domingo, 27 de febrero de 2011

Los niños están en desventaja en la escuela, frente a las niñas, y mucho más si tienes TDAH

Leon Trahtemberg


La escuela está diseñada para las niñas

Como padre de Niño con TDAH, cuantas veces he pensado que la escuela está diseñada para las niñas, pues infinitas. Cuantas veces he pensado que pensar así es políticamente incorrecto, pues infinitas. Cuantas veces he pensado que si dijera esto en público practicamente podrían sancionarme por agresión verbal, con penas grandes, pues infinitas. Cuantas veces he pensado que debería de llevar al niño con TDAH a un colegio especializado en TDAH, pues infinitas, pero siempre me he encontrado con que no hay colegios solo para niños, ni hay colegios especializados en TDAH. Asi que a seguir sufriendo y recibiendo castigos humillatorios tanto el niño como el padre.
Pongamos un ejemplo de mi hijo con TDAH, a quien su enfermedad le impide enfocarse en una tarea. Como ya dijimos, es un ferrari, con frenos de bicibleta, y piensa en el futbol, futbol, ganar, correr, amigos... y luego está la niña perfecta, con su muñequita rosa, y un juguetito rosa que le han regalado. Mi hijo con TDAH, cuando sale de clase, solo piensa en el futbol, y su balón nuevo, por lo que sale corriendo hacia el campo, y no ve a nadie en medio. La niña perfecta con su muñequita rosa, también sale de clase, muy tranquilita, pensando en su regalito, y también sin pensar en nadie mas. En esto, se cruzan en el pasillo, y mi hijo no pensaba en el camino, solo en el balón, y la niña solo pensaba en su meñequita rosa, pero ya que ninguno ha pensado, se chocan los dos por el punto común que es el pasillo. ¿Qué pasa? pues que el balón sale por los aires, y que la muñequita rosa sale por los aires. Es decir, ninguno de los niños ha pensado, ambos juguetes importantes para los niños sale por los aires. Pero ¿Cual es el resultado normal de la escuela actual? ESPULSAR DOS DÍAS AL NIÑO CON TDAH A SU CASA, POR PEGAR A LA NIÑA, NOTA AL PADRE SIENDO CONVOCADO A UNA REUNIÓN URGENTE EN EL COLEGIO, Y HUMILLACIÓN AL PADRE POR PARTE DEL DIRECTOR DEL COLEGIO, DICIENDO QUE LA PROXIMA VEZ QUE OCURRA ESO, EL NIÑO SERÁ EXPULSADO.
Solo recordar que la Asociación de TDAH de Las Palmas de G.C. ha pedido al Gobierno de Canarias que nombre un intermediario entre colegio y padres con niños con TDAH, para poder negociar con el intermediario, ya que negociar con el resto, siempre saldremos perdiendo. Lógicamente el Gobierno Canario se ha hecho el loco.
En fin, esta es la noticia de Perú, que me ha hecho ilusión leer, ya que veo que aunque haya mucha distancia, hay alguien más que piensa como yo.
LIMA En un fascinante video de TED, Ali Carr-Chellman demuestra cómo es que los niños que van a la escuela están en clara desventaja frente a las niñas, lo que les genera mucha frustración e impacta negativamente a lo largo de su vida escolar y universitaria. A pesar de que en estos tiempos aún las mujeres ganan menos que los hombres en empleos similares y tienen más dificultades escolares en ciencias y matemáticas que sus pares varones, en los hechos en la escuela estadounidense los niños de 3 a 13 años tienen todas las desventajas frente a las niñas (aunque la analogía con cualquier otro país como el Perú también parece válida).

Muestra las estadísticas del "Proyecto 100 Niñas". Por cada 100 niñas que dejan la escuela, hay 250 niños. Por cada 100 niñas expulsadas de la escuela, hay 335 niños. Por cada 100 niñas que reciben educación especial, hay 217 niños en similar situación. Por cada 100 niñas con problemas de aprendizaje, hay 276 niños con esas dificultades. Por cada 100 niñas con diagnóstico de trastorno emocional, hay 324 niños. Los niños tienen cuatro veces más diagnósticos de Trastornos por Déficit de Atención con Hiperactividad (TDAH) que las niñas. Estas cifras crecen en las poblaciones pobres.

Los programas que estimulan a las mujeres a mejorar en matemáticas y ciencias han dado buenos resultados y están cerrando las brechas; sin embargo, no hay programas que hagan algo para cerrar las brechas de desventaja de los varones.

El mensaje de Ali Carr es que hay que cambiar la cultura escolar para que acepte mejor a los niños. Por ejemplo, diseñar mejores juegos, incluyendo los videojuegos, incorporar más docentes hombres en inicial y primaria, revisar las políticas de tolerancia cero frente a juguetes que se consideran agresivos (lanzas, cuchillos, soldaditos de plástico), descomprimir los contenidos curriculares para dar más confort y más tiempo de maduración a los varones, etc. En suma, los niños que van a la escuela deben sentirse inteligentes, hábiles, capaces de tener logros; de lo contrario, registrarán huellas negativas en su autoestima que los dejarán marcados para toda su vida.

lunes, 21 de febrero de 2011

Una vez que sabemos que el TDAH está en ADN, pues es fácil ir averiguandolo desde el nacimiento

 A baby's health in the first minutes after birth may be linked to his or her risk of developing attention-deficit hyperactivity disorder (ADHD) later on, a new study suggests.

The findings, reported in the Journal of Pediatrics, suggest that the so-called Apgar score assigned to all newborns in the first five minutes of life may give some hint of a child's future risk of ADHD, a condition that involves attention problems and impulsive behavior.

A newborn's Apgar score is based on several physical signs, including breathing, heart rate and muscle tone. A score of 7 or higher is considered normal, with a 9 or 10 indicating that the baby is in the "best possible condition."

In the new study, researchers found that among more than 980,000 Danish children, the risk of developing ADHD climbed as Apgar scores dropped.

Compared with children whose scores had been a 9 or 10, those with a 5 or 6 had a 63 percent higher risk of ADHD. And those with an Apgar of 1 to 4 had a 75 percent greater risk.

In the U.S., surveys have found that nearly one in 10 school-aged kids have been diagnosed with the condition, according to the Centers for Disease Control and Prevention.

Exactly what the new findings mean is unclear. An abnormal Apgar score could reflect some sort of stress during pregnancy or birth -- like decreased oxygen supply -- that might contribute to ADHD development down the road, the researchers speculate.

"There may be a sharing of causes of low Apgar score and ADHD, but our analyses do not point (to) any specific factor here," Dr. Carsten Obel, one of the researchers on the work, told Reuters Health in an email.

A number of studies have linked preterm birth to an increased risk of ADHD, although the reasons aren't clear, noted Obel, of Aarhus University in Denmark.

Both preterm birth and a low Apgar score may be markers of less-than-optimal fetal development, he explained.

The findings are based on Danish national registry data for 980,902 children born between 1988 and 2001. Of those children, 8,234 were diagnosed with ADHD -- most of them boys.

Even after the researchers accounted for factors like preterm birth, family income and mothers' smoking and education levels, the risk of ADHD was higher among kids with Apgar scores below 7.

Still, the vast majority of children in the study were not diagnosed with ADHD, regardless of Apgar score. And it's not clear whether the Apgar-ADHD link might eventually have any practical implications.

In this study group, Obel said, the ability of a child's score to predict ADHD was not that strong.

"We do not find that the predictive value is so good that we routinely should inform parents who (have) a child with a low Apgar score about the higher risk of ADHD," Obel said.

Future studies, he said, could try to undercover the reasons for the link between Apgar score and ADHD. Large population studies might also be able to look at how combinations of factors -- like low Apgar score plus a family history of ADHD -- come into play.

SOURCE: bit.ly/el6Hjs Journal of Pediatrics, online January 18, 2011.

miércoles, 16 de febrero de 2011

Analizando el movimiento espejo, se puede saber la severidad del TDAH

Abnormal Hand Control May be Hint of ADHD Severity

Measurements of hand movement control may help determine the severity of attention deficit hyperactivity disorder (ADHD) in children, according to joint studies published in the February 15, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology. ADHD is a brain disorder characterized by impulsiveness, hyperactivity, such as not being able to sit still, and inattention or difficulty staying focused.

The studies were led by Stewart H. Mostofsky, MD, with the Kennedy Krieger Institute in Baltimore and Donald L. Gilbert, MD, MS, with Cincinnati Children's Hospital Medical Center in Cincinnati.

For the first study, researchers examined mirror overflow movements in 25 boys and girls between the ages of eight and 13 with ADHD and 25 boys and girls without the disorder. Mirror movements are characterized by the inability to move one side of the body without moving the other. All children were right-handed. Using video and a device that recorded finger position, the researchers measured differences in how the children tapped their fingers.

The children with ADHD experienced more mirror movements than the children without ADHD. During left-handed finger tapping, children with ADHD showed more than twice as much mirror overflow than children without ADHD. The differences were particularly prominent for boys with ADHD, who showed nearly four times as much mirror overflow than boys without ADHD on one of the two measures used in the study.

In the second study, scientists applied transcranial magnetic stimulation (TMS) to the motor control area of the brain in 49 children with ADHD and 49 children without ADHD, all right-handed and ages 8 to 12. TMS technology allows scientists to activate brain cells with magnetic pulses in order to measure brain activity.

The study found that the brain's short-interval cortical inhibition (SICI), which is an important "braking mechanism" in the brain, was reduced by 40 percent in children with ADHD compared to those without the disorder. On motor development tests, those with ADHD scored nearly 60 percent worse compared to those children without ADHD. Importantly, the scientists also found that the amount of reduced inhibition in the motor area of the brain was strongly associated with the severity of ADHD symptoms reported by the parents.

"These studies are an important step toward understanding how ADHD affects communication between the brain and other parts of the body," said Jonathan W. Mink, MD, PhD, with the University of Rochester Medical Center in New York in an accompanying editorial. Mink is also an associate editor of Neurology. "These findings show that mirror movements are likely a marker of abnormal development of motor control that improves with age and is more prominent in boys. They also provide a more specific way to measure ADHD. The hope is that, ultimately, these studies and others will guide us toward development and testing of new therapies."

The studies were supported by the National Institutes of Health.

The American Academy of Neurology, an association of more than 22,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as epilepsy, dystonia, migraine, Huntington's disease, and dementia.

For more information about the American Academy of Neurology, visit http://www.aan.com

martes, 15 de febrero de 2011

Se sigue avanzando en el conocimiento del TDAH

Implicación del transportador vesicular de monoaminas en el TDAH

IMPLICACIÓN DEL TRANSPORTADOR VESICULAR DE MONOAMINAS EN EL TDAH
G. Lorenzo Sanz. Unidad de Neurodesarrollo. Neurología infantil. Servicio de Pediatría. Hospital Universitario Ramón y Cajal. IRYCIS. Universidad de Alcalá. Madrid

INTRODUCCIÓN
El trastorno por déficit de atención con hiperactividad (TDAH) es el desorden más prevalente del neurodesarrollo en la infancia (alrededor del 5% de la población mundial). Las manifestaciones se inician en la infancia, y el 40-60% de estos niños tendrán síntomas también en la edad adulta. Aunque no se ha demostrado un marcador biológico, existen numerosas evidencias genéticas y de neuroimagen que apoyan la presencia de una alteración neurobiológica en este trastorno.
Los estudios iniciales en familiares y en gemelos monocigóticos demostraron la alta heredabilidad de este trastorno (alrededor del 76%).
Los primeros estudios moleculares pusieron de manifiesto la implicación del gen del receptor D4 de dopamina (DRD4) y del transportador de la dopamina (DA) situado en la membrana plasmática de la terminación presináptica (DAT1), en la génesis del TDAH, sustentando el fuerte papel que la DA tiene en la biopatología del trastorno. Pero la falta de respuesta al tratamiento con fármacos dopaminérgicos en el 30% de los pacientes, así como la respuesta parcial en un grupo significativo de respondedores, hizo pensar que otras moléculas debían estar implicadas en la neurobiología del TDAH.
Recientes trabajos de revisión y estudios meta-analíticos concluyen que los neurotransmisores y moduladores de la neuroplasticidad más implicados en el TDAH pueden ser, además del DRD4 y del DAT1, el receptor D5 de dopamina (DRD5), la dopamina beta-hidroxilasa (DBH), el transportador de serotonina (5-HTT), el receptor 1B de serotonina (HTRB1B) y la proteína sinaptosomal 25 (SNAP25), situada en la terminación neuronal presináptica y que es necesaria para la regulación y liberación del neurotransmisor.
Se han demostrado mediante resonancia magnética cuantitativa alteraciones anatómicas, tanto en niños como en adolescentes con TDAH, evidenciándose una disminución del volumen cerebral total, o una reducción en el volumen del hemisferio cerebral derecho, núcleo caudado, hemisferios cerebelosos y lóbulo postero-inferior de vermix cerebeloso.


CARACTERÍSTICAS DEL TRANSPORTADOR VESICULAR DE MONOAMINAS Y  SU PAPEL EN LA NEUROTRANSMISIÓN
Los  transportadores vesiculares de monoaminas (VMATs) son proteínas localizadas en las vesículas sinápticas, cuya función es la introducción de las aminas biógenas desde el citoplasma celular al interior de dichas vesículas, para posteriormente poder ser liberadas. Desde el punto de vista molecular se han clonado y secuenciado los cDNAs que codifican para el VMAT, identificándose dos isoformas, el tipo1 (VMAT1) y el tipo 2 (VMAT2).
El VMAT2 se expresa principalmente en neuronas monoaminérgicas del SNC de humanos y roedores y en neuronas postgangliónicas del sistema simpático. También se ha descrito su presencia en al menos dos poblaciones de células endocrinas. Sin embargo, el VMAT-1 se encuentra de forma predominante en células neuroendocrinas, como las células cromafines de la médula adrenal y las células enterocromafines del tracto intestinal.
La dihidrotetrabenazina (DHTBZ) es un potente inhibidor del VMAT-2 que se une con alta afinidad a este transportador. La DHTBZ marcada radiactivamente se ha utilizado como ligando para cuantificar VMAT-2 en cerebro humano, en cerebro de vaca y de ratón.
Se ha descrito que el transporte de la serotonina en plaquetas es similar al de las células cerebrales, por lo que el transporte en plaquetas se utiliza como un modelo periférico del transporte de la serotonina en el cerebro. Por otra parte se ha confirmado la existencia de un mRNA del VMAT cerebral en plaquetas humanas y la codificación de las secuencias de los cDNAs, cerebral y plaquetario son idénticas. Además, hay estudios bioquímicos que han caracterizado el transportador VMAT2 en plaquetas humanas. Todos estos trabajos apoyan la cuantificación del VMAT2 plaquetario como un modelo periférico de la actividad del VMAT2 cerebral y se utiliza para estudiar las enfermedades neuropsiquiatricas relacionadas con el metabolismo de las bioaminas.

IMPLICACIÓN DEL VMAT2 EN LA NEUROPROTECCIÓN
Como ya se ha comentado el VMAT2 en el SNC, es el encargado de secuestrar la DA citosólica y llevarla al interior de las vesículas sinápticas. Además, se le ha atribuido un papel neuroprotector. Una proporción de la DA que se recapta hacia el interior de la célula presináptica tras un estímulo nervioso se degrada enzimáticamente a través de la MAO.  La desaminación oxidativa de las monoaminas en el citosol, rinde peróxido de hidrógeno que es tóxico.
Existen diversas evidencias experimentales que apoyan esta teoría neuroprotectora del VMAT2 así como numerosos trabajos describen el efecto neuroprotector que producen diferentes agentes farmacológicos aumentando la actividad del VMAT2.
Todos estos resultados sugieren que el papel del VMAT-2 es de capital importancia en los trastornos en los que la DA está involucrada. La reducción de la actividad del VMAT2 puede disminuir la eficacia en la recaptación vesicular y la liberación de DA, lo que provocaría una alteración de la neurotransmisión dopaminérgica y contribuiría a la neurodegeneración celular por aumento de la DA citosólica. Por otro lado, si se pudiese regular la actividad del VMAT2, y así controlar la concentración de DA en las vesículas,  podríamos actuar sobre la neurotransmisión y la neuroprotección.
Por ello, considerando el papel que juegan la dopamina y otras monoaminas (noradrenalina, serotonina) en el TDAH, y que el metilfenidato, un tratamiento habitual de estos pacientes, puede modificar la actividad del VMAT2, sería lógico pensar que este transportador esté involucrado en la patogenia del TDAH.

EL VMAT2 EN EL TDAH Y EN OTROS TRASTORNOS NEUROPSIQUIÁTRICOS
El grupo de Rehavi,  basándose en la alta afinidad de la dihidro-tetrabenacina por el VMAT2, y determinando la cantidad de dicho transportador en plaquetas, ha llevado a cabo diferentes estudios para investigar de forma cuantitativa la neurotransmisión dopaminérgica en el TDAH y en otros trastornos neuropsiquiátricos. Estos autores describieron que pacientes con depresión mayor tenían un incremento de densidad de VMAT2 en plaquetas, sugiriendo que este hallazgo podría ser un reflejo del menor turnover de monoaminas.
Posteriormente documentaron que niños y adolescentes diagnosticados de TDAH tenían menor densidad de VMAT2 en plaquetas (Figura 1). No obstante los autores no determinaron que esta reducción de VMAT2 tuviese un significado etiológico, ya que también podría ser un epifenómeno, como resultado del tratamiento con fármacos monoaminérgicos que los pacientes habían recibido hasta dos meses antes de realizar el estudio.

COmparativa de densidad de VMAT2 en sujetos con TDAH y controles sanos
Fig. 1.- Densidad de VMAT2 en sujetos con TDAH y controles (760±140 vs. 913±202 fmol/ mg proteína, t=2.13, df=23, P<0.05)



Este mismo equipo de investigadores ha documentado una menor concentración de VMAT2 plaquetario en una serie de niños y adolescentes varones con síndrome de Tourette respecto a un grupo control. Suponiendo que estos resultados sean superponibles a lo que está ocurriendo a nivel cerebral, los autores sugieren que esta disminución de VMAT2 podría servir como un mecanismo neuroprotector para prevenir la sobreactividad dopaminérgica y disminuir la actividad motora.
Nuestro objetivo será medir la cantidad de VMAT2 plaquetario en una muestra de niños diagnosticados de TDAH, que no hayan recibido nunca tratamiento con fármacos monoaminérgicos, y ver si existen diferencias respecto a una muestra control. De existir diferencias, pensamos que este dato podría tener interés tanto para el diagnóstico como para el seguimiento de los pacientes que reciban tratamiento farmacológico específico, ya que podría darnos una información cuantitativa de la actividad dopaminérgica en los pacientes con TDAH.
Considerando la elevada heterogeneidad de este trastorno también es posible que no existan diferencias en el conjunto de todos los pacientes, pero si entre determinados endofenotipos de TDAH.
Por otro lado, la determinación de la cantidad de VMAT2 en plaquetas, de este mismo grupo de pacientes después de recibir tratamiento farmacológico específico, podría informarnos de si se ha producido alguna modificación en la actividad dopaminérgica o de si existen diferencias entre los pacientes con buena o mala respuesta al tratamiento farmacológico.

BIBLIOGRAFIA

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Diego A. Forero, MD; Gonzalo H. Arboleda, MD, PhD; Rafael Vasquez, MD;
Humberto Arboleda, MD, MSc. Candidate genes involved in neural plasticity and the risk for attention-deficit hyperactivity disorder: a meta-analysis of 8 common variants.J Psychiatry Neurosci. 2009; 34(5): 361-6.

Ian R. Gizer, Courtney Ficks,  Irwin D. Waldman.Candidate gene studies of ADHD: a meta-analytic review. Hum Genet. 2009; 126: 51-90.

Castellanos, F.X., Giedd, J.N., Eckburg, P., Marsh, W.L., Vaituzis, A.C., Kaysen, D., Hamburger, S.D., Rapoport, J.L., Quantitative morphology of the caudate nucleus in attention deficit hyperactivity disorder. Am. J. Psychiatry 1994; 151: 1791–1796.

Semrud-Clikeman, M., Filipek, P.A., Biederman, J., Steingard, R., Kennedy, D., Renshaw, P., Bekken, K. Attention-deficit hyperactivity disorder: magnetic resonance imaging morphometric analysis of the corpus callosum. J. Am. Acad. Child Adolesc. Psychiatry 1994; 33: 875–881.

Castellanos, F.X., Giedd, J.N., Marsh, W.L., Hamburger, S.D., Vaituzis, A.C., Dickstein, D.P., Sarfatti, S.E., Vauss, Y.C., Snell, J.W., Lange, N., Kaysen, D., Krain, A.L., Ritchie, G.F., Rajapakse, J.C., Rapoport, J.L. Quantitative brain magnetic resonance imaging in attention-deficit hyperactivity disorder. Arch. Gen. Psychiatry 1996b; 53: 607–616.

Filipek, P.A., Semrud-Clikeman, M., Steingard, R.J., Renshaw, P.F., Kennedy, D.N., Biederman, J. Volumetric MRI analysis comparing subjects having attention-deficit hyperactivity disorder with normal controls. Neurology 1997; 48: 589–601.

Mackie, S., Shaw, P., Lenroot, R., Pierson, R., Greenstein, D.K., Nugent III, T.F., Sharp, W.S., Giedd, J.N., Rapoport, J.L. Cerebellar development and clinical outcome in attention deficit hyperactivity disorder. Am. J. Psychiatry 2007; 164: 647–655.



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Sandoval V, Riddle EL, Hanson GR, Fleckenstein AE. Methylphenidate alters vesicular monoamine transport and prevents methamphetamine-induced dopaminergic deficits. J Pharmacol Exp. Ther. 2002; 304: 1181-1187.

Zucker M, Weizman A, Rehavi M. Characterization of high-affinity [3H]TBZOH binding to the human platelet vesicular monoamine transporter. 2001. Life Sci. 2001; 69: 2311-2317.

Zucker M., Aviv A., Shelef A., Weizman A., Rehavi M. Elevated platelet vesicular monoamine transporter density in untreated patients diagnosed with major depression. Psychiatry Res. 2002a; 112: 251– 256.

Paz Toren, Moshe Rehavi, Anat Luski, Netta Roz, Nathaniel Laor, Michal Lask, Abraham Weizman. Decreased platelet vesicular monoamine transporter density in children and adolescents with attention deficit/hyperactivity disorder. Eur. Neuropsychopharmacol. 2005; 15: 159– 162

David H. Ben-Dor, Sharon Zimmerman, Jonathan Sever, Neta Roz, Alan Apter, Moshe Rehavi, Abraham Weizman. Reduced platelet vesicular monoamine transporter density in Tourette's syndrome pediatric male patients. Eur. Neuropsychopharmacol. 2007; 17: 523–526

genetica tdah neurologia tdah testimonios tdah neurolinguistica tdah revisiones tdah en el aula vejez tdah 

domingo, 13 de febrero de 2011

TDAH ¿Entre la locura y la creatividad?

La creatividad y la locura

Byron

Byron era loco, malo y peligroso de conocer, según una de sus amantes.

Byron era "loco, malo y peligroso de conocer" según una de sus amantes; a Keats, el amor obsesivo lo llevó al paroxismo y Sylvia Plath puso fin a su propia vida.

La depresión y la locura son temas recurrentes a lo largo de la historia de la poesía.

La incidencia de los trastornos del estado de ánimo, suicidio e internación en hospitales psiquiátricos fue de 20 veces más alta entre los principales poetas británicos e irlandeses entre 1600 y 1800, según un estudio realizado por el psicólogo Kay Redfield Jamison.

En otras palabras, los poetas tienen 20 veces más probabilidades de terminar en un asilo que el resto de la población... y eso es sólo los poetas.

A algunos artistas, eso no les preocupa: a mediados de 1800, Emily Dickinson declaró que "mucha locura es juicio divino", mientras que Edgar Allan Poe señaló que aún no se había determinado si "la locura era o no la más excelsa inteligencia".

Cualquiera que sea la respuesta, la ciencia ha tratado de entender la razón de esa alta incidencia de enfermedades mentales.

Un estudio reciente encontró patrones similares en el cerebro de los artistas trabajando a los de los esquizofrénicos. Otro estudio encontró que los estudiantes creativos comparten más rasgos de personalidad con pacientes bipolares que los menos creativos.

Conflicto creativo

"Los hombres me han llamado loco; pero aún no está determinada la cuestión de si la locura es o no la más excelsa inteligencia"

Edgar Allan Poe

Muchos psicólogos han tratado de definir lo que hace que alguien sea creativo o no, y cómo eso se puede calcular.

Se han hecho experimentos midiendo cuántas ideas se le ocurren a los participantes cuando se les pregunta cómo pueden utilizar un ladrillo, pero el modelo de Joy Paul Guilford de la creatividad, publicado en 1950, es el que todavía se utiliza más a menudo.

Guilford fue el primero en clasificar a la creatividad como una característica independiente de la inteligencia (entendida como el cociente intelectual).

Según él, la fluidez, la flexibilidad y la originalidad de las ideas, junto con la capacidad para elaborar sobre ellas, constituyen las características de los individuos creadores.

"La creatividad viene, sin duda, de no dejarse limitar por las reglas o aceptar las restricciones que la sociedad impone sobre nosotros", le dijo el psicólogo Gary Fitzgibbon a la BBC.

"Por supuesto, entre más alguien viole las reglas, más probable es que se le perciba como un 'enfermo mental'", agregó.

El poeta Luke Wright tiene que estar relajado para poder escribir.

Entonces, ¿es la enfermedad mental lo que lleva a la gente al arte o es el arte el que lleva a la gente a la enfermedad mental?

"Mucha de la creatividad proviene de un conflicto en algún lugar de tu mente", le dijo a la BBC el poeta Luke Wright.

"No creo que uno tiene que estar 'loco' para ser poeta, pero si la mente está viva, entonces se puede producir tanto reacciones positivas como negativas. Eso puede ser maravilloso, pero también puede significar que encajar en la vida 'normal' sea difícil".

Aunque, con el aumento del diagnóstico de trastorno mental, la idea de lo "normal" se ha vuelto más difícil.

Según la Oficina del Censo de Estados Unidos, alrededor del 1% de la población de ese país tiene esquizofrenia; el déficit de atención con hiperactividad (TDAH) afecta a un estimado de 4% de los adultos y 2,5% de los habitantes sufren de trastorno bipolar.

Un tipo feliz

No obstante, hay quienes consideran que expresar las emociones y experimentar los altibajos de la vida es positivo.

Muchos artistas han sufrido enfermedades mentales.

"Tengo poemas sobre todo tipo de temas oscuros, pero en general soy un tipo muy feliz", le aseguró a la BBC el artista de la palabra hablada y músico Scroobius Pip.

"En mi vida cotidiana, no me la paso discutiendo el asesinato, el suicidio y el abuso conyugal con mis compañeros... hablo de fútbol y cosas normales. Es importante sentir una gran variedad de emociones y es genial para la mente y el alma.

"Y si hay un montón de poetas que sufren enfermedades mentales, el expresar, escribir y compartir sus sentimientos, les puede ayudar".

De hecho, la Junta de Verificación de Terapia del Arte británica avala esa opinión, pues dice que el arte puede "reducir la ansiedad y aumentar el autoestima".

sábado, 12 de febrero de 2011

Simplemente la gente que tiene TDAH tiene un mapa genético diferente.

Susan Smalley, Ph.D., is a professor in the department of psychiatry and biobehavioral sciences at the University of California, Los Angeles, Semel Institute for Neuroscience and Human Behavior and director of its Mindful Awareness Research Center. Dr. Smalley's work has a dual focus: the genetics of attention-deficit hyperactivity disorder and the use of techniques of mindfulness in promoting well-being.

Susan Smalley

Q: Many people notice that attention-deficit hyperactivity disorder, or A.D.H.D., seems to run in families. Is it very strongly inherited?

A: It is; the heritability of A.D.H.D. is 76 percent.

Q: Does that mean that 76 percent of all cases of A.D.H.D. are inherited?

A: No — heritability is different: it's looking at the variability in the population at a particular point in time. If you think about height and you lined everybody up in the population, you could see a nice, kind of a bell-shaped curve, with very tall people at one extreme and very short people at the other extreme, and the majority of people falling in this middle place, around the average. That bell-shaped curve is the distribution of variability of height in the population.

Now, if you could measure people's genes that contribute to height, we know that 60 to 80 percent of the variability in height is due to genetic differences. That's heritability — the proportion of the total variance that's due to genes. How much of the variance in A.D.H.D. is due to genetics? That's where that 76 percent comes from.

Q: So the heritability of A.D.H.D. rivals that of height? We typically think of height as being very strongly inherited.

A: The heritability of A.D.H.D. is very high; that's a very high number, 76 percent. When we look at other psychiatric conditions — things like depression — it's more on the order of 50 percent. Autism tends to be one of the highest; it's around 90 percent.

Q: Have we located any of the specific genes that contribute to A.D.H.D.?

A: We're still at the level of trying to find the genes that might play a role in A.D.H.D. That work has yielded several likely genes that are involved in A.D.H.D., but none of them has a big effect. We were saying 76 percent of the variance is genetic. These are genes that contribute to maybe 2 percent, 5 percent — very small, small amounts.

But it's very likely that the genes that are involved in A.D.H.D. are going to be many, many more than we've identified to date, and a lot of research groups, including our own, have been actively looking throughout the whole genome for genes that might have a bigger role. It's kind of like looking for a needle in a haystack. Those are the genome-wide approaches, genome-scan approaches, to A.D.H.D.

Q: How does the genome-scan approach work?

A: There are two approaches to searching for these genes. A candidate-gene approach is when you know a gene, and you go in and you directly say, "Does this gene contribute to A.D.H.D.?" You have to have the gene; you've got to know what it is and how to look at differences in that gene. That's where we've found the handful that have played a role so far.

But the majority of discoveries for disease-gene relationships haven't really emerged from that approach. They're more often found by using the genome-wide approach — by saying, "O.K., there're 30,000 genes in the genome. Let's sample little pieces of DNA throughout the whole genome that we can study in pairs of siblings, for example, with A.D.H.D., or in relatives that we can study. Do they share a particular piece of DNA more often than you'd expect by chance?" If so, then the piece of DNA they share is going to be located really near the risk gene.

Using that approach, you don't have a clue where the gene might be, but you actively search everywhere. And my analogy is, finding a gene is about equivalent to finding a contact lens at Disneyland — sort of the ratio of the size of the gene to the size of all your DNA, or the genome. Finding a contact lens in Disneyland: that would be pretty hard. But it wouldn't be so hard if we had a really good map, and a technique for saying, "O.K., the chance that you've lost it in Space Mountain is much larger than the chance that you lost it on Tom Sawyer Island, right?"

Q: Does that type of map exist?

A: Yes. That's what a genome-wide strategy does: it samples all [areas] across the whole Disneyland park with a grid, a map. You study people who have A.D.H.D., asking which pieces of DNA they have in common among the 300,000 pieces of DNA that span the whole genome. They can be used as a marker map, to study differences in the population. It helps us locate the likely candidate gene. You still don't have the gene; you just know its location. Marker maps help you map the most likely position, in the whole genome, for a gene that contributes to A.D.H.D.
 

My lab has found strong, strong support for particular places on four chromosomes — Chromosome 5, Chromosome 6, Chromosome 16 and Chromosome 17 — that have a very high chance of having a gene that contributes a bigger effect to A.D.H.D., maybe 5 to 10 percent of the variance. There are other groups that are doing the same kind of work, and the sad part is, they're not all coming up with the same four positions. They're finding evidence on Chromosome 9, Chromosome 11 — different positions. So that probably means that there are going to be a lot of genes that contribute to A.D.H.D.

Q: How does environment interact with genes in A.D.H.D.?

A: My biggest insight into A.D.H.D. is to think of it as a kind of a neural map, a neural network, a template, if you will, of brain organization that is just not the average brain organization in the population. It's more of the extreme on this normal bell-shaped curve, the extreme end of a normal distribution. It has to do with different areas of the brain, and all of those brain neural networks are bumping up against different kinds of cultures, different kinds of school systems, etc. The degree of impairment is a function of all of those things, and no one thing alone.

We understand that the predisposition to getting a diagnosis of A.D.H.D. has a lot to do with what kind of genetic complement you're born with, and then how that genetic complement interacts with the environment throughout early development. Prenatal exposure to cigarettes, for example, may impact the genes differently when you have a genetic predisposition to A.D.H.D.. Several studies have shown that maternal smoking in pregnancy increases risk for hyperactivity-impulsivity later in life, and a recent study suggests that that effect may be greater if the fetus has a certain genotype.

Postnatally, there may be differences in childhood as well. We have interesting research showing that in families where there's a lot of conflict in the home, a lot of arguing, that has a very negative impact on kids with A.D.H.D. in terms of leading to greater impairment, greater problems.

Q: Is this where your work in mindfulness comes in?

A: Our lab studies families that have two affected kids with A.D.H.D., and then we evaluate the parents for A.D.H.D. as well. In those studies, we've found that at least half of the families have one parent affected with A.D.H.D.. We've had a great opportunity to study families that are heavily loaded with genes for A.D.H.D., and we've found a lot of interesting things. Some kids don't have a lot of psychiatric issues, or as many problems academically, or cognitively. Other families have tons of problems. What is accounting for this variability?

When we studied that, conflict in the home seemed to be really important. Having a lot of conflict made families suffer much, much more than having little conflict. So A.D.H.D. alone doesn't cause the problem, because all these families have pretty much the same constellation of A.D.H.D. Something else is going on.

So another whole hat that I wear is trying to look at tools to help people cope with stress. Can meditation be useful — mindfulness-type practices? Can those be taught and used in families or schools that kids might find themselves in to help build resiliency, help reduce stress? Can that help parents cope? We know that can reduce conflict in general, so would it be useful in families that have kids with A.D.H.D.?

We're just starting to understand what the gene-by-environment interaction is in A.D.H.D. that unfolds as we develop. Then the question is, what can we do to minimize the impairment associated with A.D.H.D. and maximize the strengths? What are the strengths of having that genetic predisposition, of being at that end of the distribution?

Q: What advice would you offer parents of children with A.D.H.D.?

A: Finding their child's strengths is really important. There's a negative impact of seeing the world differently. Anybody who's at the extreme of anything — I don't care if you're just really, really tall — you bump into a world that isn't so tall, and it's impairing. It's not easy being green; we've all got some green dimension to figure out.

So I think it helps for families to understand the genetics, but it also helps to hone in on what are the strengths, and how best to manage the weaknesses. That's the approach that we take — to recognize that the way you're wired, you can learn to find tools to help manage that brain wiring so it's more compatible with the world around you. Sometimes that requires medications, and that's O.K.; sometimes it doesn't, and that's O.K. Be very open to finding the best way to manage it for your child at this particular point in time
 
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El TDAH sigue en la edad adulta, pero ¿mejorá?

Can You Outgrow A.D.H.D.? Or Get It as an Adult?

Deanna Wheeler, a reporter for the Lake Sun Leader, did not learn that she had A.D.H.D. until she was in college. She grew up in a large family, where constant activity was the norm.Dan Gill for The New York Times Deanna Wheeler, a reporter in Missouri, did not learn that she had A.D.H.D. until she was in college. She is among those featured in Patient Voices: A.D.H.D.

If you have attention deficit hyperactivity disorder, or A.D.H.D., as a child, do symptoms ease with age? Can you have adult-onset A.D.H.D.? These are among the questions recently posed by readers of the Consults blog.

Dr. Russell A. Barkley, clinical professor of psychiatry at the Medical University of South Carolina, responds. His books include "A.D.H.D. in Adults: What the Science Says" and, most recently, "Taking Charge of Adult A.D.H.D.," both from Guilford Press.

Do A.D.H.D. Symptoms Ease With Age?

Q.

Does A.D.H.D. generally improve with age? In other words, if A.D.H.D. persists into adulthood, is it expected to improve as the brain develops into a person's late 20s?
Rhett, Charleston, S.C.

A.

Dr. Barkley responds:

Research studies following children with A.D.H.D. to adulthood, including my own 20-year follow-up of children in Wisconsin, show that the symptoms of A.D.H.D. do decline with age, both in people with A.D.H.D. and in the general population. Even so, people with the disorder continue to have far more symptoms of the disorder than we see in the general population at any age.

My own research showed that 14 percent to 35 percent of children who had A.D.H.D. could be considered to have recovered or moved to within the normal range by the time they were 27. The reason for the range of recovery percentages simply has to do with how rigorously you want to define recovery. Defined loosely, about one-third no longer meet our criteria for this disorder in young adulthood. Defined more rigorously — at least two people report that the person's symptoms are no longer severe or inappropriate and are no longer impairing — and the figure falls to about 14 percent.

So, yes, some people do outgrow A.D.H.D. But most do not. The things that have been found to predict whose disorder persists are:

  • Severe symptoms in childhood. The more severe A.D.H.D. symptoms are early in life, the more likely they are to persist into adulthood.
  • The presence of a psychiatric disorder in addition to A.D.H.D.  Those who suffered from depression or other mental illnesses along with A.D.H.D. were more likely to have symptoms of A.D.H.D. as adults.
  • Having a mother with significant psychological problems also increased the risk that symptoms will continue into adulthood.

In short, A.D.H.D. seems to persist in most — but not all — cases. Even those children we followed who had recovered from the disorder had experienced significantly more school-related problems and tended to have less formal education. These educational setbacks can carry forward and affect adult life, even if someone no longer has the disorder.

Can You Have Adult-Onset A.D.H.D.?

Q.

Is it likely that in my 60s I would develop A.D.H.D.? My executive function has gone out the window in the past few years, and my partner insists that's not the only way I show the symptoms. (Including almost constant fidgeting!) So, is there late-onset A.D.H.D.? Or did I have it all along and it only got worse in the past three to five years?
Kenny Boy, Houston

A.

Dr. Barkley responds:

There is no evidence that A.D.H.D. can come on in mid- to late life unless it is a result of a brain injury or disease, in which case it is an acquired type of A.D.H.D. But aging does result in a decline in certain executive functions that can mimic some of the symptoms of A.D.H.D.

For instance, in our 60s and onward, working memory — or the ability to hold information in the mind about what you are doing, what goals you are pursuing, and why — declines in both sexes. As working memory decreases, we become more forgetful and less attentive to our goals and plans and the intentions of our actions. These symptoms can look like the inattention we see in A.D.H.D., which also causes problems with working memory. But these later-life declines in our executive abilities are not associated with other A.D.H.D.

Diferencia entre el TDAH en hombres y mujeres

Men, Women and A.D.H.D.

Robert Cimera, a professor of special education at Kent State University, learned he had A.D.H.D. while he was working on his master's degree. He says the condition has helped him be a better teacher.David Maxwell for The New York Times Robert Cimera, a professor of special education at Kent State University, learned he had A.D.H.D. while he was working on his master's degree. He says the condition has helped him be a better teacher. He is among those featured in the Times multimedia series Patient Voices: A.D.H.D.

Do men and women exhibit different symptoms of attention deficit hyperactivity disorder, or A.D.H.D.? What about boys and girls? These are among the questions recently posed by readers of the Consults blog. Dr. Russell A. Barkley, clinical professor of psychiatry at the Medical University of South Carolina and author, most recently, of "Taking Charge of Adult A.D.H.D.," responds to one reader whose wife has a "whopping case" of A.D.H.D.

Q.

Can you talk about the way A.D.H.D. manifests in adult women as opposed to men? My wife has a whopping case of it, but even people close to her don't see it because they don't live with her and she's developed some basic coping mechanisms — and because they presume the male hyperactive version instead of the female dreamy and distractible version.
Julie, Washington, D.C.

A.

Dr. Barkley responds:

First, it is important to note that attention deficit hyperactivity disorder does not present all that much differently in women from the way it does in men. Most research on this issue has confirmed this. While symptoms may vary somewhat among children, they are virtually the same by adulthood.

In childhood, boys are three times as likely as girls to have A.D.H.D. Boys with the disorder tend to be more hyperactive and impulsive and are more likely to develop oppositional behavior, conduct problems and later delinquency than girls, though girls, too, can develop these problems. Girls, on the other hand, may be more prone to develop anxiety, depression and eating disorders — bulimia, in particular.

By adulthood, the proportion of men to women with the disorder is nearly even, and there are few differences in the symptoms. Both men and women have significant problems with executive functioning, which involves skills like time management, self-organization and problem-solving, as well as self-restraint, self-motivation and self-regulation of emotions. All of these problems can have a major effect on daily life activities, like family relations, child-rearing, managing money, functioning at work or driving.

Where men and women may differ is in the amount of time they engage in these activities – and the subsequent impact on daily life. A woman who works full time outside the home, for instance, would have more work-related difficulties, whereas a stay-at-home mother might have more problems related to home life. To the extent that women may opt for certain roles, those roles will be more greatly affected by the disorder, and vice versa for men.

In the general population, men and women may be more likely to have certain problems. For example, women may be more prone to depression and anxiety or have more emotional control problems than men, whereas antisocial behavior and problems with drug use tend to be more common in men. Men also tend to drive more than women, and hence may have more traffic accidents. These same differences in the general population are also applicable to men and women with A.D.H.D., but the disorder cannot be blamed for them.

The symptom of daydreaming, which you describe in relation to your wife, can certainly occur in A.D.H.D., but daydreaming is no more common in women than in men. But the presence of behavior does raise the possibility that the person you describe may have the inattentive type of A.D.H.D., with no hyperactivity or impulsiveness. Some clinicians and others refer to this condition as attention deficit disorder, or A.D.D., leaving out the H.

But increasingly, researchers are now referring to this condition as "sluggish cognitive tempo," or S.C.T. The term refers to a constellation of symptoms that include daydreaming, being "spacey" or easily confused, mental fogginess, or being slow-moving, lethargic or less active than usual. My own recent research shows that S.C.T. is a separate and distinct disorder from A.D.H.D. that may have different causes and may not respond as well to the same treatments. It is less impairing than A.D.H.D. but can still be a troublesome attention disorder to have. The two disorders, A.D.H.D. and S.C.T., also overlap in about 20 percent of cases. Most of the time, though, they occur separately.
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jueves, 10 de febrero de 2011

Origen del TDAH

Y entre todas las teorías, falta mencionar la de valdeandemagico según la cual el hombre moderno somos fruto de la manipulación genética. Nos cuenta Valdeandemagico que hartos de trabajar los que venían de fuera, se reunieron y decidieron modificar un ser parecido a ellos y de la tierra y hacerle medianamente inteligente para que pudiera hacer de mano de obra barata. Así empezan a manipular al mono, y otros animales, creando seres con alas, con cuernos, los conocidos luego en el futuro como mitología. Todo esto pasaba en Eridú, el caso es que al final tras mucho manipular, no conseguían grandes resultados de inteligencia, así que acabaron inseminando a una de ellas, la conocida como Eva, y de ahí salió el primer molde del homo sapiens sapiens, luego hubo que enseñarle, educarle... pero llegó un día en que los dioses con minúsculas, es decir lo que nos manipularon, vieron que las mujeres de los hombres eran tan hermosas que se acostaron con ellas, y ahí fue cuando empezaron a surgir los semidioses y con ellos las razas y las pequeñas diferencias genéticas. Así que el TDAH posíblemente lo hayamos heredado de alguien de fuera, y aporta muchos problemas en la sociedad actual, y muchos beneficios en la sociedad del futuro. Una vez que toda la información esté en la red, y el conocimiento ya no sea tan imporante, empezará a valorarse la imaginación, el ser divergente, el pensar de forma creativa, sin estar manipulado por la educación recibida, y allí ellos serán los líderes.

Articulo de http://www.suite101.com/content/an-evolutionary-psychological-view-of-the-roots-of-adhd-a345345

ADHD is Traditionally framed as a 'disorder'

ADHD is traditionally viewed as a 'disorder' displaying a set of behaviours significantly different from normal, that negatively impact in many areas of the individuals life. These negative outcomes can include; social skills, organizational ability, academic attainment, career success and criminal involvement amongst others (Barkley, 1990).

Barkley is a leading writer on ADHD and he frames the condition as abnormalities causing a disorder, for which treatment is required to suppress the symptoms. Taking a neurodevelopmental approach to its origin, he argues that the crit­i­cal deficit asso­ci­ated with ADHD is the fail­ure to develop a capac­ity for "self-regulation".

ADHD is highly heritable

ADHD's heritability of 0.8 is high, especially for a behavioural disorder. Evidence is provided by twin studies that have confirmed a strong genetic contribution to individual differences in activity levels and attention abilities (Baird, Stevenson & Williams, 2000). Couple this with the relatively high occurrence in 3-9% of the population, it has been suggested that ADHD traits were selectively advantageous in the past.

This evolutionary perspective formed an entirely new approach to the understanding and treatment of ADHD as not being pathological at all, but instead normal behaviour which was once and could still be in some contexts, adaptive.

There's a controversial debate, between two key authors in the field, Barkley with a traditional pathological view and a pop writer Hartmann, who takes an evolutionary view.

Barkley wishes to treat the individual, believing ADHD symptoms are abnormally exaggerated behaviours, causing pathological harm and requiring treatment.

Hartley on the other hand wants to change the environment to fit the individual, believing the symptoms are normal behavioural patterns, which only look exaggerated because they are now out of appropriate context.

Hartmann's hunter Vs. farmer theory of ADHD

In 1993 Hartmann proposed the metaphor of 'hunter Vs. farmer', describing those with ADHD as hunters. He suggested the behaviours associated with ADHD were misunderstood, and were in fact useful skills for hunters in the evolutionary past.

Hartmann explain that each ADHD trait can be seen positively, e.g distractibility as scanning and searching for novel stimuli and threats. Three symptom behaviours, distractibility, impulsivity and risk-taking were ideal for hunters, but detrimental to farmers. For example patience is essential for farmers to complete mundane tasks such as planting seeds. Conversely risk-taking behaviour would have been the day to day norms for hunters who risked their lives against predators and had to act quickly and on impulse in order to catch prey etc.

Hartmann's ideas quickly gained popular support from parents and media.

Children with any disorder are often stigmatized and can suffer damage to their self-esteem and confidence. Therefore any new perspective indicating ADHD to have potential benefits may lessen feelings of disability and instil pride .

The Edison gene and other ADHD related genes

Hartmann's hunter in a farmers world remained just a metaphor until 2002, when researchers found a significant positive selection for the genetic variation associated with novelty-seeking behaviour and ADHD. This gene was termed the Edison gene and was likely to have served a unique adaptive purpose for our ancestors.

A mutation was discovered by analysing the DRD4 genes of a worldwide sample, noting the degree of variation and working backwards to find the time when there was no variation at all. There is now evidence of a single mutation, that triggered a novelty seeking adaptation that is found in ADHD.

Evidence supports this, like Eisenberg et al, (2008) who looked at two tribal communities still around today, one that was still nomadic, and the other recently settled. Their findings showed that those with the DRD4/7R+ genes in both communities, were better adapted to the nomadic lifestyle than to the static lifestyle of those recently settled. They continue that the short attention span associated with this genotype may allow nomadic children to more readily learn effectively in a dynamic environment (without schools), while the same attention span interferes with classroom learning in the settled community.

Academic evolutionary support of ADHD.

Jensen (1997) is in agreement with the core assumptions of an evolutionary perspective, that a species typical design develops via natural selection, implying the behaviours evident in ADHD, are potentially adaptive responses of the organism to environmental demands.

This theory suggests ADHD tendencies are innate in everyone but are activated by differing environmental stimulus in the early days. ADHD behaviours are seen as a continuum, furthermore one that is malleable, with early development being a time for 'wiring the brain' to fit its environment.

Jensen states exploratory motor behaviour usually only occurs in the context of presumed safety. A characteristically hyperactive child will thus suppress this motor activity during times of danger, during separation from the care-giver and in situations with a high degree of novel stimuli.

Attention, often described as scanning and rapidly shifting attention in those with ADHD is necessary to monitor dangers and threats. Conversely over focused attention could indeed be maladaptive in high-threat, highly novel environments. Thus those living in environments with high risks i.e high predator to prey ratio, are likely to display increased scanning behaviours (or lack of attention).

Impulsivity, defined as a quick response without considering alternatives, can be viewed similarly. Jensen proposes early on an individual can learn to adjust the threshold and timing of responses based on the likelihood of a 'payoff' as a result of immediate, delayed or non-response and whether the response is correct.

Research and Treatment Implications for an Evolutionary perspective to ADHD.

Jensen believes as society changed, problem solving individuals would have become increasingly the most adaptive type for the environments of industrialised and organised cultures. The response ready characteristics of ADHD individuals have gradually become seen as less adaptive.

This brings entirely new research and treatment implications for ADHD. Jensen asks if a systematic and strategic approach over a period of time, could effectively modify or 'reset' the individuals early biological substrates and adapt them to the environment they current reside in.

To begin this process research must be done to determine the periods of greatest plasticity and ascertain which children are most susceptible given their biologically selected substrate and their environment, to 'up-regulate' to ADHD type traits.

ADHD individuals may have been really important to our survival!

One final thought is just how important ADHD individuals may have been to our survival- The personalities of those with ADHD may have predisposed them to migration. Active, restless and adventure-seeking individuals would have pioneered the migrations that populated the earth. (Bridgeman, 2003).

The hypothesis generates a testable prediction, that the frequency of the gene should be greatest in groups that moved farthest from the African cradle of humanity. This is proven by rarity of the gene in the African bushmen, the closest group left to ancestral populations and highest in south America, about as far from Africa as one can migrate! (Bridgeman, 2003).

It seems a shame that the gene that may have caused our ancestors to explore to the farthest corners of the earth, is now recognised by the disruptive behaviour it causes in schools. It seems currently that psychiatrists are drugging children by the millions to suppress symptoms that may well be a part of the normal range of adaptive human behaviour.

Hay otra condición que se manifiesta con una firma neuroeléctrica que consiste en exceso de ondas cerebrales lentas y la escasez de ondas rápidas en la corteza prefrontal. Se trata del TDAH

¿En qué se parecen los efectos de los videojuegos a los de la terapia para el TDAH?
Vídeojuegos y tecnología: aliados eternos

La industria de los videojuegos en el mundo a sido y es muy prolífica. En los últimos 10 años, hemos visto un crecimiento casi exponencial en los tipos de juegos y en la tecnología de juegos. Hemos recorrido un largo camino desde el recordado juego de Pac Man. Existe una continuidad de los videojuegos. En un extremo están los que estimulan las vías de aprendizaje y por otro los que estimulan el sistema límbico. El sistema límbico es el responsable de preparar el cuerpo para luchar o huir en caso de amenaza (de supervivencia). Los videojuegos como Sim City(es un juego de construcción de ciudades) enseñan habilidades a los jugadores como la organización, planificación y la estrategia. Por el contrario, los videojuegos, como Doom(juego de disparos) y Quake(similar al Doom), estimulan en gran medida el sistema límbico. Hay muchas herramientas tecnologicas que los videos juegos han mantenido hasta el día de hoy. Como la tecnología en mejoramiento gráfico, controladores e indicadores que hacen muy realista cada tipo de juego. Con gráficos superiores los juegos son muy realistas y por lo tanto proporcionalmente aumentan la estimulación del jugador. Cuanto mayor sea el estímulo, mayor es la excitación emocional, a pesar de que el jugador sabe conscientemente que es sólo un juego.


Cambios neuroquimicos

Hay dos importantes neuroquímicos producidos en grandes cantidades por juegos de vídeo: la norepinefrina y la dopamina. La primera se asocia con la respuesta de la lucha o la huida, la segunda estimula directamente los centros de placer.

Los juegos de vídeo son tan emocionantes, y en algún nivel se sienten reales, y para el cerebro, en un sentido, lo son. En una situación de peligro real, el cerebro le dice al cuerpo que este listo para la acción. Se inunda el cuerpo con adrenalina, que aumenta la tasa de respiración, la constricción de los vasos sanguíneos, y la frecuencia cardiaca y la presión arterial aumenta ya que la adrenalina es liberada también en el cerebro.

Intuitivamente, podríamos imaginar que el estado de supervivencia sería uno que conecta el cerebro, pero de hecho, ocurre lo contrario, particularmente con respecto a los lóbulos frontales, donde el pensamiento de más alto nivel se produce: estas corriendo por tu vida, y te detienes a pensar por un momento si decides ir a la izquierda. Ese momento de vacilación podría costarle su vida. En cambio, el cerebro le dice al cuerpo que termine de moverse, no pensar en cómo o dónde, sólo hazlo. Durante una descarga de adrenalina, el flujo sanguíneo a los lóbulos frontales se suprime.


Además de las altas concentraciones de productos químicos asociados a la lucha o huida en el cerebro de los videojugadores, los estudios también han encontrado importantes cantidades de dopamina. Curiosamente, la presencia de dopamina es lo suficientemente confiable que los investigadores que buscan realizar un seguimiento de la dopamina en el cerebro, han usado videojuegos para estimular su producción. Se produce en respuesta a las actividades de búsqueda de objetivos que son un componente de la mayoría de los juegos de vídeo. Nuestros cuerpos producen dopamina cuando están en la búsqueda de un objetivo. Esa es la forma de nuestro cuerpo de ayudarnos a permanecer en pista con un seguimiento, ya que la dopamina estimula directamente los centros de placer del cerebro. Una vez que el objetivo es alcanzado, la producción de dopamina cae. Pero, como sabemos, detrás de cada meta en un juego de vídeo es otro objetivo a la espera de ser alcanzado, por lo que el flujo de dopamina es continua.


Cambios neuroelectricos

Ambas cantidades excesivas de dopamina y la presencia de los productos químicos de lucha o de huida provocan una disminución en el flujo sanguíneo en la corteza prefrontal, la reducción de la actividad neuronal en esa parte del cerebro. Esta reducción en el flujo de sangre se manifiesta por un aumento en la actividad de ondas cerebrales lentas y una disminución de la actividad de las ondas rápidas en la corteza prefrontal. Los estudios con resonancia magnética y el análisis del EEG han encontrado que la gente cuando juega emocionantes juegos de vídeo consistentemente muestran este patrón de ondas cerebrales.

El aumento de la actividad de las ondas cerebrales lentas se puede comprobar en el estado disociado en el que la mayoría de la gente que juega juegos de vídeo. Ellos se sumergen en el mundo imaginario, para los jugadores, es como si estuvieran realmente en el juego y la vida real deja de existir. Muchos padres dicen que tienen gran dificultad para conseguir la atención de sus hijos cuando están jugando. Esta es la razón. La rápida disminución de la actividad de la onda en los videojuegos no es inesperado debido a que la estructura de la mayoría de los juegos emocionantes que recompensan de esta manera tan efectiva. La actividad rápida de las ondas cerebrales en los lóbulos frontales le permite a una persona inhibir una respuesta el tiempo suficiente para pensar en las consecuencias de la acción antes de actuar. Se suprime la impulsividad. En juegos de vídeo, como con la lucha de la vida real o de huida, el éxito viene con respuestas rápidas, no se mide, con planes bien pensados de acción.

Hay otra condición que se manifiesta con una firma neuroeléctrica que consiste en exceso de ondas cerebrales lentas y la escasez de ondas rápidas en la corteza prefrontal. Se trata de ADD / ADHD.


Juegos de video: Entrenamiento neuroretroalimentado con resultados negativos

El entrenamiento neuroretroalimentado utiliza la capacidad del cerebro para modificar su estructura y programación (plasticidad neuronal). Los pacientes están conectados a electrodos que miden la actividad neuroeléctrica en el cerebro. Esta actividad se muestra al paciente en una pantalla de vídeo y como el paciente altera la actividad cerebral en una dirección funcional, los cambios de imagen del vídeo se muestran para hacerles saber que han logrado el éxito.

Con el tiempo, la práctica saludable de la actividad cerebral funciona como la práctica de cualquier cosa. Los pacientes mejoran en él, hasta que, finalmente, se convierte en la cosa más natural del mundo.

Cuando el entrenamiento neuroretroalimentado se utiliza para corregir el TDAH, los umbrales del equipo se establecen para premiar la ausencia de ondas cerebrales lentas y el correspondiente aumento de la actividad rápida de ondas en la corteza frontal. Este es el perfil de la actividad cerebral saludable.

Los juegos de video producen ondas cerebrales que son lo contrario de lo que es deseable para el funcionamiento saludable. Mirándolo desde esa perspectiva, los juegos de vídeo son en realidad la "terapia de neuroretroalimentación" que produce resultados negativos. Mientras que los pacientes con neuroterapia podrían pasar 60 minutos a la semana para mejorar su cerebro a un estado saludable, los jugadores fuertes de vídeo deben pasar horas y horas cada día de entrenamiento para que su cerebro funcione como alguien que sufre con TDAH.

Para los adolescentes sin TDAH o sin una vulnerabilidad con el TDAH, los juegos de vídeo emocionantes y moderados pueden no presentar riesgos graves. Sin embargo, para las personas con TDAH o con una predisposición a ella, los juegos de vídeo extremadamente emocionantes pueden ser equivalentes a un consumo alcoholico incipiente cada vez que se juega.

Hay muchos usuarios habituales de los videojuegos con extrema emocion que son a menudo socialmente rechazados aunado a la falta de madurez para su edad, tienen ansiedad y problemas de ira, van mal en la escuela, estos pacientes son difíciles de tratar y algunos no responden bien a los medicamentos. No puede haber un "huevo y la gallina" dice el viejo dicho. Tal vez los niños con estos problemas se sienten atraídos por los juegos fuertes. Pero también es posible que los juegos fuertes sean la causa del problema o lo empeoren aún más

miércoles, 9 de febrero de 2011

Nuestros hijos con TDAH tienen imaginación, muuuuucha imaginación

Parents who've claimed for years that their kids with ADHD are more creative are getting some scientific backup from a new study, which found that subjects with the disorder have enhanced creative abilities.

A new study, published Wednesday in the Journal of Personality and Individual Differences, finds some truth in the increasingly popular theory that along with the thorns of Attention Deficit Hyperactivity Disorder comes a rose: increased creativity.

Article - Schwartz ADHD A new study implies that ADHD actually increases creative problem solving among children. Credit: Getty Images

Until now the ADHD-creativity link has been an oft-repeated rumor, seen by some as something exhausted parents cling to for consolation. Dr. Holly White and her colleagues at the University of Memphis set out to find out how much truth there was to the supposed link, and discovered that their subjects with ADHD showed marked differences both in their creative abilities and their approaches to creative problem solving.

"Creativity" is a slippery term, of course, often falling under the category of "we know it when we see it." That definition is not good enough for proper science, however, and in recent years, standardized tests that measure creativity have focused on "divergent" and "convergent" thinking. Divergent thinking is the ability to generate spontaneous, often unexpected ideas or solutions, and test questions calculate originality, elaboration, and flexibility. Convergent thinking, on the other hand, is understood as divergent thinking's opposite: the kind of thought process that allows you to narrow down your options to one correct answer. This kind of thinking boosts your SAT score but not necessarily your prospects for a career in poetry.

In part because ADHD's hallmark characteristics include a lack of constraint, intellectually as well as behaviorally, studies have consistently found that people with ADHD often excel at divergent thinking but struggle with convergent thinking.

"The key seems to be the inhibitory control—the same thing that allows somebody to not be distracted—which possibly could put a mental wall between what is right in front of them and other possibilities."

These classifications, however, barely begin to capture what we mean when we talk about creativity. Divergent and convergent thinking, and the standardized tests that measure them, are well-suited to a laboratory setting; how well they translate to the real world is another matter.

White and her colleagues wanted to address exactly that in their new research: Does ADHD really have the holy grail of upsides?

For their investigation, White and her team recruited 60 undergrads at the University of Memphis, exactly half of whom had an ADHD diagnosis.

One of the tasks the subjects completed is called the Creative Achievement Questionnaire, originally developed by Sandy Carson at Harvard. In it, subjects are asked highly specific questions about their past achievements in 10 creative domains, including drama, humor, science, writing, and cooking, among others. An example of a question on the CAQ: Whether the subject's "work has won a prize at a juried art show." The specificity of the questions is designed to limit the vulnerability of the responses to the subjective interpretations of the people answering them.

White and her team found that overall, with scores from all 10 domains combined, the subjects with ADHD had significantly higher scores than those without the diagnosis. Interestingly, White said she also noticed a distinctive pattern, one not included in the study: ADHD subjects were more likely to excel at certain creative domains than at others. The performing arts in particular were their forte. Although White did not find statistically significant differences here, she definitely noticed the trend. Her ADHD subjects were particularly masterful when the talent in question involved a lack of inhibition.

The other measure White used that differs from most past studies is called the FourSight Thinking Profile, developed by Gerard Puccio in 2002. This questionnaire—which, like the CAQ, depends on self-reporting by the subjects it's administered to—is designed to explore "preference for each phase of creative problem solving." The measure conceptualizes creative problem solving in four phases: clarification—"let's look at this problem," as White puts it; brainstorming; developing and refining of ideas; and implementing the arrived-at solutions.

For each phase, a name: the Clarifier, the Ideator, the Developer, and the Implementer.

Here, again, White came up with significant findings. Her ADHD subjects markedly gravitated toward the Ideator and Developer styles; her non-ADHD subjects toward the Clarifier role. She found no difference between her groups for the Implementer.

One notable thing about the FourSight Thinking Profile is that it does not measure ability but preferences. Thus, for example, it asks the extent to which subjects "enjoy taking the necessary steps to put my ideas into actions."

White notes that she found no significant differences between those students with ADHD who were on medication and those who were not. Exactly why this should be is an interesting question that, for the time being, she has no answers for.

As for why exactly her subjects with ADHD showed such marked differences in their creative abilities and their approaches to creative problem solving, White zeroes in on the question of inhibition.

ADHD, she says, "tends to just increase the amount of collisions between all of your ideas, so at any given time, you have more potential processes being activated and you're less likely to rule out any options. It's hard to know where this operates—like someone coming up with an idea and saying, 'No, that's not a good idea,' and not even writing it down, versus, they don't even think about it because they're inhibiting it. But the key seems to be the inhibitory control—the same thing that allows somebody to not be distracted—which possibly could put a mental wall between what is right in front of them and other possibilities."

However big an upside to ADHD White's new study reveals, there's an important caveat to keep in mind. Her subjects—students who have managed to graduate high school, matriculate to a private university, and are motivated and organized enough to sign up for a psychology study—are not representative of the typical ADHD trajectory.

"The first thing I do when I see a study like this is I look at who the sample is, and that creates a little bit of an interesting issue in terms of interpreting it," says Dr. Steven Kurtz, senior director of the ADHD and Disruptive Behavior Disorders Center at the Child Mind Institute in New York. "The subset of folks who have ADHD who are there have been able already to exceed a bunch of hurdles."

Dr. Kurtz emphasizes that ADHD presents so many challenges for children—focus, task completion, perseverance—that getting through high school successfully is a feat that requires proper support from both family and educators.

"When I read this, I thought of Kinko's. You know why?" Dr. Kurtz asks. "Because the guy who started Kinko's, who is an 11 on a scale of 1 to 10 of ADHD... was able to think outside the box. He had an extremely high IQ, an incredible amount of support, and the appropriate accommodation in school."

Casey Schwartz is a graduate of Brown University and has a master's in psychodynamic neuroscience from University College London. She has previously written for The New York Sun and ABC News. Currently, she's working on a book about the brain world. mexico tdah expertos tdah mitos tdah novedades tdah diapositivas tdah videos tdah cuento tdah motivación tdah