Chronic pain can be considered as a highly salient stimulus that continuously taxes the attentional and salience processing networks, thus interfering with cognitive abilities and, more specifically, consuming attentional resources. The aim of the paper was to explore whether and how diabetic neuropathic pain (NP) affects attentional networks. We sought to achieve this by investigating resting state functional connectivity (rsFC) in diabetic NP patients and comparing it with that of matched healthy controls. NP patients showed a widespread reduction of connectivity in both the dorsal and ventral attentional networks, as well as in the dorsal anterior cingulated cortex (ACC), typically implicated in salience processing. We also found a generalized reduction of the length of functional connections in the NP group: in all the examined networks, the Euclidian distance between connected voxels was significantly shorter in patients vs. controls. In sum, our work showed that in diabetic NP pain a parieto-fronto-cingulate network controlling attention to external stimuli is impaired. In line with previous studies, we conclude that chronic pain can disrupt the synchrony of a common pool of brain areas, involved in self monitoring, pain processing and salience detection. 2 INTRODUCTIONThe nervous system is continuously bombarded by internal and extrapersonal stimuli. The priority is to identify the most relevant among these myriad of inputs. This capacity requires a system that can integrate highly processed sensory data with visceral, autonomic, and hedonic markers [1]. Pain is inherently salient, and it demands attention and cognitive resources, as it has to be evaluated in intensity and in other qualities. Thus, attention to a salient input such as pain can be viewed as the focusing of resources on a specific stimulus. While a growing number of studies have examined the relationships between attention and pain, and their neural correlates, few studies have addressed the issue of how pain engages and modifies attention. Indeed, the majority of studies to date have focused on the effects of attention on pain, while the effects of pain on attention are practically unexplored. Lesion and neuroimaging studies employing non-painful stimuli have related attentional control to a network composed of parietal, frontal, and cingulate cortical regions [2]. Some studies have found similar patterns of cortical activation for both voluntary and involuntary attentional control mechanisms [3]. Similarly to other attentional tasks, pain engages a common group of brain regions that includes the posterior parietal, prefrontal, and anterior cingulate cortices [4]. Sharing common cognitive resources and neural correlates, pain and attention systems are likely to interact. Indeed, it has been demonstrated that experimental pain can decrease cognitive performance and task-related activity [5,6]. However, the interaction between pain and other functional networks has only recently started to be considered [7,8]. We believe a promising ...

The clinical and neurophysiologic data from 65 patients taking thalidomide were reviewed. Thalidomide sensory neurotoxicity was found to be cumulative dose dependent but occurs only when the total dose is relatively high (>20 g). The risk of developing sensory neuropathy is around 10% below this threshold but increases with higher doses.

BackgroundIn this paper we explored thalamocortical functional connectivity in a group of eight patients suffering from peripheral neuropathic pain (diabetic pain), and compared it with that of a group of healthy subjects. We hypothesized that functional interconnections between the thalamus and cortex can be altered after years of ongoing chronic neuropathic pain.ResultsFunctional connectivity was studied through a resting state functional magnetic resonance imaging (fMRI) paradigm: temporal correlations between predefined regions of interest (primary somatosensory cortex, ventral posterior lateral thalamic nucleus, medial dorsal thalamic nucleus) and the rest of the brain were systematically investigated. The patient group showed decreased resting state functional connectivity between the thalamus and the cortex.ConclusionThis supports the idea that chronic pain can alter thalamocortical connections causing a disruption of thalamic feedback, and the view of chronic pain as a thalamocortical dysrhythmia.

This study was aimed at assessing the electrophysiological signs of peripheral neuropathy in diabetes mellitus (DM) type II patients at diagnosis. Nerve conduction studies (NCS) of median, ulnar, peroneal, tibial and sural nerves were performed in 39 newly diagnosed DM subjects and compared to those of 40 healthy controls. Metabolic indices were also investigated. Electrophysiological alterations were found in 32 (82%) of the DM patients, and more than half of them (62.2%) showed multiple (two to five) abnormal parameters. Because most of the subjects (84.4%) had from two to five nerves involved, these alterations were widespread in the seven nerves evaluated. Forty-two percent of the patients had NCS alterations suggestive of distal median mononeuropathy, implying that metabolic factors in DM make the median nerve more susceptible to focal entrapment. A reduced sensory nerve action potential (SNAP) amplitude was observed in the median nerve in 70% of the patients, in the ulnar in 69% and in the sural nerve only in 22%. In the presence of a decrease in the SNAP amplitude of the ulnar or median nerve, the SNAP amplitude of the sural nerve was normal in 82 or 80% of the subjects, respectively. This finding may be in keeping with a distal involvement of the sensory fibres, as explored by routine median or ulnar NCS. No correlation was found between metabolic indices and NCS parameters. In conclusion, a high percentage of newly diagnosed DM patients show signs of neuropathy, and upper limb nerve sensory NCS seem to be more sensitive in detecting it than lower limb NCS.

Criteria for the diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) are met by the polyneuropathy associated with immunoglobulin M (IgM) paraproteinemia and anti-myelin-associated glycoprotein (MAG) antibody (MAG-CIDP). However, MAG-CIDP differs from other types of CIDP, mainly in its poorer response to treatment. The utility of terminal latency index (TLI) as an electrophysiological marker for MAG-CIDP has been debated. In this study we confirmed its diagnostic usefulness and evaluated TLI threshold values for motor nerves investigated in routine nerve conduction studies. Median, ulnar, peroneal, and tibial TLIs of 11 subjects with MAG-CIDP, 18 with CIDP, and 76 healthy controls were compared, and threshold values for MAG-CIDP evaluated as the lowest value with a likelihood ratio higher than 10. Mean TLI values and TLIs of all but the peroneal nerve were significantly lower in MAG-CIDP. Median nerve TLI of 0.26 and ulnar nerve TLI of 0.33 were identified as the threshold TLI values for MAG-CIDP.