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Functional connectivity in obsessive-compulsive disorder and its subtypes
- Arun Ravindran, Margaret Richter, Tania Jain, Lakshmi Ravindran, Neil Rector, Norman Farb
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- Journal:
- Psychological Medicine / Volume 50 / Issue 7 / May 2020
- Published online by Cambridge University Press:
- 23 May 2019, pp. 1173-1181
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Background
Obsessive-compulsive disorder (OCD) is an anxiety disorder with significant morbidity whose pathophysiology is not fully understood. Neuroimaging studies have characterized OCD in terms of elevated striatal and prefrontal reactivity to emotion provocation. This neural model may be informed by investigation of functional connectivity in OCD, identifying alterations in how sensory information is integrated into frontostriatal regions.
MethodsThe current study employed functional magnetic resonance imaging (fMRI) to compare neural activity and connectivity in 31 OCD patients (12 washing and 19 checking subtypes) and 17 healthy volunteers in an emotion provocation paradigm using visual stimuli.
ResultsOCD status was associated with hyper-activation of the posterior cingulate (PCg) in response to emotion provocation. Additionally, OCD patients demonstrated elevated PCg functional connectivity with the visual cortices and frontostriatal regions. Exploratory analyses suggested that stimulus-provoked activity and connectivity was elevated for checking subtypes in motor cortices, and elevated in washing subtypes in the anterior insula and orbitofrontal cortex.
ConclusionsThe PCg's role in moderating connectivity between the visual cortex and frontolimbic regions is muted in OCD, consistent with the PCg's suggested role in regulating attention towards emotional stimuli. Exploratory analyses suggest distinct PCg connectivity profiles in OCD subtypes, with checking linked to motor activation, but washing linked to a network supporting emotional salience. The study was not powered to fully investigate the effects of medication, patients often endorsed secondary symptom subtypes that muddied washing/checking distinctions, and the emotion provocation paradigm was of limited intensity compared to life stressors.
Serum Choline Esterase and Anxiety
- Derek Richter, Margaret Lee
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- Journal:
- Journal of Mental Science / Volume 88 / Issue 372 / July 1942
- Published online by Cambridge University Press:
- 08 February 2018, pp. 428-434
- Print publication:
- July 1942
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Following the work of Dale (1934) and Loewi (1935) on the relationship of choline esterase to the transmission of nervous impulses, a number of studies have been made of the choline esterase activity of the serum in different physiological and pathological conditions. The serum esterase activity varies considerably from one individual to another, but it generally remains very constant in any one individual even over long periods of time; it is believed to be unaffected by changes in diet, exercise, fatigue, or by menstruation. The earlier investigators were unable to correlate the esterase level with any such factor as age, sex, heart rate, blood pressure, weight, or with pathological conditions such as benign or malignant tumours, chronic infections, heart diseases or neurological conditions (v. Verebely, 1936; McGeorge, 1937); they found only a tendency to low esterase activities in acute infections (Hall and Lucas, 1937) and in advanced tuberculosi (Vahlquist, 1935).
In an investigation in which psychopathic patients were included Tod and Jones (1937) and Jones and Stadie (1939) described a number of positive correlations between the serum choline esterase and various clinical conditions. They found a high esterase activity in anxiety states and lowered activity in catatonic stupor, epilepsy, schizophrenia and also in advanced tuberculosis and carcinoma. Antopol et al. (1937, 1938) associated high serum esterase activity with thyrotoxicosis and low activities with liver disease, anaemia and hyperpyrexia. Milhorat (1938), in agreement with Jones and Stadie, attributes the low esterase activities in these conditions to the general debility, but McArdle (1940) concludes that impairment of liver function is the primary cause.
The present work was carried out with the object of obtaining further information as to the relationship between the serum choline esterase activity and anxiety.
Serum Choline Esterase and Depression
- Derek Richter, Margaret Lee
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- Journal:
- Journal of Mental Science / Volume 88 / Issue 372 / July 1942
- Published online by Cambridge University Press:
- 08 February 2018, pp. 435-439
- Print publication:
- July 1942
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While investigating the serum choline esterase activity in anxiety states, a series of successive new admissions to the Neurological Section of the Mill Hill Emergency Hospital were tested with a view to obtaining further information as to the types of cases giving abnormally high or low esterase activities.
Sera giving abnormally high esterase activity were generally found to come from patients who had been diagnosed on admission as anxiety states, but an exception was noted particularly in the case of one patient (P. M—) with the very high esterase activity of 169. This patient was described on admission as “always emotional; he feels like weeping when the National Anthem is sung; not afraid of dangers.” He complained of uncontrollable weeping in company and he had considered suicide. Both from our own observation and from that of others it appeared that he was not a particularly anxious person, but he was extremely depressed. This observation raised the question of whether anxiety is the only emotional condition in which the serum esterase activity is raised or whether it may not also be raised in severe depression.
It appeared that information on this point might be obtained by analysing the data which had accumulated in testing the new admissions, which consisted of a varied collection of patients suffering from anxiety states, depressive states, hysteria and other neurological and mixed conditions. The possibility of subsequent analytical treatment was not considered at the time when the data were collected and the diagnoses were made by more than 12 different physicians who were known to differ to some extent in their diagnostic criteria. For this reason it was hardly expected that the results would be extremely clear-cut, but in actual fact the analysis brought out surprisingly clearly the differences in serum choline esterase activity in different types of neurotics. The diagnoses were made without a previous knowledge of the esterase activities and were therefore unbiased in this respect; we are indebted to the physicians for their permission to make use of them.
Methods.—The method of estimating the serum choline esterase was the same as was described in the preceding paper (Richter and Lee, 1942), except that venous blood from the arm was used instead of capillary blood. In some of the estimations acetylcholine bromide was used instead of the chloride. The bromide ion caused a slight inhibition of the enzyme which was corrected by multiplying by the factor 1·06, which was determined empirically by carrying out estimations on the same sample of serum with the chloride and bromide at the same time. The control group consisted of the 12 normal and 12 surgical patients described in the preceding paper; the mean serum esterase activity for the 24 controls was 75 units. The various esterases occurring in blood have been described by Richter and Croft (1942).
Blood Amines
- Derek Richter, Margaret Lee
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- Journal:
- Journal of Mental Science / Volume 88 / Issue 370 / January 1942
- Published online by Cambridge University Press:
- 08 February 2018, pp. 127-133
- Print publication:
- January 1942
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In the normal individual toxic amines produced by bacterial action in the gut or elsewhere are readily destroyed by the amine oxidase, an enzyme which is present in the liver, intestine and other organs (Richter, 1938; Blaschko, Richter and Schlossmann, 1937). This process of detoxication is normally very rapid and efficient, but it has been suggested that in certain pathological conditions the detoxicating system may be defective, giving rise to an abnormally high level of toxic amines in the blood (Quastel, 1937).