Научная статья на тему 'Немоторные проявления болезни Паркинсона'

Немоторные проявления болезни Паркинсона Текст научной статьи по специальности «Клиническая медицина»

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Ключевые слова
PARKINSON''S DISEASE / НЕВРОЛОГИЯ / БОЛЕЗНЬ ПАРКИНСОНА / NEUROLOGY

Аннотация научной статьи по клинической медицине, автор научной работы — Пиллипович Анна Александровна, Гойтемирова П. У., Ноздрюхина Наталия Васильевна, Струценко Алла Анатольевна, Гарабова Наида Исагаджиевна

Parkinson's disease a chronic degenerative disease of the central nervous system, clinically manifested by a combination of hypokinesia and postural disorders with rigidity and resting tremor, and autonomic disorders and mental functions. The pathogenesis of Parkinson's disease is inhibition of the functions of dopaminergic systems of the central nervous system (stria negroid, tuberoinfundibular, olfactory, retinal, and so on). With a comprehensive defeat of dopaminergetic systems associated with the appearance not only of motor disorders, but also a wide variety of autonomic, endocrine, emotional and cognitive, that is, non-motor symptoms. The frequency and severity of non-motor disorders correlated with the duration of Parkinson's disease and the severity of motor disorders. It is important to note that many non-motorized violations appear already at the preclinical stage of Parkinson's disease, ahead of the manifestation of the classic symptoms of Parkinson's disease hypokinesia, rigidity, tremor and postural disorder. As the disease progresses, some of them become the dominant clinical significance, having a negative impact on the quality of life of patients, leading to their disability and reducing life expectancy. The period before the movement disorder can be quite long, sometimes up to 10 years, and is characterized by the appearance of non-motor symptoms. Typical non-motor symptoms of Parkinson's disease are impaired sense of smell, sleep disorders, depression, constipation, change in color perception, less pain, restless leg syndrome, apathy, fatigue, anxiety. Already in the early stages of Parkinson's disease can be detected as a violation of neurodynamic bradiphrenia and disorders of attention. For the first stage Parkinson characteristic lesion olfactory bulb, olfactory nucleus anterior, dorsal motor nucleus of the vagus nerve, peripheral ganglia, autonomic nervous system, as well as pre-and post-ganglionic sympathetic and parasympathetic structures intestinal, heart and pelvic plexus that clinically hypoosmia, constipation, the sympathetic innervation of the myocardium as vasodilation, reducing the strength of heart contractions, disorders of the heart rate variability, orthostatic hypotension. In the second stage of the disease in the degenerative process involves the nucleus of the medulla oblongata and pons, including the core of the nuclei raphe, the locus coeruleus and reticular formation. The second stage is manifested clinically disturbed sleep and wakefulness rapid eye movements during sleep, daytime sleepiness, falling asleep as well as a violation of emotional disorders as depression and apathy. Join a moderate or severe cognitive impairment, and autonomic dysfunction. For the third stage is characterized by loss of the substantia nigra, the tonsils, the basal forebrain is shown connecting motor symptoms such as distortion of fine motor skills. At the fourth step involves the degeneration of the hippocampus and temporal mesokortex. The fourth stage of Parkinson's disease is characterized by a loss of 60% of the dopaminergic neurons of the substantia nigra and a decrease in dopamine production by 80%. Symptomatology complemented tremor, rigidity, hypokinesia, different manifestations of autonomic dysfunction. In the fifth stage of the disease have shown an interest associative zones prefrontal, temporal and parietal cortex. Degeneration of the motor and sensory cortical areas is characteristic of the sixth stage of Parkinson's disease, is characterized by increasing cognitive, behavioral and psychotic disorders. Patient J. 57 years, was admitted with complaints of persistent sleep disturbances, memory loss, fatigue, "darkening" of the eyes, frequent urge to urinate, especially at night ( up to 4 times), constipation, stiffness and clumsiness, excessive salivation, sweating. From history, we know that the above complaints bother with 2011, while growing gradually in intensity. Indication of exposure to toxic substances: carbon monoxide poisoning, neuroleptic administration, repeated head injuries, and the presence of extrapyramidal disorders in relatives there. In the neurological status: general cerebral and meningeal signs are not present, the field of view at an indicative study of preservation. Eye slits are symmetrical, the pupils round, medium-sized, direct and friendly photoreaction saved. Synchronous movement of the eyeballs, a few jerky: hypometria arbitrary saccades. The weakness of convergence without diplopia. The sensitivity of the face is not reduced. Celebrated a rare blinking several "frozen" look, hypomimia. It disprosodii with elements determined bradilalia moderate and mild dysarthria. No dysphagia. Paresis not pay attention total depletion of the motor pattern. Bilateral effects of oligobradykinesia, with an emphasis on the left. Formed a "supplicant posture" of the foot while standing parallel to each other, arms bent at the elbow a few joints and given to the body. When walking is determined by the tendency to mikrobasia, aheyrokinesis on both sides. Coordination tests perform adeguately. Caused by retropulsion not overcome. The tendon and periosteal reflexes were brisk and symmetrical, no signs of pathological Iambic. Muscle tone is increased by plastic type in the axial muscles and muscles of the extremities, with an emphasis on the right. Akrohypergidrosis. Scale UPDRS: Part I = 12, Part II = 17, Part III = 43, Part IV = 0 Total score = 72. Hyun scale Yar = 3. Tilt test in the supine position for 5 minutes BP (D, S) 157/90 mm ​​Hg. Art. Ps 84 beats / min, standing for 5 minutes, blood pressure (D, S) 126/78 mm Hg. Art. Ps 78 beats / min. Schirmer test was conducted to determine production of tears 0.5mm. The amount of saliva released within 5 minutes was 6.5gr. Patient have quantified cognitive impairment using the following tests and scales: Mini Mental State Examination (MMSE) a brief assessment of mental status scale – 27 points, Frontal Assessment Batter (FAB) battery of tests on the frontal dysfunction 15 points, the test is " 5 Words" – 10 points, clock drawing test 9 points. To assess mood disorders questionnaire used Beck 12 points, Spielberger anxiety scale: 37 situational anxiety, trait anxiety 48. The level of Toronto Alexithymia Scale is 82 points. Autonomic symptoms were assessed using questionnaires and autonomic manifestations was 42 points. Symptom Index of the American Urological Association (AUA) was 8 points. Non-motor symptoms questionnaire Parkinson's disease was 10 points. Thus, on the basis of complaints, medical history, neurological status, clinical and imaging studies of the patient 's disease, Parkinson's akinetic rigid form, 3st by Hyun Yar with affective and autonomic disturbances (orthostatic hypotension, sialoreya, overactive bladder, constipation).

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Manifestation of non-motor Parkinson’s disease

Parkinson's disease a chronic degenerative disease of the central nervous system, clinically manifested by a combination of hypokinesia and postural disorders with rigidity and resting tremor, and autonomic disorders and mental functions. The pathogenesis of Parkinson's disease is inhibition of the functions of dopaminergic systems of the central nervous system (stria negroid, tuberoinfundibular, olfactory, retinal, and so on). With a comprehensive defeat of dopaminergetic systems associated with the appearance not only of motor disorders, but also a wide variety of autonomic, endocrine, emotional and cognitive, that is, non-motor symptoms. The frequency and severity of non-motor disorders correlated with the duration of Parkinson's disease and the severity of motor disorders. It is important to note that many non-motorized violations appear already at the preclinical stage of Parkinson's disease, ahead of the manifestation of the classic symptoms of Parkinson's disease hypokinesia, rigidity, tremor and postural disorder. As the disease progresses, some of them become the dominant clinical significance, having a negative impact on the quality of life of patients, leading to their disability and reducing life expectancy. The period before the movement disorder can be quite long, sometimes up to 10 years, and is characterized by the appearance of non-motor symptoms. Typical non-motor symptoms of Parkinson's disease are impaired sense of smell, sleep disorders, depression, constipation, change in color perception, less pain, restless leg syndrome, apathy, fatigue, anxiety. Already in the early stages of Parkinson's disease can be detected as a violation of neurodynamic bradiphrenia and disorders of attention. For the first stage Parkinson characteristic lesion olfactory bulb, olfactory nucleus anterior, dorsal motor nucleus of the vagus nerve, peripheral ganglia, autonomic nervous system, as well as pre-and post-ganglionic sympathetic and parasympathetic structures intestinal, heart and pelvic plexus that clinically hypoosmia, constipation, the sympathetic innervation of the myocardium as vasodilation, reducing the strength of heart contractions, disorders of the heart rate variability, orthostatic hypotension. In the second stage of the disease in the degenerative process involves the nucleus of the medulla oblongata and pons, including the core of the nuclei raphe, the locus coeruleus and reticular formation. The second stage is manifested clinically disturbed sleep and wakefulness rapid eye movements during sleep, daytime sleepiness, falling asleep as well as a violation of emotional disorders as depression and apathy. Join a moderate or severe cognitive impairment, and autonomic dysfunction. For the third stage is characterized by loss of the substantia nigra, the tonsils, the basal forebrain is shown connecting motor symptoms such as distortion of fine motor skills. At the fourth step involves the degeneration of the hippocampus and temporal mesokortex. The fourth stage of Parkinson's disease is characterized by a loss of 60% of the dopaminergic neurons of the substantia nigra and a decrease in dopamine production by 80%. Symptomatology complemented tremor, rigidity, hypokinesia, different manifestations of autonomic dysfunction. In the fifth stage of the disease have shown an interest associative zones prefrontal, temporal and parietal cortex. Degeneration of the motor and sensory cortical areas is characteristic of the sixth stage of Parkinson's disease, is characterized by increasing cognitive, behavioral and psychotic disorders. Patient J. 57 years, was admitted with complaints of persistent sleep disturbances, memory loss, fatigue, "darkening" of the eyes, frequent urge to urinate, especially at night ( up to 4 times), constipation, stiffness and clumsiness, excessive salivation, sweating. From history, we know that the above complaints bother with 2011, while growing gradually in intensity. Indication of exposure to toxic substances: carbon monoxide poisoning, neuroleptic administration, repeated head injuries, and the presence of extrapyramidal disorders in relatives there. In the neurological status: general cerebral and meningeal signs are not present, the field of view at an indicative study of preservation. Eye slits are symmetrical, the pupils round, medium-sized, direct and friendly photoreaction saved. Synchronous movement of the eyeballs, a few jerky: hypometria arbitrary saccades. The weakness of convergence without diplopia. The sensitivity of the face is not reduced. Celebrated a rare blinking several "frozen" look, hypomimia. It disprosodii with elements determined bradilalia moderate and mild dysarthria. No dysphagia. Paresis not pay attention total depletion of the motor pattern. Bilateral effects of oligobradykinesia, with an emphasis on the left. Formed a "supplicant posture" of the foot while standing parallel to each other, arms bent at the elbow a few joints and given to the body. When walking is determined by the tendency to mikrobasia, aheyrokinesis on both sides. Coordination tests perform adeguately. Caused by retropulsion not overcome. The tendon and periosteal reflexes were brisk and symmetrical, no signs of pathological Iambic. Muscle tone is increased by plastic type in the axial muscles and muscles of the extremities, with an emphasis on the right. Akrohypergidrosis. Scale UPDRS: Part I = 12, Part II = 17, Part III = 43, Part IV = 0 Total score = 72. Hyun scale Yar = 3. Tilt test in the supine position for 5 minutes BP (D, S) 157/90 mm ​​Hg. Art. Ps 84 beats / min, standing for 5 minutes, blood pressure (D, S) 126/78 mm Hg. Art. Ps 78 beats / min. Schirmer test was conducted to determine production of tears 0.5mm. The amount of saliva released within 5 minutes was 6.5gr. Patient have quantified cognitive impairment using the following tests and scales: Mini Mental State Examination (MMSE) a brief assessment of mental status scale – 27 points, Frontal Assessment Batter (FAB) battery of tests on the frontal dysfunction 15 points, the test is " 5 Words" – 10 points, clock drawing test 9 points. To assess mood disorders questionnaire used Beck 12 points, Spielberger anxiety scale: 37 situational anxiety, trait anxiety 48. The level of Toronto Alexithymia Scale is 82 points. Autonomic symptoms were assessed using questionnaires and autonomic manifestations was 42 points. Symptom Index of the American Urological Association (AUA) was 8 points. Non-motor symptoms questionnaire Parkinson's disease was 10 points. Thus, on the basis of complaints, medical history, neurological status, clinical and imaging studies of the patient 's disease, Parkinson's akinetic rigid form, 3st by Hyun Yar with affective and autonomic disturbances (orthostatic hypotension, sialoreya, overactive bladder, constipation).

Текст научной работы на тему «Немоторные проявления болезни Паркинсона»

2013, том 15 [11]

MANIFESTATION OF NON-MOTOR PARKINSON’S DISEASE.

Pillipovich A.A., Goytemirova P.U., Nozdryuhina N.V., Strutsenko A.A Garabova N.I., Cheboksarov D. V. Buntina M.A.

Department of Nervous Diseases FPPOVFirstMGMU them I.M. Sechenova Peoples' Friendship University Department of Nervous Diseases and Neurosurgery

Parkinson's disease - a chronic degenerative disease of the central nervous system, clinically manifested by a combination of hypokinesia and postural disorders with rigidity and resting tremor, and autonomic disorders and mental functions. The pathogenesis of Parkinson's disease is inhibition of the functions of dopaminergic systems of the central nervous system (stria - negroid, tuberoinfundibular, olfactory, retinal, and so on). With a comprehensive defeat of dopaminergetic systems associated with the appearance not only of motor disorders, but also a wide variety of autonomic, endocrine, emotional and cognitive, that is, non-motor symptoms. The frequency and severity of non-motor disorders correlated with the duration of Parkinson's disease and the severity of motor disorders. It is important to note that many non-motorized violations appear already at the preclinical stage of Parkinson's disease, ahead of the manifestation of the classic symptoms of Parkinson's disease - hypokinesia, rigidity, tremor and postural disorder. As the disease progresses, some of them become the dominant clinical significance, having a negative impact on the quality of life of patients,

leading to their disability and reducing life expectancy. The period before the movement disorder can be quite long, sometimes up to 10 years, and is characterized by the appearance of non-motor symptoms. Typical non-motor symptoms of Parkinson's disease are impaired sense of smell, sleep disorders, depression, constipation, change in color perception , less pain, restless leg syndrome, apathy, fatigue, anxiety . Already in the early stages of Parkinson's disease can be detected as a violation of neurodynamic bradiphrenia and disorders of attention. For the first stage Parkinson characteristic lesion olfactory bulb, olfactory nucleus anterior, dorsal motor nucleus of the vagus nerve, peripheral ganglia, autonomic nervous system, as well as pre-and post-ganglionic sympathetic and

parasympathetic structures intestinal, heart and pelvic plexus that clinically hypoosmia, constipation, the sympathetic innervation of the myocardium as vasodilation, reducing the strength of heart contractions, disorders of the heart rate variability, orthostatic hypotension. In the second stage of the disease in the degenerative process involves the nucleus of the medulla oblongata and pons, including the core

Издание зарегистрировано в Федеральной службе по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор). Свидетельство о регистрации СМИ ПИ ЭЛ № ФС77-50518

2013, том 15 [11]

of the nuclei raphe, the locus coeruleus and reticular formation. The second stage is manifested clinically disturbed sleep and wakefulness - rapid eye movements during sleep, daytime sleepiness, falling asleep as well as a violation of emotional disorders as depression and apathy. Join a moderate or severe cognitive impairment, and autonomic dysfunction. For the third stage is characterized by loss of the substantia nigra , the tonsils, the basal forebrain is shown connecting motor symptoms such as distortion of fine motor skills. At the fourth step involves the degeneration of the hippocampus and temporal mesokortex . The fourth stage of Parkinson's disease is characterized by a loss of 60% of the dopaminergic neurons of the substantia nigra and a decrease in dopamine production by 80 %. Symptomatology complemented tremor, rigidity, hypokinesia, different manifestations of autonomic dysfunction. In the fifth stage of the disease have shown an interest associative zones prefrontal, temporal and parietal cortex. Degeneration of the motor and sensory cortical areas is characteristic of the sixth stage of Parkinson's disease, is characterized by increasing cognitive, behavioral and psychotic disorders.

Patient J. 57 years, was admitted with complaints of persistent sleep disturbances, memory loss, fatigue, "darkening" of the eyes, frequent urge to urinate, especially at night ( up to 4 times), constipation, stiffness and clumsiness, excessive salivation, sweating. From history, we know that the above

complaints bother with 2011, while growing gradually in intensity. Indication of exposure to toxic substances: carbon monoxide poisoning, neuroleptic administration, repeated head injuries, and the presence of extrapyramidal disorders in relatives there. In the neurological status: general cerebral and meningeal signs are not present, the field of view at an indicative study of preservation. Eye slits are symmetrical, the pupils round, medium-sized, direct and friendly photoreaction saved. Synchronous movement of the eyeballs, a few jerky: hypometria arbitrary saccades. The weakness of convergence without diplopia. The sensitivity of the face is not reduced. Celebrated a rare blinking several "frozen" look, hypomimia. It disprosodii with elements determined bradilalia moderate and mild dysarthria. No dysphagia. Paresis not pay attention total depletion of the motor pattern. Bilateral effects of oligo-bradykinesia, with an emphasis on the left. Formed a "supplicant posture" of the foot while standing parallel to each other, arms bent at the elbow a few joints and given to the body. When walking is determined by the tendency to mikrobasia, aheyrokinesis on both sides. Coordination tests perform

adeguately. Caused by retropulsion not overcome. The tendon and periosteal reflexes were brisk and symmetrical, no signs of pathological Iambic. Muscle tone is increased by plastic type in the axial muscles and muscles of the extremities, with an emphasis on the right. Akrohypergidrosis . Scale UPDRS: Part I = 12 , Part II = 17 , Part III = 43, Part IV = 0

Издание зарегистрировано в Федеральной службе по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор). Свидетельство о регистрации СМИ ПИ ЭЛ № ФС77-50518

образование

2013, том 15 [11]

Total score = 72. Hyun - scale Yar = 3. Tilt test in the supine position for 5 minutes BP (D, S) 157/90 mm Hg. Art. Ps 84 beats / min , standing for 5 minutes, blood pressure (D, S) 126/78 mm Hg. Art. Ps 78 beats / min. Schirmer test was conducted to determine production of tears 0.5mm. The amount of saliva released within 5 minutes was 6.5gr. Patient have quantified cognitive impairment using the following tests and scales: Mini Mental State Examination (MMSE) - a brief assessment of mental status scale - 27 points , Frontal Assessment Batter (FAB) - battery of tests on the frontal dysfunction - 15 points , the test is " 5 Words" -10 points , clock drawing test - 9 points. To assess mood disorders questionnaire used Beck - 12 points, Spielberger anxiety scale: 37 situational anxiety , trait anxiety 48. The level of Toronto Alexithymia Scale is 82 points . Autonomic symptoms were assessed using questionnaires and autonomic manifestations was 42 points. Symptom Index of the American Urological Association (AUA) was 8 points. Non-motor symptoms questionnaire Parkinson's disease was 10 points. Thus, on the basis of complaints, medical history, neurological status, clinical and imaging studies of the patient 's disease, Parkinson's akinetic - rigid form, 3st by Hyun - Yar with affective and autonomic disturbances (orthostatic hypotension, sialoreya , overactive bladder, constipation).

Keywords: neurology, Parkinson's disease.

~ 3 ~

Издание зарегистрировано в Федеральной службе по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор). Свидетельство о регистрации СМИ ПИ ЭЛ N° ФС77-50518

2013, том 15 [11]

НЕМОТРНЫЕ ПРОЯВЛЕНИЯ БОЛЕЗНИ ПАРКИНСОНА.

Пиллипович А.А., Гойтемирова П. У., Ноздрюхина Н.В., Струценко А.А., Гарабова Н.И., Чебоксаров Д.В., Бунтина М.А.

Кафедра нервных болезней ФППОВ Первого МГМУ им И.М.Сеченова РУДН кафедра нервных болезней и нейрохирургии

Болезнь Паркинсона - хроническое дегенеративное заболевание ЦНС,

клинически проявляющееся сочетанием гипокинезии и постуральных нарушений с ригидностью и тремором покоя, а также нарушениями вегетативных и психических функций. В основе патогенеза болезни Паркинсона лежит угнетение функций дофаминэргических систем центральной нервной системы (стрио-негральной, тубероинфундибулярной, ольфакторной, ретинальной, и т.д.). С комплексным

поражением дофаминэргических систем связано появление не только моторных нарушений, но и широкого спектра вегетативных, эндокринных, эмоциональных и когнитивных, то есть немоторных

проявлений. Частота и тяжесть немоторных нарушений коррелирует с длительностью

болезни Паркинсона и тяжестью моторных расстройств. Важно отметить, что многие немоторные нарушения появляются уже на доклинической стадии болезни Паркинсона,

опережая манифестацию классических симптомов паркинсонизма - гипокинезию, ригидность, тремор и постуральные

нарушения. По мере прогрессирования заболевания некоторые из них приобретают доминирующее клиническое значение,

оказывая негативное влияние на качество жизни пациентов, приводя к их

инвалидизации и сокращая

продолжительность жизни. Период до появления двигательных расстройств может быть довольно длительным, иногда до 10 лет, и характеризуется появлением немоторных симптомов. Типичными немоторными

симптомами паркинсонизма являются

нарушение обоняния, расстройства сна, депрессия, запоры, изменение

цветовосприятия, реже боли, синдром

беспокойных ног, апатия, утомляемость,

тревога. Уже на начальных стадиях паркинсонизма могут быть выявлены

нейродинамические нарушения в виде

брадифрении и нарушений внимания. Для первой стадии паркинсонизма характерно

Издание зарегистрировано в Федеральной службе по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор). Свидетельство о регистрации СМИ ПИ ЭЛ № ФС77-50518

2013, том 15 [11]

поражение обонятельной луковицы, переднего ольфакторного ядра, дорсального моторного ядра блуждающего нерва, периферических ганглиев вегетативной нервной системы, а также пре- и постганглионарных симпатических и парасимпатических структур кишечного, сердечного и тазового сплетений, что клинически проявляется гипоосмией, запорами, нарушением симпатической

иннервации миокарда в виде вазодилатации, снижения силы сердечных сокращений, расстройств вариабельности сердечного ритма, ортостатической гипотензии. Во второй стадии заболевания в дегенеративный процесс вовлекаются ядра продолговатого мозга и моста, в том числе ядро шва, голубоватое пятно и ретикулярная формация. Клинически вторая стадия проявляется расстройствами сна и бодрствования -быстрыми движениями глаз во время сна, дневной сонливостью, нарушением

засыпания, а также эмоциональными

нарушениями в виде депрессии и апатии. Присоединяются умеренные или

выраженные когнитивные расстройства и

вегетативная дисфункция. Для третьей стадии характерно поражение черной субстанции, миндалин, базальных отделов переднего мозга проявляется

присоединением моторных симптомов таких как, тонкие нарушения моторики. При четвертой стадии в дегенерацию вовлекается височный мезокортекс и гиппокамп. Четвертая стадия паркинсонизма

характеризуется гибелью 60%

дофаминергических нейронов черной субстанции и уменьшением выработки дофамина на 80%. Симптоматика дополняется тремором, ригидностью, гипокинезией, разнообразными

проявлениями вегетативной дисфункции. В пятой стадии заболевания отмечается заинтересованность ассоциативных зон префронтальной, височной и теменной коры. Дегенерация моторных и сенсорных корковых отделов характерна для шестой стадии паркинсонизма, характеризующейся нарастанием когнитивных, поведенческих и психотических расстройств.

Пациент Ж. 57 лет, поступил с жалобами на стойкие нарушения сна, снижение памяти, усталость, утомляемость, «потемнение» в глазах, учащённые позывы на мочеиспускание, особенно в ночное время (до 4 раз), запоры, скованность и неловкость движений, слюнотечение, потливость. Из анамнеза известно, что вышеописанные жалобы беспокоят с 2011 г., постепенно нарастая по интенсивности. Указаний на

контакт с токсическими веществами,

отравление угарным газом, прием

нейролептиков, повторные черепно-мозговые травмы, и наличие экстрапирамидных

заболеваний у родственников нет. В

неврологическом статусе: общемозговых и менингеальных симптомов нет, поля зрения при ориентировочном исследовании сохранны. Глазные щели симметричны, зрачки округлой формы, средней величины,

~ 5 ~

Издание зарегистрировано в Федеральной службе по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор). Свидетельство о регистрации СМИ ПИ ЭЛ № ФС77-50518

2013, том 15 [11]

прямая и содружественная фотореакции сохранены. Движения глазных яблок синхронные, несколько отрывистые:

гипометрия произвольных саккад. Слабость конвергенции без диплопии.

Чувствительность на лице не нарушена. Отмечается редкое мигание, несколько «застывший» взгляд, гипомимия. Речь с элементами диспросодии, определяется умеренная брадилалия и легкая дизартрия. Дисфагии нет. Парезов нет, обращает внимание общая обедненность

двигательного рисунка. Двусторонние явления олиго-брадикинезии, с акцентом слева. Сформирована «поза просителя», стопы при стоянии расположены параллельно друг другу, руки несколько согнуты в локтевых суставах и приведены к туловищу. При ходьбе определяется тенденция к микробазии, ахейрокинез с обеих сторон. Координаторные пробы выполняет удовлетворительно. Вызванную ретропульсию не преодолевает.

Сухожильные и периостальные рефлексы живые, симметричные, патологических стопных знаков нет. Мышечный тонус повышен по пластическому типу в аксиальной мускулатуре и мышцах конечностей с акцентом справа. Акрогипергидроз. Шкала UPDRS: Часть I = 12 , Часть II = 17 , Часть III = 43 , Часть IV = 0 , Общий балл = 72 . Шкала Хен-Яра = 3 . Ортостатическая проба в положении лежа в течение 5 минут АД (р^) 157/90 мм рт. ст. Ps 84 уд/ мин, в положении стоя в течение 5

минут АД (D,S)126/78 мм рт. ст. Ps 78 уд/ мин. Тест Ширмера проводился для определения слезопродукции 0.5мм. Количество слюны выделяемой в течение 5 минут составил 6.5гр. Пациенту

проводилась количественная оценка когнитивных нарушений с применением следующих тестов и шкал: Mini Mental State Examination (MMSE) - краткая шкала оценки психического статуса - 27баллов, Frontal Assessment Batter (FAB) - батарея тестов на лобную дисфункцию - 15 баллов, тест «5 слов» - 10баллов, тест рисование часов - 9 баллов. Для оценки аффективных нарушений использовался опросник Бека - 12 баллов, шкале тревоги Спилбергера: ситуативная

тревожность 37, личностная тревожность 48. Уровень алекситимии оценивался торонтской алекситимической шкалой и составил 82 балла. Вегетативные симптомы оценивались с помощью анкеты вегетативных проявлений и составил 42 балла. Индекс симптомов Американской урологической ассоциации (AUA) составил 8 баллов. Опросник немоторных проявлений болезни

Паркинсона составил 10 баллов. Таким образом, исходя из жалоб, анамнеза заболевания, неврологического статуса, клинических и инструментальных методов исследования у пациента болезнь Паркинсона, акинетико-ригидная форма, 3ст по Хен-Яру с аффективными и вегетативными нарушениями

(ортостатическая гипотензия, сиалорея, гиперактивный мочевой пузырь, запоры).

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Издание зарегистрировано в Федеральной службе по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор). Свидетельство о регистрации СМИ ПИ ЭЛ № ФС77-50518

2013, том 15 [11]

-ЄЧЄ4&^9-

Ключевые слова: неврология, Болезнь Паркинсона.

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Издание зарегистрировано в Федеральной службе по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор). Свидетельство о регистрации СМИ ПИ ЭЛ № ФС77-50518

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