PubMed Health⌕ Search

Biomedical subjects

Li M Li

Publications and source records attributed to Li M Li.

24 records · Page 2Linked to original sources
PubMed2003

Texture analysis of hippocampal sclerosis.

UNLABELLED: Mesial temporal lobe epilepsy (MTLE) is frequently associated with refractory seizures and pathologic features of hippocampal sclerosis (HS). Quantitative magnetic resonance imaging (MRI) techniques can improve the detection and quantification of HS. The objective of this study was to evaluate whether MRI texture analysis can detect hippocampal abnormalities in patients with pathologically proven HS. METHODS: Nineteen consecutive patients who underwent surgery for refractory unilateral MTLE and had HS diagnosed on histopathology (12 right and seven left) had their preoperative MRIs evaluated. We performed texture analysis in 3-mm coronal T1-IR MRIs, focusing on the hippocampal head, by using the software MAZDA. Data were compared with those of a group of 78 normal hippocampi from 39 healthy adult volunteers through multivariate analysis of variance and selection of the most significant texture parameters. RESULTS: Overall, almost all parameters of texture could discriminate the group of hippocampi with HS and the group of contralateral hippocampi from the group of normal hippocampi, but the post hoc comparison showed no differences between HS and contralateral hippocampi. CONCLUSIONS: These results provide evidence of texture alteration in MRIs of hippocampi with HS and corroborate the hypothesis of bilaterality of hippocampal damage in patients with MTLE, but further studies are needed to investigate the lateralization power of texture analysis.

Adolescent↗
PubMed2002

Magnetic resonance imaging evidence of hippocampal sclerosis in asymptomatic, first-degree relatives of patients with familial mesial temporal lobe epilepsy.

OBJECTIVE: To investigate the presence of hippocampal atrophy (HA) and other magnetic resonance imaging (MRI) signs of hippocampal sclerosis (HS) in asymptomatic relatives of patients with familial mesial temporal lobe epilepsy (FMTLE). METHODS: We invited first-degree, asymptomatic relatives of patients with FMTLE to participate in our MRI protocol. After obtaining informed consent, all participating individuals underwent an MRI examination. Hippocampal abnormality was determined by qualitative and volumetric analyses, using a standard protocol. RESULTS: We studied 52 asymptomatic individuals (27 men), with a mean age of 32 years (range, 7-71 years), from 11 families with FMTLE. Volumetric studies showed HA in 18 (34%) of 52 individuals: 11 had left HA and 7 had bilateral HA. In addition, careful visual analysis of T1- and T2-weighted images showed additional classic MRI signs of HS (such as abnormal T2 signal and/or abnormal internal structure) in 14 of these 18 individuals. There was no age difference between individuals with and without HA (t test, P =.80). CONCLUSIONS: Our findings indicate that MRI evidence of HS is not necessarily related to seizure severity and may occur in individuals who never had seizures. In addition, these observations strongly indicate that HS in FMTLE is not a consequence of recurrent seizures and is determined by a strong genetic predisposition. The determination of seizure severity in patients with FMTLE probably depends on the interaction of different factors, both genetic and environmental.

Adolescent↗
PubMed2002

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.

Adolescent↗
PubMed2002

Association of family history of epilepsy with earlier age at seizure onset in patients with focal cortical dysplasia.

OBJECTIVE: To establish the contribution of family history of epilepsy to seizure onset in patients with focal cortical dysplasia (FCD). PATIENTS AND METHODS: From January 1998 to January 2001, we prospectively evaluated 19 consecutive patients (10 male, 9 female) with a diagnosis of FCD based on magnetic resonance imaging. All patients and at least 1 family member were directly interviewed by the same observer after completion of a semistructured questionnaire. Initially, we classified patients into 2 groups: presence or absence of family history of epilepsy. Patients with a family history of epilepsy were subdivided into 2 groups: patients with a family history of epilepsy in first-degree relatives or multiple relatives (n=5) and patients with a family history of epilepsy in relatives who were not first-degree (n=4). Statistical analysis was performed with use of the nonparametric tests Kruskal-Wallis and Kaplan-Meier (survival analysis). P=.05 was considered statistically significant. RESULTS: The ages of the patients ranged from 3 to 41 years (mean, 15.6 years). All patients had similar type and extent of cortical dysgenesis. Ages at seizure onset varied from 1 month to 22 years, with a mean of 5.8 years. Nine patients had a family history of epilepsy. The mean age at the first seizure in patients with a family history of epilepsy was 2.6 years compared with 8.5 years in those with no relatives having epilepsy (P=.02). When patients with a family history of epilepsy were classified further, the mean age at first seizure was 1.9 years for patients with a family history of epilepsy in first-degree or multiple relatives and 3.9 years for patients with a family history of epilepsy in relatives who were not first-degree compared with 8.5 years for patients with no family history of epilepsy (P=.04). CONCLUSION: Our results show that a family history of epilepsy is associated with an earlier age at seizure onset in patients with FCD. Although this is a preliminary finding and a larger sample is needed to confirm these results, we believe these observations provide evidence that genetic modifiers could become an important issue in the clinical presentation of patients with dysplastic lesions.

Adolescent↗
PubMed2002

[Idiopathic generalized epilepsies misdiagnosed as partial epilepsies].

Idiopathic generalized epilepsy (IGE) is often not recognized with serious consequences on the sufferers. We examined factors contributing to the missed diagnosis of IGE in 41 adults attending our epilepsy clinic with diagnosis of partial epilepsy who had semiology or EEG findings suggesting a possible differential diagnosis. After careful re-evaluation, the diagnosis of IGE was established in 25 patients: 22 (88%) with JME, one with juvenile absence, one with perioral myoclonia with absences, one with eyelid myoclonia with typical absences. Myoclonic jerks, the hallmark of the JME and other IGE, were not usually reported by patients or misdiagnosed as focal motor seizures. Brief and infrequent absence seizures and focal EEG abnormalities were other factors contributing to not recognizing JME. All 25 patients did not achieve seizure control before re-evaluation of diagnosis. After appropriate diagnosis of IGE and change of AED to valproate or valproic acid, 19 (76%) became seizure free and six (24%) had a significant improvement on seizure control. Association with lamotrigine provided further improvement in three of these patients. An appropriate questioning to identify myoclonic and absence seizures and a proper interpretation in the context of whole clinical constellation are essential for a correct seizure classification and diagnosis of IGE in adults.

Adolescent↗