MSD Ch. 4 Flaccid Dysarthrias, Spinal+ Cranial Nerves, Summary – Flashcards

Course and Function: The three main branches of THIS cranial nerve arise in the ganglion (of the same name) in the petrous bone of the middle cranial fossa.

Central connections from the trigeminal ganglion enter the lateral aspect of THIS and are distributed to various nuclei in the brainstem.

The peripheral distribution of cranial nerve V includes THIS sensory branch, which exits the skull through the superior orbital fissure to innervate the upper face; THIS sensory branch, which exits the skull through the foramen rotundum to supply the mid face; and THESE motor and sensory branches, which exits the skull through the foramen ovale to supply the jaw muscles, tensor tympani, and tensor veli palatini.

The tensor veli palatini is innervated by THIS branch of CN-V.

Trigeminal functions for speech are mediated through the THESE (2) branches. Sensory contributions include tactile and proprioceptive information about jaw, face, lip, and tongue movements and their relationship to stationary articulatory structures in the mouth (e.g., teeth, alveolus, palate). Motor fibers drive jaw movements during speech.

Etiologies and Localization of Lesions: Damage to cranial nerve V is usually associated with involvement of other cranial nerves. It is rarely the only cranial nerve involved in flaccid dysarthrias (see Table 4-4 ). Any disorder that affects the THIS fossa can produce weakness or sensory loss in the nerve's distribution.

Etiologies involving CN-V most often include aneurysm, infection, arteriovenous malformation (AVM), tumors in the middle fossa or cerebellopontine angle, and surgical trauma (e.g., posterior fossa, acoustic neuroma, temporomandibular joint) or nonsurgical trauma to the skull or anywhere along the nerve's course to muscle. THESE branches are most often damaged in isolation by tumors or fractures of the facial bones or skull. Disease of the neuromuscular junction can cause jaw weakness, as can disease affecting the jaw muscles themselves (myopathies).

Pain of trigeminal origin can indirectly affect speech. Trigeminal neuralgia (tic douloureux) is characterized by sudden, brief periods of THIS in one or more of the sensory divisions of the nerve. It is often idiopathic, but many cases reflect compression or irritation of the trigeminal sensory roots. Pain can be triggered by sensory input from facial or jaw movements, sometimes leading to restricted lip, face, or jaw movements during speech to avoid triggering pain.

Nonspeech Oral Mechanism: In patients with THIS form of mandibular branch lesions, the jaw will deviate to the weak side when opened, and the partly opened jaw may be pushed easily to the weak side by the examiner.

Nonspeech Oral Mechanism: In unilateral mandibular branch lesions the degree of contraction of either/both THESE (2) muscles is felt on palpation when the patient bites down may be decreased on the weak side.

Nonspeech Oral Mechanism: With THIS for of weakness, the jaw may hang open at rest. The patient may be unable to close the jaw or may move it slowly or with reduced range; may resist the examiner's attempts to open or close the jaw; or may clench the teeth strongly enough for normal masseter or temporalis contraction to be felt. Patient complaints may include chewing difficulty, drooling, and recognition that the jaw is difficult to close or move.

Nonspeech Oral Mechanism: If sensory branches are affected, patients may complain of decreased face, cheek, tongue, teeth, or palate sensation. *This can be assessed while patients' eyes are closed by asking them to indicate when light touch or pressure applied to the affected areas is detected*. Decreased sensation of undetermined origin in one or more of the peripheral branches of cranial nerve V is often referred to as THIS.

In *trigeminal sensory neuropathy*, THIS etiology is most common, but association with diabetes, sarcoidosis, and connective tissue disease has also been noted. Facial numbness is occasionally a presenting symptom in multiple sclerosis.

Speech: The effects of cranial nerve V lesions on speech are most apparent during reading, conversation, and AMRs, which stands for THIS.

During AMRs, imprecision or slowness for "puh" may be greater than that for "tuh" or "kuh." But THIS kind of prolongation may be normal.

During AMRs in patients with THIS, progressive weakening of jaw movements during speech may be observed.

THIS (1) kind of damage to the motor division of cranial nerve V generally does not perceptibly affect speech. In contrast, THIS (2) lesions can have a devastating impact on articulation. The inability to elevate a bilaterally weak jaw can reduce precision or make impossible bilabial, labiodental, lingual-dental, and lingual-alveolar articulation, as well as lip and tongue adjustments for many vowels, glides, and liquids. The speech rate can be slow, either as a direct effect of weakness or in compensation for weakness. The effects of cranial nerve V motor weakness on speech are summarized in Table 4-3 .

Lesions to the sensory portion of the mandibular branch, especially if bilateral, can reduce face, lip, lingual, and palatal sensation sufficient to cause imprecise articulation of bilabial, labiodental, lingual-alveolar, and lingual-palatal sounds. This can occur without weakness and is presumably due to reduced sensory information about articulatory movements or contacts. Technically, the articulatory distortions resulting from decreased sensation should not be classified as a dysarthria, because the source of the speech deficit is not primarily neuromotor. However, because the source is neurologic and does affect the precision of motor activity, it could be viewed as a "THIS"; the use of such a term should be accompanied by a statement that the speech deficits are presumed to reflect decreased oral sensation.

Individuals with relatively isolated severe jaw weakness sometimes hold the jaw closed to facilitate articulation in THIS way, meaning "with one's hand."

Those with mandibular branch sensory loss sometimes produce THIS kind of movement of the jaw, lips, and face during speech, presumably in an attempt to increase sensory feedback. These movements can sometimes be mistaken for, or difficult to distinguish from, hyperkinetic movement disorders.

Sensory loss is usually detectable on touch or pressure sensation testing in patients with trigeminal sensory loss and not in those with true THIS.

Finally, as noted previously, patients with trigeminal neuralgia may restrict jaw movement during speech to reduce sensation that might trigger pain. Although apparent visually, this compensatory restriction of movement may not be apparent auditorily. Mild articulatory distortions and decreased loudness or altered THIS, however, could result from such a strategy.

FIGURE 4-3

Course and Function Cranial nerve VII has motor and sensory functions, but only its motor component has a clear role in speech. Motor fibers originate in the facial nucleus in the lower third of the pons and exit the cranial cavity, along with fibers of cranial nerve VIII, through the internal auditory meatus. They pass through the facial canal , exit at the stylomastoid foramen below the ear, pass through the parotid gland, and innervate the muscles of facial expression. The facial muscles crucial for speech are those that move the lips and firm the cheeks to permit impounding of intraoral air pressure for bilabial and labiodental sounds. Etiologies and Localization of Lesions Cranial nerve VII can be damaged in isolation or along with other cranial nerves. Pathology in the brainstem and posterior fossa can cause seventh nerve damage, but a lesion anywhere along the nerve may affect its functions for speech. Because cranial nerves VI (abducens) and VII are in close proximity within the pons, especially in the floor of the fourth ventricle, lesions of both of these nerves implicate that part of the brainstem. If cranial nerves VII and VIII are involved, as they frequently are with acoustic neuromas, a lesion is suspected in the area of the internal auditory meatus where both nerves exit the brainstem. Known infectious causes of facial paralysis include, but are not limited to, herpes zoster, mononucleosis, otitis media, meningitis, Lyme disease, syphilis, sarcoidosis, Guillain-Barré syndrome, and inflammatory polyradiculoneuropathy. Common neoplastic causes include acoustic neuroma, parotid tumor, cerebellopontine angle meningioma, tumor of the facial nerve, and leptomeningeal carcinomatosis. 12 , 42 , 51 Vascular lesions and trauma can also cause cranial nerve VII lesions. Bell's palsy is a relatively common condition, accounting for a majority of acute facial palsies. Its most frequent cause is probably latent herpes viruses, 33 but autoimmune-mediated inflammatory neuropathy and swelling of the nerve induced by exposure to cold or allergic factors are other possible causes. 52 It is characterized by isolated unilateral cranial nerve VII weakness. Upper and lower facial muscles are affected, and the ability to close the eye on the affected side may be limited. Some patients also have decreased lacrimation, salivation, and taste sensation, as well as hyperacusis (possibly due to involvement of the portion of the nerve that innervates the stapedius); a small percentage of patients may have other cranial neuropathies, usually affecting the trigeminal, glossopharyngeal, or hypoglossal nerves, 9 About three quarters of patients recover normal facial function, but lasting weakness can occur. 33 Nonspeech Oral Mechanism The visible effects of unilateral cranial nerve VII lesions can be striking (Samples 57). At rest, the affected side sags and is hypotonic. The forehead may be unwrinkled, the eyebrow drooped, and the eye open and unblinking. Drooling on the affected side may occur. The nasolabial fold is often flattened, and the nasal ala may be immobile during respiration. During smiling the face retracts more toward the intact side ( Figure 4-2 ). Food may squirrel between the teeth and cheek on the weak side because of buccinator weakness. The patient may bite the cheek or lip when chewing or speaking and may have difficulty keeping food in the mouth. With milder weakness, asymmetry may be apparent only with use, as in voluntary retraction, pursing, and cheek puffing. Reduced or absent movement is apparent during voluntary , emotional, and reflexive activities. Fasciculations and atrophy may be apparent (Samples 58, 59) on the affected side. Bilateral cranial nerve VII lesions are less common than unilateral lesions. With bilateral lesions, the effects of weakness are on both sides, but they may be less apparent visually because of the symmetric appearance (one of the cases in Part IV of the accompanying website has this problem) . At rest, the mouth may be lax and the space between the upper and lower lips wider than normal. During reflexive smiling the mouth may not pull upward, giving the smile a transverse appearance . The patient may be unable to retract, purse, or puff the cheeks, or the seal on puffing may be overcome easily by the examiner. Fasciculations in the perioral area and chin may be present; patients are usually unaware of them. Patients may complain that their lips do not move well during speech and that they lose food or liquid out of their mouth when eating. Drooling during speech, when concentrating on another activity, or during eating or sleep, may be reported or observed. Abnormal movements of the face sometimes occur with cranial nerve VII lesions. They are noteworthy because they are unexpected in the context of FCP disease and may be confused with hyperkinesias of CNS origin. Synkinesis (see Figure 4-2 ) is the abnormal contraction of muscle adjacent to muscle that is contracting normally. For example, a normal reflexive or voluntary eye blink may cause simultaneous movement of lower facial muscles. It reflects aberrant branching or misdirection of regenerating axons of the facial nerve or abnormal activity of residual motor units. It is most commonly seen after recovery from Bell's palsy. 12 Hemifacial spasm is characterized by paroxysmal, rapid, irregular, usually unilateral tonic spasm of the facial muscles. It may be due to irritation of the nerve by a pulsating blood vessel in the area of the cerebellopontine angle or facial canal, but it may also be associated with tumor , vascular abnormalities, or multiple sclerosis . 12 Facial myokymia is characterized by rhythmic, undulating movements on an area of the face in which the surface of the skin moves like a "bag of worms." Such movements are more prolonged than fasciculations and reflect alternating brief contractions of adjacent motor units. They are often benign but if widespread may be associated with multiple sclerosis, brainstem tumors, syringobulbia, or demyelinating cranial neuropathies, or they may occur after head and neck radiation therapy. 39 , 52 , 67 Speech The speech tasks that are most revealing of cranial nerve VII lesions are conversational speech and reading, speech AMRs, and stress testing. A flutter of the cheeks may be evident during conversation, because hypotonicity results in less resistance to intraoral air pressure peaks during pressure sound production. Poor bilabial closure on one or both sides may be apparent. There may be a mismatch between speech AMRs for "puh" versus those for "tuh" and "kuh," with reduced precision and perhaps mild slowness of "puh" because of lip weakness. In general, precision is reduced more than speed, unless weakness is bilateral and severe. If MG is present, stress testing may generate visible and auditory perceptual deficits attributable to lower face weakness. The effect of unilateral facial nerve paralysis on speech can be more visible than audible. There may be mild distortion of bilabial and labiodental consonants and, less frequently, anterior lingual fricatives and affricates. There is usually no perceptible effect on vowels. Bilateral facial weakness can lead to distortions or complete inability to produce /p/, /b/ , /m/, /w/, /hw/, /f/, and /v/. Bilabial stop distortions are often in the direction of frication or spirantization. If lip rounding and spreading are markedly reduced, vowels may be distorted. A reduction in syllables per breath group (probably secondary to reduced lip closure for labial consonants) and reduced bilabial AMR and conversational syllable rates have been documented for one speaker with relatively isolated traumatic bilateral facial paralysis. 87 , 88 The effects of cranial nerve VII lesions on speech are summarized in Table 4-3 . Patients with unilateral and bilateral facial weakness sometimes spontaneously compensate in an effort to improve speech and physical appearance . With unilateral weakness, they may use a finger to prop up the weak side at rest and during speech or, rarely, manually assist lower lip movement when producing bilabial and labiodental sounds. Some patients exaggerate jaw closure in an effort to approximate the lips. If weakness is bilateral, severe, isolated to the face, and chronic, they may substitute lingual for bilabial consonants (e.g., t/ p). 58 Duffy, Joseph R. (2013-06-16). Motor Speech Disorders: Substrates, Differential Diagnosis, and Management (Kindle Locations 4676-4690). Elsevier Health Sciences. Kindle Edition.

Glossopharyngeal Nerve (IX) Lesions Course and Function Motor fibers of cranial nerve IX that are relevant to speech originate in the nucleus ambiguus within the reticular formation of the lateral medulla. The nerve's rootlets emerge from the medulla, exit through the jugular foramen in the posterior fossa, and eventually pass into the pharynx to innervate the stylopharyngeus muscle, which elevates the pharynx during swallowing and speech. Afferent fibers originate in the inferior ganglion in the jugular foramen and terminate in the nucleus of the tractus solitarius in the medulla; they carry sensation from the pharynx and posterior tongue and are important to the sensory component of the gag reflex. Etiologies and Localization of Lesions Cranial nerve IX is rarely damaged in isolation (at the least, cranial nerve X is also typically involved). It is susceptible to the same pathologic influences that can affect other cranial nerves in the lower brainstem. Intramedullary and extramedullary lesion localization is usually tied to Nonspeech Oral Mechanism Cranial nerve IX is assessed clinically by examining the gag reflex, particularly asymmetry in the ease with which the reflex is elicited. A reduced gag may implicate the sensory or motor components of the reflex — the sensory component if the patient reports decreased sensation in the area. However, a normal gag can be present after intracranial section of cranial nerve IX, suggesting that cranial nerve X is also involved in pharyngeal function. It is clear, however, that cranial nerve IX may be implicated in dysphagia, with lesions to it presumably affecting pharyngeal elevation during the pharyngeal phase of swallowing. Some individuals with cranial nerve IX lesions develop brief attacks of severe pain that begin in the throat and radiate down the neck to the back of the lower jaw. Pain can be triggered by swallowing or tongue protrusion. This condition is known as glossopharyngeal neuralgia. Speech The role of cranial nerve IX in speech cannot be assessed directly. The nerve probably influences resonance and perhaps phonatory functions , because lesions affect pharyngeal elevation. Because cranial nerve IX lesions are usually associated with cranial nerve X lesions, and because cranial nerve X has a crucial and relatively clearly defined role in speech, cranial nerve IX's importance in the assessment of dysarthria can be considered indeterminate for practical purposes. Duffy, Joseph R. (2013-06-16). Motor Speech Disorders: Substrates, Differential Diagnosis, and Management (Kindle Locations 4702-4715). Elsevier Health Sciences. Kindle Edition.

Vagus Nerve (X) Lesions Course and Function Cell bodies of cranial nerve X that are relevant to speech originate in the nucleus ambiguus. Cell bodies of relevant sensory fibers originate in the inferior ganglion located in or near the jugular foramen; central processes of the sensory fibers terminate in the nucleus of the tractus solitarius in the brainstem. Cranial nerve X exits the skull through the jugular foramen, along with cranial nerves IX and XI. From there it divides into the pharyngeal branch, which enters the pharynx; the superior laryngeal branch, which enters the pharynx and larynx; and the recurrent laryngeal branch, which passes down to the upper chest where it loops around the subclavian artery on the right and around the aorta on the left before traveling back up the neck to enter the larynx. The pharyngeal branch supplies the muscles of the pharynx except the stylopharyngeus (cranial nerve IX), the muscles of the soft palate except the tensor veli palatini (mandibular branch of cranial nerve V), and the palatoglossus muscle. It is responsible for pharyngeal constriction and palatal elevation and retraction during speech and swallowing. The internal laryngeal nerve, a component of the superior laryngeal nerve, transmits sensation from mucous membranes of portions of the larynx, epiglottis, base of the tongue, and aryepiglottic folds and from stretch receptors in the larynx. The external laryngeal nerve, the motor component of the superior laryngeal nerve, supplies the inferior pharyngeal constrictors and the cricothyroid muscles. Its innervation of the cricothyroid muscle is important, because cricothyroid contraction lengthens the vocal folds for pitch adjustments. The recurrent laryngeal branch of the nerve innervates all of the intrinsic laryngeal muscles except the cricothyroid. Its sensory fibers carry general sensation from the vocal folds and larynx below them. Etiologies and Localization of Lesions The localization of cranial nerve X lesions is somewhat complicated because of its long course and three major branches. The degree of weakness, positioning of paralyzed vocal folds, and degree and type of voice or resonance abnormality depend on lesion localization along the course of the nerve and whether the lesion is unilateral or bilateral. Careful consideration of signs and symptoms stemming from cranial nerve X lesions can often distinguish among lesions that are (1) intramedullary, extramedullary, or above the pharyngeal branch; (2) below the pharyngeal branch but above the superior and recurrent laryngeal branches; or (3) below the superior laryngeal branch. Vagus nerve lesions can be intramedullary, extramedullary, or extracranial. Intramedullary lesions damage the nerve in the brainstem. Extramedullary lesions damage the trunk of the nerve as it leaves the body of the brainstem but while it is still within the cranial cavity (i.e., before it exits the jugular foramen). Extracranial lesions damage the nerve after it exits the skull. It is generally the case that as the distance of a lesion from the brainstem increases, the number of muscles, structures, and functions affected by the lesion decreases. Thus, intracranial lesions are more likely than extramedullary and extracranial lesions to be bilateral or associated with multiple cranial nerve involvement. Extramedullary lesions are more likely to be unilateral but may still affect several cranial nerves (e.g., cranial nerves IX, X, and XI all exit through the jugular foramen on each side of the posterior fossa). Extracranial lesions are more likely to be isolated to cranial nerve X and perhaps only one of its branches. The most important relationships between cranial nerve X lesion loci and impairment of muscle function include the following: 1. Intramedullary, extramedullary, and extracranial lesions above the separation of the pharyngeal, superior laryngeal, and recurrent laryngeal branches affect all muscles supplied by the nerve below the level of the lesion. Therefore pharyngeal and palatal muscles supplied by the pharyngeal branch, the cricothyroid muscle supplied by the superior laryngeal branch, and the remaining intrinsic laryngeal muscles supplied by the recurrent laryngeal branch are weak or paralyzed on the side of the lesion ( Figure 4-3 ). 2. Lesions below the pharyngeal branch, but still high enough in the neck to affect the superior and recurrent branches, spare the upper pharynx and velopharyngeal mechanism but cause paralysis or weakness of the cricothyroid and other intrinsic muscles on the side of the lesion. 3. Lesions of the superior laryngeal branch but not the recurrent laryngeal or pharyngeal branches affect the cricothyroid but not the velopharyngeal mechanism or the remaining intrinsic laryngeal muscles. 4. Lesions affecting only the recurrent laryngeal nerve cause weakness or paralysis of the intrinsic laryngeal muscles on the side of the lesion, except the cricothyroid. Intramedullary and extramedullary lesions affecting cranial nerve X can be caused by tumor, infection, stroke, syringobulbia, Arnold-Chiari malformation, Guillain-Barré syndrome, polio, motor neuron disease, and other inflammatory or demyelinating diseases. 3 Not infrequently, lesions in the posterior fossa affect cranial nerves IX, X, and XI in combination. When this occurs in the area of the jugular foramen, it is called a jugular foramen syndrome. Extracranial cranial nerve X disorders can be caused by myasthenia gravis, tumors in the neck, lung or thorax; aneurysms in the aortic arch or internal carotid or subclavian artery; aortic or internal carotid artery dissection; endotracheal intubation; pulmonary or mediastinal tuberculosis; and viruses (e.g., herpes simplex virus, influenza ). 5 , 12 , 56 Surgery is a common cause of vocal fold paralysis, most often associated with thyroidectomy, carotid endarterectomy, anterior approach for cervical fusion, skull base procedures, thoracic and esophageal surgeries, and vagal nerve stimulation for seizure control. 56 Vagus nerve degeneration and dysphonia have been reported in individuals with diabetes and severe alcoholic neuropathies. 29 , 56 When unilateral vocal fold paralysis is idiopathic, a significant percentage of cases have good recovery of voice within 1 year, although recovery rates across studies are reported to range from 25% to 87%. 81 Nonspeech Oral Mechanism Unilateral pharyngeal branch lesions are manifest by the following: 1. The soft palate hangs lower on the side of the lesion. It pulls toward the nonparalyzed side on phonation (see Figure 4-3 ; also Figure 4-4 [Sample 56]). A palate that hangs low at rest but elevates symmetrically may not be weak; it may be asymmetric as a normal variant or the result of scarring Unilateral pharyngeal branch lesions are manifest by the following: 1. The soft palate hangs lower on the side of the lesion. It pulls toward the nonparalyzed side on phonation (see Figure 4-3 ; also Figure 4-4 [Sample 56]). A palate that hangs low at rest but elevates symmetrically may not be weak; it may be asymmetric as a normal variant or the result of scarring from tonsillectomy. If palatal asymmetry on phonation is ambiguous, the clinician should look for a levator "dimple" representing the point of maximum contraction of the levator veli palatini muscle. If it is centered, the palate may not be weak; if it is displaced to one side, the palate is probably weak on the opposite side. 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Accessory Nerve (XI) Lesions Course and Function The cranial portion of cranial nerve XI arises from the nucleus ambiguus, emerges from the side of the medulla, and exits the skull through the jugular foramen along with cranial nerves IX and X. It intermingles with fibers of cranial nerve X to help innervate the uvula, levator veli palatini, and intrinsic laryngeal muscles. The spinal portion arises from the first five to six cervical segments of the spinal cord, ascends and enters the posterior fossa through the foramen magnum, and then leaves the skull with fibers of cranial nerves IX and X and the cranial portion of cranial nerve XI, where it innervates the sternocleidomastoid and trapezius muscles. Etiologies and Localization of Lesions Etiologies of lesions to the cranial portion of cranial nerve XI are similar to those described for cranial nerve X. The spinal portion can be damaged by lesions in the cervical spinal cord and by compression from lesions in the area of the foramen magnum. Radical neck surgery is another source of eleventh nerve lesions. STOPPED BUT THERE'S MORE

Hypoglossal Nerve (XII) Lesions Course and Function Cranial nerve XII originates in the medulla. Its fibers exit the brainstem as a number of rootlets that converge and pass through the hypoglossal foramen just lateral to the foramen magnum . The nerve travels medial to cranial nerves IX, X, and XI in the vicinity of the common carotid artery and internal jugular vein and passes above the hyoid bone to reach the intrinsic and extrinsic muscles of the tongue. Cranial nerve XII innervates all of the intrinsic and extrinsic muscles of the tongue, except the palatoglossus (cranial nerve X). It is crucial for lingual articulatory movements, as well as chewing and swallowing. Etiologies and Localization of Lesions Hypoglossal nerve lesions can be intramedullary, extramedullary, and extracranial. They can be caused by any condition that can affect the lower cranial nerves. Lesions of the hypoglossal nerve often damage other cranial nerves, especially IX, X, and XI, but the hypoglossal nerve can be damaged in isolation. Common causes of isolated hypoglossal lesions include infection and basilar skull or neck tumor, trauma, and surgery. About 5% of carotid endarterectomies are associated with usually temporary hypoglossal nerve injury. 4 The nerve can also be damaged by carotid and vertebral artery aneurysms; carotid artery dissection; tumors in the neck, salivary glands, or base of the tongue; and radiation therapy. 12 , 44 , 63 , 82 Duffy, Joseph R. (2013-06-16). Motor Speech Disorders: Substrates, Differential Diagnosis, and Management (Kindle Locations 4902-4917). Elsevier Health Sciences. Kindle Edition.

Spinal Nerve Lesions Course, Function, and Localization of Lesions Upper cervical spinal nerves supplying the neck are indirectly implicated in voice, resonance , and articulation. The effects on speech of lesions to these nerves are indirect, usually mild, and poorly understood. Spinal nerves more directly involved in respiration are spread from the cervical through the thoracic divisions of the spinal cord. Those supplying the diaphragm arise from the third through fifth cervical segments. They combine to form the phrenic nerves, each of which innervates half of the diaphragm, the most important inspiratory respiratory muscle. Remaining inhalatory muscles are supplied by branches of the lower cervical nerves, intercostal nerves, and phrenic nerves. Muscles of forced exhalation, important for control of exhalation during speech, are innervated by motor fibers of the thoracic and intercostal nerves. Diffuse impairment of spinal nerves supplying respiratory muscles is often necessary to interfere significantly with respiration. The exception is damage to the third through fifth segments of the cervical spinal cord, which can paralyze the diaphragm bilaterally and severely compromise THERE'S MORE

Multiple Cranial Nerve Lesions When several cranial nerves are affected, the condition is often referred to as bulbar palsy. The jaw, face, lips, tongue, palate, pharynx, and larynx can be affected in varying combinations and to varying degrees, depending on the particular cranial nerves involved and whether damage is unilateral or bilateral. Conditions that affect multiple cranial nerves tend to be associated with intracranial pathology. This is because the smallest lesion that can do the most damage is in the brainstem where the cranial nerves are closer together than anywhere else along their course. This is not always the case, however, because multiple cranial nerves may be involved in neuromuscular junction diseases (e.g., myasthenia gravis), and myopathies can affect muscles in the distribution of more than one cranial nerve. Etiologies Multiple cranial nerve involvement can be caused by many of the same conditions that affect single cranial nerves . Multiple rather than single cranial nerve involvement is more common in certain diseases, however, including ALS, MG, and brainstem vascular disturbances or tumors. THERE'S MORE

SUMMARY 1. Flaccid dysarthrias reflect damage to the motor units of cranial or spinal nerves that serve speech muscles. They occur at a frequency comparable to that of other single dysarthria types. They sometimes reflect weakness in only a small number of muscles and can be isolated to lesions of single cranial or spinal nerves. Weakness and THIS are the underlying neuromuscular deficits that explain most of the abnormal speech characteristics associated with flaccid dysarthrias.

SUMMARY 2. Lesions anywhere in the motor unit can cause flaccid dysarthrias, and various etiologies can produce such lesions. Surgical trauma and THESE diseases (meaning the function or structure of the affected aspect will increasingly deteriorate over time) are common known causes, but the etiology is sometimes uncertain, particularly when only a single cranial nerve is involved. Stroke, MG, tumor, infection, demyelinating diseases, anatomic malformations, and radiation therapy effects represent other known causes.

SUMMARY 3. Speech characteristics and nonspeech examination findings differ among lesions of THESE (4) cranial nerves and spinal respiratory nerves. Examination can localize the effects of disease to one or a combination of these nerves.

SUMMARY 4. Lesions of the mandibular branch of the trigeminal nerve (V) lead to weakness of jaw muscles. When bilateral, jaw weakness can have significant effects on THIS. Lesions of the trigeminal nerve that affect sensation from the jaw, face , lips, tongue, and stationary points of articulatory contact may also affect speech, primarily articulatory precision.

SUMMARY 5. Lesions of the facial nerve (VII) can cause THIS kind of weakness and flaccid dysarthria. Unilateral weakness of the face can be associated with mild articulatory distortions. Bilateral lesions may lead to significant distortion of all consonants and vowels requiring facial movement.

SUMMARY 6. Lesions of the vagus nerve (X) can cause some of the most frequently encountered manifestations of flaccid dysarthrias. Lesions affecting the pharyngeal branch can lead to THIS form of incompetence, with hypernasality, nasal emission, and weak pressure consonant sounds. Lesions of the superior laryngeal and recurrent laryngeal branches can lead to various voice abnormalities in which perceptual attributes are consistent with weakness and hypotonia of laryngeal muscles. Lesions above the pharyngeal branch can lead to both resonatory and laryngeal incompetence, whereas lesions below the pharyngeal branch are associated with laryngeal manifestations only.

SUMMARY 7. Lesions of the hypoglossal nerve (XII) cause weakness of THIS. The resulting flaccid dysarthria is reflected in imprecise lingual articulation, with severity dependent upon the degree of weakness and whether the lesion is unilateral or bilateral.

SUMMARY 8. Lesions affecting spinal respiratory nerves can reduce respiratory support for speech. Weakness at this level can lead to reduced loudness and variability in THIS, as well as reduced phrase length per breath group.

SUMMARY 9. Phonatory and resonatory incompetence are commonly encountered distinguishing features of flaccid dysarthrias. Although they are tied to involvement of THIS cranial nerve, it is nonetheless important to attend to speech movements generated through cranial nerves V, VII, and XII. This is important both for a complete description of the speech disorder and because speech deficits isolated to single cranial or spinal nerves are possible in flaccid dysarthrias and unusual in other dysarthria types.

SUMMARY 10. Flaccid dysarthrias can be the only, the first, or among the first and most prominent manifestations of neurologic disease. Their recognition and localization to cranial and spinal nerves subserving speech can aid in THIS and diagnosis of neurologic disease. Their diagnosis and description are important to decision making for medical and behavioral management.