scholarly journals Passive Exercise of the Hind Limbs after Complete Thoracic Transection of the Spinal Cord Promotes Cortical Reorganization

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e54350 ◽  
Author(s):  
Alessandro Graziano ◽  
Guglielmo Foffani ◽  
Eric B. Knudsen ◽  
Jed Shumsky ◽  
Karen A. Moxon
2015 ◽  
Vol 30 (5) ◽  
pp. 479-489 ◽  
Author(s):  
Guglielmo Foffani ◽  
Jed Shumsky ◽  
Eric B. Knudsen ◽  
Patrick D. Ganzer ◽  
Karen A. Moxon

Background. In rat models of spinal cord injury, at least 3 different strategies can be used to promote long-term cortical reorganization: (1) active exercise above the level of the lesion; (2) passive exercise below the level of the lesion; and (3) serotonergic pharmacotherapy. Whether and how these potential therapeutic strategies—and their underlying mechanisms of action—interact remains unknown. Methods. In spinally transected adult rats, we compared the effects of active exercise above the level of the lesion (treadmill), passive exercise below the level of the lesion (bike), serotonergic pharmacotherapy (quipazine), and combinations of the above therapies (bike+quipazine, treadmill+quipazine, bike+treadmill+quipazine) on long-term cortical reorganization (9 weeks after the spinal transection). Cortical reorganization was measured as the percentage of cells recorded in the deafferented hindlimb cortex that responded to tactile stimulation of the contralateral forelimb. Results. Bike and quipazine are “competing” therapies for cortical reorganization, in the sense that quipazine limits the cortical reorganization induced by bike, whereas treadmill and quipazine are “collaborative” therapies, in the sense that the reorganization induced by quipazine combined with treadmill is greater than the reorganization induced by either quipazine or treadmill. Conclusions. These results uncover the interactive effects between active/passive exercise and serotonergic pharmacotherapy on cortical reorganization after spinal cord injury, emphasizing the importance of understanding the effects of therapeutic strategies in spinal cord injury (and in other forms of deafferentation) from an integrated system-level approach.


Development ◽  
1982 ◽  
Vol 72 (1) ◽  
pp. 269-286
Author(s):  
N. G. Laing

Counts were made of the number of motoneurons innervating the hind limbs of 10-day normal and paralysed chick embryos whose right hind limb buds had been subjected to varying degrees of amputation prior to innervation. The number of motoneurons on the intact sides of the paralysed embryos was found to be similar to the number present in normal embryos prior to the major period of motoneuron death. Since it has previously been shown that paralysis does not increase the number of motoneurons generated, this means that normal motoneuron death was largely prevented in the paralysed embryos. There were differences in the distributions of motoneurons in the rostrocaudal axis of the spinal cord between normal and paralysed embryos. Therefore, cell death does not eliminate a uniform fraction of motoneurons throughout the rostrocaudal extent of the chick embryo lumbar lateral motor column. It is also argued that there are differences in the relative contribution of the various lumbosacral levels to different parts of the limb, e.g. the shank, before and after the period of cell death. In both normal and paralysed embryos there was a linear relationship between the volume of limb muscle which developed after amputation and the number of motoneurons surviving in the spinal cord. There was no evidence of a ‘compression’ of motoneurons into the remaining muscle either after amputation alone or after amputation combined with paralysis. Motoneurons are therefore rigidly specified for certain parts of the limb. The relationship between motoneuron number and muscle volume on the amputated side differed from that of the intact side. For a similar increase in muscle volume there was a smaller increase in motoneuron number on the intact sides. This suggested a parallel to the paradoxically small increase in motoneuron number that occurs on the addition of a supernumerary limb.


2017 ◽  
Vol 37 (6) ◽  
pp. 561-569
Author(s):  
Paulo V. Peixoto ◽  
Krishna D. Oliveira ◽  
Ticiana N. França ◽  
David Driemeier ◽  
Marcos D. Duarte ◽  
...  

ABSTRACT: Following a case of iatrogenic selenium poisoning in a young pig, an experimental study was carry out. Sodium selenite was orally and parenterally administered to 13 pigs that were subdivided into three groups (G1, G2 and G3). The animals in groups G1 and G3 received sodium selenite intramuscularly (IM), G1 received a comercial formula, and G3 received sodium selenite mixed with distilled water at different dosages, and those in group G2 were fed commercial sodium selenite. Acute and subacute poisoning was observed in both groups, although the onset of clinical signs was slower in group G2. Only one pig (in group G1) that had received the highest dose showed a peracute course. Apathy, anorexia, dyspnea, vomiting, muscular tremors, proprioceptive deficit, ataxia and paresis of the hind limbs progressing to the front limbs evolving to tetraplegia were observed. Postmortem findings differed whether the animals received the injected (G1 and G3) or oral (G2) sodium selenite. The liver was moderately atrophic in some animals of G2. Some of the animals in groups G1 and G3 presented with lung edema. One pig in G3 had yellowish-brown areas in the ventral horns of the cervical intumescences of the spinal cord. The most important histological changes were present in the ventral horns of the cervical and lumbar intumescences of the spinal cord. In one animal, changes were present in the brainstem and mesencephalon. The initial lesion was a perivascular and astrocyte edema that progressing to lysis and death of astrocytes and neurons. In the chronic stage of the lesions, there were extensive areas of liquefaction necrosis with perivascular lymphocytic and histiocytic infiltration and occasional eosinophils. It seems that disruption of the blood-brain barrier due to astrocyte edema is the most likely mechanism of CNS lesion.


F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 921 ◽  
Author(s):  
Norman R. Saunders ◽  
Katarzyna M. Dziegielewska ◽  
Sophie C. Whish ◽  
Lyn A. Hinds ◽  
Benjamin J. Wheaton ◽  
...  

Background: Most animal studies of spinal cord injury are conducted in quadrupeds, usually rodents. It is unclear to what extent functional results from such studies can be translated to bipedal species such as humans because bipedal and quadrupedal locomotion involve very different patterns of spinal control of muscle coordination. Bipedalism requires upright trunk stability and coordinated postural muscle control; it has been suggested that peripheral sensory input is less important in humans than quadrupeds for recovery of locomotion following spinal injury. Methods: We used an Australian macropod marsupial, the tammar wallaby (Macropus eugenii), because tammars exhibit an upright trunk posture, human-like alternating hindlimb movement when swimming and bipedal over-ground locomotion. Regulation of their muscle movements is more similar to humans than quadrupeds. At different postnatal (P) days (P7–60) tammars received a complete mid-thoracic spinal cord transection. Morphological repair, as well as functional use of hind limbs, was studied up to the time of their pouch exit. Results: Growth of axons across the lesion restored supraspinal innervation in animals injured up to 3 weeks of age but not in animals injured after 6 weeks of age. At initial pouch exit (P180), the young injured at P7-21 were able to hop on their hind limbs similar to age-matched controls and to swim albeit with a different stroke. Those animals injured at P40-45 appeared to be incapable of normal use of hind limbs even while still in the pouch. Conclusions: Data indicate that the characteristic over-ground locomotion of tammars provides a model in which regrowth of supraspinal connections across the site of injury can be studied in a bipedal animal. Forelimb weight-bearing motion and peripheral sensory input appear not to compensate for lack of hindlimb control, as occurs in quadrupeds. Tammars may be a more appropriate model for studies of therapeutic interventions relevant to humans.


2014 ◽  
Vol 66 (5) ◽  
pp. 1323-1328
Author(s):  
P.V.T. Marinho ◽  
C.C. Zani ◽  
P.C. Jark ◽  
B.W. Minto ◽  
M.T. Costa

This study aimed to describe in detail the surgical technique of partial lateral corpectomy (PLC) associated with pediculectomy to treat an in vitroextradural chondroma. A 12-year old female Cocker Spaniel was seen in the hospital with proprioceptive ataxia of hind limbs associated with extradural compression between the 1st and 2nd lumbar vertebrae. The owner opted for euthanasia since the patient's condition changed due to simultaneous illnesses that culminated in a poor prognosis. The patient's body was formally ceded to perform experimental spinal decompression. The technique was effective to completely remove the epidural mass with minimal manipulation of the spinal cord.


2016 ◽  
Vol 40 (6) ◽  
pp. E2 ◽  
Author(s):  
Indira Devi Bhagavatula ◽  
Dhaval Shukla ◽  
Nishanth Sadashiva ◽  
Praveen Saligoudar ◽  
Chandrajit Prasad ◽  
...  

OBJECTIVE The physiological mechanisms underlying the recovery of motor function after cervical spondylotic myelopathy (CSM) surgery are poorly understood. Neuronal plasticity allows neurons to compensate for injury and disease and to adjust their activities in response to new situations or changes in their environment. Cortical reorganization as well as improvement in corticospinal conduction happens during motor recovery after stroke and spinal cord injury. In this study the authors aimed to understand the cortical changes that occur due to CSM and following CSM surgery and to correlate these changes with functional recovery by using blood oxygen level–dependent (BOLD) functional MRI (fMRI). METHODS Twenty-two patients having symptoms related to cervical cord compression due to spondylotic changes along with 12 age- and sex-matched healthy controls were included in this study. Patients underwent cervical spine MRI and BOLD fMRI at 1 month before surgery (baseline) and 6 months after surgery. RESULTS Five patients were excluded from analysis because of technical problems; thus, 17 patients made up the study cohort. The mean overall modified Japanese Orthopaedic Association score improved in patients following surgery. Mean upper-extremity, lower-extremity, and sensory scores improved significantly. In the preoperative patient group the volume of activation (VOA) was significantly higher than that in controls. The VOA after surgery was reduced as compared with that before surgery, although it remained higher than that in the control group. In the preoperative patient group, activations were noted only in the left precentral gyrus (PrCG). In the postoperative group, activations were seen in the left postcentral gyrus (PoCG), as well as the PrCG and premotor and supplementary motor cortices. In postoperative group, the VOA was higher in both the PrCG and PoCG as compared with those in the control group. CONCLUSIONS There is over-recruitment of sensorimotor cortices during nondexterous relative to dexterous movements before surgery. After surgery, there was recruitment of other cortical areas such as the PoCG and premotor and supplementary motor cortices, which correlated with improvement in dexterity, but activation in these areas was greater than that found in controls. The results show that improvement in dexterity and finer movements of the upper limbs is associated with recruitment areas other than the premotor cortex to compensate for the damage in the cervical spinal cord.


2000 ◽  
Vol 97 (26) ◽  
pp. 14703-14708 ◽  
Author(s):  
C. I. Moore ◽  
C. E. Stern ◽  
C. Dunbar ◽  
S. K. Kostyk ◽  
A. Gehi ◽  
...  

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Anitha Manohar ◽  
Guglielmo Foffani ◽  
Patrick D Ganzer ◽  
John R Bethea ◽  
Karen A Moxon

After paralyzing spinal cord injury the adult nervous system has little ability to ‘heal’ spinal connections, and it is assumed to be unable to develop extra-spinal recovery strategies to bypass the lesion. We challenge this assumption, showing that completely spinalized adult rats can recover unassisted hindlimb weight support and locomotion without explicit spinal transmission of motor commands through the lesion. This is achieved with combinations of pharmacological and physical therapies that maximize cortical reorganization, inducing an expansion of trunk motor cortex and forepaw sensory cortex into the deafferented hindlimb cortex, associated with sprouting of corticospinal axons. Lesioning the reorganized cortex reverses the recovery. Adult rats can thus develop a novel cortical sensorimotor circuit that bypasses the lesion, probably through biomechanical coupling, to partly recover unassisted hindlimb locomotion after complete spinal cord injury.


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