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.     

Traumatic oculomotor nerve palsy.

Traumatic isolated oculomotor nerve palsy is not common. Oculomotor nerve palsy without internal ophthalmoplegia (pupil sparing) is extremely rare. We report a case of this condition in a child. An 11-year-old boy was transferred to our hospital after a head injury in a traffic accident. Neuro-ophthalmic examination showed that the left eye had limited adduction, supraduction, and infraduction, incomplete convergence and left ptosis, but no internal ophthalmoplegia. Magnetic resonance imaging indicated mild bending of the ipsilateral oculomotor nerve at the posterior petroclinoid ligament. One month after injury, movement of the patient's eyes was normal on examination, but there was mild diplopia. The suggested mechanism of the oculomotor nerve palsy with pupil sparing in this case is stretching of the oculomotor nerve at the posterior petroclinoid ligament, maintaining an intact pupillomotor nerve.     

Isolated left oculomotor nerve palsy following measles

A 10-month-old boy was admitted with ptosis on the left eyelid, which rapidly occurred following a disease with rash about 20 days before admission to our hospital. By history, none of the vaccinations had been performed. On physical examination, his vital signs were stable, and he had marasmus. Isolated left oculomotor nerve palsy was diagnosed. Cranial magnetic resonance imaging was normal. Serum IgM antibody to measles virus was positive. Oculomotor nerve palsy markedly improved on the 15th day of follow-up, and complete improvement was noted on the second month of follow-up. To our knowledge, this is the first case of oculomotor nerve palsy following measles.     

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.     

MRI abnormalities of the oculomotor nerve in a case of ophthalmoplegic migraine]

A 15-year-old girl presented with headache in the left retro-orbital area associated with double vision. She had a history of migraine headaches since the age of 9, and her mother also had suffered from migraine. The patient had experienced a similar episode at the age of 13, which resolved without any treatment in a day. On examination, two days after the onset of diplopia the patient had left ptosis and paresis of inwards and downwards in the left eye. Her pupils were isocoric, and the light reflex was prompt. MRI of the brain showed thickening and enhancement of the left third nerve through the cistern portion, especially at the oculomotor midbrain exit. No cavernous sinus involvement was noted. Results of the hemogram, ESR, and CSF were normal. The oculomotor palsy resolved spontaneously within six days. A follow-up MRI two months later demonstrated a marked lessening of enhancement at the oculomotor nerve but did not completely disappeared. These serial MRI abnormalities are thought to be important and typical findings seen in the patients of ophthalmoplegic migraine.     

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 late onset group B streptococcus meningitis with transient oculomotor nerve palsy

I report here a case of late onset Group B Streptococcus (GBS) meningitis with transient oculomotor nerve palsy. The boy was admitted to our hospital at 25 days of age. On the 5th hospital day, he was found to be unable to open the left eye. Although light reflex of both the eyes was intact, the left eye was deviated to the left lateral side. We administered intravenously steroid hormone and antibiotics. His eye movements were normalized on the 30th hospital day. Oculomotor nerve palsy in this case may have been caused by vasculitis of the middle cerebral artery. This case shows that steroid hormone is effective for vascular edema complicating neonatal meningitis.     

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.     

Recurrent unilateral painful oculomotor nerve palsy with an ipsilateral posterior ethmoidal mucocele

We presented a case of 6 episodes of the right painful oculomotor nerve palsy for 10 years, accompanied by a posterior ethmoidal mucocele on the same side. No destructive bone lesions were shown on every recurrence with the brain CT. For the pathogenesis of neurological involvement in cases of mucocele, either the direct compression by an expanding mucocele or the inflammatory infiltration from a mucocele has been considered. In this case the latter mechanism is considered to be responsible for the etiology of the painful oculomotor nerve palsy. Cases of the painful oculomotor nerve palsy with paranasal lesion or history of parasinusitis are characterized by (1) predominant in male, (2) neurological manifestations unilaterally on the same side of paranasal lesion, and (3) frequent recurrence of neurological symptoms.     

A case of partial fascicular oculomotor paresis caused by midbrain infarction]

We report a 74-year-old man with an ischemic lesion in the ventral midbrain. He presented with contralateral ptosis and marked upward gaze paresis of the right eye. Neurological examination revealed partial oculomotor nerve palsy caused by impairment of the right levator palpebrae, superior rectus and inferior oblique muscles. This finding is highly suggestive of a possible lesion in the midbrain affecting the oculomotor fascicular fibers. Magnetic resonance images showed an ischemic lesion in the paramedian area of the right midbrain tegmentum. The coronal view of T 2-weighted imaging clearly demonstrated to be the site of lesions below the red nucleus. It seemed to be coincidental with the impaired site of involving the caudal part of oculomotor fascicular fibers emerging from the nucleus. This report is considered to be a typical case of partial fascicular oculomotor paresis based on impairment of the caudal part of oculomotor fascicles for the levator palpebrae, superior rectus, and inferior oblique muscles. This is a valuable case to be documented in which neurological site of lesions are consistent with those found in radiological study.     

表现为动眼神经麻痹的垂体腺瘤卒中的诊治(附15例分析)

目的探讨垂体腺瘤卒中所致颅神经麻痹的手术疗效,提高术前诊断率。方法总结从2002年4月到2012年6月,15例合并动眼神经麻痹的垂体腺瘤患者的临床资料。男10例,女5例,年龄18~68岁,平均49.6岁;病程从6 d到7年;临床症状表现为头痛,视力下降,视野缺损,动眼神经麻痹,外展神经麻痹,垂体前叶功能低下等内分泌功能紊乱等;术前均行内分泌激素测定、垂体增强磁共振;所有患者均行经蝶入路手术切除垂体肿瘤。结果术后病理结果证实15例患者均存在垂体卒中,无手术死亡病例。术后动眼神经麻痹完全恢复9例,部分恢复3例,另外3例合并外展神经麻痹术后眼肌麻痹均未恢复。66.7%的患者视力改善(6/9),83.3%的视野缺损术后改善(5/6)。所有患者均获随访,平均随访时间12.4个月(6个月至2年)。结论垂体卒中合并动眼神经麻痹需尽快手术治疗,经蝶窦入路手术减压,肿瘤切除是治疗垂体卒中所致颅神经麻痹的安全有效的治疗方法。     

Neuro-ophthalmology

Eye movement research during the last year is discussed. The review covers the fields of: memory-guided saccades in supplementary motor area lesions, and the vertical saccadic system; cerebral hemispheric localization of smooth pursuit asymmetry; oculomotor disturbances in Wallenberg's syndrome; locomotory gaze instability in vestibular dysfunction; smooth pursuit disorders in vermal infarct; physiologic end-point and rebound nystagmus and the results of surgical and optical treatment of manifest latent nystagmus; clinical/magnetic resonance imaging correlations in abnormalities of horizontal gaze; mesencephalic cholinergic nuclei in progressive supranuclear palsy; as well as mesencephalic damage in diabetic third nerve palsy, divisional oculomotor nerve paresis; and new hypotheses on eye muscle susceptibility in myasthenia gravis.     

Bilateral ptosis, bilateral upgaze and adduction paresis, and monocular downgaze paresis from a mesencephalic infarction]

We report a 57-year-old man with an ischemic lesion in the midbrain. In the acute stage, he presented with bilateral ptosis and markedly limited extraocular motion except for bilateral abduction and downward motion of the right eye. The pupillary reaction to light of his left eye also was impaired. He was admitted to our hospital, and brain MRI showed a small infarction extending from the left paramedian to the median tegmentum of the midbrain. Three weeks after admission, the ptosis and limited extraocular right eye motion had resolved. The pupillary reaction and downward motion of the left eye normalized gradually within 3 weeks. Two months after admission, ptosis and the limited left eye adduction were partially resolved, but the markedly limited upgaze of the left eye had not changed. Initial neuro-ophthalmologic findings suggested involvement of the caudal part of the oculomotor nucleus and the left oculomotor nerve within the midbrain. The pattern of neuro-ophthalmologic impairment seen in our patient led us to conclude that the caudal oculomotor nucleus and medial part of the fascicular fibers of the left oculomotor nerve probably recovered first, after which recovery of the fascicular fibers progressed laterally. The results of serial MRI were consistent with this interpretation.     

Case of pontine infarction causing alternating hemiplegia with ipsilateral abducens nerve palsy and contralateral supranuclear facial nerve palsy]

We report a 73-year-old man with alternating abducent hemiplegia (Raymond syndrome) and contralateral supranuclear facial nerve palsy. On admission, he showed lateral gaze palsy of the right eye, left supranuclear facial nerve palsy, dysarthria and left hemiparesis. Brain MRI showed an infarct that was located in the paramedian and lateral area in the base of the caudal pons on the right side. MRA showed a mild stenosis of the basilar artery. Hemiplegia and supranuclear facial nerve palsy were considered to be caused by the involvement of corticospinal tract and corticobulbar tract that run at the ventromedial area of the pons. Abducens nerve palsy was considered to be caused by the involvement of infranuclear abducens nerve fibers. There has been one previously reported case of Raymond syndrome in which MRI determined the precise location of the lesion. In this case, a small hematoma was found at the ventral and medial pontomedullary junction, whereas the infarct in our case was located in the pontine base. We considered that documentation of our case was an important contribution to determine the pathogenesis of supranuclear facial nerve palsy due to caudal pontine lesions.     

表现为神经功能缺损的3例硬脑膜动静脉瘘误诊分析

目的探讨表现为神经功能缺损的硬脑膜动静脉瘘(DAVF)的临床及影像特点,以提高对该病的诊断率。方法回顾性分析3例临床表现为神经功能缺损的DAVF患者的病例及影像资料。结果例1:发作性言语不能,右侧肢体活动不灵,误诊为TIA;例2:痴呆、双下肢行走不稳、尿失禁,既往有头部伤史,误诊为正常颅压脑积水;例3:左侧动眼神经麻痹,既往糖尿病史9年,误诊为糖尿病动眼神经麻痹。3例均经DSA证实为DAVF。前两例头部MRI重新仔细阅片,发现两侧大脑皮层存在不对称的血管流空信号,提示DAVF,第3例左侧动眼神经麻痹患者头MRI和CTA均未见异常,行全脑DSA进一步除外动脉瘤时,意外发现病因为颈外动脉系统供血的海绵窦区DAVF。结论当患者有神经功能缺损、临床表现与影像不一致、对治疗不佳时,应考虑到DAVF的可能,注意MRI上有无细微的血管形态改变,以减少误诊。     

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.     

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.     

Acute lymphoblastic leukemia presenting with oculomotor nerve palsy

A 48-year-old man presented with left ptosis and double vision. Laboratory test findings indicated acute lymphoblastic leukemia (ALL). Lymphoblastic infiltration of both cavernous sinuses was observed on pituitary gland magnetic resonance imaging. Leukemias may present by many clinical conditions, but isolated cranial nerve palsy is very rare. To our knowledge, this is the first case of ALL presenting with oculomotor nerve palsy. Clinicians should consider oculomotor nerve palsy as the first ALL indication.