Citalopram is a widely prescribed selective serotonin reuptake inhibitor (SSRI) used to treat major depressive disorder and anxiety conditions. Tardive Dyskinesia (TD) is a serious neurological disorder characterized by involuntary, repetitive body movements. This article examines the evidence connecting TD’s occurrence to the use of Citalopram.
Defining Tardive Dyskinesia
Tardive Dyskinesia (TD) is an iatrogenic movement disorder, meaning it is induced by medical treatment. It is characterized by involuntary, repetitive movements of the face, trunk, and limbs. The term “tardive” highlights the delayed onset of symptoms, which typically appear after months or years of exposure to a causative medication. TD is distinguished as a chronic condition because the movements can be irreversible.
TD differs fundamentally from acute extrapyramidal symptoms (EPS), such as acute dystonia or parkinsonism, which often appear shortly after starting a medication. Acute EPS are usually reversible with medication adjustment. However, TD symptoms may persist or worsen after the offending drug is discontinued. TD development is associated with the long-term use of medications that interfere with the brain’s dopamine signaling pathways.
Assessing the Link to Citalopram
The traditional cause of TD involves the long-term blockade of dopamine D2 receptors in the nigrostriatal pathway, associated with older antipsychotic medications. Citalopram, as an SSRI, operates by inhibiting serotonin reuptake, increasing serotonin levels, and does not directly block dopamine receptors. This distinct pharmacological profile means SSRIs have a substantially lower risk of causing TD compared to antipsychotic drugs.
Despite the difference in primary action, the risk of TD with Citalopram is not zero, as indicated by case reports. The proposed mechanism for SSRI-induced dyskinesia involves an indirect effect on the dopamine system. Increased serotonin levels are thought to exert a tonic inhibition on dopaminergic neurons in the nigrostriatal pathway. This indirect inhibition can mimic the dopamine D2 receptor blockade, potentially leading to dyskinetic movements in susceptible individuals.
The risk exists, especially in vulnerable patients. Established risk factors for developing TD include older age, female sex, and the presence of brain damage or a major affective disorder. Citalopram-induced dyskinesia has been reported both acutely and in a delayed fashion. While the absolute risk is low, this potential serious side effect warrants careful monitoring in vulnerable patient groups.
Recognizing the Physical Manifestations
The involuntary movements characteristic of TD can affect nearly any muscle group, ranging from subtle twitches to continuous, disruptive motions. Movements are often rapid and jerky or slow and writhing. The most common symptoms occur in the orofacial and buccal regions.
Orofacial Symptoms
Orofacial symptoms include repetitive actions such as:
- Lip smacking
- Tongue protrusion
- Chewing movements
- Grimacing
Patients might also exhibit uncontrolled blinking, puffing out of the cheeks, or making sucking noises. These movements are typically outside of the patient’s control and can significantly impact speech and eating.
Movements can also manifest in the limbs and trunk, though these are less frequent than facial movements. Limb involvement appears as finger wiggling, foot tapping, or complex stereotypical finger movements. Truncal movements include rocking the pelvis back and forth or swaying from side to side. Even mild symptoms can cause social embarrassment and interfere with a patient’s quality of life.
Medical Protocols for Diagnosis and Care
If involuntary movements are suspected while a patient is taking Citalopram, healthcare providers conduct a thorough assessment to confirm TD. A structured movement rating tool, such as the Abnormal Involuntary Movement Scale (AIMS), is the gold standard used for initial diagnosis and routine monitoring. The AIMS scale systematically evaluates the severity of involuntary movements across different body regions.
The primary management strategy for confirmed drug-induced TD involves reducing the dose of the offending agent or discontinuing it entirely under strict medical supervision. Discontinuation must be approached carefully, as the movements may initially be unmasked or temporarily worsen after the drug is stopped. Guidelines recommend the use of Vesicular Monoamine Transporter 2 (VMAT2) inhibitors as first-line treatment for moderate to severe TD.
These FDA-approved medications, which include valbenazine and deutetrabenazine, modulate dopamine levels in the brain to reduce involuntary movements. Patients experiencing any new or unusual movements should immediately contact their prescribing physician. Early detection and intervention offer the best chance for symptom improvement and minimize the risk of the condition becoming permanent.