Recent-recall 3 items or a brief story

remote-ask patient about historical or verifiable personal events

Memory can be impaired on many different timescales. Impaired ability to register and recall something within a few seconds after it was said is an abnormality that blends into the category of impaired attention discussed earlier. If immediate recall is intact, then difficulty with recall after about 1 to 5 minutes usually signifies damage to the limbic memory structures located in the medial temporal lobes and medial diencephalon.  Dysfunction of these structures characteristically causes anterograde amnesia, meaning difficulty remembering new facts and events occurring after lesion onset, and retrograde amnesia, meaning impaired memory of events for a period of time immediately before lesion onset, with relative sparing of earlier memories. Loss of memory without these time characteristics may signify damage to areas other than the medial temporal and medial diencephalic structures.

Calculations, Right-Left Confusion, Finger Agnosia, Agraphia

Impairment of all four of these functions in an otherwise intact patient is referred to as Gerstmann's syndrome. Since Gerstmann's syndrome is caused by lesions in the dominant parietal lobe, aphasia is often (but not always) present as well, which can make the diagnosis difficult or impossible. Each of the individual components of Gerstmann's syndrome is poorly localizing on its own, but they are worth documenting as part of the assessment of overall cognitive function:

As we have noted, abnormality of all four of these functions that is out of proportion to other cognitive deficits is strongly localizing to the dominant (usually left) parietal lobe. Otherwise, each of the individual abnormalities can be seen in many different lesions and may be present in individuals with impaired attention, language, praxis (see the next section), constructions, logic and abstraction, and so on.

The term apraxia will be used here to mean inability to follow a motor command that is not due to a primary motor deficit or a language impairment. It is apparently caused by a deficit in higher-order planning or conceptualization of the motor task. You can test for apraxia by asking the patient to do complex tasks, using commands such as "Pretend to comb you hair" or "Pretend to strike a match and blow it out" and so on. Patients with apraxia perform awkward movements that only minimally resemble those requested, despite having intact comprehension and an otherwise normal motor exam. This kind of apraxia is sometimes called ideomotor apraxia. In some patients, rather than affecting the distal extremities, apraxia can involve primarily the mouth and face, or movements of the whole body, such as walking or turning around.

Unfortunately, the term "apraxia" has also been attached to a variety of other abnormalities—for example, "constructional apraxia" in patients who have visuospatial difficulty drawing complex figures, "ocular apraxia" in patients who have difficulty directing their gaze, "dressing apraxia" in patients who have difficulty getting dressed, and so on. It is unclear at present whether these various types of "apraxia" are related in some way, or are caused by completely different mechanisms.

Although apraxia indicates brain dysfunction, it can be caused by lesions in many different regions, so exact localization is often difficult. Apraxia is commonly present in lesions affecting the language areas and adjacent structures of the dominant hemisphere. This can make it challenging to prove that the deficit is apraxia rather than impaired language comprehension. Often we can make the distinction by asking the patient to perform a task and, if he fails, demonstrating several tasks and asking him to choose the correct one.

Neglect and Constructions

Hemineglect is an abnormality in attention to one side of the universe that is not due to a primary sensory or motor disturbance. In sensory neglect, patients ignore visual, somatosensory, or auditory stimuli on the affected side, despite intact primary sensation (see Neuroanatomy through Clinical Cases, Chapter 19). This can often be demonstrated by testing for extinction on double simultaneous stimulation. Thus, patients may detect a stimulus on the affected side when presented alone, but when stimuli are presented simultaneously on both sides, only the stimulus on the unaffected side may be detected. In motor neglect, normal strength may be present, however, the patient often does not move the affected limb unless attention is strongly directed toward it. Sensory and motor neglect are usually tested as part of the visual, auditory, somatosensory, and motor exams. During the reading and writing portions of the language exam, patients may be noted to neglect one side of the page.

During the mental status exam, certain other aspects of neglect should be screened for. Patients should be asked, "Is anything wrong with you right now?" because patients with anosognosia may be strikingly unaware of severe deficits on the affected side. For example, some patients with acute stroke who are completely paralyzed on the left side believe there is nothing wrong and may even be perplexed about why they are in the hospital. Some patients do not even comprehend that affected limbs belong to them (hemi-asomatognosia). In addition, certain drawing tasks, such as asking the patient to bisect a line or draw a clock face, can demonstrate neglect. Construction tasks involving drawing complex figures or manipulating blocks or other objects in space may be abnormal as a result of neglect or other visuospatial impairments. However, constructional abilities can also be abnormal because of other cognitive difficulties, such as impaired sequencing (see next section) or apraxia.

Hemineglect is most common in lesions of the right (nondominant) parietal lobe, causing patients to neglect the left side. Left-sided neglect can also occasionally be seen in right frontal lesions, right thalamic or basal ganglia lesions, and, rarely, in lesions of the right midbrain. In left parietal lesions a much milder neglect is usually seen affecting the patient's right side. Abnormal constructions demonstrating neglect can occur with right parietal lesions. In addition, other abnormalities in constructions can occur as well, as a result of lesions in many other parts of the brain. Generally, however, impaired visuospatial function is more severe with damage to the nondominant (right) hemisphere.

Sequencing Tasks and Frontal Release Signs

Frontal lobe lesions in adults can cause the reemergence of certain primitive reflexes that are normally present in infants. These so-called frontal release signs include the grasp, snout, root, and suck reflexes. Of these reflexes, the grasp reflex is the most useful in evaluating frontal lobe dysfunction.

Patients with frontal lobe dysfunction may have particular difficulty in changing from one action to the next when asked to perform a repeated sequence of actions. For example, when asked to continue drawing a silhouette pattern of alternating triangles and squares (written alternating sequencing task), they may get stuck on one shape and keep drawing triangles. This phenomenon is called perseveration. The Luria manual sequencing task, in which the patient is asked to tap the table with a fist, open palm, and side of open hand and then to repeat the sequence as quickly as possible, is also a useful test for perseveration.

Another common finding is motor impersistence, a form of distractibility in which patients only briefly sustain a motor action in response to a command such as "Raise your arms" or "Look to the right." Ability to suppress inappropriate behaviors can be tested by the auditory Go-No-Go test, in which the patient moves a finger in response to one sound, but must keep it still in response to two sounds.

Patients with frontal lobe lesions may also exhibit very slow responses termed abulia or may have changes in personality and judgment based on sequential exams or reported by family members.

Logic and Abstraction

Can the patients solve simple problems such as the following: "If Mary is taller than Jane, and Jane is taller than Ann, who's the tallest?" How do they interpret proverbs such as "Don't cry over spilled milk"? How well can they comprehend similarities such as "How are a car and an airplane alike?" How well can they generalize and complete a series—for example, "Continue the following: AZ BY CX D_"? A more detailed evaluation can be done, when indicated, using formal neuropsychological testing batteries. Educational background must always be taken into account in interpretations of these tests.

These functions can be abnormal in damage to a variety of brain areas involving higher-order association cortex and are not well localized.

Delusions and Hallucinations

Does the patient have any delusional thought processes? Does he have auditory or visual hallucinations? Ask questions such as, "Do you ever hear things that other people don't hear or see things that other people don't see?" "Do you feel that someone is watching you or trying to hurt you?" "Do you have any special abilities or powers?"

These abnormalities can be seen in toxic or metabolic abnormalities and other causes of diffuse brain dysfunction, and in primary psychiatric disorders. In addition, abnormal sensory phenomena can be caused by focal lesions or seizures in visual, somatosensory, or auditory cortex, and thought disorders can be caused by lesions in the association cortex and limbic system.

Does the patient have signs of depression, anxiety, or mania? Signs of major depression include depressed mood, changes in eating and sleeping patterns, loss of energy and initiative, low self-esteem, poor concentration, lack of enjoyment of previously pleasurable activities, and self-destructive or suicidal thoughts and behavior. Anxiety disorders are characterized by preoccupation with worrisome thoughts. Mania causes patients to be abnormally active and cognitively disorganized.

What is Being Tested?

These disorders are often considered psychiatric in origin and may be due to imbalances in neurotransmitter systems in several different areas of the brain. However, features of these disorders are also seen in focal brain lesions and in toxic or metabolic abnormalities such as thyroid dysfunction.

Some of the most difficult and interesting diagnostic dilemmas arise because of overlap and confusion between psychiatric and neurologic disorders. Thus, depressed patients with somatization or conversion disorders (which will be discussed later in the chapter) often have complaints such as pain, numbness, weakness, or even seizurelike activity and are therefore referred to neurologists for evaluation. Likewise, neurologic disorders such as brain tumors, strokes, metabolic derangements, and so on can produce confusional states or bizarre behavior that may be misinterpreted as psychiatric in origin.

Cranial Nerves

Perhaps more than any other part of the neurologic exam, cranial nerve testing can raise red flags that suggest specific neurologic dysfunction rather than a systemic disorder. For example, there are many medical causes of lethargy, unsteadiness, headaches, or dizziness. However, any of these symptoms together with cranial nerve abnormalities strongly suggests brainstem dysfunction as the cause (see Neuroanatomy Through Clinical Cases, Chapters 12, 13 and 14). Careful testing of the cranial nerves, therefore, can reveal crucial information to help pinpoint disorders in the nervous system.

Can the patient smell coffee or soap with each nostril? Do not use noxious odors, since they may stimulate pain fibers from CN V. CN I is often not tested unless specific pathology such as a subfrontal brain tumor is suspected.

Impairment can be due to nasal obstruction, damage to the olfactory nerves in the nasal mucosa, damage to the nerves as they cross the cribriform plate, or intracranial lesions affecting the olfactory bulbs.

Examine both retinas carefully with an ophthalmoscope.

This exam allows direct visualization of damage to the retina or retinal vessels, optic nerve atrophic changes, papilledema (see Neuroanatomy through Clinical Cases, Key Clinical Concepts 5.3), and other important abnormalities.

Visual Acuity. Test visual acuity for each eye separately (by covering one eye at a time) using an eye chart.

Color Vision. Test each eye separately for ability to distinguish colors. Test for red desaturation, a sign of subtle asymmetry in optic nerve function seen, for example, in optic neuritis (see Neuroanatomy through Clinical Cases, Key Clinical Concepts 11.4), by asking the patient to cover each eye alternately while looking at a red object and report any relative dullness of the color in one eye.

Visual Fields. Test visual fields for each eye by asking the patient to fixate straight ahead and to report when a finger can be seen moving in each quadrant. Alternatively, ask the patient to report how many fingers are being shown in each quadrant. More precise mapping of visual fields can be done in the laboratory for patients who will be followed over time (see Neuroanatomy Through Clinical Cases, Key Clinical Concepts 11.2).

Visual Extinction. Test for visual extinction on double simultaneous stimulation by asking the patients how many fingers they see when fingers are presented to both sides at the same time. In visual extinction, a form of hemineglect , patients do not report seeing the fingers on the affected (usually left) side of the visual field, although they can see fingers when they are presented to that side alone.

n comatose or uncooperative patients, visual fields can be tested roughly using blink-to-threat, in which the examiner's fingers are moved rapidly towards the patient's eyes from each quadrant to see if a blink occurs.

Damage anywhere in the visual pathway from the eye to the visual cortex can cause specific deficits in the visual fields of one or both eyes (see Neuroanatomy through Clinical Cases, Figure 11.15). Importantly, some visual information from each eye crosses to the opposite side at the optic chiasm. Therefore, lesions in front of the optic chiasm (eye, optic nerve) cause visual deficits in one eye, while lesions behind the optic chiasm (optic tract, thalamus, white matter, visual cortex) cause visual field deficits that are similar for both eyes.

Visual hemineglect or extinction is usually caused by contralateral parietal lesions, and less often by frontal or thalamic lesions. Neglect is usually more robust in lesions of the right hemisphere.

CN II, III

First, record the pupil size and shape at rest. Next, note the direct response, meaning constriction of the illuminated pupil, as well as the consensual response, meaning constriction of the opposite pupil.

In an afferent pupillary defect there is a decreased direct response caused by decreased visual function in one eye. This can be demonstrated with the swinging flashlight test, in which the light is moved back and forth between the eyes every two to three seconds. The afferent pupillary defect becomes obvious when the flashlight is moved from the normal to the affected eye, and the affected pupil dilates in response to light. Under normal conditions, the pupil constricts in response to light. Brief oscillations of pupillary size called hippus occur normally in response to light which should not be confused with an afferent pupillary defect.

Finally, test the pupillary response to accommodation. Normally, the pupils constrict while fixating on an object being moved from far away to near the eyes.

Direct response (pupil illuminated). The direct response is impaired in lesions of the ipsilateral optic nerve, the pretectal area, the ipsilateral parasympathetics traveling in CN III, or the pupillary constrictor muscle of the iris.

Consensual response (contralateral pupil illuminated). The consensual response is impaired in lesions of the contralateral optic nerve, the pretectal area, the ipsilateral parasympathetics traveling in CN III, or the pupillary constrictor muscle.

Accommodation (response to looking at something moving toward the eye). Accommodation is impaired in lesions of the ipsilateral optic nerve, the ipsilateral parasympathetics traveling in CN III, or the pupillary constrictor muscle, or in bilateral lesions of the pathways from the optic tracts to the visual cortex. Accommodation is spared in lesions of the pretectal area.

Check extraocular movements (eye movements) by having the patient look in all directions without moving their head and ask them if they experiences any double vision. Test smooth pursuit by having the patient follow an object moved across their full range of horizontal and vertical eye movements. Test convergence movements by having the patient fixate on an object as it is moved slowly towards a point right between the patient's eyes. Also, observe the eyes at rest to see if there are any abnormalities such as spontaneous nystagmus (see below)or dysconjugate gaze (eyes not both fixated on the same point) resulting in diplopia (double vision).

Saccades are eye movements used to rapidly refixate from one object to another. The examiner can test saccades by holding two widely spaced targets in front of the patient (such as the examiner's thumb on one hand and index finger on the other) and asking the patient to look back and forth between the targets.

Test optokinetic nystagmus (OKN) by moving a strip with parallel stripes on it in front of the patient's eyes and asking them to watch the stripes go by. Normally, rhythmic eye movements called nystagmus occur consisting of an alternating slow phase with slow pursuit movements in the direction of strip movement, and a rapid phase with quick refixations back to midline.

In comatose or severely lethargic patients, the vestibulo-ocular reflex can be used to test whether brainstem eye movement pathways are intact. The oculocephalic reflex, a form of the vestibulo-ocular reflex, is tested by holding the eyes open and rotating the head from side to side or up and down. These maneuvers obviously should not be performed in cases of head injury or other cases of suspected cervical spine trauma unless complete cervical spine films are normal. The reflex is present if the eyes move in the opposite direction of the head movements, and it is therefore sometimes called doll's eyes. Note that in awake patients, doll's eyes are usually not present because voluntary eye movements mask the reflex. Thus, the absence of doll's eyes suggests brainstem dysfunction in the comatose patient but can be normal in the awake patient. Another, more potent stimulus of the vestibulo-ocular reflex used to evaluate comatose patients is caloric stimulation (see Neuroanatomy Through Clinical Cases, Chapter 3).

Careful testing can often identify abnormalities in individual muscles or in particular cranial nerves (oculomotor, trochlear, or abducens) in their course from the brainstem to the orbit, in the brainstem nuclei, or finally, in the higher-order centers and pathways in the cortex and brainstem that control eye movements (for more details, see Neuroanatomy Through Clinical Cases, Chapter 14). Spontaneous nystagmus can indicate toxic or metabolic conditions such as drug overdose or alcohol intoxication, or peripheral or central vestibular dysfunction.

Facial Sensation and Muscles of Mastication (CN V)

Test facial sensation using a cotton wisp and a sharp object. Also test for tactile extinction using double simultaneous stimulation.

The corneal reflex, which involves both CN V and CN VII, is tested by touching each cornea gently with a cotton wisp and observing any asymmetries in the blink response.

Feel the masseter muscles during jaw clench. Test for a jaw jerk reflex by gently tapping on the jaw with the mouth slightly open.

Facial sensation can be impaired by lesions of the trigeminal nerve (CN V), the trigeminal sensory nuclei in the brainstem, or ascending sensory pathways to the thalamus and somatosensory cortex in the postcentral gyrus (see Neuroanatomy through Clinical Cases, Chapters 7 and 12). The corneal blink reflex is mediated by polysynaptic connections in the brainstem between the trigeminal (CN V) and facial (CN VII) nerves and can be impaired by lesions anywhere in this circuit.

Extinction in the presence of intact primary sensation is usually caused by right parietal lesions.

Weakness of the muscles of mastication can be due to lesions in the upper motor neuron (UMN) pathways synapsing onto the trigeminal (CN V) motor nucleus, in the lower motor neurons (LMNs) of the trigeminal motor nucleus in the pons or as they exit the brainstem to reach the muscles of mastication, in the neuromuscular junction, or in the muscles themselves.

Presence of a jaw jerk reflex is abnormal, especially if it is prominent. It is a sign of hyperreflexia associated with lesions of UMN pathways projecting to the trigeminal motor nucleus. Both the afferent and the efferent limbs of the jaw jerk reflex are mediated by CN V.

Muscles of Facial Expression and Taste (CN VII)

Look for asymmetry in facial shape or in depth of furrows such as the nasolabial fold. Also look for asymmetries in spontaneous facial expressions and blinking. Ask patient to smile, puff out their cheeks, clench their eyes tight, wrinkle their brow, and so on. Old photographs of the patient can often aid your recognition of subtle changes.

Check taste with sugar, salt, or lemon juice on cotton swabs applied to the lateral aspect of each side of the tongue. Like olfaction, taste is often tested only when specific pathology is suspected, such as in lesions of the facial nerve, or in lesions of the gustatory nucleus (nucleus solitarius).

Facial weakness can be caused by lesions of upper motor neurons in the contralateral motor cortex or descending central nervous system pathways, lower motor neurons in the ipsilateral facial nerve nucleus (CN VII) or exiting nerve fibers, the neuromuscular junction, or the face muscles. Note that the upper motor neurons for the upper face (the upper portions of the orbicularis oculi and the frontalis muscles of the forehead) project to the facial nuclei bilaterally (see Neuroanatomy Through Clinical Cases, Figure 12.12). Therefore, upper motor neuron lesions, such as a stroke, cause contralateral face weakness sparing the forehead, while lower motor neuron lesions, such as a facial nerve injury, typically cause weakness involving the whole ipsilateral face.

Hearing and Vestibular Sense (CN VIII)

Hearing. Can the patient hear fingers rubbed together or words whispered just outside of the auditory canal and identify which ear hears the sound? A tuning fork can be used to distinguish neural from mechanical conductive hearing problems. In the Rinne test the sound heard when holding a vibrating tuning fork just outside each ear (air conduction), is compared to the sound heard when placing the tuning fork handle on each mastoid process (bone conduction). Normal individuals will hear the tone better by air conduction. In conductive hearing loss, bone conduction is greater than air conduction, because bone conduction bypasses problems in the external or middle ear. In sensorineural hearing loss, air conduction is greater than bone conduction in both ears (as in normal hearing), however, hearing is decreased in the affected ear. In the Weber test, the tuning fork is placed on the vertex of the skull in the midline, and the patient is asked to report the side where the tone sounds louder. Normally, the tone sounds equal on both sides. In sensorineural hearing loss, the tone is louder on the normal side. In conductive hearing loss, the tone is louder on the affected side. You can verify that the tone is louder on the side of conductive hearing loss on yourself by closing each ear alternately while humming.

Vestibular Sense. Vestibular sense is generally not specifically tested, except for in the following important situations:

Patients with vertigo. Barany or Hall-Pike positional testing can help distinuish peripheral from central causes of vertigo. The patient sits on the bed or examining table, and the examiner supports the patient's head as the patient lays back with one ear down, and with the head extending over the edge of the table. This maneuver does not need to be done especially briskly. The patient is asked to keep their eyes open and report any sensations of vertigo, while the examiner looks for nystagmus . This change of position causes maximal stimulation of the posterior semicircular canal of the ear that is down, and of the anterior semicircular canal of the ear that is up. The maneuver is also done with the other ear down. With peripheral lesions, there is usually a delay of a few seconds before the onset of nystagmus and vertigo. The nystagmus is horizontal or rotatory and does not change directions. Nystagmus and vertigo then fade away within about a minute. If the same maneuver is repeated, there is often adaptation, so that the nystagmus and vertigo are briefer and less intense each time. In contrast, with central lesions, the nystagmus and vertigo may begin immediately, and there tends to be no adaptation. Horizontal or rotatory nystagmus can also be seen with central lesions. However, vertical nystagmus, nystagmus that changes directions, or prominent nystagmus in the absence of vertigo are seen only in central, and not in peripheral lesions.

Patients with limitations of horizontal or vertical gaze. Testing the vestibulo-ocular reflex can help localize the lesion (see Neuroanatomy through Clinical Cases, Chapter 13). As we mentioned when discussing Extraocular Muscles the vestibulo-ocular reflex can be tested in two ways. The first is using the oculocephalic maneuver, in which the eyes are held open and the head is turned rapidly either from side to side or up and down. The second is using caloric testing, in which cold or warm water is instilled into one ear, producing asymmetric stimulation of the semicircular canals.

Patients in coma. The vestibulo-ocular reflex is often the only way to test eye movements in these patients.

What is Being Tested?

Hearing loss can be caused by lesions in the acoustic and mechanical elements of the ear, the neural elements of the cochlea, or the acoustic nerve (CN VIII). After the hearing pathways enter the brainstem, they cross over at multiple levels and ascend bilaterally to the thalamus and auditory cortex. Therefore, clinically significant unilateral hearing loss is invariably caused by peripheral neural or mechanical lesions. Abnormalities in vestibular testing can be associated with lesions in the vestibular apparatus of the inner ear, the vestibular portion of CN VIII, the vestibular nuclei in the brainstem, the cerebellum, or pathways in the brainstem (such as the medial longitudinal fasciculus) that connect the vestibular and oculomotor systems.

Palate Elevation and Gag Reflex (CN IX, X)

Does the palate elevate symmetrically when the patient says, "Aah"? Does the patient gag when the posterior pharynx is brushed? The gag reflex needs to be tested only in patients with suspected brainstem pathology, impaired consciousness, or impaired swallowing.

What is Being Tested?

Palate elevation and the gag reflex are impaired in lesions involving CN IX, CN X, the neuromuscular junction, or the pharyngeal muscles.

Muscles of Articulation (CN V, VII, IX, X, XII)

Is the patient's speech hoarse, slurred, quiet, breathy, nasal, low or high pitched, and so on? It is often important to ask if the patient's speech has changed from baseline. Note that dysarthria, or abnormal pronunciation of speech, is not the same as aphasia, which is an abnormality in language production or comprehension.

Abnormal articulation of speech can occur in lesions involving the muscles of articulation, the neuromuscular junction, or the peripheral or central portions of CN V, VII, IX, X, or XII. Furthermore, speech production can be abnormal as a result of lesions in the motor cortex, cerebellum, basal ganglia, or descending pathways to the brainstem.

Sternocleidomastoid and Trapezius Muscles (CN XI)

Ask the patient to shrug their shoulders, turn their head in both directions, and raise their head from the bed, flexing forward against the force of your hands.

Weakness in the sternocleidomastoid or trapezius muscles can be caused by lesions in the muscles, neuromuscular junction, or lower motor neurons of the accessory spinal nerve (CN XI). Unilateral upper motor neuron lesions in the cortex or descending pathways cause contralateral weakness of the trapezius, with relative sparing of sternocleidomastoid strength. This may be explained by bilateral upper motor neuron projections controlling the sternocleidomastoid, in analogy to the bilateral projections controlling the upper face.

Tongue Muscles (CN XII)

Note any atrophy or fasciculations (spontaneous quivering movements caused by firing of muscle motor units) of the tongue while it is resting on the floor of the mouth. Ask the patient to stick their tongue straight out and note whether it curves to one side or the other. Ask the patient to move their tongue from side to side and push it forcefully against the inside of each cheek.

Fasciculations and atrophy are signs of lower motor neuron lesions. Unilateral tongue weakness causes the tongue to deviate toward the weak side. Tongue weakness can result from lesions of the tongue muscles, the neuromuscular junction, the lower motor neurons of the hypoglossal nerve (CN XII), or the upper motor neurons originating in the motor cortex. Lesions of the motor cortex cause contralateral tongue weakness.

Motor Exam

The motor exam has several steps including 1. Observation, 2. Inspection, 3. Palpation, 4. Muscle tone testing, 5. Functional testing, and 6. Strength testing of individual muscle groups. Each of these steps will now be discussed in turn.

First, carefully observe the patient to detect any twitches, tremors, or other involuntary movements, as well as any unusual paucity of movement suggestive of a movement disorder (see Neuroanatomy Through Clinical Cases, Key Clinical Concepts 15.2, and 16.1). Note also the patient's posture. Next inspect several individual muscles to see if muscle wasting, hypertrophy, or fasciculations (spontaneous quivering movements caused by firing of muscle motor units) are present. The best muscles to look at for fasciculations in generalized LMN disorders are the intrinsic hand muscles, shoulder girdle, and thigh. In cases of suspected myositis, palpate the muscles to see if there is tenderness.

Next test muscle tone. Ask the patient to relax, and then passively move each limb at several joints to get a feeling for any resistance or rigidity that may be present.

Before formally testing strength in each muscle, it is useful to do a few general functional tests that help detect subtle abnormalities. Check for drift by having the patient hold up both arms or both legs and close their eyes. Check fine movements by testing rapid finger tapping, rapid hand pronation—supination (as in screwing in a light bulb), rapid hand tapping, and rapid foot tapping against the floor or other object.

Finally, test the strength of each muscle group and record it in a systematic fashion (see next section).

What is Being Tested?

Involuntary movements and tremors are commonly associated with lesions of the basal ganglia or cerebellum (see Neuroanatomy Through Clinical Cases, Key Clinical Concepts 15.2, and 16.1). Tremors can also occasionally be seen with peripheral nerve lesions.

Many parts of the motor exam can help distinguish between upper motor neuron and lower motor neuron lesions (see Neuroanatomy through Clinical Cases Chapters 2 and 6). Recall that upper motor neurons project via the corticospinal tract to lower motor neurons located in the anterior horn of the spinal cord. Signs of lower motor neuron lesions include weakness, atrophy, fasciculations, and hyporeflexia (reduced reflexes). Signs of upper motor neuron lesions include weakness, hyperreflexia (increased reflexes), and increased tone. The hyperreflexia and increased tone seen with corticospinal lesions is apparently caused by damage to pathways that travel in close association with the corticospinal tract rather than directly by damage to the corticospinal tract itself. Note that with acute upper motor neuron lesions there is often flaccid paralysis with decreased tone and decreased reflexes. With time (hours to weeks), increased tone and hyperreflexia usually develop.

Increased tone can occur in upper motor neuron lesions, but can also occur in basal ganglia dysfunction (see Neuroanatomy Through Clinical Cases, Key Clinical Concept 16.1). In addition, slow or awkward fine finger movements or toe tapping in the absence of weakness can signify a subtle abnormality of the corticospinal pathways, but can also occur in lesions of the cerebellum or basal ganglia.

Strength of Individual Muscle Groups

Patterns of weakness can help localize a lesion to a particular cortical or white matter region, spinal cord level, nerve root, peripheral nerve, or muscle. Test the strength of each muscle group and record it in a systematic fashion. It is wise to pair the testing of each muscle group immediately with testing of its contralateral counterpart to enhance detection of any asymmetries. Muscle strength is often rated on a scale of 0/5 to 5/5 as follows:

• 0/5: no contraction
• 1/5: muscle flicker, but no movement
• 2/5: movement possible, but not against gravity (test the joint in its horizontal plane)
• 3/5: movement possible against gravity, but not against resistance by the examiner
• 4/5: movement possible against some resistance by the examiner (sometimes this category is subdivided further into 4^–/5, 4/5, and 4⁺/5)
• 5/5: normal strength

While testing muscle strength, it is important to keep in mind anatomic information such as which nerves, nerve roots, and brain areas control each muscle and to allow this information to guide the exam. Also compare proximal versus distal weakness because these features can sometimes suggest muscle versus nerve disease, respectively. A detailed discussion of patterns of muscle weakness and localization is provided in Neuroanatomy through Clinical Cases Key Clinical Concepts 6.3, and in Chapters 8 and 9. In the tables below we briefly summarize some of the main actions, muscle groups, peripheral nerves, and nerve roots tested during the motor exam.

Upper Extremity Strength Testing

Lower Extremity Strength Testing

When more than one nerve root participates in an action, emphasis indicates the most important nerve roots.

Deep Tendon Reflexes

Check the deep tendon reflexes using impulses from a reflex hammer to stretch the muscle and tendon. The limbs should be in a relaxed and symmetric position, since these factors can influence reflex amplitude. As in muscle strength testing, it is important to compare each reflex immediately with its contralateral counterpart so that any asymmetries can be detected. If you cannot elicit a reflex, you can sometimes bring it out by certain reinforcement procedures. For example, have the patient gently contract the muscle being tested by raising the limb very slightly, or have them concentrate on forcefully contracting a different muscle group just at the moment when the reflex is tested. When reflexes are very brisk, clonus is sometimes seen. This is a repetitive vibratory contraction of the muscle that occurs in response to muscle and tendon stretch. Deep tendon reflexes are often rated according to the following scale:

• 0: absent reflex
• 1⁺: trace, or seen only with reinforcement
• 2⁺: normal
• 3⁺: brisk
• 4⁺: nonsustained clonus (i.e., repetitive vibratory movements)
• 5⁺: sustained clonus

Deep tendon reflexes are normal if they are 1⁺, 2⁺, or 3⁺ unless they are asymmetric or there is a dramatic difference between the arms and the legs. Reflexes rated as 0, 4⁺, or 5⁺ are usually considered abnormal. In addition to clonus, other signs of hyperreflexia include spreading of reflexes to other muscles not directly being tested and crossed adduction of the opposite leg when the medial aspect of the knee is tapped.

Deep tendon reflexes (see Neuroanatomy Through Clinical Cases, Figure 2.21) may be diminished by abnormalities in muscles, sensory neurons, lower motor neurons, and the neuromuscular junction; acute upper motor neuron lesions; and mechanical factors such as joint disease. Abnormally increased reflexes are associated with upper motor neuron lesions. Note that deep tendon reflexes can be influenced by age, metabolic factors such as thyroid dysfunction or electrolyte abnormalities, and anxiety level of the patient. The main spinal nerve roots involved in testing the deep tendon reflexes are summarized in the following table:

Deep Tendon Reflexes

Plantar Response

Finger Flexors

There is no precise hand equivalent for the plantar response, however, finger flexor reflexes can help demonstrate hyperreflexia in the upper extremities. Test finger flexors by tapping gently on the palm with the reflex hammer. Alternatively, heightened reflexes can be demonstrated by the presence of Hoffmann's sign. You can elicit this sign by holding the patient's middle finger loosely and flicking the fingernail downward, causing the finger to rebound slightly into extension. If the thumb flexes and adducts in response, Hoffmann's sign is present.

Babinski's sign is associated with upper motor neuron lesions anywhere along the corticospinal tract. Note that it may not be possible to elicit Babinski's sign if there is severe weakness of the toe extensors. Hoffmann's sign, or heightened finger flexor reflexes suggest an upper motor neuron lesion affecting the hands.

Reflexes Tested in Special Situations

Coordination and Gait

Coordination and gait are usually described under a separate section because cerebellar disorders can disrupt coordination or gait while leaving other motor functions relatively intact. There is much overlap, however, between the systems being examined in this section and those examined in the earlier general motor exam section. Keep in mind that disturbances of coordination and gait can be caused by lesions in many systems other than the cerebellum.

The term ataxia is often used to describe the abnormal movements seen in coordination disorders. In ataxia there are medium- to large-amplitude involuntary movements with an irregular oscillatory quality superimposed on and interfering with the normal smooth trajectory of movement. Overshoot is also commonly seen as part of ataxic movements and is sometimes referred to as past pointing when target-oriented movements are being discussed. Another feature of coordination disorders is dysdiadochokinesia—that is, abnormal alternating movements.

Cerebellar lesions can cause different kinds of coordination problems depending on their location. One important distinction is between truncal ataxia and appendicular ataxia. Appendicular ataxia affects movements of the extremities and is usually caused by lesions of the cerebellar hemispheres and associated pathways. Truncal ataxia affects the proximal musculature, especially that involved in gait stability, and is caused by midline damage to the cerebellar vermis and associated pathways

Appendicular Coordination

Fine movements of the hands and feet, as discussed earlier under the general motor exam, should be tested. Rapid alternating movements, such as wiping one palm alternately with the palm and dorsum of the other hand, should be tested as well. Perhaps the most popular test of coordination, however, is the finger—nose—finger test, in which the patient is asked to alternately touch their nose and the examiner's finger as quickly as possible. Ataxia is best revealed if the examiner's finger is held at the extreme of the patient's reach, and if the examiner's finger is occasionally moved suddenly to a different location. Test for overshoot by having the patient raise both arms suddenly from their lap to the level of your hand. In addition, you can apply pressure to the patient's outstretched arms and then suddenly release it. To test the accuracy of movements in a way that requires very little strength, you can draw a line on the crease of the patient's thumb and then ask the patient to touch the line repeatedly with the tip of their forefinger.

Similar tests can be done with the legs. In the heel—shin test the patient is asked to touch the heel of one foot to the opposite knee and then to drag their heel in a straight line all the way down the front of their shin and back up again. In order to eliminate the effect of gravity in moving the heel down the shin, this test should always be done in the supine position.

Normal performance of these motor tasks depends on the integrated functioning of multiple sensory and motor subsystems. These include position sense pathways, lower motor neurons, upper motor neurons, the basal ganglia, and the cerebellum. Thus, in order to convincingly demonstrate that abnormalities are due to a cerebellar lesion, one must first test for normal joint position sense, strength, and reflexes and confirm the absence of involuntary movements caused by basal ganglia lesions. As already mentioned, appendicular ataxia is usually caused by lesions of the cerebellar hemispheres and associated pathways, while truncal ataxia (see Romberg Test and Gait ) is often caused by damage to the midline cerebellar vermis and associated pathways

Romberg Test

Ask the patient to stand with their feet together (touching each other). Then ask the patient to close their eyes. Remain close at hand in case the patient begins to sway or fall.

With the eyes open, three sensory systems provide input to the cerebellum to maintain truncal stability. These are vision, proprioception, and vestibular sense. If there is a mild lesion in the vestibular or proprioception systems, the patient is usually able to compensate with the eyes open. When the patient closes their eyes, however, visual input is removed and instability can be brought out. If there is a more severe proprioceptive or vestibular lesion, or if there is a midline cerebellar lesion causing truncal instability, the patient will be unable to maintain this position even with their eyes open. Note that instability can also be seen with lesions in other parts of the nervous system such as the upper or lower motor neurons or the basal ganglia, so these should be tested for separately in other parts of the exam.

A patient's gait can be difficult to describe in a reproducible fashion. Observe the patient walking toward you and away from you in an open area with plenty of room. Note stance (how far apart the feet are), posture, stability, how high the feet are raised off the floor, trajectory of leg swing and whether there is circumduction (an arced trajectory in the medial to lateral direction), leg stiffness and degree of knee bending, arm swing, tendency to fall or swerve in any particular direction, rate and speed, difficulty initiating or stopping gait, and any involuntary movements that are brought out by walking. Turns should also be observed closely. When following a patient over several visits, it may be useful to time him walking a fixed distance, and to count the number of steps he took and the number of steps he required to turn around. The patient's ability to rise from a chair with or without assistance should also be recorded.

To bring out abnormalities in gait and balance, ask the patient to do more difficult maneuvers. Test tandem gait by asking the patient to walk a straight line while touching the heel of one foot to the toe of the other with each step. Patients with truncal ataxia caused by damage to the cerebellar vermis or associated pathways will have particular difficulty with this task, since they tend to have a wide-based, unsteady gait, and become more unsteady when attempting to keep their feet close together. To bring out subtle gait abnormalities or asymmetries, it may be appropriate in some cases to ask the patient to walk on their heels, their toes, or the insides or outsides of their feet, to stand or hop on one leg, or to walk up stairs.

Gait apraxia is a perplexing (and somewhat controversial) abnormality in which the patient is able to carry out all of the movements required for gait normally when lying down, but is unable to walk in the standing position, thought to be associated with frontal disorders or normal pressure hydrocephalus

As with tests of appendicular coordination, gait involves multiple sensory and motor systems. These include vision, proprioception, lower motor neurons, upper motor neurons, basal ganglia, the cerebellum, and higher-order motor planning systems in the association cortex. Once again, it is important to test each of these systems for normal function before concluding that a gait disturbance is caused by a cerebellar lesion.

Sensory Exam

Primary sensation - asymmetry, sensory level

Light touch is best tested with a cotton-tipped swab, but a light finger touch will often suffice, as long as care is taken to make the stimulus fairly reproducible. You can test the relative sharpness of pain by randomly alternating stimuli with the sharp or dull end of a safety pin (always use a new pin for each patient).

Temperature sensation can be tested with a cool piece of metal such as a tuning fork.

Test vibration sense by placing a vibrating tuning fork on the ball of the patient's right or left large toe or fingers and asking him to report when the vibration stops. Take care not to place the tuning fork on a bone, since bones conduct the vibration to much more proximal sites, where they can be detected by nerves far from the location being tested.

Test joint position sense by moving one of the patient's fingers or toes up and down and asking the patient to report which way it moves. Hold the digit lightly by the sides while doing this so that tactile inputs don't provide significant clues to the direction of movement. The digit should be moved very slightly because normal individuals can detect movements that are barely perceptible by eye.

Two-point discrimination can be tested with a special pair of calipers, or a bent paper clip, alternating randomly between touching the patient with one or both points. The minimal separation (in millimeters) at which the patient can distinguish these stimuli should be recorded in each extremity.

As in other parts of the exam, the patient's deficits, as well as the anatomy of the nerves, nerve roots, and central pathways, should be used to guide the exam (see Neuroanatomy through Clinical Cases Chapters 7, 8, and 9). Comparisons should be made from one side of the body to the other and from proximal to distal on each extremity. Note especially if there is a sensory level corresponding to a particular spinal segment below which sensation abruptly changes, since such a change may indicate a spinal cord lesion requiring emergency intervention. Whenever there are uncertainties in the sensory exam, or other parts of the exam, a good strategy is to repeat the relevant portions of the exam several times.

Cortical Sensation, Including Extinction

Higher-order aspects of sensation, or cortical sensation, should be tested as well. To test graphesthesia, ask the patient to close their eyes and identify letters or numbers that are being traced onto their palm or the tip of their finger. To test stereognosis, ask the patient to close their eyes and identify various objects by touch using one hand at a time. Test also for tactile extinction on double simultaneous tactile stimulation. Note that graphesthesia, stereognosis, and extinction cannot reliably be tested for unless primary sensation is intact bilaterally.

What is Being Tested?

Somatosensory deficits can be caused by lesions in peripheral nerves, nerve roots, the posterior columns or anterolateral sensory systems in the spinal cord or brainstem, the thalamus, or sensory cortex. Recall that position and vibration sense ascend in the posterior column pathway and cross over in the medulla, while pain and temperature sense cross over shortly after entering the spinal cord and then ascend in the anterolateral pathway.  Intact primary sensation with deficits in cortical sensation such as agraphesthesia or astereognosis suggests a lesion in the contralateral sensory cortex. Note, however, that severe cortical lesions can cause deficits in primary sensation as well. Extinction with intact primary sensation is a form of hemineglect that is most commonly associated with lesions of the right parietal lobe. Extinction can also be seen in right frontal or subcortical lesions, or sometimes in left hemisphere lesions causing mild right hemineglect.

The pattern of sensory loss can provide important information that helps localize lesions to particular nerves, nerve roots, and regions of the spinal cord, brainstem, thalamus, or cortex (see Neuroanatomy Through Clinical Cases, Key Clinical Concept 7.3).

In the era of modern neuroimaging methods, the neurologic exam remains an essential diagnostic tool. It is a critical way station in the clinical decision making process, dictating whether imaging studies or other tests are required. In addition, the neurologic exam enables the clinician to decide what regions should be imaged, and when emergency therapeutic interventions are needed prior to any diagnostic tests. By understanding how to perform and interpret the neurologic exam, health care professionals in all specialties can help preserve the functioning of the nervous system, vastly improving patient quality of life.