![]() The levator palpebrae superioris muscles, the superior recti, and the constrictors of the pupils are affected bilaterally with nuclear lesions. Isolated inferior rectus paresis may also occur on a supranuclear basis with a lesion selectively interrupting fibers descending from the right medial longitudinal fasciculus (MLF) to the inferior rectus subnucleus (Tezer, 2000). Lesions of the inferior rectus subnucleus, however, may also give rise to isolated weakness of the inferior rectus muscle (Chou, 1998 Lee, 2000b Tezer, 2000). For example, isolated inferior rectus paresis may develop with trauma, myasthenia gravis, or vascular disease and may also occur on a congenital or idiopathic basis (von Noorden, 1991). Paresis of an isolated muscle innervated by the oculomotor nerve almost always results from a lesion in the orbit or from disease of the muscle or neuromuscular junction. Nuclear lesions may be due to infarction, hemorrhage, tumor, infection, or trauma and, thus, should be investigated by magnetic resonance imaging (MRI). Lesions of the third nerve nucleus are rare and often associated with other signs of mesencephalic involvement, especially vertical gaze impairment (Bengel, 1994 Bogousslavsky, 1994 Chee, 1990 Gaymard, 1990 Nakao, 1998 Saeki, 2000b). Patients with TNP that worsens after the acute stage (more than 2 weeks) or who develop new neurologic findings are considered to have progressive TNP patients without resolution of TNP after 12 to 16 weeks are considered unresolved Type 4C: TNP with subnormal pupillary sphincter dysfunction and partial or complete extraocular muscle palsies Type 4B: TNP with normal pupillary sphincter and incomplete palsied extraocular muscles Type 4A: TNP with a normal pupillary sphincter with completely palsied extraocular muscles Isolated unilateral TNP, which has a clearly established temporal relationship to significant previous head trauma and does not progress, is considered traumatic in origin patients with minor head trauma are not included Systemic, infectious, or inflammatory risk factors for TNP (e.g., history of previous malignancy, giant cell arteritis, collagen vascular disease) Multiple cranial nerve palsies (including bilateral TNP) or radiculopathyīrainstem signs (e.g., hemiplegia, cerebellar signs, other cranial nerve deficits) Orbital disease (e.g., chemosis, proptosis, lid swelling, injection, and positive forced ductions)Įvidence to suggest myasthenia gravis (e.g., fatigability of the motility defect, Cogan’s lid twitch sign, orbicularis oculi weakness) Etiologies of TNPs by localization are outlined in Table 11–3. ![]() The localization of TNP is outlined in Table 11–2. We define six types of TNP in Table 11–1. ![]() ![]() Patients with evidence for myasthenia gravis (e.g., variability, fatigue, Cogan’s lid twitch sign, enhancement of ptosis) are not included in the isolated TNP group. The isolated TNPs were defined as TNPs without associated neurologic findings (e.g., headache, other cranial neuropathies). We classify TNPs as either nonisolated or isolated. Is the TNP Isolated or Nonisolated? Can the TNP Be Localized? In this section, we discuss the localization of TNPs associated with other neurologic signs (nonisolated TNPs) and TNPs without other associated neurologic or neuro-ophthalmologic deficits (isolated TNPs) (Lee, 1999). Partial TNPs may cause (in combination or isolation) variable ptosis variable paresis of eye adduction, elevation, and depression and variable pupillary involvement. The oculomotor nerve (third cranial nerve) supplies four extraocular muscles (medial, superior and inferior recti, and inferior oblique) as well as the levator of the lid, and contains parasympathetic fibers that supply the sphincter of the pupil and the ciliary body A complete peripheral third nerve palsy (TNP) thus causes ptosis, a fixed and dilated pupil, and a down (hypotropic) and out (exotropic) resting eye position. What Are the Clinical Features of a Third Cranial Nerve Palsy? ![]()
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