Clinical Neuroscience

[Anxiety in epilepsy - based on two case reports]

BARAN Brigitta, FARKAS Márta, RAJNA Péter

OCTOBER 20, 2002

Clinical Neuroscience - 2002;55(09-10)

[There are a great number of psychopathological symptoms which manifest themselves in 70-75% of epileptic patients but most of them remain unrecognised and untreated. These symptoms may affect the patients’ quality of life more negatively than the epileptic seizures themselves. Anxiety is one of the most frequently occurring interictal psychopathological symptom. A number of specialists agree that chronic epilepsy causes the amplification of endogenic seizure suppressing mechanisms which hinder the epileptic seizures and are responsible for the development of interictal psychopathological symptoms. However the physiological effects of the interictal psychopathological conditions (e.g. anxiety) have epileptogenic effect as well. There is a high chance that the conditions of epilepsy and anxiety will mutually create a destructive vicious circle and it will be illustrated by our two case reports. In our experience, before modifying the pharmacotherapy of a patient suffering from chronic epilepsy with increased frequency of seizures, the anxiety level should be defined; and if it is high it should be treated first. From our perspective, the so-called ”rational bitherapy” is very effective when a high potential antiepileptic drug is combined with an anxiety reducing method. The latter can be drug related or consists only of psychotherapy. We need more controlled clinical research to prove that inside epilepsy there are risk groups as well as conditions of high risk when the connection between anxiety and epilepsy is more than evident. The described cases seem to indicate that the existence of periictal anxiety can be a risk factor in developing later interictal anxiety.]

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KÉKESI Gabriella, HORVÁTH Gyöngyi

[It is well known that glutamate receptors have significant role in the pain transmission. The activation of N-methyl-Daspartate receptors causes persistent pain, therefore the antagonists acting on these receptors cause antinociception in chronic pain states. As the synthetic N-methyl-D-aspartate receptor antagonists have several side effects, they are not used generally in the clinical therapy. The tryptophan metabolite kynurenic acid is an endogenous antagonist of N-methyl-D-aspartate receptors. Although some data proved its neuroprotective effect, only a few studies suggest the antinociceptive potential of kynurenic acid. The goal of this review to summarise the possible role of kynurenic acid in the pain therapy based on the results of animal studies. Data available concerning this subject demonstrated that kynurenic acid is not an appropriate agent for antinociception neither in single nor in continuous administration because of its side-effect resulting in motor deficiency. On the other hand the combination of low doses of kynurenic acid and endomorphin-1 provides effective antinociception without side-effects on inflammatory pain test, thus may offer a new treatment modality in human pain therapy.]

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[Kennedy’s syndrome - bulbo-spinal muscular atrophy]

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[Kennedy syndrome is a late-onset, bulbar-spinal type of muscular atrophy, with X-linked recessive inheritance. The characteristic features of the disease become prominent in the 4-5th decades: proximal muscle wasting and weakness, bulbar signs, fasciculations in skeletal muscles, subtle signs of endocrine dysfunction, such as gynaecomastia or testicular atrophy. The electrophysiological examinations are the keypoint to the diagnosis. Electroneurography shows normal conduction velocity in peripheral nerves, but the sensory nerves usually show axonal degeneration, which causes only very mild or subclinical neurological deficits. Electromyography shows chronic anterior horn cell degeneration in skeletal muscles. Molecular genetic diagnosis was introduced in 1991, when an abnormal expansion of CAG repeat was found in the first exon of the androgen receptor gene on chromosome X with a frequency of 100% in the affected population. Since the progression is very slow and these patients can expect a normal life span, it is essential to distinguish this syndrome from other, often more severe diseases, such as ALS. There is no proven therapy for Kennedy's disease yet. This is the first case of Kennedy's disease published in Hungary.]

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