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Stroke. Sudden in onset Focal neurologic deficit Involvement of the blood vessels.

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Presentation on theme: "Stroke. Sudden in onset Focal neurologic deficit Involvement of the blood vessels."— Presentation transcript:

1 Stroke

2 Sudden in onset Focal neurologic deficit Involvement of the blood vessels

3 Temporal profiles of neurologic deficits that point to the underlying pathologic cause. -Mayo Clinic

4 Types of Stroke

5 DIFFERENTIAL DIAGNOSIS Clinical Types of Stroke in the PHILIPPINES 61.39% Ischemic 38.6% Hemorrhagic

6 Hemorrhagic Stroke Primary Intracerebral hemorrhage – Inside the brain – defective artery in the brain bursts – Bleed in the substance of the brain --. Basal ganglia (60% recurrence) 10 % recurrence at the different lobes, 10% at the cerebellum, 10% recurrence a – Secondary to hypertension Subarchanoid Hemorrhage – – Outside the brain – a blood vessel on the brain's surface ruptures and bleeds – annuerysm, AVM

7 Hemorrhagic Stroke intracerebral > subarachnoid hemorrhage Occur during stress or exertion Focal deficits rapidly evolve Confusion, coma or immediate death

8 Hemorrhagic Stroke Classic: sudden onset headache, vomiting, elevated BP Focal neurologic deficits that progress over minutes May present with agitation and lethargy but progresses to stupor or coma

9 Ischemic Stroke Thrombus forms and blocks blood flow in an artery bringing blood to part of the brain

10 Ischemic Stroke Sudden onset of a non-convulsive, FND due to CVD Embolic strokes – Deficit reaches its peak almost at once – Reverses itself within a few hours or days Thrombotic strokes – Evolve more slowly over a period of several min/hrs and occasionally days – Improve gradually over weeks or months Cerebral Hemorrhage – There is severe deficit of rapid but not necessarily instantaneous onset

11 Ischemic Stroke: Thrombotic Local Origin of Clot Usually develops at night during sleep Symptoms perceived in the morning Suspect in history of atherosclerosis, hypercoaguable states and collagen vascular disorders

12 Thrombotic 1/3 of ischemic strokes, occlude large cerebral arteries (lCA, MCA, basilar), small penetrating arteries (lacunar strokes), cerebral veins, and venous sinuses. Symptoms evolve over minutes to hrs. Often preceded by TIA in same territory causing similar deficits.

13 Ischemic Stroke: Embolic Proximal origin of clot Occurs at any time Frequently during periods of vigorous activity History of AF, valvular vegetations, thromboembolism from MI, ulcerated plaques in carotid system Seizures in 20% of cases

14 Embolic 2/3 of ischemic strokes, from thrombus in heart, aortic arch, large cerebral artery or medium sized branches of brain a. In anterior circulation usually effect MCA, in posterior circulation usually effect branch point of basilar or PCA. Produce maximal neurological deficit at onset. When TIAs precede, symptoms vary because emboli lodges in different places.

15 Ischemic Stroke Classic: sudden onset of headache, vomiting,  BP Focal neurological deficits progress over minutes May present with agitation & lethargy but progresses to stupor & coma Lacunar—small vessel disease

16 Lacunar Infarction May result to pure motor or sensory stroke Perforating arteries – Obstruction – Microatheromas – Microembolisms Site of occlusion: putamen, caudate, internal capsule, thalamus, pons, and white matter of the corona radiata High risk: HPN with atherosclerosis, DM

17 Primary (Hypertensive) Intracerebral Hemorrhage “spontaneous” brain hemorrhage Most common sites are: – The putamen and adjacent internal capsule (50%) – Central white matter of the lobes – Thalamus – A cerebellar hemisphere – Pons Cardinal features: headache, acute hypertension, and vomiting with a focal neurological deficit

18 Lobar (Nonhypertensive) Hemorrhage Anticoagulation or thrombolytic therapy, AVM, trauma, and amyloidosis of cerebral vessels Progressive worsening headache, vomiting and drowsiness with accompanying focal deficits

19 Spontaneous SAH Due to Ruptured Saccular Aneurysm 4th most frequent CVD Small, berry shaped dilatation of a surface artery Congenital defect in the internal elastic lamina and media of the vessel Severe headache of acute onset, nausea, vomiting, and signs of meningeal irritation Associated with intense physical effort or Valsalva maneuver

20 Arteriovenous Malformation (AVM) Tangle of dilated vessels that form an abnormal communication between the arterial and venous systems persistence of an embryonic pattern of blood vessels Vessels are abnormally thin and do not have the structure of normal arteries or veins Main modes of presentation: Bleeding or seizures Before rupture: chronic recurrent headache of a nondescript type or classic migraine w/ or w/o neurologic accompaniment

21 Diagnosis

22 Diagnose Clinical Presentation Neuroimaging/neurosonology Establish mechanism/s

23 Clinical Presentation WILL BE DISCUSSED BY ANOTHER TRIO

24 Neuroimaging/Neurosonology NeuroImaging Cranial CT Scan – to differentiate infarct vs hemorrhage Timing of the test  important when to do the imaging Cerebral Infarction  1 st 6 hour normal Bleeds  abnormal at the start – Cranial MRI  transmission weighted imaging Infarct  early changes (DW1) Diffusion-perfusion mismatch

25

26 Neurosonology – Carotid Duplex Examination Carotid Artery, Vertebral Artery, IMT (thickening) – Stenosis Obstruction – Transcranial Doppler Examination Blood vessels inside the brain Intracranial stenosis or occlusion non-invasive, can be repeated, accurate

27 Mechanism of stroke DISCUSSED ABOVE – HEMORRGAHIC, ISCHEMIC ETC

28 NIH Stroke Scale The National Institute of Health (NIH) stroke scale (NIHSS) is a standardized method used by physicians and other health care professionals to measure the level of impairment caused by a stroke. Assessment of whether or not the degree of disability caused by a given stroke merits treatment with tPAtPA

29 NIH Stroke Scale The NIH stroke scale measures several aspects of brain function, including consciousness, vision, sensation, movement, speech, and language. A certain number of points are given for each impairment uncovered during a focused neurological examination.

30 NIH Stroke Scale A maximal score of 42 represents the most severe and devastating stroke. Current guidelines as of 2008 allow strokes with scores greater than 4 points to be treated with tPA. 0= no stroke 1-4= minor stroke 5-15= moderate stroke 15-20= moderate/severe stroke 21-42= severe stroke

31 NIH Stroke Scale Level of Consciousness (LOC) 0-Alert 1-Drowsy 2-Stuporous 3-Coma Best Gaze 0-Normal 1-Partial gaze palsy 2-Forced deviation Best Motor Arm 0-No drift 1-Drift 2-Can't resist gravity 3-No effort against gravity LOC Answers Two Questions (Pt. asked two questions) 0-Answers correctly 1-Answers one correctly 2-Answers none LOC Commands (Patient given two commands) 0-Obeys both correctly 1-One correctly 2-Incorrect Pupillary response 0-Both react 1-One reactive 2-Neither reactive Best Visual 0-No loss 1-Partial hemianopia 2-Complete hemianopia Facial Palsy 0-Normal 1-Minor 2-Partial 3-Complete Best Motor Leg 0-No drift 1-Drift 2-Can't resist gravity 3-No effort against gravity Plantar Reflex 0-Normal 1-Equivocal 2-Extensor 3-Bilaterally extensor Limb Ataxia 0-None 1-Lower or upper 2Both Sensory 0-Normal 1-Partial loss 2-Dense loss Neglect 0-None 1-Partial 2-Complete Dysarthria 0-Normal articulation 1-Mild/moderate 2-Near unintelligible Best Language 0-No aphasia 1-Mild/moderate 2-Severe 3-Mute Change From Previous Exam same/better/wors e Change From Baseline same/better/wors e


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