Dynamic assessment of high-resolution MRI with multi-planar reconstruction increases the yeld of lesion detection in patients with patial epilepsy

To investigate the presence and type of lesions associated with partial epilepsies by routine high resolution MRI and multi-planar reconstruction (MPR) and correlate the MRI abnormalities with semiology and EEG findings. We studied 100 consecutive patients followed in the epilepsy clinic of our Hospital with partial epilepsy who underwent MRI investigation. THE MRI protocol included 6 mm sagittal T1-weighted, 3-4 mm axial T1 and T2-weighted, 3 mm coronal T1 inversion recovery and T2-weighted images that were printed on a radiographic film for routine analysis. The clinical and EEG findings were tabulated independently, and results were comapred using Chi-square of Fisher exact test when appropriate. The patients were divided into 10 groups according to their etiological classification (structural lesions) establihed by MRI. Mesial temporal sclerosis (MTS) was the largest group (40 per cent). There were 65 women and 35 men. Mean age was 23.9 (+- 5.7) years and mean age of onset of recurrent seizures was 9.9 (+-0.8) years. The most frequent risk factors were family history of seizures (23 per cent), head trauma (10 per cent), peri-natal anoxia (5 per cent) and infection (9 per cent). High resolution MRI including thin coronal slices, in addition to a "dynamic" analysis in a workstation with MPR, allowed a significant improvement in lesion detection compared to the traditional analysis with radiographic films (94 per cent versus 80 per cent) (p<0.05). The lesions previously undetected were focal cortical dysplasia and subtle MTS. There was a good concordance between MRI lesions and clinical and EEG findings. High resolution MRI including thin coronal slices, in addition to a "dynamic" analysis in a workstation with MPR allowed a significative improvement in lesion detection compared to the traditional analysis with radiographic films 94 per cent versus 80 per cent). Patients with partial epilepsy and "normal" MRI need to to investigated further with thin slices and post-processing techniques using volume acquisitions tha allow adequate multi-planar re-slicing

Massas abdominais volumosas em pediatria: ensaio iconográfico / Bulky abdominal masses in pediatrics: iconographic essay

Os autores apresentam os achados de exames de imagem de 19 pacientes pediátricos com massas abdominais volumosas. Foram selecionadas imagens de ultra-sonografia (US), tomografia computadorizada (TC) e ressonância magnética (RM). Nos 19 pacientes estudados os diagnósticos foram: hidronefrose, tumor de WiIms, neuroblastoma, carcinoma de adrenal, sarcoma, hemangioendotelioma, hepatoblastoma, hamartoma mesenquimal, carcinoma hepatocelular, cisto de colédoco, cisto esplênico, linfoma, cisto de mesentério, teratoma, hidrometrocolpos, lipoma. Os exames de imagem (US, TC e RM) são importantes ferramentas na avaliação de massas abdominais pediátricas e podem contribuir para o diagnóstico e avaliação da extensão dessas entidades.

Epilepsy and destructive brain insults in early life: a topographical classification on the basis of MRI findings.

Destructive insults of early development can lead to a wide variety of lesional patterns and are a well known cause of epilepsy. The aim of this study is to present a topographic magnetic resonance imaging (MRI) classification of these lesions in adult patients with epilepsy. Thirty-three consecutive patients were divided in three groups according to the topographic distribution of their lesion on MRI: hemispheric (H, n = 7); main arterial territory (AT, n = 18); arterial borderzone (Bdz, n = 8). We analyzed clinical, MRI and magnetic resonance angiography (MRA) data. Status epilepticus (SE) during childhood was more common in group H (7/7) than in the groups AT (1/18) and Bdz (0/8) (P < 0.001). MRA pattern of impaired flow signal in the distal segments of all three major arteries in the affected hemisphere was present in 85.7% of group H patients, and was exclusive to this group. 88.8% (16/18) of patients from group AT presented congenital motor deficit, in contrast to 37.5% (3/8) of group Bdz, and in none of group H (P < 0.001). All patients with Bdz lesions had antecedent of fetal distress, in contrast to 1/7 from group H and 5/18 of group AT (P = 0.001). The MRAs of patients with Bdz lesions were often normal except in those with larger lesions. Our data suggest that in adult patients with epilepsy due to precocious destructive brain insults, a MRI topographical classification distributes them in relatively homogenous clinical groups.

Lateralization of epileptiform discharges in patients with epilepsy and precocious destructive brain insults.

Unilateral destructive brain lesions of early development can result in compensatory thickening of the ipsilateral cranial vault. The aim of this study was to determine the frequency of these bone changes among patients with epilepsy and precocious destructive lesions, and whether a relationship exists between these changes and epileptiform discharges lateralization. Fifty-one patients had their ictal / interictal scalp EEG and skull thickness symmetry on MRI analyzed. Patients were divided into three main groups according to the topographic distribution of the lesion on the MRI: hemispheric (H) (n=9); main arterial territory (AT) (n=25); arterial borderzone (Bdz) (n=17). The EEG background activity was abnormal in 26 patients and were more frequent among patients of group H (p= 0.044). Thickening of the skull was more frequent among patients of group H (p= 0.004). Five patients (9.8%) showed discordant lateralization between epileptiform discharges and structural lesion (four of them with an abnormal background, and only two of them with skull changes). In one of these patients, ictal SPECT provided strong evidence for scalp EEG false lateralization. The findings suggest that compensatory skull thickening in patients with precocious destructive brain insults are more frequent among patients with unilateral and large lesions. However, EEG lateralization discordance among these patients seems to be more related to EEG background abnormalities and extent of cerebral damage than to skull changes.

Laterization of epileptiform discharges in patients with epilepsy and precocious destructive brain insults

Lesões cerebrais destrutivas unilaterais ocorridas em fase precoce do desenvolvimento podem resultar em espessamento compensatório da calota craniana ipsilateral. O objetivo deste estudo foi determinar a freqüência destas alterações ósseas em pacientes com epilepsia e lesões destrutivas precoces e avaliar se há associação entre estas alterações e lateralização de descargas epileptiformes. Foram analisados EEGs interictais / ictais e espessura do crânio pela RM de 51 pacientes. Os pacientes foram divididos em três grupos de acordo com a distribuição topográfica da lesão à RM: hemisférico (H) (n=9); território arterial (AT) (n=25); fronteira arterial (Bdz) (n=17). A atividade de base no EEG foi anormal em 26 pacientes e foi mais freqüente entre os pacientes do grupo H (p=0,044). Espessamento unilateral da calota craniana foi mais freqüente entre os pacientes do grupo H (p=0,004). Cinco pacientes (9,8 por cento) apresentaram discordância lateralizatória entre as descargas epileptiformes e lesão estrutural (quatro deles com atividade de base anormal, e apenas dois deles com espessamento da calota craniana). Em um destes pacientes, o SPECT ictal revelou forte evidência de falsa lateralização pelo EEG. Os achados sugerem que o espessamento compensatório da calota craniana é mais freqüente entre pacientes com lesões unilaterais e extensas. No entanto, a lateralização de descargas epileptiformes parece estar mais relacionada ao grau de alteração da atividade de base e extensão da lesão cerebral do que às alterações ósseas.

Early development destructive brain lesions and their relationship to epilepsy and hippocampal damage.

Fifty-one consecutive adult patients with epilepsy and early development destructive brain lesions were divided into three main groups according to the topographic distribution of the lesion on magnetic resonance imaging: hemispheric (H) (n=9); main arterial territory (AT) (n=25) and arterial borderzone (Bdz) (n=17). Eight (89%) patients from group H presented status epilepticus in the first 5 years of life, five of them associated with fever. Seventeen of the 25 patients from group AT (76%) had an obvious hemiparesis observed early in life. In addition, major prenatal events were significantly more common in the group AT compared with the other two groups. Among patients from group Bdz, prenatal or postnatal events were not identified, except for one patient. Conversely, nine patients from group Bdz (60%) showed a history of perinatal complications. Hippocampal atrophy (HA) was determined by visual analysis in 74.5% of all patients and by volumetry in 92%. The frequency of HA was comparable among groups, but patients from group H presented the most severe atrophy and more frequent hyperintense T2 hippocampal signal. In conclusion, these three groups of patients with early destructive lesions and epilepsy (H, AT and Bdz), appear to have distinct pathogenic mechanisms. Our data show that there is a striking association of HA with different patterns of neocortical destructive lesions of early development. This association seems to be related to a common and synchronic pathogenic mechanism. The recognition of the pattern and degree of HA among these patients with intractable seizures may influence the surgical rationale.

Crossed cerebellar atrophy in patients with precocious destructive brain insults.

OBJECTIVE: To analyze the frequency and pathogenetic factors of crossed cerebellar atrophy (CCA) in adult patients with epilepsy secondary to destructive brain insults of early development. METHODS: We studied 51 adult patients with epilepsy and precocious destructive lesions. Patients were divided into 3 groups according to the topographic distribution of their lesions on magnetic resonance imaging: group A, hemispheric (n = 9); group B, main arterial territory (n = 25); and group C, arterial border zone (n = 17). We evaluated the presence of CCA visually and with cerebellar volumetric measurement, correlating it with the clinical data. Other features shown on magnetic resonance imaging, such as the thalamus, brainstem, and middle cerebellar peduncle, were also carefully analyzed. RESULTS: Seven patients (13%) had CCA that was associated with the extent of the supratentorial lesion (6 from group A, 1 from group B, and none from group C; P<.001). Status epilepticus was present in 6 patients from group A and in none from the other groups. There was an association between the antecedent of status epilepticus and CCA (P<.001). All patients had atrophy of the cerebral peduncle ipsilateral to the supratentorial lesion and 4 had contralateral atrophy of the middle cerebellar peduncle. The duration of epilepsy was not associated with the presence of CCA (P =.20). CONCLUSIONS: Our data suggest that in patients with epilepsy and destructive insults early in life, the extent of the supratentorial lesion as well as the antecedent of status epilepticus play a major role in the pathogenesis of CCA. Recurrent seizures do not seem to be relevant to the development of CCA.

Neuroimaging of acute cerebellitis.

Acute cerebellitis is one of the main causes of acute cerebellar dysfunction in childhood and may be infectious, postinfectious, or postvaccination. The etiology of acute cerebellitis is usually viral. Varicella zoster, Epsten-Barr, rubeola, pertussis, diphtheria, and coxsackie viruses are the most frequently involved agents. Diagnosing of acute cerebellitis can sometimes be difficult because the patient may present only mild cerebellar signs and the examination of cerebrospinal fluid may be normal. The authors present the clinical and neuroimaging findings of 2 patients presenting with acute cerebellitis. Their magnetic resonance imaging showed hyperintense signal of cerebellar gray matter in T2-weighted sequences, which is a strong indication of a diagnosis of acute cerebellitis.