Schizophrenia Bulletin

Dalén,, Per

doi: 10.1093/schbul/16.3.363pmid: 2287926

Abstract Subdividing a sample of patients on the basis of family history into familial and sporadic cases is a simple research method whose purpose is often misunderstood. What it can do is to reveal etiological heterogeneity by refuting a hypothesis of homogeneity. If familial cases prove to be different from sporadic cases in some respect, the question of a refutation arises. Homogeneity is usually assumed in genetic work on schizophrenia. This assumption is also widespread outside genetic circles, but it is not necessarily true. If it is false, research into the causes of schizophrenia must be redirected. The author claims that the use of familial/sporadic subdivisions is a clinical research method that does not require genetic expertise. Geneticists may frown upon it for its lack of sophistication, but the important thing is whether it works in actual attempts to refute the homogeneity view. This content is only available as a PDF. © Oxford University Press

Dalén, Per

doi: N/Apmid: N/A

Subdividing a sample of patients on the basis of family history into familial and sporadic cases is a simple research method whose purpose is often misunderstood. What it can do is to reveal etiological heterogeneity by refuting a hypothesis of homogeneity. If familial cases prove to be different from sporadic cases in some respect, the question of a refutation arises. Homogeneity is usually assumed in genetic work on schizophrenia. This assumption is also widespread outside genetic circles, but it is not necessarily true. If it is false, research into the causes of schizophrenia must be redirected. The author claims that the use of familial/sporadic subdivisions is a clinical research method that does not require genetic expertise. Geneticists may frown upon it for its lack of sophistication, but the important thing is whether it works in actual attempts to refute the homogeneity view.

Dalén, Per

doi: 10.1093/schbul/16.3.363pmid: 2287926

Subdividing a sample of patients on the basis of family history into familial and sporadic cases is a simple research method whose purpose is often misunderstood. What it can do is to reveal etiological heterogeneity by refuting a hypothesis of homogeneity. If familial cases prove to be different from sporadic cases in some respect, the question of a refutation arises. Homogeneity is usually assumed in genetic work on schizophrenia. This assumption is also widespread outside genetic circles, but it is not necessarily true. If it is false, research into the causes of schizophrenia must be redirected. The author claims that the use of familial/sporadic subdivisions is a clinical research method that does not require genetic expertise. Geneticists may frown upon it for its lack of sophistication, but the important thing is whether it works in actual attempts to refute the homogeneity view.

Farmer,, Anne;McGuffin,, Peter;Gottesman, Irving, I.

doi: 10.1093/schbul/16.3.367pmid: 2287927

Abstract The authors defend the proposition that the simple division of schizophrenia into family history positive versus family history negative in the hope of uncovering etiological heterogeneity is too naive for a multifactorial disorder as contrasted with rare, mendelizing genetic conditions. Dalén is correct to forecast that a monolithic homogeneity view about the origins of schizophrenia is likely to be refuted and that it is important to pursue such a strategy. Using computed tomographic brain scan results and the simple dichotomy of family history positive versus family history negative as an illustration, we show the weakness (lack of statistical power) of the strategy. The problem arises from the fact that a negative family history for schizophrenia characterizes the vast majority of schizophrenic patients just as it does for insulin-dependent diabetes, another genetically influenced multifactorial disorder. A continuum from more genetic to less genetic variation in the etiology of schizophrenia fits the available familial patterns of risk. This content is only available as a PDF. © Oxford University Press

Farmer, Anne; McGuffin, Peter; Gottesman, Irving I.

doi: N/Apmid: N/A

The authors defend the proposition that the simple division of schizophrenia into family history positive versus family history negative in the hope of uncovering etiological heterogeneity is too naive for a multifactorial disorder as contrasted with rare, mendelizing genetic conditions. Dalén is correct to forecast that a monolithic homogeneity view about the origins of schizophrenia is likely to be refuted and that it is important to pursue such a strategy. Using computed tomographic brain scan results and the simple dichotomy of family history positive versus family history negative as an illustration, we show the weakness (lack of statistical power) of the strategy. The problem arises from the fact that a negative family history for schizophrenia characterizes the vast majority of schizophrenic patients just as it does for insulindependent diabetes, another genetically influenced multifactorial disorder. A continuum from more genetic to less genetic variation in the etiology of schizophrenia fits the available familial patterns of risk.

Farmer, Anne; McGuffin, Peter; Gottesman, Irving I.

doi: 10.1093/schbul/16.3.367pmid: 2287927

The authors defend the proposition that the simple division of schizophrenia into family history positive versus family history negative in the hope of uncovering etiological heterogeneity is too naive for a multifactorial disorder as contrasted with rare, mendelizing genetic conditions. Dalén is correct to forecast that a monolithic homogeneity view about the origins of schizophrenia is likely to be refuted and that it is important to pursue such a strategy. Using computed tomographic brain scan results and the simple dichotomy of family history positive versus family history negative as an illustration, we show the weakness (lack of statistical power) of the strategy. The problem arises from the fact that a negative family history for schizophrenia characterizes the vast majority of schizophrenic patients just as it does for insulindependent diabetes, another genetically influenced multifactorial disorder. A continuum from more genetic to less genetic variation in the etiology of schizophrenia fits the available familial patterns of risk.

Hyde, Alexander P.

doi: N/Apmid: N/A

This article addresses itself to the apparent conflict between those reports indicating that caffeine affects schizophrenic behavior and the present study which failed to show substantial behavior or medication changes with caffeine. It is suggested that there are important subgroups of schizophrenic patients who are unusually sensitive to caffeine’s apparent psychotogenic actions as reported in case reports and data on violence and destruction. It is also suggested that there are subgroups of schizophrenia which seem to require increased medication doses to “cover” caffeine effects.

Hyde, Alexander P.

doi: 10.1093/schbul/16.3.371pmid: 1981106

This article addresses itself to the apparent conflict between those reports indicating that caffeine affects schizophrenic behavior and the present study which failed to show substantial behavior or medication changes with caffeine. It is suggested that there are important subgroups of schizophrenic patients who are unusually sensitive to caffeine’s apparent psychotogenic actions as reported in case reports and data on violence and destruction. It is also suggested that there are subgroups of schizophrenia which seem to require increased medication doses to “cover” caffeine effects.

Hyde, Alexander, P.

doi: 10.1093/schbul/16.3.371pmid: 1981106

Abstract This article addresses itself to the apparent conflict between those reports indicating that caffeine affects schizophrenic behavior and the present study which failed to show substantial behavior or medication changes with caffeine. It is suggested that there are important subgroups of schizophrenic patients who are unusually sensitive to caffeine's apparent psychotogenic actions as reported in case reports and data on violence and destruction. It is also suggested that there are subgroups of schizophrenia which seem to require increased medication doses to “cover” caffeine effects. This content is only available as a PDF. © Oxford University Press

Koczapski, Andrzej B.; Ledwidge, Barry; Paredes, Jaime; Kogan, Claudio; Higenbottam, John

doi: N/Apmid: N/A

The authors describe intoxicationrelated behavior patterns observed among 89 chronic schizophrenic inpatients over a 5-year period. These include caffeine intoxication, water intoxication, antihistamine intoxication, nicotine withdrawal, voluntary hyperventilation, and ingestion of deodorants and aerosols. Affected patients tended to abuse multiple substances in the hospital, to have generalized polydipsia, and to have histories of drug or alcohol abuse before hospitalization. Periodic intoxication in this population may be an important contributor to the refractoriness of their psychotic symptoms.