Dominique Dive

Cerebral glucose utilization during sleep-wake cycle in man determined by positron emission tomography and [18F]2-fluoro-2-deoxy-d-glucose method

Using the [18F]fluorodeoxyglucose method and positron emission tomography, we studied cerebral glucose utilization during sleep and wakefulness in 11 young normal subjects. Each of them was studied at least thrice: during wakefulness, slow wave sleep (SWS) and rapid eye movement sleep (REMS), at 1 week intervals. Four stage 3-4 SWS and 4 REMS fulfilled the steady state conditions of the model. The control population consisted of 9 normal age-matched subjects studied twice during wakefulness at, at least, 1 week intervals. Under these conditions, the average difference between the first and the second cerebral glucose metabolic rates (CMRGlu was: -7.91 +/- 15.46%, which does not differ significantly from zero (P = 0.13). During SWS, a significant decrease in CMRGlu was observed as compared to wakefulness (mean difference: -43.80 +/- 14.10%, P less than 0.01). All brain regions were equally affected but thalamic nuclei had significantly lower glucose utilization than the average cortex. During REMS, the CMRGlu were as high as during wakefulness (mean difference: 4.30 +/- 7.40%, P = 0.35). The metabolic pattern during REMS appeared more heterogeneous than at wake. An activation of left temporal and occipital areas is suggested. It is hypothetized that energy requirements for maintaining membrane polarity are reduced during SWS because of a decreased rate of synaptic events. During REMS, cerebral glucose utilization is similar to that of wakefulness, presumably because of reactivated neurotransmission and increased need for ion gradients maintenance.

Cerebral Glucose Utilization During Stage 2 Sleep in Man

Using [18F]fluorodeoxyglucose method and positron emission tomography, we performed paired determinations of the cerebral glucose utilization at one week intervals during sleep and wakefulness, in 12 young normal subjects. During 6 of 28 sleep runs, a stable stage 2 SWS was observed that fulfilled the steady-state conditions of the model. The cerebral glucose utilization during stage 2 SWS was lower than during wakefulness, but the variation did not significantly differ from zero (mean variation: -11.5 +/- 25.57%, P = 0.28). The analysis of 89 regions of interest showed that glucose metabolism differed significantly from that observed at wake in 6 brain regions, among them both thalamic nuclei. We conclude that the brain energy metabolism is not homogeneous throughout all the stages of non-REMS but decreases from stage 2 SWS to deep SWS; we suggest that a low thalamic glucose metabolism is a metabolic feature common to both stage 2 and deep SWS, reflecting the inhibitory processes observed in the thalamus during these stages of sleep. Stage 2 SWS might protect the stability of sleep by insulating the subject from the environment and might be a prerequisite to the full development of other phases of sleep, especially deep SWS.

Cerebral Glucose Utilization During Sleep in Landau‐Kleffner Syndrome: A PET Study

Summary: : Three right‐handed male children (aged 5, 6, and 11 years) with signs, symptoms and/or history of the syndrome of acquired aphasia‐epilepsy (Landau‐Kleffner syndrome) were studied during drug‐induced, electroen‐cephalographically (EEG)‐monitored sleep by positron‐emission tomography (PET) and the [18F]fluorode‐oxyglucose (FDG) method. Our data demonstrate that in Landau‐Kleffner syndrome, cerebral glucose utilization is not normal during sleep. The metabolic pattern varied between the children but the metabolic disturbances always predominated over the temporal lobes. They were right‐sided, left‐sided, or bilateral. In the two first patients, EEG recordings showed continuous spike‐and‐wave discharges during sleep and a right‐greater‐than‐left asymmetry was observed in temporal areas. In patient 1, the asymmetry was associated with a relative increase of glucose utilization of the right posterior temporal region. In patient 2, the glucose utilization was relatively decreased in the left anterotemporal and left perisylvian regions. In patient 3, the sleep EEG showed no discharge and no significant asymmetry was observed; however, glucose utilization of both temporal lobes was decreased. Lower metabolic rates in subcortical structures than in cortex were also noted in the three children. This metabolic pattern may be related to the maturation of the central nervous system (CNS).

Reproducibility of cerebral glucose utilization measured by PET and the [18F]-2-fluoro-2-deoxy-d-glucose method in resting, healthy human subjects

The stability of cerebral glucose utilization was examined in nine right-handed, healthy men (age, 24.88±2.93 years) using positron emission tomography (PET) and the [18F]-fluorodeoxyglucose (FDG) method. Each study was run twice at intervals of 1–12 weeks with the subject at rest. The average cerebral metabolic rate for glucose (CMRGlu) was 5.40±0.71 mg/100 g per min (coefficient of variance, 13.08). The average intraindividual variation of CMRGlu was 7.91%±15.46% (P=0.13). Metabolic indices (MI: regional/mean cortical CMRGlu) were used to determine the regional cerebral metabolic distribution. The interindividual (coefficient of variance, 7.13) and intraindividual variabilities (average variation, −0.12%±8.76%) of MI were smaller than those of metabolic rates. No reproducible significant asymmetry was observed. The FDG method used with subjects at rest thus yields low intraindividual variability of both cerebral glucose consumption and regional metabolic distribution, even at an interval of several weeks. Cerebral glucose utilization measured under such conditions may act as a reliable reference for determination of the influences of physiological (activation), pharmacological or pathological processes on cerebral glucose metabolism.

Corticosteroids in the management of acute multiple sclerosis exacerbations

Multiple sclerosis (MS) is an autoimmune, inflammatory demyelinating disease of the central nervous system characterized in the majority of the patients by a relapsing-remitting disease course. For decades high-dosage corticosteroids (CS) are considered the cornerstone in the management of acute MS relapses. However, many unanswered questions remain when it comes to the exact modalities of CS administration. In this review on behalf of the Belgian Study Group for MS we define the efficacy of CS in reducing MS-related morbidity and examine whether the effect is different according to type of CS, route of administration, cumulative dosage, timing of initiation and disease course. We also review the use of CS in combination with other MS treatments and during pregnancy and lactation. Furthermore, we delineate the relevant adverse events due to a pulse CS regimen and present a decision tree that can be used when treating MS relapses in clinical practice.

A Broad Range of New Clinical Applications for a Magnetic Sensor Measuring Distance on the Human Body

This paper describes the features of a magnetic distance meter initially intended to detect sleep-related breathing efforts through the recording and analysis of jaw movements. The design of the device made it a very sensitive, non-invasive, wearable and easy-to-use motion detector. As such, it rapidly became an interesting equipment in wholly different clinical domains like radiotherapy and biomechanics. The new prospects offered by this magnetic motion-sensing solution in various clinical applications are presented and discussed here.

Motor neuron disorders : novel electrophysiologic approach (MUFDEC protocol)

Publisher Summary This chapter reviews that primary lateral sclerosis (PLS), amyotrophic lateral sclerosis (ALS), and X-linked spinobulbar muscular atrophy (Kennedys disease) are disorders characterized by progressive loss of upper motor neurons (UMN), lower motor neurons (LMN), or both. Clinically, PLS is usually considered to be a disorder of pure UMN loss, ALS mixed UMN and LMN loss, and Kennedys disease as a disorder of LMN loss. There are data suggesting a degree of LMN loss in PLS, and little is known about motor unit (MU) loss and its rate in Kennedys disease. The chapter discusses that motor unit number estimation (MUNE) is a unique neurophysiological technique that can directly assess LMN loss. It reports the results of two studies applying these techniques and tests to the subjects with PLS, ALS, and Kennedys disease. The aims of this study were: to document subclinical LMN involvement in PLS, to compare the degree of LMN loss involvement among the diseases, and to measure the respective rate of MU loss. The aims of study were: to compare two MUNE techniques, the adapted multipoint stimulation (AMPS) and the statistical technique, and attempt to explain the differences by the other parameters studied with new MUFDEC neurophysiologic protocol.

NMOSD with anti-MOG antibodies following anti-TNFα therapy: A case report

Tumor necrosis factor α (TNFα) inhibitors are highly effective and a therapeutic choice for several inflammatory diseases. Their broad and long-term use is associated with a growing number of paradoxical autoimmune events including demyelinating lesions of the central nervous system (CNS). We report and discuss a case of neuromyelitis optica spectrum disorder (NMOSD) with positive myelin oligodendrocyte glycoprotein antibodies (MOG-IgG1) following anti-TNFα therapy for a pustular psoriasis.

Is the triple stimulation technique a better quantification tool of motor dysfunction than motor evoked potentials in multiple sclerosis

The triple stimulation technique (TST) was rarely used in multiple sclerosis (MS). This study aimed to compare TST and motor evoked potentials (MEP) for the quantification of motor dysfunction. Central motor conduction based on MEP (four limbs) and TST (upper limbs) was assessed in 28 MS patients with a median Expanded Disability Status Scale (EDSS) of 4. EDSS, timed 25-foot walk (T25FW), grasping strength and motor components of the MS functional composite were evaluated. Regression analysis was used to assess the relationship between MEP, TST and clinical findings. TST was negatively correlated with EDSS (r = − 0.74, p < 0.0001) and to a lesser extent with T25FW (r = − 0.47, p < 0.05), and grasping strength (r = − 0.43, p < 0.05). A multiple regression analysis underlined the better correlation between clinical data and TST (R2 = 0.56, p < 0.0005) than with MEP (0.03 < R2 < 0.22, p > 0.05). This study evidenced the value of TST as a quantification tool of motor dysfunction. TST appeared to reflect a global disability since it was correlated not only to hand function but also to walking capacity.

Correction to: Management of immune thrombocytopenia in multiple sclerosis patients treated with alemtuzumab: a Belgian consensus

The article Management of immune thrombocytopenia in multiple sclerosis patients treated with alemtuzumab: a Belgian consensus, written by Lambert et al., was originally published electronically on the publisher’s internet portal on 27 January 2018 without open access.