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Biomedical subjects

N E Alessi

Publications and source records attributed to N E Alessi.

At least 37 records · Page 2Linked to original sources
PubMed1989

Complications of phenylpropanolamine.

Phenylpropanolamine is a sympathomimetic agent present in over 100 proprietary and prescription anorectics, nasal decongestants, psychostimulants and treatments for premenstrual syndrome. It is often found in street drugs prepared to look like amphetamines. Phenylpropanolamine has precipitated paranoid psychosis, severe anxiety, cerebrovascular accidents and hypertensive crises. Hypertensive crises can be treated with phentolamine. Psychiatric symptoms and anxiety are managed with benzodiazepines.

Humans↗
PubMed1989

Nifedipine-haloperidol combination in the treatment of Gilles de la Tourette's syndrome: a case study.

Anecdotal case reports have been published describing the use of the calcium channel blockers verapamil and nifedipine to provide rapid and dramatic relief in refractory Gilles de la Tourette's syndrome (TS). The authors' case presentation illustrates that, although these two drugs may not always work alone, they can be successfully used in combination with other medications for treating refractory TS.

Administration, Oral↗
PubMed1988

Chronic treatment with amitriptyline produces supersensitivity to nicotine.

The authors used a thermoregulation paradigm to evaluate effects of amitriptyline (AMI) on the sensitivity of a nicotinic mechanism involved in the regulation of core temperature in rats. Treatment with this tricyclic was associated with a significant increase in the hypothermic response to nicotine. Supersensitivity persisted for a minimum of 7.5 days following the last dose of AMI, and a significant proportion of animals displayed increased sensitivity after 14.5 days of abstinence. Implications for the mechanism of action of AMI are highlighted.

Amitriptyline↗
PubMed1988

Temperature as a dependent variable in the study of cholinergic mechanisms.

1. Change in core temperature over time can be used as a dependent variable when studying the effects of manipulations on neurotransmitter systems. This article focuses on the measurement of core temperature as a strategy for detecting changes in the status of cholinergic systems. 2. Cholinergic neurons participate in the process of thermoregulation and interventions affecting them alter the thermal response to cholinomimetics. For example, chronic treatment with amitriptyline, chronic swim stress and inescapable footshock supersensitize rats to the hypothermic effects of oxotremorine. 3. This is consistent with the hypothesis that the pathophysiologies of tricyclic antidepressant withdrawal phenomena and stress involve supersensitivity of muscarinic mechanisms. 4. Uses of thermoregulation paradigms for investigating the actions of lithium ion, electroconvulsive shock and substances of abuse on muscarinic mechanisms are discussed. Applications to problems in the arena of clinical research are highlighted.

Animals↗
PubMed1988

Antipsychotic withdrawal symptoms: phenomenology and pathophysiology.

The authors review the literature discribing non-dyskinetic antipsychotic withdrawal phenomena. Withdrawal of these agents can cause nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgia, paresthesia, anxiety, agitation, restlessness, and insomnia. Psychotic relapse is often presaged by increased anxiety, agitation, restlessness and insomnia, but the temporal relationship of these prodromal symptoms to reduction in the dosage or discontinuation of neuroleptics distinguishes them from the effects of abrupt withdrawal.

Antipsychotic Agents↗
PubMed1988

Panic disorder in psychiatrically hospitalized children.

In a sample of 136 psychiatrically hospitalized children, panic disorder was identified in four boys and three girls. Six had separation anxiety disorder, and four had depressive disorders. This report documents the occurrence of panic disorder in children.

Age Factors↗
PubMed1987

Amitriptyline supersensitizes a central cholinergic mechanism.

The withdrawal of tricyclic antidepressants produces symptoms characteristic of cholinergic overdrive states. The authors previously proposed that these states are the consequence of the pharmacological induction of cholinergic system supersensitivity by chronic treatment with antidepressants, combined with a reduction in the plasma level of a competitive muscarinic receptor antagonist when the dose of a tricyclic is decreased. This is consistent with the facts that all tricyclic antidepressants are antimuscarinic agents and that classical antimuscarinic compounds, such as scopolamine, up-regulate and supersensitize muscarinic cholinergic systems. The authors present evidence that chronic treatment with amitriptyline supersensitizes a central cholinergic mechanism. Core body temperature is subject to influence by a central (hypothalamic) muscarinic mechanism, which is rendered supersensitive to cholinomimetic challenge by treatment with scopolamine. The authors telemetrically measured the hypothermic responses of adult male rats to various doses of the muscarinic agonist oxotremorine before and in the course of chronic treatment with amitriptyline. Treatment with amitriptyline resulted in marked enhancement of the cholinomimetic-induced hypothermia. Methylscopolamine nitrate, a peripherally active antimuscarinic agent, did not block the hypothermic response to oxotremorine, whereas scopolamine, a centrally active antimuscarinic compound, did. This study indicates that the chronic administration of amitriptyline can produce supersensitivity of a central muscarinic cholinergic mechanism. Clinical and theoretical implications of this finding are discussed.

Amitriptyline↗
PubMed1987

Panic and depressive disorders among psychiatrically hospitalized adolescents.

Sixty-one adolescents hospitalized on an inpatient psychiatric unit were evaluated to determine whether they met criteria for panic and affective disorders according to Research Diagnostic Criteria. Ten (16%) and 15 (24%) met criteria for definite or possible panic disorder. Fifteen (24.5%) had major depressive disorder (MDD) endogenous subtype, 10 (16%) had MDD nonendogenous subtype, 8 (13%) had minor depressive disorder (mDD), and 27 (44%) had no diagnosable mood disorder. Four adolescents with definite panic disorders were diagnosed as having MDD endogenous subtype, three MDD, two mDD, and one had no diagnosable depressive disorder. The mean total score on the Hamilton Rating Scale for Depression (HRSD) was significantly higher among those subjects with definite panic attacks compared with those with either possible or no panic. Patients with definite panic disorder showed significant increases on the HRSD items of guilt, decreased work and interest, psychological and somatic anxiety, and weight loss compared to these samples.

Adolescent↗
PubMed1985

Time of origin of opioid peptide-containing neurons in the rat hypothalamus.

By using a combined technique of immunocytochemistry and [3H]thymidine autoradiography, we have determined the "birth date" of opioid peptide-containing neurons in several hypothalamic nuclei and regions. These include proopiomelanocortin (POMC) neurons (represented by ACTH immunoreactivity) in the arcuate nucleus; dynorphin A neurons in the supraoptic and paraventricular nuclei and the lateral hypothalamic area; and leu-enkephalin neurons in the periventricular, ventromedial, and medial mammillary nuclei, as well as in preoptic and perifornical areas. Arcuate POMC neurons were born very early in embryonic development, with peak heavy [3H]thymidine nuclear labelling occurring on embryonic day E12. Supraoptic and paraventricular dynorphin A neurons were also labelled relatively early (peak at E13). The lateral hypothalamic dynorphin A neurons showed peak heavy labelling also on day E12. By contrast, leu-enkephalin neurons in the periventricular nucleus and medial preoptic area exhibited peak heavy nuclear labelling on day E14. Furthermore, perifornical and ventromedial leu-enkephalin neurons were also born relatively early (peak on days E12 and E13, respectively). However, the leu-enkephalin neurons in the medial mammillary nucleus were born the latest of all cell groups studied (i.e., peak at E15). The results indicate a differential genesis of these opioid peptide-containing neuronal groups in different hypothalamic nuclei and regions.

Adrenocorticotropic Hormone↗
PubMed1985

Postnatal development of beta-endorphin immunoreactivity in the medulla oblongata of rat.

Beta-endorphin (B-END) like immunoreactivity (i.r.) levels were measured by radioimmunoassay in the medulla oblongata of developing rats on postnatal ages P1-P42 at 7 day intervals, and in adult rats. From P1 to P42, B-END i.r. increased from 77.0 +/- 1.3 fm to 900.0 +/- 21.6 fm per medulla region (Mean +/- S.E.M.). Adult levels of B-END i.r. were 852.0 +/- 17.0 fm per medulla region. When B-END i.r. was determined per unit protein during this developmental period, a statistically significant change in levels was noted. B-END i.r. dropped from P1 to P7, and then increased from P7 to P14 (P less than 0.01). From P14 through adult, levels did not change significantly. Despite a "drop-out" in the observed immunostaining of B-END neurons in caudal medulla (perikarya in the nucleus tractus solitarius) at P21, radioimmunoassayable levels of this peptide remained constant from P21 through adult per unit protein.

Animals↗
PubMed1985

Development of hypothalamic opioid neurons: a combined immunocytochemical and [3H]thymidine autoradiographic study.

Using a combined technique of immunocytochemistry and [3H]thymidine autoradiography, we have determined the "birth-date" of opioid peptide containing neurons in three hypothalamic nuclei. These include proopiomelanocortin neurons (indicated by ACTH immunoreactivity) in the arcuate nucleus, dynorphin A neurons in the supraoptic nucleus, and [Leu]enkephalin neurons in the periventricular nucleus. Arcuate proopiomelanocortin neurons were born very early in embryonic development, with peak heavy [3H]thymidine nuclear labelling occurring on embryonic day E12. Supraoptic dynorphin A neurons were also labelled relatively early (peak at E13). By contrast, [Leu]enkephalin neurons in the periventricular nucleus exhibited peak heavy nuclear labelling on day E14. The results indicate a differential genesis of these three opioid peptide containing neuronal groups in three different hypothalamic nuclei.

Adrenocorticotropic Hormone↗