Clinical Neuroscience


OLÁH László, CSÉPÁNY Tünde, BERECZKY Zsuzsanna, KERÉNYI Adrienne, MISZ Mária, KAPPELMAYER János, CSIBA László

JANUARY 20, 2005

Clinical Neuroscience - 2005;58(01-02)

[Introduction - Decreased activity of natural anticoagulants (antithrombin-III, protein C, protein S) rarely causes cerebral ischaemia, however it can be found frequently in acute phase of ischaemic stroke. The authors’ aim was to investigate whether the decreased activity of natural anticoagulants is accompanied by worsening of symptoms in ischaemic stroke. Patients and method - Sixty-eight acute ischaemic stroke patients were investigated. Severity of symptoms were assessed and followed by the NIH Stroke Scale. Antithrombin- III, protein C, protein S activities, and concentration of C-reactive protein (CRP) were measured within 48 hours after onset of ischaemic stroke. Results - Progressing stroke was found in 29% of patients. Decreased activity of at least one natural anticoagulant proteins was present in 31% of patients. Progression of stroke symptoms occured in 76% of patients with decreased natural anticoagulant activity, while this proportion was only 9% in those with normal natural coagulation inhibitor protein activity (p<0.01). Progressing stroke was also more frequent in patients with elevated CRP value (60%) than in those with normal CRP level (11%; p<0.05). Decreased activity of natural anticoagulants was more frequent in patients with elevated CRP concentration compared with patients with normal CRP. Conclusion - The results demonstrate the importance of decreased activity of natural anticoagulants in acute phase of ischaemic stroke. This abnormality was present in about 1/3 of stroke patients. The decreased activity of natural coagulant inhibitor proteins may play an important role in development of progressing stroke thus indicating unfavourable outcome.]



Further articles in this publication

Clinical Neuroscience



[Dizziness and vertigo - like headache - are the most common complaints which lead patients to visit the doctor. In spite of the headache - which may be primary (e.g. migraine) or symptomatic - dizziness and vertigo do not appear to be a separate nosologic entity but rather the symptoms of several neurological disorders. For differential diagnosis, interdisciplinary thinking and activity is needed because the vestibular, neurological and psychiatric disorders might have a common role in the development of symptoms and further overlapping can also occur. The vascular disorders of the vertebrobasilar system are discussed in detail in this review. The importance, occurrence and causes of vertigo as a warning symptom is in the focus. The author draws attention to life-threatening conditions with acute onset in cases of the posterior scale ischemia and emphasizes the importance of the correct and early diagnosis. The author tries to clear up the nihilistic aspect in treating of stroke and stresses the necessity of thrombolysis and interventional radiological procedures which may be the only chance for the recovery of the patients. The pharmacological prevention of recurrent vascular events is also important and obligatory for the clinicians.]

Clinical Neuroscience



[There is an increasing number of peripheral nerve disorders with inflammatory and immune mechanisms involved. The precise diagnosis is of utmost importance, since these patients can be successfully treated. Unfortunately, there is no specific marker for any disease of this group. The diagnosis therefore relies on the appropriate consideration of the clinical, neurophysiological and laboratory data, which requires in-depth knowledge of these diseases. In this paper we review the diagnostic criteria and treatment strategies for the major types of chronic inflammatory polyneuropathies.]

Clinical Neuroscience



[In this work the authors provide evidences for a unifying concept of the syndromes of benign focal childhood epilepsies, Landau-Kleffner syndrome, and electrical status epilepticus in sleep treating them as a spectrum of disorders with a common transient, age dependent, non lesional, genetically based epileptogenic abnormality, the nature of which is still not known. The electro-clinical features of these syndromes are congruent with the different degree involvement of the perisylvian cognitive network and with the involvement of the thalamo-cortical associative system of variable degree. These epilepsies are characterized by the abundance of regional epileptiform discharges in sharp contrast with the rare and in several cases lacking seizures. The nature and severity of interictal cognitive symptoms are closely related to localization within the network and amount of epileptic interictal discharges. Spike-wave discharges are attributed to an alternation of overexcitation (spikes) and overinhibition (waves). The recurrent overinhibition represented by the wave of the discharges may interfere with the continuous depolarization of the cells of a large population of neurons, which is a requirement of the overt seizures. The overinhibition also interfere with cognitive processes which are correlated with the continuous presence of the fast (gamma) activity, binding the required cortical areas. Hence the recurrent inhibition works against the existence of the binding fast frequency activity. This is the assumed reason for the co-existence of the relative lack of overt seizures and in the same time for the frequently observed epileptogenic cognitive deficit symptoms ("cognitive epilepsies"). The time course of these syndromes overlaps with important developmental milestones. The frequent epileptic discharges alters the evolution of the perisylvian network developing late after early childhood and is very vulnerable for any interference in this imprinting time for speech and other cognitive functions. This spectrum of disorders represents a type of age linked, mild to severe ‘epileptic encephalopathy’ limited to the perisylvian network, where the cognitive impairment is underlied by epileptic discharges interfering with cognitive development.]

Clinical Neuroscience

[EXPERIMENTAL DEMYELINATION CAUSED BY PRIMARY OLIGODENDROCYTE DYSTROPHY Regional distribution of the lesions in the nervous system of mice brain]


[Background and purpose - Heterogeneity of multiple sclerosis lesions has been recently indicated: In addition to T-cell-mediated or T-cell plus antibody-mediated autoimmune mechanisms (patterns I-II) two other patterns (III-IV) were described. Patterns III-IV are characterized by primary oligodendrocyte dystrophy, reminiscent of virus- or toxin-induced demyelination rather than autoimmunity. It was described more than 30 years ago that dietary application of a copper-chelating agent called cuprizone results in primary oligodendrocyte degeneration which is followed by demyelination. The aim of the present study was to examine the regional distribution of cuprizone induced oligodendrocyte dystrophy and demyelination in the nervous system of mice. Material a methods - Demyelination was induced in male weanling Swis-Webster mice by feeding them on a diet containing 0.6% (W/W) cuprizone bis(cyclohexanone)-oxalyldihydrazone (G. F. Smith Chemical, Columbus OH) for 8 weeks. Animals were sacrificed after 3, 7, 14, 27, 35, 56 days of cuprizone administration. Samples were taken from corpus callosum, anterior commissure, optic nerve, cervical spinal cord and sciatic nerve. Samples were examined by immunohistochemistry, in situ hybridization for myelin proteins and myelin protein mRNA-s, respectively. Conventional neuropathological stainings and electron microscopy was also performed. Results - Oligodendrocyte degeneration and demyelination followed a particular standard pattern in the central nervous system. Profound myelin loss developed in the superior cerebellar peduncle, anterior comissure and corpus callosum, whereas the optic nerves, velum medullare anterior and spinal cord showed little or no demyelination. Sciatic nerves were unaffected. No infiltration by lymphocytes or blood-brain barrier damage was observed during cuprizone treatment. Conclusion - Cuprizone induced oligodendrocyte damage and demyelination follows a particular standard pattern in the central nervous system of mice. Cuprizone induced demyelination might be considered as a model for human demyelinating disorders with primary oligodendrocyte dystrophy and apoptosis.]

Clinical Neuroscience


FARSANG Marianna, TAKÁTS Annamária, SZIRMAI Imre, KOVÁCS Tibor

[Corticobasal degeneration was described in 1968 by Rebeiz, Kolodny and Richardson, who characterized the disease as a syndrome of asymmetric akinesis and rigidity, dystonia of the upper limb, apraxia, myoclonus and dementia. Atrophy of the frontal and parietal lobe, neuronal loss, gliosis and achromatic neurones (and nowadays astrocytic plaques) are the characteristic pathological features of the disease. Corticobasal degeneration is a rare or a rarely recognized disease and it is frequently misdiagnosed as Parkinson’s disease. According to the Lang’s criteria, corticobasal degeneration can be diagnosed in the presence of rigidity and one cortical symptom (apraxia, cortical sensory loss, alien hand) or in a patient with rigidity, dystonia and focal reflex myoclonus. Exclusion criteria are early dementia (as in primary degenerative dementias), early vertical gaze problems (as in progressive supranuclear palsy), resting tremor and good, sustained therapeutic response to levodopa (as in Parkinson’s disease), severe autonomic problems (as in multiple system atrophy) and any pathology on imaging studies which might explain the clinical symptoms. It should be mentioned, that recently early dementia is recognized as an initial symptom of corticobasal degeneration. The authors present a case and review the literature to call attention to this disorder.]

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Lege Artis Medicinae

[Importance of statin therapy in stroke prevention]


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Clinical Neuroscience

[Is there any importance of the Leiden mutation in the pathogenesis of ischaemic stroke?]

PONGRÁCZ Endre, TORDAI Attila, CSORNAI Márta, BÉLA Zsuzsanna, NAGY Zoltán

[Background - There are conflicting data about the role of Leiden mutation in the pathogenesis of cerebral arterial thrombosis. In order to obtain relevant data, authors investigated the prevalency of factor V Leiden (A506G) both in healthy subjects and in a subgroup of ischaemic stroke patients. Matherial and methods - Blood samples of 171 healthy persons and 254 ischaemic stroke patients were examined by PCR method for Leiden mutation. Ischaemic lesions in the stroke group were documented by CT or MRI. A routin questionnaire was used to study the family history of vascular events (hypertension, diabetes, POAD, stroke, myocardial infarction) of patients. Conventional vascular risk factors of patients were also documented. Results - The prevalence of Leiden mutation was 7.2% in healthy persons and 11.9% in stroke patients. The OR for 254 patient was 1,45 (0.71-2.97). In the subgroup of young patients: age <50 (n=134) the OR was 1.67 (0.75-3.70) and in the elderly patients group: age >50 (n=120) the OR was 1.21 (0.50-2.89). In the family history of stroke patients having Leiden mutation (hetero- and homozigosity) the stroke prevalence was higher (p=0.01). In the ischaemic stroke group, age<50 with polymorphism a tight correlation with hyperlipidaemia (p=0.03) was found. In the group of age<50 with heterozigosity for Leiden, a lower plasma fibrinogen concentration (p=0.02) was found. The polymorphism showed no correlation with the hypertension, hyperuricaemia, migraine, diabetes mellitus, smoking, alcohol consumption and CDS status of patients. Conclusion - When comparing stroke patients to control population there is no significant increase in the frequency of Leiden mutation. Leiden mutation together with hyperlipidaemia and stroke in the family history results in high risk for ischaemic stroke in young patients.]

Lege Artis Medicinae

[New treatment option for oral anticoagulation in the prevention of cardiogenic stroke - Focus on the RE-LY trial]


[Atrial fibrillation (AF) represents the most common cause of cardioembolic stroke. The prevalence of AF increases with age and affects 10% of elderly people. AF-related stroke is usually severe and has a high mortality. The risk of stroke can be estimated on the basis of risk factors accompanying AF and age. Patients with one of the highest risk are those with AF and previous TIA or stroke. Efficient prevention is achieved by chronic anticoagulation therapy. In clinical practice, the use of vitamin K antagonists (VKA) has been the only option. The use of these agents is limited for a number of reasons, and clinicians are especially reluctant to use them in elderly patients at high risk of stroke. Consequently, of the patients with AF for whom anticoagulant therapy is indicated, only about 50-60% receives such therapy, and only half of the treated patients achieves target INR values. More than 50 years after the introduction of warfarin, data of trials with the new direct thrombin inhibitor dabigatran have been published in the past few years. In this paper, we review the results of the phase III, international RE-LY trial, published in 2009, which evaluated the preventive efficacy dabigatran etexilate in patients with AF compared with warfarin at a therapeutic dose. On the basis of the results, dabigatran used at a dose of 2×110mg daily provides the same protection as warfarin, whereas at a dose of 2×150mg it provides a signiificantly more efficient protection from AF-associated stroke and systemic embolism. In addition to its excellent preventive effect, dabigatran tretament results in a significant decrease in the risk of intracranial haemorrhages, and of other major haemorrhages. On the basis of the results, dabigatran will probably change the current treatment paradigm in the stroke prevention in patients with AF, and its introduction can substantially increase the number of patients treated efficiently and safely.]

Clinical Neuroscience

[MR investigations in stroke]

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[In the article digital imaging methods are presented with special emphasis on the use on diagnostics of cerebral circulation studies. Recently, fundamental changes have happened in this field, concerning especially the MR investigations. These changes have influenced the therapeutic strategies of ischaemic stroke. Authors give the theoretical background on the diffusion and perfusion MR imaging, emphasising the importance of their “mismatch” and its impact in the estimation of the outcome of ischaemic events. More recently, new, controversial facts arose, regarding the reasons of the introduction of the theory of so called “negative” and “positive” mismatches. As a consequence, a level of uncertainty took place in the judgement of prognostics. The leading institutions are searching the way to solve the problem which seems to be the quantitative evaluation of the diffusion, perfusion and mismatch data. The advent of the multislice spiral CT with very fast imaging and the importance of CT investigations increased. With this new kind of equipment, even perfusion studies can be performed using iodinated contrast medium.]