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]     

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.     

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.     

Nuclear oculomotor nerve syndrome and ocular tilt reaction caused by mesencephalic hematoma]

A 78-year-old man had a midbrain hemorrhage, documented by CT scan and MRI, resulting in a mild cerebellar syndrome predominant on the left upper limb, lateropulsion, and a complex ocular motor syndrome. The latter was associated with right nuclear oculomotor nerve palsy, gaze paresis to the left for voluntary saccades, and a tonic ocular tilt reaction. Pathophysiological mechanisms are discussed.     

Lymphoma as a cause of isolated oculomotor nerve palsy

We report two patients with diffuse large B-cell lymphoma with isolated oculomotor nerve palsy. This was the initial manifestation of lymphoma in one patient but in a second, the palsy appeared as a part of a generalized recurrence of lymphoma. In addition, we reviewed the clinical findings of 12 previously reported patients. Isolated oculomotor nerve palsy was most frequently associated with the large B-cell lymphoma cell type, and was not frequently associated with periorbital pain. The pupil was spared in half the patients irrespective of infiltration of the oculomotor nerve. MRI and cerebrospinal fluid cytological examinations are helpful in determining invasion of lymphoma to the oculomotor nerve, cavernous sinus, and surrounding leptomeninges.     

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.     

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.     

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.     

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.     

Neuro-ophthalmic pathological correlations in primary reticulum cell sarcoma of the nervous system

Two cases of primary reticulum cell sarcoma of the nervous system are presented because of their unusual clinicopathological correlations. Consecutive pupil-sparing third nerve paralysis was associated with tumour infiltrating the diencephalon and mesencephalon and the fascicular portions of both oculomotor nerves in the first case. Concomitant sympathetic involvement, as evidenced by relative miosis, cannot account for the preserved pupillary reactions. Preservation of the pupils was most likely the result of the intrinsic rather than compressive, third nerve involvement. In the second case involvement of the right facial colliculus was associated with the `one-and-a-half' syndrome (combined lateral gaze palsy and unilateral internuclear opthalmoplegia) and peripheral facial nerve paralysis. Terminally, the left lateral rectus muscle was also involved, and a discrete tumour implant had extended well beyond the midline.     

A case of midbrain and thalamic infarction showing Collier's sign in one side and blepharoptosis in the other side

A 68-year-old man was admitted to the hospital complaining of aphasia and right hemiparesis. Neurological examination revealed aphasia, right hemiparesis and ataxia in the left upper extremity. He showed striking ocular symptoms: intense retraction of the right eyelid (Collier's sign), complete ptosis of the left eyelid which might conceal Collier's sign, marked upward gaze palsy and slight downward gaze palsy. Vertebral angiography and MRI revealed an infarction in the left medial area and the left crus cerebri in the upper midbrain, the left subthalamic area inferomedially extending from the adjacent area to the posterior commissure and the medial area in the left thalamus resulting from occlusion of the left mesencephalic artery. From these MRI findings and the reports on pathological findings of patients with Collier's sign, we suggest that damage in the posterior commissure or its adjacent area may be responsible for the sign. Upward gaze palsy is often associated with Collier's sign because fibers mediating upward gaze may decussate in the posterior commissure. Third nerve palsy is also associated with the Collier's sign in some patients. The mechanism creating Collier's sign may be a disturbance of inhibitory fibers leading to the motoneuron pool of the levator muscle in the posterior commissure or its adjacent area.     

Oculomotor syndromes resulting from mesencephalic lesions in man

Midbrain lesions may give rise to the most complex eye movement disorders observed in clinical neurology. Three main types of dysfunction may be delineated, which may be combined: 1) intra-axial fascicular syndromes of the third and fourth cranial nerves; 2) nuclear syndromes of the third and fourth cranial nerves; 3) prenuclear and supranuclear syndromes, in which vertical gaze dysfunction is the main abnormality, but frequently with associated horizontal gaze dysfunction. The fascicular syndromes of the third nerve may be diagnosed when the oculomotor palsy is associated with some specific neurologic disturbances (syndromes of Weber, Benedikt, Claude-Nothnagel-Raymond-Cestan, Achard-Levi). The nuclear syndrome of the third nerve Is also quite suggestive, but it may be more difficult to diagnose an intra-axial fascicular or nuclear involvement of the fourth nerve. Supranuclear vertical gaze dysfunction are usually conjugate (upgaze/downgaze/vertical gaze palsies) and correspond to specific anatomical correlates. Dysconjugate vertical gaze syndromes are not as well known, are often less specific, and their topographic correlation is usually less precise; they include skew deviation and variants, slowly alternating skew deviation, see-saw nystagmus, monocular upgaze palsy, ocular tilt reaction, vertical one-and-a-half syndrome, and "V" pattern pseudobobbing. Some of these eye movement disorders are not only specific for the location of the lesion, but also for a definite etiology (for instance, acute downgaze palsy suggests bilateral infarction of the posterior thalamo-subthalamic paramedian territory).     

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.     

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.     

Claude's syndrome associated with supranuclear horizontal gaze palsy caused by dorsomedial midbrain infarction

Claude's syndrome caused by dorsal midbrain lesion is characterized by ipsilateral third nerve palsy and contralateral ataxia. To date, reports in the literature concerning Claude's syndrome associated with the midbrain paresis of horizontal gaze are rare. A 62-year-old man suddenly developed left third cranial nerve palsy, right lateral gaze palsy, and right ataxia. Intact Bell's phenomenon and preserved right horizontal oculocephalic reflex suggested the lateral gaze palsy in the right eye was supranuclear in nature. Magnetic resonance imaging (MRI) revealed an infarction in the left dorsomedial midbrain. Although the red nucleus has often been suggested as the lesion site responsible for Claude's syndrome, a lesion of the superior cerebellar peduncle just below and medial to the red nucleus could be responsible for this syndrome. This case demonstrates neurological heterogeneity of midbrain infarction.     

Isolated abducens nerve palsy caused by pontine infarction]

An 82-year-old hypertensive man suddenly developed diplopia during right lateral gaze. Neurological examination revealed right isolated abducens nerve palsy without any other findings. By cranial CT scan, a low density area over the posterior limb of right internal capsule and tortuosity of basilar artery were noted. 3 months later, his symptom disappeared and then he was well in next 2 years til he felt diplopia during left lateral gaze. On this time he showed left isolated abducens nerve palsy. Though cranial CT scan failed to find out new abnormality, T2-weighted cranial MRI disclosed high intensity spot over left pontine base located between medial lemniscus and pyramidal tract, which was supposed to coincide to fascicle of left abducens nerve Three months later, he recovered in the same manner as 2 years before. Hemilateral isolated abducens nerve palsy may be caused by many origins, but pontine infarct was not detected so much in pre-MRI era. Being the long-term prognosis of the lacunar infarction not satisfactory, it is important for the cases of isolated abducens palsy to ascertain whether there is pontine small infarction or not. So in these cases, precise examination including MRI should be needed.     

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.     

Clinical analysis of the mechanism of oculomotor nerve palsy caused by unruptured internal carotid artery posterior communicating artery aneurysm]

We analyzed the clinical course of eight female patients of oculomotor nerve palsy due to unruptured internal artery posterior (IC-PC) communicating artery aneurysm in order to speculate on the mechanism of aneurysmal rupture. Seven of the eight patients had preceding headache or ophthalmalgia, three of them deteriorated oculomotor nerve palsy and one showed worsening of ophthalmalgia. These deteriorations occurred between three to seven days after the first clinical symptom appeared. Neck clipping of aneurysm was performed for all eight patients. These aneurysms were profiled except for one patient whose aneurysm ruptured before operation. None of these seven patients had subarachnoid hemorrhage in the operative field. The patients who showed clinical deterioration had fragile aneurysm wall, wall with bleb, and one aneurysm showed minor blood leakage during operative manipulation. In the four patients who did not show clinical deterioration, aneurysm attached oculomotor nerve, these aneurysm walls were arteriosclerotic and we could not find the fragile portion during operation. Repeated minor bleeding near the oculomotor nerve or direct aneurysmal compression are the main causes of oculomotor nerve palsy with unruptured IC-PC aneurysm. Adhesion or stimulation of aneurysm on the upper border of cavernous sinus cause the headache or ophthalmalgia and these deteriorations are thought to occur gradually. However, these deteriorations occur more rapidly than ever thought and reflect acute aneurysmal growth and its direct affect on the oculomotor nerve. IC-PC aneurysm is the only aneurysm we can observe its aneurysmal growth by its unique clinical presentation. From this study, we conclude that the deterioration of oculomotor nerve palsy, preceding headache or ophthalmalgia reflects rapid growth of unruptured IC-PC aneurysm. We neurosurgeons consider it to be an urgent rupture period and should introduce surgical management to prevent its rupture and the devastating consequence of subarachnoid hemorrhage.     

Isolated oculomotor nerve palsy as the presenting clinical manifestation of a meningeal carcinomatosis: a case report

Abstract We present a previously unreported case of isolated oculomotor nerve palsy as the inaugural clinical sign of meningeal carcinomatosis (MC). Gadolinium-enhanced magnetic resonance images (MRI) were unremarkable. Cerebrospinal fluid (CSF) analysis showed malignant cells consistent with a pulmonary adenocarcinoma; the chest CT revealed a small pulmonary mass in the upper right lobe. This case highlights the importance of considering MC in all patients who develop sudden oculomotor palsy; lumbar punctures should always be performed on patients with normal MRI when other possible causes of oculomotor palsy have been ruled out.     

Isolated superior division oculomotor palsy in a child with spontaneous recovery.

A 10 year old boy with a superior division palsy of the left oculomotor nerve is reported. He had a flu-like illness 1 week before the onset. The computed tomography and magnetic resonance imaging scans were normal. Laboratory data for evaluation of infection, diabetes mellitus and myasthenia gravis were normal. The symptoms spontaneously disappeared after 2 months. The course of the illness in conjunction with the negative laboratory findings made this case an example of partial paralysis of the third nerve related to viral infection. In the literature, only several cases with isolated divisional palsy of the oculomotor nerve were found after a viral infection. Inferior division palsy has been reported in five children. Superior division palsy has been published in only two cases. Divisional palsy is more common among children and resolves spontaneously. This rare but important clinical entity is one of the differential diagnoses in oculomotor nerve palsies, particularly in children, which are neuroradiologically undiagnosed. It occurs after a viral infection and may affect a superior or inferior division alone.