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Antidepressant Medications
Published in Gary W. Jay, Practical Guide to Chronic Pain Syndromes, 2016
The major adverse effects of TCAs are secondary to cholinergic/muscarinic receptor blockade, histaminergic blockade (H1, H2), as well as blockade of the dopaminergic system. The anticholinergic side effects predominate and can include blurred vision, xerostomia, sinus tachycardia, constipation, urinary retention, confusion, and memory dysfunction. Histaminergic blockade can induce sedation, weight gain, dizziness, and hypotension. It also potentiates the effects of other CNS depressants. Alpha-1 adrenergic blockade can be associated with postural hypotension and dizziness. Blockade of dopaminergic receptors can induce extrapyramidal syndrome, dystonia, akinesia, neuroleptic malignant syndrome, tardive dyskinesia, and endocrine changes. Tachycardia and prolonged PR and QRS intervals with membrane stabilization can occur. The QT interval can become prolonged (1, 2).
Antidepressant Medications
Published in Gary W. Jay, Clinician’s Guide to Chronic Headache and Facial Pain, 2016
The major adverse effects of TCAs are secondary to cholinergic/muscarinic receptor blockade, histaminergic blockade (H1, H2), as well as blockade of the dopaminergic system. The anticholinergic side effects predominate and can include blurred vision, xerostomia, sinus tachycardia, constipation, urinary retention, confusion, and memory dysfunction. Histaminergic blockade can induce sedation, weight gain, dizziness, and hypotension. It also potentiates the effects of other CNS depressants. Alpha-1 adrenergic blockade can be associated with postural hypotension and dizziness. Blockade of dopaminergic receptors can induce extrapyramidal syndrome, dystonia, akinesia, neuroleptic malignant syndrome, tardive dyskinesia, and endocrine changes. Tachycardia and prolonged PR and QRS intervals with membrane stabilization can occur. The QT interval can become prolonged (1, 2).
Toxicology
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
The best-known examples of these are: Cholinergic syndrome which may have either a muscarinic or nicotinic pattern: Muscarinic pattern: Diarrhea (often with nausea and vomiting) excess urination, muscle fasciculation, miosis, bradycardia, bronchospasm, excessive lacrimation, excessive salivation—Mnemonic DUMBELSNicotinic pattern: Weakness tachycardia, mydriasis, hyperglycemia, hypertension, muscle fasciculations, CNS excitation.The former can be found with organophosphates including nerve gases or certain pesticides. Certain mushrooms can also have this effect.Anticholinergic syndrome: Flushing, dry skin and mucous membranes, mydriasis, loss of accommodation, and mental status changes, including convulsions, psychosis, delirium are classic manifestations. Fever, tachycardia, thirst, urinary retention are also seen. This pattern can be seen totally or partially with overdoses of atropine and similar anticholinergics. Mushrooms such as Amanita muscarina, plants like jimson weed, skeletal muscle relaxants, antipsychotics, antihistamines, or tricyclics can produce this effect.Serotonin syndrome.Extrapyramidal syndrome.Excessive sympathetic syndrome.Malignant hyperthermia.
Dyskinesia is most centrally situated in an estimated network of extrapyramidal syndrome in Asian patients with schizophrenia: findings from research on Asian psychotropic prescription patterns for antipsychotics
Published in Nordic Journal of Psychiatry, 2021
Seon-Cheol Park, Gyung-Mee Kim, Takahiro A. Kato, Mian-Yoon Chong, Shih-Ku Lin, Shu-Yu Yang, Ajit Avasthi, Sandeep Grover, Roy Abraham Kallivayalil, Yu-Tao Xiang, Kok Yoon Chee, Andi Jayalangkara Tanra, Chay Hoon Tan, Kang Sim, Norman Sartorius, Naotaka Shinfuku, Yong Chon Park, Toshiya Inada
To facilitate the clinical and pharmacological approaches for extrapyramidal syndrome, estimating their latent structure is needed. Network analysis is an analytical method to estimate the map of a collection of interrelated symptoms and explicate dynamic causal architectures of symptom clusters [8]. From a topological perspective, a network’s structure consists of nodes (symptoms) and edges (inter-connections). According to graph theory, different spatial and functional characteristics that demonstrate information about the relationships between the nodes within an estimated network are represented [9,10]. Since centrality is based on the overall interconnections of a symptom within an estimated network, central symptoms may have greater influence than peripheral symptoms. It is speculated that intertwined symptoms are more easily activated by symptoms that are centrally situated within the entire network. In terms of centrality, node strength, closeness, and betweenness are defined as the sum of all associations of a given node with all other nodes, the measure of how close a symptom is to all other symptoms, and the shortest length of a path connecting any two nodes, respectively [11,12]. Thus, the network structures of psychopathology among patients with schizophrenia have been estimated below. Alogia and avolition have been the most central domains among the negative symptoms of schizophrenia. Furthermore, blunted affect, alogia, and asociality have been the most central domains in female patients with schizophrenia, whereas alogia and avolition have been the most central domains in their male counterparts [13]. Moreover, the latent structure of negative symptoms has been estimated as an association of the five domains – anhedonia, avolition, asociality, blunted affect, and alogia [14].