The European journal of neuroscience
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We review the history of efforts to apply central thalamic deep brain stimulation (CT/DBS) to restore consciousness in patients in a coma or vegetative state by changing the arousal state. Early experimental and clinical studies, and the results of a recent single-subject human study that demonstrated both immediate behavioral facilitation and carry-over effects of CT/DBS are reviewed. ⋯ We conclude that CT/DBS should be studied as a therapeutic intervention to improve impaired cognitive function in severely brain-injured patients who, in addition to demonstrating clinical evidence of consciousness and goal-directed behavior, retain sufficient preservation of large-scale cerebral networks within the anterior forebrain. Although available data provide evidence for proof-of-concept, very significant challenges for study design and development of CT/DBS for clinical use are identified.
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Gilles de la Tourette Syndrome (GTS) is characterized by multiple motor and one or more vocal/phonic tics. Psychopathology and co-morbidity occur in approximately 80-90% of clinical cohorts. The most common psychopathologies are attention deficit hyperactivity disorder, obsessive-compulsive behaviours, obsessive-compulsive disorder, depression, anxiety and certain behavioural disorders. ⋯ This paper reviews critically and in detail all studies published to date. Only two studies on just a few patients fulfil some of the evidence-based criteria. DBS for GTS is therefore still highly experimental.
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A great deal of experimental evidence has already been accumulated that hyperpolarization-activated and cyclic nucleotide-gated cation channels (HCN) expressed by peripheral nerve fibers contribute to the initiation of nerve activities leading to pain. Complementing these findings, we have recently demonstrated that HCN subunit 2 (HCN2) channel protein is also widely expressed by axon terminals of substance P (SP)-containing peptidergic nociceptive primary afferents in laminae I-IIo of the spinal dorsal horn, and postulated that they may play a role in spinal pain processing. In the present study, we investigated how the expression of HCN2 ion channels in the spinal dorsal horn may change in inflammatory pain evoked by unilateral injection of complete Freund's adjuvant (CFA) into the hind paw of rats. ⋯ The elevation of HCN2 immunoreactivity was paralleled by an increase in SP immunoreactivity. In addition, similarly to control animals, the co-localization between HCN2 and SP immunoreactivity was remarkably high, suggesting that central axon terminals of nociceptive primary afferents that increased their SP expression in response to CFA injection into the hind paw also increased their HCN2 expression. The results indicate that HCN2 ion channel mechanisms may play a role in SP-mediated spinal pain processing not only in naive animals but also in chronic inflammatory pain.