Corea subagudo reversible por déficit de vitamina B12 / Reversible subacute chorea caused by vitamin B12 deficiency

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[Treatment of relapsing-remitting multiple sclerosis with fingolimod in routine clinical practice]. / Tratamiento de la esclerosis multiple remitente recurrente con fingolimod en la practica clinica habitual.

INTRODUCTION: Fingolimod is a selective immunosuppressant that targets the S1P receptor, and is indicated in the treatment of aggressive relapsing-remitting multiple sclerosis (RRMS) and following treatment failure with first-order drugs. AIM: To investigate the safety and effectiveness of fingolimod under the conditions of routine clinical practice. PATIENTS AND METHODS: We conducted an observational study with prospective follow-up of patients with RRMS who received fingolimod from January 2011 until February 2014. Data assessed were the annualised relapse rate (ARR), disability measured by the Expanded Disability Status Scale (EDSS), magnetic resonance activity and the appearance of side effects. RESULTS: Our sample consisted of 122 patients, 79.5% of them females and with a mean age of 26.8 years. They were classified, according to the last treatment received, as being: naive (aggressive RRMS; n = 17), previous treatment failure (n = 67) and withdrawal of natalizumab due to risk of progressive multifocal leukoencephalopathy (n = 38). After a mean follow-up of 29.9 ± 15.9 months, the ARR and the appearance of new lesions with gadolinium enhancement were reduced in both the naive and the previous treatment failure groups. There were no differences between the various subgroups as regards the progression of EDSS or the time elapsed until the first attack or treatment failure. The risk of treatment failure is higher with a baseline EDSS > 3 (hazard ratio: 4.24; p = 0.001) and presence of IgM oligoclonal bands (hazard ratio: 2.45; p < 0.022). CONCLUSIONS: Fingolimod is an effective and well-tolerated drug under conditions of routine clinical practice. Having a baseline EDSS > 3 and IgM oligoclonal bands is predictive of a poor response to fingolimod.

TITLE: Tratamiento de la esclerosis multiple remitente recurrente con fingolimod en la practica clinica habitual.Introduccion. El fingolimod es un inmunosupresor selectivo dirigido contra el receptor SP-1, indicado en el tratamiento de la esclerosis multiple remitente recurrente (EMRR) agresiva y tras el fracaso del tratamiento con farmacos de primera linea. Objetivo. Investigar la seguridad y efectividad del fingolimod en condiciones de practica clinica habitual. Pacientes y metodos. Estudio observacional con seguimiento prospectivo de pacientes con EMRR que recibieron fingolimod desde enero de 2011 hasta febrero de 2014. Se evaluo la tasa anual de brotes (TAB), la discapacidad medida por la escala expandida del estado de discapacidad (EDSS), la actividad en la resonancia magnetica y la aparicion de efectos adversos. Resultados. Incluimos 122 pacientes, el 79,5% mujeres y con una edad media de 26,8 antilde;os. Se clasificaron segun el ultimo tratamiento recibido en: naive (EMRR agresiva; n = 17), fracaso a terapias previas (n = 67) y retirada de natalizumab por riesgo de leucoencefalopatia multifocal progresiva (n = 38). Tras un seguimiento medio de 29,9 ± 15,9 meses, se redujo de forma significativa la TAB y la aparicion de nuevas lesiones con realce de gadolinio en el grupo naive y el de fracaso a terapias previas. No ha habido diferencias en la evolucion de la EDSS ni en el tiempo hasta el primer brote o el fracaso terapeutico entre los diferentes subgrupos. El riesgo a fracaso terapeutico es mayor con la EDSS basal > 3 (hazard ratio: 4,24; p = 0,001) y presencia de bandas oligoclonales IgM (hazard ratio: 2,45; p < 0,022). Conclusiones. El fingolimod es un farmaco eficaz y seguro en la EMRR en condiciones de practica clinica habitual. Tener una EDSS basal > 3 y bandas oligoclonales IgM predice una mala respuesta al fingolimod.

[Review of the novelties presented at the 26th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) (II)]. / Revision de las novedades presentadas en el XXVI Congreso del Comite Europeo para el Tratamiento e Investigacion en Esclerosis Multiple (ECTRIMS) (II).

The new insights presented at European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), held in the city of Gothenburg, Sweden, in October 2010, have been summarized at the third edition of Post-ECTRIMS meeting held in Madrid in November 2010. Encouraging findings from the 5-years follow up extension from PreCISe study confirm the benefit of early treatment with glatiramer acetate in patients with clinically isolated syndromes (CIS) against the conversion to clinically definitive multiple sclerosis and cerebral atrophy with an adequate safety and tolerability. Regarding treatment decision with escalation or induction therapy, different strategies have been proposed depending on to the characteristics of the individual patient with CIS. Findings from several of the reported studies have revealed the favorable role of combined therapy on relapse rate but not on magnetic resonance parameters in patients with recurrent-remittent multiple sclerosis. Novel therapies such as alemtuzumab, daclizumab ofatutumab or ocrelizumab have shown promising findings regarding efficacy. Nevertheless, safety findings for these emerging therapies have detected some severe adverse events, the main ones being potentially fatal opportunistic infections such as progressive multifocal leukoencephalopathy (PML) caused by JC virus, mainly linked to natalizumab treatment. In this regard, clinicians will face the assessment of he benefit-risk ratio when deciding on the adequate treatment for each patient in the clinical setting. In this regard, determination of antibodies to JC virus by a novel two-step enzyme-linked immunosorbent assay (ELISA) could provide clinicians with a useful tool to stratify PML risk in patients. Regarding non pharmacologic therapies, behavioral intervention has emerged as an effective therapy in the treatment of depression in multiple sclerosis, showing additional benefits on fatigue, disability and adherence to treatment.

Afectación de las funciones cognitivas en la esclerosis múltiple secundaria progresiva / Compromise of the cognitive functions in progressive secondary multiple sclerosis

Definir el patrón de afectación cognitiva en un grupo homogéneo de pacientes afectados de esclerosis múltiplesecundaria progresiva (EMSP). Pacientes y métodos. Se incluyó a 42 pacientes mayores de edad con el diagnóstico de EMSP y un grado similar de discapacidad, un tiempo de evolución superior a 24 meses y en tratamiento con interferón beta-1b un mínimo de tres meses. Se les administró una batería de 10 test neuropsicológicos, seleccionados para este estudio y repartidos en dos sesiones de una hora. Además, se evaluó el estado emocional con el inventario de depresión de Beck y la escala de ansiedadde Hamilton. Definimos ‘deterioro cognitivo’ como la alteración de dos o más test. Resultados. El 73,8% eran mujeres; edad media: 45 años (rango: 25-62); Expanded Disability Status Scale media: 5,4 (rango: 3,0-7,5); tiempo medio de evolución: 34,5 meses (rango: 24-80), y tiempo medio de tratamiento: 13,5 meses (rango: 3-38 ). El 78,5% padecía deterioro cognitivo. Lasfunciones más alteradas fueron: capacidad atencional, percepción visuoespacial, fluidez verbal, memoria lógica a largo y corto plazo y razonamiento abstracto. La presencia de deterioro cognitivo se relacionó con el tiempo de evolución de la enfermedad (r = 0,31; p < 0,05) pero no con la edad, el grado de discapacidad o con la duración del tratamiento. Conclusión. El deterioro cognitivo es frecuente en la EMSP; la velocidad para la adquisición y procesamiento de nueva información y las funciones ejecutivas fueron las áreas afectadas con mayor frecuencia y gravedad. La alteración de la información visuoespacial fue un hallazgodiferencial de nuestra serie que podría contribuir al diagnóstico clínico de la progresión

To define the patterns of cognitive impairment in a homogeneous group of secondary progressive multiplesclerosis (SPMS) patients. Patients and methods. Forty-two SPMS patients were included with a similar degree of disability; all had been treated with interferon beta-1b for a minimum of 3 months. They voluntarily complimented a battery of 10 neuropsychological tests selected for this study, distributed in two sessions of one hour. In addition, the emotional state was evaluatedwith the Beck Depression Inventory and the Hamilton Anxiety Scale. We considered cognitive impairment as more than two tests altered, according with previously reported studies. Results. 73.8% of patients were women; mean age was 45 years (range: 25-62); mean EDSS was 5.4 (range: 3.0-7.5); mean evolution time was 34.5 months (range: 24-80); mean treatment durationwas 13.5 months (range: 3-38). Cognitive impairment was present in 78.5% of patients. The most frequently impaired functions were: attentional capacity, visuospatial perception, verbal fluency, short-term and long-term logic memory and abstractreasoning. The presence of cognitive impairment was related to the time of evolution of the disease (r = 0.31; p < 0.05) but not with the age, the degree of disability or the treatment duration. Conclusion. Cognitive impairment in the SPMS patients is afrequent finding, being the alteration in the speed for the acquisition and processing of new information, and the abstract reasoning the most frequent and severe altered functions. The also frequent impairment of visuospatial information was a differential finding in our study that could contribute to diagnosis of clinical progression

[Compromise of the cognitive functions in progressive secondary multiple sclerosis]. / Afectación de las funciones cognitivas en la esclerosis múltiple secundaria progresiva.

AIM: To define the patterns of cognitive impairment in a homogeneous group of secondary progressive multiple sclerosis (SPMS) patients. PATIENTS AND METHODS: Forty-two SPMS patients were included with a similar degree of disability; all had been treated with interferon beta-1b for a minimum of 3 months. They voluntarily complimented a battery of 10 neuropsychological tests selected for this study, distributed in two sessions of one hour. In addition, the emotional state was evaluated with the Beck Depression Inventory and the Hamilton Anxiety Scale. We considered cognitive impairment as more than two tests altered, according with previously reported studies. RESULTS: 73.8% of patients were women; mean age was 45 years (range: 25-62); mean EDSS was 5.4 (range: 3.0-7.5); mean evolution time was 34.5 months (range: 24-80); mean treatment duration was 13.5 months (range: 3-38). Cognitive impairment was present in 78.5% of patients. The most frequently impaired functions were: attentional capacity, visuospatial perception, verbal fluency, short-term and long-term logic memory and abstract reasoning. The presence of cognitive impairment was related to the time of evolution of the disease (r = 0.31; p < 0.05) but not with the age, the degree of disability or the treatment duration. CONCLUSION: Cognitive impairment in the SPMS patients is a frequent finding, being the alteration in the speed for the acquisition and processing of new information, and the abstract reasoning the most frequent and severe altered functions. The also frequent impairment of visuospatial information was a differential finding in our study that could contribute to diagnosis of clinical progression.

Comparison of injection site pain and injection site reactions in relapsing-remitting multiple sclerosis patients treated with interferon beta-1a or 1b.

This prospective, multicentre, international, observational, cohort study compared injection site pain (ISP) and injection site reactions (ISRS) between interferon beta-1b (IFNB-1b; Betaferon) 250 microg subcutaneously every other day and interferon beta-1a (IFNB-1a; Rebif) 44 microg subcutaneously three times weekly in patients with relapsing-remitting MS. Patients started treatment within 3 months before recruitment and were on full dose of therapy at inclusion. Patients self-injected IFNB and self-assessed ISP for 15 consecutive injections immediately, 30 and 60 min after injection, using a visual analogue scale diary. Study staff assessed ISRS. Of 445 patients (valid cases), approximately 90% used autoinjectors. More patients were pain-free at all timepoints with IFNB-1b than with IFNB-1a (eg, 30 min: 42.6% versus 19.7%; P<0.0001). The mean proportion of pain-free injections was greater for IFNB-1b (eg, 30 min: 79.0%) than for IFNB-1a (53.3%; P<0.0001). The proportion of patients without ISRS was greater for IFNB-1b (second visit 51.8% versus 33.8%; P<0.0001). Compared with IFNB-1a, more IFNB-1b patients either had no pain or their ISP had no influence on treatment satisfaction (76.9% versus 64.1%; P=0.006). The impact on tolerability and patient acceptability of any new IFNB product formulations would, however, have to be evaluated in comparative studies.

[Total brain T2-hyperintense lesion-volume and the axonal damage in the normal-appearing white matter of brainstem in early lapsing-remitting multiple sclerosis]. / Relación entre el volumen lesional cerebral total en resonancia magnética secuencia T2 y el daño neuroaxonal en la sustancia blanca aparentemente normal del tronco del encéfalo en la esclerosis múltiple remitente-recurrente.

AIM: To evaluate the relationship between the total brain T2-hyperintense lesion volume (TBT2LV) and the axonal damage in the normal-appearing white matter of brainstem measured by 1H-MRS in a group of early relapsing-remitting multiple sclerosis patients. SUBJECTS AND METHODS: 40 relapsing-remitting multiple sclerosis patients and ten sex- and age-matched healthy subjects were prospectively studied for two years. T2-weighted MR and 1H-MRS imaging were acquired at time of recruitment and at year two. The TBT2LV was calculated with a semiautomatic program; N-acetylaspartate (NAA), creatine (Cr) and choline (Cho) resonances areas were integrated with jMRUI program and the ratios were calculated for four volume elements that represented the brainstem. RESULTS: At basal study we obtained an axonal loss (as a decrement of NAA/ Cho ratio) in the group of patients compared with controls (p = 0.017); this axonal loss increased at the second year of the follow-up for patients (NAA/Cho decrease, p = 0.004, and NAA/Cr decrease, p = 0.002) meanwhile control subjects had no significant metabolic changes. Higher lesion load was correlated with a poor clinical outcome, being the correlation between the basal TBT2LV and the Expanded Disability Status Scale at second year (r = 0.299; p = 0.05). Besides, axonal loss was not homogeneous for all multiple sclerosis patients, being stronger in the subgroup of patients with high basal TBT2LV (p = 0.043; ANOVA). CONCLUSION: Our data suggest that axonal damage is early in multiple sclerosis and higher in patients high basal TBT2LV, suggesting a possible relationship between these two phenomena.

Relación entre el volumen lesional cerebral total en resonancia magnética secuencia T2 y el daño neuroaxonal en la sustancia blanca aparentemente normal del tronco del encéfalo en la esclerosis múltiple remitente-recurrente

Analizar mediante espectroscopia de protón el daño neuroaxonal en la sustancia blanca aparentementenormal del tronco del encéfalo y su relación con el volumen lesional cerebral total en T2 (VLCT2) medido por resonancia magnética, en pacientes con esclerosis múltiple remitente-recurrente. Sujetos y métodos. Estudio longitudinal prospectivo comparativo a dos años de las variaciones en la concentración de N-acetilaspartato (NAA), creatina (Cr) y colina (Co), medidas por espectroscopia de protón, en 40 pacientes afectos de esclerosis múltiple remitente-recurrente y 10 personas sanas ajustadas por sexo y edad. Los metabolitos se calcularon mediante el programa jMRUI en cuatro volúmenes de interés representadosen el troncoencéfalo, y el VLCT2, con un programa semiautomático. Resultados. El estudio basal mostró daño neuroaxonal (expresado como un menor cociente NAA/Co, p = 0,017) en el grupo de pacientes frente a los controles. El daño axonal se incrementó significativamente a los dos años sólo en el grupo de pacientes (descenso del cociente NAA/Co, p =0,004, y NAA/Cr, p = 0,002). Un mayor volumen lesional basal se correlacionó con una peor evolución clínica, representada por la Expanded Disability Status Scale a los 2 años (r = 0,299; p = 0,05). La intensidad del daño neuroaxonal no fue homogénea en todos los pacientes, siendo mayor en el subgrupo de pacientes con VLCT2 basal superior (p = 0,043; ANOVA). Conclusión.Los resultados sugieren que el daño neuroaxonal aparece precozmente en la esclerosis múltiple, que es progresivo y que se relaciona al menos parcialmente con el volumen lesional cerebral

To evaluate the relationship between the total brain T2-hyperintense lesion volume (TBT2LV) and the axonaldamage in the normal-appearing white matter of brainstem measured by 1H-MRS in a group of early relapsing-remitting multiple sclerosis patients. Subjects and methods. 40 relapsing-remitting multiple sclerosis patients and ten sex- and agematchedhealthy subjects were prospectively studied for two years. T2-weighted MR and 1H-MRS imaging were acquired attime of recruitment and at year two. The TBT2LV was calculated with a semiautomatic program; N-acetylaspartate (NAA), creatine (Cr) and choline (Cho) resonances areas were integrated with jMRUI program and the ratios were calculated for four volume elements that represented the brainstem. Results. At basal study we obtained an axonal loss (as a decrement of NAA/Cho ratio) in the group of patients compared with controls (p = 0.017); this axonal loss increased at the second year of the follow-up for patients (NAA/Cho decrease, p = 0.004, and NAA/Cr decrease, p = 0.002) meanwhile control subjects had no significant metabolic changes. Higher lesion load was correlated with a poor clinical outcome, being the correlation betweenthe basal TBT2LV and the Expanded Disability Status Scale at second year (r = 0.299; p = 0.05). Besides, axonal loss was not homogeneous for all multiple sclerosis patients, being stronger in the subgroup of patients with high basal TBT2LV (p = 0.043; ANOVA). Conclusion. Our data suggest that axonal damage is early in multiple sclerosis and higher in patients highbasal TBT2LV, suggesting a possible relationship between these two phenomena

[Subacute uveomeningoencephalitis as the presenting symptom of acute infection by the human immunodeficiency virus]. / Uveomeningoencefalitis subaguda como forma de presentación de la infección aguda por el virus de la inmunodeficiencia humana.

INTRODUCTION: The uveo-meningitic syndrome, or the combination of chronic or recurrent meningitis and acute uveitis, has a specific differential diagnosis. This syndrome can be the clinical debut of systemic disorders, vasculophathies, connective tissue disorders and inmuno-mediated diseases. In patients with AIDS, the syndrome often appears in relation with an opportunist concomitant infection of the central nervous system (CNS). CASE REPORT: We present one case of subacute uveo-meningitic syndrome as symptomatic presentation of a early infection of HIV. The patient was a man, 37 years-old. He was inmunocompetent and did not know his seropositivity for HIV type 1. We relate the results of the neurologic examination and complementary tests. Only serologic test for HIV type 1 and detection of IgG anti-HIV in cerebrospinal fluid were positives. CONCLUSIONS: In patients HIV-positive the ocular infection, usually a posterior uveitis, appears together with systemic disorders or central nervous infections. In other hand, the cause of meningitic infection depends on grade of immunocompromise. Aseptic meningitis, for early stages of the disease, is usually no symptomatic. After, opportunist infections or neoplasic infiltration of CNS can be cause of meningoencephalitis. In this patient, the early infection of HIV causes an subacute uveomeningoencephalitis. Early infection of HIV increases the possibilities of aetiological diagnosis of uveomeningitic syndrome.

Uveomeningoencefalitis subaguda como forma de presentación de la infección aguda por el virus de la inmunodeficiencia humana / Subacute uveomeningoencephalitis as the presenting symptom of acute infection by the human immunodeficiency virus

Introducción. El síndrome uveomeníngeo (SUM) resulta de la combinación de una uveítis anterior y una meningitis linfocitaria, aguda recurrente o crónica. Puede corresponder al debut de una enfermedad sistémica, una vasculopatía, una enfermedad del colágeno o de procesos inmunomediados. En los pacientes con sida, acompaña con frecuencia a infecciones oportunistas del sistema nervioso central (SNC). Caso clínico. Varón de 37 años, inmunocompetente, sin conductas de riesgo, que consultó por inflamación ocular derecha y un síndrome meníngeo. Durante su evolución sufrió un déficit neurológico focal transitorio. Todas las exploraciones practicadas fueron normales con excepción del estudio licuoral, que mostró hiperproteinorraquia y ligera linfocitosis. El estudio serológico frente al VIH tipo 1 fue positivo, y se confirmó además la producción intratecal de anticuerpos IgG frente al virus. Conclusiones. En los pacientes positivos para el VIH, la infección ocular que acompaña a enfermedades sistémicas o infecciones del SNC, habitualmente, es una uveítis posterior o coriorretinitis. Por otra parte, el perfil etiológico de la infección meníngea varía en función de la afectación inmunitaria del paciente seropositivo. En las fases precoces de la enfermedad la primoinfección por el VIH suele provocar una meningitis linfocitaria que cursa de manera asintomática. En fases más avanzadas, la meningoencefalitis del paciente con sida tiene habitualmente un origen infeccioso o infiltrativo. En nuestro paciente, la infección por el VIH tuvo un debut excepcional, el de una uveomeningoencefalitis subaguda. La infección aguda por el VIH amplía las posibilidades de diagnóstico etiológico frente al SUM (AU)

Introduction. The uveo-meningitic syndrome, or the combination of chronic or recurrent meningitis and acute uveitis, has a specific differential diagnosis. This syndrome can be the clinical debut of systemic disorders, vasculophathies, connective tissue disorders and inmuno-mediated diseases. In patients with AIDS, the syndrome often appears in relation with an opportunist concomitant infection of the central nervous system (CNS). Case report.We present one case of subacute uveomeningitic syndrome as symptomatic presentation of a early infection of HIV. The patient was a man, 37 years-old. He was inmunocompetent and did not know his seropositivity for HIV type1.We relate the results of the neurologic examination and complementary tests. Only serologic test for HIV type 1 and detection of IgG anti-HIV in cerebrospinal fluid were positives. Conclusions. In patients HIV-positive the ocular infection, usually a posterior uveitis, appears together with systemic disorders or central nervous infections. In other hand, the cause of meningitic infection depends on grade of immunocompromise. Aseptic meningitis, for early stages of the disease, is usually no symptomatic. After, opportunist infections or neoplasic infiltration of CNS can be cause of meningoencephalitis. In this patient, the early infection of HIV causes an subacute uveomeningoencephalitis. Early infection of HIV increases the possibilities of aetiological diagnosis of uveomeningitic syndrome (AU)

[Pseudopolyneuritic symptoms with a medullary origin as the presenting symptom of multiple sclerosis]. / Patrón pseudopolineurítico de origen medular como forma de presentación de una esclerosis múltiple.

INTRODUCTION: Myelopathy is, frequently, the first manifestation of a multiple sclerosis (MS), being the acute transverse mielitis, partial or incomplete, the habitual clinical syndrome. Other sensitive symptoms with an origin in the spinal cord as 'steroanesthesia', 'pseudo-athetosis' or 'pseudo-radiculopathy' have been described as unusual form of presentation in MS, but not the 'pseudo-polyneuropathy', perhaps in relation with its rapid progression in an acute transverse mielitis or other sensory pattern. CASE REPORTS: We presented two patients with a 'pseudo-polyneuropathy' pattern as the first manifestation of MS. In the two cases magnetic resonance imaging showed a cervical lesion of spinal cord with a probably inflammatory origin and other similar lesions in the brain. Neurophysiological studies were normal. We think that the 'pseudo-polyneuropathy' could be caused by an antero-lateral demyelinating process in the cervical spinal cord, with affectation of the anterior comissure and the ventral portion of lateral spinothalamic pathway. CONCLUSION: The 'pseudo-polyneuropathic' syndrome is uncommon form of presentation of MS in young people. We may be capable of recognize the 'pseudo-polyneuropathy' with spinal origin and early choose the appropriate complementary examinations for a correct diagnosis and therapy.

Hipotensión intracraneal espontánea: evolución de la imagen en resonancia magnética y confirmación mediante ventriculografía isotópica / Spontaneous intracranial hypotension: progression of the images obtained by magnetic resonance and confirmation by means of a gated blood pool scan

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[Differences in the spectroscopy of the lesions of the remitting relapsing form of multiple sclerosis shown by magnetic resonance]. / Diferencias en la espectroscopía de las lesiones de esclerosis múltiple en su forma remitente recurrente mediante resonancia magnética.

INTRODUCTION: Multiple sclerosis (MS) is a chronic demyelinating disorder of the central nervous system, characterized by the presence of inflammatory lesions. OBJECTIVE: To analyze the biochemical profile of the demyelinating lesions of the initial forms of MS (remitting relapsing) by analyzing the proton magnetic resonance spectra (1H MRS) to characterize the process of demyelination and relate it to the metabolites and clinical variables analyzed. PATIENTS AND METHODS: We analyzed the largest demyelinating lesions in eight patients with remitting relapsing MS (RRMS) using the technique of single volume 1H MRS (VOI) with short echo time. The spectra of the white matter of two healthy control were used as reference. RESULTS: NAA/Cr and NAA/Cho value ratios decrease and mI/Cr one increase in all spectra lesions as compared to healthy controls. In four of the eight patients, the Cho/Cr was higher than in the controls. Qualitative and quantitative differences in the resonances of macromolecules were observed, related to the biochemistry of the process of demyelination. These differences in NAA/Cr, Cho/Cr, mI/Cr and macromolecules probably represent different stages in the evolution of the plaques. CONCLUSIONS: MRS is a non invasive technique able to observe biochemical variations related to the evolution process of demyelination. Activity of the lesion is shown by the increment of resonances around 0.9 1.3 ppm. An increase in mI seems to occur at an early stage of demyelination and later the NAA is reduced. The initial forms of MS show metabolic alterations in the plaques which are similar to the most advanced forms of MS.

Diferencias en la espectroscopía de las lesiones de esclerosis múltiple en su forma remitente-recurrente mediante resonancia magnética / Differences in the spectroscopy of the lesions of the remitting-relapsing form of multiple sclerosis shown by magnetic resonance

Introducción. La esclerosis múltiple (EM) es una enfermedad crónica desmielinizante del sistema nervioso central, caracterizada por la presencia de lesiones inflamatorias. Objetivo. Analizar el perfil bioquímico de las lesiones desmielinizantes en las formas iniciales de EM (remitente-recurrente) mediante el análisis de los espectros de resonancia magnética de protón (1H-ERM) para caracterizar el proceso de desmielinización y relacionarlo con los metabolitos y las variables clínicas analizados. Pacientes y métodos. Se analizaron las lesiones desmielinizantes de mayor tamaño en ocho enfermos con EM remitente-recurrente (EMRR) mediante la técnica de 1H-ERM de volumen único (VOI) a tiempo de eco corto. Como referencia se tomaron los espectros de sustancia blanca de dos controles sanos. Resultados. Los espectros de todas las lesiones mostraron un descenso en los cocientes NAA/Cr y NAA/Co y un aumento del mI/Cr respecto a los controles. En cuatro de los ocho pacientes la relación Co/Cr fue superior a la de los controles. Se observaron diferencias cualitativas y cuantitativas en las resonancias pertenecientes a macromoléculas, correlacionadas con la bioquímica del proceso de desmielinización. Estas diferencias en NAA/Cr, Co/Cr, mI/Cr y macromoléculas probablemente expresen diferentes estados evolutivos de las placas. Conclusiones. La ERM es una técnica incruenta capaz de observar variaciones bioquímicas relacionadas con la evolución del proceso de desmielinización. La actividad lesional se traduce en un aumento de las resonancias alrededor de 0,9-1,3 ppm. El aumento del mI parece producirse en un estado precoz de la desmielinización, para posteriormente disminuir el NAA. Las formas iniciales de EM presentan alteraciones metabólicas en sus placas similares a las formas más evolucionadas de la EM (AU)

[Axonal involvement in multiple sclerosis. Current concepts]. / Afectación axonal en la esclerosis múltiple. Conceptos actuales.

INTRODUCTION: Axon pathology in multiple sclerosis is an emerging concept, not because it is unknown but because it has been forgotten. However, clinical, functional and pathological aspects have clearly shown that it is damaged at a very early stage in development of the plaque of demyelination. There is sufficient clinical, radiological and pathological evidence to permit definition of axonal damage as the central element of the pathology and clinical features of multiple sclerosis. DEVELOPMENT AND CONCLUSIONS: Throughout this article we will see how the axon is affected in multiple sclerosis, how this affects the inflammatory response and which parameters allow us to measure axonal damage and its relation to disability. Finally we will see how a new physiopathogenic concept of multiple sclerosis appears, based on the axonal lesion, and how this fits current clinico-pathological concepts better.

Afectación axonal en la esclerosis múltiple. Conceptos actuales / Axonal involvement in multiple sclerosis. Current concepts

Introducción. La patología del axón en la esclerosis múltiple es un concepto emergente, no por desconocido sino por olvidado. Pero tanto a nivel clínico, como funcional y patológico, es un hecho plenamente demostrado que está dañado en fases muy precoces del proceso de desarrollo de la placa de desmielinización. Existen suficientes evidencias clínicas, radiológicas y patológicas que permiten definir el daño axonal como el elemento central en la patología y la clínica de la esclerosis múltiple. Desarrollo y conclusiones. A lo largo de la presente exposición veremos cómo se afecta el axón en la esclerosis múltiple, cómo determina la respuesta inflamatoria esta afectación axonal y cuáles son los parámetros que nos permiten medir el daño axonal y su relación con la discapacidad. Por último, veremos cómo se vislumbra una nueva concepción fisiopatogénica de la esclerosis múltiple basada en la lesión axonal y cómo ésta se adapta mejor a los conceptos clínico-patológicos actuales (AU)