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PubMed2026

Editor's Choice - Aquaporin-4: A Predictor and Therapeutic Target for Permanent Paraplegia after Endovascular Thoraco-abdominal Aortic Aneurysm Repair.

OBJECTIVE: Endovascular thoraco-abdominal aortic aneurysm (TAAA) repair can impair spinal cord perfusion, leading to paraplegia. The mechanisms driving this devastating complication are poorly understood. This study aimed to interrogate the cerebrospinal fluid (CSF) proteome in patients after TAAA repair to identify biomarkers that herald permanent paraplegia. It also aimed to investigate a potential therapeutic target identified by proteomics using an in vivo model of ischaemic spinal cord injury (iSCI). METHODS: CSF was collected for proteomic analysis from patients before and following TAAA repair. A differentially expressed protein identified in human paraplegic subjects was subsequently interrogated in a rodent model of iSCI. The protein composition of CSF was analysed using tandem mass tag proteomics. Neurological examinations were carried out by a blinded neurologist and T2 weighted magnetic resonance imaging (MRI) was used to measure spinal cord volume and oedema. A rodent model of iSCI was used to investigate a clinically relevant therapeutic target informed by proteomic findings. RESULTS: CSF analysis was taken from 37 patients, all of whom had aneurysm repair using a custom branched and or fenestrated device (median age 73.5 years, range 67 - 78 years; 27 men, ten women; Crawford classification: six type I, 11 type II, 15 type III, three type IV, and two type V). Five patients remained permanently paraplegic and seven recovered from transient paraplegia. The CSF of patients who remained paraplegic contained approximately fourfold more aquaporin-4 (AQP4) (41.8 ± 19.2 ng/mL, n = 5) than those who recovered from paraplegia (10.8 ± 1.3 ng/mL, n = 7; p = .005) or did not develop paraplegia (10.8 ± 1.2 ng/mL, n = 25; p = .004). Permanently paraplegic patients had CSF AQP4 levels > 15 ng/mL and this was associated with greater cord oedema on T2 weighted MRI (1.77 ± 0.19 vs. 1.03 ± 0.36; p = .032). In a rodent model of iSCI, AQP4 inhibition preserved spinal neurons and glia in the dorsal horn and intermediate zones of white matter (p = .004) and protected against ischaemia induced paraplegia (p < .001). CONCLUSION: The AQP4 level in the CSF of a patient represents a prognostic marker of permanent paraplegia after TAAA repair and highlights a novel therapeutic target. These findings represent a conceptual advance in the management of iSCI.

Paraplegia↗

PubMed1976

Recovery from experimental paraplegia after levodopa administration.

In decompression sickness and during some surgical procedures, air emboli that form sometimes cause serious damage if the gas bubbles find their way to the vital organs. Paralysis of the spinal cord is one of the most serious manifestations induced by air emboli. Exposure to compression chambers is effective in air emboli treatment, but availability of chambers is inadequate and the treatment is lengthy. Until now there has been no fully effective injectable agent that can remedy the damage caused by air embolization. In this work levodopa was chosen as an injectable drug that might help to improve recovery from experimental paraplegia because of the reported effects of levodopa on muscle tone, spasticity and locomotion. To induce air emboli, the descending aorta of rats was chronically cannulated. Two weeks later, after full recovery from surgery, air was injected through the chronically implanted cannula into unanesthetized rats (0.35 ml of air per 100 g, during 4 sec). The paraplegia (paralysis of both hind legs) was manifested 2-10 minutes later. Only animals that had total paraplegia, without any sensation, were used in the experiments. Levodopa was administered 2 minutes after paraplegia was established. The levodopa treatment was repeated each day during one week. After six days, ten levodopa treated (intra-arterially) animals in a group of twelve and six levodopa treated (intraperitoneally) animals in a group of eight recovered completely from paraplegia. In control groups only three from thirteen (untreated), or two from twelve (solvent administration) animals recovered from paraplegia.

Animals↗

PubMed1977

Homocarnosinosis. 3. Spinal fluid amino acids in familial spastic paraplegia.

Increased concentration of CSF homocarnosine has recently been found in a family with spastic paraplegia. CSF homocarnosine was therefore determined in 13 patients from other families with familial spastic paraplegia. Also examined were seven patients from families where the constellation of symptoms and signs was more complex, but also comprised spastic paraplegia, and five patients with non-familial spastic paraplegia. No changes were found in homocarnosine level. In one patient with spastic familial paraplegia clear elevation of threonine in the CSF was found. The affected brother showed no such abnormality. CSF homocarnosine elevation is thus no common denominator in familial spastic paraplegia.

Adult↗

PubMed1975

[Paraplegia following acute infrarenal aortic occlusion (author's transl)].

The clinical syndrome of paraplegia following acute occlusion of the infrarenal aorta may be caused by either ischemic spinal cord damage or ischemia of the cauda equina and sacral nerve roots and ganglia. The neurologic manifestations are similar and therefore specific anatomic diagnosis is difficult. From October 1972 to February 1975 a total of 31 patients with infrarenal aortic occlusion were treated at the Medizinische Hochschule in Hannover. In nine cases the occlusion up to the renal arteries was acute. Three of these patients presented beside acute ischemic manifestations on both legs and the lower abdominal wall, neurologic symptoms of paraplegia. The anatomic and hemodynamic aspects of ischemic spinal cord damage and those of ischemic lesions of the cauda equina and peripheral nerves are discussed. There appear to be three main mechanisms responsible for vascular paraplegia following acute infrarenal occlusion of the aorta: 1. it may be caused by thrombotic occlusion of a major radicular artery which arises below the level of occlusion. 2. it may be produced by thrombosis of a lumbar collateral acting as major supply to the cord when arteriosclerotic narrowing of the major radicular artery is present. Especially in states of severe hypotension critical interference of blood supply to the spinal cord will result. 3. Paraplegia by ischemia of the cauda and peripheral nervous tissue may also follow prolonged interruption of circulation to this area supplying spinal vessels from low lumbar and sacral arteries.

Aged↗

PubMed1979

Diagnosis and management of tuberculous paraplegia with special reference to tuberculous radiculomyelitis.

Paraplegia occurred in eight of 17 patients with central nervous system tuberculosis. In six of these paraplegia was the presenting feature. Paraplegia may complicate tuberculous meningitis, or vertebral tuberculosis, but it may also occur, as in three of our cases, as a primary localised spinal tuberculous radiculomyelitis. These cases are presented in relation to the concept that paraplegia complicating these forms of tuberculosis is caused by radiculomyelitis.

Adolescent↗

PubMed1978

Hypothalamic hypothyroidism causing spastic paraplegia: recovery following thyroid medication.

A 63-year-old woman with longstanding spastic paraplegia and neurological evidence of long tract disturbance was found to have hypothyroidism, partial diabetes insipidus, hyperprolactinemia, and gonadotropin deficiency of hypothalamic origin. Replacement therapy with thyroxine and prednisone induced complete remission of the neurological abnormalities. The association of spastic paraplegia with hypothalamic insufficiency has not been reported previously. The possibility of hypothalamic disease should be considered in cases of spastic paraplegia of unknown cause.

Brain Diseases↗

PubMed1978

Some experience with paraplegia in a small hospital in Nepal.

Paraplegia is a common problem in developing countries. They are the most pitiable group of cases seen, but they can all be offered some help, however limited one's resources. The main causes are Potts Disease, arachnoiditis, tropical spastic paraplegia, trauma, lathyrism and cord compression. The usual trauma is falling from trees and the use of trained monkeys to gather leaves and nuts whilst humorous should not be dismissed. The author saw some 35 cases of paraplegia, of which four are described--two good results and two bad. The physician going to a developing country is advised to prepare himself for the care of these cases and to be prepared to motivate staff, patients and relatives. He will find local medical assistants are kind and enthusiastic and rapidly acquire the necessary skills. Nearly all cases should receive a simple and inexpensive anti-tuberculous regime, vitamins and a very generous diet. Necessary equipment required for the home should be locally made and nothing requiring more than simple maintenance should be used.

Adult↗

PubMed1978

Traumatic rupture of the aorta and paraplegia.

During the past 10 years, 15 traumatic ruptures of the aorta isthmus have been diagnosed. The most likely mechanism is that of a brutal deceleration. Three patients developed a complete mid-thoracic flaccid paraplegia. One died in a few hours of a complete rupture, the second after a few days from renal insufficiency, the third 12 days after, having been operated upon on the same day of the accident. All had associated lesions. Diagnosis can be very difficult in these patients, especially in the first few hours. Paraplegia is here considered as an aggravation ischaemic symptom with anuria and loss of blood circulation in the lower limbs. In delayed cases the vascular mechanism of the infarction of the spinal cord is discussed, either by compression of the intercostal arteries or by direct compression of the aorta itself. In our cases, the most likely mechanism is that of an obstruction of the lumen of the aorta by a torn inner coat. These patients must be transferred as quickly as possible to a cardiovascular surgical unit and operated upon immediately. Three cases of preoperative, rapidly progressive paraplegia with neurological recovery after the operation, have been reported in the literature.

Accidents, Traffic↗

PubMed1992

Paraplegia due to a ruptured aneurysm of the distal posterior inferior cerebellar artery.

A case of paraplegia was due to a ruptured aneurysm of the distal posterior inferior cerebellar artery. The paraplegia was caused by a unilateral lesion located between the cervicomedullary junction and the C2 level, where it involved both crossed and uncrossed pyramidal fibres projecting to the lower extremities. Since a vascular lesion near the cervicomedullary junction is likely to be missed, special attention should be paid to this region when investigating subarachnoid haemorrhage with paraplegia.

Arteries↗

PubMed1975

Spinal lesions, paraplegia and the surgeon.

Thirty-six patients with spinal cord lesions and varying degrees of paraplegia were seen by the surgical team at the Angau Memorial Hospital, Lae, over a thirty month period. Because the continued presence of a spinal lesion may lead to progressive cord destruction and ischaemic myelopathy, prompt treatment is advocated. The depressing results that have followed treatment of fracture dislocations of the cervical spine and secondary neoplasm with paraplegia is recorded and some suggestions are made that may improve the outlook in future cases. Early and major surgery is advocated in the treatment of spinal abscesses, tumours, Pott's paraplegia and unstable fracture dislocations of the lumbar spine.

Abscess↗

PubMed1992

The effect of an anti-G suit on cardiovascular responses to exercise in persons with paraplegia.

The purpose of this study was to determine whether external pressure on legs and abdomen could prevent venous blood pooling in persons with paraplegia and thus positively affect their cardiovascular responses to arm exercise. To investigate this, five male subjects with paraplegia (P), with complete lesions between T6 and T12, and five male control subjects who were wheelchair bound (C) (due to a chronic lower extremity disability), performed submaximal arm-cranking exercise at 20%, 40%, and 60% of their maximal power output (Wmax), with and without an antigravity (anti-G) suit inflated to 52 mm Hg (1 psi). For P, higher preexercise systolic pressure (127 vs 117 mm Hg) was seen with the anti-G suit. At 40 and 60% Wmax, significantly lower heart rates (at 40% = 5.7%; at 60% = 10.6%) at similar cardiac outputs were seen for P with an anti-G suit. Although not significant, P also demonstrated higher stroke volumes at 40% (4.8%) and 60% (5.0%) Wmax with external pressure. For C, no differences in preexercise blood pressure or cardiovascular responses at all three exercise levels were seen with or without the anti-G suit. These data suggest that an inflated anti-G suit is able to prevent venous blood pooling and offers hemodynamic benefits in persons with paraplegia during submaximal arm-cranking exercise. In addition, this study reports a possible alternative to hosiery or functional neuromuscular stimulation that could be applied to all subjects with spinal cord injuries regardless of type or duration of the lesion or of muscle-atrophy.

Adult↗

PubMedDate not supplied

[Paraplegia as a risk following catheterization of the umbilical artery. Report of a case and bibliographic review].

A case of paraplegia in a female newborn in whom an umbilical catheter was inserted for treatment of fetal maternal isoimmunization with exchange transufsion is presented. Paraplegia was diagnosed in the fifth day after the procedure was performed. A left transfemoral angiography demonstrated the absence of the segmentary artery of Adamkiewicz at the level of T-11, which is responsible of circulation of the lower segment of the spinal cord; paraplegia was considered to be secondary to spinal cord infarction due to thrombosis; other causes of spinal block were ruled out. Review of the literature shows several reports of manifestations of thrombosis after catheterization of umbilical vessels.

Catheterization↗

PubMed1976

Injectable agent for the treatment of air emboli-induced paraplegia in rats.

Rats with air emboli-induced paraplegia were treated with dialy levodopa injections (intra-arterially or intraperitoneally). Of the control animals, 20% fully recovered from paraplegia during a period of 7 d. Of the levodopa treated animals, 85% fully recovered during the same period. It appears, therefore, that levodopa might be one of the few injectable agents enhancing recovery from air-induced paraplegia, suggesting its possible use in decompression sickness.

Animals↗

PubMed1977

Strumpell's pure familial spastic paraplegia: case study and review of the literature.

A family with pure Strumpell's familial paraplegia is presented. There were 11 afflicted members involving three generations. The mode of inheritance was dominant, the onset in the first decade, and in this family the disease was mild. Literature data from 104 families with 536 members dating from 1880 are tabulated. This report confirms others regarding mode of inheritance, age of onset, distribution between sexes, and disease manifestations. However, contrary to other reports, we found the dominant and recessive form of pure Strumpell's familial spastic paraplegia to be similar in severity. There are now clinical and pathological data supporting the separation of pure Strumpell's familial spastic paraplegia from the other heredodegenerative diseases of the nervous system.

Adolescent↗

PubMed1976

[Involvement of the peripheral motor neuron in hereditary spastic paraplegia (author's transl)].

Two patients from families with hereditary spastic paraplegia (recessive and dominant type) were examined electromyographically. It was found that the peripheral motor neuron is involved. It is assumed that in cases of infantile recessive familial spastic paraplegia the peripheral motor neuron is rather more involved than in those of the dominant type of spastic paraplegia.

Electromyography↗

PubMed1976

Spastic paraplegia associated with Addison's disease: adult variant of adreno-leukodystrophy.

Clinical and pathological features of an adult variant of adreno-leukodystrophy (ALD) are presented. A male with clinical and laboratory signs of Addison's disease (AD) developed at age 22 a slowly progressing paraplegia with slight sensory deficits in both legs and bladder and sphincter dysfunctions; he died at age 24 in an AD crisis. Autopsy revealed hyperplasia of lymphatic tissues, lymphocytic infiltrates in various organs including the CNS and adrenocortical atrophy with prominence of large ballooned, sometimes bizarre and occassionally striated cortical cells. CNS lesions consisted in incomplete demyelination of long tracts of brain stem and spinal cord with accentuation in the pyramical tracts; in these areas, perivascular cuffs of "epitheloid" histiocytic cells contained a strongly PAS-positive non-sudanophilic material. Electron microscopy demonstrated massive stroge of leaflet structures in perivascular histiocytes identical to the lamellar profiles previously described as specific for ALD. Some leaflets were found in close contact with compact lamellar arrays and with an electron-dense fingerprint material within astrocytes. In our case, the spastic paraplegia-AD syndrome which has been described previously in several clinical observations could be neuropathologically classified as an adult variant of ALD. Several differences to "classical" ALD occurring in young boys are stressed: the predominance of the endocrine disorder probably accounting for some of the perivascular lymphocyte infiltrates within the CNS; the absence of both clinical and pathological signs of diffuse cerebral involvement and the peculiar topistic pattern of CNS lesions and the very slow evolution of neurological signs paralleled by the absence of active sudanophilic demyelinating lesions. The possible mechanism of demyelination and the nature of the suggested metabolic defect in ALD are discussed. The ultrastructurally prominent leaflet structures may originate from myelin remnants, thus relating ALD to pathological storage of a myelin degradation product.

Addison Disease↗

PubMed1975

Protein patterns of cerebrospinal fluid in hereditary ataxias and hereditary spastic paraplegia.

The CSF findings in hereditary ataxias and allief disorders have hitherto mostly been reported as normal if one excludes Refsum's syndrome. The CSF-protein patterns found on isoelectric focusing and quantitative paper electrophoresis were studied in 12 patients with hereditary ataxias and hereditary spastic paraplegia. Using a recently-developed technique of isoelectric focusing of CSF-proteins in flat beds of polyacrylamide gel, the authors could show abnormal CSF-protein patterns in all but 1 of the present cases. The aberrant CSF-protein patterns found showed differences between the syndromes studied. Two unique patterns with conspicuous fractions in the acid range were observed in patients with Marie-Sanger-Brown's ataxia (mother and daughter) and Holmes' ataxia. A third CSF-protein pattern was found in a sibship with Friedreich's ataxia including a double fraction in the acid region (pI 5.9-6.1) in all 4 subjects and a highly alkaline fraction (HAF) with pI about 9.3, in 3 of them. Similar acid fractions (pI 5.9-6.1) were also detected in 3 of 4 patients with hereditary spastic paraplegia, a brother and sister showing a very similar CSF-protein pattern. Double fractions with pI 5.9-6.1 and/or HAF may also occur in other neurological diseases, mostly, however, associated with other distinctive features of their CSF-protein patterns. A possibility in the future of distinguishing hereditary CNS-diseases by examination of the CSF-protein pattern is suggested.

Abetalipoproteinemia↗

PubMed1975

Osteopetrosis associated with familial paraplegia: report of a family.

A clinical analysis of three members of a family with documented osteopetrosis and familial paraplegia is presented. All patients had a long history of increased bone density and slowly progressing paraparesis of both legs. A thorough review of the literature has revealed no other cases which presented with paraplegia without spinal cord compression. Although the etiologic factor or factors remain unknown, our review supports the contention that this is a distinct clinical entity.

Adult↗