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To reduce unnecessary laboratory testing, a three-phase intervention was designed by students to decrease serum folate laboratory testing in the inpatient setting. These included an educational phase, a personalized feedback phase, and the uncoupling of orders in the electronic medical record. Average monthly serum folate ordering decreased by 87% over the course of the intervention, from 98.4 orders per month at baseline to 12.7 per month in the last phase of the intervention. In the segmented regression analysis, joint ordering of folate and vitamin B12 significantly decreased during the intervention ([INCREMENT]slope = -4.22 tests/month, p = .0089), whereas single ordering of vitamin B12 significantly increased ([INCREMENT]slope = +5.6 tests/month; p < .001). Our intervention was successful in modifying ordering patterns to decrease testing for a deficiency that is rare in the U.S. population.

There are no standardized diagnostic criteria for psychosis associated with Parkinson's disease (PDPsy). As part of an NIH sponsored workshop, we reviewed the existing literature on PDPsy to provide criteria that distinguish PDPsy from other causes of psychosis. Based on these data, we propose provisional criteria for PDPsy in the style of the Diagnostic and Statistical Manual of Mental Disorders IV-TR. PDPsy has a well-characterized temporal and clinical profile of hallucinations and delusions, which is different than the pattern seen in other psychotic disorders such as substance induced psychosis or schizophrenia. PDPsy is associated with a poor prognosis of chronic psychosis, nursing home placement, and death. Medications used to treat Parkinson's disease (PD) contribute to PDPsy but may not be sufficient or necessary contributors to PDPsy. PDPsy is associated with Lewy bodies pathology, imbalances of monoaminergic neurotransmitters, and visuospatial processing deficits. These findings suggest that PDPsy may result from progression of the disease process underlying PD, rather than a comorbid psychiatric disorder or drug intoxication. PDPsy is not adequately described by existing criteria for psychotic disorders. We established provisional diagnostic criteria that define a constellation of clinical features not shared by other psychotic syndromes. The criteria are inclusive and contain descriptions of the full range of characteristic symptoms, chronology of onset, duration of symptoms, exclusionary diagnoses, and associated features such as dementia. These criteria require validation and may be refined, but form a starting point for studies of the epidemiology and pathophysiology of PDPsy, and are a potential indication for therapy development.

Background: Similarities between Alzheimer disease (AD) and Parkinson disease (PD) suggest a possible role for apolipoprotein E (APOE) in PD. Most previous studies seeking to establish such a link used case-control datasets and results have been inconsistent., Objective: To investigate APOE's role in PD using family-based association analyses., Methods: APOE functional polymorphisms were genotyped for 658 PD affected families, including 282 multiplex and 376 singleton families. The pedigree disequilibrium test (PDT) and the genotype-PDT were used to test the risk effect of APOE. The Monks-Kaplan test was used to evaluate the effect of APOE on age at onset of PD., Results: APOE was significantly associated with risk of developing PD. Stratified analysis revealed that APOE was most strongly associated with families with a positive PD family history (global p = 0.003). Like AD, the APOE-4 allele increases disease risk while the APOE-3 allele decreases risk. We detected a positive association of APOE-3 (p = 0.019) and a negative association of APOE-4 (p = 0.015) with age at onset in PD., Conclusions: The APOE-4 allele increases risk and decreases age at onset of PD, an association that may not be dependent upon cognitive impairment.

Objective: To analyze the role of the seminal 19th-century neurologist, Jean-Martin Charcot, in the internationalization of neurasthenia, previously known as "the American disease.", Background: The New York neurologist, George Beard, first described neurasthenia in 1869 and considered it a disorder related to the particular stress of modern civilization, most typified in the United States., Methods: Charcot's personal files on neurasthenia from the Bibliothèque Charcot, Salpêtrière Hospital, Paris, were studied and his teaching lessons and lectures were examined., Results: Charcot presented numerous cases of neurasthenia, always crediting Beard with the original name and description. Calling Beard's 1880 work a "remarkable monograph," Charcot emphasized that patients with neurasthenia also comprised the bulk of his own private practice. Focusing on the signs of sexual impotency, fatigue, and a tight band of pressure around the head, Charcot categorically distinguished patients with neurasthenica from patients with hysteria. Like Beard, Charcot concluded that the origin of neurasthenia was psychological stress and felt the European society also fostered the environment to precipitate the disease. Charcot adamantly opposed extrapolations that called for early childhood educational reforms to reduce current classroom stress. Charcot sympathized more with the treating physician than the patient, calling neurasthenics insufferable (insupportables). On the front sheet of his neurasthenia file, he wrote in large script, "Poor Beard!!", Conclusion: By emphasizing the prevalence of neurasthenia and extending Beard's observations, Charcot internationally legitimized the new diagnosis. Adding neurasthenia to the other neurologic descriptions from the United States by Hammond, Mitchell, and Dana, Charcot helped to foster the recognition of the American Neurologic School.

Background: To date, to our knowledge, there is no systematic presentation of treatment outcome in large series of patients clinically diagnosed as having corticobasal degeneration., Objective: To evaluate the clinical presentation and treatment outcome of patients clinically diagnosed as having corticobasal degeneration., Subjects: We gathered case patients seen in 8 major movement disorder clinics during the last 5 years who were diagnosed as having corticobasal ganglionic degeneration., Methods: Using a chart review method, we recorded the clinical presentation, medications used, response to medications, and adverse effects., Results: A total of 147 case patients were reviewed, 7 were autopsy proven. Parkinsonian features were present in all, other movement disorders in 89%, and higher cortical dysfunction in 93%. The most common parkinsonian sign was rigidity (92%), followed by bradykinesia (80%), gait disorder (80%), and tremor (55%). Other movement disorders were dystonia in 71% and myoclonus in 55%. Higher cortical dysfunction included dyspraxia (82%), alien limb (42%), cortical sensory loss (33%), and dementia (25%). Ninety-two percent of the case patients received dopaminergic drugs, which resulted in a beneficial effect for 24%. Parkinsonian signs were the elements improving the most and levodopa was the most effective drug. Benzodiazepines, primarily clonazepam, were administered to 47 case patients, which resulted in improvement of myoclonus in 23% and dystonia in 9%. The most frequent disabling adverse effects of drug trials in these case patients were somnolence (n = 24), gastrointestinal complaints (n = 23), confusion (n = 16), dizziness (n =12), hallucinations (n = 5), and dry mouth (n = 5)., Conclusions: Pharmacological intervention was largely ineffective in the management of corticobasal degeneration, and new treatments are needed for ameliorating the symptoms of this syndrome.

Background: Whether Parkinson disease (PD) and dementia with Lewy bodies (DLB) represent 2 distinct nosologic entities or are diverse phenotypes of Lewy body disease is subject to debate., Objectives: To determine the accuracy of the diagnoses of Lewy body disease, PD, and DLB by validating the clinical diagnoses of 6 neurologists with the neuropathologic findings and to identify early predictors of the diagnoses., Methods: Six raters who were unaware of the neuropathologic diagnoses analyzed 105 clinical vignettes corresponding to 29 cases of Lewy body disease (post hoc analysis of 15 patients with PD and 14 with DLB) and 76 patients without PD or DLB whose cases were confirmed through autopsy findings., Main Outcome Measures: Sensitivity and positive predictive value (PPV) were chosen as validity measures and the K statistic as a reliability measure., Results: Interrater reliability for the diagnoses of Lewy body disease and PD was moderate for the first visit and substantial for the last, whereas agreement for diagnosis of DLB was fair for the first visit and slight for the last. Median sensitivity for diagnosis of Lewy body disease was 56.9% for the first visit and 67.2% for the last; median PPV was 60.0% and 77.4%, respectively. Median sensitivity for the diagnosis of PD was 73.3% for the first visit and 80.0% for the last; median PPV was 45.9% and 64.1%, respectively. Median sensitivity for the diagnosis of DLB was 17.8% for the first visit and 28.6% for the last; median PPV was 75.0% for the first visit and 55.8% for the last. The raters' results were similar to those of the primary neurologists. Several features differentiated PD from DLB, predicted each disorder, and could be used as clinical pointers., Conclusions: The low PPV with relatively high sensitivity for the diagnosis of PD suggests overdiagnosis. Conversely, the extremely low sensitivity for the diagnosis of DLB suggests underdiagnosis. Although the case mix included in the study may not reflect the frequency of these disorders in practice, limiting the clinical applicability of the validity measures, the raters' results were similar to those of the primary neurologists who were not exposed to such limitations. Overall, our study confirms features suggested to predict these disorders, except for the early presence of postural imbalance, which is not indicative of either disorder.

This is a study of the status of American neurology at the beginning of the 20th century as perceived by European neurologist Georges Guillain. Guillain trained in Paris, the international "Mecca" of neurology at that time. Whereas many Americans traveled and studied in Europe, very few European neurologists made the reverse journey to the United States. In 1902 Georges Guillain, age 26, traveled to the United States with the specific aim of evaluating neurologic services in America. Recent access to Guillain's personal travel journal and an article in French that he wrote after his return to Europe provide first-hand documentation of American neurology at the turn of the century from a European perspective. Using introductory references from his teacher, Pierre Marie, Guillain visited New York, Chicago, Boston, Philadelphia, and Baltimore. He studied hospitals, outpatient departments, laboratories, and universities, comparing them with institutions in his native France and other European capitals. Guillain was particularly struck by the creative energy of American neurologists, the broad-ranging programs in research and patient care, and the strong financial support provided by local philanthropists, universities, and governments. Guillain clearly foresaw the rising international role of American neurology and the prominence it would gain by the end of his career in the 1950s.

According to the most recently available data presented in the Statistical Abstract of the United States 1994 (United States Bureau of the Census, 1994), 17,100 young Americans (15 to 44 years old) died in 1991 due to suicide. At no other time during the life span were suicide rates so high. Suicide among college and university students is estimated by some to be 50% higher than for other Americans of comparable age (Westefeld & Pattilo, 1987). Not only is suicide considered by many authors to be the number one health problem on the nation's campuses (Mathiasen, 1988), but the suicide rate for this population has tripled over the past 25 years (Hardin & Weast, 1989). Professional nursing students could perhaps be at an even higher risk for suicide than other college students. Manicini, Lavecchia, and Clegg point out that "[n]ursing students are more doubtful than other college students about their academic performance. They encounter stress in adjusting to a rigorous program of theory and practice. The reality is often far different from a prospective student's image of it" (cited in Lampkin, Cannon, & Fairchild, 1985, p. 148). Because of the longevity of contact hours spent with nursing students in both lecture and clinical milieus, nursing faculty are in a uniquely favorable position to identify and assess those students who appear to be at risk for suicide. In addition, as most nurse educators provide supportive relationships, rich with caring and trust for their students, distressed students are usually open to talking to a faculty member. If a suicidal risk is found during the assessment interview, the faculty member should then provide an immediate referral for further psychiatric evaluation and intervention. To assist faculty in the quick recall of the essential components of this helping process the acronym S.A.V.E. is used: 1. S: Suicidal behaviors. 2. A: Assessment interview. 3. V: Value student. 4. E: Evaluation-Referral.

Although Charcot and Mitchell only met once or possibly twice in Paris (1873 and 1875), they interacted in multiple ways to influence one another's research and the development of nineteenth century neurology. Charcot strongly relied on, and openly credited, Mitchell's important contributions on the fragility of bones in locomotor ataxia when he postulated his own historic concepts on neuropathic arthropathies (Charcot joints). Mitchell likewise referred to Charcot in his texts and manuscripts, although his comments were not always complementary. Most notably, Mitchell publicly criticized Charcot for wrongfully claiming precedence over Americans (i.e., Mitchell himself) in the development of isolation therapy. The two men shared many specific neurologic interests, especially the effects of trauma and disorders affecting women, including hysteria. In the development of clinical neurology as a new scientific field, Charcot and Mitchell were both strong empiricists who distrusted theory but believed that clinical medicine, and specifically neurology, required continued infusion of new data from the laboratory sciences. Both men were exemplary teachers, Mitchell primarily a preceptor and supervisor of doctors outside the university system and Charcot the first European professor of clinical neurology and head of the celebrated School of the Salpêtrière.

American universities recognized and institutionalized the emerging importance of neuroscience in medicine by establishing neurological professorships as early as the 1860s. Nearly 20 years before Charcot assumed his celebrated chaired professorship for Diseases of the Nervous System in France, Harvard University created a professorship of Physiology and Pathology of the Nervous System (1864), naming Brown-Sequard as its recipient. In 1867, the new Bellevue Hospital Medical School established a combined neurology/psychiatry chair with William A. Hammond as professor, and the University of Pennsylvania created a clinical professorship devoted specifically to neurology in 1875, naming Horatio C. Wood. Although modest in their university power base and their clinical research/laboratory programs, these American posts were internationally unique for their time and solidly entrenched neurology as a specific division in early US medical education.

Although European treatises were translated and available to American doctors interested in neurology during the 19th century, the early American neurologic textbooks were distinctive in their comprehensive integration of basic and clinical science. William A. Hammond, in 1871, published the first comprehensive American textbook of neurology, preceding the manuals by Gowers (1886) and Oppenheim (1894) by more than a decade. Four other American adult neurologic textbooks expanded on Hammond's model and incorporated other important topics, including neurologic anatomy, the formal examination, neurochemistry, and complete bibliographies. Bernard Sachs' 1895 textbook was the first pediatric neurologic textbook published in America and made significant contributions to the organization of childhood neurologic disorders. These works functioned as centralized resources for neurologic information, were influential educational tools, and helped foster a growing appreciation of the American neurologic school both nationally and internationally.