naloxone and Syndrome

The authors seek to extend understanding and treatment of hospitalized schizophrenics presenting with complications of polydipsia and dilutional hyponatremia. Attending physicians may ask the consultation/liaison psychiatrist to see schizophrenics with hyponatremically-induced delirium or other psychiatric syndromes. The referring physician may or may not have identified polydipsia and dilutional hyponatremia and their complications. This article will help the consultation/liaison psychiatrist recognize early evidence of water imbalance, describe evaluation, and provide somatic and behavioral treatment approaches to this life-threatening syndrome.. Over the past ten years, the authors have treated more than 100 patients with the polydipsia-hyponatremia syndrome. The authors discuss their and others' experience with drugs that help and hinder patients suffering from dilutional hyponatremia. They review current key articles from the polydipsia-hyponatremia syndrome literature including articles identified via Medline search 1985-94.. Schizophrenics with the polydipsia-hyponatremia syndrome most commonly present with polydipsia, polyuria, urinary incontinence, cognitive, affective, and behavioral changes, seizures, or coma. Quantitating polydipsia, hyponatremia, and diurnal changes in body weight facilitate therapeutic interventions. Treatment include patient and caregiver education, drug therapies to better treat psychosis and better treat osmotic dysregulation, behavioral interventions to interdict polydipsia, and diurnal weight monitoring.. Once recognized, acute, subacute, and chronic complications of the polydipsia-hyponatremia syndrome are readily treatable. Besides treating the patient, consultation/liaison psychiatrists can teach their medical colleagues about this syndrome. In so doing, they will enhance the quality of their patients' lives and help the internist and surgeon feel more comfortable when working with schizophrenics.

Topics: Angiotensin II; Anti-Inflammatory Agents, Non-Steroidal; Antipsychotic Agents; Carbamazepine; Cognition Disorders; Demeclocycline; Drinking Behavior; Electroconvulsive Therapy; Humans; Hyponatremia; Lithium; Mood Disorders; Naloxone; Phenytoin; Polyuria; Propranolol; Psychiatry; Psychotherapy; Schizophrenia; Sodium Chloride; Syndrome; Water Intoxication; Workforce

Colonic inertia and outlet obstruction are a major problem of constipation affecting almost solely women and are characterised by an extreme slowness of colonic transit time (less than 80 percent of the markers eliminated in five days) and by a lack of relaxation and a contraction of pelvic muscles, mainly of the pubo-rectalis, during defecation. This syndrome is associated with a high frequency of gynecological diseases (first described in 1908 by Arbuthnot Lane), galactorrhea, urological abnormalities, abnormal manometric oesophageal recordings, Raynaud's phenomenon, idiopathic oedema, orthostatic hypotension and neurological symptoms. A distinctive abnormality of the colonic myenteric plexus has been described. Medical treatment of the affection is without effect, with the exception, perhaps, of the prescription of naloxone. In the absence of other therapeutic means, subtotal colectomy with ileo-rectal and coeco-rectal anastomosis may give relative improvement.

Topics: Colectomy; Constipation; Defecation; Female; Gastrointestinal Motility; Humans; Intestinal Obstruction; Naloxone; Rectal Diseases; Syndrome; Time Factors

Topics: Bromocriptine; Climacteric; Clonidine; Dopamine; Female; Gonadotropin-Releasing Hormone; Humans; Menopause; Naloxone; Norepinephrine; Prolactin; Sulpiride; Syndrome

Endogenous opioid peptides have been implicated in the regulation of pain perception, behaviour, gastrointestinal activity and other physiological responses. However, the functional role of these peptides in the horse has yet to be elucidated. The opioid antagonist, naloxone, is often administered to infer endogenous opioid effects. In the present study, naloxone (0.75 mg/kg bodyweight) was administered to eight Thoroughbred racehorses and a number of behavioural and autonomic responses were measured. Naloxone produced rapid onset diarrhoea, restlessness, abdominal checking, tachycardia, tachypnoea, paradoxical yawning and diaphoresis. These responses described an acute abdominal distress syndrome similar to spasmodic colic. Results from this study suggest that, in the horse, endogenous opioids: 1) influence behaviour, 2) modify intestinal activity and sensation, and 3) if perturbed, may be involved in pathophysiology of colic.

Topics: Abdominal Pain; Animals; Behavior, Animal; Colic; Defecation; Diarrhea; Gastrointestinal Diseases; Heart Rate; Horse Diseases; Horses; Naloxone; Respiration; Syndrome; Yawning

In a constantly increasing world of opioid addiction, naloxone has become a topic of great discussion and use. With seemingly minimal side effects, naloxone has become one of the most wellknown and widely used reversal agents for opioid intoxication. While more common effects of using naloxone include agitation, abdominal cramps, piloerection, diarrhea, nausea, and yawning, lesser known side effects involve muscle spasms, flushing, hyperreflexia in neonates, and seizures. This case study demonstrates a side effect of rigidity secondary to IV naloxone that has not previously been documented.. A 56 year old man was brought in by EMS after being found unresponsive in a car with a bag of drugs beside him. He was given 0.5 mg naloxone IV by EMS and immediately brought to the hospital. On arrival, the pt was noted to have tight rigidity of his upper extremities, with severe flexion. This presentation was not noted before the delivery of naloxone by EMS.. While this case highlights a patient with a rare side effect of naloxone, it reminds physicians that all medications come with a cost. Of course, ABCs remain the highest priority of resuscitation, however when administering a medication to reverse a drug overdose, it is important to keep in mind all possible consequences of said agent. Recognizing that complete muscle rigidity may remain a result of naloxone administration allows physicians to perhaps save patients from further medical workup.

Topics: Adult; Analgesics, Opioid; Emergency Service, Hospital; Female; Humans; Muscle Rigidity; Naloxone; Narcotic Antagonists; Opioid-Related Disorders; Syndrome; Thoracic Wall

Repeated hypoglycemia is associated with hypoglycemia-associated autonomic failure (HAAF), a syndrome of defective counterregulation.. HAAF increases the risk of severe hypoglycemia in diabetes, although its mechanism remains unresolved. Because beta-endorphin influences the autonomic response to hypoglycemia via opioid receptor activation, we hypothesized that it is also involved in the pathogenesis of HAAF.. We asked whether opioid receptor blockade during antecedent hypoglycemia (60 mg/dl) on d 1 would prevent development of HAAF on d 2 in eight nondiabetic subjects (five males, 3 females; age, 28 +/- 3.5 yr; body mass index, 24.2 +/- 2.1 kg/m(2)). On four occasions, d 1 was: 1) two 90-min hypoglycemic clamps (N-); 2) two 90-min hypoglycemic clamps plus naloxone (N+); 3) two euglycemic 90-min clamps (C); or 4) two euglycemic 90-min clamps plus naloxone (C+).. Day 1 hypoglycemia caused marked deterioration of d 2 hormonal responses to hypoglycemia, consistent with HAAF-i.e. decreased plasma epinephrine, norepinephrine, and glucagon compared to control (C) (374 +/- 71 vs. 810 +/- 94, 307 +/- 65 vs. 686 +/- 98, and 71 +/- 9 vs. 93 +/- 4 pg/ml, respectively, P < 0.01), as well as in endogenous glucose production (24 vs. 163%; P < 0.01). In contrast, naloxone on d 1 completely prevented the defective counterregulatory responses; epinephrine, norepinephrine, and glucagon (852 +/- 82, 769 +/- 77, and 98 +/- 7 pg/ml) and endogenous glucose production recovery (167%) were identical to those after d 1 euglycemia (P < NS for all). Infusion of naloxone alone during euglycemia on d 1 (C+) had no effect on d 2 responses.. These data suggest that the opioid signaling system is a promising target for further studies to prevent HAAF.

Topics: Adult; Autonomic Nervous System Diseases; beta-Endorphin; Blood Glucose; C-Peptide; Epinephrine; Female; Glucagon; Gluconeogenesis; Humans; Hypoglycemia; Insulin; Male; Naloxone; Narcotic Antagonists; Norepinephrine; Receptors, Opioid; Syndrome

Topics: Adjuvants, Anesthesia; Adult; Anesthesia, General; Anesthetics, Intravenous; Central Nervous System Diseases; Cholinesterase Inhibitors; Electrocardiography; Female; Glucose; Glycopyrrolate; Heart Block; Heart Rate; Humans; Midazolam; Middle Aged; Naloxone; Narcotic Antagonists; Physostigmine; Propofol; Respiration, Artificial; Syndrome

Topics: Acute Disease; Adult; Beverages; Charcoal; Cholinergic Antagonists; Datura stramonium; Delirium; Humans; Male; Naloxone; Plants, Medicinal; Plants, Toxic; Psychoses, Substance-Induced; Scopolamine; Syndrome

Shapiro's syndrome comprises agenesis of the corpus callosum in association with episodic hyperhidrosis and hypothermia. We describe a 25-year-old man who is the twentieth case to be reported. There was no evidence of epilepsy, sympathetic nervous system dysfunction or inappropriate vasopressin release. However, investigation demonstrated a central defect in temperature regulation with an abnormally low hypothalamic set-point and normal homeothermic reflexes. Therapy with clonidine, an alpha 2-adrenoceptor agonist, was associated with remission of symptoms: these recurred on four occasions when clonidine was withdrawn. Clonidine therapy was also associated with a return to normal central temperature regulation. We suggest that the efficacy of clonidine reflects an action on hypothalamic thermoregulation rather than on peripheral catecholamine release. These findings have implications for the use of clonidine in other patients with Shapiro's syndrome and in more common disorders of temperature control, including perimenopausal flushing.

Topics: Adult; Agenesis of Corpus Callosum; Body Temperature Regulation; Clonidine; Humans; Hyperhidrosis; Hypothermia; Magnetic Resonance Imaging; Male; Naloxone; Syndrome; Water-Electrolyte Imbalance

We studied monocyte function in 35 consecutive patients with chronic fatigue syndrome (CFS) and 25 healthy controls. Eighty-five per cent of the patients showed monocyte dysfunction characterized by marked reduction in the number of monocytes displaying immunoreactive cytoskeletal vimentin filaments, a low phagocytosis index, and a reduced expression of HLA-DR antigens. These values increased dramatically after incubation of the patients' monocytes with the opioid antagonist naloxone. Other immunological abnormalities also noted in the patients were low lymphocyte blastogenesis and diminished numbers of monocytes displaying receptors for Fc of IgG (FcR) and C3b (CR1). These findings suggest that an increased opioid activity acting through a classical receptor mechanism is active on monocytes from a high proportion of patients with CFS and that this represents a novel example of immunomodulation by opioid peptides in human disease. We suggest that endogenous opioids are involved in the pathogenesis of the chronic fatigue syndrome.

Topics: Adult; beta-Endorphin; Fatigue; Female; HLA-DR Antigens; Humans; Male; Middle Aged; Monocytes; Naloxone; Phagocytosis; Receptors, Complement; Receptors, Fc; Syndrome; Vimentin

Topics: Cerebrovascular Disorders; Female; Hemiplegia; Humans; Hypesthesia; Infusions, Intravenous; Male; Middle Aged; Naloxone; Palliative Care; Syndrome; Thalamic Diseases

To elucidate the mechanism of hypogonadotropic hypogonadism in a patient with X-linked congenital adrenal hypoplasia, we studied the effects on serum LH and FSH of repeated iv administration of GnRH (400 micrograms, over 2 h, once a day, for 14 consecutive days), pulsatile sc administration of GnRH (5 micrograms every 90 min during days 1 approximately 56, 10 micrograms every 90 min during days 57 approximately 91) and an iv bolus injection of 10 mg of naloxone. The repeated administration of GnRH restored the hyporesponsiveness of serum FSH and increased serum testosterone level from less than 1.0 to 1.7 nmol/l, but the impaired LH response to the standard GnRH test was not improved. The pulsatile administration of GnRH for 91 consecutive days did not induce a clinical or a biochemical change of puberty. Serum testosterone remained undetectable less than 1.0 nmol/l, the hyporesponsiveness of serum LH was not improved, but basal FSH level was significantly increased and the impaired FSH response to the standard GnRH test was slightly improved. Naloxone had no effect on serum LH or FSH before or during the pulsatile administration. We conclude that hypogonadotropic hypogonadism in our patient is due to the pituitary dysfunction and that the endogenous opioid peptides may not play a role in the mechanism of inhibited gonadotropin secretions.

Topics: Adolescent; Adrenal Glands; Adrenal Insufficiency; Endorphins; Follicle Stimulating Hormone; Humans; Hypogonadism; Infant, Newborn; Luteinizing Hormone; Male; Naloxone; Pituitary Hormone-Releasing Hormones; Puberty; Syndrome; Testosterone; X Chromosome

Both thresholds of nociceptive flexion reflex and pain sensation were studied in 6 normal subjects and in 6 patients with typical thalamic pain. In these patients, on the painful side, these thresholds were found increased (98 p. 100; 89 p. 100 respectively) compared to the normal side. Values obtained in this latter did not significantly differ from those observed in normal subjects. After 8 days of indalpine treatment, the nociceptive reflex threshold was furthered increased in the painful side while the pain threshold was not modified by this drug. In the normal side, changes observed after indalpine were similar to that obtained in normal subjects. All the indalpine-induced modifications were reversed by naloxone in both patients and normals. These results are discussed in the context of the possible mechanisms of thalamic hyperpathia.

Topics: Aged; Female; Humans; Male; Middle Aged; Naloxone; Pain; Pain Measurement; Piperidines; Reflex; Sensory Thresholds; Serotonin; Syndrome; Thalamic Diseases

We present 2 cases in which naloxone, the opioid antagonist, produced urinary urgency. The mechanism of action and possible therapeutic applications are discussed.

Topics: Aged; Dementia; Humans; Male; Middle Aged; Naloxone; Parkinson Disease; Syndrome; Urination Disorders

Thirteen adult patients with established thalamic syndrome, resistant to prior analgesic and other therapy, were treated with intravenous infusions of the opiate antagonist, naloxone. A total of twenty treatments were administered with doses of naloxone varying from 4.0-8.0 mgs. Seven patients exhibited beneficial effects with the duration of the resultant pain relief ranging from four days to two and a half years. In these patients, pain and hyperpathia were completely obtunded in six out of seven and partially in one. Side effects of therapy were minimal and of short duration being mainly confined to the cardiovascular system. During therapy all patients had continuous E.C.G. monitoring. In certain ischaemic conditions of the central nervous system, endogenous opioids possibly reduce cerebral blood flow via. inhibition of the locus coeruleus and subsequent release of noradrenaline: hence naloxone by inhibiting the opioids could increase cerebral perfusion pressure. This study has shown the benefit of treating patients with cerebral ischaemic lesions with an opioid antagonist. The rapidity of onset of pain relief in these patients would appear to indicate a mode of action by increasing cerebral perfusion.

Topics: Aged; Analgesics; Female; Humans; Injections, Intravenous; Intracranial Embolism and Thrombosis; Male; Middle Aged; Naloxone; Pain, Intractable; Syndrome; Thalamus

We tested the hypothesis that suppressive effects of endogenous opiate substances are involved in certain hypogonadotropic states. For this purpose, we studied gonadotropin secretion in idiopathic hypopituitarism (five children), constitutionally delayed adolescence (five boys), and Kallmann's syndrome (three men). Endogenous opiate pathways were antagonized by the iv infusion of naloxone hydrochloride at a dose previously shown to elicit a prompt and significant increase in serum levels of LH in normal men. Under these conditions, naloxone did not increase serially sampled serum concentrations or mean urinary levels of LH: or FSH in eight patients with idiopathic hypopituitarism or Kallmann's syndrome. Gonadotropin concentrations in four of five patients with constitutional delay of adolescence also were unaffected. In one boy with clinical and biochemical indices of late pubertal development, naloxone elicited a significant increase in LH levels in blood and urine, similar to the pattern observed in normal men. In contrast to results in experimental animals, naloxone did not suppress serum PRL concentration significantly in any subject. These observations suggest that: 1) endogenous opiate mechanisms are unlikely to constitute a principal factor in maintaining hypogonadotropism in idiopathic hypopituitarism, delayed adolescence, or Kallmann's syndrome, at least acutely; 2) endogenous opiate mechanisms also cannot be implicated in the acute regulation or PRL secretion in children; and 3) the capability of adult men, but not early pubertal boys, to respond with increased gonadotropin secretion during inhibition of opiate receptors suggests that maturation of the opiate-related neuroendocrine system occurs during the course of sexual development in the human.

Topics: Adolescent; Adult; Child; Child, Preschool; Female; Follicle Stimulating Hormone; Humans; Hypogonadism; Hypopituitarism; Luteinizing Hormone; Male; Naloxone; Prolactin; Puberty, Delayed; Syndrome

A syndrome of disordered hypothalamic function with abnormal control of temperature, appetite, and thirst, hyperprolactinaemia, and inappropriate vasopressin release is described in a 13-year-old boy who, in addition, had insensitivity to pain and a more general disorder affecting mood, sleep, and control of respiration. A disturbance of the opioid peptide system is postulated. Naloxone reversed central analgesia, altered urine fluid and electrolyte excretion, modified the hormonal response to gonadotrophin-releasing and thyrotrophin-releasing hormones, and improved the auditory and visual reaction times. Specific opioid antagonists may have a therapeutic role.

Topics: Adolescent; Appetite; Body Temperature; Child; Child, Preschool; Emotions; Endorphins; Humans; Hypothalamus; Inappropriate ADH Syndrome; Male; Naloxone; Pain Insensitivity, Congenital; Respiration; Sleep; Syndrome; Thirst

Topics: Ataxia; Brain; Brain Chemistry; Brain Diseases; Cerebrospinal Fluid; Diagnosis, Differential; Endorphins; Enkephalins; Humans; Infant; Injections, Intravenous; Intellectual Disability; Male; Morphine; Naloxone; Necrosis; Spinal Cord Diseases; Syndrome

Topics: Endorphins; Humans; Morphine; Naloxone; Pain; Serotonin; Substance Withdrawal Syndrome; Substance-Related Disorders; Syndrome

Adult male Sprague-Dawley rats briefly immersed in cold water and forced to swim showed Straub tail elevation, a typical sign of opiate stimulation, upon removal. The presence of Straub tail was a function of degree of immersion and was reversed by naloxone. This suggests the Straub tail response may be a novel behavioral index of stress-induced endorphin release.

Topics: Animals; Cold Temperature; Endorphins; Male; Movement; Naloxone; Rats; Stress, Physiological; Syndrome; Tail