To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
The brain functional correlates of delusions have been relatively little studied. However, a virtual reality paradigm simulating travel on the London Underground has been found to evoke referential ideation in both healthy subjects and patients with schizophrenia, making brain activations in response to such experiences potentially identifiable.
Ninety patients with schizophrenia/schizoaffective disorder and 28 healthy controls underwent functional magnetic resonance imaging while they viewed virtual reality versions of full and empty Barcelona Metro carriages.
Compared to the empty condition, viewing the full carriage was associated with activations in the visual cortex, the cuneus and precuneus/posterior cingulate cortex, the inferior parietal cortex, the angular gyrus and parts of the middle and superior temporal cortex including the temporoparietal junction bilaterally. There were no significant differences in activation between groups. Nor were there activations associated with referentiality or presence of delusions generally in the patient group. However, patients with persecutory delusions showed a cluster of reduced activation compared to those without delusions in a region in the right temporal/occipital cortex.
Performance of the metro task is associated with a widespread pattern of activations, which does not distinguish schizophrenic patients and controls, or show an association with referentiality or delusions in general. However, the finding of a cluster of reduced activation close to the right temporoparietal junction in patients with persecutory delusions specifically is of potential interest, as this region is believed to play a role in social cognition.
The first demonstration of laser action in ruby was made in 1960 by T. H. Maiman of Hughes Research Laboratories, USA. Many laboratories worldwide began the search for lasers using different materials, operating at different wavelengths. In the UK, academia, industry and the central laboratories took up the challenge from the earliest days to develop these systems for a broad range of applications. This historical review looks at the contribution the UK has made to the advancement of the technology, the development of systems and components and their exploitation over the last 60 years.
The brain functional correlates of autobiographical recall are well established, but have been little studied in schizophrenia. Additionally, autobiographical memory is one of a small number of cognitive tasks that activates rather than de-activates the default mode network, which has been found to be dysfunctional in this disorder.
Twenty-seven schizophrenic patients and 30 healthy controls underwent functional magnetic resonance imaging while viewing cue words that evoked autobiographical memories. Control conditions included both non-memory-evoking cues and a low level baseline (cross fixation).
Compared to both non-memory evoking cues and low level baseline, autobiographical recall was associated with activation in default mode network regions in the controls including the medial frontal cortex, the posterior cingulate cortex and the hippocampus, as well as other areas. Clusters of de-activation were seen outside the default mode network. There were no activation differences between the schizophrenic patients and the controls, but the patients showed clusters of failure of de-activation in non-default mode network regions.
According to this study, patients with schizophrenia show intact activation of the default mode network and other regions associated with recall of autobiographical memories. The finding of failure of de-activation outside the network suggests that schizophrenia may be associated with a general difficulty in de-activation rather than dysfunction of the default mode network per se.
Although executive and other cognitive deficits have been found in patients with borderline personality disorder (BPD), whether these have brain functional correlates has been little studied. This study aimed to examine patterns of task-related activation and de-activation during the performance of a working memory task in patients with the disorder.
Sixty-seven DSM-IV BPD patients and 67 healthy controls underwent fMRI during the performance of the n-back task. Linear models were used to obtain maps of within-group activations and areas of differential activation between the groups.
On corrected whole-brain analysis, there were no activation differences between the BPD patients and the healthy controls during the main 2-back v. baseline contrast, but reduced activation was seen in the precentral cortex bilaterally and the left inferior parietal cortex in the 2-back v. 1-back contrast. The patients showed failure of de-activation affecting the medial frontal cortex and the precuneus, plus in other areas. The changes did not appear to be attributable to previous history of depression, which was present in nearly half the sample.
In this study, there was some, though limited, evidence for lateral frontal hypoactivation in BPD during the performance of an executive task. BPD also appears to be associated with failure of de-activation in key regions of the default mode network.
Delusional disorder has been the subject of very little investigation
using brain imaging.
To examine potential structural and/or functional brain abnormalities in
We used structural imaging (voxel-based morphometry, VBM) and functional
imaging (during performance of the n-back task and
whole-brain resting connectivity analysis) to examine 22 patients meeting
DSM-IV criteria for delusional disorder and 44 matched healthy
The patients showed grey matter reductions in the medial frontal/anterior
cingulate cortex and bilateral insula on unmodulated (but not on
modulated) VBM analysis, failure of de-activation in the medial
frontal/anterior cingulate cortex during performance of the
n-back task, and decreased resting-state connectivity
in the bilateral insula.
The findings provide evidence of brain abnormality in the medial
frontal/anterior cingulate cortex and insula in delusional disorder. A
role for the former region in the pathogenesis of delusions is consistent
with several other lines of evidence.
Little is known about how functional imaging changes in bipolar disorder
relate to different phases of the illness.
To compare cognitive task activation in participants with bipolar
disorder examined in different phases of illness.
Participants with bipolar disorder in mania (n = 38),
depression (n = 38) and euthymia (n =
38), as well as healthy controls (n = 38), underwent
functional magnetic resonance imaging during performance of the n-back
working memory task. Activations and de-activations were compared between
the bipolar subgroups and the controls, and among the bipolar subgroups.
All participants were also entered into a linear mixed-effects model.
Compared with the controls, the mania and depression subgroups, but not
the euthymia subgroup, showed reduced activation in the dorsolateral
prefrontal cortex, the parietal cortex and other areas. Compared with the
euthymia subgroup, the mania and depression subgroups showed
hypoactivation in the parietal cortex. All three bipolar subgroups showed
failure of de-activation in the ventromedial frontal cortex. Linear
mixed-effects modelling revealed a further cluster of reduced activation
in the left dorsolateral prefrontal cortex in the patients; this was
significantly more marked in the mania than in the euthymia subgroup.
Bipolar disorder is characterised by mood state-dependent hypoactivation
in the parietal cortex. Reduced dorsolateral prefrontal activation is a
further feature of mania and depression, which may improve partially in
euthymia. Failure of de-activation in the medial frontal cortex shows
The pathological basis of tardive dyskinesia is unknown. Although its clinical features implicate the basal ganglia, imaging studies have not found clear evidence that it is associated with volume changes in these or other brain structures.
To determine, using voxel-based structural imaging, whether there are regions of grey matter volume change in people with schizophrenia who also have tardive dyskinesia compared with those without tardive dyskinesia.
A total of 81 people with chronic schizophrenia, 32 with tardive dyskinesia and 49 without, were examined using magnetic resonance imaging (MRI) and whole-brain, optimised voxel-based morphometry. A comparison group of 61 healthy controls was also examined.
Compared with those without tardive dyskinesia, patients with tardive dyskinesia showed a pattern of volume reductions in predominantly subcortical regions, including the basal ganglia and the thalamus. Within the basal ganglia, volume reductions were seen in the caudate nucleus, to a lesser extent in the putamen, and only marginally in the globus pallidus. The patients with tardive dyskinesia, but not those without, showed significant volume reductions in the basal ganglia compared with the healthy controls but both groups had smaller volumes than controls in other affected areas.
The pathological process or processes that underlie the development of tardive dyskinesia are not just neurochemical in nature, but affect brain structure.
Cognitive impairment is an established feature of schizophrenia. However,
little is known about its relationship to the structural and functional
brain abnormalities that characterise the disorder.
To identify structural and/or functional brain abnormalities associated
with schizophrenic cognitive impairment.
We carried out structural magnetic resonance imaging (MRI) and
voxel-based morphometry in 26 participants who were cognitively impaired
and 23 who were cognitively preserved, all with schizophrenia, plus 39
matched controls. Nineteen of those who were cognitively impaired and 18
of those who were cognitively preserved plus 34 controls also underwent
functional MRI during performance of a working memory task.
No differences were found between the participants who were cognitively
intact and those who were cognitively impaired in lateral ventricular
volume or whole brain volume. Voxel-based morphometry also failed to
reveal clusters of significant difference in grey and white matter volume
between these two groups. However, during performance of the n-back task,
the participants who were cognitively impaired showed hypoactivation
compared with those who were cognitively intact in the dorsolateral
prefrontal cortex among other brain regions.
Cognitive impairment in schizophrenia is not a function of the structural
brain abnormality that accompanies the disorder but has correlates in
altered brain function.
The symptoms of schizophrenia are on the whole anything but subtle, but even so thought disorder stands out from amongst them. There is something about it which arouses curiosity and demands explanation. Part of the reason for this immediacy may be, as the psychologist Harvey has pointed out, that it is one of the few signs in psychiatry – an objectively observable abnormality as opposed to a subjective description of some aspect of one's inner mental state. But whatever it is, a great deal of ink has been spilled by psychiatrists trying to describe and psychologists trying to explain just what it is that makes the patient difficult to follow.
Unfortunately the answer to these questions appears to be ‘more than one thing’. The price of describing thought disorder reliably has been the acceptance of a large and unwieldy set of abnormalities, and this book has only narrowly avoided finding support for every theory ever proposed to explain it. In such circumstances integrative models are customarily reached for. For integrative one can usually read complicated, and the term model conjures up something which is not testable and accompanied by flow diagrams. Without resorting to models, and resisting any temptation to inflict flow diagrams on the reader, what follows offers some not very systematic suggestions on how the different elements of thought disorder and their underpinnings might be reduced to something more manageable.
When trying to explain thought disorder, or anything else for that matter, a good place to start is by describing the phenomenon accurately. In medicine, the customary way of doing this is by observing a suitably large number of patients who show the phenomenon in all its varied forms, and extracting the common features so as to arrive at some distillation of the essential nature of the symptom itself. This is the so-called clinical method, sometimes dignified as descriptive psychopathology in psychiatry, where the symptoms are much more individually variable than in the rest of medicine, and occasionally elevated to the status of its own discipline of ‘phenomenology’.
Traditional and greatly respected in medicine, this approach to defining thought disorder was objected to by two linguists, Rochester and Martin (1979), on the grounds that it was too dependent on inference. They levelled their criticisms particularly at Bleuler (1911), who coined the term schizophrenia and was responsible for giving what is still one of the most detailed accounts of thought disorder. In the first place, he took it as a given that the underlying abnormality was one of thought rather than of speech, and according to Rochester and Martin the uncritical acceptance of this view by those who followed him caused many problems and obscured some interesting issues. Secondly, Bleuler specified the disorder of thought as one of ‘loosening of associations’ or ‘association disturbance’, a speculative construct to which he accorded great theoretical significance.
This book reviews our knowledge of the incoherent speech which can present as a symptom of schizophrenia. This is one of the most researched symptoms in the disorder. The content covers clinical presentation, differential diagnosis and the theories proposed to account for the symptom in these 'thought disordered' patients, ranging from the psychoanalytic to there being a form of aphasia involved. The book is unique in its ability to apply linguistic and neuropsychological approaches to the understanding of this condition, and is the first book to cover comprehensively the range of clinical studies that followed the introduction of Andreasen's rating scale for what was then called thought, language and communication disorder. This book is essential reading for all those working in the field of schizophrenia and also for those interested in language and disorders of speech.
At times, thought disorder has been considered to be a symptom of, and only of, schizophrenia. Nowhere was this more true than in American psychiatry, which until comparatively recently laboured under Bleuler's (1911) dictate that it was one of the fundamental symptoms of schizophrenia. Harrow and Quinlan (1977), for example, noting that countless authors since Bleuler had ‘affirmed its importance as a central feature of this disorder’, stated that ‘some astute clinicians have believed that reliance on disordered thinking is a certain way to distinguish schizophrenics from non-schizophrenics’. This view persisted until their own and others' studies (e.g. Harrow et al., 1973; Harrow and Quinlan, 1977; Carlson and Goodwin, 1973; Taylor and Abrams, 1975) began to cast doubt on its universality in the disorder. These studies also made it clear, to nobody's surprise but their authors', that thought disorder was seen in at least one other disorder, mania.
This point was also made by Andreasen, in a typically pragmatic way, in one of her earliest studes (Andreasen et al., 1974). She showed a group of forty-two psychiatrists, psychologists and social workers at the hospital where she worked six samples of prose and asked them to decide whether thought disorder was present and what diagnosis they suspected in each case. Two of the samples were from patients with schizophrenia, two from patients with mania, and the remaining two consisted of an extract from James Joyce's Finnegans Wake and part of a poem retyped in prose form, The Perfection of Dentistry by Marvin Bell.