Which clinical and experimental data link temporal lobe epilepsy with depression?

The association of temporal lobe epilepsy with depression and other neuropsychiatric disorders has been known since the early beginnings of neurology and psychiatry. However, only recently have in vivo and ex vivo techniques such as Positron Emission Tomography, Magnetic Resonance Imaging and Magnetic Resonance Spectroscopy in combination with refined animal models and behavioral tests made it possible to identify an emerging pattern of common pathophysiological mechanisms. We now have growing evidence that in both disorders altered interaction of serotonergic and noradrenergic neurons with glutamatergic systems is associated with abnormal neuronal circuits and hyperexcitability. Neuronal hyperexcitability can possibly evoke seizure activity as well as disturbed emotions. Moreover, decreased synaptic levels of neurotransmitters and high glucocorticoid levels influence intracellular signaling pathways such as cAMP, causing disturbances of brain-derived and other neurotrophic factors. These may be associated with hippocampal atrophy seen on Magnetic Resonance Imaging and memory impairment as well as altered fear processing and transient hypertrophy of the amygdala. Positron Emission Tomography studies additionally suggest hypometabolism of glucose in temporal and frontal lobes. Last, but not least, in temporal lobe epilepsy and depression astrocytes play a role that reaches far beyond their involvement in hippocampal sclerosis and ultimately, therapeutic regulation of glial-neuronal interactions may be a target for future research. All these mechanisms are strongly intertwined and probably bidirectional such that the structural and functional alterations from one disease increase the risk for developing the other. This review provides an integrative update of the most relevant experimental and clinical data on temporal lobe epilepsy and its association with depression.     

X-Chromosomal recessive microcephaly with epilepsy,spastic tetraplegia and absent abdominal reflexes. New variety of “Paine syndrome”?

Summary Two brothers (7 years of age and 8 months respectively) are reported. They both suffered from a combination of severe microcephaly, spastic tetraplegia, clonic epileptic fits, absent abdominal cutaneous reflexes and severe mental retardation. This syndrome shows an X-chromosomal mode of inheritance. Dermatoglyphic patterns were characteristic. There was no change in aminoacids in CSF and the birth weight was high (4000g, in contrast to the cases described by Warkany et al.).

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Zusammenfassung Es wird über zwei Brüder (7 Jahre bzw. 8 Monate alt) berichtet. Beide litten an einer Kombination von schwerer Mikrocephalie, spastischer Tetraplegie, klonischen epileptischen Anf?llen, fehlenden abdominalen Hautreflexen und schwerem Schwachsinn. Es fand sich ein X-chromosomaler Erbgang. Die Dermatoglyphen zeigten einen charakteristischen Befund. Die Aminos?uren waren im Liquor cerebrospinalis nicht ver?ndert, und das Geburtsgewicht war hoch im Gegensatz zu den F?llen von Warkany et al.

     

Mitochondrial dysfunction and oxidative stress: a contributing link to acquired epilepsy?

Mitochondrial dysfunction and oxidative stress contribute to several neurologic disorders and have recently been implicated in acquired epilepsies such as temporal lobe epilepsy (TLE). Acquired epilepsy is typically initiated by a brain injury followed by a "latent period" whereby molecular, biochemical and other cellular alterations occur in the brain leading to chronic epilepsy. Mitochondrial dysfunction and oxidative stress are emerging as factors that not only occur acutely as a result of precipitating injuries such as status epilepticus (SE), but may also contribute to epileptogenesis and chronic epilepsy. Mitochondria are the primary site of reactive oxygen species (ROS) making them uniquely vulnerable to oxidative damage that may affect neuronal excitability and seizure susceptibility. This mini-review provides an overview of evidence suggesting the role of mitochondrial dysfunction and oxidative stress as acute consequences of injuries that are known to incite chronic epilepsy and their involvement in the chronic stages of acquired epilepsy.     

C.P.S.—Its Strengths and Weaknesses

The following, a supplement to the annual report of the Board of Trustees of California Physicians'' Service that was published in the March 1961 issue of California Medicine, was delivered at the 1961 Annual Session of the House of Delegates by Dr. John G. Morrison, chairman of the board.