Материал: Kaplan USMLE-1 (2013) - Anatomy

Chapter 5 • The Brain Stem

Lateral Medullary (Wallenberg) Syndrome

Lateralmedullarysyndrome results from occlusionofthe PICA (Figure IV-5-15).

Thecranial nervesornuclei involvedinthe lesion are thevestibularorthe cochle­ ar parts of CN VIII, the glossopharyngeal and the vagus nerves, and the spinal nucleus or tract ofV The long tracts involved are the spinothalamic tract and the descending hypothalamic fibers.

Spinothalamic tract lesions produce a pain and temperature sensation deficit in the contralaterallimbs andbody.

Lesions of descending hypothalamic fibers produce an ipsilateral Horner syn­ drome (i.e., miosis, ptosis, and anhidrosis).

Lesions ofthe vestibular nuclei and pathways may produce nystagmus, vertigo, nausea, and vomiting. Ifthere is a vestibular nystagmus, the fast component will be away from the side ofthe lesion.

Lesions of the vagus nerves exiting the medulla may produce dysphagia (diffi­ cultyin swallowing) orhoarseness. The palate willdroop onthe affected side, and the uvulawill deviate away from the side ofthe lesion.

Lesions ofthe glossopharyngealnerveresultin a diminished orabsentgag reflex.

Lesions ofthe spinal tract and nucleus ofthe trigeminal nerve produce a loss of just pain andtemperaturesensations on the ipsilateral side ofhalfthe face. Touch sensations from the faceandthe cornealblinkreflexwillbe intact. In lateral med­ ullary syndrome, the pain and temperature losses are alternating; these sensa­ tionsarelost fromthe face andscalp ipsilateral to the lesionbutarelost fromthe contralateral limbs and trunk.

Taste sensations maybe altered ifthe solitary nucleus is involved.

Medial Pontine Syndrome

Medial pontine syndrome results from occlusion ofparamedian branches ofthe basilar artery (Figure IV-5-16).

At a minimum, this lesion affects the exiting fibers ofthe abducens nerve and the corticospinal tract. The medial lemniscus may be affected ifthe lesion is deeper into the pons, and the facial nerve maybe affected ifthe lesion extends laterally.

The long tract signs will be the same as in medial medullary syndrome, involving the corticospinal and medial lemniscus, but the abducens nerve and the facial nerve lesions localize the lesion to the caudal pons.

Corticospinaltractlesionsproduce contralateralspastichemiparesisofbothlimbs.

Medial lemniscus lesions produce a contralateral deficit of proprioception and touch, pressure, and vibratory sensations in the limbs and body.

Lesions of the abducens nerve exiting the caudal pons produce aninternal stra­ bismus ofthe ipsilateral eye (from paralysis ofthe lateral rectus). This results in diplopia on attempted lateral gaze to the affected side.

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Section IV • Neuroscience

Lesions ofthe facial nerve exiting the caudal pons produce complete weakness of the muscles offacial expression on the side ofthe lesion.

Lesions ofthe facial nerve may also include an alteration oftaste from the anterior two-thirds ofthe tongue, loss oflacrimation (eye dryand red), and loss ofthe motor limb ofthe corneal blink reflex.

If a lesion extends dorsally to include the abducens nucleus (which includes the horizontal gaze center in the PPRF), there may be a lateral gaze paralysis in which both eyes are forcefully directed to the side contralateral to the lesion.

Lateral Pontine Syndrome

Lesions ofthe dorsolateral pons usually result from occlusion ofthe anterior in­ ferior cerebellar artery (caudal pons) or superior cerebellar artery (rostral pons). The long tracts involved will be the same as in lateral medullary syndrome, the spinothalamic tract and the descending hypothalamic fibers. The cranial nerves involved willbe the facial and vestibulocochlear in the caudal pons, the trigemi­ nal nerve in the rostral pons, and the spinal nucleus and tract ofV in both lesions (Figure IV-5-17).

Spinothalamic tract lesions produce a pain and temperature sensation deficit in the contralateral limbs and body.

Lesions of descending hypothalamic fibers produce an ipsilateral Horner syn­ drome (i.e., miosis, ptosis, and anhidrosis).

Lesions ofthe vestibular nuclei and pathways (caudal pons) produce nystagmus, vertigo, nausea, andvomiting. Again, the fastphase ofthe nystagmus willbe away from the side ofthe lesion. Lesions ofthe cochlear nucleus or auditorynerve pro­ duce an ipsilateral sensorineuralhearing loss.

Lesions ofthe spinal tract andnucleus ofthe trigeminal nerve result onlyin a loss ofpain and temperature sensations on the ipsilateral side ofhalfthe face.

Lesions ofthe facial nerve and associated structures produce ipsilateral facial pa­ ralysis, loss oftaste from the anterior two-thirds ofthe tongue, loss oflacrimation and salivation, and loss ofthe corneal reflex.

Lesions of the trigeminal nerve (rostral pons) result in complete anesthesia ofthe face on the side ofthe lesion, weakness ofmuscles ofmastication, and deviation of thejawtoward the lesioned side.

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