Effects of continuous theta burst transcranial magnetic stimulation on cortical excitability in patients with idiopathic generalized epilepsy.

INTRODUCTION: Transcranial magnetic stimulation (TMS) is a noninvasive technique for investigating cortical physiologic functions in the brain. In this study, the effects of continuous theta burst stimulation (cTBS) on motor evoked potential (MEP) parameters in patients with idiopathic generalized epilepsy (IGE) were investigated. MATERIALS AND METHODS: Fifteen patients with IGE were included. Motor threshold (MT) and cortical silent period (CSP) were determined before cTBS application. Next, cTBS was applied to the dominant (left) hemisphere M1 hand area as the first application. After 1 day, cTBS was applied first to the left M1 hand area and then to the right lateral cerebellar area as the second application. Parameters were again determined after the applications. RESULTS: There was no difference in resting MT values before and after cTBS application (p>0.05). Although CSP increased after stimulation (p<0.05), it was not significantly different between applications (p>0.05). CONCLUSION: For patients with epilepsy, cTBS is a safe technique when applied at a low intensity. The inhibitory effect of cTBS, a noninvasive technique, on cortical excitability in patients with IGE was determined using MEP parameters. The effect lasted at least 1 h. To our knowledge, this is the first study to assess the effect of cTBS on cortical excitability in patients with IGE. Our findings indicate that cTBS decreases cortical excitability in patients with IGE.

Transcallosal conduction in paroxysmal kinesigenic dyskinesia.

OBJECTIVES: Detecting whether a possible disequilibrium between the excitatory and inhibitory interhemispheric interactions in paroxysmal kinesigenic dyskinesia (PKD) exists. METHODS: This study assessed measures of motor threshold, motor evoked potential latency, the cortical silent period, the ipsilateral silent period and the transcallosal conduction time (TCT) in PKD patients. Data were compared between the clinically affected hemisphere (aH) and the fellow hemisphere (fH). RESULTS: The transcallosal conduction time from the aH to the fH was 11.8 ms (range = 2.3-20.7) and 13.6 ms (range = 2.8-67.7) from the fH to the aH. The difference in TCT in the affected side was significant (p = .019). CONCLUSION: The findings demonstrated that, although inhibitory interneurons act normally and symmetrically between the motor cortices and transcallosal inhibition was normal and symmetrical between both sides, the onset of transcallosal inhibition was asymmetrical. The affected hemisphere's inhibition toward the unaffected hemisphere is faster compared to the inhibition provided by the fellow hemisphere. These results are consistent with an inhibitory deficit in the level of interhemispheric interactions. SIGNIFICANCE: This study revealed a defect in inhibition of the motor axis could be responsible in the pathological mechanisms of kinesigenic dyskinesia.

Clinical properties of regional thalamic hemorrhages.

BACKGROUND: Thalamic hemorrhage constitutes 6% to 25% of intracerebral hemorrhages. Vascular lesions affecting the thalamus may cause a variety of clinical symptoms. This retrospective study aims to evaluate localization of hemorrhage and clinical symptoms in patients with thalamic hemorrhage. METHODS: One hundred and one patients with thalamic hemorrhage were examined retrospectively in our department. Hemorrhages were classified into 5 groups according to computed tomography: medial (thalamoperforate), anterolateral (tuberothalamic), posterolateral (thalamogeniculate), dorsal (posterior choroidal), and global. The relation between volume, localization, and penetration to adjacent structures/ventricles of hemorrhage and risk factors, clinical features, and prognosis were evaluated. RESULTS: The study group included 101 patients. Eighty-two percent of the patients had hypertension, 19.8% had diabetes mellitus, 14.9% had cardiac disease, and 5.9% had chronic renal failure. Mean blood pressure was 173/101 mm Hg. Decreased Glasgow coma scale was significantly higher in the global hemorrhage group than in all regional groups (Chi-square, 10.54; P = .002). Medial group hemorrhages had a significantly higher rate than anterolateral, posterolateral, and dorsal intraventricular expansion. Out of speech disorders, 49% of patients had a right thalamic lesion (especially dysarthria) and 51% of patients had a left thalamic lesion (mostly aphasia). CONCLUSIONS: In the study, we detected that the most important risk factor in thalamic hemorrhage is hypertension. The prognosis is worse in global and medial group hemorrhages, especially those which rupture to the ventricle, than the other groups. Thalamic lesions cause a variety of symptoms, including forms of aphasia, such as crossed dextral aphasia.

Strength-duration time constant in peripheral nerve: no abnormality in multiple sclerosis.

Objectives. To investigate the properties of the strength-duration time constant (SDTC) in multiple sclerosis (MS) patients. Methods. The SDTC and rheobase in 16 MS patients and 19 healthy controls were obtained following stimulation of the right median nerve at the wrist. Results. SDTC and rheobase values were 408.3 ± 60.0 µs and 4.0 ± 1.8 mA in MS patients, versus 408.0 ± 62.4 µs and 3.8 ± 2.1 mA in controls. The differences were not significant in SDTC or rheobase values between the patients and controls (P = 0.988 for SDTC and P = 0.722 for rheobase). Conclusion. Our study showed no abnormality in relapsing remitting MS patients in terms of SDTC, which gives some indirect information about peripheral Na(+) channel function. This may indicate that alterations in the Na(+) channel pattern in central nervous system (CNS) couldnot be shown in the peripheral nervous system (PNS) in the MS patients by SDTC. The opinion that MS can be a kind of channelopathy might be proven by performing other axonal excitability tests or SDTC in progressive forms of MS.

Time-dependent changes in the serum levels of prolactin, nesfatin-1 and ghrelin as a marker of epileptic attacks young male patients.

A relationship between hormones and seizures has been reported in animals and humans. Therefore, the purpose of this study was to investigate the association between serum levels of prolactin, nesfatin-1 and ghrelin measured different times after a seizure or non-epileptic event and compared with controls. The study included a total of 70 subjects, and of whom 18 patients had secondary generalized epilepsy (SGE), 16 patients had primary generalized epilepsy (PGE), 16 patients exhibited paroxysmal event (psychogenic) and 20 healthy males were control subjects. The first sample was taken within 5min of a seizure, with further samples taken after 1, 24, and 48h so long as the patient did not exhibit further clinically observable seizures; blood samples were taken once from control subjects. Prolactin was measured immediately using TOSOH Bioscience hormone assays. Nesfatin-1 and ghrelin peptides were measured using a commercial immunoassay kit. Patients suffering from focal epilepsy with secondary generalization and primary generalized epilepsy presented with significantly higher levels of serum prolactin and nesfatin-1 and lower ghrelin levels 5min, 1 and 24h after a seizure than patients presenting with paroxysmal events (psychogenic) and control subjects; the data were similar but not statistically significant after 48h. The present study suggests that increased serum prolactin and nesfatin-1 concentrations, decreased ghrelin concentrations could be used as markers to identify patients that have suffered a recent epileptic seizure or other paroxysmal event (psychogenic).

Lateralization of cerebral blood flow in juvenile absence seizures.

Cerebrovascular blood flow in absence seizures and flow patterns during the ictal period have not been thoroughly investigated. We aimed to evaluate cerebral blood flow changes in typical juvenile absence seizures during the ictal and postictal phases. Seizures were recorded in three patients (mean age: 21 +/- 1 years) with multiple daily typical absence seizures. Simultaneous video electroencephalography and bilateral middle cerebral artery transcranial Doppler ultrasonography recordings were conducted during seizures. Basal, ictal, and postictal blood flow velocities were recorded bilaterally, and offline analyses were performed in relation with generalized spike and wave discharges. Total of 43 seizures were recorded. Ictal increase and postictal decrease of cerebral blood flow velocities were significant for both sides (P < 0.001). The interhemispheric asymmetry in the ictal velocity increase was significant (P < 0.05). The interhemispheric asymmetry in the postictal velocity decrease was not significant (P > 0.05). The blood flow velocity increase after seizure onset indicates a vascular coupling mechanism. A sudden and then a gradual decrease in blood flow velocity, which lasted even after the seizure ceased, might suggest a preventive mechanism to avoid excessive seizure duration or even an absence status epilepticus. Significant asymmetries in increase and a symmetrical decrease may support the cortical focus theory.

Vasomotor properties of the M2 segment of the middle cerebral artery.

Vasomotor response can be tested by means of transcranial Doppler sonography. It is assumed that flow changes during hyperventilation or breath-holding are due to altered resistance caused by changes in the diameter of vessels distal to the M1 segment of the middle cerebral artery. Evaluating velocities of the M2 and M1 segments together may help elucidate the vasomotor properties of distal segments. We simultaneously evaluated the vasomotor properties of the M1 and M2 segments of the middle cerebral artery in ten healthy volunteers (mean age 21.6 +/- 0.9 years) with breath-holding and hyperventilation. The radius index (RI), defined as the ratio of the M1-M2 segment radii, was estimated after 20 s and after the maximum duration of breath-holding, as well as at the first, second, and third minute of hyperventilation, in relation to velocity ratios. RI values in the resting state were compared with the values after activation procedures. The RI estimated with basal velocities ranged from 0.72 to 0.97 (mean 0.81 +/- 0.07). The RI ranged from 0.73 to 0.97 (mean 0.82 +/- 0.07) after 20 s and 0.75 to 0.90 (mean 0.82 +/- 0.06) after the maximum duration of breath-holding. The RI was 0.72-1.02 (mean 0.85 +/- 0.11), 0.71-1.03 (mean 0.86 +/- 0.12), and 0.71-1.14 (mean 0.88 +/- 0.15) at the first, second, and third minute of hyperventilation, respectively. The differences between RI values in the resting state and during each activation procedure were not statistically significant. These results suggest that the diameter ratio of the M1-M2 segments did not change after vasomotor activation, indicating that the two segments have similar vasomotor properties.

Cerebral vasomotor reactivity in epilepsy patients.

Vasomotor reactivity, which can be defined as the cerebral vasculature response to hypoxia, is not well known in epilepsy patients. We aimed to evaluate cerebrovascular reserve in idiopathic generalized epilepsy patients using transcranial Doppler ultrasonography (TCD). The study included 20 patients and 20 healthy volunteers. Diagnosis of epilepsy was based on the observation of seizure in the video electroencephalography unit. Cerebrovascular reactivity was evaluated by means of the breath-holding index. Insonation depth and basal velocity were symmetrical and not significantly different between the two groups (p[0.05). The breath-holding index ranged from 0.62 to 4.45 (mean 2.13 +/- 0.83) in the epilepsy patients and 0.57 to 2.55 (mean 1.60 +/- 0.46) in the control group (p\0.05). Breath-holding index values showed that cerebrovascular reserve in epilepsy patients was increased, as compared to healthy individuals. Cerebrovascular reserve was increased in epilepsy patients; this should not be accepted as an abnormality, but might have been the result of an adaptive mechanism that protects the brain from hypoxic challenges due to seizure apnea.

Reinnervation cannot be interpreted as an indicator of electrophysiologic improvement in amyothrophic lateral sclerosis.

Denervation and reinnervation comprise a dynamic process that begins in the early periods of amyothrophic lateral sclerosis and lasts until the final individual motor neuron dies. A dynamic process like denervation-reinnervation that is found in the natural course of the disease can not be presented as a neurophysiologic measure. Other parameters, such as motor unit number estimation, compound muscle action potential amplitude and neurophysiologic index, seem more appropriate for therapeutic trials.