Abnormality in hippocampal signal intensity predicts atrophy in patients with systemic lupus erythematosus.

Objectives To quantify signal abnormalities in the hippocampus (Hsig) of patients with systemic lupus erythematosus (SLE) and to determine if Hsig predict hippocampal atrophy (HA) in SLE. Methods We included all SLE patients and healthy age- and sex-matched individuals with two magnetic resonance imaging (MRI) scans performed with a minimum of 1 year interval. All individuals underwent a standardized neuropsychological evaluation. Individual results were converted into standard scores and compared to normative data. SLE patients were additionally assessed for disease activity (SLE Disease Activity Index (SLEDAI)), damage (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI)), and the presence of antiphospholipid antibodies. MRI was performed on an Elscint 2 T scanner and T1 inversion recovery and T2 coronal images were used for analysis. Volumetric (HV) and signal quantification (Hsig) were determined by standardized protocols. Results We included 54 SLE patients (48 women; mean age 32.2 ± 10.56 years). Hsig were found at study entry in 15 (45.5%) patients. Hsig in the body and tail of non-atrophic hippocampi correlated with progression of volume loss during the follow-up period ( r = 0.8, p < 0.001). The presence of Hsig in the head of atrophic hippocampi correlated with progression of HA ( r = 0.73, p = 0.005) during the same period. No correlation of Hsig and disease activity or prednisone dose was observed. Conclusion HA is frequently observed in SLE patients and volume loss is progressive in a subgroup of patients. The evaluation of Hsig is an easy tool to determine patients that may have progressive hippocampal volume loss and should be followed more closely with MRI and cognitive evaluation.

Bevacizumab continuation beyond initial bevacizumab progression among recurrent glioblastoma patients.

BACKGROUND: Bevacizumab improves outcome for most recurrent glioblastoma patients, but the duration of benefit is limited and survival after initial bevacizumab progression is poor. We evaluated bevacizumab continuation beyond initial progression among recurrent glioblastoma patients as it is a common, yet unsupported practice in some countries. METHODS: We analysed outcome among all patients (n=99) who received subsequent therapy after progression on one of five consecutive, single-arm, phase II clinical trials evaluating bevacizumab regimens for recurrent glioblastoma. Of note, the five trials contained similar eligibility, treatment and assessment criteria, and achieved comparable outcome. RESULTS: The median overall survival (OS) and OS at 6 months for patients who continued bevacizumab therapy (n=55) were 5.9 months (95% confidence interval (CI): 4.4, 7.6) and 49.2% (95% CI: 35.2, 61.8), compared with 4.0 months (95% CI: 2.1, 5.4) and 29.5% (95% CI: 17.0, 43.2) for patients treated with a non-bevacizumab regimen (n=44; P=0.014). Bevacizumab continuation was an independent predictor of improved OS (hazard ratio=0.64; P=0.04). CONCLUSION: The results of our retrospective pooled analysis suggest that bevacizumab continuation beyond initial progression modestly improves survival compared with available non-bevacizumab therapy for recurrent glioblastoma patients require evaluation in an appropriately randomised, prospective trial.

Neuropsychological and neuroimaging evidences of cerebral dysfunction in stroke-free patients with atrial fibrillation: A review.

Atrial fibrillation (AF) is the most common heart arrhythmia, with the highest prevalence in the elderly. AF has been correlated with silent lesions and cognitive impairment, even in the absence of stroke. The cognitive impairment in AF represents a risk of functional decline, morbidity, mortality and high costs, constituting a public health problem due to the increasing prevalence of this arrhythmia. Cognitive analysis of patients with AF without stroke has shown poor performance in executive, memory and learning functions. The greater loss occurs in speed processing and performance of instrumental tasks leading to functional dependence. Neuroimaging studies have shown both structural and functional abnormalities in individuals with AF even in the absence of cognitive impairment. The mechanisms related to cognitive impairment and cerebral abnormalities in the AF are still a matter of discussion in the literature and, therefore, how to stop its progression is unknown. We reviewed the recent evidence about AF and dementia in patients without stroke, with special emphasis to the reported profile of cognitive dysfunction and the neuroimaging evidence of brain abnormalities.

[Prosthetic inguinal hernioplastics in day surgery. Which type of anesthesia? Our experience on 328 patients]. / Ernioplastica inguinale protesica in regime di day surgery. Quale anestesia? La nostra esperienza su 328 pazienti.

AIM: The aim of this paper is to compare local, spinal and general anesthesia with the tolerance of the patients as to pain and quality of life in the immediate postoperative period, and in the first week after the operation of prosthetic inguinal hernioplastics. METHODS: Three hundred and fifty eight patients underwent inguinal hernioplastes in day surgery regimen. The patients were divided into three groups according to the type of anesthesia and with the help of a schedule given to them. The parameters of the immediate postoperative period, such as pain nausea, vomit, cephalalgia, diuresis and the parameters in the following seven days after the operation, such as mobility, activity, pain, dejection and analgesic therapy, were compared. RESULTS: Collected data put into evidence a significative value, the mean pain value in the postoperative period, calculated on a numeric scale comprising numbers from 1 to 10. In patients who underwent a surgical procedure after a local anesthesia the mean pain value was 3.1. Comparison of postoperative symptoms highlights an asymptomatic condition in local or spinal anesthesia operated patients. Local anesthesia is generally more painful in the perioperative stage. Local anesthesia operated patients lament a longer duration of pain, in days, in the postoperative period and a longer administration of analgesics. No significance difference between mobility and quality of life has been noticed. CONCLUSION: The results of our study demonstrate that the comparison among the three types of anesthesia operated in day surgery is well balanced, as it was clearly expressed by the patients of each group. Every group was satisfied with its own anesthesia protocol.

MR Imaging Characteristics of Wingless-Type-Subgroup Pediatric Medulloblastoma.

BACKGROUND AND PURPOSE: "Transcriptionally different" medulloblastoma groups are associated with specific signaling pathway abnormalities; hence, they may present with distinct imaging manifestations. In this study, we sought to describe the MR imaging features of wingless-type-subgroup medulloblastomas with embryologic correlations. MATERIALS AND METHODS: Pre- and postoperative imaging studies of 16 patients with wingless-type-subgroup medulloblastoma were evaluated for tumor location, involvement of surrounding CSF spaces or parenchymal structures, conventional and DWI signal properties, and postsurgical damage patterns. Laterality scores were assigned to tumors at each step in the evaluation process. Continuous variables were summarized by using descriptive statistics. The Wilcoxon signed rank test was performed to compare laterality scores. To determine the interobserver variability, we computed the intraclass correlation and Cohen κ coefficients. RESULTS: Wingless-type-subgroup medulloblastomas in our series were histopathologically "classic." Wingless-type-subgroup medulloblastomas occur in specific sites, with involvement of the foramen of Luschka (75%), the fourth ventricle (68.75%), the cisterna magna (31.25%), and the cerebellopontine angle cistern (18.75%). Laterality scores were low (<2) when preoperative primary and secondary anatomic features were evaluated separately, but they increased (>2) when all pre- and postoperative anatomic features were considered. Results were statistically shown to be reproducible (interclass correlation coefficient, 0.71-0.94; Cohen κ, 0.63-1.00). On the basis of anatomic lesion patterns, 4 location-based subtypes may be distinguished: 1) midline-intraventricular, 2) midline-extraventricular, 3) off-midline-intraventricular, and 4) off-midline-extraventricular, which represent a continuum. CONCLUSIONS: Wingless-type-subgroup medulloblastomas are lateralized tumors arising from the brain stem and cerebellum around the foramen of Luschka. Our current understanding of their embryologic origins is in concordance with the spatial distribution of these tumors.

Abnormalities of hippocampal signal intensity in patients with familial mesial temporal lobe epilepsy.

Mesial temporal lobe epilepsy (MTLE) is associated with hippocampal atrophy and hippocampal signal abnormalities. In our series of familial MTLE (FMTLE), we found a high proportion of hippocampal abnormalities. To quantify signal abnormalities in patients with FMTLE we studied 152 individuals (46 of them asymptomatic) with FMTLE. We used NIH-Image for volumetry and signal quantification in coronal T1 inversion recovery and T2 for all cross-sections of the hippocampus. Values diverging by 2 or more SD from the control mean were considered abnormal. T2 hippocampal signal abnormalities were found in 52% of all individuals: 54% of affected subjects and 48% of asymptomatic subjects. T1 hippocampal signal changes were found in 34% of all individuals: 42.5% of affected subjects and 15% of asymptomatic subjects. Analysis of the hippocampal head (first three slices) revealed T2 abnormalities in 73% of all individuals (74% of affected subjects and 72% of asymptomatic subjects) and T1 abnormalities in 59% (67% of affected subjects and 41% of asymptomatic subjects). Affected individuals had smaller volumes than controls (P < 0.0001). There was no difference in hippocampal volumes between asymptomatic subjects and controls, although 39% of asymptomatic patients had hippocampal atrophy. Patients with an abnormal hippocampal signal (133 individuals) had smaller ipsilateral volume, but no linear correlation could be determined. Hippocampal signal abnormalities in FMTLE were more frequently found in the hippocampal head in both affected and asymptomatic family members, including those with normal volumes. These results indicate that subtle abnormalities leading to an abnormal hippocampal signal in FMTLE are not necessarily related to seizures and may be determined by genetic factors.

3T MRI quantification of hippocampal volume and signal in mesial temporal lobe epilepsy improves detection of hippocampal sclerosis.

BACKGROUND AND PURPOSE: In mesial temporal lobe epilepsy, MR imaging quantification of hippocampal volume and T2 signal can improve the sensitivity for detecting hippocampal sclerosis. However, the current contributions of these analyses for the diagnosis of hippocampal sclerosis in 3T MRI are not clear. Our aim was to compare visual analysis, volumetry, and signal quantification of the hippocampus for detecting hippocampal sclerosis in 3T MRI. MATERIALS AND METHODS: Two hundred three patients with mesial temporal lobe epilepsy defined by clinical and electroencephalogram criteria had 3T MRI visually analyzed by imaging epilepsy experts. As a second step, we performed automatic quantification of hippocampal volumes with FreeSurfer and T2 relaxometry with an in-house software. MRI of 79 healthy controls was used for comparison. RESULTS: Visual analysis classified 125 patients (62%) as having signs of hippocampal sclerosis and 78 (38%) as having normal MRI findings. Automatic volumetry detected atrophy in 119 (95%) patients with visually detected hippocampal sclerosis and in 10 (13%) with visually normal MR imaging findings. Relaxometry analysis detected hyperintense T2 signal in 103 (82%) patients with visually detected hippocampal sclerosis and in 15 (19%) with visually normal MR imaging findings. Considered together, volumetry plus relaxometry detected signs of hippocampal sclerosis in all except 1 (99%) patient with visually detected hippocampal sclerosis and in 22 (28%) with visually normal MR imaging findings. CONCLUSIONS: In 3T MRI visually inspected by experts, quantification of hippocampal volume and signal can increase the detection of hippocampal sclerosis in 28% of patients with mesial temporal lobe epilepsy.

Seizure frequency and lateralization affect progression of atrophy in temporal lobe epilepsy.

BACKGROUND: It is unclear which factors lead to progressive neuronal damage in mesial temporal lobe epilepsy (MTLE). The objective of this study was to evaluate whether progressive hippocampal and extrahippocampal atrophy occur in patients with MTLE and whether this atrophy is related to seizures. METHOD: We performed 2 MRI scans in 33 patients with clinical and electroencephalographic diagnosis of MTLE and in 24 healthy controls. MRI was performed in a 2-T scanner, and a T1-weighted gradient-echo sequence with 1 mm thickness was used for voxel-based morphometry analysis. Follow-up images were obtained at least 7 months after the first baseline MRI. Comparisons between the patient's follow-up and baseline MRIs, and between patients and controls, were performed. A corrected p value of 0.05 was set as the threshold for the statistical analysis. RESULTS: Follow-up MRI was performed after a median interval of 39 months (range 7-85 months). Three patients were seizure-free between the first and second MRIs. We observed progressive white and gray matter atrophy (p < 0.05) in patients with MTLE. This progression was more intense in patients with left MTLE compared with right MTLE. A higher frequency of seizures and a longer duration of epilepsy were associated with progression of gray and white matter atrophy in patients with MTLE. CONCLUSION: The progression of white and gray matter atrophy in patients with mesial temporal lobe epilepsy (MTLE) was more intense in patients with left MTLE and was associated with poorer seizure control and a longer duration of epilepsy.

Hippocampal abnormalities and seizure recurrence after antiepileptic drug withdrawal.

The authors performed hippocampal volumetry and T2 relaxometry in 84 consecutive patients with partial epilepsy from a protocol for antiepileptic drug (AED) withdrawal after at least 2 years of seizure control. Seizure recurrence after AED withdrawal was more frequent among patients with hippocampal atrophy and abnormal hippocampal T2 signal.

Patterns of hippocampal abnormalities in malformations of cortical development.

OBJECTIVE: To assess whether different types of malformation of cortical development (MCD) are associated with specific patterns of hippocampal abnormalities. METHODS: A total of 122 consecutive patients with MRI diagnosis of MCD (53 males, age range 1-58 years) were included in the study. Hippocampal measurements were made on 1-3 mm coronal T1-weighted MRIs and compared with MRIs of normal controls. RESULTS: A total of 39 patients had focal cortical dysplasia, 5 had hemimegalencephaly, 5 had lissencephaly-agyria-pachygyria, 11 had SLH, 11 had PNH, 12 had bilateral contiguous PNH, 5 had schizencephaly, and 34 had polymicrogyria. The frequency of hippocampal abnormalities in these patients with MCD was 29.5%. A small hippocampus was present in all types of MCD. Only patients with lissencephaly and SLH had an enlarged hippocampus. Abnormalities in hippocampal rotation and shape were present in all types of MCD; however, these predominated in PNH. None of the patients with lissencephaly-agyria-pachygyria or SLH had hyperintense signal on T2 or FLAIR images or abnormal hippocampal internal architecture. CONCLUSION: A small hippocampus was present in all types of MCD; however, the classic MRI characteristics of hippocampal sclerosis were often lacking. Abnormal enlargement of the hippocampus was associated with only diffuse MCD due to abnormal neuronal migration (lissencephaly-agyria-pachygyria and SLH).

Abnormalities of hippocampal signal intensity in patients with familial mesial temporal lobe epilepsy

Mesial temporal lobe epilepsy (MTLE) is associated with hippocampal atrophy and hippocampal signal abnormalities. In our series of familial MTLE (FMTLE), we found a high proportion of hippocampal abnormalities. To quantify signal abnormalities in patients with FMTLE we studied 152 individuals (46 of them asymptomatic) with FMTLE. We used NIH-Image© for volumetry and signal quantification in coronal T1 inversion recovery and T2 for all cross-sections of the hippocampus. Values diverging by 2 or more SD from the control mean were considered abnormal. T2 hippocampal signal abnormalities were found in 52 percent of all individuals: 54 percent of affected subjects and 48 percent of asymptomatic subjects. T1 hippocampal signal changes were found in 34 percent of all individuals: 42.5 percent of affected subjects and 15 percent of asymptomatic subjects. Analysis of the hippocampal head (first three slices) revealed T2 abnormalities in 73 percent of all individuals (74 percent of affected subjects and 72 percent of asymptomatic subjects) and T1 abnormalities in 59 percent (67 percent of affected subjects and 41 percent of asymptomatic subjects). Affected individuals had smaller volumes than controls (P < 0.0001). There was no difference in hippocampal volumes between asymptomatic subjects and controls, although 39 percent of asymptomatic patients had hippocampal atrophy. Patients with an abnormal hippocampal signal (133 individuals) had smaller ipsilateral volume, but no linear correlation could be determined. Hippocampal signal abnormalities in FMTLE were more frequently found in the hippocampal head in both affected and asymptomatic family members, including those with normal volumes. These results indicate that subtle abnormalities leading to an abnormal hippocampal signal in FMTLE are not necessarily related to seizures and may be determined by genetic factors.