Paresia transitoria del nervio troclear tras angioplastia percutánea

Case report

A case is presented of a 63-year-old man who suffered a unilateral isolated trochlear nerve palsy with vertical diplopia following an elective radial coronary angiography and percutaneous coronary intervention, which resolved spontaneously within 2 months.

Third cranial nerve palsy in children.

PURPOSE: To report the causes and the sensory, motor, and cosmetic results after treatment for oculomotor (third cranial nerve) palsy in children. METHODS: Review of the clinical records of children with a diagnosis of third cranial nerve palsy followed up in a university-based pediatric ophthalmology practice between 1981 and 1996. RESULTS: Forty-nine children with 53 affected eyes were followed up for a mean of 5.5 years. Third cranial nerve palsy was partial in 31 children (32 eyes) and complete in 18 children (21 eyes). The palsy was congenital in 20 eyes and caused by postnatal trauma in 17 eyes. Seventeen eyes had aberrant regeneration and four eyes with partial third cranial nerve palsy had spontaneous resolution. Thirty-six children (38 eyes) were affected before visual maturation (age 8 years), and 25 (27 eyes) had amblyopia. Of the five amblyopic eyes with quantifiable visual acuity, none had measurable improvement of Snellen visual acuity during the follow-up period. Overall, visual acuity was between 6/5 and 6/12 at the last follow-up visit in 31 eyes (58%). Ocular alignment was greatly improved after strabismus procedures, with a mean of 1.5 procedures for patients with partial third cranial nerve palsy and 2.3 procedures for those with complete palsy. Binocular function was difficult to preserve or restore but was achieved for some patients with partial third cranial nerve palsy. CONCLUSIONS: Surgical treatment of third cranial nerve palsy is frequently necessary, especially in cases of complete palsy. Multiple strabismus procedures are often needed to maintain good ocular alignment. Surgery can result in cosmetically acceptable alignment of the eyes, but it rarely results in restoration or achievement of measurable binocular function. Treatment of amblyopia is effective in maintaining the level of visual acuity present at the onset of the third cranial nerve palsy, but improvement in visual acuity is difficult to achieve.     

Case of herpes zoster ophthalmicus with abducent palsy: the cause and magnetic resonance imaging findings

PURPOSE: To report the cause and magnetic resonance imaging (MRI) findings in a case of abducent palsy following herpes zoster ophthalmicus. CASE: A 76-year-old man presented with acute onset of pain, a vesicular cutaneous eruption and herpes zoster ophthalmicus on the right side. He developed complete abducent palsy on the right side two weeks after onset. MRI with gadolinium enhancement showed Meckel's sinus, which contains the trigeminal ganglion, and the abducent nerve on the right side. The patient was treated with intravenous acyclovir and methylprednisolone. The abnormal enhancement shown on MRI vanished immediately and the ophthalmoplegia resolved significantly. CONCLUSION: This is the first reported case where an affected cranial nerve was detected next to the inflammatory cavernous sinus in ophthalmoplegia following herpes zoster ophthalmicus. These MRI findings showed that this ophthlamoplegia was induced by direct viral invasion or extension of inflammation to the ipsilateral cranial nerve. Further studies need to be performed to clarify the role of specific antiviral therapy or anti-inflammatory agents in treating this complication of herpes zoster.     

Oculomotor nerve paralysis and bilateral facial nerve paralysis as presenting signs of Lyme disease

Lyme disease is a tick-borne illness caused by the spirochete Borrelia burgdorferi . On occasions, patients with Lyme disease present with isolated cranial nerve palsies; multiple palsies have rarely been reported in the literature.We discuss the case of a patient, who presented with a third nerve palsy and bilateral seventh nerve palsies and was subsequently diagnosed as suffering from Lyme disease.To our knowledge, this is the first reported case of Lyme disease presenting with this combination of neurological signs. A 53-year-old male from the Scottish Western Isles presented with a two-day history of double vision. On examination, he was found to have a left third cranial nerve palsy and a left seventh cranial nerve palsy. Five days later, the patient developed a right seventh cranial nerve palsy. Serum and CSF enzymelinked immunosorbent assay (ELISA) and Western blot analysis were both positive for Lyme disease as was CSF polymerase chain reaction (PCR) analysis. Subsequently, the patient gave a history of multiple tick bites over the previous few years. He was commenced on appropriate antibiotic therapy and oral prednisolone. A rapid improvement in his condition was noted. This case demonstrates the importance of considering the diagnosis of Lyme disease in patients with multiple cranial neuropathies, especially those residing in, or with a history of travel to, endemic areas. In addition, it illustrates how early diagnosis, with the institution of appropriate therapy, leads to a prompt improvement in neurological symptoms and signs.     

Acute Transient Oculomotor Nerve Palsy from Presumed Cavernous Angioma in an Infant

Cavernous angiomas of the cranial nerves are extremely rare, and those of the oculomotor (third) cranial nerve are rarer still, with no previous cases having been reported in the literature. We report herein the first case of a presumed cavernous angioma involving the subarachnoid portion of the left third nerve presenting as an acute left third nerve palsy in an infant. The child was followed without intervention and the palsy completely resolved. Given the poor functional results with attempted surgical excision and the potential for spontaneous improvement in oculomotor nerve function, it is reasonable to follow patients with these lesions without intervention.     

Painful ophthalmoplegia secondary to larynx carcinoma

CASE REPORT: We present a case of metastatic larynx cancer in the cavernous sinus. It presented itself as a right sixth cranial nerve palsy which progressed into a painful ophthalmoplegia with normal CT and RNM in its early stages. DISCUSSION: We must suspect a cavernous sinus invasion in patients with cranial nerve palsies and with a history of malignancy, despite negative radiologic findings. Tumoral invasion of the skull base has been described in pharyngeal neoplasms but it is exceptional in larynx carcinomas.     

Spheniodal mucocele causing bilateral optic neuropathy and ophthalmoplegia

Sphenoid sinus mucocele comprises only 2% of all paranasal sinus mucoceles. In literature, there is a case report on sphenoidal mucocele causing bilateral optic neuropathy, with unilateral partial recovery and cranial nerve palsy, but we did not come across any literature with bilateral optic neuropathy and ophthalmoplegia together caused by spheno-ethmoidal mucocele. We present such a rare case of spheno-ethmoidal mucocele causing bilateral optic neuropathy and unilateral sixth nerve palsy who had postsurgery, unilateral good vision recovery, and complete resolution of sixth nerve palsy.     

Fascicular oculomotor nerve palsy in neuro-Beh?et's disease.

A 43-year-old man with Beh?et's disease developed a left oculomotor palsy and a right elevation paresis. His clinical picture was consistent with an isolated fascicular third cranial nerve palsy, considering the mass effect of a large left capsulothalamic lesion extending down into the mesencephalon, which was visualized by CT and (more precisely) by MRI. The patient's clinical status was improved with steroid and immunosuppressive therapy, and radiologic abnormalities resolved markedly in a month.     

Ischemic ophthalmoplegia in diabetic mellitus

Purpose : To analyze the natural course of ischemic diabetic palsies of the 3 rd , 4 th , and 6 th cranial nerves and their correlations with the status of diabetic control and retinopathy. Materials and methods : Twenty-nine patients with diabetic ophthalmoplegia, treated in Kaohsiung Medical University Hospital during the period 1996-1999, were included in the study. Data on clinical characteristics of the patients were obtained by chart review and the natural course of the cranial nerve palsies was analyzed. Laboratory studies, neuroimaging, and fundus studies were also performed. Results : Thirty-six episodes of ischemic ophthalmoplegia were recorded in 29 patients. Seventeen episodes of ophthalmoplgia occurred in patients with poor diabetic status. Third cranial nerve involvement occurred in 21 episodes, six of which (28.6%) had pupil involvement. Four patients had 4 th cranial nerve palsy and 11 episodes in nine patients involved 6 th cranial nerve palsy. Four patients had recurrent or alternate cranial nerve involvement, and three had simultaneous multiple cranial nerve involvement.The mean duration of paralysis was 2.8 ± 1.5 months with a significant difference ( p = 0.009) between the complete and incomplete palsy groups. Most of the cases had either no diabetic retinopathy ( No-DR )(55.2%) or only background diabetic retinopathy ( BDR )(34.5%). Except for average age, no significant difference was found between No-DR , BDR , and proliferative diabetic retinopathy ( PDR ) groups with respect to the duration of the palsies and fasting blood sugar levels. Age was significantly higher in the less severe diabetic retinopathy group (especially in the No-DR group). Conclusion : Cranial neuropathy with ophthalmoplegia is benign and self-limited. The oculomotor nerve was the most frequently involved in our group. Recovery time was dependent on ophthalmoplegia severity.The status of diabetic retinopathy and blood sugar level was not significantly related to the prognosis. Older diabetics (age > 63 years) had less severe retinopathy during attacks of ophthalmoplegia (p < 0.05). There might also be other risk factors, such as arteriosclerosis, inflammation, or anatomic variation, intervening in the pathogenesis of diabetic ophthalmoplegia.     

Síndrome del uno y medio de Fisher a causa de un cavernoma bulbo-protuberancial

The one and a half Fisher syndrome is produced by an unilateral lesion in the dorsal and inferior part of the pons located specifically in the pontine tegmentum. This is an area that contains the medial longitudinal fasciculus (LMF), the paramedian pontine reticular formation (PPRF) and the nucleus of the sixth cranial nerve, responsible for the horizontal movements of the gaze. Clinically it manifests with conjugate gaze palsy with internuclear ophthalmoplegia.The case is reported on a 60 year-old patient, who presented with binocular diplopia, ophthalmoplegia and paralysis of the gaze conjugated to the left. Imaging studies were performed that showed a hemi-protuberant haematoma secondary to a cavernoma. As expected, he presented with several episodes of re-bleeding with clinical worsening: headache, diplopia, tetraparesis, and hypoaesthesia in the right side of the face, as such that the microsurgical exeresis of the protuberant cavernoma was considered.     

Pupil sparing incomplete third nerve palsy secondary to a cavernous sinus meningioma: challenges in management

Background: The diagnosis of incomplete third nerve palsy can be clinically challenging because the aetiologies, as well as presentations, can be variable and subtle. The optometric clinician should be familiar with the association of third nerve palsy with compressive lesions, including the clinical presentations and management of these patients. Case report: We present a 68‐year‐old hypertensive male complaining of intermittent diplopia for the previous six months. Neurological examination revealed a mild deficit in adduction, reduced range of vertical motility and questionable ptosis, all limited to the OD. No pupillary involvement was noted. MRI revealed a cavernous sinus meningioma. The patient elected against surgery, choosing MRI every six months. Conclusion: Due to the subtle clinical presentation of incomplete pupil sparing third nerve palsy, this ophthalmoplegia may be easily overlooked. The associated aetiologies of palsy of cranial nerve three (CN3) carry increased risk of morbidity and mortality. Management should include evaluation for mass lesions and/or vascular aetiologies, regardless of pupillary involvement.     

Oculomotor palsy and papilledema with pial-dural arteriovenous malformation

A 62-year-old man presented with papilledema, a cranial bruit, and a partial left oculomotor nerve palsy. Arteriography revealed a large mixed pial-dural arteriovenous malformation involving the superior sagittal and both transverse sinuses. After the superior part of the malformation was embolized, the patient's papilledema and ocular motility disturbance resolved. The oculomotor disturbance may have been a nonspecific sign of increased intracranial pressure. Cranial auscultation should be performed in all cases of papilledema and cranial nerve palsy.     

Acquired, isolated third nerve palsies in infants with cerebrovascular malformations

PURPOSE: To report two infants with acquired, isolated third nerve palsies attributable to intracranial cerebrovascular malformations. DESIGN: Observational case report. METHODS: Two patients are described. Each was examined in a university-based pediatric ophthalmology and neuro-ophthalmology practice. RESULTS: An 8-month-old child presented with a pupil-involving partial left third nerve palsy because of a partially thrombosed fusiform aneurysm of the left internal carotid artery. A 3-month-old infant developed a right third nerve palsy from a giant arteriovenous fistula arising from an M2 branch of the right middle cerebral artery. CONCLUSION: Patients younger than 8 months and 3 months with acquired, isolated third nerve palsies resulting from intracranial cerebrovascular malformations could not be found in a MEDLINE search. In conclusion, at even this young age, acquired, isolated third nerve palsies may be the initial manifestation of an intracranial aneurysm or fistula. Magnetic resonance imaging (MRI) and MRI-angiography were adequate for detecting these processes.     

Atypical clinical presentation of oculomotor (III) nerve palsy

The atypical clinical presentations of three patients with an oculomotor (III) nerve palsy are outlined. The first patient is a 49-year-old with a painful, pupil-sparing ophthalmoplegia of sudden onset due to a pituitary adenoma which had eroded into the cavernous sinus. The second patient is a 7-year-old with a traumatic III nerve palsy who despite full recovery of her oculomotility, has been symptomatic due to a permanent internal ophthalmoplegia. The third patient is an 8-year-old who has undergone prolonged optometric therapy for an "atypical esotropia," but in fact has a congenital III nerve palsy with oculomotor synkinesis and deep amblyopia.     

Central Retinal Artery Occlusion and Third Cranial Nerve Palsy Following Nasal Septoplasty

Background

Postoperative vision loss following routine nasal surgery is an extremely rare and devastating complication. We report a case of unilateral blindness due to central retinal artery occlusion associated with third cranial nerve following septoplasty.

Case Report

We report a patient who developed an unusual central retinal artery occlusion with unilateral blindness following nasal surgery under general anesthesia. A 45-year-old man underwent a nasal septal surgery for severe epistaxis. Soon after recovery, the patient noticed loss of vision in his right eye and was unable to lift his upper eyelid. Upon ophthalmic examinations, we determined that he had right-sided third cranial nerve palsy with central retinal artery obstruction and ptosis of right upper eyelid, restriction of ocular movements, and no perception of light in the right eye. Postoperative computerized tomography scan revealed multiple fractures of the left medial orbital wall, including one near the optic canal. Ptosis and ocular defects were recovered partially, but visual loss persisted until the last follow-up.

Conclusion

This paper highlights one case of complete unilateral blindness from direct central retinal artery occlusion associated with third cranial nerve palsy following an apparently uneventful septorhinoplasty. Ophthalmologists and otolaryngologists should therefore be aware of the possible occurrence of such complications.Key Words: Central retinal artery occlusion, Third nerve palsy, Septoplasty, Nasal polypectomy, Visual loss     

Ocular myasthenia presenting as superior oblique weakness

We diagnosed ocular myasthenia in a 39-year-old man whose presenting symptom was vertical diplopia. Unrecognized weakness of the right superior oblique and secondary overaction of the right inferior oblique caused a right hypertropia, which was worse on left gaze. One week later left blepharoptosis, right medial rectus weakness, and bilateral obicularis oculi weakness were found on ocular examination. All findings were partially reversed by the injection of Tensilon. Superior oblique muscle palsy simulating a fourth cranial nerve palsy is infrequently reported in patients with ocular myasthenia. Pseudofourth nerve palsy is another sign of myasthenia gravis.     

Encephalopathy,Chiasmal Compression,Ophthalmoplegia, and Diabetes Insipidus in Pituitary Apoplexy

ABSTRACT

Pituitary apoplexy with haemorrhage is a potentially life-threatening condition, and a rare cause of third nerve palsies. The range of vision loss and ophthalmoplegia seen in cases of apoplexy reflects the variability of cranial structures compressed by mass effect. The pathophysiology of extraocular muscle limitation and facial paraesthesia occurs with compression of the cavernous sinus, which contains cranial nerves III, IV, VI, and the ophthalmic branch of V. Blood supply to adjacent structures may be also compromised, causing additional loss of function. This case report of a patient with diabetes insipidus and a third nerve palsy illustrates the anatomic basis of the presenting signs of pituitary apoplexy, and the necessity for prompt neuroimaging if it is suspected.     

Third cranial nerve palsy related to an unruptured aneurysm of the posterior communicating artery

The posterior communicating artery (PCA) aneurysm is a traditional cause of young subjects' painful ophthalmoplegia. We report the case of a patient presenting a complete, extrinsic and intrinsic, third cranial nerve palsy related to an unruptured aneurysm of the PCA. The diagnosis was made with the angio-CT, and the patient was treated with endovascular treatment for 6 days after the beginning of the cephalalgias. Recovery was complete at 8 weeks. We review the literature on the etiologies of this type of attack, the work-up, and the possible treatments.     

Diabetic complete external ophthalmoplegia

A 69-year-old diabetic patient taking oral hypoglycemic drugs and with no systemic complications presented a right peripheral facial palsy, and 2 months later a complete right external ophthalmoplegia with sparing of the pupillary function. Clinical, radiologic, and other laboratory investigation ruled out compressive, infectious, and inflammatory etiology. Four months later, after achieving good metabolic control, there was almost complete recovery of the ophthalmoplegia without signs of aberrant regeneration of the third nerve. Diabetes is proposed as the etiology of this case. A possible anatomic substrate is presented to explain the findings.     

Bilateral sixth nerve and left third nerve palsy after head trauma

CASE REPORT: To describe a case of combined bilateral cranial nerve palsy of traumatic origin. To determine the lesions that produce the symptoms is useful to define the final prognosis and the best treatment. DISCUSSION: We report the case of a patient who developed a bilateral sixth nerve and left third nerve palsy after head trauma. The underlying lesion was a diffuse axonal injury. After an observation period during which no spontaneous improvement occurred, we administered botulinum toxin with a successful clinical result. Bilateral combined traumatic cranial nerve palsies are rare. When a diffuse axonal injury is present, the chance of spontaneous resolution is poor.