Clinical Neuroscience

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NOVEMBER 30, 2011

Clinical Neuroscience - 2011;64(11-12)

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Clinical Neuroscience

[Theoretical and practical considerations of rational polytherapy in epilepsy]

RAJNA Péter

[Author analyses the consideration of rational polytherapy for epilepsy. Among the theoretical aspects he points the different effect of seizure inhibitory drugs on the epilepsy models but didn’t find data enough for the basis of any successful combination. Combinations of compounds having different way of action are more promising. Rational polytherapy can serve also the epileptic patients’ tailored therapy in the daily routine. There have already been some proved synergisms concerning drug interactions. Based on detailed analysis of side effects a possibility occurs for neutralization of side effects when anticonvulsants with side effects of opposite nature are combined. Considering both the side effect profiles and the different (somatic and psychic) habits of the patients we can create a special list of favourable combinations. Co-morbid states and their treatments play a significant role in the application of rational polytherapy. Combination of anticonvulsants of lower potential but without drug-interactions can be the choice in these cases. The non-epileptic indications of the anticonvulsants can also be utilized in polymorbid patients. Based on the theoretical and practical considerations the author defines the ten-step-cognitive-preparation-process in planning the optimal (poly)therapy. On speculative basis he suggests eight beneficial versions of seizure inhibitory rational polytherapy.]

Clinical Neuroscience

[The winners of the Schaffer Károly Prize 2010.]

Clinical Neuroscience

[Vascular or “lower body parkinsonism”. Rise and fall of one diagnosis]

SZIRMAI Imre

[The “arteriosclerotic parkinsonism”, which is called vascular parkinsonism (VP), was first described by Critchley1. The broad based slow gait, reduced stride lenght, start hesitation, freezing and paratonia was mentioned as “lower body parkinsonism” (LBP) which can be associated by slow speech, dysexecutive syndrome, and hand tremor of predominantly postural character. In VP the DAT-scan proved normal dopamine content of the striatum in contrast with Parkinson’s disease (PD). Additionally, Lewy bodies of brainstem type were not found in VP. Probability of VP increases if central type pathologic gait is prominent; the hands are slightly involved, the MRI indicates transparent periventricular white substance and/or brain atrophy. In some cases differentiation of gait apraxia and parkinsonism could be challenging. There is no rigor of the lower limbs at rest in neither of them, the disturbance of movement is evoked by the gait itself. Three subtypes of “gait ignition failure” has been recently described: (1) ignition apraxia, (2) equilibrium apraxia and (3) mixed gait apraxia. The primary progressive freesing gait was considered as a Parkinson-plus syndrome. Freesing occurs more frequently in diseases with pakinsonism than in PD. The grade of ventricle dilatation and the frontal leukoaraiosis was similar in LBP and gait apraxia. In cases of normal pressure hydrocephalus the impaired gait may mimic PD. Pathologic gait in VP can be explained by the lesions of the senso-motor association pathways in dorsal paramedian white substance within the vulnerable borderzone region. These may be colocalized with the representation of the lower extremities in the posterior third of the supplementer motor area. Rektor2 proposed to change the name of LBP to “cerebrovascular gait disorder”. Notwithstandig central type gait disorder develops also in many degenerative diseases other than cerebro-vascular origin. The neuronal net controling the regulation of movement is widespread, therefore several cortical and subcortical lesions could elicit large variations of pathologic gait, ie.: ataxia, apraxia, ignition failure, akinesis etc. In conclusion: most of the central gait disorders regarding the pathology and their appearance can not be called “parkinsonism”; these are much closer related to the localization of lesions rather than to the diagnostic categories.]

Clinical Neuroscience

[A8344G mutation of the mitochondrial DNA with typical mitochondrial encephalomyopathy with lactic acidosis and stroke like episodes syndrome]

VASTAGH Ildikó, GÁL Anikó, REMÉNYI Viktória, SEMJÉN Judit, LUKÁCS Tímea

[We report an unusual case of juvenile ischaemic stroke syndrome associated with the A8344G mutation in tRNALys gene of mitochondrial DNA. The clinical phenotype of patient was typical for MELAS (mitochondrial ecephalomyopathy with lactate acidosis and stroke like episodes). The MELAS has been related to mutation A3243G in most cases, but some other mitochondrial DNA mutations were described in the background of this syndrome as well. A 22-years-old man and his family were investigated. Throughout clinical investigation as well as Doppler sonography, neuroradiological, and immunserological examinations were performed. Molecular studies included the analysis of the Leiden, prothrombin G20210A and the most common mitochondrial DNA mutations. The DNA analysis of the proband revealed a heteroplasmic A8344G substitution in the T-loop of the tRNALys gene. The mutation could not been detected in her mother blood. We can conclude that A8344G mutation of the mitochondrial DNA resulted in juvenile ischemic stroke, which is associated only rarely to this genetic alteration. In young age onset of a stroke-like episode with undetermined etiology the mtDNA alterations always have to be excluded.]

Clinical Neuroscience

[Complementer medicine - on principles of evidence based medicine]

ORVOSI Tudományok Osztálya

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