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Incomplete Spinal Cord Injury
Published in Kelechi Eseonu, Nicolas Beresford-Cleary, Spine Surgery Vivas for the FRCS (Tr & Orth), 2022
Kelechi Eseonu, Nicolas Beresford-Cleary
The examination findings are consistent with a Brown–Sequard syndrome. The CT shows a parasagittal image showing multiple calcified thoracic discs—one of more of which are likely to have caused unilateral cord compression and this resulting pattern of injury. The pattern of deficit is due to dorsal column compression causing ipsilateral loss of fine touch, vibration, two-point discrimination and conscious proprioception. Disruption of the spinothalamic tracts causing contralateral pain, the temperature is due to the crossing of the tracts to the contralateral side after initially ascending a level. The ipsilateral weakness is caused by compression of the corticospinal tracts. At the level of the lesion, the pattern of weakness would be lower motor neurone weakness, and distal to this would be upper motor neurone weakness. Other causes of Brown–Sequard syndrome include penetrating trauma (e.g. stabbing), tumour and blunt trauma.
Trauma of the Brain and Spinal Cord
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Fernando D. Goldenberg, Ali Mansour
Brown–Sequard syndrome: often described in individuals with penetrating trauma to the spinal cord. Typical findings include loss of motor function, light touch, proprioception, and vibratory sensation ipsilateral to the injury with loss of pain and temperature sensation on the contralateral side.
Central Nervous System (Brain, Brainstem, Spinal Cord), Ears, Ocular Toxicity
Published in Tiziana Rancati, Claudio Fiorino, Modelling Radiotherapy Side Effects, 2019
Federica Palorini, Anna Cavallo, Letizia Ferella, Ester Orlandi
Late injury consists in myelopathy, typically irreversible. The symptoms range from minor motor and sensory deficits to a full-blown Brown–Séquard syndrome. The latent time to myelopathy was 18 months following a single course of treatment, and 11 months after reirradiation.
Clinico-radiological correlation and surgical outcome of idiopathic spinal cord herniation: A single centre retrospective case series
Published in The Journal of Spinal Cord Medicine, 2021
Deepak Menon, Sruthi S. Nair, Bejoy Thomas, K. Krishna Kumar, Muralidharan Nair
From our prospectively maintained data base and picture archiving system, we identified those patients who had been evaluated for myelopathy and myeloradiculopathy in whom alternative causes were excluded. Radiologically, ventral or ventrolateral displacement of spinal cord, presence of dorsal communicating dilated cerebrospinal fluid (CSF) space occupying the normal cord position(after excluding arachnoid cyst) with or without associated cord atrophy or intrinsic cord signal changes were considered features of ISCH.2 From the database, the clinical presentation of patients was obtained through chart review. Along with the clinical presentation, differential diagnosis entertained and management aspects along with the clinical status at the last follow-up was collected. We identified eight patients with ISCH over a ten-year period. Brief clinical description of representative cases presenting with Brown-Sequard syndrome, pure spastic paraparesis, radiculopathy and girdle sensation are given below. Table 1 shows a summary of the clinical and radiological features of all patients.
Blocking SP/NK1R signaling improves spinal cord hemisection by inhibiting the release of pro-inflammatory cytokines in rabbits
Published in The Journal of Spinal Cord Medicine, 2023
Yuehuan Zheng, Nannan Wang, Zhe Chen, Liqiang Shi, Xiangyang Xu
Although, the semi-sectioned spinal cord models have been widely used to simulate Brown-Séquard syndrome in rats,14 possums,15 and monkeys.16 However, the detailed procedure for the standard spinal cord hemisection (SCH) has not been described. In this study, we tentatively constructed the SCH model in rabbit for the first time, and initially explored the regulation of the SP-NK1R axis on inflammation in this model. It aims to explore whether the inhibition of SP or NK1R is expected to become a therapeutic target for patients with incomplete SCI.