LIST REFERENCES LIST REFERENCES A) HYPOGLYCEMIA 7774 K) PANIC 948 B) HYPOGLYCEMIA /CL/CO/DI 5779 L) PREMENSTRUAL TENSION 739 C) ABSTRACT ONLINE 1725807 M) PSYCHOPHYSIOLOGIC DISO 9699 D) *ON B&C 3000 N) DEPRESSION... 55938 E) 1987...88 220500 O) *SUM GHIJKLMN 115555 F) *ON D&E 100 P) *ON D&O 34 G) ANXIETY DISORDERS 3213 Q) NERVOUS SYSTEM DISEASE 10143 H) FEAR 4791 R) DEPRESSION(+) 67555 I) MENTAL DISORDERS 34958 S) *SUM GHIJKLMNQR 193253 J) NEUROLOGIC MANIFESTATI 5269 T) *ON D&S 45 *** *** *****AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY***** 81106765 Reid RL Yen SS Premenstrual syndrome. AM J OBSTET GYNECOL 1981 Jan; 139(1):85-104 The premenstrual syndrome (PMS) is a major clinical entity afflicting a large segment of the female population. Available information are descriptive in nature and the etiology of this syndrome remains unclear. In this review, both biochemical and psychosocial elements of the syndrome have been explored in an effort to redefine the pathophysiology of this seemingly multifactorial psychoneuroendocrine dysfunction. We propose that luteal phase sensitivity to and subsequent withdrawal from the central effects of the neuropeptides beta-endorphin and alpha-melanocyte-stimulating hormone result in a cascade of neuroendocrine changes within the brain-hypothalamus- pituitary complex. Modulation of neurotransmitter function by these peptides may produce alterations in mood and behavior as well as enhance pituitary release of prolactin and vasopressin. Variable gonadal steroid modulation of these responses from subject to subject likely accounts for the heterogeneous clinical manifestations of the PMS. 86127492 Mabie BC Sibai BM Severe hypoglycemia associated with the HELLP syndrome [letter] AM J OBSTET GYNECOL 1986 Jan; 154(1):211-2 *****AMERICAN JOURNAL OF PHYSIOLOGY***** 76275401 Buchanan BJ Filkins JP Hypoglycemic depression of RES function. AM J PHYSIOL 1976 Jul; 231(1):265-9 The intravascular removal rates of colloidal carbon and of biologically active endotoxin by the reticuloendothelial system (RES) were evaluated as a function of blood-glucose levels. There was a significant negative correlation of carbon clearance half time on blood glucose in both saline-treated and insulin-treated rats. Insulin hypoglycemia depressed RES carbon clearance with the maximal effect occurring at blood glucose values below 30 mg/dl. Insulin hypoglycemia also severely impaired the intravascular removal of endotoxin as evaluated by lethality bioassay in lead-sensitized rats. It is concluded that blood glucose may modulate RES phagocytic function and that the hypoglycemia of endotoxin shock may augment the shock state due to impairment of RES host defense clearance functions. *****AMERICAN JOURNAL OF PSYCHIATRY***** 85044420 Uhde TW Vittone BJ Post RM Glucose tolerance testing in panic disorder. AM J PSYCHIATRY 1984 Nov; 141(11):1461-3 Seven of nine patients with panic disorder given a standard glucose tolerance test developed symptomatic hypoglycemia but not panic attacks. These findings suggest that hypoglycemia is an unlikely cause of "spontaneous" panic attacks in this population. 84101835 Gorman JM Martinez JM Liebowitz MR Fyer AJ Klein DF Hypoglycemia and panic attacks. AM J PSYCHIATRY 1984 Jan; 141(1):101-2 Many patients with panic disorder believe hypoglycemia causes their symptoms. Of 10 patients with panic disorder given sodium lactate to induce panic, none had evidence of low blood sugar levels when they began to experience anxiety symptoms. 76158373 Ford CV Bray GA Swerdloff RS A psychiatric study of patients referred with a diagnosis of hypoglycemia. AM J PSYCHIATRY 1976 Mar; 133(3):290-4 Five-hour oral glucose tolerance tests (GTTs) differentiated 30 volunteer patients who considered themselves hypoglycemic into three major groups: those who had reactive hypoglycemia, those who were normal, and those who had diabetes. Clinical psychiatric evaluation and Minnesota Multiphasic Personality Inventory testing revealed that half of the 30 patients were experiencing a current psychiatric disorder, usually depression. Hysterical personality traits were also noted in many of the patients. The idea that reactive hypoglycemic patients have specific personality characteristics was not substantiated by the authors' data. They hypothesize that some patients with psychiatric illness may have their symptoms erroneously attributed to incidental GTT findings. 87323675 True BL Perry PJ Burns EA Profound hypoglycemia with the addition of a tricyclic antidepressant to maintenance sulfonylurea therapy. AM J PSYCHIATRY 1987 Sep; 144(9):1220-1 Cases of profound hypoglycemia after the initiation of tricyclic antidepressant therapy in two patients taking sulfonylureas are described. To the authors' knowledge, this is the first report of a potential drug interaction between tricyclic antidepressants and sulfonylureas. Department of Psychiatry College of Pharmacy University of Iowa Iowa City 52242. 86184262 Schweizer E Winokur A Rickels K Insulin-induced hypoglycemia and panic attacks. AM J PSYCHIATRY 1986 May; 143(5):654-5 To investigate whether hypoglycemia might trigger panic attacks, the authors administered intravenous insulin to 10 patients with panic disorder. All subjects developed hypoglycemia but no panic anxiety. They reported symptoms of adrenergic hyperactivity but differentiated them from spontaneous panic attacks. Department of Psychiatry University of Pennsylvania University Hospital, Philadelphia 19104 *****ANNALS OF NEUROLOGY***** 85223936 Malouf R Brust JC Hypoglycemia: causes, neurological manifestations, and outcome. ANN NEUROL 1985 May; 17(5):421-30 During a 12-month prospective study there were 125 visits to the Harlem Hospital Emergency Room for symptomatic hypoglycemia. Sixty- five patients had obtundation, stupor, or coma; 38 had confusion or bizarre behavior; 10 were dizzy or tremulous; 9 had had seizures; and 3 had suffered sudden hemiparesis. Diabetes mellitus, alcoholism, and sepsis, alone or in combination, accounted for 90% of predisposing conditions; others included fasting, terminal cancer, gastroenteritis, insulin abuse, and myxedema. Average blood glucose levels were lower among comatose than among obtunded patients, but overlap was considerable, and overall there was little correlation among cause, blood glucose levels, and symptoms. Although mortality was 11%, only one death was attributable to hypoglycemia per se, and only four survivors had focal neurological residua. Department of Neurology Harlem Hospital Center New York, NY 10037 *****BRITISH MEDICAL JOURNAL [CLINICAL RESEARCH ED.]***** 88001387 Betteridge DJ Reactive hypoglycaemia. BR MED J [CLIN RES] 1987 Aug 1; 295(6593):286-7 Rayne Institute University College of London. *****JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM***** 88008236 Ipp E Forster B Sparing of cognitive function in mild hypoglycemia: dissociation from the neuroendocrine response. J CLIN ENDOCRINOL METAB 1987 Oct; 65(4):806-10 Central nervous system function during insulin-induced reductions in plasma glucose was studied by measuring plasma epinephrine concentrations and testing cognitive function. Mild glucose reduction [mean plasma glucose, 62 +/- 3 (+/- SEM) mg/dL (3.4 +/- 0.2 mmol/L)] was induced with an iv insulin infusion at the rate of 40 mU/kg.h for 180 min in 7 normal subjects. Despite a marked increase in mean plasma epinephrine concentrations, which peaked at 426 +/- 68 pm/mL (2325 +/- 371 pmol/mL; P less than 0.001), no significant differences in cognitive function occurred as determined by a series of trail- making tests compared with the results of serial tests in a group of 17 control subjects. In contrast, when hypoglycemia was induced (plasma glucose, less than 42 mg/dL; 2.3 mmol/L) by bolus injection of insulin in 4 normal subjects, cognitive function was impaired in every subject, as demonstrated by a delay in completion of the trail- making test. The mean completion time was prolonged to 107 +/- 16% of the baseline at the time of hypoglycemia vs. 74 +/- 4% in control subjects (P less than 0.01). These findings suggest that cognitive function may be spared during mild plasma glucose reductions and is dissociated from the neuroendocrine adrenergic response that is activated under these conditions. This dissociation may be part of a homeostatic process in which overall brain function is maintained during glucoprivation, although counterregulation has already been triggered to prevent a further decrease in plasma glucose. Division of Endocrinology and Metabolism Harbor-UCLA Medical Center Torrance 90509. *****JOURNAL OF CLINICAL PSYCHIATRY***** 87279953 Raj A Sheehan DV Medical evaluation of panic attacks. J CLIN PSYCHIATRY 1987 Aug; 48(8):309-13 Panic disorder with or without agoraphobia is dominated by the occurrence of panic attacks. However, panic attacks are also reported to occur as part of the clinical picture in several medical conditions, notably thyroid disease, hypoglycemia, and pheochromocytoma. The authors examine these conditions, review the relevant literature, and offer an evaluation strategy. Routine screening is not recommended. Panic disorder is also associated with mitral-valve prolapse and temporal lobe seizures. The authors explore the possible consequences of this association and outline an evaluation strategy. Again, routine screening is not recommended. Department of Psychiatry University of South Florida College of Medicine Tampa 33613. *****JOURNAL OF PEDIATRICS***** 87140552 Phillip M Bashan N Smith CP Moses SW An algorithmic approach to diagnosis of hypoglycemia. J PEDIATR 1987 Mar; 110(3):387-90 An algorithm has been devised to facilitate the diagnostic approach to the causes of hypoglycemia. This systematic approach enables the physician to reach the final diagnosis in a logical way without subjecting the child to unnecessary and possibly hazardous investigations. The algorithm is based on the following measurements as required by each patient: concentrations of blood glucose, lactate, ketone bodies, and glucose-regulating hormones. These measurements are performed with the patient in the fasting state and after loading tests (glycerol and galactose) as needed. If indicated, an enzymatic test is performed to establish the final diagnosis. Eighteen children aged 1 month to 7 years who had persistent or recurrent hypoglycemia have been examined according to this algorithm. The correct diagnosis was arrived at in 17 patients. The diagnosis was not reached in one neonate who had glucose-6- phosphatase deficiency and initially did not have lactic acidosis; once lactic acidosis developed, his illness fitted perfectly into the algorithm. Pediatric Research Laboratory Soroka University Hospital Ben-Gurion University of the Negev Beer-Sheva Israel. *****JAMA - JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION***** 80140739 Johnson DD Dorr KE Swenson WM Service FJ Reactive hypoglycemia. JAMA 1980 Mar 21; 243(11):1151-5 The clinical characteristics and scores on the Minnesota Multiphasic Personality Inventory (MMPI) of 192 patients undergoing a five-hour oral glucose tolerance test (OGTT) for evaluation of reactive hypoglycemia were assessed. There were twice as many women as men. One hundred twenty-nine patients had spells of light-headedness, shakiness, diaphoresis, weakness, and fatigue. Hypoglycemic symptoms occurring during the test were not related to level of plasma glucose nadir or to rate of descent of glucose level. Hypoglycemia was not found when glucose levels were measured during occurrence of spontaneous symptoms in 86 patients. MMPI scores were significantly different from those of general medical patients. Both men and women evinced a conversion V profile. The five-hour OGTT seems unreliable for the diagnosis of reactive hypoglycemia, and most patients with symptoms suggestive of hypoglycemia may have emotional disturbances. *****LANCET***** 86013120 Hypoglycaemia and the nervous system [editorial] LANCET 1985 Oct 5; 2(8458):759-60 *****POSTGRADUATE MEDICINE***** 88040738 McFarland KF Baker C Ferguson SD Demystifying hypoglycemia. When is it real and how can you tell? POSTGRAD MED 1987 Nov 1; 82(6):54-5, 59-60, 63-5 Contrary to popular belief, hypoglycemia is an infrequently encountered condition and its presence is questionable until confirmed by appropriate tests. In ambulatory patients, blood glucose levels obtained during intake of a normal diet are more reliable than those obtained during a glucose tolerance test. If the blood glucose is actually abnormally low and the other two criteria of hypoglycemia are also satisfied, a search for the cause is in order. In hospitalized patients, excessive doses of insulin or oral hypoglycemic agents, the effect of drugs, or chronic renal failure are the most common causes of hypoglycemia. If these factors are absent, another chronic illness known to cause hypoglycemia may be the source. If the cause is still obscure, a thorough evaluation of the endocrine status is warranted. Department of Medicine Richland Memorial Hospital Columbia SC 29203. 86148987 Diamond S Prager J Freitag FG Diet and headache. Is there a link? POSTGRAD MED 1986 Mar; 79(4):279-86 Diet has been implicated as a source of migraine since antiquity. Now, diet is thought of as one of many factors that can trigger migraine. Improved understanding of the migraine process and an attempt to delineate the most common causes of diet-precipitated migraine have resulted in a more rational treatment strategy. We recognize that a small group of patients will have migraine after ingesting certain foods with vasoactive properties or by missing a meal; thus, we suggest a nutritional course to limit this influence. The role of allergy in migraine is not yet determined and remains controversial. Diamond Headache Clinic Chicago IL 60625 *****SURGICAL CLINICS OF NORTH AMERICA***** 87178599 Kaplan EL Arganini M Kang SJ Diagnosis and treatment of hypoglycemic disorders. SURG CLIN NORTH AM 1987 Apr; 67(2):395-410 Many other hypoglycemic states can be confused with an insulinoma. This article presents the diagnosis, localization, and therapy of these islet cell tumors. Also presented is a discussion of the role of nesidioblastosis in persistent hyperinsulinemic hypoglycemia in the neonate. Department of Surgery University of Chicago Pritzker School of Medicine Illinois. *** *** *****FORTSCHRITTE DER MEDIZIN***** 77004680 Reichenmiller HE [Leading neurological symptoms of internal diseases] FORTSCHR MED 1976 Apr 22; 94(12):670-4 (Published in GERMAN) After description of the central-nervous signs due to hypoglycemia, hypoxia, hypo- and hypercalcemia there are discussed several internal diseases with prominent neurologic symptoms like endocrine disorders of thyroid, adrenal and pituitary gland, malignant diseases especially regarding the hematopoietic system, disorders of the joints and connective tissue and metabolic disorders as acute intermittent porphyria, uremic and hepatic coma. The principal differential diagnostic considerations in this relation are being described in order to avoid severe diagnostic errors. ********** 78129940 Leggett J Favazza AR Hypoglycemia: an overview. J CLIN PSYCHIATR 1978 Jan; 39(1):51-7 Hypoglycemia was not described as a human clinical syndrome until exogenous insulin was discovered. Much of our current knowledge of the symptoms of hypoglycemia derived from the reactions of schizophrenics to insulin coma therapy in the late 1920's. The diagnosis of hypoglycemia cannot be made simply on the basis of a blood glucose level since many asymptomatic persons have levels below 50 mg/100 ml. The diagnosis should be made only if symptoms occur at the glucose nadir and are relieved by the administration of glucose. The most common organic cause of hypoglycemia is functioning islet- cell tumor. By far the most prevalent type of hypoglycemia is idiopathic (function), a condition whose pathophysiology is not understood and which has given rise to a popular lay "mythology." *****JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY***** 82143213 Lader MH Assessment methods and the differential diagnosis of anxiety. J CLIN PSYCHOPHARMACOL 1981 Nov; 1(6):342-9 Anxiety states are commonly encountered, especially in general practice. Some endocrine disorders have features in common with anxiety states, especially thyrotoxicosis and idiopathic hypoglycemia. Functional cardiovascular disorders merge into anxiety states and include a large number of ill-differentiated syndromes. Other causes of anxiety are the drug-associated conditions, such as amphetamine overdose and barbiturate withdrawal. Among neuropsychiatric illnesses, temporal lobe epilepsy and the postconcussional state commonly have anxiety as a prominent syndrome. Psychophysiological technique can be used to assess anxiety levels in a variety of clinical contexts but need cautious interpretation. Anxiety is most easily assessed using rating scales but potential users must be clear as to what they are trying to measure. For clinical anxiety assessed by the physician, the Hamilton Scale is appropriate; for self-assessments linear scales can be adapted. *****MUNCHENER MEDIZINISCHE WOCHENSCHRIFT***** 77254765 Kanig K [Applied neurochemistry (author's transl)] MUNCH MED WOCHENSCHR 1977 Jul 8; 119(27):911-8 (Published in GERMAN) Metabolic disorders may also be accompanied by neurological symptoms. Diagnosis is ofter difficult because clinical opportunities are rare. But some things can be detected even by simple means. In particular, primary biochemical disturbances are discussed, insofar as they may have an unfavorable effect on the nervous system. Among these are hypoglycemia, hyperglycemia, cerebral nutritional disorders, phenylketonuria. Wilson's disease, folic acid deficiency and acute intermittent porphyria. *****NUTRITION AND HEALTH***** 86066132 Rippere V Some varieties of food intolerance in psychiatric patients: an overview. NUTR HEALTH 1984; 3(3):125-36 Foods may cause mental and behavioural symptoms by means of a variety of mechanisms. Food allergy is only one of many of these. The paper presents a brief overview of evidence, as of early 1982, concerning cerebral allergy, food addiction, the hypoglycaemias, caffeinism, hypersensitivity to chemical food additives, reactions to vasoactive amines in foods, and reactions attributed to neuropeptides formed from foods as causes of mental symptoms, with particular reference to psychiatric patients. It is concluded that although much work in this field remains to be done, enough is already known to benefit patients now if available knowledge is applied. An individual-centred environmental approach, extending beyond dietary factors if necessary, is recommended as more likely to help than a group-centred paradigm-based approach to treatment. *****PROGRESS IN NEURO-PSYCHOPHARMACOLOGY AND BIOLOGICAL PSYCHIATRY***** 84120298 Bowen RC Differential diagnosis of anxiety disorders. PROG NEUROPSYCHOPHARMACOL BIOL PSYCHIATRY 1983; 7(4-6):605-9 The literature comparing panic disorder with natural fear, hypoglycemia, hyperthyroidism, pheochromocytoma, the hyperventilation syndrome, the mitral valve prolapse syndrome and partial complex seizures is briefly reviewed. Some features of each of these syndromes may clinically resemble panic disorder. It is concluded that: a) patients with panic disorder should be medically evaluated. b) the diagnosis of panic disorder should be based on a broad system, rather than on symptoms alone. c) diagnostic systems should include a category for "organic anxiety syndromes". *****SCANDINAVIAN JOURNAL OF CLINICAL AND LABORATORY INVESTIGATION. SUPPLEM***** 84097353 Narvanen S Role of 5-hydroxytryptamine (serotonin) in oral glucose intolerance. SCAND J CLIN LAB INVEST [SUPPL] 1983; 167:1-53 The aim of the present study was to investigate the metabolic base of psychoneurological symptoms, most notably tiredness and loss of concentration ability, appearing after carbohydrate-rich meals and during oral glucose tolerance tests. Such metabolic changes may be the cause of many accidents attributed to the "human factor". Oral glucose tolerance tests (OGTT) were performed in healthy volunteers, divided into symptomatic (n = 21) and symptom-free (n = 15) groups. Since the symptoms arising during OGTT simulate those in alcohol intoxication, a method for clinical examination of alcohol intoxication was used to separate symptom-free from symptomatic subjects. Comparison of blood glucose concentrations during OGTT revealed the symptomatic group to have higher concentrations in blood samples taken 15 min (p less than 0.05), 30 min (p less than 0.01), 45, 60 and 90 min (p less than 0.05) after intake of glucose than those having no symptoms. The symptoms began when the glucose concentration was at maximum, some 38 min (mean value) following the ingestion of glucose. The symptomatic subjects demonstrated a normal assimilation rate of glucose (mean 1.7 %/min) as tested with intravenous glucose tolerance tests and the differences in blood glucose concentrations between the groups is concluded to depend on the rate of absorption of glucose from the intestinal tract. The enterochromaffine cells of the intestinal tract are the site of biosynthesis, storage and release of 5-hydroxytryptamine (5-HT) (serotonin). In whole blood practically all of the 5-HT is of thrombocytic origin. Thrombocytes are thought to be peripheral models of 5-HT neurons in regard to 5-HT uptake, storage release and metabolism. Thrombocytes have a mechanism for 5-HT uptake analogous to the reuptake mechanism for 5-HT in the serotonergic nerve terminals. The whole blood 5-HT changes parallel changes in the 5-HT concentrations of the neurons. In this work 5-HT concentrations were measured during OGTT in whole blood to ascertain the possible relation between 5-HT changes and glucose absorption. For this purpose a reliable, fluorometric method for 5-HT was developed with the following improvements: In whole EDTA-blood the oxidation of 5-HT was prevented with ascorbic acid. The oxidation of hemoglobin iron to ferri-iron was prevented with carbon monoxide, because 5-HT, being a phenol, will otherwise form a complex with ferri-iron. Proteins were precipitated with perchloric acid and the supernatant neutralized before purification of 5-HT by cation exchange.(ABSTRACT TRUNCATED AT 400 WORDS) Connect Time = 31.62 Minutes Connect Time Charge @ $16.00/HR 8.43 Communications Charge @ 6.00/HR 3.16 Search Element @ .10 2.00 Reference Display @ .10 .40 Reference Print @ .10 2.50 Title Scan @ .05 10.35 Abstract Print @ .10 2.20 Total Search Cost $ 29.04 Printing done. Please Deactivate, Then Press .