Contenu connexe


cerebrovasular disease 2.pptx

  1. Cerebrovascular Disease Dr Mohamed Rizk Khodair Lecturer of neurology October 6 Universirty
  2. Definition: Stroke is a sudden onset focal and or generalized neurological deficit, lasting more than 24 hours. Strokes occur due to either ischemia (about 85%) or hemorrhage (15%). Transient ischemic attack (TIA) is defined as sudden onset focal neurological deficit lasting less than 24 hours.
  3. Types: A) Ischemic Stroke : Most ischemic strokes are due to thrombosis or embolism B) Hemorrhagic stroke: Intracerebral hemorrhage and Subarachnoid hemorrhage
  4. Etiology of ischemic stroke Thrombosis: The commonest cause is atherosclerosis Predisposing (Risk) Factors A stroke may happen to anybody at any age. However, if you have specific risk factors, your chances of having a stroke increase. Some stroke risk factors are modifiable, while others are not. Non-Modifiable Factors:  Older age. Incidence doubles each decade past 55 years.  Race. African American race has twofold increased risk than whites. This is partly because the African American population has a greater incidence of high blood pressure.  Gender. Strokes are more common in men. (1.25 times that of females).  History of prior stroke. There is a higher risk for having a second stroke after you have already had a stroke.  Heredity or genetics. People with a positive family history of stroke are more likely to have a stroke. Modifiable Factors:  Hypertension: 3-4 folds increase of stroke.  Dyslipidemia: high total cholesterol and low-density lipoprotein (LDL) are related to atherosclerosis and increase risk.  Diabetes mellitus (DM): 2-4, folds increase of stroke, pathogenetic factor in cerebral small vessel disease. DM produces rheological abnormalities and aggravates atherosclerosis. DM increases morbidity and mortality after  stroke.  Heart diseases  Smoking (2-3 times greater than non-smokers), heavy alcohol consumption.
  5. Embolism: Embolism (from the heart is also a common cause) include valvular disease, artificial heart valves, recent myocardial infarction, endocarditis and cardiac tumors. Also, paradoxical embolism as in a patient with an atrial septal defect or patent foramen oval. Other causes include: 1. Arterial (e.g., carotid or vertebral) dissection 2. Vasculitis 3. Hematological disorders: polycythemia, thrombocythemia, sickle cell disease, leukemia and antiphospholipid syndrome 4. Genetic disorders: as Cerebral autosomal dominant arteriopathy with subcortical infarcts and Leukoencephalopathy (CADASIL) and Mitochondrial encephalomyopathy, lactic acidosis, and Stroke-like episodes (MELAS). 5. Recreational drug use: cocaine, amphetamine 6. Hypoperfusion of the brain leading to so-called watershed or border zone infarcts as in shock, excessive blood loss, excessive hypotensive drugs, low cardiac output (as in myocardia infarction or arrhythmia),hemoconcentration( as in dehydration) . 7. Venous disease as due to cerebral venous sinus thrombosis.
  6. Clinical Picture: Symptoms and signs depend upon the occluded blood vessel.
  7. The carotid system (Anterior circulation). Blood Supply of the brain The vertebral system (Posterior circulation). .
  8. The carotid system (Anterior circulation): Each internal carotid artery enters the cranial cavity through the carotid foramen and canal to the cavernous sinus where it lies lateral to optic chiasma. The artery in the sinus gives off three small branches: - The ophthalmic artery. - The anterior choroidal artery. - The posterior communicating artery. The internal carotid artery then divides into its two terminal branches → the middle and anterior cerebral arteries.
  9. A. The middle cerebral artery gives 2 branches: Capsular branch, supplying dorsal half of internal capsule (Lenticulostriate branch of middle cerebral artery). Cortical branches: Frontal branch supplying the lower part of the motor area (face, U.L. and trunk), and the motor speech areas. Parietal branch supplying the lower part of the sensory area, the angular and supramarginal and the upper fibers of the optic radiation. lower fibers of the optic Temporal branches supplying the auditory areas and the lower fibers of the optic radiation.
  10. B. The anterior cerebral artery supplies: The anterior cerebral artery runs medially on the medial surface of the cerebral hemisphere, then around the corpus callosum as far as the parieto-occipital sulcus. This artery supplies the medial aspect of the anterior 3/5 of the cerebral hemisphere and the upper edge of the lateral surface. It gives the following branches: • Capsular branch (Heubner's artery) supplying the ventral half of the anterior limb of the internal capsule. • Cortical branches: a) Frontal branch supplying the pre-frontal area (area of mentality and inhibition of primitive reflexes). b) Paracentral branch supplying the motor and sensory areas of the L.L., and the paracentral lobule (cortical bladder center). c) Callosal branch supplying the corpus callosum.
  11. The vertebral system (Posterior circulation): Vertebral Arteries Course and branches: The left and right vertebral arteries originate from their respective subclavian arteries, on the posterosuperior aspect. The vertebral arteries then proceed to enter the transverse foramina of the spine at level C6 and continue superiorly. After passing through the transverse foramen of C1, the arteries traverse the foramen magnum. The vertebral arteries give off the following branches once within the cranial vault:  Posterior inferior cerebellar artery (PICA) – this is the largest branch of the vertebral artery and is one of three main arteries supplying the cerebellum  Anterior and posterior meningeal arteries – supply the dura mater  Anterior and posterior spinal arteries – supply the spinal cord along its entire length The vertebral arteries then converge to form one midline single artery, basilar artery, at the base of the pons, inside the cranium.
  12. Basilar Arteries Course and branches: The basilar artery runs superiorly within the central groove of the pons, giving off several branches including the pontine arteries, which supply the pons. The basilar artery anastomoses with the circle of Willis via the posterior cerebral arteries and posterior communicating arteries. Branches of posterior cerebral artery : Cortical branches supply occpital lobe and posterior communicating artery to circle of willis Capsular branche: thalamogeniculate artery ( ventral aspect of genu and posterior limb of internal capsule)
  13. Circle of Willis The terminal branches of the anterior and posterior circulation form an anastomosis to create a ring-like vascular structure known as the circle of Willis, located within the base of the cranium. The left and right internal carotid arteries continue as the middle cerebral arteries (MCA), after each giving off a branch to supply the anterior cerebral arteries (ACA). The anterior communicating artery links the two anterior cerebral arteries together. The internal carotid arteries also give off the posterior communicating arteries (PCoA), linking the middle cerebral arteries (MCA) with the posterior cerebral arteries (PCA).
  14. The Internal capsule It is a broad band of white fibers lying in the depth of the cerebral hemisphere. It is formed of: 1. The anterior limb which is placed between the caudate nucleus medially and the lentiform nucleus laterally. 2. The genu. 3. The posterior limb which is placed between the thalamus medially and the lentiform nucleus laterally. Fibers passing through the internal capsule: a) Pyramidal fibers descend in the genu, adjacent part of anterior limb and anterior 1/2 of posterior limb. The fibers supplying the arm are followed by those supplying the head, trunk, and lastly the lower limb. b) Sensory fibers from the thalamus ascend in the PL. c) Auditory and optic radiations pass in the posterior part of PL. d) Associative fibers pass in the anterior part of AL.
  15. Blood supply of the internal capsule • Upper part: MCA (lenticulostriate artery). • Lower part: Anterior limb; ACA (recurrent artery of Heubner). Posterior limb: PCA (thalamogeniculate artery).
  16. (1) Anterior circulation (carotid system) infarction A) Middle cerebral artery occlusion: Contralateral hemiparesis (face and arm > leg) Contralateral hemisensory loss (face and arm > leg) Homonymous hemianopia Contralateral gaze palsy Neglect Aphasia (if dominant hemisphere is affected)
  17. B) Anterior cerebral artery occlusion: • Contralateral hemiparesis (leg > arm) • Contralateral hemisensory loss (leg > arm) • Mental changes • Sphincteric disturbances in massive infarction
  18. (2) Posterior circulation (vertebrobasilar territory) infarct A) Posterior cerebral artery occlusion: • Contralateral homonymous hemianopia (which may be macular sparing, as this may be supplied by the middle cerebral artery). • Thalamic pain (spontaneous intractable and persistent pain). • Transient hemiparesis. • Visual agnosia.
  19. B) Posterior inferior cerebellar artery (Lateral medullary syndrome; Wallenberg syndrome) crossed hemianesthesia • Contralateral impairment of pain/temperature sensation in the limb with ipsilateral impairment of pain/temperature in the face • Ipsilateral Horner‘s syndrome • Ipsilateral cerebellar signs (ataxia), • Ipsilateral dysarthria, vertigo, vomiting, dysphagia
  20. C) Other brainstem stroke syndromes • Apart from the lateral medullary syndrome, other brainstem stroke syndromes are rare, e.g., the medial medullary syndrome which causes ipsilateral tongue weakness and contralateral hemiparesis in the arm and leg. (crossed hemiplegia) D) Lacunar strokes: These infarcts are usually less than 1 cm in diameter and are caused by the occlusion of small penetrating arteries supplying deep structures in the brain as basal ganglia, thalamus, pons. It include: • Pure motor strokes (face, arm, and leg) in the posterior limb of internal capsule. • Pure sensory stroke (thalamus). • Ataxic hemiparesis (weakness and ataxia affecting the same side) due to a pontine lesion. • Clumsy hand/dysarthria due to a lesion in the pons or internal capsule.
  21. Investigations A) Imaging studies: Should be performed within 24 hours to exclude haemorrhagic stroke and other causes, e.g., tumors. 1- CT: It is the first diagnostic tool to exclude hemorrhage , Ct is free in 1st 48 hours of onset of ischemic stroke. 2- MRI: Diffusion-weighted images (DWIs) show changes within minutes (most diagnostic tools). Useful to distinguish acute from chronic changes. 3- Imaging of extracranial vessels should be performed in all patients with TIA or stroke for diagnosis of partial or complete obstruction of the extracranial vessels as: Carotid and vertebral ultrasonography; MR or CT angiography (MRA/CTA). 4- Imaging of intracranial vessels should be performed in all patients for diagnosis of partial or complete obstruction of the intracranial vessels as: Trascranial color coded duplex; MR or CT angiography (MRA/CTA). 5- ECG and Echocardiography :for diagnosis of cardiac diseases as a cause for stroke.
  22. Normal vs ischemic vs hemorrhagic
  23. Treatment of acute ischemic stroke: A) Specific treatment 1- Thrombolysis Thrombolysis with IV rt-PA was used for the treatment of acute ischemic stroke within 3,5 hours of onset to achieve early recanalization of a thrombosed artery. 2- Antiplatelet Therapy: • Aspirin All patients should be initially treated with aspirin; 150-325 mg/day; following acute ischemic stroke unless they are being treated with thrombolytic therapy. Beyond the initial treatment period following ischemic stroke, most patients should be maintained on antiplatelet therapy to reduce the long-term risk of recurrent stroke. • Clopidogrel, Ticlopidine and combined aspirin and dipyridamole ( persantine) are acceptable alternative to aspirin.
  24. 3- Anticoagulant therapy : The goal of anticoagulation in acute ischemic stroke is to prevent early recurrent cerebral embolism as cardioembolic stroke due to atrial fibrillation or prevention of DVT due to recumbency. 4- Treatment of risk factors: as antihypertensive, control of diabetes, antiarrhythmic. 5- Dehydrating measures: especially in massive infarction. Mannitol 1-2 mg/kg/day used for 48 hours. 6- Nootropic drugs: as Piracetam (Nootropil). These drugs enhance the brain metabolism and brain oxygenation. B) General treatment: in comatose patients 1-Care of skin by changing the position of patient. 2- Care of respiration by maintaining patent airways, frequent suctions of secretions 3- Care of nutrition and fluids 4- Care of urinary bladder 5- physiotherapy
  25. ΙΙ- Hemorrhagic : It may be in the brain ‫״‬intracerebral hemorrhage or within the subarachnoid space ―subarachnoid hemorrhage.
  26. Spontaneous Intracerebral hemorrhage (ICH) ICH is the second most common form of stroke (about 15–30% of all strokes). Risk factors: Risk factors for ICH are like those with ischemic stroke: • Age; • Male gender • Hypertension • Smoking • Diabetes • Excess alcohol use.
  27. Causes of ICH: 1. Chronic hypertension. 2. Excess anticoagulant use, antiplatelet use, Thrombolytic therapy. 3. Rupture of intracranial aneurysms, arteriovenous malformations and cavernomas. 4. Hemorrhagic blood diseases as in purpura, leukemia 5. Moya Moya syndrome 6. Trauma to the head. Common sites for ICH: Basal ganglia., Thalamus, Pons, Cerebellum, Cerebrum (lobar hemorrhage) and Brainstem.
  28. Clinical picture: 1- Prodromal symptoms are related to hypertension as severe headache, vomiting, and alterations in level of consciousness as confusion may be more common. 2- The focal symptoms ad signs depend upon the site of hemorrhage. 3- Onset is usually very sudden. 4- Convulsions are common and may point to the onset of hemorrhagic stroke.
  29. Investigations: A) Imaging studies: 1. CT scan: Non contrast brain CT scan is the usual initial imaging procedure of choice. 2. CT angiography (CTA): CTA is very sensitive and specific in detecting vascular lesions (e.g., AVM or aneurysm). 3. MRI with appropriate scanning sequences.
  30. Treatment: A) Nonsurgical management: 1. Airway, breathing and circulation should be the initial focus. 2. Hypertension (HTN) should be controlled. 3. Intubate if GSC ≤ 8 as patient can‘t maintain his or her airways. 4. Monitoring of intracranial pressure and treatment of elevated ICP with dehydrating measures (as mannitol), and hyperventilation. 5. Fluid management. 6. Anticonvulsants drugs. 7. Maintain body temperature. B) Surgical treatment: 1. Evacuation of large, surfacing and manifesting ICH with imminent transtentorial herniation.. 2. Endoventricular drainage for intraventricular hemorrhage. 3. large cerebellar hemorrhage >3cm. 3. Definitive treatment of the underlying cause as AVM or aneurysm
  31. Thank you