RESUMO
Despite being a prevalent clinical condition, cauda equina concussion has not been thoroughly elucidated in the literature. The aim of this study is to delineate the etiology and pathogenesis of cauda equina concussion and its associated clinical manifestations. Patients exhibiting clinical manifestations indicative of spinal cord injury and transient neurological deficits after spinal trauma were evaluated retrospectively. The pathogenesis was elucidated through correlating clinical presentations with radiological findings. Neurological deficits were categorized into two principal groups, symmetrical and asymmetrical. Non-penetrating fractures were classified to ascertain the relationship between the type of trauma and the ensuing neurological deficits. A cohort of 82 patients was diagnosed with cauda equina concussion. Among these, 58 had experienced vertical trauma resulting from falls, while 24 had encountered axial trauma in vehicular accidents. Stable spinal fractures were identified in 52 patients across multiple levels, whereas single-level fractures were observed in 30. Asymmetrical neurological deficits were detected in 51 (62.19%) patients, with a notably higher incidence among those subjected to vertical trauma (p < 0.014). The mean recovery time was 14.25 ± 15.16 h for sensory deficits and 11.25 ± 13.36 h for motor deficits in those patients. Notably, motor deficits resolved more expeditiously than sensory deficits in all cases presenting with both. Cauda equina concussion emerges as a frequently encountered clinical phenomenon attributable to the impact of high-energy vertical forces. Neurological deficits commonly manifest asymmetrically. The rapid resolution of neurological deficits presents challenges for the diagnostic process.
RESUMO
BACKGROUND: Neural plasticity under physiological condition develops together with normal tau phosphorylation and amyloid precursor protein (APP) processing. Since restoration of PI3-kinase signaling has therapeutic potential in Alzheimer's disease, we investigated plasticity-related changes in tau and APP metabolism by the selective Rho-kinase inhibitor fasudil. METHODS: Field potentials composed of a field excitatory post-synaptic potential (fEPSP) and a population spike (PS) were recorded from a granule cell layer of the dentate gyrus. Plasticity of synaptic strength and neuronal function was induced by strong tetanic stimulation (HFS) and low-frequency stimulation (LFS) patterns. Infusions of saline or fasudil were given for 1 h starting from the application of the induction protocols. Total and phosphorylated tau levels and soluble APPα levels were measured in the hippocampus, which was removed after at least 1 h post-induction period. RESULTS: Fasudil infusion resulted in attenuation of fEPSP slope and PS amplitude in response to both HFS and LFS. Fasudil reduced total tau and phosphorylated tau at residue Thr181 in the HFS-stimulated hippocampus, while Thr231 phosphorylation was reduced by fasudil treatment in the LFS-stimulated hippocampus. Ser416 phosphorylation was increased by fasudil treatment in both HFS- and LFS-stimulated hippocampus. Fasudil significantly increased soluble APPα in LFS-stimulated hippocampus, but not in HFS-stimulated hippocampus. CONCLUSION: In light of our findings, we suggest that increased activity of Rho kinase could trigger a mechanism that goes awry during synaptic plasticity which is reversed by a Rho-kinase inhibitor. Thus, Rho-kinase inhibition might be a therapeutic target in cognitive disorders.