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Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
Childhood stroke   ped neurology view
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Childhood stroke ped neurology view

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  • BUT not go on with children because1- commonly have a brain infarction shown by brain imaging despite thetransient nature of their symptoms. 2- Children with cerebral venous sinus thrombosis (CVST) commonly present withheadache or seizures. 3- “Stroke-like episodes” without an obvious vascular cause may occur in migraine or metabolic disease but may require specific treatment. 4- Prior illness (eg, infection) or events (eg, head trauma) need not preclude a diagnosis of stroke
  • Adult risk factors: BP, DM, Obesity, atherosclerosis. Sedentary life20% hgic – 80% ischemic
  • This incidence rate of childhood stroke makes childhood stroke more common than pediatric brain tumors . Most under age of 2 ysHowever, recent research has led physicians to believe that pediatric stroke is about twice this common, affecting about 5 or 6 per 100,000 children 1/3 in newbornAlthough cerebrovascular disorders occur less often in children than in adults, recognition of stroke in children has probably increased because of the wide spread application of noninvasive diagnostic studies such as magnetic resonance imaging (MRI),magnetic resonance angiography (MRA), computed tomography (CT) and, in the neonate,cranial ultrasound studies.1-
  • Spontaneous Intraparenchymal and SAH non traumatic
  • Intrapaenchymal he might occur spontaneously
  • Pmt and neoenates with higher risk
  • Numbness or pins and needles of the face, arm or leg on one side of the body Slurring speech or difficulty finding words Brief loss of vision in one or both eyes. Children often experience different symptoms of stroke to adults, The signs and symptoms of a stroke vary depending on several factors, including the age of the child and the location and severity of the CVA. A child who is having a stroke generally experiences the same symptoms that an adult would The signs and symptoms of a stroke vary depending on several factors, including the age of the child and the location and severity of the CVA. A child who is having a stroke generally experiences the same symptoms that an adult would such as seizures, headache and fever. However, many of the symptoms of stroke in children are similar to those experienced by adults. Depending on the areas of the brain affected by stroke
  • Therefore a cascade occurs in which vwf promotes sickle red cell/endothelial cell adhesion( nidus for thrombus formation)
  • Breavment
  • Thalamic infarction
  • CT vesus MRI
  • urgent exchange transfusion should be undertaken to reduce HbS to <30% and raise hemoglobin to 10–12.5 g/dlII- if the patient has had a neurological event in the context of severe anemia (eg., splenic sequestration or aplastic crisis), or if exchange transfusion is going to be delayed for more than four hours, urgent top-up blood transfusion should be undertaken
  • Transcript

    • 1. Stroke in Children: Clinical Guidelines Prof Dr Hussein Abdeldayem Prof of Ped Neurology, Alex Univ
    • 2. CASE STUDY • 4 YS DS with TF • Sudden onset of hemiplegia
    • 3. WHO DEFINITION OF STROCK 2004 • “A clinical syndrome in which there is rapidly developing signs of focal or global disturbance of cerebral functions, lasting more than 24 hours or leading to death, with no apparent causes other than of vascular origin”
    • 4. Definition • Transient ischaemic attacks (TIAs): ‘where the neurological deficit resolves within 1 hr (previously 24 hours).
    • 5. Differs from Adult Stroke • In adult: chronic risk factors • In children: 1- congenital and developmental risk factors 2- rare 3-subtle presentation* 4- wide DD 5- no established tt *Among neonates, signs of hemiparesis are generally not seen before the first six months to one year of life
    • 6. incidence -2.5 – 3.0 children out of 100,000 affected every year. -Newborn babies can develop a stroke 28/100,000 - More in boys - Nearly half are hgic stroke One of the top ten causesof childhood deaths world wide
    • 7. types • A hemorrhagic stroke: a ruptured blood vessel bleeding into the brain. with: headache, disturb consc, vomiting • An ischaemic stroke: +++ 51% isch, 49% hgic 80% isch and 20% hgic (adult)
    • 8. Hgic Stroke
    • 9. Types (cont. ) • An ischaemic stroke : an embolism or thrombus blocks a blood vessel in the brain ++ EMBOLI: sec thrombus: minutes warning: TIA Arterial ischaemic stroke: ‘a clinical stroke syndrome due to cerebral infarction in an arterial distribution’.
    • 10. Ischemic Stroke
    • 11. types of stroke ischemic hemorrhagic thrombosis embolus Stenosis Spasm intraparenchymalsubarachnoid arterial venous I Ventricular
    • 12. Fate • About 10% of childhood strokes are fatal.
    • 13. Fate • Recurrence ( 20-30%) • Motor impairment • Seizures (10-20%) • Language, Communication • Cognition • Headache (30%) • Social interaction • Learning
    • 14. Motor impairment • Hemiparesis/hemiplegia • Spasticity (?CP) • dystonia • a mixed pattern
    • 15. Language and communication defects • language input :(receptive aphasias) • language processing (word-finding problems, grammatical problems and other aphasias), • speech production ( dysarthria ) • written language (dyslexia). • Mutism: problems of social interaction and the willingness to communicate
    • 16. Blood supply of brain
    • 17. pathophysiology • Blood supply of the brain
    • 18. • In children ischemic stroke has been most commonly reported in the distribution of the middle cerebral artery.
    • 19. Types of stroke (2) According to time of onset : 1- prenatal 2- perinatal 2- pediatric
    • 20. Prenatal and Perinatal stroke • 17 times more common than pediatric stroke beyond the newborn period. • Arterial ischemia occurring during the 3 days surround birth is reported to be responsible for 50% to 70% of congenital hemiplegic cerebral palsy. • Germinal matrix hge : prone with increase BP
    • 21. Pathophysiology • Features of perinatal period that influence coagulation state – Presence of fetal hemoglobins – Fetal proteins – High hematocrit and blood viscosity – Concentrations of procoagulant and anticoagulant proteins change with gestational and postnatal age
    • 22. Risk Factors for Perinatal Arterial Stroke • Infants : Antiprothrombin factors • in the mothers, antiphospholipid antibodies : anticardiolipin (aCL) antibodies and lupus anticoagulant (LA).,
    • 23. Prenatal Stroke • Focal cerebral infarction (stroke) secondary to intrauterine or perinatal thromboembolism related to thrombophilic disorders, especially anticardiolipin antibodies, is an important cause of hemiplegic CP Nelson Textbook of Pediatrics 18th ed
    • 24. Prenatal Stroke • Family histories suggestive of thrombosis and inherited clotting disorders may be present and evaluation of the mother may provide information valuable for future pregnancies and other family members. Nelson Textbook of Pediatrics 18th ed
    • 25. Perinatal stroke and the risk of developing childhood epilepsy. • Childhood epilepsy is frequent after perinatal stroke. Evidence of infarction on prenatal ultrasonography and a family history of epilepsy predict earlier onset of active seizures J Pediatr. 2007 Oct
    • 26. Stroke Awareness • Survival from risky disease : PMT, LK, Cyanotic CHD • Improving of radiography
    • 27. CP Neonates - <6 months • Seizures • Irritability, drowsiness, bulge AF, jitterness, apnea • Focal motor defect ( hemiparesis): >6 mo age
    • 28. CP > 6 months • As adult: focal motor, ataxia, aphasia sensation troubles • ICHge: severe headache • SAH: meningism • Developmental delay (17%- SCD)
    • 29. Potential signs • Motor Disorder • Sensory • Reflexes - focal weakness - initial hypotonia then spasticity - Abnormal plantar reflex ( Babinski’s)
    • 30. Aetiology Cong/Acq/ Idiopathic CONGENITAL: Cardiac, SCD, Coag abn ACQUIRED: • 1- TRAUMA/ drug induced • 2-VASCULAR • 3-INFLAMMATORY/autoimmune • 4-NEOPLASM • 5-systemic: METABOLIC, DEHYDRATION & DEGENERATIVE
    • 31. Coagulopathies and Hematologic Disorders RBC: SCD, polycythemia Platelets: ITP-Thrombocytosis, Protein C deficiency Protein S deficiency Factor V (Laiden) mutation Anticardiolipin antibodies Lupus anticoagulant antithrombin III deficiency Cong coagulation defects 8-9-VWF DIC Liver dysfunction with coagulation defects, Vit K defeciency Malgnancy: Leukemia Metabolic/syndrome Homocystinuria Mitochondrial disorders Sulfite oxidase deficiency Fabry’s syndrome DS Ehler’s – Danlos -Moyamoya syndrome
    • 32. Hematologic causes • Sickle cell disease: Overt or silent strokes 1-Occlusion of small vessels by deformed sickled cells 2-Membranes of SRC are abnormal ,so have a pro coagulant activity 3-VWF enhances adherence of sickle red cells to endothelium in cases of high rates of flow (linear sheer stress)
    • 33. Consequences of Arterial Occlusive Stroke in Sickle Cell Disease Age: 5 y (1-18y) 1-disturbed learning and intellectual problems 2 -Neovascularization occurs in the areas that are left underperfused by the stroke. The network of small, delicate vessels that appear as cloud-like puffs on an arteriogram are called "moyamoya
    • 34. Moyamoya disease Basal arterial occlusion with telangectasia Chronic , progressive, non inflammatory vasculopathy Bilateral slowly progressive occlusion of ICA As occlusion is slowly progressive multiple anastomosis between external & internal carotid New vascular net work at the base of the brain composed of collaterals(basillar meningeal& choroidal arteries)
    • 35. • It is not a disease but secondary to other disorders Sickle cell anaemia VSD Down syndrome TOF NFI
    • 36. MR angiography :telangectasis produces hazy appearance like a puff of smoke ( japanese word :moyamoya)
    • 37. Moyamoya disease in a 9-year-old boy. ©1999 by Radiological Society of North America
    • 38. Disorders of coagulation: 1- anticoagulant deficiency Protein c Protein s AT III 2- Factor v leiden 3- prothrombin mutation
    • 39. Protein C, Protein S, AntithrombinIII deficiency • Protein C and protein S are inhibitors of factor V(Leiden) and antithrombin III opposes the normal procoagulant activity of factors II, IX, X, XI, and XII by promoting the irreversible formation of inactive complexes of these factors. • inherited or acquired
    • 40. Congenital Heart Disease Acquired Heart Disease VSD, ASD, PDA Aortic stenosis Mitral stenosis Coarctation Cardiac rhabdomyoma Complex congenital heart defects as FT Rheumatic heart disease Prosthetic heart valve Libman-Sacks endocarditis Bacterial endocarditis Cardiomyopathy Myocarditis Atrial myxoma Arrhythmia
    • 41. Cardiac causes Cyanotic heart disease (<2 years) 1. Venus sinus thrombosis: polycythemia, dehydration ,viral illness and iron deficiency anaemia 2. Embolic arterial occlusion in children due to vegetations or RT to LT shunt Cardiomyopathy , prothetic valve ,endocarditis, cardiac cath and surgical repair
    • 42. Vasculitis Meningitis/encephalitis Systemic infection, SLE Polyarteritis nodosa Granulomatous angiitis Takayasu's arteritis Rheumatoid arthritis Dermatomyositis IBD, HUS Drug abuse (cocaine, amphetamines), Drug induced Systemic Vascular Disease Systemic hypertension Volume depletion or systemic hypotension Hypernatremia Superior vena cava syndrome Diabetes
    • 43. VasoSpastic Disorders Structural Anomalies of the Cerebrovascular System Migraine Ergot poisoning Vasospasm with subarachnoid hemorrhage Arterial fibromuscular dysplasia Agenesis or hypoplasia of the internal carotid or vertebral arteries Arteriovenous malformation AVM Hereditary hemorrhagic telangiectasia Sturge-Weber syndrome Intracranial aneurysm
    • 44. Trauma Child abuse Fat or air embolism Foreign body embolism Carotid ligation (e.g., ECMO) Vertebral occlusion following abrupt cervical rotation Blunt cervical arterial Trauma: Neck trauma, intraoral trauma Posttraumatic arterial dissection Arteriography Posttraumatic carotid cavernous fistula Coagulation defect with minor trauma Amniotic fluid/placental embolism Penetrating intracranial trauma
    • 45. Drugs: Amphetamines Cocaine Sympathomimetics L asparginase
    • 46. Inflammatory • Meningitis • Encephalitis (due to vasculitis, venous thrombosis or parenchymal necrosis) ( bacterial & varicella) • Local head and neck infection Sebrie et al 1999
    • 47. Metabolic MELAS • 1. Mitochondrial emcephalopathy, lactic acidosis, and stroke • 2. Point mutation of mitochondrial DNA • 3. Normal developmental milestones in first few years of life. • 4. Episodic vomiting, lactic acidosis, and proximal muscle weakness • 5. Stroke syndromes - migranous HA, seizures, or hemiplegia • 6. Encephalopathy/dementia are progressive. • 7. Hearing loss, visual defects, and short stature are typical Systemic Disorder Metabolic
    • 48. • Mitochondrial disorder (MELAS): Mitochondrial accumulations and abnormalities in sm of intramuscular vessels , brain arterioles and in blood vessels of choroid plexus (mitochondrial angiopathy)
    • 49. • Fabry’s disease X-linked, defniciency of alpha-galactosidase angiokeratomas, corneal and lenticular opacities, and painful acroparesthesias ,hypohydrosis, Vascular complications:(renal failure, cerebral thrombosis.?
    • 50. Homocystinuria: Thromboembolic episodes involving both large and small vessels specially brain Damage to the vascular endothelium and increased platelet adhessivness 2ry to elevated homocystine level
    • 51. Metabolic Hyperhomocysteinemia • HC is a highly reactive amino acid toxic to vascular endothelium – Pro-atherogenic and pro-thrombotic effect on blood vessels • HC can potentiate the auto-oxidation of LDL • HC is emerging as a potentially modifiable risk factor for atherosclerosis
    • 52. prothrombin gene G20210A mutation. • Prothrombin G20210A mutation is an important prothrombotic condition for venous thrombosis. Recently, some studies have also considered it to be a risk factor for arterial ischemic stroke in children. J Child Neurol.2007 Mar;22(3):329-31
    • 53. Clinical presentation • F:M = 3:2 • Girl + headache+ bilateral UMNL signs 1. Sudden hemiplegia of face and limbs associated with hemianopia ,hemianaesthesia and aphasia recovery may occur followed by new episodes of focal neurological findings on same or other side 2-recurrent TIA with episodic hemiparesis for min or hrs with no loss of consciousness
    • 54. Scope of the guidelines • the diagnosis, investigation and management of acute arterial ischaemic stroke in children beyond the neonatal period
    • 55. Stroke Guidelines 1st • Families/carers should be given actual information about their child’s condition as soon as possible after diagnosis . This should be simple and consistent, avoiding technical terms and jargon • Children should be given information about their condition at an appropriate level .
    • 56. Stroke Guidelines 2nd Presentation and diagnosis • All children with acute stroke should be referred to, or have their management discussed with, a consultant paediatric neurologist
    • 57. Stroke Guidelines 3rd Brain Imaging • Cross-sectional brain imaging is mandatory in children presenting with clinical stroke • Brain magnetic resonance imaging (MRI) is recommended for the investigation of children presenting with clinical stroke
    • 58. Stroke Guidelines 4th • If brain MRI will not be available within 48 hours, computed tomography (CT) is an acceptable initial alternative
    • 59. Stroke Guidelines 5th Further Non-invasive cerebrovascular imaging : - M R Angiography - CT angiography - ultrasound with Doppler techniques - combination MRV (magnetic resonance venography)
    • 60. Stroke Guidelines 6th • All children with clinical stroke should have regular assessment of conscious level and vital signs • Brain imaging should be undertaken urgently in children with clinical stroke who have a depressed level of consciousness at presentation or whose clinical status is deteriorating
    • 61. History Subsequent Lab
    • 62. • CBC (WBC, RBC*, Platelets) • Electrolytes • PT/PTT • Liver functions • Lipid profiles • ESR • Echocardiograph: Transthoracic cardiac echocardiography • * CSF examination Initial Lab *Hemoglobin electrophoresis
    • 63. Stroke Guidelines 8th Echocardigram: - for congenital and acquired cardiac disease - Transthoracic cardiac echocardiography should be undertaken within 48 hours after presentation in all children with arterial ischaemic stroke
    • 64. A lumbar puncture • LP will screen for metabolic derangements and CNS inflammatory and infectious disorders.
    • 65. • Prothormbic tendency factors • Other relevant tests Subsequent Lab
    • 66. prothrombotic Factors • protein C deficiency • protein S deficiency • Antithrombin III • Factor V Leiden • antiphospholipid antibodies:anticardiolipin (aCL) antibodies and lupus anticoagulant (LA)., • activated protein C resistance • lipoprotein-associated phospholipase A2 (Lp-PLA2)* • high-sensitivity C-reactive protein (hs-CRP) * • increased plasma homocysteine ( & urine) • prothrombin G20210A and MTHFR TT677 mutations and A 1298C *FDA approved for stroke recurrence
    • 67. • homocysteine levels, levels of protein C,S,and antithromin III, Leiden factor V, RPR, C reactive protein/ESR,lipid panel, troponin, creatinine kinase, electrolytes, glucose, HbA1C, diffusion weighted and perfusion weighted MR, transesophageal echocariogram, EKG with rhythm strip, CBC with platelets, chest X ray?
    • 68. Other relevant tests • ANA • HIV • Lactic acid, pyruvic acid ( blood , CSF)
    • 69. Acute care • General measures • Specific measures • Prevention/prophylaxis Recovery after stroke depends on the severity of the stroke and the speed of treatment
    • 70. Acute care general measures Stroke Guidelines 9th • Hospital • ABCD care • Temperature should be maintained within normal limits • Oxygen saturation should be maintained within normal limits
    • 71. Acute care general measures Stroke Guidelines 10th • i - swallowing safety • ii-feeding and nutrition • iii-communication • Iv- pain • v-moving and handling requirements • vi- positioning requirements • vii- risk of pressure ulcers
    • 72. Acute care general measures Pain: • Children affected by stroke should be assessed for the presence of pain using non verbal technique • All pain should be treated actively, using appropriate measures including positioning, handling, and medication Reduce intracranial tension : mannitol IV
    • 73. Specific treatment
    • 74. Acute care specific medical treatments (cont.) If diagnosed within 3 hrs: • Thrombolytics: streptokinase, tissue plasminogen activator (tPA)
    • 75. Acute care specific medical treatments • Aspirin (5 mg/kg/day)* should be given once there is radiological confirmation of arterial ischaemic stroke, except in patients with evidence of intracranial haemorrhage on imaging and those with sickle cell disease - LMWH (1 week) - Warfarin ( for 6 months) *max 300 mg
    • 76. SCD stroke 1- exchange transfusion 2- prevention: repeat transfusion 4-6 weeks to keep hemoglobin S <20- 30%
    • 77. • Neonate + noncardioembolic AIS do not use anticoagulant or aspirin • Neonate+cardioembolic AIS use anticoagulant therapy (UFH or LMWH ) for 3 months • Child+AIS treat with anticoagulant for 5-7 days or until cardio-embolic or vascular dissection has been excluded. Antithrombotic therapy in children: the Seventh ACCP Conference on Antithrombotic Chest 2004 Sep;126 (3 Suppl):645S-687S.
    • 78. Acute care specific medical treatments (cont.) • Treatment of underlying cause
    • 79. A Cardiac Source of Embolism and AIS • The decision to use anticoagulation should be discussed with a consultant paediatric cardiologist and paediatric neurologist
    • 80. 3- prevention Stroke recurrence • Arterial ischaemic stroke recurs in between 6% and 20% of all children. • The risk of recurrence* is increased in children with multiple risk factors and in those with protein C deficiency, increased levels of lipoprotein (a) and vascular disease *(Lanthier et al2000)
    • 81. Stroke recurrence Stroke Guidelines 11th 1- Aspirin • Patients with cerebral arteriopathy other than arterial dissection or moyamoya syndrome or those with sickle cell disease should be treated with aspirin (1–3 mg/kg/day)
    • 82. Stroke recurrence prevention 2- Anticoagulation • should be considered: 1- until there is evidence of vessel healing, or for a maximum of six months, in patients with arterial dissection 2- if there is recurrence of arterial ischaemic stroke despite treatment with aspirin 3- in children with cardiac sources of embolism, following discussion with the cardiologist managing the patient 4- until there is evidence of recanalisation or for a maximum of six months after cerebral venous sinus thrombosis
    • 83. Stroke recurrence In children with sickle cell disease: • should be considered: 1- regular blood transfusion (every three to six weeks) should be undertaken to maintain the HbS% <30% and the Hb between 10–12.5 g/dl (C) 2- transfusion may be stopped after two years in patients who experienced stroke in the context of a precipitating illness (eg aplastic crisis) and whose repeat vascular imaging is normal at this time (C) 3- after three years a less intensive regime maintaining HbS <50% may be sufficient for stroke prevention(C)
    • 84. Stroke recurrence Stroke Guidelines 12th moyamoya syndrome • Children should be referred for evaluation to a centre with expertise in evaluating patients for surgical re-vascularisation
    • 85. Stroke recurrence • Advice should be offered regarding preventable risk factors for arterial disease in adult life, particularly smoking, exercise and diet • Blood pressure should be measured annually to screen for hypertension
    • 86. DD of stroke like events 1- Alternating hemiplegia: 2-18 month, intermittent episodes of hemiplegia from one side to the other associated with choreoathetosis and dystonia for min or weeks and then resolve ,occasionally associated with migrain Progressive MR and developmental disabilities , poor prognosis Radiology & lab are free
    • 87. • Todds paralysis • Stroke like episodes: migraine • Focal post viral encephalitis, ADAM, HIV • hyperlipidemia • Familial hemiplegic migraine
    • 88. Rehabilitation Use of assessment measures • The assessment tools selected should be appropriate for the child’s age and developmental and functional level
    • 89. Goal of Rehabilitation • Help children with physical disabilities improve FUNCTION and PARTICIPATE more fully in family, social, educational and recreational activities.
    • 90. Rehabilitation Tools • Motor and cognitive exercises • Medications • Injections • Braces • Adaptive equipment • Referral to therapies • Referral to surgeries • Recreational involvement
    • 91. • Child +AIS+cardioembolic treat with anticoagulant 5-7 days followed by oral anticoagulant for 3-6 mon • ALL children +AIS TREAT WITH aspirin 2-5 mglkglday after the anticoagulant therapy
    • 92. - Prevention of recurrence: Low dose aspirin or oral anticoagulant for long term prophylaxis in certain conditions?
    • 93. 1. Cardiac emboli 2. Disecting aneurysm 3. Severe prothrombotic conditions 4. High grade cerebral artery stenosis
    • 94. 3- treatment of underlying cause a) For SCD: Exchange transfusion Frequent transfusion Bone marrow transplant Hydroxy urea • Moyamoya: consider revascularization • Prothrombotic :consider anticoagulant • For others :low dose asprin
    • 95. • 4- rehabilitation therapy: Speech , physiotherapy, occupational &psychotherapy

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