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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

3 children with severe renal hypertension and bilateral infarction of the optic nerves are described. 1 patient also had a transverse myelopathy. Such complications may perhaps be prevented by earlier detection of hypertension and gradual reduction of blood-pressure.
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PMID:Blindness and paraplegia in severe childhood hypertension. 8 59

Five cases of radiation myelopathy were found in a total of 10,000 cases given radiotherapy from 1968 to 1977. The clinical presentation and treatment details including the total dose, treatment volume, number of fractionations, overall time, and the RET value at the spinal cord were calculated and compared with other reports on this subject. The total number of fractionations ranged from 20 to 26 with an overall time of 32 days to 37 days. The dose received by four patients ranged from 1030 to 1900 RET, a little higher than the tolerance level of the spinal cord as compared to reported values. Two patients in this series had high blood pressure. The incidence of radiation myelopathy, already acceptably low, could possibly be reduced further by meticulous planning of radiation.
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PMID:Radiation myelopathy. 44 80

The literature dealing with radiation myelopathy is reviewed. The following points are to be noticed:radiation myelopathy is a rare complication in the radiation therapy of extraspinal tumors, nevertheless the number of case reports is increasing during the last years; probably this is due to the increasing use of high energy therapy. Already a cord dose of 1000 rad may be dangerous; with an increasing dose the risk of radiation myelopathy is increasing too. Besides the total dose the incidence of radiation myelopathy depends on the rate of delivery, the over-all time of administration, the size of the individual fraction, the field size, the size of the volume irradiated, the type of irradiation, the use of hyperbaric oxygen and some other special conditions of radiation. But the incidence of radiation myelopathy depends not only on radiation technique but also on patients' variables. Individual variations in radiosensitivity are a well known fact; this may be partly due to an inherent biologic variation of response. Moreover the incidence of radiation myelopathy may be intensified by simultaneously existing diseases - above all by hypertension- and probably by some medicaments taken simultaneously. A dependence from age, sex, and the kind of the primary tumor seems not to exist. Radiation lesions of the cervical spinal cord have been reported much more frequently than lesions of the dorsal spinal cord; lesions of the lumbal spinal cord are a very rare event. There exist different conceptions of the pathogenesis: opinions differ as to whether the effect is primarily on the connective tissue and blood vessels or on nerve cells and their axons or if the different tissues are injured simultaneously; moreover an autoimmuno-hypothesis is discussed. The clinical signs of radiation myelopathy can be grouped into two major syndromes: the transient radiation myelopathy and the delayed or chronic radiation myelopathy, which usually develops gradually with a subsequent chronic progressive course but in some cases may occur acutely after the latent period; the course is not always progressive but may be undulating and remissions have been reported in some rare cases...
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PMID:[Radiation injury of the spinal cord]. 77 Feb 97

Several conclusions seem evident from this study : firstly radiation myelopathies exist without any doubt; secondly clinical observation, even very attentive, during irradiation is perfectly blind regarding this subject; lastly, one can only, at this time, attempt to anticipate medullary accidents caused by irradiation. Radiation myelopathies exist incontestably. We report 27 new cases which are added to the more than 500 cases already analysed in the world litterature. The improvement of results of cancerology and in particular of radiotherapy make and will continue to make the number of observations published increase. However, if there is no doubt as to existence of these myelopathies, discussions persist concerning their nature : purely vascular, cytotoxic, probably mixed, perhaps maintained and prolonged by a superimposed immunologic phenomenon. Prevention is the sole method at our disposal to be effective. It must be applied as much to the patient as to the technique of irradiation. With regard to the patient treated in a medullary volume, several factors are probably favorable to the development of myelopathy and must cause one to modify eventually the technique of radiation proposed : the existence of anterior vertebral medullary pathology, whatever its nature; two ages demonstrate increased incidences : the young which have relative immaturity of tissue (we report 4 cases patients less than 25 years old), and the old, whose chances of accumulating associated pathologies are great, especially as systemic hypertension and arteriosclerosis are likely to have played a favorable role; the patients for whom restraint is difficult or who present disrupted regions anatomy are qually much more fragile. With regard to the technical plan, several factors incontestably favor the appearance of radiation myelopathy : large medullary volumes irradiated, especially when they encompass the zones of vascular medullary junction; the overlap of fields involving the spinal cord; the reduction of fields too close to the spinal cord not allowing at least 1 cm margin of relative security; the association of physical agents in the measure to which the global dosimetry is uncertain, i.e. in particular the use of high energy electrons for boost dosage, the intensity of which must be chosen with the greatest prudence; finally and most importantly, it seems desirable to us not to surpass at the level of the spinal cord, treating 5 times per week, a dose of 5 000 rads with fractions of 200 rads of 4 500 rads with fractions of 250 rads, and of 4 000 rads with fractions of 300 rads. Can one reasonable pretend always to foresee all radiation myelopathies? No, for on the one hand there exist authentic cases which have occured after doses which were below the limits of tolerance which we have indicated above, in accordance with others authors, and on the other hand, the necessity of sterilising certain inoperable tumors obliges one sometimes to deliver to region of the spinal cord aggressive doses.
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PMID:[Late progressive radiation myelopathies. A study of 27 cases]. 81 47

Five cases of chronic radiation myelopathy (four of the thoracic and one of the cervical cord) are presented together with a short summary of cases already published. The important influence of the fractionation scheme is stressed. A dose not exceeding 4400 rd in the thoracic myelon (20 X 2000 rd, 5 times per week, plus 10 X 40 rd - or 15 X 200 rd plus 15 X 90 rd, 5 times per week, - or 8 X 330 rd, three times per week, plus 15 X 80 rd 5 times per week) is considered to be a safe limit. In view of the scarcity of adequately documented cases of cervical myelopathy, it is recommended to keep dose limits about 10% lower than in the thoracic region and to avoid high single doses in curative treatments. Hypertension may increase the risk of radiation myelopathy (case nr. 5).
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PMID:The risk of chronic progressive radiation myelopathy. 98 87

An interesting case of systemic lupus erythematosus (SLE) is presented in which the clinical onset of myelopathy strongly suggested demyelinating disease. Later, intracranial hypertension developed on two occasions. Postmortem examination showed the systemic lesions of SLE. In addition, demyelinating lesions were found in the spinal cord and the optic nerve, the neuropathologic picutre of Devic's syndrome, a variant of multiple sclerosis. We question whether some of the cases showing necrotic myelopathy might have an autoimmune pathogenesis.
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PMID:A case of neuromyelitis optica (Devic's syndrome) in systemic lupus erythematosus. Clinicopathologic report and review of the literature. 98 14

Intracranial dural arteriovenous (AV) fistulas with spinal perimedullary venous drainage are rare lesions that have distinctive clinical, radiological, and therapeutic aspects. Five patients presented with an ascending myelopathy, which extended to involve the brain stem in three cases. Myelography and magnetic resonance imaging showed slightly dilated spinal perimedullary vessels. Spinal angiograms were normal in the arterial phase. Diagnosis was only possible after cerebral angiography, which demonstrated posterior fossa AV fistulas fed by meningeal arteries and draining into spinal perimedullary veins. Endovascular treatment alone resulted in angiographic obliteration of the lesion in three patients. Two patients required surgery in addition to endovascular therapy. One patient died postoperatively, and in one a transient complication of embolization was observed. Improvement after treatment was good in two cases and fair in two. Transverse sinus thrombosis was observed in three cases and was probably the cause of the aberrant venous drainage of the fistula into the spinal perimedullary veins. The pathophysiology is related to spinal cord venous hypertension. These lesions were classified as Type 5 in the Djindjian and Merland classification of dural intracranial AV fistulas. Endovascular therapy is a safe effective method in the treatment of these fistulas and should be tried first.
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PMID:Endovascular treatment of intracranial dural arteriovenous fistulas with spinal perimedullary venous drainage. 140 13

Enzyme linked Immunosorbent Assay (ELISA) was done for the detection of antibodies to Cysticercus cellulosae in 135 cerebrospinal fluid (CSF) and 152 serum samples from patients suspected clinically of neurocysticercosis (NC), neurological disorders other than NC and controls by the use of crude cyst extract antigen. This assay was compared with the standard technique of indirect haemagglutination test (IHA). The results of the two techniques were matched with retrospective analysis of proven diagnosis of these patients. ELISA and IHA was found to be positive respectively in 88 and 84 percent of CSF and 92 and 87.2 percent of serum samples from proven NC patients. The IHA technique was found to be absolutely specific for the detection of antibodies in CSF samples while cross reactions were observed with ELISA technique in CSF from 5 patients, one each suffering from disappearing CT scan lesion, tubercular meningitis (culture negative), chronic meningitis, benign intracranial hypertension and non compressive myelopathy. However possibility of neurocysticercosis cannot be absolutely ruled out in such patients. Both the techniques were found to be highly non specific for the detection of antibodies in serum samples. The study suggests that either of the two techniques may be used for the detection of antibodies in CSF samples from clinically suspected NC patients with high degree of sensitivity and specificity.
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PMID:Evaluation of enzyme linked immunosorbent--assay for the detection of anticysticercus antibodies in cerebrospinal fluid from patients with neurocysticercosis. 151 54

The authors report a series of seven patients with myelopathy who were found to have spinal dural arteriovenous (AV) fistulas in which the nidus was located at some distance from the spinal cord. The nidus was intracranial in three cases and involved a sacral nerve root sheath in the other four; in each case, the arterialized draining vein led into the coronal plexus of medullary veins. A lack of normal draining radicular veins was noted in all cases. Magnetic resonance images were obtained in four patients and demonstrated spinal cord tissue changes only in the lower thoracic cord in three cases and in the cervical cord in one, all consistent with an ischemic process secondary to venous hypertension. Five patients were managed surgically by division of the draining vein, with improvement of the neurological deficit in all. One patient was treated by embolization alone and had stabilization of her deficit. The remaining patient in the series died of unrelated systemic disease before the spinal dural AV fistula could be treated. These cases support the theory that venous hypertension is the dominant pathophysiological mechanism involved in spinal dural AV fistulas independent of their location. In patients with a suspected spinal dural AV fistula, lumbar and thoracic spinal angiography will reveal the site of the fistula in the majority of cases (88% in this series). In the remaining patients, the possibility of a remote fistula must be considered. The lack of normal venous drainage of the cord following injection in the artery of Adamkiewicz is the most reliable indicator of venous hypertension in the cord and can be helpful in making the decision to proceed with a search for a cranial or sacral arterial supply.
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PMID:Cranial and sacral dural arteriovenous fistulas as a cause of myelopathy. 154 54

A case of acute aortic dissection (AAD) presenting as sudden, transient paraplegia and severe back pain is reported. The patient was a 66-year-old male with a 10-year-history of hypertension. The pain characteristically migrated from the back to the neck and then returned to the back. He showed complete transverse myelopathy at the level of the 9th thoracic cord. Computed tomography disclosed internal displacement of aortic intimal calcifications, without abnormalities in the spinal canal, and myelography showed no spinal canal block or stenosis. Electrocardiography and chest x-ray indicated nonspecific changes of high amplitudes and mild cardiomegaly, respectively. Together, these findings suggested acute aortic dissection with spinal cord ischemia. The initial systolic blood pressure of 220 mmHg was lowered with medication, and the pain was controlled with morphine. He recovered fully and was discharged 80 days after the onset of symptoms, with no neurological deficits. AAD carries a very poor prognosis unless treated immediately. Therefore, it is very important to promptly differentiate this disorder from spinal vascular conditions that also produce back pain and paraparesis.
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PMID:Transient paraplegia caused by acute aortic dissection--case report. 169 75


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