Hormonal therapy for epilepsy.

In 2011, there are greater than 20 antiepileptic medications available. These medications work by modulating neuronal excitability. Reproductive hormones have been found to have a role in the pathogenesis and treatment of seizures by also altering neuronal excitability, especially in women with catamenial epilepsy.

Acute anti-emetic withdrawal associated with a hemorrhagic cerebellar arteriovenous malformation.

We present a 67-year-old right-handed male with a brachium pontis arteriovenous malformation on continuous anti-emetic therapy who demonstrated acute withdrawal symptoms after the abrupt discontinuation of ondansetron, a 5-HT(3) receptor antagonist. Removal of anti-emetic therapy led to the development of extreme flushing and tremor, but subsequent return of ondansetron resulted in the resolution of these symptoms. This is the first clinical report demonstrating acute withdrawal from an anti-emetic agent and we further highlight the need for future studies evaluating not only arterial supply with pressure gradients and anatomical location, but also the association with periventricular venous drainage, venous drainage stenosis, and mass effect from venous stasis as this may contribute partly to the sensitivity of the serotonergic receptors seen here.

Regression of multiple intracranial meningiomas after cessation of long-term progesterone agonist therapy.

The authors present the case of a patient that demonstrates the long-standing use of megestrol acetate, a progesterone agonist, and its association with multiple intracranial meningioma presentation. Discontinuation of megestrol acetate led to shrinkage of multiple tumors and to the complete resolution of one tumor. Histological examination demonstrated that the largest tumor had high (by > 25% of tumor cell nuclei) progesterone-positive expression, including progesterone receptor (PR) isoform B, compared with low expression of PR isoform A; there was no evidence of estrogen receptor expression and only unaccentuated collagen expression.

Association of Chiari malformation type I and tethered cord syndrome: preliminary results of sectioning filum terminale.

Objective: The pathogenesis of CM-I is incompletely understood. We describe an association of CM-I and TCS that occurs in a subset of patients with normal size of the PCF.

Methods: The prevalence of TCS was determined in a consecutively accrued cohort of 2987 patients with CM-I and 289 patients with low-lying cerebellar tonsils (LLCT).

Headache and mitochondrial disorders.

We report on 2 patients who have a mitochondrial myopathy, encephalopathy, lactic acidosis, and recurrent cerebral insults that resemble strokes (MELAS). These 2, and 9 other, reported patients share the following features: ragged red fibers evident on muscle biopsy, normal early development, short stature, seizures, and hemiparesis, hemianopia, or cortical blindness. Lactic acidemia is a common finding.

Pathogenic role of mitochondrial [correction of mitochondral] amyloid-beta peptide.

Metabolic dysfunction is one of the early features in Alzheimer's disease (AD) affected brain. Amyloid-beta peptide (Abeta), a major peptide deposited in neuritic plaques, has been considered as an important initiating molecule in the pathogenesis of AD. However, the pathogenic role of Abeta remains to be determined.

Amyloid-beta-induced mitochondrial dysfunction.

As an important molecule in the pathogenesis of Alzheimer's disease (AD), amyloid-beta (Abeta) interferes with multiple aspects of mitochondrial function, including energy metabolism failure, production of reactive oxygen species (ROS) and permeability transition pore formation. Recent studies have demonstrated that Abeta progressively accumulates within mitochondrial matrix, providing a direct link to mitochondrial toxicity. Abeta-binding alcohol dehydrogenase (ABAD) is localized to the mitochondrial matrix and binds to mitochondrial Abeta.