Side effects experienced while taking cinnarizine range from the mild to the quite severe. Possible side effects include drowsiness, sweating, dry mouth, headache, skin problems, lethargy, gastrointestinal irritation, hypersensitivity reactions, as well as movement problems/muscle rigidity, and tremor. Because cinnarizine can cause drowsiness and blurred vision, it is important that users make sure their reactions are normal before driving, operating machinery, or doing any other jobs which could be dangerous if they are not fully alert or able to see well.
Cinnarizine is also known to cause acute and chronic parkinsonism due to its affinity for D2 receptors, which strongly counter-suggests its actual usefulness for improving neurohealth. Cinnarizine's antagonistic effects of D2 dopamine receptors in the striatum leads to symptoms of depression, tremor, muscle rigidity, tardive dyskinesia, and akathisia, which are characterized as Drug-Induced Parkinson's disease and is the second leading cause of Parkinson's. Evidence suggests that it is one of the metabolites of cinnarizine, C-2, that has an active role in contributing to the development of drug-induced Parkinson's. It is also of note that an estimated 17 of 100 new Parkinson's cases are linked to administration of either cinnarizine or Flunarizine, making cinnarizine and drug-induced Parkinson's a serious issue. Those people especially at risk are elderly patients, in particular women, and patients who have been taking the drug for a longer amount of time. There is also evidence that suggests that patients with a family history of Parkinson's, or a genetic predispostion to the disease are more likely to develop the drug induced form of this disease as a result of cinnarizine treatment.
In addition to antagonizing D2 receptors, treatment with cinnarizine has also been shown to lead to reduced presynaptic dopamine and serotonin, as well as alterations in vesicular transport of dopamine. Terland et al. have shown that chronic treatment with cinnarizine builds the drug concentrations high enough that they interfere with the proton electrochemical gradient necessary for packaging dopamine into vesicles. Cinnarizine, pKa = 7.4, acts as a protonophore, which prevents the MgATP-dependent production of the electrochemical gradient crucial to the transport and storage of dopamine into vesicles, and thereby lowers the levels of dopamine in the basal ganglia neurons and leads to the Parkinson's symptoms.
Additionally, several cases of pediatric and adult cinnarizine overdose have been reported, with effects including a range of symptoms such as somnolence, coma, vomiting, hypotonia, stupor, and convulsions. The cognitive complications likely result from the antihistaminic effects of cinnarizine, while the motor effects are a product of the antidopaminergic properties. In cases of overdose, the patient should be brought to and observed in a hospital for potential neurological complications.
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