Dementia Praecox and Paraphrenia

Kraepelin, Emil

doi:10.1097/00005053-192110000-00104

Cited by 1,087 publications

(1,353 citation statements)

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“…Syphilitic insanity was common in that era, and manifestations included psychosis. When the cause was determined and these cases were recognized and separated from other forms of madness, it was possible for Kraepelin to distinguish the illness patterns on which he proposed the two major forms of chronic psychotic illness (Kraepelin, 1919). The manic-depressive psychoses were described and separated from dementia praecox.…”

Section: History Of the Concept And A Paradigm Shift: Relevance To Drmentioning

confidence: 99%

The Evolution of Drug Development in Schizophrenia: Past Issues and Future Opportunities

Carpenter

Koenig

2007

Neuropsychopharmacol

185

128

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Section: History Of the Concept And A Paradigm Shift: Relevance To Drmentioning

confidence: 99%

The Evolution of Drug Development in Schizophrenia: Past Issues and Future Opportunities

Carpenter

Koenig

2007

Neuropsychopharmacol

185

128

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“…[1][2][3][4] Among those, many fulfill the deterioration criteria of Kraepelin's dementia praecox. 5 These facts already justify the use of the term degeneration in schizophrenia. Further neurodegenerative aspects of the disease, however, are still a matter of dispute among scientists while there is overall agreement on neurodevelopmental alterations providing the ground for schizophrenia.…”

Section: Introductionmentioning

confidence: 98%

“…10,[13][14][15][16] Unfortunately, no drug up till now has been clearly shown to have lasting beneficial effects on cognition in schizophrenia. [14][15][16][17] The increasing evidence of neurodegenerative mechanisms acting in schizophrenia, particularly that derived from imaging data demonstrating progressive loss of cortical gray matter in this condition, [18][19][20] have led to a virtual renaissance of Kraepelin's dementia praecox considerations, 5 and have stimulated novel concepts of the disease, 7,[21][22][23][24][25] including therapeutic neuroprotection. 26 Based on previous observations by ourselves and others, erythropoietin (EPO) appears to be a promising candidate for neuroprotection in schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Improvement of cognitive functions in chronic schizophrenic patients by recombinant human erythropoietin

et al. 2006

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Schizophrenia is increasingly recognized as a neurodevelopmental disease with an additional degenerative component, comprising cognitive decline and loss of cortical gray matter. We hypothesized that a neuroprotective/neurotrophic add-on strategy, recombinant human erythropoietin (rhEPO) in addition to stable antipsychotic medication, may be able to improve cognitive function even in chronic schizophrenic patients. Therefore, we designed a doubleblind, placebo-controlled, randomized, multicenter, proof-of-principle (phase II) study. This study had a total duration of 2 years and an individual duration of 12 weeks with an additional safety visit at 16 weeks. Chronic schizophrenic men (N = 39) with defined cognitive deficit (X1 s.d. below normal in the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)), stable medication and disease state, were treated for 3 months with a weekly short (15 min) intravenous infusion of 40 000 IU rhEPO (N = 20) or placebo (N = 19). Main outcome measure was schizophrenia-relevant cognitive function at week 12. The neuropsychological test set (RBANS subtests delayed memory, language-semantic fluency, attention and Wisconsin Card Sorting Test (WCST-64) -perseverative errors) was applied over 2 days at baseline, 2 weeks, 4 weeks and 12 weeks of study participation. Both placebo and rhEPO patients improved in all evaluated categories. Patients receiving rhEPO showed a significant improvement over placebo patients in schizophrenia-related cognitive performance (RBANS subtests, WCST-64), but no effects on psychopathology or social functioning. Also, a significant decline in serum levels of S100B, a glial damage marker, occurred upon rhEPO. The fact that rhEPO is the first compound to exert a selective and lasting beneficial effect on cognition should encourage new treatment strategies for schizophrenia.

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“…Beginning with the concept of dementia praecox proposed by Emil Kraepelin [1], research into the physiological substrates of cognitive dysfunctions and clinical symptoms of schizophrenia has been predominantly pursued with the assumption that pathophysiological processes are to be found in alterations of circumscribed brain regions and circuits. Advances in functional and anatomical magnetic resonance imaging (MR/fMRI) have supported this hypothesis through providing a large body of work demonstrating changes in brain functioning as well anatomical parameters across cortical regions in schizophrenia.…”

Section: Introductionmentioning

confidence: 99%