The 1920s was a formative period in the development of neurosurgery in Ireland. This study examines a 1922 brain tumour case treated by Adams McConnell, father of Irish neurosurgery, that illustrates the clinical limitations and defining practices of early neurosurgical interventions. A 19-year-old female was admitted with progressive neurological symptoms, including paraesthesias, diplopia, worsening vision, persistent vomiting, and gait imbalance. On clinical examination, signs of severe raised intracranial pressure and brainstem involvement were present, including papilledema and ataxia. Following diagnostic ventriculography, the patient then underwent two surgeries, including attempts at posterior decompression and posterior fossa exploration. Her condition rapidly declined postoperatively, marked by escalating fever and tachycardia, resulting in her death. Autopsy revealed a right-sided skull base tumour originating from the Gasserian ganglion. The tumour had eroded the middle cranial fossa and extended posteriorly to compress the pons, so it was not visible to the surgeons during craniotomy. Without modern medical technology and imaging, careful history taking, meticulous clinical observations, and the neurological examination were relied on to formulate a diagnosis. This study offers a snapshot of early neurosurgery amid diagnostic constraints; through which we can appreciate the remarkable advancements in the field over the past century.

Primary intracranial Ewing sarcoma / Ewing-like sarcoma is an exceptionally rare malignant small round cell tumor. Its radiological appearance is often non-specific and may mimic other aggressive intracranial neoplasms, leading to diagnostic delay. We report the case of a young adult presenting with progressive headaches and recurrent generalized tonic-clonic seizures for six months, followed by rapid bilateral visual loss. Neurological examination revealed papilledema and decreased visual acuity, prompting brain imaging. MRI demonstrated a large aggressive frontal mass with heterogeneous enhancement, marked diffusion restriction, meningeal involvement, and significant mass effect with midline crossing. Initial staging showed no extracranial disease. Histopathology revealed a small round cell tumor with strong membranous CD99 expression consistent with an intracranial Ewing-like sarcoma. The patient received multimodal treatment including radiotherapy and VDC/IE chemotherapy. Follow-up imaging demonstrated partial tumor response. However, no visual recovery occurred, and the patient remained limited to light and shadow perception. This case highlights the diagnostic challenges of primary intracranial Ewing-like sarcoma and its potential to present with severe and irreversible visual impairment. Early neuroimaging in patients with persistent seizures is essential to avoid diagnostic delay, and molecular confirmation remains crucial for future cases.

Cryptococcal antigen (CrAg) lateral flow assays (LFA) are widely used for the rapid diagnosis of cryptococcal meningitis because of their excellent sensitivity and specificity. We report a rare case of culture- and sequencing-confirmed Cryptococcus gattii VGI meningitis in an immunocompetent 43-year-old man with persistently negative IMMY CrAg LFA and semi-quantitative CrAg SQ results in both cerebrospinal fluid (CSF) and serum. The patient presented with fever, chronic progressive headache, diplopia, and papilledema. CSF analysis demonstrated lymphocytic pleocytosis, hypoglycorrhachia, elevated protein, and budding yeast cells on direct microscopy and India ink preparation. BioFire FilmArray meningitis/encephalitis panel detected C. neoformans/gattii species complex, while fungal culture and sequencing confirmed C. gattii VGI. False-negative CrAg LFA results persisted despite serial sample dilutions up to 1:2560. This case highlights a rare diagnostic pitfall of CrAg testing and underscores the importance of integrating microscopy, culture, and molecular methods when clinical suspicion remains high despite negative antigen assays.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune demyelinating disorder of the central nervous system in which optic neuritis is a frequent manifestation. Its presentation during pregnancy may pose a diagnostic challenge because bilateral optic disc edema and headache can mimic idiopathic intracranial hypertension or hypertensive disorders of pregnancy. We report a 39-year-old primigravid woman at 31 weeks of gestation with gestational diabetes and class III obesity who presented with progressive bifrontal headache followed by transient bilateral blurred vision, dyschromatopsia, and sudden severe visual loss in the right eye. Ophthalmologic examination showed bilateral papilledema, a relative afferent pupillary defect in the right eye, and reduced visual acuity. Ultrasound demonstrated an enlarged optic nerve sheath diameter, while brain and spine magnetic resonance imaging showed no major abnormalities. Visual evoked potentials revealed bilateral conduction delay, more severe in the right eye. Lumbar puncture showed a normal opening pressure (19.5 cmH2O) and normal cerebrospinal fluid cytochemistry, but cerebrospinal fluid-restricted oligoclonal bands were detected. Given the clinical suspicion of inflammatory optic neuropathy, serum testing for demyelinating disorders was performed and was positive for anti-myelin oligodendrocyte glycoprotein (MOG) antibodies, whereas aquaporin-4 and systemic autoimmune antibodies were negative. The patient was treated with intravenous methylprednisolone followed by therapeutic plasma exchange because of limited initial response, with progressive visual recovery and no maternal or fetal complications. This case highlights that MOG-associated optic neuritis should be considered in pregnant patients with acute visual loss and bilateral optic disc edema. Intracranial hypertension was ruled out, and paraclinical studies concluded bilateral inflammatory optic neuritis. Early recognition, serologic confirmation, and timely immunotherapy are essential to improve visual outcomes. Careful postpartum follow-up is warranted because relapse risk may increase after delivery.

Optic neuritis is a severe blinding ocular disease, and identifying its etiology is crucial for selecting appropriate treatment strategies and evaluating patient prognosis. This paper reports the clinical data of a patient initially presenting with unilateral visual decline who was ultimately diagnosed with bilateral atypical optic neuritis. The patient was a 40-year-old male who presented with decreased vision in the left eye for 2 weeks. Fundus examination at admission revealed bilateral optic disc edema, leading to a diagnosis of bilateral atypical optic neuritis. Systemic examination showed a positive Treponema pallidum particle agglutination test. After a series of serological and cerebrospinal fluid examinations for syphilis, syphilitic optic neuritis was excluded. The patient showed a poor response to conventional treatment for optic neuritis. Further comprehensive brain and ocular examinations were performed. After excluding multiple possible causes of optic neuritis, mitochondrial gene testing ultimately confirmed the diagnosis of Leber hereditary optic neuropathy (LHON). For young male patients presenting with acute vision loss, bilateral involvement, and typical fundus findings, etiological investigation should be emphasized, particularly the application of genetic testing, to achieve early diagnosis and timely treatment.

Pseudo-Foster Kennedy syndrome is a rare condition characterized by unilateral papilledema with contralateral optic atrophy in the absence of an intracranial mass causing direct compression of the optic nerve. We here report the case of a 75-year-old overweight female patient (BMI 30 kg/m[2]), with poorly controlled hypertension, who presented with decreased visual acuity. The patient reported headaches evolving over 2 months. Ophthalmologic examination showed papilledema in the right eye and optic nerve atrophy in the left eye. Physical examination revealed poorly controlled arterial hypertension with a peak blood pressure of 200/110 mmHg. The patient underwent neurological examination and brain imaging, both of which revealed no abnormalities. A lumbar puncture was performed and revealed increased resistance to CSF flow (34 cmH2O). Other tests were normal. The diagnosis of pseudo-Foster Kennedy syndrome secondary to idiopathic intracranial hypertension (IIH) was established. The patient was treated with oral acetazolamide. The evolution was marked by complete resolution of papilledema and headaches, with gradual recovery of visual acuity in the right eye. Idiopathic intracranial hypertension is a rare cause of pseudo-Foster Kennedy syndrome. Only a few cases have been reported in the literature. It should be considered when this syndrome is present in order to preserve both visual and vital prognosis.