Inorganic Enuresis

What is Inorganic Enuresis?

It is characterized by involuntary urination during the day and / or night, which does not correspond to the child’s mental age. Not due to the lack of control over the function of the bladder due to neurological disorders, epileptic seizures, structural abnormalities of the urinary tract.

Causes of Inorganic Enuresis

Bladder control develops gradually, it is influenced by features of the neuromuscular system, cognitive functions, and, possibly, genetic factors. Violations of one of these components may contribute to the development of enuresis. Children suffering from enuresis are approximately twice as likely to have developmental delays. 75% of children with inorganic enuresis have close relatives suffering from enuresis, which confirms the role of genetic factors. Most children suffering from enuresis have an anatomically normal bladder, but it is functionally small. Psychological stress can increase enuresis. A big role is played by the birth of a sibling, the beginning of schooling, the breakup of a family, and the transfer to a new place of residence.

Prevalence

Enuresis affects more men than women, at any age. The disease occurs in 7% of boys and 3% of girls aged 5 years, 3% of boys and 2% of girls aged 10 and 1% of boys and is almost completely absent in girls aged 18 years. Daytime enuresis is less common than nocturnal, in about 2% of 5-year-olds. Unlike nocturnal, daytime enuresis occurs more often in girls. Mental disorders are present only in 20% of children with inorganic enuresis, most often they occur in girls or in children with day and night enuresis. In recent years, descriptions of rare forms of epilepsy appear more and more often in the literature: an epileptic variant of enuresis in children (5-12 years old).

Symptoms of Inorganic Enuresis

Inorganic enuresis can be observed from birth – “primary” (80%), or occur after a period of more than 1 year, acquired bladder control – “secondary”. Late onset is usually observed at the age of 5-7 years. Enuresis can be monosymptomatic or combined with other emotional or behavioral disorders, and is the primary diagnosis if involuntary urination is observed several times a week, or if other symptoms show a temporary connection with enuresis. Enuresis is not associated with any particular sleep phase or night time, more often it is observed in a random order. Sometimes it occurs when it is difficult to go from a slow phase of sleep to a fast one. Emotional and social problems that arise as a result of enuresis include low self-esteem, a sense of inferiority, social constraints, stiffness and family conflicts.

Diagnosis of Inorganic Enuresis

The minimum chronological age for diagnosis should be 5 years, and the minimum mental age should be 4 years.

  • Involuntary or arbitrary urination in bed or clothing can be observed during the day (F98.0) or overnight (F98.01) or observed during the night and day (F98.02).
  • At least two episodes per month for children aged 5-6 years and one event per month for older children.
  • The disorder is not associated with a physical illness (diabetes, urinary tract infections, seizures, mental retardation, schizophrenia and other mental illnesses).
  • The duration of the disorder is at least 3 months.

Differential diagnostics

It is necessary to exclude the possible organic causes of enuresis. Organic factors are most often found in children who have daytime and nocturnal enuresis, combined with frequent urination and an urgent need to empty the bladder. They include: 1) disorders of the genitourinary system – structural, neurological, infectious (uropathy, cystitis, hidden spina bifida, etc.); 2) organic disorders causing polyuria – diabetes mellitus or diabetes insipidus; 3) disorders of consciousness and sleep (intoxication, somnambulism, epileptic seizures), 4) side effects of treatment with certain antipsychotic drugs (thioridazine, etc.).

Treatment of Inorganic Enuresis

Due to the etiology of the disorder, various methods are used in treatment.

Hygiene requirements include training in using the toilet, limiting fluid intake 2 hours before bedtime, and sometimes a night waking to use the toilet.

Behavioral therapy. In the classic version – conditioning by a signal (bell, beep) the time of the onset of involuntary urination. The effect is observed in more than 50% of cases. This therapy uses hardware methods. It is reasonable to combine this treatment option with praise or reward for longer periods of abstinence.

Drug treatment

The use of Melipramine is recommended. Against the background of its administration, in 30% of patients, enuresis completely stops, and in 85% it weakens.

However, the effect is not always lasting. There are reports of the effectiveness of the use of Driptan (the active substance is oxybutrin), which has a direct antispasmodic effect on the bladder and a peripheral M-cholinolytic effect with a decrease in the hypertonus of the parasympathetic nervous system. Doses 5 – 25 mg / day.

Traditional variants of psychotherapy for enuresis in some cases are not effective.

Undifferentiated Somatoform Disorder

What is Undifferentiated Somatoform Disorder?

Undifferentiated somatoform disorder. This category should be used in cases where somatic complaints are multiple, variable and long-lasting, but at the same time, a complete and typical clinical picture of a somatized disorder is not detected. For example, the assertive and dramatic nature of the complaint may be absent, the latter may be relatively small in number, or there may be no violation of social and family functioning. The grounds for the assumption of psychological conditioning may or may not be present, but there should be no somatic basis for a psychiatric diagnosis.

Symptoms of Undifferentiated Somatoform Disorder

Symptoms resembling somatic disease, however, constant complaints despite excessive detail, vague, inaccurate and inconsistent in time. Somatic is framed by emotional instability, anxiety, low mood, not reaching the level of depression, decay of physical and mental strength, besides, irritability, a feeling of internal tension and dissatisfaction are often present. An exacerbation of the disease is provoked not by physical exertion or by changing weather conditions, but by emotionally significant stressful situations.

Diagnosis of Undifferentiated Somatoform Disorder

Criteria:

  • The presence of multiple, changing somatic symptoms in the absence of any somatic diseases that could explain these symptoms.
  • Constant concern about the symptom leads to prolonged suffering and repeated (3 or more) consultations and examinations in the outpatient clinic, and if counseling is unavailable for any reason, repeated visits to representatives of paramedicine.
  • Persistent refusal to accept a medical opinion on the absence of sufficient somatic causes of the existing symptoms or only a short-term agreement with it (up to several weeks).

Undifferentiated somatoform disorder can be diagnosed, when the minimum duration of symptoms is reduced to 6 months, criteria 1 and 3 are fully satisfied, criterion 2 can only be partially met

Important differentiation with the following disorders:

  • Somatic disorders. It is most difficult to differentiate somatoform disorder from some somatic diseases, such as multiple sclerosis, systemic lupus erythematosus, etc., beginning with nonspecific, transient manifestations. Here, the doctor needs to distinguish from a variety of clinical symptoms those that are characteristic of these diseases. Thus, multiple sclerosis often begins with transient motor, sensory (paresthesia) and visual disturbances. Hyperparathyroidism can be manifested by osteoporosis (loosening and tooth loss), and systemic lupus erythematosus often begins with polyarthritis, which is gradually joined by polyserositis.
    However, one should take into account the probability of the emergence of an independent somatic disorder in such patients, which is not lower than that of ordinary people at the same age. Particular attention in case of change of emphasis in the complaints of patients or their stability, when you need to continue surveys.
  • Affective (depressive) and anxiety disorders. Depression and anxiety of varying degrees are often accompanied by somatized disorders, but they should not be described separately unless they are sufficiently pronounced and stable to justify their own diagnosis. The appearance of multiple somatic symptoms after the age of 40 years may indicate a manifestation of primary depressive disorder.
  • Hypochondriacal Disorder. With somatisation disorder, the focus is on the symptoms themselves and their individual manifestation, while in hypochondriacal disorder, attention is directed more to the presence of the intended progressive and serious disease process, as well as its disabling consequences. In hypochondriacal disorder, the patient more often asks for examination in order to confirm the nature of the alleged disease, while a patient with somatisation disorder asks for treatment in order to remove the existing symptoms. With somatisation disorder, there is usually excessive use of drugs, whereas patients with hypochondriacal disorder are afraid of drugs, their side effects, and seek support and relief from frequent visits to various doctors.
  • Delusional disorders (such as schizophrenia with somatic delusions and depressive disorders with hypochondriacal ideas). Freakish features of ideas, combined with a smaller number of them and the more constant nature of somatic symptoms, are most typical of delusional disorders.

Longer (from 2 years) and more intense symptoms are diagnosed as somatoform disorder.

Treatment of Undifferentiated Somatoform Disorder

The main role in the treatment belongs to psychotherapy. Pharmacotherapy aims to create psychotherapy opportunities and is carried out to correct the accompanying symptoms. The choice of drugs in each case is determined by the characteristics of the symptoms and associated manifestations. The following groups of drugs are used for pharmacotherapy: drugs of the first choice are antidepressants (tricyclic and SSRI groups); second choice drugs are beta blockers and mood stabilizers; In the initial stages of treatment, a combination of antidepressant with benzodiazepine is possible; antipsychotics with sedative effect are also used as reserve medicines for severe anxiety, which can not be stopped by benzodiazepines. In addition, the treatment of somatoform disorders must be supplemented with vasoactive, nootropic drugs and vegetal stabilizers.

Disruption of Activity and Attention

What is a Disruption of Activity and Attention?

Previously called minimal brain dysfunction (MMD), hyperkinetic syndrome, minimal brain damage. This is one of the most common childhood behavioral disorders, many of which remain in adulthood.

Prevalence

The disorder is more common in boys. The relative prevalence among boys and girls from 3: 1 to 9: 1, depending on the criteria of diagnosis. Currently, the prevalence among schoolchildren is from 3 to 20%. In 30-70% of cases, the syndromes of the disorder turn into adulthood. Hyperactivity in adolescence in many decreases, even if other disorders remain, but the risk of asocial psychopathy, alcoholism and drug addiction is high.

Causes Disruption of Activity and Attention

Previously, the hyperkinetic disorder was associated with intrauterine or postnatal brain damage (“minimal brain damage”). Identified genetic predisposition to this disorder. For identical twins, concordance is higher than for dvuiaytsovyh. 20-30% of parents of patients suffered or suffer from impaired activity and attention. Congenital tendency to hyperactivity increases under the influence of certain social factors, since this behavior is more common in children living in adverse social conditions. Parents of patients are more likely to have alcoholism, asocial psychopathy, and affective disorders in the general population. The alleged causes of the disorder are associated with food allergies, prolonged lead intoxication and exposure to food additives, but these hypotheses are not supported by convincing evidence. A strong relationship was found between activity and attention disorders and insensitivity to thyroid hormones – a rare condition, based on a mutation of the thyroid hormone beta-receptor gene.

Symptoms Disruption of Activity and Attention

The diagnostic criteria for a disorder have changed somewhat over the years. Symptomatology almost always manifests itself to 5-7 years. The average age of a doctor is 8-10 years.

Manic Episode

What is a Manic Episode?

A manic episode is an affective disorder characterized by a pathologically elevated mood background and an increase in the volume and pace of physical and mental activity.

The mood of the patient is raised inadequate to the circumstances and can vary from careless gaiety to almost uncontrollable arousal. A rise in mood is accompanied by increased vigor, leading to hyperactivity, excessive volume and speed of speech production, an increase in vital drives (appetite, sex drive), and a reduced need for sleep. Perception disorders may occur. Normal social inhibition is lost, attention is not maintained, there is marked distractibility, high self-esteem, super-optimistic ideas and ideas of greatness are easily expressed. A patient has many plans, but none of them is fully implemented. Criticism is reduced or absent. The patient loses the ability to critically assess his own problems; inadequate actions with negative consequences for social status and material well-being are possible; they can perform extravagant and impractical actions, waste money or be aggressive, amorous, hypersexual, playful in inappropriate circumstances.

In some manic episodes, the patient’s condition can be described as irritated and suspicious, rather than elevated. 86% of patients with bipolar disorder experience mania with psychotic symptoms throughout their lives. At the same time, increased self-esteem and ideas of superiority turn into delusional ideas of grandeur, irritability and suspicion are transformed into delusions of persecution. In severe cases, expansive-paraphrenic experiences of grandeur or delusions about noble origins can occur. As a result, leaps of thought and verbal pressure, the speech of the patient is often incomprehensible to others.

Manic episodes are much less common than depression: according to various sources, their prevalence is 0.5-1%. Separately, it should be noted that a manic episode in cases where one or more affective episodes (depressive, manic or mixed) have already occurred in the past are diagnosed within the framework of bipolar affective disorder and are not considered independently.

Today, quite conventionally, there are three severity of manic disorders:

  • Hypomania
  • Mania without psychotic symptoms
  • Mania with psychotic symptoms

Hypomania is a mild degree of mania. There is a constant light mood elevation (at least for several days), increased vigor and activity, a sense of well-being and physical and mental productivity. Increased sociability, talkativeness, excessive familiarity, increased sexual activity and reduced need for sleep are also often noted. However, they do not lead to serious disruption or social rejection of patients. Instead of the usual euphoric sociability, irritability, increased self-esteem and rude behavior can be observed.

Concentration and attention can be upset, thus reducing the opportunities for both work and leisure. However, such a state does not prevent the emergence of new interests and vigorous activity or a moderate propensity to spend.

Mania without psychotic symptoms is a moderate degree of mania. The mood is raised inadequate circumstances and can vary from careless gaiety to almost uncontrollable arousal. Elevation of mood is accompanied by increased vigor, leading to hyperactivity, speech pressure and reduced need for sleep. Normal social inhibition is lost, attention is not maintained, there is marked distractibility, increased self-esteem, super-optimistic ideas and ideas of greatness are easily expressed.

Perception disorders may occur, such as experiencing color as especially bright (and usually beautiful), concern about the fine details of a surface or texture, subjective hyperacusis. The patient may take extravagant and impractical steps, mindlessly spend money or may become aggressive, amorous, playful in inappropriate circumstances. In some manic episodes, the mood is more irritated and suspicious than upbeat. The first attack occurs more often at the age of 15-30 years, but can be at any age from childhood to 70-80 years.

Mania with psychotic symptoms is a severe degree of mania. The clinical picture corresponds to a more severe form than mania without psychotic symptoms. Increased self-esteem and ideas of greatness can develop into nonsense, and irritability and suspicion – into the delirium of persecution. In severe cases, marked delusions of grandeur or noble descent are noted. As a result, leaps of thought and speech pressure patient’s speech becomes obscure. Heavy and prolonged physical exertion and agitation can lead to aggression or violence. Neglect of food, drink and personal hygiene can lead to a dangerous state of dehydration and neglect. Delusions and hallucinations can be classified as appropriate or inappropriate.

Manic episodes, if not treated, have a duration of 3-6 months with a high probability of relapse (manic episodes recur in 45% of cases). Approximately 80-90% of patients with manic syndromes eventually develop a depressive episode. With timely treatment, the prognosis is quite favorable: 15% of patients recover, 50-60% recover not fully (numerous relapses with good adaptation between episodes), in one third of patients there is a likelihood of the disease becoming chronic with persistent social and labor maladjustment.

Causes of the Manic Episode

The etiology of the disorder is currently not fully understood. According to most neurologists and psychiatrists, genetic factors play the most important role in the occurrence of the disease, this assumption is indicated by the high frequency of the disorder in the families of patients, the increased likelihood of developing the disease with an increase in the degree of kinship, and a 75% chance of developing the disease in monozygous twins. However, the provoking influence of environmental changes is not excluded. Among the possible etiological factors, there are: metabolic disorders of biogenic amines (serotonin, norepinephrine, dopamine), neuroendocrine disorders, sleep disorders (shortened duration, frequent awakenings, disturbed sleep-wake rhythm), and even psychosocial factors.

Symptoms Manic Episode

Criteria for a manic episode:

  • high self-esteem a sense of self-worth or grandeur;
  • reduced need for sleep;
  • increased talkativeness, obsession in conversation;
  • jumps of thoughts, feeling of “flight of thought”;
  • attention imbalance;
  • increased social, sexual activity, psychomotor excitability;
  • involvement in risky operations with securities, thoughtlessly large expenditure, etc.

A manic episode may include delirium and hallucinations including

To diagnose mania, you must have at least three of these symptoms, or four, if one of the symptoms is irritability, and the duration of the episode must be at least 2 weeks, but the diagnosis can be made for shorter periods, if the symptoms are unusually severe and come quickly.

Diagnosing Manic Episode

When diagnosing a manic episode, the clinical method is the main one. In it the main place belongs to questioning (clinical interview) and objective observation of the patient’s behavior. With the help of the inquiry, a subjective history is collected and clinical facts that determine the patient’s mental state are identified.

An objective history is collected by examining medical records, as well as from conversations with the patient’s relatives.

The purpose of collecting anamnesis is to obtain data on:

  1. hereditary mental illness;
  2. patient’s personality, features of his development, family and social status, transferred exogenous hazards, features of response to various everyday situations, mental trauma;
  3. features of the patient’s mental state.

When taking a history of a patient with a manic episode, attention should be paid to the presence of such risk factors as:

  1. episodes of affective disorders in the past;
  2. affective disorders in family history;
  3. history of suicide attempts;
  4. chronic somatic diseases;
  5. stressful changes in life circumstances;
  6. alcoholism or drug addiction.

Additional methods of examination include clinical and biochemical blood tests (including glucose, ALT, AST, alkaline phosphatase; thymol test);

Treatment of Manic Episode

Treatment in the manic state is usually stationary, the length of hospital stay depends on the rate of symptom reduction (on average, 2-3 months). Treatment is possible in semi-stationary or outpatient settings.

In the system of therapeutic measures there are three relatively independent stages:

  • relief therapy aimed at treating the current condition;
  • treatment or stabilizing (supportive) therapy aimed at preventing the exacerbation of a previous condition;
  • prophylactic therapy aimed at preventing relapse (recurrence).

At the stage of treatment therapy, lithium salts (lithium carbonate, lithium oxybate), carbamazepine, and valproic acid salts (sodium valproate) are the drugs of choice.

For sleep disorders, hypnotics (hypnotics) are added to nitrazepam, flunitrazepam, temazepam, etc.

In severe psychomotor agitation, aggressiveness, the presence of manic-delusional symptoms, antipsychotics are prescribed (usually haloperidol, which, if necessary, is administered parenterally), the dose of which is gradually reduced to the full extent as the therapeutic effect is achieved. For rapid reduction of psychomotor arousal, zuclopentixol is used. The use of neuroleptics is necessary due to the fact that the effect of mood stabilizers appears only after 7-10 days of treatment. In motor arousal and sleep disorders, neuroleptics with a sedative effect (chlorpromazine, levomepromazine, thioridazine, chlorprothixene, etc.) are used.

In the absence of effect in the first month of treatment, a transition to intensive therapy is needed: alternation of high doses of incisive neuroleptics with sedatives, the addition of parenterally administered anxiolytics (phenazepam, lorazepam). In cases of resistant mania, combination therapy with lithium salts and carbamazepine, lithium salts and clonazepam, lithium salts and valproic acid salts is possible.

At the second stage, the use of lithium salts should continue on average 4-6 months to prevent the exacerbation of the condition. Lithium carbonate or its prolonged forms are used; the concentration of lithium in the plasma is maintained in the range of 0.5-0.8 mmol / l. The question of stopping the therapy with lithium drugs is solved depending on the characteristics of the course of the disease and the need for preventive therapy.

The minimum duration of maintenance therapy is 6 months after the onset of remission. With the abolition of therapy is considered appropriate to slowly reduce the dose of the drug for at least 4 weeks.

Nightmares

Causes of Nightmares

Deeply repressed phobias, complexes, aggression can be expressed in stereotypical horrors in a dream.

Symptoms of Nightmares

Terrible and disturbing, often stereotypically repeated dreams, the contents of which the patient remembers well. It seems the pursuit, the end of the world, the metamorphosis of objects. The patient is afraid to fall asleep, as this dream can see. In children, fragments of images of sleep can intrude into reality.

Diagnostics Nightmares

Dense and anxious dreams, which the patient remembers in great detail. Clinical signs:

  1. Awakening (in the second half of sleep) with detailed and lively reproduction of dreams of bright frightening content.
  2. When you wake up, you quickly reach a normal level of wakefulness and orientation.
  3. Disorders lead to marked distress.

Differential diagnostics

Nightmares may be present in the initial stages of depression, other endogenous psychosis, and chronic pain. Usually the type of dream suggests its symbolic significance.

Nightmare Treatment

Psychotherapy, psychoanalysis, deepening of sleep with antidepressants and tranquilizers, carbamazepine are used.

Hysterical Personality Disorder

Causes of Hysterical Personality Disorder

Disorder, associated with the education of the “idol of the family” type or as a result of cultivating demonstrative traits in families in which parents try to realize their own claims for leadership in children. More common in women.

Symptoms of Hysterical Personality Disorder

Since childhood, there is a desire to be in the center of attention of children and adults, the thirst for praise and evaluation. The refusal of adults to fulfill desires in a child meets a protest reaction with a demonstration of a fall, rolling of eyes, intermittent breathing. Character is marked by demonstrativeness, theatricality, extraverted behavior in excitable, emotional personalities. Patients are not able to maintain deep long-term affection. Characterized by frequent demonstrations of bouts of irritability, tears and accusations, if the person is not the center of attention or does not receive praise or approval. The suggestibility and orientation to authorities are enhanced, the influence of surrounding circumstances or circumstances is easily formed. Excessive physical preoccupation and constant manipulative behavior to meet their needs are typical. Facial expression is characterized by excessive vividness, paramimia are possible, an expansive gesture. Bright colors and extravagance prevail in clothes and cosmetics. The pursuit of occupations that satisfy the need for demonstration. High susceptibility to dissociative disorders, including motor and disorders of consciousness, as well as the use of alcohol and other psychoactive drugs. Many mental phenomena in hysterical individuals resemble paroxysmal, therefore they are close to the epileptic circle.

Diagnosis of Hysterical Personality Disorder

It should be distinguished from organic dissociative disorders characteristic of some endocrine diseases, in particular, thyrotoxicosis and organic disorders as a result of head injuries. These disorders are characterized, in addition to hysterical characteristics, by dysmnesic, dysphoric and asthenic states, as well as by typical data of additional methods of research (neurology, EEG, CT).

Treatment for Hysterical Personality Disorder

Psychoanalysis, focused on clarifying the internal sensations of the patient, pharmacotherapy. Therapy with antiparoxysmal agents, in particular diphenin and carbamazepine.

Stuttering

What is Stuttering?

Characteristic features – frequent repetition or prolongation of sounds, syllables or words; or frequent stops, indecision in speech with violations of its smoothness and rhythmic flow.

Causes of Stuttering

The exact etiological factors are not known. Put forward a number of theories:

  • The theory of “block stuttering” (genetic, psychogenic, semantogennaya). The basis of the theory is cerebral dominance of speech centers with constitutional predisposition to the development of stuttering due to stress factors.
  • Theories of the beginning (include the theory of failure, the theory of needs and the theory of anticipation).
  • The theory of learning is based on an explanation of the principles of the nature of reinforcement.
  • Cybernetic theory (speech is an automatic process of the type of feedback. Stuttering is explained by the breakdown of feedback).
  • Theory of changes in the functional state of the brain. Stuttering is a consequence of incomplete specialization and lateralization of language functions.

Recent studies suggest that stuttering is a genetically inherited neurological disorder.

Prevalence

Stuttering suffers from 5 to 8% of children. The disorder is 3 times more common in boys than in girls. In boys, it is more stable.

Symptoms of Stuttering

Stuttering usually begins before the age of 12 years, in most cases there are two acute periods – between 2-4 and 5-7 years. It usually develops over several weeks or months, starting with repeating the initial consonants or whole words that are the beginning of a sentence. As the disorder progresses, repetitions become more frequent with stuttering on more important words and phrases. Sometimes it may be absent when reading aloud, singing, talking to pets or inanimate objects. The diagnosis is made when the duration of the disorder is at least 3 months.

Clonic-tonic stuttering (disturbed rhythm, tempo, fluency of speech) – in the form of a repetition of initial sounds or syllables (logos), at the beginning of speech clonic convulsions with the transition to tonic.

Tonic-clonic stuttering is characterized by a rhythm disturbance, smoothness of speech in the form of hesitations and stops with frequent vocal enhancement and pronounced breathing disorders associated with speech. There are additional movements in the muscles of the face, neck and limbs.

During stuttering, there are:

  • Phase 1 – preschool period. The disorder appears sporadically with long periods of normal speech. After this period, recovery may occur. During this phase, stuttering occurs when children are agitated, distressed, or when they need to talk a lot.
  • Phase 2 occurs in primary school. The disorder is chronic with very short periods of normal speech. Children are aware and painfully experiencing their disadvantage. Stuttering concerns the main parts of speech – nouns, verbs, adjectives and adverbs.
  • Phase 3 occurs after 8-9 years and lasts until adolescence. Stuttering occurs or increases only in certain situations (call to the board, buying in a store, talking on the phone, etc.). Some words and sounds are more difficult than others.
  • Phase 4 occurs in late adolescence and in adults. Expressed fear of stuttering. Typical are word substitutions and bouts of wordiness. Such children avoid situations that require verbal communication.

The course of stuttering is usually chronic, with periods of partial remission. From 50 to 80% of children with stuttering, especially in mild cases, recover.

Complications of the disorder include a decline in school performance due to shyness, fear of speech disorders; restrictions in the choice of profession. For those suffering from chronic stuttering, frustration, anxiety, and depression are typical.

Diagnosis of Stuttering

Spastic dysphonia is a speech disorder similar to stuttering, but is characterized by the presence of a pathological breathing pattern.

Unclear speech, in contrast to stuttering, is characterized by erratic and disrhythmic speech patterns in the form of quick and sharp flashes of words and phrases. When speech is unclear, there is no awareness of his lack, while those who stutter are acutely aware of their speech disorders.

Stuttering Treatment

Includes several directions. The most typical is distraction, suggestion and relaxation. Stutterers are taught to speak simultaneously with the rhythmic movements of the arms and fingers, or in a slow and monotonous manner. The effect is usually temporary.

Classical psychoanalysis, psychotherapeutic methods are not effective in the treatment of stuttering. Modern methods are based on the point of view that stuttering is a form of learned behavior that is not associated with neurotic manifestations or neurological pathology. Within these approaches, it is recommended to minimize the factors that increase stuttering, reduce secondary disturbances, convince the stutterer to talk, even with stuttering, freely, without constraint and fear, in order to avoid secondary blocks.

An effective method of self-therapy based on the premise that stuttering is a specific behavior that can be changed. This approach includes desensitization, reducing emotional reactions, fear of stuttering. Since stuttering is what a person does, and a person can learn to change what he does.

Drug treatment is of an auxiliary nature and is aimed at alleviating the symptoms of anxiety, expressed fear, depressive manifestations, and facilitating communicative interactions. Soothing, sedative, fortifying agents (valerian, motherwort, aloe vera, multivitamins and B vitamins, magnesium preparations) are applicable. In the presence of spastic forms, antispasmodics are used: mydocalm, sirdalud, myelostane, diafene, amisyl, theofedrin. Tranquilizers are used with caution, mebikar 450-900 mg / day is recommended, with short courses. Significant effect is brought by courses of dehydration.

Alternative options for drug treatment:

  • In the clonic form of stuttering, pantogam is used from 0.25 to 0.75 – 3 g / day., Courses lasting 1-4 months.
  • Carbamazepines (predominantly tegretol, timonyl, or finlepsin retird) with 0.1 g / day. up to 0.4 g / day. within 3-4 weeks, with a gradual reduction of the dose to 0.1 g / day. as a supportive treatment, with a duration of up to 1.5 – 2 months.

Complex treatment of stuttering also includes physiotherapeutic procedures, courses of general and specialized speech therapy massage, speech therapy, psychotherapy using the suggestive method.

Dysthymia (Mood Decline)

What is Dysthymia (Mood Decline)?

Dysthymia is a chronic depressive mood.

Causes of Dysthymia (Mood Decline)

The types of personalities that have dysthymia, it would be correct to call constitutional depressive. These features in them are manifested in childhood and puberty as a reaction to any difficulty, and later on endogenously.

Symptoms of Dysthymia (Mood Decline)

They are tearful, pensive and not too sociable, pessimistic. Under the influence of insignificant stresses in postpuberty, for at least two years, they have periods of constant or periodic depressive mood. Intermediate periods of normal mood rarely last longer than several weeks, the whole mood of the person is colored by subdepression. However, the level of depression is lower than with mild recurrent disorder. It is possible to identify the following symptoms of subdepression:

  • reduced energy or activity;
  • violation of the rhythm of sleep and insomnia;
  • decrease in self-confidence or feeling of inferiority;
  • difficulty concentrating, and hence the subjectively perceived loss of memory;
  • frequent tearfulness and hypersensitivity;
  • decrease in interest or pleasure from sex, other earlier pleasant and instinctive forms of activity;
  • a sense of hopelessness or despair in connection with the realization of helplessness;
  • inability to cope with the routine duties of everyday life;
  • pessimistic attitude towards the future and a negative assessment of the past;
  • social isolation;
  • decrease in talkativeness and secondary deprivation.

Diagnosis of Dysthymia (Mood Decline)

  • At least two years of persistent or recurring depressive mood. Periods of normal mood rarely last longer than a few weeks.
  • The criteria do not correspond to a mild depressive episode, since suicidal thoughts are absent.
  • During periods of depression, at least three of the following symptoms should be present: a decrease in energy or activity; insomnia; decreased self-confidence or inferiority; difficulty concentrating; frequent tearfulness; decrease in interest or pleasure from sex, other pleasant kinds of activity; sense of hopelessness or despair; inability to cope with the routine duties of everyday life; pessimistic attitude towards the future and a negative assessment of the past; social exclusion; reduced need for communication.

Differential diagnostics

It should be differentiated from a mild depressive episode, the initial stage of Alzheimer’s disease. In a mild depressive episode, suicidal thoughts and ideas are present. In the initial stages of Alzheimer’s disease and other organic disorders of depression become protracted, organics can be identified neuropsychologically and with the help of other objective research methods.

Dysthymia Treatment (Mood Decline)

With a reduced mood, Prozac, sleep deprivation treatment and enotherapy are indicated. Sometimes 2-3 sessions of nitrous oxide, amytal-caffeine disinhibition and intravenous administration of novocaine, as well as nootropic therapy, give the effect.

Dissociative Seizures

What is Dissociative Seizures?

Dissociative seizures (pseudo-fits) are seizures that very accurately mimic an epileptic seizure, but without life-threatening manifestations (dangerous falls, biting of the tongue, loss of consciousness is absent and memory is kept for events of this period, stupor or trance may occur).

Causes of Dissociative Seizures

Situational conditionality

Symptoms of Dissociative Seizures

The main feature is sudden and unexpected jerky movements, for which stereotype is not observed and a certain theatricality is characteristic. Duration from minutes to hours. The demonstrative character emphasizes what happens in the presence of outside observers and disappears when they lose interest in the patient. More often abortive forms are encountered – fainting, tears or laughter, tremor of the whole body with external signs of loss of consciousness without actually losing it. In childhood, there is a protest reaction when adults refuse to fulfill the child’s demands.

Diagnosis of Dissociative Seizures

For a reliable diagnosis, the following criteria should be:

  • The absence of a physical disorder that could explain the symptoms that characterize the disorder (but there may be physical disorders that give rise to other symptoms).
  • There is a convincing link in time between the onset of symptoms of the disorder and stressful events, problems or needs.
  • Sudden and unexpected spastic movements, resembling any variants of epileptic seizures, but without subsequent loss of consciousness.
  • Convulsions are not accompanied by a bite of the tongue, serious bruises or injuries due to a fall or involuntary urination, loss of consciousness, pupillary reaction to light is maintained.

Differential diagnosis: Should be distinguished from epileptic seizures.

Treatment of Dissociative Seizures

Emotional stress psychotherapy, psychoanalysis.

Dissociative Disorders of Motility

Causes of Dissociative Motility Disorders

Psychological stress, avoidance of conflict by flight to the disease.

Symptoms of Dissociative Motility Disorders

Full or partial paralysis of the limb (mono-, those- and paraparesis and plegia), ataxia, astasia-abasia, apraxia, akinesia, aphonia, dysarthria, blepharospasm.

Evaluation of the patient’s mental state suggests that a decrease in productivity resulting from the loss of function helps him to avoid unpleasant conflict or to express his dependence or indignation indirectly. A significant factor is the behavior aimed at attracting attention.

Diagnosis of Dissociative Motility Disorders

With dissociative paralysis, there are no pyramidal signs, disturbance of trophism and tone, and sensitivity disorders vary.

Treatment of Dissociative Motility Disorders

Psychoanalysis, hypnosis, Amital-caffeine disinhibition, behavioral therapy.

Which doctors should be consulted if you have Dissociative Motility Disorders

Psychiatrist