Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to produce syringomyelia, localized arachnoiditis was created in adult New Zealand albino rabbits and Wistar rats by the injection of kaolin into the thoracic spinal subarachnoid space and incision of the dura mater of the thoracic spinal cord. The rabbits and rats were divided into 3 groups; the control group, dural incision group (DG) and kaolin injection group (KG). Each rabbit was sacrificed at 4, 8, 12 and 16 weeks after the operation. Each rat was sacrificed at 8 and 16 weeks after the operation. Cavity formation in the cord of all rabbits was examined by ultrasound. All animals were perfused with 10% neutral beffered formalin at 150 cm H2O pressure, and histological examination was performed with Luxol fast blue (LFB) and hematoxylin and eosin (H&E) stains. Results obtained: (1) Cavity formation was noted in 6 of 16 DG of rabbit (37.5%), 5 of 16 KG of rabbit (31.2%) and 2 of 9 KG of rat (22.2%) with histological verification. With use of ultrasound, cavity was noted in 3 of 16 DG rabbits (12.5%) and 2 of 16 KG rabbits (18.8%). (2) Cavity formation was present in the cord adjacent to the marked adhesive arachnoiditis both in rabbits and in rats. (3) Cavity was noted in the ischemic area. (4) In 2 rabbits in which kaolin encircled whole surface of the spinal cord, hydromyelia was formed communicating with enlarged central canal caudad from the kaolin subarachnoid block. (5) Histological examination showed obliteration or narrowing of lumen of the small pial vessels involved in the adhesive arachnoiditis. In the cord parenchyma adjacent to the arachnoiditis, multiple spots of demyelination due secondary to ischemia demonstrated by LFB stain were noted. On the other hand, in the cord with the pia-arachnoid remained uninvolved, no demyelination was observed. (6) Localized adhesive arachnoiditis consisted of proliferation of fibrous tissue, lymphocytic infiltration and obliterating processes of small pial vessels involved in it. These data suggest that the cavitation within the cord would be induced by the ischemia, and hydromyelia would be produced by the pressure dissociation between the spinal subarachnoid space and the central canal.
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PMID:[Experimental syringomyelia in rabbits and rats after localized spinal arachnoiditis]. 129 32

Three unusual cases are reported in which communicating syringomyelia presented acutely. The first patient presented with paraplegia, the second with acute respiratory distress secondary to bilateral vocal cord paralysis, and the third with symptoms of acute brain-stem ischemia. Each patient had a communicating spinal cord syrinx associated with a posterior fossa and foramen magnum region anomaly (a huge posterior fossa arachnoid cyst in one and Chiari malformations in two). The mechanisms of craniospinal pressure dissociation and hindbrain herniation are discussed, along with other reported emergency presentations of syringomyelia.
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PMID:Acute presentations of syringomyelia. Report of three cases. 229 73

The authors review the clinical course of 29 patients who underwent syringosubarachnoid shunting for syringomyelia. Twenty-two patients presented hindbrain-related syringomyelia; seven patients had non-hindbrain-related syringomyelia secondary to trauma (four cases) and to spinal arachnoiditis (three cases). The surgical technique is described in detail. All patients showed postoperative deflation or collapse of the syrinx at follow-up magnetic resonance imaging evaluation. Symptoms stabilized in 17 cases (59%); 9 cases (31%) showed improvement in the neurological function; 3 cases (10%) presented delayed neurological deterioration, probably owing to spinal cord ischemia.
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PMID:Surgical treatment of syringomyelia: favorable results with syringosubarachnoid shunting. 247 14

This report is the first to correlate data concerning intraoperative somatosensory evoked potentials (SSEPs) and local spinal cord blood flow (ISCBF) in patients with syringomyelia. In a consecutive study, bilateral median nerve SSEPs were recorded intraoperatively in 13 patients undergoing a syrinx shunt to the posterior fossa cisterns (syringocisternostomy). ISCBF was measured in five of these patients using laser doppler flowmetry (LDF) calibrated in arbitrary units (AU). SSEP recordings obtained 30 min after syrinx decompression demonstrated a slight but consistent reduction of N20 latencies (mean change: 0.53 ms right, p < 0.003; 0.58 ms left, p < 0.001) concurrent with a similar but less consistent increase of N20 amplitudes (0.16 mV right, p = 0.256; 0.29 mV left, p = 0.03). Prior to shunting, LDF recordings from the spinal cord overlying syrinxes revealed very low ISCBF values in five of five patients (mean LDF, 13.2 AU +/- 15.3 SD). Immediately after shunting, there was a dramatic rise of ISCBF (mean LDF, 241.2 AU +/- 106.3 SD) associated with visualized hyperemia of the spinal cord and pial vessels. The ISCBF fell to intermediate levels after 2 min (157.2 AU +/- 33.0 SD) and remained at these levels during the interval of recording (5 min). Hyperventilation testing in two patients prior to shunting revealed no change in ISCBF consistent with a loss of CO2 vascular reactivity and a paradoxical increase of ISCBF in one patient 5 min after shunting. Each patient in this study experienced neurological improvement in the immediate postoperative period associated with collapse or disappearance of the syrinx on magnetic resonance imaging scans. Because syrinx shunting results in an acute decompression of the distended spinal cord, it is possible that the rapid improvement of SSEPs reflects a relief of mechanical factors such as stretching and compression of nervous tissue. However, the LDF findings in this study suggest that distended spinal cord cavities are also capable of producing regional ischemia. A significant reduction of ISCBF is a possible contributing cause of neurological injury and SSEP abnormalities. Intraoperative improvement of SSEPs and ISCBF were found to correlate well with neurological recovery following syringocisternostomy. Our results indicate that SSEP monitoring can provide useful information during surgical procedures for syringomyelia and that further experience with LDF monitoring may provide insights into the pathophysiology of this condition.
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PMID:Intraoperative improvement of somatosensory evoked potentials and local spinal cord blood flow in patients with syringomyelia. 880 32

A 30-year-old healthy woman was involved in a road traffic accident. She sustained a fracture dislocation of T11/12 with a complete Frankel A paraplegia below T11. She had no associated injuries. High Dose Methylprednisolone was administered according to the NASCIS III protocol (48 h) together with low molecular weight Heparin and gastroprotected medication. Complete transection of the spinal cord and an anterior haematoma from T11 to T12 were confirmed on X rays, CT's and MRI scans. Posterior surgical stabilisation was performed using Isola instrumentation, starting 8 h post injury. Her post surgical period was uneventful except for some episodes of low blood pressure (85/60 mmHg) from which she had no symptoms. On the 12th post operative day, while in the physiotherapy department, she complained of right scapular pain. This occurred every time she was sat up and was associated with paraesthesia of both upper limbs. Two days later she deteriorated neurologically and her level ascended initially to T8 and then to T3. MRI of the spine with and without gadolinium showed spinal cord oedema between C3 and T1. There was no evidence of haemorrhage or syringomyelia. The authors discussed this case making different hypotheses. They are mainly the following: (1) Gradually ascending ischaemia due to a vascular disorder; (2) Double spinal trauma; (3) Ischaemia related to repeated hypotensive episodes; (4) Low grade intramedullary tumour; and (5) Thrombus of the Radicularis Magna artery. The case has been recognised as being very rare and interesting. In the conclusions, the presenting author stresses the importance of adopting MRI-compatible instrumentation for the surgical stabilisation of the spine, and careful monitoring of blood pressure during the acute phase of spinal cord injury. Dr Aito agrees with Mr El Masry about the opportunity of forming a group of clinicians in order to discuss protocols to cope with this devastating complication.
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PMID:Ascending myelopathy in the early stage of spinal cord injury. 1049 Aug 52

Syringomyelia classically presents with slowly progressing dissociated sensory and upper and lower motor deficits. Atypical and acute manifestations have rarely been described. We report here on 3 patients with syringomyelia, who had acute and atypical brainstem symptoms with regard to the underlying disease. These symptoms occurred after acute elevation of the intrathoracic and intra-abdominal pressure, respectively, and remitted subsequently. Vertebrobasilar ischemia was initially suspected.
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PMID:Acute brainstem symptoms associated with cervical syringomyelia. 1060 8

The improvement of preclinical emergency medicine, better surgical and conservative therapies, and the development of intensive care units and specialized centers have improved the survival rate for patients with serious spinal cord injuries. Therefore, more sequelae of chronic spinal cord injuries such as post-traumatic spinal cord cavitations also occur. The first such case was described by Bastian in 1867. Generally, these cavitations were diagnosed from 2 months up to 32 years after the trauma. The overall prevalence of post-traumatic syringomyelia (PTS) is not known; however, with the increasing use of magnetic resonance imaging (MRI), its diagnosis has increased, ranging from 2.3% of paraplegic and tetraplegic patients in 1976 and 3.2% in 1985, to nearly 50% in a selected group of patients in 1991 and 1993. In 1995, a 4.45% incidence was reported. In our clinic we are currently treating 440 cases of syringomyelia, 140 of which are PTS. Several observations suggest more than one potential mechanism for the evolution of a post-traumatic cyst or PTS. Various factors, such as hemorrhage or, in particular, ischemia within the spinal cord, blockage of the cerebrospinal fluid (CSF) pathways around the cord or localized meningeal fibrosis either alone or in combination with other factors, may be involved. Clinically, sensory disturbances, loss of motor function, pain, and modification of the deep tendon reflexes are observed in most patients. On MRI, PTS is seen as a longitudinal, cystic cavity within the spinal cord, giving a hypointense signal on T1-weighted images and a hyperintense signal on T2-weighted images. For treatment planning it is mandatory to identify the lower and upper end of the PTS on the MRI.
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PMID:[Posttraumatic syringomyelia]. 1066 5

The role of spinal cord ischemia in the pathophysiology of syringomyelia remains undetermined. Previous reports in the literature suggest that shunting of syringes can improve spinal cord blood flow. In order to determine the effects of syrinx decompression on spinal cord blood flow in patients with syringomyelia, we prospectively measured regional spinal cord blood flow (RSCBF) intraoperatively pre and post shunting in patients with symptomatic syringomyelia using laser doppler flowmetry. Six patients with MRI documented syringomyelia were studied (three with Arnold Chiari I malformation and associated syrinx and three with post-traumatic syringomyelia). Surgery was performed on all patients with either a syringopleural or syringoperitoneal shunt. Laser doppler blood flow and somatosensory evoked potentials were monitored prior to myelotomy and after shunt insertion. Results indicate that there was a significant increase in RSCBF after decompression of the syrinx. This study supports the hypothesis that spinal cord ischemia is important in the pathophysiology of syringomyelia and confirms previous reports in the literature regarding RSCBF in syringomyelia.
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PMID:Intraoperative measurement of spinal cord blood flow in syringomyelia. 1099 7

Two cases of acute presentation of cervical syringomyelia associated with Chiari malformation are reported. In the first case, dysphagia was the main symptom; the second patient had symptoms suggesting acute brain stem ischemia. The mechanism of this acute onset of the illness is discussed.
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PMID:[Acute onset syringomyelia: two cases]. 1145 90

A review of the literature was conducted to study the pathomechanics by which Paget's Disease of bone (PD) alters the spinal structures that result in distinct spinal pathologic entities such as pagetic spinal arthritis, spinal stenosis, and other pathologies, and to assess the best treatment options and available drugs. The spine is the second most commonly affected site with PD. About one-third of patients with spinal involvement exhibit symptoms of clinical stenosis. In only 12-24% of patients with PD of the spine is back pain attributed solely to PD, while in the majority of patients back pain is either arthritic in nature or a combination of a pagetic process and coexisting arthritis. Neural element dysfunction may be attributed to compressive myelopathy by pagetic bone overgrowth, pagetic intraspinal soft tissue overgrowth, ossification of epidural fat, platybasia, spontaneous bleeding, sarcomatous degeneration and vertebral fracture or subluxation. Neural dysfunction can also result from spinal ischemia, when blood is diverted by the so-called "arterial steal syndrome". Because the effectiveness of pharmacologic treatment for pagetic spinal stenosis has been clearly demonstrated, surgical decompression should only be instituted after failure of antipagetic medical treatment. Surgery is indicated as a primary treatment when neural compression is secondary to pathologic fractures, dislocations, spontaneous epidural hematoma, syringomyelia, platybasia, or sarcomatous transformation. Since, in the majority of cases with pagetic spinal involvement, there are also coexisting osteoarthritic changes, antipagetic medical treatment alone may be disappointing. Therefore, one must be careful before attributing low back pain to PD alone. Five classes of drugs are available for the treatment of PD: bisphosphonates, calcitonins, mithramycin (plicamycin), gallium nitrate, and ipriflavone. Bisphosphonates are the most popular, and several forms have been investigated, but only the following forms have been approved for clinical use: disodium etidronate, clodronate, aledronate, risedronate, neridronate, pamidronate, tiludronate, ibadronate, aminohydroxylbutylidene bisphosphonate, olpadronate, and zoledronate. Several of these forms are still under investigation.
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PMID:Paget's disease of the spine and its management. 1171 91


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