scholarly journals Coordinated expression of the renin‐angiotensin genes in the lumbar spinal cord: lateralization and effects of unilateral brain injury

2021 ◽  
Author(s):  
Georgy Bakalkin ◽  
Anika Kahle ◽  
Daniil Sarkisyan ◽  
Hiroyuki Watanabe ◽  
Nikolay Lukoyanov ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Brain Injury ◽  
Lumbar Spinal Cord ◽  
Renin Angiotensin ◽  
Coordinated Expression ◽  
Lumbar Spinal ◽  
Unilateral Brain

scholarly journals Focal traumatic brain injury induces neuroplastic molecular responses in lumbar spinal cord

2019 ◽  
Vol 37 (2) ◽  
pp. 87-96
Author(s):  
Olga Kononenko ◽  
Hiroyuki Watanabe ◽  
Lada Stålhandske ◽  
Ann Zarelius ◽  
Fredrik Clausen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Spinal Cord ◽  
Brain Injury ◽  
Lumbar Spinal Cord ◽  
Molecular Responses ◽  
Lumbar Spinal

scholarly journals Endocrine signaling mediates asymmetric motor deficits after unilateral brain injury

2020 ◽  
Author(s):  
Nikolay Lukoyanov ◽  
Hiroyuki Watanabe ◽  
Liliana S. Carvalho ◽  
Olga Nosova ◽  
Daniil Sarkisyan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Brain Injury ◽  
Neural Control ◽  
Expression Patterns ◽  
Lumbar Spinal Cord ◽  
Motor Deficits ◽  
Postural Asymmetry ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Unilateral Brain

AbstractA paradigm in neurology is that brain injury-induced motor deficits (e.g. hemiparesis and hemiplegia) arise due to aberrant activity of descending neural pathways. We discovered that a unilateral injury of the hindlimb sensorimotor cortex of rats with completely transected thoracic spinal cord produces hindlimb postural asymmetry with contralateral flexion, and asymmetric changes in nociceptive hindlimb withdrawal reflexes and gene expression patterns in lumbar spinal cord. The injury-induced postural effects were abolished by prior hypophysectomy and were mimicked by transfusion of serum from animals with unilateral brain injury. Antagonists of the opioid and vasopressin receptors blocked formation of hindlimb postural asymmetry suggesting that these neurohormones mediate effects of brain injury on lateralized motor responses. Our data indicate that descending neural control of spinal circuits is complemented by a previously unknown humoral signaling from injured brain to the contra- and ipsilesional hindlimbs, and suggest the existence of a body side-specific neuroendocrine regulation in bilaterally symmetric animals.

scholarly journals Hindlimb motor responses to unilateral brain injury: spinal cord encoding and left-right asymmetry

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Mengliang Zhang ◽  
Hiroyuki Watanabe ◽  
Daniil Sarkisyan ◽  
Marlene Storm Andersen ◽  
Olga Nosova ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Brain Injury ◽  
Brain Lesion ◽  
Motor Deficits ◽  
Postural Asymmetry ◽  
The Asymmetry ◽  
Withdrawal Reflexes ◽  
The Right ◽  
Lumbar Spinal ◽  
Unilateral Brain

Abstract Mechanisms of motor deficits (e.g. hemiparesis and hemiplegia) secondary to stroke and traumatic brain injury remain poorly understood. In early animal studies, a unilateral lesion to the cerebellum produced postural asymmetry with ipsilateral hindlimb flexion that was retained after complete spinal cord transection. Here we demonstrate that hindlimb postural asymmetry in rats is induced by a unilateral injury of the hindlimb sensorimotor cortex, and characterize this phenomenon as a model of spinal neuroplasticity underlying asymmetric motor deficits. After cortical lesion, the asymmetry was developed due to the contralesional hindlimb flexion and persisted after decerebration and complete spinal cord transection. The asymmetry induced by the left-side brain injury was eliminated by bilateral lumbar dorsal rhizotomy, but surprisingly, the asymmetry after the right-side brain lesion was resistant to deafferentation. Pancuronium, a curare-mimetic muscle relaxant, abolished the asymmetry after the right-side lesion suggesting its dependence on the efferent drive. The contra- and ipsilesional hindlimbs displayed different musculo-articular resistance to stretch after the left but not right-side injury. The nociceptive withdrawal reflexes evoked by electrical stimulation and recorded with EMG technique were different between the left and right hindlimbs in the spinalized decerebrate rats. On this asymmetric background, a brain injury resulted in greater reflex activation on the contra- versus ipsilesional side; the difference between the limbs was higher after the right-side brain lesion. The unilateral brain injury modified expression of neuroplasticity genes analysed as readout of plastic changes, as well as robustly impaired coordination of their expression within and between the ipsi- and contralesional halves of lumbar spinal cord; the effects were more pronounced after the left side compared to the right-side injury. Our data suggest that changes in the hindlimb posture, resistance to stretch and nociceptive withdrawal reflexes are encoded by neuroplastic processes in lumbar spinal circuits induced by a unilateral brain injury. Two mechanisms, one dependent on and one independent of afferent input may mediate asymmetric hindlimb motor responses. The latter, deafferentation resistant mechanism may be based on sustained muscle contractions which often occur in patients with central lesions and which are not evoked by afferent stimulation. The unusual feature of these mechanisms is their lateralization in the spinal cord.

scholarly journals Left-right side-specific endocrine signaling complements neural pathways to mediate acute asymmetric effects of brain injury

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Nikolay Lukoyanov ◽  
Hiroyuki Watanabe ◽  
Liliana S Carvalho ◽  
Olga Kononenko ◽  
Daniil Sarkisyan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Brain Injury ◽  
Brain Injuries ◽  
Expression Patterns ◽  
Lumbar Spinal Cord ◽  
Neural Pathways ◽  
Postural Asymmetry ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Lumbar Spinal

Brain injuries can interrupt descending neural pathways that convey motor commands from the cortex to spinal motoneurons. Here, we demonstrate that a unilateral injury of the hindlimb sensorimotor cortex of rats with completely transected thoracic spinal cord produces hindlimb postural asymmetry with contralateral flexion and asymmetric hindlimb withdrawal reflexes within 3 hr, as well as asymmetry in gene expression patterns in the lumbar spinal cord. The injury-induced postural effects were abolished by hypophysectomy and were mimicked by transfusion of serum from animals with brain injury. Administration of the pituitary neurohormones β-endorphin or Arg-vasopressin-induced side-specific hindlimb responses in naive animals, while antagonists of the opioid and vasopressin receptors blocked hindlimb postural asymmetry in rats with brain injury. Thus, in addition to the well-established involvement of motor pathways descending from the brain to spinal circuits, the side-specific humoral signaling may also add to postural and reflex asymmetries seen after brain injury.

Lipomeningocele associated with diplomyelia in a dog

2018 ◽  
Vol 46 (05) ◽  
pp. 323-329 ◽  
Author(s):  
Nele Ondreka ◽  
Sara Malberg ◽  
Emma Laws ◽  
Martin Schmidt ◽  
Sabine Schulze
Keyword(s):  
Spinal Cord ◽  
Neurological Status ◽  
Split Cord Malformation ◽  
Lumbar Spinal Cord ◽  
Histopathological Diagnosis ◽  
Type I ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Subcutaneous Mass ◽  
Lumbar Spinal

SummaryA 2-year-old male neutered mixed breed dog with a body weight of 30 kg was presented for evaluation of a soft subcutaneous mass on the dorsal midline at the level of the caudal thoracic spine. A further clinical sign was intermittent pain on palpation of the area of the subcutaneous mass. The owner also described a prolonged phase of urination with repeated interruption and re-initiation of voiding. The findings of the neurological examination were consistent with a lesion localization between the 3rd thoracic and 3rd lumbar spinal cord segments. Magnetic resonance imaging revealed a spina bifida with a lipomeningocele and diplomyelia (split cord malformation type I) at the level of thoracic vertebra 11 and 12 and secondary syringomyelia above the aforementioned defects in the caudal thoracic spinal cord. Surgical resection of the lipomeningocele via a hemilaminectomy was performed. After initial deterioration of the neurological status postsurgery with paraplegia and absent deep pain sensation the dog improved within 2 weeks to non-ambulatory paraparesis with voluntary urination. Six weeks postoperatively the dog was ambulatory, according to the owner. Two years after surgery the owner recorded that the dog showed a normal gait, a normal urination and no pain. Histopathological diagnosis of the biopsied material revealed a lipomeningocele which confirmed the radiological diagnosis.

Aging process of the human lumbar spinal cord: A morphometric analysis

1996 ◽  
Vol 16 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Ming Zhou ◽  
Noboru Goto ◽  
Chen Zhang ◽  
Wei Tang
Keyword(s):  
Spinal Cord ◽  
Morphometric Analysis ◽  
Aging Process ◽  
Lumbar Spinal Cord ◽  
Lumbar Spinal

scholarly journals Multi-pronged neuromodulation intervention engages the residual motor circuitry to facilitate walking in a rat model of spinal cord injury

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Marco Bonizzato ◽  
Nicholas D. James ◽  
Galyna Pidpruzhnykova ◽  
Natalia Pavlova ◽  
Polina Shkorbatova ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Rat Model ◽  
Stress Responses ◽  
Learning Algorithm ◽  
Lumbar Spinal Cord ◽  
Cord Injury ◽  
Potential Synergy ◽  
Lumbar Spinal ◽  
Deep Brain

AbstractA spinal cord injury usually spares some components of the locomotor circuitry. Deep brain stimulation (DBS) of the midbrain locomotor region and epidural electrical stimulation of the lumbar spinal cord (EES) are being used to tap into this spared circuitry to enable locomotion in humans with spinal cord injury. While appealing, the potential synergy between DBS and EES remains unknown. Here, we report the synergistic facilitation of locomotion when DBS is combined with EES in a rat model of severe contusion spinal cord injury leading to leg paralysis. However, this synergy requires high amplitudes of DBS, which triggers forced locomotion associated with stress responses. To suppress these undesired responses, we link DBS to the intention to walk, decoded from cortical activity using a robust, rapidly calibrated unsupervised learning algorithm. This contingency amplifies the supraspinal descending command while empowering the rats into volitional walking. However, the resulting improvements may not outweigh the complex technological framework necessary to establish viable therapeutic conditions.

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