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At least 145 records · Page 8Linked to original sources
PubMed2006

Reversal of delayed-onset paraplegia with thrombectomy of an interposed graft for the intercostal artery after thoracic descending aortic aneurysm repair.

A 78-year-old woman who had previously undergone prosthetic graft replacement of the total aortic arch was admitted to repair a chronic expanding type IIIb dissecting aneurysm. Firstly the patient's abdominal aorta was replaced with a prosthetic graft without any complications, then the thoracicdescending aorta was repaired five months later. Surgery for the thoracic descending aorta was performed with distal perfusion, cerebrospinal fluid drainage, somatosensory evoked potential (SEP) monitoring and reimplantation of three pairs of intercostal arteries. During surgery, SEP showed no significant changes, and the patient awoke without paraplegia three hours after the surgery. However, she developed bilateral complete paraplegia eight hours after the surgery. Reexploration demonstrated thrombo-occlusion of the sidearm graft for reimplantation of the Th10 intercostal artery. After thrombectomy of the sidearm graft, there was gradual neurological recovery and the patient was ambulatory when discharged. Quick treatment to restore the spinal cord blood supply promoted recovery from paraplegia.

Aged↗
PubMed2000

Prevention of paraplegia in transluminally placed endoluminal prosthetic grafts for descending thoracic aortic aneurysms.

OBJECTIVE: To evaluate the efficacy of a temporary balloon occlusion test for the prevention of paraplegia following transluminally placed endoluminal prosthetic grafts for descending thoracic aortic aneurysms. SUBJECTS AND METHODS: Two occlusion balloons were inserted via the brachial and femoral arteries and positioned in the proximal and distal neck of the descending thoracic aortic aneurysms using fluoroscopy. After temporary occlusion of the thoracic aorta by inflation of both the proximal and distal balloons, the evoked spinal potential was measured for 15 mins. A maximum amplitude during temporary balloon occlusion test decreasing by more than 20% of the pre-balloon occlusion level was considered to be significant, enough to not perform transluminally placed endoluminal prosthetic grafts, but instead an open repair. The test was applied in 12 cases (9 males and 3 females, 50-86 years old). All aneurysms were located between the Th6 and Th12 with a maximum diameter of 40-70 mm, and average of 56 mm. RESULTS: The changes in maximum amplitude of evoked spinal potential remained within 20% of the value before balloon occlusion in 11 cases. Transluminally placed endoluminal prosthetic grafts were performed in these 11 cases and no instance of paraplegia or other complication relating to the test was observed. Deployment of stent-grafts was successful in 10 cases (91%). CONCLUSION: It is suggested that the preoperative measurement of evoked spinal potential during temporary balloon occlusion is clinically useful for the assessment of the risk to paraplegia occurring in transluminally placed endoluminal prosthetic grafts.

Aged↗
PubMed2000

Acute-onset nontraumatic paraplegia in childhood: fibrocartilaginous embolism or acute myelitis?

Fibrocartilaginous embolus causing acute spinal cord infarction is a rare cause of acute-onset paraplegia or quadriplegia. Few cases of survivors have been reported in the neurosurgical literature, with most reports involving postmortem or biopsy findings. There is little information on MRI findings in such patients. We present the youngest patient ever reported, and discuss the important differences between fibrocartilaginous embolus and acute myelitis of childhood. A 6-year-old girl with a history of back pain presented with sudden-onset nontraumatic paraplegia, with a clinical anterior spinal artery syndrome. Initial MRI scan revealed intervertebral disc disease at L1-2 and an incidental thoracic syrinx, but no cause for her acute-onset paraplegia was identified. Cerebrospinal fluid and other investigations were all negative. Sequential MRI scans revealed development of spinal cord expansion from T10 to the conus medullaris, with increased cord signal in the anterior aspect of the spinal cord. The intervertebral disc disease was unchanged. The imaging and clinical findings were caused by fibrocartilaginous embolus, which meant there was no need for spinal cord biopsy. The report describes the clinical and imaging criteria for diagnosis of fibrocartilaginous embolus, highlighting the case for avoiding an unnecessary biopsy. The clinical pattern in the paediatric group is discussed, with features differentiating it from acute myelitis of childhood.

Acute Disease↗
PubMed2000

A rare case of osteoporotic spine fracture associated with epidural lipomatosis causing paraplegia following long-term cortisone therapy.

Cushing's syndrome is frequently associated with osteoporosis. Therefore, the incidence of osteoporotic spine fractures is significant. They are a rare cause of paraplegic syndromes. Additionally, epidural lipomatosis may occur in those patients. The combination of both fracture and lipomatosis may cause neurological deficit. A case of a young patient suffering from drug-induced Cushing's syndrome is reported. She developed progressive paraplegia. Radiographs demonstrated kyphosis of the thoracic spine from T7 to T9 and pathologic fractures. Urgent operation was planned to stabilize and decompress the spinal cord in the area of the kyphosis. Fortunately, magnetic resonance imaging (MRI) was conducted first. It confirmed pathologic fractures of T7-9 but also showed massive epidural fat extending from the level of T1 to T9. As suspected, laminectomy alone in the area of the fracture proved to be insufficient, as shown by myelography during operation. For treatment of paraplegia in this case of symptomatic epidural lipomatosis, an expanded laminectomy was necessary to remove all the epidural fat. Having undergone this procedure, the patient is now recovering from paraplegia. Our experience suggests that care should be taken before operative treatment of patients with pathological fractures in combination with Cushing's syndrome. In addition to vertebral fractures, epidural lipomatosis has to be taken into consideration. Those patients with neurological deficits have to be treated by an extensive laminectomy.

Adult↗
PubMed1997

Evidence of a third locus in X-linked recessive spastic paraplegia.

We have investigated a family with severe X-linked spastic paraplegia and assigned the disease locus to Xq11.2-q23 by linkage and haplotype analysis. This region harbors the gene coding for proteolipid protein, which is mutated in one of the two established forms of X-linked spastic paraplegia, i.e., SPG2. We have performed extensive mutation analysis of this gene. Our failure to detect a mutation in this family suggests a third locus in X-linked recessive spastic paraplegia.

DNA-Binding Proteins↗
PubMed2006

Four mutations of the spastin gene in Japanese families with spastic paraplegia.

Hereditary spastic paraplegia (HSP) is a group of genetically heterogeneous neurodegenerative disorders characterized by slowly progressive spasticity and weakness of the lower limbs. HSP is caused by failure of development or selective degeneration of the corticospinal tracts, which contain the longest axons in humans. The most common form of HSP is caused by mutations of the spastin gene (SPAST), located on chromosome 2p21-p22, which encodes spastin, one of the ATPases associated with diverse cellular activities (AAA). In this study, we detected four causative mutations of SPAST among 14 unrelated patients with spastic paraplegia. Two missense mutations (1447A-->G, 1207C-->G) and two deletion mutations (1465delT, 1475-1476delAA) were located in the AAA cassette region. Three of these four mutations were novel. Previous reports and our results suggest that the frequency of SPAST mutations is higher among Japanese patients with autosomal dominant HSP, although SPAST mutations are also observed in patients with sporadic spastic paraplegia.

Adenosine Triphosphatases↗
PubMed2004

Early onset autosomal dominant spastic paraplegia caused by novel mutations in SPG3A.

Hereditary spastic paraplegia (HSP) is a group of neurodegenerative disorders mainly characterized by progressive spasticity of the lower limbs. The major features of HSP are a marked phenotypic variability both among and within families and an extended genetic heterogeneity. More than 20 HSP loci and 10 spastic paraplegia genes (SPG) have been identified to date, including the genes responsible for the two most frequent forms of autosomal dominant spastic paraplegia (AD-HSP), encoding spastin (SPG4) and atlastin (SPG3A), respectively. To date, only eight mutations have been described in the atlastin gene, which was reported to account for about 10% of all AD-HSP families. We investigated 15 German and French AD-HSP families, including the 3 large pedigrees that allowed the mapping and subsequent refinement of the SPG3A locus. Three novel mutations were found in exons 4, 9, and 12 of the atlastin gene and the common R239C mutation located in exon 7 was confirmed in a 7th family of European origin. Overall, the comparison of the clinical data for all SPG3A-HSP families reported to date failed to reveal any genotype/phenotype correlation as demonstrated for other forms of AD-HSP. However, it confirmed the early onset of this form of HSP, which was observed in almost all affected individuals with a mutation in the atlastin gene.

Adolescent↗
PubMed2006

Hereditary spastic paraplegia.

The hereditary spastic paraplegias (HSPs) comprise a large group of inherited neurologic disorders. HSP is classified according to the mode of inheritance, the HSP locus when known, and whether the spastic paraplegia syndrome occurs alone or is accompanied by additional neurologic or systemic abnormalities. Analysis of 11 recently discovered HSP genes provides insight into HSP pathogenesis. Hereditary spastic paraplegia is a clinical diagnosis for which laboratory confirmation is sometimes possible, and careful exclusion of alternate and co-existing disorders is an important element in HSP diagnosis. Treatment for HSP is presently limited to symptomatic reduction of muscle spasticity, reduction in urinary urgency, and strength and gait improvement through physical therapy. Prenatal genetic testing in HSP is possible for some individuals with the increasing availability of HSP gene analysis.

Diagnosis, Differential↗
PubMed1994

Spinal cord protection: development of a paraplegia-preventive solution.

We present a clinically available method to protect the spinal cord against ischemic or reperfusion injury and to prevent paraplegia after cross-clamping of the aorta. We separated 35 rabbits into five equal groups and clamped each animal's abdominal aorta distal to the left renal artery. We also occluded the aortas 2 cm above the iliac bifurcation for 45 minutes with inflated 5F balloon catheters. Through the catheter port distal to each balloon one of four different solutions was infused at 3 degrees C for 3 minutes at a rate of 5 mL/min (group I, uninfused control; group II, lactated Ringer's solution; group III, lactated Ringer's solution + 30 mg/kg of methylprednisolone; group IV, lactated Ringer's solution+methylprednisolone + 3 mL of 20% mannitol; group V, lactated Ringer's solution+methylprednisolone+mannitol + 10 mg/kg of vitamins E and C). We assessed the neurologic status of the hind limbs on the second postoperative day using Tarlov's criteria. The neurologic status in groups III, IV, and V was significantly superior to that of group I (p < 0.05, groups III versus I; p < 0.01, groups IV and V versus I). Spastic paraplegia occurred in 71% of group I, in 43% of group II, in 29% of group III, in 14% of group IV, and not at all in group V. The infusion of our specially blended solution with several spinal cord neuroprotective properties (hypothermia, methylprednisolone, mannitol, and vitamins E and C) achieved the best spinal cord protection against ischemic or reperfusion injury and prevented postoperative paraplegia.

Animals↗
PubMed1986

Anterior communicating artery aneurysm presenting with sudden paraplegia.

A case of sudden paraplegia as the first symptom of a ruptured anterior communicating artery aneurysm is reported. The sudden appearance of paraparesis or paraplegia is an exceptional event in patients with intracranial aneurysms. The various pathogenetic mechanisms are briefly discussed. The insufficient blood perfusion of both paracentral areas was the cause of paraplegia in the reported case.

Humans↗
PubMed1987

Ischemic injury to the spinal cord as a cause of transient paraplegia.

Spinal cord ischemia presenting as acute paraplegia is an uncommon occurrence not previously reported in the emergency medicine literature. Paraplegia due to spinal ischemia is seen most commonly after intraoperative aortic manipulation; however, acute hypotension and prolonged cardiopulmonary resuscitation are also reported settings. The differential diagnosis of acute, non-traumatic paraplegia includes mechanical spinal cord compression, acute transverse myelitis, and polyneuritis.

Acute Disease↗
PubMed1995

Exclusion of the candidate locus FSP1 in six families with late-onset autosomal dominant spastic paraplegia.

Hereditary spastic paraplegias are neurological hereditary conditions of unknown aetiology. In pure spastic paraplegia, most of the pedigrees display an autosomal dominant mode of inheritance. A gene for pure autosomal dominant spastic paraplegia (ADSP), termed FSP1, was mapped to chromosome 14q in a large pedigree with early-onset disease. This locus was tested by linkage analysis in six large French kindreds of ADSP with late-onset disease, using four microsatellites spanning a 9 cM interval including FSP1. FSP1 could be excluded in five of the six families, while no evidence for linkage was found in the remaining family. These results suggest that FSP1 is not involved in late onset ADSP, at least in the six families studied.

Adolescent↗
PubMed2006

[Transforaminal epidural steroid injection and paraplegia: case report and bibliographic review].

OBJECTIVES: We report a patient in whom paraplegia developed following transforaminal epidural injection of a corticosteroid and discuss the physiopathology of this complication, based on a literature survey. CASE REPORT: A 40-year-old man presented with low-back pain and symptoms of L4 radiculopathy due to degenerative disc herniation resistant to conventional medical treatment. Computed tomography revealed posterolateral L4-L5 disc protrusion. A dosage of 125 mg of hydrocortisone was given by epidural transforaminal L4-L5 left injection under radioscopy guidance. Within minutes following the injection, intense pain developed in both legs, with T12 complete paraplegia. Emergency magnetic resonance imaging (MRI) 2 hours later did not reveal spinal cord abnormalities. The patient underwent immediate surgery consisting of excising the protruding disc and extensive L3-L5 laminectomy. MRI performed 3 months later did not reveal medullar abnormalities. Six months later, the patient continued to show slow neurologic improvement, permitting him to walk with crutches and to stop intermittent self-catheterisation. DISCUSSION: The occurrence of paraplegia following epidural transforaminal injection of corticosteroids is a rare complication. To our knowledge, only 5 similar cases have been described. Most of the authors proposed that the mechanism of this complication is ischemia of the terminal cone due to accidental suppression of medullary blood supply. Direct lesion of a medullar artery, arterial spasm, or corticosteroid-induced occlusion due to undetected intra-arterial injection could lead to this medullar infarction. Anatomical variations of the path followed by the Adamkievicz artery strongly support this hypothesis.

Adult↗
PubMed2007

Effects of circuit resistance training on fitness attributes and upper-extremity pain in middle-aged men with paraplegia.

OBJECTIVE: To examine the effects of circuit resistance exercise (CRT) training on muscle strength, endurance, anaerobic power, and shoulder pain in middle-aged men with paraplegia. DESIGN: Repeated testing. SETTING: Academic medical center. PARTICIPANTS: Seven men (age range, 39-58y) with motor-complete paraplegia from T5 to T12 and confirmed shoulder pain occurring during daily activities. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Subjects underwent a 4-month CRT program using alternating resistance maneuvers and high-speed, low-resistance arm exercise. One-repetition maximal force was measured before training and monthly thereafter. Pretraining and posttraining peak oxygen uptake (Vo(2)peak) was measured by graded arm testing. Anaerobic power was measured before and after training using a 30-second Wingate Anaerobic Test. Shoulder pain was self-evaluated by an index validated for people with spinal cord injury (Wheelchair Users Shoulder Pain Index [WUSPI]). RESULTS: Strength increases ranging from 38.6% to 59.7% were observed for all maneuvers (P range, .005-.008). Vo(2)peak increased after training by 10.4% (P=.01), and peak and average anaerobic power increased by 6% (P=.001) and 8.6% (P=.005), respectively. WUSPI scores +/- standard deviation were lowered from 31.9+/-24.8 to 5.7+/-5.9 (P=.008), with 3 of 7 subjects reporting complete resolution of shoulder pain. CONCLUSIONS: CRT improves muscle strength, endurance, and anaerobic power of middle-aged men with paraplegia while significantly reducing their shoulder pain.

Activities of Daily Living↗
PubMed2005

Thin corpus callosum and amyotrophy in spastic paraplegia--case report and review of literature.

We report the clinical, structural, functional and genetic characterization of a 37-year-old Caucasian female, presenting as a sporadic case of complicated spastic paraplegia with thin corpus callosum (CC), cognitive impairment, amyotrophy of the hand muscles and a sensorimotor neuropathy and review the literature for spastic paraplegia with thin CC. Magnetic resonance imaging (MRI) examination revealed a thin CC with fronto-parietal cortical atrophy. 18Fluordesoxyglucose positron emission tomography (FDG-PET) showed reduced cortical and thalamic metabolism. By transcranial magnetic stimulation, we delineated a severe impairment of transcallosal inhibition. Sequence analysis did not reveal disease causing mutations in the genes SLC12A6 (Andermann), Spastin (SPG 4), BSCL2 (SPG 17) and Spartin (SPG 20). We reviewed the literature for HSP with thin CC and found 113 HSP patients with thin CC previously described (35 with linkage to chromosome 15q13-15). Thin CC and peripheral neuropathy often appear together in spastic paraplegia and might be indicative for combined degeneration mechanism of central and peripheral axons.

Adult↗
PubMed2004

The role of sensory and motor evoked potentials in the prognosis of Pott's paraplegia.

OBJECTIVE: In view of paucity of evoked potential changes in Pott's paraplegia, it is proposed to evaluate the role of motor and somatosensory evoked potentials in predicting the outcome. METHODS: Consecutive patients with Pott's paraplegia during 1993-2003 were subjected to detailed clinical, radiological and evoked potential study. The latter comprised of tibial somatosensory evoked potential (SEP) and motor evoked potential (MEP) study to tibialis anterior. The patients were clinically evaluated at 6 and 12 months and the outcome was defined into poor (bed ridden), partial (dependent for activities of daily living) and complete recovery (independent). The evoked potential findings were correlated with clinical and radiological findings and outcome. RESULTS: There were 39 patients whose age ranged between 16 and 70 (mean 42.1) years and 22 were females. The mean duration of symptoms was 8.2 months. Sensory motor deficit was present in 18 and pure motor signs in 21 patients. Five patients had quadriplegia and remaining had paraplegia. The muscle weakness was severe in 12 and moderate in 15 patients. In 12 patients, lower limb power was normal but they had lower limb hyper-reflexia with or without spasticity suggesting pyramidal dysfunction. Pinprick and joint position sensations were abnormal in 18 patients. MRI was abnormal in all and revealed cervical involvement in 7, thoracic in 22 and lumbar in 10 patients. Paravertebral soft tissue shadow was present in 36 and cord compression in 30 patients. Motor evoked potential was abnormal in 19 patients (unrecordable in 11 patients, 21 sides and prolonged in 8 patients, 14 sides). SEP was abnormal in 18 patients (unrecordable in 15 patients, 25 sides and prolonged central conduction in 8 patients, 9 sides). Both MEP and SEP were abnormal in 16, normal in 18, and only MEP was abnormal in 3 and only SEP in 2 patients. At 6 month 25 patients had complete, 9 partial and 5 poor recovery. At 1 year 33 had complete and 4 partial recovery. SEP and MEP abnormalities correlated with respective sensory and motor functions, vertebral level and outcome at 6 and 12 months. CONCLUSIONS: MEP and SEP both are helpful in predicting 6-month outcome. Combining SEP and MEP gives stronger correlation with 6-month outcome compared to only MEP or SEP. The potential role of evoked potentials in deciding different therapeutic strategies needs further studies.

Adolescent↗
PubMed2006

Spinal anaesthesia in a patient with hereditary spastic paraplegia: case report and literature review.

We report the use of spinal anaesthesia in a patient with hereditary spastic paraplegia who presented for manual removal of placenta following a normal vaginal delivery. This 18-year-old primigravida had been diagnosed with hereditary spastic paraplegia at 8 years of age when neurological examination revealed mild bilateral lower limb spasticity. A 25-gauge Whitacre spinal anaesthetic needle was inserted at the L3-4 intervertebral space and 0.5% plain bupivacaine 2 mL plus fentanyl 25 microg administered. The procedure was uneventful. At 24 hours postoperatively, there was full neurological recovery to pre-anaesthetic levels. The hereditary spastic paraplegias are a group of neurological disorders characterised by a slowly progressing spastic paraparesis. The neurological disorder and its anaesthetic implications are reviewed.

Adolescent↗
PubMed2005

Postoperative paraplegia secondary to the use of oxidized cellulose (Surgicel).

Iatrogenic paraplegia after thoracic surgery is a devastating complication. In this report, the authors present a case of paraplegia in a toddler after the resection of a mediastinal neuroblastoma. In this case, the paraplegia was caused by spinal cord compression after migration of oxidized cellulose into the spinal canal.

Cellulose, Oxidized↗