Withdrawal symptoms may occur after treatment with tricyclic antidepressants (e.g. imipramine, amitriptyline, desipramine), serotonin reuptake inhibitors (e.g. fluoxetine, paroxetine, sertraline) and monoamine oxidase inhibitors (e.g. phenelzine, selegiline, pargyline).
The likelihood of this syndrome depends on the dose and half-life of the drug taken, as well as the rate at which the drug is discontinued. It is most likely to occur with short-acting medications that are stopped suddenly rather than gradually discontinued. The short-acting serotonin reuptake inhibitor paroxetine is the drug that causes the most withdrawal symptoms, but these symptoms can occur with any type of antidepressant.
Unlike withdrawal syndromes that occur with opioids, alcohol and other substances of abuse, antidepressant withdrawal syndrome is diagnostic. There are no symptoms. Symptoms are vague and variable and begin within 2-4 days after the last dose of the antidepressant. Symptoms such as dizziness, ringing in the ears, “electric shocks in the head,” inability to sleep, and acute anxiety have been described for SSRIs. Before discontinuation, antidepressant use must not have caused hypomania or euphoria (one must ensure that the discontinuation syndrome is not due to mood swings brought on by previous treatment). Antidepressant withdrawal syndrome is due solely to pharmacological factors and is not related to the reinforcing effects of an antidepressant. Similarly, if an antidepressant potentiates the stimulant, abrupt discontinuation will result in stimulant withdrawal symptoms rather than the antidepressant withdrawal syndrome described here. Parkinson's tremor, muscle rigidity, akinesia (loss of movement or difficulty initiating movements) that develops within a few weeks after starting a medication (e.g. a neuroleptic), increasing the dose of the medication, or reducing the dose of the medication used to treat extrapyramidal symptoms. or bradykinesia (slowing of behavior). Patients usually received a dopamine antagonist within 72 hours before symptoms developed. Excessive sweating accompanied by hyperthermia (orally measured > 38.02C at least twice) is a distinctive feature of neuroleptic malignant syndrome, and with this feature, antipsychotic drugs may affect neurology. It differs from other worrying side effects. Extreme temperature increases, which indicate the collapse of the thermoregulatory center, mostly support the diagnosis of neuroleptic malignant syndrome. In its most severe form, described as a “lead pipe,” generalized rigidity, often unresponsive to antiparkinsonian medications, is the hallmark of this disorder, along with other symptoms of neurological concern (e.g., tremor, sialorrhea, akinesia, dystonia, trismus, myoclonus, dysarthria, dysphagia, rhabdomyolysis). may accompany this. Elevated creatine kinase at least four times the upper limit of normal values is frequently seen. Changes in level of consciousness and certain mood changes, ranging from delirium or stupor to coma, are often an early finding. Affected individuals may appear alert but confused and may not respond in a manner consistent with catatonic stupor.
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