Disease relevance of NMS

• In the present study urinary catecholamine metabolites obtained during the course of NMS were studied with respect to frequently reported signs and symptoms of NMS [1].
• A diagnosis of NMS was made, despite the absence of hyperthermia [2].
• CK-MB was elevated, as judged by E and by M, in all of 42 patients with acute myocardial infarction (AMI), and in 40 of the 42 by NMS [3].
• The ability to differentiate AMI from no infarction in patients was best with E, and was not satisfactory by NMS [3].
• In those patients in whom it is difficult to differentiate between serotonin and neuroleptic malignant syndromes, the physical examination may be helpful:clonus and hyperreflexia are more suggestive of serotonin syndrome,whereas lead-pipe rigidity is suggestive of NMS [4].

Psychiatry related information on NMS

• NMS and lethal catatonia [5].
• Although NMS has been reported in patients with diverse psychiatric diagnoses, as well as in normal subjects, patients with organic brain disorders or mood disorders, particularly when receiving lithium, may be at increased risk [6].
• NMS significantly decreased food intake (and consequently body weight) in a time-dependent manner during 12-h light period, but increased both body temperature and gross locomotor activity [7].

High impact information on NMS

• After short preincubations with N-[(3)H]methylscopolamine ([(3)H]NMS) or R(-)-[(3)H]quinuclidinyl benzilate ([(3)H]QNB), radioligand dissociation from muscarinic M(1) receptors in Chinese hamster ovary cell membranes was fast, monoexponential, and independent of the concentration of unlabeled NMS or QNB added to reveal dissociation [8].
• The effect of the synthetic toxins on the atropine-induced [3H]N-methylscopolamine (NMS) dissociation confirms that sMT7 targets the allosteric site on the M1 receptor, whereas sMT1 seems interact on the orthosteric one [9].
• We have studied the interactions of five indolocarbazoles with N-[methyl-(3)H]scopolamine (NMS) and unlabeled acetylcholine at M(1)-M(4) muscarinic receptors, using equilibrium and nonequilibrium radioligand binding studies [10].
• In human embryonic lung fibroblasts, transforming growth factor-beta 1 (TGF-beta 1) induced a time-dependent down-regulation of M2 muscarinic receptor binding sites as measured with the nonselective hydrophilic ligand [3H]N-methylscopolamine (NMS) [11].
• m1-Toxin was found to slow the dissociation of [3H]N-methyl-scopolamine (NMS) and [3H]pirenzepine from m1 muscarinic receptors expressed in the membranes of Chinese hamster ovary cells [12].

Chemical compound and disease context of NMS

• We argue that NMS and TSS are examples of a non-specific generalized neurotoxic syndrome, and not specific syndromes: and that these are subtypes of catatonia [13].
• Rhabdomyolysis associated with haloperidol without evidence of NMS [14].
• Successful treatment of NMS requires a high degree of suspicion, rapid recognition of clinical signs and symptoms and institution of therapy with dantrolene and possibly dopaminergic agonists [15].

Biological context of NMS

• Central expression of NMS appears restricted to the suprachiasmatic nucleus, and NMS has been involved in the regulation of dark-light rhythms and suppression of food intake [16].
• Our data are the first to disclose the potential implication of NMS in the regulation of gonadotropic axis, a function that may contribute to the integration of circadian rhythms, energy balance, and reproduction [16].
• Central administration of NMS evoked modest LH secretory responses in pubertal and cyclic females at diestrus, whereas exaggerated LH secretory bursts were elicited by NMS at estrus and after short-term fasting [16].
• In adult females, hypothalamic expression of NMS (which was confined to suprachiasmatic nucleus) and NMU2R significantly varied during the estrous cycle (maximum at proestrus) and was lowered after ovariectomy and enhanced after progesterone supplementation [16].
• MATERIALS AND METHODS: Competitive inhibitory effects of antimuscarinic agents on specific NMS [H] (PerkinElmer Life Sciences, Boston, Massachusetts) binding were examined in human tissue homogenates and in CHO-K1 cell membranes expressing human muscarinic receptor subtypes [17].

Anatomical context of NMS

• Expression of NMS and NMU2R genes was detected at the hypothalamus along postnatal development, with significant fluctuations of their relative levels (maximum at prepubertal stage and adulthood) [16].
• The principal findings are that (1) elevated urinary catecholamines and metabolites are a frequent but inconstant feature of NMS; (2) it is likely that sympathetic nervous system hyperactivity contributes to the picture of fulminant NMS; and (3) the role of the adrenal medulla in producing excess catecholamines during NMS is uncertain [1].
• On the other hand, MAF was less effective in depressing antigen- and mitogen-induced proliferation of human blood cells than were NMS or human serum [18].
• Muscarinic cholinergic receptors were assayed in frozen sections of the umbilical artery and vein by a radioligand binding assay technique, using [3H]-N-methyl scopolamine (NMS) as a ligand [19].
• There have been cases where the authors are convinced that the "pneumonia" or "urinary tract infection" was in fact a mild case of NMS that cleared [20].

Associations of NMS with chemical compounds

• Neuromedin s as novel putative regulator of luteinizing hormone secretion [16].
• Crossover reaction between haloperidol and amoxapine for NMS [21].
• These results do not indicate a useful role for dantrolene or bromocriptine in the treatment of NMS [22].
• Carbachol (0.1 microM to 1 mM) dose dependently displaced [3H] NMS binding and increased the intracellular calcium concentration without modification of adenylate cyclase activity [23].
• This is the first report of a zuclopenthixol-induced NMS [24].

Other interactions of NMS

• We found in one patient with a history of NMS a nucleotide substitution at codon 310 (CCG-->TCG) of exon 7 of the DRD2 gene which predicts the replacement of proline to serine in the third cytoplasmic loop of the receptor, a part of the receptor that interacts with G-proteins [25].
• Although both methods use CK-B antisera and radioiodinated CK-B, one ("M" for Mallinckrodt) uses hybridized CK-MB for calibration, while the other ("NMS" for Nuclear Medical Systems) uses CK-B [3].
• The clinical triad of fever, movement disorder, and altered mentation known as NMS represents an infrequent yet highly lethal side effect of neuroleptic therapy [26].

Analytical, diagnostic and therapeutic context of NMS

• A patient suffering from schizophrenia developed diabetic keto-acidosis and NMS after treatment with neuroleptics [27].
• In this patient, treatment of NMS with bromocriptine did not start until 10 days into hospitalization [28].
• However, insulinemia decreased more in the postoperative period in the MS group compared to the NMS group (p<0.05) [29].
• These results indicate that the application of human/mouse chimeric antibodies in two-site immunoassays is more effective for reducing interference from heterophilic antibodies than the adding of NMS or purified mouse IgG in the assay using conventional MAbs [30].
• Discontinuation of antipsychotics, maintenance of supportive therapy aimed at preventing dehydration, hemodynamic, and electrolyte imbalances, and pharmacotherapy are essential in the treatment of NMS [28].

References