Aleksandar J. Ristić

Long-Term Prognosis of Vascular Hemiballismus

Background and Purpose— The aim of this study was to prospectively evaluate the long-term prognosis of hemiballismus due to first-ever ischemic strokes. Methods— A cohort of 27 patients with hemiballismus due to first-ever ischemic strokes was followed for a mean period of 30 months (range, 5 days to 150 months). Results— During the follow-up period there were 11 deaths (44%). The survival rate was 85% (95% CI, 71% to 99%) at 6 months, 81% (95% CI, 65% to 97%) at 15 months, 51% (95% CI, 24% to 78%) at 36 months, and only 32% (95% CI, 4% to 60%) at 150 months. The survival rate free from recurrent stroke was 96% (95% CI, 87% to 100%) at 6 months, 91% (95% CI, 79% to 100%) at 12 months, 80% (95% CI, 61% to 99%) at 24 months, and 27% (95% CI, 0% to 71%) at 150 months. Conclusions— The long-term prognosis of patients with vascular hemiballismus is similar to that of other stroke patients, ie, it follows the etiologic pattern of hemiballismus.

The Frequency of Reversible Parkinsonism and Cognitive Decline Associated with Valproate Treatment: A Study of 364 Patients with Different Types of Epilepsy

Summary:  Purpose: We report the frequency of parkinsonism and cognitive decline (P/CD) in patients treated with valproate (VPA) after 1 year of treatment and at least 1 year of follow‐up.

Linking MRI postprocessing with magnetic source imaging in MRI‐negative epilepsy

MRI‐negative (MRI–) pharmacoresistant focal epilepsy (PFE) patients are most challenging for epilepsy surgical management. This study utilizes a voxel‐based MRI postprocessing technique, implemented using a morphometric analysis program (MAP), aiming to facilitate detection of subtle focal cortical dysplasia (FCD) in MRI– patients. Furthermore, the study examines the concordance between MAP‐identified regions and localization from magnetic source imaging (MSI).

Voxel-based morphometric magnetic resonance imaging (MRI) postprocessing in MRI-negative epilepsies.

In the presurgical workup of magnetic resonance imaging (MRI)‐negative (MRI− or “nonlesional”) pharmacoresistant focal epilepsy (PFE) patients, discovering a previously undetected lesion can drastically change the evaluation and likely improve surgical outcome. Our study utilizes a voxel‐based MRI postprocessing technique, implemented in a morphometric analysis program (MAP), to facilitate detection of subtle abnormalities in a consecutive cohort of MRI− surgical candidates.

Frequency analysis and clinical characterization of different types of spinocerebellar ataxia in Serbian patients

The relative frequencies of different spinocerebellar ataxias (SCAs) vary widely among different ethnic groups, presumably due to a founder effect. We investigated the relative prevalence of SCA1–3, 6–8, 12, 17; dentate–rubro–pallidoluysian atrophy; and Friedreichs ataxia (FRDA) in Serbian patients with adult‐onset (>20 years of age) hereditary and sporadic SCAs, and compared clinical features of patients with genetically confirmed SCAs. A total of 108 patients from 54 families (38 apparently dominant [ADCA] and 16 apparently recessive) with adult‐onset hereditary ataxia and 75 apparently sporadic patients were assessed. Of 38 families with ADCA, 13 (34%) were positive for an expansion in an SCA1 and 5 families (13%) for an expansion in an SCA2 allele. In 20 families (53%), no expansions have been identified in any of the analyzed genes. Gaze palsy, spasticity, and hyperreflexia were significantly more common in SCA1, whereas slow saccades, hypotonia, hyporeflexia, and dystonia prevailed in SCA2 patients. Among the 16 families with an apparently recessive mode of ataxia inheritance, 4 (25%) were identified as having the FRDA mutation. Ataxia‐causing mutations were identified in 8 (10.6%) of patients with apparently sporadic adult‐onset ataxia.

Frequency, causes and phenomenology of late seizure recurrence in patients with juvenile myoclonic epilepsy after a long period of remission

PURPOSE To determine frequency, causes, and phenomenology of late seizure recurrence (SR) in patients with juvenile myoclonic epilepsy (JME) after remission of at least 1 year. METHODS Among 2722 epileptic patients from tertiary referral center, we retrospectively identified 105 patients (62 females; mean age 22.3+/-7.2 years) with an established diagnosis of JME. All patients were treated with valproates (83.3%), or lamotrigine, topiramate, phenobarbital, add-on clobazam, or combinations (16.2%). RESULTS The median period of follow-up was 4.2+/-3.2 (range: 1-17) years. SR occurred in 74 patients (70.5%) after median period of 2.4+/-3.2 years. Twenty-two patients (29.7%) experienced myoclonic seizures (MS), 13 (17.7%) generalized tonic-clonic seizures (GTCS), 37 (50%) a combination of MS and GTCS, and two (2.6%) a combination of MS, GTCS and absence seizures. SR was associated most frequently with sleep deprivation and AED withdrawal, and rarely with alcohol intake, drug abuse, photostimulation, or menstruation. No provoking factors for SR were identified in 31.1% and 45% of cases with MS and GTCS, respectively. The majority of patients (59/74) had a single SR. A second SR occurred less frequently in patients in whom valproate dosage was increased after the first SR (p=0.0048). CONCLUSION Late SR (mainly MS and GTCS) is detected frequently after prolonged follow-up in patients with JME despite the use of best-known therapy, usually due to AED withdrawal or erratic life style. Instead of futile efforts to persuade the patient to conform to restrictive life style, it is probably more efficient to use initial higher doses of AEDs.

Cortical thickness, surface area and folding in patients with psychogenic nonepileptic seizures

OBJECTIVE To determine cortical thickness (CTh), cortical surface area (CSA), curvature and sulcal depth (SD) in patients with psychogenic nonepileptic seizures (PNES). METHODS Freesurfer software was used to identify differences between active and control group in Cth, CSA, curvature, and SD. Neuropsychological tests intending to document possible frontal lobe deficit were applied. RESULTS We included 37 patients with PNES (age 37.3±13.8; female/male 31/6; age of disease onset 26.1±10.6; age of disease duration 11.1±11.1), and 37 healthy controls (age 38.4; ±12.7; female/male 26/11). No difference in CSA and curvature was detected between groups. Patients with PNES had increased CTh in the left insula, left and right medial-orbitofrontal, and left lateral-orbitofrontal, and decreased CTh in the left and right precentral, right enthorinal, and right lateral-occipital region than healthy controls. SD was increased at the level of the left and right insula, right rostral anterior cingulate, right posterior cingulate, and left cuneus, and reduced at the level of the right and left medial-orbitofrontal sulci in patients with PNES compared to healthy controls. CONCLUSION Individuals with PNES display a distinct profile of changes in CTh, in association with increase in SD in both insula as compared to controls. Our results may contribute to the understanding of the neurobiological background of PNES. Further research, to include replication of the findings and directed to understand the role of insula is needed.

Neuroimaging characteristics of MRI‐negative orbitofrontal epilepsy with focus on voxel‐based morphometric MRI postprocessing

The orbitofrontal (OF) region is one of the least explored regions of the cerebral cortex. There are few studies on patients with electrophysiologically and surgically confirmed OF epilepsy and a negative magnetic resonance imaging (MRI) study. We aimed to examine the neuroimaging characteristics of MRI‐negative OF epilepsy with the focus on a voxel‐based morphometric MRI postprocessing technique.

Etiology of a short-term mortality in the group of 750 patients with 920 episodes of status epilepticus within a period of 10 years (1988–1997)

PURPOSE To determine the etiology of short-term mortality in patients with status epilepticus (SE). METHODS 920 episodes of SE were recorded among 750 patients in a 10-year period. According to the clinical assessment, sequence of events that led to death in a particular case showed two major causes of death: (1) underlying disease, and (2) complications caused by convulsions, therapy or coma. RESULTS Among 920 episodes of SE, 120 (13%) patients passed away. 79 patients (65.8%) died due to the underlying disease and 27 patients (22.5%) died of the combination caused by complications of underlying disease, convulsions, therapy, and/or coma. Among remaining 14 patients (11.7%), underlying disease was not the cause of death. Those 14 patients suffered complications caused by convulsions, therapy, and coma which caused death in four; therapy and coma in three; therapy in three; coma in two; and convulsions and coma in two patients, in the order already mentioned. CONCLUSIONS Among approximately 9 out of 10 patients with SE, death was the result of underlying disease. Although with very few patients, additional factors could provoke fatal complications of SE. In case of 1 among 10 patients complications caused by coma, therapy, and/or convulsions were the immediate cause of death. In case of such patients timely and adequate treatment could prevent death.

Hippocampal metabolic dysfunction in juvenile myoclonic epilepsy: 3D multivoxel spectroscopy study

PURPOSE To investigate the metabolic differences in hippocampi of patients with juvenile myoclonic epilepsy (JME) and healthy controls using magnetic resonance spectroscopy (MRS). METHODS A 3D multivoxel SE 135 MRS study on 1.5 T scanner of both hippocampi was performed in 17 patients with JME and normal brain MRI and in 19 age and sex matched controls. Three dominant signals were measured: Choline (Cho), Creatine (tCr) and N-Acetylaspartate (NAA) and expressed as ratios of Cho:tCr, NAA:tCr, NAA:Cho and NAA:(Cho+tCr). Metabolite ratios in head, body and tail of each hippocampus in the JME group of patients were compared with ratios from corresponding structures in the control group. RESULTS We found a significant difference in metabolite ratios of both hippocampi between the JME and the control groups. We detected significant differences of Cho:tCr in the head, NAA:tCr in the head, body and tail, NAA:Cho and NAA:(Cho+tCr) in the body and tail of the left hippocampus, and NAA:Cho and NAA:(Cho+tCr) in the body and tail of the right hippocampus. DISCUSSION Although not previously recognized as a part of the epileptogenic network, our results suggest that the hippocampus, well recognized as a key player in focal epilepsies, may have a certain role in the pathogenesis of JME.