The Quality of Survival after Rupture of an Anterior Cerebral Aneurysm

Logue, Valentine; Durward, Marjorie; Pratt, R. T. C.; Piercy, Malcolm; Nixon, W. L. B.

doi:10.1192/bjp.114.507.137

Cited by 107 publications

(21 citation statements)

References 10 publications

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“…Damasio and coworkers [13] have described how, in general, patients with ventromedial frontal lobe lesions exhibit an inability to initiate, organize, and carry out normal activities, and also demonstrate poor decision-making, financial mistakes, breakup of relationships, perseverative activities, and decreased spontaneity. Patients in the early stages of fvFTD also bear some resemblance to other patient groups with dysfunction principally of the orbitofrontalsubcortical circuit, for example those with ruptured anterior communicating aneurysms, orbitofrontal tumours, and inferior frontal lobe infarction [14][15][16]. In contrast, patients with dorsolateral prefrontal-subcortical dysfunction are predominantly characterized by impairments in executive function [17].…”

Section: Introductionmentioning

confidence: 99%

Comparative Cognitive Neuropsychological Studies of Frontal Lobe Function: Implications for Therapeutic Strategies in Frontal Variant Frontotemporal Dementia

Rahman

Robbins

Sahakian³

1999

Dement Geriatr Cogn Disord

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Patients with mild frontal variant frontotemporal dementia (fvFTD) who attend the clinic are usually unaware of the pervasive changes in their personality and behaviour, despite the fact it is these changes which have prompted the referral from the patient’s spouse or carer. Comparative studies across various species offer unique insights into the heterogeneous structure and functions of the prefrontal cortex, and can allow a novel approach to the precise identification of the neuropsychological deficits present in these patients. We have found that they may show marked deficits on tests sensitive to ventromedial prefrontal or orbitofrontal function, in the relative absence of impairments on tests sensitive to dorsolateral prefrontal function. We highlight important differences in the neurocognitive profile of these patients with that of patients with other neurodegenerative conditions, including basal ganglia diseases and dementia of the Alzheimer type. The specific nature of these neuropsychological deficits, together with converging evidence from clinical and neuropathological studies, may provide useful clues about the predominant locus of dysfunction in the early stages of fvFTD and possible underlying neurotransmitter abnormalities. This is important for the successful development of therapeutic intervention strategies for both cognitive and behavioural symptoms in fvFTD. Finally, we evaluate critically the rationales for therapeutic modulation of noradrenergic, serotonergic and dopaminergic neurotransmitter systems at various stages of disease.

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Section: Introductionmentioning

confidence: 99%

Comparative Cognitive Neuropsychological Studies of Frontal Lobe Function: Implications for Therapeutic Strategies in Frontal Variant Frontotemporal Dementia

Rahman

Robbins

Sahakian³

1999

Dement Geriatr Cogn Disord

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“…Lesion studies have demonstrated that damage to the orbitofrontal cortex produces disinhibition, inappropriate behavior, or emotional displays; inappropriate responses to environmental cues; and utilization behavior (Cummings, Gosenfeld, Houlihan, & McCaffrey, 1983;Kolb, 1977;Lhermitte, Pillon, & Serdaru, 1986;Logue, Durward, Pratt, Piercy, & Nixon, 1968;Rolls, 1985). OCD patients with purely obsessional or purely compulsive symptoms display such characteristics.…”

Section: Discussionmentioning

confidence: 99%

Issues surrounding the cognitive neuroscience of obsessive-compulsive disorder

Wilson

1998

Psychonomic Bulletin & Review

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Obsessive-compulsive disorder (OCD) has been studied extensively in recent years, with increased emphasis on understanding OCD's biological substrates. There has been significant progress in documenting abnormal brain function in OCD patients, particularly in the orbitofrontal cortex, basal ganglia, and thalamus. Similar progress has broadened our understanding of the cognitive and behavioral manifestations of the disorder, including deficits in set shifting, hyperattention, and visuospatial construction abilities. Unfortunately, these results have not been replicated consistently. This report comprises a review of previous attempts to characterize the neurobiology and neuropsychology of OCD, and a discussion of several factors in OCD research that can help to explain previous inconsistencies.Obsessive-compulsive disorder (OCD) is a relatively common form of psychopathology with a lifetime prevalence of2%-3% (Robins et al., 1984). Although the anatomical and behavioral regularities of the disorder have been studied extensively over the past 20 years, there has been relatively little success in the attempt to establish how the former give rise to the latter. Popular models of OCD have drawn upon a variety of disciplines, including learning theory (Mowrer, 1960), cybernetics (Pitman, 1987) and psychoanalysis (Fenichel, 1945). Often, however, these models have had relatively little to say about the dysfunctional aspects of the OCD brain. This is due in part to the fact that, until recently, the neuroanatomical substrates ofOCD were poorly understood. Although OCD researchers had long suspected the involvement of the frontal cortex and basal ganglia in OCD neuropathology, there was little empirical evidence to support such claims. Only through the use ofmodern neuroimaging techniques have many of these suspicions been confirmed.Neurobiological studies ofOCD have produced a wealth of data, but the inability to consistently replicate results has left many questions unanswered. Neuropsychological studies have similarly generated much information, but with equal uncertainty. An adequate theory ofOCD must integrate the findings from each of these two disciplines, but any such integration would be premature at the moment, given the variability present within each. The goal of this review is therefore not to provide an all-encompassing theory ofOCD expression, but rather to delineate several factors that may explain the discrepancies among previous studies of OCD. Consideration of these factors will help clarify the relevant neurobiological and neuropsycho-

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“…However, there was also no significant difference with respect to fear about recurrent hemorrhage between the 2 groups. Logue et al 24 evaluated 79 patients (66 surgically treated and 13 conservatively treated) between 7 and 101 months after SAH with a number of psychiatric tests and a psychiatric interview. In contrast to the general expectation, fear of a new hemorrhage was more common in the surgically treated patients than in those who had no documented source of hemorrhage (13 [19.6%] of 66 and 1 [7.6%] of 13, respectively).…”

Section: Sah As Psychological Traumamentioning

confidence: 99%

“…4,5,8,26,32 In particular, arousal symptoms such as concentration deficits, irritability, and a heightened startle response are not only typical symptoms of mild head injury 4,5 but also are among the most frequent late sequelae seen in patients after SAH. 15,16,[23][24][25]38 …”

Section: Assessment Of Psychological Traumatizationmentioning

confidence: 99%

Subarachnoid hemorrhage as a psychological trauma

Hütter

Kreitschmann-Andermahr

2014

JNS

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E vEn months to years after subarachnoid hemorrhage (SAH), increased irritability, personality changes, loss of interest and initiative, social problems, and emotional disturbances frequently persist. 6,15,16,23,25,28,29,31,34,35,38 These psychological changes and subjective complaints are also present even when the degree of neurological and/or cognitive impairment is relatively mild. 15,16,23,25,[28][29][30][31]35,38 Ropper and Zervas 35 and Ljunggren et al. 23 found that approximately 25% of their SAH patients with a good neurological result (Glasgow Outcome Scale [GOS] score of 1) exhibited substantial emotional maladjustment. The etiology of this psychosocial impairment has not been resolved conclusively. It can be speculated that these personality and emotional changes result directly of brain damage or can be regarded as an expression of chronic functional impairment. On the other hand, several authors have noted that the frequency and severity of emotional disturbances and personality changes after SAH are out of proportion to the typically rather moderate cognitive and neurological impairments of these patients. 15,16,23,25,[28][29][30][31]35,38 This discrepancy cannot be explained by a psychological reaction to persisting functional deficits or the social stigma associated with having had "trouble with the head." Therefore, the question about additional causes beyond brain damage for the psychological abnormalities occurring after SAH arises. Several authors have found that chronic posttraumatic stress disorder (PTSD) is far from being uncommon in patients who have experienced SAH, with rates ranging from 19% to 37% in the published literature. Object. Despite the progress made in the management of subarachnoid hemorrhage (SAH), many patients complain of persistent psychosocial and cognitive problems. The present study was performed to explore the significance of psychological traumatization by the bleeding with respect to psychosocial results after SAH.Methods. A series of 45 patients were examined in a cross-sectional study an average of 49.4 months after SAH by means of a quality-of-life questionnaire, the Beck Depression Inventory, the German version of the Impact of Event Scale (IES), and a clinical interview (Structured Clinical Interview for DSM Disorders) to make the diagnosis of chronic posttraumatic stress disorder (PTSD). Twenty-nine patients underwent surgery for treatment of a ruptured aneurysm; the remaining 16 patients had SAH of unknown origin.Results. Twelve patients (27%) exhibited PTSD, and almost two-thirds of the 45 patients in the study reported substantial fear of recurrent hemorrhage. Not only the presence of PTSD but the severity of psychological traumatization as assessed by the IES explained up to 40% of the variance of the self-and proxy-rated impairments. Multivariate analyses revealed psychological traumatization (IES) and neurological state on admission (Hunt and Hess grade) as substantial predictors of the self-and proxy-rated quality of life, explaining 31% and 42% of t...

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The Quality of Survival after Rupture of an Anterior Cerebral Aneurysm

Cited by 107 publications

References 10 publications

Comparative Cognitive Neuropsychological Studies of Frontal Lobe Function: Implications for Therapeutic Strategies in Frontal Variant Frontotemporal Dementia

Comparative Cognitive Neuropsychological Studies of Frontal Lobe Function: Implications for Therapeutic Strategies in Frontal Variant Frontotemporal Dementia

Issues surrounding the cognitive neuroscience of obsessive-compulsive disorder

Subarachnoid hemorrhage as a psychological trauma

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