Value of 7T MRI and post-processing in patients with nonlesional 3T MRI undergoing epilepsy presurgical evaluation.

OBJECTIVE: Ultra-high-field 7-Tesla (7T) magnetic resonance imaging (MRI) offers increased signal-to-noise and contrast-to-noise ratios, which may improve visualization of cortical malformations. We aim to assess the clinical value of in vivo structural 7T MRI and its post-processing for the noninvasive identification of epileptic brain lesions in patients with pharmacoresistant epilepsy and nonlesional 3T MRI who are undergoing presurgical evaluation. METHODS: Sixty-seven patients were included who had nonlesional 3T MRI by official radiology report. Epilepsy protocols were used for the 3T and 7T acquisitions. Post-processing of the 7T T1-weighted magnetization-prepared two rapid acquisition gradient echoes sequence was performed using the morphometric analysis program (MAP) with comparison to a normal database consisting of 50 healthy controls. Review of 7T was performed by an experienced board-certified neuroradiologist and at the multimodal patient management conference. The clinical significance of 7T findings was assessed based on intracranial electroencephalography (ICEEG) ictal onset, surgery, postoperative seizure outcomes, and histopathology. RESULTS: Unaided visual review of 7T detected previously unappreciated subtle lesions in 22% (15/67). When aided by 7T MAP, the total yield increased to 43% (29/67). The location of the 7T-identified lesion was identical to or contained within the ICEEG ictal onset in 13 of 16 (81%). Complete resection of the 7T-identified lesion was associated with seizure freedom (P = .03). Histopathology of the 7T-identified lesions encountered mainly focal cortical dysplasia (FCD). 7T MAP yielded 25% more lesions (6/24) than 3T MAP, and showed improved conspicuity in 46% (11/24). SIGNIFICANCE: Our data suggest a major benefit of 7T with post-processing for detecting subtle FCD lesions for patients with pharmacoresistant epilepsy and nonlesional 3T MRI.

Quantitative positron emission tomography-guided magnetic resonance imaging postprocessing in magnetic resonance imaging-negative epilepsies.

OBJECTIVE: Detection of focal cortical dysplasia (FCD) is of paramount importance in epilepsy presurgical evaluation. Our study aims at utilizing quantitative positron emission tomography (QPET) analysis to complement magnetic resonance imaging (MRI) postprocessing by a morphometric analysis program (MAP) to facilitate automated identification of subtle FCD. METHODS: We retrospectively included a consecutive cohort of surgical patients who had a negative preoperative MRI by radiology report. MAP was performed on T1-weighted volumetric sequence and QPET was performed on PET/computed tomographic data, both with comparison to scanner-specific normal databases. Concordance between MAP and QPET was assessed at a lobar level, and the significance of concordant QPET-MAP+ abnormalities was confirmed by postresective seizure outcome and histopathology. QPET thresholds of standard deviations (SDs) of -1, -2, -3, and -4 were evaluated to identify the optimal threshold for QPET-MAP analysis. RESULTS: A total of 104 patients were included. When QPET thresholds of SD = -1, -2, and -3 were used, complete resection of the QPET-MAP+ region was significantly associated with seizure-free outcome when compared with the partial resection group (P = 0.023, P < 0.001, P = 0.006) or the no resection group (P = 0.002, P < 0.001, P = 0.001). The SD threshold of -2 showed the best combination of positive rate (55%), sensitivity (0.68), specificity (0.88), positive predictive value (0.88), and negative predictive value (0.69). Surgical pathology of the resected QPET-MAP+ areas revealed mainly FCD type I. Multiple QPET-MAP+ regions were present in 12% of the patients at SD = -2. SIGNIFICANCE: Our study demonstrates a practical and effective approach to combine quantitative analyses of functional (QPET) and structural (MAP) imaging data to improve identification of subtle epileptic abnormalities. This approach can be readily adopted by epilepsy centers to improve postresective seizure outcomes for patients without apparent lesions on MRI.

Cerebral vasculitis and intracranial multiple aneurysms in a child with Lyme neuroborreliosis.

Introduction. Lyme borreliosis is a multisystem tick-borne disease caused by Borrelia burgdorferi. Neurological manifestations are reported in up to 15 % of adult patients with Lyme disease, while the frequency among children is higher. The most common manifestations are painful radiculopathy, facial nerve paresis and lymphocytic meningitis. Epileptic seizures and cerebral vasculitis with stroke or aneurysms are very rare complications. Case presentation. We describe a paediatric patient with sensorineural auditory dysfunction, headache, fatigue and epileptic seizures as sequelae of meningoencephalitis/Lyme neuroborreliosis (LNB) caused by B. burgdorferi. Brain magnetic resonance imaging revealed widespread enhancement of the leptomeninges, cranial nerves and artery walls compatible with vasculitis and disturbances in cerebrospinal fluid (CSF) circulation. The patient was treated with ceftriaxone for 2 weeks. Two years later, the patient had an ischemic stroke. Brain magnetic resonance angiography revealed multiple aneurysms, which were not present previously. The largest aneurysm was operated rapidly. The patient was treated with another course of intravenous ceftriaxone for 4 weeks and pulse therapy with corticosteroids. He recovered well. CONCLUSION: . This unique case demonstrates complications of LNB that can result in serious morbidity or even mortality. Lumbar puncture and analysis should be considered for paediatric patients with epileptic seizures or cerebrovascular events living in a Lyme borreliosis endemic area.

Lower Counts of Astroglia and Activated Microglia in Patients with Alzheimer's Disease with Regular Use of Non-Steroidal Anti-Inflammatory Drugs.

Epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAID) may have some therapeutic effect in Alzheimer's disease (AD) and experimental studies have shown that microglia activation by Abeta-peptide (Abeta-peptide. Furthermore, our results indicate that regular NSAID use is associated with significantly lower counts of astrocytes and a trend of lower counts of activated microglia in the brain tissue. The influence of NSAID use was noted in all ApoE genotypes however the trend of lower counts of glial cells with regular NSAID use was more marked in patients carrying the ApoE varepsilon 4/4 alleles. Based on our results one would anticipate that regular NSAID dosing could have a beneficial effect on the progression of the disease. However, the fact that we failed to observe significant differences for activated microglia might indicate an age or stage dependent difference in the glial response i.e. in their activation rate. More studies into age and stage related factors influencing the glial response are required if one is to devise novel pharmacological treatment strategies for AD.