Reorganization Of Somatosensory Cortex Research Articles

Rapid Bidirectional Reorganization of Cortical Microcircuits.

Mature neocortex adapts to altered sensory input by changing neural activity in cortical circuits. The underlying cellular mechanisms remain unclear. We used blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) to show reorganization in somatosensory cortex elicited by altered whisker sensory input. We found that there was rapid expansion followed by retraction of whisker cortical maps. The cellular basis for the reorganization in primary somatosensory cortex was investigated with paired electrophysiological recordings in the periphery of the expanded whisker representation. During map expansion, the chance of finding a monosynaptic connection between pairs of pyramidal neurons increased 3-fold. Despite the rapid increase in local excitatory connectivity, the average strength and synaptic dynamics did not change, which suggests that new excitatory connections rapidly acquire the properties of established excitatory connections. During map retraction, entire excitatory connections between pyramidal neurons were lost. In contrast, connectivity between pyramidal neurons and fast spiking interneurons was unchanged. Hence, the changes in local excitatory connectivity did not occur in all circuits involving pyramidal neurons. Our data show that pyramidal neurons are recruited to and eliminated from local excitatory networks over days. These findings suggest that the local excitatory connectome is dynamic in mature neocortex.

Large-scale reorganization of the somatosensory cortex following spinal cord injuries is due to brainstem plasticity

Adult mammalian brains undergo reorganization following deafferentations due to peripheral nerve, cortical or spinal cord injuries. The largest extent of cortical reorganization is seen in area 3b of the somatosensory cortex of monkeys with chronic transection of the dorsal roots or dorsal columns of the spinal cord. These injuries cause expansion of intact face inputs into the deafferented hand cortex, resulting in a change of representational boundaries by more than 7 mm. Here we show that large-scale reorganization in area 3b following spinal cord injuries is due to changes at the level of the brainstem nuclei and not due to cortical mechanisms. Selective inactivation of the reorganized cuneate nucleus of the brainstem eliminates observed face expansion in area 3b. Thus, the substrate for the observed expanded face representation in area 3b lies in the cuneate nucleus.

Rapid Experience-Dependent Plasticity following Somatosensory Damage

Studies in nonhuman primates have provided evidence of rapid neural reorganization in somatosensory cortex after brain damage [1] and amputation [2]. Furthermore, there is also evidence of experience-dependent plasticity in both human [3-5] and nonhuman primates [6] that is induced by repetitive tactile stimulation. Given the evidence of plasticity subsequent to both neural damage and tactile experience, we hypothesized that somatosensory damage could lead to increased levels of experience-dependent tactile plasticity. To examine this hypothesis, the tactile localization judgments of two individuals with left hemisphere somatosensory damage subsequent to stroke were examined. Suprathreshold tactile stimuli were presented to the hand or forearm, and the effect of the location of previous stimulation on localization judgments for subsequent stimuli was examined. Results showed that, only on the contralesional limb, even a single tactile stimulation could induce a significant perceptual shift in localization judgments for subsequent stimuli, with shifts occurring in the direction of the preceding stimulation. These results provide novel evidence of a very rapid time course for substantive perceptual changes in tactile location perception in response to simple stimulation, revealing a highly plastic and dynamic tactile system even many years after neural damage.

Síndrome del miembro fantasma: aproximación terapéutica mediante el tratamiento espejo. Experiencia de un Servicio de Geriatría

The clinical use of mirror visual feedback was initially introduced to alleviate phantom pain by restoring motor function through plastic changes in the human primary motor cortex. It is a promising novel technique that gives a new perspective to neurological rehabilitation. Using this therapy, the mirror neuron system is activated and decrease the activity of those systems that perceive protopathic pain, making somatosensory cortex reorganization possible. This paper reports the results of the mirror therapy in three patients with phantom limb pain after recent lower limb amputation, showing its analgesic effects and its benefits as a comprehensive rehabilitation instrument for lower limb amputee geriatric patients.

Pain and Plasticity: Is Chronic Pain Always Associated with Somatosensory Cortex Activity and Reorganization?

The somatosensory cortex remodels in response to sensory deprivation, with regions deprived of input invaded by neighboring representations. The degree of cortical reorganization is correlated with ongoing pain intensity, which has led to the assumption that chronic pain conditions are invariably associated with somatosensory cortex reorganization. Because the presentation and etiology of chronic pain vary, we determined whether cortical changes in human subjects are similar for differing pain types. Using functional and anatomical magnetic resonance imaging, we found that, while human patients with neuropathic pain displayed cortical reorganization and changes in somatosensory cortex activity, patients with non-neuropathic chronic pain did not. Furthermore, cortical reorganization in neuropathic pain patients was associated with changes in regional anatomy. These data, by showing that pain per se is not associated with cortical plasticity, suggest that treatments aimed at reversing cortical reorganization should only be considered for use in patients with certain types of chronic pain.

High Frequency Sensory Stimulation Improves Tactile but Not Motor Performance in Older Adults

We examined the effect of high frequency tactile stimulation (tHFS) on tactile and motor performance as well as tactile-motor interactions. Seventeen right-handed participants (66-78 years) underwent a pretest (tactile frequency and spatial discrimination task, manual dexterity test, and precision grip task) with their left hand, received 30 min of tHFS on the tips of their left index finger and thumb, and performed a posttest (control group: no stimulation). Results indicated an improvement in frequency and spatial discrimination in the experimental but not the control group. In the precision grip task, however, training effects as found for the control group seem to be blocked in the experimental group. For the manual dexterity task no effect was found. Our data indicate that tHFS positively influences tactile performance. Assuming tHFS-induced plastic reorganization in somatosensory cortex our results give further evidence to the notion of an interrelation between sensory and motor performance.

Somatosensory cortex reorganization linked to neuropathic pain

Somatosensory cortex reorganization linked to neuropathic pain

Neuropathic pain and primary somatosensory cortex reorganization following spinal cord injury

The most obvious impairments associated with spinal cord injury (SCI) are loss of sensation and motor control. However, many subjects with SCI also develop persistent neuropathic pain below the injury which is often severe, debilitating and refractory to treatment. The underlying mechanisms of persistent neuropathic SCI pain remain poorly understood. Reports in amputees describing phantom limb pain demonstrate a positive correlation between pain intensity and the amount of primary somatosensory cortex (S1) reorganization. Of note, this S1 reorganization has also been shown to reverse with pain reduction. It is unknown whether a similar association between S1 reorganization and pain intensity exists in subjects with SCI. The aim of this investigation was to determine whether the degree of S1 reorganization following SCI correlated with on-going neuropathic pain intensity. In 20 complete SCI subjects (10 with neuropathic pain, 10 without neuropathic pain) and 21 control subjects without SCI, the somatosensory cortex was mapped using functional magnetic resonance imaging during light brushing of the right little finger, thumb and lip. S1 reorganization was demonstrated in SCI subjects with the little finger activation point moving medially towards the S1 region that would normally innervate the legs. The amount of S1 reorganization in subjects with SCI significantly correlated with on-going pain intensity levels. This study provides evidence of a link between the degree of cortical reorganization and the intensity of persistent neuropathic pain following SCI. Strategies aimed at reversing somatosensory cortical reorganization may have therapeutic potential in central neuropathic pain.

Differences in Low Back Pain Behavior Are Reflected in the Cerebral Response to Tactile Stimulation of the Lower Back

Two groups of patients with chronic low back pain (cLBP) were scanned with functional magnetic resonance imaging during stimulation of the lower back; those showing 4 or 5 positive Waddell signs (WS-H) and those showing 1 or none (WS-L) as an index of pain-related illness behavior. We hypothesized that patients showing good versus poor adjustment to cLBP mobilize cortical affective-cognitive functions differently in response to sensory stimulation and show increased reorganization of somatosensory cortex corresponding to the back. Some patients with cLBP go on to develop significant disability while the majority do not, and physical disease or psychosocial factors alone do not account for the difference. Neuroimaging studies have suggested abnormalities in cortical pain modulation systems can lead to variable pain and behavioral responses, which may account for these differences. METHODS.: Fifteen WS-L and 13 WS-H patients were scanned with functional magnetic resonance imaging while receiving intense tactile stimulation to the lower back. Questionnaire measures of psychosocial function were also collected. There were no significant differences in cLBP duration or lumbar stimulation tolerance threshold between the 2 groups. Significantly more activation was seen in the WS-L versus WS-H group in regions previously associated with normal affective-cognitive processing of sensory input including posterior cingulate and parietal cortices; the magnitude of this activation negatively correlated with catastrophizing scores. WS-H patients showed a modest medial shift in primary somatosensory cortex activation relative to the WS-L group. Successful adjustment to cLBP is associated with a patient's ability to effectively engage a sensory modulation system. In patients in whom such activation does not occur, subjective lack of control maypredispose to altered affective and behavioral responses with poor adjustment to pain. Pain experience may be furthermodified by reorganization of somatosensory cortex, contributing to maintenance of the chronic pain state.

PHANTOM ARM AND LEG AFTER PONTINE HEMORRHAGE

The phantom limb appears not only after limb amputation1 but also after brain damage (known as supernumerary phantom limb [SPL]).2 A previous review1 on phantom limb following limb amputation proposed the remapping hypothesis of topographic reorganization of somatosensory cortex in which the referred sensation from the neighboring receptive field to phantoms is one of at least five possible sources for phantom sensation. On the other hand, the current theories of SPL emphasize the dissociation between established sensorimotor limb representation and marked changes in afferent and efferent signals in brain–limb communication.3,4 There is little information about SPL in patients with brainstem damage,5 which has somewhat different characteristics from phantom sensations following supratentorial cerebral lesions, as well as from phantoms following limb amputation. Here we address the contribution of the brainstem to SPL. ### Case reports. A 47-year-old woman (Case 1) and a 55-year-old man (Case 2) developed acute pontine hemorrhage (figure, A [a, b] and B [a, b]). They survived a locked-in period with complete paralysis except for vertical eye movements. The neurologic examination …

Improving human haptic performance in normal and impaired human populations through unattended activation-based learning

Human haptic performance is not fixed, but subject to major alterations through learning processes. We describe a new stimulation protocol that allows to improve haptic performance in humans in a highly systemic way through unattended activation-based learning. The so-called coactivation protocol is based upon temporal constraints of Hebbian learning where simultaneity plays a key role for the induction of plastic changes. We provide an overview about the potential of coactivation by summarizing recent findings showing that coactivation alters a broad range of basic as well as cognitively demanding types of haptic performance in parallel to cortical reorganization in somatosensory cortex. For example, coactivation applied to the tip of the index finger, or to all fingers of the dominant hand improves tactile acuity, but also haptic object recognition, and speeds up multiple-choice reaction times. Because such changes persist between 24 h and 1 week without further intervention, we interpret the underlying processes as a particular form of perceptual learning. We describe results where coactivation has been utilized for therapeutical purposes in impaired human populations, we outline new developments to optimize and extend unattended activation-based learning protocols, and we sketch the next steps necessary to apply the concept of unattended activation-based learning on a regular and reliable basis as a therapeutical tool in order to selectively interfere with impaired haptic performance.

Poster 35: High-resolution electroencephalography and reorganization of posterior cortical potentials

Objective: To test whether reorganization after spinal cord lesions is “unfavorable” because of a takeover of cortical areas representing weak or paralyzed muscles. Design: Randomized study of electroencephalograms. Setting: Spinal cord research laboratory. Participants: 16 patients with spinal cord lesions and 10 normal controls. Interventions: Subjects were instructed in moving their right middle or index fingers. The fingers were also moved in a similar manner by an operator. Voluntary movement was monitored by electromyography. Main Outcome Measures: Movement-related cortical potentials and passive movements. Results: Posterior cortical reorganization represented reinforcement of residual motor pathways from somatosensory cortex (S1) to the spinal cord, and facilitated rehabilitation. Conclusion: Motor potentials can be generated by active and passive measurements of the fingers. Reorganization of somatosensory cortex is important in deriving potentials from proprioceptive input and creating the necessary templates to activate the motor networks and electroencephalographic activity.

Multimodality functional imaging evaluation in a patient with Rasmussen's encephalitis

Rasmussen's encephalitis (RE) is a cryptogenic progressive inflammatory disorder of the brain that causes severe neurological problems, including intractable focal epilepsy. In select patients, aggressive treatment using cerebral hemispherectomy may ameliorate the devastating cognitive decline that accompanies this disease, even if the epileptic focus appears broadly distributed. We present a case of histopathologically-confirmed RE evaluated using a multimodal process that explored the physical and functional aspects of the associated epilepsy. This process included magnetic resonance imaging, single photo emission computed tomography, electroencephalography, and magnetoencephalography (MEG). The findings indicate that functional brain imaging data may greatly assist the surgical treatment decision-making process in RE, especially when structural imaging fails to reveal definitive localizing information. In addition, MEG may provide insights about the cortical reorganization of somatosensory cortex following hemispherectomy.

The effect of opioids on phantom limb pain and cortical reorganization

The efficacy of oral retarded morphine sulphate (MST ®) was tested against placebo in a double-blind crossover design in 12 patients with phantom limb pain after unilateral leg or arm amputation. Two counterbalanced treatment phases of 4 weeks each were initiated with an intravenous test infusion of MST ® or Placebo. The titration phase was 2 weeks. The dose of MST ® was titrated to at least 70 mg/day and at highest 300 mg/day. Pain intensity was assessed hourly on visual analog scales during a 4-week treatment-free phase, both treatment phases and at two follow-ups (6 and 12 months). Reorganization of somatosensory cortex, electric perception and pain thresholds as well as selective attention were measured pre- and post-treatment. A significant pain reduction was found during MST ® but not during placebo. A clinically relevant response to MST ® (pain reduction of more than 50%) was evident in 42%, a partial response (pain reduction of 25–50%) in 8% of the patients. Neuromagnetic source imaging of three patients showed initial evidence for reduced cortical reorganization under MST ® concurrent with the reduction in pain intensity. Perception and pain thresholds were not significantly altered whereas attention was significantly lower under MST ®. Thus, opioids show efficacy in the treatment of phantom limb pain and may potentially influence also cortical reorganization. These data need to be replicated in larger patient samples.

Computational model of topographic reorganization in somatosensory cortex in response to digit lesions

A biologically plausible computational model of the somatosensory system which allows the study of processes related to the reorganization of somatotopic maps was developed. The model was constructed with an input layer of tactile receptors (hand) connected to a cortical layer of pyramidal and basket cells (layer IV of area 3 b). After the formation of a map in the cortical area, the skin model was lesioned and reorganization was allowed to proceed. The results show that the model is capable of reproducing the formation of the somatotopic maps of the hand with patterns of cortical reorganization similar to those observed in primates.

Large-scale sprouting of cortical connections after peripheral injury in adult macaque monkeys.

Distributions of thalamic and cortical connections were investigated in four macaque monkeys with long-standing, accidental trauma to a forelimb, to determine whether the growth of new connections plays a role in the reorganization of somatosensory cortex that occurs after major alterations in peripheral somatosensory inputs. In each monkey, microelectrode recordings of cortical areas 3b and 1 demonstrated massive reorganizations of the cortex related to the affected limb. Injections of tracers in area 1 of these monkeys revealed normal patterns of thalamocortical connections, but markedly expanded lateral connections in areas 3b and 1. Thus, the growth of intracortical but not thalamocortical connections could account for much of the reorganization of the sensory maps in cortex.

Reorganization of Somatosensory Cortex After Nerve and Spinal Cord Injury

Somatotopic maps in the mature brain reorganize in response to deafferentation by peripheral nerve cut, amputations, or spinal lesions. Mechanisms underlying these changes may range from altered tonic inhibition and synaptic efficacy to neuronal sprouting. An understanding of these mechanisms could guide interventions that potentiate recovery from such injuries.

Perceptual significance of somatosensory cortical reorganization following peripheral denervation.

The functional significance of reorganization in somatosensory cortex following peripheral denervation has not been thoroughly addressed. In this paper, two distinct hypotheses dealing with this issue are discussed. The first is the hypothesis of functional respecification. This influential view suggests that sets of partially deafferented cortical neurons, which respond to new peripheral inputs and acquire new receptive fields, undergo corresponding changes in perceptual meaning. Excitation of these neurons by stimulation of their novel receptive fields is thought to result in a change in referral of sensation from the original (now denervated) skin fields to the newly acquired skin fields. The second hypothesis is that of functional conservation. This equally plausible alternative is that sets of partially deprived neurons, although they respond to novel peripheral inputs, retain their original perceptual meaning. Excitation of these neurons by stimulation of their new receptive fields is thought to evoke sensation formerly mediated by those neurons, and hence is still projected to the original, now denervated skin regions or phantom. Behavioral evidence strongly suggests that cortical reorganization after peripheral denervation does not result in major functional respecification, but that the original perceptual function mediated by those neurons is preserved.

Effects of Regional Anesthesia on Phantom Limb Pain Are Mirrored in Changes in Cortical Reorganization

The causes underlying phantom limb pain are still unknown. Recent studies on the consequences of nervous system damage in animals and humans reported substantial reorganization of primary somatosensory cortex subsequent to amputation, and one study showed that cortical reorganization is positively correlated with phantom limb pain. This paper examined the hypothesis of a functional relationship between cortical reorganization and phantom limb pain. Neuroelectric source imaging was used to determine changes in cortical reorganization in somatosensory cortex after anesthesia of an amputation stump produced by brachial plexus blockade in six phantom limb pain patients and four pain-free amputees. Three of six phantom limb subjects experienced a virtual elimination of current phantom pain attributable to anesthesia (mean change: 3.8 on an 11-point scale; Z = -1.83; p < 0.05) that was mirrored by a very rapid elimination of cortical reorganization in somatosensory cortex (change = 19.8 mm; t(2) = 5.60; p < 0.05). Cortical reorganization remained unchanged (mean change = 1.6 mm) in three phantom limb pain amputees whose pain was not reduced by brachial plexus blockade and in the phantom pain-free amputation controls. These findings suggest that cortical reorganization and phantom limb pain might have a causal relationship. Methods designed to alter cortical reorganization should be examined for their efficacy in the treatment of phantom limb pain.

Networks with lateral connectivity. III. Plasticity and reorganization of somatosensory cortex.

1. Mechanisms underlying cortical reorganizations were studied using a three-layered neural network model with neuronal groups already formed in the cortical layer. 2. Dynamic changes induced in cortex by behavioral training or intracortical microstimulation (ICMS) were simulated. Both manipulations resulted in reassembly of neuronal groups and formation of stimulus-dependent assemblies. Receptive fields of neurons and cortical representation of inputs also changed. Many neurons that had been weakly responsive or silent became active. 3. Several types of learning models were examined in simulating behavioral training, ICMS-induced dynamic changes, deafferentation, or cortical lesion. Each learning model most accurately reproduced features of experimental data from different manipulations, suggesting that more than one plasticity mechanism might be able to induce dynamic changes in cortex. 4. After skin or cortical stimulation ceased, as spontaneous activity continued, the stimulus-dependent assemblies gradually reverted into structure-dependent neuronal groups. However, relationships among individual neurons and identities of many neurons did not return to their original states. Thus a different set of neurons would be recruited by the same training stimulus sequence on its next presentation. 5. We also reproduced several typical long-term reorganizations caused by pathological manipulations such as cortical lesions, input loss, and digit fusion. 6. In summary, with Hebbian plasticity rules on lateral connections, the network model is capable of reproducing most characteristics of experiments on cortical reorganization. We propose that an important mechanism underlying cortical plastic changes is formation of temporary assemblies that are related to receipt of strongly synchronized localized input. Such stimulus-dependent assemblies can be dissolved by spontaneous activity after removal of the stimuli.