Do repeated courses of ECT cause brain damage detectable by MRI?
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Aged↗
Biomedical subjects
A I Scott
Publications and source records attributed to A I Scott.
Time course of cerebra; magnetic resonance changes after electroconvulsive therapy.
Nuclear magnetic resonance images of the non-dominant cerebral hemisphere were obtained in 20 unipolar depressed patients immediately before and 25 minutes after electroconvulsive therapy (ECT). T1 values rose about 1%. Repeated scanning up to 24 hours after ECT was carried out in 13 of these patients. The greatest change in magnetic resonance images was two hours after ECT, and thereafter images gradually returned to baseline values. There was no correlation between magnetic resonance changes and the time taken to become reorientated after ECT.
Adult↗
A neuroendocrine view of ECT.
"A neuroendocrine hypothesis to explain the clinical activity of convulsive therapy is described. The hypothesis is based on the diabetes/insulin model and suggests that hypothalamic dysfunction with an insufficiency of a mood-maintaining peptide is the basis for affective disorders. Repeated seizures enhance the production and release of the hypothalamic peptide antidepressin - the active principle that relieves both neuroendocrine and behavioral abnormalities.
Bipolar Disorder↗
Treatment outcome, seizure duration, and the neurophysin response to ECT.
Serum concentrations of immunoreactive neurophysin (IRN) and vasopressin-associated neurophysin (hNpI) were measured before and after the first treatment in a course of electroencephalographically monitored electroconvulsive therapy (ECT) given to 19 depressed patients. The difference (DIFF) between the serum concentrations of IRN and hNpI is equivalent to the concentration of oxytocin-associated neurophysin. Before ECT the six patients who had a good outcome at 2 months after the course of ECT had a mean serum IRN concentration one-half (p less than 0.05) and a mean serum DIFF concentration one-third (p less than 0.05) that of the 13 patients who had a poor outcome. The increase in serum DIFF concentration (but not IRN or hNpI) after the first ECT correlated with the improvement on the Hamilton Rating Scale for Depression (r = -0.73, p less than 0.005) and the Montgomery and Asberg Depression Rating Scale (r = -0.49, p less than 0.05). The peak percentage increase in serum DIFF concentrations after ECT was 4 times greater (p less than 0.001) in the good outcome group than in the poor outcome group. None of the neurophysin responses to ECT correlated with electroencephalogram-measured seizure duration.
Adult↗
Reconstitution of apo-porphobilinogen deaminase: structural changes induced by cofactor binding.
Expression of porphobilinogen deaminase in a hemB- strain of E. coli has permitted the isolation of the apoenzyme, i.e. deaminase lacking the porphobilinogen-derived dipyrromethane cofactor. Incubation of purified apoenzyme with porphobilinogen resulted in reconstitution of the covalently attached dipyrromethane cofactor, indicating no additional cofactors or enzymes are required for biosynthesis of holoenzyme. Electrophoretic and 13C-NMR spectroscopic analyses demonstrate that the apoenzyme exists in a conformationally unstable form which is converted to a highly stable tertiary structure on covalent attachment of the dipyrromethane cofactor.
Ammonia-Lyases↗
Diminished TSH release after a course of ECT: altered monoamine function or seizure activity?
The release of thyroid stimulating hormone (TSH) after the first and last treatments in a course of electroconvulsive therapy (ECT) was measured in nine depressed patients free of neuroleptic drugs. There were close correlations between altered TSH release after a course of ECT and changes in bilateral spike wave activity (r = 0.99, p less than .0.001) and total seizure length (r = 0.72, p less than 0.05) as measured by six-channel electroencephalogram. The close correlation of TSH release after ECT with seizure activity makes it unlikely that the study of TSH release will provide new insights into the mode of action of this controversial treatment.
Adult↗
Which depressed patients will respond to electroconvulsive therapy? The search for biological predictors of recovery.
A small yet significant minority of contemporary patients with endogenous depressive illness who are treated with electroconvulsive therapy (ECT) gain little or no benefit. It is argued that the use of clinical features alone may not improve the ability to predict outcome after ECT. Many biological measures have been used to attempt to identify depressed patients for whom ECT would be an effective treatment, but none has yet been shown to be superior to clinical predictors. Depressed patients show a wide range of physiological responses to the first treatment of a course of ECT. Of these physiological responses, estimations of seizure threshold and of the release of posterior pituitary peptides merit further investigation as putative predictors of recovery.
Depressive Disorder↗
Would monitoring by electroencephalogram improve the practice of electroconvulsive therapy?
Estimates of seizure length made by the treating psychiatrist were compared with estimates made by six-channel EEG in 100 electroconvulsive treatments in 22 depressed patients. In 70 treatments the doctor observed a fit which was shorter than 25 seconds. No doctor restimulated a patient in such a case and on only three occasions was the electrical stimulus increased at the next treatment. EEG monitoring revealed that only 30 of the treatments resulted in a seizure of less than 25 seconds, and this was detected in almost all cases by the treating doctor. The potential value of EEG monitoring was to identify patients whose visible seizure was short but where cerebral seizure length was satisfactory. Trainee psychiatrists often mismanage patients who have short seizures.
Cerebral Cortex↗
Status epilepticus after electroconvulsive therapy.
Status epilepticus is a rare complication of ECT. We describe a patient who suffered a prolonged seizure which required termination with intravenous diazepam. The status epilepticus was not accompanied by motor movements, and the diagnosis was made only because of simultaneous EEG monitoring. The incidence of status epilepticus after ECT may be underestimated.
Acetaminophen↗
Site-directed mutagenesis and high-resolution NMR spectroscopy of the active site of porphobilinogen deaminase.
The active site of porphobilinogen (PBG)1 deaminase (EC 4.3.1.8) from Escherichia coli has been found to contain an unusual dipyrromethane derived from four molecules of 5-aminolevulinic acid (ALA) covalently linked to Cys-224, one of the two cysteine residues conserved in E. coli and human deaminase. By use of a hemA- strain of E. coli the enzyme was enriched from [5-13C]ALA and examined by 1H-detected multiple quantum coherence spectroscopy, which revealed all of the salient features of a dipyrromethane composed of two PBG units linked head to tail and terminating in a CH2-S bond to a cysteine residue. Site-specific mutagenesis of Cys-99 and Cys-242, respectively, has shown that substitution of Ser for Cys-99 does not affect the enzymatic activity, whereas substitution of Ser for Cys-242 removes essentially all of the catalytic activity as measured by the conversion of the substrate PBG to uro'gen I. The NMR spectrum of the covalent complex of deaminase with the suicide inhibitor 2-bromo-[2,11-13C2]PBG reveals that the aninomethyl terminus of the inhibitor reacts with the enzyme's cofactor at the alpha-free pyrrole. NMR spectroscopy of the ES2 complex confirmed a PBG-derived head-to-tail dipyrromethane attached to the alpha-free pyrrole position of the enzyme. A mechanistic rationale for deaminase is presented.
Ammonia-Lyases↗
Identification of a cysteine residue as the binding site for the dipyrromethane cofactor at the active site of Escherichia coli porphobilinogen deaminase.
The dipyrromethane cofactor of Escherichia coli porphobilinogen deaminase was specifically labelled with 13C by growth of the bacteria in the presence of 5-amino[5-13C]levulinic acid. Using 13C-NMR spectroscopy, the structure of the cofactor was confirmed as a dipyrromethane made up of two linked pyrrole rings each derived from porphobilinogen. The chemical shift data indicate that one of the pyrrole rings of the cofactor is covalently linked to the deaminase enzyme through a cysteine residue. Evidence from protein chemistry studies suggest that cysteine-242 is the covalent binding site for the cofactor.
Aminolevulinic Acid↗
Analytical and preparative separation of uroporphyrin I and III by high-performance liquid chromatography.
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Chromatography, High Pressure Liquid↗
5-Aminolevulinic acid formation from glutamate via the C5 pathway in Clostridium thermoaceticum.
A cell-free extract of the anaerobic eubacterium, Clostridium thermoaceticum, catalyzes the synthesis of 5-aminolevulinic acid (ALA) from glutamate via the C5 pathway. The enzyme reaction resembles that of higher plants and algae in cofactor requirements and sensitivity to ribonuclease. From the phylogenetic distribution it is proposed that the C5 pathway evolved earlier than the ALA synthase pathway.
Aminolevulinic Acid↗
In vivo and solid state 13C nuclear magnetic resonance studies of tyrosine metabolism during insect cuticle formation.
1. Tyrosine metabolism during pupation can be followed in living Heliothis virescens larvae using nuclear magnetic resonance spectroscopy. 2. Loss of 13C signals from a label at the C-3 position of tyrosine during pupation indicates uptake of tyrosine into solid cuticle. 3. Solids 13C NMR spectroscopy of cuticle formed by insects injected with 3-13C labelled tyrosine indicates that little change in chemical shift occurs during cuticle hardening, indicating that the side chain is probably not involved in protein cross-linking.
Animals↗
13C-NMR analysis of alanine metabolism by isolated perfused livers from C3HeB/FeJ mice infected with African trypanosomes.
1. Isolated perfused livers from mice infected with Trypanosoma brucei rhodesiense formed substantially more [3-13C]-lactate from [3-13C]-alanine than livers from uninfected mice. Quantities formed by infected livers increased as infection progressed. 2. Infected livers produced more 13C-labeled glutamate and glutamine, with label scrambled between C-2 and C-3. Scrambling also produced [2,3-13C]-aspartate, [2-13C]-alanine and [2-13C]-lactate. Delayed appearance of label in C-4 of glutamate/glutamine in infected livers reflects significant endogenous stores of unlabeled acetyl CoA. 3. Although differences do exist in catabolism of [3-13C]-alanine by perfused livers from infected and control mice, trypanosomiasis does not cause permanent breakdown or blockage of hepatic alanine metabolism.
Alanine↗
Characterization of Alkaloid Uptake by Catharanthus roseus (L.) G. Don Protoplasts.
The accumulation of alkaloids by protoplasts of Catharanthus roseus (L.) G. Don var. Little Bright Eye was studied to determine the specificity of uptake and the role of ion trapping in the storage of alkaloids. Accumulation of the indole alkaloids vindoline, ajmalicine, tabersonine, and vinblastine was found to be biphasic, with an initial burst of uptake followed by a slow, prolonged phase of accumulation. The concentration and pH dependence of the initial burst of uptake for vindoline suggested that uptake occurred by simple diffusion. Uptake of nicotine was monophasic, with a half life of 5.2 minutes. The accumulation ratio (Ci/Ce) for nicotine at steady state and for the initial burst of uptake for vindoline and ajmalicine suggested that accumulation was driven by the pH gradient between the vacuole and the external assay medium. The second, sustained phase of uptake of vindoline was sensitive to inhibition by either 20 millimolar NaN(3) or 0.5 millimolar Cu(2+). In azide-treated protoplasts, the uptake for vindoline conformed to the kinetics of simple diffusion, with a half life of 4 minutes. The second phase of uptake for ajmalicine, although sensitive to inhibition by Cu(2+), was insensitive to inhibition by NaN(3). The biphasic uptake of the indole alkaloids was not due to any significant metabolism. It is concluded that accumulation and storage of the indole alkaloids is due only partly to ion trapping of the alkaloids by the low pH of the vacuole lumen. In the case of vindoline, there appears to be a specific energy-requiring uptake that is not seen with nicotine (which is not endogenous to Catharanthus). Accumulation of ajmalicine appears to involve both ion trapping and an azide-insensitive component, which may be due to complexation with organic counterions and phenolics.
Journal Article↗
Attempted strangulation during phenothiazine-induced sleep-walking and night terrors.
A patient who resumed sleep-walking as an adult is described. The failure to diagnose his disturbed nocturnal behaviour as sleep-walking kept him from his work for over 8 months, and led to a treatment which exacerbated the behaviour. The diagnosis was made when the patient attempted to strangle his wife.
Adult↗
Effects of seizure duration on serum TSH concentration after ECT.
Serum thyroid stimulating hormone (TSH) concentrations were measured by a sensitive immunoradiometric assay in 14 patients immediately before and after the first treatment of a course of electroconvulsive therapy (ECT). There was a close correlation (r = +0.70, p less than 0.01) between the increase in TSH concentration 15 min after ECT and the duration of seizure activity as measured by EEG. This observation may help clarify previous contradictory findings on the effects of ECT on TSH concentrations. There was no correlation between the increase in serum TSH concentration and the extent of recovery from depressive illness.
Aged↗