Browsing by Author "Kostić, V.S. (35239923400)"

Objective: To compare clinical characteristics of the involuntary movements in primary and symptomatic dystonias. Patients and methods: 132 consecutive patients with the diagnosis of primary dystonia and 51 consecutive patients with secondary dystonia caused by well defined structural lesion(s) of the central nervous system, with particular emphasis on the characteristics of involuntary movements. Results: Eight variables with the highest risk contribution to either symptomatic or primary dystonias were identified: dystonic movement in secondary dystonia was much more frequently presented at rest, whereas the presence of dystonic tremor, chronic inflammatory process, or peripheral trauma located in the region that is later affected by dystonia, as well as the use of sensory tricks and development of spontaneous remissions, classified the affected patients more often in the category of those with primary dystonia. Conclusion: The study identified several clinical features that may be helpful in differentiating primary from secondary dystonia.

Depression is frequently encountered in Parkinson's disease and was seen to occur in 14 of 26 patients studied. The levels of 5-hydroxyindoleacetic acid (5-HIAA), the main metabolite of serotonin (5-HT), in CSF samples of the patients were significantly lower than in those of controls. However, within the group of patients the levels of 5-HIAA in CSF samples were significantly lower in the depressive subgroup compared with the non-depressive patients. Moreover, no correlation was recorded between motor disability and depression. The results indicate that disturbed 5-HT metabolism may possibly play a role in Parkinson's disease as a predisposing factor in the development of depression. © 1987 Springer-Verlag.

Depression is frequently encountered in Parkinson's disease and was seen to occur in 14 of 26 patients studied. The levels of 5-hydroxyindoleacetic acid (5-HIAA), the main metabolite of serotonin (5-HT), in CSF samples of the patients were significantly lower than in those of controls. However, within the group of patients the levels of 5-HIAA in CSF samples were significantly lower in the depressive subgroup compared with the non-depressive patients. Moreover, no correlation was recorded between motor disability and depression. The results indicate that disturbed 5-HT metabolism may possibly play a role in Parkinson's disease as a predisposing factor in the development of depression. © 1987 Springer-Verlag.

Objective: The female sex is associated with increased stroke severity and relatively poor functional recovery. Several studies have demonstrated that women with stroke benefit more from intravenous thrombolysis compared with men, while others found the nullification of gender effect among women treated with recombinant tissue plasminogen activator (rtPA). The purpose of our study was to determine any gender differences in the efficacy and safety of systemic thrombolysis among patients with acute ischemic stroke in Serbia. Methods: Data were from the Serbian experience with intravenous thrombolysis in ischemic stroke (SETIS) study, a prospective, ongoing, multicenter, open, and observational study in Serbia of all patients who have received rtPA for acute ischemic stroke. We analyzed sex differences in the baseline characteristics, functional outcome and treatment complications. Results: Among 60 women and 96 men with stroke and treated with intravenous thrombolysis, we found that at day 90, no significant sex differences in excellent functional outcome (50.9% of women vs. 57.0% of men, p = 0.5), favorable functional outcome (61.4% of women vs. 68.8% of men, p = 0.38) or death (8.8% of women vs. 12.9% of men, p = 0.60). These results were constant even after adjustments for age, severity of basal neurological deficit and onset to treatment time. Conclusion: There were no sex differences in functional outcome at 90 days after the stroke among patients treated with IV rtPA. This finding might confirm that thrombolytic therapy nullifies usual sex differences in stroke outcome and suggests that women with stroke may benefit more from rtPA treatment. © 2009 Elsevier B.V. All rights reserved.

Twenty three patients with hemiballism and two with biballism were studied. Ischaemic and haemorrhagic strokes were the cause in most patients. Other causes were encephalitis, Sydenham's chorea, systemic lupus erythematosus, basal ganglia calcifications, non-ketotic hyperglycaemia, and tuberous sclerosis. Neuroimaging studies showed a lesion of the subthalamic nucleus in only six patients. In others, different subcortical structures were involved or the results were normal. Only two patients had "pure" hemiballism. The others had other types of dyskinesias, mainly chorea, which was present in 16 patients. The prognosis was usually good.

Background and purpose: To investigate survival rates, prognostic factors, and causes of death in Wilson disease (WD). Methods: In the years 1980-2007, a cohort of 142 patients with WD was prospectively registered (54 presented with neurologic symptoms, 49 with hepatic symptoms, 33 had mixed form, and data were missing for six patients). The duration of follow-up for patients alive was 11.1 ± 8.8 years. Results: After initiation of treatment (d-penicillamine and zinc salts), 79% of patients had a stable or improved course of disease. Despite early diagnosis and appropriate therapy, 15 patients still had a relentlessly progressive course. Thirty patients died. The cumulative probability of survival in a 15-year period for the whole group was 76.7 ± 4.9%. Better prognosis of WD was associated with male sex, younger age at onset, neurologic form of the disease, and treatment continuity. Causes of death were predominantly related to hepatic failure (16 patients), but also suicide (four patients) and cancer (three patients). Conclusion: Despite the relatively early diagnosis and treatment of our patients with WD, mortality was still considerably high. © 2009 EFNS.

Background and purpose: To investigate survival rates, prognostic factors, and causes of death in Wilson disease (WD). Methods: In the years 1980-2007, a cohort of 142 patients with WD was prospectively registered (54 presented with neurologic symptoms, 49 with hepatic symptoms, 33 had mixed form, and data were missing for six patients). The duration of follow-up for patients alive was 11.1 ± 8.8 years. Results: After initiation of treatment (d-penicillamine and zinc salts), 79% of patients had a stable or improved course of disease. Despite early diagnosis and appropriate therapy, 15 patients still had a relentlessly progressive course. Thirty patients died. The cumulative probability of survival in a 15-year period for the whole group was 76.7 ± 4.9%. Better prognosis of WD was associated with male sex, younger age at onset, neurologic form of the disease, and treatment continuity. Causes of death were predominantly related to hepatic failure (16 patients), but also suicide (four patients) and cancer (three patients). Conclusion: Despite the relatively early diagnosis and treatment of our patients with WD, mortality was still considerably high. © 2009 EFNS.

BACKGROUND AND PURPOSE: In MS, the relation between clinical and MR imaging measures is still suboptimal. We assessed the correlation of disability and specific impairment of the clinical functional system with overall and regional CNS damage in a large cohort of patients with MS with different clinical phenotypes by using a random forest approach. MATERIALS AND METHODS: Brain conventional MR imaging and DTI were performed in 172 patients with MS and 46 controls. Cervical cord MR imaging was performed in a subgroup of subjects. To evaluate whether MR imaging measures were able to correctly classify impairment in specific clinical domains, we performed a random forest analysis. RESULTS: Between-group differences were found for most of the MR imaging variables, which correlated significantly with clinical measures (r ranging from -0.57 to 0.55). The random forest analysis showed a high performance in identifying impaired versus unimpaired patients, with a global error between 7% (pyramidal functional system) and 31% (Ambulation Index) in the different outcomes considered. When considering the performance in the unimpaired and impaired groups, the random forest analysis showed a high performance in identifying patients with impaired sensory, cerebellar, and brain stem functions (error below 10%), while it performed poorly in defining impairment of visual and mental systems (error of 91% and 70%, respectively). In analyses with a good level of classification, for most functional systems, damage of the WM fiber bundles subserving their function, measured by using DTI tractography, had the highest classification power. CONCLUSIONS: Random forest analysis, especially if applied to DTI tractography data, is a valuable approach, which might contribute to overcoming the MS clinical - MR imaging paradox.

Objective: To investigate whether a specific pattern of gray matter (GM) tissue loss is associated with freezing of gait (FOG) in patients with Parkinson disease (PD). Methods: Seventeen patients with PD with FOG (PD-FOG), 20 patients with PD with no FOG (PD-noFOG), and 34 healthy control subjects were recruited. PD-FOG and PD-noFOG patients were matched on an individual basis for age, disease duration, and Hoehn and Yahr stage. Patients were also administered a comprehensive neuropsychological battery focused on executive functions. The extent and distribution ofGMatrophy were assessed using voxel-based morphometry. Results: In patients with PD, the severity of FOG correlated with frontal executive deficits. Compared with healthy control subjects, PD-FOG patients showed a distributed pattern of GM atrophy including the dorsolateral prefrontal, medial, and lateral temporal, inferior parietal, and occipital cortices. PD-noFOG patients showed only small regions of GM atrophy in the bilateral frontal and temporal cortex. The left inferior frontal gyrus, left precentral gyrus, and left inferior parietal gyrus were more atrophic in PD-FOG patients relative to both healthy control subjects and PD-noFOG patients. In PD-FOG patients, the severity of FOG was associated with GM volumes of the frontal and parietal cortices bilaterally. Conclusions: GM frontal and parietal atrophy occur in PD-FOG patients. FOG in PD seems to share with executive dysfunction and perception deficits a common pattern of structural damage to the frontal and parietal cortices. Copyright © 2012 by AAN Enterprises, Inc.

Rapid eye movement (REM) sleep latency (time from sleep onset to the first REM episode) was measured in 39 patients with idiopathic Parkinson's disease. Reduced REM sleep latency (≤65.0 min) was found in a high proportion of patients (69%). Since reduced REM sleep latency may be a trait-like abnormality relatively specific to primary depression, we evaluated this parameter in two groups of parkinsonian patients: depressed (16 patients) and non-depressed (23 patients). Its incidence was significantly higher in depressed patients with Parkinson's disease. © 1989 Springer-Verlag.

Rapid eye movement (REM) sleep latency (time from sleep onset to the first REM episode) was measured in 39 patients with idiopathic Parkinson's disease. Reduced REM sleep latency (≤65.0 min) was found in a high proportion of patients (69%). Since reduced REM sleep latency may be a trait-like abnormality relatively specific to primary depression, we evaluated this parameter in two groups of parkinsonian patients: depressed (16 patients) and non-depressed (23 patients). Its incidence was significantly higher in depressed patients with Parkinson's disease. © 1989 Springer-Verlag.

Objective: To investigate, using MRI and voxel-based morphometry (VBM), whether specific patterns of gray matter (GM) and white matter (WM) loss are associated with depression in patients with Parkinson disease (PD). Methods: Forty patients with PD and 26 healthy subjects were studied. Patients were diagnosed with depression using DSM-IV criteria. The Hamilton Depression Rating Scale (HDRS) was administered to patients. The topographic distribution of brain tissue loss in patients with PD and controls was assessed using VBM as implemented in Statistical Parametric Mapping (SPM5). Results: Twenty-four patients with PD were diagnosed as nondepressed (PD-NDep) and 16 as having depression (PD-Dep). Patient groups were similar in terms of clinical findings, except for the HDRS score (p < 0.001). Compared to controls, patients with PD showed common GM loss in the right anterior cingulate (AC) cortex and insula, and in the left middle frontal and angular gyri (p < 0.001). No regions of WM loss common to PD-NDep and PD-Dep patients relative to healthy controls were found. PD-Dep vs PD-NDep patients showed WM loss in the right AC bundle and inferior orbitofrontal (OF) region (p < 0.001). In patients with PD, HDRS score correlated with WM loss in the right inferior OF region (r =-0.51, p < 0.05). Conclusions: Tissue loss in several WM regions within the cortical-limbic network occurs in PD-Dep vs PD-NDep patients. Such pattern of brain atrophy overlaps with key regions involved in major depressive disorders, suggesting an increased vulnerability of this neural circuit in PD. This may partially account for the high prevalence of depression in PD. © 2010 by AAN Enterprises, Inc.

Not only childhoodonset, but also adult-onset primary dystonia may spread to multiple body parts. The relative risk of spread by site of onset of dystonia, important for clinical prognosis and approach, has not been well characterized. The aim of this study was to prospectively follow the spread of dystonia in 132 consecutive patients and to estimate the risk of spread by the site of onset of dystonia. The patients were included in the study if primary focal dystonia was the only sign of neurological disease other than tremor; i.e. in all patients a single body part could be identified as affected at the onset. At the end of the followup (mean duration 7.5 years; range 5.2-13.4 years), 96 patients (73%) remained focal, while 26 (20%) and 10 (7%) progressed to segmental and generalized dystonia, respectively. The highest likelihood for further spread was observed in patients with initial blepharospasm (10 out of 30 patients; 33.3%), followed by dystonia of upper extremities (32.3%), torticollis (19.6%), and laryngeal dystonia (6.7%). In addition to the highest risk for further spread of dystonia, blepharospasm was associated with the fastest rate of spread (the second region affected on average after 1.2 years). Our results demonstrated that the initial site of primary dystonia was relevant for the risk of spread. © 2007 Steinkopff-Verlag.

Not only childhoodonset, but also adult-onset primary dystonia may spread to multiple body parts. The relative risk of spread by site of onset of dystonia, important for clinical prognosis and approach, has not been well characterized. The aim of this study was to prospectively follow the spread of dystonia in 132 consecutive patients and to estimate the risk of spread by the site of onset of dystonia. The patients were included in the study if primary focal dystonia was the only sign of neurological disease other than tremor; i.e. in all patients a single body part could be identified as affected at the onset. At the end of the followup (mean duration 7.5 years; range 5.2-13.4 years), 96 patients (73%) remained focal, while 26 (20%) and 10 (7%) progressed to segmental and generalized dystonia, respectively. The highest likelihood for further spread was observed in patients with initial blepharospasm (10 out of 30 patients; 33.3%), followed by dystonia of upper extremities (32.3%), torticollis (19.6%), and laryngeal dystonia (6.7%). In addition to the highest risk for further spread of dystonia, blepharospasm was associated with the fastest rate of spread (the second region affected on average after 1.2 years). Our results demonstrated that the initial site of primary dystonia was relevant for the risk of spread. © 2007 Steinkopff-Verlag.

The aim of this study was to ascertain whether the stage of Parkinson's disease (PD) (according to the Hoehn and Yahr staging system) would affect the length of time between the introduction of levodopa therapy and appearance of levodopa-associated motor complications. Forty patients with clinically definite PD were studied. In all, clinical and therapeutic data were collected from the time of diagnosis to the time of levodopa-associated motor complications (i.e. dyskinesia, motor fluctuations). In 17 patients, levodopa could be started in Hoehn and Yahr stage I (H&Y-I; 16.2 months after the onset of PD), whilst in 13 patients levodopa could be started in H&Y-II (19.6 months after the onset of the disease) and in 10 in H&Y-III (45.1 months after the onset of PD). Cox proportional hazard regression model shows that the PD patients in whom the initial levodopa treatment was introduced at stage III develop both dyskinesias and motor fluctuations significantly earlier than the patients whose levodopa started in stage I and II of PD. The median interval to develop dyskinesias was 66, 72 and 24 months for patients in whom levodopa was introduced in stage I, II and III, respectively. These values were 64, 55 and 14 months for motor fluctuations. These findings add to the clinical arguments that favour an essential role of severity of PD at levodopa initiation as a risk factor for the development of levodopa-associated motor complications.

The aim of this study was to ascertain whether the stage of Parkinson's disease (PD) (according to the Hoehn and Yahr staging system) would affect the length of time between the introduction of levodopa therapy and appearance of levodopa-associated motor complications. Forty patients with clinically definite PD were studied. In all, clinical and therapeutic data were collected from the time of diagnosis to the time of levodopa-associated motor complications (i.e. dyskinesia, motor fluctuations). In 17 patients, levodopa could be started in Hoehn and Yahr stage I (H&Y-I; 16.2 months after the onset of PD), whilst in 13 patients levodopa could be started in H&Y-II (19.6 months after the onset of the disease) and in 10 in H&Y-III (45.1 months after the onset of PD). Cox proportional hazard regression model shows that the PD patients in whom the initial levodopa treatment was introduced at stage III develop both dyskinesias and motor fluctuations significantly earlier than the patients whose levodopa started in stage I and II of PD. The median interval to develop dyskinesias was 66, 72 and 24 months for patients in whom levodopa was introduced in stage I, II and III, respectively. These values were 64, 55 and 14 months for motor fluctuations. These findings add to the clinical arguments that favour an essential role of severity of PD at levodopa initiation as a risk factor for the development of levodopa-associated motor complications.