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To assess the relationship of aspirin use and ischemic cranial nerve palsies among patients with diabetes mellitus and hypertension.This retrospective case-control study involved 100 patients with ischemic cranial nerve palsies in association with diabetes, hypertension, or both (palsy cases) and 163 age-matched and sex-matched patients with diabetes, hypertension, or both but without ischemic cranial nerve palsies (nonpalsy control subjects). Comparisons were made with respect to duration of diabetes, dose and duration of aspirin use, dose and duration of tobacco use, and presence of cardiac or cerebrovascular disease.There were 20 oculomotor, 33 trochlear, 37 abducens, and 10 facial nerve palsy cases. The median duration of diabetes was 6 years for cases and 7 years for control subjects. There were 34 cases (34%) who had used aspirin for a mean duration of 5.5 years before the onset of the cranial nerve palsy and 49 control subjects (30.1%) who had used aspirin for a mean duration of 4.3 years. There were no significant differences between cases and control subjects for duration of diabetes (P =.94); aspirin use (P =.51), duration (P =.50), and dosage (P =.89); tobacco use (P =.73) and consumption (P =.45); and proportion of cardiac disease (P =.17). Cerebrovascular disease was significantly less common among palsy cases than nonpalsy control subjects (P.001). There was no significant difference in the odds of a patient having cranial nerve palsy in the aspirin group compared with the nonaspirin group (odds ratio, 1.12; 95% confidence interval, 0.70-2.04).Aspirin use was not associated with a reduced rate of ischemic third, fourth, sixth, and seventh nerve palsies among patients with diabetes mellitus and hypertension. Aspirin appears to be ineffective in preventing ischemic third, fourth, sixth, and seventh cranial nerve palsies. Patients with ischemic cranial nerve palsy have a significantly lower rate of strokes and transient ischemic attacks than patients who have diabetes or hypertension but who do not have a history of cranial nerve palsy.

Purpose: To determine the population-based incidence and cause of cranial nerve palsies affecting ocular motility in children in the circumscribed population of Olmsted County, Minnesota. MethodsM: The Rochester Epidemiology Project medical records linkage system captures virtually all medical care provided to Olmsted County residents. By means of this database, all cases of third, fourth, and sixth cranial nerve palsy were identified among county residents less than 18 years of age from 1978 through 1992. Medical records were reviewed to confirm the diagnosis, determine the cause, and document county residency. Incidence rates were adjusted to the age and sex distribution of the 1990 white population in the United States. Results: Over this 15-year period, 36 incidence cases of cranial nerve palsy were identified in 35 children in this defined population. The age-adjusted and sex- adjusted annual incidence of third, fourth, and sixth nerve palsies combined was 7.6 per 100,000 (95% confidence interval, 5.1 to 10.1). The most commonly affected nerve was the fourth (36%), followed by the sixth (33%), the third (22%), and multiple nerve palsies (9%). The most common cause was congenital for third and fourth nerve palsy, undetermined for sixth, and trauma for multiple nerve palsies. Although three cases were associated with neoplasia, a cranial nerve palsy was not present at the time of diagnosis in any case. Conclusions: Unlike many institutionally based referral series, our population-based study provides data on the incidence and cause of third, fourth, and sixth nerve palsies in a geographically defined population. In contrast to previous institutionally based series, nearly half the cases were congenital in origin, and in no case did intracranial neoplasia present as an isolated nerve palsy.

Purpose To study the corneal nerves in patients with chronic bullous keratopathy. Design Prospective observational case series with histologic evaluation. Methods We studied 25 eyes of 25 bullous keratopathy patients of different etiologies (17 female, 8 male; mean age, 76.3 years) as well as 6 eyes of 6 normal control subjects (5 male, 1 female; mean age, 38 years). All subjects were scanned by laser scanning confocal microscope. Five corneal buttons obtained following penetrating keratoplasty from 5 of the above patients and 6 normal control corneal buttons were stained as whole mounts with acetylcholinesterase (AChE) method for corneal nerve demonstration and scanned in multiple layers with digital pathology scanning microscope. Results The density, branching pattern, and diameter of sub-basal nerves were significantly lower in corneas with bullous keratopathy compared with normal corneas (density: 4.42 ± 1.91 mm/mm 2 vs 20.05 ± 4.24 mm/mm 2 ; branching pattern: 36.02% ± 26.57% vs 70.79% ± 10.53%; diameter: 3.07 ± 0.64 μm vs 4.57 ± 1.12 μm). Aberrations such as localized thickenings or excrescences, abnormal twisting, coiling, and looping of the (mid) stromal nerves were observed in the study group both by in vivo confocal microscopy and on histology. Conclusions Striking alterations in corneal innervation are present in corneas with bullous keratopathy that are unrelated to any specific etiology of bullous keratopathy. This study provides histologic confirmation of novel in vivo confocal microscopy findings related to corneal nerves in bullous keratopathy.

Between January 1966 and December 1988, 160 pediatric patients (age range, 0 to 17 years) were seen at the Mayo Clinic with an acquired oculomotor (35 patients), trochlear (19 patients), abducent (88 patients), or multiple (18 patients) cranial nerve palsy. The clinical findings in the 160 pediatric patients were compared with the results obtained in other reviews of cranial nerve palsies in the pediatric age group and with the adult Mayo Clinic patients with acquired cranial nerve palsies. Trauma was the most common reason for an acquired cranial nerve palsy in our pediatric group. The percentage of patients with an acquired cranial nerve palsy resulting from trauma was significantly greater in the pediatric group (42.5%) than in adults (15.4%) (P.01). The difference between the percentage of adults (15.2%) and pediatric patients (16.9%) with a cranial nerve palsy secondary to a neoplasm was not statistically significant (P = .28).

We collected data from a large series of patients with ocular palsies and compared them with data in previous series from the Mayo Clinic. The largest group of patients among 4,278 cases was that in which the cause was undetermined for a long period of follow-up. The abducens nerve was most commonly affected. The probability of establishing a diagnosis was higher in patients younger than 50 years and among those with associated neurologic findings or multiple ocular palsies. The prognosis for recovery was best in the vascular group but was better than 50% for all groups except those with tumors. Investigation may be tailored to each patient according to clinical findings and probabilities of finding a cause, and judicious clinical judgement should be exercised.

Two previous cases of cold-induced corneal edema have been reported in patients with corneal anesthesia secondary to a trigeminal nerve disorder. We studied six patients with complete unilateral corneal anesthesia after trigeminal ablation. Subjects' eyes were exposed to 4 C air from a fan for one hour. We measured corneal thickness, corneal surface temperature, and endothelial permeability to fluorescein. During cold exposure, two of the six study eyes exhibited reversible corneal swelling (11% and 26% over baseline value). All anesthetic corneas were consistently colder (13.8 +/- 0.7 C) than the contralateral corneas (21.0 +/- 1.7 C, P = .001). Baseline endothelial permeability and aqueous humor flow rates were similar in both the study and control groups. After cold exposure, the study eyes had a significant transient increase in permeability compared to the controls (7.5 +/- 2.4 x 10(-4) cm/min vs 2.9 +/- 1.4 x 10(-4) cm/min, P = .007). Baseline endothelial photomicrographs also showed increased pleomorphism (fewer hexagonal cells) in the anesthetic corneas. These data suggest that sensory denervation of the eye influences ocular temperature regulation and corneal endothelial cell morphologic characteristics. Some anesthetic corneas are prone to cold-induced edema, which may result from excessive cooling.

We studied 29 consecutive patients with acute unilateral sixth-nerve palsy, who received botulinum toxin injection to the antagonist medial rectus muscle. The average interval between onset of palsy and treatment was 40 days and the mean follow-up from the last injection was 14 months. Before treatment, esotropia in the primary position ranged from 12 to 45 prism diopters and limitation to abduction in the affected eye ranged from −2 (approximately 15 degrees lateral to midline) to −6 (15 degrees nasal to midline). After treatment, 22 of 29 patients (76%) had complete recovery of motility as determined by version testing. Of the seven patients with a residual abduction deficit, two had fusion in the primary position, three had fusion with prismatic correction, and two patients required subsequent surgery. Botulinum toxin injection seems to be an effective treatment option in cases of acute unilateral sixth-nerve palsy.

Purpose To analyze the horizontal rectus extraocular muscles (EOMs) by orbital magnetic resonance imaging (MRI) in patients with congenital cranial dysinnervation disorders that arises from abnormal development of cranial nerve nuclei or their axonal connections. Design Case series, retrospective analysis. Methods The morphology of the horizontal rectus EOMs was analyzed in orbital MRI on 4 patients with congenital oculomotor palsy, 26 with congenital superior oblique palsy, and five with Duane syndrome. Orbital imaging was performed by 1.5 tesla (T) and 3T MRI, and quasi-coronal and sagittal images perpendicular and parallel to the long axis of the orbit were obtained at slice thicknesses of 3 and 2 mm. Results The horizontal rectus EOMs were split in 4 of the 35 patients (11%). Splitting was observed in 2 of the five patients (40%) with Duane syndrome, one of the 26 patients (4%) with congenital superior oblique palsy, and 1 of the 4 patients (25%) with oculomotor palsy, but in none of the 6 normal subjects and 12 patients with acquired cranial nerve palsy. Conclusion Since splitting of the horizontal rectus EOMs was noted in patients with congenital dysinnervation disorders, including Duane syndrome, Sevel's theory that the horizontal rectus EOMs develop from the superior and inferior mesodermal complexes is considered to be reasonable.

We examined 32 children one to 15 years after virologically verified neonatal herpes simplex virus infection. Sixteen of 17 (94%) neurologically impaired children had ocular abnormalities compared to three of 15 (20%) neurologically healthy children. Disturbed oculomotor control occurred in 14 children (44%), most of whom were among those with severe handicap. Ocular morbidity was present in 13 (40%) of 32 children: one had cataracts, two had corneal scars, seven had optic atrophy, and nine had chorioretinal scars. The clinically silent chorioretinal lesions were manifest as coarse hyperpigmented areas between the equator and ora serrata. One child had suffered from acute fulminant retinitis. Twelve of 13 (93%) severely handicapped children had impaired vision, mainly because of cortical blindness. Less affected children had normal vision unless corneal scars were present. Long-term observation of patients with neonatal herpes infections is essential because ocular manifestations are not rare, and recurrences may be more common than previously reported.

To analyze the density and morphology of corneal epithelial cells and keratocytes by in vivo confocal microscopy (IVCM) in patients with herpes zoster ophthalmicus (HZO) as associated with corneal innervation.Prospective, controlled and masked cross-sectional study.setting: Single-center study.Thirty eyes with the diagnosis HZO and their contralateral clinically unaffected eyes, 15 eyes of 15 normal controls. intervention procedures: In vivo confocal microscopy and corneal esthesiometry of the central cornea.Changes in morphology and density of the superficial and basal epithelial cells and stromal keratocytes, and correlation with corneal sensation.The density of superficial epithelial cells in HZO eyes with severe sensation loss (766.5 ± 25.2 cells/mm(2)) was significantly lower than both healthy control eyes (1450.23 ± 150.83 cells/mm(2)) and contralateral unaffected eyes (1974.13 ± 298.24 cells/mm(2)) (P = .003). Superficial epithelial cell size (1162.5 μm(2)) was significantly larger in HZO eyes with severe loss of sensation, as compared to contralateral (441.46 ± 298.14) or healthy eyes (407.4 ± 47.2μm(2); all P.05). The density of basal epithelial cells, anterior keratocytes, and posterior keratocytes did not show statistical significance between patients, controls, and contralateral unaffected eyes. Changes in superficial epithelial cell density and morphology correlated strongly with corneal sensation.In vivo confocal microscopy reveals profound HZO-induced changes in the superficial epithelium, as demonstrated by increase in cell size, decrease in cell density, and squamous metaplasia. We demonstrate that these changes strongly correlate with changes in corneal innervation in eyes affected by HZO.

Purpose To report bilateral trochlear nerve palsy and its magnetic resonance imaging characteristics in a patient with an arachnoid cyst of the quadrigeminal cistern. Method We performed magnetic resonance imaging of the brainstem of a 54-year-old man who had bilateral trochlear nerve palsy and mild truncal ataxia. Results Magnetic resonance imaging disclosed an arachnoid cyst of the quadrigeminal cistern with enlargement of the lateral, third, and fourth ventricles. The tectum of the midbrain and the ambient and interpeduncular cisterns were markedly compressed by the arachnoid cyst. Conclusion These findings suggest that the bilateral trochlear nerve palsy in this patient was caused by the arachnoid cyst of the quadrigeminal cistern.

Purpose To describe a 59-year-old patient who had seven recurrent, self-limited episodes of isolated ipsilateral abducens nerve palsy in the previous 4 years. Each episode lasted between 2 and 5 weeks. Methods Systemic examination and neuroimaging studies were performed. RESULT: Repeated comprehensive examination failed to demonstrate any ocular or systemic condition apart from a lateral protrusion by dolichoectasia of the posterior portion of the cavernous left internal carotid artery, compressing the posterior left cavernous sinus. Conclusion Numerous self-limited episodes of sixth nerve palsy may be associated with structural abnormalities of the intracranial carotid vasculature.

PURPOSE: To report infraorbital nerve dysfunction after laser in situ keratomileusis. DESIGN: Observational case report. METHODS: Neuro-ophthalmologic examination with brain and orbital magnetic resonance imaging (MRI) and orbital computed tomography (CT). RESULTS: During laser in situ keratomileusis, two healthy women, aged 42 and 46 years, experienced acute onset of sharp ipsilateral cheek pain. Both cases occurred during manipulation of the eyelid speculum. Postoperatively, ipsilateral numbness and tingling or pain of the upper cheek was reported, and examination showed decreased sensation in the distribution of the infraorbital nerve. In both cases, brain and orbit MRI and orbit CT were normal. Both patients were managed medically. In one patient, mild symptoms persisted 1 year postoperatively, and in the second patient, moderate discomfort persisted 8 months postoperatively. CONCLUSION: Infraorbital nerve palsy is a potential complication of laser in situ keratomileusis. Symptoms improve but may persist.

PURPOSE: To report two cases of laser in situ keratomileusis-induced neurotrophic epitheliopathy with punctate epitheliopathy and rose bengal staining of the corneal flap. METHODS: Interventional case reports. RESULTS: A 42-year-old woman and a 37-year-old man with no preoperative symptoms or signs of dry eye developed dry eye symptoms and bilateral punctate epithelial erosions as well as rose bengal staining of the corneal flaps after laser in situ keratomileusis. Neither patient had less than 12 mm of wetting with the Schirmer test without anesthesia at any time point between development and resolution of the flap surface abnormalities. The flap surface abnormalities resolved approximately 6 months after laser in situ keratomileusis. CONCLUSIONS: Laser in situ keratomileusis-induced neurotrophic epitheliopathy may be attributable to loss of trophic influence from severed corneal nerve trunks. The condition typically resolves approximately 6 months after laser in situ keratomileusis or laser in situ keratomileusis retreatment.

Purpose: To assess the relationship between tendon anomalies and the volume of the superior oblique muscle in patients with congenital unilateral superior oblique palsy. Methods: Thirty-three patients with unilateral congenital superior oblique palsy were enrolled. Coronal, cross-sectional magnetic resonance imaging scans of the superior oblique muscle were obtained, and the volume of the paretic superior oblique muscle belly was calculated as a percentage of the superior oblique muscle belly on the normal side. The percentage volume of the affected superior oblique muscle was compared retrospectively with the angle of the vertical deviation in the primary position, the tendon looseness determined by a traction test, and other intraoperative findings. Results: When a tendon was loose, the volume of its muscle belly was significantly smaller than the belly of muscles with a normal taut tendon (Mann-Whitney U test, P = .0005). The average vertical deviation of patients assessed to have loose tendons was 4.80 prism diopters, and the deviation in patients with normal tendons was 9.90 prism diopters. The mean vertical deviation of patients with atrophic muscle belly on magnetic resonance imaging was 18.1 prism diopters, and that with normal muscle structure was 10.1 prism diopters. The cases with loose tendon as determined by the traction test after administration of general anesthesia and the cases with atrophic muscle belly had significantly larger vertical deviation in the primary position than the cases with normal tendons and muscles. (Mann-Whitney U test, P = .01 and .0196, respectively). Conclusions: The traction test is sensitive enough to detect anomalies of the superior oblique tendons. Anomalous superior oblique tendons are nearly always associated with attenuated superior oblique muscle and this information provides us with an explanation for the phenomenon of laxity of the superior oblique tendon.

PURPOSE: To describe three children with acute fourth cranial nerve palsy secondary to pseudotumor cerebri. METHODS: We reviewed the medical records of children younger than 18 years who were diagnosed with pseudotumor cerebri between 1977 and 1997. Pseudotumor cerebri was defined by normal neuro-imaging, elevated intracranial pressure measured by lumbar puncture, and normal cerebrospinal fluid composition. RESULTS: Three children with pseudotumor cerebri presented with vertical diplopia and clinical signs of fourth cranial nerve palsy including a hypertropia of the affected eye, which increased with adduction and ipsilateral head tilt. The fourth cranial nerve palsy resolved after reduction of the intracranial pressure in all three children. CONCLUSIONS: Fourth cranial nerve palsy may occur in children with pseudotumor cerebri and may be a nonspecific sign of elevated intracranial pressure.

PURPOSE: To describe the clinical features of patients with isolated unilateral trochlear nerve palsy secondary to imaging-defined schwannoma of the trochlear nerve. METHODS: A chart review of all patients seen at the Neuro-Ophthalmology Unit at Emory University since 1989. Of 221 patients with trochlear nerve palsy, six had a lesion consistent with a trochlear nerve schwannoma. RESULTS: The six patients had isolated unilateral trochlear nerve palsy. Duration of diplopia before diagnosis averaged 6 months. Magnetic resonance imaging demonstrated circumscribed, enhancing lesions along the cisternal course of the trochlear nerve, all measuring less than 5 mm in greatest dimension. Five of the patients were seen in follow-up, over periods ranging from 11 to 26 months from initial presentation (mean, 15.6 months; standard deviation, 6.0 months). All of these patients remained stable except one, who was slightly worse at 15 months by clinical measurements and magnetic resonance imaging. None of these patients have developed additional symptoms or signs of cranial nerve or central nervous system involvement. CONCLUSIONS: The differential diagnosis of an isolated unilateral fourth cranial nerve palsy should include an intrinsic neoplasm of the trochlear nerve. Magnetic resonance imaging is useful, both for diagnosis and follow-up. These patients can remain stable and may not require neurosurgical intervention.

PURPOSE: To report the occurrence of neurotrophic corneal defects after ciliary body ablation with the diode laser. METHODS: Case reports. RESULT: Neurotrophic keratitis, previously associated with cyclocryotherapy, may also be associated with ciliary body ablation with a contact diode laser. CONCLUSION: Practitioners who use the diode laser for ciliary body ablation should be aware of neurotrophic keratitis as a possible complication, especially because the patient population receiving this therapy may have diabetes, chronic eye inflammation, or other conditions predisposing to compromised corneal innervation, which is necessary for epithelial integrity.

PURPOSE: To examine the lesion associated with external ophthalmoplegia in Fisher syndrome using three-dimensional magnetic resonance imaging (3-D MRI). METHOD: Case report. A 65-year-old woman with Fisher syndrome was investigated by gadolinium-enhanced 3-D MRI. RESULT: The extramedullary portion of the left trochlear nerve was enhanced. CONCLUSION: Contrast-enhanced 3-D MRI revealed that the lesion responsible for the external ophthalmoplegia in Fisher syndrome is located in the extramedullary portion of the trochlear nerve.

Purpose To demonstrate that currently available magnetic resonance imaging techniques may verify the absence of the abducens nerve in Duane syndrome. Methods We performed magnetic resonance imaging in a 36-year-old woman with left Duane syndrome, type 1, using spoiled gradient recalled acquisition in the steady state to obtain high-resolution T1-weighted images through the abducens nerve in its subarachnoid segment. Scans were obtained in the axial plane from the medulla to the midbrain and then reformatted along the plane of the abducens nerve. Result Unilateral absence of the left abducens nerve was verified using magnetic resonance imaging. Conclusion The absence of the abducens nerve in Duane syndrome can be verified by modern magnetic resonance imaging techniques.

Purpose To describe the clinical and magnetic resonance imaging findings of a patient with Gradenigo syndrome. Methods A 4 1/2-year-old boy developed Gradenigo syndrome with unilateral facial pain, ophthalmoplegia, and facial weakness secondary to ipsilateral otitis media. The clinical, laboratory, and radiologic findings are discussed. Results The patient was treated with antibiotics and had complete resolution of symptoms and signs. Conclusion Ophthalmologists should be aware of the potential for petrosal involvement of cranial nerves secondary to otitis media and Gradenigo syndrome.

Purpose To assess magnetic resonance imaging as a diagnostic tool of neurovascular compression in a patient with abducens nerve palsy. Methods We performed magnetic resonance imaging of the brainstem of a 46-year-old patient with left abducens nerve palsy using spoiled gradient recalled acquisition in the steady state (SPGR), which allows high-resolution T weighted imaging and detection of the arteries across the plane of slices as a high-signal-intensity area. Results Computed tomography of the brain was unremarkable except for leftward shifting of the basilar artery. As disclosed by magnetic resonance imaging with the SPGR, the right vertebral artery was shifted to the left and joined with the left vertebral artery, and the left abducens nerve was compressed by the vertebral artery. No other abnormal signals were seen in the brainstem. Conclusions These findings suggest that the abducens nerve palsy in this patient was caused by vascular compression at the root exit zone. Magnetic resonance imaging with the SPGR is useful for the diagnosis of vascular compressive neuropathy.

Primary oculomotor nerve synkinesis is almost always caused by an intracavernous meningioma or aneurysm. We treated a patient who had signs of primary oculomotor nerve synkinesis from an unruptured extracavernous aneurysm located at the junction of the internal carotid artery and the posterior communicating artery. The aneurysm was successfully clipped, resulting in some improvement in ocular motility and alignment. Although most aneurysms affecting the subarachnoid portion of the oculomotor nerve cause an acute, painful oculomotor nerve paresis, such aneurysms may rarely produce painless primary oculomotor synkinesis and therefore should be considered in the differential diagnosis of this phenomenon.

Review of the clinical features of 48 patients with chordoma and 49 patients with low-grade chondrosarcoma of the skull base disclosed overlapping clinical profiles but distinctive features. Both tumors occurred at all ages but chondrosarcoma tended to occur in the third and fourth decades. Twenty-five (52%) of the patients with chordoma and 24 (49%) of the patients with chondrosarcoma had ocular symptoms (diplopia or visual impairment) as the initial manifestation of the disease. Of the 59 patients (both groups) with diplopia, the diplopia was initially intermittent in 25 (42%). Headache and diplopia from an insidious abducens nerve palsy was most common in both groups. Abducens nerve palsy occurred in 22 (46%) of the patients with chordoma and 23 (47%) of the patients with chondrosarcoma. Normal examination results were more common in patients with chordoma, whereas visual loss, facial numbness, and multiple cranial neuropathies were more common in patients with chondrosarcoma. The similarities in the clinical features of these tumors reflect their common origin at the central skull base and the vulnerability of the abducens nerves at that site. The differences reflect the tendency of chordomas to originate from the clivus and chondrosarcomas to originate from the temporal bone.

PURPOSE: To describe an unusual ophthalmic manifestion of a pituitary adenoma. METHODS: Case report. RESULTS: A 32-year-old man had left supraorbital and frontal headaches and new-onset vertical diplopia. Examination showed a left fourth nerve palsy and increased vertical fusional amplitudes. Magnetic resonance imaging disclosed a sellar mass consistent with a pituitary macroadenoma. CONCLUSION: A pituitary adenoma may rarely manifest with an isolated fourth nerve palsy.

Purpose To estimate the spontaneous recovery rate of isolated traumatic sixth-nerve palsy. Method A retrospective chart review over a 24-year period at a single institution, excluding patients who were first seen more than 6 weeks after injury, to reduce bias toward nonrecovery. Results The Kaplan-Meier survival estimate of spontaneous recovery at 6 months was 27% (95% confidence interval [CI], 5% to 44%) in unilateral traumatic sixth-nerve palsy and 12% (95% CI, 0% to 33%) in bilateral traumatic sixth-nerve palsy. Conclusion Spontaneous recovery from isolated traumatic sixth-nerve palsy may be lower than previously reported. A prospective study is needed to provide a more accurate estimate of recovery rate.

Purpose/Methods We recently encountered anterior segment ischemia in a young healthy girl with traumatic abducens nerve palsy after the Jensen procedure and ipsilateral recession of the medial rectus muscle. The patient was treated with topical dexamethasone and homatropine 2% and oral prednisone. Results/Conclusion The patient's condition improved, and six weeks postoperatively, visual acuity was 20/20. As this complication of anterior segment ischemia is potentially serious and unpredictable, we think that an alternative surgical approach should be used when treating patients with muscle palsies.

Two patients, an 81-year-old man and a 77-year-old woman, developed sixth nerve palsies after radiofrequency trigeminal gangliolysis for trigeminal neuralgia. Both sixth nerve palsies resolved spontaneously within four to seven months. The combination of postoperative trigeminal nerve deficits and transient oculomotor nerve palsies can mimic parasellar mass lesions and lead to unnecessary neuroradiologic investigation in the early postoperative period.

A prospective evaluation of ophthalmologic findings in 26 patients (25 men and one woman) with the acquired immune deficiency syndrome disclosed that 19 patients had significant ocular abnormalities. These included isolated retinal hemorrhages, cotton-wool spots, cytomegalovirus retinitis, acute retinal necrosis, cranial nerve palsies, and orbital Kaposi's sarcoma. Hemorrhages and cotton-wool spots appeared and disappeared spontaneously. Cytomegalovirus retinitis and acute retinal necrosis were progressive and destructive. The fundus findings did not correlate with the patient's general clinical status.

Two patients had paresis of the trochlear nerve contralateral to the site of lesions in the brainstem. Both patients had ipsilateral blepharoptosis and miosis suggesting oculosympathetic paresis from involvement of the descending sympathetic tract, adjacent to the fourth cranial nerve nucleus and its fascicles, in the caudal mesencephalon. Cerebral angiography documented an arteriovenous malformation of the brainstem in Case 1. Magnetic resonance imaging disclosed a lesion of high signal intensity on T 2 -weighted images involving the dorsal mesencephalon in Case 2. Involvement of the superior cerebellar peduncle produced ipsilateral dysmetria and ataxia. Lesions involving the fourth cranial nerve nucleus or its fascicles, before decussation in the superior medullary velum, and adjacent sympathetic fibers may produce an ipsilateral Horner's syndrome and contralateral superior oblique muscle paresis.

A patient with a left sensorimotor trigeminal neuropathy was found to have edema of the corneal stroma induced by cold. Examination at room temperature demonstrated an anesthetic left cornea with minimal injection of the left eye and multiple punctate epithelial erosions. Corneal thickness, mean endothelial cell size, coefficient of variation of cell size, endothelial permeability to fluorescein, and aqueous humor flow rate, measured at room temperature were similar in the two eyes. After 47 minutes in a cold room at 4 C, the corneal thickness in the left eye increased from 0.55 to 0.65 mm, whereas that of the right eye remained at 0.55 mm. During the period of maximum swelling, the left cornea had clinical stromal edema with folds in Descemet's membrane but no epithelial edema. After return to room temperature there was a gradual return to normal corneal thickness over three hours. Fluorophotometry showed no evidence of increased endothelial permeability during corneal swelling in the left eye. Specular microscopy after 15 minutes of cold exposure demonstrated many swollen and irregular endothelial cells with darkened areas between cells in the left eye. Sensory nerve deficiency in the human cornea can produce an abnormal sensitivity to cold, resulting in defective control of corneal hydration. This study suggests that this effect may be on the endothelium.