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PubMed2005

Verbal fluency deficits in multiple sclerosis.

A quantitative review of 35 studies with 3673 participants was conducted to estimate and compare the magnitude of deficits upon tests of phonemic and semantic fluency for participants with multiple sclerosis (MS) relative to healthy controls. Participants with MS were substantially but similarly impaired on tests of phonemic and semantic fluency. These deficits were larger than deficits on measures of verbal intelligence, confrontation naming and another widely used measure of executive functioning, the Wisconsin Card Sorting Test, but were of a comparable or smaller magnitude relative to deficits on the oral version of the Symbol Digit Modalities Test (SDMT). This is consistent with other research suggesting that measures of verbal fluency and the SDMT may be amongst the most sensitive neuropsychological measures to cognitive impairment in MS. Increased neurological disability and a chronic progressive (as opposed to a relapsing remitting) disease course were associated with larger deficits on tests of phonemic and semantic fluency. However, it is suggested that this latter finding is attributable to the distinct clinical features of chronic progressive and relapsing remitting sub-types. Thus, patients who follow a chronic progressive course tend to be older, have an increased duration of illness and experience greater neurological disability. Once these variables were controlled for, differences between the two sub-types were substantially attenuated.

Adult↗
PubMed1985

Normal T cell subsets and lymphocyte activity in multiple sclerosis.

Nine patients with either chronic progressive or relapsing/remitting multiple sclerosis were treated with several courses of lymphopheresis. The lymphocytes obtained by this procedure showed a significantly lower percentage of OKT3+ cells than normal controls at the beginning of therapy. This percentage increased to normal levels after five lymphopheresis treatments and then decreased during the last stages of treatment. Patients had normal levels of OKT4+ and OKT8+ cells compared to controls and these percentages showed no statistically significant changes during the course of treatment. The proliferative response of patient's lymphocytes after stimulation with concanavalin A, PHA and alloantigen was not significantly different from normal controls and these responses were unchanged during the lymphopheresis treatment. Natural killer cell activity was also normal in our patients. The results reported in this study do not suggest a basic T cell abnormality in our patients with multiple sclerosis. Furthermore, the lymphopheresis treatments did not induce any significant change in T cell numbers or functional activity in vitro.

Adult↗
PubMed1999

Language functions in patients with multiple sclerosis.

Few studies have demonstrated language impairment in patients with multiple sclerosis (MS) compared to healthy controls. The purpose of this investigation was to examine language functions, specifically naming, comprehension, and verbal fluency, in patients with MS and healthy controls to (1) determine if patients with MS demonstrate language impairment, and (2) provide clarification of MS-related language disturbance, particularly in patients with MS of differing courses. Results showed that both chronic-progressive and relapsing-remitting patients with MS performed significantly more poorly than controls on naming, aural comprehension, letter fluency, and category fluency, as well as other language-based cognitive measures. Chronic-progressive patients obtained significantly lower scores than relapsing-remitting patients on the latter three tests. The language disturbance in this MS sample may be partly explained by impairment in other verbal cognitive functions. These findings highlight the importance of assessing language abilities in patients with MS.

Adult↗
PubMed2005

Serum ferritin, transferrin and soluble transferrin receptor levels in multiple sclerosis patients.

Over the last few years, increased evidence has supported the role of iron dysregulation in the pathogenesis of multiple sclerosis (MS), as iron is essential for myelin formation and oxidative phosphorylation. We studied indices of iron metabolism, such as serum iron, ferritin, transferrin and soluble transferrin receptor (sTFR) levels in 27 MS patients. Seven patients had chronic progressive active disease (CP-A), six had chronic progressive stable (CP-S), ten had relapsing remitting active (RR-A) and four had relapsing-remitting stable (RR-S) disease. sTFR levels were found to be significantly higher in CP-A (P = 0.021) and RR-A (P < 0.004) patients than in controls. sTFR levels were also elevated in CP-S patients but did not reach significance (P = 0.064). sTFR values in RR-S patients were comparable to those found in controls (P = 0.31). Ferritin levels were significantly elevated only in CP-A patients (P < 0.002). Patients of the CP group had significantly higher ferritin values than the RR patients (P < 0.004). Haemoglobin values as well as iron and transferrin levels were within normal limits in all patients. In conclusion, the increased serum sTFR and ferritin levels in nonanaemic MS patients with active disease reflect the increased iron turnover. The mild elevation of sTFR levels in CP-S patients may indicate active inflammation with ongoing oxidative damage that is not detectable by history or examination.

Adult↗
PubMed2001

The prevalence of multiple sclerosis, distribution of clinical forms of the disease and functional status of patients in Csongrád County, Hungary.

OBJECTIVE: The aim of this study was to determine the prevalence of multiple sclerosis (MS) in the population of Csongrád County, Hungary (400,128 inhabitants) and to determine the functional status (based on the Expanded Disability Status Scale; EDSS) of the patients according to the clinical forms of the disease. METHODS: The diagnosis was established with the aid of the Poser diagnostic criteria, and the degree of physical disability was determined using the Kurtzke EDSS. RESULTS: In Csongrád County, the prevalence of MS is 62/100,000. The distribution of patients according to the clinical forms of MS was as follows: 15% had the benign form, 54% had relapsing-remitting MS, 20% had secondary chronic progressive MS and 11% had the primary chronic progressive form of MS. Sixty percent of relapsing-remitting MS patients had an EDSS score of 0-4 points and 33% had an EDSS score of 4.5-6.5 points. CONCLUSION: The distribution of patients according to the clinical forms of the disease in this representative population is comparable to results in other regions of the world.

Adolescent↗
PubMed2004

The pathogenesis of primary progressive multiple sclerosis: antibody-mediated attack and no repair?

Primary progressive multiple sclerosis (MS) differs from the more common form of MS which has an initial relapsing-remitting course in a number of ways, including pathological features, clinical course, differential diagnosis and response to treatment. The lesions in primary progressive MS tend to be more diffuse, less inflammatory and less likely to remyelinate than those occurring in relapsing-remitting MS and secondary progressive MS; there are also fewer focal lesions in the brain in primary progressive MS. Recent evidence suggests that antibodies to central nervous system (CNS) antigens have an important role in disease progression. Such antibodies could cause demyelination, inhibit remyelination and cause axonal destruction. Ongoing immune attack by autoantibody and lack of CNS repair could be responsible for the gradually increasing disability in primary progressive MS. Further research on the B-cell and autoantibody response in primary progressive MS might lead to advances in diagnosis and treatment. Inhibition of autoantibody production by inducing B-cell apoptosis with rituximab is a potential new therapy for primary progressive MS.

Autoantibodies↗
PubMed1988

Chronic progressive myelopathy: its relation to the spinal progressive form of multiple sclerosis.

The causes and clinical features of chronic progressive myelopathy (CPM) were evaluated in a retrospective study of 107 patients. A special emphasis was put on those in whom no underlying cause for the myelopathy could be determined. Of 76 such, 39 (51%) had oligoclonal immunoglobulins (Ig) in the CSF and were therefore considered as possible MS, while the remainder, without oligoclonal Ig, were designated "myelopathy of unknown origin" (MUO). Our "possible MS" group was similar clinically to reported series of proven spinal MS, and it seems therefore, that the presence of oligoclonal Ig permits the recognition of a group of patients with myelopathy who might be at a greater risk for MS. Patients with MUO differed from possible MS patients in several clinical characteristics, but most significantly in disease course and levels of functional disability which were more benign in the former. Myelopathy in possible MS patients was also of a primary pyramidal and asymmetrical nature. It is therefore suggested that the segregation of patients with CPM of undetermined origin into 2 separate groups based on the presence or absence of oligoclonal Ig might be of prognostic significance.

Adult↗
PubMed2001

[Myelopathy - Sjogren's syndrome association: analysis of clinical and radiological findings and clinical course].

Myelopathies associated with Sjögren's syndrome has been rarely described especially concerning magnetic resonance imaging (MRI) and treatment aspects. The aim of this study was to determine the clinical, laboratory and radiological features of myelopathies occurring in Sjögren's syndrome. Eleven patients were studied, 7 with an acute myelopathy and 4 with a chronic form. Acute myelopathy were clinically severe with a feature of transverse myelitis necessitating immunosuppressive drugs. On the other hand, chronic forms were closely similar to progressive multiple sclerosis (MS), for clinical and laboratory data. In 7 cases optic neuritis was found associated with myelopathy and fulfilled the diagnostic criteria of Devic's syndrome in 4 cases. The diagnosis of myelopathy associated with Sjögren's syndrome may be difficult especially compared with MS, HTLV1 or HIV myelopathy and sarcoidosis, in the chronic form but also with other vasculitis, MS or viral infection in the acute forms. However, in this last form, magnetic resonance imaging and cerebrospinal fluid data should bring to the diagnosis of Sjögren syndrome and confirmed by appropriate tests. This diagnosis will have direct consequences for an early treatment by immunosuppressive drugs.

Adult↗
PubMed2004

Management of secondary-progressive multiple sclerosis.

The majority of patients with relapse-onset multiple sclerosis (MS) will go on to develop secondary-progressive MS (SPMS) disease, with approximately 50% developing SPMS after 10 years. It remains unknown whether the relapsing and progressive phases of MS differ qualitatively. The pathogenesis of SPMS is poorly understood. The specific role that inflammation plays in disease progression is not well defined. Immunosuppressive therapies, which are capable of reducing or stopping clinical relapses and suppressing MRI activity, generally do not stop disease progression. Recent natural history studies suggest that disease progression occurs regardless of the presence of superimposed relapses. However, poor recovery from clinical relapses does account for the acquisition of disability. Therefore, stopping relapses with appropriate therapy delays the acquisition of disability but does not necessarily delay or prevent the development of SPMS. At present, the only disease-modifying therapies licensed for use in SPMS are interferon-beta-1b in Europe and the US, and mitoxantrone in the US. These agents can only be recommended for patients who continue to have relapses. Symptomatic therapies remain the cornerstone of treatment for patients with SPMS. Delivering high-quality, effective symptomatic therapies requires a multidisciplinary approach. The aim of symptomatic therapies should not only be to reduce neurological impairments but also to decrease disability and handicap and to improve the emotional well-being and health-related quality of life of patients with SPMS.

Adjuvants, Immunologic↗
PubMed2005

[A case of primary progressive multiple sclerosis with onset of memory impairment].

We report a 52-year-old woman with primary progressive multiple sclerosis (PPMS) presenting with chronic progressive memory impairment. From a couple of years prior to admission, she had developed impairment of her short-term memory. For example, she forgot her nephew's name, and spoke the same phrases again and again. She also sometimes forgot to turn off her gas stove and forgot things she bought in shops. Moreover, her mental activity gradually decreased and she became apathetic. However, she did not note her memory impairment, and had no hallucinations. She was admitted to our hospital on 20 May, 2003 because donepezil had been ineffective for treating her memory impairment. Neurologically, she showed bilateral horizontal gaze nystagmus, mild limb ataxia on the left and mildly ataxic gait. Neuropsychological examinations showed mildly impaired cognitive function, e.g., MMSE 25/30, WAIS-R full IQ 69 and especially in verbal short memory, which may represent temporal lobe dysfunction. Moreover, Benton's visual memory test revealed marked visual short-term memory impairment, while impaired performance on a Kana picking up test suggested mild to moderate attention impairment, which could have represented frontal lobe dysfunction. Brain MRI showed multiple T2-high plaque lesions close to the bilateral lateral ventricles, and bilateral optic nerve lesions enhanced by gadolinium. Also, spinal cord MRI showed a gadolinium enhanced lesion at Th5 on the left. Cerebral spinal fluid (CSF) examination showed normal cell count and protein level, and undetectable oligoclonal bands (OCB), but an elevated IgG index (1.1, normal < 0.85). Visual evoked potentials (VEPs) showed prolonged P100 latency bilaterally, indicating subclinical optic nerve lesions. She was thus diagnosed as having PPMS according to McDonald's diagnostic criteria for MS. 99mTc Single photon emission computed tomography (SPECT) showed a decreased cerebral blood flow (CBF) in the bilateral frontal and temporal lobes, which was consistent with her clinical features. PPMS patients generally present with chronic progressive spastic paraparesis and/or cerebellar ataxia. Cognitive impairments observed in PPMS are generally thought to be due to white matter lesions, i.e., subcortical dementia. However, some recent reports have shown MS patients with short-term memory impairment (antegrade amnesia) similar to cortical dementias such as Alzheimer's disease (AD). In such MS cases, visual short-term memory impairment seems characteristic of their cognitive impairment compared to AD cases. As well, the present case showed visual memory impairment as evaluated by Benton's memory test. Parietal and frontal lobes are reported to be important for verbal and visual working memory, respectively. Thus, in the present case, decreased CBF in the frontal and temporal lobes, which could have been due to a disconnection between cortices and subcortices caused by the white matter lesions, is consistent with the type of her cognitive dysfunction, i.e., notable visual memory impairment. PPMS may thus be an important disease as a differential diagnosis for chronic progressive dementia. Further neuropsychological and functional imaging studies will be necessary to achieve a better understanding of the mechanisms of cognitive impairment in PPMS.

Brain↗
PubMed1995

Frequency of anti-nuclear antibodies in multiple sclerosis.

We found anti-nuclear antibodies (ANA) in 26.7% of 150 relapsing-remitting and in 30.4% of 23 chronic progressive definite multiple sclerosis (MS) patients by retrospective chart review. These patients did not have systemic lupus erythematosus. Since ANA are not pathogenically relevant in MS, they are false-positive, and likely reflect systemic immune dysregulation in MS.

Adult↗
PubMed2003

Successful treatment of intrathecal morphine overdose.

A 47-year-old woman was diagnosed with secondary progressive multiple sclerosis, and was treated with intrathecal morphine for chronic pain via a slow-release subcutaneous pump. She accidentally received a 35-ml (510 mg) bolus injection of morphine by this route, which led to status epilepticus. She was treated with continuous intravenous naloxone infusion, and with medication to control hypertension and stop the seizure activity. The outcome was excellent, and the patient returned to her neurological baseline. This report describes the complications and the successful treatment of intrathecal morphine overdose. In order to prevent these serious errors, it is vital that only care providers who are proficient with these devices perform the refilling procedure.

Analgesics, Opioid↗