Neurobiology of Epileptogenesis in the Temporal Lobe

Molecular and network changes that are proposed to underlie the development of spontaneous seizures are best understood in subjects with symptomatic aetiology for temporal lobe epilepsy (TLE). Symptomatic TLE typically develops in three phases (Fig. 1): b

  • PDF / 2,720,756 Bytes
  • 20 Pages / 482 x 692 pts Page_size
  • 16 Downloads / 177 Views

DOWNLOAD

REPORT


With 3 Figures Contents Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Reorganisation of Neuronal Circuitries Underlying Epileptogenesis in the Hippocampus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy........... ................. .................................... Neuronal Loss.......................................................... Neurogenesis.............. .............................................. Gliosis.............. ..................................................... Axonal Plasticity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Dendritic Plasticity ..................................................... Reorganisation of Neuronal Circuitries in the Amygdala. . . . . . . . . . . . . . . . Anatomy................................................................ Neuronal Loss.. ................. ....... ................................ Reorganisation of Neuronal Circuitries in the Entorinal Cortex. . .. . .. . . Anatomy................................................................ Neuronal Loss and Sprouting.......................................... Conclusions................................................................ Acknowledgements........................................................ References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . J. D. Pickard et al. (eds.), Advances and Technical Standards in Neurosurgery © Springer-Verlag/Wien 2002

4

5 5 7 8 8 9 10 11 11 13 14 14 15 15 16 16

4

L.

JUTILA

et al.

Introduction

Molecular and network changes that are proposed to underlie the development of spontaneous seizures are best understood in subjects with symptomatic aetiology for temporal lobe epilepsy (TLE). Symptomatic TLE typically develops in three phases (Fig. I): brain damage --+ latency phase or epileptogenesis --+ appearance of spontaneous seizures or epilepsy which can be easy to control or turn out to be drug-refractory over the time.

EPILEPTIC PROCESS

I NEURONAL DAMAGE I - neuronal damage (acute, delayed) - neurogenesis - plasticity (axonal, dendritic) - gliosis - molecular reorganization

LATENCY PERIOD (epileptogenesls)

Epileptogenic lesion: Head trauma Stroke Infection Status epilepticus

....... ... . ...........

TLE WITH GOOD SEIZURE CONTROL

.....

••••

EPILEPSY (spontaneous seizures)

.

.. .. -." :. ?. ............. •• . .-

-.....,.

..

DRUGREFRACTORY TLE

SECONDARY EPILEPTOGENESIS (mirror focus)

Fig. 1. Epileptic process includes three stages: brain injury (trauma, stroke, infection, status epilepticus) --+ latency period (epileptogenesis) --+ spontaneous seizures (epilepsy). Some data suggest the induction of secondary epileptogenesis and development of mirror focus in some patients even though this issue is still under a dispute [61]. Other altern