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PubMed2001

Central and peripheral haemodynamics in individuals with paraplegia during light and heavy exercise.

The purpose of this study was to analyse lower leg skin blood flow (laser Doppler flowmetry) in five individuals with high-level paraplegia (T5-T9), six participants with low-level paraplegia (T10-T12) and six able-bodied controls during 3-minute light and heavy arm-cranking exercises (approximately 15% and 80% peak power output, respectively). Throughout light exercise, cutaneous vasoconstriction was shown for the control group (-20%), but not the low-level (+62%) or the high-level paraplegic group (+33%). During heavy exercise, vasoconstriction was initially found for controls followed by an increase in skin blood flow during the last 2 minutes, whereas the participants with paraplegia demonstrated skin blood flow increases. Skin blood flow responses were not related to lesion level. Metabolic parameters were not different among the three groups, but heart rates for participants with paraplegia were higher during heavy exercise than in controls. These results suggest impaired sympathetic vasoconstriction in individuals with paraplegia during exercise.

Adult↗
PubMed2003

Nontraumatic acute complete paraplegia resulting from cervical disc herniation: a case report.

STUDY DESIGN: A case report of nontraumatic acute complete paraplegia resulting from cervical disc herniation. OBJECTIVES: To describe a rare case of nontraumatic paraplegia resulting from enlargement of a herniated disc in the cervical spine and to outline appropriate management of a patient with severe spinal cord compression secondary to disc herniation with developmental spinal canal stenosis. SUMMARY OF BACKGROUND DATA: Acute progression of myelopathy into complete paraplegia resulting from disc herniation is rare. There are only four reported cases of nontraumatic acute myelopathy secondary to cervical disc herniation. No other report has described magnetic resonance imaging findings noted before and after the onset of acute myelopathy. METHODS: A cervical disc herniation at C6-C7 is reported in a 29-year-old man who had nontraumatic acute complete paraplegia. Neurologic and magnetic resonance imaging findings are evaluated and discussed. RESULTS: Disc herniation at C6-C7 enlarged nontraumatically, resulting in complete paraplegia. Emergent anterior decompression followed by secondary posterior multilevel decompression was performed. Magnetic resonance imaging studies revealed localized high signal intensity change in the spinal cord. No neurologic recovery was achieved 3 years post-surgery. CONCLUSION: We emphasize that there is a possibility of acute, irreversible progression of paralysis secondary to nontraumatic enlargement of cervical disc herniation with canal stenosis. In these cases, immediate early decompressive surgery is crucial to the prevention of severe myelopathy.

Acute Disease↗
PubMed2005

Prognosis of conservatively treated patients with Pott's paraplegia: logistic regression analysis.

OBJECTIVE: To evaluate the prognostic significance of various clinical, radiological, and neurophysiological findings in conservatively treated patients with Pott's paraplegia, using multiple regression analysis. METHODS: The study included 43 patients with Pott's paraplegia, managed conservatively. The diagnosis of Pott's spine was based on clinical, magnetic resonance imaging, and computed tomography or ultrasound guided aspiration biopsy. All patients were examined clinically, and motor evoked potentials (MEPs) to lower limbs and tibial somatosensory evoked potentials (SEP) were recorded. Outcome at six months was defined as good or poor. For evaluating predictors of outcome, 15 clinical, investigative, and evoked potential variables were analysed, using multiple logistic regression analysis. RESULTS: The age range of the patients was 16-70 years, and 22 were female. Mild spasticity with hyperreflexia only was seen in 13 patients. In the remaining, weakness was severe in eight, and moderate and mild in 11 patients each. Twenty patients had loss of joint position sensation. MEP and SEP were abnormal in 19 and 18 patients, respectively. On multiple regression analysis, the best model predicting six month outcome included power, paraplegia score, SEP, and MEP. CONCLUSION: Patients with Pott's paraplegia are likely to recover completely by six months if they have mild weakness, lower paraplegia score and normal SEPs and MEPs.

Adolescent↗
PubMed2000

Ventilatory and respiratory muscle responses to hypercapnia in patients with paraplegia.

To evaluate ventilatory and respiratory muscle responses to hypercapnia in patients with paraplegia with paralysis of abdominal muscles, we studied seven patients with complete transection of the midthoracic cord (Th6-Th7) and six normal subjects. Minute ventilation (V E) and mean inspiratory flow responses to hypercapnia were similar in normal subjects and patients with paraplegia, but in the latter, at any given level of end-tidal CO(2) partial pressure (PET(CO(2))), tidal volume (VT) was reduced and frequency was increased. In normal subjects during hypercapnia, end-expiratory transpulmonary pressure (PL) and abdominal volume at end expiration decreased markedly, whereas end-expiratory volume of the rib cage (Vrc,E) remained constant, suggesting progressive recruitment of abdominal muscles. In patients with paraplegia compared to normal subjects the decrease in end-expiratory PL was reduced, and it was associated with a decrease in Vrc,E, suggesting recruitment of rib cage expiratory muscles. For a PET(CO(2)) of 70 mm Hg the estimated expiratory muscle contribution to VT was 10.3 and 28.4% (p < 0.02) in patients with paraplegia and normal subjects, respectively. We conclude that the V E-CO(2) relationship is preserved in patients with paraplegia with the development of a rapid and shallow pattern of breathing. This suggests that expiratory muscle paralysis elicits adaptation of the ventilatory control system similar to that observed in patients with generalized respiratory muscle weakness.

Adult↗
PubMed2002

Spastic paraplegia, ataxia, mental retardation (SPAR): a novel genetic disorder.

OBJECTIVE: To describe a kindred with a dominantly inherited neurologic disorder manifested either as uncomplicated spastic paraplegia or ataxia, spastic paraplegia, and mental retardation. METHODS: Neurologic examinations and molecular genetic analysis (exclusion of known SCA and HSP genes and loci; and trinucleotide repeat expansion detection [RED]) were performed in six affected and four unaffected subjects in this family. MRI, electromyography (EMG), and nerve conduction studies were performed in three affected subjects. RESULTS: The phenotype of this dominantly inherited syndrome varied in succeeding generations. Pure spastic paraplegia was present in the earliest generation; subsequent generations had ataxia and mental retardation. MRI showed marked atrophy of the spinal cord in all patients and cerebellar atrophy in those with ataxia. Laboratory analysis showed that the disorder was not caused by mutations in genes that cause SCA-1, SCA-2, SCA-3, SCA-6, SCA-7, SCA-8, and SCA-12; not linked to other known loci for autosomal dominant ataxia (SCA-4, SCA-5, SCA-10, SCA-11, SCA-13, SCA-14, and SCA-16); and not linked to known loci for autosomal dominant hereditary spastic paraplegia (HSP) (SPG-3, SPG-4, SPG-6, SPG-8, SPG-9, SPG-10, SPG-12, and SPG-13) or autosomal recessive HSP SPG-7. Analysis of intergenerational differences in age at onset of symptoms suggests genetic anticipation. Using RED, the authors did not detect expanded CAG, CCT, TGG, or CGT repeats that segregate with the disease. CONCLUSIONS: The authors describe an unusual, dominantly inherited neurologic disorder in which the phenotype (pure spastic paraplegia or spastic ataxia with variable mental retardation) differed in subsequent generations. The molecular explanation for apparent genetic anticipation does not appear to involve trinucleotide repeat expansion.

Adolescent↗
PubMed2006

Autonomic recovery from peak arm exercise in fit and unfit individuals with paraplegia.

INTRODUCTION: Altered autonomic cardiovascular control in persons with paraplegia may reflect peripheral sympathetic denervation caused by the injury or deconditioning due to skeletal muscle paralysis. Parameters of autonomic cardiovascular control may be improved in fit persons with paraplegia similar to effects reported in the noninjured population. PURPOSE: To determine differences in resting and recovery HR and cardiac autonomic control in fit and unfit individuals with paraplegia. METHODS: Eighteen healthy males with paraplegia below T6 were studied; nine participated in aerobic exercise conditioning (fit: >or=30 min.d, >or=3 d.wk, >or=6 months), and nine were sedentary (unfit). Analysis of heart rate variability (HRV) was used to determine spectral power (ln transformed) in the high- (lnHF) and low-frequency (lnLF) bandwidths, and the LF/HF ratio was calculated. Data were collected at baseline (BL) and at 2, 10, 30, 60, and 90 min of recovery from peak arm cycle ergometry. RESULTS: The relative intensity achieved on the peak exercise test was comparable between the groups (i.e., 88% peak predicted HR). However, peak watts (P<0.001) and oxygen consumption (P<0.01) were higher in the fit compared with the unfit group (56 and 51%, respectively). Recovery lnHF was increased (P<0.05), and recovery lnLF (P<0.01) and LF/HF (P<0.05) were reduced in the fit compared with the unfit group. Mean recovery autonomic activity was not different from BL in the fit group. In the unfit group, mean recovery lnHF was reduced, and mean recovery lnLF and LF/HF remained elevated above BL. CONCLUSION: These data suggest that fit individuals with paraplegia have improved cardiac autonomic control during the postexercise recovery period compared with their unfit counterparts.

Adult↗
PubMed2001

[A family of hereditary spastic paraplegia with dementia, ataxia, and dystonia].

We reported three siblings with complicated hereditary spastic paraplegia. The striking features in these patients were characterized by early onset of gait disturbance, mental deficiency, and dystonia. The most likely diagnosis was Mast syndrome. Patient 1: A 44 years-old woman. She first developed gait disturbances at age of 8. She was admitted in our hospital because of progressive spastic paraplegia. Neurological examination revealed mental deficiency, saccadic pursuit eye movement, speech disturbance of cerebellar type, ataxia, and spastic paraplegia. She showed also dystonia in the face, tongue, and trunk. MRI showed cerebellar atrophy. Patient 2: A 51 years-old brother of the patient 1. He had mentally retarded. Late teens he developed gait disturbance. Gradually he manifested spastic paraplegia, dysarthria, dysphasia, mental deficiency, and ataxia. He also showed incontinence of urine and feces. Then he became bedridden, apathetic, and showed forced crying. MRI showed diffuse brain atrophy. Patient 3: A 48 year-old woman. This woman, a sister of the patient 1, showed progressive gait disturbance and dysarthria. She also developed incontinence, apathy, and dystonia. She became bedridden, responding to simple questions with only occasional single-word answers. Her speech was slurred, and spastic paraplegia was noted. MRI showed diffuse brain atrophy including marked atrophy of the cerebellum.

Brain↗
PubMed2003

Acute postoperative paraplegia complicating with emergency graft replacement of the ascending aorta for the type a dissection.

Postoperative paraplegia complicating with type A dissection is extremely rare. We describe a case of acute paraplegia after emergency graft replacement of the ascending aorta for type A dissection. A 63 year-old hypertensive man presented to hospital with chest pain. A chest computed tomography demonstrated an aortic dissection of the ascending aorta with mild pericardial effusion. Under deep hypothermic circulatory arrest with concomitant antegrade selective cerebral perfusion, the ascending aorta was replaced. The patient regained consciousness six hours after operation, however, he was complicated with paraplegia. All sensation was lost below the level of Th12. The cause of the paraplegia was assumed to be a thrombotic occlusion of costal arteries, which originated from the false lumen. Spinal fluid was drained for three days. Hyperbaric oxygenation therapy was started four days after onset of paraplegia. Fortunately, our patient recovered gradually, and he was doing well and was walking independently at one-year follow-up. (Ann Thorac Cardiovasc Surg 2003; 9: 330-3)

Acute Disease↗
PubMed1991

[A new type of complicated form of hereditary spastic paraplegia showing mental deterioration, quadriplegia with muscular atrophy, sensory disturbance, extrapyramidal disorders, and epilepsy].

UNLABELLED: This study proposes a new type of complicated form of hereditary spastic paraplegia (HSP) and some problems on a clinico-pathological classification of HSP. The present study includes three male and two female patients from two families (A and B). In the family A, four siblings (two males and two females) were affected. Spastic paraplegia developed as an initial symptom. In the family B, a man was affected with spastic paraplegia which had started at the age of eleven. His two half-sisters are normal. All parents in two pedigrees are healthy. The parents in the family B are first cousins. CLINICAL FEATURES: Their physical development was normal, but all of them showed mild mental retardation. Gait disturbance due to spastic paraplegia and mental deterioration developed at the age of high teens. At the age of high 20's, they became unable to walk, because of progressive spastic paraplegia and other complicated neurological impairments including pyramidal disorders in the upper limbs, generalized neurogenic muscular atrophy, sensory disturbance and bradykinesia. Some cases showed rigidity and/or spasticity. At the age of high 30's, they became bed-ridden, because of quadriplegia with generalized muscular atrophy. Three cases in the family A suffered from convulsions which started at the high 30's. Mild athetoid movement in the face and neck was observed in three cases in the family A. All patients became apathetic and indifferent at least by the age of 40. Laboratory findings and data: CT scan yielded brain atrophy and dilatation of the lateral ventricles, atrophy of the corpus callosum and hyperostosis of the cranium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Is paraplegia after repair of coarctation of the aorta due principally to distal hypotension during aortic cross-clamping?

The hypothesis is presented that paraplegia after coarctation of the aorta is principally due to hypotension of sufficient severity and duration. In a group of 103 patients who underwent surgery during a 10-year period, the distal aortic pressure was maintained above 60 mm Hg while the aorta was cross-clamped or the period of cross-clamping was limited to less than 20 minutes. No neurologic problems occurred. In 17 of the 103 cases aortic pressure decreased below 60 mm Hg, occurring in 8% of patients with the aorta occluded below the left subclavian artery but in 30% of those occluded above. Therapeutic measures used in the 17 patients included infusion of metaraminol in five and limiting cross-clamp time to less than 20 minutes in 11. The theory is proposed that ligation of intercostal arteries in a patient with coarctation cannot injure the spinal cord because the normal direction of blood flow is reversed. Certainly, in patients without a coarctation, such as thoracic aneurysms, ligation of a critical intercostal artery may injure the spinal cord. However, in patients with coarctation the direction of blood flow is reversed, blood flowing from the intercostals into the distal aorta. The vague relationship long noted between development of collateral circulation, including rib notching, and the frequency of paraplegia probably depends not on the presence of enlarged intercostal arteries but on whether their temporary occlusion at the time of aortic cross-clamping results in distal hypotension. Data with somatosensory-evoked potentials measured during operations on the thoracic aorta in 25 patients found no changes in sensory potentials as long as the distal aortic pressure remained above 60 mm Hg, but a gradual disappearance was found at lower pressures. In five of six patients with large thoracicoabdominal aneurysms in whom sensory potentials were absent for longer than 30 minutes, paraplegia resulted. Use of somatosensory potentials provides a significant method for evaluating methods to protect from paraplegia. This method should be far more productive than are simple clinical experiences because the fortunate rare occurrence of paraplegia, one in 200, greatly limits available data.

Aorta, Thoracic↗
PubMed1995

[Syphilitic thoracic aortic aneurysm with destruction of vertebral body, producing numbness of lower extremities and paraplegia].

Numbness and paraplegia are uncommon complaints in patient with thoracic aortic aneurysm (TAA). The patient was a 64-year-old man. He suffered numbness and gait disturbance (paraplegia). The blood examination showed no positive findings except a Wassermann was positive. Roentgen examination of the chest showed two abnormal shadows like tumors. The CT and MRI revealed destruction of the vertebral bodies and TAAs adjacent to the spinal cord. After the graft replacement was performed, numbness and paraplegia disappeared. This suggests that in our patient the TAAs destruct the vertebral body and produce pressure on the spinal cord, causing numbness and paraplegia. We experienced a rare case of the syphilitic TAA producing bone destruction, numbness and paraplegia.

Aortic Aneurysm, Thoracic↗
PubMed1995

Paraplegia at the Tikur Anbessa Teaching Hospital: a seven year retrospective study of 164 cases.

Admission analysis of adult non-traumatic paraplegia and paraparesis from 1981 to 1988 was carried out. Information was collected from charts of 223 consecutive admissions according to a pre-set protocol. Paraplegia or paraparesis was responsible for 164(13.4%) of all neurological admissions over the study period. The median age of the patients was 36 years with a male to female ratio of 1.7:1. Tuberculosis was the leading cause of paraplegia or paraparesis accounting for 47% of the cases. Tumours (20%), Landry-Guillain-Barre' syndrome (12.2%) and tropical spastic paraparesis (TSP) (9.8%) were important but less frequent causes in this series. Other causes like disc prolapse, transverse myelitis, spinal artery stroke and fluorosis were rarely encountered. Vertebral deformity (88.1%), vertebral tenderness (88.1%) and abnormal plain spinal X-ray (89%) were the most helpful findings in the diagnosis of tuberculous paraplegia. Nearly all cases of tuberculous paraplegia were treated medically alone. However, the outcome of treatment as judged by the treating physicians was good with a significant response recorded in 78%.

Adult↗
PubMed2004

Three novel mutations of the spastin gene in Chinese patients with hereditary spastic paraplegia.

BACKGROUND: Hereditary spastic paraplegia is a group of genetically heterogeneous neurodegenerative disorders characterized by progressive spasticity of the lower limbs. The most common form of hereditary spastic paraplegia is caused by mutations in the spastin gene (SPG4), which encodes spastin, an adenosine triphosphatase associated with various cellular activities protein. OBJECTIVE: To investigate the Chinese patients with hereditary spastic paraplegia for mutations in SPG4. METHODS: DNA samples from 31 unrelated patients were analyzed for mutations in SPG4 by single-strand conformation polymorphism analysis and direct sequencing. All DNA samples were screened for mutations by the polymerase chain reaction, followed by electrophoresis and silver staining. Each new variant identified was analyzed in 50 control subjects to determine whether it is a polymorphism or a mutation. RESULTS: Three novel mutations were detected in 4 affected individuals, including 2 missense mutations (T1258A and A1293G) and 1 deletion mutation (1668-1670delCTA). CONCLUSIONS: To our knowledge, this is the first report of SPG4 mutations in the People's Republic of China. The percentage of involved Chinese families with autosomal dominant hereditary spastic paraplegia with an SPG4 mutation is 18% (4/22), lower than the estimated 40% linked to this locus.

Adenosine Triphosphatases↗
PubMed2007

Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia.

Extramedullary tumors, also known as granulocytic sarcomas (GS), occur most frequently in acute myelogenous leukemia (AML). They may signal the onset of the accelerated phase of chronic myelogenous leukemia (CML) or the blastic transformation of a myeloproliferative disorder. Occasionally, a GS may be the presenting sign of undiagnosed AML, and rarely the presenting sign of undiagnosed CML or aleukemic leukemia. Paraplegia due to a spinal cord GS is an extremely rare presentation of undiagnosed leukemia. This is the first case report of paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed CML. A 53-year-old woman reported back pain for 6 days, rapidly progressing to paraplegia. Physical examination noted a large abdominal mass and flaccid paralysis in both lower extremities. Spinal MRI revealed a T4-T6 vertebral mass causing spinal stenosis and cord compression. Tumor debulking and laminectomy were performed emergently. The tumor consisted of noncohesive blast cells. The CBC revealed a leukocyte count of 238,300/microl and a differential consistent with CML. Reexamination of the patient found that the abdominal mass was a giant spleen. Further immunohistochemical studies of the tumor were consistent with extramedullary acute megakaryoblastic blast transformation of CML. Although extramedullary blast crises herald the accelerated phases in approximately 10% of CML cases, megakaryoblastic blast transformation of CML accounts for less than 3% of these cases. The combination of acute paraplegia and megakaryoblastic transformation in a previously undiagnosed patient with CML is extremely rare and may pose a diagnostic dilemma.

Combined Modality Therapy↗
PubMed2005

Mapping of a new form of pure autosomal recessive spastic paraplegia (SPG28).

Pure hereditary spastic paraplegias are characterized by isolated and progressive spasticity in the lower limbs. We mapped the spastic paraplegia 28 (SPG28) locus to chromosome 14q21.3-q22.3 in a Moroccan family with autosomal recessive hereditary spastic paraplegia. Affected patients experienced development of progressive spastic gait during childhood and required help walking in their early 40s. Nine additional hereditary spastic paraplegia families were not linked to this locus, demonstrating further genetic heterogeneity. No mutations were found in exons of GCH1 and SPG3A, two genes from the candidate region involved in movement disorders.

Adult↗
PubMed1997

Effect of nitroglycerin and cerebrospinal fluid drainage on spinal cord perfusion pressure and paraplegia during aortic cross-clamping.

When sodium nitroprusside (SNP) is used to control proximal blood pressure (Px-BP) during cross-clamping (AXC) of the thoracic aorta, it decreases spinal cord perfusion pressure (SCPP) by reducing distal aortic pressure (Ds-BP) and increasing cerebrospinal fluid pressure (CSFP). The decrease cannot be reversed by CSF drainage (CSFD) because such drainage is limited by a reduction in compliance of the spinal canal. Nitroglycerin can also be used to control Px-BP, but its effect on CSF dynamics has not previously been investigated. In the present study we have compared the effects of NTG alone and in combination with CSFD, with SNP and CSFD. Each group (Gp) of six dogs was treated with SNP + CSFD (Gp 1), NTG alone (Gp 2), and NTG + CSFD (Gp 3). Left carotid and right femoral arteries were catheterized to monitor Px-BP and Ds-BP, respectively. CSFP was monitored and CSF was drained through a spinal needle placed in the cisterna cerebellomedullaris. The thoracic aorta was cross-clamped via a left thoracotomy for 60 min. Data were acquired at baseline, during aortic occlusion, and 24 hr after surgery. There were no significant differences in any measurements among the three groups before AXC; after AXC, Px-BP was maintained between 85 and 95 mm Hg in all groups. Ds-BP was significantly lower in Gp 1 than Gp 2 and 3 (7 +/- 2 mm Hg vs. 13 +/- 3 mm Hg and 17 +/- 2 mm Hg, respectively P < 0.05). CSFP did not differ between Gp 1 and 2 (10 +/- 3 mm Hg vs. 9 +/- 1 mm Hg, P > 0.05). CSFD effectively kept CSFP at zero values in Gp 3 during AXC, but not in Gp 1. SCPP was significantly higher in Gp 3 than in Gp 1 and 2 (17 +/- 2 mm Hg vs -3 +/- 4 mm Hg and 4 +/- 1 mm Hg, respectively, P < 0.05). All animals in Gp 1 and 2 suffered paraplegia, as opposed to none in Gp 3. NTG causes paraplegia by decreasing SCPP. When used in conjunction with CSFD, it controls Px-BP without causing paraplegia. CSFD cannot counteract the negative effects of SNP on SCPP; therefore, SNP contributes to postoperative paraplegia. The effects of NTG on cerebrospinal fluid dynamics are different from those of SNP. We caution surgeons against the use of NTG without CSFD during aortic cross-clamping.

Animals↗
PubMed2006

[Paraplegia after acute thoracic pain].

Severe neurological complications such as spinal cord ischemia and paraplegia can occur with acute aortic dissection in 3%. This report describes the case of a 67-year old patient with delayed onset of paraplegia 8 h after acute chest pain. Contrast enhanced computed tomography documented Stanford type B dissection confined to a short segment of the aorta. Furthermore, magnetic resonance imaging revealed intraspinal intraaxial hematoma of the myelon, which can explain the neurological complication. This case shows that even in the scenario of acute aortic dissection other mechanisms for paraplegia may be operational than dissection itself. Paraplegia in this case results from intramyelon bleeding preceding aortic dissection.

Acute Disease↗
PubMed2004

Iatrogenic paraplegia in spinal surgery.

INTRODUCTION: Paraplegia as a result of a surgical spinal procedure is a rare complication. The risk cannot be precisely quantified due to the lack of current data. The aim of this study was to record a sufficiently large number of major spinal operations, especially extended methods in scoliosis surgery. Hereby, a reliable statement regarding the risk of severe neurological complications with these surgical techniques should be possible. First, a retrospective analysis of patients from a German spine centre (spinal fusion) and a survey of 17 German centres of spinal surgery were conducted for the retrospective acquisition of severe iatrogenic neurological complications. MATERIALS AND METHODS: The study included 1194 patients who underwent a spinal fusion during the period 1992-2002. The incidents of postoperative paraplegia are described in detail, and case studies done. Possible causes, methods of intraoperative monitoring and options of therapy are discussed according to research in relevant publications. Additionally, severe neurological complications of 3115 spinal operations were recorded in a standardised survey conducted throughout major German spinal centres. RESULTS: Of the 1194 patients surveyed, 7 (0.59%) experienced a postsurgical complete or incomplete paraplegia. In 3 of the recorded cases, the cause could be identified. The survey of 3115 scoliosis surgeries showed that iatrogenic paraplegia occurred with a frequency of 0.55%. The risks associated with short spinal fusions (0.14%), cervical discectomies (0.07%) and lumbar discectomies (0.03%) are considerably less. CONCLUSION: Operative treatment of scoliosis with a high degree of correction carries a risk of neurological complications of about 0.5%. Mechanical as well as ischaemic damage to the spinal cord can be detected early by means of consistent intraoperative neuromonitoring.

Adolescent↗