Augmentation of seizure induction in electroconvulsive therapy: a clinical reappraisal

OBJECTIVE: Missed or abortive seizures during electroconvulsive therapy (ECT) may preclude completion of an effective course of treatment in some cases. Seizure augmentation, using proconvulsant agents, has been used to overcome resistance to the induction and continuation of seizure activity. In this review, we analyze published clinical data on the effects and safety of seizure augmentation techniques. METHOD: Clinical studies and case reports were obtained through a MEDLINE literature search from 1966 to 2001, cross-referencing ECT and proconvulsant agents. Article references were also scanned for relevant studies. RESULTS AND CONCLUSIONS: Data from clinical trials indicate that augmentation facilitates seizure induction when maximal electrical stimuli fail. Anesthetic modifications, including hyperventilation and substitution with etomidate, ketamine, or other agents, often are successful in overcoming seizure resistance and compare favorably with the use of caffeine. In a few studies, augmentation enabled the use of lower stimulus intensities and fewer treatments without loss of efficacy, even in patients not resistant to seizure induction. However, effects of proconvulsants must be reconciled with increasing evidence of the importance of stimulus dosing relative to seizure threshold and other parameters, now considered key to the efficacy of ECT. Further investigations of pharmacologic augmentation could facilitate the administration of ECT and could provide further insights concerning parameters of seizure efficacy and the mechanism of action underlying convulsive therapies.     

Regional brain bioamine levels under hyperbaric oxygen in two unequally susceptible strains of mice

BACKGROUND: Hyperbaric oxygen (HBO) increases monoamine deamination with related toxic products which aggravates hyperbaric oxygen (HBO) neurotoxicity. However, the possibility of some protective action of monoamines balanced by the toxicity of their metabolites have received little attention. HYPOTHESIS: To try to unmask this protective action, we compared brain monoamine levels in two strains of mice differing in HBO-sensitivity and their sensitivity to HBO after norepinephrine (NE) depletion by N-(2-chloroethyl)-N-ethyl-2-bromo benzylamine (DSP4). METHODS: Mice were exposed to 6 ATA O2 for 90 min (C57 strain) and 24 min (HBO-sensitive CD1 strain) so that 50% of mice of each strain had preconvulsive symptoms when decompressed and 50%), had one generalized convulsion. After microwave sacrifice, monoamines in the cerebral cortex, the striatum and the brainstem were analyzed. Another series studied the effect of DSP4 on the delay to symptoms of these HBO)-exposed mice. RESULTS: NE normoxic levels in the striatum were greater in the HBO-sensitive CD1 than in the C57 strain. Under HBO, NE levels in the striatum and the cortex of CD1 fell without any concomitant increase in its metabolite whereas in the C57 strain, NE decreased less and its metabolite increased. There was no strain difference and little change in the NE levels in the brainstem. The increase in toxicity induced by DSP4 was highly significant in both strains; moreover C57 strain was more affected than CD1. CONCLUSION: Monoamine depletion before HBO aggravates HBO neurotoxicity. As monoamine deamination is known to be toxic, this demonstrates that monoaminergic activation is protective. The greater toxicity of DSP4 in the C57 strain suggests the involvement of monoamines in the strain-differential susceptibility to HBO. The lower sensitivity of CD1 mice to DSP4 may be related to a combination of less NE activation under HBO that in C57 and greater activation of peroxidation and amino acids in CD1 sensitive strain.     

Difficult reintubation during a Fantoni's tracheostomy resolved using a laryngeal mask

We report the failure of a reintubation under direct laryngoscopy, during a percutaneous tracheostomy by Fantoni method. After the accidental per-procedural extubation and in front of an unpredicted difficult conventional endotracheal intubation, a laryngeal mask was used as an airway intubator conduit for the blind passage of the set's ventilation tube. This ventilation tube is a 40 cm long, 4 mm internal diameter special catheter with low pressure cuff, included into the TLT kit. The end of the procedure was uneventful.     

Structural variability and originality of the Bordetella endotoxins

Structural studies of Bordetella endotoxins (LPSs) have revealed remarkable differences: (i) between their LPSs and those of other bacterial pathogens; (ii) among the LPSs of the seven identified Bordetella species; and (iii) among the LPSs of some Bordetella strains. The lipid As have the "classical" bisphosphorylated diglucosamine backbone but tend to have fewer and species-specific fatty acid components compared to those of other genera. Nevertheless, three strains of B. bronchiseptica have at least three different fatty acid distributions; however, the recently identified B. hinzii and B. trematum LPSs had identical lipid A structures. The B. pertussis core is a dodecasaccharide multi-branched structure bearing amino and carboxylic groups. Another unusual feature is the presence of free amino sugars in the central core region and a complex distal trisaccharide unit containing five amino groups of which four are acetylated and one is methylated. The B. pertussis LPS does not have O-chains and that of B. trematum had only a single O-unit, unlike the LPSs of all the other species of the smooth-type. The O-chain-free cores of non-B. pertussis LPSs were always built on the B. pertussis core model but most were species-specifically incomplete. The LPS structures of three B. bronchiseptica strains were found to be different from each other. The O-chains of B. bronchiseptica and B. parapertussis were almost identical and had some features in common with B. hinzii O-chain. Serological analyses are consistent with the determined LPS structures.     

Two types of chloride cells in the gill epithelium of a freshwater-adapted euryhaline fish: Lebistes reticulatus; their modifications during adaptation to saltwater

Two types of chloride cells were identified in the gill epithelium of freshwater-adapted guppies. One type, referred to as an “α-chloride cell,” was a pale, elongated cell located at the base of the secondary lamella in close contact with the arterioarterial pillar capillaries. In its cytoplasm, membranous tubules in continuity with its basolateral plasma membrane formed an extended tridimensional network. The vesiculotubular system (Pisam: Anat. Rec. 200:401–414, 1981) consisted of a few tubules and vesicles located next to the apical plasma membrane. A second type, referred to as a “β-chloride cell,” was a darker, ovoid cell located in the interlamellar region of the primary epithelium facing the central venous sinus. Membranous tubules in continuity with the basolateral plasma membrane were unevenly distributed in the cytoplasm. A prominent vesiculotubular system composed of numerous vesicles and tubules was found between the Golgi apparatus and the apical surface. During seawater adaptation, the α-chloride cells increased in size and progressively transformed into characteristic “sea-water α-chloride cells” with a well-developed, regular, tight tubular network and numerous vesicles and tubules of the vesiculotubular system accumulated below the apical pit. The α-chloride cells underwent a progressive degeneration and disappeared. Thus, in freshwater-adapted guppies, there are two types of chloride cells, α and β, respectively, related to the arterial and the venous vessels, whereas in seawater-adapted fishes, a single type of cell, the α-chloride cell, was related to both the arterial and venous channels.