Tonic pupil caused by adenoid cystic carcinoma versus postradiation changes to the ciliary ganglion.

A tonic pupil, without other features of an oculomotor neuropathy, is due to a lesion in the ciliary ganglion or short ciliary nerves. Here, we present a case of a tonic pupil in a woman with radiation-treated adenoid cystic carcinoma of the nasopharynx with perineural spread and skull base involvement. This a rare case of a tonic pupil caused by direct invasion of the ciliary ganglion or postradiation effects.

Spontaneous spinal epidural abscess in patients 50 years of age and older: a 15-year institutional perspective and review of the literature: clinical article.

Object: A spinal epidural abscess (SEA) is a rare but severe infection requiring prompt recognition and management. The incidence of SEA has doubled in the past decade, owing to an aging population and to increased use of spinal instrumentation and vascular access. The optimal management of SEAs in patients 50 years of age and older remains a matter of considerable debate.

Evidence for astrocytes as a potential source of the glutamate excess in temporal lobe epilepsy.

Increased extracellular brain glutamate has been implicated in the pathophysiology of human refractory temporal lobe epilepsy (TLE), but the cause of the excessive glutamate is unknown. Prior studies by us and others have shown that the glutamate degrading enzyme glutamine synthetase (GS) is deficient in astrocytes in the epileptogenic hippocampal formation in a subset of patients with TLE. We have postulated that the loss of GS in TLE leads to increased glutamate in astrocytes with elevated concentrations of extracellular glutamate and recurrent seizures as the ultimate end-points.

Altered expression of brain monocarboxylate transporter 1 in models of temporal lobe epilepsy.

Monocarboxylate transporter 1 (MCT1) facilitates the transport of monocarboxylate fuels (lactate, pyruvate and ketone bodies) and acidic drugs, such as valproic acid, across cell membranes. We recently reported that MCT1 is deficient on microvessels in the epileptogenic hippocampal formation in patients with medication-refractory temporal lobe epilepsy (TLE). To further define the role of MCT1 in the pathophysiology of TLE, we used immunohistochemistry and stereological analysis to localize and quantify the transporter in the hippocampal formation in three novel and highly relevant rat models of TLE and in nonepileptic control animals.