Functional involvement of cerebral cortex in adult sleepwalking

The pathophysiology of adult sleepwalking is still poorly understood. However, it is widely accepted that sleepwalking is a disorder of arousal. Arousal circuits widely project to the cortex, including motor cortex. We hypothesized that functional abnormality of these circuits could lead to changes in cortical excitability in sleepwalkers, even during wakefulness. We used transcranial magnetic stimulation (TMS) to examine the excitability of the human motor cortex during wakefulness in a group of adult sleepwalkers. When compared with the healthy control group, short interval intracortical inhibition (SICI), cortical silent period (CSP) duration, and short latency afferent inhibition (SAI) were reduced in adult sleepwalkers during wakefulness. Mean CSP duration was shorter in patients than in controls (80.9 +/- 41 ms vs. 139.4 +/- 37 ms; p = 0.0040). Mean SICI was significantly reduced in patients than in controls (73.5 +/- 38.4% vs. 36.7 +/- 13.1%; p = 0.0061). Mean SAI was also significantly reduced in patients than in controls (65.8 +/- 14.2% vs. 42.8 +/- 16.9%; p = 0.0053). This neurophysiological study suggests that there are alterations in sleepwalkers consistent with an impaired efficiency of inhibitory circuits during wakefulness. This inhibitory impairment could represent the neurophysiological correlate of brain "abnormalities" of sleepwalkers like "immaturity" of some neural circuits, synapses, or receptors.     

Long-lasting effects of transcranial static magnetic field stimulation on motor cortex excitability

Background

Transcranial static magnetic field stimulation (tSMS) was recently added to the family of inhibitory non-invasive brain stimulation techniques. However, the application of tSMS for 10–20?min over the motor cortex (M1) induces only short-lasting effects that revert within few minutes.

Effects of replacement therapy on sleep architecture in children with growth hormone deficiency

ObjectiveChildren with GH deficiency (GHD) show a general decrease in electroencephalographic (EEG) arousability represented by a significant global decrease in Cyclic Alternating Pattern (CAP). The aim of the present study was to evaluate if sleep structure is influenced by GH substitutive therapy by analyzing the classical sleep architecture parameters and sleep microstructure by means of CAP.Subjects and methodsLaboratory polysomnographic sleep recordings were obtained from five children affected by GHD (two girls and three boys; mean age: 4.6 ± 3.1 years), at baseline and after GH therapy, and from 10 normal healthy children (four girls and six boys, mean age: 5.6 ± 2.2 years).ResultsCompared to controls, GHD subjects showed a reduced total sleep time with increased wakefulness and a consequent decrease in sleep efficiency; GH therapy was associated with an increase of the awakenings/hour and a large effect size was evident for sleep latency, sleep efficiency, and stage N3, which were decreased, and for stage W, which was increased. CAP appeared to be globally reduced and all phase A subtypes and CAP cycle showed a longer duration in GHD children vs. controls. GH substitutive treatment was followed by an increase in CAP rate (total, in N2, and in N3); additionally, A1 index was also significantly increased, especially during stage N3, with a very large effect size. On the other hand, A2 and A3 index and CAP cycle mean duration were reduced.ConclusionSleep stage architecture seems to be influenced by the GH status, but the analysis of sleep microstructure by means of CAP reveals an enhancement of EEG slow oscillations in GHD patients (demonstrated by an increase in CAP rate and A1 index during N3) after the start of GH replacement therapy. These findings deserve to be verified in a larger trial.     

Effect of diagnostic labeling and causal explanations on medical students' views about treatments for psychosis and the need to share information with service users

This study examines whether medical students' views of treatments for ‘schizophrenia’ and of patients' rights to be informed about their condition and their medication were influenced by diagnostic labeling and causal explanations and whether they differed over medical training. Three hundred and eighty-one Italian students attending their first or fifth/sixth year of medical studies read a vignette portraying someone who met diagnostic criteria for ‘schizophrenia’ and completed a self-report questionnaire. The study found that labeling the case as ‘schizophrenia’ and naming heredity among its causes were associated with confidence in psychiatrists and psychiatric drugs. Naming psychological traumas among the causes was associated with confidence in psychologists and greater acknowledgment of users' right to be informed about drugs. Compared to first year students, those at their fifth/sixth-year of studies more strongly endorsed drugs, had less confidence in psychologists and family support, and were less keen to share information on drugs with patients. These findings highlight that students' beliefs vary during training and are significantly related to diagnostic labeling and belief in a biogenetic causal model. Psychiatric curricula for medical students should include greater integration of psychological and medical aspects in clinical management of ‘schizophrenia’; more information on the psychosocial causes of mental health problems.     

Dietary and nutritional indications in hepatic encephalopathy

The restriction of dietary protein has long been considered a main stay in the therapy of hepatic encephalopathy. More recently it has been recognized that protein energy malnutrition is frequent in advanced liver disease and may adversely affect the patients’outcome. Moreover studies on inter-organ ammonia exchange in liver cirrhosis have shown that the muscle may have a crucial role in ammonia detoxification. In light of these evidences nutritional guidelines have proposed that protein restriction should be avoided in patients with hepatic encephalopathy as protein requirement is even increased in cirrhotic patients. Survey about the current clinical practice show that protein restriction is still considered advisable in patients with hepatic encephalopathy, however a recent trial evidenced that a low protein diet in patients hospitalized for acute hepatic encephalopathy exacerbates protein breakdown without inducing any specific clinical benefit when compared to a normal protein regimen. The relevance of an adequate protein intake and possible strategies to implement protein tolerance are also discussed. From the 13 International Symposium on Hepatic Encephalopathy and Nitrogen Metabolism held in Abano Terme, Padova 28th April 1st May 2008     

Quantitative functional magnetic resonance imaging of brain activity using bolus-tracking arterial spin labeling

Blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI) is the most widely used method for mapping neural activity in the brain. The interpretation of altered BOLD signals is problematic when cerebral blood flow (CBF) or cerebral blood volume change because of aging and/or neurodegenerative diseases. In this study, a recently developed quantitative arterial spin labeling (ASL) approach, bolus-tracking ASL (btASL), was applied to an fMRI experiment in the rat brain. The mean transit time (MTT), capillary transit time (CTT), relative cerebral blood volume of labeled water (rCBV_lw), relative cerebral blood flow (rCBF), and perfusion coefficient in the forelimb region of the somatosensory cortex were quantified during neuronal activation and in the resting state. The average MTT and CTT were 1.939±0.175 and 1.606±0.106 secs, respectively, in the resting state. Both times decreased significantly to 1.616±0.207 and 1.305±0.201 secs, respectively, during activation. The rCBV_lw, rCBF, and perfusion coefficient increased on average by a factor of 1.123±0.006, 1.353±0.078, and 1.479±0.148, respectively, during activation. In contrast to BOLD techniques, btASL yields physiologically relevant indices of the functional hyperemia that accompanies neuronal activation.     

Motor cortex hyperexcitability to transcranial magnetic stimulation in Alzheimer's disease

OBJECTIVES: Recent transcranial magnetic stimulation (TMS) studies demonstrate that motor cortex excitability is increased in Alzheimer's disease (AD) and that intracortical inhibitory phenomena are impaired. The aim of the present study was to determine whether hyperexcitability is due to the impairment of intracortical inhibitory circuits or to an independent abnormality of excitatory circuits. METHODS: We assessed the excitability of the motor cortex with TMS in 28 patients with AD using several TMS paradigms and compared the data of cortical excitability (evaluated by measuring resting motor threshold) with the amount of motor cortex disinhibition as evaluated using the test for motor cortex cholinergic inhibition (short latency afferent inhibition) and GABAergic inhibition (short latency intracortical inhibition). The data in AD patients were also compared with that from 12 age matched healthy individuals. RESULTS: The mean resting motor threshold was significantly lower in AD patients than in controls. The amount of short latency afferent inhibition was significantly smaller in AD patients than in normal controls. There was also a tendency for AD patients to have less pronounced short latency intracortical inhibition than controls, but this difference was not significant. There was no correlation between resting motor threshold and measures of either short latency afferent or intracortical inhibition (r = -0.19 and 0.18 respectively, NS). In 14 AD patients the electrophysiological study was repeated after a single oral dose of the cholinesterase inhibitor rivastigmine. Resting motor threshold was not significantly modified by the administration of rivastigmine. In contrast, short latency afferent inhibition from the median nerve was significantly increased by the administration of rivastigmine. CONCLUSIONS: The change in threshold did not seem to correlate with dysfunction of inhibitory intracortical cholinergic and GABAergic circuits, nor with the central cholinergic activity. We propose that the hyperexcitability of the motor cortex is caused by an abnormality of intracortical excitatory circuits.