Fatal neurogenic pulmonary edema in a patient with progressive multiple sclerosis.

We report a case of fatal neurogenic pulmonary edema in progressive multiple sclerosis (MS). The patient had one isolated relapse-like episode. Six years later progressive disease began, lasting 5 years until unexpected death during sleep. Medico-legal autopsy revealed pulmonary edema and neuropathological examination showed infiltrations with lymphocytes and microglia in the respiratory centers of the medulla. More classical demyelinated lesions were found in the white matter of spinal cord and in the gray matter of the brain along with disseminated perivascular lymphocytic infiltrates. Medullary inflammation in progressive MS may result in sudden fatal respiratory failure.

The AMPA antagonist NBQX provides partial protection of rat cerebellar Purkinje cells after cardiac arrest and resuscitation.

Purkinje cell loss in adult rats resuscitated following cardiac arrest is analogous to that seen following human cardiac arrest. Administration of the competitive AMPA antagonist NBQX to rats resuscitated after 10 min duration cardiac arrest rescued 21.5% of the vulnerable Purkinje cell population. These results support the hypothesis that sustained postischemic overexcitation of AMPA receptors may be a driving force in the process of Purkinje cell degeneration.

The AMPA antagonist NBQX protects thalamic reticular neurons from degeneration following cardiac arrest in rats.

Thalamic reticular (RT) neurons are selectively vulnerable to degeneration following global ischemia. The degenerative mechanism is thought to involve an excitotoxic component, mediated in part by sustained post-ischemic activation of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate) type excitatory amino acid (EAA) receptors. In order to test this hypothesis, the selective competitive AMPA type EAA antagonist NBQX (2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F) quinoxalinedione) was administered at 30 mg/kg to rats 1, 3, and 6 h after resuscitation from 10 min cardiac arrest. NBQX treatment resulted in a 2-fold increase of spared RT neurons, from a mean density of 3.6 +/- 0.8 x 10(3) neurons/mm3 in cardiac arrest cases to 7.4 +/- 1.1 x 10(3) neurons/mm3 in the NBQX treated group, which represents sparing of 41.7% of the normal population of RT neurons, and protection of 26.9% of vulnerable RT neurons. Neurons within the central core of the RT manifest both a higher degree of vulnerability to ischemic degeneration, > 92% loss, and a higher sensitivity to sparing following NBQX administration, 460% increased sparing, than neuronal sub-populations in the medial or lateral 1/3 of the RT. Protection by post-arrest administration of NBQX suggests that sustained post-arrest stimulation of AMPA receptors is an important component in the process of ischemic degeneration of RT neurons.