PMID- 11233674

OWN - NLM
STAT- MEDLINE
DCOM- 20010531
LR - 20131121
IS - 0300-9009 (Print)
IS - 0300-9009 (Linking)
VI - 100
IP - 4
DP - 2000 Dec
TI - Pathophysiology of epilepsy.
PG - 201-13
AB - This work reviews the current knowledge on epileptogenesis and
pathophysiology of
epilepsy. Recently, gene defects underlying four monogenic epilepsies
(generalized
epilepsy with febrile seizures, autosomal dominant nocturnal frontal lobe
epilepsy,
benign familial neonatal convulsions and episodic ataxia type 1 with partial
seizures) have been identified, shedding new light on the pathophysiology of
epilepsy as these diseases are caused by ion channel mutations. Although
epileptic
syndromes differ pathophysiologically, common ictogenesis-related
characteristics as
increased neuronal excitability and synchronicity are shared as well as
mechanisms
involved in interictal-ictal transition. Emerging insights point to
alterations of
synaptic functions and intrinsic properties of neurons as common mechanisms
underlying hyperexcitability. This work also reviews the neurochemical
mechanisms of
epilepsy. An imbalance between glutamate and gamma-aminobutyric acid
neurotransmitter systems can lead to hyperexcitability but catecholaminergic
neurotransmitter systems and opioid peptides were shown to play a role in
epileptogenesis as well. An overview of currently available anti-epileptic
drugs and
their presumed mechanisms of action is given as an illustration of the
neurochemistry of epileptogenesis. Most anti-epileptic drugs exert their
anti-epileptic properties through only a few neurochemical mechanisms that
are
meanwhile basic pathophysiological mechanisms thought to cause seizures.
FAU - Engelborghs, S
AU - Engelborghs S
AD - Department of Neurology, A.Z. Middelheim, Antwerp, Belgium.
FAU - D'Hooge, R
AU - D'Hooge R
FAU - De Deyn, P P
AU - De Deyn PP
LA - eng
PT - Journal Article
PT - Research Support, Non-U.S. Gov't
PT - Review
PL - Italy
TA - Acta Neurol Belg
JT - Acta neurologica Belgica
JID - 0247035
RN - 0 (Anticonvulsants)
RN - 0 (Catecholamines)
RN - 0 (Ion Channels)
RN - 0 (Receptors, AMPA)
RN - 0 (Receptors, GABA)
RN - 0 (Receptors, Glutamate)
RN - 0 (glutamate receptor ionotropic, AMPA 3)
RN - 3KX376GY7L (Glutamic Acid)
RN - 56-12-2 (gamma-Aminobutyric Acid)
RN - 9NEZ333N27 (Sodium)
RN - RWP5GA015D (Potassium)
RN - SY7Q814VUP (Calcium)
SB - IM
MH - Adult
MH - Animals
MH - Anticonvulsants/pharmacology
MH - Autoimmune Diseases/immunology/physiopathology
MH - Calcium/physiology
MH - Catecholamines/physiology
MH - Cell Movement
MH - Child
MH - Child, Preschool
MH - Electroencephalography
MH - Encephalitis/immunology/physiopathology
MH - Epilepsies, Partial/etiology/physiopathology
MH - Epilepsy/classification/drug therapy/etiology/genetics/*physiopathology
MH - Epilepsy, Temporal Lobe/physiopathology
MH - Genes, Dominant
MH - Genetic Predisposition to Disease
MH - Glutamic Acid/physiology
MH - Hamartoma/complications
MH - Humans
MH - Infant
MH - Infant, Newborn
MH - Ion Channels/drug effects/genetics/physiology
MH - Kindling, Neurologic
MH - Membrane Potentials
MH - Neurons/pathology/physiology
MH - Potassium/physiology
MH - Rats
MH - Receptors, AMPA/immunology
MH - Receptors, GABA/drug effects/physiology
MH - Receptors, Glutamate/drug effects
MH - Sodium/physiology
MH - Spasms, Infantile/genetics/physiopathology
MH - Syndrome
MH - Thalamic Diseases/complications
MH - gamma-Aminobutyric Acid/physiology
RF - 88
EDAT- 2001/03/10 10:00
MHDA- 2001/06/02 10:01
CRDT- 2001/03/10 10:00
PHST- 2001/03/10 10:00 [pubmed]
PHST- 2001/06/02 10:01 [medline]
PHST- 2001/03/10 10:00 [entrez]
PST - ppublish
SO - Acta Neurol Belg. 2000 Dec;100(4):201-13.