Tim Crow (1980) suggested that positive symptoms may be the result of a disturbance of neurotransmitter mechanisms, whereas negative symptoms may be due to a structural abnormality in the brain.
Structural Abnormalities in Schizophrenia
PET, CAT and MRI imaging of live schizophrenic brains has revealed:
- Larger than average ventricles, particularly on the left side of the brain (Cannon & Marco, 1994).
- Research has failed, however to link this to negative symptomatology. Only 5 of 18 studies reviewed by Lewis (1990) found a significant relationship. It may be too crude a measure of structural abnormality.
- Small frontal lobes, cerebrums, and craniums
- Decreased blood flow in the frontal lobes
- A lack of ability to activate the frontal lobes during frontal tasks (Andreasen, 1992).
These have all been linked to negative symptoms in schizophrenic patients (Liddle & Morris, 1991).
Post mortem tissue analysis has also revealed chronic abnormalities in the orientation of cells in the hippocampi of schizophrenics; these have not been found in degenerative disorders such as Alzheimer's disease or Huntington’s chorea, so schizophrenia may be a developmental disorder, where the abnormalities occur during embryogenesis when cells are migrating (Kovelman & Schiebel, 1984).
That schizophrenia is due to abnormalities that occur in the developing embryo is supported by the finding that schizophrenics are more likely to have minor physical abnormalities such as dermatological (skin) and craniofacial malformation (abnormal formation of the skull and face), although these seem to be markers of general early neuromaldevelopment rather than of a specific disorder like schizophrenia (Ismail et al, 2000).
Crow (1980) originally believed that the structural abnormalities were caused by a viral infection. This is because research has shown that more sufferers of schizophrenia are born during early spring and late winter than during the summer (Hare, 1988).
Mednick et al (1988) studied the Asian flu epidemic of 1957: In the early spring of 1958, they found, there was a doubling in the number of births of people who would later be diagnosed as schizophrenic. This has also been found in similar studies (e.g., Adams et al., 1993). Nevertheless, some studies have found no effect of flu epidemics on schizophrenia rates.
Crow now believes, however, that a virus is not responsible for the abnormalities. Instead he believes that the genetic mechanism for the development of language (esp. hemispheric specialisation) is responsible. According to Crow: “The brain changes in schizophrenia can be seen to include an ‘arrest of development’ of cerebral asymmetry”.
Nevertheless, the glial cell theory of Moises, Zoega & Gottesman (2002) may offer a plausible mechanism for the abnormal development of the schizophrenic brain. This theory combines genetic and viral influences on the development of schizophrenia.
Moises, Zoega & Gottesman (2002) have found genes that code for growth factors that affect the development of glial cells in chromosome areas associated with schizophrenia. They suggest that this may result in unhealthy glial cells and, thus, weaken communication between neurons. They also propose that viruses such as human herpes virus 6 may further weaken deficient glial cells (see “Abnormal Brain Structure”). Recent research using diffusion tensor imaging has supported the glial cell theory.
