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N Sternić

Publications and source records attributed to N Sternić.

15 recordsLinked to original sources
PubMed2001

Bereitschaftspotential in depressed and non-depressed patients with Parkinson's disease.

Impaired initiation and slowed execution of movements are two of the principal characteristics of Parkinson's disease (PD). A similar pattern of movement impairments (psychomotor retardation) can be seen frequently in patients with idiopathic depression. In addition, affective disorders have been frequently reported in patients with different basal ganglia disorders. The aim of this study was to determine whether there are some particularities in the cerebral electrical activity during the preparation and execution of voluntary internally paced movements (i.e., Bereitschaftspotential, BP) in depressed PD patients, which can distinguish them from non-depressed PD patients, as well as from healthy controls. The BPs were recorded in 16 patients with idiopathic PD, eight of whom were depressed (PD-D), and eight of whom were not (PD-ND). Additional recordings were taken from a group of eight age- and sex-matched healthy subjects. Depression was classified using the Research Diagnostic Criteria and the two PD groups were matched for age, disease severity, and disease duration. The amplitudes and slopes of the BPs from PD patients were generally smaller than in controls, but there was no specific pattern of BP changes that distinguished depressed from non-depressed PD patients. In addition, there was no particular association between measures of depression severity and BP parameters. The data suggest that presence of depression in PD might not have any additional deteriorating influence on already impaired preparation for self-paced spontaneous movements.

Adult↗
PubMed2000

Single center experience on eversion versus standard carotid endarterectomy: a prospective non-randomized study.

BACKGROUND AND PURPOSE: The prospective studies that have compared the outcomes of eversion and standard longitudinal carotid endarcterectomy (CEA) have been few and small and available data to reach definitive conclusions are still scarce. This prospective, non-randomized study sought to compare eversion and standard CEA for early and late mortality and morbidity and the incidence of late restenosis. METHODS: Between 1992 and 1997, we performed 2806 CEAs in 2469 patients (2124 eversion CEAs in 1859 patients and 682 standard CEAs in 610 patients). All patients underwent preoperative neurological examination and cervical duplex scanning. Patients were followed up by neurological evaluation and duplex scanning at 1 and 6months after CEA, and yearly afterwards. RESULTS: Demographics and neurologic inidications for CEA were similar in both groups. Mean clamping time was shorter in the eversion CEA group (13.5+/-6.1 vs 19.9+/-19.1min, P<0.001). Early (30-day) postoperative mortality due to major stroke was lower after eversion CEA (10/2124 vs 9/682, P=0. 037), as well as total cardiovascular mortality (16/2124 vs 12/682, P=0.038). Early carotid occlusion was more frequent in standard CEA group (12/2124 vs 11/682, P=0.017), as well as total early morbidity (112/2124 vs 53/682, P<0.001). During follow-up (mean 56 months, range 6-92), restenosis rate was lower in the eversion CEA group (0. 5 vs 1.8%, P=0.006). CONCLUSIONS: Our data indicate that eversion CEA as compared to standard CEA technique is associated with lower total cardiovascular perioperative mortality and mortality due to major stroke, shorter clamping time, lower early occlusion rate, and lower late restenosis rate.

Aged↗
PubMed1994

Effect of age at onset on frequency of depression in Parkinson's disease.

In a consecutive series of 169 outpatients with Parkinson's disease the frequency of depression was compared in two groups: those who developed Parkinson's disease before the age of 50, and those who developed the disease after 50. Major depression was found in 36% of patients with early onset and in 16% of patients with late onset Parkinson's disease. This significant difference disappeared when both groups were matched for duration of Parkinson's disease. A stepwise regression analysis in both the early onset and the late onset Parkinson's disease showed a significant correlation only between depression scores and the impairment scores of activities of daily living.

Adult↗
PubMed1993

Sudden hearing loss as the initial monosymptom of multiple sclerosis.

Hearing loss is an uncommon symptom in multiple sclerosis. We report two patients in whom unilateral sudden hearing loss was the first monosymptomatic manifestation of multiple sclerosis. We confirmed the initial central auditory dysfunction suggested by audiometric findings and brainstem auditory evoked potentials by MRI, which showed a unilateral pontine lesion in one patient and a lesion in the medulla oblongata in the other.

Adult↗
PubMed1990

Auditory event-related potentials in different types of dementia.

Auditory event-related potentials were recorded in demented, drug-free patients with Huntington's disease and Alzheimer's disease, as well as in demented and nondemented patients with Parkinson's disease, who were matched for age, duration and stage of the disease. The normal P3 latency at a given age was predicted by using an age regression equation that had been calculated on the basis of the findings in 42 normal adults. Using this procedure, a prolonged P3 latency was found in about two thirds of demented patients, irrespectively of the underlying disease. Although the prolonged P3 latency proved to be useful electrophysiological correlate of dementing illness, no differences were found between the observed groups in respect to other components of the auditory event-related potentials (N1 and P2).

Adult↗
PubMedDate not supplied

Multiple sclerosis as the cause of sudden 'pontine' deafness.

Sudden deafness is rarely ascribed to multiple sclerosis (MS). Sudden deafness and tinnitus were the initial symptoms of MS for the two patients described in this paper. A sensorineural hearing loss was present in one ear in both patients. Brainstem responses (BSRs) showed only the first three waves for the first patient, and only wave I for the second. Magnetic resonance imaging showed focuses of demyelination in the pons (case 1) and on the borderline between medulla and pons (case 2). The placement of plaques and the involvement of the BSR-generating acoustic afferent pathways are discussed. The hearing level measured by tonal audiometry recovered after 1 month in both patients and remained stable during 1 year. BSRs remained pathological after 1 month as well as after 1 year. Sudden hearing loss and tinnitus might be the initial symptoms of MS.

Adult↗
PubMedDate not supplied

[Clinico-genetic study of type I spinocerebelllar ataxia].

Inherited, autosomal-dominant cerebellar ataxia (ADCA) comprises a genetically and clinically heterogenous group of neurodegenerative disorders. Clinical classification of these disorders was an important step [2] in differentiation among several types, the most common one being ADCA-I, accompanied with supranuclear ophthalmoplegia, optic nerve atrophy, symptoms of the basal ganglia lesions, dementia and amyotrophia. Molecular-genetic studies indicated genetic heterogeneity of ADCA-I with mutations of genetic loci on chromosome 6p (spinocerebellar ataxia type 1; SCA1), 12q (SCA2), 14q (SCA3), 19p (SCA6) and 16q (SCA4) [3]. Spinocerebellar ataxia type 1 (SCA1) is characterized by cerebellar ataxia, ophthalmoplegia and pyramidal signs [4], but also with other neurological findings that tend to prevent clinical differentiation among patients with SCA1, SCA2 and SCA3. The mutation inducing SCA1 is an instable expansion of trinucleotide (CAG) repeats in the coding region on chromosome 6 [5]. Herein, we report clinical features in patients from two families with SCA1: family I with 15 and family II with 8 affected members in 4 consecutive generations. The acceptable data (history, examination and/or insight into medical records) were obtained for 9 patients in family I and 7 patients in family II. The age at the onset of the disease was 37.8 +/- 11.3 years (mean value +/- SD) (range: 27-60) for all the patients, or 31.8 +/- 10.7 years (range: 7-60) for family I and 45.0 +/- 8.4 years (range: 35-55) for family II. Duration of the disease was 8.9 +/- 4.6 years (range: 3-15); 10.8 +/- 4.1 (range 5-15) and 5.7 +/- 3.8 years (range: 3-10) for families I and II, respectively. The mean number of CAG repeats in the mutated allele for SCA1 of the affected individuals was 50.5 +/- 6.2 (range 45-64). A significant inverse correlation (p < 0.05) was noted between the number of CAG repeats and the age at the onset of the disease (Figure 3). Similarity of initial symptoms in SCA1 was noted. They include simultaneous gait-related problems and dysarthria (usually slurred speech). Occurrence of other neurological signs (Table 3) was also predictable in most cases and depended on the phase of SCA1 at the time of examination. Generally, it is believed that intra- and interfamilial phenotypic heterogeneity in SCA1 is lower than in SCA2 and SCA3 [12]). In conclusion, typical clinical manifestations of SCA1, at least in early phases of the disease, according to our study, include gait ataxia, dysarthria, brisk muscle reflexes and marked hand ataxia; the age at the onset of the disease was inverse, and clinical progression was directly related to the number of CAG repeats in the mutated allele on chromosome 6. Nevertheless, significant differences in clinical properties of this inherited disease are possible among different affected families.

Adolescent↗
PubMedDate not supplied

[Buspirone in the treatment of cerebellar ataxia].

Ataxia is defined as a disturbance which, quite independent of any motor weakness, alters direction and extent of voluntary movement and impairs the sustained voluntary of reflex muscle contraction necessary for maintaining postiue and equilibrium [1]. Since pathophysiological basis of cerebeller ataxia is still not completely clear, the current therapeutic attempts are mainly symptom-oriented [3]. One possible approach could be a modification of potentially involved neurotransmitter systems of the cerebellum, where particularly interesting is the serotonergic system. However, attempts with levorotatory form of tryptophan (5-HT precursors) proved to be ineffective [4, 5]. Since receptors in the cerebellum are mainly of 5-HTIA subtype, the use of specific agonists might be a more reasonable therapy [6]. The study initially involved 11 patients, but only 9 completed the protocol due to unfavorable side effects. Our open label prospective study lasted for 15 weeks. The patients were tested before the beginning of the treatment (initial visit), at 7th (first visit) and 11th week (second visit) of continuous therapy, and eventually at 15th week (final visit). The daily dose was 40 mg at the first and 60 mg at the second visit. We used the evaluation scale gurposed for cerebellar functions testing (speech, gait, coordination and ocular movements). Significant improvement of cerebellar ataxia in patients under buspiron therapy has been noted. We analyzed the results obtained from our 9 patients (4 females and 5 males), of which 6 patients suffered from cerebellar degeneration, one from multiple sclerosis, one from Ramsey-Hunt syndrome, and one from pontine myelinolysis. At the initial visit the patient score was 18.9 (SD = 7.3), subsequently, at the iirst visit the score was 15.4 (SD = 8), while the second visit yielded the score of 12.9 (SD = 8.2), and finally, after a two-weeks lasting wash-out period, it was 17.7 (SD = 7.1) (Table 1). It was found that patients exhibiting mild ataxia showed a better improvement in comparison to the patients who had marked cerebellar symptoms at the beginning of the treatment (Table 2). In conclusion, our prospective study shows that buspiron treatment improves cerebellar symptoms.

Adult↗
PubMedDate not supplied

[Gilles de la Tourette's syndrome].

Gilles de la Tourette's syndrome (GTS) is characterized with motor and vocal tics, initiating before 21 years of age, lasting for over a year and are associated with diverse behavioral disorders. The study analyzes features of 12 our GTS patients with mean age at the onset of the disease of 12.0 years, while the exact diagnosis was established only after 9.5 years (2-33 years). In 11 out of 12 patients the disease started with motor or vocal tics, while in completely developed clinical picture of GTS the permanently present tics were associated with coprolalia (6 patients), echolalia, copropraxia (in 2 patients, respectively), attention deficits (9 patients), obsessive-compulsive disorders (8 patients) etv. The role of neuroleptic therapy was discussed according to our experience and other reported studies. In our study, haloperidol had good therapeutical effect in 64% of the treated patients.

Adolescent↗
PubMedDate not supplied

[Comparison of administration of low doses of bromocriptine and levodopa in the early treatment of Parkinson disease].

Results og an open, controlled three-month clinical trial of therapeutical efficacy of a combination of a low doses of levodopa/carbidopa and bromocriptine in 20 de novo patients with Parkinson's disease (PD) are presented. All patients received the same daily doses of levodopa/carbidopa (250 mg), while daily dosage of bromocriptine was gradually increased from 1.25 mg to 30 mg. Owing to development of adverse effects 3 patients dropped out of the study, while in 70% of the patients who completed the protocol improvement of motor functioning exceeded 50%. Those with bradykinesia and rigidity responded most favorably. For all our patients the mean daily dose of bromocriptine was 26.25 mg. The most common adverse effects of the therapy were orthostatic hypotension (7 pts) and nausea (5 pts). The results of the study coincide with the hypothesis that comparative administration of low doses of bromocriptine and levodopa is the best approach to treatment of early phases of PD.

Aged↗
PubMedDate not supplied

[Aneurysms of the carotid arteries].

The aim of the paper is the presentation of the treatment of aneurysms of the extracranial carotid artery and review of literature. Aneurysms of extracranial carotid arteries (common carotid artery, external carotid artery and cervical part of the internal carotid artery) are very rate [1, 2]. In 1979 McCollum from the Baylor University (Houston, Texas) reported 37 cases over a 21-year period [3]. Moreau from France reported 38 cases over a 24-year period [4]. Mayo clinic experience includes 25 cases in the 40-year period [5]. According to Schechter 835 extracranial carotid artery aneurysms were reported in literature until 1977. These and the other aneurysms of the extracranial carotid artery can be partially or completely thrombosed, can cause distal embolization, or compression of adjacent structures, and can be ruptured [4, 9]. Therefore, the mortality rate in non operated patients with carotid artery aneurysm is 70% [10]. Over the period from January 1, 1985 to December 31, 1996 at the Centre of Vascular Surgery within the Institute of Cardiovascular Diseases of the Serbian Clinical Centre in Belgrade, 12 patients with 13 extracranial carotid artery aneurysms were treated. Nine of them (75%) were males and 3 (25%) females, average age 58.22 (21-82) years. There were two traumatic (gunshot wounds) and one anastomotic (after carotid subclavian bypass with PTFE graft) pseudoaneurysms, and 10 true atherosclerotic aneurysm. Three (23%) aneurysms were on the common and 9 (77%) on the cervical part of the internal carotid artery. Two (15%) aneurysms were in the form of asymptomatic pulsatile neck mass, 7 (54%) with CVI or TIA, three (23%) with compression of the cranial nerves and one (8%) was ruptured. Twelve (92%) patients were treated surgically, while one asymptomatic aneurysm in a 82-year old female patient was not operated due to high risk. The intraoperative findings revealed one complete and 11 partial thromboses of the aneurysmal sac. In 3 patients with fusiform aneurysms, thrombectomy and aneurysmorrhaphy were performed. One traumatic pseudoaneurysm was treated with aneurysmectomy and lateral suture of the artery. In 3 patients aneurysmectomy and end to end anastomosis were done, while in three aneurysmectomy and saphenous vein graft interposition. In case of ruptured aneurysm of the internal carotid artery aneurysmetomy and arterial ligature were carried out, while in case of anastomotic pseudoaneurysm after carotid subclavian bypass, aneurysmectomy and new carotid subclavian bypass with PTFE graft, were performed. During the study no intrahospital mortality was recorded. One patient died 5 years after the operation due to myocardial infarction. The mean follow-up period was 4 years and 2 months (6 months to 11 years). The early and late potency rates were 100%. Two (17%) CVI and two transient cranial nerve paresies were noticed immediately after the operation. In literature male/female ration in patients with extracranial carotid artery aneurysms is 2:1 [2, 4, 7], but in our study it was 5:1. One (10%) of our patients had a bilateral carotid artery aneurysm. According to literature data the incidence of bilateral localization of extracranial carotid artery aneurysms with atherosclerotic origin is 21% [1]. Of 12 surgically treated aneurysms in our study, 9 were of atherosclerotic origin, two were traumatic and one anastomotic pseudoaneurysms. Today, most of true extracranial carotid artery aneurysms are of atherosclerotic origin [7, 20-25]. However, true extracranial carotid artery aneurysms can be developed due to: infection of the arterial wall (mycotic forms) [26-37]; nonspecific [23] or irradiation arteritis [38], fibromuscular dysplasia [4, 8, 15, 16, 39]. The most frequent types of false extracranial carotid artery aneurysms are traumatic pseudoaneurysms [32, 50-54] and anastomotic pseudoaneurysms [53, 59, 60]. There are also dissecting extracranial carotid artery aneurysms developed after isolated spontaneous d

Adult↗
PubMedDate not supplied

[Importance of the number of trinucleotide repeat expansions in the clinical manifestations of Huntington's chorea].

INTRODUCTION: In 1993 the gene responsible for Huntington's disease (IT15) was isolated [5]. It was mapped to the tip of the short arm of chromosome 4 and within its coding sequence, near the 5' end, it contained a certain number of trinicleotide (CAG)n (cytosine-adenine-guanine) repeats (Figure 1). This gene codes for a protein (348 kd) called "huntington" that is widely expressed, and its sequence is not related to any protein [6]. The normal range of (CAG)n repeat numbers within IT15 was reported to be between 6 and 37 [6]. Mutation responsible for Huntington's disease implied expansion of (CAG)n repeats: in patients with Huntington's disease the pathologic range was determined to be between 35 and 121 repeats [7-10]. PATIENTS AND METHODS: In this study we correlated the age at onset, rate of progression and initial symptoms of Huntington's disease with the number of trinucleotide (CAG)n repeats in IT15. DNA was isolated from peripheral blood leukocytes of patients fulfilling clinical criteria for definite and probable Huntington's disease [2]. Genetic verification of Huntington's disease was made by the previously described and modified PRC (polymerase chain reaction) technique [17, 18]. In our laboratory a gene with 40 or more repeats was considered as a marker of Huntington's disease. RESULTS: The study comprised 26 patients (11 women and 15 men). At the onset of Huntington's disease they were between 19 and 66 years old (36.6 12.8 years), with the duration of the disease between 1 and 15 years (5.8 4.3 years). The number of (CAG)n, repeats in IT15 ranged between 40 and 95 (49.9 14.1). The negative correlation between the (CAG)n, count in the expanded allele and the age at onset of the disease has been confirmed. Regression analysis showed the correlation coefficient of -0.54 (p = 0.012). The effect of trinucleotide (CAG)n, repeats on the initial clinical manifestations and rate of progression of Huntington's disease is only one of the growing group of "CAG-repeat" disorders that also include entities such as spinocerebellar ataxia-type 1 and 3, spinobulbar muscular atrophy and dentato-rubo-pallidoluysian atrophy [6].

Adult↗