Patterns of visual loss are the key to anatomic localization. Strictly monocular defects map to the prechiasmal sensory visual system. Bitemporal hemianopia is the signature of damage to the optic chiasm. Incongruous homonymous hemianopia points to an optic tract lesion. The closer a lesion gets to the occipital cortex, the more congruous or similar are the patterns of homonymous hemianopia. Understanding these patterns will add an important dimension to the clinician's localization arsenal. Perimetry is the quantitation of the visual field. This is done with a perimeter and usually involves estimating visual thresholds with a range of light stimuli. It is used clinically to map patterns of visual loss due to damage to the sensory visual system. This chapter discusses the types of perimetric testing and the underlying psychophysics of perimetry. This is followed by the interpretation of perimetric results, the relevant visual system anatomy, and patterns of loss helpful for neurologic localization. Lastly, the difficult issue of deciding whether the visual field has changed is reviewed.

We report the case of a 30-year-old woman with no relevant medical history who presented with a new-onset headache associated with nausea, vomiting, photophobia, phonophobia, and right nasal hemianopsia. Ocular point of care ultrasound (POCUS) examination revealed a hyperechoic lesion adhered to the vascular layer that did not move with eye movements. The patient was referred to ophthalmology, where choroidal melanoma was confirmed. Extension studies showed no metastases, and enucleation was performed. This case highlighted the importance of ocular POCUS in the diagnostic approach to this patient.

We report a case of Foster Kennedy Syndrome (FKS) caused by a frontal lobe tumor in which the optic disc (OD) shape was first monitored by optical coherence tomography (OCT) before and after tumor removal. A 56-year-old male complained of decreased vision in the left eye and an abnormal visual field in both eyes. The OD showed swelling and redness in the right eye and paleness in the left eye. OCT was used to measure the thickness of the retinal nerve fiber layer (RNFL) and the optic nerve head (ONH). The average OD thickness in the right and left eyes was 647 and 335 μm, respectively. Goldmann perimetry revealed an enlarged Mariotte blind spot with paracentral scotoma in the right eye and central absolute scotoma with horizontal hemianopsia in the left eye. FKS was suspected, and MRI revealed a lobulated mass outside the brain parenchyma of the anterior base of the skull, severely compressing both the frontal lobes and the corpus callosum. The patient underwent surgery for tumor removal. Six months after surgery, the visual field improved, but a central scotoma remained in the left eye. The OD thickness in the right and left eyes was 360 and 279 μm, respectively. RNFL thickness decreased preoperatively in both eyes, reaching the atrophic range in the left eye. In conclusion, OCT analysis revealed edema in the swollen OD and in the atrophic one in FKS. Notably, the ONH may be within the normal range in the early stages of the disease.

Following right brain damage, some patients experience anosognosia, which is a deficit of self-awareness affecting motor, somatosensory, or visual functions on the left side of the body. While domain dissociations in anosognosia have been studied extensively, the time course of recovery remains poorly understood. This study examines the longitudinal recovery time course of anosognosia in two patients presenting hemiplegia, hemianesthesia, and visual field defect after right brain damage. Anosognosia was assessed using the Bisiach four-point scale, a self-assessment of daily life activities, and interview reports. At onset, both patients exhibited complete anosognosia for left motor, somatosensory and visual field deficit. Anosognosia for hemiplegia recovered first, and was followed by recovery of anosognosia for hemianesthesia, while anosognosia for visual field defect persisted longer. This study provides evidence for differences in the time course of recovery of anosognosia for motor and sensory deficits. These findings question underlying mechanisms of awareness deficits: domain-specific or unitary models.

Pituitary neuroendocrine tumors, formerly referred to as pituitary adenomas, are common intracranial neoplasms. Most are benign and slow-growing. Clinical manifestations typically arise from hormonal hypersecretion or mass effect on adjacent structures. Hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion is an uncommon presentation of pituitary tumors and has been rarely reported. We present the case of a 35-year-old woman with a history of secondary amenorrhea and infertility who exhibited progressive headache and recurrent presyncope episodes. Laboratory tests showed that the patient had severe hyponatremia (sodium {Na}: 121 mmol/L), low serum osmolality (252 mOsm/kg), inappropriately elevated urine osmolality (748 mOsm/kg), elevated urinary sodium (112 mEq/L), hypouricemia (1.9 mg/dL), and a fractional excretion of uric acid of 11.66%, consistent with syndrome of inappropriate antidiuretic hormone secretion. Hormonal assessment indicated hypogonadotropic hypogonadism characterized by diminished levels of follicle-stimulating hormone, luteinizing hormone, and estradiol. Magnetic resonance imaging of the brain showed a sellar mass measuring 19 × 31 × 32 mm with a suprasellar extension and compression of the optic chiasm. Visual field testing corroborated bitemporal hemianopsia. The patient had an endoscopic transsphenoidal resection of the lesion. Histopathological examination identified a plurihormonal mature pituitary neuroendocrine tumor of gonadotroph lineage, exhibiting positive immunohistochemical staining for SF-1 and INSM1, negative expression for Pit-1, and a Ki-67 proliferation index of 10%. This case illustrates an uncommon manifestation of a gonadotroph pituitary neuroendocrine tumor presenting as severe hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion. Identifying this unusual presentation is crucial, as prompt diagnosis and intervention may avert considerable neurological, metabolic, and visual complications.

Rathke's cleft cysts are benign epithelial-lined sellar and suprasellar lesions that are often incidental findings but can cause visual deficits, hypopituitarism, and headaches when they enlarge and compress adjacent structures. Recurrence after surgical treatment remains challenging despite various surgical approaches. Marsupialization has emerged as an alternative technique for complex recurrent cases, establishing permanent communication between the cyst and the nasal cavity while minimizing surgical risk. We present a case of a 76-year-old man with type 2 diabetes mellitus, a history of meningeal tuberculosis, and panhypopituitarism who experienced progressive visual decline following multiple failed Rathke's cleft cyst surgeries. Ophthalmological evaluation revealed right temporal hemianopsia and reduced visual acuity, and magnetic resonance imaging confirmed a recurrent sellar-suprasellar lesion compressing the optic chiasm. Revision endoscopic endonasal surgery was performed using the marsupialization technique, including a type III sphenoidotomy, cyst aperture, dural membrane eversion toward the nasal cavity, and nasoseptal flap placement on the cyst floor. Surgery was completed without complications. At eight-month follow-up, the patient demonstrated complete resolution of hemianopsia, improved visual acuity, and stable postoperative changes without cyst reaccumulation on imaging. Endoscopic transnasal marsupialization represents a safe and effective therapeutic option for recurrent Rathke's cleft cysts, particularly following multiple failed interventions, providing permanent drainage while minimizing manipulation of delicate neurovascular structures. It may also potentially reduce recurrence rates and improve functional outcomes in complex cases.

A homonymous visual field defect (homonymous hemianopia) is the most common visual dysfunction after a cerebrovascular accident and is associated with involvement of the postchiasmatic pathways (usually the optic radiation or peristriate cortex). Patients with hemianopia experience difficulties with daily activities, such as navigation, visual search, recognition of people and objects, and reading. This review presents current data on use and effectiveness of various non-drug methods for neurorehabilitation in patients with homonymous visual field defects, including approaches for compensation, replacement, and recovery (trainings for restoring vision, stimulus response practices, systematic training of eye movement, use of immersive technologies, multisensory and transcranial non-invasive stimulation, etc.), as well as analyzes the available scientific data on the neurophysiological basis of recovery of patients with hemianopia after a cerebrovascular accident. Activation of neuroplasticity mechanisms underlying rehabilitation in homonymous hemianopia after stroke, and targeted management of cortical reorganization processes, help achieve the best recovery of visual functions.

Metastasis to the pituitary gland is rare, occurring in approximately 1% of pituitary tumors resected via transsphenoidal surgery. We present the second report of metastatic high-grade serous ovarian carcinoma to the pituitary gland, presenting with diabetes insipidus and bilateral hemianopsia. An 86-year-old female patient presented with complaints of dizziness, vertigo, vision changes (peripheral field vision loss), loss of taste, extreme thirst, and fatigue. Urine studies revealed hypotonic hyponatremia, which was consistent with diabetes insipidus. The pituitary magnetic resonance imaging (MRI) scan revealed a sellar and suprasellar hypoenhancing lesion compressing the optic chiasm. The intrasellar portion was heterogeneous, whereas a nodular component along the stalk demonstrated more solid, mild enhancement. The lesion measured 1.8 cm craniocaudally and 7 mm medial-laterally. The lesion presented with compression on the optic chiasm and edema in the proximal optic tracts and hypothalamus. This was a new finding compared with the MRI of the cervical spine as well as prior head computed tomography. An endoscopic transsphenoidal approach to resect the sellar and suprasellar parts of the lesion was performed. Pathology results revealed metastatic adenocarcinoma to the anterior pituitary gland with large areas of necrosis. Immunohistochemistry results revealed that the tumor cells were positive for pankeratin, keratin 7, PAX8, WT1, and estrogen receptor with null-type tumor protein p53 labeling, and negative for keratin 20, TTF1, Napsin-A, GATA3, CDX2, synaptophysin, chromogranin, p16, p63, KIT, and progesterone receptor. The final diagnosis was metastatic adenocarcinoma of Mullerian origin. Following diagnosis, a metastatic workup was done, including a whole-body positron emission tomography (PET) scan, which revealed a 5.1 cm right adnexal ovoid mass and numerous scattered liver metastases. Additionally, the PET scan revealed hypermetabolic right supraclavicular, paratracheal, celiac, and upper aortocaval nodes, consistent with metastatic disease. This report highlights high-grade serous ovarian carcinoma with pituitary metastasis as the initial presentation of systemic cancer.

Hyperosmolar hyperglycemic state (HHS) is a severe complication of uncontrolled diabetes, often presenting with nonlocalizing neurologic symptoms such as encephalopathy. Rarely, focal neurologic deficits like hemianopsia can occur, even with serum osmolality below the diagnostic threshold for HHS. We report two cases of hyperglycemic patients with borderline serum osmolality presenting with neuro-ophthalmologic symptoms. Case 1 involved a 43-year-old male with type 1 diabetes who developed right-sided visual disturbances and was found to have cortical T2/FLAIR hyperintensity and subcortical hypointensity in the left temporal lobe and posterior cingulate gyrus. Case 2 involved a 64-year-old female with untreated type 2 diabetes and hypertension who presented with bright flashes and left homonymous hemianopsia. MRI revealed subtle cortical T2/FLAIR hyperintensity and subcortical hypointensity in the right occipital lobe, findings initially missed on radiological review. In both cases, symptoms resolved with glycemic control and treatment. These cases underscore the importance of recognizing neuro-ophthalmic symptoms as potential manifestations of hyperglycemia, even when serum osmolality is below the diagnostic threshold for HHS. The structural brain changes demonstrated by subtle radiographic findings corresponded to the patients' focal neuro-ophthalmic deficits. The reversibility of these findings with glycemic control highlights the critical need for early recognition and intervention.