[While 10% of healthy men had sexual dysfunctions, male epilepsy patients experience sexual problems in 40-70%. The cause of sexual dysfunction in epilepsy is multifactorial, but there are three main factors: the epilepsy itself, antiepileptic treatment and psychiatrical/psychic problems. Antiepileptics with hepatic enzyme induction potential (carbamazepine, phenytoin) enhance the metabolism of sexual steroids. Valproic acid as an enzyme inhibitor and drug with high protein binding affinity elevates the free serum levels of androgenes. Certain antiepileptic drugs may have negative cognitive side effects, some of them can induce psychiatric disorders. These drugs can facilitate male sexual dysfunctions through these psychic side effects. The metabolic and endocrine alterations caused by carbamazepin may return to normal level after replacement of carbamazepin with oxcarbazepine. After an oxcarbazepin-carbamazepin replacement, carbamazepin-induced impotency can be cured. According some new data lamotrigine can also help in sexual dysfunction. The therapy of sexual dysfunction in epilepsy depends on its cause. In cases of hormonal alterations, the fist step is a change of antiepileptic regimen. Instead of enzymeinductor antiepileptics and valproate, new antiepileptic drugs should be prescribed. At present, the most investigated antiepileptic drug is the oxcarbazepine with positive effect on antiepileptic-induced male sexual dysfunction, however, lamotrigine seems to be also beneficial. If the hormonal and sexual dysfunctions cannot be eliminated by drug changes, androgenic therapy or bromocriptin may be required. Testosteron may not only be beneficial on sexual functions, but can reduce also the seizure frequency. Independent of etiology, erectile dysfunctions can be successfully treated by sildenafil.]

[Abstracts of the 8th congress of the hungarian epilepsy league Pecs 25-27 may 2006]

[A 36 year-old male patient developed sudden double vision and gait imbalance. Neurological examination revealed gaze paresis upward and on the left side downward (vertical “oneand- a-half”-syndrome), horizontal gaze nystagmus on the left bulbus directed to left. The MRI revealed bilateral thalamic and left midbrain ischemic lesions. The brainstem auditory and visual evoked responses were normally configured. Optokinetic nystagmus test found rightward, upward and downward hypometric saccades, convergence-retraction nystagmus - which was not visible at physical neurological examination - saccadic smooth pursuit eye movement and pseudoabducent palsy on both sides. The complex gaze disturbance was attributed to the lesions in the intralaminar nuclei of the thalamus and in the pretectal and rostromedial tegmentum of the mesencephalon. Infarcts may have been due to a variant artery: i.e. the thalamoperforant and the superior paramedian mesencephalic arteries originate with common branch from one of the communicant basilar artery. The authors discuss the mechanism of complex gaze palsy and call attention to the diagnostic value of optokinetic nystagmus examination.]