Abstract
Epilepsy is a chronic neurological disorder which is manifested at some times and masked at others. Sleep-waking state physiology is one of the most well documented factoKs affecting the clinical expression or suppression of human epilepsy1,2. Specifically, non-rapid-eye-movement (NREM) sleep and the gradual process of awakening from NREM sleep are the most vulnerable periods for seizures, especially convulsions. Moreover, the type of epilepsy is an important consideration in the timing of convulsions. Temporal lobe epilepsy with secondary generalized convulsions is the most common pure sleep epilepsy, with convulsions occurring in NREM or the transition from NREM to rapid-eye-movement (REM) sleep in nearly 60% of the patients2. In contrast, over 90% of patients with primary generalizgd, “petit mal” epilepsy display convulsions exclusively after awakening2. Finally, type of epilepsy is not a factor in the suppression of seizures during REM sleep. REM sleep is the most anti-epileptic state in the sleep-wake cycle for all generalized electrographic (EEG) and clinical seizures1.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
M.N. Shouse, Seizures and epilepsy during sleep, in: “Principles and Practice of Sleep Medicine,” M.H. Kryger, T. Roth and W.C. Dement, eds., Saunders, Philadelphia, 1989.
D. Janz, The grand mal epilepsies and the sleeping-waking cycle, Epilepsia 3: 69 (1962).
J.A. Wada and S. Sato, Generalized convulsive seizures induced by daily stimulation of the amygdala in cat: correlative electroencephalographic and behavioral features, Neurology 24: 565 (1974).
P. Gloor, Generalized epilepsy with spike-wave discharge: A reinterpretation of its electrographic and clinical manifestations, Epilepsia 20: 571 (1977).
S.L. Moshe, E.F. Sperber and B.J. Albala, Kindling as a model of epilepsy in developing animals, in: “Kindling and Synaptic Plasticity: The legacy of Graham Goddard,” F. Morrell, ed., Dirkhauser, Boston, in press.
M.N. Shouse, Differences between two feline epilepsy models in sleep and waking state disorders, state dependency of seizures and seizure susceptibility: Amygdala kindling interferes with systemic penicillin epilepsy, Epilepsia 28: 399 (1987).
W.J. West, On a peculiar form of infantile convulsion, Lancet 1: 724 (1841).
M. Steriade, Ascending control of motor cortex responsiveness, Electroenceph. Clin. Neurophysiol. 26: 25 (1969).
M. Steriade, Ascending control of thalamic and cortical responsiveness, Int. Rev. Neurobiol. 12: 87 (1970).
M. Shouse, Thalamocortical mechanisms of state-dependent seizures during amygdala kindling and systemic penicillin epilepsy in cats, Brain Res. 425: 198 (1987).
M. Shouse, State disorders and state dependent seizures in amygdala kindled cats, Exp. Neurol. 92: 601 (1986).
J. M. Siegel, Brainstem mechanisms generating REM sleep, in: “Principles and Practice of Sleep Medicine,” M.H. Kryger, T. Roth and W.C. Dement, eds., Saunders, Philadelphia, 1989.
J.A Wada and M. Sato. Effects of unilateral lesions in the midbrain reticular formation on kindled amygdaloid convulsions in cats. Epilepsia 16: 693 (1975).
M.N. Shouse and M.B. Sterman. Sleep pathology in experimental epilepsy, in: “Sleep and Epilepsy,” M.B. Sterman, M.N. Shouse and P. Passouant, eds., Academic Press, New York, 1982.
M.N. Shouse and M.B. Sterman, Changes in seizure susceptibility, sleep time and sleep spindles following thalamic and cerebellar lesions, Electroenceph. Clin. Neurophysiol. 46: 1 (1979).
S. Mullan, G. Valiati, J. Karasick and M. Mailias, Thalamic lesions for the control of epilepsy, Arch. Neurol. 16: 277 (1967).
W.R Hess, Diencephalon-Autonomic and Extrapyramidal Functions, “Grune and Stratton, New York, 1954. Consciousness Symposium” J.F. Freshaye, ed., Blackwell, Oxford, 1954.
R. S. Szymusiak, T. Iriye and D. J. McGinty, Sleep-waking discharge of neurons in the posterior lateral hypothalamic area of cats. Brain Res. Bull. In Press, 1989.
C.B. Saper, Organization of cerebral cortical afferent systems in the rat. II. Hypothalamocortical projections, J. Comp. Neurol. 237: 21, (1985).
M.N. Shouse, J.M. Siegel, M.F. Wu, R.S. Szymusiak and A.R. Morrison. Mechanisms of seizure suppression during rapid-eye-movement (REM) sleep in cats. Brain Res., In Press, 1989.
C.H. Vanderwolf and T.E. Robinson, Reticulocortical activity and behavior: A critique of the arousal theory and a new synthesis (with commentaries), Behay. Brain Sci. 4: 459 (1981).
M. Jouvet and F. Delorme, Locus coeruleus et sommeil paradoxique, C.R. Soc. Biol. 159: 4790 (1988).
J.C. Hendricks, A. R. Morrison and G. L. Mann, Different behaviors during paradoxical sleep without atonia depend on pontine lesions site. Brain Res. 239: 81 (1982).
M. E. Corcoran, J.A Wada, A. Wake, and H Urstad. Research note: Failure of atropine to retard amygdala kindling. Exp. Neurobiol. 51: 271 (1976).
B.E Jones and H. H. Webster. Neurotoxic lesions of the dorsolateral pontomesencephalic tegmentum-Cholinergic cell area in the cat. I. Effect upon the cholinergic innervation of the brain, Brain Res., 458: 285 (1989)
S.R. Vincent and P. B. Reiner, The immunohistochemical localization of choline acetyltransferase in the cat brain, Brain Res. Bull. 18: 371 (1987).
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1990 Plenum Press, New York
About this chapter
Cite this chapter
Shouse, M.N. et al. (1990). Basic Mechanisms Underlying Seizure-Prone and Seizure-Resistant Sleep and Awakening States in Feline Kindled and Penicillin Epilepsy. In: Wada, J.A. (eds) Kindling 4. Advances in Behavioral Biology, vol 37. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5796-4_23
Download citation
DOI: https://doi.org/10.1007/978-1-4684-5796-4_23
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4684-5798-8
Online ISBN: 978-1-4684-5796-4
eBook Packages: Springer Book Archive