localization of stroke, CVS, stroke, for post graduates

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New localization of stroke syndromes
1.Clinical localization of the site of the lesion.
2.Identifying the vascular territory and the vessel involved.
3.Correlating with the imaging findings.

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localization of stroke, CVS, stroke, for post graduates

  1. 1. Localization of stroke syndromes Dr.M.Dhanaraj
  2. 2. Localization of stroke syndromes Three steps 1.Clinical localization of the site of the lesion. 2.Identifying the vascular territory and the vessel involved. 3.Correlating with the imaging findings.
  3. 3. Clinical localization of stroke syndromes Prerequisites 1.Functional anatomy of brain. 2.Blood supply to the different parts of brain.
  4. 4. Blood supply of brain-Carotid Arteries
  5. 5. Vertebral artery Circle of willis Blood supply of brain – vertebral artery and circle of Willis
  6. 6. Blood supply of brain
  7. 7. ANTERIOR CIRCULATION STROKE SYNDROMES
  8. 8. Anterior circulation
  9. 9. Blood supply-Lateral view
  10. 10. Blood supply-Medial view
  11. 11. Blood supply-Coronal view
  12. 12. Blood supply-Axial view
  13. 13. Middle cerebral artery infarction - superior branch Clinical features 1.Contralateral hemiplegia – face and upper limb more involved than lower limb. 2. Contralateral hemisensory loss. 3.Conjugate gaze paresis(patient looks towards the side of lesion. 4.Broca’s dysphasia (if left sided)
  14. 14. Middle cerebral artery infarction - Inferior branch Clinical features 1.Contralateral hemianopia. 2.Wernicke’s dysphasia ( if left sided ) 3.Left spatial neglect ( if right sided )
  15. 15. Middle cerebral artery infarction - stem occlusion Clinical features 1.Contralateral hemiplegia 2. Contralateral hemisensory loss 3. Contralateral gaze palsy 4. Contralateral hemianopia 5.Global dysphasia (Left sided lesion) 6.Anosognosia and amorphosynthesis (Right sided lesion) 7.Altered sensorium (due to edema)
  16. 16. Middle cerebral artery infarction - Clinical features 1.Contralateral hemiparesis 2.Contralateral sensory loss 3.Transcortical motor / sensory aphasia ( left sided lesion) Lenticular striate artery occlusion
  17. 17. Anterior cerebral artery infarction Clinical features 1.Contralateral a.paralysis of leg and foot with paresis of arm b.cortical sensory loss over leg and foot c.presence of primitive reflexes 2.Urinary incontinence 3.Gait apraxia 4.Mutism, delay and lack of spontaneity of motor acts 5.Apraxia of left sided limbs(with left sided lesion and corpus callosum involvement)
  18. 18. Internal carotid artery infarction Clinical features Variable - based on the collaterals and mechanism of stroke (embolism, extension of thrombus , low flow) 1.Amaurosis fugax 2. Watershed infarctions 3.MCA/ACA- either alone or in combinations
  19. 19. Posterior circulation stroke syndromes
  20. 20. Posterior circulation Lateral view
  21. 21. Posterior circulation
  22. 22. Medulla
  23. 23. Lateral medullary syndrome A. IPSILATERAL 1.Xth cranial nerve palsy 2.Cerebellar signs 3.Horner’s syndrome 4.Impaired pain, temperature and touch on the upper half of face B. CONTRA LATERAL 1.Impaired pain and temperature over the body
  24. 24. Medial medullary syndrome A.IPSILATERAL 1.XIIth nerve palsy B.CONTRALATERAL 1.Hemiplegia – sparing the face 2.Hemianaesthesia sparing the face.
  25. 25. Pons-Lower
  26. 26. Medial pontine syndrome – occlusion of paramedian branch of basilar artery A.IPSILATERAL 1.Gaze paresis 2.Cerebellar signs B.CONTRALATERAL 1.Hemiparesis 2.Hemianaesthesia
  27. 27. Lateral pontine syndrome-occlusion of anterior inferior cerebellar artery A.IPSILATERAL 1.LMN VIIth nerve palsy 2.Gaze palsy 3.Deafness,tinnitus 4.Cerebellar signs B.CONTRALATERAL 1.Impairment of pain and temperature on the body
  28. 28. MID BRAIN
  29. 29. Weber syndrome-occlusion of perforating branch of posterior cerebral artery Clinical features 1.Ipsilateral a.3rd nerve palsy 2.Contralateral a.hemiplegia
  30. 30. Benedikt syndrome-occlusion of perforating branch of posterior cerebral Clinical features 1.Ipsilateral a.3rd nerve palsy 2.Contralateral a.cerebellar ataxia
  31. 31. Thalamus-occlusion of thalamo geniculate branches of posterior cerebral artery Contralateral 1.Sensory loss 2.Spontaneous pain 3.Choreo athetosis 4.Ataxic tremor 5.Mild hemiparesisTHALAMUS
  32. 32. Occipital lobe-optic pathway and visual reflexes
  33. 33. Occipital lobe-occlusion of left calcarine artery Clinical features 1.Right Hemianopia
  34. 34. Occipital lobe-occlusion of both calcarine arteries Clinical features 1.Bilateral hemianopia- cortical blindness (light reflex preserved)
  35. 35. Left occipital lobe with corpus callosum infarction Left Clinical features 1.Right hemianopia 2.Alexia without agraphia
  36. 36. Basilar artery occlusion Clinical features 1.Paralysis of all four limbs 2.Bulbar paralysis 3.Eye movements abnormalities 4.Nystagmus 5.Coma Note: The neurological deficit is variable depending upon the ischemia – modifying factors.
  37. 37. Differentiating features between anterior and posterior circulation stroke Clinical features Posterior circulation Anterior circulation A.History 1.Vertigo Present Absent 2.Unsteadiness Present Absent B.Physical findings 1.Crossed hemiplegia Present Absent 2.Bilateral deficits Present Absent 3.Cerebellar signs Present Absent 4.Ocular findings(LMN/INO/Gaze deviation to paralysed side) Present Absent 5.Dissociated sensory loss Present Absent 6.Sensory loss over V1 and V2 Present Absent 7.Horners syndrome Present Absent
  38. 38. Importance of clinical localisation of stroke 1. Careful clinical evaluation in combination with imaging helps to find out the etiology of stroke and plan the appropriate treatment. 2. Clinical observations in correlation with imaging helps to understand neurology / neurophysiology better. Note:Neurological examination must be tailored according to the clinical scenario .
  39. 39. Limitations of clinical localisation of stroke syndromes 1. A single syndrome may occur due to lesion at different sites Eg. Pure motor hemiplegia 2.A vascular occlusion at a specific site can produce varying clinical manifestations. 3.Clinical examination may not detect very small or multiple infarctions(as in SBE). Note:Imaging is very useful in the above situations.

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