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Guillermo Enríquez CoronelEnc.Clinica de M.A, IMSS PUE Delegado por Mexico, MDS
DIAGNOSTICO Y TRATAMIENTO ENFERMEDAD DE PARKINSON
www.drguillermoenriquezcoronel.org
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Enfermedad de Parkinson
La E.P es un sindrome heterogéneo caracterizado por varios síntomas motores y No motores.
Rasgos cardinales, son, rigidez, bradicinesia, temblor de reposo , alteración de la marcha y inestabilidad postural
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Enfermedad de Parkinson
Rasgos No motores son: daño en la olfacción , autonómica , sueño, estado de animo, cognitivo.
Degeneración de neuronas del mesencéfalo pars compacta, locus coeruleus , colinérgicas , núcleo basal de Meynert, núcleo motor dorsal del vago, de medula espinal y sistema nervioso autonómico periférico
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Barcelona ,España
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Preguntas?
¿ Como hacer el Dx. de Parkinson?
¿Qué no es Parkinson?
¿ Con que fármaco inicio el tratamiento E. P.
¿Funciona la Neuroproteccion?
¿ Saber reconocer y tratar las fluctuaciones y las disquinesias en Parkinson???????
Cuando solicitar la cirugía de E.P. y cual método es el adecuado: ablación vs DBS
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Parkinson’s Disease PathologyLewy bodies
-synuclein Ubiquitin
Tofaris & Spillantini. Mov Disord 2005;20 Suppl 12:S37-44.
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ETIOLOGIA
Factores Genéticos
Factores del medio ambiente
Patogénesis
Stress Oxidativo
Disfunción Mitocondrial
Excito-toxicidad
Inflamación
FORMACION DE CUERPOS DE LEWY
DISFUNCION NEURONAL
APOPTOSIS
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ANTIOXIDANTES ( VIT E ,C , QUELANTES DE HIERRO
INHIBIDORES DE MONOAMINO OXIDASA TIPO B, RASAGILINA, SELEGILINE
AGENTES BIOENERGETICOS COENZIMA Q 10
AGENTES ANTIGLUTAMATERGICOS N METIL D ASPARTATO NMDA ANTAGONISTAS
BLOQUEADORES DE CANALES DE CALCIO
AGENTES ANTI-INFLAMATORIOS COX 2,INHIBIDORES DE CASPASAS, PROPARGILAMINAS
ENLACES A PROTEOSOMALES, FACTORES TROFICOS, AGONISTAS DOPA ,
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Diagnostico temprano EPI
Con base al Banco de Cerebros de UK, el Dx de la EP es incorrecto , con una sensibilidad de 93 %, una especificidad de 46 %, comparado al Dx final en 3 años
El SPECT era 78 % sensible pero mas especifico 97 %
Mov. Disord Dic 31 , 2008
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Diagnostico temprano EPI
Aproximadamente 5-10 % de paciente con EP son mal diagnosticados con otra enfermedad.
20 % de paciente diagnósticos como EP tienen diagnósticos alternativos.
JNNP 2000; 68, 434-440
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NEUROLOGY 2009;72 (Suppl 4):S1–S136
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Heiko Braak
Propone que la EPI inicia no en el SNC sustancia nigra sino en el tallo cerebral y bulbo olfatorio
Estadio 1 : se comprometen areas no motoras bulbo olfatorio, y complejo nuclear motor del lX y X par, plexo mienterico.
Estadio 2: extensión al puente , locus coeruleus, núcleos del rafe, y parte magnocellar de la formación reticular
NEUROLOGY 2009;72 (Suppl 4):S1–S136
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Parkinson
Trast.-Movimiento
Demencia
Trast.- Autonomico
Dolor
Parestesias
PsicosisAislamiento social
Trastornos-sueño
Depresion
Ansiedad
Apatía
Alucinaciones
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Atrofia sistémica múltiple
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PSP
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Parkinson
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Anthony E. Lang, MD NEUROLOGY 2009;72(Suppl 2):S39–S43
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Anthony E. Lang, MD
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Curr Opin Neurol 20:477–483. 2007 Lippincott Williams & Wilkins.a
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Síntomas motores en la EPTratamiento sintomático
Inhibidores de la monoaminooxidasa (MAO) B
• Selegilina, rasagilina
Fármacos no dopaminérgicos• Anticolinérgicos: benzhexol,trihexifenidilo
• Antagonista del glutamato:amantadina
Levodopa
• Inhibidores de la descarboxilasa: benseracida, carbidopa
• Inhibidores de la catecol-O-metiltransferasa (COMT): entacapona, tolcapona
Agonistas de la dopamina
• No derivados del ergot: pramipexol, ropinirol, rotigotina,apomorfina
• Derivados del ergot: bromocriptina, cabergolina, lisurida, pergolida
Nirenberg MJ, Fahn S. En: Principles of Treatment in Parkinson’s Disease; 2005.
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AGONISTAS DOPAMINERGICOS
CALM-PD
REAL PET ( ropirinol, levodopa)
ELLDOPA
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ARCH NEUROL/VOL 56, MAY 1999
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CALM-PD 4-YEAR IMAGING STUDY
Kenneth L. Marek, MD
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Conclusiones
Patients initially treated with pramipexole demonstrated a reduction in the percentage loss from baseline of striatal [123I] -CIT uptake, a marker of dopamine neuron degeneration, of approximately 40% compared with those initially treated with levodopa during a 46-month evaluation period
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DATATOP
No fue posible determinar si, el retraso del tiempo a utilizar dopaminergicos en el grupo con Selegiline , era el resultado de una situación sintomática o por efecto neuroprotector
Ann. Neurología 1996, 39, 29- 36
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DATATOP
En el grupo de extensión , mostro que el grupo tratado con selegiline, alcanzo la incapacidad mas pronto que el grupo no tratado con selegiline, sugiriendo que cualquier ventaja de selegiline NO ERA SOSTENIDA
Ann. Neurology 1996, 39, 29- 36
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SINDEPAR
Sinemet –deprenil- parlodel
Selegiline y levodopa
Placebo y levodopa
Selegiline y bromocriptina
Placebo y bromocriptina
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SINDEPAR
UPDRS era peor en pacientes con placebo que en esos con selegiline
Concluye con un efecto Neuroprotector de selegiline
Ann Neurol 1995 ,38, 1-7
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8080
Subtipos de receptores dopaminérgicos
Receptores similares a D1 Receptores similares a D2
D1 D2
D5 D3
D4
Missale C, et al. Physiol Rev 1998;78:189-225. Poewe W. En: Principles of Treatment in Parkinson’s Disease; 2005.
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Agonistas Dopaminergicos
Derivados del Ergot
Bromocriptina
Cabergolina
Dihidroergocriptina
Lisurida
Pergolide
No derivados del Ergot
Apomorfina
Piribedil
Pramipexol
Ropirinol
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Dr. Kulisewsky
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Dr. Linazasoro
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Movement Disorders, Vol. 20, No. 5, 2005
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Apomorfina
Potente D1,D2
Via sublingual intranasal, rectal, subcutanea e IV
Se da frecuentemente por vía subcutánea en paciente con fluctuaciones en Europa.
Mejoría del off
99
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Piribedil
No ergot agonista mixto D2 y D3
Vida larga de 20 hrs
Util en algunos países
100
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101
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Movement Disorders, Vol. 20, No. 5, 2005
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103
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104
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105105
Agonistas de la dopamina como terapia adyuvante de la levodopa
Permiten usar dosis reducidas de levodopa
Mejoran las fluctuaciones motoras
Prolongan el periodo “on”
Mejoran la función “on”
El pramipexol mejora los síntomas depresivos
Weintraub D, et al. Am J Manag Care 2008;14(2 Suppl):S49-58. Lemke MR. Eur J Neurol 2008;15 Suppl 2:9-14. Barone P, et al. Mov Disorder 2009;24 Suppl 1:S347, Mo-248.
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107
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108
Pramipexol de liberación prolongada en la EP avanzadaConclusión sobre la eficacia
• Se demostró la superioridad del pramipexol LP vs. el placebo en la Semana 18 tanto para el punto final primario (UPDRS II+III) como para el punto final secundario clave (periodo “off”)
• Se demostró el mantenimiento de la eficacia después de 33 semanas de tratamiento
• La eficacia del pramipexol LP fue comparable con la del pramipexol LI, al usar una dosis media diaria y una distribución de dosis similares, y con una duración de tratamiento comparable
108
Schapira AHW, et al. Movement Disorder Society 13th International Congress, Paris, France, June 7-11, 2009, Poster We-199.
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123
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124
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Fenómeno Wearing-off
Es un incremento en el acortamiento del periodo de beneficio, seguido en cada dosis de Levodopa y es el mas común tipo de fluctuaciones motoras vistas en la Enfermedad de Parkinson.
Síntomas sensoriales, Psiquiátricos, autonómicos y fluctuaciones motoras.
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Wearing-off, Tratamiento
Mas frecuentes dosis de Levodopa
Utilizar un inhibidor de COMT
Utilizar un Agonista dopaminergico
Utilizar Levodopa de Liberacion controlada
Diagnosis and Management of Parkinson,s Disease
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Agentes No dopaminergicos para síntomas No motores
Urgencias urinaria: oxibutina, tolterodina,
Impotencia: sildenafil
Gastrointestinal, constipacion:fibra
Nausea: domperidona
Sialorrea: propantelina, toxina botulinica
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PARKINSON
Tratamiento Quirurgico
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Tratamiento Quirurgico en la Enfermedad de Pakinson
Talamotomia
Palidotomia
Estimulación cerebral profunda
Trasplante de células productoras de dopamina.
Gama-Knife
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Lesiones Ablativas
Talamotomia
Palidotomia
subtalamotomia
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Estimulación cerebral profunda
VIM del tálamo
Globo pálido interno
Núcleo subtalamico
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Cirugía de Parkinson
Unilateral
Bilateral
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Talamotomia, ventajas
Beneficio anti-temblor
Posible efecto anti-disquinesia
No requiere seguimiento
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Talamotomia: desventajas
No mejora rigidez ni bradicinesia , marcha o postura
Posible daño a estructuras cercanas
Procedimiento bilateral es asociado a riesgo de disartria , disfagia y daño cognitivo.
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Palidotomia: ventajas
Mejora la disquinesia contrlateral
Modesta mejoría de los rasgos Parkinsonianos
No requiere seguimiento
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Palidotomia : desventajas
Riesgo de lesión de estructuras cercanas
Procedimiento bilateral es asociado a riesgo de disfagia , disartria y daño cognitivo
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Subtalamotomia : ventajas
Mejora rasgos Parkinsonianos
Reduce la disquinesia
No requiere seguimiento
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Subtalamotomia: Desventajas
Riesgo de daño a estructuras vecinas
Procedimiento bilateral , con riesgo de disartria , disfagia y daño cognitivo.
Riesgo de Hemibalismo
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DBS: ventajas
No requiere realizar lesiones destructivas
Puede ser realizada de manera bilateral con seguridad en comparación a lesiones ablativas .
Puede regularse a máximo beneficio y mínima adversidad
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DBS:desventajas
MUY CARA
Ajustes de estimulación
Puede haber complicaciones : disartria y disfunción de movimientos oculares , problemas mecánicos del estimulador , e infección.
Necesidad periódica de reemplazo de pila
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Selección del paciente para cirugía Diagnostico de Parkinson
Edad
Duración de la enfermedad
Severidad de la enfermedad
Respuesta a levo-dopa
Daño cognitivo
Enfermedad Psiquiátrica
Habilidad del cirujano
Costo
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Arch Neurol. 2011;68(2):165-171. Published onlineOctober 11, 2010. doi:10.1001/archneurol.2010.260
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Trasplantes de Células de medula adrenal autólogas
• Iniciado por Neurocirujanos suecos en 1982
• Los reportes iniciales eran promisorios
• Los estudios posteriores no demostraron mejoría en escala motora UPDRS
• Pobre sobrevida del injerto
•Alta morbilidad y mortalidad cercana al 10%
•Técnica abandonada en el presente
Walter, Vitek, Lancet neurol 2004; 3: 719-28
Ahlskog Neurology 2007; 69:1701-1711
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Trasplante de Células Fetales de Mesencéfalo.
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Trasplante de Células Epiteliales Pigmentadas de Retina (Esferamina)
• Células localizadas en la lamina interna neural de la retina que producen dopamina
• Implantadas por estereotaxia en el estriado
• Mejoría en ratones, primates no humanos y humanos
• Estudio piloto de 6 pacientes mostraron 48% de mejoría en motor-UPDRS después de los 6 y 12 meses de la implantación
• Están en progresos ensayos controlados aleatorizados en norte América
Watts et al neurology 2002(suppl 7);58:A241
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Trasplantes de Células madres Embrionicas
• La tecnología de células madre es capaz de generar poblaciones puras de neuronas dopaminérgicas nigrales
• Se han Reportado algunos casos con éxito sin embargo aún hay muchas interrogantes:
Es posible generar grandes cantidades de células que se diferencien a neuronas nigrales?
Que posibilidad hay de que las células trasplantadas originen neoplasias del SNC?
Cual es la respuesta inmune al trasplante?
Nader Sin N Engl J Med 2005;353:811-22Schwarz J Neurol 2002William Langston. J Clin Invest.2005;115:23 25Ahlskog Neurology 2007; 69:1701-1711
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Terapia Génica con el gen del GNDF
• En modelos primates de parkinsonismo con MPTP
• Mediante un vector lentiviral se inyecto el gen de GNDF
•Se logró incremento en la producción de factor neurotrófico derivado de células glíales en el estriado y sustancia negra
•Se asocio a mejoría en los síntomas parkinsónicos
• El estudio histológico demostró colaterilización de las células dopaminérgicas nigroestriatales
Kordower JH et al. Science2000;290:767-73.
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Neurology® 2008;70:1996–2003
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186
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190
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Puebla 2010
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Puebla 2011
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SEXTO CURSO DE PARKINSON EN PUEBLA , MARZO 2012
Dr. Alberto Spay
ESTAN INVITADOS A PUEBLA
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