Generalized periodic epileptiform discharges: etiologies, relationship to status epilepticus, and prognosis.

Generalized periodic epileptiform discharges (GPEDs) are generalized, synchronous electrographic discharges. This study investigates etiologies, relationship to status epilepticus (SE), and the prognosis for patients with GPEDs. All EEGs with GPEDs performed at Duke University Medical Center between January 1994 and October 1995 were identified. Clinical histories and EEGs were reviewed. They were divided into groups depending on the etiology of the GPEDs, whether the patients were in SE or not, and whether they were alive or not at discharge. A comparison of histories and GPED characteristics among groups was undertaken using parametric and nonparametric t tests. Twenty-five patients were enrolled: 7 (28%) had toxic-metabolic encephalopathy, 10 (40%) had anoxia and toxic-metabolic encephalopathy, and 8 (32%) had a primary neurologic process. Eight patients (32%) were in SE. In the SE group, GPED amplitude was higher (110 versus 80 microV, P < 0.05), GPED duration was longer (0.5 versus 0.3 seconds, P < 0.05), and inter-GPED amplitude was higher (34 versus 17 microV, P < 0.05). Nine patients (36%) were alive at discharge; they were more likely to be younger (51 versus 68 years, P < 0.05), have a better mental status at the time of their EEG, and have a higher inter-GPED amplitude (33 versus 18 microV, P < 0.05). A variety of conditions, including SE, can cause GPEDs. Intergroup differences in historic and GPED features exist between those patients in SE and those not in SE and those with good and poor prognoses.

Depression in sleep disorders clinics.

PURPOSE: The purpose of this paper was to determine the incidence of depression in our sleep disorders clinics (and it's relation to patient characteristics) and to determine whether the incidence of depression varies in patients with and without sleep apnea. METHODS: The Beck Depression Inventory (BDI) was administered to evaluate patients for depression. We reviewed records of all new patients between November, 1995 and May, 1996 and determined their BDI scores and polysomnogram (PSC) results. Patients were divided based on their respiratory disturbance index (RDI); a cut off value of 15 was chosen. Patients were re-divided based on the BDI score (13 or greater suggestive of depression). The age, sex, body mass index (BMI), BDI or RDI (as appropriate) and arousal indices were compared. RESULTS: Sixty-three patients were enrolled; 29% were depressed. BDI scores and PSG data were available in 42 patients. Those with a high RDI had significantly lower BDI scores and higher arousal indices. Those with a high and low BDI scores were not significantly different in any of the parameters evaluated. CONCLUSIONS: Symptoms of depression are commonly seen in a sleep clinic. In patients with symptoms suggestive of SA but with low RDI scores, a diagnosis of depression should be entertained. The presence of depression, however, should not negatively influence a decision to perform PSG.

Structure of the gene for cartilage matrix protein, a modular protein of the extracellular matrix. Exon/intron organization, unusual splice sites, and relation to alpha chains of beta 2 integrins, von Willebrand factor, complement factors B and C2, and epidermal growth factor.

The entire gene for chicken cartilage matrix protein (CMP) has been isolated and characterized by restriction mapping, electron microscopy, nuclease S1 mapping, and sequence analysis. The gene, which is present in a single copy in the chicken genome, is 18 kilobase pairs long and comprises eight exons and seven introns. It has two transcription initiation sites, 8 base pairs from each other. A sequence very homologous to the consensus nuclear factor III binding-site sequence, a CAT- and a TATA-like sequence are found in the promoter region and ATTAAA is used as a polyadenylation signal. The nucleotide sequence defines a primary translation product of 493 amino acids which consists of a 23-amino acid signal peptide and two large repeated domains connected by an epidermal growth factor module. Amino acid sequences homologous to those of the repeated domains are present in the type A repeats of von Willebrand factor, complement factors B and C2, and in the alpha chains of the integrins Mac-1, p150,95, and LFA-1. The exon-intron structure indicates that the CMP gene may have arisen by exon duplication and exon shuffling during evolution. The GT-AG splice rule cannot be applied for the excision of the last intron of the CMP pre-mRNA. The donor splice site of intron G is basically different from the consensus sequence indicating that a novel type of splicing mechanism might exist in cartilage.