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Mark Solms

Publications and source records attributed to Mark Solms.

7 recordsLinked to original sources
PubMed2005

Apolipoprotein E variants and cognition in healthy individuals: a critical opinion.

The epsilon4 allele of apolipoprotein E (ApoE) is a well-established risk factor for late onset Alzheimer's disease (AD). This knowledge has generated interest in the role of ApoE variants in normal cognition. Varying degrees of cognitive dysfunction have been described in non-demented individuals with one or two epsilon4 alleles leading to suggestions that the gene plays a role in normal cognition or helps calibrate the aging process. In this paper, these hypotheses are critically evaluated. It is argued that ApoE variants play no role in cognitive development. Given the differential neurocognitive sequelae of normal aging and AD, we also suggest that accelerated aging is unlikely to account for the pattern of deficits observed in non-demented epsilon4 allele carriers. We conclude that the neuropsychological dysfunction reported in non-demented epsilon4 carriers is most likely to be the result of incipient AD.

Apolipoproteins E↗
PubMed2005

Neuropsychological dysfunction in bipolar affective disorder: a critical opinion.

Data from the imaging literature have led to suggestions that permanent structural brain changes may be associated with bipolar disorder. Individuals diagnosed with bipolar disorder display deficits on a range of neuropsychological tasks in both the acute and euthymic phases of illness, and correlations between experienced number of affective episodes and task performance are commonly reported. These findings have renewed interest in the neuropsychological profile of individuals with bipolar disorder, with deficits of attention, learning and memory, and executive function, asserted to be present. This paper critically reviews five different potential causes of neurocognitive dysfunction in bipolar disorder: (i) iatrogenic, (ii) acute functional changes associated with depression or mania, (iii) permanent structural lesions of a neurodegenerative origin, (iv) permanent structural lesions that are neurodevelopmental in origin, and (v) permanent functional changes that are most likely genetic in origin. Although the potential cognitive effects of residual symptomatology and long-term medication use cannot be entirely excluded, we conclude that functional changes associated with genetically driven population variation in critical neural networks underpin both the neurocognitive and affective symptoms of bipolar disorder. The philosophical implications of this conclusion for neuropsychology are briefly discussed.

Bipolar Disorder↗
PubMed2005

Neurocognitive function as an endophenotype for genetic studies of bipolar affective disorder.

The genetic basis of bipolar affective disorder remains opaque despite years of intensive investigation. One of the most serious difficulties for genetic research is the enormous phenotypic heterogeneity of psychiatric illnesses. As a response to this problem, geneticists have searched for alternative strategies to identify those individuals at genetic risk for developing the disorder. One approach is to use endophenotypes or intermediate traits. Gottesman and Gould (2003), in their discussion of endophenotypes, suggest five criteria that should be characteristic of a trait in order for it to qualify as an endophenotype. These five criteria are used in order to assess the viability of using measures of neuropsychological dysfunction as endophenotypes for genetic studies of bipolar disorder. A review of the literature suggests that executive dysfunction is characteristic of people with bipolar disorder in both the acute and chronic stages of the illness, that neurocognitive function is influenced by genetic factors and that neuropsychological deficits have been reported in the nonaffected relatives of bipolar probands. Nevertheless, it is unclear whether neuropsychological dysfunction co-segregates with affectively ill individuals. We conclude that the use of neurocognitive markers of bipolar illness suffers from a number of serious drawbacks but given the absence of more appropriate endophenotypes, the neuropsychological profiling of probands and their relatives may nevertheless prove to be a worthwhile exercise.

Bipolar Disorder↗
PubMed2004

Wishful reality distortions in confabulation: a case report.

Several theories have been proposed to account for the complex cognitive mechanisms underlying the various forms and manifestations of confabulation. As regards the content of confabulations, deficit accounts explain what is lacking in the confabulations, but accounts of the positive features of the content may also be required to explain what remains. There is reason to believe that the content of confabulations is not motivationally neutral; in particular, they appear to "improve" the world experienced by the patient, making it more pleasant than the reality of the situation demands. The present study investigated the content of the confabulations of a neurological patient, ES: a 56-year-old man, who developed a striking confabulatory syndrome following removal of a meningioma in the pituitary and suprasellar region. ES's cognitive abilities were severely compromised, and he confabulated continuously and bizarrely. Raters presented with transcriptions of ES's confabulations found them to represent significantly more pleasant experiences than their corresponding, misrepresented realities. This finding suggests that confabulations include motivated (or "wishful") content. The influence of this motivational feature of confabulation must be considered in parallel with the memory and executive deficits which contribute to the mechanism of confabulation.

Affect↗
PubMed2004

Freud returns.

Explore the source record for details and available documents.

Brain↗
PubMed2004

Dissociative identity disorder associated with mania and change in handedness.

OBJECTIVE: To investigate the overlap between dissociative and bipolar disorders with reference to their neurophysiological foundations. BACKGROUND: Case reports of anomalous lateralization and shifts in handedness associated with both affective and dissociative conditions have intermittently surfaced in the literature. The two disorders are, however, usually considered to be distinct psychopathological entities. METHOD: A case of co-occurring bipolar disorder and dissociative identity disorder (DID) is presented. RESULTS: The "switch" in personality coincided with manic or hypomanic symptoms and was associated with a change in handedness. CONCLUSIONS: A parallel between the "personality" shifts that characterize DID and the mood fluctuations that underlie bipolar disorder is drawn, suggesting some nosological overlap between the two disorders. The possibility that these two psychiatric conditions share a similar neurophysiological architecture is also raised.

Adolescent↗