Risk factors for the development of secondary intracranial hypertension in acute cerebral venous thrombosis.

PURPOSE: Intracranial hypertension (IH) can complicate cerebral venous thrombosis (CVT), potentially causing permanent visual loss. Current knowledge on risk factors for the development of IH following CVT is scarce. We applied a compound classifier (CSF opening pressure > 25 cmH2O, papilledema, or optic disc protrusion on MRI) as a surrogate for IH and studied the predictive value of thrombus location, the number of thrombosed segments, and thrombus volume. METHODS: We prospectively included 26 patients with acute CVT and complete MRI data. IH was defined by CSF opening pressure > 25 cmH2O, papilledema, or optic disc protrusion on MRI. Using high-resolution contrast-enhanced venography, we determined the thrombus location, number of thrombosed segments, and thrombus volume. We analyzed their association with IH by logistic regression, their predictive power by the area under the receiver operating characteristic curve, and their association with CSF opening pressure by linear regression. RESULTS: IH occurred in 46% of CVT patients and was associated with higher thrombus volume (AUC 0.759, p = 0.025) and superior sagittal sinus thrombosis both alone (OR 2.086, p = 0.049) and combined with transverse sinus thrombosis (OR 2.014, p = 0.028). Effects in patients presenting CSF opening pressure > 25 cm H2O and the compound classifier were consistent. Thrombus volume > 4 ml was the single most important predictor of higher CSF opening pressure (ß = 0.566, p = 0.035), increasing IH risk. CONCLUSION: Larger thrombus volume, dominant transverse sinus occlusion, and extensive superior sagittal combined with transverse sinus thrombosis were associated with IH. Thrombus volumetry might identify patients at risk for IH and direct further clinical evaluation.

Diagnosis of idiopathic intracranial hypertension - the importance of excluding secondary causes: A systematic review.

BACKGROUND: Idiopathic intracranial hypertension is characterized by increased intracranial pressure without any pathological findings on neuroimaging, except for signs of high intracranial pressure. Before diagnosing idiopathic intracranial hypertension secondary causes of increased intracranial pressure should be excluded. OBJECTIVE: to characterize the phenotype of patients with secondary intracranial hypertension and to identify possible risk factors for secondary intracranial hypertension. METHODS: We have systematically searched the PubMed database. The publications were analyzed according to the patient phenotype, age, gender, comorbidities, body mass index/weight status, and additional medication. The results are summarized in four categories: medication, infection, hormonal induced intracranial hypertension and miscellaneous groups of diseases related to sIH. RESULTS: We identified 105 eligible papers which included 272 cases. There were 49.6% pediatric cases. Among the adult group,70.9% were women. A total of 40.4% of all cases were obese or overweight, 27% among adults and 13.4% among pediatric cases. Increased BMI and recent weight gain, anemia, renal diseases and hypertension were the most frequent comorbidities related to sIH. CONCLUSION: Among sIH patients, 40.4% were obese or overweight; two thirds were women. We recommend that even patients with a typical IIH phenotype should be screened for secondary causes.

Quantification of foveal avascular zone area and macular vascular density changes in papilledema by swept-source optical coherence tomography angiography.

This work provide objective measures of foveal avascular zone area and macular vascular density by swept-source optical coherence tomography angiography during the follow-up of a patient with papilledema due to secondary intracranial hypertension.

Headache in Guillain-Barré Syndrome: Diagnostic and Management Implications.

Headache is an uncommon symptom in Guillain-Barré syndrome (GBS). We review four clinical settings related to GBS in which headache may be present. We focus on pathophysiological explanations, alerting the clinician to further potential investigations and treatment. Most reports of headache in GBS occur in the context of the posterior reversible encephalopathy syndrome, an increasingly recognized dysautonomia-related GBS complication. Less frequent is headache in the setting of increased intracranial pressure and papilledema (secondary intracranial hypertension), Miller Fisher syndrome, and cerebral venous sinus thrombosis. Rarely, headache can occur secondary to aseptic meningitis from IVIg use.

Cerebral Venous Thrombosis in Patients With Traumatic Brain Injury: Epidemiology and Outcome.

The natural history and epidemiological aspects of traumatic cerebral venous thrombosis (CVT) are not fully understood. Due to the concomitant occurrence with intracranial hemorrhages, guidelines for medical treatment have been highly controversial. In this study, our objective was to carry out an analysis description of the population and to conduct a literature review. A prospectively gathered radiology registry data of patients hospitalized at the tertiary hospital of Centro Hospitalar Universitário do São João, Porto, Portugal, between 2016 and 2021 was carried out. All patients with traumatic brain injury (TBI) and concomitant CVT were identified. CVT was confirmed by CT venogram. Demographic, clinical, and radiological data and their medical management were reported. In-hospital complications and treatment outcomes were compared between patients measured by the Glasgow Outcome Score Extended (GOSE) at discharge and GOSE at three months. There were 41 patients with traumatic CVT admitted to this study. The majority (45.2%) had a hyperdense signal near the lateral sinus at admission, and only 26.2% presented with skull fractures. Of this cohort, 95% had experienced lateral sinus thrombosis. Twenty-five patients (60%) had occlusive venous thrombosis. Venous infarct was the main complication following CVT. Thirty-two patients (78%) were anticoagulated after CVT and four developed complications. At the three-month follow-up after discharge, 28.2% had good recovery (GOSE > 6). This study revealed a higher incidence of CVT in severe TBI and a mild association with skull fractures. There is a higher incidence of CVT in the lateral sinus. Management was inconsistent, with no difference in outcome without or with anticoagulation. Larger, prospective cohort studies are required to better comprehend this condition and determine evidence-based guidelines.

Acute Fulminant Cerebral Edema in a Child With Suspected Meningoencephalitis.

Acute fulminant cerebral edema (AFCE) is a recently identified encephalitis type associated with significant morbimortality. Described as rare, limited data exists on its early detection and treatment. This paper describes a case of AFCE that progressed to unresponsive intracranial hypertension. A previously healthy four-year-old boy presented with fever, myalgias, and neurological symptoms. Diagnostic assessments showed cerebrospinal fluid abnormalities, and despite medical interventions, his condition deteriorated rapidly and developed severe cerebral edema and herniation within 24 hours. A decompressive craniectomy was attempted to decrease intracranial pressure, without success. This case emphasizes the urgency of early AFCE recognition and effective management strategies given its severe prognosis, aiming to improve understanding and spur further research.

Diffusion Mri in Intracranial Hypertension: Quantitative Assesment.

PURPOSE: Intracranial hypertension (IH) is a neurological disease that is characterized by increased intracranial pressure. Idiopathic intracranial hypertension (IIH) is characterized by an increase in intracranial pressure without an underlying neuroradiological cause (1-3). The IH that is associated with a reason such as a mass, hydrocephalus, or drug use, is referred to as secondary intracranial hypertension (SIH). We aimed to detect determine whether the increased intracranial pressure causes a change in the diffusion values of brain in the diffusion MRI images. METHODS: The study includes 24 consecutive patients that were diagnosed with IIH and 18 consecutive patients that were diagnosed with secondary intracranial hypertension (SIH). The control group included 24 patients. Measurement of apparent diffusion coefficient (ADC) was performed using DWI sections obtained from subcortical white matter and the cortex of the frontal lobe in the basal ganglia plane, caudate nucleus head, thalamus, the posterior leg of the internal capsule, corpus callosum splenium; in the centrum semiovale plane, from the central white matter region. with 1.5T MRI using b=500s/mm2 and b=1000s/mm2 values both in patients and control groups. Mean ADC values were compared between IIH, SIH patients and control groups. RESULTS: The ADC values from the head of the caudate nucleus and the cortex were significantly higher in the IIH group, compared to the control group. When the ADC values of the SIH and control groups were compared, it was found that some of the ADC measurements (subcortical white matter, cortex and semioval center) were significantly different. The comparison of the IIH and the SIH groups revealed that the ADC measurements central white matter in the centrum semiovale, the subcortical white matter and the posterior leg of the internal capsule were significantly different. Conclusions: We have found increased diffusion IIH and SIH patients, which supports the development of brain edema. Even though the mechanism of the brain edema in IIH are not entirely clear, it is thought that the mechanism is different from the brain edema caused by a mass or a sinus thrombosis.

Secondary intracranial hypertension in aplastic anemia: A case report and review of current concepts.

Intracranial hypertension (IH) when detected mandates prompt and appropriate therapy to avoid permanent visual impairment. We report a 7-year-old boy who presented to the emergency services with purpuric rashes and bruises. Peripheral blood smear and bone marrow aspiration confirmed the diagnosis of aplastic anemia. During admission, the child developed headache, nausea, vomiting, and diplopia. Ophthalmic examination revealed intermittent esotropia and bilateral papilledema. The findings on neuroimaging and lumbar puncture led to the diagnosis of secondary IH (SIH). The intracranial pressure normalized on treatment with oral acetazolamide, oral furosemide, and intravenous dexamethasone.

Update on the application of optic nerve sheath fenestration.

BACKGROUND: With the ongoing development of surgical procedures and instruments, the safety of optic nerve sheath fenestration (ONSF) has been improved. OBJECTIVE: Through the past three decades, progress has been made in preventing visual loss from chronic optic nerve swelling in idiopathic intracranial hypertension (IIH), secondary intracranial hypertension and local optic nerve diseases. We now review the updated application of ONSF in those diseases. METHODS: The application of ONSF in papilledema due to IIH, secondary intracranial hypertension to cerebral venous sinus occlusion, Cryptococcal meningitis, and intracranial mass or tumors is reviewed. Additionally, the potential benefits of ONSF in local optic neuropathy from optic nerve sheath meningioma, optic nerve drusen, traumatic optic neuropathy and optic nerve/sheath biopsy are also described. RESULTS: Although ONSF has little or no effect on intracranial pressure, it is a safe, relative easy and effective surgical procedure to prevent or reverse visual loss in IIH. When other treatment modalities fail to timely protect vision, ONSF can be useful in protecting visual function or delay visual loss in secondary intracranial hypertension. CONCLUSION: We recommend that ONSF should be considered as a meaningful alternative or an adjunct therapy to reduce or delay the visual morbidity of these diseases, although the use of ONSF for some of them remains controversial.

Idiopathic intracranial hypertension in children: Diagnostic and management approach.

Idiopathic intracranial hypertension (IIH) is a rare neurological disorder in children. It is characterized by raised intracranial pressure (ICP) in the absence of brain parenchymal lesion, vascular malformations, hydrocephalus, or central nervous system (CNS) infection. The diagnosis is usually confirmed by high opening pressure of cerebrospinal fluid (CSF) with exclusion of secondary causes of intracranial hypertension. If not treated properly, it may lead to severe visual dysfunction. Here we review the etiology, clinical presentation, diagnostic criteria and management of IIH in children through illustration of the clinical and radiological presentation of a 13-year-old overweight girl who presented with severe headache, diplopia and bilateral papilledema. Otherwise, she had unremarkable neurological and systemic examinations. Lumbar puncture showed a high CSF opening pressure (360-540 mmH2O). Her investigations showed normal complete blood count (CBC), normal renal, liver, and thyroid function tests. Cerebrospinal fluid (CSF) and blood chemistry were unremarkable. Magnetic resonant image (MRI) of the brain demonstrated empty sella turcica, tortuous optic nerves, and flattening of the posterior sclera. Magnetic resonant venography (MRV) showed focal narrowing of the distal transverse sinuses and absence of venous sinus thrombosis. She required treatment with acetazolamide and prednisolone. With medical treatment, weight reduction, and exercise, our patient had a remarkable improvement in her symptoms with resolution of papilledema in two months. This review highlights the importance of early recognition and management of IIH to prevent permanent visual loss.