CC BY
84
ш
М1ЖНАРОДНИЙ НЕВРОЛОГ1ЧНИЙ ЖУРНАЛ
INTERNATIONAL NEUROLOGICAL JOURNAL 1
МЕЖДУНАРОДНЫЙ НЕВРОЛОГИЧЕСКИЙ ЖУРНАЛ ОРИГШАЛЬШ ДОСЛЩЖЕННЯ /ORIGINAL RESEARCHES/
UDC 616.831-005.1-031.79-092-07
S.M. Vinychuk1, O.Ye. Fartushna2 1Oleksandrivska Clinical Hospital, Kyiv, Ukraine 2Ukrainian Military Medical Academy, Kyiv, Ukraine
DOI: 10.22141/2224-0713.6.100.2018.146450
Crossed cerebellar diaschisis in acute stroke patients:
case analysis and report
Abstract. Background. Stroke represents a high-risk condition for long-term disability and death. The role of diaschisis in the severity of acute neurological deficit and spontaneous stroke recovery is significant. However, currently there are not enough published prospective, hospital-based, cohort studies that report and analyze clinical characteristics of crossed cerebellar diaschisis in acute stroke patients. Moreover, modern stroke treatment may change clinical representation of diaschisis. The purpose of this study is to determine the features of the clinical manifestations of crossed cerebellar diaschisis after acute cerebral stroke and to improve the efficiency of its diagnosis by comparing the obtained data with the results of the magnetic resonance imaging findings. Materials and methods. We prospectively recruited 124 acute stroke patients, who were admitted to a single department of the academic tertiary care hospital in Kyiv, Ukraine. The primary outcome was the combined incidence of stroke and diaschisis. In the secondary analyses, we studied pathophysiological, anatomical, and clinical features specific to crossed cerebellar diaschisis in a cohort of acute stroke patients with diaschisis. Results. Among 124 selected acute stroke patients admitted to the department, 42 (33.9 %) persons were diagnosed with different forms of diaschisis: cerebrospinal (n = 22), commissural (n = 4), crossed cerebellar (n = 5), crossed cerebellar-hemispheric (n = 6), crossed andponto-cerebellar diaschisis (n = 5). We have conducted a detailed pathophysiological and clinical analysis of crossed cerebellar diaschisis in acute ischemic stroke patients, described clinical manifestations of crossed cerebellar diaschisis. Utilizing the von Monakow theory of diaschisis, we found a scientific explanation for the pathophysiology of clinical manifestations of that remote form of diaschisis. Conclusions. Results of this study showed that cerebellar infarction is associated not only with typical symptoms of cerebellar lesion, but also with paresis, disturbances of sensitivity, and higher mental functions. Further study of the issues addressed in this article will help to improve the diagnosis and management of patients with acute cerebellar stroke. Keywords: crossed cerebellar diaschisis; cerebellar stroke; cerebellum; remote diaschisis; forms of diaschisis; clinical manifestations; diagnosis, case report
Introduction
Stroke is the second leading global cause of death behind heart disease, accounting for 11.8 % oftotal deaths worldwide [1—5]. Each year, about 795,000 people experience a new or recurrent stroke [6—9]. Approximately 610,000 of these are first-time attacks, and 185,000 are recurrent attacks [10—15]. In 2013, worldwide prevalence of stroke was 25.7 million, with 10.3 million people having a first stroke [16—22].
For decades, the concept of diaschisis coined by von Monakow in 1914 to describe the neurophysiologi-
cal changes that occur distant to a focal brain lesion was placed at the center of the understanding of brain function [23—29]. Until the late 1970s, this concept triggered widespread clinical interest to describe symptoms and signs which primary stroke lesion could not fully explain [30]. However, after the first imaging studies that only partially confirmed the clinical significance of diaschisis, the concept of diaschisis became neglected and subsequently disappeared from mainstream research in clinical neuroscience [31].
© «Ммнародний невролопчний журнал» / «Международный неврологический журнал» / «International Neurological Journal» («Mezdunarodnyj nevrologiieskij zurnal»), 2018 © Видавець Заславський О.Ю. / Издатель Заславский А.Ю. / Publisher Zaslavsky O.Yu., 2018
Для кореспонденци: Фартушна Олена £вгешвна, кандидат медичних наук, старший викладач кафедри авiацiйно'í, морсько!' медицини та психофвюлоп% УкраТнська вмськово-медична академiя, вул. Мельникова, 24, м. КиТ'в, 04050, УкраТ'на; e-mail: [email protected]
For correspondence: Olena Fartushna, PhD, Senior Lecturer at the Department of aviation marine medicine and psychophysiology, Ukrainian Military Medical Academy, Melnikova st., 24, Kyiv, 04050, Ukraine; e-mail: [email protected]
OpiiriHaAbHi gocaigffieHHi /Original Researches/
The development of new imaging techniques allows a clear visualization and deeper understanding of structural and functional connectivity between brain areas which are distant to the primary lesion. These techniques have consequently revitalized the concept of diaschisis. Presently, one of the most promising techniques is neuromodulation utilizing transcranial magnetic stimulation. Once this last technique becomes successful, the concept of diaschisis will regain all the clinical respectability that was unobtainable during decades of research.
Remote diaschisis focusing on specific networks seems to relate more consistently to the clinical findings, especially after stroke in the motor and attentional networks. Normalization of remote connectivity changes in these networks is associated with better recovery [26]. Therefore, neuro-physiological changes distant to the lesion should be the target of therapeutic strategies, and specific clinical characteristics of diaschisis should be well understood and promptly recognized by clinicians.
The purpose was to conduct a prospective hospital-based cohort study in acute stroke patients in order to analyze clinical features of all forms of distant diaschisis in modern treatment.
Materials and methods
The materials and methods of this study have been reported in detail previously [32, 33]. We have conducted a prospective, hospital-based, cohort study of patients with newly diagnosed acute ischemic stroke (n = 124) who were admitted to the department of cerebrovascular diseases of the University hospital (Oleksandrivska Clinical Hospital, Kyiv, Ukraine) within the first 24 hours after the stroke occurred. All cases were reviewed by at least two board-certified neurologists trained in cerebrovascular diseases.
All participants underwent standardized examination to obtain: clinical history, 12-lead electrocardiogram, blood testing (blood chemistry, thyroid, renal, and hepatic function, complete blood count, serum glucose, coagulation studies), carotid Doppler ultrasound (carotid duplex (Multigon 500M, USA) or carotid triplex (Aloka SSD-4000, Japan)), computed tomography of the head (Toshiba Activion 16 Multislice CT system, Nasu, Japan) and 1.5T brain magnetic resonance imaging (MRI), magnetic resonance angiography (Vantage MRI System, Japan) within 24—72 hours after the onset of symptoms and in dynamics during the period of maximum severity of symptoms. A chest radiograph was done if pulmonary disease or heart failure was suspected.
Stroke was defined according to criteria of the World Health Organization, American Heart Association/American Stroke Association guidelines for adult stroke and was confirmed by neuroimaging [34, 35]. The etiology of stroke was classified according to the TOAST (trial of ORG 10172 in acute stroke treatment) criteria [36]. The National Institutes of Health Stroke Scale, modified Rankin scale, Bar-thel index were used in all participants based on the data available upon admission and in their respective medical records. Secondary stroke prevention was prescribed according to the American Heart Association/American
_INJ]
Stroke Association and the European Stroke Organisation guidelines, immediately after the stroke diagnosis was made [36-44].
Parametric and non-parametric univariate analyses were performed with x2, Fisher's exact, Mann-Whitney U, and Student t tests, as appropriate. The log-rank test was used for univariate comparisons of event-free survival between groups. A two-sided p < 0.05 was considered significant for all analyses. All statistical analyses were performed using IBM SPSS Statistics Version 22 (IBM, Armonk, NY).
Results and discussion
In total, 124 patients aged 28 to 84 years with acute ischemic stroke were screened. The localization of primary stroke lesion confirmed by neuroimaging was as follows: cerebral hemispheres (n = 68), brainstem (n = 11), cerebellum (n = 45).
Among the 124 patients, 42 persons (22 men and 20 women) were diagnosed with remote diaschisis. These 42 patients had a mean age of 60.8 ± 12.5 years (from 32 to 84 years). The localization of primary brain lesion in the study group was as follows: brain hemisphere (n = 31), pons Varolii (n = 5), cerebellar hemisphere (n = 6).
Based on the localization of primary brain lesion and considering secondary dysfunction of brain neighboring structures, we have analyzed and described clinical manifestations and characteristics of the following forms of remote diaschisis: cerebrospinal (n = 22), commissural (n = 4), crossed cerebellar (n = 5), crossed cerebellar-hemispheric (n = 6), and ponto-cerebellar diaschisis (n = 5). Clinical features of cerebrospinal and commissural diaschisis were analyzed in detail in our previous publications [33]. This article deals with the analysis of clinical manifestation and course of crossed cerebellar diaschisis.
Crossed cerebellar diaschisis was detected in 5 patients. It arose with an acute hemispheric territorial infarction. The localization of the primary stroke lesion was as follows: cortex of frontoparietal lobe (n = 4), inner capsule and basal ganglia (n = 1). The clinical manifestation of stroke was determined not only by the localization of primary stroke lesion and its size, but also by the MRI-proved ischemic focus (diaschisis) in the contralateral cerebellar hemisphere.
Synchronous or sequential diaschisis (acute ischemic injury of structures that are anatomically and functionally connected, but remote to the primary brain lesion) caused more severe neurological deficit compared to that expected from the primary brain lesion. Clinically, patients were diagnosed with hemiparesis and hemihypesthesia on the side opposite to the primary brain lesion. Diaschisis was manifested clinically with the symptoms of hemiataxia in these patients. For illustration, we present a clinical case of patient E., who has developed regional ischemic stroke with hemorrhagic transformation (Fig. 1).
Neurological deficit in crossed cerebellar diaschisis composed a syndrome of motor and ataxic hemiparesis — hemi-paresis-hemiataxia. The main mechanism of its occurrence is damage at the level of the first corticopontine neuron of
6
MimHapoAHHH HeBponoriHHHH mypHaa ISSN 2224-0713 (print), ISSN 2307-1419 (online) № 6 (100), 2018
Figure 1. Patient E., 57 years old: a — brain MRI, axial projection, T2-weighted image. In the cortical and subcortical areas of the posterior frontal, parietal, and temporal lobes of the right hemisphere, a section of ischemic lesion is visualized, sized 100 x 50 x 30 mm, with a non-uniform MR-signal due to hemorrhagic transformation. In the right thalamus, a focus of ischemia was detected; b — diffusion-weighted MRI, axial projection: in the anterior regions of the left cerebellar hemisphere (branch of the upper cerebellar artery), the focus (arrow) of the lacunar infarction is clearly identified
the cortico-cerebellar path, which causes the dissociation of its parts and dissolution. This results in deactivation of the afferent impulses from the brain lesion in the cerebral hemisphere to the cross-pontine-cerebellar path in the pons. Because of this deactivation, the function of the pathway returns to the phylogenetically lower level (Fig. 2).
Damage of the corticopontine neuron (i.e., ischemic damage (diaschisis)) at the level of different parts of the cerebral cortex (mainly, in frontal or parietal lobe of brain hemisphere) led to the deactivation of afferent impulses to the cross-pontine-cerebellar pathway in the pons. This deactivation causes a decrease in blood flow and metabolic depression in cerebellar hemisphere opposite to the stroke brain lesion (i.e., opposite to the brain hemisphere with the primary damage). Contralateral hypoperfusion in the cerebellum was detected in 58 % of patients with hemispheric stroke [26].
Conclusions
Isolated cerebellar infarctions often cause crossed cere-bellar-hemispheric diaschisis in the contralateral cortex of the frontal or frontoparietal lobe of the brain accompanied by structural and morphological findings on MRI in 87.5 % of observations. Neurologists should know that cerebellar stroke can manifest not only in typical symptoms of cerebellar dysfunction (dizziness, disorders of static and coordination, dysmetria, intentional tremor, nystagmus, dysarthria), but also in the remote symptoms such as paresis of limbs, impaired sensitivity and mental functions caused by a cross-hemispheric diaschisis.
Conflicts of interests. Authors declare no conflicts of interests that might be construed to influence the results or interpretation of their manuscript.
Figure 2. Scheme of afferent connections of the cerebellum and the mechanism of crossed cerebellar diaschisis development in patients with hemispheric stroke and lesion located in the frontal or parietal lobe
Оригшальш дослщження /Original Researches/
Author contributions
S.M. Vinychuk — study concept and design, interpretation of data, data acquisition; O. Ye. Fartushna — article concept and design, literature overview, data acquisition, interpretation of data, and drafting the article.
References
1. Feigin V.L. Global and regional burden of stroke during 1990—2010: findings from the Global Burden of Disease Study 2010/ V.L. Feigin, M.H. Forouz,anfar, R. Krishnamurthi [et al.]// The Lancet. — 2014. — Vol. 383(9913). — P. 245-254.
2. Mackay J. The atlas of heart disease and stroke / J. Mackay, G.A. Mensah. — Geneva: World Health Organization and Center for Disease Control and Prevention, 2004. — 112p.
3. Benjamin E.J. On behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics — 2018 update: a report from the American Heart Association / E.J. Ben -jamin, S.S. Virani, C.W. Callaway [et al.] // Circulation. — 2018. — Vol. 137(12). — P. e67-e492.
4. Thrift A.G. Global stroke statistics / A.G. Thrift, T. Thayaba-ranathan, G. Howard [et al.] // International Journal of Stroke. — 2017. — № 12(1). — P. 13-32.
5. Вничук С.М. Гострий meMiuHuü нсульт / С.М. Вничук, М.М. Прокотв. — К. : Наукова думка, 2006. — 286 с.
6. World Stroke Organization. Facts and Figures about Stroke. — Режим доступу: http://www.world-stroke.org/component/content/ article/16-forpatients/84-facts-and-figures-about-stroke
7. Snow S.J. Stroke and t-PA — triggering new paradigms of care / S.J. Snow // The New England Journal of Medicine. — 2016. — № 374(9). — P. 809.
8. Евтушенко С.К. Новые факторы риска развития инсульта у лиц молодого возраста / С.К. Евтушенко, Д.А. Филимонов, И.С. Евтушенко // Журнал неврологии и психиатрии им. С. С. Корсакова. Спецвыпуск. — 2015. — Т. 115, № 12. — С. 3-12.
9. Фартушна O.G. Виявлення таусунення васкулярних чин-нитв ризику — важливий напрямок первинног профыактики транзиторних iшемiчних атак та/чи нсульту/ O.G. Фартушна, С.М. Вничук // Украгнський медичний часопис. — 2015. — № 1(105). — С. 23-27.
10. Benjamin E.J. On behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics — 2017 update: a report from the American Heart Association / E.J. Benjamin, M.J. Blaha, S.E. Chiuve [et al.]// Circulation. — 2017. — № 135. — P. 229-445.
11. Feigin V.L. Global burden of stroke / V.L. Feigin, B. Nor-rving, G.A. Mensah// Circulation Research. — 2017. — № 120(3). — Р. 439-448.
12. Wilkins E. European cardiovascular disease statistics 2017/ Е. Wilkins, L. Wilson, K. Wickramasinghe [et al.]. — Brussels: European Heart Network, 2017. — 188p.
13. Lees R. Vascular cognitive impairment/vascular dementia. The pattern of cognitive impairment in stroke survivors with carotid stenosis / R. Lees, F. McGrane, O. Fartushna, N.M. Broomfield, T.J. Quinn, K. Dani, K. Forbes, J. Dawson // International Journal of Stroke. — 2014. — № 9. — P. 323-324.
14. Вничук С.М. Ранняреабштацы тсля гострих iшемiчних порушеньмозковогокровообку /С.М. Вничук, O.G. Фартушна//
_INJ]
Мiжнародний неврологiчний журнал. — 2016. — № 8(86). — С. 34-39.
15. Фартушна O.G. Актуальтсть проблеми цереброваску-лярних захворювань, транзиторних шемiчних атак та вдоско-налення гх дiагностики в системi охорони здоров'я в Украгт / O.G. Фартушна, М.М. Прокотв//Проблеми вшськовог охорони пращ: Зб. наук. праць Украгнськог вшськово-медичног акаде-мй/ За ред. проф. В.Я. Быого. — К. : УВМА, 2007. — Вип. 19. — С. 335-342.
16. GBD 2016 Causes of Death Collaborators. Global, regional, and national age-sex specific mortality for 264 causes of death, 1980—2016: a systematic analysis for the Global Burden of Disease Study 2016// The Lancet. — 2017. — № 390(10100). — P. 11511210.
17. Wang H. Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980—2015: a systematic analysis for the Global Burden of Disease Study 2015/H. Wang, M. Naghavi, C. Allen [et al.]// The Lancet. — 2016. — № 388(10053). — P. 1459-1544.
18. Fartushna O.Y. Emergency therapeutic approach as a secondary prevention of an acute ischemic stroke in patients with TIA / Fartushna O.Y. // XX World Neurological Congress, 12—17.11.2011. — Marrakesh, Morocco, 2011. — P. 167.
19. Фартушна O.G. Транзиторт шемiчm атаки/O.G. Фартушна, С.М. Вничук. — К.: ВД«Авщена», 2014. — 216с.
20. Фартушна O.G. Модифжащя поведнкових чинниювризику як складова первинног профыактики транзиторних ше-мiчних атак та/чи нсульту/ O.G. Фартушна, С.М. Вничук// Украгнський медичний часопис. — 2014. — № 6(104) — XI/XII. — С. 42-44.
21. Фартушна O.G. Епiдемiологiя транзиторних iшемiч-них атак в стрyктyрi гострих порушень мозкового кровообку в Украгт та нших крагнах/ O.G. Фартушна, С.М. Вничук// Мiжнародний неврологiчний журнал. — 2017. — № 5(91). — С. 105-111.
22. Фартушна O.G. Патогенетичт тдтипи транзиторних iшемiчних атак: особливостi неврологiчног клтки, гемодинамжи талжування[Текст]:Дис... канд. мед. наук: 14.01.15/Фартушна Oлена Gвгенiвна; Нац. мед. ун-т iм. O.O. Богомольця. — К., 2012. — 217арк.:рис., табл. — Бiблiогр.: арк. 187-217.
23. Jagella C. 100 Jahre Neurologie an der Universität Zürich 1894 bis 1994 — Constantin von Monakow (1853 bis 1930) / C. Jagella, H. Isler, K. Hess // Schweizer Archiv fur Neurologie und Psychiatrie. — 1994. — Vol. 145 (suppl. 1). — P. 1-61.
24. Seitz R.J. The role of diaschisis in stroke recovery / R.J. Seitz, N.P. Azari, U. Knorr [et al.]// Stroke. — 1999 Sep. — № 30(9). — P. 1844-50.
25. Monakow von C. Die Lokalisation im Grosshirm und der Ablau der Function dürch korticale Herde / Monakow von C. — Wiesbaden: J.F. Bergmann, 1914. — 1033 s.
26. Виничук С.М. Диашиз при мозговом инсульте. — К.: OЖИВА, 2017. — 64 c.
27. Vinychuk S.M. Diaschisis: brief historical review / S.M. Vinychuk, O.Ye. Fartushna // International Neurological Journal. — 2018. — № 4(98). — С. 11-16.
28. Вничук С.М. Iсторiя Кигвськог неврологiчног школи / С.М. Вничук, O.G. Фартушна. — К.:Едванс-Прщт, 2015. — 55с.
29. Carrera E. Diaschisis: past, present, future / E. Carrera, G. Tononi//Brain. — 1911. — Vol. 137(9). — P. 2408-2422.
8
М1жнародний невролопчний журнал, ISSH 2224-0713 (print), ISSH 2307-1419 (online) № 6 (100), 2018
fiNJj
Оригшальш досл1дження /Original Researches/
30. Engelhardt E. Shock, diaschisis and von Monakow/E. Engelhardt, M.M. Gomes // Arq. Neuropsiquiatr. — 2013. — Vol. 71. — P. 487-489.
31. Finger S. The von Monakow concept of diaschisis: origins and perspectives / S. Finger, P.J. Koehler, C. Jagella // Archiv Neurologie. — 2004. — Vol. 61. — P. 283-288.
32. Виничук С.М. Диашиз и его роль в развитии реф-лекторно-двигательных расстройств при мозговом инсульте // Укратський медичний часопис. — 2013. — №2. — С. 143-147.
33. Vinychuk S.M. Cerebrospinal and commissural diaschisis in acute stroke patients: case analysis / S.M. Vinychuk, O.Ye. Fartushna // International Neurological Journal. — 2018. — № 5(99).
34. Kernan W.N. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association / W.N. Kernan, B. Ovbiagele, H.R. Black [et al.] // Stroke. — 2014. — № 45. — P. 2160-2236.
35. Aho K. Cerebrovascular disease in the community: results of a WHO collaborative study / K. Aho, P. Harmsen, S. Ha-tano [et al.] // Bull. World Health Organ. — 1980. — № 58. — P. 113-130.
36. Adams H.P. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment / H.P. Adams, B. H. Bendixen, L.J. Kappelle [et al.]// Stroke. — 1993. — № 24. — P. 35-41.
37. Sacco R.L. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of this guideline / R.L. Sacco, R. Adams, G. Albers [et al.]// Stroke. — 2006. — № 37. — P. 577- 617.
38. Ringleb P. European Stroke Organisation 2008 guidelines for managing acute cerebral infarction or transient ischemic attack. Part 1 / P. Ringleb, P.D. Schellinger, W. Hacke [et al.]//Der Nervenarzt. — 2008. — № 79. — P. 936-957.
39. Fartushnaya E.E. Reducing the risk of recurrent ischemic stroke, after transient ischaemic attack along with neuroprotective and antiaggregant therapy / E.E. Fartushnaya, S.M. Vinichuk // XIV International Congress of Rehabilitation Medicine and Immunorehabilitation, 16—21.10. 2009: Abstract. — Tel-Aviv, Israel, 2009. — Р. 67.
40. Fartushna O.Ye. Brain injury in patients with acute TIA: clinical features in different TIA subtypes / O.Ye. Fartushna, S.M. Vinychuk //International Neurological Journal. — 2017. — № 3(89). — P. 13-18.
41. Вничук С.М. Аторвастатин та його роль у профыак-тищ та лжувант meMi4Hux порушень мозкового кровообiгу / С.М. Вшичук, O.G. Фартушна // Здоров 'я Украши. — 2015. — № 9. — С. 3.
42. Фартушна O.G. Використання оптимальноiдози препарату Торвакард — важливий напрямок зниження ризику розви-тку повторних транзиторних шeмiчних атак та/чи тсульту / O.G. Фартушна, С.М. Вничук // Семейная медицина. — 2015. — № 3. — С. 223-227.
43. Вiничук С.М. Диференцшоване лжування транзиторних шeмiчних атак — ефективний спосб профыактики повторних гострихцеребральнихподш/ С.М. Вничук, O.G. Фартушна // Мiжнародний нeврологiчний журнал. — 2014. — № 6. — С. 87-92. — Режим доступу: http://nbuv.gov.ua/UJRN/ Mnzh_2014_6_15
44. Вничук С.М. Освтт програми профыактики транзиторних шeмiчних атак та/чи iнcульту / С.М. Вничук, O.G. Фартушна//Укр. мед. часопис. — 2014. — № 5. — С. 49-51.
Received 10.04.2018 ■
Вничук С.М.1, Фартушна О.£.2
Юлександр'тська 1^мчна лкарня, м. Кив, Украна
2Укра'1нська вйськово-медична академя, м. Кив, Украна
Перехресно-мозочковий Ai^^ у па^енлв i3 гострим шсультом: OHöAi3 та презентащя кл^чних випадюв
Резюме. Актуальтсть. Спонтанне вщновлення невролопч-них функцш шсля шсульту пояснюеться феноменом д1ашизу й пов'язане з реоргашзащею в моторних та премоторних да-лянках кори головного мозку. Однак на сьогодш опублшова-но недостатньо проспективних когортних досладжень, у яких наведено та проанал1зовано клш1ко-нейров1зуал1зацшш характеристики перехресно-мозочкового д1ашизу в пащенпв iз гострим шем1чним шсультом. Мета досл&женняг визна-чення особливостей клшчних прояв1в перехресно-мозочко-вого д1ашизу в пащенйв iз гострим шем1чним шсультом та пщвищення ефективносп його д1агностики шляхом зютав-лення отриманих даних з результатами магнитно-резонансно! томографи. Матерiалu та методы. Ми провели проспек-тивне госттальне когортне дослщження пащенпв iз гострим шем1чним шсультом (п = 124), яю були госштатзоваш у вщ-дшення цереброваскулярних захворювань Олександр1всько! клшчно! лшарш м. Ки!ва протягом перших 24 годин з мо-
менту розвитку шсульту. Ум пащенти пройшли комплексне клшко-невролопчне, лабораторне, ультразвукове i нейровь зуатзацшне обстеження. Результаты. Серед 124 хворих i3 гострим iшемiчним шсультом перехресно-мозочковий дiашиз був дiагностований у 5 (4,03 %) пащенпв. Ми проанатзували патофiзiологiчнi, анатомiчнi та клiнiко-нейровiзуалiзацiйнi особливосп перехресно-мозочкового дiашиза в пащенпв iз гострим iшемiчним шсультом. Висновки. Семютика гострого шсульту визначаеться не тшьки первинним шфарктом мозоч-ку, а й дiашизом, що обумовлюе бшьш серйозний невролопч-ний дефщит. Перехресно-мозочковий дiашиз асоцшеться не тшьки з характерними симптомами ураження мозочку, але й парезом кшщвок, порушеннями чутливосй та вищих функцш мозку.
K™40Bi слова: перехресно-мозочковий дiашиз; шсульт мо-зочка; мозочок; дистантний дiашиз; форми дiашизу; клшчш прояви; дiагностика; клшчний випадок
Оригшальш дослщження /Опдта1 КезеагсЬез/ НМЛ]
Виничук С.М.1, Фартушная Е.Е.2
1Александровская клиническая больница, г. Киев, Украина 2Украинская военно-медицинская академия, г. Киев, Украина
Перекрестно-мозжечковый диашиз у пациентов с острым инсультом: анализ и презентация клинических случаев
Резюме. Актуальность. Спонтанное восстановление неврологических функций после инсульта объясняется феноменом диашиза и связано с реорганизацией в моторных и премоторных участках коры головного мозга. Однако в настоящее время опубликовано недостаточно проспективных когортных исследований, в которых представлены и проанализированы клинико-нейровизуализационные характеристики перекрестно-мозжечкового диашиза у пациентов с острым ишемическим инсультом. Цель исследования: определение особенностей клинических проявлений перекрестно-мозжечкового диашиза у пациентов с острым ишемическим инсультом и повышение эффективности его диагностики путем сопоставления полученных данных с результатами магнитно-резонансной томографии. Материалы и методы. Мы провели проспективное госпитальное когортное исследование пациентов с острым ишемическим инсультом (п = 124), госпитализированных в отделение цереброваскулярных заболеваний Александровской клинической больницы г. Киева в течение первых 24 часов по-
сле развития инсульта. Все пациенты прошли комплексное клинико-неврологическое, лабораторное, ультразвуковое и нейровизуализационное обследование. Результаты. Среди 124 больных с острым ишемическим инсультом перекрестно-мозжечковый диашиз был диагностирован у 5 (4,03 %) пациентов. Мы проанализировали патофизиологические, анатомические и клинико-нейровизуализационные особенности перекрестно-мозжечкового диашиза у пациентов с острым ишемическим инсультом. Выводы. Семиотика острого инсульта определяется не только первичным инфарктом мозжечка, но и диашизом, что обусловливает более серьезный неврологический дефицит. Перекрестно-мозжечковый диа-шиз ассоциируется не только с характерными симптомами поражения мозжечка, но и с парезом конечностей, нарушениями чувствительности и высших функций мозга. Ключевые слова: перекрестно-мозжечковый диашиз; инсульт мозжечка; мозжечок; дистантный диашиз; формы диа-шиза; клинические проявления; диагностика; клинический случай
10
М1жнародний невролопчний журнал, ЕвН 2224-0713 (ргИ), ВвН 2307-1419 (опИпе) № 6 (100), 2018
