Conduction In Nerve Fibers Research Articles

Influence of rehabilitation nursing intervention on blood pressure control and quality of life of elderly patients with hypertension in general practice

Hypertensive cerebral hemorrhage is a typical cerebral microhemorrhage. Due to severe brain injury, the physiological conduction of nerve fibers is interrupted, and clinical symptoms lead to local nerve defects, such as dizziness, headache, disturbance of consciousness, aphasia, and hemiplegia. In recent years, with the improvement of medical level, the mortality rate of hypertensive cerebral hemorrhage has decreased significantly. However, disability rates in long-term clinical studies of survival suggest that rehabilitation measures have a significant impact on promoting the recovery of neurological function.

Towards a more accurate quasi-static approximation of the electric potential for neurostimulation with kilohertz-frequency sources * *This work has been partially supported by ANID Millennium Science Initiative Program through Millennium Nucleus for Applied Control and Inverse Problems NCN19-161.

Objective. Our goal was to determine the conditions for which a more precise calculation of the electric potential than the quasi-static approximation may be needed in models of electrical neurostimulation, particularly for signals with kilohertz-frequency components. Approach. We conducted a comprehensive quantitative study of the differences in nerve fiber activation and conduction block when using the quasi-static and Helmholtz approximations for the electric potential in a model of electrical neurostimulation. Main results. We first show that the potentials generated by sources of unbalanced pulses exhibit different transients as compared to those of charge-balanced pulses, and this is disregarded by the quasi-static assumption. Secondly, relative errors for current-distance curves were below 3%, while for strength-duration curves these ranged between 1%–17%, but could be improved to less than 3% across the range of pulse duration by providing a corrected quasi-static conductivity. Third, we extended our analysis to trains of pulses and reported a ‘congruence area’ below 700 Hz, where the fidelity of fiber responses is maximal for supra-threshold stimulation. Further examination of waveforms and polarities revealed similar fidelities in the congruence area, but significant differences were observed beyond this area. However, the spike-train distance revealed differences in activation patterns when comparing the response generated by each model. Finally, in simulations of conduction-block, we found that block thresholds exhibited errors above 20% for repetition rates above 10 kHz. Yet, employing a corrected value of the conductivity improved the agreement between models, with errors no greater than 8%. Significance. Our results emphasize that the quasi-static approximation cannot be naively extended to electrical stimulation with high-frequency components, and notable differences can be observed in activation patterns. As well, we introduce a methodology to obtain more precise model responses using the quasi-static approach, retaining its simplicity, which can be a valuable resource in computational neuroengineering.

Serum Uric Acid Levels Are Related to Diabetic Peripheral Neuropathy, Especially for Motor Conduction Velocity of Tibial Nerve in Type 2 Diabetes Mellitus Patients.

Oxidative stress is one of the most critical factors that contribute to the pathogenesis of neuronal damage, including diabetic peripheral neuropathy (DPN). Uric acid is a kind of natural antioxidant that plays a major role in the antioxidant capacity against oxidative stress. Here, we aim to determine the role of serum uric acid (SUA) in the DPN of patients with type 2 diabetes mellitus (T2DM). Patients and Methods. 106 patients with T2DM were recruited and divided into the DPN group and the control group. Clinical parameters, especially for motor nerve fiber conduction velocity and sensory nerve fiber conduction velocity, were collected. Differences between T2DM patients with and without DPN were compared. Correlation and regression analyses were performed to explore the association between SUA and DPN. Compare with 57 patients with DPN, 49 patients without DPN showed lower HbA1c and elevated SUA levels. Additionally, SUA levels are negatively associated with the motor conduction velocity of tibial nerve with or without adjusting for HbA1c. Besides, it is suggested that decreased SUA levels may influence the motor conduction speed of the tibial nerve by multiple linear regression analysis. Moreover, we demonstrated that decreased SUA level is a risk factor for DPN in patients with T2DM by binary logistic regression analysis. Lower SUA is a risk factor for DPN in patients with T2DM. Additionally, decreased SUA may influence the damage of peripheral neuropathy, especially for motor conduction velocity of the tibial nerve.

Effect of body mass index on ulnar nerve conduction velocity among medical students

Background: Obesity and overweight incidence is increasing among the medical students. The main reason for obesity among medical students is sedentary lifestyle, unhealthy food intake and stress. Increase in subcutaneous fat impairs the conduction in nerve fibers. Body mass index (BMI) is an easy tool to assess the obesity as it is noninvasive and non-expensive. Nerve conduction studies are the tools for assessing the performance of the nervous system. Aims and Objectives: The aim of the study was to evaluate the effect of obesity on the ulnar nerve conduction velocity among medical students. Materials and Methods: A total of 50 medical students were recruited for the study and the study was done in the Department of Physiology, ESIC Medical College, Hyderabad. Two groups were made Group A (n = 25 with BMI 18.5–24.9) and Group B (n = 25 with BMI >25). AD instrument was used for data acquisition for right ulnar nerve conduction velocity in both the groups. Results from both the groups were compared. Results: Nerve conduction velocity among the Group B students (50.95 ± 15.91) was decreased compared to Group A students (57.56 ± 14.79) but the decrease in nerve conduction velocity was not significant (P = 0.28). Conclusions: Nerve conduction velocity gets impaired with obesity among medical students, but further studies need to be done with more sample size.

Inhibitory Actions of Clinical Analgesics, Analgesic Adjuvants, and Plant-Derived Analgesics on Nerve Action Potential Conduction

The action potential (AP) conduction in nerve fibers plays a crucial role in transmitting nociceptive information from the periphery to the cerebral cortex. Nerve AP conduction inhibition possibly results in analgesia. It is well-known that many analgesics suppress nerve AP conduction and voltage-dependent sodium and potassium channels that are involved in producing APs. The compound action potential (CAP) recorded from a bundle of nerve fibers is a guide for knowing if analgesics affect nerve AP conduction. This entry mentions the inhibitory effects of clinically used analgesics, analgesic adjuvants, and plant-derived analgesics on fast-conducting CAPs and voltage-dependent sodium and potassium channels. The efficacies of their effects were compared among the compounds, and it was revealed that some of the compounds have similar efficacies in suppressing CAPs. It is suggested that analgesics-induced nerve AP conduction inhibition may contribute to at least a part of their analgesic effects.

Effectiveness of pupillography for assessing the state of autonomic nervous system and the choice of treatment for accommodative disorders in children

AbstractPurposeFor the first time, the values of indices of accommodation, direct and friendly pupillary reactions were determined – the maximal (Smax) and minimal (Smin) area of the healthy children aged 6 to 18 years depending on their age and tone of the autonomic nervous system (2016).Methods269 healthy children, 130 children with spasm of accommodation and 79 children with accommodation weakness were obsovered. We used the computer pupillography OК‐2 for registration of direct, consensual and accommodative convergent‐pupillary reaction.ResultsDifference between Smax values in children with accommodation spasm (23.94 ± SD 5.5 mm2, DI 95% 22.8–25.0) and with accommodation weakness (49.3 ± SD13.8 mm2, DI 95% 47.1–51.6) was revealed, that can be considered as a criterion for choosing the type of treatment. In accommodation spasm, the pupil area (Smax) in the range 22.8–25.0 mm2 and the general vagotonia (according to the Kerdo index) treatment by mydriatics should be appointed. In weak accommodation, Smax in the range of 47.1–51.6 mm2 and general sympathotonia, transcranial electrical stimulation and phosphenelectrostimulation are indicated. Phosphenelectrostimulation (FES) and ETRANS had unidirectional influence – an increase in the uncorrected visual acuity at a distance of 33% and 49% respectively, an improvement in accommodation reserves of 2.8–4.1 D in patients with accommodative dysfunctions.ConclusionsThe mechanisms of action of electrostimulation, where one of the key roles is the improvement of conduction of nerve fibers. In accommodation spasm and the general vagotonia treatment by mydriatics should be appointed.

Reversible alteration of brainstem auditory evoked potential in iron deficient anemic patients in response to treatment

Background: Iron deficiency anemia is associated with central and peripheral nervous system disturbances. Iron is an essential component of brain growth, myelination, nerve impulse conduction, protein synthesis, hormone production, fundamental aspects of cellular energy metabolism and is involved in neurotransmitter synthesis including serotonin, norepinephrine and dopamine. Hence, its deficiency adversely affects motor performance, mental development as well as cognitive and behavioral functions. Since myelination is concerned with conduction in nerve fibers, iron deficiency potentially impairs neuronal transmission and leads to functional neurodeficit like hearing loss.Methods: BAEP was recorded using RMS EMG EP MK2 machine in patients of iron deficiency anemia with haemoglobin less than 10.9 g/dl between 18-50 years of age who were followed up after 3 months of treatment and compared with 30 age and sex matched controls.Results: BAEP absolute and interpeak latencies were prolonged in IDA patients as compared to the control groups which was reversible with iron replacement therapy.Conclusions: Increased absolute and interpeak latencies of BAEP indicates impairment of auditory pathways in IDA patients. Thus, the electrophysiological study of BAEP provides an objective method for monitoring the function of CNS, especially the auditory function in iron deficiency anemia patients before and after iron replacement therapy. It is a non-invasive test for early diagnosis and therefore early treatment to prevent complications.

Inhibition of Fast Nerve Conduction Produced by Analgesics and Analgesic Adjuvants-Possible Involvement in Pain Alleviation.

Nociceptive information is transmitted from the periphery to the cerebral cortex mainly by action potential (AP) conduction in nerve fibers and chemical transmission at synapses. Although this nociceptive transmission is largely inhibited at synapses by analgesics and their adjuvants, it is possible that the antinociceptive drugs inhibit nerve AP conduction, contributing to their antinociceptive effects. Many of the drugs are reported to inhibit the nerve conduction of AP and voltage-gated Na+ and K+ channels involved in its production. Compound action potential (CAP) is a useful measure to know whether drugs act on nerve AP conduction. Clinically-used analgesics and analgesic adjuvants (opioids, non-steroidal anti-inflammatory drugs, α2-adrenoceptor agonists, antiepileptics, antidepressants and local anesthetics) were found to inhibit fast-conducting CAPs recorded from the frog sciatic nerve by using the air-gap method. Similar actions were produced by antinociceptive plant-derived chemicals. Their inhibitory actions depended on the concentrations and chemical structures of the drugs. This review article will mention the inhibitory actions of the antinociceptive compounds on CAPs in frog and mammalian peripheral (particularly, sciatic) nerves and on voltage-gated Na+ and K+ channels involved in AP production. Nerve AP conduction inhibition produced by analgesics and analgesic adjuvants is suggested to contribute to at least a part of their antinociceptive effects.

Signal Modeling and Simulation of Temporal Dispersion and Conduction Block in Motor Nerves.

Electroneurography is a well-established diagnostic test for supporting the diagnosis of disorders of myelinated peripheral nerves. Neurophysiological quantities are automatically calculated and are used to determine the pathology of the nerve (axonal damage) or its sheath (myelin damage). Specific differential diagnostic criteria are derived from time-domain normative data, which result primarily from a computer simulation in the early 1990s based on animal data, namely rats. However, the rat signals studied differ significantly from those of humans because of anatomical differences. We present a model-based simulation of nerve conduction in healthy and pathological motor nerves. In contrast to earlier simulations, the present model is based on motor unit action potentials extracted from real human measurements facilitating the generation of realistic signals, starting from a conduction velocity distribution. In addition to the modeling of healthy nerves, we model a hereditary peripheral nerve disease as well as an acute and a chronic inflammatory demyelinating condition. Quantitative signal differences based on standard variables in the time-domain are presented. The findings for the demyelinating conditions demonstrate amplitude reductions of 71% and 65% between the distal and proximal responses, which result from an increase in the variance of the nerve fiber conduction velocities. The simulation results closely match those of empirical measurements, indicating that the signal model captures relevant pathological mechanisms. An amplitude reduction of more than 50% in demyelinating conditions is in accordance with routine measurements and shows that temporal dispersion is quite well-modeled compared to previous simulation models. The simulation outcomes can serve as the basis for an improved pathophysiological understanding of peripheral nerve disorders and should aid neurophysiologists to refine their diagnostic armamentarium resulting in a more precise differential diagnosis.

The mechanosensitive ion channel TRAAK is localized to the mammalian node of Ranvier.

TRAAK is a membrane tension-activated K+ channel that has been associated through behavioral studies to mechanical nociception. We used specific monoclonal antibodies in mice to show that TRAAK is localized exclusively to nodes of Ranvier, the action potential propagating elements of myelinated nerve fibers. Approximately 80 percent of myelinated nerve fibers throughout the central and peripheral nervous system contain TRAAK in what is likely an all-nodes or no-nodes per axon fashion. TRAAK is not observed at the axon initial segment where action potentials are first generated. We used polyclonal antibodies, the TRAAK inhibitor RU2 and node clamp amplifiers to demonstrate the presence and functional properties of TRAAK in rat nerve fibers. TRAAK contributes to the 'leak' K+ current in mammalian nerve fiber conduction by hyperpolarizing the resting membrane potential, thereby increasing Na+ channel availability for action potential propagation. We speculate on why nodes of Ranvier contain a mechanosensitive K+ channel.

Adding Clonidine to Ropivacaine in Brachial Plexus Block for Upper Limb Surgeries: Study of Hemodynamic Variables

Background: Ropivacaine is a long acting amide local anaesthetic agent. It was first synthesized in 1957 along with bupivacaine and mepivacaine. It is a pure S-enantiomer while bupivacaine is a racemic mixture. Ropivacaine causes reversible inhibition of sodium ion influx, and thereby blocks impulse conduction in nerve fibres. This action is potentiated by dose-dependent inhibition of potassium channels. Subjects and Methods: This study was conducted on 60 patients undergoing upper limb surgeries aged between 18 to 55 years under supraclavicular block. Informed written consent was taken. Result values were recorded using a preset proforma. Results: There were 24 patients in Group R and 23 patients in Group RC belonging to ASA Grade I, and 6 patients in Group R and 7 patients in Group RC belonging to ASA Grade II which was considered statistically not significant. Conclusion: The combination produces improved analgesia, resulting in a prolonged effect and stable hemodynamics.

Inside the Scrambler Therapy, a Noninvasive Treatment of Chronic Neuropathic and Cancer Pain: From the Gate Control Theory to the Active Principle of Information.

Scrambler therapy (ST) is an electro-analgesia therapy for the noninvasive treatment of chronic neuropathic and cancer pain based on a new generation of medical device that uses 5 artificial neurons and is based on a novel theoretical model the differs from gate control theory. The active principle with Scrambler Therapy is such that synthetic “non-pain” information is transmitted by C fiber surface receptors. This is a different theoretical mechanism than the traditional electric stimulation of A-Beta fibers to produce paresthesia and/or block the conduction of nerve fibers to produce an analgesic effect, that is, via TENS (transcutaneous electrical nerve stimulation) machines. Scrambler therapy was developed to treat chronic neuropathic pain and cancer pain resistant to opioids and other types of treatments. The goal of Scrambler Therapy is to eliminate pain during treatment and allow for long-lasting analgesia after a series of 10 to 12 consecutive treatments performed over a 2-week period. The aim of this review is to clarify the underlying theory of Scrambler Therapy and describe the appropriate usage method that maximizes its effectiveness while reducing bias and deepen the explanation of the artificial neuron technology associated with Scrambler Therapy.

PO-177 Effect of rational exercise on delaying brain aging and its mechanism analysis

PO-177 Effect of rational exercise on delaying brain aging and its mechanism analysis

T34. Diagnosing patients with carpal tunnel syndrome: Do you need needle EMG?

Introduction Carpal tunnel syndrome (CTS) is a common diagnosis that requires a thorough clinical history and examination. Electrodiagnostic (EDX) evaluation with nerve conduction studies (NCS) is frequently performed to assist the ordering physician when considering additional therapies or surgical intervention. It is a sensitive tool to examine median nerve dysfunction and aids in distinguishing CTS from cervical radiculopathy (CR) by identifying selective slowing of the conduction of median nerve fibers across the carpal tunnel. Some argue that if the NCS shows evidence of CTS, then needle EMG is not necessary. Current practice guidelines consider needle EMG to be an optional test better suited to exclude concurrent causes (cervical radiculopathy) of the patient’s symptoms for improving diagnostic sensitivity. We set out to determine the number of suspected CTS patients with evidence of CTS on NCS who also have concurrent needle EMG evidence of cervical radiculopathy. We aimed to further explore whether clinical examination performed by physicians ordering EDX could distinguish between the diagnoses of CTS and CR before testing is performed. Methods A retrospective chart review of 606 cases of CTS and CR in the Mayo Clinic Arizona EMG Laboratory from January 2015 to January 2016 was performed. Clinical notes of referring physicians for EMG/NCS and final EMG/NCS reports were reviewed for referring diagnoses, clinical history, physical exam and EMG diagnoses. Results Out of 472 patients diagnosed with CTS, 19.1% also had a concurrent diagnosis of CR confirmed by needle EMG ( n = 90). 17.2% of suspected CTS based on clinical assessment were not confirmed after electrodiagnostic testing ( n = 104). 29.0% of suspected CR patients were not confirmed after electrodiagnostic testing ( n = 176). 12 clinical assessment data points (clinical history and physical exam findings) felt to represent a common evaluation of diagnoses of CTS were compiled. These included cervicogenic pain, radicular pain, hand paresthesias, nocturnal pain, symptoms worse with activity, symptoms relieved by shaking out hands (“flick” sign), myotomal weakness, dermatomal sensory abnormalities, hyporeflexia, loss of sensation in the median nerve distribution, thenar atrophy, and hand weakness. The only clinical finding found to have a clinically significant association with both CTS and CR was hand paresthesias ( p = 0.001). Conclusion This series demonstrated that 19% of patients seen with CTS have an associated cervical radiculopathy. Without needle electromyography, these concurrent diagnoses would be missed, which can affect subsequent management and therapy. Clinical assessment alone may not be enough to distinguish between CTS and CR, as has been demonstrated in previous studies. Even though practice guidelines allude to optional needle EMG, this data provides a strong argument in favor of performing both NCS and needle EMG in patients with suspected CTS.

S165. Henneman’s size principle for the motor neurons recruitment of human spinal reflex: Evidences from a study of H reflexes during acute compression/ischemia

Introduction In H reflex studies, H waves are recruited from the reflex-elicited depolarization of the Alpha motor neurons, which follows the Henneman’s size principle that the small motor neurons are responsible for the early portion of the recruitment of the H-reflex. However, there has not been a successful experiment in human with EMG techniques to demonstrate this principle. The goal of this study is to demonstrate that small motor fibers are responsible for the elicitation of the H-reflex in the soleus and flexor carpi radialis (FCR) muscles by blocking the conduction of large motor nerve fibers of the tibial and median nerve using partial ischemia via blood pressure cuff. Methods This prospective study recruited 8 health resident physicians (4 m, 4 F). Electrical stimulation to the tibial nerve at the popliteal fossa, with recording from the soleus and to median nerve at above the elbow with recording from FCR was titrated to elicit both M and H waves, with ratios of amplitudes at 1:1. Compression by a blood pressure cuff was placed at the proximal tibia during tibial nerve stimulations, and at the forearm just distal to the elbow for median nerve stimulation. Stimulations with pulse duration of 1 ms at intervals of 2 s were delivered to the two nerves before, during, and post compression/ischemia. Results In all the subjects tested, during blood pressure cuff inflation, the M-waves of the two muscles consistently demonstrated significant loss of amplitude (or disappeared) with mild increase of latency, while the H-reflex showed no, or very mild amplitude reductions without changes in latency. After blood pressure cuff deflation, the M-waves immediately returned to their previous amplitude and latency patterns. There was a significant dissociation between the changes of M and H waves during acute partial compression/ischemia. Conclusion Acute compression/ischemia instantly causes nerve conduction block of the tibial and median nerves motor fibers and reduces the amplitude of the M waves, but not the H-reflexes. M waves elicited by electrical stimulation recruit large motor fibers first, and are more susceptible to the ischemic blockade applied. By contrast, the H reflex first recruits small motor neurons, with their smaller motor nerve fibers less susceptible to partial acute compression/ischemia. This experiment demonstrates the Henneman’s size principle that the smallest motor units are recruited first during spinal reflexes and volitional muscle contraction. It is also of important significance in the application of motor rehabilitation with therapeutic and functional electrical stimulation of nerves and muscles.

Compound action potential inhibition produced by various antidepressants in the frog sciatic nerve

Although an inhibition of action potential conduction in nerve fibers possibly contributes to at least a part of antinociception produced by analgesics and the adjuvants, it has not been fully examined yet how the conduction inhibition differs in extent among their drugs. We investigated the effects of various antidepressants used as analgesic adjuvants on compound action potentials (CAPs) recorded from the frog sciatic nerve by using the air-gap method. The results were compared with those of the other adjuvants that were reported previously. Antidepressants, duloxetine (serotonin and noradrenaline reuptake inhibitor, SNRI), fluoxetine (selective serotonin reuptake inhibitor, SSRI), amitriptyline (tricyclic tertiary amine), desipramine (tricyclic secondary amine) and maprotiline (tetracyclic secondary amine), reduced the peak amplitude of the CAP with half-maximal inhibitory concentration (IC50) values of 0.23, 1.5, 0.26, 1.6 and 0.95mM, respectively. Trazodone (non-SNRI, -SSRI, -tricyclic and -tetracyclic antidepressant) at 1.0mM reduced CAP amplitude by about 50%. The duloxetine and amitriptyline values were comparable to those of lamotrigine and carbamazepine (antiepileptics), dexmedetomidine (α2-adrenoceptor agonist) and ropivacaine, levobupivacaine and pramoxine (local anesthetics). The fluoxetine, desipramine, maprotiline and trazodone values were similar to those of oxymetazoline (α2-adrenoceptor agonist) and lidocaine, cocaine, procaine and prilocaine (local anesthetics). The antidepressants’ IC50 values were much larger than that of tetracaine (local anesthetic). In conclusion, the six antidepressants inhibited CAPs with efficacies comparable to some antiepileptics, α2-adrenoceptor agonists and local anesthetics. It was suggested that antidepressants inhibit nerve conduction with efficacies comparable to those of the other adjuvants.

NaV1.7 and pain: contribution of peripheral nerves.

The sodium channel NaV1.7 contributes to action potential (AP) generation and propagation. Loss-of-function mutations in patients lead to congenital indifference to pain, though it remains unclear where on the way from sensory terminals to central nervous system the signalling is disrupted. We confirm that conditional deletion of NaV1.7 in advillin-expressing sensory neurons leads to impaired heat and mechanical nociception in behavioural tests. With single-fiber recordings from isolated skin, we found (1) a significantly lower prevalence of heat responsiveness to normally mechanosensitive C-fibers, although (2) the rare heat responses seemed quite vigorous, and (3) heat-induced calcitonin gene-related peptide release was normal. In biophysical respects, although electrical excitability, rheobase, and chronaxy were normal, (4) axonal conduction velocity was 20% slower than in congenic wild-type mice (5) and when challenged with double pulses (<100 milliseconds interval), the second AP showed more pronounced latency increase (6). On prolonged electrical stimulation at 2 Hz, (7) activity-dependent slowing of nerve fiber conduction was markedly less, and (8) was less likely to result in conduction failure of the mutant single fibers. Finally, recording of compound APs from the whole saphenous nerve confirmed slower conduction and less activity-dependent slowing as well as the functional absence of a large subpopulation of C-fibers (9) in conditional NaV1.7 knockouts. In conclusion, the clear deficits in somatic primary afferent functions shown in our study may be complemented by previously reported synaptic dysfunction and opioidergic inhibition, together accounting for the complete insensitivity to pain in the human mutants lacking NaV1.7.

Neurobiological Mechanism of Acupuncture for Relieving Visceral Pain of Gastrointestinal Origin.

It is currently accepted that the neural transduction pathways of gastrointestinal (GI) visceral pain include the peripheral and central pathways. Existing research on the neurological mechanism of electroacupuncture (EA) in the treatment of GI visceral pain has primarily been concerned with the regulation of relevant transduction pathways. The generation of pain involves a series of processes, including energy transduction of stimulatory signals in the sensory nerve endings (signal transduction), subsequent conduction in primary afferent nerve fibers of dorsal root ganglia, and transmission to spinal dorsal horn neurons, the ascending transmission of sensory signals in the central nervous system, and the processing of sensory signals in the cerebral cortex. Numerous peripheral neurotransmitters, neuropeptides, and cytokines participate in the analgesic process of EA in visceral pain. Although EA has excellent efficacy in the treatment of GI visceral pain, the pathogenesis of the disease and the analgesic mechanism of the treatment have not been elucidated. In recent years, research has examined the pathogenesis of GI visceral pain and its influencing factors and has explored the neural transduction pathways of this disease.

Effects of acute tryptophan depletion on central processing of CT-targeted and discriminatory touch in humans.

C-tactile afferents (CTs) are slowly conducting nerve fibres, present only in hairy skin. They are optimally activated by slow, gentle stroking touch, such as those experienced during a caress. CT stimulation activates affective processing brain regions, alluding to their role in affective touch perception. We tested a theory that CT-activating touch engages the pro-social functions of serotonin, by determining whether reducing serotonin, through acute tryptophan depletion, diminishes subjective pleasantness and affective brain responses to gentle touch. A tryptophan depleting amino acid drink was administered to 16 healthy females, with a further 14 receiving a control drink. After 4h, participants underwent an fMRI scan, during which time CT-innervated forearm skin and CT non-innervated finger skin was stroked with three brushes of differing texture, at CT-optimal force and velocity. Pleasantness ratings were obtained post scanning. The control group showed a greater response in ipsilateral orbitofrontal cortex to CT-activating forearm touch compared to touch to the finger where CTs are absent. This differential response was not present in the tryptophan depleted group. This interaction effect was significant. In addition, control participants showed a differential primary somatosensory cortex response to brush texture applied to the finger, a purely discriminatory touch response, which was not observed in the tryptophan depleted group. This interaction effect was also significant. Pleasantness ratings were similar across treatment groups. These results implicate serotonin in the differentiation between CT-activating and purely discriminatory touch responses. Such effects could contribute to some of the social abnormalities seen in psychiatric disorders associated with abnormal serotonin function.

Dexmedetomidine augments the effect of lidocaine: power spectrum and nerve conduction velocity distribution study.

BackgroundIn this study, the individual and combined inhibitory effects of dexmedetomidine and lidocaine on the conduction group of isolated nerve were investigated by determining conduction velocity distribution (CVD) and power spectrum.MethodsElectrophysiological compound action potential (CAP) recordings were conducted on isolated rat sciatic nerve before (Con) and 20 minutes after exposure to 1 mM lidocaine (Lido), 21pM dexmedetomidine (Dex) and their combination (Lido + Dex). Then for CVD, mathematical model and for power spectrum Fast Fourier analysis were conducted.ResultsDexmedetomidine alone made no significant difference in shape and duration of CAPs as compared to Con, on the other hand lidocaine depresses amplitude and prolongs the duration of CAPs, but not more than combination of dexmedetomidine and lidocaine can do.Lidocaine caused a shift in the CVD histogram to relatively slower conducting group significantly while dexmedetomidine did not cause any significant change as compared to Control. Lidocaine, when combined with dexmedetomidine revealed a remarkable effect on the whole CVD histogram by causing almost complete blockage of fast conducting nerve fibers. The relative number of fibers in CVD is conserved for separate applications of anesthetics, but not for their combination.As in CVD, power spectrum shifted from higher to lower frequency region by lidocaine and significantly for lidocaine combined with dexmedetomidine application. Shifts for dexmedetomidine applied group were seen beggarly.ConclusionsWe have concluded that dexmedetomidine alone did not influence nerve conduction, but when it is used with lidocaine it augments neural conduction blockage effect, especially on fast conducting nerve fibers.