Joseph B. Green

An electromyographic study of mirror movements

ASSOCIATED MOVEMENTS, or synkineses, may occur normally in young children and abnormally in a variety of psychiatric and neurologic disorders. The latter include hemiplegia, athetosis, and the Klippel-Feil syndrome.1-3 Synkineses between the upper extremities appear to be of two types. Active movement of one arm may be accompanied by reflex posturing of the opposite arm, often with participation of the contralateral leg, neck, and trunk. This type of associated movement resembles the syncinbsies globales or spasmodiques described by Mane and Foix4 and the tonicdiffuse synkineses of DeAjuriaguerra and Stambak.5 Such tonic or postural reflexes were well described by Walshe in hemiplegics.1 He noted that some degree of spasticity was required for them to be present. However, contralateral posturing involving proximal niusculature may normally persist into aduIt life and may be manifest during strenuous effort.6 The second type of contralateral synkinesis consists of imitative movements of one limb when its opposite carries out rapid movements. This mirroring is evident in grasping, adduction of the fingers, and in pronation-supination of the forearm. These are the syncinbsies dimitation of Marie and Foix,4 also called tonickinetic by DeAjuriaguerra and Stambak.5 Mirror or imitative movements are gradually lost in the course of development and are rarely present in the normal individual over 14 years of age.7 They may persist in the neurologically handicapped and in some individuals as a familial trait.a.9 In hemiplegia, particularly, the affected side may mirror the movements of the sound limb, and at times the paretic extremity can be moved only if accompanied by movement of the normal limb. The physiological basis of mirror movements is not well understood. Meyer, noting their occurrence in a variety of spatially separated lesions of the nervous system, postulated a release phenomenon resulting from a destructive or developmental lesion somewhere in the course of long neural pathways.9 These pathways, he thought, though closely related anatomically, were not identical with the pyramidal tracts because so-called pyramidal signs, while frequent, were not invariably present in cases of synkinesis. Since disease or defect of the pyramidal pathways is often associated with mirror movements, it seems reasonable to suppose that these discrete distal movements may be based anatomically on nonpyramidal pathways utilized in the course of voluntary motor function. In the investigation to be reported, clinical observation of synkinetic movements was supplemented by electromyography. The temporal relationships between muscular activity on the active and “imitative” sides and the spatial distributions involved are better defined by this method. Such measurements have neurophysiologic implications concerning movements which will be discussed in the light of new information about descending brainstem pathways.

Cerebrospinal Fluid Glutamic Oxalacetic Transaminase Activity in Neurologic Disease

THE ESTIMATION of glutamic oxalacetic transaminase* activity in the serum has become a valuable aid in the diagnosis of diseases involving necrosis of tissue especially rich in this enzyme.ls2 It is thought that the cells of such tissue, when disrupted, release transaminase (and other enzymes) into the blood. Whatever the mechanism of liberation, this increase over the normal serum level can be readily determined. The magnitude of transaminase activity has been shown to correlate with the amount of cellular necr~sis .~ This enzymatic determination has found its greatest applicability in the diagnosis and prognosis of myocardial infar~t ion.~.~ It has been useful in the evaluation of liver disease, particularly in the early stages of hepatitis.6 Both the heart and liver are organs containing abundant transaminase. The brain ranks with both of these in its transaminase content.? Therefore, it was considered probable that necrosis of brain tissue, as exemplified by infarction, would release significant quantities of intracellular enzymes, among these transaminase, into the serum and the cerebrospinal fluid. This hypothesis has been tested in preliminary clinical studies a t this hospital,R as well as in an experimental project by Wakim and Fleisher.@ Cerebral infarctions resulted in significant increases of transaminase activity in the spinal fluid clinically and experimentally. Wakim and Fleisher found smaller and inconstant elevations of serum activity in dogs, while patients examined at this institution failed to show serum changes. The purpose of this paper is to extend and amplify these observations in clinical cerebral infarctions and, by surveying other neurologic diseases, to evaluate the role of the estimation of spinal fluid transaminase activity in differential diagnosis. This is a report of significant transaminase data obtained from some 400 cerebrospinal fluid analyses.

Phenytoin prolongs far‐field somatosensory and auditory evoked potential interpeak latencies

Far-field auditory and somatosensory evoked potentials were recorded in 163 epileptic patients and 31 normal controls. Analysis of variance revealed significant effects on interpeak latencies of age, sex, and phenytoin levels in three ranges: subtherapeutic, therapeutic, and toxic. Toxic levels of phenytoin may affect peripheral and central axons, slowing conduction. Therapeutic levels of phenytoin may prolong far-field interpeak latencies by acting on synapses.

Association of behavior disorder with an electroencephalographic focus in children without seizures.

THE PURPOSE of this communication is to report a series of 10 children who had abnormal electroencephalograms characteristic of the interictal epileptic state bu t who had not had any recognizable type of epileptic seizure a t the time of initial study. These 10 were selected from a group of one hundred and thirty children, all of whom had been referred for study and electroencephalograms because of behavior disorder or suspected mental retardation. In many cases, the referral was initiated by a school psychologist after testing suggested a n “organic” mental disorder. All electroencephalograms were performed with a standard Grass 8-channel machine. No sedation or activation technics other than spontaneous sleep were employed. The children were followed for periods u p to two years in the Pediatric Neurology Clinic of this hospital. Anticonvulsant drugs were prescribed for all children, and clinical observations of the effect of this therapy were recorded. T h e children, because of similarities in clinical features, were divisible into 3 groups, and their case histories, which follow, will be so arranged.

Relation of respiratory water loss to coughing after exercise

Exercise has been shown to result in bronchoconstriction, the extent of which is related to respiratory heat loss. Some normal subjects report coughing after exercise, and to determine whether this might also be related to respiratory heat loss, we monitored cough frequency after hyperpnea with air of varying temperature and water content in seven such subjects. Hyperpnea with fully saturated air at 37 degrees failed to provoke coughing and was not associated with heat loss or water loss. Hyperpnea with dry air at 37 degrees C resulted in more water loss (P less than 0.0005), less heat loss (P less than 0.01), and more coughing (P less than 0.001) than hyperpnea with subfreezing air. Hyperpnea with ambient air was associated with a similar cough frequency and water loss but with less heat loss (P less than 0.001) than hyperpnea with subfreezing air. There was a direct relation between cough frequency and respiratory water loss but no consistent relation between cough frequency and respiratory heat loss. This study indicates that coughing after hyperpnea with poorly conditioned air is related to the overall rate of respiratory water loss. Since strenuous exercise is associated with marked hyperpnea, coughing after exercise may also result from respiratory water loss.

The simultaneous determination of multiple anticonvulsant drug levels by gas-liquid chromatography. Method and clinical application.

The clinical usefulness of blood level determinations of antiepileptic drugs has been emphasized in a recent review by Rose et al.’ The technique of gas-liquid chromatography (GLC) has made possible rapid and accurate determination of serum levels without interference between drugs as in older ultraviolet methods.’-’ By a modification of the GLC method described by MacGee,6 it has been possible to determine simultaneously several anticonvulsant drug levels and to assay quantitatively as many as ten different compounds from a single extraction of serum. Results are available promptly, often the same day, so that drug dosage may be adjusted at the time the patient is seen or shortly afterward. Questions of intoxication are resolved promptly. The control of seizures is expedited by more rapidly reaching the therapeutic range of a drug, and the risk of overdosage is reduced. This report will attempt to indicate how experience with over 1,000 determinations of serum anticonvulsant levels has favorably influenced the management of epilepsy. A brief description of the GLC method used will be presented; for further details MacGee’s original paper should be consulted.

Return of EEG activity after electrocerebral silence: two case reports

Two cases, both children, are described, in which there was a return of the electroencephalogram after a period of electrocerebral silence. One child survived for six weeks. Electroencephalographic technique and instrumentation adequately excluded non-cerebral potentials as a source of confusion in the second case. Hypothermia and drug overdosage, known to reversibly depress the electroencephalogram, were not present in either case. The return of EEG activity was associated with improvement in neurological status. It is concluded that the EEG should always be repeated after electrocerebral silence before the determination of cerebral death, and that the applicability of adult criteria of brain death to children is questionable.

The middle latency auditory evoked potential may be abnormal in dementia

The P1 potential (50 msec) of the middle latency auditory evoked potential was lacking in 12 of 31 (39%) patients with probable Alzheimers disease and seven of 12 (58%) demented patients with Parkinsons disease. Component P1 was not present in one normal control subject and one nondemented Parkinsons disease patient. Clinical and experimental evidence suggests that abnormalities of P1 in dementia may be due to cholinergic dysfunction.

Seizures on closing the eyes. Electroencephalographic studies.

EPILEPTIC SEIZURES provoked by closing the eyes have been called an “exceptional type of visual reflex epilepsy” by Gastaut and Tassinari, who described two cases.’ A previously reported study* of self-induced epilepsy suggested an important role of voluntary eye closure in triggering paroxysms of spikes and slow waves on the electroencephalogram. One patient could induce seizures by closing his eyes, even in total darkness. Experience with additional cases has confirmed these observations and has indicated a complex relationship between eye closure and photosensitivity in the production of seizures.

The P1 component of the middle latency auditory potential may differentiate a brainstem subgroup of Alzheimer disease.

The P1 component of the middle latency auditory evoked potential (MLAEP) was found to be absent in 47.5% of 101 patients with Alzheimer disease (AD). Lack of a P1 component recently has been associated with a more rapid decline in cognitive performance. The blink reflex (BR) was tested in 36 patients with probable AD and 17 elderly control subjects. All subjects also underwent P1 recording. Patients lacking a P1 potential showed a significant increase in latency of the contralateral R2 response of the BR. The P1 component and the R2 response may differentiate a subgroup of AD patients with involvement of the brainstem, especially the reticular formation.