Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SCLEROSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,261 records · Page 70Linked to original sources
PubMed1995

The loss of 40-kDa chromosomal protein in tuberous sclerosis lesions.

Tuberous sclerosis is an genetic disease characterized by systemic hamartomas. Some of the cultured cells derived from tuberous sclerosis show the distinct chromosomal disarrangement and abnormal cell division. To detect the proteins responsible for this phenomenon, we investigated many nuclear components related to cell division. 40-kDa protein (p40) recognized by one monoclonal antibody M108, which was present in nucleus, chromosomes and cytoplasm of many vertebrate culture cells, significantly decreased in the tuberous sclerosis cells. Immunoblot analysis revealed that in all the fractions the quantity of p40 of severe tuberous sclerosis cells was approximately 4 times less than p40 in normal fibroblasts.

Antibodies, Monoclonal↗
PubMed1984

Spatio-temporal processing in multiple sclerosis.

The processing of spatial and temporal detail was investigated in patients with multiple sclerosis. Normal observers and 13 patients with optic neuritis secondary to multiple sclerosis performed a battery of visual tests that included contrast sensitivity, temporal integration, evoked potentials, and visual masking. The multiple sclerosis patients exhibited losses of pattern processing, and these deficits became more noticeable when the patterns were presented briefly. Moreover, these patients exhibited diverse response patterns for the different visual tests. For some, temporal integration functions appeared severely attenuated, while evoked potential latency was within normal limits. Others displayed poor performance in the visual masking test, yet contrast sensitivity functions were comparable to those of the control group. We suggest that a battery of tests that incorporates spatial as well as temporal stimuli is necessary for the detection of visual dysfunction in multiple sclerosis.

Adult↗
PubMed1987

Cerebellar sclerosis in pediatric cancer patients.

Cerebral cortical sclerosis is an acquired condition that has rarely been described in cancer patients. We reviewed necropsy findings in all children with cancer who died at the Children's Hospital of Philadelphia during the 20 year period 1963-1982 and found cerebellar sclerosis in 14 children with cancer (12 with acute lymphoblastic leukemia, 1 each with neuroblastoma and osteogenic sarcoma). The lesions were focal (3), multifocal (9) or diffuse (2). They occurred more frequently in children with acute lymphoblastic leukemia who had received intravenous methotrexate therapy. Ten of these 12 children had also received whole brain irradiation. The pathogenesis of the cerebellar sclerosis is unknown, but it is possible that extrinsic cerebellar compression by tumor or chronically increased intracranial pressure may have played a role in 6, ischemia/hypoxia in 3, and methotrexate toxicity in 2. No clear associations could be ascertained in 3. Methotrexate may be a previously unrecognized cause of cerebellar cortical injury. In addition, oncologic treatment regimens that include other central nervous system-penetrating drugs and irradiation may sensitize cerebellar cortex and make it more susceptible to other cerebellar sclerosis-causative factors.

Cerebellum↗
PubMedDate not supplied

Angiomyolipomas of the liver in tuberous sclerosis.

Although the association of tuberous sclerosis and renal angiomyolipomas is well established, the occurrence of hepatic hamartomatous lesions in this disease is less well documented. We describe two cases of tuberous sclerosis with associated multiple intrahepatic angiomyolipomas, and we review the literature on this subject. Radiologically, angiomyolipomas can range from entirely lipomatous to completely solid, features which are present in our cases. A characteristic finding of the hepatic involvement in this disease appears to be the multiplicity of the lesions. We suggest that in the setting of tuberous sclerosis it is reasonable to assume that intrahepatic lesions represent angiomyolipomas. However, in nontuberous sclerosis patients with similar findings malignancy cannot be excluded.

Adult↗
PubMed1982

Modulation of immunity in multiple sclerosis: a double-blind levamisole-placebo controlled study in 85 patients.

Levamisole seems to regulate cell-mediated immunity by restoring T-cell function. Since a deficiency of T lymphocytes has been described by various authors in multiple sclerosis patients. Of the 85 patients involved in the trial, evaluation of functional and neurological scores was possible in 54 (32 with placebo and 22 with levamisole). The mean follow-up period was 2 years. This double-blind controlled study indicates that both neurological function and disability significantly deteriorated in the placebo-treated patients, but remained fairly stable in the levamisole-treated group. Since the difference between both groups was not significant, no levamisole effect was demonstrated on progression in multiple sclerosis. With the exception of one case of granulocytopenia (which had no clinical effect), no drug-related changes could be demonstrated. This contrasts with the general impression that this immunomodulator agent might be harmful to patients with multiple sclerosis. The fact that during this blind study both annual relapse rate and disability score remained more stable in treated patients with severe disability suggests that, while waiting for a more effective treatment, long-term levamisole therapy could be useful in patients with multiple sclerosis.

Adolescent↗
PubMed1987

Multiple sclerosis and Hashimoto's thyroiditis.

A case of multiple sclerosis and Hashimoto's thyroiditis confirmed by cytology is reported. The association of multiple sclerosis with other autoimmune diseases is infrequent but supports the immune hypothesis of the pathogenesis of multiple sclerosis. The authors suggest the inclusion of immunological tests in the screening of all patients diagnosed as having multiple sclerosis.

Adult↗
PubMed1987

Trauma and multiple sclerosis. An hypothesis.

An obligatory event in the pathogenesis of the multiple sclerosis plaque appears to be an increase in the permeability of the blood-brain barrier. Neuropathological observations of the brain of persons suffering from concussion after relatively minor head injury, as well as of animals subjected to experimental brain injury, have shown that alterations of the blood-brain barrier constitute a common result of such trauma. It is postulated that the alterations of the blood-brain barrier secondary to trauma of the brain or spinal cord of patients with already established multiple sclerosis may result in an exacerbation or recurrence of a previously symptomatic plaque, in the appearance of symptoms from a silent lesion, or in the formation of a new plaque in such an area of selected vulnerability. In other persons injury to the nervous system may cause the development of multiple sclerosis plaques in the previously damaged areas when the disease has its onset after the trauma. There is no evidence to support the idea that trauma ever causes multiple sclerosis.

Adult↗
PubMed1979

Intrathecal IgG synthesis in multiple sclerosis and other neurological diseases: a comparative evaluation by IgG-index and isoelectric focusing.

Intrathecal IgG synthesis has been investigated by determining the IgG index and by isoelectric focusing in 30 cases of definite multiple sclerosis, in 15 cases of probable multiple sclerosis and in 128 patients affected by other neurological diseases. The blood-brain barrier function was evaluated at the same time by serum albumin/CSF albumin quotient and isoelectric focusing. The IgG index was found elevated in 73.3% of definite multiple sclerosis patients, while oligoclonal IgG bands occurred in 90%. In the other neurological diseases the IgG index was abnormally increased in 35.1% but IgG bands were present only in cerebrospinal fluid (CSF) in 1.5% and both in the CSF and serum in 7% of patients. The high capacity of isoelectric focusing to detect IgG oligoclonal bands in the CSF is pointed out as an extremely useful diagnostic tool in multiple sclerosis.

Adult↗
PubMed1987

Autosomal dominant type of endosteal hyperostosis with unusual manifestations of sclerosis of the jaw bones.

We report three cases of autosomal dominant type endosteal hyperostosis which occurred in one Japanese family. A new pattern of sclerotic changes in the jaw bones is evident. In all members of the family there was a symmetrical thickening of the diaphyseal cortices of the long bones. The affected bones were only minimally widened and the epiphyses and metaphyses were spared. Endosteal sclerosis of the neurocranium was present with loss of the diploë. The sclerotic changes included enlargement and mottled sclerosis of both the maxilla and mandible, with multiple embedded teeth and odontomas. The ramus of the mandible was spared. Severe sclerosis of the jaw bones was present only in a 28-year-old woman. The 2-year-son showed only focal sclerosis in the mandible, and his grandmother had minimal changes in the skeleton.

Adult↗
PubMed1994

The effect of methylprednisolone on monocyte eicosanoid production in patients with multiple sclerosis.

The in vitro effect of methylprednisolone on prostaglandin E2 (PGE2), leukotriene B4 (LTB4) and thromboxane B2 (TXB2) synthesis by adherent monocytes was examined using samples of peripheral blood from 15 patients with multiple sclerosis and 18 normal controls. Eicosanoid production by monocytes was reduced in patients compared with controls and there was a dose-dependent inhibitory effect of methylprednisolone on eicosanoid production in both groups. In vitro production of PGE2 and TXB2 but not LTB4 was reduced in patients with multiple sclerosis following intravenous treatment with methylprednisolone compared with pretreatment samples. In a separate cohort of 20 patients with multiple sclerosis and 15 controls, the in vitro inhibition of PGE2 release by methylprednisolone was not associated with reduced pokeweed-mitogen-stimulated immunoglobulin G synthesis by peripheral blood mononuclear cells. These results suggest that methylprednisolone inhibits monocyte-macrophage function, but this effect is not specific to patients with multiple sclerosis.

Adult↗
PubMed1992

Evidence for increased lipid peroxidation in multiple sclerosis.

Pentane and ethane are degradation products of unsaturated fatty acids which are released during lipid peroxidation. In order to assess whether multiple sclerosis is associated with lipid peroxidation, we measured pentane and ethane excretion by 16 patients with multiple sclerosis and compared them to healthy control subjects. Patients with acute exacerbation of multiple sclerosis had significantly higher concentrations of pentane (10.5 +/- 4.2 nmol/l)(p less than 0.01) compared to either patients in remission (4.5 +/- 1.7 nmol/l) or control subjects (4.9 +/- 1.1 nmol/l). The concentrations of ethane were not significantly different among these groups. Of the patients with acute exacerbation who later achieved remission, the pentane excretion also returned to normal (5.6 +/- 0.9 nmol/l). One patient who failed to reachieve clinical remission continued to excrete large amounts of pentane. We conclude that oxygen free radical activity is enhanced during exacerbation of multiple sclerosis.

Breath Tests↗
PubMed1995

Discriminative power of visual evoked potential characteristics in multiple sclerosis.

To investigate the discriminative power of pattern-reversal visual evoked potential characteristics (peak latencies and amplitude) and to test whether the addition of visual evoked potential amplitude can increase the power of the visual evoked potential in the diagnosis of multiple sclerosis, we retrospectively studied visual evoked potentials in 59 patients with definite multiple sclerosis and 126 control subjects. Two check sizes (17' and 10') were used. Females had significantly higher amplitudes and shorter latencies than males. N80 latency showed a gradual increase and P100 amplitude a decrease with age. P100 latency was stable between the ages of 20 and 55 years but was increased in childhood and the elderly. The significance of visual evoked potential peak latencies and amplitude in separating the two groups was investigated by means of a (multivariate) discriminant analysis. The visual evoked potential with a pattern of 10' could be measured in 58% of patients with multiple sclerosis. The exclusive use of the P100 amplitude in the discriminant analysis resulted in a percentage of correctly classified cases of 84%, whereas for P100 and N80 latency it was 85% and 90%, respectively. With the 17' pattern, the N80 latency yielded also a higher correct percentage than did the P100 latency. Although N80 latency is, to a greater extent than P100 latency, influenced by age, sex and size of stimulus pattern, when these influences are accounted for, the N80 latency is a more sensitive measure than P100 latency in the classification of multiple sclerosis. Combined use of latency and amplitude for discriminant analysis yielded no significant improvement of the percentage of correctly classified cases.

Adolescent↗
PubMed1984

Coarctation of the aorta and renal artery stenosis in tuberous sclerosis.

Among neurocutaneous disorders, coarctation of the abdominal aorta and renal artery stenosis have traditionally been associated with neurofibromatosis. We report a 5-year-old girl who, during the evaluation of asymptomatic hypertension, was discovered to have bilateral renal artery stenosis, coarctation of the abdominal aorta, renal cysts and typical skin lesions of tuberous sclerosis. Renal vascular hypertension has not been reported previously in tuberous sclerosis. We conclude that the tuberous sclerosis complex should be expanded to include vascular malformations and that hypertension should not be assumed to be secondary to renal hamartomata or cysts in patients with tuberous sclerosis.

Aortic Coarctation↗
PubMed1984

A review of the etiology of multiple sclerosis.

The geographic distribution of multiple sclerosis and the influence of migration on the risk of contracting it point to an environmental factor as cause of the disease. This environmental factor might be a virus which might produce the demyelination process through an autoimmune reaction against components of the central nervous system. The other possible cause of multiple sclerosis is a genetic susceptibility, inferred from the higher risk for the disease found among relatives of patients with multiple sclerosis and on the association between the disease and some histocompatibility antigens of the HLA system. Both theories seem to be correct, with the environmental factors(s) causing multiple sclerosis only in the presence of a genetic susceptibility.

Age Factors↗
PubMed1997

[Physical trauma and multiple sclerosis].

Without a more detailed knowledge of etiology and pathogenesis of multiple sclerosis final conclusions regarding an association between physical trauma and the onset or course of multiple sclerosis cannot be drawn. Only a few prospective studies which are appropriately designed to prove a putative correlation have been published. A critical review of these studies and some case reports, in the light of the current pathophysiological concepts of multiple sclerosis, does not indicate a causal relationship between physical trauma and onset of multiple sclerosis or exacerbations.

Central Nervous System↗
PubMed1999

[Interferon beta-1b for treatment of secondary chronic progressive multiple sclerosis].

Several phase III studies have proven that the beta-interferons have positive effects on the number and severity of acute exacerbations of relapsing remitting multiple sclerosis. Recently the first study on the effectiveness of interferon beta-1b in secondary progressive multiple sclerosis was published. In a multicenter, double-blind, randomized, Placebo-controlled study 718 patients with secondary progressive multiple sclerosis and an expanded disability status scale (EDSS) value between 3.0 and 6.5 were treated with either 8 Mio.interferon beta-1b or Placebo subcutaneously every second day for two to three years. The primary study end-point was the time until confirmed progression of the disease as signified by a one point increase of the EDSS value (for initial EDSS values between 3.0 and 5.5) or 0.5 point increase when the initial EDSS value was between 6.0 and 6.5. After two years an interim analysis showed a highly significant difference in delay of disease progression by nine to twelve months for the treatment group (p = 0.0008). This means that interferon beta-1b is the first recombinant beta-interferon to be shown effective in the treatment of secondary progressive multiple sclerosis.

Adjuvants, Immunologic↗
PubMed1997

Reduced bone mass and fat-free mass in women with multiple sclerosis: effects of ambulatory status and glucocorticoid Use.

Multiple sclerosis (MS) is associated with reduced bone mass and vitamin D deficiency. The underlying pathophysiology of the bone disease is uncertain, however, acute and long-term glucocorticoid use, progressive immobilization, vitamin D deficiency, and possibly skeletal muscle atrophy are likely to be determinants. The aims of this study were to determine (a) whether multiple sclerosis is associated with reduced fat-free mass and (b) whether in patients with multiple sclerosis, ambulation ability or glucocorticoid use is associated with bone mass and/or fat-free mass. Seventy-one female patients with MS were compared with 71 healthy, age-matched female controls. Total body bone mineral content (TBBMC, kg), fat mass (FM, kg), and fat-free mass (FFM, kg) were measured using dual X-ray absorptiometry. Disability status was graded according to the Kurtzke Expanded Disability Status Scale (EDSS) as ambulatory, with or without aide (EDSS score of 0 to 6.5), or predominantly wheelchair bound (EDSS score > 6.5). The patients with MS, when compared to age-comparable controls, had deficits in TBBMC ( approximately 8%, -0.3 +/- 0.1 SD, P < 0.04) and FFM ( approximately 5%, -0.3 +/- 0.1 SD, P < 0.01). Both TBBMC and FFM were negatively associated with EDSS score (r = 0.33, P < 0.01, and r = 0.41, P < 0.01, respectively). Patients with MS who were nonambulatory had even greater deficits in TBBMC and FFM as compared with age-matched controls (-0.6 +/- 0.1 SD, P < 0.01, and -0.6 +/- 0. 1 SD, P < 0.01, respectively). By contrast, as compared with age-comparable controls, ambulatory patients with MS had no deficits in bone mass or soft tissue mass. When compared with ambulatory patients with MS, nonambulatory patients with MS had deficits in TBBMC and FFM (P < 0.01 and P < 0.01, respectively). The difference in TBBMC was largely caused by the difference in fat-free mass, whereas the difference in FFM was largely caused by the difference in glucocorticoid use based on analysis of covariance. We conclude that in patients with multiple sclerosis, physical disuse is the main determinant for the reduction in bone mass. Glucocorticoid treatment is the major determinant of the reduction in fat-free mass and thus also contributes to the reduction in bone mass.

Adipose Tissue↗
PubMed2004

MR spectroscopy of cervical spinal cord in patients with multiple sclerosis.

MR spectroscopy (MRS) of the brain in patients with multiple sclerosis has been well studied. However, in vivo MRS of the spinal cord in patients with MR spectroscopy has not been reported to our knowledge. We performed MRS of normal-appearing cervical spinal cords in multiple sclerosis patients and in healthy controls. N-acetyl aspartate was shown to be reduced within the cervical spinal cord of multiple sclerosis patients when compared with healthy controls. This finding supports axonal loss and damage within even normal-appearing spinal cords of multiple sclerosis patients.

Adult↗