Ropper, Allan H. and Brown, Robert H., Principles of Neurology, 8th Ed. NY: McGraw-Hill, 2005.

We studied the behavioral, cognitive, and neuroimaging characteristics of obsessive-compulsive disorder (OCD) in 13 patients with focal brain lesions (acquired OCD) and compared their clinical features and the severity of obsessive and compulsive (OC) symptoms with patients with idiopathic OCD. Both OCD groups were further compared with matched normal controls on a series of neuropsychological tests. Patients with acquired OCD had a negative familial history and later age at onset of OCD symptoms than patients with idiopathic OCD. The two OCD groups showed relatively similar clinical phenomenology, severity of OC symptoms, and profile of neuropsychological deficits. Compared with normal control subjects, both OCD groups showed cognitive deficits affecting attention, intellectual function, memory, word retrieval, and motor and executive functions. Eight of the 13 patients with acquired OCD had abnormal neurologic examinations, whereas only 3 of the 13 patients with idiopathic OCD had abnormal neurologic examinations. Neuroimaging in the acquired OCD group disclosed a variety of lesions involving exclusively the cerebral cortex (frontal, temporal, or cingulate regions), the basal ganglia, or both. These results suggest that acquired and idiopathic OCDs may share a common pathophysiologic mechanism, and that structural damage to specific frontal-limbic-subcortical circuits plays an important role in the pathogenesis of acquired OCD.

The pharmacological efficacy of serotonergic-acting drugs suggest that patients with obsessive-compulsive disorder (OCD) may have alterations in their cerebral serotonergic (5-HT) receptor system, and previous neuroimaging studies of OCD patients have shown abnormalities in several fronto-subcortical regions. In this study we investigated cerebral 5-HT(2A) receptor binding in 15 untreated OCD patients and in 15 age- and gender-matched healthy volunteers by magnetic resonance imaging and [(18)F]altanserin positron emission tomography (PET). Eleven of the patients were rescanned with PET after receiving treatment with a selective serotonin reuptake inhibitor (SSRI). The distribution volumes of specific tracer binding (DV(3)') were calculated for 12 brain regions, and comparisons were made between: (1) healthy volunteers vs. untreated OCD patients, (2) healthy volunteers vs. treated OCD patients, and (3) OCD patients before and during treatment. When comparing the distribution volume for specific fronto-subcortical brain regions, significantly higher values were recorded in the caudate nuclei in OCD patients (DV(3)': 0.24+/-0.14) compared to the healthy control group (DV(3)': 0.15+/-0.13) (p<0.05, Wilcoxon matched-pairs test). This difference between groups was not present after treatment with SSRIs. There was no correlation between the severity of OCD symptoms and 5-HT(2A )receptor binding. An increase in 5-HT(2A) receptor binding is found in the caudate nuclei of untreated patients with OCD. The up-regulation in 5-HT(2A) receptors might be compensatory for a lack of serotonin in the feedback loop between the thalamus and orbito-frontal cortex, the caudate nuclei, and the globus pallidus.

Berthier ML. Unidad de Neurología Conductual, Hospital Clínico Universitario, Universidad de Málaga, España. mberthier@telenet.es INTRODUCTION: Although obsessive-compulsive symptoms are uncommon among patients with neurological diseases, structural neuroimaging (CAT or MRI) disclose focal brain lesions in some patients. However, little is know about the clinical phenomenology of obsessive-compulsive symptoms and the cognitive deficits that occur in neurological conditions. OBJECTIVE: To review the cognitive functioning of patients who develop an obsessive-compulsive disorder (OCD) in association with focal brain lesions. DEVELOPMENT: In the present study, the author review recent studies which suggest that OCD associated with brain lesions is relatively similar to idiopathic or 'functional' OCD (i.e., OCD unassociated with gross brain damage). Idiopathic and acquired forms of OCD are clinically heterogeneous. The content of obsessions and compulsions in acquired OCD depends, at least in part, of the causative lesion, whereas the pattern of cognitive deficits is more homogeneous affecting attention, general intelligence, verbal and visuospatial memory, and executive function. CONCLUSION: It is suggested that the study of different subgroups of patients with acquired OCD would detect differences in the phenomenology of obsessions and compulsions as well as in the pattern of cognitive deficits. Moreover, this approach can improve our understanding about the pathophysiological mechanisms underlying idiopathic OCD.

There are people in Oregon prisons because the voices told them to do it, but they were not really schizophrenic voices. The voices could be explained by the criminal misuse of a subliminal activation system. People can be programmed with subliminal training messages to commit crimes. Hidden perpetration of crimes with subliminal training is not detected with ordinary psychological screening. The electronic system causes organic impairment of the brain. Evidence of such impairment can be found in Kip Kinkel and Ray Perkins. They were programmed to kill.

The electromagnetic assault of a subliminal training system causes a particular set of neurological impairments, like a signature. Areas of of the brain that process auditory and visual perception are overloaded by chronic subliminal activation. This results in poor spelling and visual retention. The coordination of one hand is impaired. If this is the dominant hand, then handwriting will be impaired. The prefrontal lobe, the area that chooses between self-motivation and external input, is impaired by the electronic thought control system.

Persistent and hidden electronic coercion interferes with emotional development. Kinkel was three years behind at age 15. Perkins was four years behind at age 14. The chronic distortion of perception and the social isolation that are imposed by the subliminal training may lead to poor reality testing.

A clinical state of paranoia is typical in these cases and could logically be the result of an inability to identify hidden interference with the defendant's social learning skills.

Although hidden perpetrators go to elaborate effort to create a false conduct disorder, these unfortunate defendants are discovered to be psychotic. After the crime is committed, the psychosis wears off. Dr. Sack found that Kinkel was developing a psychosis instead of a conduct disorder (Sentencing, pp. 699, 704). Perkins did not have a real conduct disorder either.

Kinkel had an impaired sense of touch in the left hand. this indicates an impairment in the right parietal lobe (Sentencing, p. 588). Kinkel had impairment of the prefrontal lobe. When this area is impaired, one looses ability to choose between self-motivation and external input (Sentencing, 586). The right frontal area was the most impaired (Sentencing, p. 589).

Poor spelling is a sign of impairment of auditory processing. Persistent bombardment by electronic coercion systems can cause this. Perkins took the WRAT-R in June, 2002. He was 14 years old. His reading and math were sixth grade level. His spelling was fourth grade level. His IQ was 84 (State's Exhibit 18). Kinkel was uncommonly bright, but his spelling was very poor. He was in advanced classes for other subjects, but had to go to special classes for spelling.

Kinkel's reading was not good. He had a low visual memory. Kinkel had a nerve impairment of the left hand.

Perkins was tested in detention in June, 2002. His over all IQ on the Wechsler intelligence test was 84. His lowest score was on the Coding scale. Students who have visual-motor coordination delays or a weak visual recall ability will score low on this scale. He processes visual information and reproduces it much slower than other students. This impaired his penmanship. His level of processing of visual information and reproducing it motorically was at age 10 years, 3 months (Psychoeducational Evaluation). He was 14 years old.

Of Perkins, one teacher, Janice Nason, said, "He could hardly spell. He had capabilities, but he didn't have belief in himself." (Naffziger, p. 8).

Another teacher said reading was Perkins' biggest problem (Naffziger, p. 11).

Perkins' handwriting was poor. He had an impairment of motor control of his right hand.

In June, 2002, Perkins was tested with the Wechsler intelligence test. His IQ was 84. The mean for the general population is 100. His lowest score on the subtests was for Coding. People who score low on scoring have difficulty interpreting or organizing visually perceived materials when under pressure. Students who have visual-motor corrdination delays or a weak visual recall ability will score low on this scale. He processes visual information and reproduces it much slower than other students. This impaired his penmanship. His level of processing of visual information and reproducing it motorically was at age 10 years, 3 months (Psychoeducational Evaluation). Perkins was 14 years old.

Kinkel had an impaired sense of touch in the left hand. this indicates an impairment in the right parietal lobe (Sentencing, p. 588). Kinkel had impairment of the prefrontal lobe. When this area is impaired, one looses ability to choose between self-motivation and external input (Sentencing, 586). The right frontal area was the most impaired (Sentencing, p. 589). Poor spelling is a sign of impairment of auditory processing. Electronic coercion systems do this. Perkins took the WRAT-R in June, 2002. He was 14 years old. His reading and math were sixth grade level. His spelling was fourth grade level. His IQ was 84 (State's Exhibit 18). Kinkel was uncommonly bright, but his spelling was very poor. He was in advanced classes for other subjects, but had to go to special classes for spelling.

Kinkel's reading was not good. He had a low visual memory. He couldn't remember what he read.

A neurological exam with appropriate psychological tests would shed some light on how the impairment makes the defendants more susceptible to being trained against their will.

Contested Remand Hearing, Case no. JV 8244, Coos County Circuit Court, Oregon, transcript at Court of Appeals, Salem.

Clark, Diane Martha, Letter to Judge Barron, Coos County Circuit Court, June 6, 2002.

Elman, Steven B., Letter to Judge Barron, Coos County Circuit Court, June 2, 2002.

Lange, R. Kristina, "Remand Report," August 14, 2002.

Lange, R. Kristina, Notes, State's Exhibit 13, Case no. JV 8244, Coos County Circuit Court, Oregon Court of Appeals, Salem.

Naffziger, Joyce, Investigative Report, Naffziger Investigations, Eugene, Oregon.

Naffziger, Joyce, Memorandum, July 23, 2002, Defense Exhibit 101.

Perkins, Raymond, A., Journal, State's Exhibit 5.

Psychoeducational Evaluation, August 5, 2002, State's Exhibit 18.

Sack, William H., Letter to Gregory J. Hazarabedian, July 5, 2002.

Sasser, Michael S., Psychiatric Evaluation on Raymond Perkins, June 12, 2002, State's Exhibit 10.

Sentencing Hearing, State v. Kinkel, Kipland P., Lane County Circuit Court, transcript at Oregon Court of Appeals, Salem.

State v. Perkins, Raymond A., Oregon Court of Appeals, Salem, Case no. A119589, transcripts and exhibits from Coos County Circuit Court, Case no. JV 8244.

State's Exhibit 18, Case no. JV 8244, Coos County Circuit Court, Oregon Court of Appeals, Salem.

True, Donald, Letter to Greg Hazarabedian, August 26, 2002.

Waiver Hearing Memorandum of the Coos County District Attorney.

Copyright © 2004 Daniel A. Montgomery

Dan Montgomery
kryptox@sonic.net