ABSTRACT
The term mild cognitive impairment (MCI) defines an intermediate state between normal aging and dementia. Vascular cognitive impairment refers to a decline in cognitive function that is caused by or associated with vascular disease and comprises all the spectrum of cognitive impairments, from MCI of vascular origin to vascular dementia. One of the available treatments for cognitive impairment is cytidine diphosphate-choline (CDP-Choline), or citicoline. The objective of the present manuscript is to provide complete evidence about the efficacy of citicoline for MCI, especially of vascular origin, but also due to other neurodegenerative disorders. Citicoline is a pharmaceutical product constituted by the combination of 2 natural molecules (cytidine and choline) and is marketed as a food supplement. It has been proposed to provide neuroprotective effects through diverse mechanisms of action. Taking into account the available literature, citicoline has shown a consistent improvement in cognitive function in patients with MCI, especially of vascular origin. Moreover, it provides beneficial effects on vascular, Alzheimer, and mixed dementias, stroke sequelae, intracerebral hemorrhages, traumatic brain injuries, and neurodegenerative diseases. Long-term treatment with citicoline has also been demonstrated to be well-tolerated and has not been associated with severe adverse events. Citicoline is a safe, well-tolerated, and promising agent with evidenced neuroprotective properties.
ABSTRACT
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Subject(s)
Humans , Male , Female , Hypercholesterolemia/chemically induced , Hypercholesterolemia/complications , Lipid Metabolism , Lipid Metabolism Disorders/chemically induced , Lipid Metabolism Disorders/complications , Lipid Metabolism Disorders/diagnosis , Anticonvulsants/adverse effects , Aminoimidazole Carboxamide/adverse effects , Epilepsy/complications , Epilepsy/drug therapy , Retrospective Studies , Chemotherapy, Adjuvant/methods , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/prevention & control , Risk FactorsABSTRACT
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Subject(s)
Humans , Anticonvulsants/adverse effects , Hyponatremia/chemically induced , Epilepsy/drug therapy , Carbamazepine/adverse effects , Retrospective StudiesSubject(s)
Anticonvulsants/therapeutic use , Carbamazepine/analogs & derivatives , Carbamazepine/adverse effects , Dibenzazepines/therapeutic use , Hyponatremia/prevention & control , Adult , Anticonvulsants/adverse effects , Carbamazepine/administration & dosage , Carbamazepine/therapeutic use , Dibenzazepines/adverse effects , Drug Substitution , Drug Therapy, Combination , Epilepsies, Partial/blood , Epilepsies, Partial/drug therapy , Female , Humans , Hyponatremia/chemically induced , Male , Middle Aged , Retrospective Studies , Therapeutic EquivalencyABSTRACT
OBJECTIVE: To evaluate the effect of different migraine prophylaxis medications on subject responsiveness to almotriptan. BACKGROUND: There is evidence supporting an increase of responsiveness of symptomatic medications for migraine attacks by some prophylactic treatments although this has not been probed. METHODS: A total of 345 patients (230 women, mean age 37.3) with episodic or chronic migraine were classified according to the prophylaxis they were taking in the following groups: (1) no prophylactic medication; (2) propranolol; (3) topiramate; (4) flunarizine. Decrease in Analogical Visual Scale and pain-free at 2 hours after almotriptan intake was assessed at 2 months. Side effects and discontinuation or treatment were also assessed. RESULTS: Headache severity was reduced 4.2 in control group, 5.3 in propranolol group, 4.1 in topiramate group, and 4.0 in flunarizine group, whereas pain-free status was achieved in 37.3%, 48.7%, 36.1%, and 38.1% respectively. These two parameters were statistically significative between propranolol and control groups. Side effects were similar in all groups. CONCLUSIONS: Our results displayed a higher efficacy of almotriptan in propranolol group and we hypothesized it may be due to a common mechanism of action at serotoninergic receptors.
Subject(s)
Flunarizine/pharmacology , Fructose/analogs & derivatives , Migraine Disorders/drug therapy , Propranolol/pharmacology , Serotonin Receptor Agonists/pharmacology , Tryptamines/pharmacology , Adolescent , Adrenergic beta-Antagonists/pharmacology , Adult , Anticonvulsants/pharmacology , Calcium Channel Blockers/pharmacology , Drug Interactions/physiology , Drug Therapy, Combination , Female , Fructose/pharmacology , Humans , Male , Middle Aged , Migraine Disorders/physiopathology , Migraine Disorders/prevention & control , Pain Measurement , Topiramate , Treatment Outcome , Young AdultABSTRACT
INTRODUCTION: Topiramate is a sulfamate-substituted monosaccharide that has proven efficacy in reducing migraine attacks frequency and severity and has similar mechanisms of action and side effects profile to zonisamide. Although there are some studies suggesting a potential role of this drug in migraine prophylaxis, data are still scarce. We evaluate the efficacy and safety of zonisamide for migraine prevention in patients refractory to topiramate. METHODS: Sixty-three patients were initiated on 50 mg/d zonisamide dosage, which was titrated to 400 mg/d, as tolerated. Number of migraine attacks, headache severity (according to a 1- to 10-point visual analog scale), and use of acute medication were tested before and 2 and 6 months after the initiation of zonisamide. Demographic data, dose of the medication, duration of the treatment, and adverse events were also collected and analyzed. RESULTS: Statistically significant improvement in number of migraine attacks, headache severity, and use of acute medication reduction was obtained after the second month of zonisamide therapy and carried through month 6 of treatment. Fifteen patients reported adverse events, the most common of which was concentration difficulties. CONCLUSIONS: These results suggest that zonisamide is effective and well tolerated for migraine prevention in patients refractory to topiramate. With the exception of the inhibition of T-type calcium channels by zonisamide, its mechanisms of action seem to be very similar to topiramate's. We suggest the potential role of these channels in the pathophysiology of migraine.
