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.     

Dissection of the intracranial internal carotid artery producing isolated oculomotor nerve palsy with sparing of pupil

Dissection of the internal carotid artery usually occurs in the cervical segment, but rarely may involve the artery in the intracranial course (1). The clinical course of intracranial dissection is often catastrophic, with rapid onset of profound neurological deficit, as a result of middle and/or anterior cerebral artery involvement. When this occurs the mortality rate is generally considered high. We describe a case of intracranial internal carotid artery dissection following trivial trauma presented with an isolated painful pupillary sparing oculomotor nerve palsy.     

Sphenoid sinus mucocele with recurrent visual disturbance]

We presented a case with sphenoid sinus mucocele associated with recurrent visual disturbance on the same side. A 22-year-old female showed two episodes of visual disturbance on the left eye for three months. She was diagnosed as acute retrobulbar optic neuritis and was treated with cortico-steroid. In two episodes visual disturbance improved in a week. MRI showed a mucocele in the left sphenoid sinus. No destruction of left optic canal was found in roentgenogram and the left optic nerve showed swelling with high intensity in T2-weighted MRI. Therefore the expansion of inflammation or edema in optic canal rather than direct compression by expanding mucocele was considered as pathogenesis of the visual disturbance. In a case of recurrent and unilateral visual disturbance, a mucocele of posterior paranasal sinus should be suspected in the differential diagnosis.     

Ocular signs due to an oculomotor intranuclear lesion: palsy of adduction and contralateral eye elevation.

Reports on ocular signs of discrete oculomotor nuclear lesions have been rare. This is a case report of a patient with the sudden onset of limited adduction on the left side and bilateral elevation palsy, more pronounced on the right side. The symptoms lasted for 3 days. Neuroimaging study did not reveal a responsible lesion. The patient was diagnosed as having a lacunar infarct. It is neuroanatomically established that the oculomotor subnucleus to the superior rectus muscle primarily cross-innervates the muscle. The palsy of adduction and contralateral supraduction is most plausibly explained by a partial oculomotor nuclear lesion. This patient demonstrated the intranuclear close arrangement of the nerves for the superior and medial rectus muscles. This case reminds us of the clinical importance of basic anatomy based neurological examinations in this computer orientated, high tech era.     

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.     

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.     

Tuberculous meningitis with initial manifestation of isolated oculomotor nerve palsy

Tuberculous meningitis (TB meningitis) is a subacute meningitis known for its various form of initial manifestations, which often make early diagnosis difficult. The present case report demonstrates a patient with TB meningitis, who had initial manifestation of isolated right oculomotor nerve palsy. High vigilance is needed in diagnosing TB meningitis. A 75 year-old female was hospitalized due to acute onset of right side ptosis. Thorough neurological examination at admission revealed isolated right oculomotor nerve palsy. Brain magnetic resonance imaging and cerebral angiography showed no specific finding. Lumbar puncture was performed two days later due to low grade fever. Cerebrospinal fluid (CSF) study and the polymerase chain reaction on CSF confirmed the diagnosis of TB meningitis. Because TB meningitis is a chronic disease, cranial nerve palsies are common manifestations. This report suggests that TB meningitis should be a disease of differential diagnosis for isolated oculomotor nerve palsy.     

Midbrain infarction presenting isolated inferior rectus nuclear palsy]

We presented a patient of isolated inferior rectus muscle palsy from midbrain lacunar infarction involving the oculomotor nucleus. The patient noticed sudden onset diplopia gazing to the right side, especially to the right-lower direction. He did not have any other symptom, and neurological examination revealed no other findings. Brain MRI documented the focal hyperintense lesion on T2-weighted images in the right-median midbrain ventral to the aqueduct at the level of the superior colliculus. This lesion involved the right oculomotor nucleus, especially the dorso-lateral subnucleus extend to the inferior rectus muscle. The oculomotor nuclear complex consists of one unpaired subnucleus and four paired subnuclei. Among them, the inferior rectus subnucleus lies dorso-laterally. So nucleus lesion may cause isolated weakness of one of muscles innervated by the oculomotor nerve. Among them the isolated inferior rectus muscle palsy can occur relatively.     

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.     

Intra-axial involvement of the common oculomotor nerve in mesencephalic infarctions

Mesencephalic infarcts are rarely limited to the midbrain, and usually extend rostrally to the thalamus. This fact explains why an elective palsy of the oculomotor nerve is exceedingly uncommon in brainstem infarcts. We studied 4 cases with a unilateral infarct apparently restricted to the middle mesencephalon, with intra-axial involvement of the oculomotor nerve. In 2 cases with a fascicular lesion, there was a contralateral hemiparesis or hemi-ataxia, so that it is possible to term them Weber's syndrome and Claude's syndrome. In the 2 other cases, we suggest that a nuclear syndrome of the oculomotor nerve was present, because of bilateral involvement of the rectus superior in both cases, of the levator palpebrae in one case, and of the parasympathetic pupillary fibres in the other, although the infarct was unilateral. There are several clinical variants of the intra-axial syndrome of the oculomotor nerve which can be differentiated according to the uni or bilaterality of the oculomotor palsy, the pupillary disturbances, and the type of associated neurological dysfunction. The nuclear syndrome corresponds to an infarction of the median arterial area, which is directly supplied by the most distal part of the basilar artery. The fascicular syndromes correspond to infarction of the paramedian and intermediolateral areas supplied by the first part of the posterior cerebral artery (basilar communicating or mesencephalic artery). As the paramedian thalamic arteries also originate from the basilar communicating artery, most infarcts also involve the upper midbrain and the thalamus, producing supranuclear oculomotor disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mucocele of the sphenoid sinus: A rare cause of reversible 3rd nerve palsy

Ophthalmoplegia due to 3^rd nerve palsy is a common occurrence, and is usually a sign of diabetes mellitus or a serious intracranial disease. We report a rare case of pupil sparing 3^rd nerve palsy caused by mucocele of the sphenoid sinus. The patient regained 3^rd nerve functions after successful decompression of the mucocele. Early and correct diagnosis of this relatively benign condition is important to prevent permanent neurological deficits, including visual loss by optic nerve atrophy. Etiology, clinical manifestations and treatment of the sphenoid mucoceles is discussed and available literature is reviewed.     

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]     

Abduction of the eyeballs palsy as a first sign of subarachnoid hemorrhage from ruptured posterior inferior cerebellar artery aneurysm: a case report

The authors present a rare case of the abduction of the eyeballs palsy caused by subarachnoid hemorrhage from ruptured posterior-inferior cerebellar artery aneurysm, which appeared as a first sign of hemorrhage. Aneurysm was clipped. During three days after the operation, oculomotor lesions appeared persistent, no consciousness deterioration or other focal signs were observed. On the third day after the operation asystolic cardiac arrest appeared. Control CT scan did not reveal any pathological changes responsible for such deterioration. The patient died. In our case after an analysis of the mechanism and pathophysiology of this lesion in our opinion that palsy might be caused by influence of extravasated blood after hemorrhage. This thesis is adequate to the reviewed literature on this problem. Nevertheless, the compression of the abducent nerve as the reason cannot be excluded, e.g. rapid enlargement of the aneurysm or the compression of the brain stem near the nerve. Posthemorrhagic lesion of the brain stem may have been the reason of this lesion, caused by penetration of the blood into the ventricle during subarachnoidal hemorrhage. Although these lesions are very rare, subarachnoid hemorrhage should be taken into consideration when the patient with eyeballs abduction palsy is admitted to a neurosurgical or neurological department.     

Fascicular arrangement within the oculomotor nerve MRI analysis of a midbrain infarct.

The fascicular arrangement of the oculomotor nerve within the midbrain is not adequately elucidated in humans. We treated a patient with a partial oculomotor palsy who had impaired adduction and supraduction on the left side, which were attributed to an ipsilateral lacunar infarct. CT and MRI revealed a discrete lesion in the centre of the midbrain tegmentum in the rostrocaudal plane. This case suggests that the oculomotor fibres for extraocular movement are located in the middle of the the midbrain, and supports the fascicular proximity of the superior and medial rectus muscles. The fascicular arrangement of the midbrain oculomotor nerve is speculated to be pupillary component, extraocular movement and eyelid elevation in that rostrocaudal order, based on the previous reports of neuro-ophthalmological impairment and MRI findings, which are analogous to the nuclear arrangement proposed by Warwick.     

Isolated nuclear oculomotor nerve syndrome due to mesencephalic hematoma

Unilateral third nerve palsy with bilateral superior rectus paresis and bilateral ptosis is a typical condition for nuclear oculomotor nerve syndrome. We report a case of nuclear oculomotor nerve syndrome due to midbrain hemorrhage, as a rare cause. A 73-year-old man presented with an abrupt onset of double vision and difficulty opening his eyes. He had uncontrolled hypertension in his history. Neurological examination revealed right oculomotor palsy with impairment of bilateral upward gaze and bilateral ptosis. MRI showed a mesencephalic area of increased T1 signal and decreased T2 signal consistent with a subacute hematoma. It is emphasized that isolated mesencephalic hemorrhage may be the cause of the nuclear oculomotor nerve syndrome without associated neurological signs.     

Nuclear syndrome of the common oculomotor nerve after skull injury

A case of a nuclear syndrome of the oculomotor nerve due to trauma is reported. There was 3rd nerve palsy on the ipsilateral side, a superior rectus muscle palsy on the contralateral side and a bilateral ptosis. The location was confirmed by magnetic resonance imaging and CT.     

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.     

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.     

Crossed innervation of the superior rectus.

We studied two patients which showed a paralysis of the oculomotor nerve on one side and isolated paralysis of the superior rectus on the other side. On the side of oculomotor nerve paralysis, midbrain infarct extending from the paramedian tegmentum to crus cerebri was demonstrated in one case who showed no recovery, and a small lacuna in midbrain tegmentum in another one who showed complete recovery. On the side of isolated paralysis of the superior rectus, no lesion was demonstrated by CT and MRI, and no clinical signs of the involvement of fiber tracts or nuclei were evident in both cases. A unilateral lesion of oculomotor nerve nucleus caused a paralysis of the contralateral superior rectus.     

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.