A twenty megapixel projection display system takes advantage of a micro electro‐mechanical systems (MEMS) based grating light modulator (GLM). In a GLM a laser beam is diffracted by an array of thousands of closely spaced parallel ribbons that simultaneously “paint” an entire column of pixels. The grating light modulator contains only a single column of microscopic ribbons because each pixel can be switched in as little as 100 nanoseconds. This leaves more than enough time to scan the column across a wide image. The present system consists of a linear array of 4096 pixels scanned to produce a projected image 4096 by 5120 pixels in size. Red, green, and blue fiber lasers, using nonlinear optical frequency conversion, provide about 10 watts per color enabling full color video projection onto large screens. A number of these systems have been delivered to planetarium and flight simulator customers.

According to the two currently most popular biological hypotheses, schizophrenic symptoms result from a hyperactivity in dopaminergic neurotransmission or from a hypoactivity in GABAergic neurotransmission. Since diazepam is known to reduce dopamine release and to potentiate GABA, the possible beneficial effects of diazepam were tested in ten hospitalized chronic schizophrenic patients who were resistant to standard neuroleptic treatment. High doses of diazepam, up to 200 mg/day initially, but smaller maintenance doses (less than 55 mg/day diazepam in eight of the ten patients) were added to the previous neuroleptic medication of these patients. The diazepam dose was adjusted daily to avoid oversedation. The effects of diazepam treatment on the mental status were assessed weekly for 12 weeks by the Brief Psychiatric Rating Scale (BPRS), the physician's Clinical Global Impressions Scale (CGI), and the Psychotic inpatient Profile Scale (PIP). For additional documentation, videotapes of mental status interviews were obtained at baseline and during diazepam treatment. These videotapes were rated blind by an independent psychiatrist. The addition of diazepam produced a marked improvement in three, a moderate improvent in four, a mild improvement in one and no change in two of the ten patients. Four of the ten patients were so much improved that they were discharged from the hospital. No side effects were noted, except for one patient who became confused and disoriented on 160 mg diazepam/day. Oversedation was avoided in the other patients, whose maximum daily dose of diazepam was 100 mg or higher, by reducing the diazepam dose within 1 week after the maximum daily dose was reached. It is concluded that diazepam may be of use in the treatment of schizophrenia and that further controlled clinical studies are warranted.

1.1. Verapamil, a papaverine calcium channel blocker, has been used effectively and safely in the treatment of angina pectoris and auricular arrhythmias, and more recently in the treatment of mania.2.2. Many antipsychotic drugs show calcium channel blocking effects similar to verapamil's.3.3. A 41 year old male schizophrenic, only partially responsive to haloperidol decanoate and oral haloperidol, was given increasing doses of verapamil concomitantly, and monitored clinically and by the BPRS, electrocardiogramme, and other laboratory measures.4.4. The patient's total BPRS score dropped from 79 to 41 and remained stable, after initial worsening at lower doses, at verapamil 80 mg po qid. Mild fatigue was the only side effect. Further investigation of verapamil in the treatment of schizophrenia is warranted.

Publisher Summary This chapter presents some of the evidence from animal and clinical studies, implicating cholecystokinin (CCK)-peptides in the pathophysiology of schizophrenia. CCK pathways are extensively distributed throughout the CNS. CCK-immunoreactivity (CCK-IR) is co-localized with dopamine (DA) in some DA neurons projecting to limbic structures. The extent of the co-localization is species dependent. The co-existence of CCK and DA is of interest in view of the DA hypothesis of schizophrenia and the putative role of limbic dysfunction in the pathophysiology of this disorder. Several biochemicals, electrophysiological, and behavioral studies point to an interaction between CCK and DA. Some studies point to an inhibitory effect of CCK peptides on DA function, which would be compatible with a potential antischizophrenic action, others point to an enhancement. CCK peptides show a neuroleptic-like profile in several screening tests for neuroleptics but not in all studies. Cerebrospinal fluid (CSF) CCK-IR is described as being unchanged or decreased in schizophrenia. Autopsy studies have shown significant decreases, increases, or no change in brain CCK-IR in schizophrenia.

CCK-IR is co-localized with DA in some DA neurons projecting to limbic structures. The extent of the co-localization is species dependent. The co-localization of CCK and DA is of interest in view of the DA hypothesis of schizophrenia and the putative role of limbic dysfunction in the pathophysiology of this disorder. In animals biochemical, electrophysiological and behavioural studies point to an interaction between CCK and DA. Whereas some investigations point to an inhibitory effect on DA function, which would be compatible with a potential antischizophrenic action, others point to an enhancement or no effect. CCK peptides show a neuroleptic-like profile in several screening tests for neuroleptics but not in all studies. In man there is endocrinological evidence for an inhibitory effect of CCK-33 and CCK-8 on DA function. However, alternate explanations are possible. CSF CCK-IR is unchanged or decreased in schizophrenia. Autopsy investigations have shown significant decreases, increases or no change in brain CCK-IR concentrations and a decrease in CCK-33 binding in schizophrenia. Eight of 11 clinical trials with CER, CCK-8 or CCK-33 have shown a therapeutic effect in schizophrenia; only two of these eight trials have been double-blind studies. The three controlled investigations which have shown no effect have used only small patient populations. None of the trials have used an active placebo. It is difficult to reconcile the apparent long duration of antipsychotic activity with the short half-life of the peptides and problems of the peptides in crossing the blood brain barrier. Despite these apparent anomalies information to date is sufficiently impressive to warrant further detailed investigation of CCK-DA-interactions and the evaluation of the clinical effects of a variety of CCK peptides and related compounds, natural and synthetic, which may more easily cross the blood brain barrier and which may show regional selectivity in site of action in brain.

Annals of the New York Academy of SciencesVolume 448, Issue 1 p. 535-541 Clinical and Neuroendocrine Studies with Cholecystokinin Peptides N. P. V. NAIR, N. P. V. NAIR Douglas Hospital Research Centre Verdun, Quebec, Canada Departrnent of Psychiatry Faculty of Medicine, McGill University Montreal, Quebec, CanadaSearch for more papers by this authorD. BLOOM, D. BLOOM Douglas Hospital Research Centre Verdun, Quebec, Canada Departrnent of Psychiatry Faculty of Medicine, McGill University Montreal, Quebec, CanadaSearch for more papers by this authorS. LAL, S. LAL Douglas Hospital Research Centre Verdun, Quebec, Canada Departrnent of Psychiatry Faculty of Medicine, McGill University Montreal, Quebec, CanadaSearch for more papers by this authorG. DEBONNEL, G. DEBONNEL Philippe Pinel Institute Montreal, Quebec, CanadaSearch for more papers by this authorG. SCHWARTZ, G. SCHWARTZ Douglas Hospital Research Centre Verdun, Quebec, CanadaSearch for more papers by this authorS. MOSTICYAN, S. MOSTICYAN Douglas Hospital Research Centre Verdun, Quebec, CanadaSearch for more papers by this author N. P. V. NAIR, N. P. V. NAIR Douglas Hospital Research Centre Verdun, Quebec, Canada Departrnent of Psychiatry Faculty of Medicine, McGill University Montreal, Quebec, CanadaSearch for more papers by this authorD. BLOOM, D. BLOOM Douglas Hospital Research Centre Verdun, Quebec, Canada Departrnent of Psychiatry Faculty of Medicine, McGill University Montreal, Quebec, CanadaSearch for more papers by this authorS. LAL, S. LAL Douglas Hospital Research Centre Verdun, Quebec, Canada Departrnent of Psychiatry Faculty of Medicine, McGill University Montreal, Quebec, CanadaSearch for more papers by this authorG. DEBONNEL, G. DEBONNEL Philippe Pinel Institute Montreal, Quebec, CanadaSearch for more papers by this authorG. SCHWARTZ, G. SCHWARTZ Douglas Hospital Research Centre Verdun, Quebec, CanadaSearch for more papers by this authorS. MOSTICYAN, S. MOSTICYAN Douglas Hospital Research Centre Verdun, Quebec, CanadaSearch for more papers by this author First published: July 1985 https://doi.org/10.1111/j.1749-6632.1985.tb29946.xCitations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume448, Issue1Neuronal CholecystokininJuly 1985Pages 535-541 RelatedInformation

Antipsychotic properties of cholecystokinin have been suggested both in laboratory studies and in some open clinical trials, mainly in patients suffering from chronic schizophrenia. Eighteen patients (14 males, 4 females) meeting Research Diagnostic Criteria for schizophrenia had been receiving neuroleptics at a dosage that had not changed for 3 months, and to which the patients were at best only partially responsive. The patients were randomized into groups that received weekly intravenous injections of 10 micrograms of CCK-8 or normal saline over 8 weeks. Neuroleptic medication was unchanged for the study. Baseline and weekly assessments were carried out using the Brief Psychiatric Rating Scale (BPRS) and the Schizophrenia Subscale of the Present State Examination (SS-PSE). Analysis of covariance revealed significant differences between CCK-8 and placebo over the study period on the Thought Disturbance Factor and Total Score of the BPRS, and on the Nuclear Syndrome, Total Delusion Factor, and Total Score of the SS-PSE. No important side effects were noted. It is concluded that CCK-8 has definite antipsychotic properties in patients with chronic schizophrenia. Clinical trials in neuroleptic-free patients are warranted.