A video-polygraphic analysis of the cataplectic attack.

OBJECTIVES AND METHODS: To perform a video-polygraphic analysis of 11 cataplectic attacks in a 39-year-old narcoleptic patient, correlating clinical manifestations with polygraphic findings. Polygraphic recordings monitored EEG, EMG activity from several cranial, trunk, upper and lower limbs muscles, eye movements, EKG, thoracic respiration. RESULTS: Eleven attacks were recorded, all of them lasting less than 1 min and ending with the fall of the patient to the ground. We identified, based on the video-polygraphic analysis of the episodes, 3 phases: initial phase, characterized essentially by arrest of eye movements and phasic, massive, inhibitory muscular events; falling phase, characterized by a rhythmic pattern of suppressions and enhancements of muscular activity, leading to the fall; atonic phase, characterized by complete muscle atonia. Six episodes out of 11 were associated with bradycardia, that was maximal during the atonic phase. CONCLUSIONS: Analysis of the muscular phenomena that characterize cataplectic attacks in a standing patient suggests that the cataplectic fall occurs with a pattern that might result from the interaction between neuronal networks mediating muscular atonia of REM sleep and neural structures subserving postural control.

Effects of chronic levodopa and pergolide treatment on cortical excitability in patients with Parkinson's disease: a transcranial magnetic stimulation study.

OBJECTIVES: Transcranial magnetic stimulation was used to assess the effects of chronic levodopa and pergolide treatment on motor cortex excitability in Parkinson disease (PD). METHODS: Motor thresholds, intracortical inhibition and facilitation were studied at baseline and after 6 and 12 months of therapy in 10 PD patients and compared to 7 age-matched controls. RESULTS: At baseline, there was significantly less intracortical inhibition with only a slight reduction of intracortical facilitation in PD as compared to controls. Relative to pretreatment condition, levodopa restored intracortical inhibition for 12 months while pergolide did not. Intracortical facilitation was always within the normal range. Motor thresholds were unchanged in both groups of patients over 12 months. Clinically, levodopa and pergolide improved motor Unified Parkinson's disease rating scale (UPDRS) scores at 6 months but only levodopa maintained benefit at 12 months as compared to baseline. CONCLUSIONS: Levodopa and pergolide differentially affected cortical inhibitory circuits at 12 months. The progressive deterioration of restored intracortical inhibition with pergolide may be due to the development of tolerance and down-regulation of dopamine receptors.

Facilitation of rhythmic events in progressive myoclonus epilepsy: a transcranial magnetic stimulation study.

Twelve subjects with progressive myoclonus epilepsy (PME) were studied with transcranial magnetic stimulation (TMS), using single and paired magnetic stimuli at different interstimulus intervals (ISIs), and polygraphic recording. Motor threshold (T) and silent period (SP) were normal. Paired TMS showed a loss of inhibition at 100-150 ms ISI and a marked facilitation at 50 ms ISI of conditioned motor evoked potential (MEP). Polygraphic analysis showed 20 Hz oscillatory activity over the sensorimotor area coupled to contralateral myoclonic jerks. These findings suggest a condition of increased supraspinal excitability and support the evidence of a cortical rhythm in the range of 20 Hz. No direct evidence exists that these findings are mediated by the same intracortical pathway. Furthermore, the normal SP and T suggest that the abnormal excitability is not a constant feature but is evident during rhythmic events.

Motor evoked responses to paired cortical magnetic stimulation in Parkinson's disease.

We evaluated cortical excitability in patients with Parkinson's disease (PD) using paired magnetic stimulation. This recent technique allows to study the cortical inhibition after motor evoked potential (MEP) and its modulation at different intensities of stimulation and interstimulus intervals (ISIs). At low stimulus intensity and at ISIs of 40-75 ms we observed, in PD patients, a greater test MEP inhibition, which might be due to a lower facilitatory effect of conditioning MEP on the motor cortex. At high stimulus intensity, in PD patients, a consistent inhibition of test MEP persisted and, at ISIs of 75-150 ms, it did not reach the amplitude of conditioning MEP as in normal subjects. Some clinical and neurophysiological features, like a silent period of shorter duration, demonstrated in PD patients a decrease of the inhibitory input to the motor cortex. On the contrary, the persistence of test-MEP inhibition at high stimulus intensity could also suggest a prevalence of inhibitory activity when an effective and phasic activation of the corticospinal system is required.