Search

El Dolor en los relatos de la mujer: Fibromialgia (Dra Ingrid Brunke)

Loading...

Flash Player 9 (or above) is needed to view presentations.
We have detected that you do not have it on your computer. To install it, go here.

0 comments

Post a comment

    Post a comment
    Embed Video
    Edit your comment Cancel

    Notes on slide 1

    Se seguirá este esquema

    Heinroth in 1818 described “mixtures; Griesinger (1845) middle form. Mixed states was use by Jules Falret. In his monograph, Weygandt (1899) who worked with Kraepelin, distinguished three forms of mixed episode: manic stupor, agitated melancholia: depression with flight of ideas and agitation, and unproductive mania: elated mood, increased motor activity, and inhibition of thinking Kraepelin linked mania and depressive illness in 1899 in his book, which was translated to English in 1921. He distinguished between two general classes of mixed states: Transitional forms: a stage in between when depression changes to mania and vice versa. Autonomous form: a mixed disorder on its own: “the most unfavourable form of manic-depressive insanity” The course is longer, with a tendency to chronicity, as compared with other types of manic-depressive insanity. The modern definitions can be subdivided as follows: Broad definitions: the presence of a single depressive symptom within a manic episode is considered sufficient for diagnosis of a mixed episode (Swann et al., 1997) Narrow or strict definitions: Only the co-existence of the full or cardinal symptomatology of a manic and a depressive episode allows the diagnosis of a mixed episode. (DSM-IV)‏ Moderate definitions: the co-existence of the full syndromes of mania and melancholia is not necessary: prominent depressive symptoms within a manic or hypomanic state is sufficient. The Cincinnati, Pisa and Vienna criteria belong to this category. (Berber, McElroy, Bauer, Perugi)‏

    Heinroth in 1818 described “mixtures; Griesinger (1845) middle form. Mixed states was use by Jules Falret. In his monograph, Weygandt (1899) who worked with Kraepelin, distinguished three forms of mixed episode: manic stupor, agitated melancholia: depression with flight of ideas and agitation, and unproductive mania: elated mood, increased motor activity, and inhibition of thinking Kraepelin linked mania and depressive illness in 1899 in his book, which was translated to English in 1921. He distinguished between two general classes of mixed states: Transitional forms: a stage in between when depression changes to mania and vice versa. Autonomous form: a mixed disorder on its own: “the most unfavourable form of manic-depressive insanity” The course is longer, with a tendency to chronicity, as compared with other types of manic-depressive insanity. The modern definitions can be subdivided as follows: Broad definitions: the presence of a single depressive symptom within a manic episode is considered sufficient for diagnosis of a mixed episode (Swann et al., 1997) Narrow or strict definitions: Only the co-existence of the full or cardinal symptomatology of a manic and a depressive episode allows the diagnosis of a mixed episode. (DSM-IV)‏ Moderate definitions: the co-existence of the full syndromes of mania and melancholia is not necessary: prominent depressive symptoms within a manic or hypomanic state is sufficient. The Cincinnati, Pisa and Vienna criteria belong to this category. (Berber, McElroy, Bauer, Perugi)‏

    Heinroth in 1818 described “mixtures; Griesinger (1845) middle form. Mixed states was use by Jules Falret. In his monograph, Weygandt (1899) who worked with Kraepelin, distinguished three forms of mixed episode: manic stupor, agitated melancholia: depression with flight of ideas and agitation, and unproductive mania: elated mood, increased motor activity, and inhibition of thinking Kraepelin linked mania and depressive illness in 1899 in his book, which was translated to English in 1921. He distinguished between two general classes of mixed states: Transitional forms: a stage in between when depression changes to mania and vice versa. Autonomous form: a mixed disorder on its own: “the most unfavourable form of manic-depressive insanity” The course is longer, with a tendency to chronicity, as compared with other types of manic-depressive insanity. The modern definitions can be subdivided as follows: Broad definitions: the presence of a single depressive symptom within a manic episode is considered sufficient for diagnosis of a mixed episode (Swann et al., 1997) Narrow or strict definitions: Only the co-existence of the full or cardinal symptomatology of a manic and a depressive episode allows the diagnosis of a mixed episode. (DSM-IV)‏ Moderate definitions: the co-existence of the full syndromes of mania and melancholia is not necessary: prominent depressive symptoms within a manic or hypomanic state is sufficient. The Cincinnati, Pisa and Vienna criteria belong to this category. (Berber, McElroy, Bauer, Perugi)‏

    Heinroth in 1818 described “mixtures; Griesinger (1845) middle form. Mixed states was use by Jules Falret. In his monograph, Weygandt (1899) who worked with Kraepelin, distinguished three forms of mixed episode: manic stupor, agitated melancholia: depression with flight of ideas and agitation, and unproductive mania: elated mood, increased motor activity, and inhibition of thinking Kraepelin linked mania and depressive illness in 1899 in his book, which was translated to English in 1921. He distinguished between two general classes of mixed states: Transitional forms: a stage in between when depression changes to mania and vice versa. Autonomous form: a mixed disorder on its own: “the most unfavourable form of manic-depressive insanity” The course is longer, with a tendency to chronicity, as compared with other types of manic-depressive insanity. The modern definitions can be subdivided as follows: Broad definitions: the presence of a single depressive symptom within a manic episode is considered sufficient for diagnosis of a mixed episode (Swann et al., 1997) Narrow or strict definitions: Only the co-existence of the full or cardinal symptomatology of a manic and a depressive episode allows the diagnosis of a mixed episode. (DSM-IV)‏ Moderate definitions: the co-existence of the full syndromes of mania and melancholia is not necessary: prominent depressive symptoms within a manic or hypomanic state is sufficient. The Cincinnati, Pisa and Vienna criteria belong to this category. (Berber, McElroy, Bauer, Perugi)‏

    Heinroth in 1818 described “mixtures; Griesinger (1845) middle form. Mixed states was use by Jules Falret. In his monograph, Weygandt (1899) who worked with Kraepelin, distinguished three forms of mixed episode: manic stupor, agitated melancholia: depression with flight of ideas and agitation, and unproductive mania: elated mood, increased motor activity, and inhibition of thinking Kraepelin linked mania and depressive illness in 1899 in his book, which was translated to English in 1921. He distinguished between two general classes of mixed states: Transitional forms: a stage in between when depression changes to mania and vice versa. Autonomous form: a mixed disorder on its own: “the most unfavourable form of manic-depressive insanity” The course is longer, with a tendency to chronicity, as compared with other types of manic-depressive insanity. The modern definitions can be subdivided as follows: Broad definitions: the presence of a single depressive symptom within a manic episode is considered sufficient for diagnosis of a mixed episode (Swann et al., 1997) Narrow or strict definitions: Only the co-existence of the full or cardinal symptomatology of a manic and a depressive episode allows the diagnosis of a mixed episode. (DSM-IV)‏ Moderate definitions: the co-existence of the full syndromes of mania and melancholia is not necessary: prominent depressive symptoms within a manic or hypomanic state is sufficient. The Cincinnati, Pisa and Vienna criteria belong to this category. (Berber, McElroy, Bauer, Perugi)‏

    Heinroth in 1818 described “mixtures; Griesinger (1845) middle form. Mixed states was use by Jules Falret. In his monograph, Weygandt (1899) who worked with Kraepelin, distinguished three forms of mixed episode: manic stupor, agitated melancholia: depression with flight of ideas and agitation, and unproductive mania: elated mood, increased motor activity, and inhibition of thinking Kraepelin linked mania and depressive illness in 1899 in his book, which was translated to English in 1921. He distinguished between two general classes of mixed states: Transitional forms: a stage in between when depression changes to mania and vice versa. Autonomous form: a mixed disorder on its own: “the most unfavourable form of manic-depressive insanity” The course is longer, with a tendency to chronicity, as compared with other types of manic-depressive insanity. The modern definitions can be subdivided as follows: Broad definitions: the presence of a single depressive symptom within a manic episode is considered sufficient for diagnosis of a mixed episode (Swann et al., 1997) Narrow or strict definitions: Only the co-existence of the full or cardinal symptomatology of a manic and a depressive episode allows the diagnosis of a mixed episode. (DSM-IV)‏ Moderate definitions: the co-existence of the full syndromes of mania and melancholia is not necessary: prominent depressive symptoms within a manic or hypomanic state is sufficient. The Cincinnati, Pisa and Vienna criteria belong to this category. (Berber, McElroy, Bauer, Perugi)‏

    Se seguirá este esquema

    Se seguirá este esquema

    Se seguirá este esquema

    Referencias: 1. Taylor CP, Angelotti T, Fauman E. Pharmacology and mechanism of action of pregabalin: The calcium channel alpha 2 -delta subunit as a target for antiepileptic drug discovery. Epilepsy Res . 2007;73:137-150. 2. Field MJ, Cox PJ, Stott E et al. Identification of the alpha 2-delta subunit of voltage-dependant calcium channels as a molecular target for dolor mediating the analgesic actions of pregabalin. Proc Natl Acad Sci . 2006;46:17537-17542. 3. Fehrenbacher JC, Taylor CP, Vasko MR. Pregabalin and gabapentin reduce release of substance P and CGRP from rat spinal tissues only after inflammation or activation of protein kinase C. dolor . 2003;105:133-141. Aunque el mecanismo exacto de acción de la pregabalina es desconocido, los resultados de los modelos animales sugieren que la unión a la subunidad  2 -  puede estar asociada con el efecto de la pregabalina en el alivio sintomático del dolor por FM. 1,2 La pregabalina se une selectivamente a la subunidad  2 -  de los canales de calcio de las neuronas en el cerebro y en el sistema nervioso central 1 A medida que esta se une, la pregabalina reduce la liberación de varios neurotransmisores en las neuronas hiperexcitadas, incluyendo sustancia P, glutamato, y noradrenalina 1 Los estudios preclínicos sugieren que es a través de esta modulación de la hiperexcitabilidad neuronal que sus efectos analgésicos y anticonvulsivos se logran 1 La pregabalina no es un bloqueante del canal de calcio vascular; esta no afecta significativamente la presión arterial o la función cardiaca 1,2 La pregabalina no es activa en el receptor del ácido gamma-aminobutírico (GABA) 3 Los bloqueadores del canal de calcio se unen a una subunidad de los canales de calcio de tipo L y directamente bloquean al poro

    Terapias no farmacológicas que han mostrado ser efectivas en el manejo de la FM. 1 Las opciones terapéuticas no farmacológicas con un fuerte nivel de evidencia para su eficacia incluyen: educación del paciente, ejercicio aeróbico, y terapia conductual cognitiva (CBT) 1 Se ha demostrado que el ejercicio aeróbico moderadamente intenso mejora el dolor y los umbrales de dolor por presión en los puntos sensibles. 2 La progresión gradual del ejercicio debería ser aconsejada para evitar la exacerbación de los síntomas 3 Se ha demostrado que la educación intensiva del paciente con FM mejora el dolor, el sueño, la fatiga, y la calidad de vida en pacientes con FM 1 Referencias: 1. Goldenberg DL, Burckhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA . 2004;292:2388-2395. 2. Busch AJ, Schachter CL, Peloso PMJ, Bombardier C. Exercise for treating fibromyalgia syndrome. Cochrane Database Syst Rev . 2002;CD003786. 3. Burckhardt CS, Goldenberg D, Crofford L, et al. Guideline for the Management of Fibromyalgia Syndrome dolor in Adults and Children . APS Clinical Practice Guidelines Series, No.4. Glenview, IL: American dolor Society; 2005.

    1 Favorite

    El Dolor en los relatos de la mujer: Fibromialgia (Dra Ingrid Brunke) - Presentation Transcript

    1. El dolor en los relatos de la mujer: FIBROMIALGIA apsa Capítulo de Interconsulta y Psiquiatría de Enlace Dra Ingrid Brunke 2009
      • “… me duele todo…”
      • “… pero como me ven de pie, suponen que no tengo nada…”
      • “ ...y debo seguir adelante...
      • “ ...y como mis análisis y placas son normales, insisten en que no tengo nada..”
      • “ ...y debo seguir adelante...
      • “ ...y además me dicen que todo “está en mi cabeza”....
      • “ ...y debo seguir adelante...”
    6.  
    7. FIBROMIALGIA
      • Crónica, costosa en su tratamiento
      • Debilitante, puede llegar a ser invalidante
      • Prevalencia 2%
      • Población femenina
      • De largo derrotero en la consulta multidisciplinaria: clínicos, reumatólogos, traumatólogos, psiquiatras, etc
    8. Colegio Americano de reumatología – 1990 Criterios diagnósticos de Fibromialgia dispareunia Síntomas afectivos Trastornos del sueño Astenia cefalea parestesias 11 de 18 ptos dolorosos positivos Sindromes asociados
    9. FIBROMIALGIA
    10. PSICOPATOLOGIA
      • Sobreadaptadas
      • Comorbilidad con trastornos de personalidad (narcisista, obsesiva, histriónica,dependiente...)‏
      • Comorbilidad en eje I fundamentalmente con trastorno adaptativo, trastornos por ansiedad generalizada y distimia,
      • Hipótesis: depresión enmascarada. Situaciones de stress previo desencadenante.
    11. Evolución del concepto de fibromialgia
      • Giullaume de Baillou (1592): “reumatismo muscular”
      • Robert Burton (1621): Asociación entre dolor y fatiga, con depresión melancólica
      • R. Manningham (1750): Asociación entre astenia, dolor y febrícula en mujeres de clase media / alta
      • William Balfour (1824): Relación entre reumatismo y nódulos dolorosos “inflamatorios”
    12. Evolución del concepto de fibromialgia
      • Dupuy (1865): “neuromialgia”: dolor muscular, afebril, no articular, sin causa orgánica
      • George Miller Beard (1880): “Neurastenia” y “Mioastenia”
      • Sigmund Freud (1894): Neurastenia en sus estudios sobre las neurosis. “La neurastenia y la neurosis de angustia” (1895)‏
      • Sir William Richard Gowers (1904): Clase magistral y publicación en el British Medical Journal sobre una entidad a la que llama “Fibrositis”
    13. Evolución del concepto de fibromialgia
      • William Osler (1909): Reumatismo muscular Sostiene que: no significa con certeza que los tejidos musculares sean el lugar de la enfermedad
      • Sir Thomas Lewis y John H Kellgren (1936): “trigger points” o puntos gatillo
      • JL Halliday (1937): “Reumatismo psicosomático”
      • Edward Boland (1947): “Reumatismo psicógeno”
    14. Evolución del concepto de fibromialgia
      • Hugh A Smythe (1972): Sistematización de los puntos dolorosos. Separa dolor localizado de dolor generalizado (bases modernas...)‏
      • Kahler Hench (1976): FIBROMIALGIA
      • Harvey Moldofsky (1976): Estudios del sueño.‏ Relación del triptofano con intensidad del dolor
      • JAMA (1987): Credibilidad de su existencia
      • Robert Bennet (1989): Primer capítulo sobre FM en texto de reumatología
    15. ...y la historia continúa...
      • ‏ ...con los estudios de Bennet, Yunus, Jon Russel, Daniel Clauw y Lesly Arnold...
      • ...han podido demostrar que la FM sería una enfermedad neurológica, con alteraciones en la conducción de las vías de inhibición o excitación dolorosas‏... ( TODO ESTÁ EN TU CABEZA ....)‏
    16. ......fisiopatología.....
      • ... con deficit de la actividad serotoninérgica y noradrenérgica y aumento de los niveles de neurotransmisión excitatoria del glutamato y sustancia P...
      • ...y sería poligénica..se encontró polimorfismo para los genes receptores de los recptores 5HT 2A y DA D4, y para los transportadores de serotonina... (MAS FRECUENTE EN MUJERES)‏
    17. .....por ello....
      • Los tratamientos dirigidos al alivio de los síntomas
      • periféricos son menos efectivos que los que actúan a
      • nivel central. (por ejemplo: antiinflamatorios)‏
      • Serán efectivos los medicamentos que aumentan los
      • niveles de noradrenalina y serotonina y aquellos que
      • reduzcan los niveles de neurotransmisión excitatoria.
    18. Fibromialgia
      • Fuerte evidencia de mejoría con antidepresivos duales y
      • anticonvulsivantes.
      • Evidencia media con tramadol, ISRS, oxibato sódico,
      • agonistas DOPA.
      • Baja evidencia con opioides, corticoides, AINE,
      • benzodiazepinas e hipnóticos.
      • Arnold et al Arthritis Rheum 2004; 50: 944-952
    19. Duloxetina ‏
      • Inhibidor potente de la recaptación de serotonina y noradrenalina
      • Aumenta los niveles extracelulares de ambas en corteza prefrontal e hipotálamo
      • Tiene debil afinidad por el sitio involucrado en la recaptación de dopamina
      • Tiene una mayor afinidad por los sitios transportadores de serotonina y noradrenalina comparado con otros antidepresivos.
      • Wong et al. Prog Drug Res2002;58:169-222.
    20. La Pregabalina Se Une a la Subunidad  2 -  de los Canales de Ca 2+ Dependientes del Voltaje en el Sistema Nervioso Central Representación esquemática del mecanismo de acción propuesto para pregabalina Taylor. Epilepsy Res. 2007;73:137-150.
      • La pregabalina se une selectivamente a la subunidad  2 -  de los Canales de Ca 2+ dependientes del Voltaje
        • Modula el ingreso de calcio en la neuronas hiperexcitadas
        • Reduce la liberación de neurotransmisores excitatorios (glutamato, sustancia P, noradrenalina)‏
        • El efecto farmacológico requiere la unión a este sitio en los modelos animales
        • Actualmente se desconoce la significancia clínica de estas observaciones en humanos
      Neurotransmisores Postsináptica Canal de Ca 2+ Subunidad  2 -  Presináptica Pregabalina Presináptica Postsináptica Neurotransmisores Canal de Ca 2+ Subunidad  2 - 
    21. Terapias No Farmacológicas
      • Educación del Paciente
        • mejora el dolor, el sueño, la fatiga y la calidad de vida de los pacientes con FM
      • Ejercicio aeróbico
        • Incrementar el rendimiento aeróbico modifica el umbral de presión de dolor en los puntos sensibles, y de percepción dolorosas.
      • Psicoterapia conductual cognitiva ‏
        • Hay evidencia de mejoría en el dolor, la fatiga, el estado de ánimo y la función física
    SlideShare Zeitgeist 2009

    + capitulointerconsultacapitulointerconsulta Nominate

    custom

    809 views, 1 favs, 2 embeds more stats

    Trabajo presentado en el Congreso de Psiquiatría ( more

    More info about this document

    © All Rights Reserved

    Go to text version

    • Total Views 809
      • 743 on SlideShare
      • 66 from embeds
    • Comments 0
    • Favorites 1
    • Downloads 0
    Most viewed embeds
    • 41 views on http://capitulointerconsulta.blogspot.com
    • 25 views on http://vesta-salud.blogspot.com

    more

    All embeds
    • 41 views on http://capitulointerconsulta.blogspot.com
    • 25 views on http://vesta-salud.blogspot.com

    less

    Flagged as inappropriate Flag as inappropriate
    Flag as inappropriate

    Select your reason for flagging this presentation as inappropriate. If needed, use the feedback form to let us know more details.

    Cancel
    File a copyright complaint
    Having problems? Go to our helpdesk?

    Categories

    Tags

    -->
    Search
    RSS Feed
    What's new?

    © 2009 SlideShare Inc. All Rights Reserved