Optic Chiasm Lesions Research Articles

Bitemporal Hemianopia with Optic Chiasm Lesion: An Uncommon Presentation of MOGAD

Bitemporal Hemianopia with Optic Chiasm Lesion: An Uncommon Presentation of MOGAD

How should visual function monitoring be performed and interpreted in surgery for suprasellar tumors?

Preservation of visual function is important in surgery for suprasellar tumors. Visual evoked potentials (VEPs) are expected to play an important role in monitoring visual function during surgery. Given the lack of information in this field, the authors aimed to investigate the effects of optic nerve compression caused by suprasellar tumors to understand the possible usefulness of VEP monitoring using off-response (OFR) VEP. Eleven healthy volunteers who underwent surgery for standard record confirmation and 32 patients with optic chiasm lesions who underwent surgery were examined. Preoperative, postoperative, and intraoperative VEPs were recorded. Propofol anesthesia was administered during intraoperative VEP monitoring. Patients who underwent surgery were monitored using the same stimulation method during surgery. Light stimulation was given from a luminant pad on the eyelids, and low-intensity stimulation with continuous 500-msec emission and 500 msec off was performed. The luminescence intensity of the stimulation was at a maximum of 8000 lx with three attenuation steps, each of which was recorded repeatedly. The OFR potentials and delay latencies decreased as stimulus intensity decreased. In the patient with temporal hemianopia, monocular stimulation produced the highest OFR in the contralateral occipital lobe of the stimulated eye. The authors recorded preoperative, intraoperative, and postoperative VEP in 32 patients and observed intraoperative changes in 23 patients. In the cases where VEP declined during intraoperative recording, it recovered when surgery was discontinued. Furthermore, 3 patients eventually achieved a higher VEP than that achieved at the beginning of the surgery, and rapid recovery was confirmed with visual field examination immediately after surgery. Of the 5 patients in whom VEP did not recover during surgery, 3 showed decreased visual field and acuity after surgery. In 15 cases, potential dropped temporarily but returned to the original potential, and their visual field recovered after surgery. OFR has a diagnostic element in the visual field, in which the maximal potential was recorded on the opposite side of the stimulus with monocular stimulation. Unambiguous determination required stimulation of different intensities in both eyes or 1 eye and multiple recording electrodes placed in the occiput. Monitoring the OFR provides real-time alerts, making it a valuable tool for visual function evaluation in suprasellar surgery.

Opportunities and challenges in the diagnosis and treatment of optic chiasm lesions: a clinical and research perspective

The optic chiasm is a critical component of the visual pathway, and lesions in the pituitary and sellar regions can cause irreversible damage to a patient's visual function, resulting in a significant decrease in their quality of life. As a result, neuro-ophthalmology evaluation is a crucial part of the multidisciplinary treatment of pituitary diseases. However, due to the significant variation in the anatomical structure of the optic chiasm and the sellar region, as well as the complexity of the injury mechanism, chiasm injury can result in diverse manifestations and severity levels, which can make it difficult to correlate with anatomical parameters. In recent years, research has increasingly focused on the early recognition of optic chiasm compression, the prediction of visual function after intervention, and the long-term neurodegenerative effects, while optical coherence tomography (OCT), electrophysiological examinations, and functional magnetic resonance imaging are currently the most commonly used methods for evaluating sellar region lesions. However, the role of these methods, represented by OCT, in clinical diagnosis and treatment, still lacks high-level clinical evidence support, and the evaluation and prediction of optic chiasm function remain key areas for further study. In addition to compression lesions, lesions such as inflammation, infiltration, and demyelination in the sellar region, caused by systemic multi-system diseases, can also lead to visual function damage and require recognition in clinical practice.

Diagnosis of postretinal blindness caused by intracranial disease in three dogs

In this report, we provide clinical information on the diagnosis of postretinal blindness in veterinary ophthalmology. We have diagnosed three dogs with postretinal blindness (bilateral in one case and in the left eye in two cases). The electroretinogram results were normal and the optic axis was relatively clear in all cases. Our findings indicate that the reason for the blindness in these dogs was an intracranial lesion. Fundus photography did not reveal any significant changes, except in the optic disc. A normal optic disc, an optic disc that appeared to be smaller than that in the other eye, and a severely hyperemic and edematous optic disc were seen in cases 1, 2, and 3, respectively. On magnetic resonance imaging, two dogs had optic chiasm lesions (one a tumor, one inflammation) and the remaining dog had inflammation in the right optic tract and occipital lobe even though bright flash electroretinograms were normal. Magnetic resonance imaging and electroretinography can be used as diagnostic tools for detection and localization of central nervous system lesions in the visual pathways.

Ganglion cell layer complex measurements in compressive optic neuropathy.

Neuroophthalmologists and neurosurgeons are often asked by their patients what their visual prognosis will be after decompression of an optic chiasm lesion. Previous methods have been studied but have not provided consistent guidance. However, a recent algorithm which allows for retinal ganglion cell analysis from optical coherence tomography (OCT) may be more helpful. Recent studies have shown that ganglion cell layer complex (GCC) measurements from OCT strongly correlate with the visual field loss associated with compressive optic neuropathies. For example, GCC measurements show corresponding binasal thinning with bitemporal hemianopia. Some investigators have also shown that more preserved GCC thickness is preoperatively associated with better postsurgical outcome. Interestingly, some patients experience almost complete recovery of visual fields despite considerable GCC thinning, and others may have GCC loss before they develop demonstrable visual field defects. GCC measurements on OCT strongly correlate with visual field defects from optic chiasm compressive lesions and may help with regard to prognosis following treatment. However, considerable visual recovery is possible despite persistent GCC loss.

Damage to the optic chiasm in myelin oligodendrocyte glycoprotein-experimental autoimmune encephalomyelitis mice.

Optic chiasm lesions in myelin oligodendrocyte glycoprotein (MOG)–experimental autoimmune encephalomyelitis (EAE) mice were characterized using magnetic resonance imaging (MRI) and validated using electron microscopy (EM). MR images were collected from 3 days after induction to remission, approximately 20 days after induction. Hematoxylin and eosin, solochrome cyanin–stained sections, and EM images were obtained from the optic chiasms of some mice approximately 4 days after disease onset when their scores were thought to be the highest. T2-weighted imaging and apparent diffusion coefficient map hyperintensities corresponded to abnormalities in the optic chiasms of EAE mice. Mixed inflammation was concentrated at the lateral surface. Degeneration of oligodendrocytes, myelin, and early axonal damage were also apparent. A marked increase in chiasm thickness was observed. T2-weighted and diffusion-weighted MRI can detect abnormalities in the optic chiasms of MOG-EAE mice. MRI is an important method in the study of this model toward understanding optic neuritis.

The Influence of “Blind” Distractors on Eye Movement Trajectories in Visual Hemifield Defects

There is evidence that some visual information in blind regions may still be processed in patients with hemifield defects after cerebral lesions ("blindsight"). We tested the hypothesis that, in the absence of retinogeniculostriate processing, residual retinotectal processing may still be detected as modifications of saccades to seen targets by irrelevant distractors in the blind hemifield. Six patients were presented with distractors in the blind and intact portions of their visual field and participants were instructed to make eye movements to targets in the intact field. Eye movements were recorded to determine if blind-field distractors caused deviation in saccadic trajectories. No deviation was found in one patient with an optic chiasm lesion, which affect both retinotectal and retinogeniculostriate pathways. In five patients with lesions of the optic radiations or the striate cortex, the results were mixed, with two of the five patients showing significant deviations of saccadic trajectory away from the "blind" distractor. In a second experiment, two of the five patients were tested with the target and the distractor more closely aligned. Both patients showed a "global effect," in that saccades deviated toward the distractor, but the effect was stronger in the patient who also showed significant trajectory deviation in the first experiment. Although our study confirms that distractor effects on saccadic trajectory can occur in patients with damage to the retinogeniculostriate visual pathway but preserved retinotectal projections, there remain questions regarding what additional factors are required for these effects to manifest themselves in a given patient.

Imagerie des urgences en neuro-ophtalmologie

MRI often is mandatory in the diagnostic work-up of visual loss, visual field alterations and oculomotor problems. It is performed emergently in patients with painful diplopia associated to mydriasis, to exclude aneurysm, or in patients with painful Horner syndrome to exclude dissection of the internal carotid artery. CT scan in emergency remains useful in case of acute lateral hemianopsia or acute post traumatic visual loss. Progressive neuro-ophthalmological symptoms may require imaging examination in a short delay to define the therapeutic strategy: monocular transient blindness (dissection or carotid stenosis), progressive visual loss (optic nerve compression), bitemporal hemianopsia (optic chiasm lesion), painful visual loss (optic neuritis). A very precise clinical indication is helpful for the choice of imaging protocol and to improve its diagnosis value.

CT of cerebral abnormalities in precocious puberty.

True precocious puberty occurs as a result of the premature release of luteinizing hormone-releasing hormone from the hypothalamus, which stimulates the secretion of the pituitary gonadotropins, which in turn stimulate the gonadal sex steroids. The differential diagnosis of true precocious puberty includes cerebral and idiopathic categories. This differentiation, which cannot be made endocrinologically due to similarities in pituitary gonadotropin and sex steroid levels, may be facilitated by high-resolution CT. A CT study of 90 children (73 girls and 17 boys) with true precocious puberty was performed at the NIH to detect cerebral causes of their precocious puberty. Thirty-four cerebral abnormalities were demonstrated in 32 children, 16 boys and 16 girls. These included hypothalamic hamartomas (17), hypothalamic astrocytoma (one), optic chiasm lesions (six), ventricular abnormalities (eight), arachnoid cyst (one), and teratoma (one). The CT appearance of these cerebral abnormalities is discussed and related to the endocrinologic findings and natural history of true precocious puberty. A practical neuroradiologic approach to the evaluation of children with precocious puberty is presented.

Hypothalamic mediation of growth hormone and adrenal stress response in the squirrel monkey.

Hypothalamic lesions were produced in the squirrel monkey in order to identify the neural pathways by which the emotional stimulus of capture and the stress of ether anesthesia bring about growth hormone (GH) hypersecretion. Plasma GH levels were determined by human GH radioimmunoassay. As an index of pituitary-adrenal activation in these animals, plasma corticoids were measured by competitive binding assay. In unlesioned animals capture led to increased release of GH and to adrenal cortical activation. Chair restraint was followed by continued adrenal cortical hypersecretion unaccompanied Tjy GH discharge, while ether anesthesia induced GH discharge without a significant increase in adrenocortical secretion. Growth hormone responses to capture and ether anesthesia were blocked by relatively small lesions in either anterior or posterior median eminence, while adrenal responses to capture and chair restraint were blocked by lesions in the posterior median eminence in 3 animals. Lesions of the inferior third of the mammillary bodies blocked GH and adrenal responses to capture. GH responses to ether were greatly enhanced in 3 animals with midline optic chiasm lesions and in one animal with a mammillary body lesion, suggesting that structures in these regions may have an inhibiting effect on GH responses. (Endocrinology89: 694, 1971)