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Interesting cases of young stroke

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  • 1. Interesting cases of young stroke Prof.S.RAMASAMY’s unit Dr.A.Prakash
  • 2. Case 1
    • 35 year old male Mr. Arul, businessman
    • c/o inability to use right UL & LL since previous day night
    • c/o inability to talk since previous day night.
    • h/o right facial lag with deviation of the mouth to the left side.
    • No h/s/o sensory disturbances.
    • No h/s/o autonomic disturbances.
    • No h/s/o cerebellar symptoms.
    • No h/s/o cortical sensory disturbances.
    • No h/s/o meningitis.
    • No h/o wasting/twitching.
  • 3.
    • A known alcoholic for past 2 years; weekly twice
    • Not a smoker.
    • Not a k/c of DM/HTN/CAD/BA/CVA/seizure.
    • No h/o chronic drug intake.
    • No relevant family history.
  • 4. General examination
    • Conscious, aphasic, not dyspnoeic, afebrile, response to oral commands,
    • No pallor/cyanosis/clubbing/jaundice/PE/GLA
    • JVP not elevated
    • Hydration adequate
    • no neurocutaneous markers
    • Vitals: BP-110/80mmHg, PR-88/min, felt in all peripheral vessels, left carotid pulse feeble, RR-16/min, Temp N
  • 5. Examination of CNS
    • HFs- aphasic
    • Cranial nerves- right sided UMN facial palsy
    • Motor system- f/o right sided hemiplegia
    • Sensory system normal
    • No Cerebellar signs
    • No signs of meningeal irritation
    • Spine & cranium normal
  • 6. Examination of other system
    • CVS- S1, S2 +, no murmur, left carotid bruit +
    • RS- NVBS +, no added sounds.
    • Abdomen –soft, no organomegaly.
  • 7. Provisional diagnosis
    • CVA/ RIGHT HEMIPLEGIA/ RIGHT UMN FACIAL PALSY/ YOUNG STROKE-?CAUSE.
  • 8. CASE 2
    • Krishnamoorthy 34 year old male, shopkeeper,
    • c/o inability to use left UL & LL since previous night
    • c/o facial lag on the left side with deviation of angle of mouth to right side
    • No h/o loss/difficulty in speech..
    • No h/s/o sensory disturbances.
    • No h/s/o autonomic disturbances.
    • No h/s/o cerebellar symptoms.
    • No h/s/o cortical sensory disturbances.
    • No h/s/o meningitis.
    • No h/o wasting/twitching.
  • 9.
    • Not an alcoholic/smoker.
    • Not a k/c of HTN/DM/CVA/IHD/BA/PT/seizure.
    • No h/o chronic drug intake.
    • No relevant family history.
  • 10. General examination
    • Conscious, drowsy, not dyspnoeic, afebrile, response to oral commands,
    • No pallor/cyanosis/clubbing/jaundice/PE/GLA
    • JVP not elevated.
    • Hydration adequate.,
    • no neurocutaneous markers.
    • Vitals: BP-120/80mmHg, PR-80/min, RR-16/min, Temp N
  • 11. Examination of CNS
    • HFs- NORMAL
    • Cranial nerves- LEFT sided UMN facial palsy
    • Motor system- f/o left sided hemiparesis.
    • Sensory system normal.
    • No Cerebellar signs.
    • No signs of meningeal irritation.
    • Spine & cranium normal.
  • 12. Examination of other systems
    • CVS- S1, S2 +, no murmur,
    • RS- NVBS +, no added sounds.
    • Abdomen –soft, no organomegaly.
  • 13. Provisional diagnosis
    • CVA/LEFT SIDED HEMIPARESIS/LEFT UMN FACIAL PALSY/ YOUNG STROKE-?CAUSE.
  • 14. INVESTIGATIONS INVESTIGATIONS CASE 1 CASE 2 HB 11.8 12.2 TC 7600 6800 DC P66, L33, E1 P71, L26, E2 PLATELET 1.4 LAKS 1.6 LAKS PCV 35% 37% RBC 3.9 MILLION 3.6 MILLION ESR 8/22 10/26 PERIPHERAL SMEAR NORMAL NORMAL
  • 15. INVESTIGATIONS CASE 1 CASE 2 BLOOD SUGAR 113 MG% 97 UREA 22 25 SR CREATININE 0.8 0.8 Na 134 137 K 3.8 3.8 Cl 106 102 HCO3 23 23 urinalysis SUG NIL, ALB NIL, 1-2 PC SUG NIL, ALB NIL, 2-4 PC PT/APTT 17 (C 12-15), 25 (C 26-39) 16 , 25
  • 16. LIPID PROFILE CASE 1 CASE 2 TOTAL CHOLESTEROL 173 mg% 185 TRIGLYCERIDES 129 136 HDL 39 42 LDL 99 88 VLDL 35 30
  • 17. investigations Case 1 Case 2 HIV NR NR RHEUM ATOLOGICAL PROFILE ANA NEG NEG RAF NEG NEG ACLA IgG IgM IgA APLA IgM IgG 2.88 GPL/ml (N <10) 3.04 MPL/ml(N <7) 3.2 APL/ml (N <15) NOT DETECTABLE ( N <15) 3 U/ml (N <15) 5.6 4.8 3.3 NOT DETECTABLE 3.4 u/ml LA NEG NEG
  • 18. INVESTIGATIONS CASE 1 CASE 2 BLEEDING TIME 3 MIN 4 MIN PROTEIN C 142.1 (n 70-140) 90 PROTEIN S 138.4 (N 60-150) 110 ANTI THROMBIN III 24 (n 22-39MG/DL) 26 HOMOCYSTEINE 126.8 (n 5-16) 150.4
  • 19. INVESTIGATIONS CASE 1 CASE 2 CAROTID DOPPLER PLAQUE IN LEFT CAROTID BULB NORMAL ECHO NORMAL NORMAL CT BRAIN NORMAL RIGHT SIDED INFARCT MRI BRAIN LEFT MCA INFARCT CXR NAD NAD
  • 20. OPINION CASE 1 CASE 2 CARDIOLOGY ECHO- N CARDIAC STATUCS NORMAL ECHO –N CARDIAC STATUS NORMAL NEUROLOGY CVA/RIGHT HEMIPLEGIA/ RIGHT UMN FACIAL PALSY/ YOUING STROKE DUE TO HYPERHOMOCYSTENEMIA CVA/LEFT HEMIPARESIS/ LEFT UMN FACIAL PALSY/ YOUNG STROKE DUE OT HYPERHOMOCYSTENEMIA OPHTHALMOLOGY LENS- N, FUNDUS- N, LENS- N, FUNDUS-N
  • 21. DIAGNOSIS
    • YOUNG STROKE DUE TO HYPERHOMOCYSTINEMIA.
  • 22. Young stroke
    • A stroke or CVA is defined by this abrupt onset of a neurologic deficit, that is attributable to a focal vascular cause as occurred if neurological signs & symptoms last for >24 hrs.
    • Young stroke means stroke occurring in persons < 40 years of age.
  • 23. Causes of young stroke
    • Premature atherosclerosis
    • Cardiovascular causes
    • RHD
    • Infective endocarditis
    • Embolism
    • Prosthestic valve
    • MVPS
    • Left atrial myxoma
    • Specific arteritis – TB, sypilis
    • Nonspecific arteritis- aortoarteritis, moya moya ds, takayasu, trauma, drugs
    • Collagen vascular diseases- SLE, APLAS, spontaneous dissection of carotid
    • Inborn errors of metabolism- homocystinuria, fabrys angiokeratosis
    • hematological causes- sickle cell ds, ITP,
  • 24. THROMBOPILIA
    • CONGENITAL-
    • Activated protein c resistant syndrome (factor V leiden mutation)
    • Protein C & S deficiency
    • Antithrombin III def
    • Hyperhomocystinemia (MTHFR mutation)
    • TPA def
    • Hyperfibrinogenemia
    • Factor XII def
    • Increased conc of factor VIII
    • Heparin cofactor II def
    • Prothrombin gene mutation
  • 25. Acquired
    • Increased age
    • Cancer
    • Pregnancy
    • OCP &HRT
    • APLAS
    • Nephrotic syndrome
    • Myeloproliferative disorder
    • PNH
    • Hyperhomocystinemia
    • Increased factor VIII
    • Heparin induced trombocytopenia
    • Increased viscosity
  • 26. Approach to iscemic stroke
    • Emergent (for Rx purpose)
    • History & physical examination
    • CT brain
    • ECG
    • CBC
    • PT & aPTT
    • Blood sugar
    • Serum electrolytes
    • RFT
    • urinalysis
  • 27.
    • Non-emergent ( to r/o causes)
    • LAB INVESTIGATIONS
    • Serum lipid profile
    • ESR
    • HIV serology
    • Rheumatological profile –ANA, RA, ACLA, LA
    • SPECIAL HEMATOLOGICAL STUDIES
    • HB electrophoresis
    • BT & Thrombin time
    • Protein C & S
    • Antithrombin III
    • Serum fibrinogen
  • 28.
    • Imaging study
    • Carotid doppler
    • MRI brain
    • ECHO
    • Cerebral angiograpy
  • 29. Approac to a Hemorragic stroke
    • Emergent (for Rx purpose)
    • History & physical examination
    • CT brain
    • ECG
    • CBC
    • PT & aPTT
    • Blood sugar
    • Serum electrolytes
    • RFT
    • urinalysis
  • 30.
    • Non emergent
    • LAB INVESTIGATIONS
    • Serum lipid profile
    • ESR
    • HIV serology
    • Hematology
    • Peripheral smear
    • HB electrophoresis
    • Imaging
    • CT brain
    • Echo
    • MRI brain
    • Cerebral angiograpy
  • 31.
    • Non emergent
    • LAB INVESTIGATIONS
    • Serum lipid profile
    • ESR
    • IV serology
    • Hematology
    • Peripheral smear
    • HB electrophoresis
    • Imaging
    • CT brain
    • Eco
    • MRI brain
    • Cerebral angiograpy
  • 32. Homocystinuria
    • Homocysteine is an intermediate product in the metabolism of amino acid metheonine
    • Homocystinemia can be caused by an error in metabolism of sulfur containing amino acid
    • Causes of elevated homocysteine level---
    • A genetic defect in MTHFR gene
    • nutritional def of folate ,vit. B12, vit. B6
  • 33.
    • Homocystinuria classified in to 4 types
    • Classic homocystinuria due to reduced activity of cystathionine beta synthase (the pyridoxol phosphate dependent enzyme that condenses homocystein with serine to form cystathionine
    • Clinical features
    • Dislocated optic lenses, MR, marfanoid habitus, osteoporosis, life threatening thrombotic vascular diseases
    • Classic homocystinuria can be diagnosed with analysis of plasma amino acids showing elevated metheonine, and presence of free homocystein. Total plasma homocystein is also extremely elevated usually >100 micromol
  • 34. Treatment
    • Special diet restricted in protein & metheonine & supplemented with cystein
    • Oral pyridoxine (25-500 mg/d)
    • Folate def should be prevented by adequate supplementation
    • Betaine is also effective in reducing homocysteine level in pyridoxine unresponsive patient
  • 35. Other form of homocysteinuria
    • Due to result of impaired remethylation of homocystein to metheonine---
    • Metheonine synthase def- MR, hypotonia, seizures, megaloblastic anemia
    • Two essential cofactor def (5-methyl THF & methyl cobalamine)
    • Changes of homocystein levels are also observed with increased age, smoking, post menopausal women, renal failure, hypothyroidism, leukemias, IBD, psoriasis, during therapy with drugs such as methotrexate, N2O, isoniazid and some anti epileptic agent
  • 36. pathophysiology
    • homocystein acts as an atherogenic & thrombophilic agent
    • An increased in plasma homocystein represents is an independent risk factor for coronary, cerebro vascular & peripheral arterial disease as well for DVT
    • homocystein is synergistic with hypertension & smoking and it is additive with other risk factor that predispose to arterial disease
    • In defective MTHFR gene causes premature Atherosclerosis as well as stroke in affected individuals
  • 37.
    • Cell culture studies suggest that homocystein may have prothrombotic on endothelium & vascular smooth muscle
    • Mild hyperomocystinemia is an independent risk factor for increased carotid artery wall thickeness & plaque formation
    • It also increases endothelial cell injury, platelet aggregation, and abnormalities of the clotting cascade by activations of factor V, X, XII
  • 38.
    • Studies supportive for elevated homocystein is an independent risk factor for young stroke.
    • Framingham study: the relative risk for stroke associated with non-fasting levels of 14.24 to 219.84 micromol/L compared with level of 4.13 to 9.25 micromol/L was 1.82 (95% confidence interval ).
    • Rotterdom study: relationship between elevated homocystein levels in the elderly as well as young, the risk of stroke and myocardial infarction are found a risk of increase of 6 -7% for every 1 micromol/L increse in total plasma homocystein..
    • In another case control study of 80 patients with stroke between the age of 18 to 44 years, a 4.8 fold of increase of iscemic stroke was found in those with post-metheonine load elevations in palsma homocystein levels.
  • 39.
    • Hyperhomocysteine level is an independent risk factor for young stroke .
  • 40.
    • THANK YOU