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PubMed1992

The association of cervical spondylosis and multiple sclerosis.

The diagnostic and therapeutic considerations produced by the coexistence of cervical spondylosis and multiple sclerosis are complex. We have encountered six patients, affected by both multiple sclerosis and cervical spondylosis, in whom neurosurgical procedures were performed. The diagnosis of multiple sclerosis was confirmed by a combination of clinical, neuroimmunologic, electrophysiologic, and neuroradiologic findings. The diagnosis of spondylosis with spinal cord compromise was confirmed by myelography and computed tomographic scan in all cases, and by magnetic resonance imaging in four. Surgery was followed by lasting clinical improvement in two patients, transient improvement in one, and no change in the other three. Our experience confirms that multiple sclerosis and cervical spondylosis can coexist and suggests that this coexistence may result in an interaction that compounds the deleterious effect on the nervous system. Diagnostic evaluations of patients, particularly young patients, with symptoms of cervical spondylosis should include consideration of the possible coexistence of multiple sclerosis. The evaluation of a patient with known multiple sclerosis who develops new signs of cervical spinal cord dysfunction should always include spinal neuroimaging studies. When progression of symptoms coincides with documented progression of anatomic compression, surgical intervention can yield good results.

Adult↗
PubMed2006

Clinical characteristics of cortical multiple sclerosis.

There are several articles in this special issue in which authors eloquently describe neurobehavioural and cognitive complications of multiple sclerosis with relevant neuropsychological assessments and neuroimaging findings. However behavioural and cognitive presentation of multiple sclerosis remains poorly understood. Two years ago, we reported a series of patients with multiple sclerosis who presented with neurobehavioural symptoms and had neuropsychological deficits consistent with cortical dysfunction. Based on previous case reports, pathological studies of cerebral cortex in multiple sclerosis and advanced neuroimaging studies we suggested that neurobehavioural presentation of multiple sclerosis represents a new variant called "cortical multiple sclerosis". The condition is characterised by predominant or exclusive cortical pathology presenting with neurobehavioural symptoms, such as depression, amnesia or distinct cortical syndromes. Since the publication of our report, there has been further neuroimaging and neuropathological findings that further supported the above concept. In addition, observation of more patients with this condition helped us to formulate a logical approach in the detection of these patients. This article focuses on their clinical characteristics.

Behavioral Symptoms↗
PubMed2006

Tuberous sclerosis with open lipped schizencephaly.

Tuberous sclerosis is a multisystem disorder that is transmitted in an autosomal dominant fashion. It affects approximately 1 in 10,000 live births. A growing body of evidence implicates a defect of cell maturation and migration in the pathogenesis of many of the lesions in tuberous sclerosis affecting the central nervous system. There have been numerous case reports of various abnormalities of neuronal migration associated with tuberous sclerosis. To our knowledge, there has only been one case of schizencephaly reported in a patient with tuberous sclerosis. The present report describes a male with tuberous sclerosis and an extensive open lipped schizencephalic cleft affecting his right frontoparietal lobe. This case supports the hypothesis that the cerebral lesions in tuberous sclerosis are secondary to a defect in neuronal maturation and migration.

Abnormalities, Multiple↗
PubMed2006

Multiple sclerosis with childhood onset: report of 21 cases in Taiwan.

Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system. However, the clinical features of childhood-onset multiple sclerosis in Asia have been rarely reported. This report presents our experience in 21 patients with multiple sclerosis (15 females, 6 males, mean age 12.4 +/- 4.5 years) in Taiwan with the onset age before 18. The most common presenting symptoms were limb weakness (62%) and visual disturbance (43%). Poly-symptomatic presentations were found in 16 (76%) patients. Magnetic resonance imaging demonstrated basal ganglion involvement in 33.3% of the patients. Neuroimaging and neurophysiologic evaluations revealed optic nerve involvement in 13 (62%) patients. Only one child had the optico-spinal form. Eighteen (86%) patients had a relapsing remission course, whereas three (14%) patients had secondary progressive course. Three (14%) patients initially diagnosed with acute disseminated encephalomyelitis developed multiple sclerosis after 4 months, 2 years, and 6 years, respectively. In conclusion, childhood multiple sclerosis in Taiwan is frequently poly-symptomatic, and is characterized by a higher ratio of optic nerve and basal ganglion involvement. However, the optico-spinal form of multiple sclerosis occurs rarely in children in Taiwan. Our experience suggests that the chance of relapsing should not be overlooked in patients presenting with clinical and neuroimaging findings suggestive of acute disseminated encephalomyelitis.

Adolescent↗
PubMed2000

Aberrant forms of alpha(2)-macroglobulin purified from patients with multiple sclerosis.

The biochemical properties of alpha(2)-macroglobulin were investigated in four patients with multiple sclerosis and compared to alpha(2)-macroglobulin from healthy controls. An impaired stability of alpha(2)-macroglobulin from the multiple sclerosis patients was demonstrated as a spontaneous conversion to an electrophoretic"fast" form of alpha(2)-macroglobulin upon purification and storage, with a concomitant decrease in functional capacity to inhibit proteinases. The ability to form complexes with proteinases was significantly reduced in alpha(2)-macroglobulin purified from the multiple sclerosis patients. The aberrant molecular arrangements of the protein were not due to proteinase cleavages in the bait regions of alpha(2)-macroglobulin, as demonstrated by gel electrophoresis and protein sequencing. The number of functional thiol esters, however, was reduced in alpha(2)-macroglobulin purified from the multiple sclerosis patients, an observation compatible with the impaired proteinase binding property. Furthermore, differences in isoelectric points were observed between alpha(2)-macroglobulin from the multiple sclerosis patients and alpha(2)-macroglobulin from healthy controls. The results suggest that aberrant forms of alpha(2)-macroglobulin may be present in patients with multiple sclerosis.

Adult↗
PubMed1998

Effects of influenza vaccination and influenza illness on exacerbations in multiple sclerosis.

Despite reports that influenza vaccination appears to be safe in multiple sclerosis there is uncertainty which patients may benefit from it. By using a questionnaire we compared the effects of influenza illness (1995-1996 season) and influenza vaccination (autumn of 1996) on neurologic symptoms in patients with multiple sclerosis registered in the Groningen Multiple Sclerosis Data Bank. No clinically relevant effects were reported in 53 patients with primary progressive multiple sclerosis, either following vaccination or the illness. In a group of 180 patients with relapsing multiple sclerosis, an exacerbation occurred within the following 6 weeks in 33% after influenza illness, whereas it occurred in only 5% after vaccination. The exacerbation rate following influenza illness was significantly higher regardless of whether patients were essentially restricted to wheelchair or not. Because of a substantial greater risk of relapse after influenza illness than after vaccination, annual influenza vaccination should be offered routinely to all patients with relapsing multiple sclerosis.

Adult↗
PubMed1994

Role of limited evaluation and aggressive medical management in multiple sclerosis: a review of 113 patients.

Multiple sclerosis has frequent urological manifestations. Medical management, based on clinical symptoms and urodynamic findings, incorporates clean intermittent catheterization, oral pharmacological agents (that is oral oxybutynin) or their combination (the desired end point of treatment being complete retention with clean intermittent catheterization). Our objectives were to evaluate the efficacy of medical management in multiple sclerosis patients, determine the incidence of hydronephrosis at presentation and during treatment, and evaluate the impact of electromyography on patient management. We reviewed retrospectively 113 patients with documented multiple sclerosis (mean age 45 years, range 20 to 75 years and mean followup 41 months, range 6 to 136 months). Presenting symptoms were irritative alone or combined with obstructive symptoms in 94 patients (83%). On cystometrography 79 patients (70%) had detrusor hyperreflexia and 17 (15%) had an areflexic bladder. Coaxial needle electromyography was performed on 54 patients and 15 (28%) had detrusor-sphincter dyssynergia. Patients with detrusor-sphincter dyssynergia had more advanced neurological disease. A total of 105 patients had radiological imaging of the upper tracts. Only 7 patients (6.6%) had hydronephrosis at presentation and all were stable or improved with medical management. No patient had hydronephrosis with aggressive medical management. No patient with detrusor-sphincter dyssynergia had hydronephrosis or elevated creatinine levels at presentation or during treatment. Medical management failed in 8 patients (7%) who required surgical intervention. Limited evaluation (voiding symptoms, post-void residual and cystometrography) of multiple sclerosis patients is sufficient to formulate an effective treatment program. Electromyography is not necessary in the routine evaluation of patients with documented multiple sclerosis. After baseline upper tract imaging, routine yearly evaluations are unnecessary (unless initially abnormal or indicated by a change in clinical status). Medical management of patients with multiple sclerosis is safe and effective. In this series, no patient had hydronephrosis on therapy, and only 7% of the patients failed aggressive medical management and required surgical intervention.

Adult↗
PubMedDate not supplied

Interferon beta-1a for brain tissue loss in patients at presentation with syndromes suggestive of multiple sclerosis: a randomised, double-blind, placebo-controlled trial.

BACKGROUND: In patients who present with clinically isolated syndromes suggestive of multiple sclerosis, interferon beta-1a is effective in delaying evolution to clinically definite disease and in reducing MRI-measured disease activity. We aimed to assess whether this drug can also reduce the rate of brain volume decrease in such patients enrolled in the ETOMS (early treatment of multiple sclerosis) trial. METHODS: MRI data for brain volume measurements at baseline, month 12, and month 24 were available from 131, 111, and 112 patients assigned treatment (22 microg interferon beta-1a), and 132, 98, and 99 patients assigned placebo respectively. Normalised brain parenchymal volume (NBV) at baseline and percentage brain volume changes (PBVC) were measured with a fully-automated segmentation technique. The primary endpoint was conversion to clinically definite multiple sclerosis due to clinical relapse. Analysis was by intention to treat. FINDINGS: 41 (31%) of 131 patients on interferon beta-1a and 62 (47%) of 132 on placebo converted to clinically definite multiple sclerosis (odds ratio 0.52 [95% CI 0.31-0.86], p=0.0115). Mean PBVC for patients on placebo was -0.83% during the first year, -0.67% during the second year, and -1.68% during the entire study period. Respective values for treated patients were -0.62%, -0.61%, and -1.18%. The changes in brain volume were significant in both groups at all timepoints. A significant treatment effect was detected for month 24 versus baseline values (p=0.0031). The number of new T2 lesions formed during the first year correlated weakly with PBVC during the second year. INTERPRETATION: Early treatment with interferon beta-1a is effective in reducing conversion to clinically definite multiple sclerosis and in slowing progressive loss of brain tissue in patients with clinically isolated syndromes. The modest correlation between new lesion formation and brain volume decrease suggests that inflammatory and neurodegenerative processes are, at least partly, dissociated from the earliest clinical stage of multiple sclerosis onwards.

Adolescent↗
PubMed1989

Tuberous sclerosis: aberrant proline sensitivity of skin fibroblasts.

Cultured skin fibroblasts from patients with tuberous sclerosis were analyzed as to their sensitivities to proline, glutamic acid and arginine, and their analogues by means of a cell growth study. A difference was observed between tuberous sclerosis and normal cells when proline was added. Skin fibroblasts derived from normal-appearing skin of tuberous sclerosis patients exhibited sensitivity to proline. Skin fibroblasts derived from tumorous skin of tuberous sclerosis patients exhibited resistance to proline in the cell growth study and was found to be rather sensitive to proline in a colony formation study. This aberrant sensitivity to proline of tuberous sclerosis cells may indicate abnormal proline metabolism in tuberous sclerosis patients.

Arginine↗
PubMed2001

Vagal nerve stimulation in tuberous sclerosis complex patients.

This is an open-label, retrospective, multicenter study to determine the outcome of intermittent stimulation of the left vagal nerve in children with tuberous sclerosis complex and medically refractory epilepsy. The records of all children treated with vagal nerve stimulation were reviewed in five pediatric epilepsy centers to locate those with tuberous sclerosis complex who had been treated with vagal nerve stimulation for at least 6 months. These patients were compared with (1) a series of patients obtained from the literature, (2) 10 similar control patients with epilepsy obtained from a registry of patients receiving vagal nerve stimulation, and (3) four published series of tuberous sclerosis complex patients whose epilepsy was surgically managed. Ten tuberous sclerosis complex patients with medically refractory epilepsy treated with vagal nerve stimulation were found. Nine experienced at least a 50% reduction in seizure frequency, and half had a 90% or greater reduction in seizure frequency. No adverse events were encountered. Comparison with published and registry patients revealed improved seizure control in the tuberous sclerosis complex patients. Comparison with the group undergoing seizure surgery demonstrated improved outcomes after surgery. Vagal nerve stimulation appears to be an effective and well-tolerated adjunctive therapy in patients with tuberous sclerosis complex and seizures refractory to medical therapy. Resective surgery has a better prospect for improved seizure control.

Adolescent↗
PubMed1998

Chemical analysis of multiple sclerosis lesions by FT-IR microspectroscopy.

Fourier transform infrared microspectroscopy can be used to collect infrared spectra from microscopic regions of tissue sections. If spectra are collected along a grid pattern, then maps of chemical functional groups can be produced and correlated to tissue histopathology. In the present study, white matter from multiple sclerosis and control brains were examined. Mapping experiments were designed such that 17 spectra were collected at 200 microm intervals along a line that was partially or wholly within a multiple sclerosis lesion site or within a representative white matter region of control tissue. Data analysis was based on earlier in vitro studies which found that the carbonyl at 1740 cm(-1) increases when lipids become oxidized (Free Rad. Biol. Med. 16:591-601, 1994), and the amide I peak at approximately 1660 cm(-1) broadens when proteins become oxidized (FEBS Let. 362:165-170, 1995). The results indicated that the C=O to CH2 ratio (1740 cm(-1):1468 cm(-1)) was elevated at several collection points in lesion sites from multiple sclerosis brains compared to values from white matter of control brains. Inspection of the amide I peak at 1657 cm(-1) revealed that it was broadened towards 1652 cm(-1) in multiple sclerosis tissues but not control tissues. These results suggest that lipids and proteins could be oxidized at active multiple sclerosis lesion sites. The localization of these products to lesion sites supports a role for free radicals in the pathogenesis of multiple sclerosis.

Aged↗
PubMed2006

Sex ratio of multiple sclerosis in Canada: a longitudinal study.

BACKGROUND: Incidence of multiple sclerosis is thought to be increasing, but this notion has been difficult to substantiate. In a longitudinal population-based dataset of patients with multiple sclerosis obtained over more than three decades, we did not show a difference in time to diagnosis by sex. We reasoned that if a sex-specific change in incidence was occurring, the female to male sex ratio would serve as a surrogate of incidence change. METHODS: Since environmental risk factors seem to act early in life, we calculated sex ratios by birth year in 27 074 Canadian patients with multiple sclerosis identified as part of a longitudinal population-based dataset. FINDINGS: The female to male sex ratio by year of birth has been increasing for at least 50 years and now exceeds 3.2:1 in Canada. Year of birth was a significant predictor for sex ratio (p<0.0001, chi(2)=124.4; rank correlation r=0.84). INTERPRETATION: The substantial increase in the female to male sex ratio in Canada seems to result from a disproportional increase in incidence of multiple sclerosis in women. This rapid change must have environmental origins even if it is associated with a gene-environment interaction, and implies that a large proportion of multiple sclerosis cases may be preventable in situ. Although the reasons why incidence of the disease is increasing are unknown, there are major implications for health-care provision because lifetime costs of multiple sclerosis exceed pound1 million per case in the UK.

Adult↗
PubMed2006

Endostatin peptide, an inhibitor of angiogenesis, prevents the progression of peritoneal sclerosis in a mouse experimental model.

Peritoneal sclerosis is a major and serious complication in patients on long-term continuous ambulatory peritoneal dialysis (PD). The involvement of angiogenesis and proangiogenic factors such as vascular endothelial growth factor (VEGF)-A in progressing peritoneal sclerosis has been reported. We previously reported the therapeutic efficacy of endostatin peptide, a potent inhibitor of angiogenesis derived from type XVIII collagen, in a mouse diabetic nephropathy model. Here, we examined the therapeutic effect of endostatin peptide in preventing progression in a mouse peritoneal sclerosis model. Male ICR mice received intraperitoneal injections of chlorhexidine gluconate (CG) every other day to induce peritoneal sclerosis. Endostatin peptide (1 or 4 mg/kg/day) was administered via subcutaneously implanted osmotic minipumps. Peritoneal sclerosis (day 24) was significantly suppressed by endostatin peptide in a dose-dependent manner. Peritoneal accumulation of type III collagen was significantly suppressed by endostatin peptide. Increase in the number of CD31(+) blood vessels, F4/80(+) monocyte/macrophage accumulation, and 5-bromodeoxyuridine(+) proliferating cells was significantly inhibited by endostatin peptide. Increase in peritoneal expression of VEGF-A, profibrotic transforming growth factor-beta1, and alpha-smooth muscle actin was suppressed by endostatin peptide. Immunoreactivity for endogenous endostatin (whole molecule) and endostatin receptor alpha5beta1-integrin was increased and colocalized to CD31(+) blood vessels in the thickened peritonea of CG-injected mice. These results demonstrate the potential use of antiangiogenic endostatin peptide as a novel therapeutic agent in preventing peritoneal sclerosis, a severe complication in patients undergoing long-term PD.

Actins↗
PubMed2003

[Therapy of day time fatigue in patients with multiple sclerosis].

Fatigue is the most common symptom of multiple sclerosis. 75%-90% of patients with multiple sclerosis report having fatigue, and 50%-60% describe it as the worst symptom of their disease. Fatigue is significantly associated with reduced quality of life and is also a major reason for unemployment, especially for patients with otherwise minor disability. The mechanisms underlying abnormal levels of fatigue in multiple sclerosis are poorly understood. To date, drug treatment has been only partially successful in alleviating fatigue, and effects vary widely from patient to patient. Amantadine and modafinil showed to be effective in the treatment of fatigue in some studies. Non-pharmacological management of fatigue in multiple sclerosis includes inpatient rehabilitation and endurance training. There is also evidence, that pulsing electromagnetic fields may improve fatigue associated with multiple sclerosis. This paper summarizes the recent literature on pathophysiology, diagnosis and therapy of the most common symptom of multiple sclerosis.

Central Nervous System Stimulants↗
PubMed2001

Ankle images digital analysis (AIDA): digital measurement of joint space width and subchondral sclerosis on standard radiographs.

OBJECTIVE: Reliable evaluation of joint space width and subchondral sclerosis of osteoarthritic joints is difficult. The present study describes a new digital method to analyse standard radiographs of the ankle. DESIGN: Standardized radiographs were taken of the ankle of 12 patients with severe osteoarthritis (OA) under full weight-bearing conditions, before treatment and 1 year after initiation of treatment. Treatment consisted of 3 months distraction of the tibio-talar joint, for which clinical benefit has been shown previously. The width of the joint space was measured on digitized images of the radiographs by means of the newly developed semi-automatic digital technique called AIDA (Ankle Images Digital Analysis) and by means of the most widely used conventional analogue measurements. In addition, AIDA was used to assess subchondral sclerosis by measuring the intensity of the radiograph at fixed positions at the bone-cartilage interface. RESULTS: AIDA appeared to be a reliable method for measuring small changes in joint space width and subchondral sclerosis because the intra- and interobserver variation was small. Mean JSW for two observers was 1.96 and 2.00 mm, with mean differences between two observations of 0.05 and -0.01, respectively. Mean subchondral sclerosis in the tibia was 1.52 and 1.61 with mean differences between two observations of, respectively, 0.00 and 0.03. In addition to conventional measurements, AIDA could demonstrate a decrease in subchondral sclerosis as a result of joint distraction of 71% and 69% after 1 year for talus and tibia, respectively. CONCLUSION: The use of AIDA is preferable to the conventional analogue method for evaluating the severity of ankle OA, because the method provides quantitative data not only for the joint space width but also for subchondral sclerosis.

Ankle Joint↗
PubMed1998

Axonal transection in the lesions of multiple sclerosis.

BACKGROUND: Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system and is the most common cause of neurologic disability in young adults. Despite antiinflammatory or immunosuppressive therapy, most patients have progressive neurologic deterioration that may reflect axonal loss. We conducted pathological studies of brain tissues to define the changes in axons in patients with multiple sclerosis. METHODS: Brain tissue was obtained at autopsy from 11 patients with multiple sclerosis and 4 subjects without brain disease. Fourteen active multiple-sclerosis lesions, 33 chronic active lesions, and samples of normal-appearing white matter were examined for demyelination, inflammation, and axonal pathologic changes by immunohistochemistry and confocal microscopy. Axonal transection, identified by the presence of terminal axonal ovoids, was detected in all 47 lesions and quantified in 18 lesions. RESULTS: Transected axons were a consistent feature of the lesions of multiple sclerosis, and their frequency was related to the degree of inflammation within the lesion. The number of transected axons per cubic millimeter of tissue averaged 11,236 in active lesions, 3138 at the hypocellular edges of chronic active lesions, 875 in the hypocellular centers of chronic active lesions, and less than 1 in normal-appearing white matter from the control brains. CONCLUSIONS: Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.

Adolescent↗
PubMed1996

Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions.

Mutations in the human Cu,Zn superoxide dismutase gene (SOD1) are found in 20% of kindreds with familial amyotrophic lateral sclerosis. Transgenic mice (line G1H) expressing a human SOD1 containing a mutation of Gly-93 --> Ala (G93A) develop a motor neuron disease similar to familial amyotrophic lateral sclerosis, but transgenic mice (line N1029) expressing a wild-type human SOD1 transgene do not. Because neurofilament (NF)-rich inclusions in spinal motor neurons are characteristic of amyotrophic lateral sclerosis, we asked whether mutant G1H and/or N1029 mice develop similar NF lesions. NF inclusions (i.e., spheroids, Lewy body-like inclusions) were first detected in spinal cord motor neurons of the G1H mice at 82 days of age about the time these mice first showed clinical evidence of disease. Other neuronal intermediate filament proteins (alpha-internexin, peripherin) also accumulated in these spheroids. The onset of accumulations of ubiquitin immunoreactivity in the G1H mice paralleled the emergence of vacuoles and NF-rich spheroids in neurons, but they did not colocalize exclusively with spheroids. In contrast, NF inclusions were not seen in the N1029 mice until they were 132 days old, and ubiquitin immunoreactivity was not increased in the N1029 mice even at 199 days of age. Astrocytosis in spinal cord was associated with a marked increase in glial fibrillary acidic protein immunoreactivity in the G1H mice, but not in the N1029 mice. Finally, comparative studies revealed a striking similarity between the cytoskeletal pathology in the G1H transgenic mice and in patients with amyotrophic lateral sclerosis. These findings link a specific SOD1 mutation with alterations in the neuronal cytoskeleton of patients with amyotrophic lateral sclerosis. Thus, neuronal cytoskeletal abnormalities may be implicated in the pathogenesis of human familial amyotrophic lateral sclerosis.

Aging↗
PubMed1995

Pregnancy is associated with a lower risk of onset and a better prognosis in multiple sclerosis.

The effects of pregnancy were studied in a multiple sclerosis incidence cohort. In order to eliminate interaction bias between the disease and pregnancy, analysis of the risk of relapse during pregnancy and the puerperium was limited to the onset bout, using fecundity figures for Sweden. The risk of onset bout was significantly reduced during pregnancy while the risk of onset bout in the post-partum period did not differ significantly from the risk during non-pregnancy periods. We also found a decreased risk of multiple sclerosis onset in parous compared with nulliparous women. The association between nulliparity and multiple sclerosis tended to increase with age. Furthermore, the effect of pregnancy on the long-term prognosis in established multiple sclerosis was analysed by comparing the risk of change from a relapsing-remitting to a chronic progressive course and the risk of reaching level 6 of the Disability Status Scale in women with pregnancy after multiple sclerosis onset with that in non-pregnant control patients, matched for neurological deficit, disease duration and age. There was a significantly decreased risk of a progressive course in women who were pregnant after multiple sclerosis onset.

Adolescent↗