Biomedical subjects

E Kurca

Publications and source records attributed to E Kurca.

12 recordsLinked to original sources

PubMed2006

Impaired cognitive functions in mild traumatic brain injury patients with normal and pathologic magnetic resonance imaging.

INTRODUCTION: Mild traumatic brain injury (MTBI) is a common neurological (neurotraumatological) diagnosis. As well as different subjective symptoms, many patients develop neuropsychological dysfunction with objective impairment of attention, memory and certain executive functions. Magnetic resonance imaging (MRI) is not routinely used in MTBI patients despite its proven greater sensitivity and specificity in comparison with computed tomography (CT). METHODS: The patient group consisted of 30 persons with MTBI and the control group consisted of 30 sex- and age-matched healthy volunteers. Both groups underwent neurological examination, neuropsychological testing (including the Postconcussion Symptoms Scale questionnaire, PCSS) and brain MRI (the patient group within 96 h after injury). RESULTS: The analyzed groups did not differ significantly in terms of sex, age, or level or duration of education. MRI pathological findings (traumatic and nonspecific) were present in nine patients. Traumatic lesions were found in seven patients. Nonspecific white matter lesions were found in five healthy controls. There were significant differences between MTBI patients and controls in terms of subjective symptoms (PCSS) and selected neuropsychological tests. Statistically significant neuropsychological differences were found between MTBI patients with true traumatic lesions and MTBI patients with nonspecific lesions. CONCLUSION: There is evidence that MTBI patients with true traumatic MRI lesions are neuropsychologically different from MTBI patients with nonspecific MRI lesions or normal brain MRI. These results support the hypothesis that some acute MTBI signs and symptoms have a real organic basis which can be detected by selected new MRI modalities.

Adult↗

PubMed2005

[Contemporary view on mild brain injuries in adult population].

Mild brain injury is one of the most common neurological a neurotraumatological diagnoses. The pathophysiological basis of mild brain injury is frequently a diffuse axonal damage of variable degree. In the acute phase of mild brain injury we have to identify 1% of patients who will undergo neurosurgery because of vital need. The analysis of patient's personal history, screening of risk factors, neuropsychological testing and imaging methods (CT, MRI) are irreplaceable in the diagnostic process of mild brain injury. Though the mild brain injury is currently considered as an irrelevant traumatic event, approximately 10% of patients develop the so-called post-concussion syndrome.

Brain Concussion↗

PubMed2004

Sympathetic skin response: review of the method and its clinical use.

Sympathetic skin response (SSR) represents a potential generated in skin sweat glands; it originates by activation of the reflex arch with different kinds of stimuli. The potential of rapid habituation after repeated stimuli is formed by biphasic or triphasic slow wave activity with relatively stable latency and variable amplitude. In healthy subjects younger than 60 years of age the response is always present in all extremities. SSR is most frequently used in diagnosing the functional impairment of non-myelinated postganglionic sudomotor sympathetic fibers in peripheral neuropathies. In this study a more complex and informative view on the anatomical and physiological substrates of SSR, its character, normal values and technique are presented, focusing on problems in evaluation of the response and factors that have influence on it. Based on personal experience normative latency and amplitude values of SSR in a group of 20 healthy individuals (x +/- SD), upper extremities: 1.48 +/- 0.80 sec., 444 +/- 167 microV, respectively; lower extremities: 2.06 +/- 0.93 sec., 203 +/- 87.4 microV, respectively) and recommendations for qualitative evaluation preference--the presence or absence of the response--over quantitative evaluation of latency and amplitude of the response in practical clinical use of the method are presented. (Tab. 1, Fig. 2, Ref. 148.).

Adolescent↗

PubMed2004

Clinically unapparent central motor pathways lesion in patients with type I diabetes mellitus. A transcranial magnetic stimulation study.

OBJECTIVE: There is an evidence of central nervous system (CNS) involvement in diabetic patients. The aim of the study was to determine a conduction slowing in CNS pathways using a transcranial magnetic stimulation (TMS) and F-wave latency measurement. METHODS: Diabetic patients and a control group, both without clinical symptoms and signs of CNS lesion were evaluated. Motor evoked potentials were recorded from upper and lower extremities and central conduction time (CCT) was calculated according to formula: CCT = MEP-[0.5x(F-M-1)+M]. Obtained results and data from literature were compared. RESULTS: There was a significant prolongation of CCT recorded from lower extremities. The prolongation of CCT recorded from upper extremities was not statistically significant. Our results correlate with previously published data. CONCLUSION: In spite of missing clinical signs of CNS lesion in diabetic patients, a significant prolongation of CCT compared to control group and literature data was recorded. We assume a presence of diffuse subclinical CNS lesion induced by metabolic changes in DM. Difference between CCT obtained from upper and lower extremities implicate, that changes are analogical to peripheral neuropathies ("central length-dependent injury?"). Measurement of CCT using TMS could become a complementary electrophysiological method for assessment of subclinical CNS involvement in diabetic patients. (Tab. 4, Ref. 17.)

Adolescent↗

PubMed2002

Pathogenesis of alcoholic neuropathy.

Chronic alcoholism is a medical, economical and social problem. Motility and mental function disorders are among the complications of chronic alcoholism and have been known for more than two centuries as "alcoholic paralysis", and are caused by alcoholic neuropathy. The pathogenesis of alcoholic neuropathy does not appear to be identical with central nervous system disorders which are caused by chronic alcoholism and it seems that it results from a failure of the protection barrier systems in the peripheral nervous system. To the pathogenesis of alcoholic neuropathy includes: 1. direct toxic effects of alcohol on the cellular population of the central nervous system and other tissues, especially of parenchymatous organs (in particular of the liver), 2. indirect metabolic and exotoxic changes mediated by malabsorption, maldigestion and secondary caloric and energy deprivation, 3. effects of genetic factors. (Fig. 2, Ref. 23.)

Alcoholic Neuropathy↗

PubMed2002

Neuromodulative treatment of overactive bladder--noninvasive tibial nerve stimulation.

BACKGROUND: Conservative treatment of overactive bladder employes behavioral or invasive neuromodulatory inhibition of miction reflex and administration of anticholinergic drugs. MAIN PURPOSE: The aim of this study was to use non-invasive stimulation of the tibial nerve with the intention to achieve desired therapeutic effects without iatrogenic nerve damage using a superficial electrostimulation. METHODS: All patients suffered from overactive bladder (OAB) without bladder outlet obstruction. OAB was examined by the Behavioral urge score BUS (0.0--the best and 1.0--the worst score), the International prostate symptom score IPSS (0--the best and 35--the worst score) and the Incontinence quality of life questionnaire IQOL (0.0--the worst and 1.0--the best index). The patients were divided into 3 groups: Group I--patients with electrode attached behind the medial ankle of the left lower extremity. The intensity of stimulation corresponded to 70% of the maximum amplitude of response from musculus abductor hallucis. Frequency of stimulation was 1 Hz and duration of the square impulse was 0.1 ms. Surface stimulation lasted 30 minutes and was repeated once a week. Group II--patients were treated by oral oxybutynin 5 mg t.i.d. Group III--patients without treatment. The BUS, IPSS, and IQOL were repeated after the treatment. RESULTS: The study included 28 females of average age 54 year (range 45 to 63). Mean IPSS was 17 (range 12 to 21), mean index of quality of life IQOL was 30 (range 12 to 78) and mean BUS score was 0.68 (range 0.50 to 0.86). Group I with stimulation did achieve statistically significant changes following the treatment: decrease of mean IPSS from 17 +/- 3 points to 6 +/- 4 points after the treatment, increase in mean IQOL from 36 +/- 10 to 68 +/- 20 and decrease of mean BUS from 0.65 +/- 0.12 to 0.43 +/- 0.16. Group II had similar statistically significant differences after the treatment of OAB. Group III noted no changes in the complaints. CONCLUSION: Noninvasive stimulation had improved subjective symptom related to overactive bladder, had no adverse events and was well tolerated. (Fig. 1, Tab. 1, Ref. 18.).

Female↗

PubMed2001

Unique case of eleven Bell's palsy episodes.

Bell's palsy (BP) is a peripheral facial nerve paralysis of unknown etiology. It is not a life-threatening condition; however, incomplete recovery may leave an individual stigmatized functionally, occupationally as well as socially. Recurrent paralyses are seldom, noted in 7-8% of all BP cases. More than two BP relapses are even less frequent. Adour et al. (1977) reported only two patients with four BP episodes from 1700 patients. Only one patient with more than four BP recurrences in the group containing 2414 BP cases were reported by Yanagihara et al. (1984). The highest reported number of BP recurrences in the accessible literature has been nine. We are presenting an unusual patient who suffered a total of eleven relapses of an idiopathic facial nerve palsy. Description of the case along with review of the relevant literature are discussed.

Adult↗

PubMed2000

Possible extrapyramidal system degradation in Parkinson's disease.

Extrapyramidal system, a rich network of nerve and glial cells consists of subcortical and cortical grey matter. The system serves as an integrator of unaware, automatic, repeated, spontaneous, complicated and purposeful motor samples. Muscle tone regulation and its distribution is another decisive extrapyramidal function. This review article concerns to some degradation mechanisms in extrapyramidal system, as either the programmed cell death or apoptosis. The physiologic extracellular decreasing signals creating apoptosis (nerve growth factor--fall) are either genetically expressed or there are neuropathophysiologic processes that may activate pathways leading to apoptosis, namely oxidative stress, glutamate toxicity and calcium homeostasis disruption. The level of dopamine transporter expression (mRNA, methyl-phenyl-pyridinium) might determine the vulnerability of the nigral neurons to the Parkinsonian insult. The most common clinical picture of extrapyramidal disorder-Parkinson's disease-consists of an active dopamine cell death-apoptosis, which is partially programmed like as programmed cell death and partially accidentally installed chain of events. Without morphological criteria, biochemical indicators such as laddered DNA fragmentation pattern and/or the requirement for macromolecular synthesis merely suggest but do not provide unequivocal evidence for apoptosis. There are either genetic or acquired conditions creating unbalance of Bax/Bcl-2 families-proapoptotic and prooncogenic factors, respectively. The first Bax gene cooperates with other genes coding the new transmembrane proteins into the mitochondrial megapores determinating transition by means of death receptors. Bcl-2 codes prooncogenic mitoses and tissue proliferation. The neuroprotective hypothesis of the dopamine agonist action is a very attractive working hypothesis and some of its tenets are derived from the oxidative stress hypothesis for neurodegeneration, but this hypothesis is still controversial.

Aged↗

PubMed2000

Four quantitative EMG methods and theirs individual parameter diagnostic value.

Quantitative electromyography (EMG) usage in daily clinical medicine can exclude the investigation results influencing by the electromyographer's subjective factor in needle EMG. The aim of our study was to compare the diagnostic efficiency of these quantitative EMG methods which have found some more consistent application in routine neurologic practice. We have investigated 35 healthy subjects and 59 patients with two basic types of neuromuscular disorders (neuropathies and myopathies) by means of four quantitative EMG methods: 1--modified Buchthal's low threshold MUAPs (motor unit action potentials) analysis; 2--interference EMG pattern Dorfman's and McGill's limited decomposition; 3--interference EMG pattern spectral analysis; 4--interference EMG pattern turns-amplitude analysis. In results analysis parameter's 95% confidence intervals were calculated by Campbell and Gardner and the difference between three subject groups (controls, neuropathies, myopathies) was evaluated by special multidimensional statistics (Hotelling T2 test) using simultaneously all tested parameters of four quantitative EMG methods. The modified Buchthal's low threshold MUAPs analysis was the most effective method in discovering neuropathy and myopathy with area as the best discriminating parameter. The diagnostic power in neuropathies may be increased using selected quantitative EMG methods or theirs individual parameters combinations. Several aspects of applyied quantitative EMG methods and aquired data statistical analysis are discussed.

Action Potentials↗

PubMed1999

[Leber's hereditary optic neuropathy].

BACKGROUND: Leber's hereditary neuropathy of the optic nerve (LHON) is manifested by bilateral affection of the eyes with acute or subacute loss of vision. The disease is caused by point mutations in the mitochondrial DNA (mtDNA) and is one of the most frequent mitochondrial diseases in the population. In patients with LHON 18 different point mutations in the mtDNA were described which correlate partly with the rate of progression of the disease and the severity and prognosis of the final affection of vision. METHODS AND RESULTS: The submitted paper deals with the results of molecular genetic examinations in three families with clinical manifestations of LHON. In three patients in the first family a homoplasmic mutation of mtDNA G3460A was found. In the second family in a young man with severely impaired vision a heteroplasmic mutation G3460A was found associated with a higher ratio of mutated mtDNA molecules than in his mother who is clinically healthy. In the third family the presence of homoplasmic mutation of mtDNA in position G11778A was detected. CONCLUSIONS: The diagnosis of LHON and genetic counselling in affected families should be based on close collaboration of ophthalmological and genetic departments with specialized laboratories engaged in molecular biological diagnosis of mitochondrial diseases.

DNA, Mitochondrial↗

PubMed1999

[Leber's hereditary optic nerve neuropathy].

The authors present a case report of 26 years old man with bilateral optic nerve neuropathy. Detection of heteroplasmic mutation of mitochondrial DNA at G3460A site confirmed the suspicion on Lebers hereditary optic nerve neuropathy (LHON). Genetic and environmental factors of the disease and various accompanying neurologic and other symptoms, which can together with the optic nerve defect participate in the development of of the LOHN clinical pattern are discussed. (Ref. 12.)

Adult↗

PubMed1997

[Local immune defects--products of free oxygen radicals].

The discussion about the supporting task of four main active oxygen dependent mechanisms mediating and modulating immune signals was included in the work, along with the discussion on antioxidants influencing these mechanisms. The former include xanthine-oxidase, cyclooxygenase, lipoxygenase, aldehyde oxygenase metabolic chains. Currently, we are just beginning to realize that active oxygen and antioxidants can modulate the induction of physiological signals, and that these effects are not limited to the immune system. The effects of antioxidant treatment could represent neutralization of harmful radicals, albeit they can simply represent modulation of complex biochemical events which are essential parts of normal metabolism. Some natural antioxidants, e.g. alfa-to-copherol, ascorbic acid and beta-carotens are very good means of the primary prevention, but with acute failure of local antioxidants, they do not prevent the excessive production of proliferative inflammatory tissue. Tirilazad-mesylate has threefold beneficial influences: first as an inhibitor of the creation of oxygen radicals, second as a scavenger or quencher of free oxygen radicals, and finally in the arrangement of the defects in the phospholipid bilayer and possible receptors of macrophages, as well as T cells. The drug is suitable for active modulation of locally changed immune reactions and thus it rejects harmful proliferative inflammation in the subdural space. Until recently it has been eliminated by surgical procedure. The authors expel the thick (0.8 cm) subdural collection of the proliferative inflammatory product by tandem treatment which includes methylprednisolon+tirilazad-mesylate for three days, followed by fourteen days of methylprednisolon, which was gradually decreased in daily oral doses. This is a revolutionary change in the treatment of similar intracranial processes. (Fig. 4, Ref. 21.)

Anti-Inflammatory Agents↗