Françoise Lotstra

Brain hypometabolism of glucose in anorexia nervosa: A PET scan study

Cerebral glucose metabolism was studied in 20 underweight anorectic girls and in 10 age- and sex-matched healthy volunteers using positron emission tomography with (18-F)-fluorodeoxy-glucose. Both groups were scanned during rest, with eye closed and with low ambient noise. Compared to controls, the underweight anorectic group showed a global hypometabolism (p = .002) and an absolute (p < .001) as well as relative (p < .01) hypometabolism of glucose in cortical regions, with the most significant differences found in the frontal and the parietal cortices. Within the underweight anorectic and the control groups, no correlations were found between absolute or relative rCMRGlu and BMI, anxiety scores, or Hamilton scores of depression. Different factors might explain this reduction of glucose metabolism in anorexia nervosa. It might be the consequence of neurophysiological or morphological aspects of anorexia nervosa and/or the result of some associated symptoms such as anxiety or depressed feelings. Supported by cognitive studies, we can also hypothesize a primary corticocerebral dysfunctioning in anorexia nervosa.

Brain hypometabolism of glucose in anorexia nervosa: normalization after weight gain.

Using positron emission tomography and (18-F)-fluorodeoxyglucose, we studied cerebral glucose metabolism in 10 anorectic girls within their underweight state and after weight gain. Ten age- and sex-matched healthy volunteers were used as controls. Both groups were scanned during rest, eyes closed and with low ambient noise. In absolute values, the underweight anorectic patients, when compared to control subjects, showed a global (p = 0.002) and regional (p < or = 0.001) hypometabolism of glucose which normalized with weight gain. In relative values, no global difference could be assessed between underweight anorectic patients and controls but a trend can, nevertheless, be observed toward parietal and superior frontal cortex hypometabolism associated with a relative hypermetabolism in the caudate nuclei and in the inferior frontal cortex. After weight gain, all regions normalized for absolute and relative values, although a trend appears toward relative parietal hypometabolism and inferior frontal cortex hypermetabolism in weight gain anorectic patients. Absolute brain glucose hypometabolism might result from neuroendocrinological or morphological aspects of anorexia nervosa or might be the expression of altered neurotransmission following deficient nutritional state. As some differences exists in relative values in underweight patients and tend to persist in weight gain states, this could support a potential abnormal cerebral functioning, a different reaction to starvation within several regions of the brain or different restoration rates according to the region.

Brain glucose metabolism in anorexia nervosa and affective disorders: influence of weight loss or depressive symptomatology.

Relationships between eating and affective disorders remain complex and unclear. Brain glucose metabolism of anorectic patients has been demonstrated to be reduced both globally and regionally, with a particular relative hypometabolism in the parietal cortex. To explore the possible influence of weight loss or depressive symptomatology on brain metabolism, we studied age- and sex-matched low-weight anorectic and depressed patients, normal-weight depressed patients, and healthy volunteers. Absolute global and regional glucose activity levels were reduced in low-weight patients, with the lowest values being found for anorectic patients. In relative values, anorectic patients showed a significant parietal hypometabolism in comparison to control subjects while they had higher metabolism in the caudate nuclei when compared with the other groups. Absolute hypometabolism of glucose seems to be a consequence of low weight as it was found in both low-weight anorectic and low-weight depressive patients. In addition, absolute glucose values were significantly correlated with body mass index in all subjects. Future positron emission tomographic studies in psychiatric patients should control for alimentary parameters.

Brain hypometabolism of glucose in bulimia nervosa

OBJECTIVE A cerebral function lateralization has been described in bulimic patients in positron emission tomography (PET) studies realized during a specific cognitive task. The purpose of this study was to evaluate, at rest, brain glucose metabolism in patients with bulimia nervosa. METHOD PET with (18-F)-fluorodeoxyglucose was used to evaluate cerebral glucose metabolism in 11 normal-weight bulimic girls compared to 11 age- and sex-matched healthy volunteers. Patients were diagnosed following DSM-IV and were off psychoactive medication. RESULTS In comparison with control subjects, bulimic patients showed global and regional absolute hypometabolism of glucose. In relative values, only parietal cortex metabolism was significantly lower in bulimic patients. No correlation was found within groups for absolute or relative cerebral glucose metabolic rates (rCMRglu) and body mass index (BMI), anxiety scores, or Hamilton scores of depression. DISCUSSION Since previous studies have demonstrated similar disturbances in anorectic patients, we hypothesized that these observations could be a consequence of neurobiological perturbations following nutritional deficiencies or a particular cerebral dysfunction in eating disorders.

Brain hypometabolism of glucose in low-weight depressed patients and in anorectic patients: a consequence of starvation?

As low-weight anorectic patients presented a global as well as a regional absolute hypometabolism of glucose, we investigated a population of ten age- and sex-matched low-weight depressed patients without anorexia nervosa to evaluate the impact of weight loss on cerebral glucose metabolism evaluated by positron emission tomography and [18F]-fluorodeoxyglucose. Ten age- and sex-matched healthy volunteers were used as controls. Absolute global and regional glucose activity was significantly lower in anorectic and low weight depressed patients than in control subjects. Anorectic patients compared with normal control subjects also showed lower relative metabolism of glucose in the parietal cortex. Within patients, absolute hypometabolism of glucose seems to be a consequence of low-weight while there is a positive correlation between absolute metabolism of glucose and body mass index.

Regional cerebral glucose metabolism in akinetic catatonia and after remission

K L Kahlbaum published in 1874 the first recorded description of catatonia. Akinetic catatonia is now defined as a neuropsychiatric syndrome principally characterised by akinesia, mutism, stupor, and catalepsy.1 Even if some advances have been made in the recognition of catatonia, in particular by the development of different rating scales,1 the pathophysiology of this syndrome is not clearly established. A right handed 14 year old girl presented with akinetic catatonia during an episode of depression in the context of a bipolar type I disorder. Her catatonic status was characterised by akinesia with brief episodic spontaneous stereotyped movements, mutism, no spontaneous oral intake, catalepsy, waxy flexibility, and stupor with brief occasional eye contacts. This corresponded to a total score of 19 on the Northoff Catatonia Scale.1 Electroencephalogram performed one day after onset of symptoms showed diffuse theta activity with sporadic diffuse delta activity. Cerebral magnetic resonance imaging was normal. Brain positron emission tomographies (PET) were obtained on a CTI-Siemens HR+ tomograph. A first PET (PET1) using [18F]-fluorodeoxyglucose (FDG) was performed on day 2 in a drug free state. Thereafter, intramuscular injection of 2 mg of lorazepam induced rapid clinical remission of the akinetic phase. Oral lorazepam was then given (3.75 mg/day) during five days. On day 8, a second PET with FDG was performed while the patient was treated by olanzapine (15 mg/day) and presented hyperactivity, logorrhoea, and disinhibition characterised …

Co‐existence of Cholecystokinin‐ or Gastrin‐like Peptides with Other Peptides in the Hypophysis and the Hypothalamus

The presence of cholecystokinin and gastrin has been reported in the hypothalamohypophyseal system. These peptides present a peculiar distribution in the hypothalamic nuclei, the median eminence, and the neurohypophysis. CCK and gastrin have close relationships with other peptides like oxytocin, CRF, vasopressin, and the enkephalins; these relationships vary in different projecting areas and in different types of hypothalamic neurons. The functional role of G-CCK in neurosecretion seems to be linked to the role of these closely associated peptides and certainly deserves further investigation.

Changes in neurohypophysial cholecystokinin content during oestrous cycle in the rat

Cholecystokinin content in the neurointermediate lobe of the rat pituitary was measured by radioimmunoassay during the different stages of the oestrous cycle. Higher levels were observed in pro-oestrus and oestrus than in metoestrus and dioestrus rats. This difference is similar to the variation observed in the same circumstance concerning oxytocin in the neurohypophysis and neurosecretory activity in magnocellular neurons. These results are discussed in relation to the coexistence of oxytocin and cholecystokinin in neurons of the hypothalamoneurohypophysial system.

Decrease of vasoactive intestinal peptide, methionine-enkephalin, substance P and increase of neuropeptide Y immunoreactive nerve fibres in aganglionic colon of Hirschsprung's disease.

Ganglionic and aganglionic full-thickness samples, at 4 levels of the colon of 26 infants with Hirschsprungs disease, were studied by immunohistochemistry. In the distal part of the aganglionic bowel, we observe a decrease of substance P and vasoactive intestinal peptide, an absence of methionine-enkephalin and an increase in neuropeptide Y nerve fibres. When detected, substance P and vasointestinal peptide are mainly present in abnormal bundle nerve fibres. In the middle part of the aganglionic bowel, a slight increase in the number of normal nerve fibres containing substance P, methionine-enkephalin and vasoactive intestinal peptide is observed. Some vasoactive intestinal peptide abnormal bundle nerve fibres are detected. They are less numerous than in the distal part. In the proximal ganglionic bowel, the number of vasoactive intestinal peptide, substance P and methionine-enkephalin normal nerve fibres is increased compared to the middle aganglionic segment but is slightly lower than in the normal colon. Again vasoactive intestinal peptide abnormal bundle nerve fibres are present at that level and are also detected in more proximal ganglionic bowel up to the hepatic flexure of the colon. Thus, abnormal distribution of neuropeptides is also found in more proximal ganglionic bowel and not only in the aganglionic segment of bowel usually specific of Hirschsprungs disease.

Cholecystokinin distribution in the human striatum and related subcortical structures

The distribution of cholecystokinin immunoreactive nerve cell bodies and processes is reported in the human striatum and adjacent structures such as the claustrum, the pallidum, the bed nucleus of the stria terminalis and the substantia innominata. Cholecystokinin-positive terminals are present in the striatum where they are arranged in a patchy pattern. Cholecystokinin-positive somata are observed in the claustrum and in the bed nucleus of the stria terminalis but not in the striatum, the pallidum or the substantia innominata. Dense networks of cholecystokinin-positive woolly fibres are present in the bed nucleus of the stria terminalis and the substantia innominata. These results suggested that cholecystokinin is involved in the compartmental organization of the human striatum. This compartmentalization has functional and pathological implications. Involvement of the cholecystokinin system in some basal ganglia diseases is therefore expected. Presence of neuronal cholecystokinin in the accumbens nucleus, bed nucleus of the stria terminalis and substantia innominata also suggests that this peptide may interact at different levels in the human limbic system.