Pallidal deep brain stimulation for patients with myoclonus-dystonia without SGCE mutations.

BACKGROUND: Pallidal deep brain stimulation (GPi-DBS) is effective for treating myoclonus and dystonia caused by SGCE mutations (DYT-SGCE, DYT11). However, it is unknown whether GPi-DBS is effective for the treatment of myoclonus-dystonia which is not associated with the SGCE gene mutations. In this study, we investigated the efficacy of GPi-DBS in treating myoclonus-dystonia in SGCE mutation-negative cases. METHODS: Three patients with myoclonus-dystonia without SGCE mutations who underwent GPi-DBS were evaluated preoperatively and 6 months postoperatively using the Unified Myoclonus Rating Scale (UMRS) and Fahn-Marsden Dystonia Rating Scale (FMDRS) for myoclonus and dystonia, respectively. In two of the three patients, myoclonus was more evident during action. Myoclonus was predominant at rest in the other patient, and he was unaware of his dystonia symptoms. The results were compared with those of the four DYT-SGCE cases. RESULTS: The mean UMRS score in patients with myoclonus-dystonia without SGCE mutations improved from 61.7 to 33.7 pre- and postoperatively, respectively, and the mean FMDRS score improved from 7.2 to 4.5. However, the degree of improvement in myoclonus-dystonia in patients without SGCE mutations was inferior to that in patients with DYT-SGCE (the UMRS score improved by 45% and 69%, respectively). CONCLUSIONS: GPi-DBS is effective for treating myoclonus-dystonia in patients with and without SGCE mutations. GPi-DBS should be considered as a treatment option for myoclonus-dystonia without SGCE mutations.

Age- and sex-related oculomotor manifestation of dopamine deficiency in Segawa disease.

OBJECTIVE: To investigate the oculomotor manifestations of Segawa disease (SD), considered to represent mild dopamine deficiency and discuss their pathophysiological basis. METHODS: We recorded visually- (VGS) and memory-guided saccade (MGS) tasks in 31 SD patients and 153 age-matched control subjects to study how basal ganglia (BG) dysfunction in SD evolves with age for male and female subjects. RESULTS: SD patients were impaired in initiating MGS, showing longer latencies with occasional failure. Patients showed impaired ability to suppress reflexive saccades; saccades to cues presented in MGS were more frequent and showed a shorter latency than in control subjects. These findings were more prominent in male patients, particularly between 13 and 25 years. Additionally, male patients showed larger delay in MGS latency in trials preceded by saccades to cue than those unpreceded. CONCLUSIONS: The findings can be explained by a dysfunction of the BG-direct pathway impinging on superior colliculus (SC) due to dopamine deficiency. The disturbed inhibitory control of saccades may be explained by increased SC responsivity to visual stimuli. SIGNIFICANCE: Oculomotor abnormalities in SD can be explained by dysfunction of the BG inhibitory pathways reaching SC, with a delayed maturation in male SD patients, consistent with previous pathological/physiological studies.

The Pathophysiology of Gilles de la Tourette Syndrome: Changes in Saccade Performance by Low-Dose L-Dopa and Dopamine Receptor Blockers.

AIM: To elucidate the pathophysiology of Gilles de la Tourette syndrome (GTS), which is associated with prior use of dopamine receptor antagonists (blockers) and treatment by L-Dopa, through saccade performance. METHOD: In 226 male GTS patients (5-14 years), we followed vocal and motor tics and obsessive-compulsive disorder (OCD) after discontinuing blockers at the first visit starting with low-dose L-Dopa. We recorded visual- (VGS) and memory-guided saccades (MGS) in 110 patients and 26 normal participants. RESULTS: At the first visit, prior blocker users exhibited more severe vocal tics and OCD, but not motor tics, which persisted during follow-up. Patients treated with L-Dopa showed greater improvement of motor tics, but not vocal tics and OCD. Patients with and without blocker use showed similarly impaired MGS performance, while patients with blocker use showed more prominently impaired inhibitory control of saccades, associated with vocal tics and OCD. DISCUSSION: Impaired MGS performance suggested a mild hypodopaminergic state causing reduced direct pathway activity in the (oculo-)motor loops of the basal ganglia-thalamocortical circuit. Blocker use may aggravate vocal tics and OCD due to disinhibition within the associative and limbic loops. The findings provide a rationale for discouraging blocker use and using low-dose L-Dopa in GTS.

Deciphering the saccade velocity profile of progressive supranuclear palsy: A sign of latent cerebellar/brainstem dysfunction?

OBJECTIVE: To study whether the velocity profile of horizontal saccades could be used as an indicator of brainstem and cerebellar output dysfunction, depending on progressive supranuclear palsy (PSP) subtype. METHODS: We compared the velocity profiles in 32 PSP patients of various subtypes with 38 age-matched normal subjects, including Richardson syndrome (RS), PSP-parkinsonism (PSPp), and pure akinesia (PAGF), and cerebellar subtypes of PSP (PSPc). RESULTS: PSP patients showed reduced peak velocity along with increased duration, especially in the deceleration phase. This alteration was more prominent for larger target eccentricities (20-30 degrees), and correlated with disease severity. The changes were most pronounced in PSPc patients, with irregular increases and decreases in velocity profile, followed by RS patients, whereas the change was smaller in PSPp and normal in PAGF patients. CONCLUSIONS: Saccade velocity profile can be an indicator of brainstem and/or cerebellar output. Altered velocity profile of PSP patients may reflect the pathology in the brainstem, but may also reflect cerebellar dysfunction, most prominently in PSPc. SIGNIFICANCE: Saccade velocity profile may be used as an indicator of latent cerebellar/brainstem dysfunction.

Differentiating early Parkinson's disease and multiple system atrophy with parkinsonism by saccade velocity profiles.

OBJECTIVE: Patients with Parkinson's disease (PD) and multiple system atrophy both present predominantly with parkinsonism at early stages, whereas cerebellar symptoms are largely masked in multiple system atrophy with parkinsonism (MSAP). We sought to determine whether the velocity profiles of saccades could be used to differentiate between these two disorders, revealing the underlying basal ganglia and/or cerebellar dysfunction and brainstem pathology in these disorders. METHODS: Sixteen MSA-P patients, 63 PD patients, and 36 age-matched normal subjects performed the visually guided (VGS) and memory-guided saccade (MGS) tasks. Targets were presented at eccentricities of 5, 10, 20, and 30 degrees. The amplitude, peak velocity, and duration of saccades were compared among subject groups. Duration was further subdivided into acceleration and deceleration periods, corresponding to the times before and after peak velocity. These parameters correlated with the severity of Parkinsonism as assessed by the UPDRS motor score. RESULTS: Hypometria predominated in both PD and MSAP patients, whereas hypermetria, frequently noted in cerebellar ataxia, was rarely observed. Saccades in MSAP were characterized both by prolonged acceleration and deceleration periods with reduced peak velocity. In contrast, the velocity profile of PD patients was characterized mainly by the prolonged deceleration period. The changes observed in velocity profiles of MGS deteriorated with advancing severity of parkinsonism in MSAP and PD patients. CONCLUSION: Saccade profiles provide useful information for differentiating between PD and MSAP at early stages. While the changes in velocity profiles may be explained by the cerebellar and brainstem pathology in MSAP, the changes in velocity profile in both PD and MSAP correlated significantly with increasing severity of Parkinsonism in both disorders, suggesting a link with striatonigral pathology. SIGNIFICANCE: The differential changes in saccade velocity profiles of MSAP and PD may be used as a measure indexing the progression of cerebellar and basal ganglia dysfunction as well as for assessing the functional improvement when clinical treatment becomes available.

Effect of subthalamic nucleus deep brain stimulation on visual scanning.

OBJECTIVE: Deep brain stimulation (DBS) can provide insights into the workings of the basal ganglia (BG) by interfering with their function. In patients with Parkinson's disease (PD) treated with DBS of the subthalamic nucleus, we studied the effect of DBS on scanning eye movements. METHODS: In the visual memory task, subjects viewed images of various complexities for later recall. In visual search tasks, subjects looked for and fixated one odd target ring, embedded among 48 Landolt rings, which either stood out or not from the distractors. We compared the parameters of scanning saccades when DBS was on and off. RESULTS: In the visual memory task, DBS increased the amplitude of saccades scanning simple but not complex drawings. In the visual search tasks, DBS showed no effect on saccade amplitude or frequency. CONCLUSIONS: Saccades when viewing simple images were affected by DBS since they are internally guided saccades, for which the involvement of BG is large. In contrast, saccades when viewing complex images or during visual search, made with the help of visual cues in the images (externally guided saccades) and less dependent on BG, were resistant to the effect of DBS. SIGNIFICANCE: DBS affects saccades differentially depending on the task.

Does the Clock Tick Slower or Faster in Parkinson's Disease? - Insights Gained From the Synchronized Tapping Task.

The rhythm of the internal clock is considered to be determined by the basal ganglia, with some studies suggesting slower internal clock in Parkinson's disease (PD). However, patients may also show motor hastening when they walk (festination) or are engaged in repetitive tapping, indicating faster ticking of the internal clock. Is the internal clock slower or faster in PD? The purpose of this study was to answer this question, i.e., how fast and slow a rhythm they can synchronize with, especially with reference to the limit of sensorimotor synchronization or temporal integration, representing the threshold of slower pace they can entrain into their motor actions, which is known to lie between 2 and 3 s in normal subjects but not yet studied in PD. We employed a synchronized tapping task that required subjects to tap the key in synchrony with repetitive tones at fixed interstimulus intervals (ISI) between 200 and 4800 ms. Twenty normal subjects and sixteen PD patients were enrolled, who were classified into early and advanced PD groups by UPDRS-III (early: 15 or less, advanced: more than 15). The ISI at which the response changes from synchronizing with the tones to lagging behind them was considered to be the limit of temporal integration. Early PD patients responded ahead of the tones (negative asynchrony), which became more apparent with repeated tapping. This suggested "faster" ticking clock even in the presence of the pacing tones. In normal subjects, the limit of temporal integration was around 2-3 s: below this, subjects could synchronize with the tones, while above it they had difficulty in synchronization. In early PD patients, the limit of temporal integration was significantly longer than in normal subjects, pointing to their enhanced ability to synchronize also with slower paces of tones, but advanced PD patients had significantly shortened limits, suggesting that advanced patients lost this ability. In conclusion, the limit of temporal integration is initially longer but gets shorter as the disease progresses. It can be explained by the hastening of the internal clock at the earlier stages of PD, followed by the loss of temporal integration.

Resting-State Pallidal-Cortical Oscillatory Couplings in Patients With Predominant Phasic and Tonic Dystonia.

Pallidal deep brain stimulation (DBS) improves the symptoms of dystonia. The improvement processes of dystonic movements (phasic symptoms) and tonic symptoms differ. Phasic symptoms improve rapidly after starting DBS treatment, but tonic symptoms improve gradually. This difference implies distinct neuronal mechanisms for phasic and tonic symptoms in the underlying cortico-basal ganglia neuronal network. Phasic symptoms are related to the pallido-thalamo-cortical pathway. The pathway related to tonic symptoms has been assumed to be different from that for phasic symptoms. In the present study, local field potentials of the globus pallidus internus (GPi) and globus pallidus externus (GPe) and electroencephalograms from the motor cortex (MCx) were recorded in 19 dystonia patients to analyze the differences between the two types of symptoms. The 19 patients were divided into two groups, 10 with predominant phasic symptoms (phasic patients) and 9 with predominant tonic symptoms (tonic patients). To investigate the distinct features of oscillations and functional couplings across the GPi, GPe, and MCx by clinical phenotype, power and coherence were calculated over the delta (2-4 Hz), theta (5-7 Hz), alpha (8-13 Hz), and beta (14-35 Hz) frequencies. In phasic patients, the alpha spectral peaks emerged in the GPi oscillatory activities, and alpha GPi coherence with the GPe and MCx was higher than in tonic patients. On the other hand, delta GPi oscillatory activities were prominent, and delta GPi-GPe coherence was significantly higher in tonic than in phasic patients. However, there was no significant delta coherence between the GPi/GPe and MCx in tonic patients. These results suggest that different pathophysiological cortico-pallidal oscillations are related to tonic and phasic symptoms.

A significant correlation between cauda equina conduction time and cerebrospinal fluid protein in chronic inflammatory demyelinating polyradiculoneuropathy.

We investigated the relationship between the involvement of the cauda equina in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and the increment of cerebrospinal fluid (CSF) protein. We measured cauda equina conduction time (CECT) in 14 CIDP patients using magnetic stimulation with a MATS coil. Statistical analysis revealed that CECT and CSF protein had a significant positive linear correlation. Conduction time of the peripheral nerve trunk, in contrast, had no significant linear correlation with CSF protein. We revealed that the involvement of the cauda equina and increment of CSF protein are closely related. In CIDP cases with elevated CSF protein, spinal nerves including the cauda equina are very likely involved.

Safety of repetitive transcranial magnetic stimulation in patients with implanted cortical electrodes. An ex-vivo study and report of a case.

OBJECTIVE: To evaluate the safety of repetitive transcranial magnetic stimulation (rTMS) in patients with implanted subdural cortical electrodes. METHODS: We performed ex-vivo experiments to test the temperature, displacement and current induced in the electrodes with single pulse transcranial magnetic stimulation (TMS) from 10 to 100% of stimulator output and tested a typical rTMS protocol used in a clinical setting. We then used rTMS to the motor cortex to treat a patient with refractory post-herpetic neuralgia who had previously been implanted with a subdural motor cortical electrode for pain management. The rTMS protocol consisted of ten sessions of 2000 stimuli at 20Hz and 90% of resting motor threshold. RESULTS: The ex-vivo study showed an increase in the coil temperature of 2°C, a maximum induced charge density of 30.4µC/cm2/phase, and no electrode displacement with TMS. There was no serious adverse effect associated with rTMS treatment of the patient. Cortical tremor was observed in the intervals between trains of stimuli during one treatment session. CONCLUSIONS: TMS was safe in a patient with implanted Medtronic Resume II electrode (model 3587A) subdural cortical electrode. SIGNIFICANCE: TMS may be used as a therapeutic, diagnostic or research tool in patients this type of with implanted cortical electrodes.

Distinguishing spinocerebellar ataxia with pure cerebellar manifestation from multiple system atrophy (MSA-C) through saccade profiles.

OBJECTIVE: Patients with spinocerebellar ataxia with pure cerebellar presentation (SCD) and multiple system atrophy (MSA-C) show similar symptoms at early stages, although cerebellofugal pathology predominates in SCD, and cerebellopetal pathology in MSA-C. We studied whether saccade velocity profiles, which reflect the accelerating and braking functions of the cerebellum, can differentiate these two disorders. METHODS: We recorded visually guided (VGS) and memory guided saccades (MGS) in 29 MSA-C patients, 12 SCD patients, and 92 age-matched normal subjects, and compared their amplitude, peak velocity and duration (accelerating and decelerating phases). RESULTS: Hypometria predominated in VGS and MGS of MSA-C, whereas hypometria was less marked in SCD, with hypermetria frequently noted in MGS. Peak velocity was reduced, and deteriorated with advancing disease both in SCD and MSA-C groups at smaller target eccentricities. The deceleration phase was prolonged in SCD compared to MSA-C and normal groups at larger target eccentricities, which deteriorated with advancing disease. CONCLUSION: Saccades in MSA-C were characterized by a more prominent acceleration deficit and those in SCD by a more prominent braking defect, possibly caused by the cerebellopetal and cerebellofugal pathologies, respectively. SIGNIFICANCE: Saccade profiles provide important information regarding the accelerating and braking signals of the cerebellum in spinocerebellar ataxia.

Is multiple system atrophy with cerebellar ataxia (MSA-C) like spinocerebellar ataxia and multiple system atrophy with parkinsonism (MSA-P) like Parkinson's disease? - A saccade study on pathophysiology.

OBJECTIVE: Patients with multiple system atrophy (MSA) are classified into those mainly manifesting cerebellar ataxia (MSA-C) and those mainly manifesting parkinsonism (MSA-P). Pathophysiological bases of these subtypes remain unclear. We hypothesized that MSA-C patients would resemble spinocerebellar degeneration patients and MSA-P patients would resemble Parkinson's disease (PD) patients in saccade abnormalities. METHODS: We recorded visually guided and memory guided saccades (MGS) in 27 MSA-C and 15 MSA-P patients, as well as 50 age-matched normal subjects, 14 spinocerebellar degeneration patients showing pure cerebellar symptoms (SCD) and 61 Parkinson's disease (PD) patients. RESULTS: Saccade parameters of both tasks showed similar changes with progressing disease in SCD and MSA-C patients, as did those of MSA-C and MSA-P patients, although hypometria was slightly more pronounced in MSA-P. In both subtypes of MSA, latency and success rate of MGS were stable throughout disease stages, whereas they deteriorated progressively with progressing disease in PD. CONCLUSIONS: Pathophysiology underlying MSA-C and MSA-P is similar as viewed from saccade performance. The MGS performance in MSA was preserved. However, MSA-P patients showed more marked hypometria, suggesting a mixture of basal ganglia pathophysiology. SIGNIFICANCE: The similarity of saccade performance between MSA-C and MSA-P may reflect common olivopontocerebellar pathology, while the direct pathway of the basal ganglia is relatively spared compared with PD, even in MSA-P.

Modulation of Beta oscillations in the subthalamic nucleus with prosaccades and antisaccades in Parkinson's disease.

Increased oscillations in the beta band are thought to be related to motor symptoms of Parkinson's disease (PD). Previous studies have shown that beta-band desynchronization in the subthalamic nucleus (STN) is reduced just before and during limb movements. While the STN is part of the basal ganglia (BG)-thalamocortical circuit controlling limb movements, it is also part of the BG-brainstem projection controlling saccadic eye movements. Late-stage PD patients have deficits in saccades in addition to difficulties with limb movements arising from impaired functions of the BG. We investigated saccade-related changes in beta-band (15-30 Hz) oscillatory activities in the human STN while PD patients performed visually guided prosaccades and antisaccades, the latter requiring suppression of reflexive responses and volitional initiation of saccades. We recorded local field potentials from deep brain stimulation electrodes implanted in the STN in human PD patients 1-5 d after surgery and compared prosaccades and antisaccades with these and with limb movements. Saccade-related beta-band desynchronizations were observed just before and during saccades in all subjects, suggesting that reduction of beta-band oscillatory activity in the STN is related to preparation and execution of saccades. Furthermore, beta-band desynchronizations for antisaccades started earlier, were sustained for longer periods, were of greater magnitude, and were observed more often than prosaccades. Beta-band desynchronization in the STN may reflect the additional processes associated with suppression of reflexive responses and volitional execution of saccades in the opposite direction.

Cortical hemoglobin concentration changes underneath the coil after single-pulse transcranial magnetic stimulation: a near-infrared spectroscopy study.

Using near-infrared spectroscopy (NIRS) and multichannel probes, we studied hemoglobin (Hb) concentration changes when single-pulse transcranial magnetic stimulation (TMS) was applied over the left hemisphere primary motor cortex (M1). Seventeen measurement probes were centered over left M1. Subjects were studied in both active and relaxed conditions, with TMS intensity set at 100%, 120%, and 140% of the active motor threshold. The magnetic coils were placed so as to induce anteromedially directed currents in the brain. Hb concentration changes were more prominent at channels over M1 and posterior to it. Importantly, Hb concentration changes at M1 after TMS differed depending on whether the target muscle was in an active or relaxed condition. In the relaxed condition, Hb concentration increased up to 3-6 s after TMS, peaking at ∼6 s, and returned to the baseline. In the active condition, a smaller increase in Hb concentrations continued up to 3-6 s after TMS (early activation), followed by a decrease in Hb concentration from 9 to 12 s after TMS (delayed deactivation). Hb concentration changes in the active condition at higher stimulus intensities were more pronounced at locations posterior to M1 than at M1. We conclude that early activation occurs when M1 is activated transsynaptically. The relatively late deactivation may result from the prolonged inhibition of the cerebral cortex after activation. The posterior-dominant activation at higher intensities in the active condition may result from an additional activation of the sensory cortex due to afferent inputs from muscle contraction evoked by the TMS.

Deterioration of horizontal saccades in progressive supranuclear palsy.

OBJECTIVE: To investigate horizontal saccade changes according to disease stage in patients with progressive supranuclear palsy (PSP). METHODS: We studied visually and memory guided saccades (VGS and MGS) in 36 PSP patients at various disease stages, and compared results with those in 66 Parkinson's disease (PD) patients and 58 age-matched normal controls. RESULTS: Both vertical and horizontal saccades were affected in PSP patients, usually manifesting as "slow saccades" but sometimes as a sequence of small amplitude saccades with relatively well preserved velocities. Disease progression caused saccade amplitude reduction in PSP but not PD patients. In contrast, VGS and MGS latencies were comparable between PSP and PD patients, as were the frequencies of saccades to cue, suggesting that voluntary initiation and inhibitory control of saccades are similar in both disorders. Hypermetria was rarely observed in PSP patients with cerebellar ataxia (PSPc patients). CONCLUSIONS: The progressively reduced accuracy of horizontal saccades in PSP suggests a brainstem oculomotor pathology that includes the superior colliculus and/or paramedian pontine reticular formation. In contrast, the functioning of the oculomotor system above the brainstem was similar between PSP and PD patients. SIGNIFICANCE: These findings may reflect a brainstem oculomotor pathology.

Where do neurologists look when viewing brain CT images? An eye-tracking study involving stroke cases.

The aim of this study was to investigate where neurologists look when they view brain computed tomography (CT) images and to evaluate how they deploy their visual attention by comparing their gaze distribution with saliency maps. Brain CT images showing cerebrovascular accidents were presented to 12 neurologists and 12 control subjects. The subjects' ocular fixation positions were recorded using an eye-tracking device (Eyelink 1000). Heat maps were created based on the eye-fixation patterns of each group and compared between the two groups. The heat maps revealed that the areas on which control subjects frequently fixated often coincided with areas identified as outstanding in saliency maps, while the areas on which neurologists frequently fixated often did not. Dwell time in regions of interest (ROI) was likewise compared between the two groups, revealing that, although dwell time on large lesions was not different between the two groups, dwell time in clinically important areas with low salience was longer in neurologists than in controls. Therefore it appears that neurologists intentionally scan clinically important areas when reading brain CT images showing cerebrovascular accidents. Both neurologists and control subjects used the "bottom-up salience" form of visual attention, although the neurologists more effectively used the "top-down instruction" form.

Initiation and inhibitory control of saccades with the progression of Parkinson's disease - changes in three major drives converging on the superior colliculus.

The cardinal pathophysiology of Parkinson's disease (PD) is considered to be the increase in the activities of basal ganglia (BG) output nuclei, which excessively inhibits the thalamus and superior colliculus (SC) and causes preferential impairment of internal over external movements. Here we recorded saccade performance in 66 patients with PD and 87 age-matched controls, and studied how the abnormality changed with disease progression. PD patients were impaired not only in memory guided saccades, but also in visually guided saccades, beginning in the relatively early stages of the disease. On the other hand, they were impaired in suppressing reflexive saccades (saccades to cue). All these changes deteriorated with disease progression. The frequency of reflexive saccades showed a negative correlation with the latency of visually guided saccades and Unified Parkinson's Disease Rating Scale motor subscores reflecting dopaminergic function. We suggest that three major drives converging on SC determine the saccade abnormalities in PD. The impairment in visually and memory guided saccades may be caused by the excessive inhibition of the SC due to the increased BG output and the decreased activity of the frontal cortex-BG circuit. The impaired suppression of reflexive saccades may be explained if the excessive inhibition of SC is "leaky." Changes in saccade parameters suggest that frontal cortex-BG circuit activity decreases with disease progression, whereas SC inhibition stays relatively mild in comparison throughout the course of the disease. Finally, SC disinhibition due to leaky suppression may represent functional compensation from neural structures outside BG, leading to hyper-reflexivity of saccades and milder clinical symptoms.

Small saccades restrict visual scanning area in Parkinson's disease.

The purpose of this study was to investigate abnormalities in visual scanning when Parkinson's disease patients view images of varying complexity. Eighteen nondemented Parkinson's disease patients and 18 normal subjects participated in the study. The ocular fixation position during viewing visual images was recorded using an eye-tracking device. The number of saccades, duration of fixation, amplitude of saccades, and scanned area in Parkinson's disease patients were compared with those in normal subjects. We also investigated whether the number of saccades, duration of fixation, or amplitude of saccades influenced the scanned area. While scanning images of varying complexity, Parkinson's disease patients made fewer saccades with smaller amplitude and longer fixation compared with normal subjects. As image complexity increased, the number of saccades and duration of fixation gradually approached those of normal subjects. Nevertheless, the scanned area in Parkinson's disease patients was consistently smaller than that in normal subjects. The scanned area significantly correlated with saccade amplitude in most images. Importantly, although Parkinson's disease patients cannot make frequent saccades when viewing simple figures, they can increase the saccade number and reduce their fixation duration when viewing more complex figures, making use of the abundant visual cues in such figures, suggesting the existence of ocular kinesie paradoxale. Nevertheless, both the saccade amplitude and the scanned area were consistently smaller than those of normal subjects for all levels of visual complexity. This indicates that small saccade amplitude is the main cause of impaired visual scanning in Parkinson's disease patients.

The effect of electromagnetic field emitted by a mobile phone on the inhibitory control of saccades.

OBJECTIVE: To investigate whether exposure to a pulsed high-frequency electromagnetic field (pulsed EMF) emitted by a mobile phone has short-term effects on the inhibitory control of saccades. METHODS: A double-blind, counterbalanced crossover study design was employed. We assessed the performance of 10 normal subjects on antisaccade (AS) and cued saccade (CUED) tasks as well as two types of overlap saccade (OL1, OL2) task before and after 30 min of exposure to EMF emitted by a mobile phone or sham exposure. RESULTS: After EMF or sham exposure, we observed a slight but significant shortening of latency in the CUED and OL2 tasks. AS amplitude decreased as well as the saccade velocities in the AS, CUED, and OL1 tasks after exposure. These changes occurred regardless of whether exposure was real or sham. The frequencies of pro-saccades in the AS task, saccades to cue in the CUED task, and prematurely initiated saccades in the overlap (OL2) task did not change significantly after real or sham EMF exposure. CONCLUSIONS: Thirty minutes of mobile phone exposure has no significant short-term effect on the inhibitory control of saccades. SIGNIFICANCE: The cortical processing responsible for saccade inhibition is not affected by exposure to EMF emitted by a mobile phone.

Prominent cauda equina involvement in patients with chronic inflammatory demyelinating polyradiculoneuropathy.

In chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), it has not been well known which segment of the peripheral nerves, distal or proximal, is more often involved in electrophysiological examination. This study compares nerve conductions at proximal segments with those at distal segments in 11 patients with CIDP. To obtain cauda euqina conduciton time (CECT), compound muscle action potentials (CMAPs) were elicited by magnetic stimulation using a MATS coil from the abductor hallucis muscle. CECT was prolonged in 9 patients (81.8%), whereas the ankle-knee conduction was delayed in 4 (36.4%). The proximal segments are more frequently involved than the distal segments in this disorder.