EEG abnormalities during treatment with tadalafil, a phosphodiesterase type 5 inhibitor.

OBJECTIVE: Tadalafil is a selective phosphodiesterase type 5 (PDE-5) inhibitor approved for the treatment of erectile dysfunction. Less is known about the electroencephalography (EEG) effects of PDE-5 inhibitors, and the present study, therefore, examined the risk of EEG abnormalities associated with tadalafil. METHOD: EEG recordings from 35 erectile dysfunction patients taking tadalafil (20 mg) were graded for severity of EEG abnormalities (at admission, 2 and 48 hours after tadalafil administration). RESULTS: At admission, there were no EEG abnormalities. At second EEG, abnormalities occurred in 12 (34.3%) of the 35 patients. Eight (22.9%) patients had mild and four (11.4%) patients had moderate EEG abnormalities. At third EEG, one (2.9%) patient had mild and one (2.9%) patient had moderate EEG abnormalities. CONCLUSION: PDE-5 inhibitors may produce EEG abnormalities. Although the exact role of PDE in altering susceptibility to seizure remains unclear, epileptic seizures may occur during treatment with PDE inhibitors.

Caffeic acid phenethyl ester protects rabbit brains against permanent focal ischemia by antioxidant action: a biochemical and planimetric study.

The present study was conducted to investigate whether caffeic acid phenethyl ester (CAPE), an active component of propolis extract, has a protective effect on brain injury after focal permanent cerebral ischemia, and to determine the possible antioxidant mechanisms. Cerebral infarction in adult male New Zealand rabbits was induced by microsurgical procedures producing right focal permanent middle cerebral artery occlusion (pMCAO). CAPE was administered to the treatment group after pMCAO at a dose of 10 micromol kg(-1) once a day intraperitoneally for 7 days. Neurological deficits were evaluated, using a modified six-point scale. Spectrophotometric assay was used to determine the contents of malondialdehyde (MDA), glutathione (GSH), catalase (CAT), nitric oxide (NO) and xanthine oxidase (XO). In the ipsilateral hemisphere, the infarct volume of the brain was assessed in brain slices stained with heamatoxylen and eosin. The results showed that treatment with CAPE significantly reduced the percentage of infarction in the ipsilateral hemisphere compared with the ischemia group. CAPE treatment significantly attenuated the elevation of plasma MDA, CAT and XO content (p<0.05), whereas it significantly increased the levels of plasma GSH and NO (p<0.05). Therefore, subacute CAPE administration plays a protective role in focal pMCAO due to attenuation of lipid peroxidation and its antioxidant activity. All of these findings suggest that CAPE provides neuroprotection against cerebral ischemia injury through its antioxidant action.

The co-occurrence of Chiari type 1 malformation with syringomyelia and total situs inversus.

BACKGROUND: Total situs inversus (TSI) is a rare congenital anomaly that often occurs concomitantly with other disorders. TSI is the complete left-to-right inversion of the thoracic and abdominal organs. It develops due to an abnormal rotation of the cardiac tube during embryogenesis, the mechanism of which is of unknown mechanism. Syringomyelia (SM) is an uncommon disease of the spinal cord and is known as the occurrence of a cystic space in the middle of the spinal cord. SM occurs due to spinal cord injury, a primary tumor of the spinal cord, or an extramedullary lesion at the foramen magnum such as a Chiari type 1 malformation (CM1). In the literature there has been reported association of CM1 and SM (CM1/SM) with known genetic syndromes. CASE REPORT: We report a 33-year-old female with CM1/SM coexisting with TSI. Our patient presented with pain in the neck, arm, and upper back. She had no trauma history. There was dysesthesia in the cervical-2 dermatomes. Radiological tools revealed that CM1/SM with TSI accompanied by no other abnormality. CONCLUSIONS: It can be suggested that the existence of this case indicates that genetic factors may influence the pathogenesis of some CM1/SM cases.

Autonomic dysfunction and cardiac repolarization abnormalities in patients with migraine attacks.

The clinical symptoms of migraine are widely accepted to be related to the involvement of the autonomic nervous system, and especially to dysfunction in the regulation of the circulatory system and autonomic balance. Disturbance of the autonomic nervous system is a primary characteristic of migraine Therefore, patients with migraine have a variety of symptoms, such as vasodilatation (flushing), pilo-erection, nausea, vomiting, diarrhea, cutaneous vasoconstriction (pallor), and diaphoresis. The electrocardiographic changes seen during a migraine attack compared with the pain-free period could be secondary to reversible disturbances of the state of autonomic innervation of the heart and coronary arteries. Dysfunction of ANS may affect atrial and ventricular repolarization. For instance, increased sympathetic activity causes sinus tachycardia, but increased parasympathetic activity causes sinus bradycardia, atrioventricular block, and ST-segment and T-wave abnormalities. Comprehensive electrocardiographic analyses have been providing more details in terms of the detection of abnormalities in atrial and ventricular repolarization which potentially may result in arrhythmias in patients with migraine. However, there is no information in literature reporting the frequency of cardiac arrhythmias in migraine patients who had cardiac repolarization abnormalities. In this review, detailed electrocardiographic findings and their relation with the autonomic nervous system, including recent observations, have been evaluated. However, further studies are needed to investigate the association between autonomic dysregulation and cardiac repolarization abnormalities in patients with migraine.

Evaluation of oxidative stress and inflammation in long term Brucella melitensis infection.

The Brucella genus is able to cause chronic infection in a wide range of mammals including humans. Oxidative events, lipid peroxidation and inflammatory response against Brucella infection have not yet been well elucidated in vivo. We have investigated oxidative/antioxidative status and nitric oxide production in plasma, brain, liver and spleen during a 60 day period of B. melitensis infection in a rat model. In addition, inducible nitric oxide synthase (iNOS), IL-10, IL-12, IFN-gamma and TNF-alpha mRNA transcriptions were analyzed by semiquantitative reverse transcriptase PCR (RT-PCR) in brain samples. Animals were infected with B. melitensis and sacrificed at 7th, 15th, 30th, 45th and 60th day of post-inoculation. Malondialdehyde (MDA), as an indicator of lipid peroxidation, and nitric oxide (NO) concentrations were significantly increased after Brucella inoculation and began to decline to basal levels from 45th day in plasma, liver and spleen. However, iNOS transcription was not induced during the infection period in brains. In contrast, MDA level was increased in brain during the late phase of infection without any change in NO production. The infection did not alter the antioxidant enzyme activities in the tissues; although significantly increased catalase activity was observed between days 30 and 45 in the liver. Transcription analyses demonstrated that IL-10, IL-12 and IFN-gamma mRNA level were not induced in the brain. Only TNF-alpha mRNA was weakly up-regulated in brain 30 days after pathogen inoculation. The results obtained in this study demonstrate that B. melitensis induces lipid peroxidation and NO production in the liver and spleen in the early days of infection, but that these levels subsequently decline. Moreover, Brucella does not appear to induce antioxidant enzyme activities and inflammation during two months of infection. However, the pathogen does stimulate cerebral lipid peroxidation in the late phase of infection without causing significant inflammation.

Tear film tests in Parkinson's disease patients.

OBJECTIVE: Parkinson's disease (PD) has both motor and nonmotor features. Parkinson's disease patients are prone to dry eye due to both autonomic dysfunction and motor symptoms affecting blinking. This study was conducted to investigate the changes in tear functions in PD patients. DESIGN: Nonrandomized, prospective, clinical study. PARTICIPANTS: Fifty-six eyes of 56 consecutive patients with PD were studied. Thirty-six eyes of age-matched non-PD patients without pathology affecting tear tests were examined as control subjects. INTERVENTION: Modified Hoehn-Yahr (H-Y) scale, blink rate (BR), and tear tests were examined. MAIN OUTCOME MEASURES: Modified H-Y scale, BR, dry eye assessment questionnaire, meibomian gland evaluation, tear meniscus height, tear breakup time, fluorescein stain, rose bengal stain, Schirmer's test, and phenol red thread test. RESULTS: Overall tear function abnormalities were significantly more common in PD patients (P = 0.001, Mann-Whitney U test). Each test was found to be significantly disturbed in PD patients relative to controls (P<0.05, Mann-Whitney U test). Each PD patient had at least 1 abnormal test. Overall tear function abnormalities as assessed by the total abnormal test count correlated with the H-Y score (P<0.001, Spearman rho correlation). Parkinson's disease patients' mean BR (12.7+/-7.42 per minute) was significantly less than the controls' (21.8+/-7.37) (P<0.01, Student's t test). The abnormality in each tear test, except those for meibomian gland function and tear meniscus height, was significantly related to the H-Y scores (P<0.05, chi2 linear-by-linear association). CONCLUSION: The results of this study indicate that PD is associated with disturbances in tear function. With the exception of meibomian gland disease and tear meniscus height, the tests were found to have a linear association with the H-Y scale, which may be attributed to associated dysfunctions of PD.