Cerebral obesity: causes, symptoms, diagnosis, treatment

The following forms of cerebral obesity are observed: the Itenko-Cushing's disease, adiposogenital dystrophy, the Lawrence-Moon-Barde-Biddle syndrome, the Morgani-Steward-Morel, Prader-Willy, Klein-Levin, Alstrem-Halgren, Edwards, Barraker-Siemens dyspnoea, , Madelung's disease, a mixed form of obesity.

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

[1], [2], [3], [4], [5], [6]

Causes of cerebral obesity

Causes of cerebral obesity can be:

1. pathology of the hypothalamus as a result of tumor, inflammatory, posttraumatic lesions and increased intracranial pressure;
2. violation of hypothalamic control over pituitary functions, as is the case with the syndrome of the "empty" Turkish saddle;
3. the constitutional biochemical defectiveness of the hypothalamus and its connections, decompensated under the influence of unfavorable external factors (improper diet and physical activity, hormonal changes, emotional stress).

Cerebral obesity, resulting from the decompensation of a constitutionally conditioned defect in the cerebral regulation of eating behavior and energy metabolism, is the most common in clinical practice.

[7], [8], [9], [10], [11], [12], [13], [14], [15]

Pathogenesis of cerebral obesity

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

Symptoms of cerebral obesity

Generalized fat distribution is noted. Excess body weight, as a rule, is combined with other neuro-exchange-endocrine manifestations: a decrease in the function of the sexual glands (oligo and amenorrhea, infertility, anovulatory menstrual cycle, decreased secretion of the vaginal glands), secondary hypercorticism (hirsutism, trophic skin changes - cyanotic shade, acne, hypertension), a violation of carbohydrate metabolism (a tendency to hyperglycaemia on an empty stomach, a violation of the glucose tolerance test), a violation of water-salt metabolism (fluid retention in organizma with obvious or latent edema or pastosity of the feet and legs). 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, daytime undeveloped hypersomnia combined with disturbances in night sleep, decreased sexual desire.

Vegetative disorders in cerebral obesity are always vividly represented. The tendency to sympathoadrenal reactions in the cardiovascular system (elevated blood pressure figures, tachycardia), especially when performing physical exertion, is due to a new level of adaptation of autonomic devices to excess body weight. However, this is not limited to permanent vegetative disorders, which are also manifested by increased sweating, increased skin greasiness, propensity to constipation, periodic subfebrile condition.

In addition, patients have a pronounced psycho-vegetative syndrome, which is manifested by excessive provision of any kind of mental activity, and also - in 30% of cases - paroxysmal vegetative manifestations. Paroxysms are either sympathoadrenal or mixed and, as a rule, are found in patients with anxiety-phobic disorders. Syncopal states are quite rare and are noted in patients who had a tendency to them from early childhood. Psychopathological disorders are highly polymorphic, more often represented as anxiety-depressive and senestopatic-hypochondriacal manifestations. Possible manifestations of a hysterical circle.

Algic manifestations are widely represented, mainly psihalgii chronic course in the form of: tension headaches, cardialgia, pain in the back and neck. The pain in the back and neck can be vertebrogenic in nature or refer to myofascial pain syndromes. As a rule, the most vivid psycho-vegetative and algic disorders are typical for patients with anxiety-depressive and hypochondriacal disorders.

It should be borne in mind that overeating in patients with cerebral obesity can be not only a reflection of increased appetite and hunger, but also serve as a kind of protective mechanism against stressful influences. So, often patients with obesity eat to calm down and get rid of the state of discomfort with nervous tension, boredom, loneliness, reduced mood, poor physical condition. Food distracts, soothes, relieves inner tension, brings a sense of satisfaction and joy. Thus, the hyperphagic response to stress occurs not only as a result of increased appetite and hunger, but is also a form of stereotyped response to stress. In these cases, the discharge of affective stress is achieved by increased intake of food. Our researches have shown, that the beginning of similar food behavior is promoted initially by the raised appetite since a birth and wrong education.

It is assumed that the role of emotion-related eating behavior is played not only by the conditioned reflex mechanism (incorrect learning), but also by the specificity of neurochemical cerebral regulation with a deficiency of serotonergic systems. In this case, the use of high-carbon, easily assimilated food promotes a rapid increase in the blood of carbohydrates followed by hyperinsulinemia. Due to hyperinsulinemia, the permeability of the blood-brain barrier to amino acids changes with increasing permeability for tryptophan. As a result, the amount of tryptophan in the central nervous system increases, which leads to an increase in the synthesis of serotonin. Thus, the intake of carbohydrate-rich food is for patients a kind of medicine that regulates the level and exchange of serotonin in the central nervous system. It is with an increase in serotonin in the central nervous system that the states of satiety and emotional comfort appearing in patients after emotional food are associated.

In addition to emotive eating behavior, for obese, so-called external eating behavior is characteristic. It manifests an increased and preferential response not to internal, but to external stimuli for food intake (type of food, food advertising, well-served table, the kind of person who takes food). Saturation in obese is sharply reduced, fast absorption of food, evening overeating, rare and abundant meals are characteristic.

In a number of patients with cerebral obesity, it is not possible to identify the fact of overeating. The hormonal studies made it possible to reveal in these patients a decreased level of somatotropin with an inadequate decrease in emotional stress, an elevated level of cortisol with its excessive increase in response to emotional stress, not associated with a corresponding increase in ACTH. These data made it possible to consider that motivational disorders predominate in patients with a hyperphagic reaction to stress, neuro-exchange-endocrine disorders predominate in patients without such a reaction.

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

Differential diagnosis: first of all it is necessary to exclude the endocrine forms of obesity - hypothyroidism, Itzenko-Cushing syndrome, hypogenital obesity, obesity in hyperinsulinism. In the exogenously-constitutional form of obesity, as a rule, hypothalamic-pituitary manifestations are found. The question of the primary or secondary nature of these manifestations to date has no unambiguous answer. We are of the opinion that even in the exogenously-constitutional form of obesity, there is a primary dysfunction of the cerebral link of regulation. Apparently, these two forms of obesity are not characterized by qualitative signs, but only by the degree of cerebral dysfunction.

Treatment of cerebral obesity

Treatment of obesity should be aimed at eliminating the cause that caused hypothalamic-pituitary dysfunction. Traditional therapeutic approaches to treatment are used in the tumor process, neuroinfectious and post-traumatic lesions. With the constitutional defectiveness of the hypothalamus, non-specific types of therapy are used, the main of which are various dietary measures, increased physical activity, a change in the abnormal eating and motional stereotype. Prolonged dosed fasting can be recommended to all patients without hyperphagic reaction to stress. In the presence of such a reaction to the appointment of dosed starvation should be approached differentially. It is advisable to perform a test daily fasting and, depending on the patient's well-being, recommend or do not recommend a further course of treatment before the appointment of a dosed fasting. In the case of an increase in anxiety disorders during trial daily fasting, further treatment with this method is not indicated.

Apply different types of pharmacotherapy. Treatment with anorexigenic drugs amphetamine-type (fepranone, desopimon) is contraindicated. It is not recommended to use anorexanth adrenergic action, close in its properties to amphetamines (mazindol, teronak). These drugs increase the stress-availability of patients, increase anxiety disorders, decompensate psycho-vegetative manifestations and psychopathological disorders. At the same time, food intake sometimes does not decrease, but increases, as patients with emotive eating behavior do not eat as a result of increased appetite, but "seize" anxiety, bad mood, etc.

In recent years, anorectic agents of the new generation, related to serotonin agonists - fenfluramine (mini-fat) or dexfenfluramine (isoline), have been successfully used. Usually used doses are 60 mg of a mini-pore or 30 mg of isoline per day for three to six months. These funds are fundamentally different from the anorexants of the previous generation. They contribute to increased satiety, reduce the manifestations of emotionogenic eating behavior, stimulate fat metabolism processes, normalize hormonal status, and not addictive. Contraindications for the treatment of 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 reduction in thyroid function. In such cases, appoint thyroid in small doses (0.05 g 2 times a day for 20 days). With simultaneous edematous syndrome, it is recommended to take veroshpiron 0,025 g 3 times a day for 1-2 months. The use of other diuretics is not shown. Intramuscular injections of adiposin 50 UU are often widely used 12 times a day, usually for 20 days. Apply treatment with adiposone on the background of a low-calorie diet.

Recommended drugs that affect tissue metabolism: methionine 2 tablets 3 times a day, vitamins B (vitamins B6 and B15 are preferred). To correct vegetative disorders, alpha and beta adrenoblockers, pyrroxane and anaprilin, are used. It is necessary to use means that improve cerebral hemodynamics: stugeron (cinnarizine), komplamin (theonikol, xanthinal nicotinate), cavinton. As a rule, they are appointed for 2-3 months. 2 tablets 3 times a day. It should be used 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 in 1-2 months. And aminalon by 0.25 g 3-4 times a day for 2-3 months.

Treatment of obesity must necessarily include the use of psychotropic drugs, which, acting on neurochemical processes, not only contribute to the normalization of psychopathological disorders, but also in a number of cases improve neuroendocrinal processes. The use of psychotropic drugs is also necessary to prevent the undesirable consequences of diet therapy. It should not be forgotten that the lack of the ability to satisfy the dominant food motivation is a significant stressor for obese patients while dieting. There is a significant number of clinical observations with the appearance (or intensification) of psychopathological and vegetative disorders with a decrease in body weight with subsequent refusal of patients from therapy. Especially essential is the therapy with psychotropic drugs in patients with hyperphagic stress reaction, in which a decrease in the body's stress-free availability and a decrease in psychopathological manifestations leads to a significant decrease in the food intake. Psychotropic drugs are prescribed strictly individually, based on the nature of emotional and personality disorders; apply them for a period of six months. Usually, small neuroleptics such as sonapax are used in combination with daytime tranquilizers (mesapam) or antidepressants. Preferred antidepressants are the new generation related to selective serotonin agonists, namely, serotonin reuptake inhibitors in the presynaptic membrane: fluoxetine (prozac), sertraline (zoloft). Recommended doses: 20 mg 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 up to 3 months. Antidepressants of this series in addition to stopping psychopathological, psycho vegetative and algic manifestations contribute to the normalization of eating behavior, the disappearance of hyperphagic reaction to stress, cause anorectic reactions, lead to a decrease in body weight. These drugs should not be prescribed together with antidepressants of other groups and anorexigenic agents of any action. A very topical method of treatment is psychotherapy.

The main goal of psychotherapy is to increase the stress-stability of patients, to create a new food and motor stereotype, to learn the differentiation of the motives of various modalities (hunger and affective states), to increase self-esteem of patients, and to develop higher needs. Various kinds of psychotherapeutic influence are applied. Behavioral and rational psychotherapy, bodily-oriented methods come to the fore. Treatment of obesity should always be comprehensive and include diet therapy, physiotherapy methods of treatment, exercise therapy, behavioral therapy, pharmacotherapy. Treatment is long. Patients should be under medical supervision for years.