poor cooperation. Failure to perform an act is not evidence of apraxia. To be apractic the act must be performed incorrectly, or components of the act must be performed imprecisely. Parts of the act might be omitted, sequenced abnormally, or incorrectly oriented in space. There are three types of testing: (1) gesture (“Show me how you would throw a ball”); (2) imitation (“Watch how I point upward, then you do it”); and (3) use of an actual object (“Here is a spoon. Show me how you would use it”).
Apraxias are traditionally classified as limb-kinetic, ideational, and ideomotor. With limb-kinetic apraxia the act is understood but motor execution is faulty. With ideational apraxia the idea of the act—the neural representation of the act, or engram—is disrupted. With ideomotor apraxia the idea of the act and the motor components of its execution are functionally disconnected. Such patients might be unable to imitate using a hammer but able to accurately describe its use and, if given a hammer, use it correctly.
Gnosia and Spatial Manipulation
Agnosia is a failure of recognition not explained by impaired primary sensation (tactile, visual, auditory) or cognitive impairment. It has been described as “perception stripped of its meaning.” Agnosia differs from anomia in that the patient not only fails to name an object but also cannot select it from a group or match it to a picture. With tactile agnosia (astereognosis), touch threshold is normal yet patients cannot identify what they are touching.
Comparable agnosias exist in the visual and auditory spheres. However, because the responsible lesions are likely to be bilateral, visual and auditory agnosias are rare. Simultanagnosia is the inability to recognize the meaning of a whole scene or object, even though its individual components are correctly recognized.
The left hemisphere usually processes language and the right hemisphere processes spatial information. Right hemispheric (particularly parietal) lesions impair spatial perception and manipulation; patients have difficulty reading maps or finding their way about (topographagnosia), or difficulty copying simple pictures or shapes or drawing simple objects such as a flower or a clock face (constructional apraxia or apractagnosia).
Even more striking is spatial hemineglect syndrome. Patients with damage to the right hemisphere may ignore objects to the left of midline, including the left side of the body (personal neglect syndrome). They may fail to recognize severe hemiplegia (anosognosia) or even to acknowledge left body parts as their own (asomatognosia). Asked to bisect a line, such patients indicate a point to the right of midline. A copied picture might be missing the left half, and a drawn clock face might have all the numbers neatly arranged on the right.
A subtle manifestation of spatial neglect is extinction. Patients are able to recognize a stimulus (visual, auditory, or tactile) on either side when it is presented alone but unable to recognize the stimulus when it is presented on one side while the opposite side is also stimulated.
Cranial Nerve Function
Several of the cranial nerves are multifunctional; their motor, sensory, and autonomic functions must be assessed separately. The optic nerve is actually a central nervous system tract, and the accessory nerve is anatomically an aberrant spinal nerve (the motor neurons reside in the upper spinal cord).
Olfactory Nerve (Cranial N. I)
When patients complain that foods no longer taste right, the first step is to look into the nose for possible obstruction of airflow. Each nostril is then tested separately, using non-noxious odorants such as coffee or soap. (Pungent substances such as ammonia will stimulate trigeminal nociceptors.) Failure to smell anything is termed anosmia. Unpleasant distortion of an innocuous odorant is termed parosmia.
There are several cerebral representations for olfaction in the brain. As a result anosmia is most often secondary to local nasal disease, or to lesions affecting olfactory fibers as they pass through the cribriform plate (see Figure 32-1).
Optic Nerve (Cranial N. II)
Visual Acuity
Visual acuity is tested with Snellen’s chart (at 20 feet) or a hand-held card (at 14 inches). The eyes are tested separately; if acuity is severely reduced, finger counting, detection of hand movement, or light perception should be assessed. Refractive errors are identified by having patients wear their glasses or look through a pinhole. Inspection of the eyes and funduscopic examination will often identify ocular lesions impairing acuity, such as corneal scarring, cataracts, glaucoma, diabetic retinopathy, or macular degeneration.
Visual Fields
The eyes are tested separately. The examiner faces the patient and holds an object equidistant between the patient’s and the examiner’s eyes to compare his or her own experience with that of the patient. A test object is moved slowly inward from the periphery, and the patient is asked to indicate when it is first seen; or the patient can be told to count fingers in different visual quadrants. Stimuli are presented simultaneously to the right and left fields to identify spatial neglect (extinction).
Visual field testing provides very accurate localization of structural lesions (see Figure 25-5). Monocular visual impairment, including either field defect or scotoma (an area of visual loss surrounded by preserved vision), localizes a lesion to the optic nerve, the retina, or other ocular structures. Bitemporal hemianopia, if caused by a single lesion, places that lesion at the optic chiasm. Homonymous hemianopia, quad-rantanopia, or bilateral congruent scotomas indicate a lesion behind the chiasm in the contralateral optic tract, lateral geniculate nucleus of the thalamus, optic radiation, or primary visual cortex.
Funduscopy
Using an ophthalmoscope, the examiner focuses successively on the cornea, anterior chamber, lens, and vitreous body, and then surveys the optic disk, retinal vessels, and the retina itself. Optic atrophy refers to disk pallor; its many causes include glaucoma, optic nerve compression, infarction, and multiple sclerosis.
In papilledema (optic disk swelling) the disk margins become blurred and elevated. Papilledema can be the result of local pathology, for example the inflammatory demyelination of optic neuritis, in which case visual acuity is acutely impaired by swelling of the optic nerve head. When papilledema is the result of increased intracranial pressure, the normal blind spot becomes enlarged but visual acuity is not initially affected; over time, however, the visual fields become constricted and visual acuity is impaired. In addition, the ratio of the diameter of retinal veins to arteries (normally approximately 3:2) increases, and there may be retinal hemorrhages and whitish exudates.
Other abnormalities identified by funduscopy include arterial narrowing (hypertension), exudates (diabetes mellitus, blood dyscrasias), microaneurysms (diabetes mellitus), subhyaloid hemorrhages (located between the retina and the vitreous membrane and associated with subarachnoid hemorrhage), tubercles and other granulomas, phakomas (glial collections, associated with the hereditary diseases neurofibromatosis and tuberous sclerosis), pigmentary changes (retinitis pigmentosa), and emboli (seen within arteriolar branches of the central retinal artery).
Oculomotor, Trochlear, and Abducens Nerves (Cranial N. III, IV, VI)
Pupils
The pupillary light reflex is tested by directing a bright light into each eye and observing the bilateral response. Both pupils should constrict to bright light in either eye. The accommodation reflex and pupillary near response are tested by having the patient converge onto an object held close to the eyes; the pupils should constrict.
Anisocoria (unequal pupils) signifies either a parasympathetic lesion affecting the larger pupil or a sympathetic lesion affecting the smaller pupil. A parasympathetic lesion is indicated by marked pupillary dilatation, loss of the light reflex, or both, as well as involvement of extraocular muscles innervated by the oculomotor nerve. A sympathetic lesion is indicated by pupillary constriction, preservation of the light reflex, and signs of Horner syndrome (ptosis and, in some cases, loss of sweating over the ipsilateral face). A pupil with both parasympathetic and sympathetic denervation will be mid-position and unreactive to light.
A unilateral lesion involving the optic nerve or retina is indicated when neither pupil constricts in response to light directed into the affected eye, but both pupils constrict when light is directed into the unaffected eye (afferent pupillary defect). The pupils react equally because the pupillary light reflex is consensual (Figure B–2A; and see Figure 45-7).
Figure B-2 Multiple sclerosis produces protean symptoms that wax and wane.
A. A common early symptom of multiple sclerosis (MS) is transient blurred vision in one eye as a result of optic neuritis, inflammation of the optic nerve that occurs during the acute phase of an MS lesion. 1. Shining a light in the normal eye produces both direct and consensual pupillary constriction, but when the light is swung to the affected eye, both pupils dilate because the patient perceives a relative dimming of light intensity. This is referred to as a de-afferented pupil. At no time with a de-afferented pupil is there anisocoria. A positive “swinging flashlight test” indicates a de-afferented pupil. 2. To determine the site of the lesion the examiner must use an ophthalmoscope to evaluate the possibility of a corneal or lenticular opacity, vitreous hemorrhage, retinal detachment, or ischemic retinopathy. 3. If the funduscopic examination is normal, or reveals a slight elevation or blurring of the optic nerve head, the lesion is localized to the visual pathway behind the eye. Lack of a homonymous visual field defect involving the other eye localizes the lesion proximal to the optic chiasm, therefore placing the lesion in the retrobulbar segment of the optic nerve consistent with the diagnosis of optic neuritis.
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