Tardive Dyskinesia
A condition affecting the nervous system, often caused by long-term use of some psychiatric drugs.
Tardive dyskinesia is caused by long-term use of neuroleptic drugs, which are used to treat psychiatric conditions.
Tardive dyskinesia causes repetitive, involuntary movements, such as grimacing and eye blinking.
Stopping or tapering drugs that may be contributing to involuntary repetitive movements can help. In rare cases, botulinum toxin, deep brain stimulation, or medications can help.
Cluster Number:
Wiki Number: PW216
Diagnosis: Tardive Dyskinesia
US Patients: 30% of those taking antipsychotic medicines
World Patients:
Sex Ratio: M;F+
Age Onset: elderly
Brain Area:
Symptoms: involuntary, repetitive body movements: rapid-jerking or slow-writhing; grimacing, smacking lips, sticking out tongue, eye-blinking
Progression: walking is difficult or impossible due to excess leg movement
Causes: reactions to narcoleptic drugs; reactions to long-term-use of dopamine-receptor-blocking medications; antipsychotics
Medications: supersensitivity to dopamine becomes in the nigrostriatal pathway;discontinuing the narcoleptics helps; valbenazing, etc.
Therapies: No therapies listed; newer antipsychotic drugs cause less dyskinesia than the first generation of antipsychotic drugs did.
Youtube Video: Meet Jeff, Living with Tardive Dyskinesia
Amazon or Library Book:
Ultimate Medical Guide to Tardive Dyskinesia
Click the book to link or order from Amazon.
4 CURRENT ARTICLES
FROM PUBMED
The world-wide medical research
reports chosen for each diagnosis
Clicking each title opens the
PubMed article’s summary-abstract.
- Inhibition of VMAT2 by β2-adrenergic agonists, antagonists, and the atypical antipsychotic ziprasidoneby Svein Isungset Støve on November 23, 2022
Vesicular monoamine transporter 2 (VMAT2) is responsible for packing monoamine neurotransmitters into synaptic vesicles for storage and subsequent neurotransmission. VMAT2 inhibitors are approved for symptomatic treatment of tardive dyskinesia and Huntington's chorea, but despite being much-studied inhibitors their exact binding site and mechanism behind binding and inhibition of monoamine transport are not known. Here we report the identification of several approved drugs, notably β2-adrenergic...
- Clinical phenomenology and pathophysiology of daytime and nighttime imperative movementsby A O Akhmadulina on November 22, 2022
Imperative movements have an intermediate position between voluntary and involuntary movements and are also referred to as semi-voluntary, or induced. Their common characteristic is the urge, forcing the patient to perform an action that can have a different duration and degree of complexity - from a short twitch (with tics) to prolonged episodes of general motor restlessness (for example, akathisia or stereotypes). The ability to slow down this movement for a short or longer period of time by...
- Risperidone Abruption-Induced Tardive Dyskinesia in a Six-Year-Old Male Patient With Known Autism and Attention Deficit Hyperactivity Disorder: A Case Reportby Abdullah H Alhamoud on November 21, 2022
As a serotonin-dopamine antagonist, risperidone is less likely than traditional antipsychotics to result in tardive dyskinesia (TD). There are not many reports of risperidone abruption-induced TD. Herein we report a new case of tardive dyskinesia induced by a sudden stop of risperidone during the treatment of an autistic patient with attention deficit hyperactivity disorder (ADHD) on risperidone. He was presented to the emergency department in King Fahd Central Hospital in Jazan, Saudi Arabia,...
- Filgrastim, a Recombinant Form of Granulocyte Colony-stimulating Factor, Ameliorates 3-nitropropionic Acid and Haloperidol-induced Striatal Neurotoxicity in Ratsby Vikrant Rahi on November 17, 2022
Striatal neurotoxicity is the pathological hallmark for a heterogeneous group of movement disorders like Tardive dyskinesia (TD) and Huntington's disease (HD). Both diseases are characterized by progressive impairment in motor function. TD and HD share common features at both cellular and subcellular levels. Filgrastim, a recombinant methionyl granulocyte colony-stimulating factor (GCSF), shows neuroprotective properties in in-vivo models of movement disorders. This study seeks to evaluate the...