T1- or T2-weighted magnetic resonance imaging: what is the best choice to evaluate atrophy of the hippocampus?

BACKGROUND AND PURPOSE: Magnetic resonance imaging is part of the diagnostic criteria for Alzheimer's disease (AD) through the evaluation of hippocampal atrophy. The objective of this study was to evaluate which sequence of T1-weighted (T1WI) and T2-weighted (T2WI) imaging allowed the best visual evaluation of hippocampal atrophy. METHODS: Visual qualitative ratings of the hippocampus of 100 patients with mild cognitive impairment (MCI) and 50 patients with AD were made independently by four operators according to the medial temporal lobe atrophy score based either on T1WI or T2WI. These two evaluations were compared in terms of interobserver reproducibility, concordance with a quantitative volumetric measure, discrimination power between AD and MCI groups, and correlation with several neuropsychological tests. RESULTS: The medial temporal lobe atrophy score evaluated on either T1WI or T2WI exhibited similar interobserver variability and accordance with quantitative volumetric evaluation. However, the visual evaluation on T2WI seemed to provide better discrimination power between AD and MCI groups for both left (T1WI, P = 0.0001; T2WI, P = 7.072 × 10-5 ) and right (T1WI, P = 0.008; T2WI, P = 0.001) hippocampus, and a higher overall correlation with neuropsychological tests. CONCLUSIONS: The present study suggests that T2WI provides a more adequate visual rating of hippocampal atrophy.

Do we know how to diagnose epilepsy early in Alzheimer's disease?

Epilepsy is an increasingly recognized comorbidity in Alzheimer's disease (AD). First described as generalized in dementia patients, epileptic AD patients are nowadays fully described in earlier stages of the disease (with mild or subjective cognitive impairment). At such early stages, patients may present not only with generalized seizures, but also with focal seizures (commonly localized in the frontal or temporal lobe). Thus, partial or generalized epilepsy is part of the semiological spectrum of AD that should be borne in mind at all stages of disease to ensure early identification and prevent the risk of repeated seizures (such as accidents, injury, progression of cognitive impairment). This review of the available (and still growing) literature shows that there are already sufficient data to inform physicians on seizure semiology, and on the diagnostic value of electroencephalography and brain imaging. Taken together, these tools can help to rapidly identify epilepsy in AD patients. Nevertheless, epilepsy diagnosis can be challenging, and test medication is sometimes necessary. Some cerebrospinal fluid biomarkers (or their ratios) may also prove to be good predictors of seizures in AD, but further studies are needed. Epilepsy in AD patients is frequently pharmacosensitive, and a good response can be obtained with standard doses of antiepileptic drugs. For all these reasons and based on our review of the literature, it appears that, at present, the diagnosis of epilepsy in AD is not only possible at any stage of the disease, but also to be recommended to improve the patient's prognosis.

Exploring anterograde memory: a volumetric MRI study in patients with mild cognitive impairment.

BACKGROUND: The aim of this volumetric study was to explore the neuroanatomical correlates of the Free and Cued Selective Reminding Test (FCSRT) and the Delayed Matching-to-Sample-48 items (DMS-48), two tests widely used in France to assess verbal and visual anterograde memory. We wanted to determine to what extent the two tests rely on the medial temporal lobe, and could therefore be predictive of Alzheimer's disease, in which pathological changes typically start in this region. METHODS: We analysed data from a cohort of 138 patients with mild cognitive impairment participating in a longitudinal multicentre clinical research study. Verbal memory was assessed using the FCSRT and visual recognition memory was evaluated using the DMS-48. Performances on these two tests were correlated to local grey matter atrophy via structural MRI using voxel-based morphometry. RESULTS: Our results confirm the existence of a positive correlation between the volume of the medial temporal lobe and the performance on the FCSRT, prominently on the left, and the performance on the DMS-48, on the right, for the whole group of patients (family-wise error, P < 0.05). Interestingly, this region remained implicated only in the subgroup of patients who had deficient scores on the cued recall of the FCSRT, whereas the free recall was associated with prefrontal aspects. For the DMS-48, it was only implicated for the group of patients whose performances declined between the immediate and delayed trial. Conversely, temporo-parietal cortices were implicated when no decline was observed. Within the medial temporal lobe, the parahippocampal gyrus was prominently involved for the FCSRT and the immediate trial of the DMS-48, whereas the hippocampus was solely involved for the delayed trial of the DMS-48. CONCLUSIONS: The two tests are able to detect an amnestic profile of the medial temporal type, under the condition that the scores remain deficient after the cued recall of the FCSRT or decline on the delayed recognition trial of the DMS-48. Strategic retrieval as well as perceptual/attentional processes, supported by prefrontal and temporo-parietal cortices, were also found to have an impact on the performances. Finally, the implication of the hippocampus appears time dependent, triggered by a longer delay than the parahippocampus, rather than determined by the sense of recollection or the encoding strength associated with the memory trace.

[Cognitive and affective theory of mind in Lewy body dementia: A preliminary study]. / Théorie de l'esprit cognitive et affective dans la démence à corps de Lewy : une étude préliminaire.

INTRODUCTION: 'Theory of Mind' refers to the ability to attribute mental states, thoughts (cognitive component) or feelings (affective component), to others. This function has been studied in many neurodegenerative diseases; however, to our knowledge no studies investigating theory of mind in dementia with Lewy Bodies (DLB) have been published. The aim of our study was to search theory of mind deficits in patients with DLB. METHODS: Seven patients with DLB (DLB group), at the stage of mild dementia or mild cognitive impairments, and seven healthy elderly adults (control group) were included in the study. After a global cognitive assessment, we used the Faux Pas Recognition test to assess the cognitive component of theory of mind, and the Reading the Mind in the Eyes test for the assessment of affective component. RESULTS: We found a significant difference between the two groups for the Faux Pas test with an average score of 35.6 for the DLB group and 48.3 for the control group (P=0.04). Scores were particularly low in the DLB group for the last question of the test concerning empathy (42.9% versus 85%, P=0.01). There was not a significant difference between the two groups for the Reading the Mind in the Eyes test (P=0.077). DISCUSSION: This preliminary study showed early impairments of theory of mind in the DLB. The cognitive component seems more affected than the affective component in this pathology. This pattern is consistent with the pattern found in Parkinson's disease, but differs from other neurodegenerative diseases as Alzheimer's disease or frontotemporal lobe dementia. These patterns may help to differentiate DLB from these diseases. Further study is needed to confirm these results and to compare with other dementias.

[Syndrome of transient epileptic amnesia and epileptic amnesic syndrome: the same entity?]. / Le syndrome of transient epileptic amnesia et l'epileptic amnesic syndrome sont-ils une même entité ?

A chronic subjective cognitive impairment can be symptomatic of temporal lobe epilepsy (TLE); it is thereby frequently reversible with the use of antiepileptic monotherapy. In this field, two distinct syndromes have been described: the Epileptic Amnesic Syndrome (EAS) and the Syndrome of Transient Epileptic Amnesia. Their diagnostic criteria have much in common but identification of STEA is based only on transient amnesic attacks. On the contrary, EAS takes into account subtle temporal lobe seizures. Here, we report a case where chronic cognitive disturbances were combined with very limited temporal lobe seizures while amnesic attacks were lacking. Antiepileptic drug treatment led to normalization of cognitive function. The criteria of STEA were not applicable because of the lack of transient amnesia in the patients' medical history. Considering brief episodes of flashbacks and abdominal pain as possibly seizure-related, the criteria of EAS were more operative: they allowed proper investigation to confirm TLE in our patient.

[Peripheral neuropathies after bariatric surgery]. / Polyneuropathies après chirurgie bariatrique.

INTRODUCTION: Peripheral neuropathies sometimes complicate bariatric surgery. PATIENTS AND METHODS: We report the detailed clinical, electrophysiological, biological and histological characteristics of five patients who developed peripheral neuropathy after bariatric surgery. RESULTS: Three patients presented with small fiber neuropathy, one presented with axonal polyneuropathy, and one with demyelinating polyradiculoneuropathy. All patients had in common prominent neuropathic pain, massive weight loss, and multiple nutritional deficiencies. The pathophysiology of postbariatric surgery polyneuropathies is complex and involves nutritional, infectious and dysimmune mechanisms. CONCLUSION: The spectrum of peripheral neuropathies complicating bariatric surgery is wide, and includes pure small fiber neuropathy, axonal polyneuropathy, and demyelinating polyradiculoneuropathy. Treatment is mainly preventive, but sometimes surgical revision is needed.

[Sepsis associated encephalopathy]. / Encéphalopathie associée au sepsis.

The sepsis associated encephalopathy (SAE) is a common cause of delirium, accompanied by hyperthermia or not. It is defined as a diffuse cerebral dysfunction induced by the systemic response to the infection without clinical or laboratory evidence of direct infectious involvement of the central nervous system. It is, thus, a diagnosis of exclusion. The pathogenic mechanisms underlying SAE are now better understood: it involves, at least, an intense inflammation of the central nervous system and a major impairment of the blood brain barrier. At the present time, clinical, biological and radiological characteristics of SAE have been sufficiently described to ensure rapid identification, but prognosis remains severe. Proper management requires treatment as early as possible of the infectious site and accompanying systemic inflammatory response. When appropriately conducted, minimal consequences or complete recovery can be expected.