Oculomotor nerve

The cell bodies of parasympathetic preganglionic neurons are located in the brainstem and the sacral spinal cord. Parasympathetic outflow is channeled from the brainstem (1) through the third cranial nerve (oculomotor n.) via the ciliary ganglion to the eye (2) through the seventh cranial nerve (facial n.) via the pterygopalatine and submaxillary... 

The pupil is supplied with constrictor fibres from the parasympathetic system (via the Illrd or oculomotor nerve and the ciliary ganglion) and with dilator fibres from the sympathetic system (the upper thoracic nerves to the sympathetic and to the inferior and superior cervical ganglia fig. 8). 

The muscle fibres of the ciliary bodies are innervated by the mrd or oculomotor nerve. As explained above, when these fibres contract they allow the lens to take up its natural shape. Direct stimulation of the Illrd nerve therefore produces accommodation for near objects. Parasympathomimetic drugs have a similar action, whereas atropine paralyses this effect and so accommodates the lens for seeing distant objects. 

Action on eye Morphine causes constriction of pupil (miosis) due to action on oculomotor nerve nucleus. 

Morphine causes miosis by stimulating the oculomotor nerve... 

Miosis is a characteristic symptom of opiate administration, and while tolerance develops to many of the pharmacological effects of this class of drugs, tolerance to the miotic effects occurs at a much slower rate. Miosis is due to an excitatory action of the autonomic segment of the nucleus of the oculomotor nerve, an effect attributed to the stimulation of the mu receptors. In general, it would appear that the actions of morphine and its analogues on the brain, spinal cord and gastrointestinal tract are due to stimulation of the mu receptors. 

PP, peripeduncular nucleus PR, prerubral field Reth, retroethmoid nucleus RMC, red nucleus, magnocellular RPC, red nucleus, parvocellular scp, superior cerebellar peduncle SNC, substantia nigra, compact part SNL, substantia nigra, lateral part SNR, substantia nigra, reticular part SPFPC, subparafascicular thalamic nucleus, parvocellular part SuML, supramammillary nucleus, lateral part VTA, ventral tegmental area VTM, ventral tuberomammillary nucleus ZID, zona incerta, dorsal part ZIV, zona incerta, ventral part 3, oculomotor nucleus 3n, oculomotor nerve or its root. Reproduced with permission from Paxinos and Watson (1998) and Paxinos et al. (1999). 

A previously healthy 16-year-old man developed an unsteady gait and double vision. His symptoms began 5 minutes after intranasal amfetamine (actually amfetamine cut with cocaine). He had a left-sided internuclear ophthalmoplegia, an incomplete fascicular paresis of the left oculomotor nerve, and saccadic vertical smooth pursuit. Cranial MRI showed a leftsided hyperintense lesion near the midline of the mesencephalon. A repeat MRI scan 9 days later showed that the lesion was much smaller. He made a full recovery within 3 weeks. 

The posterior cerebral artery encircles the midbrain close to the oculomotor nerve at the level of the tentorium and supplies the inferior part of the temporal lobe, and the occipital lobe (Marinkovic et al. 1987). Many small perforating arteries arise from the proximal portion of the posterior cerebral artery to supply the midbrain, thalamus, hypothalamus and geniculate bodies. Sometimes a single perforating artery supplies the medial part of each thalamus, or both sides of the midbrain. In approximately 15% of individuals, the posterior cerebral artery is a direct continuation of the posterior commrmicating artery, its main blood supply then coming from the internal carotid artery rather than the basilar artery. 

Fig. 5.1. Brain CT images showing a large hypodense (arrows) edematous cerebral infarct in the distribution of the middle cerebral artery, with midline shift. Such large infarcts cause herniation of the cingulate gyrus under the falx cerebri of the ispsilateral uncus under the tentorium to compress the oculomotor nerve, posterior cerebral artery and brainstem and of the contralateral cerebral peduncle to cause ipsilateral hemiparesis.

Lesion Location Pupil Responses Anisocoria Field Nerve Defects Head Near Reflex Oculomotor Involvement Accommodation Disease or Syndrome... 

One girl in her third year, who had been immunized against tuberculosis at birth, developed an abscess of the associated lymph nodes (which were extirpated) and some weeks later developed intestinal BCG dissemination, which appeared to be cured by tuberculostatic treatment. Despite this, at the age of 22 years she developed a leftsided hemiplegia due to aneurysms and thrombosis of cerebral arteries, and 4 years later an oculomotor nerve paralysis was diagnosed. She died at 26 from recurrent intestinal BCG dissemination, which developed at the end of a pregnancy (a healthy premature child was bom). 

The autopsy confirmed the diagnoses and showed acid-fast bacilli in the adventitia of the basilar artery the paralysis of the oculomotor nerve was caused by the brain lesion. Defective function of macrophages was suggested as the possible cause of the underlying immunological abnormality (81). 

Other isolated reports of ophthalmic abnormalities refer to optic neuritis with blurring of vision, cortical blindness with fatal encephalopathy, mononeural abducent nerve paralysis, and complete but reversible bilateral oculomotor nerve paralysis (SED-13,1096) (94-97). 

Bauherz G, Soeur M, Lustman F. Oculomotor nerve paralysis induced by alpha Il-interferon. Acta Neurol Belg 1990 90(2) 111-14. 

Morphine and most opioids cause papillary constriction, which may be due to an excitatory action on the autonomic segment of the nucleus of the oculomotor nerve. Tolerance to this miotic effect is not usual. 

Isolated case reports of Guillain-Barre syndrome after HDC vaccine have been published (SED-11, 684) (SEDA-15, 356) (3). Polyneuropathy and oculomotor nerve impairment have been reported after Russian cell-culture vaccine (SEDA-12, 284). 

COX-1 Constitutive form of cyclooxygenase enzyme. COX-2 Inducible form of cyclooxygenase enzyme, cranial nerve Any of 12 pairs of nerves that arise directly from the brain I (olfactory) II (optic) III (oculomotor) IV (trochlear) V (trigeminal) VI (abducens) VII (facial) VIII (vestibulocochlear) IX (glossopharyngeal) X (vagus) XI (accessory) XII (hypoglossal). They comprise part of the peripheral nervous stem. 

Ml primary motor cortex 7-34, 81-89, 112-116 M2 secondary motor cortex 6-34, 80-86, 114-116 m5 motor root of the trigeminal nerve 46-59, 84-85, 90-97 MA3 medial accessory oculomotor nucleus 40-43, 79-80, 101-103 mcer middle cerebral artery 81 mch medial corticohypothalamic tract 21-22, 98-101 MCLH magnocellular nucleus of the lateral hypothalamus 31-33, 83, 94-95... 

III. Oculomotor. (Cranial nerves III, IV, and VI have similar functions and are tested as a unit.) Eye movements Patient is asked to watch a light as it moved up, down, and on both sides, while eye... 

Adverse effects of drugs may involve external ocular functions and structures, such as oculomotor function, eyeUds, lacrimation, conjunctiva, and cornea or internal structures, such as trabecular meshwork, cihary body, iris, lens, retina, and optic nerve. Higher-than-therapeutic doses and long duration of administration enhance the incidence of drug-induced oculotoxicity. 

Not only peripheral sensorimotor neuropathies are beneficially affected by the ACTH 4-9 analog Org 2766 but autonomic neuropathies, such as the crushed parasympathetic fibers of the oculomotor nerve are responsive to treatment with this neuropeptide, especially in the initial stages of regeneration. However, if the oculomotor nerve is sectioned, systemic treatment with Org 2766 improves neither the rate nor quality of functional recovery as determined by pupil diameter (Vandertop et al., 1994). 

Vandertop, W.P., de Vries, W.B., Notermans, N.C., Tulleken, C.A.F. and Gispen, W.H. (1994). Experimentally induced autonomic neuropathy beneficial effects of a systemic ACTH 4—9 analog on oculomotor nerve regeneration. Rest. Neurol. Neurosci. 7 37—43. 

The mydriatic action of atropine is not due to an effect on the contractility of the sphincter muscle, since direct electrical stimulation of this muscle in the atropinized eye leads to constriction of the pupil. Stimulation of the postganglionic fibers of the oculomotor nerve is, however, without effect in the fully atropinized eye. Atropine must therefore either prevent the normal action of the nerve itself or block the receptors which respond to acetylcholine liberated at the nerve ending. But pilocarpine still produces miosis after degeneration of the oculomotor nerve, and this effect is reversed by atropine. Consequently, atropine must act upon the receptor mechanism it does not interfere with the nerve itself but blocks the action of the chemical transmitter by means of which the nerve affects the sphincter muscle. 

---