Subject(s)
Gait Disorders, Neurologic/physiopathology , Gait Disorders, Neurologic/therapy , Muscle Weakness/physiopathology , Muscle Weakness/therapy , Muscular Diseases/physiopathology , Muscular Diseases/therapy , Myasthenic Syndromes, Congenital/physiopathology , Myasthenic Syndromes, Congenital/therapy , Age Distribution , Aged , Disease Progression , Ephedrine/pharmacology , Ephedrine/therapeutic use , Extremities/physiopathology , Female , Gait Disorders, Neurologic/etiology , Genetic Predisposition to Disease , Horner Syndrome/genetics , Humans , Muscle Proteins/genetics , Muscle Weakness/etiology , Muscle, Skeletal/physiopathology , Muscular Diseases/genetics , Myasthenic Syndromes, Congenital/diagnosis , Neuromuscular Junction/geneticsABSTRACT
PURPOSE: To evaluate the use of EEG responses to transcranial magnetic stimulation (TMS-EEG responses) as a noninvasive tool for the diagnosis of focal epilepsy. METHODS: Fifteen patients and 15 healthy subjects were studied. TMS at an intensity set at resting corticomotor threshold were delivered at the standard EEG electrode positions. For each position, EEG responses to TMS were evaluated before and after averaging EEG recordings synchronized with the TMS pulse. RESULTS: Two types of TMS-EEG responses were seen: (A) early responses: consisting of a single slow wave seen after the TMS pulse; and (B) late TMS-EEG responses, which were subclassified into (b.1) delayed responses: waveforms resembling interictal epileptiform discharges induced by TMS; or (b.2) repetitive responses: onset of a new rhythym induced by TMS. Early responses were observed in patients and healthy subjects when stimulating at various sites and were considered normal responses to TMS. Late TMS-EEG responses were not seen in healthy subjects, whereas they were seen in 11 of the 15 epileptic patients. Late TMS-EEG responses occurred when stimulating the epileptogenic side in eight out of the nine patients who had lateralized late TMS-EEG responses. The combined use of late TMS-EEG responses and interictal scalp EEG would have suggested the diagnosis of focal epilepsy in all patients, despite the absence of late TMS-EEG responses in four patients and the presence of normal interictal scalp EEG in three. CONCLUSIONS: TMS-EEG responses can identify epileptogenic cortex and may substantially improve the diagnosis of focal epilepsy, particularly, if combined with standard EEG studies.
Subject(s)
Brain Mapping/methods , Cerebral Cortex/physiopathology , Electroencephalography/statistics & numerical data , Epilepsies, Partial/diagnosis , Epilepsies, Partial/physiopathology , Transcranial Magnetic Stimulation/statistics & numerical data , Adolescent , Adult , Control Groups , Electrodes, Implanted , Electroencephalography/methods , Female , Frontal Lobe/physiopathology , Functional Laterality/physiology , Humans , Male , Middle Aged , Monitoring, Physiologic/methods , Monitoring, Physiologic/statistics & numerical data , Prefrontal Cortex/physiopathology , Preoperative Care/methods , Transcranial Magnetic Stimulation/methodsABSTRACT
Recent studies have demonstrated acquired muscle inexcitability in critical illness myopathy (CIM) and have used direct muscle stimulation (DMS) techniques to distinguish neuropathy from myopathy as a cause of weakness in the critically ill. The mechanisms underlying weakness in CIM are incompletely understood and DMS is only semiquantitative. We report results from a series of 32 patients with CIM and demonstrate significant slowing of muscle-fiber conduction velocity (MFCV) and muscle-fiber conduction block during the acute phase of CIM, which correlates with prolonged compound muscle action potential (CMAP) duration, clinical severity, and course. We also used a paired stimulation technique to explore the excitability of individual muscle fibers in vivo. We demonstrate altered muscle-fiber excitability in CIM patients. Serial studies help define the course of these pathophysiological changes. Parallels are made between CIM and hypokalemic periodic paralysis. Our findings provide further evidence for muscle membrane dysfunction being the principal underlying abnormality in CIM.
