CNS

1. Acute stroke (Brain attack)
Based on ABC of stroke
Updated on 10th
March 2003 based on
RCP guidelines (2002/feb)

2. WHO definition
Clinical syndrome typified by rapidly
deveoloping signs of local or global
disturbance of cerebral functions, lasting
more than 24hrs or leading to death with
no apparent causes other than of
vascular
origin

3. Introduction
 Stoke: sudden neurological deficit of presumed
vascular origin
 It’s a syndrome rather than a single disease
 Acute stroke is now a treatable condition that
deserves specialised attention
 A senior clinician should review all pts with
presumed stroke (class B recommendation)
 Drug Rx and specialised care both influence
survival and recovary

4. Assesing the patient
 Pts should be assessed at hospital
immediately after stroke
 Hyperacute treatments such as thrombolysis
must be administered within 3-6 hrs
 Stroke is a clinical diagnosis, but imaging is
required to differentiate between ischemic
and primary intracerebral h’age
 Following can be used to diagnose and
predict prognosis
 Eivdence of motor, sensory or cortical dysfunction
 Hemianopia

5. Pathophysiology
 For practical purposes – 2 types of stroke
(after excluding SAH)
 Ischaemic: 85%
 1ry h’age: 15%
 H’ge causes direct neuronal injury and
pressure effect causes adjacent ischemia
 1ry ischaemia results from atheroembolic
occlusion or embolism
 Usual sources of emboli are LA in pts with AF
or LV in MI/LVF

6. Pathophysiology
 Vessel occlusion from atherosclerosis
 Typically in internal carotid just above carotid
bifurcation
 If form small vessel – small vessel disease deep
wihin the brain
 Ischaemia causes direct neuronal injury from

Lack of oxygenation

Lack of nutritional support

Cascade of neurochemical events that lead to spreading
damage

Ischaemia may be reversible if reperfusion is obtained
quickly (3-6hrs)

Chemical injuries may be interrupted by various
neuroprotective drugs (unproved in humans)

7. Symptoms and signs of stroke
 Anterior circulation strokes
 Unilateral weakness
 Unilateral sensory loss or inattention
 Isolated dysarthria
 Dysphasia
 Vision

Homonymous hemianopia

Monocular blindness

Visual inattention

8. Symptoms and signs of stroke
 Posterior circulation strokes
 Isolated homonymous hemianopea
 Diplopia and disconjugate eyes
 Nausea and vomiting
 Unilateral or bilateral weakness and/or sensory
loss
 No specific signs
 Dysphagia
 Incontinence
 Loss of consciousness

9. Characteristics of subtypes of
stroke
Lacunar PACI TACI Post
Signs Motor or
sensory
only
2 of the
following:
motor or
sensory,
cortical,
hemianop
ia
All of:
motor or
sensory
cortical,
hemian
opea
Hemian
opia,
brainste
m,
cerebell
ar
%dead at
1yr
10 20 60 20
%depend
at 1 yr
25 30 35 20

10. Anterior cerebral stroke
 Ant cerebral artery gives a branch called ‘recurrent artery of
Huebner’ immediately after its origin
 If present it contributes to the supply of internal capsule
 Two ant cerebral arteries are joined together by ant
communicating artery
 Ant cerebral artery occlusions are rare
 If there is no recurrent artery
 Face, arm will not be affected
 Entire leg area of the cortex is destroyed
 So it causes flaccid paralysis of the leg with cortical sensory loss
 If there is recurrent artery & block occurs proximal to its origin
 Ant internal capsule will also be affected

UMN Facial weakness, spastic arms and useless flaccid leg

The arm has good potential for recovary, because the cortical control is
there

But the leg has no potential for recovary as the cortical control is lost

11. Anterior cerebral stroke
 Perforating artery occlusion
 If the recurrent artery Huebner is present and
occluded weakness of face & arm will be present
 Even if the dominant hemisphere is affected
dysphasia will not occur, because the cortex is
spared
 Terminal branch occlusion
 Terminal vessels supply mainly the cortex
controlling the legs, so the motor & sensory
function will be affected
 Pt may not walk at all
 Less severe intellectual & sphincte involvement
than with main trunck occlusion

12. Anterior cerebral stroke
 Because of the affection of precentral gyrus
 Incontinence of urine is common – when there is desire to
pass they cannot control
 Incontinence with flaccid leg weakness can mimick cauda
equinal lesion
 But the reflexes will return and plantar will be upgoing with
time
 Considerable memory and intellectual deficits may be
there
 If there is evidence of weakness of other leg also (ie,
that the lesion is not strictly unilateral) a parasagital
tumor should be excluded
 Vascular occclusions affecting hemispheres should
not produce B/L signs

13. Middle cerebral artery
occlusion
 Massive infarction of the bulk of hemisphere
 There is considerable cerebral oedema
 Coma & eventual death
 If non dominant hemisphere
 Severe dyspraxia or
 Denial of existance of the left side
 If dominant hemisphere is affected
 Global dysphasia
 Motor:
 Destroys both pyramidal & extrapyramidal mechanisms
producing flaccid weakness of face & arm with little or no
chance of recovary
 The leg cortex is spared, but rarely recovers significantly

14. Middle cerebral artery
occlusion
 Hemianaesthesia & hemianopia are associated with
hemiparesis
 Devastating type of stroke
 Minimal chance of recovary
 High chance of death due to cerebral odema, unresponsive
to steroids or osmotic agents
 It is similar to total occlusion of carotid artery in the
neck
 With cross circulation via ant communicating artery
 With normal vertebro basilar artery
 The anastomoses could be so efficient that pt may
not have any neurological deficits

15. Signs to be looked for
 Conscious level
 Neurological signs
 BP
 HR/rhythm
 Heart murmurs
 Peripheral pulses
 Systemic signs of infection or neoplasm

16. Death rate after stroke
30 days 1 year 5 years
Ischaemic
stroke
10 23 52
ICH 52 62 70
SAH 45 48 52

17. Conditions that can mimick stroke
Diagnosis Diagnostic features
Decompression of previous stroke Evidence of infection such as
urinary or respiratory tract;
metabolic dist.
Cerebral neoplasm (1ry or 2ry) Less abrupt; 1ry tumor or 2ry (lung
or breast CA)
SAH Recent head injury
Epileptic seizures Possible previous fits
Traumatic brain injury H/O trauma
migraine Less abrupt onset; followed by
headache; young pt
Multiple sclerosis Less abrupt onset, possible
previous epi
Cerebral abscess Infection

18. Investigations of stroke
 All should have a CTwithin 48hrs to distiguish
between ischaemic and h’gic stroke
 Imaging should be urgent in
 Depressed conscious level, fluctuating symptoms,
papilloedema, neck stiffness, fever, severe
headache, previous trauma, anticoagulant
treatment or bleeding diathesis (B)

19.  MRI is superior, because it also assess blood
flow and perfusion of the brain/detect wether
lesion is old or new and identify carotid
stenosis
 Imaging will also identify stroke mimicking
conditions
 But a low grade glioma could still be difficult
to be differentiated from cerebral infarction

20. Investigations of stroke
 All patients
 CT/MRI
 ECG
 CXR
 FBC
 Clotting screen
 SE/creatinine
 Plasma glucose

21. Investigations of stroke
 Sub groups
 Carotid duplex scanning
 ECHO
 Thrombophilia screen
 Immunology screen
 Syphillis serology
 Cerebral angiography (Rarely)

22. Investigations – to what extent
 Depends on several factors
 Likely degree of recovary
 Presence of obvious risk factors
 Age of the pt (younger pts likely to have
identifiable cause such as inflammatory or
clotting dissorder)
 Ix better be restricted to tests that will
help in the management

23. Stroke unit
 Stroke unit should be centred in a hospital
 Should be staffed by
 Multidisciplinary team with expertise in stroke care (A)
 Team should work to agreed protocols for common problems (A)
 Should provide educational programmes for staff, pts and carers
 Stroke unit trialist’s collobaration
 Stroke units compared to alternatives showed reduction in odds ration for death
recorded at follow up (OR 0.86)
 Odds ratio of death, instituitionalised care and death or dependency were significantly
less
 Outcomes were independent of age, gender and stroke severity and appeared to be
better in stroke units based in a geographincally discrete ward
 No increase in hospital stay in stroke unit
 In a study where patients were randomly assigned to stroke unit care, general wards
with stroke team support, or domiciliary stroke care, mortality and institutionalisation
rates at one year were lower in patients who received care on the stroke ward
 The benefits of stroke unit care have been shown to persist at 10 years after initial
stroke

24.  Early supported discharge from hospital to a
specialist rehabilitation team providing care at
home is feasible for selected pts (A)
 If the pt can transfer from bed to chair, can be
sent home and equally effective specialised
multidisciplinary care could be given at home
(A)
 Patients should only be managed at home if
acute assessment guidelines can be adhered
to and the services organised for home are
flexible, and part of a specialist stroke service
(A)

25.  The guidelines do allow for the management of some patients in the
community, particularly those with transient ischaemia attacks (TIAs)
and strokes with good recovery
 The consensus was that these patients could be managed at home
provided they had access to a neurovascular clinic within two weeks
(C)
 More than one TIA within a short period (crescendo TIA) requires
admission to hospital (C)
 The guidelines are not prescriptive in defining a short period but the
authors consider that recurrent TIAs within one week merit admission
 The guidelines recommend that families are involved in the decision
making process and have input into future plans for the patient (C)
 Caring for a stroke patient can be very difficult & emotional distress is
seen in 55% of caregivers at six months after stroke
 Caregivers are more likely to be depressed if the patients are severely
dependent or emotionally distressed themselves
 The stroke team must be alert to recognising carer stress and helping
carers in this difficult situation (B)
 Disseminating information about the nature of stroke and on relevant
local and national services improves patient and carer knowledge (A)
 Introduction of stroke family support workers increases the quality of life

27. Emergency management
 Within the 1st
hour after cerebral
ischaemia, part of the brain is under
threat of death
 The densly ischaemic area will
inevitably die, but there is also tissue
that could be salvaged
 At this stage oxygenation,
haemodynamic and metabolic factors
are crucial

28. Management
 Restore vascular anatomy
 Thrombolysis
 Angioplasty/stent
 Antiplatelets/anticoagulants
 Stop ischaemic neurones dying
 Prevent complications
 DVT
 MI
 Infection
 Seccondary prevention

29. Emergency management
 The emergency managemet of stroke requires
 Medical stabilisation
 Assesment of factors that may lead to complications

Swallowing

hydration
 It is important to keep physiological variables such as
hydration,
 temperature, nutrition, and oxygenation within normal range
 in the acute phase of stroke (C)
 Thrombolysis may be considered
 Stroke units are associated with better outcome

30. Early Rx of ischemic stroke
 General care
 Specific Rx: thrombolysis, anticoagulants,
antiplatelets, neuroprotective agents
 Emergency aproach
 Stroke unit care
 Treatment of complications
 Treatment of co-morbidity
 Rehabilitation

31. Swallowing and feeding
 Dysphagia in ~35%
 Unrecognised in mild stroke
 But associated with poor outcome

Aspiration

Pnuemonia

Poor nutrition
 Presence of gag reflex is a poor guide and therefor formal assesment is
essential
 Fluids are more difficult to swallow than solids
 They should be fed through NG or percutaneous endoscopic feeding tube
 Most pts will not need enteral feeding beyond a few weeks
 However when and how optimally to feed dysphagic pts is yet to be determined
 Dysphagia Mx involves:
 Initial swallow screen
 Diet modification
 Compensatory swallowing techniques
-reduces aspiration pneumonia

32.  Malnutrition is also common and is seen in 30% of
patients one week after stroke
 Routine oral or enteral protein supplementation
improves nutritional indices but there is no evidence
that it affects outcome
 In the dysphagic patient, enteral nutrition can be
supplied by either nasogastric tube or percutaneous
endoscopic gastrostomy
 There is some evidence that percutaneous
endoscopic gastrostomy feeding is superior to
nasogastric feeding,36 but its insertion requires an
invasive procedure.
 Questions concerning the most effective nutritional
route as well as the timing of nutritional intervention
after stroke are being addressed in a large
randomised controlled trial, the FOOD trial
 Information is available at
http://www.dcn.ed.ac.uk/food.

33. Communication and speech
 Stroke can affect communication and speech in a
variety of ways, including
 impaired motor speech production (dysarthria)
 impaired language skills (dysphasia)
 Impaired planning and execution of motor speech
(articulatory dyspraxia)
 Deficits can be subtle and every patient with a
communication difficulty needs to be assessed by a
speech and language therapist
 Speech therapy input is effective at improving
communication, with short, intensive courses of
speech therapy lasting 4–8 weeks proving most
beneficial

34. Acute treatment of stroke
 Asprin: in most patients
 2 large trials (160-300mg/d by PO/NG/ Rectum) started within
48hrs of stroke, reduces subsequent death and disability
 NNT- 77 (reducing risk by reducing reinfarction)
 For 1000 pts –

12 avoid death and dependency

Risk of h’age minimal (1-2/1000)

Early asprin is beneficial
 In a study where patients were randomly assigned to stroke
 unit care, general wards with stroke team support, or
 Patients with acute ischaemic stroke should receive aspirin (160–
300 mg) as soon as possible after stroke if a diagnosis of
haemorrhage is considered unlikely (A)
 But CT/MRI is essential before asprin
 But if CT is not availble and ischaemic stroke is highly suspected may give
asprin

35.  IST(International Stroke Trial) and
CAST (Chinese acute stroke trial)
combined
 40,000 pts
 Significant decrease in death and
dependency at 6/12 if asprin is given
immediately
 13 more pts alive per 1000 Rxed
 Increase in ICH – 2 per 1000
 Reduction in recurrence - 7 per 1000

36. Acute treatment of stroke
 Heparin (conventional or LMWH)
 Trials did not show any improved outcome.
But useful certain groups of pts
 Prophylactic:

Previous venous thromboembolism

Morbid obesity
 Therapeutic:

Carotid artery dissection

Embolic, recurrent transient ischaemic attacks

37.  Anticoagulation has no net benefit
 Decreases recurrent ischaemic stroke (9
per 1000 Rxed) and pulmonary emboli (4
per 1000 Rxed)
 But 9 per 1000 increase in ICH
 But it has definitive place in 2ry prevention
 Immediate anticoagulation in AF is not
advised
 RCP guidelines: start anticoagulation 14d
after the acute event (A)
 There is evidence for acute anticoagulation
in the specific stroke syndrome of cerebral
venous thrombosis

38. Acute treatment of stroke
 Thrombolysis
 Standard acute Rx in USA, Australia and most
european countries
 Type of drug and timing important
 NINDS trial: Alteplase (tPA) within 3 hrs increases
the chances of near complete recovary (NNT-7)
 3-4x increase in ICH
 20% reduction in death and dependency
 Rx after 6 hrs less effective (NNT-12)
 Complications: intra or extracranial h’age

39. Acute treatment of stroke
 Contra indications to thrombolysis:

Seizure at onset

Pre Rx BP >185/110

Major infarct on CT

Previous ICH

Recent MI

Recent or intended surgery

Use of anticoagulants

40. Acute treatment of stroke
 Withhold antihypertensives for 10 days
 Indications for early Rx of high BP
 Evidence of pre existing HBP

Documented previous HT:clinic recors etc

Evidence of target organ damage
Hypertensive retinopathy, LVH on ECG
 Evidence of hypertensive emergancy

HT encephalopathy

LVF
 BP is very high

SBP >220-240

DBP >120

41. Complications of stroke
 Hyperglycaemia**
 Hypertension**
 Fever**
 Infarct extension or
bleeding
 Cerebral oedema
 Herniation
 coning
 Aspiration
 Pneumonia
 UTI
 Cardiac
dysrrhythmia
 Recurrence
 DVT
 PE

42.  Mood disorders are common after stroke and
difficult to diagnose due to speech problems
 Crying after minimal provocation is common,
may be due to emotionalism and may be
treated by fluexetine (A)
 Pain after stroke varies in type, origin and
modes of treatment
 Some related to stroke damage – neuropathic or
central pain (responds to tricyclics)
 Mechanical pain due to immobility or exacerbation
of pre-existing osteoarthritis
 Shoulder pain is seen in 30%
 Rx should begin with simple analgesia and proper
handling techniques

43. Venous thrombolism
 Is common after stroke and studies using
radiolabelled fibrinogen leg scanning suggest that
deep vein thrombosis occurs in up to 50% of patients
with hemiplegia
 The guidelines recommend that aspirin (75–300 mg
daily) should be used (A) (in non-haemorrhagic
strokes)
 Compression stockings should be applied to patients
with weak or paralysed legs (A)
 The final recommendation on the length of stocking
to be used awaits results from the on-going CLOTs
trial.

44. Spasticity
 Spasticity is a motor disorder characterised by a velocity dependent
increase in tonic stretch reflexes
 It may lead to secondary complications such as muscle and joint
contractures
 Management requires several coordinated interventions including
physiotherapy, drug treatment, and patient education
 Physiotherapy using isokinetic strength training can improve strength
and gait velocity without increasing spasticity
 Drug therapy with either baclofen or tinzanadine as an adjunct to
physiotherapy has been shown to reduce spasticity
 In patients with disabling or symptomatically distressing symptoms,
botulinum toxin is safe and effective & can be targeted to individual
muscles
 The guidelines indicate that spasticity should be treated if causing
symptoms, though functional benefit is uncertain (B)

45. Mx of increased IC pressure
 Elevate head by 30 degrees
 Avoid or correct aggravating factors
 Hypoxia
 hyperglycemia
 Moderate fluid restriction
 Avoid hyperosmolar fluids eg: dextrose
 Osmotic agents: eg: manitol; as indicated
 Hyperventillation
 IV barbiturates
 NO STEROIDS
 Neuroprotective agents are not proved to be effective

46. Rehabilitation
 Aims
 Restore function
 Reduce the effects of stroke on pt and theirs
carers
 Regain independence and maximise ability in all
activities of daily living
 Should start early during recovery
 Once pt is medically stable, should be
transferred to a stroke rehabilitation unit
 Formal rehabilitation at a centre reduces
death, disability and hospital stay (NNT-12)

47.  A physiotherapist with expertise in neurodisability should
coordinate treatment to improve movement performance of
patients with stroke (C)
 The effectiveness of motor and strength rehabilitation is being
underpinned by new evidence based
 Progressive resistive exercise studies have also been shown to
improve gait, strength, activity, and mood
 There is some evidence that increased intensity of therapist
input improves outcome but some patients cannot tolerate
intense therapist input
 The guidelines recommend that patients receive as much as
they find tolerable and at least every working day (B)
 It is vital that patients have the opportunity to practise
rehabilitation tasks
 The need for special equipment such as a wheelchair or
adapted cutlery should be assessed on an individual basis as
review by an occupational therapist with specialist knowledge in
neurological disability can significantly reduce disability and
handicap (B)
 The provision of hoists or adaptation of the home environment
may prevent the patient going to institutional care

48. Secondary prevention
 Should start shortly after admission,
except BP control
 All pts should be offered
 Life style guidance
 Stop smoking
 Reduce saturated fat, alcohol and salt
 Asprin for life

49. Stroke secondary prevention

50. Introduction
 A second stroke will not necessarily be
of the same type as the initial event
 Pts with previous stroke commonly
suffer other vascular events like MI
 Effective 2ry prevention depends on
attention to all modifiable risk factors
and treating the cuase of initial stroke

51. Four questions should be
answered
 Is it acute cerebrovascular disease
 Is it ischaemic or Haemorrhagic
 Cardioembolic or vascular aetiology
 Anterior or posterior circulation

52. Is it acute CVA
 Key features are
 Focal neurological deficit
 Sudden onset
 Absence of an alternative explanation
 Exclude stroke mimicking conditions

53. Ischaemic or haemorrhagic
 History or examination cannot reliably distinguish
 A small bleed can produce transient symptoms
 Imaging is essential
 H’age is immediately apparent on CT, but over few
weeks it becomes indistinguishable from infarction
 Small bleeds may be missed after one week
 MRI has a greater sensitivity for brain stem,
cerebellar and small ischaemic strokes
 Can also identify h’gic stroke and remains diagnostic
long after signs have disappeared

54. Sub cortical h’age with TIA D0 and D8

55. Correct imaging techniques
Symp <1h Symp >1h
onset<2w
Symp>1hr
onset>2w
Abrupt onset,
typical CVA
Image only if
anticoagulation
proposed
CT MRI
Insidious onset
suspicious of
tumor
NA CT with
contrast
CT contrast
Insidious onset
suggestive of
multiple
sclerosis
NA MRI MRI

56. Cardioembolic or vascular
aetiology
 25% are due to embolism from heart or major
vessels
 Embolic stroke can affect any vascular
territory
 Certain features should prompt search for
embolic source
 TOE is justified if the results are unequivocal
or index of suspicion is high

57. Embolic causes of stroke
found on echo
 MS
 LAH (>4cm)
 Dyskinetic or akinetic LV
 Severe global LV dysfunction
 Valvular vegetation
 LA/LV thrombi
 MV calcification
 Calcific aortic valve or stenosis predispose to
embolism but may not justify anticoagulation

58. Justification for echo
 AF
 HF
 MI within 3/12
 ECG abnormalities
 MI
 IHD
 BBB
 Heart murmur
 Peripheral embolism
 Clinical events in >2
territories
 R & L hemisphere
 Ant & post circulation
 >/= cotical events (in
same territory) unless
severe carotid disease

59. Anterior or posterior
circulation
 Ant circulation (Carotids)
 Cerebral hemispheres
 Post circulation (Vertebro basillar) supplies
the
 Brain stem
 Cerebellum
 Occipital lobe
 If ant circulation stroke
 Carotid doppler to decide on endarterectomy

60. Risk of recurrence after stroke
or TIA
 Stroke:
 8% per year
 TIA
 8% risk of stroke in the first month
 5% risk of stroke a year thereafter
 5% risk of MI a year

61. Modifiable risk factors for
stroke
 HBP
 Smoking
 DM
 Diet: high salt & fat,
low K & vitamins
 Excess alcohol
 Morbid obesity
 Low physical
exercise
 Low temperature
 Cholesterol
concentrations –
atleast in pts with
CAD

62. Management of risk factors
 Smoking:
 Important correctable risk factors
 Risk returns to that of a non smoker within
3-5 yrs of cessation

63. Management of risk factors
 Blood pressure
 Immediate reduction may be deleterious
 Long term risk is inversely related to BP achieved
 HT should be treated 1 or 2 weeks after the stroke
 Rx reduces

Recurrence of fatal and non fatal stroke by 28%
 Pts at high risk of further stroke derive greatest
benefit (eg: elederly)
 Target BP recommended by British Hypertension
Society is <140/85

64. BP threshold for Rx

65.  PROGRESS study:
 Pts with history of stroke or TIA were treated with
antihypertensives irrespective of baseline BP
 Pts treated with Perindropril and indapamide had a
reduction in BP of 12/5
 And reduced stroke risk of 43%
 There were similar reductions in hypertensives
and non-hypertensives
 HOPE study
 32% relative risk reduction in 1ry and 2ry stroke
prevention in 9297 high risk pts with ramipril
 Base line BP was 139/79
 Reduction in BP was only 3.8/2.8
 Efficacy of ACEI may explained by anti-
inflammatory effect and plaque stabilization

66. Management of risk factors
 Role of cholesterol – contraversial
 But statins reduce risk of stroke in pts
with CAD
 Use of statins after a athersclerotic
stroke or TIA probably reduces
recurrent events and IHD
 Since stroke pts are high risk pts cost
Rx may be justified

67. Heart protection study
 Over 20,000 pts with high risk of vascular disease
aged 40-80
 There were 1820 pts with history of non disabling
stroke or TIA
 All were randomised to simvastatin 40mg/d or
placebo for 5 years, independent of baseline
cholesterol
 Simvastatin pts showed highly significant 25%
reduction in incidence rate of 1st
stroke
 The benefits were seen across all age ranges and
base line cholesterol levels

68. Management of risk factors
 Diabetes:
 Confers substantial dissadvantage for

Survival

Functioning outcome on pts with acute stroke

Plasma glucose should be normalised early

BP targets for diabetics are lower

69. BP targets for non diabetic
and diabetic stroke pts
No DM DM
Titrate to DBP </=85 </=80
Optimal BP <140/85 <130/80
Suboptimal BP >/=150/90 >/=140/85

70. Management of risk factors
 Hyperhomocystenemia:
 Linked to premature vascular disease
 Easily lowered with vitamin supplements

Folic acid

Pyridoxine
 Although value of lowering homocysteine
level has not been proven, younger pts
with high plasma homocysteine levels may
benefit

71. Anti platelet & anticoagulation
therapy
 Warfarin:
 Pts with AF should receive warfarin if there are no
CI – INR 2-3
 Pts with other sources of cardiac embolism also
benefit from warfarin
 Pts with mechanical prosthetic valve require INR
of 2.5-4.5
 If warfarin is not suitable asprin 300mg daily
should be given, but it’s a less effective alternative

72. Main contraindications to long
term warfarin treatment
 GI bleeding
 Active peptic ulcer
 Frequent falls
 Alcohol misuse
 History of ICH
 Age by itself is not a contraindication

73. Anti platelet & anticoagulation
therapy
 Asprin
 All other pts should receive antiplatelet Rx as first line
 Benefits of asprin conclusively proven
 ASA – initial dose of 300mg & followed by 75mg/d
 Dipyridamol
 Dipyridamole MR 200mg BD has independent and additive
effect to low dose asprin in preventing stroke, but not
coronary events or overall mortality
 So routine addition of dipyridamol may be cost effective
 Dipyridamol alone does not prevent cardiac events

74. Anti platelet & anticoagulation
therapy
 Clopidogrel:

Inhibits ADP receptors

Well tolerated and slightly more effective than
asprin

Not cost effective as 1st
line Rx

So should be used in pts with true intolerance
to asprin (allergy or intractable side effects on
low dose enteric coated asprin with or without
antiulcer drugs)

75.  There is no clear evidence for
superiority of one antiplatelet agent
over another or for combination
antiplatelet therapy in cerebrovascular
disease
 But if a patient on one antiplatelet agent
experiences a recurrent stroke then it is
better to add a second antiplatelet
agent

76. Treatment protocol

77. Carotid surgery
 Benefit from endarterctomy upto 12 months after the
event in pts with ipsilateral severe carotid stenosis
 Surgical risk
 Operative mortality in pts with severe disease -- 1%
 Risk of death or disabling stroke <4%
 Risk of death or any stroke <7.5%
 Surgical risk less in busy units
 Surgeons must quote their own risk, rather than the
trial results
 Any pt with carotid territory symptom should be
considered a potetial candidate and doppler USS
should be done, if fit for surgery
 Presence or absence of carotid bruit is irrelavent

78. Indications for carotid
endarteractomy
 Surgery indicated
 Carotid territory symp within 6/12 and
ipsilateral 70-99% stenosis
 Carotid territory symp within 12/12 &
ipsilateral 80-99% stenosis
 Surgery not indicated:
 Carotid territory symp and an ipsilateral 0-
69% stenosis
 Complete occlusion of the carotid artery

79. Carotid angiogram tight stenosis of
internal carotid

80. Before & after endarterectomy

81.  Succesful surgery is not major surgery,
so pts can leave hospital within 24hrs
 Neither clinical nor USS surveilance
prevents late stroke, so most pts are
discharged from followup after 6/52
 The operation should only be carried
out by a specialist with a proved low
complication rate (A)
Carotid surgery

82. Angioplasty
 indications:
 Fibromuscular dysplasia
 Radiation injury
 Symp stenosis after carotid endartartectomy
 advantages:
 Less hospital stay
 Less cranial N injury
 Less wound complications
 Less cardiovascular morbidity
 Dissadvantage:
 Embolic stroke at the time of surgery
 Recurrent stenosis

83. Complex cases that may
require hospital referral
case Possibel treatment
Recurrent stroke or TIA despite
antiplatelet treatment
High dose ASA, addition of
Dipyridamol substitution or addition of
clopidegrel or sub or add of warfarin
Recurrent embolic events despite
adequate warfarin
Consider adding low dose asprin
Recurrent non haemodynaemic symp
from severe carotid stenosis or
serious I/C stenosis despite antriplalet
Rx
Consider warfarin
HT or inoperable severe carotid
stenosis
Consider cerebral blood flow
monitoring before anti HT

84. Summary of management of
stroke
 Admit to stroke unit – improves survival &
dependency
 Immediate CT
 Leg stockings (CLOTS trial)
 Asprin 300mg stat and 75mg thereafter
 Avoid heparin
 Thrombolysis (Randamise)
 Relaxed about BP
 Nursing, swallowing and nutrition