After section of a peripheral nerve a series of processes occurs in the distal stump involving all of its constituents and leading to a breakdown of the axons and their myelin sheaths. This process was first studied by Waller (1852) and is generally known as " Wallerian degeneration ". The first part of Waller's law states that after cutting a nerve degeneration occurs in the distal stump and that degeneration is due to disconnection of the nerve trunk from its " trophic " centre, i.e., the nerve cell.Although it is almost 100 years since this law was conceived, the mechanism of degeneration is still not clear. In order to understand the process it is necessary to investigate the nature of this " trophic influence ". Only in this way can the question, Why does a nerve fibre degenerate ? be solved.Wallerian degeneration results after a certain time in failure of transmission of nerve impulses. The time at which this failure of transmission of nerve impulses can be recorded is apparently not a constant value. It is for instance known that both the metabolic rate and temperature influence the rate of degeneration (Muralt, 1945). Additional information about the factors affecting the rate of degeneration should help in understanding the mechanism of "Wallerian degeneration".It is necessary first to define clearly the criteria of degeneration used. After nerve section degeneration in the physiological sense appears primarily when the nerve fibre will no longer transmit impulses. As a physiological criterion we are therefore using the time at which failure of transmission of nerve impulses can be recorded. A much more complicated problem is the evaluation of the criteria of degeneration in the morphological sense. Muralt (1945) (Johnson, McNabb, and Rossiter, 1949). Valuable quantitative criteria are given by the changes of acetylcholine content in the degenerating nerve (Muralt and Schulthess, 1944), or of cholinesterase content in the degenerating nerve (Sawyer, 1946). Data about enzyme activity in a degenerating nerve will certainly acquire great importance.In this paper we have used physiological and morphological criteria in an attempt to study quantitatively the factors which affect degeneration of peripheral nerve fibres. Methods Rabbits, guinea-pigs, and rats were used in our experiments. In rabbits the peroneal, tibial and, in some experiments, the sural, nerves were used, whereas in rats and guinea-pigs the experiments were done with the whole sciatic nerve. The nerves were cut at an initial operation and, at different times after nerve section, the wounds were reopened and the nerves excised. The excised nerves were placed on platinum electrodes in a thermostat. The temperature of the chamber varied from 36 to 380 C. but was approximately constant for any

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INTRODUCTIONPreviods experiments ( I , 2) showed that flickering light, enforcing its rhythm to the whole EEG, influences in healthy man intea-vals of conditioned reflexes to time, in specific relation to flicker frequency, accordifig to the so-called rule of octaves. It was concluded from these experiments that cerebral rhythms, especially the a-rhythm, represent apparently the reference pacemaker, the "biological pendulum'' of time sense in man, for measuring time periods in the range of seconds and minutes.It is a well known fact from human pathology that alterations of cerebral rhythms occur in various kinds of epilepsy, particularly in seizures or even subclinical paroxysms characterized by slow EEG rhythms (not mentioning true paroxysms).The problem of this paper is whether in epileptics there is a correlation between the alterations of the time sense and those of the EEG rhythms. A preliminary communication already appeared (3). METHODSIn addition to our usual laboratory procedure on a 14-channelelectroencephalograph, the patient lying at rest, with several eye openings and a hyperventilation lasting 3 4 min, simultaneous testing of time sense was performed by the method of free production of intervals. According to the instruction given in advance the patient pressed the key at regular intervals during the whole procedure. The intervals had to last about 15-20 sec, their actual duration was chosen by the patient, who had to see only to their regularity. The pressing of the key was recorded simultaneously with the EEG.No special training was performed. Up to the present our work is based on 45 records from 41 patients, among them 32 epileptics (9 children), all treated with drug combinations. RBSULTSAlthough during the examination in most records (27) several prolonged intervals occurred from time to time, obviously as nonspecific reactions, e.g. to eye opening, to instruction about hyperventilation, etc., time intervals varied quite insignificantly, Epilepsia, 3 (1962) 323-328 Epilepsia, 3 (1962) 323-328

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