[Orexin, sleep and appetite regulation: a review]. / Orexina, regolazione del sonno e dell'appetito: una rassegna.

Since 1998, two research groups independently reported the discovery of two novel hypothalamic neuropeptides, called hypocretin-1 and hypocretin-2, respectively many studies have been carried out about their possible functions. One group named these new peptides orexins (A and B) after the Greek word for appetite, since they found that central administration of orexins potently increased food intake in rats. However hypocretins/ orexins are involved in various hypothalamic mechanisms, such as energy homeostasis, neuroendocrine functions, appetite and satiety regulation, vigilance and defence behaviour, sleep and wake regulation. Here is a review of the recent literature, showing some recent discoveries about the link between orexin system, sleep regulation and appetite regulation.

Influence of cholinergic circuitries in generation of high-frequency somatosensory evoked potentials.

OBJECTIVE: High-frequency oscillations (HFOs) evoked by upper limb stimulation reflect highly synchronised spikes generated in the somatosensory human system. Since acetylcholine produces differential modulation in subgroups of neurons, we would determine whether cholinergic drive influences HFOs. METHODS: We recorded somatosensory evoked potentials (SEPs) from 31 scalp electrodes in 7 healthy volunteers, before and after single administration of rivastigmine, an inhibitor of central acetylcholinesterase. Right median nerve SEPs have been analysed after digital narrow bandpass filtering (500-700 Hz). Raw data were further submitted to Brain Electrical Source analysis (BESA) to evaluate the respective contribution of lemniscal, thalamic and cortical sources. Lastly, we analysed by Fast Fourier transform spectral changes after drug administration in the 10-30 ms latency range. RESULTS: Rivastigmine administration caused a significant increase of HFOs in the 18-28 ms latency range. Wavelets occurring before the onset latency of the conventional N20 SEP did not show any significant change. A similar increase concerned the strength of cortical dipolar sources in our BESA model. Lastly, we found a significant power increase of the frequency peak at about 600 Hz in P3-F3 traces after drug intake. CONCLUSIONS: Our findings demonstrate that the cortical component of HFOs is significantly enhanced by cholinergic activation. Pyramidal chattering cells, which are capable to discharge high-frequency bursts, are mainly modulated by cholinergic inputs; by contrast, acetylcholine does not modify the firing rate of fast-spiking GABAergic interneurons. We thus discuss the hypothesis that cortical HFOs are mainly generated by specialised pyramidal cells.

Sleep disorders in childhood: a review.

Several studies in the last ten years have been directed towards a better understanding of sleep disorders in childhood. Defining sleep disorders in this age is difficult in dependence of relevant differences in sleep patterns at subsequent developmental stages. In new-borns total sleep time is fairly equal during night and day. Normally, day-time sleep gradually decreases over the first three years of life, such that night-time sleep progressively increases till the age of four, and similar to adult sleep-time by adolescence. The most frequent sleep disorders observed in childhood are parasomnias, that, thought to be a CNS sign of immaturity, tend to be quite predictable, recurring in the same families and not even influenced by environmental stimuli. These disorders included: a) arousal disorders, that generally emerge from delta sleep or relate to arousals occurring during NREM sleep, very common in childhood and fairly common in adulthood either; b) somnambulism and somniloquy, that have many common characteristics: first of all, they have the potential to generate a great sense of discomfort and fear in parents watching a child who suddenly sits up in bed eyes-opened but 'unseeing'; c) nocturnal enuresis, that is substantially not a problem of depth of sleep, despite many parents believe. Although narcolepsy is more common in adolescence, many studies have demonstrated that narcoleptic symptoms may begin in childhood. Narcoleptic symptoms in children are similar in their appearance to those predominant in adults, but their expression may be different because of CNS maturational factors. Historical descriptions of the OSAS evidenced since the beginning the importance of neurobehavioral complications associated with the cessation of airflow at the nose and mouth accompanied by respiratory effort, deriving from upper airway obstruction which occurs during sleep.

[Depression in epilepsy: symptom or syndrome?]. / La depressione in epilessia: sintomo o malattia?

An occurrence of depression or depressive symptomatology has been reported in 30% of patients with epilepsy. Depression has been reported peri- and interictally. To make a differentiation may be difficult in patients with frequent seizures. However, complex partial seizures, particularly if are located on temporal lobe, appear to be etiologic factors, especially in men with left-sided epileptic foci. Depression is also more frequent in patients treated with polytherapy, particularly with phenobarbital and vigabatrin. The depression appears to be endogenous and has also been described in patients with temporal lobectomy. Underlying risk factors (genetic, metabolic, etc) and some psychosocial condition also play a part and may explain the increased rates of depression in patients with epilepsy. Treatment approaches include psychotherapy, rationalization of antiepileptic drug medication and antidepressant treatment. The use of antidepressant treatment, in these patients, still raises uncertainties because of the widespread persuasion that this drugs exacerbated seizures. This adverse event is relatively uncommon at therapeutic dosages, and its incidence with some of most frequently used antidepressant drugs is close to that of spontaneous seizures calculated for the general population, but the incidence may rise up to 30-40% after overdosage. On the basis of the data reported in literature, it appears fair to say that maprotiline and amoxapine show the greatest seizure risk, whereas trazodone, fluoxetine and fluvoxamine show the least. The data also showed that antidepressant drugs may display both convulsant and anticonvulsant effect and it is likely that the most important factor to assess the effect of a given antidepressant drug in terms of inhibition-excitation is drug dosage. Nevertheless, further studies are needed in this field, both to clarify the complex modulating effects of antidepressants on seizure threshold and to identify clearer and safer guidelines to manage the treatment of patients with epilepsy and concomitant depression.

Natural history of carpal tunnel syndrome according to the neurophysiological classification.

Although many studies on carpal tunnel syndrome (CTS) have been reported, few data on the natural history of CTS are available. Knowledge of the natural course of the disease has significant clinical and therapeutic value. We prospectively followed up 80 cases of untreated CTS. The evaluation was based on self-administered questionnaires and on neurophysiological investigation. According to the neurophysiological classification, cases of CTS were divided into six groups on the basis of impairment severity: negative, minimal, mild, moderate, severe, and extreme. Disease worsening was inversely related to severity of nerve entrapment. On the contrary, improvement was proportionally related to nerve function impairment (except for extreme cases that never improved), and about one-third of mild and moderate cases improved. Most minimally cases remained neurophysiologically unchanged. We hypothesize that in a good percentage of CTS cases, nerve impairment is self-limited. Our data suggest the utility of further studies on the natural course of this common disease.