pathophysiology of seizure

SEI UREZ

TJIARN[MD]

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY OF SEIZURE

EXCESSIVELY SYCHRONOUS AND SUSTAINED DISCHARGE OF A GROUP OF NEURONS

Engelborghs, S., D’ Hooge, R., & De Deyn, P. P. (2000). Pathophysiology of epilepsy. University of Antwerp. Antwerp, Belgium


RAPID AND CONTINUOUS FIRING OF ACTION POTENTIALS FROM A SMALL GROUP OF ABNORMAL ,

DEPOLARIZED, NEURONS

Fischer, J. (1998). Drug Therapy of Epilepsy. University of Illinois, Chicago.


MANIFESTATIONS VARY, DEPENDING ON THE

EPILEPTIC SEIZURE FOCI

Berne, R. M., Levy, M. N., Koeppen, B. M., & Stanton, B. A. (2004). Physiology. (5th ed.). United States of America, Elsevier.

RECRUITMENT OF ADJACENT NEURONS (NEURONS WITH WHICH THEY FORM CONNECTIONS WITH)


PERSISTENT INCREASE IN NEURONAL ACTIVITY



PEDIATRICS IN REVIEW October 1, 1998 vol. 19 no. 10 342-351 doi: 10.1542/pir.19-10-342


ASSOCIATION WITH TRAUMA, OXYGEN DEPRIVATION, TUMORS, INFECTION,

METABOLIC DERANGEMENTS


None found in half of epileptic patients


DISORDERS OF NEURONAL MIGRATION LINKED WITH GENETIC OR INTRAUTERINE

CAUSES


Agyria or PachygyriaNeuronal Heterotopia


DISORDERS OF NEURONAL MIGRATION LINKED WITH GENETIC OR INTRAUTERINE

CAUSES


= Epileptogenic Foci (Diffuse Hyperexcitability) (Chevassus au Louis et al., 1999)

Imaging features of tuberous sclerosis. Axial T2 -weighted MRI (left) and contrast-enhanced axial T1 -weighted MRI (right). The image on the left shows multiple focal areas of broadened gyri, blurring of the gray-white junction and increased signal in the subcortical white matter typical of cortical tubers. The image on the right shows multiple subependymal nodules (arrows) consistent with subependymal hamartoma and a large enhancing lesion at the right foramen of Monro consistent with a giant cell astrocytoma. MRI, magnetic resonance imaging


KINDLING PHENOMENON


REPETITIVE SUBCONVULSIVE STIMULATION

ROLE IN EPILEPTIC EPISODES POST BRAIN INJURIES

KINDLING PHENOMENON


* CONCEPT: SPARK > FLAME > BONFIRE

* STIMULUS INDUCED SYNCHRONOUS ADs


NEUROCHEMICAL MECHANISMS


GABA HYPOTHESIS = reduced GABAergic inhibition results to epileptic episodes (vv.)

GABA HYPOTHESIS

Decreased GABA releaseDesensitized receptors

http://www.medscape.org/viewarticle/570744_3

GABA HYPOTHESIS


* EVIDENCE OF DECREASING AMPLITUDE OF INHIBITORY POST SYNAPTIC POTENTIALS (IPSPs) WITH REPETITIVE ACTIVATION OF

CORTICAL UNITSDecreased GABA releaseDesensitized receptors

GABA HYPOTHESIS


* INHIBITORY EFFECTS OF GUANIDO COMPOUNDS AND PENICILLIN (etc.) ON

GABAergic TRANSMISSION

*** uremic complications = ANTAGONIST




GLUTAMATE = activation of ionotropic and metabotropic postsynaptic glutamate

receptors is proconvulsant

GLUTAMATE


* INCREASED SENSITIVITY OF NMDA receptors

*** uremic complications = AGONISt

* ENHANCED ENTRY OF Ca2+ INTO NEURONS

GLUTAMATE

http://www.medscape.org/viewarticle/570744_3




CATECHOLAMINESDopamine vs Norepinephrine in epileptic rats and patients


ROLE OF SUBSTANTIA NIGRA

MARKED INCREASE IN METABOLIC ACTIVITY = COMMON FEATURE AMONG GENERALIZED

TYPES OF Sz


ICTOGENESISEXCITABILITY, A KEY FEATURE

- CAUSE: ALTERED MEMBRANE PROPERTY- SUBOPTIMAL REGULATION OF ENVIRONMENT, ECF IONS- ENHANCEMENT OF EXCITABILITY


ICTOGENESIS

EXCITABILITY FROM INDIVIDUAL NEURONSEXCITABILITY FROM NEURONAL MICROENVIRONMENTEPILEPTIC CELL PROLIFERATION



INTERICTAL-ICTAL TRANSITION


MECHANISMS THAT CAUSE SIGNAL AMPLIFICATION, SYNCHRONICITY, AND

SPREAD OF ACTIVITY




ALTERATIONS IN IONIC MICROENVIRONMENTINCREASED POTASSIUM = EXCITABILITY; DECREASED EXTRACELLULAR CALCIUM




DECREASED SIZE OF EXTRACELLULAR SPACEPROMOTING EHAPTIC INTERACTIONS




EHAPTIC INTERACTIONS* CURRENTS FROM EXCITED NEURONS CAUSE

ADJACENT NEURONS TO SHARE THE EXCITEMENT




FAILURE OF ION TRANSPORTNa-K pump : regulatory role in neuronal excitability

Cl-K co-transport : Cl Concentration; GABA




PRESYNAPTIC TERMINAL BURSTING• Amount of NT release = depolarization• Synchronization due to abnormal Action Potential bursts

at axonal arborizations of thalamocortical relay cells




SYNAPTIC MECHANISM: DECREASED EFFECTIVENESS OF INHIBITORY SYNAPTIC

MECHANISMS / FACILITATION OF EXCITATORY MECHANISMS


MANIFESTATIONS VARY, DEPENDING ON THE

EPILEPTIC SEIZURE FOCI


pathophysiology of seizure

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