pathways, and so it stands to reason that the third one, which transmits messages to the frontal lobes, also becomes dysfunctional over time. If so, researchers could expect to find a global decline in brain function in patients diagnosed with tardive dyskinesia, and from 1979 to 2000, more than two dozen studies found that to be the case. “The relationship appears to be linear,” reported Medical College of Virginia psychiatrist James Wade in 1987. “Individuals with severe forms of the disorder are most impaired cognitively.” 48 Researchers determined that tardive dyskinesia was associated with a worsening of the negative symptoms of schizophrenia (emotional disengagement); psychosocial impairment; and a decline in memory, visual retention, and the capacity to learn. People with TD lose their “road map of consciousness,” concluded one investigator. 49 Investigators have dubbed this long-term cognitive deterioration tardivedementia; in 1994, researchers found that three-fourths of medicated schizophrenia patients seventy years and older suffer from a brain pathology associated with Alzheimer’s disease. 50
MRI studies
The invention of magnetic resonance imaging technology provided researchers with the opportunity to measure volumes of brain structures in people diagnosed with schizophrenia, and while they hoped to identify abnormalities that might characterize the illness, they ended up documenting instead the effect of antipsychotics on brain volumes. In a series of studies from 1994 to 1998, investigators reported that the drugs caused basal ganglion structures and the thalamus to swell, and the frontal lobes to shrink, with these changes in volumes “dose related.” 51 Then, in 1998, Raquel Gur at the University of Pennsylvania Medical Center reported that the swelling of the basal ganglia and thalamus was “associated with greater severity of both negative and positive symptoms.” 52
This last study provided a very clear picture of an iatrogenic process. The antipsychotic causes a change in brain volumes, and as this occurs, the patient becomes more psychotic (known as the “positive symptoms” of schizophrenia) and more emotionally disengaged (“negative symptoms”). The MRI studies showed that antipsychotics worsen the very symptoms they are supposed to treat, and that this worsening begins to occur during the first three years that patients are on the drugs.
Modeling psychosis
As part of their investigations of schizophrenia, researchers have sought to develop biological “models” of psychosis, and one way they have done that is to study the brain changes induced by various drugs—amphetamines, angel dust, etc.—that can trigger delusions and hallucinations. They also have developed ways to induce psychotic-like behaviors in rats and other animals. Lesions to the hippocampus can cause such disturbed behaviors; certain genes can be “knocked out” to produce such symptoms. In 2005, PhilipSeeman reported that
all
of these psychotic triggers cause an increase in D 2 receptors in the brain that have a “HIGH affinity” for dopamine, and by that, he meant that the receptors bound quite easily with the neurotransmitter. These “results imply that there may be many pathways to psychosis, including multiple gene mutations, drug abuse, or brain injury, all of which may converge via D 2 HIGH to elicit psychotic symptoms,” he wrote. 53
Seeman reasoned that this is why antipsychotics work: They block D 2 receptors. But in his research, he also found that these drugs, including the newer ones like Zyprexa and Risperdal, double the density of “high affinity” D 2 receptors. They induce the same abnormality that angel dust does, and thus this research confirms what Lars Martensson observed in 1984: Taking a neuroleptic is like having a “psychosis inducing agent built into the brain.”
Nancy Andreasen’s longitudinal MRI study
In 1989, Nancy Andreasen, a psychiatry professor at the University
MRI studies
The invention of magnetic resonance imaging technology provided researchers with the opportunity to measure volumes of brain structures in people diagnosed with schizophrenia, and while they hoped to identify abnormalities that might characterize the illness, they ended up documenting instead the effect of antipsychotics on brain volumes. In a series of studies from 1994 to 1998, investigators reported that the drugs caused basal ganglion structures and the thalamus to swell, and the frontal lobes to shrink, with these changes in volumes “dose related.” 51 Then, in 1998, Raquel Gur at the University of Pennsylvania Medical Center reported that the swelling of the basal ganglia and thalamus was “associated with greater severity of both negative and positive symptoms.” 52
This last study provided a very clear picture of an iatrogenic process. The antipsychotic causes a change in brain volumes, and as this occurs, the patient becomes more psychotic (known as the “positive symptoms” of schizophrenia) and more emotionally disengaged (“negative symptoms”). The MRI studies showed that antipsychotics worsen the very symptoms they are supposed to treat, and that this worsening begins to occur during the first three years that patients are on the drugs.
Modeling psychosis
As part of their investigations of schizophrenia, researchers have sought to develop biological “models” of psychosis, and one way they have done that is to study the brain changes induced by various drugs—amphetamines, angel dust, etc.—that can trigger delusions and hallucinations. They also have developed ways to induce psychotic-like behaviors in rats and other animals. Lesions to the hippocampus can cause such disturbed behaviors; certain genes can be “knocked out” to produce such symptoms. In 2005, PhilipSeeman reported that
all
of these psychotic triggers cause an increase in D 2 receptors in the brain that have a “HIGH affinity” for dopamine, and by that, he meant that the receptors bound quite easily with the neurotransmitter. These “results imply that there may be many pathways to psychosis, including multiple gene mutations, drug abuse, or brain injury, all of which may converge via D 2 HIGH to elicit psychotic symptoms,” he wrote. 53
Seeman reasoned that this is why antipsychotics work: They block D 2 receptors. But in his research, he also found that these drugs, including the newer ones like Zyprexa and Risperdal, double the density of “high affinity” D 2 receptors. They induce the same abnormality that angel dust does, and thus this research confirms what Lars Martensson observed in 1984: Taking a neuroleptic is like having a “psychosis inducing agent built into the brain.”
Nancy Andreasen’s longitudinal MRI study
In 1989, Nancy Andreasen, a psychiatry professor at the University
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