Paranoid Schizophrenia is different from other types of schizophrenia in that speech is not disorganized, affect is not flat, and there is no catatonic behavior. What is prominent in paranoid schizophrenia is a preoccupation with one or more delusions (fixed false ideas that are not congruent with ones culture) which generally include a sense of persecution or being singled out, deep fear and hyper-arousal due to a sense of danger, and a corresponding tendency to ‘connect the dots’ into a fixed delusion. This is often accompanied by auditory hallucinations, which can command the person to behave in an aggressive violent or aloof manner.
The Biology of Schizophrenia
Despite years of research, we know relatively little about the biology of schizophrenia. This is due to poor funding of research, inaccessibility of the live brain for study until recently, and a disorganized research approach (Carpenter, 1993). It appears now, however, that researchers are on the verge of rapid progress in understanding the biology of schizophrenia due to improved techniques for studying the brain in both live and post mortem subjects, improved organization of research, and recent validation of the concept of the ‘symptom domains’. These domains include positive symptoms (hallucinations and delusions), cognitive and attentional impairment, and enduring deficit or negative symptoms (inability to integrate sensory information, decreased social and physical pleasure).
For the purpose of organizing the different biological theories of schizophrenia, biological theorists can be divided into two camps: ‘lumpers and splitters’. The ‘lumpers’ propose that the three symptom domains may be the result of one underlying abnormality. This would be analogous to how syphilis or Lyme disease has different clinical appearances depending on which organ systems are affected by the common underlying infection.
In schizophrenia research, the general consensus is that patients manifest a deficit in integrative functioning in the central nervous system. One biological theory of schizophrenia hypothesizes that the disorder is the result of one underlying defect. In this schema (Wexler, 1991), when schizophrenics are presented with almost any task that activates a group of cortical neurons, there is a failure of those neurons to recruit, activate, connect, or link to, additional cortical brain regions. It appears that this process is at least part of how conscious mental associations are made.
Normally such linkage would help to prepare the individual for additional responses, or to elaborate on a particular response. In this theoretical framework a symptom such as poor social interaction results from the inability to elaborate responses in a conversation (poverty of speech or thought). Another theory in the ‘lumpers’ camp is that frontal cortex dopamine activity is abnormally low. Since frontal cortex neurons normally inhibit the deeper subcortical dopamine neurons, this low activity level results in a failure to suppress dopamine activity in the subcortical regions. The result is hallucinations and/or delusions due excess dopamine activity in the subcortical areas. Supporting this theory is the fact that high doses of amphetamines can cause psychosis by increasing the amount of subcortical dopamine activity. The oldest theory in this camp is the almost 30-year-old dopamine hypothesis of schizophrenia (below), which is currently viewed as too simplistic.
In the other camp, the ‘splitters’ contend that it is also possible that schizophrenia is a syndrome in which a common clinical appearance is caused by several different disease processes (similar to diabetes as discussed above). In this schema (Crow, 1980), one could think of a schizophrenic as having the quite unfortunate inheritance of three semi-independent genes. These genetic defects would then cause a cluster of symptoms. Each of these genes would be responsible for the separate symptom domains of schizophrenia. Since these symptom domains occur in isolation from each other as well as together in the schizophrenic (e.g., schizotypy [odd speech and behavior; social aloofness, isolation, anxiety and guardedness] attention deficit disorder [attention, working memory, and other cognitive deficits], and affective disturbances [flattened, inappropriate affect and anhedonia]), the patient might be thought of as having a combination of genetic vulnerabilities.
Genetics of Schizophrenia
That there is a genetic vulnerability to schizophrenia is not in doubt for a variety of reasons. It has been shown that the siblings of schizophrenic patients have an increased risk of the disorder only when they are biological siblings, not adopted. What this genetic vulnerability is, of course, is not known, as no single gene has been identified as a risk factor for schizophrenia. That the gene(s) involved interact with some environmental factor is clear since identical twins share the disorder only about 50% of the time.
According to Schwartz (1988), an individual has an 8% risk of schizophrenia if their sibling is schizophrenic, a 12% risk if one parent is affected, a 14% risk of sharing the disorder in fraternal twins, 39% risk if both parents are affected, and 47% risk when two individuals share the same exact genes. To explain the less than 100% concordance in identical twins some authors (Barr, 1990) hypothesize viral, obstetric, nutritional triggers, which may release the genetic vulnerability.