Inhibitory control is an important component of executive function that allows for the suppression of actions and resistance to interference from irrelevant stimuli. Dysfunctional inhibitory control is increasingly being recognised as an important component to a number of neuropsychiatric disorders. This paper reviews neuropsychological and neuroimaging research which documents impaired inhibitory control in Attention Deficit Hyperactivity Disorder, Autism, Tourette’s syndrome, Obsessive-Compulsive Disorder, and Schizophrenia, with a focus on different patterns of impaired cognitive and motor inhibition and related activity in the fronto-striatal circuitry.
Inhibitory control can be defined as a range of mechanisms that allow the suppression of previously activated cognitions and inappropriate actions and resistance to interference from irrelevant stimuli (Bjorklund & Harnishfegar, 1995). Essentially, inhibitory control is the ability to suppress the processing or expression of information that would disrupt the efficient completion of the goal at hand (Dempster, 1992). This key executive function allows for the control of complex cognition and behaviour and is essential for effective interaction with our environment (Burke et al., 1991). Inhibitory control is important in attention, memory, and intelligence and is related to social competence and emotional regulation (Kochanska et al., 1996). Inhibitory control is also related to impairment in a range of different neuropsychiatric disorders (Peterson et al., 1998), producing different patterns of deficits in clinical populations. This essay will examine inhibitory control as evidenced by neuropsychological findings and attempt to examine the neural correlates of such deficits, focusing on five neuropsychiatric disorders in which inhibitory control is particularly important: Attention Deficit Hyperactivity Disorder, Autism, Tourette’s syndrome, Obsessive-Compulsive Disorder, and Schizophrenia.
Attention Deficit Hyperactivity Disorder (ADHD) is a mental illness usually beginning in childhood, consisting of symptoms of inattention, impulsiveness, and hyperactivity that are inappropriate for the child’s age (APA, 2000). Inhibitory control is increasingly being recognised as central to ADHD, as a defining characteristic of ADHD is a persistent inability to control behaviour in a number of areas (Durston, 2003). Barkley (1997) proposed that an initial inability to inhibit a inappropriate pre-potent response causes all the other cognitive deficits observed in ADHD, such as problems with working memory. Thus, for Barkley, ADHD is a disorder that is mediated entirely by poor inhibitory control. In everyday settings, ADHD children demonstrate high levels of behaviour signalling poor inhibitory control, such as talking to themselves (Berk & Potts, 1991). They also have problems stopping specific behaviours when asked to do so (Barkley & Ullman, 1975) and have problems resisting temptation (Hinshaw, Simmel & Heller, 1995) and delaying gratification (Barkley & Ullman, 1975). A number of experimental findings also demonstrate poor inhibitory control in ADHD. In tasks requiring inhibition of a prepotent response, ADHD subjects commit more errors of commission (Vaidya et al., 1998) and demonstrate higher levels of interference suppression (Scheres et al., 2003). Performance is impaired on tasks of motor inhibition, such as delayed response tasks (Sonuga-Barke et al. 1992) and stop-signal tasks (Schachar & Logan, 1990). ADHD children also show deficits on cognitive inhibition tasks such as the Wisconsin Card Sorting Test and Stroop Test (Barkley, Grodzinsky, & DuPaul, 1992). Deficient inhibitory control is also apparent in those at risk of ADHD (Crosbie & Schachar, 2001), suggesting that it may be a causal factor. Whilst most models accept that inhibitory control is not the sole causal factor for ADHD symptomatology (Willicutt et al., 2005), it is certainly a key symptom in the illness, which is ameliorated through successful medication-based treatment (Aron et al., 2003).
Neuroimaging research is beginning to shed light on the neurological mechanisms underlying impaired inhibitory control in ADHD. During a Go/NoGo task, striatal activation has been found to be reduced in children and adolescents with ADHD (Durston et al., 2003; Rubia et al., 1999), whilst activity in ventrolateral prefrontal cortical areas is increased (Schulz et al., 2004). Using the same task, prefrontal cortical activity has been found to be reduced in ADHD children (Durston et al., 2003). This suggests fronto-striatal deficits mediate impaired motor inhibitory control in ADHD. Cognitive inhibition has also been studied, with reduced anterior cingulate cortex activity apparent during performance of the Stroop Task in ADHD adolescents (Bush et al., 1999). Research using transcranial magnetic stimulation suggests impaired inhibitory mechanisms in the motor regulation system in ADHD (Moll et al., 2000). Event-Related-Potential studies have shown reduced N2 amplitudes during NoGo trials in ADHD, and that wave amplitude correlates with performance (Overtoom et al., 2002). Finally, research has suggested greater frontal involvement in correct NoGo trials (Vaidya et al., 1998), essentially suggesting a greater effort to correctly inhibit a response.
Autism is a pervasive developmental disorder characterised by deficits in language and social interactions and repetitive stereotyped behaviour, with an onset usually before age 3 (APA, 2000). In recent years the executive function model of autism (Ozonoff et al., 1991) has received increasing interest. Within this executive function model, inhibitory control has been found to be disrupted in autism. A number of the symptoms of autism such as context-inappropriate behaviour suggest that response inhibition processes are impaired (Kana et al., 2007). Prepotent inhibition as measured by the Go/NoGo task has been found to be impaired in autistic individuals, even after controlling for IQ (Ozonoff et al., 1994). Performance on the NEPSY Knock-Tap task further demonstrates such deficits (Joseph, McGrath & Tager-Flusberg, 2005), as does performance on eye-movement inhibition tasks (Luna et al., 2006). Cognitive inhibition also appears to be impaired, as those with autism perform poorly on the Stroop task (Kleinhans, Akshoomoff & Delis, 2005) and Wisconsin Card Sorting Task (Ozonoff & McEvoy, 1994). Increased preservative behaviour on cognitive inhibition tasks is also apparent (Ozonoff, Pennington & Rogers, 1991; Prior & Hoffman, 1990). Failures of inhibition of a prepotent response appear to be particularly persistent in autism (Ozonoff et al., 1994). In normal children, inhibitory control has been found to be strongly related to the development of theory of mind (Carlson & Moses, 2001; Carlson, Moses & Claxton, 2004). Therefore it is plausible that an early deficit in inhibitory control may represent a causal factor for impaired theory of mind in autism. Inhibitory control impairments have been hypothesised to underlie a number of autistic symptoms, such as repetitive behaviours and obsessionality (Schmitz et al, 2006), cognitive and motor inflexibility (Baron-Cohen, 2004), and language deficits (Joseph & Tager-Flusberg, 2004).
There is also research suggesting a neurological basis for such impairments in inhibitory control in autism. Anagnostou et al. (2006) used an fMRI scanner during performance of a Go/Nogo task in autistic individuals, finding that subjects displayed decreased activation in the caudate nucleus and anterior cingulate cortex. This suggests that problems with frontostriatal circuitry in autism may relate to repetitive behaviours. Kana et al. (2007) replicated this finding of decreased activation in the anterior cingulate cortex and also found that autistic individuals show poor synchronisation between elements of the inhibition network, namely the insula and anterior and middle cingulate gyrus. Sub-activation was also found in inferior frontal and right inferior parietal regions. The authors suggest that this indicates that in autism, inhibitory neural mechanisms are under-activated and poorly synchronised, so that inhibition is successfully achieved by voluntary control rather than automatic mechanisms (Kana et al., 2007). This is further supported by the finding that autistic individuals show increased activation in the left insula, left inferior, and orbital frontal gyrus, suggesting an increased effort to inhibit responses (Schmitz et al., 2006).
Tourette’s syndrome (TS) is a neuropsychiatric disorder characterised by chronic vocal and motor tics (APA, 2000), which usually present at 5-7 years old (Robertson, 2000). A number of symptoms in TS such as ecoholalia, echopraxia, copropraxia, coprolalia, repetitive movement, urges to perform socially inappropriate acts, and other ‘disinhibited’ behaviours suggest a failure of inhibitory control (Cohen & Leckman, 1992; Kurlan et al., 1996). As such it has been suggested that impaired inhibitory control may relate to the core symptoms of TS (Rankins, Bradshaw & Georgiou-Karistianis, 2006). Until recently, such behaviours and tics were assumed to be involuntary, representing a total failure of inhibitory control. However, recent evidence suggests that these behaviours are at least partially voluntary, suggesting compromised but intact inhibitory control mechanisms. TS patients are impaired in interrupting the execution of intended movements and have difficulty in not processing irrelevant distracter stimuli when instructed to do so (Baron-Cohen et al., 1994; Ozonoff et al., 1998). Abnormalities of movement and timing errors on anti-saccade eye movement trials suggest an inability to inhibit planned motor sequences (LeVasseur et al., 2001). TS patients show increased negative priming, with increased severity of symptoms predicting poorer performance (Ozonoff et al., 1998). Work using the Simon effect paradigm suggests that impaired inhibitory control becomes more pronounced with increasing complex demands (Rankins et al., 2006). Children with TS have been shown to be impaired in their ability to inhibit both motor and verbal prepotent responses (Baron-Cohen et al., 1994).
Such inhibitory control impairments in TS have traditionally been thought to reflect impaired neurological mechanisms, and research is increasingly demonstrating this to be the case. Tic suppression has been found to relate to activity in the basal ganglia and thalamus and the prefrontal cortex (Peterson et al., 1998), suggesting these areas are important for inhibitory control over unwanted impulses. Event-related potentials during performance of a STOP-signal paradigm suggest that impaired frontal inhibitory mechanisms are present in TS (Johannes et al., 2001). The inability of TS patients to inhibit the completion of already planned motor programmes has been related to altered cortical-basal ganglia circuitry (LeVasseur et al., 2001). Peterson et al. (1998) found a number of additional active areas during tic suppression, including the right posterior cingulate, ventral putamen, and ventral globus pallidus and increased activity in right anterior cingulated, right midfrontal cortex, and right ventral caudate. Such activity was correlated with symptom severity, especially in subcortical regions. The authors consequently suggested that successful tic inhibition depends on cortical-striato-thalamo-cortical circuitry (Peterson et al., 1998). Structural abnormalities have been found in the orbital frontal cortex (Peterson et al., 2001), a region implicated in inhibitory control, and the size of the orbital frontal cortex correlates with symptom severity (Goldman-Rakic, 1987), suggesting the importance of disrupted orbitofrontal inhibitory control mechanisms in TS.
Obsessive-Compulsive Disorder (OCD) is a mental illness characterised by obsessions and compulsions that are inappropriate, frequent, and sufficiently intense to cause distress (APA, 2000). OCD has long been hypothesised to be the result of a dysfunction in inhibitory control mechanisms (Chamberlain et al., 2005). Many of the key symptoms and clinical features of OCD such as intrusive and troubling thoughts and compulsive and repetitive behaviours strongly suggest inhibitory impairment (Krikorian, Zimmerman & Fleck, 2004). On a number of different tasks, patients with OCD demonstrate impaired inhibitory control. In oculomotor tasks requiring the suppression of eye movements, OCD patients are impaired (Rosenberg et al., 1997). OCD patients commit more errors on tasks requiring response inhibition (Bannon et al., 2002) and demonstrate decreased response inhibition when instructed to respond to a stimuli that has previously been ignored (Enright & Beech, 1993). Cognitive inhibition appears to be disrupted in OCD, with poor performance on the Stroop test (Penades et al., 2005). Findings using the negative priming paradigm further support this, and such deficits may be particularly strong for those with symptoms involving compulsive checking (Enright, 1996). Motor inhibitory control also appears to be jeopardised, with OCD patients showing poor performance on the Go/NoGo task (Penades et al., 2007; Watkins et al., 2005), and such measures correlating with symptom severity (Bannon et al., 2002). Such motor impulsivity present not only in OCD patients but also in their relatives, suggesting that impaired motor inhibition may represent an endophenotype for OCD (Chamberlain et al., 2007). Such problems with cognitive and motor inhibitory control may underlie not only the primary symptoms of OCD but also the secondary executive function deficits observed in the disorder (Logan & Cowan, 1984).
Such impairments in cognitive and motor inhibition are in line with neuropsychological models of OCD that suggest poor functioning of the frontostriatal circuits of the brain which mediate functions of inhibitory control (Penades et al., 2007). In particular, inhibitory failings on tasks such as the Go/NoGo task suggest a lateral orbitofrontal loop dysfunction in OCD. During NoGo trials, Herrmann et al. (2003) found reduced frontal electrical activity in OCD patients, and such activity was negatively correlated with symptom severity. Malloy et al. (1989) found that during a Go/NoGo task, the P300 event-related potential had a significantly lower amplitude in OCD patients, and Johannes et al. (2001) found altered event-related potentials during a STOP signal paradigm, suggesting a decreased frontal activity may underlie decreased inhibition in the illness. fMRI research has demonstrated that during a Stop task, OCD patients show reduced activity in a number of areas including the basal ganglia and right orbitofrontal cortex and reduced frontal and tempoparietal activity during interference inhibition (Woolley et al., 2008). These findings suggest that dysregulation of the temporparietal areas of the brain underlie impaired cognitive inhibition observed in OCD, whilst attenuated frontostriatothalamic activity underlies impaired motor inhibition. Reduced activation of the anterior cingulate during an inhibitory task has also been demonstrated (Maltby et al., 2005), and symptom severity has been found to be negatively correlated with anterior cingulate gyri activity during such tasks (Roth et al., 2007). Different types of inhibitory control impairment underlie types of symptoms in OCD, and research suggests that such symptom dimensions may have distinct neural correlates (Mataix-Cols et al., 2004).
Schizophrenia is a mental illness characterised by a wide range of symptoms including hallucinations and delusions, disordered thinking, poverty of speech, impaired emotional reactivity, and avolition (APA, 2000). A number of neuropsychological deficits have been observed in this disorder, and impaired inhibitory control is increasingly being recognised as an important marker. Schizophrenia is strongly associated with an inability to inhibit prepotent responses once commenced (Ford et al., 2004; Roberts & Pennington, 1996), and such impairment has been described as a core feature of schizophrenia (Brownstein et al., 2003). Patients have severe difficulty in inhibiting automatic eye movement by suppressing prosaccades (Clementz, McDowell & Zisook, 1994; Clementz & Sweeney, 1990) and make more errors on NoGo trials (Kiehl et al., 2000), suggesting impaired motor inhibition. Deficits are also found on measures of cognitive inhibition, in particular the Stroop task (Braver et al, 2001; Everett, Latplante & Thomas, 1989) and negative priming paradigm (Salo et al., 1997). Such impairments are found in those who have a genetic predisposition to schizophrenia (Ross et al., 1998), and as such a failure of inhibitory control has been hypothesised to represent a key endophenotype for schizophrenia (Cadenhead et al., 2002). Poor inhibitory control may also explain high levels of co-morbid substance abuse associated with the disorder (Chambers, Krystal & Self, 2001) and predict violent offending in patients (Enticott et al., 2008). Impaired intentional control of intrusive cognitions has been linked to a predisposition to hallucinations (Paulik, Badcock & Murray, 2008) and frequency of hallucinations in schizophrenic patients (Waters et al., 2006). Poor inhibitory control also predicts poor occupational and social outcome (Reeder et al., 2004) and greater symptom severity (Donohue et al., 2006). Impaired inhibitory control is particularly evident in patients with high levels of negative symptoms (Ettinger et al., 2006; Karoumi, Ventre-Dominey & Dalery, 1998).
Research is increasingly documenting the neural correlates of such poor inhibitory control mechanisms in schizophrenia. Ford et al. (2004) found that healthy participants showed a wider range of activity during NoGo trials than did schizophrenic subjects, suggesting a less complex neural mechanism for inhibiting responses in schizophrenia. Rubia et al. (2001) showed that even when schizophrenic subjects performed equally well as controls on NoGo trials, they showed reduced activation in the anterior cingulated cortex and left rostral dorsolateral prefrontal cortex. Similar effects have been found in the thalamus and putamen (Rubia et al., 2001) and right ventrolateral prefrontal cortex (Kaladjian et al., 2007), suggesting that neural mechanisms involved in inhibiting prepotent motor responses are consistently underactive in schizophrenia. Schizophrenic patients also demonstrate reduced anterior cingulate activation during performance on measures of cognitive inhibition such as the Stroop task (Kerns et al., 2005) and the continuous performance task (Fallgatter et al., 2003). White matter abnormalities in the right inferior frontal gyrus have been found to predict impulsivity in schizophrenia (Hoptman et al., 2002), and it has been suggested that such impulsivity results from dysfunction of fronto-temporo-limbic circuits (Hoptman et al., 2004).
In conclusion, deficient cognitive and motor inhibitory control represents a key component of a number of different neuropsychiatric disorders. Inhibitory control deficits have been proposed to represent a main symptom in ADHD, from which all secondary symptoms and cognitive deficits arise. Poor response inhibition is evident in autism through a variety of both motor and cognitive tasks and may be a significant neuropsychological casual factor. Recent evidence suggests that tics in Tourette’s syndrome are voluntary and are due to an impaired ability to control such impulses. In OCD, inhibitory control appears to be related to an inability to stop inappropriate thoughts intruding, and consequently relate to the compulsions that characterise the illness. In schizophrenia, a wide range of symptoms such as hallucinations may be related to poor inhibitory control, in particular an inability to inhibit prepotent responses. Within all these disorders, fMRI and Event-related potentials have demonstrated functional and occasionally structural deficits in fronto-striatal circuitry. Such deficits are observed in terms of reduced activation, increased activation, and reduced inter-connectivity between regions. Such findings demonstrate the importance of this system in effective inhibitory control and give insight into how impairment of this system result in symptoms of disinhibition commonly observed in psychiatric patients. As such, focusing on the neural correlates of impaired inhibitory control in clinical populations may lead to important new therapeutic and pharmacological treatments.
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