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Objective To evaluate the impact of the US Air Force suicide prevention programme on risk of suicide and other outcomes that share underlying risk factors. Design Cohort study with quasi-experimental design and analysis of cohorts before (1990-6) and after (1997-2002) the intervention. Participants 5 260 292 US Air Force personnel (around 84% were men). Intervention A multilayered intervention targeted at reducing risk factors and enhancing factors considered protective. The intervention consisted of removing the stigma of seeking help for a mental health or psychosocial problem, enhancing understanding of mental health, and changing policies and social norms. Main outcome measures Relative risk reductions (the prevented fraction) for suicide and other outcomes hypothesised to be sensitive to broadly based community prevention efforts, (family violence, accidental death, homicide). Additional outcomes not exclusively associated with suicide were included because of the comprehensiveness of the programme. Results Implementation of the programme was associated with a sustained decline in the rate of suicide and other adverse outcomes. A 33% relative risk reduction was observed for suicide after the intervention; reductions for other outcomes ranged from 18-54%. Conclusion A systemic intervention aimed at changing social norms about seeking help and incorporating training in suicide prevention has a considerable impact on promotion of mental health. The impact on adverse outcomes in addition to suicide strengthens the conclusion that the programme was responsible for these reductions in risk.

Background: Later-life depressive disorders are a major public health problem in primary care settings. A validated screening instrument might aid in the recognition of depression. However, available findings from younger patients may not generalize to older persons, and existing studies of screening instruments in older patient samples have suffered substantial methodological limitations. Methods: One hundred thirty patients 60 years or older attending 3 primary care internists' practices participated in the study. Two screening scales were used: the Center for Epidemiologic Studies—Depression Scale (CES-D) and the Geriatric Depression Scale (GDS). The Structured Clinical Interview for the Diagnostic and statistical Manual of Mental Disorders, Third Edition, Revised , was used to establish "gold standard" diagnoses including major and minor depressive disorders. Receiver operating curve analysis was used to determine each scale's operating characteristics. Results: Both the CES-D and the GDS had excellent properties in screening for major depression. The optimum cutoff point for the CES-D was 21, yielding a sensitivity of 92% and a specificity of 87%. The optimum cutoff point for the GDS was 10, yielding a sensitivity of 100% and a specificity of 84%. A shorter version of the GDS had a sensitivity of 92% and a specificity of 81% using a cutoff point of 5. All scales lost accuracy when used to detect minor depression or the presence of any depressive diagnosis. Conclusions: The CES-D and the GDS have excellent properties for use as screening instruments for major depression in older primary care patients. Because the GDS's yes or no format may ease administration, primary care clinicians should consider its routine use in their practices. Arch Intern Med. 1997;157:449-454

The bond between patient and doctor is frequently tested by life's challenges. It must be strong enough to buoy the patient until calmer times arrive, and should prove rewarding and renewing for both participants. Too many times, however, there is no bond or it has no substance beyond superficial convention. Patients admitted to acute care hospitals frequently do not know their physicians. In this era of entrepreneurial medicine, business principles are applied. Medicine and government together focus on productivity and "units of service." Rationing, benefit plans, and cost containment have taken center stage in the public arena. It is within this broad and unsettled context that the national debate regarding "rational suicide" and "physician-assisted suicide" has arisen. Whether people have the right to thoughtfully choose the time and means of their death, and what role physicians should play in the process are overlapping, but not identical issues. Ironically, they are

DEPRESSION in the aging and the aged is a major public health problem. It causes suffering to many who go undiagnosed, and it burdens families and institutions providing care for the elderly by disabling those who might otherwise be able-bodied. What makes depression in the elderly so insidious is that neither the victim nor the health care provider may recognize its symptoms in the context of the multiple physical problems of many elderly people. Depressed mood, the typical signature of depression, may be less prominent than other depressive symptoms such as loss of appetite, sleeplessness, anergia, and loss of interest in, and enjoyment of, the normal pursuits of life. There is a wide spectrum of depressive symptoms as well as types of available therapies. Because of the many physical illnesses and social and economic problems of the elderly, individual health care providers often conclude that depression is a normal consequence

Abuse of 4-propyloxy-4-phenyl-N-methylpiperidine, a meperidine congener, produced parkinsonism in a 23-year-old man. Unlike other drug-induced motor disturbances, the syndrome persisted for 18 months and responded to drugs that stimulate dopamine receptors. Biogenic amines and metabolites in the cerebrospinal fluid and microscopic evaluation of the brain at necropsy were consistent with damage to aminergic neurons in the substantia nigra.

The effects of haloperidol on the release of prolactin, growth hormone, and luteinizing hormone during sleep were studied in an adolescent male who had Gilles de la Tourette's disease and delayed onset of puberty. At doses of 5 and 2 mg, haloperidol led to an increase of prolactin secretion and a suppression of luteinizing hormone release. Growth hormone was unaffected. Despite these changes, the patient had normal secondary sexual development consistent with puberty.

Age-related changes in memory functions are observed clinically and in the experimental psychology laboratory. The commonly used notion of "benign senescent forgetfulness" implies that such changes are part of "normal" aging and not associated with central nervous system pathology. Some investigators have advocated a diagnostic category, age-associated memory impairment, to define the memory loss that appears in healthy, elderly individuals. These concepts are problematic from a number of perspectives and need to be clarified and more rigorously investigated.

The neurochemistry of memory remains to be determined. Acetylcholine may be one of the neuotransmitters which mediates memory function, since the anticholinergic drug scopolamine produces amnesia in man. This study of scopolamine-induced memory deficits further defines those cognitive processes which are disrupted. The drug does not diminish attention, as assessed with an auditory vigilance task, or initial signal detection. More complex auditory decoding is affected, however. Scopolamine impairs aspects of initial memory acquisition (e. g., encoding and consolidation) and spontaneous memory retrieval. Retention is unaffected. Precise delineation of the neurochemistry of human memory will require comparative studies of amnesia-producing compounds, systematically examining the neuropsychological processes impaired by each.

This study investigates whether a brief educational program, provided to spouses of patients with Alzheimer's disease, improved the caregivers' coping skills; it also questions whether the gender of the spouse had an effect on coping ability. The sample consisted of 40 spouses who were caring for the Alzheimer patient at home, 20 who participated in the educational program, and 20 controls. The instrument used for the study was the Health Specific Family Coping Index (HSFCI). This instrument provided a quantitative assessment of overall family coping with both potential and actual health problems in the psychosocial and physical domains of health. It is rated in nine domains: physical independence, therapeutic competence, knowledge of the condition, application of principles of personal hygiene, attitude toward health care, emotional competence, family living patterns, physical environment, and use of community resources. A home visit was made by a registered nurse prior to the educational intervention and at the end of the four-week intervention period. The HSFCI was completed at each visit. There were no pretreatment differences between the intervention and control groups in coping ability. Findings indicate that the educational program was beneficial in assisting spouses to feel greater competence in the face of the disease process and to function with greater independence. In the treatment group, the greatest significant increase was in the knowledge domain, followed by therapeutic competence and emotional competence. There was no overall relationship between gender of the spouse and coping ability.

We carried out a controlled clinical trial to examine the potential of baclofen to slow the functional decline of patients with early Huntington's disease (HD). The basis of the trial was: (1) the hypothesis that excitatory amino acid neurotransmission mediates the neuronal degeneration of HD, (2) preclinical evidence that baclofen retards corticostriatal release of glutamate and aspartate, and (3) reports that baclofen produces short-term clinical benefits in some HD patients. Sixty patients with early HD were randomized to chronic baclofen, 60 mg/day, or placebo treatments and followed systematically for up to 42 months. Total functional capacity was not favorably influenced by baclofen treatment. Factors that contributed, although nonsignificantly, to a more rapid rate of total functional capacity decline included younger age (less than 35 years), earlier stage (stage I) of illness, paternal inheritance of the HD gene, and baclofen treatment. Our patients declined at a pace slower than that observed in other prospective studies, a finding likely due to selection criteria, avoidance of neuroleptic therapy, and strong psychosocial support.

Several previous studies have suggested a possible dissociation in the ability of patients with Alzheimer's Disease (AD) to utilize syntactic versus semantic information. This report describes a controlled experimental investigation of AD subjects' ability to process syntactic and semantic information. Thirteen mildly and moderately impaired AD patients were compared with 17 age- and education-matched elderly controls. Two tasks required subjects to identify and correct sentential errors; a third was a homophone spelling task. Results of the first task indicated that AD subjects were equivalent to controls in their ability to detect various types of sentential errors. When performing the second task, AD subjects were impaired in their ability to correct both types of errors, although there was a tendency for better performance with syntactically-based corrections. The third (homophone-spelling) task did not reveal a statistically significant differential sensitivity of AD subjects to syntactic versus semantic information. However, there was again a tendency for the former to be more easily processed. Results are discussed in terms of possible mechanisms which may underlie variations in the language-related performance of AD subjects.

Patients with Huntington's disease (HD) commonly have concomitant depressive disorders. Prompted by reports of elevated corticotropin releasing factor (CRF) and reduced 5-hydroxyindoleacetic acid (5-HIAA) concentrations in lumbar cerebrospinal fluid (CSF) of patients with major depression, these CSF constituents were examined in 56 nonmedicated patients who were in the early stages of HD. Elevated CRF concentrations were found in patients with HD in comparison with a control group of 21 subjects without neurologic illness. The CSF 5-HIAA concentrations in patients with HD did not differ from that in four normal volunteers. Patients with HD who had depressive disorders (major depression or dysthymia) did not differ from those without depression with respect to CSF 5-HIAA or CRF concentration. However, a positive correlation was observed between severity of major depression and CRF concentration. These findings suggest that the depression associated with HD may differ neurochemically from that seen in other major depressive disorders, and support the notion that clinically significant depressive symptoms reflect heterogeneous pathophysiologic conditions with different neurochemical correlates.

A dominant major gene was supported by analyses of 50 large extended Tourette syndrome (TS) pedigrees and by a subset of families defined by proband's clinical response to the neuroleptic drug haloperidol. Relatives were defined as affected if they ever had tics or TS. Assuming a nearly even sex ratio for TS and related symptoms resulted in the best fit of the genetic model to observed rates in families.

Fifty patients with Tourette syndrome were evaluated; data included family history, clinical characteristics, response to haloperidol, and side effects during haloperidol therapy. Sixteen patients had a family history of Tourette syndrome, and another 16 had a family history of tics. Twenty-four families had more than 2 members with Tourette syndrome or tics. There was no preponderance of families with a Jewish, Eastern European background in this sample. Thirty-four patients had obsessive-compulsive behavior. Among the 50 patients there was a high frequency of sleep disturbance, learning disability, self-destructive behavior, inappropriate sexual activity, and antisocial behavior. Family history was significantly related to the occurrence of sleep disturbance, obsessive-compulsive behavior, haloperidol response, and the frequency of side effects caused by haloperidol. The precise mode of genetic transmission in familial Tourette syndrome remains to be determined.

Twenty patients with major depressive disorder defined by the Research Diagnostic Criteria were given a range of neuropsychological tests and evaluated with the dexamethasone suppression test (DST). No correlation was found between results on the DST and cognitive impairment.

The effect of a single oral dose of choline chloride (10g) on two kinds of memory measures (serial learning and a selective reminding task) was studied in 10 normal volunteers. Choline decreased significantly the number of trials required to master a serial learning word test. On the selective reminding task only the recall of poorly imageable words (which are ordinarily difficult to remember) was enhanced by choline. Words which were highly imageable (and ordinarily easy to remember) were unaffected. The degree of enhancement with choline correlated inversely with performance of subjects on placebo. Our data indicate that brain acetylcholine may play a facilitatory role in encoding and storage of specific information items in man.

Five kindreds with multiple individuals manifesting Tourette syndrome (TS) or related abnormal movements were evaluated for linkage between TS and HLA-A, B, C and DR antigens. Families were selected to have a constellation of affected individuals which gave the appearance of transmission of a major susceptibility gene. All kindreds had at least two clearly affected first or second degree relatives. Although developmental neurobehavioral disorders are candidates for showing a relationship to specific tissue antigens, we found no evidence for a close linkage between a gene locus determining susceptibility to TS and the HLA loci.

Neuropsychology has traditionally focused on circumscribed brain lesions and their behavioral consequences, Huntington’s disease (HD), like other progressive dementing disorders, is a dynamic, evolving constellation of symptoms where clinical and research questions are inevitably confounded by problems such as stage of illness, rate of progression, and the interplay of one neuropsychological dysfunction with another. Qualitative and quantitative studies of the neuropsychological impairment in HD struggle to capture this dynamism.

Plasma prolactin levels were measured in 7 patients with Huntington's disease (HD) and 8 age matched controls after the random, oral administration of 1) placebo, 2) chlorpromazine 100 mg, 3) carbidopa 50 mg followed by levodopa 200 mg, and 4) bromocriptine 1 mg. After placebo, HD patients had significantly higher prolactin levels than controls at all times except 180, 240, and 360 minutes. Controls showed a significant suppression of prolactin release at 180 and 240 minutes after levodopa/carbidopa and at 180, 240, and 360 minutes after bromocriptine. In contrast, HD patients demonstrated no change after both levodopa/carbidopa and bromocriptine. Both groups showed a sustained elevation after CPZ, but despite having an initially higher baseline and an earlier response, the maximum prolactin levels of HD patients were significantly less than those of controls. This data suggest that HD patients may have a diminished number of hypothalamic-pituitary dopamine receptors for the regulation PRL secretion.

Tourette's syndrome (TS) has become the focus of more intensive investigation in recent years as a model neuropsychiatric disorder with precisely defined clinical diagnostic criteria and symptoms which are often responsive to pharmacotherapeutic intervention. In this provocative study, six TS patients were given doses of d-amphetamine, l-amphetamine, and haloperidol, in order to evaluate whether acute drug administration might provide a means of further clarifying the neurochemical pathophysiology of TS. Our patients experienced a heterogeneous array of responses, which precluded inferences regarding the neurochemistry of TS. Our results, however, illuminated many of the difficulties which confront investigators wishing to do behavioral pharmacologic research with TS patients, and provided insight into the complex nature of this neurobehavioral disorder.

Twelve patients with abnormal involuntary movement disorders were treated with clozapine in a double-blind, placebo-controlled trial. The cohort consisted of individuals with Gilles de la Tourette's syndrome, Huntington's disease, and atypical persistent dyskinesia that was drug induced. Two subjects were dropped from the protocol due to complications. Two patients with Huntington's disease showed a marked decrease in movements; other individuals obtained no significant therapeutic benefits. Seven of the 10 patients completing the trial experienced moderate or marked side effects.

Thirty patients with Huntington's disease, a genetically transmitted neuropsychiatric disorder that can be diagnosed reliably, were evaluated systematically for psychopathology, followed for extended periods, and treated with psychopharmacological medications when necessary. DSM-III criteria were used for establishing syndromic diagnoses. Twenty-four individuals demonstrated substantial behavioral abnormalities, including affective and schizophrenic syndromes, changes of personality, and disorders that could not be classified adequately. Pharmacotherapy was modestly beneficial in some cases. Consideration of the array of behavioral disturbances encountered in this pathogenetically unified disorder suggests that a dimensional approach to symptom classification might prove more useful heuristically than present typological methods.

• The literature describing pseudodementia was reviewed and a definition for this neuropsychiatric syndrome is formulated. It is defined as an intellectual impairment in patients with a primary psychiatric disorder, in which the features of intellectual abnormality resemble, at least in part, those of a neuropathologically induced cognitive deficit. This neuropsychological impairment is reversible, and there is no apparent primary neuropathological process that leads to the genesis of this disturbance. Data from published reports and preliminary findings presented here suggest that the intellectual impairment of patients with pseudodementia resembles subcortical dementia in many of its features.

• Tourette syndrome (TS) is a complex neurobehavioral disorder that has recently become a topic for clinical, genetic, neurochemical, and therapeutic research. Substantial progress has been made defining the clinical features of the disorder, establishing its familial nature, and documenting its response to pharmacotherapeutic intervention. Despite these advances, significant problems remain. The separation between TS and other syndromes is imprecise, and there are no uniformly accepted criteria for measuring response to treatment. Although family studies are promising, no mechanism of genetic transmission has been defined and the number of available revealing kindred for future DNA linkage studies is small. Clinical neurochemical investigations have been hampered by poor design and small subject samples; detailed postmortem neurochemical and pathological studies of brains from patients with TS have not been undertaken thus far. Careful application of newer research technologies combined with appropriately chosen subjects with TS may add to our understanding of the physiologic, anatomic, and genetic factors that contribute to this intriguing disorder. Future postmortem central nervous system studies will be essential.

This study compared the intellectual deficits of patients who had the earliest stages of Huntington's disease (HD) with those of mildly or moderately affected patients suffering from multiple sclerosis; both groups were matched for age, education, and ability to function. Twenty-one HD patients, 30 multiple sclerosis subjects, and 15 matched controls were evaluated neuropsychologically; all were free of psychoactive medications. The two patient groups showed similar overall patterns of impairment, though the HD group had greater verbal and nonverbal memory deficits. The HD patients also demonstrated significant dyscalculia and showed indications of developing problems in language usage and copying. These results are discussed in light of each disorder's neuropathologic substrate.

The potential motivation of criminal addicts for methadone treatment was tested in the New York City Correctional Institute for Men. Of 165 inmates seen, all with records of five or more jail sentences, 116 (70 per cent) applied for treatment after a single interview. None of them had previously made application to the methadone program. Of 18 randomly selected from all applicants with release dates between January 1 and April 30, 1968, 12 were started on methadone before they left jail and then referred to the program for aftercare. None of them became readdicted to heroin, and nine of 12 had no further convictions during the 50 weeks of follow-up study. All of an untreated control group became readdicted after release from jail, and 15 of 16 were convicted of new crimes during the same follow-up period.

Martin L. Albert (Ed.): Clinical Neurology of Aging. Oxford University Press, New York, 1984. 544 pages. ISBN 0-19-503287-x. $55.00.

To the Editor.— The note by Mizrahi et al (Archives1980;37:780) describing tardive dyskinesia in a child with Gilles de la Tourette's disease (TD) prompts us to report three other cases that we have observed, in addition to one that we reported previously.1 Report of Cases.— Case1.—An 8-year-old boy first received treatment with haloperidol after referral for the sudden onset of incessant coprolalia. Prior to that time, he had eye tics that began six months after beginning treatment with methylphenidate for symptoms of hyperactivity. His haloperidol dosage was gradually increased to 5 to 6 mg/day, which provided beneficial (but not complete) suppression of tics. Performance in school was unaffected by this dosage, although his family noted increased appetite and weight gain. He was followed up for two years, with regular monitoring of his TD symptoms as well as repeated dosage reduction to evaluate the possible emergence of drug-induced