[Multiple dural arteriovenous fistulas showing isolated subcortical white matter T2 hyperintensity with gadolinium enhancement].

We describe a 44-year-old man with a complaint of atonic seizures of the left upper limb, followed by generalized seizures. Brain MRI showed isolated juxtacortical white matter T2 hyperintensity with gadolinium (Gd) enhancement of the adjacent cortical gray matter and subcortical white matter in the right frontal convexity. Treatment with levetiracetam was effective for seizure suppression, and he had no other neurological abnormalities. Human leukocyte antigen typing revealed B54 and Cw1, which indicated the possibility of neuro-Sweet disease. However, a general examination, which included vital signs and eye and skin findings, was normal. A cerebrospinal fluid test showed a mild elevation in protein levels without pleocytosis and a normal range of interleukin-6. Electroencephalography showed intermittent slow waves without epileptic discharge in the bilateral temporal lobes. We detected subtle flow voids in the pia mater of the left frontal lobe, which suggested cerebrovascular disease, and specifically, the possibility of dural arteriovenous fistulas. Computed tomography angiography showed abnormally dilated perimedullary veins in the left frontal lobe. Cerebral angiography confirmed the existence of four dural arteriovenous fistulas, which included two retrograde leptomeningeal venous drainages in the right frontal cortical veins supplied by the anterior branch of the right middle meningeal artery. The other dural arteriovenous fistulas were retrograde leptomeningeal venous drainages in the left frontal cortical veins supplied by the anterior and posterior convexity branches of the left middle meningeal artery. The patient underwent successful endovascular embolization of all dural arteriovenous fistulas with Onyx injection. A follow-up MRI showed gradual improvement of the T2 hyperintensity and Gd enhancement. He remained seizure-free for 2 years following endovascular embolization.

Applying the 2022 optic neuritis criteria to noninflammatory optic neuropathies with optic nerve T2-hyperintensity: an observational study.

INTRODUCTION: Recent diagnostic criteria for optic neuritis include T2-hyperintensity of the optic nerve (ON), even without associated contrast enhancement. However, isolated ON-T2-hyperintensity is a nonspecific finding found in any optic neuropathy or severe retinopathy. We applied the 2022 optic neuritis diagnostic criteria to a cohort of patients with noninflammatory optic neuropathy and ON-T2-hyperintensity in at least one eye, to assess the rate of optic neuritis misdiagnosis using these criteria. METHODS: Retrospective study of consecutive patients who underwent brain/orbit MRI with/without contrast between 07/01/2019 and 06/30/2022. Patients with ON-T2-hyperintensity in at least one eye were included. The 2022 optic neuritis diagnostic criteria were applied to patients with noninflammatory optic neuropathies who had an ophthalmologic examination available for review. RESULTS: Of 150 patients included, 85/150 had compressive optic neuropathy; 32/150 had glaucoma; 12/150 had papilledema; 8/150 had hereditary (3), radiation-induced (3), nutritional (1), traumatic (1) optic neuropathies (none fulfilled the criteria); 13/150 had ischemic optic neuropathy and 4 fulfilled the criteria as definite optic neuritis due to contrast enhancement of the ON head. Seven additional patients would have satisfied the diagnostic criteria if red flags for alternative diagnoses had been overlooked. DISCUSSION: The application of the 2022 optic neuritis diagnostic criteria in patients with noninflammatory optic neuropathy and ON-T2-hyperintensity in at least one ON resulted in misdiagnosis of optic neuritis in only 4 patients because of ON head enhancement, all with nonarteritic anterior ischemic optic neuropathy. Neuro-ophthalmologic evaluation and exclusion of the ON head as a location in the MRI criteria would have prevented optic neuritis misdiagnosis in our study.

Influence of Blood Pressure on Acute Cervical Spinal Cord Injury Without Fracture and Dislocation: Results From a Retrospective Analysis.

OBJECTIVE: The objective of this study was to investigate the influence of blood pressure on the severity and functional recovery of patients with acute cervical spinal cord injury (SCI) without fracture and dislocation. METHODS: A retrospective case control study analyzed the data of 40 patients admitted to our orthopedics department (Beijing Tiantan Hospital, Capital Medical University) from January 2013 to February 2021. They were diagnosed as acute cervical SCI without fracture and dislocation. Gender, age, height, weight, history of hypertension, postinjury American Spinal Injury Association grade, postinjury modified Japanese Orthopaedic Association (mJOA) score, postoperative mJOA score, 1-year follow-up mJOA score, preoperative mean arterial pressure (MAP), intramedullary T2 hyperintensity, and hyponatremia were collected. The patients were divided into groups and subgroups based on their history of hypertension and preoperative MAP. The effects of history of hypertension and preoperative MAP on the incidence of T2 hyperintensity, hyponatremia, the improvement rate of the postoperative mJOA and 1-year follow-up mJOA scores were analyzed. RESULTS: Patients with history of hypertension had a lower incidence of intramedullary T2 hyperintensity than patients without history of hypertension (P < 0.05). Patients with history of hypertension and patients with a higher preoperative MAP had better neurological recovery at 1 year of follow-up (P < 0.05). CONCLUSIONS: Blood pressure has great influence on acute cervical SCI without fracture and dislocation. Maintaining a higher preoperative MAP is advantageous for better recovery after SCI. Attention should be paid to the dynamic management of blood pressure to avoid the adverse effects of hypotension after SCI.

Automated signal intensity analysis of the spinal cord for detection of degenerative cervical myelopathy - a matched-pair MRI study.

PURPOSE: Detection of T2 hyperintensities in suspected degenerative cervical myelopathy (DCM) is done subjectively in clinical practice. To gain objective quantification for dedicated treatment, signal intensity analysis of the spinal cord is purposeful. We investigated fully automated quantification of the T2 signal intensity (T2-SI) of the spinal cord using a high-resolution MRI segmentation. METHODS: Matched-pair analysis of prospective acquired cervical 3D T2-weighted sequences of 114 symptomatic patients and 88 healthy volunteers. Cervical spinal cord was segmented automatically through a trained convolutional neuronal network with subsequent T2-SI registration slice-by-slice. Received T2-SI curves were subdivided for each cervical level from C2 to C7. Additionally, all levels were subjectively classified concerning a present T2 hyperintensity. For T2-positive levels, corresponding T2-SI curves were compared to curves of age-matched volunteers at the identical level. RESULTS: Forty-nine patients showed subjective T2 hyperintensities at any level. The corresponding T2-SI curves showed higher signal variabilities reflected by standard deviation (18.51 vs. 7.47 a.u.; p < 0.001) and range (56.09 vs. 24.34 a.u.; p < 0.001) compared to matched controls. Percentage of the range from the mean absolute T2-SI per cervical level, introduced as "T2 myelopathy index" (T2-MI), was correspondingly significantly higher in T2-positive segments (23.99% vs. 10.85%; p < 0.001). ROC analysis indicated excellent differentiation for all three parameters (AUC 0.865-0.920). CONCLUSION: This fully automated T2-SI quantification of the spinal cord revealed significantly increased signal variability for DCM patients compared to healthy volunteers. This innovative procedure and the applied parameters showed sufficient diagnostic accuracy, potentially diagnosing radiological DCM more objective to optimize treatment recommendation. TRIAL REGISTRATION: DRKS00012962 (17.01.2018) and DRKS00017351 (28.05.2019).

Preoperative Magnetic Resonance Imaging Signal Intensity Classification Is Associated With Clinical Presentation and Surgical Outcomes in Myelopathy Caused by Thoracic Ossification of Ligamentum Flavum: A Multicenter Study.

STUDY DESIGN: Retrospective Cohort Study. OBJECTIVES: To explore whether classification of the increased signal intensity (ISI) on magnetic resonance imaging (MRI) correlates with clinical presentations and outcomes in symptomatic thoracic ossification of ligamentum flavum (T-OLF) patients. METHODS: All patients with symptomatic T-OLF who underwent laminectomy at four institutions were reviewed. The ISI on preoperative T2-weighted MRI was divided into 3 groups, Grade 0, none; Grade 1, light (obscure); and Grade 2, intense (bright). Neurological function before surgery and at follow-up was evaluated by the revised Japanese Orthopedic Association (JOA) score. Patients' demographics, clinical manifestations, and surgical outcomes were compared. RESULTS: A total of 94 patients were involved. Preoperative MRI showed 32 patients in Grade 0, 39 patients in Grade 1, and 23 patients in Grade 2. Low extremities numbness, weakness, and clinical signs were less frequent in Grade 0 patients. The grade of ISI was correlated with the duration of symptoms and cord compression. Grade 0 patients had a better preoperative JOA score than those with ISI changes, while Grade 2 patients showed worse neurological recovery, longer duration of operation, more intraoperative blood loss, and a higher incidence of perioperative complications. CONCLUSION: The classification of ISI is an effective parameter for preoperatively assessing cord compression, clinical severity, and surgical outcomes in T-OLF patients. Grade 0 patients have relatively mild neurological impairment but are more likely to be misdiagnosed. Grade 2 indicates the worst clinical impairment and neurological recovery, and implies a risky and challenging surgery.

A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage.

AIMS: White matter (WM) injury is a critical factor associated with worse outcomes following subarachnoid hemorrhage (SAH). However, the detailed pathological changes are not completely understood. This study investigates temporal changes in the corpus callosum (CC), including WM edema and oligodendrocyte death after SAH, and the role of lipocalin-2 (LCN2) in those changes. METHODS: Subarachnoid hemorrhage was induced in adult wild-type or LCN2 knockout mice via endovascular perforation. Magnetic resonance imaging was performed 4 hours, 1 day, and 8 days after SAH, and T2 hyperintensity changes within the CC were quantified to represent WM edema. Immunofluorescence staining was performed to evaluate oligodendrocyte death and proliferation. RESULTS: Subarachnoid hemorrhage induced significant CC T2 hyperintensity at 4 hours and 1 day that diminished significantly by 8 days post-procedure. Comparing changes between the 4 hours and 1 day, each individual mouse had an increase in CC T2 hyperintensity volume. Oligodendrocyte death was observed at 4 hours, 1 day, and 8 days after SAH induction, and there was progressive loss of mature oligodendrocytes, while immature oligodendrocytes/oligodendrocyte precursor cells (OPCs) proliferated back to baseline by Day 8 after SAH. Moreover, LCN2 knockout attenuated WM edema and oligodendrocyte death at 24 hours after SAH. CONCLUSIONS: Subarachnoid hemorrhage leads to T2 hyperintensity change within the CC, which indicates WM edema. Oligodendrocyte death was observed in the CC within 1 day of SAH, with a partial recovery by Day 8. SAH-induced WM injury was alleviated in an LCN2 knockout mouse model.

Analysis of risk factors for C5 nerve root paralysis after posterior cervical decompression.

BACKGROUND: C5 nerve root paralysis is a nonnegligible complication after posterior cervical spine surgery (PCSS). The cause of its occurrence remains controversial. The purpose of this study was to analyse the incidence of and risk factors for C5 nerve root paralysis after posterior cervical decompression. METHODS: We retrospectively analysed the clinical data of 640 patients who underwent PCSS in the Department of Orthopaedics, Affiliated Hospital of Qingdao University from September 2013 to September 2019. According to the status of C5 nerve root paralysis after surgery, all patients were divided into paralysis and normal groups. Univariate and multivariate analyses were used to determine the independent risk factors for C5 nerve root paralysis. A receiver operating characteristic (ROC) curve was used to demonstrate the discrimination of all independent risk factors. RESULTS: Multivariate logistic regression analysis revealed that male sex, preoperative cervical spine curvature, posterior longitudinal ligament ossification, and preoperative C4/5 spinal cord hyperintensity were independent risk factors for paralysis, whereas the width of the intervertebral foramina was an independent protective factor for paralysis. The area under the curve (AUC) values of the T2 signal change at C4-C5, sex, cervical foramina width, curvature and posterior longitudinal ligament ossification were 0.706, 0.633, 0.617, 0.637, and 0.569, respectively. CONCLUSIONS: Male patients with C4-C5 intervertebral foramina stenosis, preoperative C4-C5 spinal cord T2 high signal, combined with OPLL, and higher preoperative cervical spine curvature are more likely to develop C5 nerve root paralysis after surgery. Among the above five risk factors, T2 hyperintensity change in C4-C5 exhibits the highest correlation with C5 paralysis and strong diagnostic power. It seems necessary to inform patients who have had cervical spine T2 hyperintensity before surgery of C5 nerve root paralysis after surgery, especially those with altered spinal cord T2 signals in the C4-C5 segment.

Risk factors for rapid progressive neurological deterioration in patients with cervical spondylotic myelopathy.

BACKGROUND: The rapid progressive cervical spondylotic myelopathy (rp-CSM) which had a course of CSM less than 1 month and suffered rapidly progressive neurological deterioration had few reports. Therefore, it is important for us to recognize the pathophysiology of CSM especially the rp-CSM. The study aimed to investigate the risk factors for rapidly progressive (rp) neurological deterioration in patients with cervical spondylotic myelopathy (CSM). METHODS: A total of 159 patients were reviewed and divided into an rp-CSM group and a chronic-CSM (c-CSM) group. Various clinical indexes, including age, sex, Japanese Orthopaedic Association (JOA) score, intramedullary MR T2-hyperintensity, congenital/degenerative spinal stenosis, and local type of ossification of the posterior longitudinal ligament (OPLL), were analyzed, and independent risk factors were investigated. RESULTS: Thirty-four of 159 patients (21.4%) were diagnosed with rp-CSM. All patients were followed up for a mean of 68.56 ± 14.00 months in the rp-CSM group and 62.66 ± 19.95 months in the c-CSM group. No significant difference was found in sex, mean age, smoking and drinking status, diabetes mellitus (DM), hypertension, surgery time, blood loss, JOA score, degenerative spinal stenosis, or OPLL (local). Univariate analyses demonstrated that rp-CSM patients tended to have MR T2-hyperintensity, longer hospital stay, shorter waiting time for surgery, more congenital spinal stenosis, and worse neurological function and to prefer more posterior surgeries than c-CSM patients. A multiple logistic regression analysis showed that congenital spinal stenosis and MR T2-hyperintensity were independently related to the presence of rp-CSM. CONCLUSIONS: MR T2-hyperintensity and congenital spinal stenosis were risk factors for rp-CSM. Although neurological function deteriorates rapidly, early surgical decompression is recommended and can achieve good neurological recovery after surgery, indicating that rp-CSM could be a reversible condition.

Spinal adhesive arachnoiditis mimicking sarcoid myelitis with nodular dural enhancement: A case report.

Spinal adhesive arachnoiditis (SAA) is a rare, but often devastating, cause of compressive myelopathy. We report a patient with SAA resulting in a longitudinally extensive T2-hyperintense spinal cord lesion with initial nodular pial and dural enhancement mimicking neurosarcoidosis. Neurologists should be aware of this entity, especially in patients who have pertinent risk factors, such as prior meningitis, spinal cord trauma, or surgery.

Long-segment transverse myelitis in an immunocompetent patient due to varicella zoster virus reactivation.

Transverse myelitis is a segmental, full-thickness inflammation of the spinal cord with various etiologies including varicella zoster virus infection. Symptoms can manifest as sensory deficits, severe lower back pain radiating down the legs, bowel/bladder incontinence, and extremity weakness. This case report is unique in that it highlights a patient who developed long-segment transverse myelitis after a varicella zoster virus infection which has not been previously reported in the literature.

White matter T2 hyperintensities and blood-brain barrier disruption in the hyperacute stage of subarachnoid hemorrhage in male mice: The role of lipocalin-2.

AIMS: The current study examined whether white matter injury occurs in the hyperacute (4 hours) phase after subarachnoid hemorrhage (SAH) and the potential role of blood-brain barrier (BBB) disruption and an acute phase protein, lipocalin 2 (LCN2), in that injury. METHODS: Subarachnoid hemorrhage was induced by endovascular perforation in adult mice. First, wild-type (WT) mice underwent MRI 4 hours after SAH to detect white matter T2 hyperintensities. Second, changes in LCN2 expression and BBB disruption associated with the MRI findings were examined. Third, SAH-induced white matter injury at 4 hours was compared in WT and LCN2 knockout (LCN2 KO) mice. RESULTS: At 4 hours, most animals had uni- or bilateral white matter T2 hyperintensities after SAH in WT mice that were associated with BBB disruption and LCN2 upregulation. However, some disruption and LCN2 upregulation was also found in mice with no T2-hyperintensity lesion. In contrast, there were no white matter T2 hyperintensities in LCN2 KO mice after SAH. LCN2 deficiency also attenuated BBB disruption, myelin damage, and oligodendrocyte loss. CONCLUSIONS: Subarachnoid hemorrhage causes very early BBB disruption and LCN2 expression in white matter that is associated with and may precede T2 hyperintensities. LCN2 deletion attenuates MRI changes and pathological changes in white matter after SAH.

Clinics in diagnostic imaging (190). Subacute combined degeneration of the spinal cord (SCD).

A 54-year-old man presented with progressive onset of lower limb paraesthesias, sensory ataxia, gait instability and lower limb weakness. Laboratory findings revealed low serum B12 levels. Magnetic resonance imaging showed long-segment symmetrically increased T2 signal within the dorsal columns of the spinal cord in the lower thoracic spine. The conglomeration of findings was consistent with a diagnosis of subacute combined degeneration of the spinal cord (SCD). Aside from mild residual paraesthesias, the patient's symptoms largely resolved after treatment with intramuscular injections of vitamin B12. The clinical presentation, pathophysiology, clinical and radiologic differential diagnosis, and management of SCD were described.

Adult-Onset Orbital Sinus Pericranii with T2 Hyperintensity Lesion: A Case Report.

Sinus pericranii is a rare vascular anomaly, and most cases occur in children and develop at the midline. In previous reports of sinus pericranii, T2 hyperintensity lesion has not been regarded as a common sequela. We report an extremely rare case of orbital sinus pericranii with associated T2 hyperintensity lesion. A 50-year-old man was admitted to our hospital with a history of right upper eyelid swelling that had been present for several years. Computed tomography, magnetic resonance imaging, and digital subtraction angiography demonstrated a connection between the lesion and normal cerebral venous system. Thus, we diagnosed the lesion as a sinus pericranii despite its atypical features. We elected to observe the patient, and the lesion had remained the same size without any adverse events, such as hemorrhage, occurring throughout the 5-year follow-up. An atypical sinus pericranii should be considered in patients with a soft compressible swelling on the head, even if the lesion is located off the midline.

Radiologic and histologic features of the T2 hyperintensity rim of meningiomas on magnetic resonance images.

A hyperintensity rim is often seen at the brain-tumor interface of meningiomas upon T2-weighted (T2WI) magnetic resonance imaging (MRI), and it is referred to as the cerebrospinal fluid (CSF) space; however, the true nature of the rim remains unclear. We surveyed the MRI findings and the histopathologic characteristics of such rims. Our study population consisted of 53 consecutive patients who underwent meningioma removal at our hospital. The intensity of the rim on MRI scans obtained with different imaging sequences was assessed in all patients. We used 22 tumors for histopathologic investigation: tissue samples were acquired from both the tumor surface and from a deep intratumoral site. Of the 53 meningiomas, 37 (69.8%) manifested a hyperintensity rim on T2WI (T2-rim). The other 16 showed neither a hyperintense nor a hypointense rim on their T2WI. An enhancement effect corresponding to the rim was observed in 28 of the 37 (75.7%) T2-rim positive tumors. While 9 among the 37 tumors with a T2-rim (24.3%) did not show rim enhancement, they showed low intensity on fluid-attenuated inversion recovery (FLAIR) images. The microvascular density in the tumor capsule was significantly greater in the 12 T2-rim and rim enhancement positive tumors than in 10 tumors that were T2-rim negative or T2-rim positive, but rim enhancement-negative ( p < 0.001, Mann-Whitney U test). We found that 75.7% of T2 hyperintense rims that were detected at the brain-meningioma interface reflected a microvascular-rich capsule layer, rather than the CSF space.

Fluid signal changes around the knee on MRI are associated with increased volumes of subcutaneous fat: a case-control study.

BACKGROUND: Fluid in the subcutaneous fat is a common finding anterior to the knee on MRI. This may be caused by chronic low-grade shearing injuries in patients who are overweight. The purpose of this study was to determine if there is a difference in the amount of subcutaneous fat around the knee between patients with these appearances and controls. METHODS: This was a retrospective case-control study. Following a sample size calculation on pilot data, eighteen sequential patients demonstrating hyper-intense subcutaneous signal changes around the knee on fat-saturated T2-weighted MRI were identified from PACS (18 females, mean age 45, range 31-62). Age and gender-matched patients without abnormal T2 MR signal changes were selected. Two observers independently drew regions of interest representing cross-sectional areas of bone and fat. The location of T2 signal hyper-intense lesions was characterized by consensus. RESULTS: Inter and intra-rater intraclass reproducibility was "excellent" (ICC > 0.8). The mean cross-sectional area of bone for patients with T2 hyper-intense lesions was 31.79cm2 (SD 2.57) and for controls 30.11cm2 (SD 3.20) which was not significantly different (p = 0.09). The median cross-sectional area of fat for the study group was 62.29cm2 (IQR 57.1-66.5) and for controls was 32.77cm2 (IQR 24.8-32.3) which was significantly different (p < 0.0001). Consensus agreement demonstrated all T2 hyper-intense lesions were anterior to the knee extensor mechanism. CONCLUSION: Subcutaneous fluid around the knee is associated with an increased amount of subcutaneous fat, anterior to the knee extensor mechanism. This may be caused by shearing injuries in fat with reduced elasticity associated with metabolic syndrome.

Imaging in Myotonic Dystrophy Type 1 - Case Reports.

Myotonic dystrophy type 1 (DM1) is the most common of the muscular dystrophies. It is an autosomal dominant neuromuscular disorder with multisystem involvement, including the central nervous system. Two DNA-proven cases are presented. Patients reported are siblings showing features of DM1 on magnetic resonance imaging (MRI). These features include T2 and FLAIR hyperintensities in the periventricular, deep, and subcortical white matter, with frequent involvement of the anterior temporal lobe. Other features include general brain atrophy and enlarged Virchow-Robin spaces. Subcortical white matter lesions anterior in the temporal lobe are the most specific imaging finding, and a short differential diagnosis is discussed.

Multidimensional Analysis of Magnetic Resonance Imaging Predicts Early Impairment in Thoracic and Thoracolumbar Spinal Cord Injury.

Literature examining magnetic resonance imaging (MRI) in acute spinal cord injury (SCI) has focused on cervical SCI. Reproducible systems have been developed for MRI-based grading; however, it is unclear how they apply to thoracic SCI. Our hypothesis is that MRI measures will group as coherent multivariate principal component (PC) ensembles, and that distinct PCs and individual variables will show discriminant validity for predicting early impairment in thoracic SCI. We undertook a retrospective cohort study of 25 patients with acute thoracic SCI who underwent MRI on admission and had American Spinal Injury Association Impairment Scale (AIS) assessment at hospital discharge. Imaging variables of axial grade, sagittal grade, length of injury, thoracolumbar injury classification system (TLICS), maximum canal compromise (MCC), and maximum spinal cord compression (MSCC) were collected. We performed an analytical workflow to detect multivariate PC patterns followed by explicit hypothesis testing to predict AIS at discharge. All imaging variables loaded positively on PC1 (64.3% of variance), which was highly related to AIS at discharge. MCC, MSCC, and TLICS also loaded positively on PC2 (22.7% of variance), while variables concerning cord signal abnormality loaded negatively on PC2. PC2 was highly related to the patient undergoing surgical decompression. Variables of signal abnormality were all negatively correlated with AIS at discharge with the highest level of correlation for axial grade as assessed with the Brain and Spinal Injury Center (BASIC) score. A multiple variable model identified BASIC as the only statistically significant predictor of AIS at discharge, signifying that BASIC best captured the variance in AIS within our study population. Our study provides evidence of convergent validity, construct validity, and clinical predictive validity for the sampled MRI measures of SCI when applied in acute thoracic and thoracolumbar SCI.

Gliomatosis Cerebri in the Brain of a Cat.

An eight-year-old, neutered, female, long-haired cat was presented with a three-week history of progressive lethargy, unlocalized pain in the cervical and lumbar spine, and unwillingness to move. An MRI (magnetic resonance imaging) of the brain revealed poorly circumscribed regions of non-contrast-enhancing heterogeneous T2 hyperintensity within the ventral forebrain and midbrain. A mass effect and evidence of increased intracranial pressure, including transtentorial herniation of the midbrain and herniation of the cerebellar vermis through the foramen magnum, were also observed. Due to progressive clinical decline and MRI results, the cat was humanely euthanized. Gross examination of the brain confirmed caudal transtentorial and foramen magnum herniation. The ventral aspect of the forebrain, midbrain, and brainstem were soft and had loss of detail, but lacked a grossly discernible mass. Histopathological examination found a poorly delineated neoplastic mass composed of hyperchromatic cells with indistinct cytoplasm, ovoid to elongate or curved nuclei, and indistinct nucleoli. The cells lacked immunoreactivity for Olig2, GFAP, Iba1, CD3, and Pax5. Based on the cellular morphology, immunolabeling characteristics, and anatomical location, a diagnosis of gliomatosis cerebri was made. Although uncommon, gliomatosis cerebri should be considered as a differential diagnosis in cats with central nervous system disease.

Hypertrophic olivary degeneration - a report of two cases.

Hypertrophic olivary degeneration (HOD) is seen following lesions in the Guillain-Mollaret triangle. This is unique because the inferior olivary nucleus hypertrophies following degeneration unlike the typical atrophy seen in other structures. We report two cases of HOD in two different clinical scenarios.