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24.04.2026, Friday, 11:30-13:00
Medical University of Gdańsk, Studenckie Koło Naukowe Neurochirurgii
"Subarachnoid Hemorrhage: Is It the Only Cause?"
Posterior fossa arteriovenous malformations are rare, representing only 5–15% of all AVMs, with an incidence in the population of 2 per 10,000. Because of the presence of vital structures in this confined area, AVMs of posterior fossa are life-threatening. We present the case of a 31-year-old female patient, admitted for a subarachnoid haemorrhage with atypical presentation in whom angiography showed a Spetzler–Martin grade 3 AVM associated with AICA treated with embolization.
Our aim is to highlight the surgical and diagnostic difficulties, review diagnostic possibilities and summarize the management options.
The study is a retrospective case report. Clinical, laboratory, and imaging data were obtained from the patient’s medical records. Diagnostic procedures were performed according to standard clinical practice.
The case provides an excellent illustration of the importance of thorough analysis. Although the reported headache does not in any way suggest or evoke the possibility of subarachnoid hemorrhage, it turned out that the patient was admitted to the department with precisely this clinical presentation. On the other hand, there are two peaks in age at presentation of AVM, one in childhood and another at age 30 to 50, into which our patient fits perfectly, as her SAH originated from an AVM. This highlights the importance of a multidimensional perspective when evaluating such cases. A second highly significant aspect emphasized by this case is the crucial role of grading scales in determining the optimal treatment strategy.
The case underlines several key points. Firstly, the need for accurate diagnostic imaging, preferably including thin-section MRI, to improve the detection of small vessel abnormalities and guide therapeutic planning. Secondly, the central role of angioarchitecture and Spetzler–Martin grading in treatment selection, and thirdly, the fact that not all lesions require immediate intervention, as some may undergo spontaneous regression.
Medical University of Gdańsk, Student's Scientific Circle of Neurosurgery
"Dural Arteriovenous Fistula Mimicking Carotid Cavernous Fistula: An Atypical Cause of Ocular Symptoms – A Case Report."
Cranial dural arteriovenous fistulas (dAVFs) are rare vascular anomalies characterized by abnormal connections between dural arteries and venous sinuses or cortical veins. Their clinical manifestations depend primarily on venous drainage patterns. Although carotid cavernous fistulas (CCFs) are classically associated with ocular symptoms such as chemosis, proptosis, and elevated intraocular pressure, similar presentations caused by dAVFs are uncommon and may lead to misdiagnosis.
To present a case of a cranial dAVF mimicking a carotid cavernous fistula and to highlight the importance of accurate differential diagnosis in patients presenting with ocular symptoms suggestive of CCF.
We report the case of an 83-year-old male with a 4-month history of progressive left-sided exophthalmos, lacrimation, and conjunctival redness. Initial imaging suggested a carotid cavernous fistula. However, detailed digital subtraction angiography (DSA) was performed to further evaluate the vascular lesion and determine the exact angioarchitecture and venous drainage pattern.
Angiographic studies revealed multiple dural arteriovenous fistulas draining into the left sigmoid sinus with retrograde cortical venous reflux, classified as Cognard IIb and Borden II. The patient underwent endovascular embolization using Onyx 18, which resulted in complete occlusion of the fistulas. The postoperative course was uneventful, and the patient was discharged in good clinical condition without neurological deficits.
This case underscores the necessity of including dAVFs in the differential diagnosis of patients presenting with ocular symptoms typically attributed to CCFs. Failure to recognize a dAVF with retrograde cortical venous drainage may delay treatment and increase the risk of hemorrhage or neurological deterioration. Comprehensive angiographic evaluation and early endovascular intervention are crucial for achieving favorable clinical outcomes.
Institute of Psychology, Jagiellonian University, Kraków;
Doctoral School of Social Sciences, Jagiellonian University, Kraków
"EEG signatures of late-stage amyotrophic lateral sclerosis resemble patterns characteristic for unresponsive wakefulness syndrome."
Amyotrophic lateral sclerosis (ALS) is a progressive, incurable neurodegenerative disease characterized by loss of motor neurons, leading to muscle weakness, respiratory failure, and death. Although the cerebral cortex has traditionally been considered relatively preserved, accumulating evidence indicates that cognitive impairment may occur in a substantial proportion of patients. This suggests neurodegeneration may extend beyond the motor system and involve cortical networks, potentially contributing to altered consciousness and EEG patterns resembling unresponsive wakefulness syndrome (UWS) – a syndrome defined by wakefulness without awareness.
This case study evaluated auditory system functioning and covert consciousness using electrophysiological measures in a 45-year-old woman diagnosed with ALS six years prior to assessment.
The protocol included resting-state (RS) EEG, 40-Hz auditory steady-state responses (ASSR), and a passive auditory oddball paradigm. Before EEG recording, auditory screening was performed, including otoacoustic emissions and auditory brainstem responses.
RS EEG was dominated by 1–3 Hz delta oscillations with an undifferentiated 1/f spectrum, predominantly over prefrontal regions, resembling frontal intermittent rhythmic delta activity. No event-related responses were detected in the oddball paradigm, and ASSR responses were absent. Auditory testing revealed no measurable otoacoustic or brainstem responses.
Findings indicate severe cortical dysfunction and provide no electrophysiological evidence of covert consciousness. The neurophysiological profile is consistent with a clinical presentation resembling UWS in end-stage ALS.
University Clinical Centre, Department of Adult Neurology, 17 Smoluchowskiego St., Gdansk, Poland
"Severe seronegative Miller Fisher Syndrome complicated by acute respiratory failure: A case report."
Miller Fisher syndrome (MFS) is a rare variant of Guillain-Barre syndrome characterized by ophthalmoplegia, ataxia, and areflexia. Although MFS typically has a mild clinical course , severe life-threatening presentations can occur.
The aim is to present an unusual, life-threatening case of seronegative MFS complicated by rapid respiratory failure, highlighting the crucial role of clinical evaluation when laboratory confirmation is absent.
A 48-year-old male presented with dysarthria, gait ataxia, and diplopia , preceded by fever and cough. Examination revealed bilateral ophthalmoplegia, four-limb ataxia, and areflexia. Initial cerebrospinal fluid analysis and head magnetic resonance imaging were unremarkable. Electroneurography showed axonal-demyelinating damage with conduction blocks. Ganglioside immunoblot antibodies were negative.
MFS diagnosis was established based on the clinical presentation. The patient developed acute respiratory failure requiring endotracheal intubation , mechanical ventilation , and a subsequent tracheostomy. Treatment included intravenous immunoglobulins and antibiotics for concurrent pneumonia. Over the following weeks, significant clinical improvement was observed. The patient was successfully decannulated and regained independent ambulation.
While MFS is generally considered a benign condition, clinicians must remain vigilant for atypical courses involving rapid respiratory decline. Furthermore, a severe clinical manifestation can occur in seronegative patients, where diagnosis must rely strictly on the clinical evaluation. Prompt intensive care and timely immunotherapy are crucial.
