Neuropsychology has been applied to the area of mental health with three principal objectives: the identification of underlying neuropathology for research purposes; differential diagnosis of specific psychiatric syndromes; and the monitoring of cognitive changes in the course of treatment to assess modifications in cognitive ability, neurotoxic effects and learning. Attempts to identify, measure and localize cognitive disorders occurring in psychiatric syndromes have largely concerned developmental neuropsychiatric disorders, depression, schizophrenia, obsessive-compulsive disorder, neu-rodegenerative diseases of ageing and, to a lesser extent, traumatic stress disorders. These conditions will be the principal focus of this review.
This section does not aim to present a comprehensive overview of the neuropsychology of childhood mental disorders. Rather, two important neuropsychiatric disorders illustrate the diversity of this field.
Autism involves disturbance of reciprocal social interaction, disturbance of communication, including expressive and receptive language, and extreme behavioural restriction , Although autism is frequently associated with mental retardation , a more specific pattern of cognitive deficit was proposed by Hermelin and O'Connor , characterized by difficulty in perceiving order and meaning in events . Broadly consistent with this are observations which have demonstrated that autism is a frontal lobe disturbance with involvement of the amygdala [6, 7], neuropsychological evidence of impaired executive function [8, 9], and the proposal that autistic children lack a "theory of mind'', i.e. ability to understand the thinking of others from the social context .
Imaging studies have shown that some frontal and basal ganglia regions are smaller in children with attention deficit hyperactivity disorder (ADHD) than in controls, consistent with neuropsychological evidence of impaired executive function (see  for a review). Although poor performance of hyperactive children on neuropsychological tests of attention has been reported , other work has focused on response initiation and inhibition. The rate of inhibition failure in a "go-no go'' task was high in ADHD , a finding which is consistent with the construct of impulsiveness, i.e. reduced ability or willingness to inhibit inappropriate actions and to wait for a delayed consequence . However, subsequent work suggests that the response style in children with ADHD may be inefficient (slow and inaccurate) rather than impulsive (fast and inaccurate) [11, 14, 15].
Neuropsychological deficits are now recognized to be a common and significant feature of depressive disorder, resembling the profile of cognitive deficiencies seen in traumatic brain injury . Attentional, executive and secondary memory functioning are the areas principally affected [17-21]. Two different patterns of attentional deficit have been described in depression: distractor inhibition, and deficits in the processing of resources, that is, the central executive component of working memory . Memory disorder in depression is principally due to a retrieval rather than encoding deficit , but has not been consistently reported, perhaps because testing is often limited to verbal or visual stimuli, and there is some evidence to suggest the deficit may in some cases be related to dysfunction in a single hemisphere [17,24].
The association of neuropsychological tests with neuroimaging (positron emission tomography, PET, and magnetic resonance imaging, MRI) indicate dysfunction of frontostriatal circuits, the mediotemporal lobe, hippocampus and cingulate as the principal underlying neuroanatomical correlates of cognitive impairment in depression [16, 19, 25-27], Abnormal responses to negative feedback are observed in depressed patients compared to normal subjects and those with other forms of psychopathology, which may in part explain the link between mood and cognition , At a biological level, this link has been attributed to interactions between the serotonergic system and the hypothalamic-pituitary-adrenal axis [28, 29],
Not all depressed subjects show the same patterns of neuropsychological deficits, suggesting either a dominant role of moderating variables  or the existence of subtypes of depressive disorder, Different patterns of neuropsychological deficit have been identified, for example for major depression with and without psychotic features, the former showing significantly greater impairment in attention, psychomotor speed, response inhibition and verbal rather than visual secondary memory [25, 30, 31], There is also some evidence to suggest the possibility of a late-onset form of depression linked to cerebrovascular pathology evidenced as white matter lesions on T2-weighted MRI scans, These are associated with a separate pattern of cognitive deficits, characterized by significantly poorer performance on frontal executive, language and secondary verbal memory tasks , However, unrecognized subclinical dementia may be a confounding factor in identifying a specific pattern of neuropsychological deficit in this group,
Neuropsychological tests have also been used in the differential diagnosis of unipolar depression and chronic fatigue syndrome , and to measure treatment effects with electroconvulsive therapy [34, 35], transcranial magnetic stimulation  and pharmacological intervention [37, 38],
Studies of bipolar depression have been less common, Clinical studies suggest that memory functioning in mania is usually intact and that the principal area of cognitive disorder is in executive function, notably impaired judgement, Functional imaging using PET and verbal fluency tests shows rostral and orbitofrontal cortex activation during manic episodes , with poorer performance on neuropsychological tests being associated with small prefrontal and hippocampal volume [40, 41],
Neuropsychological impairment is virtually universal in schizophrenia, and is usually evident early in the disorder, Overall, schizophrenic patients perform worse than subjects with psychotic affective disorders , notably on tests of attention, Compared to normal control subjects, they are seen to have specific difficulties in the complex integration of stimuli, conceptual shifting, response initiation and inhibition, verbal fluency, ability to imitate, and encoding and retrieval in secondary verbal memory [24, 43-46]. Attention and memory disorders in childhood have been further demonstrated to be significant predictors of schizophrenia in mid-adulthood , suggesting that the cognitive deficits precede the onset of clinical symptoms. Atten-tional deficits and retroactive inhibition are also observed more frequently in otherwise symptom-free relatives of persons with schizophrenia [43, 48].
Cognitive functioning in schizophrenia is seen to be further impaired in the presence of obsessive-compulsive disorder [49, 50], particularly in frontal lobe executive functions, raising the possibility that this group may constitute a separate subtype of schizophrenia. The co-occurrence of depression also alters the cognitive profile in schizophrenia, leading to significantly greater impairment in attention . On the other hand, paranoid schizophrenia has been associated with less cognitive impairment than other forms of the disorder, although these findings have not been consistently supported .
Several attempts have been made to relate specific cognitive disorders to symptomatology in schizophrenia. Referring to the three-factor model of symptom complexes of hallucinations/delusions, disorganization of behaviour and thought, and negative symptoms, a number of studies have reported specific patterns of deficit. Psychotic symptoms appear to be unrelated to cognitive deficits, whereas disorganized thoughts and behaviour appear to be associated with lower IQ, and negative symptoms to problems of verbal and visual memory, verbal fluency and visual-motor sequencing [53, 54]. Deficits in verbal fluency have also been observed in conjunction with negative symptoms . The Continuous Performance and Wisconsin Card Sorting Tests (both tests of frontal functioning) have been described as putative indicators for the predisposition to develop negative symptoms .
Abnormality on the Wisconsin test is the most commonly reported deficit in schizophrenia, and has been assumed to reflect dorsolateral prefrontal cortex dysfunction [57, 58]. Functional imaging and morphometric studies point, however, to more widespread neuropathology, such that the cognitive deficits seen in schizophrenia are now considered to be the result of dysfunction in cortico-subcortical connectivity with a neurotransmitter imbalance in the thalamic-prefrontal motor cortex and basal ganglia .
Once considered to be related to unresolved internal conflict, obsessive-compulsive disorder (OCD) is now regarded as a model of neuropsychiatric disorder, with complex information processing deficits which go beyond the effects of any associated mood disturbance. Low overall performance on cognitive tests has also been found to be significantly associated with the presence of neurological soft signs . At the neuropsychological and physiological level, OCD in fact shares many of the features of Tourette's syndrome: lack of laterality, bilateral or left frontal lobe dysfunction, shortened rapid eye movement (REM) sleep latency and abnormal glucose metabolism in the caudate nucleus . Studies of children with OCD indicate no impairment differences on neuropsychological testing , suggesting that information processing circuits may not be disturbed in very early stages of the illness. It is perhaps difficult, however, to determine the extent of damage in children, given that such studies are carried out before full maturation of the frontal cortex, and in the face of the high neuronal plasticity present in younger brains.
The neuropsychological disturbances of OCD are principally characterized by a frontal lobe syndrome with accompanying difficulties in motor initiation, shifting and frequent perseverative errors [63-65], a profile commonly observed in lesions of the orbitofrontal cortex. A case study described by Simpson and Baldwin  of sudden-onset OCD with frontal lobe signs showed in fact low activation in the left orbitofrontal region on single photon emission computed tomography (SPECT). Spatial recognition and spatial working memory deficits consistent with frontostriatal dysfunction have also been consistently observed [65, 67]. Clinical observations of qualitative aspects of test performance by Veale et al.  also point to frontostriatal involvement, namely distractability in the face of competing stimuli, excessive monitoring and rigidity in tasks requiring change of set. The authors refer to this pattern of behaviours as dysfunction of the "supervising attentional system''. Supporting evidence for anatomical localization has come from clinical follow-up studies of subjects undergoing ventromedial frontal leucotomy, subjects with frontostriatal lesions showing the most striking improvement .
Visual and praxic memory deficits have been linked by Tallis  to checking behaviour, but a subsequent study found a relationship only with symptom severity and not with checking . Motor slowing has also been observed in some studies , which has been limited to psycho-motor tasks involving the fronto-subcortical system and thus cannot be simply attributed to interference due to thought intrusion. Disassociation on neuropsychological testing has been found between the orbitofrontal deficits observed in OCD and the dorsolateral functions observed in schizophrenia, the dorsolateral prefrontal cortex being apparently spared in OCD .
Cognitive impairment is observed in a range of neurodegenerative diseases, and neuropsychological assessment is routinely used to document this impairment in detail. However, the rapid growth of the world's elderly population has brought a focusing on dementia as a major public health burden, leading to a massive research effort to understand its aetiology and to generate effective therapies. One particular contribution made by neuro-psychology has been to the discussion of whether the multiple diseases encompassed by the term "dementia" are discrete or overlapping entities. An older distinction was made between cognitive function in the "cortical" dementia of Alzheimer's disease (AD) and that in "subcortical" dementia, such as occurs in progressive supranuclear palsy . More recently, Spinnler and Della Sala  have proposed an alternative dichotomy of instrumental cortical (retrorolandic) dementias (e.g. AD) and dysexecutive cortical (prefrontal) dementias with (e.g. Huntington's chorea) or without (e.g. Pick's disease) subcortical damage.
A more difficult issue has been the distinction between AD and vascular dementia. Again, there has been considerable debate over whether these are distinct diseases or variant consequences of common risk factors , or whether vascular dementia is in fact of valid nosological status . To some extent, however, neuropsychological research has identified a distinct cognitive profile in this disease. This is suggestive of predominantly subcortical damage, and is characterized by cognitive slowing and disorders of retrieval and attention  and executive impairment , with relative sparing of cortical functions such as those underlying aphasia, apraxia and agnosia . However, comorbidity in vascular disease complicates the attempt to separate neuropsychological features of vascular dementia, neurodegenerative dementias and other pathologies .
Finally, neuropsychology has been influential in defining the nature of mild cognitive decline in ageing. To a large extent this relates to normal ageing and is therefore beyond the scope of the present chapter. However, neuropsychology has played a role in the prediction of dementia [e.g. 78-80], as well as an essential part in the formulation of research criteria for subclinical states such as age-associated memory impairment  and ageing-associated cognitive decline [82, 83].
Stress disorder is characterized by sleep disturbance, emotional numbing and symptoms of autonomic instability, depression and cognitive disorder. There has been some interest in recent years in the cognitive consequences of exposure to stress. This area has received less attention, however, than other psychiatric syndromes, despite a high prevalence in the general population of 0.5% for men and 1.2% for women . This is perhaps because the affective component is initially the principal presenting cause of disability.
In the longer term, however, cognitive disorder may seriously impair reintegration into working life.
Clinical observations of cognitive impairment following adverse life events have been paralleled by biological observations that exposure to severe stress, notably maternal separation in childhood and combat-related post-traumatic stress disorder, leads to increases in glucocorticoids, hippo-campal damage and subsequently disorders of memory [85, 86]. An 8% reduction in right hippocampal volume has, for example, been observed in war veterans with stress disorder . Two principal areas of cognitive functioning appear to be affected in stress disorders: attention and organization of sequential stimuli, and secondary declarative memory. As subjects experiencing severe stress have also usually been exposed to physical trauma such as head injury, and are also at high risk for drug and alcohol dependency, it is often difficult for the neuropsychologist to attribute test performance difficulties specifically to psychological stress-related changes in the CNS. Hickling et al.  have, however, demonstrated that subjects with post-traumatic stress syndrome following motor vehicle accidents have impairment of secondary declarative memory independently of physical injury. Beckham et al.  have found, for example, significant difficulties on tests of working memory central executive functioning in Vietnam veterans, controlling for drug effects and comorbid conditions.
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