Paraplejía compresiva de un año de evolución. ¿Es posible la recuperación mediante tratamiento quirúrgico? / Compressive paraplegia of one year of evolution. Is recovery possible by surgical treatment?

Introducción: La recuperación de la función motora luego de una lesión medular depende de varios factores como el nivel de la lesión, la extensión del daño, el tiempo de evolución y la edad del paciente. Mayormente la literatura hace referencia a la población adulta y poco existe publicado en pediatría. Objetivo: Reportar y enfatizar la utilidad de la cirugía en una paciente de 7 años con paraplejia por compresión tumoral de larga evolución con posterior recuperación neurológica. Presentación del caso: Paciente femenina de 7 años con paraplejía de larga evolución secundaria a una lesión neoplásica extradural torácica que presentó recuperación neurológica completa en el postoperatorio. Conclusión: Se reporta un caso clínico de una paciente con historia clínica de un año de paraplejia por compresión medular tumoral y recuperación completa luego de la remoción quirúrgica.

Introduction: The recovery of motor function after a spinal cord injury depends on several factors such as the level of the injury, the extent of the damage, the time of evolution and the age of the patient. Most of the literature refers to the adult population and there is little published in pediatrics. Objective: To report and emphasize the utility of surgery in a 7-year-old patient with long-standing tumor compression paraplegia with subsequent neurological recovery. Case presentation: 7-year-old female patient with long-standing paraplegia secondary to a thoracic extradural neoplastic lesion who presented complete neurological recovery in the postoperative period. Conclusion: A clinical case of a patient with a one-year medical history of paraplegia due to tumor spinal cord compression and complete recovery after surgical excision is reported.

Toxoplasmosis intramedular en una paciente con coinfección por VIH y tuberculosis / Intramedullary toxoplasmosis in HIV-tuberculosis co-infected patient

The most common clinical presentation of Toxoplasma gondii in HIV patients is encephalitis; however, the intramedullary involvement has been reported in a few cases. We report a case of intramedullary toxoplasmosis in a female patient diagnosed with HIV/tuberculosis co-infection, and history of poor adherence to antiretroviral therapy. The patient developed subacute paraparesis with compromise of sensory function and urinary sphincter. The nuclear magnetic resonance evaluation showed a single intramedullary ring-enhanced lesion at the T-8 level which was solved after an anti-Toxoplasma therapy with trimethoprim/sulfamethoxazole.

El compromiso encefálico por Toxoplasma gondii en pacientes con VIH es la localización más frecuente, no obstante, la localización intramedular ha sido escasamente reportada. Comunicamos un caso de toxoplasmosis intramedular en una mujer con diagnóstico de coinfección por VIH y tuberculosis, con mala adherencia a la terapia antirretroviral, que desarrolló de forma subaguda un cuadro de paraparesia con compromiso sensitivo y de esfínteres. La resonancia magnética mostró una lesión única intramedular con captación de contraste periférico en anillo a nivel T-8, que se resolvió tras recibir tratamiento anti-toxoplasmosis con cotrimoxazol.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy with spinal cord lesion: A case report and literature review

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy(CADASIL)is a common hereditary disease caused by NOTCH3 gene. The major clinical manifestations includerecurrent small-vessel ischaemic events, migraine, dementia and mood disturbance. Herein, wereport a 32-years-old male presented with right leg weakness and persistent migraine. We carried outneurological exams, genetic testing, blood and cerebrospinal fluid analysis (CSF) as well as magneticresonance imaging (MRI) for the brain and spinal cord. There were no anti-aquaporin-4 antibodiesand oligoclonal bands in the CSF and blood investigations were within the normal range. MRI scansrevealed multiple hyperintense regions in the brain and longitudinally hyperintense signal in spinal cord.Further, we identified a c.383G>A(p.Cys128Tyr) mutation in NOTCH3 gene. Therefore, the patientwas diagnosed with CADASIL concurrent with spinal cord lesion. The patient’s condition slightlyimproved after two weeks treatment with daily dosage of 0.5 g citicoline and 75 mg clopidogrel.

Cervical Disc Herniation and Central Horner Syndrome

Central Horner syndrome is a rare condition, comprising a unique pathophysiological phenomenon. It results from vascular lesions, head or thoracic trauma. We describe a case of Horner syndrome associated to cervical disc herniation, and first-order neuron compression. To our knowledge, this is the second case reported to date in the literature.

A síndrome de Horner central é uma condição rara, que compreende um fenómeno fisiopatológico singular. Resulta de lesões vasculares, trauma cerebral ou torácico. Descrevemos um caso de síndrome de Horner associado a hérnia de disco cervical, com lesão de primeiro neurónio. De acordo com a revisão, é o segundo caso reportado na literatura.

A Case of Intrinsic Spinal Cord Lesions Complicating Epidural Anesthesia

No abstract available.

Repair of spinal cord lesion of rats by using of chitosan tube combined with the bio-active carrier system / 中国康复理论与实践

@#ObjectiveTo study the effect the chitosan tube combined with the bio active carrier system on inducing nerve axon regeneration of rats with spinal cord injury.Methods50 female Wister rats were characterized by the right spinal cord hemisections at the seventh and eighth thoracic segment to make the model of spinal cord hemisection. The chitosan tube serving as a regenerative loculus was implanted in the defect location of the experimental models.In the experimental group,the bio active carrier system was injected into the chitosan tube,while in control group injected nothing.The drua was sutured to restore cerebrospinal fluid circulation.Results6 months and 12 months after operation,the regenerative nerve axon had passed the defect area of spinal cord in the experiment group. According to WGA-HRP anterograde axonal tracing study, some TMB-positive axons were observed in the distal graft host interface,and came into the host environment. TEM-ultrastructure indicate some neonate synapse, myelinated nerve fibers.In the control group,few regenerative axon could be seen, there was no regenerative axon pass the middle of the tube.ConclusionsThe chitosan tube in which the bio active carrier system was injected can induce the spinal cord nerve axon regeneration.

Changes in the Motor Evoked Potentials Produced by Stimulation of Reticulospinal Tract Neurons in the Chronic Spinal Cord Injury of Rat / 대한척추외과학회지

STUDY DESIGN: There is a prospective study of 80 Sprague-Dawley rats which were made at the spinal cord lesion T5/6 level, sparing only one ventral quadrant. We monitered medullary reticulospinal neurons(RtN) evoked potentials at the L2/3 level which laminectomy was performed. OBJECTIVE: to investigate changes in the physiological responses of motor neurons to stimulation of the medullary reticular formation following partial spinal cord lesions sparing only the ventral quadrant. SUMMERY AND BACK GROUND DATA: There were many report that the animals with spinal cord lesion recovered well-coordi-nated fourlimb locomotion within 2-3 weeks. The time course of the functional recovery of this hindlimb locomotion was cor-related with the recovery of motor evoked potentials(MEP), which originate from reticular nuclei. Therefore, it was hypothe-sized that the return of locomotor function after incomplete spinal cord injury may partially rely on the reorganization of descending inputs to ventral horn neurons previously occupied by damaged afferents. MATERIALS AND METHODS: Total 80 Sprague-Dawley rats were used in this study. Under sterile conditions, spinal cord lesions were made at the T5/6 level using a No. 11 blade, sparing only one ventral quadrant. The animals allowed to survive from one day to 61 days. To monitor RtN evoked potentials, laminectomies were performed at L2/3 level. Field potentials were recorded using a glass microelectrode filled with 2 M NaCl(1.5-2.0 M Ohm). Cord dorsum potentials were also epidurally monitored at L2/3 using a pair of teflon-coated wires. The gigantocellular reticular nucleus ipsilateral to the spared ventral cord was stimulated using a monopolar tungsten microelectrode. RESULTS: The field potentials generated in the ventral horn of the lumbar cord were recorded bilaterally. In some animals field potentials were monitored just before and right after the spinal cord lesion. 1) Following spinal cord lesion at T5/6, the amplitude of RtN evoked potentials declined significantly in the L2/3 ventral gray matter of the completely lesioned side. Field potentials monitored below the ipsilaterally spared ventral quadrant remained unchanged. Depressed RtN evoked potentials in the ventral cord gradually increased during the next four weeks, and finally reached greater than 4 times of the amplitude monitored on the contralateral side. 2) The sites in which field potentials could be monitored in the lumbar spinal cord were mapped. In normal rats, the largest field was monitored near the ventral margin of the gray matter. On the other hand, in spinal cord injured ani-mals, the largest field potentials were located in more dorsal aspects of the ventral horn, suggesting a structural reorganization of the descending inputs has taken place. CONCLUSION: The RtN evoked potentials in the ventral horn increased gradually for several weeks after the injury. The returned RtN evoked potentials below the completely lesioned side of spinal cord were larger than those seen in normal spinal cord. The time course of returning evoked potentials below the lesioned side of the spinal cord seems to coincide with the resti-tution of same-side hindlimb locomotion.