Journal articles: 'Paraplegia'

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Rodenbaugh, David W., Heidi L. Collins, Dustin G. Nowacek, and Stephen E. DiCarlo. "Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 6 (December 2003): H2605—H2613. http://dx.doi.org/10.1152/ajpheart.00319.2003.

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Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias. To test this hypothesis, intact ( n = 10) and paraplegic ( n = 6) male Wistar rats were chronically instrumented to measure atrioventricular (AV) interval, sinus cycle length, sinus node recovery time (SNRT), SNRT corrected for spontaneous sinus cycle (cSNRT), Wenckebach cycle length (WCL), and the electrical stimulation threshold to induce ventricular arrhythmias. In addition, relative protein abundance and mRNA expression for sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA), phospholamban, and the Na/Ca exchanger were determined in intact ( n = 8) and paraplegic ( n = 8) rats. Paraplegia significantly ( P < 0.05) reduced AV interval (–25%), sinus cycle length (–24%), SNRT (–28%), cSNRT (–53%), WCL (–19%), and the electrical stimulation threshold to induce ventricular arrhythmia (–48%). Paraplegia significantly increased the relative protein abundances of SERCA (45%) and the Na/Ca exchanger (40%) and decreased phospholamban levels (–28%). In contrast, only the relative mRNA expression of the Na/Ca exchanger was increased (25%) in paraplegic rats. These data demonstrate that paraplegia enhances cardiac electrophysiological properties and alters Ca2+ regulatory proteins in a manner that increases susceptibility to ventricular arrhythmias.

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Lin, Xiang, Hui-Zhen Su, En-Lin Dong, Xiao-Hong Lin, Miao Zhao, Can Yang, Chong Wang, et al. "Stop-gain mutations in UBAP1 cause pure autosomal-dominant spastic paraplegia." Brain 142, no. 8 (June 15, 2019): 2238–52. http://dx.doi.org/10.1093/brain/awz158.

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Abstract Hereditary spastic paraplegias refer to a heterogeneous group of neurodegenerative disorders resulting from degeneration of the corticospinal tract. Clinical characterization of patients with hereditary spastic paraplegias represents progressive spasticity, exaggerated reflexes and muscular weakness. Here, to expand on the increasingly broad pools of previously unknown hereditary spastic paraplegia causative genes and subtypes, we performed whole exome sequencing for six affected and two unaffected individuals from two unrelated Chinese families with an autosomal dominant hereditary spastic paraplegia and lacking mutations in known hereditary spastic paraplegia implicated genes. The exome sequencing revealed two stop-gain mutations, c.247_248insGTGAATTC (p.I83Sfs*11) and c.526G>T (p.E176*), in the ubiquitin-associated protein 1 (UBAP1) gene, which co-segregated with the spastic paraplegia. We also identified two UBAP1 frameshift mutations, c.324_325delCA (p.H108Qfs*10) and c.425_426delAG (p.K143Sfs*15), in two unrelated families from an additional 38 Chinese pedigrees with autosomal dominant hereditary spastic paraplegias and lacking mutations in known causative genes. The primary disease presentation was a pure lower limb predominant spastic paraplegia. In vivo downregulation of Ubap1 in zebrafish causes abnormal organismal morphology, inhibited motor neuron outgrowth, decreased mobility, and shorter lifespan. UBAP1 is incorporated into endosomal sorting complexes required for transport complex I and binds ubiquitin to function in endosome sorting. Patient-derived truncated form(s) of UBAP1 cause aberrant endosome clustering, pronounced endosome enlargement, and cytoplasmic accumulation of ubiquitinated proteins in HeLa cells and wild-type mouse cortical neuron cultures. Biochemical and immunocytochemical experiments in cultured cortical neurons derived from transgenic Ubap1flox mice confirmed that disruption of UBAP1 leads to dysregulation of both early endosome processing and ubiquitinated protein sorting. Strikingly, deletion of Ubap1 promotes neurodegeneration, potentially mediated by apoptosis. Our study provides genetic and biochemical evidence that mutations in UBAP1 can cause pure autosomal dominant spastic paraplegia.

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Giacomini, Leonardo, Roger Neves Mathias, Andrei Fernandes Joaquim, Mateus Dal Fabbro, Enrico Ghizoni, and Helder Tedeschi. "Is there a right time for surgery in paraplegic patients secondary to non traumatic spinal cord compression?" Einstein (São Paulo) 10, no. 4 (December 2012): 508–11. http://dx.doi.org/10.1590/s1679-45082012000400020.

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Paraplegia is a well-defined state of complete motor deficit in lower limbs, regardless of sensory involvement. The cause of paraplegia usually guides treatment, however, some controversies remain about the time and benefits for spinal cord decompression in nontraumatic paraplegic patients, especially after 48 hours of the onset of paraplegia. The objective of this study was to evaluate the benefits of spinal cord decompression in such patients. We describe three patients with paraplegia secondary to non-traumatic spinal cord compression without sensory deficits, and who were surgically treated after more than 48 hours of the onset of symptoms. All patients, even those with paraplegia during more than 48 hours, had benefits from spinal cord decompression like recovery of gait ability. The duration of paraplegia, which influences prognosis, is not a contra-indication for surgery. The preservation of sensitivity in this group of patients should be considered as a positive prognostic factor when surgery is taken into account.

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Elegbe, Oloruntoba, Mirdhu Wickremaratchi, and Martyn Hinchcliffe. "The Patient with Acute Paraplegia: A Problem-Based Review." Acute Medicine Journal 10, no. 1 (January 1, 2011): 40–44. http://dx.doi.org/10.52964/amja.0462.

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Acute paraplegia is an emergency requiring immediate assessment by the acute medical team because of the need to rule out compressive lesions of the cord for which intervention may preserve neurological function and limit persistent disability. In addition acute paraplegia could be complicated by life-threatening problems. These require prompt recognition and treatment to prevent further deterioration. The following clinical scenario, based on a real case of acute paraplegia seen by the authors is aimed at providing a problem-based approach to the management of patients presenting with acute paraplegic weakness.

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Ashry, Ahmed, Ayman Tarek Mahmoud, and Mohamed Gabr. "Delayed recovery from paraplegia following resections of thoracic meningiomas." Surgical Neurology International 11 (October 2, 2020): 321. http://dx.doi.org/10.25259/sni_575_2020.

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Background: In this retrospective study, we evaluated the patterns of postoperative recovery for patients who were initially paraplegic before the excision of thoracic spine meningiomas. We also determined how the various prognostic factors impacted outcomes. Methods: Twenty patients with paraplegia underwent surgical excision of thoracic spine meningiomas at 2016– 2019. Patients’ demographics, clinical, radiological data, operative details, histopathology, and postoperative complications were recorded; patients were reassessed at 6 months and 1 year postoperatively. Results: Fourteen patients improved postoperatively, becoming, ambulatory with/without assistance; only six remained paraplegic. Poor prognostic factors for postoperative motor recovery included larger tumor size, longer duration of preoperative symptoms/paraplegia, and greater severity of sensory loss. Conclusion: For 6/20 patients with thoracic meningiomas, poor postoperative recovery of motor function correlated with larger tumor size, longer duration of preoperative symptoms/paraplegia, and more severe sensory loss.

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Wecht, Jill M., Ronald E. De Meersman, Joseph P. Weir, Ann M. Spungen, and William A. Bauman. "Cardiac homeostasis is independent of calf venous compliance in subjects with paraplegia." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (June 1, 2003): H2393—H2399. http://dx.doi.org/10.1152/ajpheart.01115.2002.

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The purpose of this study was to examine cardiac hemodynamics during acute head-up tilt (HUT) and calf venous function during acute head-down tilt (HDT) in subjects with paraplegia compared with sedentary nondisabled controls. Nineteen paraplegic males (below T6) and nine age-, height-, and weight-matched control subjects participated. Heart rate, stroke volume, and cardiac output were assessed using the noninvasive acetylene uptake method. Venous vascular function of the calf was assessed using venous occlusion plethysmography. After supine measurements were collected, the table was moved to 10° HDT followed by the three levels of HUT (10, 35, and 75°) in random order. Cardiac hemodynamics were similar between the groups at all positions. Calf circumference was significantly reduced in the paraplegic group compared with the control group ( P < 0.001). Venous capacitance and compliance were significantly reduced in the paraplegic compared with control group at supine and HDT. Neither venous capacitance ( P = 0.37) nor compliance ( P = 0.19) increased from supine with 10° HDT in the paraplegic group. A significant linear relationship was established between supine venous compliance and supine cardiac output in the control group ( r = 0.80, P < 0.02) but not in the paraplegic group. The findings of reduced calf circumference and similar venous capacitance at supine rest and 10° HDT in the paraplegic group imply that structural changes may have limited venous dispensability in individuals with chronic paraplegia. Furthermore, the lack of a relationship between supine venous compliance and supine cardiac output suggests that cardiac homeostasis does not rely on venous compliance in subjects with paraplegia.

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Olmez, Akgun, and Haluk Topaloglu. "HEREDITARY SPASTIC PARAPLEGIA: PATHOGENESIS AND PATHOPHYSIOLOGY." National Journal of Neurology 1, no. 05 (July 30, 2014): 10–22. http://dx.doi.org/10.61788/njn.v1i14.01.

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- Hereditary spastic paraplegias constitute a larger group of disorders than expected. - Autosomal dominant types are mainly composed of SPAST, Atlastin (SPG3A) and REEP1 mutations. Genetic testing is suggested mainly for these genes. - The most common autosomal recessive type is SPG11, hereditary spastic paraplegia with thin corpus callosum, but SPG15 shares the same clinical features with SPG11. Genetic testing should be done for both if thin corpus callosum is present in patients. - How different genes with many different biological functions, including axonal transport, mitochondrial functions, fatty acid and cholesterol pathways and DNA repair defects, cause hereditary spastic paraplegia is still unknown.

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Mussa, S., S. Kakar, and G. Bentley. "Total Hip Arthroplasty for Late Hip Dislocation in Paraplegia." HIP International 12, no. 3 (July 2002): 338–41. http://dx.doi.org/10.1177/112070000201200310.

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Late hip dislocation is uncommon, particularly in the context of paraplegia. We report a case in which total hip arthroplasty with a semi-constrained acetabular component was a successful treatment for this condition. A review of the literature revealed that this method of treatment had not been previously described in paraplegics. For patients with late hip dislocation in spastic paraplegia, total hip arthroplasty with a semi-constrained acetabular component, combined with adequate adductor release and obturator neurectomy is recommended.

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Mesquita Junior, Nelson, Flavia Natalia Marques Kingerski, Giovana Liz Marioto, Fabio Alex Fonseca Viegas, Suzelaine Fidelis da Silva Mesquita, and Sonia Perreto. "Prevalence of deep vein thrombosis in patients with paraplegia caused by traumas." Jornal Vascular Brasileiro 12, no. 4 (October 21, 2013): 271–77. http://dx.doi.org/10.1590/jvb.2013.051.

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BACKGROUND: Deep vein thrombosis is a common disease among people who are immobilized. Immobility is inherent to paraplegia and leads to venous stasis, which is one of the factors covered by Virchow's triad describing its development. Trauma is the primary cause of paraplegia and is currently increasing at a rate of 4% per year. OBJECTIVE: To determine the prevalence of deep vein thrombosis in paraplegic patients whose paraplegia was caused by traumas, using color Doppler ultrasonography for diagnosis. METHODS: This was a cross-sectional observational study of 30 trauma-induced paraplegia patients, selected after analysis of medical records at the neurosurgery department of a University Hospital in Curitiba, Brazil, and by a proactive survey of associations that care for the physically disabled. The prevalence of deep vein thrombosis was analyzed using 95% confidence intervals. RESULTS: Spinal cord trauma was the cause of paraplegia in 29 patients. The most common cause of trauma was gunshot wounding, reported by 17 patients. Deep vein thrombosis was diagnosed by color Doppler ultrasonography in 14 patients in the sample. The most often affected vein was the posterior tibial, in 11 patients. The left lower limb was involved three times more often than the right. Edema was observed in 25 individuals, cyanosis in 14, ulcers in 8 and localized increase in temperature in 13. CONCLUSIONS: Deep vein thrombosis was prevalent, occurring in 46.7% of the patients.

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Komachali, Sajad Rafiee, Zakieh Siahpoosh, and Mansoor Salehi. "Two novel mutations in ALDH18A1 and SPG11 gene found by whole-exome sequencing in spastic paraplegia disease patients in Iran." Genomics & Informatics 20, no. 3 (September 30, 2022): e30. http://dx.doi.org/10.5808/gi.22030.

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Hereditary spastic paraplegia is a not common inherited neurological disorder with heterogeneous clinical expressions. ALDH18A1 (located on 10q24.1) gene-related spastic paraplegias (SPG9A and SPG9B) are rare metabolic disorders caused by dominant and recessive mutations that have been found recently. Autosomal recessive hereditary spastic paraplegia is a common and clinical type of familial spastic paraplegia linked to the SPG11 locus (locates on 15q21.1). There are different symptoms of spastic paraplegia, such as muscle atrophy, moderate MR, short stature, balance problem, and lower limb weakness. Our first proband involves a 45 years old man and our second proband involves a 20 years old woman both are affected by spastic paraplegia disease. Genomic DNA was extracted from the peripheral blood of the patients, their parents, and their siblings using a filter-based methodology and quantified and used for molecular analysis and sequencing. Sequencing libraries were generated using Agilent SureSelect Human All ExonV7 kit, and the qualified libraries are fed into NovaSeq 6000 Illumina sequencers. Sanger sequencing was performed by an ABI prism 3730 sequencer. Here, for the first time, we report two cases, the first one which contains likely pathogenic NM_002860: c.475C>T: p.R159X mutation of the ALDH18A1 and the second one has likely pathogenic NM_001160227.2: c.5454dupA: p.Glu1819Argfs Ter11 mutation of the SPG11 gene and also was identified by the whole-exome sequencing and confirmed by Sanger sequencing. Our aim with this study was to confirm that these two novel variants are direct causes of spastic paraplegia.

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Shin, Sanghoon, Jinyoung Park, Juntaek Hong, and Jung Hyun Park. "Improved gait speed in spastic paraplegia: a new modality." BMJ Supportive & Palliative Care 10, no. 4 (June 14, 2019): e41-e41. http://dx.doi.org/10.1136/bmjspcare-2018-001738.

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ObjectivesThe gait disturbance in spastic paraplegic patients lowers the gait speed, increases fall risk and eventually lower the quality of life. This study aims to investigate the effect of electrical twitch obtaining intramuscular stimulation (ETOIMS) on spastic paraplegic patients’ gait speed and pattern.MethodsA prospective short-term cohort study was designed in the outpatient clinic of the department of rehabilitation in a tertiary hospital. Patients with spastic paraplegia (N=5) were participated, including spinal cord tumour (N=2), cervical myelitis (N=1), hereditary spastic paraplegia (NIPA1 mutation; N=1) and spinal cord injury (N=1). The participants underwent ETOIMS. The target muscles were the bilateral quadratus lumborum, multifidus inserting to the L4 and L5 spinous process, and gluteus medius. Gait speed, gait pattern and subjective symptoms, including pain scores (measured by visual analogue scale), were compared before and immediately after the intervention.ResultsAll patients subjectively reported reduced stiffness during walking and alleviated muscular pain in the lower back and gluteal area. After one session of ETOIMS, patient 1–4 showed 57%, 29%, 33% and 6 % improvement in gait speed, respectively, and all patients showed increased pelvic dissociation.ConclusionsThe ETOIMS can be effective in improving gait speed and stability by relaxing the muscles or alleviating the pain in the lower back and gluteal area in spastic paraplegic patients.

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Olmez, Akgun, and Haluk Topaloglu. "Hereditary spastic paraplegia:Pathogenesis and pathophysiology." NATIONAL JOURNAL OF NEUROLOGY, no. 5 (December 4, 2018): 1–13. http://dx.doi.org/10.28942/nnj.v1i5.105.

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Hereditary spastic paraplegias constitute a larger group of disorders than expected. Autosomal dominant types are mainly composed of SPAST, Atlastin (SPG3A) and REEP1 Genetic testing is suggested mainly for these genes. The most common autosomal recessive type is SPG11, hereditary spastic paraplegia with thin corpus callosum, but SPG15 shares the same clinical features with SPG11. Genetic testing should be done for both if thin corpus callosum is present in patients. How different genes with many different biological functions, including axonal transport, mitochondrial functions, fatty acid and cholesterol pathways and DNA repair defects, cause hereditary spastic paraplegia is still unknown.

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Lujan, Heidi L., Ying Chen, and Stephen E. DiCarlo. "Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemia-induced ventricular tachycardia in conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 5 (May 2009): H1364—H1372. http://dx.doi.org/10.1152/ajpheart.01286.2008.

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Midthoracic spinal cord injury is associated with ventricular arrhythmias that are mediated, in part, by enhanced cardiac sympathetic activity. Furthermore, it is well known that sympathetic neurons have a lifelong requirement for nerve growth factor (NGF). NGF is a neurotrophin that supports the survival and differentiation of sympathetic neurons and enhances target innervation. Therefore, we tested the hypothesis that paraplegia is associated with an increased cardiac NGF content, sympathetic tonus, and susceptibility to ischemia-induced ventricular tachyarrhythmias. Intact and paraplegic (6–9 wk posttransection, T5 spinal cord transection) rats were instrumented with a radiotelemetry device for recording arterial pressure, temperature, and ECG, and a snare was placed around the left main coronary artery. Following recovery, the susceptibility to ventricular arrhythmias (coronary artery occlusion) was determined in intact and paraplegic rats. In additional groups of matched intact and paraplegic rats, cardiac nerve growth factor content (ELISA) and cardiac sympathetic tonus were determined. Paraplegia, compared with intact, increased cardiac nerve growth factor content (2,146 ± 286 vs. 180 ± 36 pg/ml, P < 0.05) and cardiac sympathetic tonus (154 ± 4 vs. 68 ± 4 beats/min, P < 0.05) and decreased the ventricular arrhythmia threshold (3.6 ± 0.2 vs. 4.9 ± 0.2 min, P < 0.05). Thus altered autonomic behavior increases the susceptibility to ventricular arrhythmias in paraplegic rats.

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Dreyer, Hans C., Erin L. Glynn, Heidi L. Lujan, Christopher S. Fry, Stephen E. DiCarlo, and Blake B. Rasmussen. "Chronic paraplegia-induced muscle atrophy downregulates the mTOR/S6K1 signaling pathway." Journal of Applied Physiology 104, no. 1 (January 2008): 27–33. http://dx.doi.org/10.1152/japplphysiol.00736.2007.

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Ribosomal S6 kinase 1 (S6K1) is a downstream component of the mammalian target of rapamycin (mTOR) signaling pathway and plays a regulatory role in translation initiation, protein synthesis, and muscle hypertrophy. AMP-activated protein kinase (AMPK) is a cellular energy sensor, a negative regulator of mTOR, and an inhibitor of protein synthesis. The purpose of this study was to determine whether the hypertrophy/cell growth-associated mTOR pathway was downregulated during muscle atrophy associated with chronic paraplegia. Soleus muscle was collected from male Sprague-Dawley rats 10 wk following complete T4–T5 spinal cord transection (paraplegic) and from sham-operated (control) rats. We utilized immunoprecipitation and Western blotting techniques to measure upstream [AMPK, Akt/protein kinase B (PKB)] and downstream components of the mTOR signaling pathway [mTOR, S6K1, SKAR, 4E-binding protein 1 (4E-BP1), and eukaryotic initiation factor (eIF) 4G and 2α]. Paraplegia was associated with significant soleus muscle atrophy (174 ± 8 vs. 240 ± 13 mg; P < 0.05). There was a reduction in phosphorylation of mTOR, S6K1, and eIF4G ( P < 0.05) with no change in Akt/PKB or 4E-BP1 ( P > 0.05). Total protein abundance of mTOR, S6K1, eIF2α, and Akt/PKB was decreased, and increased for SKAR ( P < 0.05), whereas 4E-BP1 and eIF4G did not change ( P > 0.05). S6K1 activity was significantly reduced in the paraplegic group ( P < 0.05); however, AMPKα2 activity was not altered (3.5 ± 0.4 vs. 3.7 ± 0.5 pmol·mg−1·min−1, control vs. paraplegic rats). We conclude that paraplegia-induced muscle atrophy in rats is associated with a general downregulation of the mTOR signaling pathway. Therefore, in addition to upregulation of atrophy signaling during muscle wasting, downregulation of muscle cell growth/hypertrophy-associated signaling appears to be an important component of long-term muscle loss.

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Garcia-Berlanga, Jesus Eduardo, Mariana Moscovich, Isaac Jair Palacios, Alejandro Banegas-Lagos, Augusto Rojas-Martinez, and Daniel Martinez-Ramirez. "CAPN1 Variants as Cause of Hereditary Spastic Paraplegia Type 76." Case Reports in Neurological Medicine 2019 (July 1, 2019): 1–5. http://dx.doi.org/10.1155/2019/7615605.

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Background. Autosomal recessive hereditary spastic paraplegias (HSP) are a rare group of hereditary neurodegenerative disorders characterized by spasticity with or without other symptoms. SPG11 gene is the most common cause of autosomal recessive HSP. We report a case of autosomal recessive spastic paraplegia type 76 due to heterozygous variants of CAPN1 in an Argentinean subject. Case Presentation. A 38-year-old Argentinean female presented with progressive gait problems and instability of 15-year duration. Oculomotor abnormalities, ataxia, bradykinesia, cervical dystonia, and lower limb pyramidal signs were observed. Brain MRI was unremarkable. Whole-exome sequencing analysis identified two heterozygous variants in CAPN1. Conclusions. Clinicians should screen for CAPN1 mutation in a young female patient without significant family history with a spastic paraplegia syndrome associated with other symptoms.

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Akhtar, Ammara, Sobia Nazir Choudhry, Rana Muhammad Mateen, and Mureed Hussain. "Genetics A Comprehensive In Silico Analysis of Deleterious SNPs of Paraplegin Protein Associated with Hereditary Spastic Paraplegia through Mitochondrial Dysfunction." BioScientific Review 2, no. 2 (June 9, 2020): 1–14. http://dx.doi.org/10.32350/bsr.0202.01.

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Hereditary spastic paraplegia (HSP) is a heterogenous neurological disorder primarily associated with progressive spasticity. Paraplegin is a mitochondrial protein and mutations in this protein can lead to HSP. In this study, in silico analysis was carried out to identify the pathogenic variants of SPG7 (paraplegin protein). To find novel pathogenic mutations, missense and splicing variants were collected from gnomAD database and passed through a detailed and stringent analysis with the help of a variety of bioinformatic tools. The list of mutations was examined and compared in ClinVar. Altogether, 14 missense mutations and 18 splicing mutations were obtained and these mutations were predicted to have the potential of disrupting the normal structural and functional properties of paraplegin protein.

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Peters, Siert TA, Marieke J. Witvliet, Anke Vennegoor, Birkitt ten Tusscher, Bauke Boden, and Frank W. Bloemers. "The fat embolism syndrome as a cause of paraplegia." SAGE Open Medical Case Reports 6 (January 1, 2018): 2050313X1878931. http://dx.doi.org/10.1177/2050313x18789318.

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The fat embolism syndrome is a well-known complication in trauma patients. We describe a rare case of traumatic fat embolism that leads to paraplegia. A 19-year-old male motorcycle accident victim was presented to our hospital. After stabilization and trauma survey, he was diagnosed with bilateral femur fractures, a spleen laceration and a tear in the inferior vena cava, for which damage control surgery was performed. Post-operatively, the patient became paraplegic and developed a fluctuating consciousness, respiratory distress and petechiae. Fat embolism syndrome was considered as the most plausible cause of the paraplegia. The fat embolism syndrome is seen in approximately 1% of trauma patients, mostly those with bilateral fractures of the femur. Prevention of the syndrome depends on early stabilization of fractures. However, even with optimal care, this syndrome can still occur and may have dramatic consequences, as we demonstrate in this case.

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Gongati, Nissi Chrysolite, Vikas Agrawal, and Sonal Agrawal. "First SPG48 case report in India with a novel mutation." IP Indian Journal of Neurosciences 9, no. 1 (April 15, 2023): 56–58. http://dx.doi.org/10.18231/j.ijn.2023.010.

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The hereditary spastic paraplegias (HSP) are a large group of inherited neurologic disorders that share the primary symptom of difficulty in walking due to weakness and spasticity in the lower limbs. Spastic paraplegia-48 (SPG48) is an autosomal recessive neurologic disorder characterized by spasticity of the lower limbs resulting in gait difficulties. Biallelic mutations in AP5Z1 are known to cause this complex form of hereditary spastic paraplegia (HSP) referred to as SPG48 (MIM#613647). Most patients have onset in mid- or late-adulthood, although childhood onset has been reported in 1 patient. Additional features may include parkinsonism, urinary incontinence, neuropathy, and mild cognitive impairment. We report a 49-year-old male with SPG48 with a novel mutation. This is the first SPG48 case report in an Indian patient and to the best of our knowledge this mutation is the first to be reported worldwide.

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Srivastava, Sudhir, Aditya Raj, Rishi Agarwal, Sunil Bhosale, and Nandan Marathe. "Management dilemma of tuberculous paraplegia in pregnancy – A case report and review of literature." Surgical Neurology International 11 (December 29, 2020): 470. http://dx.doi.org/10.25259/sni_772_2020.

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Background: Tuberculosis (TB)/tuberculous spondylodiscitis of the spine causing paraplegia in the 2nd trimester of pregnancy is rare and poses significant management dilemmas. Pregnancy, a relatively immunocompromised state with high hormonal levels, may prompt rapid TB destruction of a vertebral body resulting in an acute/ profound neurological deficit. Here, a pregnant paraplegic mother was diagnosed with spondylodiscitis that warranted immediate decompression/fusion to achieve neurological recovery. Case Description: A 26-year-old female was 23 weeks pregnant when she presented with an acute spastic paraplegia (complete motor, sensory deficit, and sphincter loss). Operative decompression utilized a Versatile Approach along with a “Hartshill rectangle” for fusion and sublaminar wiring. This procedure accomplished simultaneous anterior and posterior fixation with a single approach without the need for intraoperative radiologic imaging. Although the pregnancy was continued with an uneventful perioperative period, intra-uterine fetal demise was documented 1 month postoperatively. Within 18 postoperative months the patient was neurologically intact, and fusion was confirmed on a computed tomography scan. Conclusion: A 23-week pregnant female acutely became paraplegic due to T5 tuberculous spondylitis confirmed on an X-ray (only source of radiation), and magnetic resonance imaging. Following a decompression/ instrumented fusion performed without fluoroscopic guidance, the patient regained full neurological function. However, 1 month postoperatively, the fetus spontaneously aborted.

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Açikgöz, B., O. E. Özcan, D. Belen, A. Erbengi, and T. Özgen. "Surgery for progressive Pott's paraplegia (tuberculous paraplegia)." Spinal Cord 29, no. 8 (October 1991): 537–41. http://dx.doi.org/10.1038/sc.1991.77.

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Azevedo, ERFBM, KC Alonso, and A. Cliquet. "Body composition assessment by bioelectrical impedance analysis and body mass index in individuals with chronic spinal cord injury." Journal of Electrical Bioimpedance 7, no. 1 (August 8, 2019): 2–5. http://dx.doi.org/10.5617/jeb.2421.

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Abstract Purpose: To assess body composition and obesity in individuals with spinal cord injury (SCI) who practice and do not practice physical activity using body mass index (BMI) and bioelectrical impedance analysis (BIA). Methods: 39 patients with SCI went through BIA evaluation and BMI was assessed. Patients were divided into four groups according to injury level (paraplegia or tetraplegia) and physical activity achievement (active or inactive). Results: 22 individuals with paraplegia (7 active and 15 inactive) and 17 with tetraplegia (5 active and 12 inactive) were evaluated. BMI, fat percentage, fat mass, lean tissue mass, total body water (TBW), and TBW percentage were assessed in groups. Tetraplegic inactive groups showed higher fat percentage featuring obesity. For paraplegic active group mean fat percentage was 19.61% (±9.27) and mean fat mass was 16.66 kg (±9.71) and for paraplegic inactive group fat percentage was 23.27% (±5.94) and fat mass 18.59 kg (±7.58). For tetraplegic groups in active group the fat percentage was 17.14% (±6.32) and fat mass was 11.22 kg (±5.16) and for inactive group mean fat percentage was 33.68% (±4.74) and fat mass was 25.59 kg (±2.91). When paraplegic and tetraplegic inactive groups were compared differences were observed in fat percentage (p = 0.0003) and fat mass (p = 0.0084). Also, when tetraplegic groups (activeXinactive) were compared differences in percentage (p = 0.0019) and fat mass (p = 0.034) were observed. Only for the paraplegic inactive group BMI result was higher than 25 kg/m2. Conclusion: BMI does not discriminate between obesity levels in individuals with SCI and physical activity can improve body composition and prevent obesity in SCI patients.

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Liang, Hai-Feng, Hao Xu, Meng-Na Zhan, Jian Xiao, Juan Li, and Qin-Ming Fei. "Thoracic giant cell tumor after two total en bloc spondylectomies including one emergency surgery: A case report." World Journal of Clinical Cases 12, no. 16 (June 6, 2024): 2894–903. http://dx.doi.org/10.12998/wjcc.v12.i16.2894.

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BACKGROUND For patients with acute paraplegia caused by spinal giant cell tumor (GCT) who require emergency decompressive surgery, there is still a lack of relevant reports on surgical options. This study is the first to present the case of an acute paraplegic patient with a thoracic spinal GCT who underwent an emergency total en bloc spondylectomy (TES). Despite tumor recurrence, three-level TES was repeated after denosumab therapy. CASE SUMMARY A 27-year-old female patient who underwent single-level TES in an emergency presented with sudden severe back pain and acute paraplegia due to a thoracic spinal tumor. After emergency TES, the patient's spinal cord function recovered, and permanent paralysis was avoided. The postoperative histopathological examination revealed that the excised neoplasm was a rare GCT. Unfortunately, the tumor recurred 9 months after the first surgery. After 12 months of denosumab therapy, the tumor size was reduced, and tumor calcification. To prevent recurrent tumor progression and provide a possible cure, a three-level TES was performed again. The patient returned to an active lifestyle 1 month after the second surgery, and no recurrence of GCT was found at the last follow-up. CONCLUSION This patient with acute paraplegia underwent TES twice, including once in an emergency, and achieved good therapeutic results. TES in emergency surgery is feasible and safe when conditions permit; however, it may increase the risk of tumor recurrence.

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Cuchanski, Mathieu, and Kelly Jo Baldwin. "Mutation in KIF5A c.610C>T Causing Hereditary Spastic Paraplegia with Axonal Sensorimotor Neuropathy." Case Reports in Neurology 10, no. 2 (July 4, 2018): 165–68. http://dx.doi.org/10.1159/000490456.

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Hereditary spastic paraplegias (HSP) are a rare heterogeneous group of inherited neurodegenerative diseases characterized by progressive lower extremity spasticity and weakness. Mutations of the kinesin family member 5A (KIF5A) gene lead to a spectrum of phenotypes ranging from spastic paraplegia type 10 to Charcot-Marie Tooth Disease type 2. We report the second known case of a mutation in the KIF5A gene at c.610C>T presenting with HSP plus an axonal sensorimotor neuropathy.

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Atorino, Luigia, Laura Silvestri, Mirko Koppen, Laura Cassina, Andrea Ballabio, Roberto Marconi, Thomas Langer, and Giorgio Casari. "Loss of m-AAA protease in mitochondria causes complex I deficiency and increased sensitivity to oxidative stress in hereditary spastic paraplegia." Journal of Cell Biology 163, no. 4 (November 17, 2003): 777–87. http://dx.doi.org/10.1083/jcb.200304112.

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Mmutations in paraplegin, a putative mitochondrial metallopeptidase of the AAA family, cause an autosomal recessive form of hereditary spastic paraplegia (HSP). Here, we analyze the function of paraplegin at the cellular level and characterize the phenotypic defects of HSP patients' cells lacking this protein. We demonstrate that paraplegin coassembles with a homologous protein, AFG3L2, in the mitochondrial inner membrane. These two proteins form a high molecular mass complex, which we show to be aberrant in HSP fibroblasts. The loss of this complex causes a reduced complex I activity in mitochondria and an increased sensitivity to oxidant stress, which can both be rescued by exogenous expression of wild-type paraplegin. Furthermore, complementation studies in yeast demonstrate functional conservation of the human paraplegin–AFG3L2 complex with the yeast m-AAA protease and assign proteolytic activity to this structure. These results shed new light on the molecular pathogenesis of HSP and functionally link AFG3L2 to this neurodegenerative disease.

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Silva, Gelson Aguiar da, Juliana Neves da Costa, and Thelma Leite de Araujo. "Cuidado de enfermagem ao portador de paraplegia à luz do modelo de adaptação de Roy." Revista de Enfermagem UFPE on line 3, no. 3 (July 3, 2009): 656. http://dx.doi.org/10.5205/reuol.149-181-1-rv.0303200929.

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ABSTRACT Objective: to analyze the nursing care adequacy to the paraplegic carrier based on the Model of Adaptation of Roy. Method: case study, qualitative character carried through with a traumatic paraplegic carrier, in phase of medullar shock, in public institution in Fortaleza city, Ceará, Brazil, from October to November 2007. It’s used the process of nursing proposed by Roy, who understands in: behaviors evaluation, stimulus evaluation, nursing diagnosis, goals establishment, interventions and evaluation. Results: it had been identified alterations in the physiological mode, the presence of interference from internal stimulus, connected to the proper spinal cord injury and of external stimulus to the socioeconomic conditions of this individual in the adaptation to its new life condition. Conclusion: the alterations related to the autoconcept mode, performance role and interdependence are at risk constant of appearance, thus needing the implementation of specific interventions of nursing to this patient, with propose to minimize the problems with the involvement and the family’s participation during the rehabilitation. Descriptors: models theoretical; nursing care; paraplegic; rehabilitation.RESUMOObjetivo: teve como objetivo analisar a adequação do cuidado de enfermagem ao paciente com lesão medular baseado no Modelo de Adaptação de Roy. Método: estudo de caso, de caráter qualitativo realizado com um paciente paraplégico traumático, em fase de choque medular, em instituição pública de Fortaleza, Ceará, no período de outubro a novembro de 2007. Utilizou-se o processo de enfermagem proposto por Roy, que compreende em: avaliação de comportamentos, avaliação de estímulos, diagnóstico de enfermagem, estabelecimento de metas, intervenções e avaliação. Resultados: a partir dos resultados, foram identificadas alterações no modo fisiológico, a presença de interferência dos estímulos internos, relacionados à própria lesão medular e de estímulos externos às condições socioeconômicas deste indivíduo na adaptação à sua nova condição de vida. Conclusão: considera-se que as alterações relacionadas aos modos de autotoconceito, desempenho de papéis e interdependência estão em risco constante de aparecimento, necessitando assim da implementação de intervenções de enfermagem específicas à este tipo de paciente, objetivando minimizar os problemas com o envolvimento e a participação da família durante a reabilitação. Descritores: modelos teóricos; cuidados de enfermagem; paraplegia; reabilitação.RESUMENObjetivo: el analizar la adequacion del cuidado del enfermería la un portador de paraplejia traumática basado en el modelo de la adaptación de Roy. Método: estudio del caso, del carácter cualitativo llevado con un portador de paraplejia traumática, en la fase del shock medular, en una institución pública del Fortaleza, Ceará, en el período de octubre a noviembre de 2007. Fue utilizado el proceso del enfermería propuesto pero Roy, en quien entiende: evaluación de comportamientos, evaluación de estímulos, diagnósticos del enfermería, establecimiento de metas, intervenciones y evaluación. Resultados: fueron dentificadas las alteraciones en el modo fisiológico, la presencia de interferencia de los estímulos internos, relacionado con la propia lesión medular y del los estímulos externos a las condiciones socioeconómicas de este individuo en la adaptación a su nueva condición de la vida. Conclusión: se considera que las alteraciones relacionada con los modos del autoconcepto, desempeño de papel y la interdependencia son en riesgo constante del aparecimiento, necesitando así de la implementación de intervenciones del enfermería especificas al este tipo de paciente, objetivando reducir al mínimo los problemas con el envolvement y la participación de la familia durante la rehabilitación. Descriptores: modelos teóricos; atención de enfermería; paraplejia; rehabilitación.

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Peters, Jan, Hans-Christian Köhler, André Gutcke, and Christoph Schulze. "Fixing a Subtrochanteric Femoral Fracture with a Humerus Nail." Ortopedia Traumatologia Rehabilitacja 24, no. 2 (April 30, 2022): 133–37. http://dx.doi.org/10.5604/01.3001.0015.8375.

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A 17-year-old paraplegic patient sustained a subtrochanteric femoral fracture due to inadequate trauma. The unusual anatomical conditions associated with his congenital paraplegia did not allow treatment with a standard intramedullary implant for the femur. Because his soft tissues were already compromised, alternative options like plate osteosynthesis were considered unfavourable as a salvage procedure. Therefore, we used an implant designed for the humerus. A satisfactory result of osteosynthesis was achieved despite varus deformity, shortening and rotational error.

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Attri, JoginderPal, Ranjana Khetarpal, RajinderPal Singh, and Lipsy Bansal. "Hysterical paraplegia." Karnataka Anaesthesia Journal 1, no. 4 (2015): 208. http://dx.doi.org/10.4103/2394-6954.180657.

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Abbassioun, K., A. Amirjamshidi, and M. Zamanianpour. "Curable paraplegia." Neurosurgery 17, no. 3 (September 1985): 528. http://dx.doi.org/10.1097/00006123-198509000-00025.

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Lockwood, Annette M. "Spastic Paraplegia." Neurology Now 4, no. 3 (May 2008): 9. http://dx.doi.org/10.1097/01.nnn.0000324745.83988.de.

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&NA;. "Spastic Paraplegia." Neurology Now 4, no. 3 (May 2008): 9. http://dx.doi.org/10.1097/01.nnn.0000324746.66062.4e.

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Baker, J. H., and J. R. Silver. "Hysterical paraplegia." Journal of Neurology, Neurosurgery & Psychiatry 50, no. 4 (April 1, 1987): 375–82. http://dx.doi.org/10.1136/jnnp.50.4.375.

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Moon, Myung-Sang, Kee-Yong Ha, Doo-Hoon Sun, Jeong-Lim Moon, Young-Wan Moon, and Jin-Hwa Chung. "Pott's Paraplegia." Clinical Orthopaedics and Related Research 323 (February 1996): 122–28. http://dx.doi.org/10.1097/00003086-199602000-00017.

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Vacca, Vincent M. "Acute paraplegia." Nursing 37, no. 6 (June 2007): 64. http://dx.doi.org/10.1097/01.nurse.0000271827.99980.e8.

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Yu, John S., M. Priscilla Short, James Schumacher, Paul H. Chapman, and Griffith R. Harsh. "Intramedullary hemorrhage in spinal cord hemangioblastoma." Journal of Neurosurgery 81, no. 6 (December 1994): 937–40. http://dx.doi.org/10.3171/jns.1994.81.6.0937.

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✓ The authors describe two cases of intramedullary hemorrhage caused by thoracic hemangioblastoma. Both patients presented with acute paraplegia. The lesion in the first case was diagnosed by myelography and in the second by magnetic resonance imaging. Emergency surgical evacuation of the intramedullary hematoma and tumor was performed in these patients. Hemangioblastoma was confirmed by histopathological examination in both cases. Both patients remain paraplegic after 7 and 1 years, respectively. Intramedullary hemorrhage is a rare and devastating effect of spinal hemangioblastoma.

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Koppen, Mirko, Metodi D. Metodiev, Giorgio Casari, Elena I. Rugarli, and Thomas Langer. "Variable and Tissue-Specific Subunit Composition of Mitochondrial m-AAA Protease Complexes Linked to Hereditary Spastic Paraplegia." Molecular and Cellular Biology 27, no. 2 (November 13, 2006): 758–67. http://dx.doi.org/10.1128/mcb.01470-06.

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ABSTRACT The m-AAA protease, an ATP-dependent proteolytic complex in the mitochondrial inner membrane, controls protein quality and regulates ribosome assembly, thus exerting essential housekeeping functions within mitochondria. Mutations in the m-AAA protease subunit paraplegin cause axonal degeneration in hereditary spastic paraplegia (HSP), but the basis for the unexpected tissue specificity is not understood. Paraplegin assembles with homologous Afg3l2 subunits into hetero-oligomeric complexes which can substitute for yeast m-AAA proteases, demonstrating functional conservation. The function of a third paralogue, Afg3l1 expressed in mouse, is unknown. Here, we analyze the assembly of paraplegin into m-AAA complexes and monitor consequences of paraplegin deficiency in HSP fibroblasts and in a mouse model for HSP. Our findings reveal variability in the assembly of m-AAA proteases in mitochondria in different tissues. Homo-oligomeric Afg3l1 and Afg3l2 complexes and hetero-oligomeric assemblies of both proteins with paraplegin can be formed. Yeast complementation studies demonstrate the proteolytic activity of these assemblies. Paraplegin deficiency in HSP does not result in the loss of m-AAA protease activity in brain mitochondria. Rather, homo-oligomeric Afg3l2 complexes accumulate, and these complexes can substitute for housekeeping functions of paraplegin-containing m-AAA complexes. We therefore propose that the formation of m-AAA proteases with altered substrate specificities leads to axonal degeneration in HSP.

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Graciani, Zodja, Silvana Santos, Lucia Inês Macedo-Souza, Carlos Bandeira de Mello Monteiro, Maria Isabel Veras, Simone Amorim, Mayana Zatz, and Fernando Kok. "Motor and functional evaluation of patients with spastic paraplegia, optic atrophy, and neuropathy (SPOAN)." Arquivos de Neuro-Psiquiatria 68, no. 1 (February 2010): 03–06. http://dx.doi.org/10.1590/s0004-282x2010000100002.

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Spastic paraplegia, optic atrophy, and neuropathy (SPOAN) is an autosomal recessive complicated form of hereditary spastic paraplegia, which is clinically defined by congenital optic atrophy, infancy-onset progressive spastic paraplegia and peripheral neuropathy. In this study, which included 61 individuals (age 5-72 years, 42 females) affected by SPOAN, a comprehensive motor and functional evaluation was performed, using modified Barthel index, modified Ashworth scale, hand grip strength measured with a hydraulic dynamometer and two hereditary spastic paraplegia scales. Modified Barthel index, which evaluate several functional aspects, was more sensitive to disclose disease progression than the spastic paraplegia scales. Spasticity showed a bimodal distribution, with both grades 1 (minimum) and 4 (maximum). Hand grip strength showed a moderate inverse correlation with age. Combination of early onset spastic paraplegia and progressive polyneuropathy make SPOAN disability overwhelming.

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Nielsen, Lasse Fisker, Frank Pott, Allan Lohse, Monica Nicole Talibi, and Markus Harboe Olsen. "Cerebral fat emboli in a patient with paraplegia caused by bilateral femur fractures." BMJ Case Reports 17, no. 1 (January 2024): e257702. http://dx.doi.org/10.1136/bcr-2023-257702.

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Cerebral fat embolism is a rare cause of stroke and therefore an overlooked diagnosis. Often it is seen as a consequence of major bone fractures or after arthroplasty, and can lead to respiratory or circulatory collapse. We present a case of a patient with a history of paraplegia after a thoracic spinal cord injury that developed cerebral fat embolism following a bilateral femur fracture. Since the patient was paraplegic and with an altered mental state upon admission, femoral bone fractures were not initially suspected. The case shows the difficulties in diagnosing this condition.

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Alayafi, Hassan Ali, Mubarak Alruwaili, Talal Khalid Aljumah, Ali Alshehri, Deema Alrasheed, Muhannad Faleh Alanazi, Raed AlRuwaili, et al. "Mycoplasma pneumoniae and Schistosoma mansoni co-infection in a young patient with extensive longitudinal acute transverse myelitis." Journal of Infection in Developing Countries 16, no. 12 (December 31, 2022): 1933–38. http://dx.doi.org/10.3855/jidc.17023.

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Introduction: Acute transverse myelitis is an uncommon inflammatory, intramedullary, disorder of the spinal cord. Spastic paraplegia, impaired sphincter functions, and sensory loss, with sensory level, are the clinical manifestations of this devastating disorder. The utilization of magnetic resonant imaging (MRI) contributes to the surge in the diagnosis of more ATM cases. Although the causes of ATM are numerous, both Mycoplasma pneumoniae and Schistosoma mansoni are uncommon causes and their co-existence in the same patient has not been reported before in Saudi Arabia. Case: We report a 25-year-old ATM male patient presented with a history of sudden onset severe low back pain. Within four hours from the onset of the back pain, he became completely paraplegic with impaired functions of the bowel and urinary bladder sphincter. Furthermore, he lost all modalities of sensory functions in the lower limbs. His examination revealed spastic complete paraplegia with sensory level at T6. Clinical neurological examination revealed normal upper limbs and brain functions. The MRI of the cervico-dorsal spine showed extensive longitudinal hyperintense lesion extending from the upper cervical segments to the lower dorsal segments (extensive longitudinal transverse myelitis). A post-infectious immune-mediated predisposition was highly suspected due to the very high titers of anti-Mycoplasma pneumoniae IgM and IgG that were detected. The immunosuppressant therapy did not improve his paraplegia. A spinal cord biopsy revealed the presence of several Schistosoma mansoni ova surrounded by chronic inflammatory reactions and reactive gliosis. Conclusions: Both Mycoplasma pneumoniae and Schistosoma mansoni should be investigated in cases with extensive longitudinal ATM.

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Cheng, Zeyi, Jin Xu, and Yingqiang Guo. "The Potential Causes of Paraplegia after Coronary Artery Bypass Grafting: A Literature Review." Heart Surgery Forum 24, no. 3 (May 25, 2021): E487—E492. http://dx.doi.org/10.1532/hsf.3731.

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Paraplegia is an unpredictable neurologic complication after coronary artery bypass grafting (CABG) surgery. It is rare but fatal, and the mechanism still is unclear. We aimed to make a summary of the possible causes of paraplegia after CABG. Pubmed database was searched from January 1, 1978 to December 31, 2019, and 14 studies were finally included. Paraplegia after CABG is a multifactorial consequence, but spinal cord ischemia is the key pathological factor to postoperative paraplegia.

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Liu, Zhao-Quan, Jen-Hsien Liao, and Chih-Ju Chang. "Paraplegia after Hypotension with Pneumothorax Episode during Thoracic Spine Tumor Surgery." Case Reports in Neurological Medicine 2021 (October 23, 2021): 1–5. http://dx.doi.org/10.1155/2021/2232769.

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Paraplegia after spine surgery is a catastrophic complication. Here, we present a patient who, following laminectomy and fusion for decompression of metastatic tumor, developed paraplegia. We tried to find out the possible reason for the paraplegia. Due to prolonged hypotension during operation and new onset of pneumothorax, we think that intraoperative prolonged hypotension leads to the spinal cord ischemia which may cause neurological deterioration of paraplegia. Maintaining hemodynamic stability during spinal surgery is very important.

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Woźniewicz, Agnieszka, Joanna Kalinowska, Małgorzata Anna Basińska, and Bogdan Pietrulewicz. "Personal resources and daily life fatigue in caregivers of persons with paraplegia." Polish Journal of Applied Psychology 12, no. 4 (December 1, 2014): 29–40. http://dx.doi.org/10.1515/pjap-2015-0019.

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Abstract Taking care of a paraplegic may contribute to the caregiver’s fatigue. Sixty family caregivers participated in our study, out of which 30 provided care for paraplegics in hospital, and 30 for paraplegics at home. The Orientation to Life Qestionnaire (SOC-29) was used to measure individual sense of coherence, The Life Orientation Test - Revised for dispositional optimism, The Polish Resiliency Assessment Scale for resiliency, and The Daily Life Fatigue Questionnaire for daily life fatigue. In order to collect data about caregivers an individual examination was applied. People with higher personal resource levels such as sense of coherence, optimism and resiliency are characterized by less severe daily life fatigue.

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Whigham, Heidi M., Gary W. Ellison, and John Graham. "Aortic foreign body resulting in ischemic neuromyopathy and development of collateral circulation in a cat." Journal of the American Veterinary Medical Association 213, no. 6 (September 15, 1998): 829–32. http://dx.doi.org/10.2460/javma.1998.213.06.829.

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Ischemic neuromyopathy and paraplegia in cats are commonly associated with aortic thromboembolism. Occlusion of the abdominal aorta by a foreign body may also result in ischemic neuromyopathy and paraplegia; however, the prognosis for cats with paraplegia secondary to an aortic foreign body may be better than that for cats with paraplegia secondary to aortic thromboembolism. Collateral circulation may develop as a result of aortic occlusion by a foreign body. Progression of the collateral circulation may allow for clinical improvement without surgical intervention.

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Thiele, Clare E. "Ruptured Spinal Arteriovenous Malformation: A Rare Cause of Paraplegia in Pregnancy." Case Reports in Obstetrics and Gynecology 2018 (August 9, 2018): 1–4. http://dx.doi.org/10.1155/2018/6096483.

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Background. Ruptured spinal arteriovenous malformation (AVM) is a rare cause of paraplegia in pregnancy, with only a few case reports describing complications from spinal AVMs during pregnancy in the literature. Case. A 32-year-old woman presented at 37 weeks gestation with back pain and rapidly progressive lower limb neurological symptoms. MRI showed a previously undiagnosed spinal AVM at T8. A healthy girl was delivered by caesarean under general anaesthesia to facilitate further investigation. After spinal angiography, it was concluded the most likely aetiology was acute rupture of an intra- and perimedullary AVM with associated haemorrhage at T8 secondary to venous compression from the enlarged uterus at L5 causing high pressure within the AVM and subsequent rupture. The neurosurgical and interventional radiology teams felt the lesion was not amenable to surgical or endovascular intervention. The patient remained paraplegic with no sign of neurological recovery six months after delivery. Conclusion. While new onset paraplegia during pregnancy secondary to ruptured spinal AVM is very rare, it is important to discuss these cases to inform future practice. In contrast to previous case reports, our patient did not spontaneously recover after delivery and was not amenable to surgical or endovascular treatment.

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Hadzsiev, Kinga, László Balikó, Katalin Komlósi, Anett Lőcsei-Fekete, Györgyi Csábi, Judit Bene, Péter Kisfali, and Béla Melegh. "Genetic testing of hereditary spastic paraplegia." Orvosi Hetilap 156, no. 3 (January 2015): 113–17. http://dx.doi.org/10.1556/oh.2015.30014.

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Introduction: Hereditary spastic paraplegia is the overall term for clinically and genetically diverse disorders characterized with progressive and variable severe lower extremity spasticity. The most common causes of autosomal dominantly inherited hereditary spastic paraplegias are different mutations of the spastin gene with variable incidence in different ethnic groups, ranging between 15–40%. Mutations in the spastin gene lead to loss of spastins function, causing progressive neuronal failure, which results in axon degeneration finally. Aim: The molecular testing of spastin gene is available in the institution of the authors since January, 2014. The experience gained with the examination of the first eleven patients is described in this article. Method: After polymerase chain reaction, Sanger sequencing was performed to examine the 17 exons of the spastin gene. Multiplex ligation-dependent probe amplification was performed to detect greater rearrangements in the spastin gene. Eight of the patients were examined in the genetic counseling clinic of the authors and after detailed phenotype assessment spastin gene testing was obtained. The other three patients were referred to the laboratory from different outpatient clinics. Results: Out of the 11 examined patients, four different pathogenic mutations were found in 5 patients. Conclusions: The first Hungarian data, gained with the examination of spastin gene are presented in this article. The five patients, in whom mutations were detected, represent 45.5% of all tested patients with hereditary spastic paraplegia, which is similar to those published in the international literature. Molecular testing and subsequent detailed genotype-phenotype correlations of the Hungarian patients may serve valuable new information about the disease, which later on may influence our therapeutic possibilities and decisions. Orv. Hetil., 2015, 156(3), 113–117.

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Hanjarwati, Astri. "Aksesibilitas Layanan Publik bagi Penyandang Paraplegia Korban Bencana Gempa Bumi DIY di Kabupaten Bantul." INKLUSI 10, no. 2 (October 19, 2023): 159–74. http://dx.doi.org/10.14421/ijds.100202.

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The research explores how people with paraplegia, a disability caused by the 2006 eartquake in Bantul Regency, Indonesia, access public services. They have spinal injuries that affect their mobility. It is crucial for ensuring access to public services for people with paraplegia is vital for their post-disaster recovery and resilience. The research uses a mixed method by combining data collected through a survey and in-depth interviews, observation, and documentation studies. The research involved 44 people with paraplegia as primary data sources. The research finds that, (1) Health services are free and the bulildings are wheelchair friendly for people with paraplegia; (2) Education services are available, but not inclusive and segregate students with disabilities; (3) Places of worship and mobility infrastructure are mostly accessible, but some need improvement. Penelitian ini mengeksplorasi bagaimana penyandang paraplegia, suatu disabilitas yang disebabkan oleh gempa bumi tahun 2006 di Kabupaten Bantul, Indonesia, mengakses layanan publik. Mereka mengalami cedera tulang belakang yang mempengaruhi mobilitas mereka. Sangat penting untuk memastikan akses layanan publik bagi penyandang paraplegia demi pemulihan dan ketahanan pasca bencana. Penelitian ini menggunakan metode campuran dengan menggabungkan data yang dikumpulkan melalui survei dan wawancara mendalam, observasi, dan studi dokumentasi. Penelitian ini melibatkan 44 penyandang paraplegia sebagai narasumber data primer. Hasil penelitian ini menemukan bahwa, (1) Layanan kesehatan dapat diakses secara gratis dan bangunan ramah bagi pengguna kursi roda termasuk penyandang paraplegia; (2) Layanan pendidikan tersedia, tetapi belum inklusif dan memisahkan siswa dengan disabilitas; (3) Tempat ibadah dan infrastruktur mobilitas sebagian besar dapat diakses, tetapi beberapa perlu perbaikan.

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Murala, Sireesha, Elanagan Nagarajan, and Pradeep C. Bollu. "Hereditary spastic paraplegia." Neurological Sciences 42, no. 3 (January 13, 2021): 883–94. http://dx.doi.org/10.1007/s10072-020-04981-7.

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Sorbie, Charles. "Exercise and Paraplegia." Orthopedics 23, no. 12 (December 2000): 1244. http://dx.doi.org/10.3928/0147-7447-20001201-07.

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Popov, N. M. "Paraplegia spinalis syphilitica." Neurology Bulletin VIII, no. 2 (December 24, 2020): 76–98. http://dx.doi.org/10.17816/nb52842.

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Landau, W., and St Louis. "Denervation in paraplegia." Neurology 42, no. 12 (December 1, 1992): 2306. http://dx.doi.org/10.1212/wnl.42.12.2306.

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Rubin, M., W. F. Brown, and M. Aisen. "Denervation in paraplegia." Neurology 42, no. 12 (December 1, 1992): 2306. http://dx.doi.org/10.1212/wnl.42.12.2306-a.

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Journal articles on the topic 'Paraplegia'

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