ABSTRACT
BACKGROUND: Cognitive impairment is one of the side effects of using anticholinergic medicines for overactive bladder; however, its incidence has not been fully reported. We experienced two elderly Japanese patients with overactive bladder who had temporary cognitive impairment caused by anticholinergic medicines. CASE PRESENTATION: The first case was a 79-year-old female patient to whom imidafenacin (0.2 mg) was administered daily to control her frequent micturition and urgency. She was taking the following medicines: etizolam, triazolam, captopril, bisoprolol, and amlodipine besylate. Her Hasegawa dementia rating scale-revised was impaired from 26/30 to 17/30 and recovered to 25/30 after the imidafenacin treatment was stopped. The second case was an 82-year-old female patient to whom imidafenacin (0.2 mg) was administered daily for frequent micturition and urgency. She was taking the following medicines: losartan potassium and clenbuterol. Her Hasegawa dementia rating scale-revised decreased from 28/30 to 19/30 and recovered to 24/30 after the imidafenacin treatment was stopped. In our patients who were taking multiple medicines, there is a possibility that medicines other than anticholinergics may have caused cognitive impairment. We need to keep in mind that many elderly people take multiple medicines because of comorbidity. CONCLUSIONS: Anticholinergic medicines can cause cognitive impairment in elderly people, and attention should be paid to cognition when elderly overactive bladder patients are treated with anticholinergic medicines.
Subject(s)
Cholinergic Antagonists/adverse effects , Cognition Disorders/chemically induced , Cognition/drug effects , Imidazoles/adverse effects , Urinary Bladder, Overactive/drug therapy , Urinary Incontinence, Urge/drug therapy , Aged , Aged, 80 and over , Cognition Disorders/diagnosis , Cognition Disorders/psychology , Female , Humans , Polypharmacy , Risk Factors , Time Factors , Urinary Bladder, Overactive/diagnosis , Urinary Bladder, Overactive/physiopathology , Urinary Incontinence, Urge/diagnosis , Urinary Incontinence, Urge/physiopathology , Urination/drug effectsABSTRACT
Japanese encephalitis (JE) virus is a mosquito-borne virus belonging to the flavivirus family, including the West Nile and St Louis encephalitis viruses endemic to North America. JE virus is prevalent in East Asian countries and can cause acute lethal encephalitis. Although vaccination programs have decreased the incidence of JE in Japan, the cases that do occur are often fatal or associated with considerable clinical sequelae. We report, for the first time to our knowledge, a patient who had repetitive bouts of hyperthermia in the summertime after recovery from acute JE. An insulin challenge test revealed only marginal increases in the levels of beta-endorphin and growth hormone, indicating partial medial hypothalamic dysfunction. Magnetic resonance imaging showed T2 hyperintensity in both thalamic paraventricular subcortical regions, known to project to the hypothalamic paraventricular nucleus. We thus attributed the episodes of hyperthermia to secondary hypothalamic impairment with thalamic lesions.
Subject(s)
Encephalitis, Japanese/complications , Fever/etiology , Hypothalamic Diseases/diagnosis , Hypothalamic Diseases/etiology , Brain/pathology , Female , Humans , Hypothalamic Diseases/pathology , Middle AgedABSTRACT
We investigated three genotypes (AA, AT, and TT) produced by signal peptide polymorphism of the alpha-1-antichymotrypsin (ACT) gene in 105 patients with multiple system atrophy (MSA) and age-matched controls. The frequency of ACT-AA genotype was significantly higher in patients with MSA (20.0%) than in controls (10.5%). The onset of MSA was significantly earlier and the disease progressed significantly faster in patients with ACT-AA genotype than in those with non-ACT-AA genotypes. The ACT concentration in cerebrospinal fluid was increased in patients with ACT-AA. To our knowledge, this is the first study to show that the ACT-AA genotype is a risk factor and modulating factor for MSA. Our findings suggest the involvement of ACT-relating inflammatory process in the pathogenesis of MSA.
