Thomas L. Kurt

Neuropsychological Correlates of Gulf War Syndrome

As part of a comprehensive multispecialty project, the present study reports on the neurocognitive and psychological function of veterans who report Persian Gulf War-related symptoms. The neuropsychological and psychological performances of 26 ill Gulf War veterans were compared to 20 well veterans from the same military unit. Neurocognitive functions assessed included intelligence, abstraction and problem-solving, attention and concentration, memory and learning, language and visual-spatial function, and sensorimotor abilities. Psychological function was measured by self-report questionnaires. Results indicated global and consistently poorer intellectual and neurocognitive function among the ill veterans compared to the control veterans. A generalized pattern of neuropsychological deficit was evident for the ill veterans. Psychological profiles of the ill veterans were similar to those in general medical patients. Based on these findings and results from the multispecialty investigation, we conclude that some of the ill veterans have experienced neurotoxic injury resulting in chronic neuropsychological impairment that is related to their service in the Persian Gulf War.

Epidemiological association in US veterans between Gulf War illness and exposures to anticholinesterases

To investigate complaints of Gulf War veterans, epidemiologic, case-control and animal modeling studies were performed. Looking for OPIDP variants, our epidemiologic project studied 249 Naval Reserve construction battalion (CB24) men. Extensive surveys were drawn for symptoms and exposures. An existing test (PAI) was used for neuropsychologic. Using FACTOR, LOGISTIC and FREQ in 6.07 SAS, symptom clusters were sought with high eigenvalues from orthogonally rotated two-stage factor analysis. After factor loadings and Kaiser measure for sampling adequacy (0.82), three major and three minor symptom clusters were identified. Internally consistent by Cronbachs coefficient, these were labeled syndromes: (1) impaired cognition; (2) confusion-ataxia; (3) arthro-myo-neuropathy; (4) phobia-apraxia; (5) fever-adenopathy; and (6) weakness-incontinence. Syndrome variants identified 63 patients (63/249, 25%) with 91 syndromes. With pyridostigmine bromide as the drug in these drug-chemical exposures, syndrome chemicals were: (1) pesticide-containing flea and tick collars (P < 0.001); (2) alarms from chemical weapons attacks (P < 0.001), being in a sector later found to have nerve agent exposure (P < 0.04); and (3) insect repellent (DEET) (P < 0.001). From CB24, 23 cases, 10 deployed and 10 non-deployed controls were studied. Auditory evoked potentials showed dysfunction (P < 0.02), nystagmic velocity on rotation testing, asymmetry on saccadic velocity (P < 0.04), somatosensory evoked potentials both sides (right P < 0.03, left P < 0.005) and synstagmic velocity after caloric stimulation bilaterally (P-range, 0.02-0.04). Brain dysfunction was shown on the Halstead Impairment Index (P < 0.01), General Neuropsychological Deficit Scale (P < 0.03) and Trail Making part B (P < 0.03). Butylcholinesterase phenotypes did not trend for inherent abnormalities. Parallel hen studies at Duke University established similar drug-chemical delayed neurotoxicity. These investigations lend credibility that sublethal exposures to drug-chemical combinations caused delayed-onset neurotoxic variants.

Multiple Chemical Sensitivities–A Syndrome of Pseudotoxicity Manifest as Exposure Perceived Symptoms

The history of and nomenclature of the multiple chemical sensitivities are reviewed. The authors definition of multiple chemical sensitivity is a symptom complex 1) triggered by odor or a perceived exposure; 2) occurring at exposure levels below those of allergic sensitivity or irritation; 3) analogous to the symptoms of panic disorder as defined by DSM-IV-R; 4) lacking objective clinic pathologic criteria; and 5) responsive to panic disorder management.

Fatal Iatrogenic Iodine Toxicity in a Nine-Week-Old Infant

BACKGROUND Povidone-iodine has been used since the 1950s for various labelled uses as a topical antiseptic. The toxicity of an excessive dose in internal use is described in this case report. CASE REPORT A 9-week old infant was treated for colic by a pediatric gastroenterologist with loperamide and the elimination of nonhuman milk. Without improvement he was hospitalized and given an enema of 50 mL of povidone-iodine diluted in 250 mL of a bowel irrigant. The enema was promptly expelled and 50 mL of the described solution was given hourly for three doses by nasogastric tube. The infant was found lifeless three hours after the last dose and resuscitation was unsuccessful. Autopsy showed a corroded and necrotic intestinal tract, serous fluid in body cavities, a blood total iodine of 14,600 micrograms/dL, protein-bound iodine of 3,400 micrograms/dL and inorganic iodine of 11,700 micrograms/dL.

Severe ethanol intoxication in an adolescent

A 15-year-old boy presented to the emergency department with status epilepticus and a blood ethanol concentration of 757 mg/dL. Mechanical ventilation and substantial amounts of benzodiazepines were required. His hospital course was complicated by aspiration pneumonia, but he had no episodes of hypoglycemia. He received 2.8 hours of hemodialysis, which increased the rate of ethanol elimination, but there is no evidence that hemodialysis improved his clinical outcome. To our knowledge, this is the highest blood ethanol level reported in a child or adolescent who survived.

Pertussis immunization for medical personnel.

Excerpt To the editor: Your February issue presents observations from the USPHS Center for Disease Control on the frequency of pertussis in adults and recommendations for immunization (Ann Intern M...

Herbal Supplements-Drug Interactions: Scientific and Regulatory Perspectives

Medical Toxicology of Natural Substances is a hardcover reference text by Donald G. Barceloux, MD, the coauthor of Medical Toxicology: Diagnosis and Treatment of Human Poisoning (first edition, 1988), which is still a staple reference in the discipline of clinical toxicology. Barceloux combines his expertise in medical toxicology and emergency medicine with his skills as an author to address the significant and challenging natural toxins that are associated with morbidity and mortality. This is an essential reference text for medical libraries, poison and drug information centers, clinical toxicologists, and anyone who manages patients who may be exposed to natural toxins. With the increasing use of alternative medicine, this book would be a useful addition to medical practice libraries and emergency departments. The book is divided into five sections (foodborne and microbial toxins, fungal toxins, medicinal herbs and essential oils, toxic plants, and venomous animals) and 185 chapters. There is a relatively equal distribution of content for each of the sections, with the exception of the fungal toxins section that comprises only 55 pages, but the topics are covered sufficiently. A strength of the reference is the consistency between and among chapters – each monograph follows a template, making it easier to navigate from chapter to chapter and between sections. Barceloux is the primary author, with a few chapters on food contamination, food additives, and bacteria being contributed by Cyrus Rangan, MD; therefore, the style and format of the contributions are consistent throughout. Additional strengths of the book include placing each toxin in perspective with regard to its potential morbidity and mortality, focused but comprehensive chapters, and extensive contemporary referencing. Most of the chapters are concise, and this allows the clinician to review the chapter quickly, which is especially important in the arena of acute care such as in a poison information center or emergency department where patient care decisions must be made expeditiously. The most prominent limitation of the reference is the indexing and cross-indexing of terms, which poses a problem in searching for the various natural toxins. For example, the terms Araceae, Arum, Epripremnum, Philodendron, and Caladium are not indexed. To find information on these botanicals, the chapter on Dieffenbachia species must be reviewed. Therefore, a clinician may not be able to locate the desired information, unless they are aware that these botanicals, such as the Dieffenbachia species, contain oxalates, and are astute enough to find the entry in the table of contents, which diminishes the usefulness of the reference to those without botanical or toxicology expertise. Other examples that include no index terms for common botanicals are Euphorbia pulcherrima (Poinsettia), oak but not Quercus, capsaicin but not jalapeño, holly but not Ilex, and so on. However, using the table of contents as the search tool circumvents some of the inadequate indexing. The chapter on tickborne illness was brief, especially in view of the epidemic nature of Lyme disease; hanta virus was not included; there was no mention of West Nile Virus from mosquitoes; rabies was not covered; freshwater algae was not addressed; there was no discussion of the caustic manchineel tree (Euphorobia cotinifolia). However, these omissions do not diminish the importance and the overall quality of the reference. While all the information included in this book can be found in a multitude of hard-copy references and online resources, this is the only book that combines a comprehensive review of the major natural toxins into a single, authoritative, contemporary, and easy to read reference.