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Sensory Cranial Nerve Lesion

Dalam dokumen Neuroanatomy for the Neuroscientist (Halaman 184-187)

Nerve to Fourth and Sixth Pharyngeal Arch

B. Sensory Cranial Nerve Lesion

Cranial Nerve V Lesions:

a. In the main sensory root of the trigeminal nerve, in its course within or external to the midpons, cranial nerve V lesions will produce ipsilateral deficits in pain, temperature, and touch over the face.

b. In the descending spinal tract of the trigeminal nerve or of its associated nucleus, cranial nerve V lesions will produce an ipsilateral deficit in pain and temperature sensation over the face, with sparing of facial touch sensation. These structures are situated close to the lateral spinothalamic tract; the combination of contralateral pain and temperature deficit over the body and extremities with ipsilateral pain and temperature deficit over the face is frequently found as a consequence of lesions that involve the dorsal lateral tegmental portion of the medulla (e.g., infarction of the territory of the posterior inferior cerebellar artery, which supplies this sector).

A similar combination might be found in the infarction of the dorsolateral tegmen-tum of the caudal pons—the territory of the anterior inferior cerebellar artery.

c. The descending spinal tract (analogous to and, in a sense, the direct continuation of Lissauer’s tract) and associated nucleus (analogous to the substantia gelati-nosa) descend into the upper cervical spinal cord. Although there is considerable overlap, the primary trigeminal fibers synapse on the nucleus of the descending spinal nucleus at the following levels:

Mandibular division fibers at a lower pontine–upper medullary level Maxillary division at a medullary level

Ophthalmic division fibers at a lower medullary and upper cervical cord level There is overlap at the upper cervical cord level between the upper cervical segment pain fibers and the ophthalmic division pain fibers. It is not surprising, then, that pain originating in C2 and C3 roots or segments of the spinal cord and, for example, the pain of C2 and C3 (occipital neuralgia) is often referred to the orbit.

d. The secondary pain fibers decussate and join the ventral secondary trigeminal tract (also labeled trigeminothalamic or quintothalamic tract), which, at a medul-lary level, is located just lateral to the medial lemniscus. At a pontine and mid-brain location, the secondary trigeminal tract is just lateral to and essentially continuous with the medial lemniscus and adjacent to the lateral spinothalamic path. A lesion that involves this tract would then usually produce contralateral deficits in pain and temperature over a variable portion of the face in association with a contralateral deficit in pain and temperature and/or position and vibration over the affected arm, leg, and trunk.

VI. Cranial Nerve Case Histories

Cranial Nerve Case due to an Aneuyrsm

A cranial nerve case resulting from a subarachnoid hemorrhage secondary to an aneurysm at the junction of the posterior communicating and internal carotid arter-ies is presented in Fig. 17.8, Case 17.4.

Cranial Nerve Case History 5.1

This 28-year-old single, black, right-handed female reported approximately 21 days of sudden lancinating jabs of pain plus a duller more steady pain involv-ing the right maxillary and mandibular distribution. She was very aware that she could trigger her pain by touching her nose or the skin over the maxillary or mandibular area. The pain was so severe that talking; chewing, or eating would l trigger episodes. As a result, she has not been eating a great deal.

There was no clear-cut extension of pain into the eye, although some of the background pain did spread into the supraorbital area and back toward the interauricular line.

Two years prior to admission, she had a less severe episode in the same dis-tribution that lasted 3 weeks. She denied any tearing of the eye or nasal stuffi-ness. She had no tingling of the face, change in hearing, facial paralysis, or diplopia.

Neurological examination: Mental status, motor system (including gait and cerebellar system) and sensory system were intact.

Cranial nerves were not remarkable except for findings relevant to the right fifth cranial nerve. Although touch and pain sensation over the face was normal, there were clear-cut exquisite trigger points producing sharp pains on light tactile stimu-lation of the nose or other maxillary areas as well the mandibular skin areas and the lower molars.

Subsequent course: Evaluation by a dentist indicated no relevant dental disease.

Clinical diagnosis: Trigeminal neuralgia: maxillary and mandibular divisions.

Cranial Nerve Case History 5.2

A 44-year-old, right-handed physician developed, over 24 hours, increasing pain in the right supraorbital and orbital areas. Edema of the eyelid developed within 36 hours. Erythematous, edematous skin lesions developed over the right supraorbital area and the anterior half of the right side of the scalp. Edema of the lid was suffi-cient to produce closure of the lid. Significant cervical lymphadenopathy, neck pain, and low-grade fever developed. The acute pain gradually subsided over 2

weeks, but the skin lesion persisted. The skin lesion crusted and gradually cleared over 4 weeks. Occasional episodes of right supraorbital pain continued to occur for 1 year. Faded, depressed scars were still present 24 years after the acute episode.

Clinical diagnosis: Ophthalmic herpes zoster.

Cranial Nerve Case History 5.3

A 37-year-old, right-handed, white housewife was referred for emergency room consultation regarding left facial paralysis. Three days prior to evaluation, the patient had developed a dull pain above and behind the left ear. She then noted occasional muscle twitching about the left lower lip and some vague stiffness on the left side of the face. On the morning of the evaluation, the patient noted she had difficulty with eye closure on the left. She noted that she was drooling from the left side of her mouth. She denied any alteration in sensation over the face and any actual deficit in hearing and denied any tinnitus. She had no crusting in the ear and no actual pain within the ear.

Neurological examination: Cranial nerves: The patient had an incomplete paralysis of the entire left side of the face. She had sufficient eye closures sitting or recumbent to cover the cornea. She was able to have minor elevation of the eyebrow in forehead wrinkling. She had minimal elevation of the lower lip in smiling. Taste for sugar was slightly decreased but not absent on the left side of the tongue (ante-rior two-thirds). All other cranial nerves were intact. Examination of the external canal and of the tympanic membranes demonstrated no abnormality.

Motor system, reflexes, sensory system, and mental state: All intact.

Clinical diagnosis: Bell’s palsy related to involvement of the peripheral portion of the facial nerve. This usually transient impairment of a facial nerve is the result of swelling of the nerve within the relatively narrow bony facial canal. The etiology of this swelling is often uncertain, but infections with the herpes simplex virus or the spirochete agents producing Lyme’s disease have been implicated. In many cases, treatment with steroids will relieve these symptoms. More precise localiza-tion depends on whether motor funclocaliza-tion alone is involved, as opposed to addilocaliza-tional involvement of taste from the anterior two-thirds of the tongue, or of parasympa-thetic supply to the facial and salivary glands.

Dalam dokumen Neuroanatomy for the Neuroscientist (Halaman 184-187)