TRATAMIENTO FARMACOLOGICO T DEFICIT ATENCIONAL

UNIVERSIDAD DE CHILE / FACULTAD DE MEDICINA

TDAH: Manejo farmacológico

Dra. Carolina Heresi Neuropediatra


Menú

•  Objetivos del tratamiento •  Manejo farmacológico

– Psicoestimulantes – Otras alternativas

•  Conclusiones


Manejo: Principios

•  Manejo como condición crónica •  Establecer objetivos

– Niño, familia, colegio

•  Tratamiento farmacológico – Monoterapia

•  Terapia conductual – Conductas oposicionistas persistentes

Rapley, NEJM 2005 352;2:165


Manejo: Principios

•  Manejo como condición crónica •  Establecer objetivos

– Niño, familia, colegio

•  Tratamiento farmacológico – Monoterapia

•  Terapia conductual – Conductas oposicionistas persistentes Hábitos: horario tareas, pantalla, SUEÑO


¿Cuáles pueden ser los objetivos del manejo?


Objetivos

•  Mejorar relaciones – Familia, compañeros, profesores

•  Disminuir conducta disruptiva •  Mejorar la calidad y eficiencia trabajo

académico •  Aumentar la independencia •  Mejorar autoestinma •  Aumentar seguridad

Rapley, NEJM 2005 352;2:165


Manejo Farmacológico


¿Cómo se regula la atención?


Atención: Normal

SOSTENIDA

•  Atención en UNA tarea •  Largo aliento

DIVIDIDA

•  Atención en varios estímulos

•  Corto aliento


Atención: TDAH

SOSTENIDA


DIVIDIDA




Dopamina

Dopamina:

•  Liberación Fásica: orientación de la atención

•  Liberación Tónica: atención sostenida

•  Genes TDAH


Atención: TDAH

SOSTENIDA


DIVIDIDA




Atención: TDAH

SOSTENIDA


DIVIDIDA



Metilfenidato


Psicoestimulantes •  Metilfenidato

–  Aumenta Dopamina y NorA espacio sináptico –  Bloquea transportador DAT –  Aumenta descargas Dopamina en relación a

una tarea, por lo que la hace más relevante –  0,3-0,8 mg/kg/d, 1-2 dosis

•  Anfetamina –  Bloquea recapatación Dopamina y NorA –  Aumenta liberación Dopamina –  Inhibe MAO (disminuye metabolismo Dopamina) –  0,15-0,5 mg/kg/d


¿Qué hace el Metilfenidato?

•  Mejora la impulsividad, atención sostenida, memoria de trabajo

•  Efecto en U invertida:





of performance in a cognition/learning task, while classroombehavior was improved across a wider dose range. However,subsequent studies generally failed to observe differentialsensitivity to MPH dose across a range of cognitive tasksversus overt behavior in ADHD patients (94–96). Importantly,Sprague and Sleator (93) used a memory task that involvedshort delays (seconds), typical of PFC-dependent workingmemory tasks, while subsequent studies examined otherforms of cognition (94). MPH was also observed to producea narrow inverted-U shaped improvement in a PFC-dependenttest of response inhibition in ADHD patients while eliciting agenerally linear dose-dependent improvement in behavioral/motor activity (96).

These observations could suggest that psychostimulantsexert differential dose-dependent effects on PFC-dependentversus PFC-independent processes. However, when thedose-dependent actions of MPH were compared acrossworking memory and sustained attention tasks, two PFC-dependent tasks (97) (Figure S2 in Supplement 1), a narrower,left-shifted inverted-U curve was observed for working mem-ory versus sustained attention (98) (Figure 6). A similar shift indose response curves across these tasks occurs with MPHinfusion directly into the dmPFC (99). Prior studies havesuggested that PFC NE may differentially regulate flexibleversus focused attention (100,101). Sustained attentionrequires little cognitive flexibility, relative to working memory.

However, when examined in a PFC-dependent attentionalset-shifting task typically used to measure flexible attention(102,103), MPH elicited dose-dependent improvements inperformance identical to sustained attention (98) (Figure 6).Collectively, these observations indicate that differing PFC-dependent cognitive processes display differing dose sensi-tivity to MPH that are not predicted by the degree to whichthey are associated with cognitive flexibility.

As reviewed above, noradrenergic α2 receptors improve,while α1 receptors impair, working memory (104). In contrast,α1 receptors improve attentional set shifting, while α2receptors have little impact in this task (100). These observa-tions suggest the hypothesis that the narrow versus broadinverted-U shaped actions of psychostimulants describedabove involve differential activation of α2 receptors versusα1 receptors, respectively. Consistent with this, MPH-inducedimprovement in working memory is dependent on α2-recep-tors [see above (104)], while MPH-induced improvement insustained attention is dependent on α1 receptors (98).

IMPLICATIONS FOR DIVERGENT DOSE-RESPONSECURVES ACROSS PFC-DEPENDENT PROCESSES

Preclinically, the differential dose sensitivity of PFC-dependenttasks to psychostimulants suggests that not all PFC-depen-dent tasks are well suited for ADHD-focused drug discoveryprograms. Extensive evidence demonstrates that the pharma-cology of working memory mirrors the pharmacology ofADHD: all approved ADHD-related drugs, including α2 ago-nists (105), low-dose psychostimulants (5,25), and selectiveNE reuptake blockers (e.g., atomoxetine) (34) improve workingmemory. For psychostimulants, their beneficial effects onworking memory only occur across a narrow range of dosesthat produce clinically relevant plasma concentrations (32,33,37,105,106). Thus, delayed response tests of working memoryare a well-suited preclinical tool for identifying potentiallyefficacious compounds for use in ADHD and possibly otherclinical conditions associated with PFC dysfunction.

In contrast, in sustained attention, attentional set shifting, andfive-choice serial reaction time tests, MPH exerts maximal bene-ficial actions at higher, behaviorally activating, and impulsivity-promoting doses that result in blood concentrations that exceedthe clinically relevant range (33,37,107,108) (Figure 1). Moreover,limited observations indicate that α2 agonists lack beneficial effectson attentional set shifting (100), as well as sustained attention(JL Berkowitz, Ph.D., BD Waterhouse, Ph.D., JS Shumsky, Ph.D.,unpublished observations, 2011). Thus, the potential utility of thesetests in an ADHD-focused preclinical program is less clear.

Clinically, as suggested by Sprague and Sleator (93) andTannock et al. (96), differential actions of psychostimulantsacross cognitive processes raise the question of whetherdoses that are optimal for controlling classroom behaviorimpair, or no longer improve, cognitive/behavioral processesimportant for other functional domains. For example, largelyanecdotal evidence suggests that cognitive constriction oroverfocusing can be a side effect of psychostimulant treat-ment (96). This action may be related to the ability of higherdoses of MPH to improve attentional processes while impair-ing certain forms of cognitive flexibility evinced in tests ofworking memory and response inhibition (96,98,107). If so, the

Figure 6. Different prefrontal cortex dependent cognitive tasks showdifferential sensitivity to methylphenidate (MPH). Methylphenidate exerts arelatively narrow inverted-U shaped facilitation of working memory perfor-mance (A), with maximal improvement seen following .5 mg/kg intraperito-neal. In contrast, MPH exerts a right-shifted dose-dependent facilitation ofsustained attention (A) and attentional set shifting (B). Importantly, doses thatimprove sustained attention and attentional set shifting impair performance inworking memory (2.0 mg/kg). *p , .05; **p , .01 compared with vehicle(VEH) treatment. [Data reproduced with permission from Berridge et al. (98).]

Psychostimulant Cognitive Enhancement: Role of the PFC

Biological Psychiatry ]]], 2014; ]:]]]–]]] www.sobp.org/journal 7

BiologicalPsychiatry

Spencer, 2014. h/p://dx.doi.org/10.1016/j.biopsych.2014.09.013





of performance in a cognition/learning task, while classroombehavior was improved across a wider dose range. However,subsequent studies generally failed to observe differentialsensitivity to MPH dose across a range of cognitive tasksversus overt behavior in ADHD patients (94–96). Importantly,Sprague and Sleator (93) used a memory task that involvedshort delays (seconds), typical of PFC-dependent workingmemory tasks, while subsequent studies examined otherforms of cognition (94). MPH was also observed to producea narrow inverted-U shaped improvement in a PFC-dependenttest of response inhibition in ADHD patients while eliciting agenerally linear dose-dependent improvement in behavioral/motor activity (96).

These observations could suggest that psychostimulantsexert differential dose-dependent effects on PFC-dependentversus PFC-independent processes. However, when thedose-dependent actions of MPH were compared acrossworking memory and sustained attention tasks, two PFC-dependent tasks (97) (Figure S2 in Supplement 1), a narrower,left-shifted inverted-U curve was observed for working mem-ory versus sustained attention (98) (Figure 6). A similar shift indose response curves across these tasks occurs with MPHinfusion directly into the dmPFC (99). Prior studies havesuggested that PFC NE may differentially regulate flexibleversus focused attention (100,101). Sustained attentionrequires little cognitive flexibility, relative to working memory.

However, when examined in a PFC-dependent attentionalset-shifting task typically used to measure flexible attention(102,103), MPH elicited dose-dependent improvements inperformance identical to sustained attention (98) (Figure 6).Collectively, these observations indicate that differing PFC-dependent cognitive processes display differing dose sensi-tivity to MPH that are not predicted by the degree to whichthey are associated with cognitive flexibility.

As reviewed above, noradrenergic α2 receptors improve,while α1 receptors impair, working memory (104). In contrast,α1 receptors improve attentional set shifting, while α2receptors have little impact in this task (100). These observa-tions suggest the hypothesis that the narrow versus broadinverted-U shaped actions of psychostimulants describedabove involve differential activation of α2 receptors versusα1 receptors, respectively. Consistent with this, MPH-inducedimprovement in working memory is dependent on α2-recep-tors [see above (104)], while MPH-induced improvement insustained attention is dependent on α1 receptors (98).

IMPLICATIONS FOR DIVERGENT DOSE-RESPONSECURVES ACROSS PFC-DEPENDENT PROCESSES

Preclinically, the differential dose sensitivity of PFC-dependenttasks to psychostimulants suggests that not all PFC-depen-dent tasks are well suited for ADHD-focused drug discoveryprograms. Extensive evidence demonstrates that the pharma-cology of working memory mirrors the pharmacology ofADHD: all approved ADHD-related drugs, including α2 ago-nists (105), low-dose psychostimulants (5,25), and selectiveNE reuptake blockers (e.g., atomoxetine) (34) improve workingmemory. For psychostimulants, their beneficial effects onworking memory only occur across a narrow range of dosesthat produce clinically relevant plasma concentrations (32,33,37,105,106). Thus, delayed response tests of working memoryare a well-suited preclinical tool for identifying potentiallyefficacious compounds for use in ADHD and possibly otherclinical conditions associated with PFC dysfunction.

In contrast, in sustained attention, attentional set shifting, andfive-choice serial reaction time tests, MPH exerts maximal bene-ficial actions at higher, behaviorally activating, and impulsivity-promoting doses that result in blood concentrations that exceedthe clinically relevant range (33,37,107,108) (Figure 1). Moreover,limited observations indicate that α2 agonists lack beneficial effectson attentional set shifting (100), as well as sustained attention(JL Berkowitz, Ph.D., BD Waterhouse, Ph.D., JS Shumsky, Ph.D.,unpublished observations, 2011). Thus, the potential utility of thesetests in an ADHD-focused preclinical program is less clear.

Clinically, as suggested by Sprague and Sleator (93) andTannock et al. (96), differential actions of psychostimulantsacross cognitive processes raise the question of whetherdoses that are optimal for controlling classroom behaviorimpair, or no longer improve, cognitive/behavioral processesimportant for other functional domains. For example, largelyanecdotal evidence suggests that cognitive constriction oroverfocusing can be a side effect of psychostimulant treat-ment (96). This action may be related to the ability of higherdoses of MPH to improve attentional processes while impair-ing certain forms of cognitive flexibility evinced in tests ofworking memory and response inhibition (96,98,107). If so, the

Figure 6. Different prefrontal cortex dependent cognitive tasks showdifferential sensitivity to methylphenidate (MPH). Methylphenidate exerts arelatively narrow inverted-U shaped facilitation of working memory perfor-mance (A), with maximal improvement seen following .5 mg/kg intraperito-neal. In contrast, MPH exerts a right-shifted dose-dependent facilitation ofsustained attention (A) and attentional set shifting (B). Importantly, doses thatimprove sustained attention and attentional set shifting impair performance inworking memory (2.0 mg/kg). *p , .05; **p , .01 compared with vehicle(VEH) treatment. [Data reproduced with permission from Berridge et al. (98).]

Psychostimulant Cognitive Enhancement: Role of the PFC

Biological Psychiatry ]]], 2014; ]:]]]–]]] www.sobp.org/journal 7

BiologicalPsychiatry

Spencer, 2014. h/p://dx.doi.org/10.1016/j.biopsych.2014.09.013


Psicoestimulantes

•  Respuesta depende de: – TDAH/TDA – Dosis (por Kg) – Duración del efecto

•  Metabolismo propio del niño •  Presentación farmacológica

•  No hay tolerancia largo plazo


Psicoestimulantes •  Respuesta depende

de: –  TDAH/TDA – Dosis (por Kg) – Duración del efecto

•  Metabolismo propio del niño

•  Presentación farmacológica

•  No hay tolerancia largo plazo

MUY IMPORTANTE!!

Monitorizar la terapia en el tiempo:

Control médico

Reporte escolar


Psicoestimulantes

•  Reacciones adversas: – Conocidas – Leves en general

– Apetito disminuido – Cefalea – Aumento presión arterial –  Agitación, irritabilidad, mareos, alergia, temblor, otros


Otras alternativas

•  Atomoxetina –  Disminuye la recaptura NorAdrenalina –  Aumenta niveles sinápticos NorA y Dopamina en corteza

prefrontal (no en estriado: no adicción) –  0,5 a 1,2mg/kg/d, titulación lenta –  Eficacia similar a metilfenidato, segunda línea

–  Meta-análisis: Atomoxetina vs metilfenidato •  Mejor respuesta en MFD liberación prolongada (Hanwella, 2011)


Otras alternativas

•  Modafinilo –  Mecanismo poco claro (potencia activ alfa1 adrenérgica,

y dopamina) –  Mejora la VIGILIA: uso en Narcolepsia –  NO está aprobado para uso en TDAH en niños por RAM

dermatológicos GRAVES

•  Otros: clonidina, pemolina


Preguntas frecuentes

•  ¿Cuanto tiempo hay que tomarlo? •  ¿Afectan el crecimiento? •  ¿Provocan adicción? •  ¿Favorecen otras adicciones?

•  Uso en Epilepsia •  Uso en Dislexia


Adicciones ¿Cuál es la relación con los psicoestimulantes?

–  Anfetaminas en altas dosis disminuyen adicción a cocaína

–  En niños con TDAH el tratamiento protege contra el trastorno por uso de sustancias

–  Potencial adictivo psicoestimulantes no está establecido en niños

–  Preferir liberación prolongada y uso regular (no basado en la necesidad)

Himanshu, J Clin Psychiatry 2007,68S11:23)


Pediatrics 2003;111:179 –185

•  Meta-análisis –  6 estudios –  Niños, adolescentes y adultos con TDAH –  Prevalencia Tr uso sustancias en adolescentes y adultos

(no nicotina), seguimiento mínimo 4 años –  674 expuestos/360 no expuestos a piscoestimulantes

–  En 4/6 estudios se explicita similares características grupo tratado/no tratado


Pediatrics 2003;111:179 –185

•  Meta-análisis –  6 estudios –  Niños, adolescentes y adultos con TDAH –  Prevalencia Tr uso sustancias en adolescentes y

adultos (no nicotina), seguim min 4 años –  674 expuestos/360 no expuestos piscoestimulantes

–  En 4/6 estudios se explicita similares características grupo tratado/no tratado

Tratamiento con psicoestimulantes reduce el riesgo de Tr uso de sustancias 1.9 veces (IC95% 1,1-3,6).

Mayor impacto en adolescentes (OR:5,8) que en adultos (OR 1,4)






Condiciones especiales

•  Epilepsia (Dunn, Semin Pediatr Neurol 2006,12:222-228)

–  30-40% niños con epilepsia tiene TDA/H –  Psicoestimulantes hasta ahora son seguros y

eficaces (epilepsia controlada)






Dislexia

•  Psicoestimulantes – Mejoran memoria trabajo – Favorecen procesamiento fonológico

– Considerar uso en dislexia y TDA, incluso si los síntomas de TDAH son leves.


Guías Clínicas


•  Pre-escolares: terapia conductual, Metilfenidato

•  Escolares y Adolescentes: Psicoestimulantes + terapia conductual, otros fármacos 2ª línea

•  Considerar TDAH condición crónica y buscar comorbilidad

CLINICAL PRACTICE GUIDELINE

ADHD: Clinical Practice Guideline for the Diagnosis,Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents

abstract +

Attention-deficit/hyperactivity disorder (ADHD) is the most commonneurobehavioral disorder of childhood and can profoundly affect theacademic achievement, well-being, and social interactions of children;the American Academy of Pediatrics first published clinical recommen-dations for the diagnosis and evaluation of ADHD in children in 2000;recommendations for treatment followed in 2001. Pediatrics 2011;128:1007–1022

Summary of key action statements:

1. The primary care clinician should initiate an evaluation for ADHD forany child 4 through 18 years of age who presents with academic orbehavioral problems and symptoms of inattention, hyperactivity, orimpulsivity (quality of evidence B/strong recommendation).

2. To make a diagnosis of ADHD, the primary care clinician shoulddetermine that Diagnostic and Statistical Manual of Mental Disor-ders, Fourth Edition criteria have been met (including documenta-tion of impairment in more than 1 major setting); informationshould be obtained primarily from reports from parents or guard-ians, teachers, and other school and mental health clinicians in-volved in the child’s care. The primary care clinician should also ruleout any alternative cause (quality of evidence B/strongrecommendation).

3. In the evaluation of a child for ADHD, the primary care clinicianshould include assessment for other conditions that might coexistwith ADHD, including emotional or behavioral (eg, anxiety, depres-sive, oppositional defiant, and conduct disorders), developmental(eg, learning and language disorders or other neurodevelopmentaldisorders), and physical (eg, tics, sleep apnea) conditions (quality ofevidence B/strong recommendation).

4. The primary care clinician should recognize ADHD as a chroniccondition and, therefore, consider children and adolescentswith ADHD as children and youth with special health care needs.Management of children and youth with special health careneeds should follow the principles of the chronic care model andthe medical home (quality of evidence B/strong recommendation).

SUBCOMMITTEE ON ATTENTION-DEFICIT/HYPERACTIVITYDISORDER, STEERING COMMITTEE ON QUALITYIMPROVEMENT AND MANAGEMENTKEY WORDSattention-deficit/hyperactivity disorder, children, adolescents,preschool, behavioral therapy, medication

ABBREVIATIONSAAP—American Academy of PediatricsADHD—attention-deficit/hyperactivity disorderDSM-PC—Diagnostic and Statistical Manual for Primary CareCDC—Centers for Disease Control and PreventionFDA—Food and Drug AdministrationDSM-IV—Diagnostic and Statistical Manual of Mental Disorders,Fourth EditionMTA—Multimodal Therapy of ADHD

This document is copyrighted and is property of the AmericanAcademy of Pediatrics and its Board of Directors. All authorshave filed conflict of interest statements with the AmericanAcademy of Pediatrics. Any conflicts have been resolved througha process approved by the Board of Directors. The AmericanAcademy of Pediatrics has neither solicited nor accepted anycommercial involvement in the development of the content ofthis publication.

The recommendations in this report do not indicate an exclusivecourse of treatment or serve as a standard of medical care.Variations, taking into account individual circumstances, may beappropriate.

www.pediatrics.org/cgi/doi/10.1542/peds.2011-2654

doi:10.1542/peds.2011-2654

All clinical practice guidelines from the American Academy ofPediatrics automatically expire 5 years after publication unlessreaffirmed, revised, or retired at or before that time.

PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

Copyright © 2011 by the American Academy of Pediatrics

FROM THE AMERICAN ACADEMY OF PEDIATRICS

Guidance for the Clinician inRendering Pediatric Care

PEDIATRICS Volume 128, Number 5, November 2011 1007 by guest on March 26, 2012pediatrics.aappublications.orgDownloaded from

Pediatrics 2011, 128: 1007-‐1022


En Chile •  Guía Mineduc (Nov 2009)

•  Minsal –  Programa “Tr hipercinéSco de la conducta” (Consultorios, COSAM)

– Atención Hospitalaria (PsicoesSmulantes)


Se han propuesto otros manejos…


Flores de Bach

•  Dr. Edward Bach (1886-1936) –  La energía de las flores puede restaurar los

estados negativos que causan enfermedad –  Flores frescas en agua, con Brandy como

preservante

•  Actualmente con amplia difusión fuera del ámbito médico


Flores de Bach •  Revisión Sistemática (2011)

–  Edzard Ernst, Dpto. Medicina Complementaria, U. Exeter/U. Plymouth

– 86 artículos sobre Flores de Bach •  Se eligieron sólo los ensayos clínicos

controlados (7/86) •  Sólo uno en niños con TDA (Pintov, 2005)

–  SIN DIFERENCIA ENTRE FLORES BACH Y PLACEBO

but at other issues (e.g., expectancy) were excluded [14,15].

Data were validated and extracted by the author ac-cording to predefined criteria (table 1). When informationwas insufficient, the authors of the study in question wereapproached to obtain more details. Methodological qualitywas assessed using the Jadad scale [16], which quantifiesthe likelihood of bias inherent in trials on the basis of theirdescription of randomisation, blinding, and withdrawals;this score ranges from a minimum of 0 to a maximum of 5points. The validity of the primary trials was estimated ona score ranging from 0 to 3 points (one point was given fora positive answer for each of the three questions: Was thestudy sample relevant? Was the intervention appropriate?Was the outcome measure suitable?). Due to the statisticaland clinical heterogeneity of the primary data, no statisticalpooling was performed.ADHD = attention deficit hyperactivity disorderVAS = visual analogue scale

Results

Seven RCTs met the inclusion criteria [17–23]. Three ofthem [17–19] had already been available for the previoussystematic review [5] and four had been included in the re-views by Thaler et al. [6] or Halberstein et al. [7]. Figure 1provides a flow chart of the articles located and included.

Figure 1

Flow chart of publications.

Table 1Randomised clinical trials of Flower Remedies (Flower Remedies).Reference Study design Jadad

scoreValidityscore

Sample Interventions Main outcomemeasures

Main result Comment

von Rühle(1995)[17]

RCT, 3 parallelgroups(not placebocontrolled, notdouble-blinded)

2 3 24 pregnantwomen withoverdue births

Individualised flowerremedies dailyup to date of birth,attention control group (noflower remedies),no such therapies,(all groups had standardcarein addition)

Time to birth,type of birth,use of medicationduring birth,anxiety during birth,well-being

Significantly lessmedication wasused in group A(p = 0.032)

Birth was delayed in group A by5.1 days, in groups B by 6.6and in group C by 4.4 days

Armstrong(1999)[18]

RCT, double-blind,2 parallel arms

5 3 100 healthyUniversitystudents sittingexams

‘Rescue Remedy’ (1–4doses during7 days before and duringexams)placebo (same treatmentschedule)

Anxiety measured withSpielberger State-Trait-Anxiety Inventory(SSTAI)

No significantdifferencesbetween groups

Study suffered from high drop-out rate

Walach(2001)[19]

RCT, double-blind, cross-over

5 3 51 healthystudents sittingexams

Rescue Remedy (4 dropsdaily for2 weeks or more ifnecessary)placebo (same treatmentschedule)

Anxiety measured withText-Anxiety Inventory


Primary authors conclude thatflower remedies are“an effective placebo”

Pintov(2005)[20]

RCT, double-blind,2 parallel arms

4 3 40 schoolchildrenwith ADHD

A) Rescue Remedy (4 drops4x perday for 3 months)B) placebo (same treatmentschedule)

Performanceevaluatedby teacher (Conner’squestionnaire)


17 drop outs

Toyota(2006)[21]

RCT, double-blind,2 parallelgroups

3 3 40 surgicalpatients

A) Rescue Remedy indrinking waterB) drinking water withoutRescueRemedy

Anxiety and tension(VAS)


Write-up is unclear in severalaspects

Halberstein(2007)[22]

RCT, double-blind,2 parallelgroups

2 3 111 studentsunder stressfulexam situa-tion

A) Rescue Remedy (5doses during a3 hour class)B) placebo

Anxiety measured withSSTAI


A subanalysis of high anxietystudents favouredA over B

Forshaw(2009)[23]

RCT, single-blind,3 parallelgroups

4 3 62 studentsunderexperimentalstress

Rescue Remedy (4 drops inwater)Placebo (pure water +participants were told that itcontained Rescue Remedy)Placebo (pure water +participants were told that itwas water)

Stress (VAS) No significantdifferencesbetween groups

All groups reported stressreduction regardless oftreatment

Review article Swiss Med Wkly. 2010;140:w13079

Swiss Medical Weekly · PDF of the online version · www.smw.ch Page 2 of 4


Gamalate (y alternativas)

•  Vitamina B6 + GABA + GABOB + Bromhidrato de glutamato de magnesio

•  No es claro que atraviesen BHE

•  NO existen estudios –  En animales –  En niños ni adultos sanos –  En niños ni adultos con TDA


Conclusiones


Tratamiento

•  Orientado por objetivos •  Estrategias ambientales •  Manejo farmacológico

–  Tiene indicaciones claras –  Es eficaz y seguro (pero no hace magia) –  No se relaciona con adicciones –  Siempre debe monitorizarse y ajustarse según

necesidad: CONTROL MÉDICO

Health & Medicine

TRATAMIENTO FARMACOLOGICO T DEFICIT ATENCIONAL