C nociceptor activity in human nerve during painful and non painful skin stimulation.

Percutaneous recordings from more than one hundred single C fibres have been performed in the radial nerve of conscious human subjects. All these fibres belong to the poly-modal C nociceptor group, being excited by mechanical and thermal and also by chemical stimulation. Conduction velocities showed a monophasic distribution with a mean value of 0.86 m/s (SD: 0.17). The mechanical threshold, measured with von Frey hairs, varied between 2.3 and 13.1 g. The receptive field was circular or elliptical; for 33 units the mean axes were 6 mm and 7 mm. Mechanically evoked C fibre discharge even up to more than 10 spikes/s was not necessarily accompanied by pain sensation. Nettle sting evoked an irregular C fibre discharge (maximum 10 spikes/s) accompanied by a pricking and burning sensation; the sensation of itch which was sometimes reported, was not correlated with the discharge frequency. C fibre activation by a chemical irritant (paint remover) also evoked an irregular discharge (maximum 3 to 6 spikes/s), accompanied by pricking and burning pain sensation. The C threshold for radiant heat usually lay below the subject's pain threshold. Increasing skin temperature produced increasing neural firing rate. The mean spike frequency rarely exceeded two spikes/s even with stimuli evoking strong heat pain. The occurrence of subjective heat pain response could be as well predicted from th C fibre spike frequency as from the skin temperature. It is concluded that nociceptive C input provoked by thermal or chemical stimuli correlates well with pain sensation. However, similar C input provided by mechanical stimulation which activates also A beta mechanoreceptors, did not necessarily produce pain sensation.     

Pseudoseizures as a complication of painful cervical ribs

An 8-year-old girl is described who presented with seizures. These were subsequently found to be pseudoseizures, with no EEG changes. They were provoked by pain from cervical ribs. This cause of pain-provoked pseudoseizures has not previously been described.     

Attention-deficit/hyperactivity disorder (ADHD) and adaptation night as determinants of sleep patterns in children

Sleep problems are a prominent feature in children with attention-deficit/hyperactivity disorder (ADHD) but their relationships to sleep structure are not consistent across studies. We aimed at further examining the sleep architecture in children with ADHD, while considering the role of the first-night effect (FNE) as a possible confounder. Twenty unmedicated children with ADHD combined type (8?C15?years old; mean 11.24, SD 2.31) and 19 healthy controls, matched for age and gender, underwent polysomnography during an adaptation and a consecutive second night. ADHD and controls displayed a typical FNE without group differences. Independently of testing night, children with ADHD spent more time in sleep and had shortened rapid eye movement (REM) sleep latency and a greater amount of REM sleep relative to controls. However, the increased REM sleep amount in ADHD children was more expressed in the second night when it was also significantly related to scores of inattention and hyperactivity. Our results (1) document similar sleep adaptation processes in children with ADHD and typically developing children, (2) reveal that REM sleep changes in association with ADHD-specific psychopathology may characterize sleep in ADHD children, which is evident only when the FNE is accounted for, (3) indicate that ADHD psychopathology and adaptation night may exert opposite effects on REM sleep in children. These results may prompt the awareness of clinicians about the importance of actual sleep alterations and their precise evaluation in children with ADHD, which could significantly contribute to better diagnostic, treatment and early prevention strategies.     

Attention deficit hyperactivity disorder: dissociation and adaptation (a theoretical presentation and case study).

Attention deficit hyperactivity disorder has become an increasingly common diagnosis among both schoolchildren and adults. Much of the literature on attention deficit hyperactivity disorder indicates that it is untreatable without the use of psychostimulant medication. With the goal of moving away from the incurable disease model of ADHD, this paper explores the possibility of adaptive aspects to ADHD, specifically regarding creativity. Using the new model allows the focus of therapy to shift to treatment of the whole person and the alleviation of problem behaviors. A case study is presented to illustrate this hypothesis in conjunction with the successful treatment of a case of ADHD in an adult using cognitive-behavioral therapy and clinical hypnosis.     

Hyperfocusing as a dimension of adult attention deficit hyperactivity disorder

Patients with Attention Deficit Hyperactivity Disorder (ADHD) suffer not only from inability to focus but also from inability to shift attention for events that trigger their interests. This phenomenon is called “hyperfocusing”. Previous literature about hyperfocusing is scarce and relies mainly on case reports. The study aimed to investigate and compare the severity of hyperfocusing in adult ADHD with and without psycho-stimulant use. ADHD (DSM-IV-TR) patients either psycho-stimulant naive (n = 53) or on psycho-stimulants (n = 79) from two ADHD clinics were recruited. The control group (n = 65) consisted of healthy university students. A socio-demographic form, the Beck Depression Inventory, the Wender-Utah Rating Scale, the Adult ADHD Self- Report Scale and the Hyperfocusing Scale were applied to the participants. There was no difference between total Hyperfocusing Scale and Adult ADHD Self- Report Scale scores of two patient groups, but both have higher scores than controls (p < 0.001). Hyperfocusing is higher in adult ADHD and there was no difference between stimulant-naive patients or patients on stimulants. Hyperfocusing can be defined as a separate dimension of adult ADHD.     

Role of a novel nociceptor autocrine mechanism in chronic pain

We have previously shown, in the rat, that neuropathic and inflammatory events produce a neuroplastic change in nociceptor function whereby a subsequent exposure to a proinflammatory mediator (e.g. prostaglandin E₂; PGE₂) produces markedly prolonged mechanical hyperalgesia. While the initial approximately 30 min of this prolonged PGE₂ hyperalgesia remains PKA‐dependent, it subsequently switches to become dependent on protein kinase C epsilon (PKCε). In this study we tested the hypothesis that the delayed onset, PKCε‐mediated, component of PGE₂ hyperalgesia is generated by the active release of a nucleotide from the peripheral terminal of the primed nociceptor and this nucleotide is then metabolized to produce adenosine, which acts on a Gi‐coupled A1 adenosine receptor on the nociceptor to generate PKCε‐dependent hyperalgesia. We report that inhibitors of ATP‐binding cassette transporters, of ecto‐5′‐phosphodiesterase and ecto‐5′nucleotidase (enzymes involved in the metabolism of cyclic nucleotides to adenosine) and of A1 adenosine receptors each eliminated the late, but not the early, phase of PGE₂‐induced hyperalgesia in primed animals. A second model of chronic pain induced by transient attenuation of G‐protein‐coupled receptor kinase 2, in which the prolongation of PGE₂ hyperalgesia is not PKCε‐dependent, was not attenuated by inhibitors of any of these mechanisms. Based on these results we propose a contribution of an autocrine mechanism, in the peripheral terminal of the nociceptor, in the hyperalgesic priming model of chronic pain.     

Acute aortic dissection presenting as painful paraplegia

Aortic dissection is a rare potentially life threatening condition. Neurological complications such as paraplegia as presenting manifestation of aortic dissection are exceedingly rare. We describe a 60-year-old man who presented with acute onset paraplegia with bladder involvement, constricting pain in the lower abdomen, bradycardia and succumbed rapidly within 14h of onset of symptoms. Autopsy revealed an unexpected cause of paraplegia with extensive aortic dissection extending from origin to iliac bifurcation (DeBakey type I). The aorta showed extensive atherosclerosis causing medial destruction and dissection. The spinal cord in the vulnerable watershed zone of T12-L1 downwards revealed ischemic softening. No infarcts were seen in other organs as he succumbed rapidly to cardiac tamponade. Acute aortic dissection presenting as paraplegia though rare, should be considered in patients presenting with sudden onset paraplegia with associated severe pain and absent pulses. Prompt diagnosis and timely intervention may help save life and limb.     

Tianeptine as a slightly effective therapeutic option for attention-deficit hyperactivity disorder

OBJECTIVE: Because of the hypotonic side effect of clonidine, the use of tianeptine was studied as an alternative because of its longer excretion half-life, decreased sedative side effects and more selective binding profile. METHOD: We rated sixty-eight psychiatric outpatients diagnosed with attention-deficit hyperactivity disorder (ADHD) at baseline and while taking tianeptine to determine its efficacy as a treatment for ADHD and used comparisons of Conners' parent ratings within each subject to measure behavioral changes in the subjects. RESULTS: During tianeptine treatment, patients' mean scores improved significantly overall, and also for Conners' Hyperactivity, Inattention and Immaturity factors. CONCLUSIONS: This preliminary study indicates that tianeptine might be a slightly effective beneficial and useful treatment for ADHD, reducing hyperactive behaviors and enabling greater attentional ability with minimal side effects.     

Pain as an evolutionary necessity

The proposed title “Pain as an evolutionary necessity” could lead to a broad debate with implications covering many chapters of the medicine and particularly of clinical neurology. In the present perspective, the discussion will focus on migraine and cluster headache chosen as elective examples of biological and not only clinical conditions, that unveil the bond between pain and necessity. Migraine, cluster headache, and perhaps other primary headaches begin to be depicted in terms of recurrent activation of innate bio-behavioral specific patterns, with a crucial and highly conserved evolutionarily adaptive significance. The pan-mammalian sickness behavior and the fight or flight response, selectively activated by different kinds of pain, are here proposed as paradigmatic of migraine and cluster headache attacks associated behaviors, allowing to reformulate these forms as the inappropriate recurrent presentation of coordinated allostatic processes, modeled along million of years of natural evolution. In this light, all the multifaceted characteristics of migraine and cluster headache attacks can be reinterpreted as complex and integrated allostatic defensive reactions to an inescapable or to an escapable pain, respectively aimed to the restoration of biologic homeostasis through a temporary disengagement from active interaction with environment (migraine associated sickness behavior) or, on the contrary, to promote the coordinated biological changes preparatory to emergency and defensive behaviors (cluster headache-related fight or flight response).

     

Micromechanical adaptation as a treatment for spinal cord injury

<正>Spinal cord injury:Thus far injury of the spinal cord is incurable and, in the majority of cases, a devastating and life-changing event. The worldwide incidence rate of spinal cord injury(SCI) ranges from 250,000 to 900,000 (www.who.int, 2013; Ku-     

Attention-deficit hyperactivity disorder as a potentially aggravating factor in borderline personality disorder

BACKGROUND: Clinical experience suggests that people with borderline personality disorder often meet criteria for attention-deficit hyperactivity disorder (ADHD). However, empirical data are sparse. AIMS: To establish the prevalence of childhood and adult ADHD in a group of women with borderline personality disorder and to investigate the psychopathology and childhood experiences of those with and without ADHD. METHOD: We assessed women seeking treatment for borderline personality disorder (n=118) for childhood and adult ADHD, co-occurring Axis I and Axis II disorders, severity of borderline symptomatology and traumatic childhood experiences. RESULTS: Childhood (41.5%) and adult (16.1%) ADHD prevalence was high. Childhood ADHD was associated with emotional abuse in childhood and greater severity of adult borderline symptoms. Adult ADHD was associated with greater risk for co-occurring Axis I and II disorders. CONCLUSIONS: Adults with severe borderline personality disorder frequently show a history of childhood ADHD symptomatology. Persisting ADHD correlates with frequency of co-occurring Axis I and II disorders. Severity of borderline symptomatology in adulthood is associated with emotional abuse in childhood. Further studies are needed to differentiate any potential causal relationship between ADHD and borderline personality disorder.     

Attention-deficit/hyperactivity disorder (ADHD) as a noradrenergic disorder.

This review revisits the thesis that a dysregulation of the central noradrenergic networks may underlie the pathophysiology of ADHD. We review the pertinent neurobiological and pharmacological literature on ADHD. The noradrenergic system has been intimately associated with the modulation of higher cortical functions including attention, alertness, vigilance and executive function. Noradrenergic activation is known to profoundly affect the performance of attention, especially the maintenance of arousal, a cognitive function known to be deficient in ADHD. Data from family, adoption, twin, and segregation analysis strongly support a genetic hypothesis for this disorder. Although molecular genetic studies of ADHD are relatively new and far from definitive, several replicated reports have found associations between ADHD with DAT and D4 receptor genes. Brain imaging studies fit well with the idea that dysfunction in fronto-subcortical pathways occurs in ADHD with its underlying dysregulation of noradrenergic function. A wealth of pharmacological data (within and without the stimulant literature) provides strong evidence for selective clinical activity in ADHD for drugs with noradrenergic and dopaminergic pharmacological profiles. Available research provides compelling theoretic, basic biologic and clinical support for the notion that ADHD is a brain disorder of likely genetic etiology with etiologic and pathophysiologic heterogeneity. Neurobiological and pharmacological data provide compelling support for a noradrenergic hypothesis of ADHD and suggest that drugs with noradrenergic activity may play an important role in the therapeutics of this disorder.