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A. Kumar, 2016 - Tia & Stroke
A. Kumar, 2016 - Tia & Stroke
Cerebrovascular Disease
Residual
Risk
Factors XX TIA XX Stroke XX Deficit
Primary Secondary
Prevention Prevention
CVS
Spectrum
Funny turns TIA Stroke Stroke/
Fatality/Palliation
Low / High risk Minor/moderate Severe
Isolated symptoms
Dizziness
Light headedness
ABCD2 score
Blurry vision <3 / >46
Gen weakness
Problematic:
1. Most TIA symptoms very short lived9
2. If longer symptoms, minimal resolve10,11
3. Half with TIA have evidence of recent infarction on MRI (DWI)12
Hence:
AHA/ASA: Tissue based, focal neurological dysfunction, brain, spinal
cord, retinal ischemia without infarction8
• Mimics:
A) Neurologic
1. Migraine with neurological symptoms
2. Seizure with Todd’s paralysis
3. Sensory march of amyloid angiopathy
B) Metabolic
4. Hypoglycaemia or Hyperglycaemia
5. Hyponatremia
C) Functional
ABCD2 Score 7
BP >140/90 1
Clinical symptoms
(max 2 pts)
Speech 1
Duration >60 mins
2
(max 2 pts)
10-59 mins 1
Diabetes 1
Total 7
5
Moderate Risk 5.9%
4
3
Low Risk 2 1.2%
1
0
• Laboratory17 - FBC
- U&E’s
- Glucose
• ECG
• Brain Imaging: CT Head, MRI Brain
• Carotid Duplex
• Case-by-case investigations (i.e: young stroke)
16. Nguyen Hhuynh et al Neurology 2005; 65:1799
17. Rothwell PM et al Lancet 2007;370:1432
Laboratory
FBC 1. Hb High
Polycythemia, 65g, 200g/L
Low Infection
3. Platelets High
Thrombocytosis (x106)
Seizures
2. Glucose High
Ketotic coma
591 Patients
Participant Population
Phase 1 Phase 2
Between April 1, 2002 – Sept 30, 2004 Between Oct 1, 2004 – March 31,
Phase of delayed assessment and treatment 2007 delay of assessment and treatment
Reduced
GP Study Clinic
Phone
310 281
Report and Assessed and treated
recommendations
Appointment Patient
Modifiable: Non-modifiable:
Hypertension Age
Diabetes Gender
Smoking Family history
Dyslipidemia
AF
Other lifestyle
factors19
• Note: Different risk factors in young vs older Patients
Hypertension
• Single biggest risk factor!!
- (~1/5 in NZ>15yrs)5
- 50% CAD, Heart failure
- 62% Strokes20
• Atherosclerotic disease & stroke: complex, but appears weak risk factor36
• Weak positive association with ischaemic strokes with high levels (>7mmol)37,38
Ischaemic Haemorrhage
10-30%
70-90%
- HTN
- Thrombus - Amyloid
- Embolus
- Hypoperfusion
Many Sources of variance affecting stoke
outcome - Heterogeniety
]
– Hypertension
– Ruptured saccular aneurysm MAJORITY
– Amyloid angiopathy
– Vascular Malformations
40% Site
10%
5%
1%
Ischaemic Stroke
Classification 58
58.BamfordJ et al Lancet22;337(8756):1521-6,1991
Lacunar Infarct (LACI)
Classification
• LACI – 5 Major syndromes 89
- Pure motor
- Pure Sensory
- Mixed
- Dysarthria clumsy hand
- Ataxic hemiparesis
• Small discrete infarcted area - penetrating artery occlusion.
• Lipohyalanosis – HT,?DM, embolism
• Due to location normally don’t affect higher cortical cognitive
function.
89 Jamary OF et al Lacunar infarcts UpToDate Aug20,2013
Regional Brain Syndrome
•Frontal lobe Parietal Lobe
Broca’s
area
Occipital
Temporal Lobe Wernicke’s area
Lobe
How to test?
• History
• Examination
– Cranial Nerves, Limbs, Gait
– Suspected higher centres
• Speech
• Memory
• Reading, comprehension
• Writing, calculation, drawing
• Gnosia, graphaesthesia, praxia
• Primitive reflexes
Diagnosis
MCA Strokes
• Left Parietal (Dominant) • Right (Non dominant)
• Aphasia/Speech + • Aparaxia
– Receptive /Fluent
(temporal lobe)
• Plus contralateral
- motor
– Expressive/Non fluent
(frontal lobe) - sensory
• Left right disorientation
• Finger Agnosia
• Plus contralateral
- motor
- sensory Astreognosis
Agraphesthesia
2 point discrimination
Dominant parietal lobe signs
–
Acalculia 25+14 = 42
– Agraphia
• Agraphaesthesia
• Sensory inattention
Other parietal lobe signs
• Tactile agnosia
• Apraxia
– Dressing
– Constructional
• Spatial neglect
• Inferior homonymous quadrantanopia
Other parietal lobe signs
• Tactile agnosia
• Apraxia
– Dressing
– Constructional
• Spatial neglect
• Inferior homonymous quadrantanopia
Temporal lobe signs
• Memory
– Short-term
– Long-term
• Superior homonymous quadrantanopia
Diagnosis
ACA Strokes
• Secondary prevention
• Aspirin (A) RRR 18% NNT 83 (IST, CAST trials)
• Clopidogrel (C)
• Dipyridamole (D) RRR 17%
• Dual (A + C) RRR ~33%, MATCH, CAPRIE
• Dual (A + D) RRR 33%, ESPSII, ESPIRIT
– >80% NNT 5
– 70-80% NNT 8
– *50-69% NNT 15 (men)
– on same side as stroke
– patient otherwise well
– low surgical risk
• Incidence - 6-32%62
• Recurrent strokes worse impact64
• Silent cerebral infarcts,AF,HT
• Rehab –difficult, ?what,?how Safety net
62. Ivan CS et al Stroke 2004;35:1264
63. Desmond DW et al Stroke 2002;33:2254
64. Srikanth VK et al Stroke 2006; 37:2479
Take home message 1
1. PSD is a clinical, not strictly
pathophysiological, definition (emphasis on
stroke)
2. PSD is heterogeneous in terms of mechanisms
(SVD, large vessel, strategic sites, multiple
lesions)
3. PSD is frequent (a major consequence of
stroke)
4. A history of stroke doubles the risk of incident
dementia
Take home message 2
1. A number of risk factors for PSD exists
2. Dementia is only part of the spectrum of
the cognitive consequences of stroke
(consider also mild cognitive impairment
– MCI)
3. Need of identifying and harmonizing
instruments for detecting post-stroke
MCI as early as possible in the disease
course
Cerebrovascular disease
Future exciting!!
Therapies:
A) Medical/surgical
– Acute stroke therapies, Thrombolysis, Thrombolysis plus (ultrasound)86,
clot retrival85, Stents87 - extracranial, intracranial, hemicranectomy79,
shunt80
B) Technology
- Telemedicine65, Facebook, robotic assisted82
C) MDT
- Circuit training83, Targeted therapy81, utilising assistants/equivalents
• Research
• - Laboratory
• - Collaborative multicenter trials- Psychiatric, Stroke physicians /
Rehabilitation / Neurologists
65. Johansson et al Telemed Telecare 2011;17:1-6
66. Vahedi K et al Lancet Neurol 2007;6:215
67. Broderick J et al Stroke 2007;38:2001
Remember!!!
• Time is Brain, Action is salvation
• Move - talk field – work field !!
• Treat immediately, aggressively
• Holistic team effort - maximize Gain
- minimize disability
- insync,
coordinated
• Thank you
Acknowledgements
• Steven C. Cramer, MD. Professor, Depts.
Neurology, Anatomy & Neurobiology, and
Physical Medicine & Rehabilitation. Vice Chair
for Research, Dept. Neurology Clinical Director,
Sue & Bill Gross Stem Cell Research Centre.
Director, Neuroimaging Core, Inst for Clinical
Translational Science. University of California,
Irvine
Acknowledgements cont
• Prof. Gert Kwakkel Chair Neuro-rehabilitation VU
University Medical Centre, Amsterdam & UMC Utrecht,
ESC conference, London May 2013
• Dr Alex Leff, Clinical senior lecturer & consultant
neurologist. Institute of Neurology & Institute of
Cognitive Neuroscience. National Hospital for
Neurology & Neurosurgery, ESC conference May 2013
References
1. Louis R Caplan et al UpToDate:Feb26,2014
2. Steven C Cramer ,”Brain repair after stroke” ESC conf,London , June 2013
3. Hacke et al NEJM 2008;359:1317
4. NINDS Study Group NEJM 1995;333:1581
5. 5 www.stroke.org,nz/preventing-stroke
6. Johnston SC et al Lancet 2007;369:283
7. Rothwell PM et al Neurology 2005; 64:817
8. Easton JD et al Stroke 2009;40:2276
9. Caplan LR et al Curr Atheroscler Rep 2006;8:276
10.Albers GW et al NEJM 2002;347:1713
11.Caplan LR et al Arch Neuo 2007;64:1080
12.12 Redgrave JN et al Stroke 2007;38:1482.
13. Montgomery BM et al Arch Intern Med 1964 ;114:680
14. Bos MJ et al JAMA 2007 ;298:2877
15. Cochrane T et al Neurology 2005;65:1140
16. Nguyen Hhuynh et al Neurology 2005; 65:1799
17.Rothwell PM et al Lancet 2007;370:1432
18. Flemings KD et al Mayo Clin Proc 2004;79:1071
References cont
19.Furie KL et al Stroke 2011; 42:227 ,AHA/ASA 2011 Guidelines
20. Manic G et al, Oct 2013,vol31,Journal of Hypertension, ESH/ESC, 2013 Practice Guidelines.
21. Aburto Net al BMJ,2013 346
22. PROGRESS Collaborative Group, Lancet 2001;358:13;1033
23.INERACT II,SAMPARIS
24. Arvanitakis Z et al, Neurology 2006;67:1960
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35.Suls JM et al Am J prev Med 2012;42:655
36. Piechowski-J et al Stroke 2004;35:1523
37. Iso H et al NEJM 1989;320:904
38. Lindenstrom E et al BMJ 1994;309:11
References cont
39 Amarenco P et al NEJM 2006; 355:549
40 Atrial Fibrillation Investigators (AFI) Group Arch Intern Med 1994;154:1449
41. Anderson DC et al Stroke 2002;33:1963
42. Harrison MJ et al Stroke 1984 ;15:441
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44. Cullinane M et al Stroke 1998 ;29:1810
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46.Rosand J et al Arch Intern Med 2004;164:880
47.Van Staa et al J Thromb Haemost 2011;9:39
48.Jamary O et al UpToDate Oct 16;2013
49. Rothwell PM et al Lancet 2004; 363:915
50. Furie KL et al Stroke 2011;42:227
51. McCarron MO et al Neurology 1999;53:1308
52. Schneider JA et al Stroke 2005 ;36:954
53. Sturgeon JD et alStroke 2005;36:2484
54. Eikelboom JW et al Stroke 2000;31:1069
55. J Neurosurg 1994 Jan;80(1):51-7
56. Cerebrovasc Dis 1999 Mar-Apr;9(2):102-8
57. Caplan LR Caplan’s Stroke 4th ed 2009.p22
58. BamfordJ et al Lancet22;337(8756):1521-6,1991
59. NEJM 333:1581-7
References cont