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Challenges for logopedic work with speechless children

20 Apr 2018

Recently, specialists are increasingly confronted with speechless children, i.e. with children who do not have speech. They have a complex organic disorder, which greatly complicates the logopedic work with them. For a full-fledged development of speech, it is necessary: innate linguistic ability, primarily preserved intellect, stimuli from the external environment, motivation for speech, the usefulness of the conductive pathways between the individual analyzers for which information is transmitted. In the brain there are speech zones: the posterior parts of the lower frontal gyrus; temporal gyrus; lower parietal region; as well as a zone located at the junction of the parietal, temporal and occipital regions of the left, dominant hemisphere by speech.

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Who can be called a non-talkative, speechless child?

A group of no-speech children is not homogeneous. It includes children with motor and sensory alalia, with a temporary delay in speech development, early childhood autism, intellectual insufficiency, infantile cerebral palsy, and hearing impairment. However, for all these children, there is a lack of motivation for speech activity, a lack of basic ideas about the meanings of objects and phenomena of the surrounding reality, an inadequacy of communicative, regulating, planning speech functions, a lack of sensorimotor level of speech activity.

Thus, at the initial stages of working with non-speaking children, its goals and tasks will be similar, regardless of etiopathogenesis and mechanisms of speech disturbance. At the present stage of the development of special education, it is urgent to develop educational programs and pedagogical technologies that ensure the comprehensive development of children with developmental disabilities.

The main goals of speech therapy with non-speaking children at the initial stages are: development of speech initiative, creation of motivation for speech activity simultaneously with enrichment of internal and external vocabulary; the formation of a child's ability to create an internal plan, a program of utterance (at first - primitive).

Logopedic work with non-speaking children provides a corrective effect, both on speech activity and on non-verbal psychic processes, on the emotional and personal development of the child.

The main tasks of corrective work with non-speaking children at the initial stage:

1. Stimulation of speech and mental activity.

2. Development of emotional communication with an adult. Expression of the teacher at each stage of the exercise with a no-speech child contributes to the development of imitation and emotionally adjusts children to speech and speech production.

3. Improving the ability to imitate the actions (echopraxia) of an adult, peers and speech imitation - echolalia.

4.Development and correction of psycho-physiological basis of speech activity: different types of perception, physiological and speech breathing, articulatory skills.

5. Formation of motivational and motivational level of speech activity.

6. Formation of internal and external lexicon (nominative, predicative, and attributive), providing minimal communication.

7. Formation of the initial skills of grammatical (morphological and syntactic) structuring of the speech message.

8. Prevention of secondary speech disorders.

The implementation of the tasks of speech therapy with non-speech children occurs in the process of using the following means:

- Games and exercises that activate all higher mental functions;

-Games and exercises regulating the muscle tone of children, allowing to correct the behavior of children, to affect the emotional-personal sphere;

-self-independent game activity;

-Igra, forming the structure of speech activity at all levels (from motivational-incentive to executive);

-Specifically organized correctional-developing environment;

-Organized family education of children.

Thus, a speech from a non-speaking child can only be triggered by using both all analyzer systems and the targeted impact of parents and professionals.


What is the difference between a speech therapist and a Defectologist?

19 Apr 2018

The defectologist can begin work with children of one-year-old age, and the speech therapist starts to study with kids from three years old. Speech therapist corrects and develops speech, puts sounds and pronunciation, while the defectologist is engaged in the lag in the development of the child, caused by various disorders, and helps the kid to know the world.

Cortexin for speech development

So, for example, the speech therapist will not teach the child color, he will pronounce their names, striving for correct pronunciation, while the defectologist's task is to familiarize the baby with the flowers and learn the name of each of them. That is, in fact, a defectologist is a broad-profile specialist, while a speech therapist is only responsible for correcting speech disorders.

1.Defectologist works with problem and sick children, the speech therapist deals exclusively with healthy children.

2.Defektolog starts to study with one-year-olds, the speech therapist begins to work with children when they reach three years.

3.Defectologist - a specialist in a wide profile, speech therapist - a narrow-profile specialist.


Problem of defective sound-pronunciation

18 Apr 2018

The problem of defective sound reproduction is also relevant in adulthood.

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Is it possible to correct the violation of sound reproduction in an adult? Of course!
But there are some conditions: to make the correct sound come into independent speech (automated), it is necessary to have a very great desire, and therefore motivation. Because in adulthood, the interactions between the articulatory zone of the cerebral cortex and the muscles of the articulation organs are already extremely strong (in contrast to preschool children, in which such connections, as they master the sounds of their native language, are just beginning to form). The sound setting in adults occurs, as a rule, faster than in children, but an adult will need more (in comparison with the child) the number of independent classes to fix the correct pronunciation and huge self-control at a long stage. With a positive attitude and some persistence, the new sound is automated and you will be self-sufficient, as all familiar will pay attention to your updated, clear pronunciation. Believe me, the efforts are worth it!

Another problem that an adult may face is a voice disturbance. Such violations can be organic or functional, arise rapidly (as a result of stress, disease, surgical intervention) or increase gradually. With this problem (especially with a sharp loss of voice), in no case should you delay the visit to the otolaryngologist, but against the background of the prescribed treatment, to the phoniatrist and the speech therapist. Here (as in the case of aphasia) the most important role is played by the time factor of contacting a specialist. In the future, the speech therapist will teach you how to perform the necessary vocal and breathing exercises to restore and strengthen the voice.

In adulthood, stammering is less likely to occur, most often in the remission stage it passes from childhood or adolescence. An adult can alleviate his condition by significantly reducing or completely eliminating the stumbling in speech under the guidance of a speech therapist. But since stuttering requires an integrated approach, it must be understood that along with the speech therapist needs to receive the support of a neurologist who will pick up a mild nerve-supporting treatment, and perhaps (with a pronounced stutter), recommend an additional examination. Often a good result is obtained if the psychologist also works in parallel with the patient.

Speech restoration in patients with aphasia is one of the most difficult areas of speech therapy with adults. Aphasia is amenable to logopedic correction, although the results depend not only on the qualification of the specialist, but also most significantly on the severity of the lesion of the speech centers of the cerebral cortex and the time to call on the speech therapist (extremely preferably the first six months or a year), as well as the patient's personal qualities and desire for lessons. However, with timely access to a specialist, there is the possibility of a significant restoration of speech functions. Speech therapist will conduct a survey and make a plan of work based on the causes of aphasia, since the methods of speech therapy correction for various forms of aphasia have their own peculiarities in each specific case. I assure you, at home, relatives and relatives will be able to deal with aphasias according to the tasks of the speech therapist, achieving good results in restoring speech.


The Mysterious World of Neuropeptides

17 Apr 2018

Hormones are the most famous regulators of processes in the body. Their functions and chemical structure have been studied quite well, which makes it possible to create medications on their basis and successfully carry out, for example, substitution therapy. On the second place in the illumination are located neurotransmitters. These compounds preferentially link the nerve cells to each other, thereby activating or inhibiting various regions and processes. Influence on neurotransmitters is somewhat more complicated, but many drugs have been developed that affect metabolism, ejection, reverse capture, etc., hence the neurotransmitter system is adjustable.

Human peptides

At this stage in the development of medicine and pharmacology, the neuropeptides are least studied and controlled. Nevertheless, they take an active part in almost all processes in the body, regulate the most important behavioral and adaptive reactions, control circadian rhythms, food and sexual behavior, affect hormones and neurotransmitters. It is impossible to ignore this topic, as well as to collect all the data on it. According to the results of the studies, the data does not always coincide, sometimes they are directly opposite, which makes the description of neuropeptides difficult, due to the lack of a single classification, there is still much confusion. Thus, information on neuropeptides is not systematized enough, nevertheless this material is the most complete in Russian and includes a significant number of compounds not listed in other reviews.

Neuropeptides (NP) - biologically active compounds that participate in the regulation of metabolism, maintenance of homeostasis, affect immune processes, play an important role in the mechanisms of memory, learning, sleep, etc. The NP is characterized by a relatively short sequence of a chain consisting of amino acid residues, as a rule, it is 5-52 elements.

NPs are formed as a result of sequential hydrolytic decomposition of the precursor peptide, for example, several substances can form from the same initial molecule, which at each stage may have biological activity different from the initial and final products. The NP precursors are synthesized in the body of the cell by translating the gene encoding the peptide, then the proteases point split the long molecule into shorter chains that can later undergo transformation or remain unchanged. If it is a neuron, then the NP is transported to the presynaptic terminal, from which it is released into the synaptic cleft. Some neuropeptides are able to perform the functions of mediators, carrying out a direct transmission of the nerve impulse, others change the metabolism of the cell, acting as a neuromodulator. NP can transmit the signal not only to close distances, the receptors to some of them are at a sufficient distance from the site of synthesis, which makes it possible to compare them with hormones. The functions of many NPs duplicate each other, nevertheless everyone has a unique spectrum of activity. This feature allows you to more accurately transmit the signal and regulate the interaction of different parts of the body, coordinate a complex system of continuously occurring processes that somehow affect each other and require constant corrections. The vast majority of neuropeptides affect the "slow" metabotropic receptors associated with G-proteins. In addition, NP can change the activity of each other and some hormones (more often inhibit or activate their synthesis), which leads to the launch of cascade reactions.

Many neuropeptides are synthesized to a greater or lesser degree in various organs and tissues, and only some of them are strictly specific for certain zones. Distribution of NP in the body is not uniform, there are places that are most characteristic for each substance, but in small amounts they are determined in virtually all tissues. In the neural tissue, NPs are present in unmyelinated C-type fibers and small A-delta-type myelinated fibers. In the spinal cord, NPs are synthesized by the cells of the dorsal horns of the ganglia, then transported along the axons to the nerve endings, where they can act as neurotransmitters. In synaptic terminals, NPs are able to act together with non-protein neurotransmitters. A neuropeptide may be colocalized with one or more mediators, which leads to some enhancement or modification of the action. If their selection coincides in time, then the effect depends on both of them, but they can also be separated separately, which leads to the realization of the biological effect of each of them separately from each other.

At present, there is no complete and comprehensive classification of NPs. Attempts were made to develop it on the basis of the chemical structure, functions or place of synthesis. However, many NPs are able to perform several functions depending on the location, similar in structure of the compound - responsible for different processes, and various substances of origin being agonists. NP found in any tissues were not always specific to them and were later found in other organs. In addition, at the moment, new compounds are opening, which can not be attributed to any of the existing groups, since their functions are not fully understood. The classification of NPs by families can be regarded as the most complete and functional, since it takes into account the greatest number of features of these substances.

Classification of Neuropeptides:

  • Hypothalamic liberins and statins
  • Opioid peptides
  • Melanocortins
  • Vasopressin-tocine
  • Pancreatic peptides
  • Glucagon secretions
  • Cholecystokinin
  • Tachykinins
  • Motilin
  • Neurotensins
  • Bombesins
  • Kininy
  • Angiotensins
  • Peptides encoded by a gene similar to the calcitonin gene
  • Atriopeptides
  • Endozepines
  • Galanin
  • Endothelins

Hypothalamic liberins and statins
Tyroliberin, corticoliberin, lyuliberin, somatoliberin, somatostatin, melanostatin. The first family includes neuropeptides synthesized by the hypothalamus. They were combined into one group according to the topological feature and had mainly the function of stimulation (liberins) or inhibition (statins) of the synthesis of pituitary hormones. According to the chemical structure, the hypothalamic neuropeptides differ considerably from each other and have different precursors. In addition to influencing the structures remote from the site of synthesis, the NPs of this group can influence neighboring neurons, depressing or vice versa stimulating each other's formation. As they studied, representatives of the first family were found in other organs and tissues and found the ability to influence the emotional state, food and sexual behavior, the regulation of the sleep-wake cycle, the provision and launch of stress-protective mechanisms, the stimulation of immune processes, neurogenesis and many others.

Opioid peptides
The family of opioid peptides is characteristic of the majority of representatives of the amino acid sequence Tyr-Gly-Gly-Phe. Accordingly, OP works on opioid receptors, mainly μ (MOP), δ (DOP), and κ (KOP), associated with G-proteins. Due to the ability to bind to the listed receptors, OPs have a naloxone-inhibiting, morphine-like analgesic and sedative effect. EP have a variety of biological effects. With regard to the impact on behavior, they have the ability to influence aggression, motivation for satisfaction, sexual attraction, food saturation, stressor adaptive processes, drug dependence, sedation, modulation of pain sensitivity, etc. In addition, they participate in neurodegenerative processes, damage to brain tissue due to trauma and ischemia.

Opioid peptides (OP) are widely distributed in the central and peripheral nervous systems, GIT, serum, are produced not only by neurons, but also by cells of the endocrine and immune systems. Most opioid peptides are formed from common protein progenitors - proopiomelanocortin (α-MSH, γ-MSH, β-MSH, ACTH, β-endorphin, α-endorphin, γ-endorphin, β-lipoprotein (β-LPH), γ-LPH , CLIP), prodinorphine (dinorphin A, dinorphin B, α-neoendorfin, β-neoendorfin, dinorphin-32, leimorfin), preproenkephalin (leu-enkephalin, meth-enkephalin, amidorfin, adrenorphine, peptide B, peptide E, peptide F), prepro- nociceptin, preproorpharin (nociceptin (orfanin FQ)), prepro-NPFF (NP FF, NP AF, NP SF), and others.

Enkephalins are short peptide chains, from 5 amino acid residues. Typical members of the family are leu-enkephalin and met-enkephalin, named for the fifth amino acid, respectively leucine and methionine. In addition, the group includes DTLET and DAMGO. They act mainly on the δ-opioid receptors. Both neuropeptides have a pronounced morphine-like analgesic, sedative effect. They take part in the formation of behavioral reactions. Their participation in many neurodegenerative pathologies is proved.

Endorphins α and β are products of hydrolysis of POMC and contain 16 and 31 amino acid residues, respectively. They participate in the motivation of alcoholic behavior, nociceptive reactions, stress response, regulation of circadian rhythms. Β-endorphin is less specific to receptors and can activate to a greater or lesser extent all three of the number of opioids.

Dinorphins are formed during the conversion of prodinorphine and contain in their structure a sequence of leu-enkephalin. The most important action is the central and peripheral nociceptive process. The group includes dinorfin A and dinorfin B (rimorphin), containing respectively 17 and 13 amino acid residues. In addition, α-, β-neoendorfin is formed. All of them activate mainly κ-opioid receptors. Their selectivity is due to the presence of arginine and lysine at the C-terminus. If the precursor proteolysis does not take place completely, a so-called "big" dinorphine is formed, which includes dinorphine A and B, and has the same properties, but is more selective for BCD.

Dermorphin and deltorphin-specific agonists of the μ- and δ-opioid receptors, respectively, consisting of 7 amino acid residues. They participate in reducing the threshold of epileptic readiness, have a pronounced analgesic effect, stimulate the release of β-endorphin. They differ in the presence of the D-amino acid in the second position, which makes them more resistant to enzymatic hydrolysis.

Hemorphins are products of proteolytic decomposition of hemoglobin, have an affinity for μ-opioid receptors. Participate in the analgesic reaction and the development of euphoria after exercise.

Endomorphin-1 and -2 are tetrapeptides, show the greatest specificity for the μ-opioid receptors from the family. Have a pronounced and long analgesic effect.

Nocystatin contains 17 amino acid residues in its composition. Reduces pain sensitivity. Studies are under way to create on its basis analgesic agents that are not addictive and morphine-like addiction.

Β-Casamorphin consists of 7 amino acid residues and is formed by the hydrolysis of casein. It is able to activate μ-opioid receptors, stimulate the immune system and increase food intake.

Leumorfin (leimorfin) is formed from the precursor of preprodinorphin. Have sufficient affinity for opioid receptors and for biological action is comparable with other OP.

Adrenorphine is synthesized mainly in the adrenal glands. Has the ability to influence nociceptive processes, as well as other peptides of the family.

A group of peptides with anti-opioid activity enhance the pain response, increase anxiety, stimulate the release of ACTH and corticosterone, inhibit morphine-induced effects. Prevent the formation of dependence on alcohol and morphine, affect the development of withdrawal syndrome in animals with morphine dependence.

Presented are:

Neuropeptides AF and SF consist of 18 and 11 amino acid residues, respectively. The neuropeptide FA consists of 8 amino acid residues. Receptors to it are located mainly in the spinal and supraspinal zones containing a large number of endogenous opioids.

Nociceptin (Orphanin FQ) - consists of 17 amino acid residues and has a structure similar to that of opioid peptides. The receptors for nociceptin are similar to opioid receptors, linked to adenylate cyclase. When these receptors are activated, potassium channels are activated and calcium is inhibited. Nociceptin and its receptors are most widely represented in the cortex, olfactory nuclei, amygdala, hippocampal formation and dorsal horns of the spinal cord. Takes part in the processes of memory, learning, stressful reactions. In experimental models showed the ability to reduce anxiety. Activation of the nociceptin receptors leads to analgesia, but it interferes with the action of opioids.

Adrenocorticotropin (ACTH) is a hormone synthesized in the anterior pituitary gland, the main function of which is stimulation of adrenal corticosteroid production. It is proved that he is able to synthesize and other parts of the brain, and in addition to the hormonal function to act as a neurotransmitter, to participate in the regulation of higher cortical functions such as memory, attention, training.

A-β-γ-melanotropins (melanocyte-stimulating hormones) are formed from proopiomelanocortin. Synthesis occurs most intensively in the median lobe of the pituitary gland. The receptors for MSH are associated with G-proteins and are divided into 2 types: MCHR1 and MCHR2. The expression of Type 1 receptors is highest in the cortex, hippocampus, amygdala and nucleus accumbent, suggesting that these neuropeptides are involved in the development of pathologies such as mood disorders and schizophrenia. This is confirmed by the introduction of antagonists to this type of receptor, which caused anxiolytic and antidepressant effects. A-MSH stimulates the formation of pigment in the skin, participates in mental processes - memory and learning, sleep, aggression, modulates inflammation in the brain, blocks the synthesis of gliosis of tumor necrosis factor. Γ-MSG has a lesser effect on the pigment metabolism, but enhances the steroidogenic function of ACTH. All MSG are able to participate in the regulation of gastrointestinal function, immune processes, cell growth and mitosis, and eating behavior.

Vasopressin and oxytocin are produced in the hypothalamus, along the axons enter the posterior lobe of the pituitary gland, from which they are released into the blood. They have a strong effect on the formation of behavioral reactions, such as affection, sexual, parental behavior. Under stress, they participate in the creation of protective mechanisms. In addition, they can influence blood pressure, reduce smooth muscle, metabolism.

Mesotocin, isotocin, vasotocin is composed of 10 amino acid residues, having a common initial sequence of 6 amino acids. Synthesize mainly in the posterior lobe of the pituitary gland together with oxytocin and vasopressin and are similar to them for biological effects, but less active.

Predecessors - preprovazopressin-neurofizin II (vasopressin, neurofizin II), preproxitocin-neurofizin I (oxytocin, neurofizin I).

Pancreatic peptides
The neuropeptide Y consists of 36 amino acid residues. Distributed in the brain (hypothalamic and cortical regions, hippocampus, thalamus) and peripheral nervous system, postganglionic sympathetic fibers, adrenal glands, megakaryocytes and platelets. There is evidence of a change in the distribution of NP in the neuronal population of the prefrontal cortex in ontogenesis in pathological disorders. Oppressing the selection of the transmitter from the nerve endings. The effect is manifested by hypotension, hypothermia and respiratory depression, secretion of water and electrolytes in the intestine, regulation of circadian rhythms and motivational behavior. Is able to participate in the regulation of eating behavior, so, with its chronic introduction into the central nervous system, the body weight increased. During the period of food intake decrease, the amount of neuropeptide Y in arched and paraventricular nuclei increased. With the breakdown of the neuropeptide Y, the resulting substances can act as its agonists and antagonists, which is determined by their chemical structure.

The tyrosine tyrosine peptide (PYY) has a similar structure to the neuropeptide Y and differs from it with the additional amino acid residue -Tyr. By function, they are just as similar and competing for binding to the same receptors.

Pancreatic polypeptide (PPY) is synthesized by PP-cells of the islets of Langerhans pancreas. It has 36 amino acid residues. By the mechanism of action it is a cholecystokinin antagonist, suppresses the secretory activity of pancreatic cells and stimulates the production of gastric juice, delaying food in the stomach.

The precursors are prepro-NPY (NPY), prepro-PPY (PPY), prepro-PYY (PYY).

Glucagon secretions
Glitsentinya is an intermediate product of the formation of glucagon from preproglucagon. Until the end of its properties are not studied, it is assumed that the spectrum of its activity is similar to that of glucagon.

Glucagon (GRP) contains 27 amino acid residues. The largest amounts are contained in the gastrointestinal tract and brain, secreted by some tumors, where it stimulates mitosis, has a trophic effect on normal and neoplastic cells, including autocrine stimulation of small cell lung cancer proliferation. Participates in the regulation of glucose metabolism, with an increase in its level stimulates the synthesis of insulin and inhibits eating behavior. In the central nervous system improves the processes of memory formation, takes part in the body's response to stress. It takes care of the regulation of sleep-wake cycles, body temperature, appetite and satiety. Modulates the activity of macrophages. Regulates the secretion of pancreatic and hydrochloric acid enzymes in the stomach, stimulates the contraction of smooth muscles and the release of certain intestinal hormones, including gastrin.

VIP (vasoactive intestinal peptide) consists of 28 amino acid residues. Widely represented in the central nervous system, especially in the cerebral cortex, where it participates in the formation of behavioral reactions, has a positive effect on the processes of learning and memory, sexual behavior. Can act as a mediator in serotonergic and cholinergic systems. On the periphery causes the expansion of the bronchi, vessels (including cerebral).

Secretin contains 27 amino acid residues. It is mainly produced by brain structures, adrenals and intestines. Most strongly, its effect is manifested in the cells of the gastrointestinal tract, where it leads to relaxation of smooth muscles and increased secretion of hormones by the pancreas.

Gastrin is mainly produced by G-cells of the stomach and pancreas. A "large" gastrin is formed, which consists of 34 amino acid residues, gastrin-17 and gastrin 14, which contain respectively 17 and 14 amino acids. On the functions performed they are similar, since all contain the same active center. Increase the secretion of hydrochloric acid, pepsin, bicarbonates, secretin, cholecystokinin, somatostatin and some other peptides involved in digestion. Stops the emptying of the stomach. It leads to the expansion of the stomach vessels by increasing the production of prostaglandin E. Participates in the regulation of eating behavior, reducing the motivation for food search.

Predecessors - preprogastrin (gastrin), preproglycagon (glycinthin, glucagon), preprosecretin (secretin), prepro-VIP (VIP).

Cholecystokinin contains 33 amino acid residues. Influencing the structure of the central nervous system affects the emotional state, leads to the activation of behavior aimed at obtaining food, has an antidepressant effect. It is of great importance in the regulation of the functions of the gastrointestinal tract - it stimulates secretion in the pancreas, motility of the gallbladder and intestines. In the decay of cholecystokinin, products that have their own action are formed. Some of them can reduce the effects of morphine and enkephalins with respect to pain sensitivity. Preecessor is preprocholecystocinin.

This group includes NPs that have a β-preprotachykinin precursor and contain the-Gly-Leu-Met sequence at the C-terminus. Biological effects are mediated by exposure to receptors associated with G-protein. Tahikinins can also act as neurotransmitters and are widely represented in various tissues of the body. The main physiological effects are the regulation of the tone of the smooth muscles of the intestine, bronchi, participate in behavioral reactions, nociceptive processes, inflammatory processes.

The substance contains in its composition 11 amino acid residues. It was opened in 1931. and is the most studied of the family. It is synthesized mainly in the central nervous system - the amygdala, the septum, the hippocampus, the hypothalamus and the gray matter in the brain water pipeline, which are involved in the formation of anxiety and depression. Occurs in the posterior horns of the spinal cord is a neuromodulator in primary afferent fibers and unmyelinated C-type fibers. It has a wide spectrum of physiological effects - it can influence the blood pressure level, capillary permeability, smooth muscle contraction, possesses secretory action, participates in the control of secretion of prolactin and digestive hormones. The synthesis of substance P is enhanced by dopamine: thus, it was revealed that when dopanergic fibers are damaged, mRNA expression is reduced, which corresponds not only to the formation of substance P, but also to enkephalins and dinorphine. Participates in the transmission of a pain signal. The ability of substance P to influence training, sleep, resistance to stress is studied.

Neurokinins (A, B and K) are similar in their effects to substance P, but have a different specificity for the receptors. They change the excitability of nerve cells, have the ability to exert an anti-inflammatory effect - their effect leads to vasodilation and increase in their permeability, the release of prostaglandin E2, cytokines and amines by mast cells and leukocytes. In addition to these physiological effects, they participate in the transmission of a nerve impulse.

Cassinin consists of 12 amino acid residues. Takes part in lowering blood pressure, stimulating contraction of smooth muscles. There is evidence that cassinin has anticonvulsant activity.

In its composition contains 22 amino acid residues. It is produced mainly in the gastrointestinal tract, where it affects mainly the motor function - it strengthens the tone of the lower sphincter-esophagus, stimulates the emptying of the stomach and the motility of the large intestine. Stimulates the production of insulin and somatostatin by the pancreas. In the central nervous system, the highest concentration is found in the hippocampus. The effect of motilin on mental functions has not been studied enough, it is assumed that it affects food behavior.

The predecessor is prepromotilin.

Neurotensin is found mainly in the hypothalamus, mesocorticolimbic and nigrostriatic zones, ventral cover, septum, cingulate gyrus, small intestinal mucosa. The peptide has a strong hypotensive effect, leads to a reduction in smooth muscle, reduces body temperature, increases the glucose and glucagon content, can bind to mast cell receptors. Neurotensin has in some sense a hormonal action - in the pituitary gland enhances the secretion of LH and FSH. There are data on its ability to influence sexual behavior, the development of stress reactions and nociceptive processes. It is established that dysfunction in the neurotensin system occurs in mental illnesses, in particular schizophrenia. It is assumed that the effect on its metabolism can have an effect in psychotic states, without causing at the same time an increase in weight and cataleptic manifestations. However, clinically significant evidence for this was not obtained. Associated with dopaminergic, serotonergic, GABAergic, glutamatergic and cholinergic systems.

Neuromedins N and U (NMN, NMU) are secreted in the cells of the central nervous system and gastrointestinal tract. Receptors to them are located in neurons, cells of the small intestine, pancreas, stomach, lymphocytes, monocytes, muscle fibers of the uterus. Exposure to NMU leads to a decrease in body weight by reducing appetite. In the regulation of immune processes increases inflammation, activating the mast cells. NMN can act as a neurotransmitter.

Xenopsy is involved in the regulation of smooth muscle tone.

The precursor is propreneurotensin.

Bombesin consists of 14 amino acid residues. It is a powerful activator of the hypothalamic-pituitary-adrenal axis, participates in the regulation of the body's stress reaction, affects the memorization processes. In addition, it regulates the consumption of ethanol. Physiological effects consist in vasoconstriction, decrease in body temperature, regulation of secretory processes in the gastrointestinal tract, takes part in autocrine stimulation of cell proliferation and growth of small lung cancer cells.

Gastrin-releasing peptide (GRP) consists of 27 amino acid residues. It is common in the brain tissue, intestines, lungs, immune system, and others. Its main functions can be called regulation of sleep-wake cycles, thermoregulation, effects on appetite and satiety, modulation of macrophage activity, increased secretion of enzymes by the pancreas, hydrochloric acid in the stomach , a reduction in smooth muscles, the release of gastrin in the intestine, and participation in the regulation of respiration at the level of the brainstem. GRP stimulates the mitotic activity of cells, including small cell lung cancer.

Litorin has many properties of the family, in particular, the ability to regulate body temperature.

Kinins have a wide spectrum of activity and are a link in the regulation of vascular tone, blood coagulation and fibrinolysis. They are synthesized in most tissues, including the CNS.

Bradykinin consists of 9 amino acid residues. Its effect leads to relaxation of the smooth muscles of the walls of the vessels, bronchi, uterus, intestine. It takes part in the regulation of hemostasis, electrolyte balance, permeability of capillaries, local inflammatory reactions and pain sensitivity. The muscle fibers outside the vessels act in the opposite way, leading to their constriction, which is important in the development of inflammation and pain intensification.

Kallidin consists of 10 amino acid residues and differs from bradykinin by the presence of a lysine residue at the beginning of the chain. By physiological effects similar to bradykinin.

The predecessor is the kininogen.

Angiotensins I, II, III are synthesized in the central nervous system and other tissues and organs. The most studied functions of these peptides are the regulation of the state of the cardiovascular system, water-salt metabolism, and blood pressure. Angiotensins are products of sequential hydrolytic cleavage from the terminal portion of several amino acids. Thus, angiotensin II is formed from angiotensin II and further with a shortening of the chain. The most powerful of the group is angiotensin II, which is formed under the influence of renin and PDA. It plays a role in the formation of mechanisms of arterial hypertension. It is part of the renin-angiotensin-aldosterone system. It is associated with the adrenergic system and tachykinins by the mechanism of action. It has been proven that angiotensins participate in learning processes, memory formation, motivation, internal reinforcement, pain sensitivity and control of emotions.

The precursor is the preprotein angiotensinogen.

Peptides encoded by a gene similar to the calcitonin gene
Calcitonin (contrinsular hormone) consists of 32 amino acid residues. It is produced mainly by C-cells of the thyroid gland. Calcitonin-like immunoreactivity is found in the pituitary gland, cerebrospinal fluid, lungs, thymus, intestine, liver, bladder. In the brain, the highest content of calcitonin is found in the zone surrounding the posterior part of the hypothalamus, mid elevation and pituitary gland. He takes an active part in the regulation of the water-salt balance. Reduces the content of calcium and phosphorus in the blood plasma, which leads to a change in the metabolism and activity of cell membranes. Has analgesic and anorectic effect, leads to vasodilation, hypotension, hyperglycemia, stimulates gluconeogenesis and glycogenolysis.

Calcitonin-gene-related peptide (CGRP) consists of 37 amino acid residues. In fairly large amounts, it occurs in the central and peripheral nervous, cardiovascular, genitourinary, GIT and C-cells of the thyroid gland. Has the ability to influence blood pressure, depending on the attendant factors leads to hypo- or hypertension, is a strong vasodilator, causes tachycardia, is involved in maintaining the tone of the coronary vessels and modulating the pain sensitivity, affects food behavior and cerebral circulation.

The precursor is prepro-CALC (calcitonin).

The peptide inhibitor of diazepam binding (DBI) consists of a large number of amino acids. Biological activity has both DBI itself and its fragments - endozepin-6 and octadecaneuropeptide (6 and 18 amino acid residues in its composition, respectively). These peptides are in large numbers in the central nervous system and are ligands of benzodiazepine receptors. By structure - strong antagonists GABA, which determines their biological effects. The level of endozapines increases in brain tissue under stress and aging. It has been proved that these peptides play a role in the formation of reactions to stress and the development of anxiety states - when intragastric administration has an anxiogenic and proconflicogenic effect, the search for their antagonists can lead to the creation of a new type of anti-anxiety drugs.

The predecessor is BDI in isoforms 1, 2, 3.

Galanin consists of 29 amino acid residues. Receptors to it are located in the hippocampus, hypothalamus, amygdala, preoptic zone, supraoptic, arcuate nucleus. Receptors are divided into 3 types and they are all associated with G-protein. In experiments it was shown that when exposed to galanin receptors, anxiolytic and antidepressant effects can be obtained. When combined with other substances, it can exert the most diverse influence - when colocalized with acetylcholine takes part in mnestic processes, the role in the development of Alzheimer's disease, with noradrenaline - the formation of social status, with vasopressin and oxytocin in supraoptic and paraventricular nuclei acquires the ability to influence osmoregulation. Formed in the hypothalamus stimulates the secretion of LH and takes part in the regulation of the feedback of the HGH axis. It is able to inhibit the secretion of glutamate and the electrical activity of the arcuate nucleus.

The predecessor is pre-progalanin.

Endothelin I, II, III are synthesized predominantly in the vascular endothelium, their expression is present in the neural tissue. They are powerful vasoconstrictors. Together with other peptides and hormones play an important role in the regulation of the endothelium, the development of renal ischemia, hypertension, bronchial asthma, heart failure and cerebral vascular pathologies. The main active peptide of the group is endothelin I. Endothelins have different precursors expressed by different genes.

In addition to the neuropeptides represented in this classification, there are a large number of compounds not included in it. To date, several hundred NPs have been opened, which for various reasons can not be attributed to existing groups. Here are some of them.

Orexins belong to the group of hypothalamic peptides and include orexin A and orexin B, consisting of 33 and 28 amino acid residues, respectively. Both peptides interact with the OXR1 and OXR2 receptors. Neurons secreting orexins are contained in the perifornical zone of the lateral hypothalamic field. Despite the fact that there are not many of them, these neurons strongly branch, having connections with various parts of the brain, such as paraventricular, dorsomedial arcuate nucleus of the hypothalamus, blue spot, posterior hypothalamic field, spinal cord. Orexins control food intake, participate in the regulation of circadian rhythms and the development of stress reactions, sexual behavior. Their concentration in the hypothalamus increases with fasting, but intracerebral administration causes only a brief increase in appetite without a noticeable effect on the total amount of food consumed. Narcolepsy and catalepsy are associated with the absence of orexin, as they can inhibit both phases of sleep and prolong the period of wakefulness. Orexins increase the activity of the sympathetic nervous system and maintain muscle tone, which is important with increasing physical activity and maintaining it at a high level. In addition, they can positively influence the secretion of HGH-axis hormones. It is assumed that orexins can play a role in the development of diseases such as Huntington's chorea, Parkinson's disease, obstructive sleep apnea syndrome, type II diabetes.

Leptin consists of 35 amino acid residues. The predecessor is preproleptin. It is synthesized mainly in adipocytes and only in small amounts in other organs and tissues, including such parts of the brain as the cortex, hippocampus, cerebellum, basal ganglia, trunk. The greatest number of receptors for leptin in the brain is concentrated in the ventrobasal and ventromedial hypothalamus. With the accumulation of white adipose tissue in the body, the content of leptin increases and, accordingly, when fasting decreases. The peptide plays an important role in food behavior and energy metabolism - it reduces the need for food, suppresses appetite and speeds up the metabolic processes at the periphery. Directly or indirectly regulates the synthesis of hormones that affect food behavior, reducing the synthesis of oryxigenic and increasing anorexigenic. There is evidence that leptin may act as a neuroprotective agent, a neuroplastic factor. Leptin inhibits the development of excitotoxicity of glutamate and limits the damage caused by oxidative stress. In the hippocampus, under the influence of the hippocampus, the formation of free radicals is suppressed. In dopaminergic neurons it is able to stabilize mitochondrial membranes and to limit the phenomena of oxidative stress due to expression of uncoupling proteins of UCP2. Limits apoptosis in cells. Has an anticonvulsant effect. Affects memory processes, contributing to the consolidation of short-term and long-term. It is suggested that a reduction in leptin levels may be positively associated with the development of Alzheimer's disease, because it limits amyloidogenesis, by inhibiting β-secretase and activating α-secretase, and also participates in τ-phosphorylation processes, reducing the formation of abnormal τ-protein, facilitating elimination β-amyloid. It is suggested that it may be important in the development of Huntington's chorea and Parkinson's disease. In addition, it regulates blood pressure and vascular tone.

DSIP (delta-sleep-inducing peptide)
DSIP (delta-sleep-inducing peptide) consists of 9 amino acid residues. Until now, the gene, its coding, predecessor and specific receptors with the genes encoding them has not been identified. DSIP is found in the neurons of Brock's diagonal ligament, the ventral septum, the anterior hypothalamus, in the areas with gonadotropin-releasing hormone-reactivity, melanin concentrating hormone, thyroid-stimulating hormone, peptides of the secretory cells of the gastrointestinal tract, melanocorticotropes of the intermediate lobe of the pituitary gland, brainstem, pituitary and epiphysis; has specific differences in localization. Often, DSIP is colocalized with catecholamines in the chromafin granules of the adrenal medulla. With intraperitoneal administration of its rats, an increase in the content of norepinephrine and serotonin in the cerebral cortex and an increase in adrenaline without a change in the concentration of dopamine have been established, due to which it can exert a inhibitory effect on the central nervous system. There are data on stimulation of GABA production and prophylaxis. DSIP blocks the stimulating effect of glutamate by reducing the sensitivity of the "fast" ionotropic NMDA receptors of the glutamatergic system of the brain and the subsequent reduction of glutamate stress-induced excitotoxicity. Has a membrane-stabilizing effect on neuronal, erythrocyte and leukocyte membranes. Increases the activity of c-Fos gene expression, which is a marker of neuronal activity, of various parts of the limbic system, playing a trigger role in the development of emotional reactions to stress and forming their neurotransmitter integration, which leads to activation of somatovegetative manifestations. It has an anti-stress action and helps to create a state of "pre-adaptation".

The involvement of DSIP in the regulation of sleep-wake cycles is controversial, different authors provide various data, from the ability to suppress to stimulation of sleep phases. Has antiepileptic and anticonvulsant activity. The peptide can participate in analgesic processes by enhancing the binding of met-enkephalin to the OP. Enhances the release of melatonin by cleaving the remainder of tryptophan from the terminal portion of the molecule. It affects the decrease in MAO activity, inhibition of corticoliberin synthesis, stimulation of the synthesis of somatotropin, somatostatin and lylyberyrin. Determines naloxone-dependent analgesia. It is able to reduce the level of lipids and cholesterol, the cholesterol coefficient of atherogenicity. DSIP is able to prevent oxidative modification of proteins during physiological aging. Has hyperglycemic activity, which may be due to an increase in the concentration of catecholamines, which reduce the release of insulin against the background of increased production of glucagon.

PACAP (a peptide that activates pituitary adenylate cyclase)
PACAP (a peptide that activates pituitary adenylate cyclase) contains 38 amino acid residues. The structure and functions are similar to VIP. PACAP is widely distributed in brain structures and peripheral organs, including the endocrine system. The greatest number of neurons containing a peptide is found in the hypothalamus, in particular in the supraoptic and paraventricular nuclei synthesizing vasopressin and oxytocin. The peptide stimulates their production by activation of cAMP. Can act in the hypothalamus as a neurotransmitter and neuromodulator in the regulation of hormone secretion. Modulates vasopressin and oxytocin in the regulation of blood pressure and osmosis of cells, takes part in modulating the function of the cerebellum with physical activity. It is suggested that PACAP is involved in regulating the rhythm of melatonin production in the pituitary and, accordingly, affects circadian rhythms. Participates in the regulation of food behavior, having an anorexigenic effect by activating cAMP in supraoptic and paraventricular nuclei. It is important in ontogenesis, inhibiting the programmed apoptosis in the developing brain, stimulating the growth of neurites, decreasing the number of mitotically dividing cells and promoting the differentiation of neuroblasts, has a neuroprotective effect in neurotoxicity caused by an increased concentration of glutamate. Consequently, in the developing brain, PACAP acts as a neurotrophic factor, and in the developed brain as a neuroprotective agent. By activating the pituitary adenylate cyclase, the peptide stimulates the release of hormones.

BINP (neurotrophic peptide from the damaged brain)
BINP consists of 13 amino acid residues. It protects brain cells from excitotoxicity of glutamate, promotes survival of cholinergic neurons of the septum and dopaminergic neurons of mesencephalon in the primary culture of the neonatal brain.

It is difficult to overestimate the role of neuropeptides. Their study over time could open prospects for the creation of drugs and artificial regulators of the body's processes. Now a lot of research is being done and attempts are being made to create preparations based on them, but the matter is complicated by the insufficient study of all the properties of neuropeptides and their interaction with other systems. As an example of such studies, the following table can be cited.

Examples of the results of II and III phases of clinical trials of ligandine neuropeptide receptors in mental disorders.


One of the main causes of developing demension

16 Apr 2018

Scientists have confirmed that traumatic brain damage is associated with an increased risk of dementia. In addition, the maximum risk increases in patients with multiple traumatic brain injuries, they emphasize.

The study analyzed data for almost 2.8 million patients, 132,000 (4.7%) of which had at least one traumatic brain injury in 1977-2013, and 126.7 thousand ( 4,5%) was diagnosed with dementia during 1999-2013. After adjusting for socio-demographic factors and co-morbidities, including neurological and psychiatric factors, the researchers found that, compared with persons who did not have traumatic brain damage, the risk of developing dementia was 24% higher in patients who underwent similar injuries. In patients with five or more traumatic brain damage, the risk increased more than threefold. Moreover, even a single case of light traumatic brain damage increased the likelihood of developing dementia by 17%.
However, the authors of the study from the Medical School of Washington University noted earlier that the absolute risk of developing dementia under the age of 50 remained relatively low. More efforts are needed to prevent traumatic brain damage and identify strategies to reduce the risk of subsequent dementia.


Speech therapist tips

13 Apr 2018

If you want to the speech of your baby was smooth, clear, expressive and beautiful, listen to the advice of a speech therapist:

1) Say it yourself expressively and correctly, do not let yourself speak quickly, too loudly, incorrectly uttering sounds. Be an example of the right speech for your child;

2) Everyone has heard about the dangers of a pacifier. She really can do much harm to the baby, if he often and for a long time keeps it in his mouth. The nipple can provoke the formation of a high palate, which distorts the pronunciation of sounds. In addition, the dummy simply prevents the child from talking;

3) Do not imitate the so-called autonomous (child) speech of the baby. Talk with the baby in a normal language - and he will soon realize that it is more correct.
If the child stubbornly does not want to talk, although he knows how, refuse to understand his gestures and facial expressions. Only respond when the child uses speech.

4) If the child does not correctly pronounce sounds and words, do not scold him and do not make harsh remarks. So you can achieve complete rejection of the child from communication.


Anti-Nootropics. How to make a person stupid?

12 Apr 2018

You are used to analyzing nootropics and other topics related to improving the quality of life, the quality of the intellect. But today we will go from the opposite. We will analyze the most popular ways of temporary deterioration of intellectual abilities!

Cortexin, cerebrolysin buy

At the beginning
- A huge request to take the release with some humor.

- Most substances are expected in medium-high doses. In the low, it does not do much harm.


Let's start with a simple and understandable to everyone! Everyone knows that alcohol significantly changes human behavior. The effect of alcohol extends to the neurotransmitters GABA, Dopamine and Serotonin. With a significant increase in these substances, there is some effect of stupor and a growing sense of self-importance.

As a substance, alcohol itself is present initially in our body, and therefore is not an alien compound. The whole question is in the dosage of pure ethyl alcohol. So, 10 g for women and 20 for men are even considered useful, that is, 20-40 g of vodka can be called nootropic. Of course, with an irregular reception.

But who can stop after the first glass? Practice shows that the willpower of people is weak, so further - more. Add here the rate of withdrawal of alcohol from the blood, an average of 7 grams per hour and the speed of the maximum effects in 20-40 minutes, it turns out the situation "Drink and not drunk, you want more!". In an hour this person will lose tens of% of his IQ) What is not an anti-nootrops ?!)))

The most direct and coarse effect of stupor! These are substances that reduce acetylcholine. But nootropics often increase it on the contrary. A sharp decrease in this neurotransmitter leads to: confusion, nausea, thirst for water, slight hallucinations and poor eyesight.

Popular anticholinergics are: cyclodol, atropine, scopolamine, dicycloverin from trigan-d.

Perhaps you've heard in the movies or maybe from acquaintances about the so-called "truth serum", about a substance that can erase memory for several hours or days. And it's not a failure in memory as from alcohol. Everything is much more serious.

The substance that is capable of this - Scopolamine, just from the group of anticholinergics. With a high dosage of this substance, the person has a block of protection, he speaks the truth easier, memory becomes worse, and overall health is terrible. At too high a dose - death. And as we have said repeatedly, all the poison and the entire medicine, depending on the dosage. Even scopolamine in small doses is used in medicine.

Created for killing first of all dopamine. Often given to mentally ill people, their neuroleptics lead to a norm, are used in medical practice, if a shift has started due to the use of narcotic psychostimulants, Tipo Amphetamine. Substances do not treat the disorder, but stop the symptoms.

Popular antipsychotics: Aminazine and Haloperidol.
When the permissible dosage is exceeded or when used by healthy people, depressive states develop, inhibition appears, prolactin increases. There is no stupidity here, but the effect of turning into a plant. You think slowly, move slowly and speak slowly and all against the background of a complete lack of positive. The problem is also in a large half-life, in short, they act up to several days.

A soft, kind and easy way to reduce the intellect. There is no tin as from anticholinergics or antipsychotics. In the release of oxytocin, we generally gave a study of its similarity to Ecstasy, but without dependence.

In the world, Oxytocin is called a "molecule of morality", in subjects under oxytocin, empathy, empathy and empathy sharply increase. It's easier to communicate with people, less aggression. But where is dullness you ask? It is complex and manifests itself in some kind of credulity, infalty, and a slight memory impairment. Therefore I said that it is a soft and kind substance.

In the studies used for application to the skin, hair or when instilled in the nose. 10-15 units of substance. In one pharmacy ampoule 5 units. And yes, in medicine this substance is for the stimulation of childbirth, so you can not be pregnant! On the other hand, pregnant women are given intramuscularly, but it is better to be safe. Oxytocin increases even in a man when he becomes a parent.

Bottom line:

Here are the substances that can stupefy a person:

- Alcohol, the most famous way of getting into an altered state

- Cholinolytics, in the literal sense of "antinotropy", the most severe and merciless

- Neuroleptics, slow down thoughts and body, develop depresnyak

- Oxytocin, light variant. Kindness, sociality, memory loss.

Remember that the effects are directly proportional to the dosage! Even a microdose of anticholinergic can improve well-being and intelligence in some settings.

Well, I hope you liked the release! Write your antinotopes) Good luck and see you soon


Cortexin - Nootropics from the Brain of Animals

11 Apr 2018

Neuropeptide nootropic - Cortexin.

Cortexin effects

Recall that this group of neuropeptides can be attributed and Semax with Selank and Noopept and Cerebrolysin / Cerebrolysate.

This group of nootropics is often criticized for a poor evidence base, and it really is. In general, nootropics have a weak base for the treatment of some kind of intellectual disturbance. We did the issue on this subject "Hayter's Nootropics" and its essence is that the brain is extremely complicated, and there is no such tablet to work on all the memory mechanisms and improve it, as an example. In this case, no one cancels the principle of work of each nootropic.

Imagine the brain as auto, and each nootropic as an auto element. And say, if you know for sure that the wheel is punched, the nootropus X patches it, and the nootropic Y dips fuel, but the car will still be with the punctured wheel, although the nootropic Y also had a positive effect.

Neuroprotective effect
Or the effect of protecting the nerve cells. It is known that with age the number of nerve cells decreases, and although they are capable of recovery, neurogenesis, the rate of dying goes faster. Often, closer to old age, this leads to intellectual disabilities. One of the ways of such apoptosis - the death of nerve cells, is the activity of so-called caspases. Cortexin is able to inhibit or turn off certain caspases, which is best preserved by neurons.

Yes, apparently it was difficult!) More clearly, under cortexin, all that kills nerve cells - will kill less. This includes the effects of alcohol and other drugs, senile changes, and other negative effects on the brain.

Even in conditions with a lack of oxygen, cortexin is able to maintain an optimal working state, so it can help in sports.

This is the second main effect that all neuropeptides are famous for. Means the creation of new nerve cells through stimulation in the cerebral cortex of the transcription of neurotrophins (NGF, BDNF). Consider brain renewal. Which is extremely effective if there are any brain injuries. And in ordinary life, visiting new places, new activities, physical training also improve neurogenesis. In short, this is a useful effect for any person.

Anti-stress action
In at least 2 studies, there was a change in the level of cortisol, one of the main stress hormones. More precisely, if the level is too high, it decreases. Therefore, you feel less nervous.

There was another mention that Cortexin can increase serotonin. The main antidepressant neurotransmitter. There is no direct connection with stress, but there is one type of depression, this can also be attributed to stress.

Other Action
Data on the positive effects in the treatment of the effects of chronic alcoholism.

A study of neurasthenia in adolescent girls showed an improvement in 80% of cases, although without a placebo group.

A recent study in 2018 showed an excellent combination of Memantine and Cortexin and a significant improvement in intellectual function in patients with ischemia.

Effects of Cortexin
This is a more subjective point, from personal experience and feedback on the network:

- Striving for novelty

An unusual effect, manifested in a great desire to hammer the information. And do not just turn the tape, but rather read books, learn languages or programs, attend courses. It seems that the degree of interest in any case is increased by several points.

- Humanity

At first I wanted to write rationality, but this is not a crude logic. Strongly growing and emotionality, empathy. In this case, there is a similar phenibut effect of less aggression and relaxation. So emotions are not in the negative side.

- Dreams

Sometimes they even fret, it's all too realistic. And after awakening, a few more seconds are needed to return to the familiar reality.

- Reduction of animal motivation

This is both a bad and good effect, less concerned with the instinct of "Dominate, Conquer, Humiliate." Less motivation for sports and parties for the whole night, more to the intellect and to the quality of social contacts, rather than quantity.

For the sake of justice, I will immediately inform you that these effects can also be attributed to Cerebrolysin, Selank and Noopept (in descending order) so that the detective does not wake up in you and does not look for advertising for something specific.

The Cortexin course
The substance has a few contraindications and side effects, read the instructions.

It is used intramuscularly / intravenously. And yes, if you are not under the supervision of a doctor, then no intravenous infusion, this is very dangerous!

There's still a way to prepare the solution!

Usually a course or every day of 10 mg intramuscularly, or every other day. Total injections 10. In the gluteus muscle. If you decide - be sure to read how to do the injections in order to avoid getting into the vessel. Effects appear immediately, but more noticeable by the end of the course and after it.

- Cortexin is a neuropeptide, similar to other nootropics from the same group.

- Works as a neuroprotector, increases neurogenesis, antistress effect. At least, there are studies on these items.

- In medicine it is used for a number of diseases, mainly associated with ischemia, stroke and encephalopathy.

- Subjective effects: the desire for novelty, dreams and reduction of animal motivation.

- The course consists of injections of 10 mg per day

Well, the substance is unusual and interesting! If used - tell us what and how, confirm or deny the information!



10 Apr 2018

A drug of the brain of pigs, positioned by the manufacturer as a medicine. It refers to nootropic drugs, complex drugs with neurotrophic activity, is proposed for use in the treatment of patients with various neurological diseases, such as ischemic and hemorrhagic strokes, vascular dementia, including Alzheimer's disease. It is a complex of low molecular weight peptides obtained by enzymatic cleavage of purified porcine brain substance proteins. The active fraction is represented by peptides whose molecular weight does not exceed 10,000 daltons. In connection with the complex nature of cerebrolysin, the exact mechanism of its action remains unknown.


- Active ingredient: hydrolyzate brain pig.
- Dosage form: injection.

The drug has been produced and studied since the early 1970s, is the main product of the Austrian pharmaceutical company EVER Neuro Pharma, which besides this drug produces a drug intended for the treatment of Parkinson's disease, and nutritional supplements. The international name of the drug is absent.

According to the authoritative organization Cochrane Collaboration in randomized clinical trials of cerebrolysin, no improvement in the status of patients from taking the drug has been reported. Based on the results of a double-blind, randomized, placebo-controlled study in 2011, patients with mild to moderate vascular dementia demonstrated that patients who received Cerebrolysin as a supplement to acetylsalicylic acid therapy experienced significant improvements in all primary outcome parameters compared to baseline level and with the same parameters in the placebo group. Main conclusions: can be recommended for inclusion in regional forms of treatment for patients with vascular dementia.

For more than 40 years, cerebrolysin has been widely used in Russia and CIS countries. For many years (since 1992) is on the government's list of vital and essential medicines.

In the United States, the Food and Drug Administration (FDA) is not registered, but has the status of a new drug approved by the FDA for private clinical use.

The composition of the drug includes low-molecular biologically active neuropeptides, which are able to penetrate the blood-brain barrier and to go directly to the nerve cells. The drug has an organ-specific multimodal effect on the brain.

~ Neurotrophic activity ~
The drug has proven neurotrophic activity, similar to the action of natural factors of neuronal growth, but manifested in conditions of peripheral administration. It has the effect of neurotrophic stimulation of neurons of the peripheral and central nervous system.

~ Metabolic regulation ~
Increases the efficiency of aerobic energy metabolism of the brain, improves intracellular protein synthesis in the developing and aging brain.

~ Neuroprotection ~
It protects neurons from damaging effects of lactic acidosis, prevents the formation of free radicals, improves survival and prevents the death of neurons in conditions of hypoxia and ischemia, reduces the damaging neurotoxic effect of excitatory amino acids (glutamate).

~ Functional neuromodulation ~
Has a positive effect on violations of cognitive functions and memory processes.

Indications: disorders of the central nervous system: traumatic brain and spinal cord injuries, ischemic stroke, Alzheimer's disease, chronic cerebrovascular insufficiency, mental retardation in children, hyperactivity and attention deficit in children, dementia syndrome of various genesis.

Contraindications: status epilepticus, acute renal failure, individual intolerance of the drug.

Efficiency mark:
A randomized controlled study of the safety of cerebrolysin, conducted at the Christian-Doppler Hospital in Salzburg, with neuroprotective treatment of patients with acute cerebrovascular accident showed that the drug is safe and well tolerated in patients with acute stroke. The results, despite the small sample size, indicate a potential effect of treatment with cerebrolysin in acute stroke.

In 2007, a meta-analysis of the effectiveness of cerebrolysin in the treatment of Alzheimer's disease was conducted at the Department of Pharmacology and Biostatistics of Shanghai Jiaotong University Medical College. Six randomized, double-blind, placebo-controlled clinical trials were examined using standard meta-analysis methods. The analysis found that cerebrolysin can significantly improve the overall condition of patients with mild and moderate Alzheimer's disease. The effectiveness of the action of cerebrolysin on cognitive functions requires further study.

A multi-center, randomized, placebo-controlled, double-blind clinical study of cerebrolysin in 2011 after the stroke did not show a difference in the final outcome of treatment with cerebrolysin compared with placebo in the treatment of ischemic stroke. However, after the stratification of the results of the severity of the patients' condition, a decrease in mortality was observed for 90 days after the stroke by 10% compared to the control group (mortality in the placebo group was 20.2%, in the cerebrolysin group 10.5 %). This result should be confirmed by further clinical studies.


Delayed Speech Development

04 Apr 2018

Delayed speech development (PID) and delayed psycho-speech development (PID) are not independent diseases, but only certain symptoms. At the same time, the prevalence of this diagnosis has recently become an epidemic.

We list the main:

- A child at 4 months emotionally does not respond to gestures of adults and does not come alive when his mother addresses him.

- In 8-9 months he does not babble (he does not repeat ba-ba-ba, pa-pa-ta, etc. of combinations), in a year is extremely quiet and almost does not make sounds.

- In a year and a half he does not speak and does not understand simple words, for example, "mom" or "dad", names of surrounding objects. He can not fulfill simple requests like "go here", "sit down".

- In two years he uses only a few separate words and does not try to repeat new words.

- In 2.5 years in the active vocabulary less than 20 words and word-of-mouth. Does not know the names of the surrounding objects and body parts. It can not, at the request, show a familiar object or bring something. He does not know how to write phrases from two words (for example, "give water").

- A three-year-old is hardly understood even by his relatives. He does not say simple sentences, does not understand simple explanations or stories about events in the past or the future.

"At three, he talks too fast, swallowing the words." Or, on the contrary, very slowly, stretching them, although there is no such speech at home.

- In three years he speaks mostly phrases from cartoons and books, but does not build his own proposals. Mirror repeats what adults say to him, even to the point.

If the child has a delay in speech development, then his mental development is violated, and by the age of 5 the diagnosis usually changes to another: the delay of psycho-speech development.

As a rule, the delay in verbal and psycho-speech development is a consequence of brain, central nervous system, genetic or mental disorders. But why they arise, and most importantly, why more often in recent times, classical medicine can not explain.

As a therapy, medications are most often prescribed, which improve metabolic processes in brain cells, microcirculation of blood and impulses in nerve fibers. Such drugs as cortexin, actovegin, coguitum, neuromultivitis, lecithin, really contribute to the restoration of normal functioning of the central and peripheral nervous system.

Often, magnetotherapy, electroreflexotherapy is used to restore certain areas of the brain responsible for mental and speech development. Sometimes unconventional methods are also connected: hippotherapy (treatment with horse riding and training with horses), dolphin therapy.

An important role is played by the work of the defectologist (psychologist), which is aimed at raising the child's mental development level. Art therapy (treatment with the help of drawing), musterapy (treatment with the help of music), subject-sensory therapy can be used in this case: in the cerebral cortex the center of speech and the center of manual motility are located close, and with the development of fine manual motility, the development of the speech center . And, of course, you need to work with a speech therapist.

Complex treatment of a neurologist, speech therapist and psychologist, as a rule, helps to significantly improve the basic indicators of speech and mental development in general. Nevertheless, classical methods do not reveal and, accordingly, do not eliminate a number of initial violations that lead to speech underdevelopment. In other words, these methods are not enough.

According to studies conducted under the guidance of the Institute of Osteopathy, speech disorders in children are accompanied in 100% of cases and, most likely, result from structural damage to the skull and spine.

These injuries most often cause problems during pregnancy and childbirth: premature, prolonged or rapid delivery, a long anhydrous period during labor, birth asphyxia, birth trauma. And, probably, it is the spread of various methods of stimulation in childbirth and the popularity of cesarean section, even without medical indications, that cause the growth of the number of speech development delays.

However, the reasons can be and others: domestic, sports traumas, sometimes even an easy cuff can cause a number of infringements in work of a brain of the child. The result is the same: different areas of the brain start to work incorrectly or not actively. Delays in speech and mental development mean that the sites responsible for speech and intellect have suffered.

And here it is important to know: structural, mechanical damage to the skull and spine can not simply be eliminated with medication, psychotherapy or logopedic work. They can be corrected only physically, manually. This is what osteopathy is doing - human mechanics.

An osteopathic physician, when examined, identifies the affected child as a result of genera or other causes of the zone and acts on them, restoring their correct position and restoring their freedom of movement. As a rule, these are the zones that are most injured in the process of childbirth, namely: 1-2 cervical vertebra, cervico-thoracic spine, occipital-temporal sutures, intraosseous injuries of the occipital bone, main seam in the skull.

As a result, the function of the bone, nervous system and blood supply is restored. Normal blood microcirculation and metabolism in brain cells. As a result, brain nutrition is improved, its work is normalized, behavior and speech are changed. In my practice, the effectiveness of osteopathic treatment with a delay in speech and mental development is 70%. There is also documented statistics.

The Institute of Osteopathy conducted a study of children diagnosed with "dysarthria" - a general hypoplasia of speech. Half of the children (control group) underwent classical treatment with a neurologist, speech therapist and psychologist, and half (experimental) with a speech therapist and an osteopath. After three months, a comprehensive examination showed: osteopathic treatment was more effective than medication.

In the experimental group receiving osteopathic treatment, all the indices were better: emotional excitement decreased in 78% of the children (56% in the control group), restlessness in 61% (45% in the control group), speech impairment in 89% (72% in the control group).

Absolutely in all children of the osteopathic group, the independent speech and the state of the speech apparatus improved (in comparison with 94% and 78% of the children in the control group).

Psycho-speech development improved in 72% (61% in the control group), intelligence increased in 56% (45% in the control group), attention was strengthened in 45% (33% in the control group).

At the same time, in children, who were treated with osteopaths, naturally, the number of disorders at the level of the body structures decreased. This allows us to hope that in the future their development will be more harmonious.

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