Bilateral Intraorbital Arachnoid Cysts of the Optic Nerves and Coloboma of the Optic Nerve Ends

1984 ◽  
Vol 4 (3) ◽  
pp. 165-168 ◽  
Author(s):  
R. Wijngaarde ◽  
G. Blaauw ◽  
A. Van Balen
Author(s):  
Taner Arpaci ◽  
Barbaros S. Karagun

Background: Leukemia is the most common pediatric malignancy. Central Nervous System (CNS) is the most frequently involved extramedullary location at diagnosis and at relapse. </P><P> Objective: To determine if Magnetic Resonance Imaging (MRI) findings of optic nerves should contribute to early detection of CNS relapse in pediatric leukemia. Methods: Twenty patients (10 boys, 10 girls; mean age 8,3 years, range 4-16 years) with proven CNS relapse of leukemia followed up between 2009 and 2017 in our institution were included. Orbital MRI exams performed before and during CNS relapse were reviewed retrospectively. Forty optic nerves with Optic Nerve Sheaths (ONS) and Optic Nerve Heads (ONH) were evaluated on fat-suppressed T2-weighted TSE axial MR images. ONS diameter was measured from the point 10 mm posterior to the globe. ONS distension and ONH configuration were graded as 0, 1 and 2. Results: Before CNS relapse, right mean ONS diameter was 4.52 mm and left was 4.61 mm which were 5.68 mm and 5.66 mm respectively during CNS relapse showing a mean increase of 25% on right and 22% on left. During CNS relapse, ONS showed grade 0 distension in 15%, grade 1 in 60%, grade 2 in 25% and ONH demonstrated grade 0 configuration in 70%, grade 1 in 25% and grade 2 in 5% of the patients. Conclusion: MRI findings of optic nerves may contribute to diagnose CNS relapse by demonstrating elevated intracranial pressure in children with leukemia.


2021 ◽  
Author(s):  
Giulio Zuccoli

Abstract Purpose Until now, the diagnosis of optic nerves hemorrhages in abusive head trauma (AHT) has been obtained only in the postmortem setting. The aim of the IRB-approved study was to assess the presence of optic nerves hemorrhages in AHT patients using 3D-SWI. Methods Thirteen children with a final confirmed multidisciplinary diagnosis of AHT underwent coronal and axial 3D-SWI imaging of the orbits. The presence of optic nerve sheath (ONS) hemorrhages was defined by thickening and marked 3D-SWI hypointensity of the ONS, resulting in mass effect upon the CSF space. Optic nerve (ON) hemorrhages were defined by areas of susceptibility artifacts in the ON parenchyma. Superficial siderosis was defined by susceptibility artifact coating the ON. Furthermore, data about post-traumatic deformity of the ONS at the head of the optic nerve were collected. Results The average age of the population was 7.9 ± 5.9 months old. The average GCS was 11.8 ± 4.5. The male to female ratio was 7:6. ONS hemorrhages were identified in 69.2% of cases. Superficial siderosis and ON hemorrhages were identified in 38.5 and 76.9% of cases, respectively. 3D-SWI also depicted traumatic deformity of the ONS at the level of the optic nerve head in 10 cases (76.9%). No statistical correlations were identified between RetCam findings and 3D-SWI findings or GCS and ON hemorrhages. Conclusion This research shows that dedicated MRI with volumetric SWI of the orbits can depict hemorrhages in the ON, ONS, and ONS injury, in AHT victims.


1996 ◽  
Vol 76 (5) ◽  
pp. 3264-3273 ◽  
Author(s):  
R. Fern ◽  
J. A. Black ◽  
B. R. Ransom ◽  
S. G. Waxman

1. The affect of extracellular Cd2+ on CNS white matter was studied using an isolated rat optic nerve preparation. A 100-min exposure to 200 microM Cd2+ reduced the area of the compound action potential (CAP) recorded from the optic nerve to 32.6 +/- 3.8% (mean +/- SE) of the preexposure area, compared with a reduction to 74.9 +/- 2.9% after 100 min in control conditions (P > 0.001). This CAP reduction was not reversed after 120 min of reperfusion with Cd(2+)-free solution, or by perfusion with Cd2+ chelators. 2. Cd(2+)-induced CAP loss occurred in the absence of extracellular Ca2+. Increasing extracellular Ca2+ concentration to 16 mM, however, prevented Cd(2+)-induced CAP loss. Once evident, Cd(2+)-induced CAP reduction could not subsequently be reversed by addition of 16 mM Ca2+. 3. Low concentrations of Cd2+ (60 microM) did not significantly reduce CAP area. This concentration of Cd2+ combined with high extracellular K+ (30 mM) caused CAP loss that was blocked by 10 microM nifedipine, an antagonist of L-type voltage-gated Ca2+ channels. 4. Treatment with pharmacological inhibitors of membrane proteins known to be inhibited by Cd2+ did not affect the CAP. These included inhibitors of voltage-gated Ca2+ channels, Ca(2+)-activated K+ channels, Ca(2+)-ATPase and the Na+/Ca2+ exchanger. 5. Treatment with pharmacological agents that inhibit calmodulin or disrupt tubulin, two intracellular proteins affected by Cd2+, did not affect CAP area. 6. The effect of Cd2+ was not prevented by pretreatment with (+)-cyanidanol-3, an agent that prevents Cd(2+)-induced lipid peroxidation. 7. Treatment with antimycin A, a inhibitor of mitochondrial respiration, resulted in irreversible CAP reduction with a time course and extent similar to that produced by 200 microM Cd2+. Cd(2+)-induced CAP reduction was prevented by 1 mM cysteine, which prevents Cd(2+)-induced disruption of mitochondrial respiration. 8. The ultrastructure of optic nerves exposed to 200 microM Cd2+ for 100 min was characterized by swollen mitochondria with disrupted cristae and dissolution of microtubules, which were replaced by flocculent debris. Occasional regions of axonal swelling and empty spaces beneath the myelin also were found. Qualitatively similar changes in mitochondria and cytoskeletal elements were found in optic nerves exposed to antimycin A for 100 min. Astrocytes also displayed disrupted mitochondria and had an electron-lucent appearance under both conditions. 9. The neurological injury produced by exposure to Cd2+ is characterized by lesions of CNS white matter. Our results indicate that Cd(2+)-induced white matter injury in vitro results largely from disruption of mitochondrial respiration after Cd2+ influx through routes that include voltage-gated Ca2+ channels.


2021 ◽  
Vol 21 (86) ◽  
pp. e194-e199
Author(s):  
Mustafa Devran Aybar ◽  
◽  
Onder Turna ◽  

Introduction: In this study, we attempt to determine the diagnostic performance of shear wave elastography of the optic nerve and adjacent fat tissue in patients with optic neuritis. Methods: The study included a patient group consisting of 72 eyes of 36 patients who were diagnosed with unilateral optic neuritis, and an age-matched control group of 36 eyes of 18 healthy subjects. The patient group consisted of 25 multiple sclerosis patients and 11 recurrent isolated optic neuritis patients. The mean shear wave elastography values of the optic nerves and intraorbital fat tissue adjacent optic nerves were recorded using m/s and kPa as units. ROC curve analysis was performed, and the diagnostic accuracy of shear wave elastography values was determined. Results: The mean shear wave elastography values of the optic nerves with neuritis (2.49 ± 0.41 m/s and 17.56 ± 4.42 kPa) were significantly higher than the values of the contralateral normal optic nerves (1.71 ± 0.32 m/s and 9.02 ± 2.34 kPa) (p = 0.006 and p = 0.004, respectively) in the optic neuritis group. The mean shear wave elastography values of intraorbital fat tissue adjacent optic nerves with neuritis (1.87 ± 0.32 m/s and 9.65 ± 1.12 kPa) were significantly higher than the values of the contralateral normal side (1.47 ± 0.27 m/s and 6.78 ± 1.14 kPa) (p = 0.025 and p = 0.022, respectively) in the optic neuritis group. ROC curve analysis showed a high diagnostic accuracy for determining optic neuritis with shear wave elastography values of the optic nerves (AUC 0.955 [95% CI, 0.933–0.978] in m/s and AUC 0.967 [95% CI, 0.940–0.985] in kPa). Conclusions: Shear wave elastography may be an important alternative diagnostic tool in the diagnosis of optic neuritis.


2006 ◽  
Vol 96 (6) ◽  
pp. 2827-2829 ◽  
Author(s):  
Bernice Grafstein

This essay looks at the historical significance of two APS classic papers that are freely available online: Sperry RW. Optic nerve regeneration with return of vision in anurans. J Neurophysiol 7: 57–69, 1944 ( http://jn.physiology.org/cgi/reprint/7/1/57 ). Sperry RW. Restoration of vision after crossing of optic nerves and after contralateral transplantation of eye. J Neurophysiol 8: 15–28, 1945 ( http://jn.physiology.org/cgi/reprint/8/1/15 ).


2004 ◽  
Vol 91 (2) ◽  
pp. 1025-1035 ◽  
Author(s):  
Chuan-Li Zhang ◽  
Yakov Verbny ◽  
Sameh A. Malek ◽  
Peter K. Stys ◽  
Shing Yan Chiu

Receptor-mediated calcium signaling in axons of mouse and rat optic nerves was examined by selectively staining the axonal population with a calcium indicator. Nicotine (1-50 μM) induced an axonal calcium elevation that was eliminated when calcium was removed from the bath, suggesting that nicotine induces calcium influx into axons. The nicotine response was blocked by d-tubocurarine and mecamylamine but not α-bungarotoxin, indicating the presence of calcium permeable, non-α7 nicotinic acetylcholine receptor (nAChR) subtype. Agonist efficacy order for eliciting the axonal nAChR calcium response was cytisine ∼ nicotine >> acetylcholine. The nicotine-mediated calcium response was attenuated during the process of normal myelination, decreasing by approximately 10-fold from P1 (premyelinated) to P30 (myelinated). Nicotine also caused a rapid reduction in the compound action potential in neonatal optic nerves, consistent with a shunting of the membrane after opening of the nonspecific cationic nicotinic channels. Voltagegated calcium channels contributed little to the axonal calcium elevation during nAChR activation. During repetitive stimulations, the compound action potential in neonatal mouse optic nerves underwent a gradual reduction in amplitude that could be partially prevented by d-tubocurarine, suggesting an activity-dependent release of acetylcholine that activates axonal AChRs. We conclude that mammalian optic nerve axons express nAChRs and suggest that these receptors are activated in an activity-dependent fashion during optic nerve development to modulate axon excitability and biology.


1990 ◽  
Vol 5 (1) ◽  
pp. 99-104 ◽  
Author(s):  
Glen Jeffery

AbstractThe course of optic axons that take different routes at the chiasm have been traced through horizontally sectioned optic nerves in the cat, after unilateral injections of horseradish peroxide into the optic tract. Behind the eye and for most of the course of the nerve, nearly all of the axons that remain uncrossed at the chiasm are located in a retinotopically appropriate position, in the lateral aspect of the nerve. However, in the most caudal segment of the nerve an increasing proportion of these axons are located in regions that are retinotopically inappropriate. Just before the nerve joins the chiasm, uncrossed axons can be found across the full medio-lateral extent of the nerve, although there is still a relative increase in their density laterally.Labeled axons that cross at the chiasm course in a relatively parallel manner along the greater proportion of the nerve. However, in the caudal segment of the nerve their relative positions change and they appear to course in an irregular manner. This occurs where the uncrossed projection becomes increasingly more widespread.Axons in the optic nerve are grouped into fascicules. This pattern of organization also changes in the caudal region of the nerve. Although clear fascicular patterns are present along the greater part of the nerve, they become progressively less distinct caudally. The change in the pattern of fasciculation occurs over the same region of the nerve as the relative changes in axon trajectory and distribution.These results demonstrate that irrespective of chiasmatic route, optic axons in the cat are reorganized in the caudal segment of the nerve. This reorganization is not confined to changes in relative axon position, but is reflected in the structure of the nerve by the change of axon grouping from a fascicular to a non-fascicular arrangement.


Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 239-239
Author(s):  
Fahad A Alkherayf ◽  
David Houlden ◽  
Chantal Turgeon ◽  
Charles B Agbi ◽  
Andre Lamothe ◽  
...  

Abstract INTRODUCTION Optic nerve/chiasmal injury is a devastating outcome that may happen during endoscopic surgery. A key goal of endoscopic skull-base surgery is visual improvement. Currently, however, there is limited intraoperative visual pathway monitoring. We examine a novel technique that uses continuous flash visual evoked potentials (FVEPs). METHODS Eyes were stimulated by light stimulators (3 LEDs on each side, 640 nm peak wavelength, 10 ms pulse width, 3000 mCd of luminous intensity). Uniform illumination was placed over eyelids. Recording electrodes were placed at Oz-Fz. The filter cuts were = 5 Hz and 100 Hz with amplifier gain 20,000 or 50,000. EEG was recorded. Recordings were correlated to pre and post operative VFs and acuity. Dropping in the FVEP was examined in relation to intraoperative events. A drop of 50% from the base line was considered positive. RESULTS >101 patients had FVEPs in addition to other neurophysiologic monitoring. Patients demographic data, co-morbidities, diagnosis, surgical approach, length of surgery, MAP, and blood loss during surgery were recorded. All patients' visual acuity and field deficits were evaluated by neuro-ophthalmologist before their surgery and within 30 days after surgery. In our cohort, one patient had true positive pre-chiasmatic while another patient had false negative test result. However, the latter patient's deficit was post chiasmatic with no optic nerve or chiasmal injury. Another patient had false positive test (drop of 60%). Eight patients had transient changes related to traction of the chiasm or optic nerves. For predicting optic nerve or chiasmal injury, our study showed sensitivity of 100% (CI2.5-100), specificity of 99% (CI94.5-99.97) and negative predicted value of 100%. CONCLUSION FVEP is reproducible throughout surgery and can predict the post surgical outcome. Additionally, we found that FVEP is transiently affected by different stages of surgery. Further validation is required given the small number of optic/chiasmal injuries in our study.


2002 ◽  
Vol 87 (3) ◽  
pp. 1376-1385 ◽  
Author(s):  
Jerome Devaux ◽  
Maurice Gola ◽  
Guy Jacquet ◽  
Marcel Crest

Four blockers of voltage-gated potassium channels (Kv channels) were tested on the compound action potentials (CAPs) of rat optic nerves in an attempt to determine the regulation of Kv channel expression during the process of myelination. Before myelination occurred, 4-aminopyridine (4-AP) increased the amplitude, duration, and refractory period of the CAPs. On the basis of their pharmacological sensitivity, 4-AP-sensitive channels were divided in two groups, the one sensitive to kaliotoxin (KTX), dendrotoxin-I (DTX-I), and 4-AP, and the other sensitive only to 4-AP. In addition, tetraethylammonium chloride (TEA) applied alone broadened the CAPs. At the onset of myelination, DTX-I induced a more pronounced effect than KTX; this indicates that a fourth group of channels sensitive to 4-AP and DTX-I but insensitive to KTX had developed. The effects of KTX and DTX-I gradually disappeared during the period of myelination. Electron microscope findings showed that the disappearance of these effects was correlated with the ongoing process of myelination. This was confirmed by the fact that DTX-I and KTX enlarged the CAPs of demyelinated adult optic nerves. These results show that KTX- and DTX-sensitive channels are sequestrated in paranodal regions. During the process of myelination, KTX had less pronounced effects than DTX-I on demyelinated nerves, which suggests that the density of the KTX-sensitive channels decreased during this process. By contrast, 4-AP increased the amplitude, duration, and refractory period of the CAPs at all the ages tested and to a greater extent than KTX and DTX-I. The effects of TEA alone also gradually disappeared during this period. However, effects of TEA on CAPs were observed when this substance was applied after 4-AP to the adult optic nerve; this shows that TEA-sensitive channels are not masked by the myelin sheath. In conclusion, the process of myelination seems to play an important part in the regulation and setting of Kv channels in optic nerve axons.


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