(1/84) Gradenigo's syndrome.

Gradenigo's syndrome, which is characterised by the triad of suppurative otitis media, pain in the distribution of the trigeminal nerve, and abducens nerve palsy may give rise to potentially fatal complications. Knowledge of the aetiology and appropriate investigations can lead to early diagnosis. A case is reported which illustrates this.  (+info)

(2/84) Transsphenoidal computer-navigation-assisted deflation of a balloon after endovascular occlusion of a direct carotid cavernous sinus fistula.

SUMMARY: A 49-year-old woman with a direct posttraumatic carotid cavernous fistula (CCF) was treated with detachable balloons via a transcarotid route. After the procedure, her intracranial bruit, conjunctival injection, and orbital congestion were cured, but the preexistent sixth nerve palsy deteriorated. CT showed one balloon positioned in the posterior portion of the right cavernous sinus and was regarded to be responsible for nerve compression. After surgical exposure by use of a transnasal-transsphenoidal approach under 3D navigation control, this balloon was deflated by puncture with a 22-gauge needle. The previously described symptoms resolved after balloon deflation. This report presents a rare complication of endovascular treatment of direct CCF and a new microsurgical approach to a balloon in a case of nerve compression.  (+info)

(3/84) Giant ocular nerve neurofibroma of the cavernous sinus: a series of 5 cases.

Five cases of giant cavernous sinus neurofibroma arising from the ocular cranial nerves are reported. These patients collected over a period of 5 years consisted of 3 males and 2 females with an age range of 9 to 40 years and a mean of 20.6 years. Clinically, all patients presented with ocular palsies over a long period (mean 3.4 years). All of them underwent a frontotemporal craniotomy along with an orbito-zygomatic osteotomy and excision of the tumour. In patients with extension of the tumour into the orbit, the superior orbital fissure was drilled, the tenon's capsule was cut and the intraorbital portion was excised. The management of these tumours is discussed and the literature reviewed.  (+info)

(4/84) Abduction paresis with rostral pontine and/or mesencephalic lesions: Pseudoabducens palsy and its relation to the so-called posterior internuclear ophthalmoplegia of Lutz.

BACKGROUND: The existence of a prenuclear abduction paresis is still debated. METHODS: In a retrospective design, we identified 22 patients with isolated unilateral (n = 20) or bilateral (n = 2) abduction paresis and electrophysiologic abnormalities indicating rostral pontine and/or mesencephalic lesions. Another 11 patients had unilateral abduction paresis with additional ocular motor abnormalities indicating midbrain dysfunction. Eight of these 11 patients also had electrophysiological abnormalities supporting this location. Electrophysiological examinations in all patients included masseter and blink reflexes (MassR, BlinkR), brainstem auditory evoked potentials (BAEP), and direct current elctro-oculography (EOG). RESULTS: Unilateral MassR abnormalities in patients with unilateral abduction paresis were seen in 17 patients and were almost always (in 16 of 17 patients) on the side of the abduction paresis. Another 11 patients had bilateral MassR abnormalities. BlinkR was always normal. EOG disclosed slowed abduction saccades in the non-paretic eye in 6 patients and slowed saccades to the side opposite to the abduction paresis in another 5 patients. Re-examinations were done in 27 patients showing normalization or improvement of masseter reflex abnormalities in 18 of 20 patients and in all patients with EOG abnormalities. This was always associated with clinical improvement. CONCLUSIONS: Electrophysiologically documented or clinically evident rostral pontine and/or mesencephalic lesions in our patients exclude an infranuclear intrapontine 6th nerve lesion and indicate the existence of an abduction paresis of prenuclear origin. An increased tone of the antagonistic medial rectus muscle during lateral gaze either by abnormal convergence or impaired medial rectus inhibition seems most likely.  (+info)

(5/84) Idiopathic giant cell granulomatous hypophysitis with hypopituitarism, right abducens nerve paresis and masked diabetes insipidus.

A 38-year-old man presented with headache, fever, and double vision associated with right abducens nerve paresis. He had neither nuchal rigidity nor visual field defect. Laboratory data revealed elevated erythrocyte sedimentation rate (ESR), eosinophilia, and lymphocytic pleocytosis in the cerebrospinal fluid (CSF). Provocation tests of pituitary hormones showed partial hypopituitarism. Magnetic resonance imaging (MRI) revealed swelling of the hypophysis and a mass lesion expanding into the right cavernous sinus. The supplement dose of dexamethasone for hypothalamic hypocortisolism manifested diabetes insipidus. Biopsy, carried out through the transsphenoidal approach, revealed giant cell granuloma. Systemic granulomatous diseases were ruled out, and the lesion was considered to be idiopathic giant cell granulomatous hypophysitis. Right abducens nerve paresis, diabetes insipidus and dysfunction of the anterior lobe were amended by the treatment with prednisolone for 4 months, and findings of the pituitary gland and stalk were normalized. The present case shows that glucocorticoid has an effect on amendment of idiopathic giant cell granulomatous hypophysitis.  (+info)

(6/84) Primitive trigeminal artery variant aneurysm treated with Guglielmi detachable coils--case report.

A 69-year-old woman had suffered from diplopia on right lateral gaze for the last 4 months due to right abducens nerve paresis. Right carotid angiography showed a cavernous internal carotid artery (ICA) aneurysm of 17 x 16 x 14 mm size and a primitive trigeminal artery (PTA) variant supplying the territory of the posterior inferior cerebellar artery. Intraluminal occlusion of the aneurysm was performed with 15 Guglielmi detachable coils. The flow of the PTA variant and the ICA was preserved. Right abducens nerve paresis improved partially. PTA variant is a primitive artery originating from the cavernous ICA supplying the cerebellum without opacification of the basilar artery. Only four of the 67 cases of PTA variant were associated with an aneurysm of the PTA variant. The possibility of this rare association should be considered when treating cavernous portion aneurysm because of the risk of cerebellar ischemia.  (+info)

(7/84) Isolated abducens nerve paresis associated with incomplete Horner's syndrome caused by petrous apex fracture--case report and anatomical study.

A 17-year-old male presented with a wound on the right temporal region, oozing hemorrhagic necrotic brain tissue and cerebrospinal fluid, following a fall. Computed tomography showed temporoparietal and petrous apex fractures on the right. Neurological examination revealed abducens nerve paresis, ptosis, and myosis on the right side. The patient was treated surgically for the removal of the free bony fragments at the fracture site and to close the dural tear. The abducens nerve paresis, ptosis, and myosis persisted at the 3rd monthly postoperative follow-up examination. The anatomy of the abducens nerve at the petroclival region was studied in four cadaveric heads. Two silicone-injected heads were used for microsurgical dissections and two for histological sections. The abducens nerve has three different angulations in the petroclival region, located at the dural entrance porus, the petrous apex, and the lateral wall of the cavernous segment of the internal carotid artery. The abducens nerve had fine anastomoses with the trigeminal nerve and the periarterial sympathetic plexus. There were fibrous connections extending inside the venous space of the petroclival area. The abducens nerve seems to be vulnerable to damage in the petroclival region, either directly by trauma to its dural porus and petrous apex or indirectly by stretching of the nerve through the nervous and/or fibrous connections. Concurrent functional loss of the abducens nerve and the periarterial sympathetic plexus clinically manifested as incomplete Horner's syndrome in our patient.  (+info)

(8/84) Adaptations and deficits in the vestibulo-ocular reflex after sixth nerve palsy.

PURPOSE: The effects of paralytic strabismus on the vestibulo-ocular reflex (VOR) have not been systematically investigated in humans. The purpose of this study was to analyze the VOR in patients with unilateral peripheral sixth nerve palsy. METHODS: Twenty-one patients with unilateral peripheral sixth nerve palsy (6 severe, 7 moderate, 8 mild) and 15 normal subjects were studied. Subjects made sinusoidal +/-10 degrees head-on-body rotations in yaw and pitch at approximately 0.5 and 2 Hz, and in roll at approximately 0.5, 1, and 2 Hz. Eye movement recordings were obtained using magnetic scleral search coils in each eye in darkness and during monocular viewing in light. Static torsional VOR gains, defined as change in torsional eye position divided by change in head position during sustained head roll, were also measured. RESULTS: In all patients, horizontal VOR gains in darkness were decreased in the paretic eye in both abduction and adduction, but remained normal in the nonparetic eye in both directions. In light, horizontal visually enhanced VOR (VVOR) gains were normal in both eyes in moderate and mild palsy. In severe palsy, horizontal VVOR gains remained low in the paretic eye during viewing with either eye, whereas those in the nonparetic eye were higher than normal when the paretic eye viewed. Vertical VOR and VVOR were normal, but dynamic and static torsional VOR and VVOR gains were reduced in both eyes in all patients. CONCLUSIONS: In darkness, horizontal VOR gains were reduced during abduction of the paretic eye in all patients, as anticipated in sixth nerve palsy. Gains were also reduced during adduction of the paretic eye, suggesting that innervation to the medial rectus has changed. After severe palsy, vision did not increase abducting or adducting horizontal VVOR gains to normal in the paretic eye, but caused secondary increase in VVOR gains to values above unity in the nonparetic eye, when the paretic eye fixated. In mild and moderate palsy, vision enhanced the VOR in the paretic eye but caused no change in the nonparetic eye, suggesting a monocular readjustment of innervation selectively to the paretic eye. Vertical VOR and VVOR gains were normal, indicating that the lateral rectus did not have significant vertical actions through the excursions that we tested (+/-10 degrees ). Reduced torsional VOR gains in the paretic eye can be explained by the esotropia in sixth nerve palsy. Torsional VOR gain normally varies with vergence. We attribute the reduced torsional gains in the paretic eye to the mechanism that normally lowers it during convergence. The low torsional gains in the nonparetic eye may be an adaptation to reduce torsional disparity between the two eyes.  (+info)

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