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Journal ArticleDOI

REVIEW ■ : Reorganization of Sensory Systems of Primates after Injury:

01 Mar 1997-The Neuroscientist (SAGE Publications)-Vol. 3, Iss: 2, pp 123-130
TL;DR: The orderly representations of sensory surfaces in the brains of adult mammals have the capacity to reor ganize after injuries that deprive these representations of some of their normal sources of activation.
Abstract: The orderly representations of sensory surfaces in the brains of adult mammals have the capacity to reor ganize after injuries that deprive these representations of some of their normal sources of activation. Such reorganizations can be produced by injury that occurs peripherally, such as nerve damage or amputation, or after injury to the CNS, such as spinal cord damage or cortical lesion. These changes likely are mediated by a number of different mechanisms, and can be extensive and involve the growth of new connections. Finally, some types of reorganizations may help mediate the recovery of lost functions, whereas others may lead to sensory abnormalities and perceptual errors. NEUROSCIENTIST 3:123-130, 1997
Citations
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Journal ArticleDOI
TL;DR: Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function, and the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans.
Abstract: Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis). Evidence from numerous sources demonstrates that neural development extends from the embryonic period through adolescence. In general, the sequence of events is comparable among species, although the time scales are considerably different. Developmental exposure of animals or humans to numerous agents (e.g., X-ray irradiation, methylazoxymethanol, ethanol, lead, methyl mercury, or chlorpyrifos) demonstrates that interference with one or more of these developmental processes can lead to developmental neurotoxicity. Different behavioral domains (e.g., sensory, motor, and various cognitive functions) are subserved by different brain areas. Although there are important differences between the rodent and human brain, analogous structures can be identified. Moreover, the ontogeny of specific behaviors can be used to draw inferences regarding the maturation of specific brain structures or neural circuits in rodents and primates, including humans. Furthermore, various clinical disorders in humans (e.g., schizophrenia, dyslexia, epilepsy, and autism) may also be the result of interference with normal ontogeny of developmental processes in the nervous system. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function. This concern is compounded by the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans.

2,659 citations

Journal ArticleDOI
01 Jun 2000-Stroke
TL;DR: This is the first demonstration in humans of a long-term alteration in brain function associated with a therapy-induced improvement in the rehabilitation of movement after neurological injury.
Abstract: Background and Purpose—Injury-induced cortical reorganization is a widely recognized phenomenon. In contrast, there is almost no information on treatment-induced plastic changes in the human brain. The aim of the present study was to evaluate reorganization in the motor cortex of stroke patients that was induced with an efficacious rehabilitation treatment. Methods—We used focal transcranial magnetic stimulation to map the cortical motor output area of a hand muscle on both sides in 13 stroke patients in the chronic stage of their illness before and after a 12-day-period of constraint-induced movement therapy. Results—Before treatment, the cortical representation area of the affected hand muscle was significantly smaller than the contralateral side. After treatment, the muscle output area size in the affected hemisphere was significantly enlarged, corresponding to a greatly improved motor performance of the paretic limb. Shifts of the center of the output map in the affected hemisphere suggested the recru...

1,390 citations

Journal ArticleDOI
TL;DR: An animal model for investigating stimulus-induced rCBF responses in the rat is developed and it is shown that there is a progressive and selective activation of somatosensory and limbic system structures in the brain and brainstem following the subcutaneous injection of formalin.
Abstract: Pain is a unified experience composed of interacting discriminative, affective-motivational, and cognitive components, each of which is mediated and modulated through forebrain mechanisms acting at spinal, brainstem, and cerebral levels. The size of the human forebrain in relation to the spinal cord gives anatomical emphasis to forebrain control over nociceptive processing. Human forebrain pathology can cause pain without the activation of nociceptors. Functional imaging of the normal human brain with positron emission tomography (PET) shows synaptically induced increases in regional cerebral blood flow (rCBF) in several regions specifically during pain. We have examined the variables of gender, type of noxious stimulus, and the origin of nociceptive input as potential determinants of the pattern and intensity of rCBF responses. The structures most consistently activated across genders and during contact heat pain, cold pain, cutaneous laser pain or intramuscular pain were the contralateral insula and anterior cingulate cortex, the bilateral thalamus and premotor cortex, and the cerebellar vermis. These regions are commonly activated in PET studies of pain conducted by other investigators, and the intensity of the brain rCBF response correlates parametrically with perceived pain intensity. To complement the human studies, we developed an animal model for investigating stimulus-induced rCBF responses in the rat. In accord with behavioral measures and the results of human PET, there is a progressive and selective activation of somatosensory and limbic system structures in the brain and brainstem following the subcutaneous injection of formalin. The animal model and human PET studies should be mutually reinforcing and thus facilitate progress in understanding forebrain mechanisms of normal and pathological pain.

371 citations

Journal Article
TL;DR: In this article, magnetic source imaging revealed that the topographic representation in the somatosensory cortex of upper extremity amputees was shifted an average of 1.5 cm toward the area that would normally receive input from the now absent nerves supplying the hand and fingers.
Abstract: MAGNETIC source imaging revealed that the topographic representation in the somatosensory cortex of the face area in upper extremity amputees was shifted an average of 1.5 cm toward the area that would normally receive input from the now absent nerves supplying the hand and fingers. Observed alterat

348 citations

Journal ArticleDOI
TL;DR: The study indicates that oromandibular-facial trauma, including dental procedures, may precipitate the onset of OMD, especially in predisposed people, and prompt recognition and treatment may prevent further complications.
Abstract: OBJECTIVES—Oromandibular dystonia (OMD) is a focal dystonia manifested by involuntary muscle contractions producing repetitive, patterned mouth, jaw, and tongue movements. Dystonia is usually idiopathic (primary), but in some cases it follows peripheral injury. Peripherally induced cervical and limb dystonia is well recognised, and the aim of this study was to characterise peripherally induced OMD. METHODS—The following inclusion criteria were used for peripherally induced OMD: (1) the onset of the dystonia was within a few days or months (up to 1 year) after the injury; (2) the trauma was well documented by the patient's history or a review of their medical and dental records; and (3) the onset of dystonia was anatomically related to the site of injury (facial and oral). RESULTS—Twenty seven patients were identified in the database with OMD, temporally and anatomically related to prior injury or surgery. No additional precipitant other than trauma could be detected. None of the patients had any litigation pending. The mean age at onset was 50.11 (SD 14.15) (range 23-74) years and there was a 2:1 female preponderance. Mean latency between the initial trauma and the onset of OMD was 65 days (range 1 day-1 year). Ten (37%) patients had some evidence of predisposing factors such as family history of movement disorders, prior exposure to neuroleptic drugs, and associated dystonia affecting other regions or essential tremor. When compared with 21 patients with primary OMD, there was no difference for age at onset, female preponderance, and phenomenology. The frequency of dystonic writer's cramp, spasmodic dysphonia, bruxism, essential tremor, and family history of movement disorder, however, was lower in the post-traumatic group (p<0.05). In both groups the response to botulinum toxin treatment was superior to medical therapy (p<0.005). Surgical intervention for temporomandibular disorders was more frequent in the post-traumatic group and was associated with worsening of dystonia. CONCLUSION—The study indicates that oromandibular-facial trauma, including dental procedures, may precipitate the onset of OMD, especially in predisposed people. Prompt recognition and treatment may prevent further complications.

157 citations

References
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Journal ArticleDOI
30 Sep 1982-Nature
TL;DR: The present results demonstrate that the lesion-induced functional reorganization is brought about not by new axonal growth but probably by local changes at the periphery of the dendrites.
Abstract: Physiological mapping of the retino-geniculate projections in adult cats which had previously undergone partial retinal lesioning have demonstrated a delayed spread of excitation into regions initially deafferented1. Anatomical studies in the adult cat2–5 and monkey6 have, however, not revealed any new axonal growth. The present results demonstrate that the lesion-induced functional reorganization is brought about not by new axonal growth but probably by local changes at the periphery of the dendrites.

68 citations


Additional excerpts

  • ...These incomplete recoveries indicate that under some conditions of sensory deprivation, appreciable axonal growth, other than local synapse formation or redistribution, does not occur (18)....

    [...]

Book ChapterDOI
01 Jan 1976
TL;DR: Following deafferentation of both forelimbs by dorsal rhizotomy, motorically mature rhesus monkeys are able to make extensive use of the affected extremities, both for patterned activity (e.g., ambulation, climbing) and for independent use ofThe deafferentialed members.
Abstract: Following deafferentation of both forelimbs by dorsal rhizotomy, motorically mature rhesus monkeys are able to make extensive use of the affected extremities, both for patterned activity (e.g., ambulation, climbing) and for independent use of the deafferented members. Limb deafferentation does, however, result in a clearly apparent motor deficit, particularly in the fine control and timing of movement.

65 citations


"REVIEW ■ : Reorganization of Sensor..." refers background in this paper

  • ...arm, forearm, and hand, for a study of movement control in macaque monkeys (19), microelectrode recordings revealed that the extensive deprived zone in area 3b of somatosensory cortex (as well as those in adjoining somatosensory areas) had become completely reactivated by remaining sensory inputs, largely those from the face (Fig....

    [...]

Journal ArticleDOI
TL;DR: Experiments employing peripheral injuries or other manipulations indicate that these maps are capable of extensive reorganization, and a number of candidate mechanisms for these changes have been suggested, providing avenues for further research.

62 citations


"REVIEW ■ : Reorganization of Sensor..." refers background in this paper

  • ...eters, are dynamically maintained by the adjustments in the balance of excitatory and inhibitory events (4-7)....

    [...]

Journal ArticleDOI
TL;DR: There is somatotopic disorder both in the regenerated median nerve and in reactivated cortex, indicating that primary somatosensory cortex does not reorganize to compensate fully for peripheral reinnervation errors in these adult primates.
Abstract: The fidelity of median nerve regeneration and the consequent effects of regeneration errors on cortical organization were determined in combined anatomical and electrophysiological studies. In three adult macaque monkeys, the median nerve was cut, sutured, and allowed to regenerate for 7-13 months. After regeneration, distributions of afferents to the dorsal horn of the spinal cord and the cuneate nucleus of the brainstem were determined by making injections of horseradish peroxidase conjugates into the distal phalanges of digit 1 or 2. While label from a single digit on the normal hand was confined to the appropriate locations in the median nerve territories of the dorsal horn and cuneate nucleus, label from the reinnervated digits spread out to cover most of the median nerve territories in those structures. These results are consistent with the interpretation that some proportion of primary sensory fibers normally innervating other digits and pads of median nerve skin erroneously reinnervated the skin of the injected digits. In the same monkeys, microelectrodes were used to record from an array of closely spaced sites across the representation of the hand in area 3b of somatosensory cortex. The reactivation pattern was abnormal, with neurons at many recording sites having more than one receptive field, larger than normal receptive fields, or receptive fields at abnormal skin locations. Thus, there is somatotopic disorder both in the regenerated median nerve and in reactivated cortex, indicating that primary somatosensory cortex does not reorganize to compensate fully for peripheral reinnervation errors in these adult primates. Nevertheless, the organization of receptive fields in area 3b suggests the existence of some central selection of synapses.

62 citations


"REVIEW ■ : Reorganization of Sensor..." refers background in this paper

  • ...cause errors in nerve regeneration are relayed to cortex and they are largely uncorrected in adult primates (55)....

    [...]

Journal ArticleDOI
TL;DR: Parabrachial activation enhanced the visual responses of almost all geniculate cells, and this enhancement included both increased depth of modulation and greater response rates.
Abstract: 1. The lateral geniculate nucleus is the primary thalamic relay for the transfer of retinal signals to the visual cortex. Geniculate cells are heavily innervated from nonretinal sources, and these modify retinogeniculate transmission. A major ascending projection to the lateral geniculate nucleus arises from cholinergic cells in the parabrachial region of the brain stem. This is an important pathway in the ascending control of arousal. In an in vivo preparation, we used extracellular recordings to study the effects of electrical activation of the parabrachial region on the spontaneous activity and visual responses of X and Y cells in the lateral geniculate nucleus of the cat. 2. We studied the effects of two patterns of parabrachial activation on the spontaneous activity of geniculate cells. Burst stimulation consisted of a short pulse at high frequency (16 ms at 250 Hz). Train stimulation was of longer duration at lower frequency (e.g., 1 s at 50 Hz). The firing rate of almost all geniculate cells was enhanced by either pattern of stimulation. However, the burst pattern of stimulation elicited a short, modulated response with excitatory and inhibitory epochs. We found that the different epochs could differentially modulate the visual responses to drifting gratings. Thus the temporal alignment of the brain stem and visual stimuli was critical with burst stimulation, and varied alignments could dramatically confound the results. In comparison, the train pattern of stimulation consistently produced a relatively flat plateau of increased firing, after a short initial period of more variable effects. We used the less confounding pattern of train stimuli to study the effects of parabrachial activation on visual responses. 3. Our main emphasis was to examine the parabrachial effects on the visual responses of geniculate cells. For most visual stimuli, we used drifting sine wave gratings that varied in spatial frequency; these evoked modulated responses from the geniculate cells. Parabrachial activation enhanced the visual responses of almost all geniculate cells, and this enhancement included both increased depth of modulation and greater response rates. 4. Our results were incorporated quantitatively into a difference-of-Gaussians model of visual receptive fields in order to study the parabrachial effects on the spatial structure of the receptive field. This model fit our data well and provided measures of the response amplitude and radius of the receptive field center (Kc and Rc, respectively) and the response amplitude and radius of the receptive field surround (Ks and Rs, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)

61 citations