Directed Neurological Examination Cranial Nerve Xi

The examination of cranial nerve (CN) XI consists of two parts: observation (at rest and during action) and palpation. Abnormal findings include atrophy; fasciculations; neck or shoulder deviation; and limitations in range, strength, or speed of motion.

Examiners should observe the neck and back while the patient is seated or standing, paying particular attention to the SCM muscle and the upper portion of the trapezius muscle. Atrophy or asymmetry should be noted. Fasciculations may be present with nuclear or lower motor neuron lesions. A unilateral paralysis of the SCM muscle causes little if any change in the position of the head while in the resting state. Bilateral paralysis may cause the neck to fall backward. Paralysis of the upper or middle portion of the trapezius muscle may alter the position of the scapula (.Fig 14-3 ). The upper part of the scapula may fall laterally away from the shoulder and vertebral column, and the interior part may be drawn inward. y , y

The speed, strength, and range of motion should be assessed. The major action of the SCM muscle, through its sternal head, is to turn the head to the opposite side.y , y Additionally, through its clavicular head, the SCM tilts the

Figure 14-2 The origin and innervation of CN XII.

head to the ipsilateral side. To examine the right SCM muscle, the patient should turn the chin completely toward the left shoulder, and the examiner should attempt to overcome the movement. During this maneuver, it is important for the examiner to press against the patient's cheek rather than the mandible, because with the latter maneuver, one is testing not only the SCM but also the lateral pterygoid muscle (CN V) as well. y The SCM muscle is also involved in neck flexion, and when both SCM muscles act simultaneously, the result is to bring the head forward and downward. This movement may be tested by asking the patient to flex the neck while the examiner exerts firm pressure on the forehead.y

To assess the strength of the rostral portion of the trapezius muscle, the patient should elevate or shrug the shoulders and maintain this movement against resistance.^ The rostral portion of the trapezius muscle also retracts the head and draws it to the ipsilateral side, y and this movement may be tested as well. The rostral and middle portions of the trapezius muscle normally stabilize the scapula, and a lesion of CN XI may cause winging of this structure. This muscle action is tested by asking the patient to extend the arms forward and horizontally. CN XI lesions cause winging of the scapula, although to a milder degree than that seen with dysfunction of the serratus anterior muscle. y

The SCM and the trapezius muscles should be palpated for the presence of atrophy or hypertrophy. Proper palpation of the sternal head of the SCM muscle is aided by asking the patient to turn the head to the opposite side against resistance. When activated, the right SCM turns the chin to the left. y , y

A unilateral hemispherical lesion does not usually cause marked deviation of the head, although some weakness may be present. In cortical or subcortical strokes, the head can deviate to the side of the lesion, away from the hemiparetic body, making rehabilitation efforts frustrating. Atrophy and fasciculations are not present in an upper motor neuron lesion.y Irritative cortical foci may result in seizures accompanied by forced deviation of the head to the contralateral side. y A unilateral supranuclear lesion in the upper brain stem may produce dissociated weakness, with ipsilateral weakness of the sternal head of the SCM and contralateral weakness of the trapezius.^ Nuclear lesions of CN XI are rare. These lesions result in muscle weakness as well as atrophy and fasciculations. Unilateral nerve lesions produce weakness of the involved muscles as well as some deviation and possibly winging of the scapula. Bilateral nerve lesions result in diminished ability to rotate the neck, and the neck may fall either backward or forward, depending on whether the SCMs or trapezeii muscles are more involved. Because other cervical muscles such as the scaleni and splenii play a major role in neck deviation, flexion, and extension, a complete paralysis of neck muscles does not occur even with bilateral lesions of CN XI.y

Figure 14-3 Lesion of the right spinal accessory nerve resulting in displacement of the right scapula.

CRANIAL NERVE XII

The examination of CN XII consists of three parts: observation, palpation, and percussion. The examiner should assess the tongue for atrophy; fasciculations; deviation; limitations in the range, strength, or speed of motion; and involuntary movements.

The tongue is observed as it rests in the mouth, with attention to atrophy, fasciculations, deviation, tremor, myoclonus, or chorea (see Chapter34 ). Atrophy, if present, may be particularly noticeable at the tip or borders of the tongue, resulting in a scalloped appearance with multiple small folds ( Fig 1.4:4 ). [9] , [n' A fine rippling of the tongue due to incomplete relaxation should not be confused with fasciculations. y Even while the tongue is "resting" in the floor of the mouth, there is some activity of the styloglossus muscles. These muscles pull the tongue upward and backward. When there is a unilateral hypoglossal nerve lesion, the resting tongue may deviate slightly away from the side of the lesion because of unopposed action of the styloglossus muscles. y

The tongue should be observed during protrusion. The examiner should note atrophy, tremor, chorea, or deviation. The genioglossus muscle causes protrusion of the apex of the tongue. When there is a unilateral lesion of the hypoglossal nerve, the protruding tongue deviates toward the side of the lesion owing to the unopposed action of the normal genioglossus muscle. y , y When there are complete bilateral nuclear or hypoglossal nerve lesions, the patient is unable to protrude the tongue at all. In general, when examining the protruding tongue for deviation, it is very important to choose appropriate landmarks. y , y For example, if the lips are used as a landmark, in the setting of unilateral facial weakness, the tongue may falsely appear to deviate toward the weak side. A more appropriate landmark in this and most other settings is the space between the two upper central incisors. This space should be aligned with the median raphe of the tongue. y , y

The tongue is observed during movements other than protrusion. First, the speed and range of motion should be assessed by asking the patient to wiggle the tongue rapidly from side to side, and to point the tip upward and downward. Second, the strength of tongue motion should be assessed by asking the patient to press the tip of the tongue sideways against the inside of the cheek, while the examiner exerts opposing pressure by placing an index finger on the outer aspect of the cheek. y Third, speech, and particularly lingual sounds, should be assessed for the presence of dysarthria.

Palpation and percussion comprise the final aspects of the examination of the tongue. Palpation of the tongue between the examiner's thumb and index finger sometimes confirms the presence of atrophy.y , y When a diagnosis of myotonia is being considered, the tongue should be tapped with a percussion hammer. A myotonic response is characterized by a contraction that is very slow to disappear. [8]

In a unilateral supranuclear lesion, the tongue may deviate toward the contralateral side; however, atrophy and fasciculations are not present. In a unilateral nuclear or hypoglossal nerve lesion, the tongue is atrophic on the ipsilateral side. On protrusion, it clearly deviates toward the side of the nuclear or nerve lesion. [9 In this setting, speech, swallowing, and respirations should be unaffected. If there are bilateral nuclear or nerve lesions, the tongue is diffusely atrophic, and the patient is unable to protrude the tongue at all. Additionally, articulation (especially lingual sounds) may be impaired, with slurred and indistinct speech. Swallowing and respiration may be impaired as the tongue falls back into the pharynx. y Fasciculations may

Figure 14-4 Lesion of the left hypoglossal nerve resulting in weakness and atrophy of the left half of the tongue.

be present either unilaterally or bilaterally in progressive disorders that involve the nucleus (e.g., amyotrophic lateral sclerosis or syringobulbia). Forced deviation of the tongue may be a manifestation of a seizure, and involuntary movements of the tongue may be a feature of myoclonus, or rarely Parkinson's disease (tremor), Huntington's disease (chorea), or tardive dyskinesia or tardive dystonia (oral-buccal-lingual movements). y

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