外伤性动眼神经麻痹的临床特点分析

目的总结轻型颅脑损伤所致动眼神经麻痹后的临床特点。方法通过眼外肌运动、眼睑活动、瞳孔大小分析20例轻型颅脑损伤患者动眼神经麻痹的严重程度及功能恢复,随访时间平均为14.2月(3个月~2年)。结果 15名男性患者和5名女性患者纳入此次研究。最常见的外伤原因是交通事故65.4%(13例);眼内肌麻痹是最常见的临床症状;上睑下垂、眼外肌麻痹和眼内肌麻痹的恢复率分别是95%(19例),83.3%(17例)和50%(10例)。结论眼球活动受限是影响轻型颅脑损伤动眼神经麻痹患者生活质量的一个主要因素;蝶骨骨折可能是一个潜在的机制参与了外伤性动眼神经麻痹的发生。     

Pupil sparing in oculomotor palsy: A brief review

The clinical dictum that pupil sparing in oculomotor nerve palsy predicts an extraaxial ischemic lesion while pupil involvement predicts an extraaxial compressive lesion has some important exceptions. Two case reports and a review of the literature disclose that pupil sparing occurs in a small proportion of intraaxial and compressve subarachnoid oculomotor nerve lesions and in a large proportion of compressive cavernous sinus oculomotor nerve lesions. Careful examination is also necessary to separate examples of apparent pupil sparing in cases of aberrant regeneration and in some instances of cavernous sinus compression.     

A patient with reversible pupil-sparing Weber's syndrome

This is a case report of a lady who presented with pupil-sparing Weber's syndrome. She had left oculomotor nerve palsy with normal pupil and right hemiparesis. The patient subsequently made a good recovery. An ischemic lesion of the lower mid-brain was demonstrated on the MRI scan of the brain, which corresponds to the motor nucleus of the oculomotor nerve. The article also describes the neuroanatomy of the oculomotor nerve and how its partial lesions lead to sparing of the pupil. In addition, this case report documents that a pupil-sparing Weber's syndrome could be reversible.     

Oculomotor nerve palsy due to small midbrain infarct--functional topography based on MRI findings]

This is a report of 3 cases presented with oculomotor nerve palsy caused by small midbrain infarct. The aim of this report is to clarify the functional topography of intranuclear and intrafascicular portion of the oculomotor nerve with MRI. Three cases are 2 males and 1 female, ranging 51 to 68 years in age. Except for the long tract signs at the acute stage, cardinal sings were all eye-related, incomplete in 1 case and pupil sparing-type in 2 cases. In MRI, the size of the lesion extended 5 to 12 mm. In the incomplete palsy case, the infarction extended from the level immediately below the 3rd ventricle into the whole length of midbrain, whereas in the pupil-sparing types, more limited lesion excluding the upper part of the midbrain was noted. Anatomically the longitudinal size of the nucleus is 10mm and nerves functionally related to pupil reaction, eye motion and eyelid elevation are arranged in rosrocaudal order. Therefore, it is speculated that in midbrain, intrafascicular location of nerve fibers associated with pupil reaction is rostral and oculomotor nerve palsy of pupil sparing type is caused by the lesion excluding the rostral midbrain. MRI findings of the present 3 cases are compatible with this speculation. The lowest border of red nucleus is at the level of superior colliculus, whereas oculomotor nucleus has its lowest margin at the inferior colliculus. Therefore, red nucleus becomes an informative landmark to visualized the level of oculomotor nerve injury, since the red nucleus is clearly demonstrated in high intensity in T2 weighted image.     

Internal Carotid Artery Occlusion Causing Acute Cranial Neuropathies

A 54-year-old male with a history of left posterior parietal ischemic stroke, epilepsy, tobacco and marijuana smoking, and alcohol abuse, presented with acute left visual loss and diplopia. On examination, he had reduced left visual acuity and a left oculomotor nerve palsy. CT angiogram from aortic arch to circle of Willis identified extensive thrombus occluding the left common and internal carotid arteries, extending to the left ophthalmic artery. This case demonstrates acute visual loss from ophthalmic artery occlusion, and left oculomotor nerve palsy from occlusion of the inferolateral trunk of the internal carotid artery (cavernous sinus portion).     

Incomplete oculomotor nerve palsy in the subarachnoid space caused by traumatic brain injury

A patient with traumatic brain injury showed incomplete oculomotor nerve palsy in the subarachnoid space. A 12-year-old girl was hospitalized after a head injury. Neuro-ophthalmic examination showed that the left eye had a ptosis and pupillary involvement. An MRI indicated an intracranial hematoma at the basilar portion of the left temple. The ptosis and pupillary involvement improved after elimination of the hematoma. The presentation patterns are best explained by topographic organization of the third nerve fiber within the subarachnoid space. This case suggests that the topographic organization of the third nerve should be considered in diagnosis of oculomotor nerve palsy.     

Waking up from Coronary Bypass Surgery and One Eye does not Move Right

Introduction

Complications of coronary artery bypass graft surgery (CABG) include acute oculomotor nerve palsy secondary to ischemic stroke and pituitary apoplexy. These can present with impairment of extraocular muscle function as well as involvement or sparing of the pupil.

Case Report

We report the case of a 58-year-old male admitted for elective CABG surgery for severe coronary artery disease and found to have a pupil-sparing partial oculomotor palsy post-procedure. Neurological examination revealed left pupil-sparing isolated medial rectus and levator palpebrae superioris paresis. Magnetic resonance imaging demonstrated acute midbrain infarction.

Conclusion

Acute pupil-sparing partial oculomotor nerve palsy should be recognized as a neurological complication of cardiac surgery. Pupillary involvement can be helpful in identifying the underlying etiology.     

Presentation of a cavernous angioma with an oculomotor nuclear syndrome: a case report

INTRODUCTION: The nuclear syndrome of the oculomotor nerve, first described in 1981, is characterized by ipsilateral third nerve palsy and elevation paresis of the contralateral eye. CASE REPORT: A 59-year-old man suddenly developed diplopia and headache. Neurological examination showed nuclear ophthalmoplegia of the left third nerve without any other neurological abnormality. MRI findings demonstrated a typical, popcorn-like, smoothly circumscribed left posterior lesion. Surgical resection was not performed because of the deep localization. Spontaneous bleeding developed. CONCLUSION: This neuro-ophthalmological complication of a cavernous angioma, as seen in our patient, has rarely been described in the literature. The clinical presentation and anatomic elements of the nuclear oculomotor syndrome are discussed. This exceptional localization provides a useful illustration of anatomoclinical correlations.     

Successful steroid pulse therapy for acute unilateral oculomotor nerve palsy associated with norovirus infection

We report a 4-year-old boy who developed acute unilateral oculomotor nerve palsy following Norovirus infection. He visited our hospital because of diplopia three weeks after Norovirus gastroenteritis. Physical examination showed only the left oculomotor nerve palsy. Enhanced MRI of the brain and cerebrospinal fluid examination revealed no abnormality. Anti GQlb antibody was negative. Because blepharoptosis and ophthalmoplegia progressed rapidly, we performed three courses of steroid pulse therapy (methylpredonisolone 30 mg/kg x 3 day/course) combined with vitamin B6. Autonomic dysfunction (isocorea, light reflex) began to improve in several days and subsequently extraocular movements (blepharoptosis, infraduction supraduction, adducent in order) resolved completely in one month. Idiopathic oculomotor paralysis is usually believed to be selflimited, but steroid pulse therapy should to be considered in cases ocular paralysis is so severe or progressive that immune-mediated mechanism was presumed.     

Ophthalmoplegic migraine: MRI findings. Case report

Ophthalmoplegic migraine is a rare syndrome in which headache is associated with ophthalmoplegia and third, fourth or sixth cranial nerves palsy. It occurs most frequently in childhood and teenagers. At magnetic resonance imaging (MRI) with gadolinium (GD-DTPA) it may be observed a transitory enhancement of the affected nerve. We present the case of a male teenager, 16 years old, with typical medical history and enhanced signal at left oculomotor nerve in cisternal portion at MRI weighted in T1 with GD-DTPA. On the control exam, eighteen months later, there was no remarkable lesion. The enhancement of oculomotor nerve at MRI is always pathological and among the differential diagnosis we must include: neoplasia (lymphoma and leukemia), infections (AIDS, syphilis), inflammatory process (sarcoidose and Tolosa-Hunt syndrome) and vascular (posterior communicating artery aneurysm).     

不同治疗方法对后交通动脉瘤预后的影响

目的探讨手术治疗和栓塞这两种不同治疗方法对后交通动脉瘤的动眼神经麻痹症状的改善。方法对8年来的102例完全动眼神经麻痹的后交通动脉瘤患者回顾性分析，研究治疗方法与动眼神经功能恢复的程度的关系。结果手术组58例治疗后，动眼神经功能完全恢复19例，部分恢复29例。无恢复10例。栓塞组44例治疗后有6例完全恢复，部分恢复20例，无恢复18例。结论手术治疗后交通动脉瘤后的动眼神经功能的恢复率和部分恢复率都明显高于栓塞治疗。     

A case of multiple fusiform aneurysms presenting homonymous hemianopsia (author's transl)

Fusiform Aneurysms are encountered in elderly persons with advanced arteriosclerosis. When they are enlarged to compress the neighboring structures, they may resemble tumors symptomatically. Especially when situated in close relation to the optic nerve or chiasmatic region, pituitary tumor is likely to be suspected. This is a case of 62 year old female with a giant fusiform aneurysm of the right internal carotid artery extending to the middle cerebral artery which caused left homonymous hemianopsia and a large aneurysm in the cavernous portion of the left internal carotid artery with fusiform extension of the distal portion of the carotid artery which presented left blepharoptosis, dilated pupil and total ophthalmoplegia. The basilar artery and the right meningohypophyseal artery showed fusiform dilatation as well. Systemic atherosclerotic change, abdominal aortic aneurysm, nephrosclerosis were also accompanied. The computed tomography demonstrated the aneurysms distinctly. Left oculomotor palsy disappeared after six months with residue of left homonymous hemianopsia. Surgical intervention was not attempted, because of the widely distributed constitutional aneurysms in the whole body.     

Isolated oculomotor nerve palsy in lymphoma

We report a patient with non-Hodgkin's lymphoma who developed a unilateral left oculomotor nerve palsy. Only eyelid lifting and vertical gaze were involved. Lateral gaze or sizes and light reactions of pupils were not involved. Magnetic resonance imaging revealed an enhancement of an upper part of left cavernous sinus and the posterior clinoid process. It was conceivable that lymphoma invaded the upper branch of oculomotor nerve. Such neurological symptoms in cases of oculomotor nerve palsy by lymphoma have not been reported previously. Because cranial neuropathy could occur as the first sign of lymphoma, lymphoma is an important differential diagnosis for the partial oculomotor palsy such as our present case.     

A neuro-Behcet's lesion in oculomotor nerve nucleus

OBJECTIVE: Fascicular oculomotor nerve involvement is occasionally seen in Behcet's disease, but nuclear involvement is very rare. CASE PRESENTATION: A 25-year-old woman presented with the Behcet's symptoms and the left eye problems. Physical examination revealed muco-cutaneous lesions, eyelid ptosis, mydriasis, upward and medial gaze palsy and lateral deviation on the left eye. Serologic tests were positive. An inflammatory lesion was detected in the left oculomotor nerve nucleus on magnetic resonance imaging. Neuro-Behcet's disease was considered the most likely diagnosis. RESULT: Dexamethasone treatment was ordered. Muco-cutaneal lesions, laboratory abnormalities were normalized after 1 year; but oculomotor nerve palsy persisted in spite of improvement in radiological findings. CONCLUSION: Clinical signs of oculomotor nerve palsy may persist despite the radiological improvement.     

A case of Tolosa-Hunt syndrome accompanied by facial and vestibular nerve damage]

A 37-year old man, who had repeatedly suffered from transient ophthalmoplegia in his left eye at the age of 29 and 36, developed left painful ophthalmoplegia accompanied by ipsilateral facial nerve palsy in August, 1991. Neurological examination revealed involvement of the left oculomotor, trochlear, ophthalmic division of the trigeminal, abducens, facial and vestibular nerves. Gadolinium-enhanced MRI which was taken at the acute phase of the illness demonstrated markedly enhanced left cavernous sinus and adjacent thickened dura mater in the middle cranial fossa. At the remission phase after starting corticosteroid therapy, these enhanced lesions were no longer observed even in enhanced MRI studies. We diagnosed him as suffering from Tolosa-Hunt syndrome presently accompanied by facial and vestibular nerve damage because of his history of illness, confined lesion in the left cavernous sinus and steroid-induced remission. We concluded that Tolosa-Hunt syndrome may be accompanied by damage of other cranial nerves in its course and that repeated gadolinium-enhanced MRIs are necessary for diagnosis and observation of the patients.     

Midbrain arteriovenous malformation causing bilateral total ophthalmoplegia as an initial ocular symptom--a case report

A 61-year-old woman is presented with a bilateral total ophthalmoplegia as an initial ocular symptom, caused by a midbrain hematoma. She complained of acute headache, nausea, vomiting and bilateral closure of her eyelids. Examination on admission showed meningeal irritation; mild consciousness disturbance; bilateral total ophthalmoplegia; left hemiparesis; ataxia in all extremities, more marked to the left. Computed tomography demonstrated a small hematoma in the midbrain tegmentum. Angiography demonstrated midbrain arteriovenous malformation, and she was treated conservatively. Abduction of both eyes and adduction of the left eye appeared on the next day of the ictus, and after that, improved gradually. Left ptosis had improved since one week after the ictus. Light reflex of the left pupil had seen 5 days after the ictus. At the same time, the left pupil revealed an oval-shape. Right internal ophthalmoplegia continued to exist. One year later, the right eye deviated externally, and the left deviated inferio-medially. Abduction of both eyes was normal. Infraduction of both eyes was seen, but limited on the left. Upgaze paresis remained unchanged, and adduction of the right eye was absent. Adduction of the left eye showed almost full recovery. There was right complete ptosis, but left ptosis became indefinite. These ocular findings indicated typical right oculomotor paresis plus superior rectus paresis of the left eye, which suggested a destructive lesion in the right oculomotor nucleus. Also, her left extremities showed a hemiparesis as a pyramidal tract sign (Weber's syndrome) and an ataxia as a cerebellar sign (Claude's syndrome).(ABSTRACT TRUNCATED AT 250 WORDS)     

Oculomotor nerve palsy as an initial manifestation of polycythemia vera

In polycythemia vera (PV), even though thrombotic complications are common, ophthalmoplegia rarely occurs, and oculomotor nerve palsy has not been described as an initial manifestation. We present a 53-year-old woman who developed right oculomotor nerve palsy and investigation disclosed PV as the cause of ophthalmoplegia. MRI also revealed an acute silent infarction in the right frontal subcortex. PV may manifest with oculomotor nerve palsy owing to a thrombotic complication and should be considered in the differential diagnosis of acute ophthalmoplegia.     

Isolated oculomotor nerve palsy in lymphoma

Abstract

We report a patient with non-Hodgkin’s lymphoma who developed a unilateral left oculomotor nerve palsy. Only eyelid lifting and vertical gaze were involved. Lateral gaze or sizes and light reactions of pupils were not involved. Magnetic resonance imaging revealed an enhancement of an upper part of left cavernous sinus and the posterior clinoid process. It was conceivable that lymphoma invaded the upper branch of oculomotor nerve. Such neurological symptoms in cases of oculomotor nerve palsy by lymphoma have not been reported previously. Because cranial neuropathy could occur as the first sign of lymphoma, lymphoma is an important differential diagnosis for the partial oculomotor palsy such as our present case. [Neurol Res 2000; 22: 347-348]     

Isolated nuclear oculomotor nerve palsy due to mesencephalic infarction

A patient with unilateral nuclear oculomotor palsy due to midbrain infarction is described. A 46-year-old man was admitted because of difficulty in opening right eye and double vision noticed when he awoke in that morning. On admission, neurological examination revealed total right oculomotor palsy with slight impairment of left upward gaze. There were no other neurologic abnormalities at all. Brain CT and cerebral angiograms were also normal. Magnetic resonance imaging (MRI) performed on the ninth day, however, demonstrated high signal intensity in the right tegmentum of the mesencephalon on T2-weighted images, which was shown more clearly after the administration of Gadolinium-DPTA. He was diagnosed as nuclear third nerve palsy caused by midbrain infarction. The majority of isolated oculomotor nerve palsy has been reported to be caused by extraaxial lesion. When the oculomotor palsy is caused by intraaxial ischemic lesion, it is usually accompanied by other brain stem signs, because abundant nuclei and fibers are present adjacent to the oculomotor nucleus and nerve in the mesencephalon. The present case clarified that such a small infarct disclosed only by MRI can cause isolated oculomotor nerve palsy. It is emphasized that the intraaxial ischemic lesion should be ruled out by using the sophisticated diagnostic aid before making diagnosis of peripheral lesion. This is the first report of the isolated third nerve palsy resulting from mesencephalic ischemic lesion in the Japanese.     

A case of left third nerve palsy and contralateral vertical gaze palsy with medial midbrain infarction]

An 81-year-old man developed oculomotor nerve palsy of the left eye and vertical gaze palsy of the right eye due to left medial midbrain infarction. His left eyelid was ptotic and the pupil was dilated. His right eye showed normal horizontal movement and Bell's phenomenon was preserved although the oculocephalic reflex was incomplete. There were no other abnormal neurological findings. The brain MRI revealed a high-intensity lesion in left medial midbrain on T2 weighted image. This lesion involved the oculomotor nerve nucleus, the interstitial nucleus of Cajal, and the rostral intersititial nucleus of the medial longitudinal fasciculus (riMLF). We thought that upward gaze palsy of the right eye was resulted from the infarction of the left riMLF or disruption of the axonal collateral of upward gaze fibers in the left oculomotor nucleus. Downward gaze palsy was resulted from the damage of the downward gaze fibers before their decussation, or the damage of the left interstitial nucleus of Cajal. This case provides evidence that unilateral lesion of the midbrain could cause contralateral vertical gaze palsy.