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Dr Kazi Ashraful Islam
Assistant Professor
Institute of Paediatric Neurodisorder & Autism,
BSMMU
Hemiplegia
Acute Chronic
 ASS
 ICSOL
 ADEM
 ICSOL
 RE
 HHE
 CP
ASS
Ischemic Hemorrhagic
 Coagulopathy
 Protein C,Protein S
deficiency, Factor V laden
 Iron deficiency
 Dehydration
 Arteriopathy – Moya moya
 Matabolic
 MELAS
 Homocystenuria
 Factor deficiency –
hemophilia A, B
 Thrombocytopenia –ITP
 Rupture of AV malformation
History
 Duration
 Onset
 Progression
 Vomiting – ICSOL, Hemorrhage
 Headache – ICSOL, Hemorrhage, CSVT
 Fever – Abscess, Tuberculoma
 H/O fever – ADS
 Similar illness in the past – Alternating hemiplegia in
infancy, MELAS, Homocystenuria, Moyamoya
 Family history – CVD,
 Past medical illness CHD, NS, SLE, Blood transfusion,
Dirrhoea, Veircela infection
Physical findings
 Temp
 Pulse
 BP
 Speech - dysarthria
 Cranial nerve palsy
 LL/UL – UMNL
 Cerebellar sign
 Gait – hemiplegic
Definition
 Stroke is defined as sudden occlusion or rupture of
cerebral arteries or veins resulting in focal cerebral
damage and clinical neurological deficit.
 According to WHO
 Rapidly developing clinical signs of focal (or global)
disturbances of cerebral function, lasting more than 24
hours or leading to death with no apparent cause other
than vascular origin.
 Brain received blood via –
 Cerebral hemisphere – through circle of Willis formed
by the paired anterior cerebral arteries, paired middle
cerebral arteries (anterior circulation from ICA) and
paired posterior cerebral arteries ( posterior circulation
from vertebral arteries/basilar artery)
 Basal ganglia, thalamus & midline brain stem – through
perforating arteries
 Lateral brain stem & cerebellum – circumferential
arteries – AICA, PICA & superior cerebellar arteries
Blood supply of Brain
Epidemiology
 Incidence 5/100000/yr
 1 in 2000 newborn
Risk factors for AIS
 Arteriopathy
 Congenital heart disease
 Hematological
 Metabolic & genetic
AIS
 Formation of thrombus
 Occlusion of vessels
 Cerebral damage
Risk Factors CSVT
 Prothromboitic conditions
 Dehydration
 Iron deficiency anaemia
 Drugs & Toxins
 Acute systemic illness
 Chronic systemic illness
 Nephrotic syndrome
 Inborn errors of metabolism
Cortical
 Weakness more in the legs
Capsular
 Complete hemiplegia
 Facial palsy
 Hemianaesthesia
 Homonymous hemianopia
Thalamic
 Hemianaesthesia
 Involuntary Movement
Midbrain
 Ophthalmoplegia (ipsilateral)
 Facial palsy (contralateral)
Pontine
 Horner’s syndrome
 Facial palsy (LMN)
 Weakness and loss of pain - contralateral
Ipsilateral
General examination
 Vital signs
 Pulse, BP, Temp
 Anaemia, Cyanosis
 Skin survey
Investigations
 CT/MRI
 CBC
 PBF
 Echocardiogram
 Protein C, Protein S, Anti thrombin III
 Lipid profile
 ANA
 Metabolic screening
 MRA, MRV, MRS
Others investigations
 According to initial report & etiology
Infarction
Hemorrhage
T1 T2
Hyper acute
<24
Iso Iso to hyper
Acute
1 – 3 days
Iso to hypo Hypo
Early subacute
3 – 7 days
Hyper Hyper
Late subacute
7 – 28 days
Hyper
Relevant Investigations
 PT
 APTT
 Factor Assay
Tuberculoma
Abscess
AIS - Imaging
•CT scan – Low detection rate for ischaemia (16% - 56%)
better to exclude hemorrhage
•MRI – Imaging of choice for AIS
DWI – showed hyperintencity
ADC – showed hypointensity
T2/FLAIR – hyperintensity (appears latter)
MRA
• MRA –
• Abrupt cutoff – embolic
• Narrowing or irregularity - arteriopathy
• Contrast MRA – concentric vessels wall enhancement arteriopathy
• CA –
• Sting, double lumen, intimal flap – dissection
• Sting of beads – vasculitis/arteriopathy
CSVT - Imaging
•CT scan – Filling defect (better for deep CSVT)
•Contrast CT – Empty delta sign
•MRI –
•FLAIR – vasogenic edema
•DWI – cytotoxic edema/infarction
•SWI - hemorrhage
•MRV – Filing defect
MRA
MRI
Management
 Neuropotection
 Control of seizure
 Maintain temperature
 Maintain normal glycaemic status
 Oxygen inhalation
 Thrombolytic & anti coagulant
 Physiotherapy
 Treatment of cause
MMS
• Rx
• Surgical
• Didect revascularization (synangiosis) doing
anastomosis of extra cranial (superficial temporal with
branch of affected vessels (MCA) ; indirect
revascularization placement of superficial temporal
artery on the surface of brain: pial synangiosis
• Symptomatic
• Associated symdrome – DS, NF1, Post radiation,
congenital
Counseling
 Rehabilitation
Moyamoya Disease
(Steno occlusive disease)
•Occlusion of branch of IC artery at circle of willis and
developedment of extensive collaterals at the base of the skull :
lenticulostrait branch
•Occlusion may occur in distal ICA, MCA
•Stroke in water shed zone
•C/F
•Headache, HTN, TIAs
•Sign of ischemia
•Aphasia
•Dysarthia
•Hemiparesis
•seizure
•Inv
•MRI - multiple infarct, vascular flow void
•MRA – absent involved vessels (conventional angiography to
see collaterals)

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Acute Stroke Syndrome.pptx

  • 1. Dr Kazi Ashraful Islam Assistant Professor Institute of Paediatric Neurodisorder & Autism, BSMMU
  • 2. Hemiplegia Acute Chronic  ASS  ICSOL  ADEM  ICSOL  RE  HHE  CP
  • 3. ASS Ischemic Hemorrhagic  Coagulopathy  Protein C,Protein S deficiency, Factor V laden  Iron deficiency  Dehydration  Arteriopathy – Moya moya  Matabolic  MELAS  Homocystenuria  Factor deficiency – hemophilia A, B  Thrombocytopenia –ITP  Rupture of AV malformation
  • 4. History  Duration  Onset  Progression  Vomiting – ICSOL, Hemorrhage  Headache – ICSOL, Hemorrhage, CSVT  Fever – Abscess, Tuberculoma  H/O fever – ADS  Similar illness in the past – Alternating hemiplegia in infancy, MELAS, Homocystenuria, Moyamoya  Family history – CVD,  Past medical illness CHD, NS, SLE, Blood transfusion, Dirrhoea, Veircela infection
  • 5. Physical findings  Temp  Pulse  BP  Speech - dysarthria  Cranial nerve palsy  LL/UL – UMNL  Cerebellar sign  Gait – hemiplegic
  • 6. Definition  Stroke is defined as sudden occlusion or rupture of cerebral arteries or veins resulting in focal cerebral damage and clinical neurological deficit.  According to WHO  Rapidly developing clinical signs of focal (or global) disturbances of cerebral function, lasting more than 24 hours or leading to death with no apparent cause other than vascular origin.
  • 7.  Brain received blood via –  Cerebral hemisphere – through circle of Willis formed by the paired anterior cerebral arteries, paired middle cerebral arteries (anterior circulation from ICA) and paired posterior cerebral arteries ( posterior circulation from vertebral arteries/basilar artery)  Basal ganglia, thalamus & midline brain stem – through perforating arteries  Lateral brain stem & cerebellum – circumferential arteries – AICA, PICA & superior cerebellar arteries
  • 8.
  • 10.
  • 12. Risk factors for AIS  Arteriopathy  Congenital heart disease  Hematological  Metabolic & genetic
  • 13. AIS  Formation of thrombus  Occlusion of vessels  Cerebral damage
  • 14. Risk Factors CSVT  Prothromboitic conditions  Dehydration  Iron deficiency anaemia  Drugs & Toxins  Acute systemic illness  Chronic systemic illness  Nephrotic syndrome  Inborn errors of metabolism
  • 15.
  • 17. Capsular  Complete hemiplegia  Facial palsy  Hemianaesthesia  Homonymous hemianopia
  • 19. Midbrain  Ophthalmoplegia (ipsilateral)  Facial palsy (contralateral)
  • 20. Pontine  Horner’s syndrome  Facial palsy (LMN)  Weakness and loss of pain - contralateral Ipsilateral
  • 21.
  • 22.
  • 23. General examination  Vital signs  Pulse, BP, Temp  Anaemia, Cyanosis  Skin survey
  • 24. Investigations  CT/MRI  CBC  PBF  Echocardiogram  Protein C, Protein S, Anti thrombin III  Lipid profile  ANA  Metabolic screening  MRA, MRV, MRS
  • 25. Others investigations  According to initial report & etiology
  • 28. T1 T2 Hyper acute <24 Iso Iso to hyper Acute 1 – 3 days Iso to hypo Hypo Early subacute 3 – 7 days Hyper Hyper Late subacute 7 – 28 days Hyper
  • 29. Relevant Investigations  PT  APTT  Factor Assay
  • 30.
  • 33.
  • 34.
  • 35.
  • 36. AIS - Imaging •CT scan – Low detection rate for ischaemia (16% - 56%) better to exclude hemorrhage •MRI – Imaging of choice for AIS DWI – showed hyperintencity ADC – showed hypointensity T2/FLAIR – hyperintensity (appears latter)
  • 37. MRA • MRA – • Abrupt cutoff – embolic • Narrowing or irregularity - arteriopathy • Contrast MRA – concentric vessels wall enhancement arteriopathy • CA – • Sting, double lumen, intimal flap – dissection • Sting of beads – vasculitis/arteriopathy
  • 38.
  • 39. CSVT - Imaging •CT scan – Filling defect (better for deep CSVT) •Contrast CT – Empty delta sign •MRI – •FLAIR – vasogenic edema •DWI – cytotoxic edema/infarction •SWI - hemorrhage •MRV – Filing defect
  • 40.
  • 41. MRA
  • 42.
  • 43. MRI
  • 44. Management  Neuropotection  Control of seizure  Maintain temperature  Maintain normal glycaemic status  Oxygen inhalation  Thrombolytic & anti coagulant  Physiotherapy  Treatment of cause
  • 45. MMS • Rx • Surgical • Didect revascularization (synangiosis) doing anastomosis of extra cranial (superficial temporal with branch of affected vessels (MCA) ; indirect revascularization placement of superficial temporal artery on the surface of brain: pial synangiosis • Symptomatic • Associated symdrome – DS, NF1, Post radiation, congenital
  • 47. Moyamoya Disease (Steno occlusive disease) •Occlusion of branch of IC artery at circle of willis and developedment of extensive collaterals at the base of the skull : lenticulostrait branch •Occlusion may occur in distal ICA, MCA •Stroke in water shed zone •C/F •Headache, HTN, TIAs •Sign of ischemia •Aphasia •Dysarthia •Hemiparesis •seizure •Inv •MRI - multiple infarct, vascular flow void •MRA – absent involved vessels (conventional angiography to see collaterals)