Transcript 12-Stroke 2014

• Case 1 : A 56 years old man diabetic and HT ; presents to
EU with sudden onset right sided weakness and aphasia
of one hour duration .no loss consciousness , mild
headache .He is controlling sphincter
• On exam: general: un remarkable apart of irregular pulse.
BP= 160/100
• Medical : abnormal heart sound??
• Neurological : aphasic but conscious
• Cranial R. facial upper motor palsy
• No meningeal signs
• Motor : Right sever hemi paresis grade 2 in UL and grade
3 in LL
• Approach
• Emergency ----------------?? See guideline in EU
• Which system? most likely diagnosis
• Where is lesion upper or lower ? Localization.
• Ischemia or bleeding
• Anterior circulation or posterior circulation
• Causes of CVA?
STROKE
• It is third common cause of death after
cancer and IHD in developed countries, the
annual incidence of stroke above the age of
45 years in UK is about 350/100 000.
• CVA: is a clinical syndrome characterized by
acute onset *N. deficit resulting from
disturbance in cerebral circulation*.
• How we can understand CVA?
anterior, posterior & middle cerebral arteries
Circle of Willis
Stroke in young
• Stroke affecting old age ,common cause is
atherosclerosis that progressed with aging,
but if the CVA occurs under the age of 40
years you have to think about other causes
and intensive investigation needed to know
the causes:
• Accelerated atherosclerosis. HT, DM---• Embolic from cardiac origin or carotid
dissection
• Vasculitis like SLE ,APL syndrome-----• Others ,like thrombophilia ,congenital
malformation :AVM, ------and idiopathic
stroke
Pathological Classification
of cerebral vascular
accidents
1. focal cerebral ischemia
(the most often)
(thrombosis & embolism)
2. intracerebral
hemorrhage
3. Subarachnoid
hemorrhage –neurosurg.
CLASSIFICATION OF STROKE SYNDROME
• Pathological classification
1-ischemic (80-85%) . can be
large V.D :80% of cases (thrombosis &embolic) which affect medium
and large size aa .
small VD: 20% of ischemic stroke called lacunar stroke which is due
to lipohyalinotic degeneration of small penetrating aa seen mainly in
HT.
2-hemorrhagic(15-20%) which is either
hypertensive bleed due to high BP ,seen at 4 (now 5) common sites
:basal ganglia ,thalamus, cerebellum and pons. Less commonly Sub
cortical or lobar.
non HT bleed: SAH, bleeding tendency, drug therapy, traumatic and
amyloid angiopathy.
Q: How you can differentiate between H. versus I. stroke? clinically
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CLINICAL CLASSIFICATION of ischemia:
in term of duration and residue of ND
1.Transient Ischemic Attack?----it is a major risk factor for disabling stroke ,about 13 folds increase as
a risk of having stroke in next year.
2-Reversible Ischemic ND(RIND)?---3-Completed Stroke?-----
Aetiology ( acute ischemic
stroke)
A- vascular
• 1-atherosclerosis: common cause of ischemic stroke affecting extracranial aa in the neck and at the base of brain.
The pathogenesis involving injury endothelium accumulation off
cholesterol (LDLP) ------fatty streaks -----fibrous plague (lipid laden
foam cell)+ platelets -----atheromatous lesion which carry risk of
thrombus formation especially if ulcerated.
What are the factors that accelerate the atherosclerosis? Quiz?
• 2-fibromuscular dysplasia: traumatic or congenital
segmental non-atherogenic thinning of tunica media with
fragmentation of elastica lamina alternating with ring of muscle
hyperplasia within media ,female > male ,ECBV>ICBV ,ICA>VA and
usually bilateral .
• 3-inflammatory disorder:
giant cell arteritis
SLE&APL syndrome
PA nodosa
granulomatous angiitis
syphilis arteritis
AIDS-direct OR by opportunistic
infection
or endocarditis
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4-carotid or vertebral artery dissection:
can be spontaneous or traumatic-----pain in head and
neck+ND
TIA or stroke
5- lacunar stroke: pure sensory, motor ,ataxic H. ,and clumsy hand
syndrome.
6-drug abuse: cocaine and amphetamine mainly causing bleeding
(may be within hours of intake from vasospasm rupture or
vasculitis), stroke or SAH are less common .Heroin is causing
embolic stroke from endocarditis.
7-moya –moya disease:=progressive multiple IC arterial occlusion:
there is bilateral narrowing of ICA as primary (idiopathic-genetic) or
secondary as may be seen in sickle cell A or basal meningitis.
Diagnosis : typical angiographic pattern of collateral circulation
look like smoke.
8-migraine :
rare cause of ischemic stroke seen in complicated migraine with
genetic Aetiology (run in families) .also seen with use of
contraceptive pile .
9-venous sinus thrombosis: less frequently seen in comparism to A,
stroke. We think about it in special clinical setup that predispose to
cause venous occlusion. the patient is more toxic ,fever ,headache
disturb consciousness ,PD, and seizure.
The feature depending on severity and onset of occlusion and site
is very important factors. causes???? As any venous thrombosis it
is important to think about Behcet's disease in male and post
partum complication in female
B-Cardiac causes:
• Mural thrombosis; as complication of MI or cardiomyopathy.
• rheumatic heart dis. as ms .
• arrhythmias: AF ,sick sinus ,the others likely to cause pan
cerebral hypoperfusion.
• endocarditis:
• infective (bacterial or fungal) :during active stage or few
months after antibiotic cure.
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Nonbacterial (marantic): in setup of systemic malignancy
MVP:
Paradoxical emboli: ASD &PFO
atrial myxoma:
prosthetic valve :artificial one.
c.hematological disorder:
• thrombocytosis
polycythemia
• sickle C .A.
Leucocytosis
• hypercoaguable state like APL syndrome ,LA, protein S or C
deficiency.
Pathophysiology of ischemic stroke
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When there is occlusion of BV the brain tissue
supplied by that BV got ischemia. the effect
depending on severity of ischemia ,duration , and
potency and patency of collateral circulation.
As a result ,the patient may develop on of the
following:
no symptom
TIA: the flow is return before cellular death
stroke :the flow is not returned in which there will
be area of dead tissue(<50ml/100gm BT) which is
surrounded by an area of ischemia (viable but not
functioning) called ischemic penumbra.
Our aim in approaching any case of stroke is to
save or to make IP area viable and functioning by
keeping balanced homeostasis (Bp, B.sugar and
good oxygenation).
Histo: Cascade of cellular changes in ischemia:
there is ATPase pump failure------influx of sodium
and water------cytotoxic edema and release of
excitatory aa mainly glutamate---further ca +2
influx----more damage.
The process fatherly worsened by anaerobic
production of lactic A and fall in tissue PH
.restoration of BF may cause hemorrhage in
ischemic area (hemorrhagic
transformation)
especially in embolic stroke.
Pathophysiology of Intracerebral bleeding
The damage here depending upon bleeding severity ,as the neurons
structurally disrupted and WM fibers are splits apart (pushed) .the big
hematoma can cause sever increase in ICP and conning.
RISK FACTORS FOR ISCHEMIC
STROKES ? How to prevent stroke
• UNMODIFIABLE
• MODIFIABLE
Avoid And Stop
Promote and encourage
Weight loss
Smoking
exercise
Contraceptive Pill
Life style modification
Alcohol Intake
Early diagnosis and treatment
hypertension
hyperlipedemia
hyperglycemia
• Is it stroke? Sudden onset ND ?If it is ,Answer: is it---?
• *Hemorrhagic? is it HT bleed or non HT?
----- high BP, meningeal S, sever H., and altered consciousness
• *Ischemic? which clinical type ie :TIA ,RIND--------etc? large or
small VD (lacunars) ?is it anterior or post circulation? How?
• drop attack ,crossed hemiparesis, dysartheria, vertigo, ataxia,
diplopia ,dysphagia, cranial nerve palsy and altered conscious
goes with posterior .
• cortical sensory loss ,aphasia goes with anterior C. : is this
absolute?
• We have to ask is it thrombotic or embolic? how?
If onset is stepwise over minutes or hours, preceded by TIA is go
with thrombosis.
If it is sudden with max. deficit at the onset ,not preceded by TIA ,
presence of cardiac lesion and hemorrhagic transformation in
CT scan are consistent with embolic.
• Seizure? seen in 10-25% ,more with embolic , cortical lesion
and permanent ND (up to 50%).
• Headache? seen more with bleeding and in 15-25% of I. stroke
Clinico-anatomic correlation to decide which V is involved
anterior, posterior & middle cerebral arteries
Clinico-anatomic correlation to decide which V is involved
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ANTERIOR CIRCULATION
1.ACA :
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Uncommon?
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Contralateral hemiparesis affecting LL>UL with sensory defect
affecting LL +affection of sphincter control resulting from loss of
inhibitory control on bladder reflex.
2.MCA:
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Main stem: contralateral hemiplegia (dense) +global aphasia if
dominant H. is affected
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Deep lenticulostriate a: contralateral dense sensory-motor H. with
or with out capsular aphasia AND transcortical aphasia (repetition
intact) if D. H is affected.
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superior division: contralateral weakness affecting face ,arm (UL)
&hand sparing leg, no VF defect, motor or expressive aphasia if
dominant H. affected.
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Inferior division:
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-Weakness less prominent.
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-VF defect contralateral ,sensory dysfunction include marked
cortical sensory dysfunction (look to 2nd lecture)
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-spatial thought disorder---lack of awareness that deficit is exist
(anisoagnosia) , neglect or and failure to recognize contralateral
limb
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-in D.H affection----sensory aphasia & Gersmann syndrome
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((agraphia ---acalculia----left right disorient.----finger agnosia)
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-non-D H affection----dressing apraxia, constructional apraxia and
3.ICA occlusion:20% of cases.
-may be asymptomatic
-ophthalmic a: range from Amurosis fugax (TIA) to
permanent V. loss due to affection of retinal a. and
ciliary a. (AION).
-features of MCA&ACA occlusion
*trans-cortical: motor or sensory or global
*subcortical aphasias ( left thalamic and putamen)
POSTERIOR CIRCULATION
1. PCA: depending on site of occlusion
• Distal part------cortical dysfunction-----contra lateral
H. H more dense superiorly
• More proximal-----will affect subthalamus ,thalamus,
midbrain and cranial nerves.
• Clinical feature: vertical gaze palsy,3rd nerve palsy,
inter N. ophthalmoplegia and vertical skew
deviation of eye .Distal part features can be seen
also.
• Dominant H .--------anomic aphasia, alexia without
agraphia, and V. agnosia =inability to identify object
in seen in L side of V. field caused by lesion
affecting corpus callosum which connect the R. V.
cortex from language area in dominant H.
• bilateral ----Balint’s syndrome (bilateral parietaloccipital lesion)+ memory disturbance+ inability to
recognize familiar faces (prospagoagnosia)+ variety
of exotic V. and behavioral changes.
• *visual inattention +optic ataxia =neither H. can
represent location or spatially guided movement.
(failure to send impulse to frontal area)
• Balint's syndrome ?due to bilateral parietal-occipital
infarction ,the pt. not moving the eyes voluntarily but
reflexly (reflex EM).=psychic paralysis of gaze, the
patient appear to have ataxia in reaching an object
(optic ataxia) ,he is looking to detailed aspect of
picture without looking for it’s meaning of picture
(asimultagnosia)
• Anton’s syndrome ?bilateral O . infarction -----cortical blindness with denial
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Basilar artery? Serious ?either thrombosis or embolic
Variety of clinical syndrome, some are incompatible with life ,can
produce bilateral N. involvement with coma or disturbance of cons.
Occlusion of both vertebral aa or lone congenital vertebral a can
produce same CF.
*stenosis or occlusion of subclavian a. before it has given rise to VA
Lead to subclavian steal syndrome? As the blood passes from VA into
distal subclavian a. with physical exercise of ipsilateral limb .
Is it predictive of stroke in VB distribution? Pt usually asymptomatic .
• 1-basilar thrombotic occlusion;
• -it affect proximal portion which supply the pons (tegmentum)
produces
• unilateral or bilateral 6th nerve palsy & ataxia
• horizontal gaze palsy
• pupil is constricted ?
• vertical N. and ocular bobbing.
• Some time the infarction affecting basis pontis with sparing of
tegmentum ,end result is locked in syndrome (pt is cons.,
tetraplegic, only moves eye vertically to command& EEG is
normal to differentiate it from persistent vegetative state due
diffuse cortical damage due any cause like diffuse cortical anoxia
or ischemia ) =Hemiplegia or quadriplegia usually present with
disturbed cons. May be coma ,which should differentiated from
pontine bleed in which the patient is comatose ,hyperthermic
with pinpoint pupil but reacting to light ,diagnosis by CT scan.
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2-Basilar a. embolism? affecting distal seg. rarely proximal seg.
The origin of emboli either BA or VA. ascend up to be arrested at
bifurcation of 2 PCA. Leading to:
--immediate loss of cons. (thalami and RAS)
--unilateral or bilateral 3rd nerve palsy (midbrain) &ataxia
--hemiplegia or quadriplegia (cerebral p.)
--features of one or both occipital lobe dysfunction? emboli may
dislodge and ascend up to occlude one or both PCA .
posterior inferior cerebellar a.? pica syndrome (Wallenberg’s) due to
atheromatous lesion thrombosis, less likely embolic of pica or VA.
ipsilaterally :ataxia, diplopia vertigo and nystagmus, Horner’s
syndrome, deafness, facial sensory loss,dysphagia ,and hoarseness
of voice, loss of taste.
controlateral there is sensory loss in UL &LL. (crossed sensory loss)
Balint’s Syndrome ?due to bilateral parietal-occipital infarction ,the pt.
not moving the eyes voluntarily but reflexly (reflex EM).=psychic
paralysis of gaze, the patient appear to have ataxia in reaching an
object (optic ataxia) ,he is looking to detailed aspect of picture without
looking for it’s meaning of picture (asimultagnosia)
Anton’s syndrome ?bilateral O . infarction ------cortical blindness with
denial.
Alexia without agraphia
Visual agnosia
• lacunar infarction?20%?cause?CF?
What are the important points you have to look in
physical examination?
• General examination: look for the signs which are suggestive of
underlying systemic disorder especially treatable one ex;
polycythemia.
• BP---HT is well risk factor for stroke
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---comparism of BP and pulse on 2 sides?
• Examination of the neck?
• Careful cardiac examination?
• Palpation of temporal A?
• Neurological examination: may be Normal as in TIA
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N. deficit : you have to define anatomic site involved that may suggest
the cause, if it is in ant. Circulation :angiographic evaluation may
suggest surgically correctable cause, while in post. Circulation
different action is taken. LOOK FOR
– cognitive function assessment: is of significant in ACA disease
specially in cortical lesion, speech is affected also.
-Ophthalmoscope examination; - retina may provide a hint to an embolic
phenomenon in RA
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-Optic disc for PD
v. field defect
ocular palsies, nystagmus, and INO ----in posterior circulation.
Hemiparesis
sensory defect including cortical one.
cerebellar signs.
Investigations
a-to confirm diagnosis
b-to evaluate for the cause
c-general assess.
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CT scan
MRI specially for posterior circulation ischemia.
Conventional angiography (DSA ) when it is needed.
Ultrasonography: Doppler US .
cardiac assessment?
Lumbar puncture
Blood tests CBP&,ESR and screen for vasculitis in young
* biochemical assessment----*lipid profile-----*serology specially in stroke in young.
Management of acute stroke in EU?
• Ensure ABCDE (vital signs, oxygen saturation, urine output)
• Keep the patients in 30 degree position unless the patient had
feature of impending herniation
• IV line ----draw blood for blood sugar , urea and creatinine ,
HB.
• ECG for any cardiac problem specially ischemia
• History: onset in minutes and progression
• If thrombolytic therapy is available ---send for all blood profile
• Control high blood pressure (only if MAP> 120 mm Hg) and
sugar before sending patient to CT scan
• Control fit if present with 10 mg diazepam over 5min infusion
,can be repeated if fit persistent with monitoring RR
• Send for CT brain to confirm diagnosis.
• No mannitol or dexamethason should be given in 1st 3 days
• Subsequent treatment: depending on type of stroke-physician
decision.
• General measure:
• Nursing measures –should be initiated with particular emphasis
on reducing the risk of complication resulting from immobility
such as pneumonia ,DVT, and UTI
• Early physical, occupational and speech therapy.
• Early assessment of swallowing ability reduce morbidity.
• Prevention and treatment of hyperthermia.
• Early observation of post stroke depression.
• Primary stroke prevention
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Identification & reduction of stroke risk factors are crucial to
decrease the incidence of stroke ,including treatment of DM ,HT
,cardiac disease and Hyperlipedemia also stop smoking
,contraceptive pill ……….etc
• Rehabilitation
• The main cause of death among stroke patient are related to
medical complication (MI, pneumonia ,sepsis and P. embolism
• R. program should be started from the onset of stroke.
• management of cerebral edema? Only in cases of big
cerebral ischemia there is edema enough to cause brain shift
an d herniation that necessitate incubation and
hyperventilation produce transient c. vasoconstriction and may
reduce ICP. Manitol infusion acts by reducing the volume of
surrounding unaffected brain but it’s effect is also transient.
corticosteroid is of no help in cytotoxic edema.
• Hypertensive encephalopathy
• It is diffuse cerebral effect of sever hypertension that are
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not caused by ischemia or bleed and it is potentially reversible
upon controlling of BP.
Patient presented with H. ,visual blurring , confusion and
drowsiness. seizure may develop.
On exam.: the BP is very high (240/150) with papilledema and
retinal bleed on fundoscopic examination.
CT &MRI is often revealed diffuse C. edema with predilection to
occipital lobe.
Treatment : is a medical emergency ,you have to reduce BP
urgently but smoothly to avoid hypotension by using sodium
nitroprusside.
This condition clinically and pathophysiologically is similar to
eclmapsia.
Specific medical therapy
• Thrombolytic Therapy.
• Use of anticoagulation: heparin or nadroparin
(enoxiparin)
and warfarin.
• INDICATION-although AP therapy remains the treatment of
choice to prevent recurrent thrombo-embolism in majority of
patient with stroke the AC is indicated in cases of stroke in set
up of AF, cardiac ischemia ,progressing or stroke in
evolution (propagated thrombus).
• To use AC you need :CT scan to exclude IC bleed or SAH ,
baseline PT ,PTT &platelet count .Screening for
hypercoaguable state may indicted in some cases.
• ow we predict progression at onset and pt. may have TIA?
Difficult
• history of active PU or uncontrolled HT (systolic BP>200)
preclude use of AC in stroke, unless the benefit out weight the
risks.
• Atrial fibrillation& cardiac disease
• In setting of valvular heart disease(17 fold
risk/year) -------AC with warfarin to INR
reaching 2-3
• In setting of non valvular AF with no other
risk factors-----ASA 325mg/day is effective
• Patient with prosthetic valve -----long term
AC is important.
• Patient with bacterial endocarditis-----AC
should be avoided
TIA:
-may indicate an impending stroke, so the treatment should include:
Prophylactic therapy with antiplatelet like aspirin, ticlopedine or
clopidogrel has been shown to prevent secondary events.
Patient with evidence of thrombo-embolism(*cardiac or carotid) or *VB
ischemia
*patient with V-B ischemia clinically-------MRI
No VB stenosis------ASA
VB stenosis-----angiography---- stenosis confirmed-----AC (INR=3)
*pt. with cardiac thrombo-embolic---do TEE-----thrombus-------AC (INR 3)
NO thrombus---holter monitor for underlying episodic arrhythmia (AF)
in this case give AC otherwise ASA or AP is quite enough
*carotid stenosis:
asymptomatic stenosis <60%-----ASA
>70 % with or without*symptom of ischemia in that vascular
distribution---c. endarterectomy is indicated
60-70% stenosis (moderate) asymptomatic-----medical versus surgery
decided on individual case-by-case basis even If it is symptomatic?
Decision of surgery vs. medical therapy in C stenosis is not easy
?operative risk (medical condition, surgical morbidity and mortality,
personal experience, &degree of stenosis) should weight against risk
of future stroke. operative risk should be less than 6%.
Identification & reduction of stroke risk factors are crucial to decrease the
incidence---------etc
PROBLEMS WITH TRANSLATING NEUROPROTECTION TO
THE CLINIC: THERAPEUTIC WINDOW
THE LONDON HELICOPTER
EMERGENCY MEDICAL SERVICE
(HEMS)
HEMS can reach anywhere inside the
M25 motorway within 15 minutes
– Thrombolytic therapy
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-patient presented within 3 hours of ischemic stroke should be
evaluated for iv recombinant tissue plasminogen activators(rt-PA)?
Clinical Evaluations: to use it there should be NO----surgery <14 d
-stroke or head trauma in
90 days
-H/O cerebral bleeding
-BP > 185/110 (should be below
175/100 )
-Rapidly improvement
-hemorrhage <12 d
-seizure at onset
-AC within 48 hr
lab . evaluations : no treatment if there is ----sever anemia
-platelet count<100000/cu.mm
-PT >15 sec.
–glucose<50 or >400 mg/dl
radiological evaluation: no treatment if
*CT-scan is positive for blood or non-stroke disease.
Strategies for it’s use ----you have to explain to the patient or family
that there is 6% risk of symptomatic IC bleeding and 50% chance of
little or no disability compared to 38% chance without rt-PA.
-careful monitoring of BP and blood sugar
-no aspirin or AC use 24 hours after rt-PA administration.
-we give 0.9 mg/kg , max:90 mg
the results is promising ,but the use of intra-arterial thrombolytic
therapy is under investigation( reteplase- - - ),or use it with
neuroprotective agent (glutamate antagonist) may prolong therapeutic
window >3 hr, or use it with aspirin or other new platelet glycoprotein
11b/111a antagonist is under evaluation .
Antiplatelet:
• Aspirin: is act through irreversible inhibition of cyclooxygenase enzyme ----inhibition of thromboxane A2 (a platelet
aggregating and PG vasoconstriction properties).
• Ticlopedine: block ADP receptor on P. preventing cascade
activation of GP11b/111a complex on P. (clopidogrel have same
effect) that lead to binding of fibrinogen to P. .It is given in dose
of 25o twice .low incidence reversible neutropnia (BM
suppression) should be followed, skin rash and diarrhea.
• Is it more effective than aspirin? when indicated.
• Dipyridamole: P. phosphodiesterase inhibition which inhibit
breakdown of cAMP which inhibits P. aggregation .
• Clopidogrel: 75 mg daily ,proved to be effective in some studies
especially if combined with aspirin in patient at high risk of
CVS events ,but risk of bleeding is high. It should be stopped
few days before surgery.
• Abciximb: monoclonal antibody to block GP111b/111a
receptors complex activation .
Neurotropic drugs : neuroaids ,citicholine
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Surgical treatment: ?
• SAH? Angio---------------surgery as early as possible
• ICH???????????
• CEREBELLAR H.?
Case 1 :
• 56 years old man diabetic and HT ; presents with right
sided weakness and aphasia of one hour duration .no loss
consciousness , mild headache .he is controlling sphincter
• On exam: general: un remarkable apart of irregular pulse.
BP= 160/100
• Medical : abnormal heart sound??
• Neurological : aphasic but conscious
• Cranial R. facial upper motor palsy
• No meningeal signs
• Motor : right sever hemi paresis grade 2 in UL and grade 3
in LL
• Approach
• Emergency ----------------??
• WHICH SYSTEM? MOST LIKELY diagnosis
• Where is lesion upper or lower ? Where about.
• Ischemia or bleeding
• Anterior circulation or posterior circulation
• Causes of CVA?