1 What is the purpose of the neurologic exam?

To localize lesions—that is, to identify the precise site of damage. This is rooted in the eloquence of the nervous system (i.e., the unique property that the brain, spinal cord, and peripheral nerves have of “talking to us”) insofar as each section performs such a discrete function that any loss can be easily traced back to its level. Hence, neuro signs (and symptoms) accurately localize lesions. And this also is why the neuro exam is the bedside tool with the highest sensitivity, specificity, and likelihood ratios. Yet, in contrast to other parts of the exam where inspection or palpation are key, the neurologic exam relies on deductive skills and specific maneuvers. Hence, it is difficult to perform but rewarding. It also is long—at least 1 solid hour.

2 What are the most important components of the neurologic exam?

3 What is dementia?

An acquired and persistent cognitive impairment that compromises multiple domains of intellectual function (such as memory, language, etc.—basically, awareness [i.e., the content of consciousness]) while preserving instead perception and arousal (i.e., the level of consciousness). Hence dementia is not coma. Dementia is not delirium either, since this is instead an acute and often reversible confusional state seen in 20% of elderly patients hospitalized for intercurrent illnesses. Dementia is painfully common, affecting 3–11% of adults older than 65, and its prevalence does increase with aging, so that one third of subjects older than 80 (and one half of those older than 90) will eventually suffer from it—something to look forward to. It can be toxic, metabolic, degenerative, inflammatory, infective, or vascular. The earliest signs are often subtle, usually involving short-term memory but otherwise sparing the bulk of the exam. As the disease progresses, frontal release signs appear.

4 What are frontal release signs?

They are the reemergence of primitive reflexes (i.e., signs that are normally present in infants, but resurface in adults only as a result of diffuse frontal lobe disease). Release signs/reflexes include snouting, rooting, sucking, and grasping. Of these, the most sensitive is grasping. To elicit it, place your index and middle fingers in the patient’s palm, apply some pressure, and then slowly withdraw them between the patient’s thumb and index finger. An abnormal response (involuntary squeezing of the examiner’s fingers—with no habituation after three successive strokes) strongly argues for a lesion in the frontal lobes or the deep nuclei and subcortical white matter. Though not too sensitive (13%), it has specificity close to 100%. Contrary to other primitive reflexes (such as palmomental or glabellar), grasp is never seen in normal subjects.

5 What are the snouting, rooting, and sucking reflexes?

6 What is the palmomental reflex?

A brief and involuntary contraction of the ipsilateral mentalis muscle, wrinkles and pushes-up the chin boss, while at the same time curving the lower lip upward in an inverted “U.” This is elicited by stroking the patient’s palm (thenar eminence) with a blunt object, from proximal to distal. As a release sign, it is often seen in Parkinson’s (where it correlates with degree of akinesia), but also in 3–70% of older normal individuals. Note that the muscle is called “mentalis,” because its voluntary contraction is often associated with thinking or concentration. Its nerve supply is provided by the facialis (CN VII).

7 What is the glabellar reflex?

Another primitive (or “release”) reflex, very much like the grasp and palmomental. It involves V and VII, and is elicited by repetitively tapping on the patient’s glabella (between the eyebrows). The normal response is a brief contraction of the orbicularis, producing a few blinks after the initial taps that stop after subsequent taps—usually fewer than five. In cases of frontal release, there is instead no habituation. Hence, blinking persists as long as tapping continues. This occurs in late extrapyramidal disorders (Parkinson), but also in 3–33% of older normal subjects.

8 How do you separate “normal” primitive reflexes from the pathologic ones?

By judging them like people: by the company they keep. Hence, a “normal” palmomental or glabellar reflex will occur in subjects with otherwise a normal neurologic exam. Thus, they will be isolated. In fact, only fewer than 12% of normal individuals have two primitive reflexes, and fewer than 2% have three. Moreover, normal primitive reflexes tend to fade with repetition (i.e., they are fatigable). Only 1% of “normal” subjects will continue to exhibit a palmomental reflex after five stimulations. In contrast, patients with real pathology have no habituation.

9 How long does it take to do a complete mental status examination?

It can take hours and even days. Yet, for clinical purposes the crucial components can be tested rather quickly. These include (1) level of consciousness, (2) orientation, (3) registration, (4) memory (recall), (5) attention and calculation, (7) intelligence, and (6) language.

10 What are the most important levels of consciousness? How do they deteriorate?

There are four levels of consciousness. In increasing degree of deterioration they are:

11 What is orientation? How do you assess it?

Orientation is the patients’ cognizance of their status in time, place, and person. To assess it, ask them to state the year/date/day/month of interview, their location, and their name (state/county/city/hospital/floor). In organic diseases, the sense of time is the first to be lost, while the sense of person is the last one. Hence, patients who are oriented to time and place but do not know who they are tend to be more psychologic than organic.

12 What is memory? How do you assess it?

Memory is the ability to register and recall prior sensory input. For testing purposes:

Most normal subjects can remember three objects after a brief distraction (recent memory). Acute encephalopathies impair all aspects of memory (both recent and remote). Dementia disrupts instead recent memory and attention span, while preserving remote memory.

13 How do you assess attention and calculation?

By spelling “world” backward or doing serial 7’s (i.e., counting backward from 100, in installments of 7, and ending after five subtractions—that is, at 65).

14 How can one efficiently examine all aspects of mental status?

Through a battery of carefully analyzed and validated questions, such as the Folstein Mini Mental Status Examination (MMSE). This consists of 11 items that can be easily administered in 5–10 minutes and are either sensitive for dementia (but not specific), or specific but not sensitive. They evaluate the most important mental status domains (orientation, registration, attention/calculation, recall, and language), with a final score of 0–30 (<23 being abnormal).

15 How reliable is the MMSE in assessing cognitive function?

Quite reliable. In fact, it has strong likelihood ratios for identifying dementia impairments. It is also valuable for follow-up, even though only significant for large changes (>4    points).

16 What is the clock-drawing test?

Another mental status test. It provides patients with a preprinted circle (4    inches in diameter), asking them to “draw a clock.” No further instruction and unlimited time are given. Normal subjects will draw all 12 numbers, even though not necessarily with proper hands or symmetric spaces between them. Missing one number is still acceptable, but absent figures, irrelevant figures, or unusual arrangements/counterclockwise orientation of figures are not. An abnormal clock-drawing test has high specificity for dementia, but low sensitivity (being positive in only 50% of patients).

17 How do you test for delirium?

By looking for (1) acute and fluctuating change in mental status; (2) difficulty in staying focused or keeping track of what is being said; (3) altered level of consciousness (both in defect and in excess); and (4) disorganized thinking, with flights of ideas, often irrelevant and illogical. Hence, delirious patients exhibit a change in both mental status and the ability to stay focused. They also may have disorganized thinking or altered level of consciousness.

18 What is intelligence? How do you test it?

Intelligence is the ability to problem-solve by applying previous knowledge to a new situation and then using reason. It can be tested through calculations (serial 7 calculations), vocabulary, fund of knowledge, abstraction (use of proverbs), and judgment (like what to do with a found wallet).

19 What are the components of language? How do you assess them?

Language involves not only speech (verbal language), but also comprehension (of what is being spoken to you), reading, and writing. Hence, the ability to use language is one of the most complex functions of the human brain, whose correct assessment must test all of its aspects. Speech impairments include dysphonia, dysarthria, and aphasia.

20 What is dysphonia?

Dysphonia is difficulty in phonation. The voice is usually hoarse, but in the most severe cases, it may be altogether absent (aphonia, mutism). Causes include laryngitis (common cold), hypothyroidism (thickening of the vocal cords from myxedematous deposits), unilateral recurrent laryngeal nerve paralysis, and lesions of the vagus nerve. Reading, writing, and understanding are intact.

21 What is dysarthria?

From the Greek dys (difficulty) and arthros (articulation), this is a speech disturbance characterized by difficulty in articulating sounds and words. Hence, the quality of speech is impaired and typically slurred, but its content remains intact. Dysarthria is a motor impairment with intact cortical/subcortical language capacity. It usually results from paralysis/spasticity of the muscles of phonation (pharyngeal, palatal, lingual, or facial), but also can be observed in cerebellar disease or simple emotional stress. Contrary to most types of aphasia, dysarthria (and mutism) preserves the capacity to read, write, and understand speech.

22 What is cerebellar speech?

Another disorder of articulation of sound, rather than ideation or perception (ataxic speech).

23 Beside cerebellar speech, what are the two most important types of dysarthria?

Table 19-1 Dysarthria and Possible Cranial Nerve Involvement

24 What is aphasia?

From the Greek aphatos (speechless), this is an acquired disturbance of language, including its production and comprehension. Hence, it should not be confused with mutism (the inability to produce sounds) or dysarthria (the weakness/incoordination of speech muscles). In both of these cases, the problem is in the “machinery” of language, not in its ideation or comprehension.

25 What are the most important defects in aphasia?

26 What are the clinical differences between fluent and nonfluent aphasia?

id=”p0300″/>Pearl. Wernicke’s aphasia is fluent, with impaired repetition and impaired comprehension. Broca’s aphasia is instead nonfluent, with impaired repetition and intact comprehension.

27 Summarize the common aphasias

See Table 19-2.

Table 19-2 Common Aphasias

28 Who was Broca?

Pierre P. Broca (1824–1880) was a French surgeon with a prolific career in medicine and neurology. A pioneer in many areas, he described rickets as a nutritional disorder before Virchow, Duchenne’s dystrophy before Duchenne, and even the use of hypnotism as a surgical adjuvant. He also was responsible for introducing to France the use of the microscope for cancer diagnosis. An anthropologist with Darwinian sympathies, Broca founded the first Anthropological Society of France and his own anthropological institute. He married the daughter of Dr. Lugol (of Lugol iodine fame) and died at 56 of myocardial infarction.

29 Who was Wernicke?

Karl Wernicke (1848–1905) was a German physician born in what is now Poland. A graduate of Breslau (now the Polish Wroclaw), he described his aphasia in a book written when he was only 26. His interest in localizing lesions was then summarized (sort of) in a three-volume textbook published in 1881, which also contained the description of an encephalopathy caused by alcoholic thiamine deficiency (ataxia, confusion, nystagmus, ophthalmoplegia, and peripheral neuritis). This was later redubbed Wernicke’s encephalopathy (with Korsakoff describing instead the psychotic manifestations of the disease). A cold and aloof man, Wernicke died also at 56, of injuries reported while biking in the Thuringian forest.

30 What is perserveration?

The difficulty in performing a repeated sequence of actions. Frontal lobe patients, for example, cannot switch easily from one task to the next. Instead, they perseverate. For example, when asked to draw a silhouette pattern of alternating triangles and squares, they get stuck on one shape and draw only triangles or squares. A good test of perseveration is Luria’s manual sequencing task, wherein patients are asked to tap sequentially the table with a fist, then an open palm, and finally the side of the open hand. Frontal lobe patients cannot rapidly repeat the sequence.

31 What is cortical dementia? What is subcortical dementia?

32 What is dyspraxia?

The inability to perform tasks requiring fine motor skills, such as drawing, buttoning, writing, and speaking (verbal dyspraxia). From the Greek dys (difficulty in) and praxis (doing).

33 What is agnosia?

The inability to recognize objects by touch alone (a, lack of; and gnosia, recognition).

34 What is the role of cranial nerve examination?

An important one, since all cranial nerves have discrete functions that permit accurate localization of lesions based only on exam. Yet detailed testing of all cranial nerves is time consuming. Hence, it is unnecessary unless symptoms point toward a specific nerve problem.

35 How do you test CN I (olfactory nerve)?

By asking patients to close their eyes, occlude one nostril, and then smell through the open naris a distinctive scent—like cinnamon, cloves, or peppermint. Transient anosmia is common, usually resulting from simple colds or intercurrent sinus infection. Chronic anosmia (especially if congenital) is instead quite important (see Chapter 6, question 33). Note that anosmia can also be seen in frontal/temporal lobectomies or Parkinson’s disease.

36 How do you test CN II (optic nerve)?

By funduscopy and color recognition (through Ishihara chart or a common and colorful object), but also by two bedside maneuvers, each testing a separate function of the optic nerve:

37 How do you test CN III, IV, and VI?

Together, since oculomotor (III), trochlear (IV), and abducens (VI) work in concert to produce the various eye movements. To test them, ask patients to hold the head stationary while following your finger as it moves through the main directions of gaze: left-up, left-middle, left-down, and right-up, right-middle, and right-down. Normal eyes move symmetrically and smoothly. Any restriction or double vision (from inability of the eyes to move together) suggests damage to III, IV, or VI (see Chapter 4, questions 84–90).

38 What abnormal eye movements result from damage to CN III, IV, or VI?

39 How do you test CN V (trigeminal nerve)?

It depends on whether you are testing a motor or sensory component. The divisions of the trigeminal nerve are shown in Figure 19-1.

Figure 19-1 Divisions of the trigeminal nerve.

(From Swartz MH: Textbook of Physical Diagnosis: History and Examination, 4th ed. Philadelphia, WB Saunders, 2002, Fig. 20–10.)

40 Where are the sensory and motor nuclei of the trigeminal nerve?

They are both in the pons. Yet the sensory also extends into the cervical cord.

41 How do you test the sensory function of CN V?

By pinprick or light touch over the areas of distribution of the trigeminal branches: upper (supplied by V1, or ophthalmic; forehead), mid (V2, or maxillary; cheek), and lower (V3, or mandibular; jaw). Sensory function of the ophthalmic branch is also tested by the corneal reflex (see question 58).

42 How do you test the motor function of CN V?

By feeling the masseters during teeth clinching. Contraction must be strong and symmetric.

43 What are the manifestations of trigeminal motor deficit?

44 What is the significance of unilateral trigeminal motor deficit?

It indicates nerve compression (bony metastases) or an ipsilateral pontine lesion. Since trigeminal motor nuclei receive bilateral cortical innervation, hemispheric strokes will not affect them. Hence, bilateral masseter weakness suggests bilateral hemispheric disease (pseudobulbar palsy).

45 What is the significance of a sensory deficit of the trigeminal nerve?

It depends on whether it involves both the face and body, or only the face:

46 What is Hutchinson’s sign?

It is the presence of herpetic vesicles on the nasal tip of patients with ophthalmic zoster—an ominous sign, since it suggests higher risk of ocular complications (uveitis and keratitis). This is because the nasal tip, the cornea, and the iris all share the nasociliary branch of the trigeminus. Patients with nasal tip involvement have a 75% chance of ocular involvement (tearing, irritation, photophobia). Still, Hutchinson’s is a rather specific (82%), but poorly sensitive (57%), sign.

47 What is the jaw-jerk reflex?

A reflex that tests the integrity of sensory (afferent) and motor (efferent) components of the V. To test for it, place your index finger (or tongue depressor) over the patients’ chin, while asking them to keep their mouth slightly open. Then, gently tap the index finger with your reflex hammer. Abnormal responses include jaw deviation or brisk closure. Exaggerated masseteric contraction, often with clonus, suggests upper motor neuron pathology (i.e., above the trigeminal nucleus in the mid-pons). This occurs in 70% of pseudobulbar palsy patients (see below, question 65).

48 How do you test CN VII (facial nerve)?

Through the muscles of facial expression. Damage to CN VII causes inability to wrinkle the forehead, tightly close the eye (Fig. 19-2), or smile. It also causes facial asymmetry (i.e., ipsilateral widening of the palpebral fissure and sagging of the nasolabial fold).

Figure 19-2 A and B, Testing the strength of eyelid closure.

(From Swartz MH: Textbook of Physical Diagnosis: History and Examination, 4th ed. Philadelphia, WB Saunders, 2002, Fig. 20–15.)

49 What determines the difference between central and peripheral lesions of the VII?

It’s the difference in control of upper versus lower facial muscles: the upper being supplied by brain stem motor neurons (controlled by both sides of the cortex), whereas the lower are supplied by brain stem motor neurons (controlled by only one side of the cortex).

50 What are the signs of central lesions of the facial nerve?

Central lesions (i.e., involving either the cortical/upper motor neuron or its pyramidal tracts) result in contralateral weakness of only the lower half of the face. Thus, patients cannot smile (the face draws to the opposite side as they try to do so) or fully open the mouth, but can still wrinkle the forehead and close the eyes. This lower facial weakness only relates to intentional movements (i.e., those originating in the motor cortex). Emotional movements are typically spared, since they originate in the thalamus and frontal lobe.

51 What are the signs of peripheral lesions of the facial nerve?

Peripheral lesions (i.e., involving either the brain stem/lower motor neuron or the nerve itself) result instead in ipsilateral weakness of the entire hemiface. Thus, patients can neither smile, nor open the mouth, nor wrinkle the forehead. Eye closure also is impaired, and the ipsilateral palpebral fissure is wider. Bell’s phenomenon is present too. Weakness affects both volitional and emotional movements. Separating “central” from “peripheral” facial weakness is clinically very important.

52 Are there any other functions of CN VII that can be affected?

Yes. CN VII also controls the anterior two thirds of the tongue, the stapedius muscle, and the lacrimal gland. Hence, its lesions may impair taste, hearing, and tearing.

53 What about ptosis?

This is actually due to lesions of either CN III (which controls the levator palpebrae) or the sympathetic nerves (which control the Mueller muscle). Do not confuse levator palpebrae with orbicularis, which is instead supplied by the VII. Hence, lesions of VII will compromise corneal or glabellar reflexes, but not ptosis.

54 What is Bell’s palsy?

A peripheral mononeuropathy of CN VII. Since it involves the nerve directly (i.e., peripheral damage), Bell’s causes paralysis of both lower and upper facial muscles. Hence, there is ipsilateral inability to smile, open the mouth wide, or wrinkle the forehead. Bell’s also causes dysfunction in (1) taste (reduced in one half of the cases); (2) hearing (hyperacusis in 20–30%); and (3) tearing (usually increased, due to weakness of the orbicularis, but sometimes reduced as a result of lacrimal gland dysfunction). In 20% of cases, Bell’s also may present with facial hyperesthesia due to concomitant trigeminal involvement.

55 What are the causes of Bell’s palsy?

Peripheral paralysis of the VII has been described in infectious mononucleosis, herpes zoster, Guillain-Barré syndrome, parotid neoplasms, sarcoidosis, diabetes, or, occasionally, a cerebellopontine tumor. Yet, by definition Bell’s is idiopathic, in fact probably viral. This is not an uncommon condition, which even affected heartthrob George Clooney while still in high school.

56 What is Bell’s phenomenon?

It is the upward rotation of the eyeball, triggered by contraction of the ipsilateral orbicularis. This is usually invisible, since contraction of the orbicularis shuts the eye. Note that Bell’s phenomenon is a completely normal event, occurring in anyone as a result of synkinesis (from the Greek syn, together, and kinesis, motion), a fancy term for an involuntary motion that accompanies a voluntary one. Examples of synkinesis include the movement of a closed eye that accompanies that of the contralateral open eye or the movement of the arms as a result of leg motion during walking. What makes Bell’s phenomenon so unusual is that in patients with peripheral facial paralysis, the eyelid on the affected side is unable to close as a result of weakness of the orbicularis. Hence, the physiologic upward rotation of the eyeball becomes suddenly visible.

57 Who was Bell?

Sir Charles Bell (1774–1842) was a Scottish neurophysiologist and surgeon. He was not the same Dr. Bell who taught medicine in Edinburgh and made a big impression on young Conan Doyle (thus becoming the accidental model for Sherlock Holmes). That was Joseph Bell, a mesmerizing teacher who even tried his analytical powers on the mystery of Jack the Ripper, the Whitechapel killer of 1888. Charles Bell was instead the soft-spoken son of an Episcopal minister, who after being denied a position in Edinburgh, left for London in 1801. There, he made a name for himself as an artist, thanks to his “Essays on the Anatomy of Painting.” He also attended the military hospital of Haslar, where he had plenty of opportunities to treat the casualties of Wellington’s peninsular campaign. This triggered a lifelong fascination with war, and what it can do to human body and psyche. In 1815, while operating on Waterloo’s wounded, he made sketches and drawings that can still be viewed at the Royal College of Surgeons in Edinburgh. He eventually moved back to his native Scotland, but only after founding the Middlesex Hospital and Medical School. He is remembered not only for his palsy and phenomenon, but also for Bell’s law, which states that the anterior spinal roots carry motor fibers, whereas the posterior carry sensory fibers, including proprioception. He also named the “sense of position” as the “sixth sense”—eventually renamed proprioception by Sherrington.

58 What is the corneal reflex?

A bedside test of CN V and VII. To elicit it, ask patients to look away (so that they cannot see what the examiner is doing), and then use a cotton wisp to gently touch the edge of their cornea. The normal response is a protective reflexive blinking, which is bilateral (i.e., both eyes blink after stimulation of one) and requires the integrity of both V and VII: the ipsilateral V must be intact to receive sensation from the cornea, whereas both facial nerves must be intact to convey the motor response (hence the blinking of both eyes). This is a risky reflex since it can cause corneal damage.

59 What is the significance of an abnormal corneal reflex?

It depends on the response. If the ipsilateral eye does not blink after corneal stimulation (while the contralateral does), the most likely explanation is unilateral facial nerve dysfunction. Conversely, if both eyes fail to blink, the explanation is unilateral trigeminal nerve dysfunction, typically in the ipsilateral brain stem. An absent corneal reflex is especially helpful in cases of unilateral sensorineural hearing loss, since it suggests a lesion of the cerebellopontine angle—like an acoustic neurinoma. Yet, an abnormal corneal reflex is poorly sensitive, since it requires a tumor >2    cm. It is not specific either, being absent in 10% of normal elderly subjects.

60 How do you test CN VIII (acoustic/vestibular nerve)?

It depends on the function you want to test, vestibular or auditory:

61 How do we maintain balance?

Through a complex circuitry that requires intact positional sense input (vision, vestibular, and proprioceptive receptors/pathways), intact sensorimotor integration (cerebellum), and intact motor output (basal ganglia/corticospinal/pyramidal tract). If there is vestibular or proprioceptive damage, the patient will be able to compensate by relying on vision. Yet, darkness (or closed eyes) will remove this compensatory input and thus cause the patient to sway and possibly fall. Conversely, if there is intrinsic cerebellar disease, the patient will be unable to compensate even with open eyes. Hence, Romberg is not a cerebellar test since patients with cerebellar ataxia will not maintain balance even when they can see. It is instead a test for proprioceptive receptors and pathways. Thus, it will be positive in conditions of sensory ataxia (i.e., affecting [1] the sensory nerves (peripheral neuropathy) and/or [2] the dorsal columns of the spinal cord [tabes dorsalis]).

62 How do you perform the Romberg test?

Ask patients to first stand up with the heels together, eyes open, and arms by the side. Note any swaying. Then ask them to close their eyes. Observe for a full minute. Normal patients may sway a little more with the eyes closed, but will not fall. Vestibular patients will sway a lot more with the eyes closed but will not fall. Sensory ataxia patients will instead sway and fall with the eyes closed.

63 Who was Romberg?

Moritz Heinrich Romberg (1795–1873) was a well-respected Jewish physician who studied and practiced in Berlin, where he distinguished himself as “officer to the indigent” during the cholera epidemics of 1831 and 1837. A popular and beloved teacher, Romberg translated into German the works of Sir Charles Bell, and then wrote a three-volume textbook of neurologic diseases centered on the relation between altered structure and symptoms and signs. He reported his homonymous maneuver in an 1846 description of tabes dorsalis:

64 What is the anatomy of CN IX (glossopharyngeal) and CN X (vagus)? How do you test them?

Axons from several brain stem nuclei mingle together to emerge from the neuraxis through two separate nerves, named by early neuroanatomists as glossopharyngeal (IX) and vagal (X) (the vagus was so termed since, as a vagabond, it wanders long distances in the body). In reality, the origin of the two nerves is essentially identical. Function also is similar: motor control of the palate and pharynx (plus, for the IX, sensory supply to the pharynx and posterior third of the tongue). Hence, their clinical testing is not entirely separable. Since the brain stem nuclei of these two nerves receive bilateral innervation from the cortex, their dysfunction results from one of three possibilities: (1) bilateral damage to the cortex or pyramidal tracts (pseudobulbar palsy), (2) brain stem disease (lateral medullary syndrome), or (3) peripheral nerve lesions (jugular foramen syndrome). You can test IX and X by asking patients to say “ahhh” or “ehhh” (see Chapter 6, questions 53 and 54) while observing whether the velum of the palate rises symmetrically. Alternatively, you can use the gag and palatal reflexes. The latter is elicited by touching the patient’s palate with a cotton swab, which causes elevation of the soft palate and ipsilateral deviation of the uvula. The gag is instead triggered by touching the posterior wall of the pharynx (or alternatively, the tonsillar area or base of the tongue). It causes tongue retraction and elevation/constriction of the pharyngeal musculature. In unilateral CN IX and X paralysis, these reflexes result in deviation of the uvula toward the normal side. Lesions of the IX also will result in loss of taste in the posterior third of the tongue, and loss of pain and touch sensations in the same area plus the soft palate and pharyngeal walls. Conversely, unilateral paralysis of CN X’s recurrent laryngeal nerve will cause hoarseness. Bilateral paralysis will cause stridor (requiring tracheostomy).

65 What is pseudobulbar palsy?

The result of bilateral damage to the pyramidal tracts supplying the nuclei of CN IX and X. This is due to lacunar disease of the internal capsule, and presents with paralysis of both the palate and pharynx (i.e., loss of the gag reflex), but also the tongue, face, and chewing muscles. As a result, patients will be dysarthric, dysphagic, and unable to control facial expression. There also will be spasmodic (and inappropriate) laughing and crying.