**2. EEG-biofeedback in ADHD**

Attention deficit/ hyperactivity disorder (ADHD) is a psychiatric disorder, characterized by symptoms of inattention and/or impulsivity and hyperactivity. These symptoms frequently co-exist with emotional, behavioural and learning deficits such as conduct disorder and oppositional defiant disorder, anxiety disorders and major depressive disorder (Barry et al., 2003). Prevalence in school-aged children is fairly high (3–12%) (Brown et al., 2001) and 30– 50% of these children will continue to experience symptoms into adulthood (Barry et al., 2003; Monastra, 2005). DSM-IV criteria allow the distinction of three ADHD subtypes: (1) the predominantly inattentive type, (2) the predominantly hyperactive-impulsive type and (3) the combined type, which exhibits symptoms of both inattention and hyperactivityimpulsivity (DSM-IV-TR; American Psychiatric Association, 2000).

Pharmacological intervention based on psychostimulant medication leads to a reduction of ADHD symptoms by increasing CNS arousal (Satterfield et al., 1974), but lacks long-term efficacy (Faraone & Buitelaar, 2010; Faraone & Glatt, 2010; Molina et al., 2009) and introduces adverse effects in 20-50% of the patients (Charach et al., 2004; Efron et al., 1997; Goldstein & Goldstein, 1990). Still, 35–45% of the patients with an "inattentive" type of ADHD and 10–30% of those diagnosed as "combined" type do not respond to medication, limiting the effectiveness of pharmaceutical intervention (Barkley, 1998; Hermens et al., 2006; Swanson et al., 1993). EEG biofeedback therapy for ADHD is one proposed alternative treatment and aims at restoring CNS arousal imbalances by training participants to suppress EEG rhythms associated with underarousal and enhance those rhythms associated with attention (J. F. Lubar & Shouse, 1976; Monastra et al., 2005; Thompson & Thompson, 1998).

### **2.1 Training duration and feedback**

An EBF training session consists of repeated training blocks of typically 3 minutes, each starting with a measure of baseline activity, like 5 minutes eyes-closed rest (J. O. Lubar & Lubar, 1984), within the specified frequency band in order to establish a target threshold value (Table 2). The participant will then attempt to match or exceed this value during a subsequent feedback trial by modulating activity within the set frequency band. The participant need not be aware of the underlying parameter(s) and is merely instructed to meet/exceed the threshold. Participants are encouraged to find their own optimal strategy to alter the brain activity. When the participant successfully exceeds the threshold, e.g., for 0.5 s (Monastra, 2005), a reward signal indicating success (e.g. a bonus point that can be traded for money or toys) is presented to reinforce learning. ADHD patients prefer smaller and immediate rewards to delayed, but larger ones (Loo & Barkley, 2005; Marco et al., 2009; Tripp & Alsop, 2001) and as the ADHD population largely consists of children, feedback protocols often involve video games where success is rewarded instantly (Drechsler et al., 2007; Leins et al., 2007).

#### **2.2 Target brain activity**

Spontaneous (resting-state) EEG profiles of ADHD children differ significantly from those of normally developing children, especially increased theta/beta ratio but also lowered alpha band activity has been reported (Barry & Clarke, 2009; Barry et al., 2003; Barry et al., 2009; Barry et al., 2003; Clarke et al., 2002; Clarke et al., 2001).

Attention deficit/ hyperactivity disorder (ADHD) is a psychiatric disorder, characterized by symptoms of inattention and/or impulsivity and hyperactivity. These symptoms frequently co-exist with emotional, behavioural and learning deficits such as conduct disorder and oppositional defiant disorder, anxiety disorders and major depressive disorder (Barry et al., 2003). Prevalence in school-aged children is fairly high (3–12%) (Brown et al., 2001) and 30– 50% of these children will continue to experience symptoms into adulthood (Barry et al., 2003; Monastra, 2005). DSM-IV criteria allow the distinction of three ADHD subtypes: (1) the predominantly inattentive type, (2) the predominantly hyperactive-impulsive type and (3) the combined type, which exhibits symptoms of both inattention and hyperactivity-

Pharmacological intervention based on psychostimulant medication leads to a reduction of ADHD symptoms by increasing CNS arousal (Satterfield et al., 1974), but lacks long-term efficacy (Faraone & Buitelaar, 2010; Faraone & Glatt, 2010; Molina et al., 2009) and introduces adverse effects in 20-50% of the patients (Charach et al., 2004; Efron et al., 1997; Goldstein & Goldstein, 1990). Still, 35–45% of the patients with an "inattentive" type of ADHD and 10–30% of those diagnosed as "combined" type do not respond to medication, limiting the effectiveness of pharmaceutical intervention (Barkley, 1998; Hermens et al., 2006; Swanson et al., 1993). EEG biofeedback therapy for ADHD is one proposed alternative treatment and aims at restoring CNS arousal imbalances by training participants to suppress EEG rhythms associated with underarousal and enhance those rhythms associated with attention (J. F. Lubar & Shouse, 1976; Monastra et al., 2005; Thompson & Thompson, 1998).

An EBF training session consists of repeated training blocks of typically 3 minutes, each starting with a measure of baseline activity, like 5 minutes eyes-closed rest (J. O. Lubar & Lubar, 1984), within the specified frequency band in order to establish a target threshold value (Table 2). The participant will then attempt to match or exceed this value during a subsequent feedback trial by modulating activity within the set frequency band. The participant need not be aware of the underlying parameter(s) and is merely instructed to meet/exceed the threshold. Participants are encouraged to find their own optimal strategy to alter the brain activity. When the participant successfully exceeds the threshold, e.g., for 0.5 s (Monastra, 2005), a reward signal indicating success (e.g. a bonus point that can be traded for money or toys) is presented to reinforce learning. ADHD patients prefer smaller and immediate rewards to delayed, but larger ones (Loo & Barkley, 2005; Marco et al., 2009; Tripp & Alsop, 2001) and as the ADHD population largely consists of children, feedback protocols often involve video games where success is rewarded instantly (Drechsler et al.,

Spontaneous (resting-state) EEG profiles of ADHD children differ significantly from those of normally developing children, especially increased theta/beta ratio but also lowered alpha band activity has been reported (Barry & Clarke, 2009; Barry et al., 2003; Barry et al., 2009;

impulsivity (DSM-IV-TR; American Psychiatric Association, 2000).

**2. EEG-biofeedback in ADHD** 

**2.1 Training duration and feedback** 

2007; Leins et al., 2007).

**2.2 Target brain activity** 

Barry et al., 2003; Clarke et al., 2002; Clarke et al., 2001).

The increased theta/beta ratio has been proposed as a characteristic biomarker for CNS underarousal (Mann et al., 1992), whereas the SMR has been classically described as reflecting motor inhibition (Sterman & Friar, 1972; Sterman et al., 1970). The vast majority of EBF studies has been inspired by a two-phase protocol of Lubar et al. (1984), in which participants where first trained to increase their SMR and later to inhibit theta activity while simultaneously increasing beta activity (Beauregard & Levesque, 2006; Carmody et al., 2000; Fuchs et al., 2003; Gevensleben et al., 2009; Heywood & Beale, 2003; Holtmann et al., 2009; Kaiser, 1997; Kaiser & Othmer, 2000; Kropotov et al., 2005; La Vaque et al., 2002; Leins et al., 2007; Levesque et al., 2006; Linden et al., 1996; J.F. Lubar et al., 1995; Monastra et al., 2002; Rossiter, 2004; Rossiter, 1998; Rossiter & La Vaque, 1995; Strehl et al., 2006; Thompson & Thompson, 1998).

Fig. 2. Brain activity profiles in children with ADHD differ from healthy controls. Theta/beta-band activity ratio is strongly elevated in ADHD, but differs in spatial localization between combined (AD/HDcom) and inattentive (AD/HDin) subtypes. (From: Barry et al., 2003.).

In recent years, however, an interesting new target for EBF has been found in the form of slow cortical potentials (SCPs). These slow event-related DC shifts represent excitation thresholds of large neuronal assemblies and training ADHD patients to increase SCPs robustly improves symptoms of ADHD (Doehnert et al., 2008; Drechsler et al., 2007; Gevensleben et al., 2009; Heinrich et al., 2007; Kropotov et al., 2005; Leins et al., 2007; Siniatchkin et al., 2000; Strehl et al., 2006).

EEG-Biofeedback as a Tool to Modulate Arousal:

affected by the arousal dysfunction.

**3. EBF as treatment of insomnia** 

insomnia and complete the vicious circle.

**2.3 Efficacy of EEG-biofeedback in the treatment of ADHD** 

any reported adverse effects so far (Leins et al., 2007; Monastra et al., 2005).

Trends and Perspectives for Treatment of ADHD and Insomnia 437

The first study of EBF in ADHD (J. F. Lubar & Shouse, 1976) reported improved attention and normalized levels of arousal, together with improved grades and achievement scores for the (eight) children under treatment. Subsequent studies have reported similarly positive results, showing improvements of behaviour, attention and impulsivity (Alhambra et al., 1995; Carmody et al., 2000; Drechsler et al., 2007; Gevensleben et al., 2010; Gevensleben et al., 2009; Heinrich et al., 2004; Kaiser & Othmer, 2000; Kropotov et al., 2005; Leins et al., 2007; Linden et al., 1996; J.F. Lubar et al., 1995; J. F. Lubar, 1991; Rossiter, 1998; Rossiter & La Vaque, 1995; Strehl, et al., 2006; Thompson & Thompson, 1998; Doehnert et al., 2008). Efficacy of EBF is comparable to psychostimulant medication and group (CBT) therapy programs with effects lasting 6 months and longer (Fuchs et al., 2003; Gani et al., 2009; Gevensleben et al., 2010; Kaiser, 1997; Leins et al., 2007; Linden et al., 1996; J.F. Lubar et al., 1995; Monastra et al., 2002; Rossiter & La Vaque, 1995; Thompson & Thompson, 1998). Overall, EBF treatment results in clinical improvement in about 75% of the cases, without

It should be noted, however, that the use of the theta/beta ratio as marker of general arousal has been questioned, because it does not correlate with skin conductance level (R.J. Barry & Clarke, 2009; R.J. Barry et al., 2009). Similarly, SCPs are no direct correlates of arousal but rather represent attentional processes (Siniatchkin et al., 2000). This raises the interesting notion that in ADHD, EBF may not restore or modulate arousal systems per se, but compensate underarousal by strengthening cognitive functions that have been negatively

Insomnia is a most pervasive disorder, affecting about 15% of the general population while 6% meet clinical (DSM-IV) criteria (Ohayon, 2002) and interferes with cognition, quality of life, job performance and represents a multi-billion dollar burden on healthcare providers (Daley et al., 2009; Ebben & Spielman, 2009; Edinger et al., 2004). Insomnia can be subdivided into primary and co-morbid insomnia with the most salient symptoms being difficulty initiating and/or maintaining sleep (Espie, 2007). Causes of primary insomnia include physiological, cognitive and behavioural factors (Espie, 2007). Symptoms and

To better understand the possible therapeutic targets of insomnia, the so-called "3P model" has been proposed (Ebben & Spielman, 2009). This model specifies three categories of factors influencing the risk at developing or worsening insomnia: predisposing, precipitating and perpetuating factors. The first category constitutes genetic factors or personality traits, such as increased basal level of anxiety or hyperarousal (Drake et al., 2004), whereas precipitating events represent work and educational stress together with health and emotional problems (Bastien et al., 2004). Finally, perpetuating factors, such as continuous stress and poor sleep hygiene, may cause the actual transition to chronic

Pharmacological treatment of insomnia with sedative-hypnotic agents has seen a steady decline over the past (Aldrich, 1992; Walsh & Schweitzer, 1999), because of side effects, discontinuation discomfort, and the risk of developing drug tolerance or dependency (Ebben & Spielman, 2009; Walsh & Schweitzer, 1999). Alternative treatment options that have been met with success are cognitive-behavioural therapy (CBT) (Ebben & Spielman, 2009; Espie, 1999; Morin et al., 1999; Morin et al., 1994; Murtagh & Greenwood, 1995; Siebern & Manber, 2010) or treatments

duration are related to severity and persistence of stressors (Morin et al., 2006).


  **P/R/B= Placebo/Randomized/Blind (- = no, + = yes). N(m):** Number of participants (males)**, Freq.:**  Target frequency (increase/decrease) of EBF condition(s).

Table 2. EBF therapy focused at treating ADHD is an active field of research.

**/Ref** 

CPz & Cz/A2

C3 or C4/A1+A2

C3/A2 or C4/A1

**Freq. Stim/** 

 

SMR 

 

Cz/A1+A2 SCP Visual

 SCP

Cz/A1+A2 SCP Visual

 SCP

Cz/A1 SMR

**Reward** 

Visual & auditory /Money

Visual & auditory /Points

Visual & auditory

Visual & auditory (video game)

/Points

Visual /Points

/Points

Visual 2x9

**#Ses./ Dur.** 

43 (34– 50) / 30–40 min

36 / 30-60 min

40 or >60 /30 or 36 min

40 / 60 min

2x15 /2x45 min

30 /60 min

2x15 /2x45 min

/2x 50 min

**N (m) Age Electrodes**

 

 

 

 

 

  [ CF3,CF4/ A1+A2 

Cz/A1+A2

Cz/A1+A2

 

 

 

Table 2. EBF therapy focused at treating ADHD is an active field of research.

 **P/R/B= Placebo/Randomized/Blind (- = no, + = yes). N(m):** Number of participants (males)**, Freq.:** 

**Study Control** 

Monastra et al., 2002

Fuchs et al., 2003

Rossiter, 2004

Lévesque et al., 2006

Drechsler et al., 2007

Leins et al., 2007

Doehnert et al., 2008

Gevensleben et al., 2009

**P/R/B**




+/+/-





Target frequency (increase/decrease) of EBF condition(s).

 

 

 

 

 

 

 

 
