| 1. |
- Eckerström, Carl, et al.
(författare)
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Small baseline volume of left hippocampus is associated with subsequent conversion of MCI into dementia. The Göteborg MCI study.
- 2008
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Ingår i: Journal of the Neurological Sciences. - : Elsevier BV. - 0022-510X .- 1878-5883. ; 272:1-2, s. 48-59
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Tidskriftsartikel (refereegranskat)abstract
- Background: Earlier studies have reported that hippocampal atrophy can to some extent predict which patients with mild cognitive impairment (MCI) will subsequently convert to dementia, and that converters have an enhanced rate of hippocampal volume loss. Objective: To further validate the hypothesis that hippocampal atrophy predicts conversion from MCI to dementia, to relate baseline hippocampal volume to different forms of dementia, and to investigate the role of hippocampal side differences and rate of volume loss over time. Patients: The subjects (N = 68) include patients with MCI at baseline and progression to dementia at the two-year follow-up (N = 21), stable MCI patients (N = 21), and controls (N = 26). Among the progressing patients, 13 were diagnosed as having AD. Methods: The Göteborg MCI study is a clinically based longitudinal study with biannual clinical assessments. Hippocampal volumetry was performed manually on the MRI investigations at baseline and at the two-year follow-up. Results: Hippocampal volumetry could predict conversion to dementia in both the AD and the non-AD subgroup of converters. Left hippocampal volume in particular discriminated between converting and stable MCI. Cut off points for individual discrimination were shown to be potentially useful. The converting MCI group had a significantly higher rate of hippocampal volume loss as compared to the stable MCI group. Conclusions: In MCI patients, hippocampal volumetry at baseline gives prognostic information about possible development of AD and non-AD dementia. Contrary to earlier studies, we found that left hippocampal volume has the best predictive power. Reliable predictions appear to be possible in many individual cases.
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| 2. |
- Malmgren, Helge, 1945
(författare)
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Classical Rorschach
- 2004
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Ingår i: Internet.
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- These web pages are devoted to the presentation and promotion of the Rorschach method, concentrating on the way it has been practiced within the classical European tradition - from Hermann Rorschach himself in 1921, via Ewald Bohm in the 1950's, 1960's and 1970's, and to the contemporary workers in the Rorschach-Bohm tradition. You can here find basic information about Hermann Rorschach, about the different Rorschach traditions and the essential differences between them, and about the current scientific debate about the Rorschach test. There are also some links to other Web pages devoted to the Rorschach method. The information on these pages has been carefully selected so that it can be made publicly available without interferring with the clinical and scientific use of the Rorschach test. Hence no specific information about the test procedure, about response categories and so on has been included, and of course no pictures of the Rorschach cards are shown.
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| 3. |
- Malmgren, Helge, 1945
(författare)
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Descartes visdom : Descartes' wisdom
- 2005
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Ingår i: Svenska Läkaresällskapets Riksstämma, 30/11–2/12 2005.
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- A. Damasio's bestseller "Descartes' error" is based on a fundamental confusion. The famous words of Descartes, "I think, therefore I am", is a statement about epistemological order: the first statement is his ground for believing the second. However, Damasio interprets it as a causal statement to the effect that thinking causes bodily processes, and argues that causation goes the other way. Through this confusion, Damasio fails to see the wisdom of Descartes that has survived centuries of criticism: that our knowledge about our own consciousness is not derived from knowledge of physical processes.
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| 4. |
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| 5. |
- Malmgren, Helge, 1945
(författare)
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Rorschach’s idea of a “movement” response in the light of recent philosophy and psychology of perception
- 2000
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Ingår i: Rorschachiana. Yearbook of the International Rorschach Society. - 1192-5604. ; 24, s. 1-27
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Tidskriftsartikel (refereegranskat)abstract
- The proper definition of the kinesthetic or movement (M) category has been the subject of many controversies within the Rorschach community; see, for example, the discussion between Kramer and Exner (Kramer, 1991; Exner, 1991). The present paper elucidates the nature of movement responses by means of a theoretical analysis of some of the key concepts involved. This analysis in part is of a philosophical character, but I also bring in several recent results from the psychology and neurophysiology of perception which in my opinion are crucial to a correct understanding of the movement responses. The first two parts of the essay describe the basic controversy between those Rorschach theorists who – like Hermann Rorschach himself and Ewald Bohm – hold that kinesthetic identification is a necessary ingredient in any movement response, and those – like John Exner – who want to drop this condition from the definition. This controversy is shown to involve another fundamental issue, namely: In what sense is movement a determinant, and what should be meant by a determinant? The third section also discusses a main objection against keeping Rorschach’s original definition: its reliance on introspective criteria. The fourth part takes a historical perspective, describing the philosophical and psychological tradition called associationism, discussing certain ideas concerning kinesthetic sensibility brought forward within that tradition, and finally analyzing the nature and extent of Hermann Rorschach’s commitment to associationism, especially as manifested in his doctoral dissertation. Some main elements of the 20th-century psychological and philosophical critique of associationism are outlined in Sections 5–6, and the relevance of this critique for the definition of a movement response is explained. Converging evidence from different sources, such as child psychology and clinical and primate neuropsychology, is then brought together in Section 7 to show that recent work on perception supports Hermann Rorschach’s basic intuition about the M category. In Section 8, a new definition of movement responses is given in terms of practical perception and immediate visuo-motor couplings. Finally, in Section 9, the possible use of Rorschach data in the experimental analysis of motion-from-form perception is pointed out.
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| 7. |
- Eckerström, Carl, et al.
(författare)
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The Göteborg MCI study – absolute and normalized hippocampal volumes in the prediction of dementia
- 2007
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Ingår i: The Annual General Meeting of the Swedish Society of Medicine, Nov. 28-30, 2007.
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Mild cognitive impairment (MCI) is a state where the cognitive functions are more impaired than what would be expected from aging alone but not enough to be described as dementia. In our material, there was an overrepresentation of men in the stable MCI group and an overrepre-sentation of women in the two other groups. Normalization of the data removed the gender-related differences in hippocampal volume and allowed for better utilization of the data. Hippocampal volumetry predicts conversion to dementia in MCI patients.
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| 8. |
- Malmgren, Helge, 1945
(författare)
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Hypotesen om schizofreni som en "hjärnsjukdom" återstår att visa
- 2007
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Ingår i: Läkartidningen. - 0023-7205. ; 204, s. 2152-5
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Tidskriftsartikel (refereegranskat)abstract
- - De senaste decenniernas hjärnforskning har påvisat många avvikelser i schizofrena patienters hjärnor jämfört med friska personer och patienter som har andra psykiska sjukdomar. - Fynden får inte utan vidare tolkas som att de icke-genetiska faktorerna i schizofreniernas etiologi är i traditionell mening ”organiska”. Även psykogena tillstånd, exempelvis sorgereaktioner och inlärda kunskaper, innebär förändringar i hjärnan. - Att beskriva schizofreni som en ”hjärnsjukdom” enbart på grund av påvisbara hjärnförändringar är därför att göra sig skyldig till ett felslut. - Symptomatologin vid schizofreni har endast ytliga likheter med symptombilderna vid de psykosyndrom som vi säkert vet är somatogena. - Den samlade evidensen talar för att det finns samband mellan fetala och perinatala skadefaktorer och senare utveckling av schizofreni. Sambanden är dock generellt svaga och det är inte klarlagt i vilken utsträckning de är kausala. - Någon substantiell evidens för att schizofrena patienter skulle ha varit utsatta för fler hjärnskador, hjärnsjukdomar eller allmäninfektioner senare i livet finns inte. - De forskningsresultat som finns talar därför mot hypotesen att schizofreni är en hjärnsjukdom (i betydelsen av ett uteslutande organiskt betingat syndrom), och gör det istället troligt att många fall av schizofreni har en avsevärd psykogen komponent.
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| 9. |
- Malmgren, Helge, 1945
(författare)
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Is schizophrenia a brain disease? : Är schizofreni en hjärnsjukdom?
- 2006
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Ingår i: Philosophy, Psychiatry and the Neurosciences: 9th International Conference on Philosophy, Psychiatry and Psychopathology. Leiden, June 29, 2006.
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Recent advances in brain imaging techniques have made it possible to discern changes in brain morphology and function in several different psychiatric disorders. Should such results be taken as evidence for an “organic” etiology of these disorders? A well-known objection says that the visible physical changes could be effects instead of causes. An even more important possibility, which is usually overlooked, is that the observable anatomic or physiological changes may be the immediate biological substrate of the psychiatric condition. Even the paradigmatically “psychogenic” condition which consists in the possession of learned knowledge has such a substrate. This substrate has been observed by imaging methods, but no one (I hope) would draw the conclusion that the possession of learned knowledge is not a mental state, or that it is not mentally caused. Similarly, the observation that, e.g., schizophrenia is accompanied by observable changes of the brain must not be taken as proof that schizophrenia is not a mental disorder, or that the non-hereditary etiological component in schizophrenia (which accounts for some 50% of the variance) is “organic” in nature. For the latter conclusion, one would need support from independent findings of such exogenic or endogenic biological and physical events in the patient’s history as could lead to organic lesions. Notably, the evidence for an overrepresentation of such events in the history of schizophrenic patients is scarce. My conclusion is that the total evidence is quite compatible with the possibility that schizophrenia is a mental disorder with an strong psychogenic component.
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