There will be a judge for everything against the Jews.
For liveliness. For mind. For stoop.
For the fact that a Jewish woman shot at the leader.
Because she missed.
So later the poet wrote.
Who is Fanny Kaplan?
This woman in Soviet times became a symbol of "absolute evil." The stronger the authority of Lenin's personality grew in the country, the more demonic the figure of the one who raised her hand against the leader of the world proletariat looked.
Conversely, for those who did not like Soviet power, the person of a little woman who tried to destroy the communist tyrant aroused deep respect.
And in folklore Fanny Kaplan completed the top three "Lenin's women" along with Nadezhda Krupskaya and Inessa Armand. There was even a legend that those very shots were not a political assassination at all, but the revenge of a rejected woman.
Love and revolution
So who is Fanny Kaplan really and why did she shoot Lenin?
She was born in Ukraine, in the Volyn province, on February 10, 1890. Her father was Chaim Roitblat who worked as a teacher in a Jewish elementary school. The future terrorist was then called Feiga Khaimovna Roytblat.
A deeply religious Jewish family, in which, in addition to Feiga, there were seven more children, was not prosperous. And that's putting it mildly. The prospects for a poor Jewish girl in Tsarist Russia, where anti-Semitism at that time was practically elevated to the rank of state policy, were not very many.
Therefore, there is nothing surprising in the fact that as a teenager, Feiga became involved in the activities of revolutionary circles. Most of all, she was drawn to the anarchists. It was in their ranks that the 15-year-old girl met the first Russian revolution.
She changed her real name to the pseudonym Fanny Kaplan, acquired the party nickname "Dora" and plunged headlong into the revolutionary struggle. The ardor of the girl was complemented by a feeling of falling in love - her comrade-in-arms became her chosen one Victor Garsky, he is Yakov Shmidman.
Together they were preparing a major terrorist attack - an attempt on the life of the Kyiv Governor-General Sukhomlinov. If Garsky had a certain experience behind him, then for Fanny this action should have been a debut. However, everything ended in complete failure.
December 22, 1906 in the Kyiv hotel "Kupecheskaya" there was a powerful explosion. The gendarmes who arrived at the scene found a wounded woman at the explosion site, who was Fanny Kaplan. It was not difficult for experienced professionals to determine that an improvised device exploded.
How exactly this happened and who was to blame is unknown. However, Garsky, leaving his comrade-in-arms and beloved, fled. Fanny, on the other hand, fell into the hands of the gendarmes with a shell shock, wounds to her arms and legs, and a pistol was also found in her room.
ten years of hell
By that time, the tsarist authorities did not stand on ceremony in the means of suppressing revolutionary uprisings. 16-year-old Fanny Kaplan was awaiting trial, which sentenced her to death. However, given her age, her death was replaced with indefinite hard labor.
I must say that during interrogations, Fanny showed her character, not telling anything about her lover who betrayed her, or about other associates.
And then there was Transbaikalia, Maltsev hard labor prison, and then the most terrible in Russia Akatui hard labor. This is how a girl who did not have time to see anything in life, who did not show herself in anything in the revolution, ended up in a real earthly hell.
The consequences of the injury and overwork led to the fact that Fanny in January 1909 was completely blind. She tried to commit suicide, but she failed. The prison administration, making sure that the girl did not feign loss of vision, gave her some indulgences in her work. Three years later, vision was partially restored.
Surprisingly, in hard labor Fanny continued to think about politics. She was seriously influenced by other prisoners, primarily a socialist-revolutionary Maria Spiridonova. It was she who, in 1918, shortly before the assassination attempt on Lenin, would raise a revolt of the Left Socialist-Revolutionaries against the Bolsheviks in Moscow, which would fail.
Fanny Kaplan no longer considers herself an anarchist, but a Socialist-Revolutionary. However, for those sentenced to indefinite hard labor, is there a difference?
Freedom to her, like other political prisoners, brought the February Revolution. Having entered hard labor at the age of 16, she was released at the age of 27. However, those who saw her after her release considered her a deep old woman - overwork in the mines and the consequences of the injury affected.
From Ulyanovsk to Ulyanovsk
There is no home, no family - Fanny's relatives moved to America back in 1911. The closest to her were those with whom she went through hard labor.
The provisional government took care of the prisoner of tsarism - she received a ticket to Evpatoria, where a sanatorium was opened for former political prisoners.
There, in the summer of 1917, Fanny, who had recovered and cheered up, met Ulyanov. But not with Vladimir, but with his brother Dmitry. They still argue about the relationship between Fanny and the leader’s brother, but one thing is known for sure - thanks to Ulyanov Jr., Kaplan received a referral to Dr. Girshman’s Kharkov eye clinic.
The operation in Kharkov helped - Kaplan began to see better. In the Crimea, she gets a job as the head of courses for the training of workers of volost zemstvos.
This was hardly what Fanny dreamed of. But she was sure that her fate would change. Here the Constituent Assembly convenes, in which the Socialist-Revolutionaries will have the majority, and then ...
But in October 1917, the Bolshevik revolution broke out, which violated all the plans of both the Socialist-Revolutionaries in general and Fanny in particular.
In February 1918, when it became clear that there would definitely be no Constituent Assembly, Kaplan decided to act. If at the dawn of her revolutionary career she did not kill the governor-general, then why not make up for this omission by killing Lenin.
For the Socialist-Revolutionary Party, individual terror was the usual method of struggle, so that Fanny had more than enough like-minded people among his party comrades. And the situation was extremely acute - the Treaty of Brest-Litovsk with Germany forced many to turn away from the Bolsheviks, and the defeat of the Left Social Revolutionaries in July 1918 gave rise to many who wanted to settle not only political, but also personal scores with Lenin and other prominent Bolsheviks.
For a woman without a family and children who went through a hard labor hell, putting her life at stake again was a common thing. Moreover, the chances of success were very high.
One step away from success
At that time, there was no modern idea of \u200b\u200bthe protection of top officials. Half a century before the assassination attempt on Lenin Alexander II almost grabbed a bullet from a terrorist Dmitry Karakozov. The king was saved not by security, but by the intervention of a bystander. The guards did not save the Austrian Archduke Ferdinand whose death triggered the outbreak of the First World War.
Yes, and Lenin himself, who miraculously survived in August 1918, almost died six months later. His car was stopped by ordinary robbers, they threw the leader of the proletariat along with the driver into the street and drove away.
Under these conditions, even a well-known politician could be killed by any determined person, let alone something, and Fanny Kaplan's determination was not to be taken. It was not a hindrance and poor eyesight - it was necessary to shoot from a short distance.
The circumstances of what happened on August 30, 1918 are still being debated. Versions are put forward, one more fantastic than the other - staging, Sverdlov's conspiracy, "second shooter", etc., etc.
Fanny Kaplan herself also let in fog, pleading guilty during the arrest, but did not tell anything about those who helped her. No wonder - she was also silent 12 years before, after the explosion in Kyiv.
She explained her actions simply and logically: Lenin was a traitor to the revolution, and his life pushed back the onset of socialism for decades. With her shots, Fanny tried to remove this obstacle.
That evening, Lenin, like other Bolshevik leaders, spoke at the Friday rallies at the factories. In the morning in Petrograd as a terrorist Leonid Kannegiser the head of the Petrograd Cheka was killed Moses Uritsky. Despite this, Lenin did not change his plans. A brilliant orator, Lenin spoke at a rally at the Michelson factory and, surrounded by workers, moved to the exit. He was about to get into the car when a woman approached him with a question. While Lenin was talking to her, Kaplan approached him from behind and fired three shots. Two bullets hit the neck and arm of the Bolshevik leader, the third hit a woman who was talking to him.
Legend of Kaplan
The seriously wounded Lenin was sent to the Kremlin, Kaplan was detained a few minutes later. According to witnesses, Fanny said: "I have done my duty and I will die with valor." During interrogations, she insisted that she acted alone.
There was no long investigation, which makes some researchers assure that Fanny knew too much, and they hastened to get rid of her.
But, perhaps, everything is simpler - the Bolsheviks, furious with the murder of Uritsky and the attempt on Lenin, officially announced the beginning of the "Red Terror", which was supposed to hit their ideological and class enemies. In this situation, they were not going to burden themselves with judicial investigative ceremonies. September 3, 1918 Chairman of the All-Russian Central Executive Committee Yakov Sverdlov gave a verbal order: to shoot Kaplan. Commandant of the Kremlin Pavel Malkov led Fanny Kaplan to the yard of the auto-combat detachment named after the All-Russian Central Executive Committee, where he personally shot her to the sound of running cars.
Fanny's body was pushed into a tar barrel, doused with gasoline and burned near the walls of the Kremlin.
Not spoiled by fame during her lifetime, Fanny Kaplan became famous after her death. For the Soviet people, she became "terrorist number one." Her story is overgrown with legends - someone allegedly saw her alive years after the execution, either on Solovki, or in Kazakhstan, or somewhere in the Caucasus. Today, rock bands are named after her, and she is the subject of countless anecdotes, historical books, and films.
Does she deserve it? Probably not. But the Greek Herostratus also at one time sentenced to oblivion, but everything turned out exactly the opposite. The story has its own, special sense of humor.
Kaplan G., Sadok B. Clinical psychiatry. Download
TRANSLATION FROM ENGLISH ADDEDPARTICIPANTS OF THE RUSSIAN EDITION
Editor-in-Chief - Tatyana Borisovna Dmitrieva, Corresponding Member. RAMS, professor
Editors and authors of additions
Aleksandrovsky Yuriy Anatolievich, Dr. med. Sciences, Professor - Managing Editor
Avedisova Alla Sergeevna, Ph.D. honey. Sciences (Ch. 15, 24) Bardenshtein Leonid Mikhailovich, Doctor of Medicine. Sci., Professor (Ch. 9, 10) Vandysh-Bubko Vasiliy Vasilievich, Dr. med. Sciences (Ch. 3, 4) Guryeva Valeria Alexandrovna, Doctor of Medicine. sciences, professor (ch. 20)
Enikeev Iskander Derdovich, Ph.D. honey. in Medicine, Fellow of the American Psychiatric Association, M.D., Ph.D. (translation editor)
Igonin Andrey Leonidovich, Dr. sciences, professor (ch. 5)
Kekelidze Zurab Ilyich, Dr. med. sciences (ch. 19, 22, 25)
Klimenko Tatyana Valentinovna, doctor of medical sciences sciences (ch. 6)
Kogan Boris Mikhailovich, Dr. sciences (ch. 27)
Kolosov Vladimir Petrovich, Ph.D. honey. sciences (ch. 23)
Kondratiev Fedor Viktorovich, Dr. sciences, professor (ch. 7, 8)
Romasenko Lyubov Vladimirovna, Dr. Sciences (Ch. 11, 12, 14, 17)
Tkachenko Andrey Anatolievich, Dr. sciences (ch. 13)
Shishkov Sergey Nikolaevich, Ph.D. legal sciences (ch. 26)
Shostakovich Boris Vladimirovich, Dr. Sciences, Professor (Ch. 16, 18)GEOTAR MEDICINE Moscow 1998
UDC 616. 89 (075 8) BBK56 14Ya73 P86
ISBN 5-88816-010-5
PocketHandbookofClinicalPsychiatry//HaroldIKaplan, BenjaminJSadock//Baltimore, Williams & Wilkins - ISBN 0-683-04583-0Recommended by the Ministry of Health of the Russian Federation as a teaching aid for students of medical universities, interns, residents, medical cadets of institutions of additional professional education.
Translation of the 2nd edition of the "Concise Guide to Clinical Psychiatry" by the world-famous authors G Kaplan and B Sadok (1996, publishing house "Williams & Wilkins") The publication has been supplemented and adapted by leading Russian psychiatrists in accordance with the characteristics and traditions of Russian psychiatry. The book covers modern scientific and practical information on key aspects of the etiology, symptoms, diagnosis and treatment of all forms of mental pathology. The text is concise, accessible, accompanied by a large number of tables that facilitate the perception of the material.
The book is intended for psychiatrists, general practitioners and medical students
The rights to this publication belong to the publishing house GEOTAR MEDICINE Reproduction and distribution in any form of part or the whole publication cannot be carried out without the written permission of the publisher
FOREWORD
Acquaintance with the basics of clinical disciplines taught in medical schools around the world is of great importance for expanding the horizons of medical students and young doctors.
Despite the fact that modern medicine is basically international, in many countries it retains its own traditions and schools, and the level of development of medical science largely depends on the material and technical capabilities of healthcare.
This determines the regional and national peculiarities of understanding and solving medical, diagnostic, preventive, and rehabilitation problems, which sometimes creates difficulties for specialists from different countries in finding a common language for professional communication.All this is clearly manifested in the example of modern psychiatry. Today, various classification and diagnostic schemes are used in medical institutions in the United States (DSM-IV-R), European countries (ICD-10), in Russia, where ICD-9 is still used.
At the same time, there are a large number of comments accepted in each country and options for approaches for making a psychiatric diagnosis.
One of the main ways to overcome these differences is to get acquainted with fundamental scientific publications, primarily with guidelines for students and doctors published in foreign countries.Unfortunately, modern foreign manuals on psychiatry have hardly been translated in Russia until recently. Known from annotated translations, they did not give a complete picture of the author's positions and did not always represent the essence of their approaches to understanding the foundations of psychopathology.
The publication in Russia of the American manual on psychiatry by G. Kaplan and B. Sadok, repeatedly reprinted in many countries of the world, undertaken by the young publishing house GEOTAR MEDICINE, is a significant event in Russian psychiatry for a number of reasons.
Firstly, this book allows you to "according to the original source" to get acquainted with the principles and main methodological approaches in making a diagnosis and conducting a "standardized" treatment of mentally ill patients, adopted in the United States and many English-speaking countries.
Secondly, the book is written taking into account the current trend of convergence of psychiatry with other areas of clinical medicine and is aimed not only at a qualified psychiatrist, but also at a general practitioner. In this regard, it can become an important tool in our country for specialists in various clinical disciplines, as well as for district and family doctors.
Thirdly, the book is notable for its methodological clarity and complete coverage of all the major clinical problems of modern psychiatry. Its 27 main chapters and good reference support allow you to navigate almost all issues of diagnosis, therapy and rehabilitation of the mentally ill.
The published guide is not limited to the translation of the author's text. A large team of highly qualified specialists worked on its adaptation for the Russian reader and addition (in agreement with the authors), who by right could become co-authors of individual chapters of the guide. All additions and comments to the translation are in italics in the text.
"Clinical Psychiatry" is published in Russia shortly after the Russian-American meeting of specialists in the field of psychiatry (Moscow, September 1997), who discussed issues of interaction within the Healthcare Committee of the Russian-American Commission on Economic and Technological Cooperation ("Gore-Chernomyrdin Commission" ).
At this meeting, specific areas of cooperation in the field of scientific research and practical psychiatry were outlined. Among them, translations of scientific and educational literature are of great importance. The publication of the book by G. Kaplan and B. Sadok is a real fulfillment of the cooperation plan, contributing to the expansion of contacts between domestic psychiatrists and American colleagues.
I would like to express my confidence that this book will have a large number of interested, thinking readers and it will contribute to the mutual enrichment of Russian and American psychiatry.
Chief Editor
Minister of Health of Russia
Corresponding Member of the Russian Academy of Medical Sciences, Professor T.E. Dmitrieva
Content
1. Diagnosis and classification in psychiatry .............................................. .............................. thirteen
I. Introduction ............................................... ................................................. ................... thirteen
II. Classification of mental disorders .............................................................. ................... fourteen
2. Psychiatric examination: medical history, mental state, clinical signs and symptoms .................................................................. .............................................. 23
I. Introduction ............................................... ................................................. ................. 23
II. Methodology of the clinical interview .......................................................... ................... 23
III. Psychiatric medical history ............................................................... ........................... 25
IV. Mental condition................................................ .............................................. 26
V. Somatic and neurological examination .............................................................. ........ thirty
VI. Recording Findings from the Medical History and Evaluation of Mental Status ....................... 30
VII. Definitions (definitions) of signs and symptoms found during the examination of the mental state .............................................................. ......................... 34
3. Delirium, dementia, amnestic and other cognitive disorders and mental disorders due to somatic and neurological diseases............................................................... ................................................. ................................. 43
I. Introduction ............................................... ................................................. ................. 43
II. Clinical examination .............................................................. ............................................... 44
III. Delirium .................................................. ................................................. ................. 44
IV. Dementia ................................................. ................................................. ............... 47
V. Dementia in Alzheimer's disease (TWO).................................................. ................... 51
VI. Vascular dementia .............................................................. ............................................... 54
VII. Pick's disease................................................... ................................................. .......... 57
VIII. Creutzfeldt-Jakob disease .............................................................. ................................. 57
IX. Huntington's disease (progressive hereditary chorea, Huntington's chorea) ................................................. ................. 57
X. Parkinson's disease (shaking palsy).................................................................. .............. 58
XI. Other dementias................................................... ................................................. ..59
XII. Amnestic disorders .................................................................. ................................... 59
XIII. Transient global amnesia .............................................................. ........................... 61
XIV. Mental disorders due to somatic or neurological diseases.................................................................................. ................................................. ...... 61
XV. Other pathological conditions ............................................................... ................................... 62
4. Neuropsychiatric aspects of HIV infection .............................................................. ................. 67
I. Introduction ............................................... ................................................. ................... 67
II. Clinical manifestations of CNS damage .............................................................. ................... 69
III. Psychopathological syndromes .............................................................. ................................. 70
IV. Treatment................................................. ................................................. ................. 71
5. Substance Use Disorders ..............................................................75
I. Introduction ............................................... ................................................. ................. 75
II. Opioids .................................................. ................................................. ................... 84
III. Sedatives, hypnotics and anxiolytics .............................................................. 87
IV. Stimulants (phenamine and substances similar in their effect to phenamine) .................................................................. ................................................. ................... 89
V. Cocaine ............................................... ................................................. ................... 90
VI. Cannabis.................................................. ................................................. ............... 91
VII. Hallucinogens .................................................................. ................................................. ..... 92
VIII. PCP ................................................. ................................................. ....................... 93
IX. Inhalants ............................................... ................................................. .................94
X. Caffeine ............................................................... ................................................. ...................... 95
XI. Nicotine................................................. ................................................. ................... 95
6. Alcohol use disorders .............................................................. .......... 97
I. Introduction ........................................: ..... ................................................. ................. 97
II. Alcohol dependence and alcohol abuse ............................................................. 98
III. Alcohol intoxication (alcohol intoxication).................................................................. .104
IV. Psychotic disorder with hallucinations caused by alcohol .............................. 106
V. Alcoholic withdrawal syndrome.................................................................... .................................... 106
VI. Alcohol withdrawal syndrome with delirium (delirium tremens).................................................................. 106
VII. Persistent amnestic disorder caused by alcohol .............................................. 108
VIII. Persistent alcohol-induced dementia .............................................................. ................. 109
7. Schizophrenia ............................................... ................................................. ................... 111
I. Definition ............................................................... ................................................. .......... 111
II. Historical information ................................................................ ................................................. 111
III. Diagnosis and symptoms ............................................................... ................................................. 111
IV. Types of schizophrenia .............................................................. ................................................. .114
V. Epidemiology ............................................................... ................................................. ...... 116
VI. Etiology................................................. ................................................. .............. 117
VII. Laboratory and psychological research............................................................... ...... 119
VIII. Pathophysiological features .............................................................. ......................... 120
IX. Psychodynamic factors .................................................................. ................................. 120
X. Differential diagnosis .................................................................. ................................... 121
XI. Course and prognosis ............................................... ................................................. .. 122
XII. Treatment................................................. ................................................. ................ 123
8. Delusional and other psychotic disorders .............................................. .............. 129
I. Brad ............................................... ................................................. ......................... 129
II. Schizophreniform disorder .............................................................. ......................... 133
III. Schizoaffective disorder .............................................................. ............................. 134
IV. Brief psychotic disorder .............................................................. ........ 135
V. Induced psychotic disorder .............................................................. ............ 136
VI. Postpartum psychosis .................................................................. ............................................. 137
VII. Psychotic disorder, unspecified ....................................................................... .............. 138
9. Mood disorders............................................................... ............................................... 141
I. Introduction ............................................... ................................................. ................ 141
II. Diagnosis, signs and symptoms ............................................... ................................. 141
III. Epidemiology................................................. ................................................. .... 148
IV. Etiology................................................. ................................................. ............. 149
V. Laboratory and psychological research............................................................... ........ 150
VI. Psychodynamics ................................................................ ................................................. ..... 151
VII. Differential diagnosis .................................................................. ................................. 151
VIII. Course and prognosis ............................................... ................................................. 154
IX. Treatment................................................. ................................................. ................ 155
10. Anxiety disorders............................................................... ............................................. 161
I. Definition ............................................................... ................................................. .......... 161
II. Diagnosis and symptoms ............................................................... ................................................. 161
III. Epidemiology................................................. ................................................. .... 163
IV. Etiology................................................. ................................................. ............ 170
V. Psychological research............................................................... ................................. 171
VI. Laboratory research................................................ ................................. 171
VII. Pathophysiological features .............................................................. ......................... 171
VIII. Psychodynamics ................................................................ ................................................. .... 172
IX. Differential diagnosis .................................................................. ................................. 173
X. Course and forecast .................................................. ................................................. ...... 175
XI. Treatment................................................. ................................................. ................. 176
11. Somatotrophic Disorders, Mimic Disorders and Simulation .................................179
I. Somatoform disorders............................................................... .................................... 179
II. Factitious Disorders .................................................................. ...................................... 191
III. Simulation................................................. ................................................. .............. 193
12. Dissociative disorders............................................................... ................................... 195
I. Introduction ............................................... ................................................. ................. 195
II. Dissociative amnesia .................................................................. ......................................... 196
III. Dissociative fugue .............................................................. ................................................. 199
IV. Dissociative Identity Disorder.................................................................... ......... 201
V. Depersonalization disorder............................................................... ....................... 203
IV. Dissociative disorder, unspecified ............................................................... ............ 204
13. Sexual dysfunctions, gender identity disorders and paraphilias... 205
I. Sexual dysfunctions............................................................... .............................. 205
II. Gender Identification Disorders .............................................................. ...................... 214
III. Paraphilia ............................................................ ................................................. ............. 220
14. Disorders associated with gray hair .............................................. ................................... 223
I. Introduction ............................................... ................................................. ................. 223
II. Anorexia nervosa .............................................................. ................................................. .. 223
III. Bulimia Nervosa .............................................................. ................................................. .... 227
15. Sleep disorders.................................................... ................................................. ........ 231
I. Introduction ............................................... ................................................. ................. 231
II. Primary sleep disorders .............................................................. ................................... 233
III. Sleep Disorders Associated with Psychiatric Disorders...............................................241
IV. Other sleep disorders .............................................................. ................................................. 241
16. Violation of control over impulses and disorders of adjustment .......................................... 243
I. Violation of control over impulses .............................................. ...................... 243
II. Adjustment Disorders .................................................................. ................................................... 248
17. Psychosomatic disorders and disorders associated with the action of psychogenic factors .............................................................. ................................................. ........... 251
I. Psychosomatic disorders ............................................................... ............................... 251
II. Psychiatry by type of consultation-interaction .............................................. ..... 261
III. Special conditions for the treatment of therapeutic patients .............................................. ....263
IV. Pain................................................. ................................................. ......................... 265
V. Analgesia ............................................................... ................................................. ................. 266
VI. Alternative (non-traditional) medicine .................................................................. .................266
18. Personality disorders............................................................... ................................................. 269
I. Introduction ............................................... ................................................. ................. 269
II. Personality disorders with manifestations of eccentricity and eccentricity .................................271
III. Disorders with manifestations of theatricality, emotionality and lability ... 275
IV. Personality Disorders with Manifestations of Anxiety and Fear ..........................................282
V. Other personality disorders .............................................................. ...................................... 286
19. Suicides, excitement and other medical emergencies .................................................................. .... 289
I. Introduction ............................................... ................................................. ................. 289
II. Self-defense-precautions to be taken by the doctor.....289
III. Preventing Harm to Yourself and Others.................................................................. 290
IV. Other Conditions Requiring Urgent Psychiatric Care .................................................293
20. Disorders of infancy, childhood and adolescence ............................................. 309
I. Principles of diagnostic assessment of the condition of children and adolescents .............................. 309
II. Child development................................................ ................................................. .... 313
III. Mental retardation................................................ ................................................. 321
IV. General developmental disorders .............................................................. ...............................327
V. Disorders of learning, motor skills and communication...............................................331
VI. Attention Deficit Disorders and Destructive Behavior............................334
VII. Behavioral disorders in infancy and early childhood due to gray hair...... 339
VIII. Tic Disorders .............................................................. ......................................... 340
IX. Disorders of excretory functions .............................................................. .................... 342
X. Other disorders of infancy, childhood and adolescence .............................. 344
XI. Other disorders occurring in childhood and adolescence ...................... 346
XII. Other Disorders Occurring in Childhood .............................................................. 347
21. Geriatric psychiatry............................................................... ................................... 349
I. Introduction ............................................... ................................................. ................. 349
II. Epidemiology................................................. ................................................. ...... 349
III. Medical aspects .................................................................. ............................................... 349
IV. Clinical Syndromes .................................................................. ............................................. 350
V. Psychotherapy of the elderly .............................................. ................................... 364
22. Bereavement and death .............................................. ................................................. 367
I. Grief, grief and bereavement .............................................. ......................................... 367
II. Death and dying .............................................................. ................................................. ... 370
23. Psychotherapy .............................................................. ................................................. .............. 373
I. Introduction ............................................... ................................................. ................. 373
II. Psychoanalysis and psychoanalytic psychotherapy .............................................................. ... 373
III. Behavioral Therapy .................................................................. ................................... 375
IV. Cognitive Therapy .................................................................. ............................................... 376
V. Family therapy............................................................... ................................................. ... 377
VI. Interpersonal Therapy .................................................................. .................................... 377
VII. Group therapy .................................................................. ................................................. 377
VIII. Couples Therapy or Marriage Therapy .............................................. ...............................379
24. Psychopharmacology and other types of biological therapy .............................................................. 383
I. Basic principles of psychopharmacology .............................................. ................. 383
II. Anxiolytics and hypnotics .............................................................. .................................... 387
III. Antipsychotic drugs .................................................................. ................................. 395
IV. Antidepressants .................................................................. ................................................. .411
V. Anti-manic drugs............................................................... ................................. 425
VI. Other drugs ................................................................ ................................................. .428
VII. EST.................................................. ................................................. ....................... 431
VIII. Psychosurgery ................................................................ ................................................. ..... 434
25. Movement disorders caused by the influence of drugs ... 435
I. Introduction ............................................... ................................................. ................ 435
II. Parkinsonism caused by neuroleptics .............................................................. ............. 435
III. Acute dystonia caused by neuroleptics .............................................................. ........... 437
IV. Acute akathisia caused by neuroleptics .............................................................. ............ 437
V. Tardive dyskinesia caused by antipsychotics .............................................................. ........ 438
VI. Malignant neuroleptic syndrome ............................................................. ......... 440
VII. Postural tremor associated with drug exposure .......... 441
VIII. Hyperthermic syndromes .................................................................. ................................. 441
26. Legal aspects of psychiatry .............................................. ................................. 443
I. Introduction ............................................... ................................................. ................. 443
II. Legal aspects of psychiatric practice .............................................................. ..... 444
III. Legal Aspects of Child and Adolescent Psychiatry.................................................... 449
IV. Legal Aspects of Psychiatry and Civil Law....................................................... 450
V. Legal Aspects of Psychiatry and Criminal Law .......................................................... .. 451
VI. Conclusion................................................. ................................................. ............ 452
27. Laboratory research in psychiatry .............................................. .................... 453
I. Introduction ............................................... ................................................. ................. 453
II. Screening tests for somatic diseases .............................................................. ... 454
III. Drugs used to treat psychiatric disorders..............................................454
IV. Laboratory research................................................ .................................... 457
V. Other laboratory tests .................................................................. ...................... 466
28. Handbook............................................... ................................................. ................. 477
I. Abbreviations ............................................................... ................................................. .......... 477
II. Glossary of terms................................................... ................................................. ... 478
III. DSM-IV Classification............................................................... ............................................. 488
IV. Author's guide ................................................................ ............................................... 505
(Vengerov)
Big biographical encyclopedia. 2009 .
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Kaplan, Isaac Mikhailovich Poster for the film "My Dear Man" Isaac Mikhailovich Kaplan (December 12, 1924, Moscow 1997, St. Petersburg) Soviet film artist. Graduated from the art faculty of VGIK. Since 1954, the artist of the film studio "L ... Wikipedia
Bars, leopard. It was preserved among the Tatars Mishars (Meshcheryakov) in the surname Kaplanov. Anthropolexeme. Tatar, Turkic, Muslim male names. Glossary of terms ... Dictionary of personal names
Fanny Efimovna (real name and first name Roytblat Feiga Khaimovna) (1887 1918), a participant in the revolutionary movement, joined the anarchists. In 1907 she was sentenced to eternal penal servitude (served in Akatus and other prisons). In 1917, a seriously ill patient was released ... Russian history
Exist., Number of synonyms: 1 priest (65) ASIS Synonym Dictionary. V.N. Trishin. 2013 ... Synonym dictionary
kaplan- or CHAPLAN capelan m. Fish for cod bait. Luchinsky 1879 ... Historical Dictionary of Gallicisms of the Russian Language
Fanny Kaplan in 1918 Fanny Efimovna Kaplan (Feiga Khaimovna Roytblat, February 10, 1890 September 3, 1918) was a member of the Russian revolutionary movement, known mainly as the perpetrator of the attempt on Lenin's life. In various ... ... Wikipedia
Anatoly Lvovich Kaplan Birth name: Tankhum Leivikovich Date of birth: January 10, 1903 Place of birth ... Wikipedia
Books
- Leningrad. Anatoly Kaplan, Anatoly Kaplan. The lithographic cycle LENINGRAD by Anatoly Kaplan has long been recognized as one of the best examples of fine art dedicated to our city. Kaplan began work on the cycle immediately ...
- Leningrad. Anatoly Kaplan, Kaplan Anatoly. The lithographic cycle "Leningrad" by Anatoly Kaplan (1903-1980) has long been recognized as one of the best examples of fine art dedicated to the great city. To work on the Kaplan cycle ...
n1.doc
Kaplan G.I., Sadok B.J. Clinical Psychiatry. In 2 tons. T. 1. - Per. from English. V.B. Sagittarius. – M.: Medicine, 1994, 672 p.MENTAL RETARDATION
DEFINITION
Mental retardation (retardation) is a behavioral syndrome that does not have a single etiology, mechanism, dynamics or prognosis. This definition of mental retardation has gone through the years and is still in the process of being refined. It reflects the views and attitudes of society in relation to mental retardation, as well as diagnostic methods and the state of medical science.
There are two main conceptual approaches to the definition of mental retardation: biomedical and sociocultural and adaptation models. Adherents of the biomedical model, especially in the United States, argue that the presence of major changes in the brain is essential for a diagnosis of mental retardation. On the contrary, supporters of the sociocultural and adaptive model emphasize the importance of social function and the general ability to adapt to accepted norms.
In table. all violations observed in infancy and preschool years, learning difficulties at school age and poor social and professional adaptation in adulthood are given.
Table. Characteristics of the development of the mentally retarded, the table includes chronological age, degree of retardation, level of intellectual, speech and social functioning)
| Degree of mental retardation | Maturity and development in preschool age (0-5) | School age (6-20). Training and education | Adult period (21 years and older). Adequacy of social and speech spheres |
| deep | Strong retardation; minimal ability to function in the sensorimotor sphere; the need for nanny care; the need for constant assistance and supervision | There is some motor activity; may respond to some attempts to educate him or her about self-care | Some development of the motor sphere and speech; may learn some self-care skills very limitedly; babysitter required |
| heavy | Poor motor development; speech is minimal; usually cannot learn self-care; few or no opportunities to teach communication skills | Can speak or learn to communicate; can be taught basic hygiene skills; unable to learn to speak | Can partially learn self-care under close supervision; can be taught the simplest rules of self-defense under control |
| Moderate | Can speak and learn to communicate; poorly oriented socially; good motor development; self-care skills can be taught; can be limited to moderate assistance and control | Can learn social and professional skills; rarely develops beyond 2nd grade in learning; can learn to navigate familiar places independently | Can self-employed in unskilled or semi-skilled work under appropriate conditions; needs protection and help with the slightest stress |
| Light | There may be social skills and ability to communicate; minimal retardation in sensorimotor areas; often does not differ from the norm at an older age | Can achieve some academic achievement, up to the 6th grade level, which is reached in late adolescence; success can be achieved in teaching appropriate social behavior | Can usually achieve adequate social and language skills for minimal self-care, but needs guidance and assistance under social and economic stress |
This table includes both the dsm-III-R and the American Association for Mental Defects (AAUD) criteria.
According to the 1983 definition given in the AAUD, mental retardation characterizes a level of intellectual development that is significantly reduced compared to the average, which is the result of or associated with concomitant disorders of adaptive behavior and manifests itself during the period of development. The definition of AAUD is almost identical to the definition of dsm-Sh-R, which describes the essential features of mental retardation as follows:
1) a significant decrease in the overall level of intellectual development, accompanied by
2) a significant deficit or impairment of adaptive functions,
3) when the marked changes appear before the age of 18 years.
The following are diagnostic mental retardation criteria for dsm-W-R:
A. General intellectual development is significantly below average: 10 is equal to 70 or less on an individually presented test of 10 (for children, a clinically significant decrease in intellectual development is stated, since there are no tests with a numerical expression of this indicator).
B. Accompanying impairment or deficiency in the child's adaptive function, i.e., lack of the adaptability expected at her age and in this cultural group in areas such as professional activity and responsibility, communication, performance of daily duties, personal independence and self-satisfaction.
C. Onset of impairment before age 18.
The diagnosis is made regardless of whether there is a concomitant physical or other mental illness. "General intelligence" is defined by standard intelligence tests, and "significantly below average" is defined as an IQ of approximately 70 or less, or two standard deviations below the mean for a particular test.
TERMINOLOGY
The term "mental retardation" is often used as an equivalent to the term "mental deficiency". The World Health Organization (WHO) has recommended the term "mental subnormality" which includes two distinct categories: mental retardation and mental deficiency. Mental retardation, according to the WHO nosology, is used to diagnose a subnormal function secondary to its cause, while mental deficiency is the legal term applied to subjects with an IQ below 70.
The term "dementia" has been used frequently in the past, especially in American literature, and is still used in the UK to refer to mild forms of mental retardation. "Oligophrenia" is usually used in the USSR, Scandinavia and other countries of Western Europe. The term "amentia" no longer occurs in modern psychiatry, except in isolated cases when it comes to the terminal state of the degenerative process.
CLASSIFICATION
The degree or level of mental retardation is expressed in various terms. dsm-III-R contains four subtypes of mental retardation, reflecting the degree of intellectual impairment: mild mental retardation, moderately severe mental retardation, severe mental retardation, and global mental retardation. The degrees of mental retardation are indicated in Table. 2 (according to IQ gradations).
Table 2. The severity of mental retardation on a scale of 10
In addition, the dsm-III-R lists "non-specific mental retardation" as a subtype intended for those individuals who are strongly suspected of having an intellectual disability but cannot be tested on standard intelligence tests, who have significant impairments, or who are uncommunicative. . This subtype can be applied to infants who are clinically marked with significantly lower than average intelligence, but for whom impairment cannot be computed numerically because quantitative tests are not available (eg, Bailey, Cattal). This subtype should not be used if the estimated IQ is greater than 70.
EPIDEMIOLOGY
The presence of mental retardation at a given time among the entire population is approximately 1%. Calculating this number accurately is very difficult, since it is impossible to establish when a given person was diagnosed with mental retardation. In many cases, retardation may be "latent" for a long time before it is recognized, either due to good adaptation or the previous diagnosis will not be confirmed at some point in the patient's life. Most often this diagnosis is made to children of school age, and the maximum falls on the age of 10-14 years. Mental retardation is more common (about 1/2 times) in men than in women.
ETIOLOGICAL FACTORS AND SYNDROMES
At the present level of development of science, it has been established that approximately 25% of cases of mental retardation are due to biological abnormalities. Chromosomal and metabolic disorders such as Down's disease and phenylketonuria are the most common mental retardation disorders. The mental retardation associated with these disorders is usually diagnosed at birth or relatively early childhood and ranges in severity from moderate to severe.
In the remaining 75% of cases, no biological causes can be identified. The level of intellectual impairment in these cases is lighter; I values? range from 50 to 70. Mild mental retardation is usually not diagnosed until the child starts school. In cases of mild mental retardation, this disorder usually occurs in both parents and siblings.
Significant dominance of cases of mild mental retardation is noted among the lower socio-economic strata of society, and the reason for this is unclear. However, it can be noted that psychosocial deprivation, such as deprivation in the areas of social, linguistic and intellectual stimulation, contributes to mental retardation, although the biological etiology of this is unknown. At the current level of knowledge, it can be assumed that there are three types of etiological factors, either alone or in combination with each other: genetic factors, environmental factors (eg, malnutrition) and early childhood experiences.
PRENATAL FACTORS
An important condition for the proper development of the embryo is the physical and psychological health of the mother during pregnancy and during breastfeeding. Chronic diseases and pathological conditions of the mother affect the normal development of the fetus, its nervous system; these conditions include untreated diabetes, anemia, emphysema, hypertension, and chronic alcohol and drug use. Infections transmitted by the mother during pregnancy, especially viral infections, can cause damage to the fetus and mental retardation. The degree of impairment depends on variables such as prenatal age of the fetus and the severity of the disease. Although the pathological influence of many infections on the central nervous system of the fetus has been noted, three types of infections are particularly strongly correlated with a high risk of mental retardation: rubella measles, cytomegalic inclusion disease, and syphilis.
Rubella measles
Rubella has replaced syphilis as the leading cause of congenital disorders and mental retardation associated with maternal infections. Babies of infected mothers may present with a range of abnormalities, including congenital heart disease, cataracts, deafness, microcephaly, and microphthalmos. The time period is a critical factor, since the length and frequency of complications are inversely correlated with the gestational age at the time of the mother's illness. When a mother has an infection in the first trimester of pregnancy, 10 to 15% of babies are born with abnormalities, but the incidence of abnormalities rises sharply to almost 50% when the infection develops in the first month of pregnancy. The situation is often complicated by the so-clinical forms of the infection, which often go unrecognized. Rubella in the mother can be prevented by immunization.
Cytomegalic inclusion disease
In many cases, cytomegalic inclusion disease is latent in the mother. Among the children are stillborn, while the living have jaundice, microcephaly and hepatosplenomegaly, and radiographically detected intracerebral calcification, microcephaly or hydrocephalus. The diagnosis is confirmed by a positive culture of the virus from material taken from the pharynx or urine, as well as by the regeneration of inclusion cells in the urine.
Syphilis
Syphilis in pregnant women was considered the main cause of various neuropathological disorders in their offspring, including mental retardation. Currently, the incidence of complications due to syphilis fluctuates along with the incidence of syphilis in the general population. Recent studies have shown that in many US cities the situation is still far from encouraging.
Other diseases
Another recognized cause of fetal disease is toxoplasmosis transmitted to the fetus from the mother. This is a rather rare condition, which, however, often ends in the birth of a child with an intellectual disability or other brain disorders. There is evidence of damage to the fetus also in connection with the mother's hepatitis.
AIDS is now a major public health concern, and intensive research is underway into how it affects fetal and newborn development. The pregnancy of a woman with AIDS ends in fetal death, stillbirth, spontaneous miscarriage, or death of the infant within the first few years of life. Since the virus is known to have a direct damaging effect on the brain, it is assumed that children born to such mothers may have various types of brain damage with varying degrees of mental retardation.
The role of maternal infections during pregnancy, such as influenza, viral acute respiratory infections, pneumonia, and urinary tract infections, in causing intellectual disability is under investigation, and there are as yet no clear results.
Complications of pregnancy
Toxicosis of pregnancy and untreated diabetes in the mother pose a danger to the fetus and sometimes result in mental retardation. Vaginal bleeding, placental abruption, and cord prolapse can damage the fetal brain by causing anoxia.
Concerning the potential teratogenic effect of pharmacological substances administered during pregnancy, much has been said in connection with the thalidomide tragedy (a substance that caused a high percentage of birth defects when given to pregnant women). So far, with the exception of metabolites used to treat cancer, no other known substances cause damage to the central nervous system of the fetus, but nevertheless, caution and restriction of drugs prescribed to pregnant women have been shown. Lithium use and excessive alcohol consumption during pregnancy have been shown in some cases to be associated with neonatal impairment, especially of the cardiovascular system.
CHROMOSOME PATHOLOGY
Autosomal chromosome abnormalities have also been associated with mental retardation, although sex chromosome abnormalities do not always cause mental retardation (eg, Turner's syndrome with X0 and Klinefelter's syndrome with variations in XXY, XXXY, or XXYY). Some children with Turner syndrome have normal or increased intelligence.
Down syndrome
Down syndrome was first described by the English physician Langdon Down in 1866 and was based on physical characteristics associated with subnormal mental development. Since then, Down's syndrome has remained the most thoroughly studied and often discussed mental retardation syndrome. Children with this syndrome were previously called Mongoloids based on their physical features—slanting eyes, epicanthal folds, and flat noses.
Despite the fact that over the past 100 years a huge number of theories and hypotheses have appeared, the cause of Down syndrome remains unknown. It is generally accepted that there are several factors that can cause this disease and that are associated with a violation in the chromosomes; this is the late age of the mother, perhaps the older age of the father and the influence of radiation. The problems of causation have been further complicated by the recent discovery of three types of abnormal chromosomes in Down syndrome:
1. Patients with trisomy 21 (3 of chromosome 21, instead of the usual 2) represent the absolute majority; they have 47 chromosomes, with one extra chromosome 21. The maternal karyotype is normal. Nondisjunction during miosis, appearing for an unknown reason, is now considered to be associated with this disorder.
2. Nondisjunction, observed every time after fertilization in every cell division, is a condition in which both normal and trisomic cells are found in various tissues.
3. During translocation, there is a fusion of 2 chromosomes, mainly 21 and 15, as a result of which only 46 chromosomes appear, despite the presence of extrachromosome 21. This disorder, unlike trisomy 21, is usually congenital, and the translocation chromosome can be found in healthy parents and siblings. These carriers, which do not reveal any pathological manifestations, have only 45 chromosomes.
The incidence of Down syndrome in the US is approximately 1 in every 700 births. In his original work, Down noted that the frequency of this disease is 10% among all patients with mental retardation. It is of interest that today about 10% of patients with Down syndrome are in hospitals for the mentally retarded. For a middle-aged mother (over 32), the risk of having a child with Down syndrome is approximately 1 in 100 if there is only trisomy, but the risk increases to 1:3 when translocation occurs. These factors are of particular interest for genetic counseling.
Amniocentesis, in which amniotic fluid is drained transabdominally from the amniotic sac between the 14th and 16th weeks of pregnancy, is a useful criterion for diagnosing an abnormality in the infant, especially Down's syndrome. Amniotic fluid cells, mostly germinal in origin, are grown for cytogenetic and biochemical studies. Many hereditary disorders can be predicted using this method, and the only method of preventing the birth of a sick child is therapeutic termination of pregnancy. Preferably, amniocentesis should occur in all pregnant women over 35 years of age. Fortunately, most chromosomal abnormalities occur only once in a family.
Mental retardation is the main feature of Down syndrome. Most patients are classified as moderately or severely retarded, with only a minority having an IQ of less than 50. Mental development appears to be normal from birth to 6 months of age. Scores 10 gradually decline from about normal at age 1 to about 30 at older ages. This decline in intelligence can be real and obvious. It may happen that infant tests do not detect the full extent of the defect, which is only detected by more subtle testing methods used in childhood. In accordance with many data, patients with Down syndrome are calm, good-natured and sociable, which facilitates their adaptation at home. The picture, however, changes during adolescence, especially if the children live in boarding schools; they may present with a variety of emotional, behavioral, and (rarely) psychotic disorders.
The diagnosis of Down syndrome is relatively easy in older children, but is often more difficult in newborns. The most serious features are general hypotension, oblique palpebral fissures, excess skin on the neck, small flattened skull, high cheekbones, and protruding tongue. The hands are wide and thick, with one transverse palmar crease, and short small fingers, rounded inwards. The Moro reflex is weak or absent. More than 100 signs and stigmas have been described in Down syndrome, but collectively they rarely occur in the same person.
The predicted life span is about 12 years. With the advent of antibiotics, however, only a few die from infections at a young age, but most patients do not live past the age of 40, when they already accumulate many signs that are not compatible with life, in particular, aging, reminiscent of the picture characteristic of Alzheimer's disease. Despite the many methods proposed, no type of treatment has proven to be effective.
Disease (syndrome) of a cat's cry
Children suffering from crying cat disease are distinguished by the absence of part of the 5th chromosome. They are characterized by severe mental retardation and many stigmas often associated with chromosomal abnormalities such as microcephaly, low ear position, oblique palpebral fissures, hypertelorism, and micrognathia. A characteristic cry, reminiscent of a cat, is associated with defects in the pharynx, gave the name to this syndrome, but gradually, over the years, the cry stops.
Other syndromes of autosomal disorders associated with mental retardation have a significantly lower prevalence than Down's syndrome. Various types of disorders of autosomal and sex chromosomes and the syndromes caused by them are presented in Table. 21.
GENETIC DEFECTS
Phenylketonuria
Phenylketonuria (PKU) was first described by Falling in 1934 as an exemplary metabolic error of an innate nature. PKU is transmitted as a simple recessive Mendelian congenital characteristic and occurs approximately 1 in every 10,000 to 15,000 live births. For parents who already have a child with PKU, the chance that the next child will also be affected is 1 in every 4-5 subsequent pregnancies. Although this disease occurs predominantly in people of Northern European origin, a few cases have been described among Negroes, Jews, and Asians. The frequency of occurrence of this disorder among defective patients in shelters is about 1%.
Table 3. Thirty-five important syndromes in various types of mental retardation (retardation)
| Syndrome | Disorders important for the diagnosis | mental retardation | short stature | Type of genetic transmission |
||
| craniofacial | skeletal | Other |
||||
| Aarsky syndrome | Hypertelorism; wide nasal bridge, anteverted nostrils, long philtrum | Short arms and legs; slight webbing between fingers, short stature | Scrotal "veil" over the penis | + | X-adjoining semi-dominant |
|
| Aper syndrome (acrocephalosyndactyly) | craniosynostosis; intermittent midfacial hypoplasia, hypertelrism | syndactyly; extension of the distal ends of the fingers and toes | ± | autosomal dominant |
||
| Cerebral gigantism (Sotos syndrome) | Big head; protruding forehead; narrow lower jaw | Big hands and feet | Significant at an early age, poor coordination | ± | ? |
|
| Cockayne syndrome | Face with pointed features; sunken eyes; thin nose, prognathia; retinal degeneration | Elongated limbs with large arms and legs; flexion defect | hypotrichosis; photosensitivity; thinning of the subcutaneous layer of the retina; hearing loss | + | + | autosomal recessive |
| Cohen's syndrome | Hypoplasia of the mandible with prominent central incisors | Narrow arms and legs | Hypotension; obesity | + | ± | ? autosomal recessive |
| Cornelia de Lange syndrome | Synophrysis (united eyebrows); thin, downturned lower lip; long philtrum; nostrils turned anteriorly; microcephaly | Small or irregularly shaped hands and feet; thumb is proximal | hirsutism | + | + | ? |
| Lejeune's syndrome ("cat's cry disease") | Epicanthal folds or oblique palpebral fissures; round face; hypertelorism; microcephaly | Short metacarpals or metatarsals; four fingers on the hand | In infancy, they make cat-like cries | + | + | ? |
| Croiseau syndrome (craniofacial dysostosis) | Proptosis with superficial eye sockets; hypoplasia of the upper jaw; Craniosynostosis | autosomal dominant |
||||
| Down's disease | Sloping forward, vertically, towards the palpebral fissures; the middle part of the face is small; epicanthal folds | Short arms; clinodactyly of the fifth finger (little finger); four fingers on the hand | Hypotension; additional folds of skin at the back of the neck | + | + | 21 Trisomy |
| Dubovitz Syndrome | small face; lateral displacement of the lower inner corner of the eye; ptosis; wide back of the nose; rare hair; microcephaly | baby eczema | ± | ++ | ? autosomal recessive |
|
| fetal alcohol syndrome | Short palpebral fissures; hypoplasia of the middle part of the face; microcephaly | ± Heart involvement; mild motor dysfunction | + | + | ||
| Fetal hydantoin syndrome (Dilanthia) | Hypertelorism; short nose; sometimes split lip | Hypoplastic nails, especially on the little finger | Heart failure | ± | ± | |
| Goldenhar syndrome | Hypoplasia of the zygomatic bone (molar hypoplasia); macrostomia (large oral fissure); micrognathia; epibulbar dermoid or lipodermoid; protruding auricles with periauricular polyps | Vertebral anomalies | ? |
|||
| Pigmentation disorders | ±tooth defect; ear deformity; ± patchy baldness | Skin pigmentation "speckled", in the form of cobwebs or in the form of flowers | ± | ? Dominant X-adjoining Lethal for men |
||
| Syndrome Beedle | retinal pigmentation | polydactyly; syndactyly | Obesity; seizures; hypogenitalism | ± | ± | autosomal recessive |
| Linear Nevus | nevus sebaceous, on the face or neck | ±Seizures | + | ± | ? |
|
| Lowe's syndrome | Cataract | Kidney tubular dysfunction | Hypotension | ++ | + | X-adjoining recessive |
| Mobius syndrome (congenital facial diplegia) | A face devoid of any expression; eye paralysis | ± Clubfoot; syndactyly | ± | ± | ? |
|
| Neurofibromatosis | ± Ocular gliomas; neubromas of the auditory pathway | ± bone damage, pseudarthrosis | neurofibromas; "coffee spots"; seizures | ± | autosomal dominant |
|
| Syndrome Noonan | Growth of the back of the neck; protruding auricles; hypertelorism | Thorax, forming a cavity; elbows turned out | Cryptorchidism; stenosis of the pulmonary artery | ± | + | ? |
| Prader-Willi Syndrome | Oblique palpebral fissure upward, vertical | Small hands and feet | Hypotension; especially in infancy; then polyphagia and obesity; hypogenitalism | + | + | ? |
| Robin syndrome | Micrognathia; omission of the tongue; splitting of the sky; "u" shape | ±Cardiac anomalies | ? |
|||
| Rubell syndrome | Cataract; retinal pigmentation; eye deformity | sensorineural deafness; open ductus arteriosus | ± | ± | ||
| Rubinstein-Taybi Syndrome | Oblique palpebral fissures (strabismus); hypoplasia of the upper jaw; microcephaly | Wide thumbs and toes | Abnormal gait | + | + | ? |
| Seckel syndrome | Hypoplasia of the face; protruding nose; microcephaly | Many small joints and pathology of the skeletal system | + | + | autosomal recessive |
|
| Sjögren-Larsson syndrome | Spasticity, especially of the legs | Ichthyosis | + | + | autosomal recessive |
|
| Smith-Lemli-Opitz syndrome | Anteverted nostrils and/or eyelid ptosis | Syndactyly of the 2nd and 3rd toes | Hypospadias; cryptorchidism | + | + | autosomal recessive |
| Sturge-Weber Syndrome | Flat hemangioma of the face, most commonly spreading along the trigeminal nerve | Meningeal hemangiomas with seizures | ||||
| Tritcher-Collins syndrome (mandibulofacital dysostosis) | Hypoplasia of the zygomatic bones and lower jaw; slanted downward palpebral fissures; defect of the lower eyelid; protruding ears | autosomal dominant |
||||
| Trisomy 18 | Microstomia; short palpebral fissures; protruding auricles; elongated skull | Clenched hands, the 2nd finger is located above the third; low temples at the fingertips; short chest | Cryptorchidism; congenital heart disease | + | + | Trisomy 18 |
| Trisomy 13 | Defects of the eyes, nose, lips, ears and forehead of the holoprosencephalic type | polydactyly; narrow curved nail beds at the fingers | Skin defects located on the back of the scalp | + | + | Trisomy 13 |
| Tuberous sclerosis | Knots on the skin of the neck from lilac-pink to brown | ± bone damage | Seizures, intracranial calcification | ± | autosomal dominant |
|
| Waardenburg syndrome | Lateral displacement of the inner corner of the eye and cavity | Partial albinism; white strand of hair; heterochromia of the iris; vitiligo; ± deafness | ||||
| Williams syndrome | Full lips; small nose with anteverted nostrils; iris dysplasia | Mild nail hypoplasia | ± Hypercalcemia in infancy; stenosis of the superior aortic valve | + | + | ? |
| cerebrohepatorenal zellweger syndrome | high forehead; flat face | Hypotension; hepatomegaly; death in early infancy | + | + | autosomal recessive |
|
The main metabolic defect in PKU is the inability to convert phenylalanine, an essential amino acid, to paratyrosine due to the absence or inactivated state of the hepatic enzyme phenylalanine hydroxylase, which catalyzes the conversion. Recently, two other types of hyperfinyl alaninemia have been described. One is associated with a deficiency of the enzyme dihydropteridine reductase and the other is associated with a deficiency of the biopterin cofactor. The first defect can be found in fibroblasts and the biopterin in body fluids. Both of these rare disorders are associated with great risk to life.
Most patients with PKU have severe mental retardation, but some have borderline or normal intelligence. Approximately 1/3 of patients experience eczema, vomiting, nausea, and seizures. Although the clinical picture varies, typical manifestations for children with PKU are hyperactivity, erratic, unpredictable behavior that is difficult to manage. These children are characterized by tantrums and bizarre movements of the body, upper limbs, and mannered hand gestures, and their behavior sometimes resembles that of autistic or schizophrenic children. Verbal and non-verbal communication is usually severely impaired. Coordination and perceptual abilities are also significantly impaired.
Previously, the diagnosis of this disease was based on a study of urine: phenylpyruvic acid in the urine reacts with a solution of ferric chloride, resulting in a bright green color. However, this test has limitations in that it cannot detect the presence of phenylpyruvic acid in the urine before the baby is 5 or 6 weeks old, and it may test positive with other amino acids. Recently, a more reliable test has been developed that uses a bacteriological method to detect phenylalanine in the blood.
Early diagnosis is very important, as the administration of a low-phenylalanine diet, used since 1955, greatly improves both behavior and normal development. The best results are obtained with early diagnosis and initiation of dietary therapy until the child is 6 months old.
However, diet therapy is not without a certain degree of risk. Phenylalanine is an essential amino acid and its deficiency in the diet can lead to serious disorders such as anemia, hypoglycemia, edema and even death. PKU diet therapy can often be stopped at age 5-6 years, although there are no other ways to change the metabolism to maintain normal blood levels of phenylalanine. Children diagnosed before 3 months of age and treated with an appropriate diet may have normal intelligence. If not treated at an early age, dieting for older children and adolescents does not appear to affect the rate of mental retardation. However, the diet will reduce their level of irritability and pathological EEG changes and improve social adaptation and attention.
Parents of children with PKU and some of their siblings are normal and are heterozygous carriers of the pathology. The disease can be detected using a phenylalanine tolerance test, which is very important for genetic counseling given to these individuals.
Maple syrup disease, Menkes syndrome
Clinical symptoms of Menkes disease appear within the first week of life. Infants are rapidly impaired and develop decerebrate rigidity, seizures, irregular breathing, and hypoglycemia. If left untreated, most patients die in the first months of life, and those who survive suffer from severe mental retardation. Some variation is noted, with short-term ataxia and only a mild degree of mental retardation.
Treatment follows the principle established for PKU and consists of a diet very low in the three amino acids leucine, isoleucine and valine.
Other Enzyme-Related Disorders
Some enzyme deficiency disorders also cause mental retardation, and more diseases are now being identified as belonging to this group. These include Hartnup's disease, galactosemia, and diseases associated with the accumulation of glycogen.
Diseases acquired in childhood
Sometimes a child's developmental status changes dramatically as a result of a specific disease or physical injury. In retrospect, it is somewhat difficult to judge how completely normal the child's development was before the disturbances occurred, but the child's reversal signs of development or loss of skills clearly have a different, new origin.
infections
Most severe infections affect the integrative abilities of the brain; such infections include encephalitis and meningitis. Measles encephalitis is reduced to nothing by the use of measles vaccine, and the frequency of other bacterial infections of the central nervous system is significantly reduced by antibacterial substances. Most cases of encephalitis are caused by viruses. It is sometimes useful to look at the problem in retrospect to assess the possible contribution of encephalitis to a previous illness that was accompanied by high fever and long-term encephalopathy. Late-diagnosed meningitis followed by antibiotic therapy or significant complications can seriously affect a child's cognitive development. The phenomena of thrombosis and suppuration inside the skull, secondary to septicemia, are rare today, but they are quite common in children.
Head injury
The most well-known cause of head injury in children is accidents with different machines; as a result, there is a violation of mental development, seizures. However, most injuries in children occur at home, such as falling from a table, from open windows, or down stairs. Physical punishment can also cause head injury.
Other reasons
Brain damage from cardiac arrest during anesthesia is rare. One of the reasons for the complete or partial violation of the type of decortication is asphyxia, which appears when the child was close to drowning. Chronic lead exposure is a well-known cause of intellectual and learning disabilities. Intracranial tumors of various types and origins, either by themselves or as a result of the influence of surgery or chemotherapy of these tumors, can also have a negative effect on brain function.
SOCIO-CULTURAL AND ENVIRONMENTAL IMPACTS
It is well known that a mild degree of mental retardation predominates in persons belonging to the culturally backward, lower socioeconomic classes, and that similar manifestations of mental retardation are often observed in members of the same family and relatives. In these cases, no biological cause is found.
In any case, it is clear that children from poor, socio-culturally backward families are potentially exposed to potentially pathogenic and developmentally negative conditions. Prenatal development takes place in conditions of poor medical care and malnutrition of the mother. Pregnant teenagers often give birth without the necessary obstetric care, they are not fully developed physically, and children are born with very small body weight, premature. Lack of proper postpartum care, poor nutrition, exposure to toxic substances such as lead, and physical trauma are common. The unstable situation of the family, frequent movements and the change of many persons who care for the child equally badly are typical of these cases. Moreover, mothers from such families often do not have sufficient education and do not know the methods necessary to provide the child with the necessary conditions.
Another unresolved issue is the impact of severe mental illness in parents. It has been suggested that such illnesses adversely affect the child's care, provision of the right environment, including sufficient levels of stimulation, and other aspects of the environment, which together create an increased risk of impaired development of the child. It is known that children of parents suffering from affective disorders are at high risk of developing these same diseases. Recent studies also show that such children have an increased risk of developing motor and other developmental disorders, delays in these functions, but this does not mean the inevitability of the development of mental retardation.
MENTAL DISORDERS AND MENTAL RETARDATION
Personality and Behavioral Patterns
The most common misconception among professionals and the public is that mentally retarded individuals are a homogeneous group. In fact, mentally retarded individuals exhibit more personality styles and behaviors than others. For example, subjects with a mild degree of mental retardation, who live on their own and only someone looks after them, are self-supporting and are closer to their non-retarded colleagues than to severely disabled individuals who are wholly cared for. -or other. Another erroneous opinion is the opinion that maladaptive individuals from among those suffering from mental retardation necessarily suffered some kind of organic disease, or have a congenital inferiority, and not acquired in the process of life.
All kinds of behavioral and personality disorders that are present in persons suffering from mental retardation are also found in untreated patients with mental disorders. However, some behaviors are more likely to be expected in the mentally retarded due to their cognitive deficits and lifestyle. Mentally retarded individuals often have egocentrism and conservatism of thought associated with cognitive deficits, especially with difficulty in forming hypotheses and abstract thinking.
Organic disorders, i.e., signs of neurological disorders, usually cannot be directly related to behavior patterns, especially in mild or moderate degrees of organic damage. Such neurological disorders are more common in patients with severe mental retardation. They may have motor disinhibition and weakening of attention with periods of its loss. Contrary to popular belief, aggression is not a mandatory manifestation and is not even very typical for patients with mental retardation.
The main factor influencing the behavior of the mentally retarded seems to be the environment and the sensations experienced. In this regard, shelters with insensitive, inhumane and unskilled personnel are the most pathogenic. Some patients, however, try to respond to mistreatment by displaying aggression and other forms of negative behavior. Overprotectiveness, usually carried out by parents, often leads to the development of dependence, low frustration tolerance, feelings of inferiority and low self-esteem.
Exposure to mental disorders
Negative self-image and low self-esteem are probably the most typical personality traits of retarded individuals, especially those who are mild to moderately retarded. They are well aware of their difference from others, and that they have not lived up to the expectations of parents and society and are lagging behind their peers and siblings.
Defense against intolerable feelings of inferiority, low self-esteem and anxiety is often inadequate and maladaptive and can lead to behavioral disturbances. Some of these teenagers and youths commit crimes and show aggression.
The conflict between the expected self-image and the actual self-image can be a source of lifelong stress and anxiety for persons with mild mental retardation who are aware of their inferiority. A strong dependence on those who care about them does not allow the formation of an idea of oneself as an independent person and, in a certain sense, prevents the distinction between ideas about oneself and others as independent categories. Their communication is associated with significant difficulties, which further increase the feeling of their own inferiority and frustration in such persons. Typical for them is inappropriate behavior such as aggression and autism. Low self-esteem in individuals with mild or moderate mental retardation predisposes them to depression.
Concerning the incidence of mental illness in mentally retarded individuals, there are no sufficiently convincing data, especially because of methodological difficulties. However, according to available information, such individuals are at a very high risk of developing mental disorders; it varies from 40 to 75%.
Among young people suffering from mild or moderate mental retardation, the most common diagnoses are: adjustment disorders, mood disorders and psychoses; among children, mood disorders, anxiety disorders and pervasive developmental disorders predominate.
DIAGNOSIS
Story
In most cases, information provided by parents or persons directly caring for a mentally retarded person is the only source of information, so every effort must be made to ensure that they are reliable. The history of the development of pregnancy, work, birth, the presence of incest or mental illness in the family deserve special interest. Parents should also indicate milestones in the child's development. This is especially difficult as the parents are biased and often show anxiety. It is very important to clarify the issue of the emotional climate in the family and its sociocultural basis, which is important for assessing clinical results.
Psychiatric conversation
Two factors are extremely important in a conversation with a patient: the attitude of the doctor and the manner of communication on the part of the patient. The doctor should be guided by the patient's mental age, since he can fully determine the patient's capabilities. A mentally retarded subject whose mental age is defined as 10 years is not the same as a 10 year old child. If he is treated like a child, some of the mentally retarded find anger, resentment and do not want to communicate. On the other hand, more passive and dependent individuals may take on the role of a child that they think is required of them. In both cases, reliable data cannot be obtained. The verbal capabilities of the patient, including receptive and expressive language, should be clarified). as soon as possible through observation, communication, verbal and non-verbal, with those caring for the patient, as well as from the medical history. In this regard, it is often helpful to see the patient and caregivers together early. If the patient communicates using sign language, the caregiver may be present during the conversation with the doctor as an interpreter.
Retarded individuals feel throughout their lives that they do not understand many things, and may experience great anxiety before talking with a doctor. The physician and caregivers should try to give such a patient a clear, precise and friendly explanation of the diagnostic process, especially for those patients who use receptive language. It is necessary to avoid such a situation when it seems to the patient that the reason for the meeting with the doctor is his bad behavior. In a language accessible to the sick person, you should express your support and praise him according to his age and understanding. Leading questions should be avoided, as retarded persons may be suggestible and will want to please others. To get them to stick to the issue under discussion, you need to give unobtrusive instructions, structure and reinforce the topic.
It is necessary to assess the mobility of a sick child and establish the facts of the presence of distractibility and impaired perception and memory. It is important to note the use of speech, the assessment of reality and the ability to generalize one's feelings, distracting from them.
The nature and maturity of the child's defenses—especially the use of excessive defenses—avoidance, repression, denial, introjection, and isolation must be described. Sublimation potential, frustration tolerance, and control over one's impulses, especially motor, aggressive, and sexual urges, should also be assessed. Also important is the idea of oneself and its role in the development of self-confidence and perseverance, perseverance and the desire to know the unknown.
In general, the psychiatric examination of a mentally retarded child should answer the question of how he copes with various tasks at various stages of personal development. Failure to do so or regression can be profiled to allow logical planning for guidance and correction.
Physical examination
On the part of some parts of the body and organs, there may be deviations characteristic of mentally retarded persons, which sometimes have a prenatal origin. For example, head configuration and size are often indicative of manifestations such as microcephaly, hydrocephalus, and Down syndrome. The patient's face sometimes has features that facilitate the diagnosis of mental retardation, such as hypertelorism, a flat nose, prominent superciliary ridges, epicanthal folds, corneal turbidity, retinal changes, low-lying, small or shapeless ears, protruding tongue, large spaces between teeth. A facial expression that can be described as stupid is not always adequate and should not be relied upon unless there are other supporting signs. Skin and hair color and density, high-arched palate, thyroid size, and torso and limb size are further areas of study. Head circumference measurement should be part of the clinical study.
Dermatoglyphics or hand drawing may be another diagnostic tool, as an atypical pattern of sulcus and flexion fold is often found in retarded children. Pathological dermatoglyphics can often be found in individuals with chromosomal abnormalities and in children with measles rubella.
Neurological examination
When neurological disturbances occur, their frequency and severity are inversely correlated with the degree of retardation. Many children with severe mental retardation do not show neurological abnormalities, and, on the contrary, about 25% of all children with cerebral palsy have normal intelligence.
Disturbances in the motor area are manifested by pathology of muscle tone (spasticity or hypotension), reflexes (hyperreflexia) and involuntary movements (choreoathetosis). Minor violations in this area are manifested by awkwardness and poor coordination.
Secondary disorders may include deafness, ranging from a slight impairment of the ability to hear to. significant cortical deafness. Visual impairments can range from blindness to disturbances in spatial representation, pattern recognition, and body schema representation.
The worst prognosis is in infants who exhibit a combination of inactivity, generalized hypotension, and over-responsiveness to stimuli. In older children, markers of brain damage are often hyperactivity, short attention spans, distractibility, and low frustration tolerance.
In general, the younger the child at the time of the study, the more caution should be exercised in predicting the future, as the potential for brain recovery in infants is very high. The most adequate approach to predicting abilities can be considered a survey of the development of the child at regular intervals.
The pneumoencephalogram is a somewhat dangerous method of investigation and is rarely used in the mentally retarded, and has now been replaced by computed tomography. Incidental findings—intrinsic hydrocephalus, cortical atrophy, or porencephaly found in severely retarded people with organic brain damage—are not considered important features in the overall picture.
X-ray examination of the skull, usually performed in such cases, helps to understand only a few cases, such as those associated with craniosynostosis, hydrocephalus, cortical atrophy and other factors resulting from intracranial calcification (for example, toxoplasmosis, pineal sclerosis, cerebral angiomatosis and hypoparathyroidism).
The electroencephalogram (EEG) should be interpreted very carefully in cases of mental retardation. The exception is patients with hyperarrhythmia or grand mal seizures, in which the EEG allows diagnosis and treatment. In most other cases, a diffuse cerebral disorder causes nonspecific EEG changes characterized by slow activity with bursts of peaks and sharp waves or abrupt wave complexes. The confusion surrounding the significance of the EEG for the diagnosis of mental retardation may be evident from reports of frequent EEG abnormalities in Down's syndrome, the percentage of which varies around 25 for most patients with this disease.
Laboratory tests
Laboratory tests include urine and blood tests for metabolic disorders.
Enzyme pathology in chromosomal disorders, especially Down's disease, promises to be an important diagnostic test. Determination of the karyotype in the genetic laboratory is indicated in all cases where there is a suspicion of chromosomal disorders.
Assessment of auditory and speech functions
Assessment of auditory and speech functions should always be done. The development of speech can be a key criterion in the study of the mentally retarded. Various hearing impairments are often found in the mentally retarded; however, in some cases, these disorders themselves can contribute to the development of mental retardation. Unfortunately, commonly used methods for assessing the ability to see and hear require the patient to be sociable, and therefore they often cannot be used in people with severe mental retardation.
Psychological assessment
Researching physicians may use several methods for infants and toddlers. As with many areas of mental retardation, there is controversy regarding the value of psychological tests in infants. The correlation of pathological disorders observed during infancy with subsequent disorders is very low according to some authors, while data from other authors indicate a high correlation. There is general agreement that the correlation increases in direct relation to the age of the child at the time of the survey.
Geometric copying, Goodenough's "Draw a Man" test, the Koch cube test, and geometric puzzles can all be used as rapid screening tests for hand-eye coordination.
Psychological testing, performed by a qualified professional, is part of the standard screening for mental retardation. The Gesell, Bailey, and Catell tests are often used on children. For children, the Stanford-Binet tests and the Wechsler Mental Development Scaling are also intended. Both tests are criticized for reflecting the cultural development of the child and testing mainly the level of academic education, and not the adequacy of adaptability to the social conditions of life; they are also criticized for their unsuitability for testing children with IQs below 50. Some try to overcome the language barrier of the mentally retarded by using picture tests, of which the Peabody Vocabulary Test is the most commonly used.
Often these tests are useful in detecting brain damage, such as the Bender-Gestalt test and the Benton visual information retention test. In addition, it is necessary to conduct a psychological study of perceptual, motor, linguistic and cognitive abilities. Information on motivational, emotional and interpersonal factors is also important.
DIFFERENTIAL DIAGNOSIS
Children from disadvantaged backgrounds who receive inadequate stimulation from the environment may show motor and mental retardation, which may disappear when they are provided with enriched stimulation in early childhood. A range of sensory impairments, especially deafness and blindness, can be mistaken for mental retardation if no compensation for the defect is offered during testing. Speech defects and cerebral palsy often make a child appear mentally retarded, even if his intelligence is borderline or normal.
Chronic disabling diseases can cause isolated lesions, such as the inability to learn to read (alexia), writing (agraphia), communication (aphasia), and some others that can be observed in individuals with normal or even high intelligence.
Children with specific developmental disabilities have a delay or lack of ability in one area, such as reading or language acquisition, but children may develop normally in other areas. In contrast, children with mental retardation show a general delay in many areas of development.
A disorder in the form of a pervasive developmental disorder manifests itself as an incorrect development of many mental functions in time, in severity and sequence, while these functions are basic for the subsequent development of professional skills and language acquisition. There are also severe qualitative disorders that are pathological for any stage of development. In mental retardation, however, there is generalized mental retardation, and such children behave as if they are going through an earlier stage of development. Mental retardation can coexist with specific developmental disorders and often with pervasive developmental disorders.
The most important differential diagnosis is between children with mental retardation, organic brain damage, early childhood autism, childhood schizophrenia, and, according to some authors, Heller's disease. The confusion stems from the fact that data on early childhood development are often unavailable or unreliable, and when they are assessed, it seems that many children show the same oddities and stereotypes in behavior, mutism, echolalia, and their general level of development is reduced. By the time these children reach the doctor, it is practically irrelevant whether the developmental delay is secondary to primary early childhood autism or whether the personality and behavioral disorders are secondary to organic brain damage or mental retardation. When ego functions are retarded or atrophied in some other way, the physician must first of all focus on the lack of contact with the child, which must be overcome until all corrective educational measures have proved useless.
Mental retardation has been associated with several heterogeneous groups of disorders and a variety of psychosocial factors. The best treatment for mental retardation is primary, secondary and tertiary prevention based on the preventive medical model.
Primary Warning
Primary prevention refers to the desire and action taken to limit the factors and conditions that lead to the development of mental retardation disorders. Such measures include:
1) upbringing and education aimed at increasing knowledge about mental retardation and its causes,
2) continuous efforts by medical professionals to improve the knowledge of police officers dealing with public health issues,
3) a law that ensures optimal care for mothers and children, and
4) eradication of known disorders that can cause damage to the central nervous system. Family and genetic counseling should help reduce the incidence of mental retardation in families where there are already cases of genetic disorders with mental retardation.
For children and mothers of low socioeconomic status, appropriate prenatal and postnatal conditions and various environmental enrichment programs and social assistance should be provided to minimize medical and psychosocial complications.
Secondary and tertiary warning
If a disorder associated with mental retardation has already been identified, it should be treated to shorten the duration of illness (secondary warning) and minimize residual effects or consequences of mental impairment (tertiary warning).
Hereditary metabolic or endocrine disorders such as PKU and hypothyroidism can be successfully treated early with diet or hormone therapy.
Mentally retarded children often exhibit emotional and behavioral disturbances requiring psychiatric treatment. These children have limited cognitive and social abilities requiring intervention and modified psychiatric treatment based on the child's IQ. Play therapy and opportunities to form social group communication can help these children manage their internal conflicts.
Behavioral therapies, especially positive reinforcement, have been shown to be effective in modifying some maladaptive behaviors. Sometimes it is possible to get rid of target symptoms or reduce them with the help of psychotropic drugs; for example, this is possible in relation to hyperactive and impulsive behavior, anxiety and depression.
Parents need constant counseling or, if indicated, family therapy. Parents should be given the opportunity to express their guilt, despair, anguish, repeated denial, and rage at the child's defect and future. The physician should be prepared to provide parents with the necessary information and provide medical information on etiology, treatment, and other necessary issues (eg, special treatment and correction of sensory defects).
