Presentasi anatomi batang otak dan cerebelum

anatomi batang otak

1. CEREBELLUM

2. Ho rizontal fis s ure v e rmis Pri mary fis s ure Hemisphere External surface of cerebellum

3. The cerebellum is connected to Brain stem by three peduncles Superior cerebellar peduncle Midbr ain M i ddle ce r ebel l ar pedu n cel Pon s Inferior cerebellar peduncle Medulla ablon g ata

4. L O B E S O F C E R EBE L LUM Divisions of lobes Anatom i cal Flocculonodular lobe Anterior lobe Posterior lobe P o s t eri o r l o b e Flocculonodular lobe I n f e rio r s u r f ace Anterior lobe Superior surface Anterior lobe P o s t e rio r lo b e

5. Paleocerebellum Neocerebellum Archicerebellum Division of lobes…..contd .

6. Archi-cerebellu m posterior lobe ( Vestibular part) It is formed of the flocculo- nodular lobe + associated fastigial nuclei , lying on inf. Surface in front of postero-lateral fissure. Embryologically , it is the oldest part of cerebellum. It receives afferent Fibres. From vestibular apparatus of internal ear Via vestibulo-cerebellar tracts. It is concerned with equlibrium Neocerebellum Archicerebellum P aleo c e r e b el l um

7. Archicerebellum …….contd . It has connections with vestibular & reticular nuclei of brain stem through the inferior cerebellar peduncle. Afferent vestibular Fibres . Pass from vestibular nuclei in pons & medulla to the cortex of ipsilateral flocculo-nodular lobe. Efferent cortical (purkinje cell) Fibres. Project to fastigial nucleus, which projects to vestibular nuclei & reticular formation. It affects the L.M.system bilaterally via descending vestibulo-spinal & reticulo- spinal tracts.

8. Paleo-cerebellum (spinal part) : it is f orme d o f midline vermis + surrounding paravermis + globose & emboliform nuclei. It receives afferent proprio- ceptive impulses from Ms.& tendons Via spino-cerebellar tracts (dorsal & ventral) mainly. it sends efferents to red nucleus of midbrain. it is concerned with muscle tone Paleocerebellum

9. It is concerned with muscle tone & posture. . Afferents spinal Fibres consist of dorsal & ventral spino- cerebellar tract from muscle, joint & cutaneous receptors to enter the cortex of ipsilateral vermis & para vermis Via inferior & superior cerebellar peduncles . Efferents cortical fibres pass to globose & emboliform nuclei, then Via sup. C. peduncle to contra-lateral red nucleus of midbrain to give rise descending rubro-spinal tract.

10. Neo-cerebellum (cerebral part) It is the remaining largest part of cerebellum. It includes the most 2-cerebellar hemispheres + dendate nuclei . It receives afferent impulses from the cerebral cortex+pons Via cerebro-ponto- cerebellar pathway. it sends efferents to Ventro lateral nucleus of thalamus. •it controls voluntary movements (muscle coordination). Neocerebellum

11. It is concerned with muscular coordination. It receives afferents from cerebral cortex involved in planning of movement- to pontine nuclei ,cross to opposite side Via middle Cerebellar peduncle to end in lateral parts of cerebellum ( cerebro-ponto-cerebellar tract). Neo-cerebellar efferents project to dendate nucleus ,which in turn projects to contra-lateral red nucleus & ventral lateral nucleus of thalamus ,then to motor cortex of frontal lobe, giving rise descending cortico-spinal & cortico- bulbar pathways. Efferents of dentate nucleus form a major part of superior C. peduncle.

12. PERJALANAN HERNIASI

13. Definisi Suatu kondisi bergesernya suatu struktur otak dari satu lokasi ke lokasi lain melalui struktur intrakranial Menyebabkan penekanan struktur otak lainnya sehingga menimbulkan gejala yang dapat diobservasi

14. Etiologi Stroke infark yang luas Stroke perdarahan Trauma kepala (EDH, SDH, SAH) Tumor otak Hidrosefalus Infeksi otak

15. Tipe Herniasi Otak Herniasi sentral / transtentorial Herniasi uncal Herniasi cingulate / subfalcine Herniasi upward cerebellar Herniasi tonsillar Herniasi transcalvarial ( eksternal )

16. Herniasi Sentral

17. Herniasi Sentral / Transtentorial Perjalanan penyakit lebih kronik daripada herniasi uncal Sering disebabkan tumor otak di lobus frontal, parietal, atau oksipital Diensefalon dan mid brain tertekan ke bawah melalui insisura tentorium Diensefalon tertekan dari kranial  robekan pada infundibulum (pituitary stalk)  gangguan endokrin

18. Fase Diensefalon Kesadaran Letargik , kadang agitasi (delirium) Pernafasan Cheyne -Stokes Pupil Miosis (1-3mm), Refleks cahaya positif Okulomotor Konjugasi normal atau posisi sedikit divergen  ; Konjugasi normal menunjukkan batang otak masih intak . Doll’s eyes positif . Upgaze terganggu karena penekanan kolikulus superior dan pretectum ( Parinaud’s syndrome ) Motorik Respons terhadap nyeri masih baik , Babinski bilateral , tonus otot sedikit meningkat . Pada fase akhir dari tahap ini akan menunjukkan pose dekortikasi .

19. Fase Diensefalon

20. Fase Mesensefalon -Pons Bagian Atas Kesadaran Somnolen - Sopor Pernafasan Central Neurogenic Hiperventilation ( teratur , cepat , dan dangkal ) Pupil Mid-Dilatasi (3-5mm), posisi di tengah ( fixed ) Okulomotor Doll’s eyes menurun , kadang diskonjugasi Motorik Pose dekortikasi ( kadang timbul spontan )

21. Fase Mesensefalon -Pons Bagian Atas

22. Fase Pons Bagian Bawah-Medulla Oblongata Kesadaran Sopor - Coma Pernafasan Cluster/ Apneustik Pupil Mid-Dilatasi (3-5mm), posisi di tengah ( fixed ) Okulomotor Doll’s eyes negatif Motorik Deserebrasi

23. Fase Pons Bagian Bawah - Medulla Oblongata

24. Fase Medulla Oblongata Kesadaran Coma Pernafasan Lambat , ireguler , gasping. Kadang hiperpnea bergantian dengan apnea ( apneustic ) atau ataksik Pupil Dilatasi maksimal (>5mm) Okulomotor Doll’s eyes negatif Motorik Flasid , no response

25. Herniasi Uncal

26. Herniasi Uncal Terjadi pada peningkatan tekanan intrakranial yang cepat Sering ditemukan pada lesi di daerah fossa media bagian lateral atau lobus temporal yang menyebabkan penekanan uncus dan hipokampus Gejala khas dari herniasi unkal adalah penurunan kesadaran yang semakin memberat , dilatasi pupil ipsilateral dan hemiplegi kontralateral

27. Fase Early Oculomotor Kesadaran Delirium - Somnolen Pernafasan Normal Pupil Anisokor minimal ( pupil yang dilatasi , ipsilateral dengan lesi , pada 85% populasi ) Okulomotor Doll’s eyes normal atau diskonjugasi Motorik Respons terhadap nyeri masih normal , Babinski kontralateral

28. Fase Early Oculomotor

29. Fase Late Oculomotor Kesadaran Sopor - Coma Pernafasan Central neurogenic hyperventilation, kadang Cheyne-Stokes Pupil Dilatasi maksimal Okulomotor External oculomotor ophthalmoplegia (EOO) Motorik Biasanya menunjukkan hemiparesis kontralateral . Tetapi pedunculus serebri kontralateral tertekan oleh tentorium dapat menyebabkan hemiparesis ipsilateral ( Kernohan’s phenomenon ). Pada fase lanjut akan menunjukkan pose deserebrasi ( jarang dekortikasi )

30. Fase Late Oculomotor

31. Herniasi Cingulate

32. Herniasi Cingulate / Subfalcine Herniasi girus cingulate melalui bagian bawah falx serebri Biasanya asimtomatik Pada herniasi cingulate/ subfalcine , derajat dari midline shift berhubungan dengan prognosis pasien . Bila midline shift < 5 mm prognosisinya baik , bila midline shift >15 mm prognosisinya jelek

33. Herniasi Upward Cerebellar

34. Herniasi Upward Cerebellar Sering disebabkan karena adanya massa di fossa posterior Vermis serebelaris tertekan ke kranial melewati tentorium hingga menekan mesensefalon dan kadang menekan arteri serebelaris superior Kadang dapat juga menekan aqueductus Sylvii hingga menyebabkan hidrosefalus

35. Herniasi Tonsilar

36. Herniasi Tonsilar Disebabkan karena penonjolan dari tonsil serebelum melewati foramen magnum Dapat menekan medula oblongata hingga menyebabkan henti nafas Bisa terjadi pada lesi supra- maupun infratentorial Sering disebabkan karena tindakan lumbal punksi pada pasien dengan tekanan intrakranial yang tinggi

37. Herniasi Eksternal

38. Herniasi transcalvarial /EKSTERNAL Herniasi Transcalvarial /External paling jarang terjadi dari semua tipe herniasi . Paling sering disebabkan karena post operasi dan lesi cranial pasca trauma

39. IMPENDING Herniasi

40. IMPENDING Herniasi Ditandai dengan Trias Cushing Peningkatan tekanan darah Bradikardi Pola napas ireguler Gejala pada tahap Diensefalon

41. There are three particular ways by which herniation can occur through the tentorial notch: Uncal herniation Central herniation Upward herniation

42. 3. KAPAN PENGGUNAAN DAPT? Patients with severe intracranial stenosis in the vascular territory of ischemic stroke or transient ischemic attack should not receive angioplasty and stenting as a first-line therapy for preventing recurrence. Aggressive medical management of risk factors and short-term dual antiplatelet therapy are preferred. Dual antiplatelet therapy is not recommended long term, and short term, dual antiplatelet therapy is recommended only in very specific patients, including those with early arriving minor stroke and high-risk transient ischemic attack or severe symptomatic intracranial stenosis. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association

43. 3. MEKANISME KERJA ANTITROMBOTIK

44. ASPIRIN Aspirin works by irreversibly inhibiting the enzyme cyclo -oxygenase (COX-1) which is required to make the precursors of thromboxane within platelets. This reduces thromboxane synthesis. Thromboxane is required to facilitate platelet aggregation and to stimulate further platelet activation.

45. DYPIRIDAMOLE Dipyridamole appears to act in vivo by synergistically modifying several biochemical pathways, including: a) inhibition of platelet cAMP -phosphodiesterase; b) potentiation of adenosine inhibition of platelet function by blocking reuptake by vascular and blood cells, and subsequent degradation of adenosine; and possibly, c) potentiation of PGI2 antiaggregatory activity and enhancement of PGI2 biosynthesis. These independent processes inhibit platelet function by increasing platelet cAMP through both a reduction in enzymatic cAMP -degradation, and stimulation of cAMP formation via activation of adenylcyclase by adenosine and possibly PGI2.

46. CILOSTAZOLE Cilostazol is classified as an antiplatelet agent because it inhibits the platelet aggregation induced by collagen, 5'-adenosine diphosphate (ADP), epinephrine, and arachidonic acid. Unlike other antiplatelet agents cilostazol not only inhibits platelet function but also improves endothelial cell function.

47. CLOPIDOGREL Clopidogrel , a thienopyridine derivative, binds specifically and irreversibly to the platelet P2RY12 purinergic receptor, inhibiting ADP-mediated platelet activation and aggregation [1,2]. After oral administration, clopidogrel is rapidly absorbed. The antiaggregating property of clopidogrel is caused by an inhibition of the binding of ADP to its platelet receptors, and more specifically to the low affinity receptors, the high affinity binding sites being unaffected by clopidogrel .

48. ABCIXIMAB The antibody fragment of abciximab  binds nonselectively and inhibits the activity of activated GP IIb / IIIa receptors, thereby preventing the formation of the cross-linkages necessary for the development of a platelet aggregate