Effect of Comprehensive Nursing on Traumatic Paraplegia Patients by Evaluation of Magnetic Resonance Imaging Features.

This research aimed to discuss the comprehensive nursing under the Omaha system in the treatment of patients with traumatic paraplegia (TP) and the changes in magnetic resonance imaging (MRI) features of patients. In total, 60 patients with TP were included as the research objects, and they were randomly divided into the experimental group (Omaha system-based comprehensive nursing) and the control group (routine nursing). All the objects underwent parallel MRI multisequence scanning. The scores of the quality of life, role change, mental health, care, oral hygiene, skin, neuromusculoskeletal (NMS) system, defecation function, urination function, contagion/infection, nutrition, healthcare supervision, and rest/sleep pattern in the experimental group were all significantly higher than those in the control group 3 months and 6 months after discharge (P < 0.05). The caregiving burden scores in the experimental group 3 months and 6 months after discharge from the hospital were 48.67 ± 6.97 and 43.40 ± 4.97, respectively, statistically lower than those in the control group (52.83 ± 6.37; 50.07 ± 7.14) (P < 0.05). On admission, MRI showed that the white lines disappeared from the compression of the dural sac, the spinal cord was compressed, and the intramedullary signal was abnormal. Then, six months after discharge, MRI showed that the compression of the dural sac was relieved, and the double white lines recovered. The apparent diffusion coefficient (ADC) of patients in the experimental group 6 months after discharge (1.063 ± 0.148) was highly lower than that in the control group (1.325 ± 0.245), with a difference of statistical significance (P < 0.05). In conclusion, comprehensive nursing under the Omaha system could improve the clinical treatment effect of patients with spinal cord injury (SCI) effectively, reduce the incidence of complications, and improve the quality of life and nursing outcomes of patients.

Heavily T2-weighted imaging findings of spinal cord swelling in dogs with intervertebral disc extrusion.

ABSTRACT: This study investigated causes of attenuation of cerebrospinal fluid (CSF) signal on heavily T2-weighted (T2W) images in dogs with thoracolumbar disc extrusion. Medical records and magnetic resonance images were retrospectively reviewed. Dogs were classified into the following grades; grade 1, non-ambulatory paraparesis; grade 2, paraplegia with deep pain perception and grade 3, paraplegia without deep pain perception. The length of intramedullary T2W hyperintensity of the spinal cord, cranial/ caudal expansion of extradural compressive materials (ECM), and the CSF signal attenuation were measured. Ratios to the second lumbar vertebra (L2) were calculated for the length of intramedullary T2W hyperintensity (T2W:L2), cranial/caudal expansion of ECM (ECML:L2), and CSF signal attenuation (CSF:L2). The dogs were classified into focal or extended T2W hyperintensity groups according to the length [focal, shorter than length of L2; extended, longer than L2]. The area of EMC and the spinal canal were measured on transverse images at the lesion deriving occupancy ratio. The correlation between CSF:L2 and other data were analysed, and CSF:L2 was compared between the grades. In dogs with intramedullary T2W hyperintensity, the locations of CSF attenuation and the hyperintensity were compared if those locations were matched. Fifty-five dogs were included, 36 of which showed intramedullary T2W hyperintensity. Twenty-two of 36 dogs were considered as match of the location of the CSF attenuation and hyperintensity. CSF:L2 was significantly correlated with T2W:L2 in dogs with extended T2W hyperintensity (p = 0.0002), while CSF:L2 was significantly correlated with ECML:L2 in dogs with focal or no T2W hyperintensity (p = 0.0103 and p = 0.0364, respectively). CSF:L2 in grade 3 was significantly greater than those in patients who were grade 1 or 2 (both p < 0.001). In conclusion, higher CSF:L2, which was frequently seen in grade 3, would be most consistent with a higher T2W:L2 which might indicate spinal cord swelling.

White Matter Alterations in Spastic Paraplegia Type 5: A Multiparametric Structural MRI Study and Correlations with Biochemical Measurements.

BACKGROUND AND PURPOSE: In spastic paraplegia type 5, spinal cord atrophy and white matter signal abnormalities in the brain are the main MR imaging alterations. However, the specific mechanism remains unclear. We explored the microstructural changes occurring in spastic paraplegia type 5 and assessed the relation between MR imaging and clinical data. MATERIALS AND METHODS: Seventeen patients with spastic paraplegia type 5 and 17 healthy controls were scanned with DTI and T1 mapping on a 3T MR imaging scanner. Fractional anisotropy, mean diffusivity, radial diffusivity, axial diffusivity, and T1 values were obtained using Tract-Based Spatial Statistics and the Spinal Cord Toolbox. Neurofilament light and myelin basic protein in the CSF were measured. The differences in MR imaging and biochemical data between patients with spastic paraplegia type 5 and healthy controls were compared using the Student t test. RESULTS: A widespread reduction of fractional anisotropy values and an elevation of mean diffusivity, T1, and radial diffusivity values were found in most cervical, T4, and T5 spinal cords; corona radiata; optic radiations; and internal capsules in spastic paraplegia type 5. A variation in axial diffusivity values was shown only in C2, C6, and the corona radiata but not in the gray matter. The levels of neurofilament light and myelin basic protein were higher in those with spastic paraplegia type 5 than in healthy controls (myelin basic protein, 3507 [SD, 2291] versus 127 [SD, 219] pg/mL; neurofilament light, 617 [SD, 207] versus 265 [SD, 187] pg/mL; P < .001). No correlation was found between the clinical data and MR imaging-derived measures. CONCLUSIONS: Multiparametric MR imaging and biochemical indicators demonstrated that demyelination (mainly) and axonal loss led to the white matter integrity loss without gray matter injury in spastic paraplegia type 5.

Supraspinal nociceptive networks in neuropathic pain after spinal cord injury.

Neuropathic pain following spinal cord injury involves plastic changes along the whole neuroaxis. Current neuroimaging studies have identified grey matter volume (GMV) and resting-state functional connectivity changes of pain processing regions related to neuropathic pain intensity in spinal cord injury subjects. However, the relationship between the underlying neural processes and pain extent, a complementary characteristic of neuropathic pain, is unknown. We therefore aimed to reveal the neural markers of widespread neuropathic pain in spinal cord injury subjects and hypothesized that those with greater pain extent will show higher GMV and stronger connectivity within pain related regions. Thus, 29 chronic paraplegic subjects and 25 healthy controls underwent clinical and electrophysiological examinations combined with neuroimaging. Paraplegics were demarcated based on neuropathic pain and were thoroughly matched demographically. Our findings indicate that (a) spinal cord injury subjects with neuropathic pain display stronger connectivity between prefrontal cortices and regions involved with sensory integration and multimodal processing, (b) greater neuropathic pain extent, is associated with stronger connectivity between the posterior insular cortex and thalamic sub-regions which partake in the lateral pain system and (c) greater intensity of neuropathic pain is related to stronger connectivity of regions involved with multimodal integration and the affective-motivational component of pain. Overall, this study provides neuroimaging evidence that the pain phenotype of spinal cord injury subjects is related to the underlying function of their resting brain.

Dolor torácico y paraplejía de aparición súbita: un caso de infarto medular / Sudden thoracic pain and paraplegia: a case of spinal cord infarction

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Tubercular longitudinally extensive transverse myelitis with lower motor neuron paralysis.

Transverse myelitis typically extends two or less spinal segments, whereas longitudinal extensive transverse myelitis (LETM) extends three or more spinal segments in length and may occasionally span all the segments of the spinal cord. We present a case of spinal tuberculosis presenting with LETM with true lower motor neuron-type flaccid paraplegia.

Familia española portadora de una mutación en heterocigosis compuesta en el gen SPG7: de la incertidumbre a la realidad clínica / A Spanish family with a compound heterozygous mutation in SPG7: From uncertainty to clinical reality

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Extravascular risk factors in the prognostic evaluation for spinal cord injury during thoraco-abdominal aortic aneurysm exclusion: a case report.

BACKGROUND: The etiology of delayed-onset spinal cord injury (SCI) following endovascular repair of thoraco-abdominal aortic aneurysms (TAAA) is still unclear and may be related to multiple factors. Extravascular factors, such as lumbar spinal stenosis (LSS), may play a significant role in the selection of patient at risk of SCI. In this report we describe a case of paraplegia following thoracic endovascular aortic repair (TEVAR) in a patient suffering from severe and symptomatic LSS and undergoing staged endovascular repair of a TAAA. CASE PRESENTATION: A 70-year-old man was admitted to our department with an asymptomatic type III TAAA in previous open repair for abdominal aortic aneurysm. The patient complained of buttock and thigh claudication in the absence of defects in the pelvic perfusion; a spinal magnetic resonance angiography (MRA) showed a severe narrowing of the lumbar canal.. After 24 h from first-step procedure (TEVAR) paraplegia was detected. A cerebrospinal fluid (CSF) drainage was then placed with incomplete recovery. CONCLUSIONS: Stenotic damage to the spinal cord is thought to be the result of direct compression of the neural elements and ischemic disruption of arterial and venous structures surrounding the spinal cord. This comorbidity may constitute an additional anatomic risk factor in those patients currently recognized as prognostically associated to the development of SCI.

Unusual Manifestation of Spinal Epidural Arteriovenous Fistula as Sudden Paraplegia.

BACKGROUND: Spinal epidural arteriovenous fistulas (SEDAVFs) are a rare entity that cause gradual progression of neurological dysfunction. We present a case of SEDAVF with acute exacerbation of paraplegia that was successfully treated with emergency transarterial embolization. CASE DESCRIPTION: A 73-year-old man presented with low back pain, numbness in the lower extremities, and gait disturbance. T2-weighted magnetic resonance imaging revealed edema of the thoracolumbar spinal cord. Computed tomography angiography showed that the SEDAVF was fed by an expanded left L1 artery, epidural venous plexus at the left L1-2 intervertebral foramen, and intradural venous drainage. The patient suddenly developed severe paraplegia 2 days later. We performed emergency spinal angiography followed by transarterial embolization. The postoperative course was uneventful, and his preoperative symptoms improved. CONCLUSIONS: SEDAVFs may result in acute exacerbation that can be treated with an endovascular intervention-a rapid and effective means of obliterating shunts.

A rare case of isolated cauda equina Nocardia farcinica infection.

Nocardia is a Gram-positive, partially acid-fast, catalase-positive, and urease-positive bacterium that grows aerobically. We present an extremely rare case of cauda equina syndrome due to isolated intramedullary Nocardia farcinica infection. A 44-year-old male presented with low backache and gradually progressive weakness in bilateral lower limbs followed by paraplegia. He was found to have a well-defined, sharply demarcated ring-enhancing lesion located from T11-T12 to L3 vertebral body. He underwent laminectomy and decompression. The histopathological examination revealed a Gram-positive filamentous organism that looks like Nocardia. The culture report was suggestive of Nocardia farcinica. He was then treated with antibiotics and had a remarkable clinical and radiological improvement.

Decompensation of a Thoracic Meningioma Below the Operated Level: A Dramatic and Unexpected Complication.

BACKGROUND: Paraplegia after lumbar spinal surgery has been previously described. It was generally provoked by a missed thoracic compression because of degenerative processes, arachnoid cyst, and spinal cord tumor such as meningioma. We describe here a case of a patient with neurofibromatosis type 2 (NF-2) with multiple spinal meningiomas that developed postoperative paraplegia because of decompensation of spinal cord compression below and far from the operated level. CASE DESCRIPTION: A 54-year-old woman with NF-2 was followed-up for multiple spinal meningiomas (C7-T1, T6-7, T9-10 levels). Surgery for the symptomatic and larger lesion (C7-T1) was scheduled. Postoperatively, the patient was found to have paraplegia with sensor anesthesia below the level of the T6 vertebra. An urgent spinal magnetic resonance imaging (MRI) scan was performed revealing the absence of complication at the operated level (C7-T1) but the appearance of a marked intramedullary hyperintensity at the T6-7 level. An urgent T6-7 laminectomy and removal of the meningioma was performed. The postoperative phase was marked by a poor recuperation. Spinal MRI scan at 3 months clearly showed a severely injured spinal cord at the T6-7 level consistent with the neurologic status of the patient. CONCLUSIONS: We report here the first case of acute neurologic deterioration after decompensation of a spinal cord compression below the operated level in spinal intradural surgery. Neurosurgeons must be aware of this possible complication when treating patients with multiple spinal meningiomas.

Case-Control Study of Ultrasound Evaluation of Acute Median Nerve Response to Upper Extremity Circuit Training in Spinal Cord Injury.

OBJECTIVE: Individuals with spinal cord injury (SCI) often present signs and symptoms of median nerve (MN) pathology. Preclinical signs identification of MN pathology might facilitate early intervention to prevent or delay carpal tunnel syndrome in SCI. We assessed if ultrasound parameters changed in response to upper extremity (UE) circuit training exercise in individuals with paraplegia and able-bodied individuals. DESIGN: Case-control study. PARTICIPANTS: Adults (N=32) with paraplegia (n=16) and age- and sex-matched able-bodied controls (n=16). INTERVENTION: Circuit training exercise. MAIN OUTCOME MEASURES: MN ultrasound evaluation at the pisiform and radius before and after UE exercise. Ultrasound parameters included cross-sectional area (CSA), and gray scale (GS). Data presented as mean ± SD. RESULTS: Pre-exercise CSAs were larger in SCI at the radius (12.0±2.9 vs 9.0±2.1; P=.003), but not the pisiform (9.8±3.1 vs 9.1±1.7; P=.431). There were no statistical differences in MN response to exercise between groups (all P≥.293). Across participants, CSA changes were inversely associated with their pre-exercise values at the pisiform (r=-0.648; P<.001) and the radius (r=-0.366; P=.043). Participants with pre-exercise CSA values ≥10.00 mm2 at the pisiform responded to exercise with decreases in CSA (mean change ± SD, -2.0±1.5; P=.002) and GS (-2.8±6.2; P=.029). Participants with pre-exercise CSA ≤9.99 mm2 at the pisiform responded to exercise with no change in CSA (mean change ± SD, 0.7±2.5; P=.002) and increased GS (3.2±7.2; P=.029). CONCLUSIONS: CSA exercise response was more strongly related to pre-exercise MN values than presence or absence of SCI.

Complete paraplegia with diffuse osteolytic skeletal metastases: an uncommon presentation of carcinoma of the prostate.

INTRODUCTION: Skeletal metastases of advanced prostatic cancer are usually osteoblastic in appearance. Osteolytic secondaries are an uncommon entity. In such scenarios, it is important to differentiate prostatic metastases from other pathologies which give an identical radiological appearance, such as multiple myeloma. Another important point to remember is that neurological complications secondary to prostatic metastases are quite uncommon. CASE PRESENTATION: We describe a man with advanced prostatic carcinoma who presented to us with an uncommon combination of sudden onset complete paraplegia associated with diminished sensation in the lower half of the body and diffuse osteolytic lesions in the entire skeletal system. On detailed workup, it was found that his prostatic specific antigen (PSA) was grossly elevated. Markers for multiple myeloma were negative. Accordingly, computerized tomography of the abdomen was performed. The latter revealed an enlarged prostate gland infiltrating into the bladder base. Histopathological analysis from the prostate as well as the bone marrow showed an identical picture thereby confirming our diagnosis. The individual underwent palliative spinal canal decompression following which he was put on anti-androgenic treatment. At one year follow up, he was ambulatory and able to walk with use of crutches. DISCUSSION: To the best of our knowledge, this is the first reported case of osteolytic prostatic metastases presenting as complete paraplegia. In this situation, in addition to evaluation for prostate CA, we also recommend screening for multiple myeloma as the clinico-radiological profile of the two diseases are similar but their management is very different.

Spinal cord injury after the use of ecstasy in a young male.

INTRODUCTION: Ecstasy is a commonly used party drug and is the second most popular drug after marijuana among youngsters. Serious health hazards have been described including cardiac diseases, neurological complications, multi-organ failure, and even death. Spinal cord injury/dysfunction (SCI/D) is rarely described as a result of ecstasy ingestion. CASE PRESENTATION: We present a case of a 19-year-old male patient who was admitted to our rehabilitation center, after developing a T11 AIS B SCI/D following recreational use of ecstasy. DISCUSSION: In our case magnetic resonance imaging was inconclusive due to artifacts caused by metallic rods used for surgical scoliosis treatment in the past. This individual received no surgical or pharmacological treatments; however, it is questionable whether any specific treatments would have been beneficial. Ecstasy ingestion leads to a serotonin surge and induces microvascular changes. Neurovascular hemorrhage, subarachnoid hemorrhage, de novo aneurysm formation, and subsequent rupture can occur. 5-hydroxytryptamine, which comes from serotonergic terminals, is a very potent vasoconstrictive amine and can thus lead to prolonged vasoconstriction and ischemia. It is most likely that the SCI/D in our case is the result of an ischemic event following the vasoconstrictive effects of ecstasy ingestion. It is important to stress the possible consequences of recreational ecstasy usage and in unexplained SCI/D, one should consider the possibility of drug-related causes.