Tactile sensibility in the human hand: relative and absolute densities of four types of mechanoreceptive units in glabrous skin.

Nevner tetthet på sensoriske nerver i huden.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1281571/

1. Single unit impulses were recorded with percutaneously inserted tungsten needle electrodes from the median nerve in conscious human subjects.
2. A sample of 334 low threshold mechanoreceptive units innervating the glabrous skin area of the hand were studied. In accordance with earlier investigations, the units were separated into four groups on the basis of their adaptation and receptive field properties: RA, PC, SA I and SA II units.
3. The locations of the receptive fields of individual units were determined and the relative unit densities within various skin regions were calculated. The over-all density was found to increase in the proximo-distal direction. There was a slight increase from the palm to the main part of the finger and an abrupt increase from the main part of the finger to the finger tip. The relative densities in these three regions were 1, 1.6, 4.2.
4. The differences in over-all density were essentially accounted for by the two types of units characterized by small and well defined receptive fields, the RA and SA I units, whereas the PC and SA II units were almost evenly distributed over the whole glabrous skin area.
5. The spatial distribution of densities supports the idea that the RA and SA I units account for spatial acuity in psychophysical tests. This capacity is known to increase in distal direction along the hand.
6. On the basis of histological data regarding the number of myelinated fibres in the median nerve, a model of the absolute unit density was proposed. It was estimated that the density of low threshold mechanoreceptive units at the finger tip is as high as 241 u./cm2, whereas in the palm it is only 58 u./cm2.

A model accounting for effects of vibratory amplitude on responses of cutaneous mechanoreceptors in macaque monkey

Nevner vibrasjonens effekt på alle sensoriske nerver i huden. Gammel studie fra 80-tallet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1250344/

1. A mechanoreceptor model, developed in the preceding paper (Freeman & Johnson, 1982), was used to study the effects of vibratory intensity and frequency on the responses of slowly adapting, rapidly adapting and Pacinian afferents in monkey hairless skin. As in the previous paper almost all of the response properties studied here were accounted for by the equivalent circuit model; changes in membrane time constant and amplitude sensitivity accounted for the differences between the three mechanoreceptive fibre types.

2. The stimulus—response function of primary concern was the relationship between impulse rate and vibratory amplitude. This relationship had the same general form in each of the three fibre types. Amplitudes, I, less than I0 produced no impulse on any stimulus cycles. Amplitudes greater than I1produced one impulse on every cycle. As I rose from I0 to I1 the impulse rate rose monotonically from 0 to 1 impulse/cycle. For each fibre type the form of this ramp depended on the stimulus frequency.

3. At stimulus frequencies low in the frequency range of each fibre type the (I0, I1) ramp tended to be steep and sigmoidal in shape. Two or more impulses occurred on some cycles and none on others.

4. At intermediate frequencies the (I0, I1) ramps became linear with at most one impulse on each cycle. A short plateau appeared at 0·5 impulses/cycle (i.e. there was a range of intensities yielding one impulse on alternate cycles). All of these response properties at low and intermediate frequencies were explained by the model.

5. At higher frequencies the (I0, I1) ramps became shallower and developed discontinuities in slope at impulse rates of 0·5 impulses/cycle. At stimulus frequencies greater than 20 Hz for SAs and RAs, the upper segment of the (I0, I1) slope became steeper. For frequencies greater than 80 Hz, the upper segments of the Pacinian (I0, I1) slopes were shallower than the lower segments. These effects suggested transient periods of hyperexcitability following each action potential, and reductions in sensitivity due to high impulse rates, respectively.

6. The model’s membrane time constant was adjusted to match the observed reduction in the (I0, I1) slope with increasing stimulus frequency. The time constants required for least-squares fitting were 58, 29 and 4·2 msec for slowly adapting, rapidly adapting and Pacinian afferents, respectively; these values are of the same order as those obtained in the preceding paper.

7. Receptor sensitivity varied across the frequency spectrum, slow adaptors being most sensitive at low frequencies, rapidly adapting units at mid-range, and Pacinians at the high frequencies. According to the model, the high frequency roll-off in a receptor’s tuning curve is due to the current integrating properties of receptor membrane, and the low frequency roll-off is due to a high pass filter, presumably mechanical, situated in the tissues between the stimulus probe and receptor membrane.

8. Impulse phase advances with increasing stimulus intensity in both receptor and model. The ability of the model to fit both the rate—intensity function and phase advance functions in individual receptors is demonstrated.

The Effect of Surface Wave Propagation on Neural Responses to Vibration in Primate Glabrous Skin

Studie som nevner at vibrasjon sprer seg i huden og forsterker signalene opp til hjernen. Men har bare 1 mm kontaktflate og forholder seg til høy frekvens (opp til 400 Hz)og pacini celler. Mye interessant likevel.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278420/

«First, we find that these waves substantially amplify the neural response to the stimulus»

«Second, we show that surface waves result in a reduction of the temporal patterning in the response of afferent populations, particularly at frequencies over 200 Hz, but the degree of temporal blurring is relatively small compared to that observed in the response of S1 neurons.»

«Third, despite these two factors, the structure of the waveform is well preserved in the form of the surface waves, suggesting that surface waves should enhance the perception of simple and complex skin oscillations.»

Because tactile perception relies on the response of large populations of receptors distributed across the skin, we seek to characterize how a mechanical deformation of the skin at one location affects the skin at another.

First, we show that a vibration applied to the fingertip travels at least the length of the finger and that the rate at which it decays is dependent on stimulus frequency.

We show that this skin resonance can lead to a two-fold increase in the strength of the response of a simulated afferent population.

Second, the rate at which vibrations propagate across the skin is dependent on the stimulus frequency and plateaus at 7 m/s. The resulting delay in neural activation across locations does not substantially blur the temporal patterning in simulated populations of afferents for frequencies less than 200 Hz, which has important implications about how vibratory frequency is encoded in the responses of somatosensory neurons.

Third, we show that, despite the dependence of decay rate and propagation speed on frequency, the waveform of a complex vibration is well preserved as it travels across the skin. Our results suggest, then, that the propagation of surface waves promotes the encoding of spectrally complex vibrations as the entire neural population is exposed to essentially the same stimulus.

Pathophysiology of Nerve Compression Syndromes: Response of Peripheral Nerves to Loading

Om nerve compression syndrome, som sannsynligvis er årsaken til de fleste plager folk kommer til behandling for. Nevner hvordan nervevev påvirkes i løpet av timer, dager og uker. Nevner de 3 gradene av kompresjon og hvilke symptomer de gir.

http://ergo.berkeley.edu/docs/1999rempeljbjs.pdf

Nerve compression syndromes involve peripheral- nerve dysfunction that is due to localized interference of microvascular function and structural changes in the nerve or adjacent tissues.

When tissues are subjected to load or pressure, they deform and pressure gradients are formed, redistribut- ing the compressed tissue toward areas of lower pres- sure. Nerve compression syndromes usually occur at sites where the nerve passes through a tight tunnel formed by stiff tissue boundaries. The resultant con- fined space limits movement of tissue and can lead to sustained tissue pressure gradients. Space-occupying structures or lesions (for example, lumbrical muscles, tu- mors, and cysts) can cause nerve compression injury, as can conditions associated with accumulation of fluid (for example, pregnancy, congestive heart failure, and muscle compartment syndromes) or accumulation of extracellular matrix (for example, acromegaly, myx- edema hypothyroidism, and mucopolysaccharidosis)76.

Although nerve injuries related to vibration occur near the region of exposure, the symptoms may be manifest at another site, where the nerve may be constricted.

Other conditions, such as diabetes mellitus, may increase the likelihood that a compressed nerve will undergo a pathological response. In addition, there may be an in- flammatory reaction that may impair the normal gliding of the nerve.

Lying next to the myelinated nerve fibers are many nonmyelinated fibers associated with one Schwann cell. Myelinated and nonmyelinated nerve fibers are organized in bundles, called fascicles, which are surrounded by a strong membrane called the peri- neurial membrane, consisting of laminae of flattened cells.

Between the nerve fibers and their basal mem- brane is an intrafascicular connective tissue known as the endoneurium. The quantity of the connective-tissue components may vary between nerves and also along the length of the same nerve. For example, nerves lo- cated superficially in the limb or parts of the nerve that cross a joint contain a greater quantity of connective tissue, possibly as a response to repeated loading76.

The propagation of impulses in the nerve fibers as well as the communication and nutritional transport sys- tem in the neuron (axonal transport) requires an ade- quate energy supply. Therefore, the peripheral nerve contains a well developed microvascular system with vascular plexuses in all of its layers of connective tis- sue36,38. The vessels approach the nerve trunk segmen- tally and have a coiled configuration so that the vascular supply is not impaired during normal gliding or excur- sion of the nerve trunk. When the vessels reach the nerve trunk, they divide into branches that run longi- tudinally in various layers of the epineurium and they also form numerous collateral connections to vessels in the perineurial sheath. When the vessels pass through the perineurium into the endoneurium, which contains primarily capillaries, they often go through the perineu- rium obliquely, thereby constituting a possible valve mechanism36,38.

The perineurial layer and the endoneurial vessels play an important role in protecting the nerve fibers in the fascicles. The endoneurial milieu is protected by a blood-nerve barrier, and the tissue pressure in the fascicle (endoneurial fluid pressure) is slightly positive50.

The median and ulnar nerves may glide 7.3 and 9.8 millimeters, respectively, during full flexion and extension of the elbow, and the extent of excursion of these nerves just proximal to the wrist is even more pronounced (14.5 and 13.8 millimeters, respectively)90. In relation to the flexor retinaculum, the median nerve can move a maximum of 9.6 millimeters during wrist flexion and somewhat less during wrist extension; it also moves during motion of the fingers48.

Acute Effects of Nerve Compression (Effects within Hours)
In animal experiments, low-magnitude extraneural compression was noted to decrease intraneural micro- vascular flow, impair axonal transport, and alter nerve structure and function. Extraneural pressures of 2.7 kilo- pascals (twenty millimeters of mercury), induced with use of miniature inflatable cuffs, reduced epineurial ve- nule blood flow68. At pressures of 10.7 kilopascals (eighty millimeters of mercury), all intraneural blood flow ceased. Similarly, pressures of 4.0 kilopascals (thirty mil- limeters of mercury) inhibited both fast and slow ante- grade as well as retrograde axonal transport8.

In subjects with different blood pres- sures, the critical extraneural pressure threshold above which nerve function was blocked was 4.0 kilopascals (thirty millimeters of mercury) less than the diastolic pressure. This finding, combined with the observation that carpal tunnel syndrome may manifest with the treat- ment of hypertension17, provides additional support for an ischemic mechanism of acute nerve dysfunction.

Short-Term Effects of Nerve Compression (Effects within Days)
Com- pression of 4.0 kilopascals led to an elevated endoneu- rial pressure, which persisted for twenty-four hours after release of the cuff. Furthermore, the endoneurial pres- sures at twenty-four hours after release of the cuff increased with increasing durations of compression. His- tological examination demonstrated endoneurial edema in the nerves that had been subjected to eight hours of compression but not in those subjected to shorter dura- tions. Eight hours of compression led to an increase of the endoneurial pressures to levels that can reduce in- traneural blood flow51.

The study demonstrated that, af- ter low elevations of extraneural pressure for only two hours, endoneurial fluid pressures increased rapidly and the increases persisted for at least an additional twentyfour hours40. These effects probably are due to the in- creased vascular permeability of the epineurial and en- doneurial vessels after compression. Other studies have demonstrated that ischemia alters the structure of the endothelial and basement membranes over a similar time-frame2.

Long-Term Effects of Nerve Compression (Effects within Weeks)
Edema was visible in the sub- perineurial space within four hours in all compression subgroups, and it persisted for the entire duration of the study. Inflammation and fibrin deposits occurred within hours after compression, followed by prolifera- tion of endoneurial fibroblasts and capillary endothe- lial cells. Vigorous proliferation of fibrous tissue was noted within days, and marked fibrosis and sheets of fibrous tissue were seen extending to adjacent structures at twenty-eight days. Endoneurial invasion of mast cells and macrophages was noted, especially at twenty-eight days. Axonal degeneration was noted in the nerves sub- jected to 10.7 kilopascals of compression and, to a lesser extent, in those subjected to 4.0 kilopascals of compres- sion. It rarely was seen in the nerves subjected to 1.3 kilopascals of compression. Axonal degeneration was associated with the degree of endoneurial edema. De- myelination and Schwann-cell necrosis at seven and ten days was followed by remyelination at fourteen and twenty-eight days. Demyelination was prominent in the nerves subjected to 4.0 kilopascals of compres- sion and, to a lesser extent, in those subjected to1.3 kilo- pascals of compression.

The tension of the ligatures or the inner diameter of the tube generally was selected so that blood flow was not visibly restricted. The re- sponse of nerves to compression in these studies was similar to that in the experiments involving compression with a cuff. For example, the application of loose liga- tures around the sciatic nerve led to perineurial edema with proliferation of endothelial cells and demyelina- tion within the first few days, to proliferation of fibro- blasts and macrophages as well as degeneration of distal nerve fibers and the beginning of nerve sprouts within one week, to invasion by fibrous tissue and remyelina- tion at two weeks, to regeneration of nerve fibers as well as thickening of the perineurium and the vessel walls at six weeks, and to remyelination of distal nerve segments at twelve weeks73.

Applica- tion of silicone tubes with a wide internal diameter can induce increased expression of interleukin-1 and trans- forming growth factor beta-1 in the nerve cell bodies in the dorsal root ganglia, but the relevance of this finding remains to be clarified92. The limitations of these models are that (1) the effects of the tissue inflammatory reac- tion to the device (foreign-body reaction) usually are not considered but do occur29 and (2) it is not possible to measure or control the applied extraneural pressure. However, these observational studies provide some in- sight into the biological response of the nerve to chronic low-grade compression.

In a few case reports on patients in whom a nerve segment was resected, the nerve at the site of the injury was compared with a nerve at a site proximal or distal to the injury47,55,82. In each instance, there was thickening of the walls of the microvessels in the endo- neurium and perineurium as well as epineurial and peri- neurial edema, thickening, and fibrosis at the site of the injury. Thinning of the myelin also was noted, along with evidence of degeneration and regeneration of fibers. The patients in these reports had advanced stages of compression syndrome. Earlier in the course of the dis- ease, a segment of the nerve usually is compressed with disturbance of the microcirculation, which is restored immediately after transection of the flexor retinaculum. There is usually both an immediate and a delayed return of nerve function, indicating the importance of ischemia in the early stages of compression syndrome43.

The tissues that lie next to a nerve, within a confined space (for example, synovial tissue within the carpal tunnel), are more easily obtained and can provide infor- mation on the response of these tissues to compres- sion18,20,32,53,61,69,70,91.
The im- portant findings were increased edema and vascular sclerosis (endothelial thickening) in samples from the patients, who were between the ages of nineteen and seventy-nine years. Inflammatory cell infiltrates (lym- phocytes and histiocytes) were observed in only 10 per- cent (seventeen) of the 177 samples. Surprisingly, the prevalence of fibrosis (3 percent [five of 177]) was much lower than the prevalences of 33 percent (fifteen of forty-five) to 100 percent (twenty-one of twenty-one) reported in the other studies.

The initial symptoms of compres- sion of the median nerve at the wrist (carpal tunnel syndrome) usually are intermittent paresthesia and def- icits of sensation that occur primarily at night (stage I). These symptoms probably are due to changes in the intraneural microcirculation that are associated with some edema, which disappears during the day.
Progres- sive compression leads to more severe and constant symptoms that do not disappear during the day (stage II); these include paresthesia and numbness, impaired dexterity, and, possibly, muscle weakness. During this stage, the microcirculation may be altered throughout the day by edema and there may be morphological changes such as segmental demyelination.
In the final stage (stage III), there are more pronounced morpho- logical changes accompanied by degeneration of the nerve fibers; these changes manifest as constant pain with atrophy of the median-nerve-innervated thenar muscles and permanent sensory dysfunction.

In a study of the ulnar nerve at the elbow, localized areas of strain (nerve-stretching) of greater than 10 percent were observed in some cadav- eric arms83. A strain of 6 to 8 percent can limit blood flow in a nerve or can alter nerve function5,37,59.

Overview
First, elevated extraneural pressures can, within min- utes or hours, inhibit intraneural microvascular blood flow, axonal transport, and nerve function and also can cause endoneurial edema with increased intrafascicular pressure and displacement of myelin, in a dose-response manner. Pressures of 2.7 kilopascals (twenty millimeters of mercury) can limit epineurial blood flow, pressures of 4.0 kilopascals (thirty millimeters of mercury) can limit axonal transport and can cause nerve dysfunction and endoneurial edema, and pressures of 6.7 kilopascals (fifty millimeters of mercury) can alter the structure of myelin sheaths.

Second, on the basis of several animal models, it is apparent that low-magnitude, short-duration extraneu- ral pressure (for example, 4.0 kilopascals [thirty millime-
ters of mercury] applied for two hours) can initiate a process of nerve injury and repair and can cause struc- tural tissue changes that persist for at least one month.

The cascade of the bio- logical response to compression includes endoneurial edema, demyelination, inflammation, distal axonal de- generation, fibrosis, growth of new axons, remyelination, and thickening of the perineurium and endothelium. The degree of axonal degeneration is associated with the amount of endoneurial edema.

Third, in healthy people, non-neutral positions of the fingers, wrist, and forearm and loading of the fingertips can elevate extraneural pressure in the carpal tunnel in a dose-response manner. For example, fingertip pinch forces of five, ten, and fifteen newtons can elevate pres- sures to 4.0, 5.6, and 6.6 kilopascals

Fourth, in a rat model, exposure of the hindlimb to vibration for four to five hours per day for five days can cause intraneural edema, structural changes in my- elinated and unmyelinated fibers in the sciatic nerve, and functional changes both in nerve fibers and in non- neuronal cells.

Fifth, exposure to vibrating hand tools at work can lead to permanent nerve injury with structural neuronal changes in finger nerves as well as in the nerve trunks just proximal to the wrist. The relationships between the duration of exposure, the magnitude of the vibration, and structural changes in the nerve are unknown.

Processing of Vibrotactile Inputs From Hairy Skin by Neurons of the Dorsal Column Nuclei in the Cat

Nevner at det hårsekk-nerver som reagerer på lavfrekvent vibrasjon (<50 Hz) og at signalene blir sterkere med høyere intensitet. Spesielt ved lave frekvenser <20 Hz er grensen for aktivering av nerveendene lav, med sterkere aktivering ved høyere intensiteter. Lav frekvens, høy amplitude gir sterkest respons! Viser hvordan signalene går opp til hjernen.

http://m.jn.physiology.org/content/95/3/1451.full

Dynamically sensitive tactile neurons of the DCN the input of which came from hairy skin could be divided into two classes, one associated with hair follicle afferent (HFA) input, the other with Pacinian corpuscle (PC) input. The HFA-related class was most sensitive to low-frequency (<50 Hz) vibration and had a graded response output as a function of vibrotactile intensity changes.

In conclusion, the functional capacities of these two classes of cuneate neuron appear to account for behavioral vibrotactile frequency discriminative performance in hairy skin, in contrast to the limited capacities of vibrotactile-sensitive neurons within the spinocervical tract system.

However, tactile information derived from the hairy skin is well represented within the spinocervical pathwayBrown 1981; Brown and Franz 1969) and in the responses of neurons within its target structure, the lateral cervical nucleus (Craig and Tapper 1978; Downie et al. 1988), in addition to its substantial representation within the dorsal column-lemniscal pathway (Brown et al. 1974; Dykes et al. 1982; Golovchinsky 1980; Gordon and Jukes 1964; Perl et al. 1962).

Although tactile information from both the glabrous and hairy skin regions is conveyed over the dorsal column pathway to higher centers, there are known to be marked differences between these two skin regions in human vibrotactile detection thresholds with those on the hairy skin of the forearm being approximately an order of magnitude higher than those for the glabrous finger tips (Merzenich and Harrington 1969; Talbot et al. 1968).

At low vibrotactile frequencies (≤100 Hz), the input from hairy skin comes from afferents associated with hair follicles, the hair follicle afferent (HFA) fibers (Burgess et al. 1968; Merzenich and Harrington 1969), whereas that from glabrous skin arises from rapidly adapting intradermal receptors, known as Meissner corpuscles in primates (Brown and Iggo 1967; Talbot et al. 1968).

As neurons of this class had circumscribed RFs that remained stable on the skin surface, even when it was possible to displace the skin across the underlying tissues, and were most sensitive to vibration at low frequencies (usually <50 Hz), they appeared to derive their input selectively or predominantly from HFA fibers. The remaining dynamically sensitive neurons (15/36) could often be activated with manual tapping stimuli from widespread regions of the limb or even the experimental table, and in circumstances in which the skin could be displaced, it appeared that responsiveness was associated with subcutaneous sources.

The vibration-sensitive neurons with lowest vibrotactile thresholds at frequencies of ≤50 Hz appeared to be activated selectively by HFA inputs and displayed a graded responsiveness as a function of changes in vibration intensity. The impulse traces of Fig. 3 show the range of responsiveness for one HFA neuron and its gradation of output as a function of amplitude increases at vibration frequencies of 10–100 Hz. Responses occur sporadically on some cycles at low-amplitude, become more regular, and, at low vibration frequencies (≤20 Hz), give way to pairs or bursts of spikes on individual cycles at the higher amplitudes, such that the firing rates usually exceed the vibration frequency in this low range of stimulus frequencies.


Quantification of the response (in imp/s) as a function of the vibration amplitude permitted construction of stimulus-response relations (Fig. 4A) which, for a different, but representative neuron of this HFA-related type, show that thresholds are lowest (5–20 μm) in the frequency range 5–50 Hz

Furthermore, the graded relations apparent at 5–100 Hz in Fig. 4Afor this particular neuron, and, at 20 Hz, for seven different HFA-related neurons in Fig. 4B, ensure that, at these low frequencies, individual neurons of this class can contribute a sensitive signal of the changing intensity of vibrotactile perturbations in the hairy skin.


B: stimulus-response relations plotting, for another neuron, the mean response (imp/s) as a function of vibration amplitude at a range of frequencies.


A: values for 12 HFA neurons; B: 10 PC neurons; and C: for the mean ± SE threshold as a function of vibration frequency for the 2 classes.


Phaselocking of this neuron’s response was retained at frequencies ranging ≤75 Hz, but at higher frequencies, the failure rate increased on individual cycles, in particular, at vibration frequencies >30 Hz.


However, a switch-over occurs ∼50 Hz with values for HFA neurons falling below those for PC neurons at the higher frequencies.

The natural tactile stimuli most frequently encountered on the hairy skin of the arms and legs are likely to arise from objects brushing across the skin surface or its projecting hairs (e.g., see discussion in Gynther et al. 1995). These moving stimuli will set up various forms of complex vibrational disturbance in the skin that will generate spatiotemporal patterns of sensory inputs that we interpret as the nature and texture of the contacted object.

One dynamically sensitive class was most sensitive to vibration frequencies <50–80 Hz, had RFs within the hairy skin itself, and appeared to derive its peripheral input from the HFA class of afferent fibers.

The cuneate neurons driven selectively by the HFA class of peripheral afferents were most tightly phaselocked in response to vibratory disturbances in the hairy skin at frequencies ≤50 Hz. Furthermore, their impulse levels enabled them to respond at these frequencies in a cycle-by-cycle manner, thus replicating in their impulse pattern the periodicity inherent in the vibration stimulus.

The HFA-related class of cuneate neuron appeared to have a similar capacity for signaling vibrotactile frequency information to that of the RA class of neurons associated with low-frequency vibrotactile inputs from the glabrous skin (Connor et al. 1984; Douglas et al. 1978; Ferrington et al. 1987a, 1988) as percentage entrainment measures for responses to different vibration frequencies ≤50 Hz had average values in the range, 87–93%, for HFA neurons (Fig. 11) in comparison with values of ∼85–97% for RA neurons examined in an earlier study from our laboratory (Fig. 11B in Douglas et al. 1978).

The capacity to encode information about the frequency parameter of vibrotactile events in the impulse patterns of individual neurons appears to be well retained at the next level of the dorsal column-lemniscal pathway, in the ventralposterolateral (VPL) nucleus of the thalamus (Ghosh et al. 1992). From here, the information is conveyed over a parallel projection network to two principal cerebral cortical target regions, the primary and secondary somatosensory areas of the cortex (SI and SII, respectively) (Bennett et al. 1980; Ferrington and Rowe 1980b; Fisher et al. 1983; Mackie et al. 1996; Rowe et al. 1985; Turman et al. 1992, 1995; Zhang et al. 1996, 2001a,b).

This breakdown of a cycle-by-cycle impulse patterning at the cortical level for higher-frequency vibrotactile disturbances may mean (if impulse patterning is the crucial neural substrate for frequency recognition) that frequency coding in the range above ∼100 Hz may be dependent on a concatenation of thalamo-cortical events that include the presence of patterned activity at the thalamic level (Ghosh et al. 1992; Rowe 1990).

It is clear from both the earlier analyses of glabrous skin vibrotactile coding mechanisms in the DCN and from the present analysis for hairy skin that individual neurons in this tactile sensory pathway, relaying through the gracile and cuneate nuclei have a much greater capacity for signaling reliably the intensive and frequency parameters of vibrotactile stimuli than do their counterparts within the parallel spinocervical ascending system (Sahai et al. 2006).

Functional MRI of working memory and selective attention in vibrotactile frequency discrimination

Viktig studie som nevner hvordan vibrasjoner på huden påvirker tilsvarende område i hjernen og hvilken relasjon dette har til hukommelse og kinestetisk oppmerksomhet. De kaller det vibrotactile memory. Denne bekrefter også at 25Hz aktiverer Meissner corpulses første og fremst. Nevner også at tidperspektivet i stimuleringen er viktig siden det aktiverer bilateralt insula (har med prosessering av følelser å gjøre). Den nevner også at hjernens «default network» dempes når vi blir oppmerksomme på vibrasjon, ganske likt det som skjer når vi mediterer.

http://www.biomedcentral.com/1471-2202/8/48

Focal lesions of the frontal, parietal and temporal lobe may interfere with tactile working memory and attention. To characterise the neural correlates of intact vibrotactile working memory and attention, functional MRI was conducted in 12 healthy young adults.

These results support the notion that working memory and attention are organised in partly overlapping neural circuits. In contrast to previous reports in the visual or auditory domain, this study emphasises the involvement of the anterior insula in vibrotactile working memory and selective attention.

Faced with a continuous stream of afferent data, somatosensory processing requires not only the analysis of the properties of tactile stimuli, but also the extraction and encoding of novel, relevant information [1]. The integration of tactile information retrieved from cutaneous afferents, traditionally attributed to the primary (SI) and secondary somatosensory cortices (SII), has been extensively studied [2]. In contrast, the neural basis of tactile working memory and tactile selective attention is less well known.

These higher-level cognitive processes are nevertheless crucial for managing many challenges of every-day life. Pulling out a key from a coat pocket in the dark requires, amongst others, exploratory finger movements, attention to tactile information derived from the exploring hand (and not, e.g., from the other hand holding a bag), storage of this information in working memory, and integration of the successively obtained tactile information. Studies on patients with focal lesions suggest that the prefrontal cortex [3,4], right parietal cortex[5] and thalamus [6] are involved in the inhibition of task-irrelevant tactile information. Lesions of the medial temporal lobe, in contrast, have been shown to impair tactile working memory in patients [7].


Brain activation associated with processing of the probe. The figure shows brain activation and deactivation associated with the processing of the probe (either 25 Hz or higher) across all conditions (clustered activation images with an overall corrected p < 0.05). Activated areas are colour-coded in yellow and red, deactivated areas are displayed in blue. Activation is seen in the left cerebellar hemisphere (1), the bilateral anterior insula (2, 3), the bilateral head of the caudate nucleus and the globus pallidus (4, 5), the bilateral thalamus (6, 7), the right inferior frontal cortex (8), the anterior cingulate cortex (9), the left (contralateral) sensorimotor cortex (10), the right posterior parietal cortex (11) and the supplementary motor area (12). Deactivation was found in the right parahippocampal gyrus (13), the bilateral medial frontal gyrus (14), the right cuneus (15), the bilateral posterior cingulate gyrus (16), the bilateral precuneus (16) and the left superior frontal gyrus (17). Brain images are shown in radiological convention (the right hemisphere is seen on the left side of the image).

The results of the present study demonstrate that vibrotactile frequency discrimination is associated with the activation of distributed neural networks, in particular the central somatosensory pathways, the motor system, and the polymodal frontal, parietal and insular cortices (Fig. 1).

The chosen vibrotactile stimuli with a frequency around 25 Hz activate primarily Meissner’s corpuscles, located in the dermal-epidermal junction of the superficial glabrous skin [10].

Based on these reports, it is hypothesised that the bilateral anterior insula is involved in the analysis of the temporal aspects of vibrotactile stimuli. In support of this hypothesis, passive vibrotactile stimulation without discrimination between stimuli of different frequency [1318,30] did not activate the anterior insula.

Compared with baseline, vibrotactile frequency discrimination was associated with deactivation in the frontal cortex (medial and superior frontal gyrus), the cuneus, the precuneus, the parahippocampal area and the posterior cingulate gyrus (Fig 3). These areas probably reflect a widespread neuronal network that is consistently activated during rest or during less demanding tasks, termed the default mode network [31].

The present study demonstrates that vibrotactile frequency discrimination is associated with the activation of distributed neural circuits including the somatomotor system, and polymodal frontal, parietal, and insular areas.

Stimulus-dependent spatial patterns of response in SI cortex

Enda en viktig studie som viser hvordan vibrasjon-stimuli i huden påvirker tilsvarende område i hjernen. Går dypere inn i hva som spesifikt skjer i selve det aktiverte området. Legges til som ekstra referanse.

http://www.biomedcentral.com/1471-2202/6/47

Afferent projections from skin to primary somatosensory cortex (SI) are well known to form a fine map of the body surface in SI. In this map, a skin locus provides afferent input to an extensive cortical region in SI [1,2]. In particular, the direct connectivity between somatosensory thalamus and SI cortex is now recognized to be much more spatially distributed than previously believed (e.g., in primates the ventrobasal thalamic region which receives its input from a single digit projects to an extensive, 20 mm2 sector of SI cortex – [3,4]).

The intrinsic SI excitatory connections link not only neighboring but also widely separated regions of somatosensory cortex[5]. These connections ensure that many members of widely distributed neuronal populations interact extensively within milliseconds after the onset of stimulus-evoked thalamocortical drive. Thus it is not surprising to find that the processing of even a very local skin stimulus is associated with SI activation over several sq. millimeters of cortical area, as revealed, for example, with optical imaging techniques [610].

Together these considerations suggest that the spatial pattern of activity evoked in SI by even the smallest stimuli might be structurally more complex than a typically envisioned basic bell-shaped pattern. A closer inspection of such patterns might reveal certain spatial formations within them with significant functional implications.

Observations of the spatial patterns of SI cortical response within an activated region, such as those evoked by flutter stimulation of the skin, suggest that evoked cortical activity within such a territory is not evenly distributed. Furthermore, the cortical activity patterns change in a manner that appears to be dependent upon stimulus conditions. The observed spatiointensive fractionation on a sub-macrocolumnar scale of the SI response to skin stimulation might be the product of local competitive interactions within the stimulus-activated SI region, and as such can lead to new insights about the functional interactions that take place in the SI cortex.