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Cerebral obesity: causes, symptoms, diagnosis, treatment

Medical expert of the article

Endocrinologist
, medical expert
Last reviewed: 04.07.2025

The following forms of cerebral obesity are observed: Itsenko-Cushing's disease, adiposogenital dystrophy, Lawrence-Moon-Bardet-Biedl syndrome, Morgagni-Steward-Morel, Prader-Willi, Kleine-Levin, Alstrom-Halgren, Edwards, Barraquer-Siemens lipodystrophy, Dercum's disease, Madelung's disease, mixed form of obesity.

Mixed form of cerebral obesity (one of the most common clinical forms)

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Causes of cerebral obesity

Causes of cerebral obesity may be:

  1. pathology of the hypothalamus as a result of tumor, inflammatory, post-traumatic damage and increased intracranial pressure;
  2. disruption of hypothalamic control over pituitary functions, as occurs in the syndrome of the "empty" sella turcica;
  3. constitutional biochemical defect of the hypothalamus and its connections, decompensated under the influence of unfavorable environmental factors (improper diet and physical activity, hormonal changes, emotional stress).

Cerebral obesity, which occurs as a result of decompensation of a constitutionally determined defect in cerebral regulation of eating behavior and energy metabolism, is the most common in clinical practice.

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Pathogenesis of cerebral obesity

Dysfunction of the cerebral system of eating behavior and endocrine-metabolic processes, mainly at the level of the hypothalamic-pituitary link of regulation. In case of pathology of eating behavior, insufficiency of serotonergic mediator systems is assumed.

Symptoms of cerebral obesity

Generalized distribution of fat is noted. Excess body weight is usually combined with other neuroendocrine-metabolic manifestations: decreased function of the sex glands (oligo- and amenorrhea, infertility, anovulatory menstrual cycle, decreased secretion of the vaginal glands), secondary hypercorticism (hirsutism, trophic changes in the skin - purple-bluish stretch marks, acne, arterial hypertension), carbohydrate metabolism disorders (tendency to fasting hyperglycemia, impaired glucose tolerance test), water-salt metabolism disorders (fluid retention in the body with obvious or hidden edema or pastosity of the feet and shins). Motivational disorders are manifested by increased appetite (there may be a pronounced hyperphagic reaction to stress, which is observed in 50% of patients), increased thirst, mild daytime hypersomnia combined with disturbances in night sleep, and decreased sexual desire.

Vegetative disorders are always clearly represented in cerebral obesity. The tendency to sympathoadrenal reactions in the cardiovascular system (elevated blood pressure, tachycardia), especially when performing physical activity, is due to a new level of adaptation of the vegetative apparatus to excess body weight. However, this does not exhaust the permanent vegetative disorders, which are also manifested by increased sweating, increased oiliness of the skin, a tendency to constipation, and periodic subfebrile condition.

In addition, patients have a pronounced psychovegetative syndrome, which is manifested by excessive provision of any types of mental activity, as well as - in 30% of cases - paroxysmal vegetative manifestations. Paroxysms are either sympathoadrenal or mixed in nature and, as a rule, are found in patients with anxiety-phobic disorders. Syncopal states are quite rare and are observed in patients who have had a tendency to them since early childhood. Psychopathological disorders are very polymorphic, most often represented by anxiety-depressive and senestopathic-hypochondriacal manifestations. Manifestations of the hysterical circle are possible.

Algic manifestations are widely represented, mainly chronic psychalgia in the form of tension headaches, cardialgia, back and neck pain. Back and neck pain can be of a vertebrogenic nature or relate to myofascial pain syndromes. As a rule, the most striking psychovegetative and algic disorders are characteristic of patients with anxiety-depressive and hypochondriacal disorders.

It should be borne in mind that overeating in patients with cerebral obesity may not only be a reflection of increased appetite and hunger, but also serve as a kind of defense mechanism against stressful influences. Thus, obese patients often eat to calm down and get rid of the state of discomfort during nervous tension, boredom, loneliness, low mood, poor somatic condition. Food distracts, soothes, relieves internal tension, brings a feeling of satisfaction and joy. Thus, the hyperphagic reaction to stress occurs not only as a result of increased appetite and hunger, but is also a form of stereotypical response to stress. In these cases, the release of affective tension is achieved by increased food intake. Our studies have shown that the formation of such eating behavior is facilitated by an initially increased appetite from birth and improper upbringing.

It is assumed that not only the conditioned reflex mechanism (incorrect learning) plays a role in the origin of emotiogenic eating behavior, but also the specificity of neurochemical cerebral regulation with insufficiency of serotonergic systems. At the same time, the intake of high-carbon, easily digestible food contributes to a rapid increase in blood carbons with subsequent hyperinsulinemia. Due to hyperinsulinemia, the permeability of the blood-brain barrier to amino acids changes with an increase in permeability for tryptophan. As a result, the amount of tryptophan in the central nervous system increases, which leads to an increase in serotonin synthesis. Thus, the intake of carbohydrate-rich food is a kind of medicine for patients, regulating the level and metabolism of serotonin in the central nervous system. It is with an increase in the level of serotonin in the central nervous system that the state of satiety and emotional comfort that appears in patients after emotiogenic food is associated.

In addition to emotional eating behavior, obese people are characterized by so-called external eating behavior. It manifests itself in an increased and predominant response not to internal, but to external stimuli for eating (the type of food, food advertising, a well-set table, the type of person eating). The satiety of obese people is sharply reduced, they are characterized by rapid absorption of food, evening overeating, rare and abundant meals.

In a number of patients with cerebral obesity, it is not possible to detect the fact of overeating. Hormonal studies have revealed in these patients a reduced level of somatotropin with an inadequate decrease during emotional stress, an increased level of cortisol with its excessive increase in response to emotional stress, not counteracted by a corresponding increase in ACTH. These data allowed us to consider that in patients with a hyperphagic reaction to stress, motivational disorders predominate, while in patients without such a reaction, neurometabolic-endocrine disorders predominate.

Cerebral obesity can be combined with syndromes of idiopathic edema, diabetes insipidus, persistent lactorea-amenorrhea (PLA).

Differential diagnosis: first of all, it is necessary to exclude endocrine forms of obesity - hypothyroidism, Itsenko-Cushing syndrome, hypogenital obesity, obesity with hyperinsulinism. In the exogenous-constitutional form of obesity, as a rule, hypothalamic-pituitary manifestations are detected. The question of the primary or secondary nature of these manifestations does not have a clear answer to date. We are of the opinion that in the exogenous-constitutional form of obesity, there is also a primary dysfunction of the cerebral regulation link. Apparently, these two forms of obesity differ not in qualitative features, but only in the degree of cerebral dysfunction.

Treatment of cerebral obesity

Treatment of obesity should be aimed at eliminating the cause of hypothalamic-pituitary dysfunction. Traditional therapeutic approaches to treatment of tumors, neuroinfectious and post-traumatic lesions are used. In case of constitutional hypothalamic deficiency, non-specific types of therapy are used, the main ones being various dietary measures, increased physical activity, changing the incorrect eating and motor stereotype. Long-term dosed fasting can be recommended to all patients without a hyperphagic reaction to stress. In the presence of such a reaction, the prescription of dosed fasting should be approached differentially. It is advisable to conduct a trial daily fasting before prescribing treatment with dosed fasting and, depending on the patient's well-being, recommend or not recommend a further course of treatment. In case of an increase in anxiety disorders during a trial daily fasting, further treatment with this method is not indicated.

Various types of pharmacotherapy are used. Treatment with anorexigenic drugs of the amphetamine series (fepranon, desopimone) is contraindicated. The use of adrenergic anorexants, similar in their properties to amphetamines (mazindol, teronac), is not recommended. These drugs increase the stress sensitivity of patients, increase anxiety disorders, decompensate psychovegetative manifestations and psychopathological disorders. At the same time, food intake sometimes does not decrease, but increases, since patients with emotional eating behavior eat not as a result of increased appetite, but "eat away" anxiety, bad mood, etc.

In recent years, new generation anorexigenic agents related to serotonin agonists - fenfluramine (miniphage) or dexfenfluramine (isolipan) - have been successfully used. The usual doses are 60 mg of miniphage or 30 mg of isolipan per day for three to six months. These agents are fundamentally different from the previous generation of anorexants. They help to increase satiety, reduce manifestations of emotional eating behavior, stimulate fat metabolism processes, normalize hormonal status, and are not addictive. Contraindications for treatment with serotonergic anorexants are depressive disorders, panic attacks (vegetative paroxysms), severe liver and kidney pathology. The use of thyroid hormones is recommended only with a verified decrease in thyroid function. In such cases, thyroidin is prescribed in small doses (0.05 g 2 times a day for 20 days). In case of simultaneous edematous syndrome, it is recommended to take veroshpiron 0.025 g 3 times a day for 1-2 months. The use of other diuretic drugs is not indicated. Intramuscular injections of adiposin 50 U 12 times a day, usually for 20 days, are widely used. Treatment with adiposin is used against the background of a low-calorie diet.

Recommended drugs that affect tissue metabolism: methionine 2 tablets 3 times a day, B vitamins (preferably vitamins B6 and B15). Alpha- and beta-blockers - pyrroxane and anaprilin - are used to correct autonomic disorders. It is necessary to use drugs that improve cerebral hemodynamics: stugeron (cinnarizine), complamine (theonikol, xanthinol nicotinate), cavinton. As a rule, they are prescribed for 2-3 months, 2 tablets 3 times a day. It is necessary to use drugs that improve metabolic processes in the brain and its blood supply: nootropil (piracetam) 0.4 g 6 times a day for 2-3 months with subsequent repeated courses after 1-2 months and aminalon 0.25 g 3-4 times a day for 2-3 months.

Treatment of obesity must necessarily include the use of psychotropic drugs, which, by affecting neurochemical processes, not only help to normalize psychopathological disorders, but also in some cases improve neuroendocrine processes. The use of psychotropic drugs is also necessary to prevent undesirable consequences of diet therapy. It should not be forgotten that the inability to satisfy the dominant food motivation is a significant stress factor for obese patients when dieting. A significant number of clinical observations are known with the appearance (or intensification) of psychopathological and vegetative disorders with weight loss, followed by the refusal of patients to undergo therapy. Psychotropic therapy is especially important in patients with a hyperphagic reaction to stress, in which a decrease in the body's stress availability and a decrease in psychopathological manifestations leads to a significant decrease in the amount of food consumed. Psychotropic drugs are prescribed strictly individually, based on the nature of emotional and personal disorders; they are used for a long time for six months. Usually minor neuroleptics such as sonapax are used in combination with daytime tranquilizers (mesapam) or antidepressants. Preferred are new generation antidepressants, which are selective serotonin agonists, namely serotonin reuptake inhibitors in the presynaptic membrane: fluoxetine (prozac), sertraline (zoloft). Recommended doses: 20 mg of prozac once a day for 2-3 months; zoloft from 50 to 10 mg per day, the dose is taken in three doses, the duration of therapy is up to 3 months. Antidepressants of this series, in addition to relieving psychopathological, psychovegetative and algic manifestations, help to normalize eating behavior, eliminate the hyperphagic reaction to stress, cause anorectic reactions, and lead to weight loss. These drugs should not be prescribed together with antidepressants of other groups and anorexigenic agents of any action. Psychotherapy is a very relevant method of treatment.

The main goal of psychotherapy is to increase the stress resistance of patients, create a new food and motor stereotype, teach differentiation of impulses of different modalities (hunger and affective states), increase self-esteem of patients, and develop higher needs. Various types of psychotherapeutic influence are used. Behavioral and rational psychotherapy, body-oriented methods come to the fore. Treatment of obesity should always be comprehensive and include diet therapy, physiotherapeutic methods of influence, exercise therapy, behavioral therapy, and pharmacotherapy. The treatment is long-term. Patients should be under the supervision of a doctor for years.


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