cerebrovascular diseases (2)

8/3/2019 Cerebrovascular Diseases (2)

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CEREBROVASCULAR

DISEASES

FADARE B.AMBChB


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OUTLINE

INTRODUCTION

EPIDEMIOLOGY

RISK FACTORS

PATHOGENESIS CLINICAL FEATURES

MANAGEMENT

COMPLICATIONS

DIFFERENTIAL DIAGNOSIS PROGNOSIS

CONCLUSION


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Cerebrovascular disease is

defined as a sudden onset of a

neurologic deficit that is

attributable to a focal vascular

cause.


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CVD could be:

Stroke: sudden focal neurologicdeficit of vascular origin that lasts

more than 24hrs or results in thedeath of the patient.

Transient IschemicAttack(TIA):


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Current thinking

Any neurologic deficit >1hr is not likelyto be TIA

Any demonstrable cerebral infarction,irrespective of the time=stroke=brainattack

RIND= CITS(Cerebral Infarction with

Transient Symptoms) CIND=Cerebral Infarction with No

Deficit)


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EPIDEMIOLOGY

3RD leading cause of death in the westerncountries & is the most common cause of severephysical disability

Annual incidence of 180-300 per 100 000 3RD commonest neurological condition in Nigeria .

6-41% of neurological admission.

4-10% of hospital mortality in Nigeria. An important cause of mortality and morbidity

affecting the patient, family, & society.


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CLINICAL CLASSIFICATION

TIA

STROKE

PROGRESSING STROKE OR STROKE INEVOLUTION

COMPLETED STROKE


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CLASSIFICATION

Ischemic

Thrombotic

Embolic

Hemorrhagic

Intracranial hemorrhage

SAH


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RISK FACTORS

NON-MODIFIABLE

Increasing age

Male gender & PM womenBlack race

+ve Family hx

Past hx of TIA or strokeGenetics: deletion polymorphism of ACE

gene


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RISK FACTORS

MODIFIABLEUndiagnosed Hypertension Obesity

Diabetes sedentary lifestyle

Hrt dx [MI,IE,VHD,CMTy,CHD,AF] dyslipidemiaHemoglobinopathy protein C&S def

Smoking thrombocytopenia

Heavy alcohol homocystinuria

OCPPolycythemia

Infections eg HIV


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Common causes of ischemic stroke

Thrombosis:small vessel(lacunar), largevessel

Embolic occlusion:Artery-to-artery(Carotid

bifurcation,Aortic arch,Arterialdissection);Cardioembolic(Atrialfibrillation,Mural thrombus,MI,DCM,ValvularlesionS(MS,Mechanical valve,Bacterial

endocarditis) Paradoxical embolus(ASD,Patent foramen

ovale,Atrial septal aneurysm)


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CAUSES OF HEMORRHAGIC CVD

Charcot-Bouchard microaneurysms

Amyloid angiopathy

Impaired bld clotting(anticoagulant tx,bld dyscrasias, thrombolytic tx)

Vascular anomaly( AV malformatn,carvernous hemangioma)

Substance abuse(cocaine,amphetamines, alcohol)


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PATHOGENESIS

A fall in cerebral blood flow to zerocauses death of brain tissue within 4 to

10 min; values 16 to 18 mL/100 g tissueper min cause infarction within an hour;and values 20 mL/100 g tissue per mincause ischemia without infarction

unless prolonged for several hours ordays.


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PENUMBRA: an area of ischemic tissue

surrounding the core region of infarction that is

reversibly dysfunctional.

UMBRA: ischemic AND infarcted area

Cellular death occurs via two distinct pathways:

Necrotic pathway

Apoptotic pathway

Depolarization and glutamate release lead to the

intracellular influx of calcium


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Worsens infarction: fever and

hyperglycemia(bld

glucose>11.1mmol/L)

Neuroprotective: hypothermia; drugs

that block the excitatory amino acid

pathways


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CLINICAL FEATURES

Neurological deficit: hx, examinatn

Anosognosia:loss of appreciation thatsomething is wrong

Cerebral lesions: unilateral motor deficit, highercerebral fxn deficit, visual field defect.

Brain stem or cerebellar lesions:ataxia,diplopia,vertigo &/orbilateral weakness.

Reduced conscious level: large volume lesion incerebral hemisphere, brain stem lesion orcomplications.


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GENERAL EXAMINATION OF STROKE

PATIENTS

Skin: xanthelasma, rashes, limb ischemia

Eyes: HTN, DM, retinal emboli, arcus senilis

CVS: irregular pulse, BP, JVP, murmurs. Respiratory: pulmonary edema, respiratory

infections

Abdomen: urinary retentn locomotor


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Ischemic stroke features

Thrombotic : usually occurs on

waking up in the morning or while

the px is resting with a gradualworsening of symptoms(stroke in

evolution). Px may be completely

paralyzed by the evening.


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Ischemic stroke ctd

Embolic stroke

Sudden onset

Deficit complete at onset


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Hemorrhagic stroke features

Occurs at the peak of activity

Sever h/ache

Vomiting

Assotd with high BP

Neck stiffness in SAH

Maximal deficit at onset


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WORLD HEALTH CRITERIA

Level of activity

Headache

Vomiting

LOC

Level of BP

Blood in the CSF


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SIRIRAJ CRITERIA

2.5(LOC)+2(h/ache)+2(vomiting)+0.5(DBP)-3(atheroma marker)-12

Atheroma markers: DM, angina, intermittent

claudication LOC:0=fully conscious

1=drowsy or stuporous

2=comatose

h/ache or vommiting0=absent

1=present


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Siriraj criteria

>/=1 : hemorrhagic stroke


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Transient ischemic attack(TIA)

Symptoms


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STROKE SYNDROMES


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STROKE SYNDROMES

Middle cerebral aa strokeHemiparesis

Hemi-anaesthesia

Homonymous hemianopia

7th&12th NN involvement: ipsilateralUMNL

Dysphasia/aphasia in dominant lobeaffectation

Dysarthria:CN 7,9,9,10,cerebellum


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Middle cerebral aa ctd

Gerstmann syndrome(non-dominanthemisphere affectation):

Acalculia

Alexia

Right leg disorientation

Finger agnosia

hemineglect


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Partial syndromes of MCA stroke

hand, or arm and hand, weakness alone(brachial syndrome)

facial weakness with nonfluent (Broca) aphasia

without arm weakness (frontal opercularsyndrome).

A combination of sensory disturbance, motorweakness, and nonfluent aphasia suggests thatan embolus has occluded the proximal superiordivision and infarcted large portions of thefrontal and parietal cortices.


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fluent (Wernickes) aphasia withoutweakness, the inferior division of theMCA supplying the posterior part

(temporal cortex) of the dominanthemisphere is probably involved.

Hemineglect or spatial agnosia without

weakness indicates that the inferiordivision of the MCA in the nondominanthemisphere is involve.


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LACUNAR INFARCTION

Occlusion of a lenticulostriate vessel

produces small-vessel (lacunar)

stroke within the internal capsuleproducing pure motor stroke or

sensory-motor stroke contralateral

to the lesion.


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MANIFESTATIONS OF LACUNAR

INFARCTS Pure motor hemiparesis from an infarct in the posterior

limb of the internal capsule or basis pontis

pure sensory stroke from an infarct in the ventrolateralthalamus

ataxic hemiparesis from an infarct in the base of the pons a clumsy hand or arm due to infarction in the base of the

pons or in the genu of the internal capsule

pure motor hemiparesis with motor (Brocas) aphasia parkinsonism and hemiballismus :affectation ofglobus pallidus

and putamen


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ACA STROKE SYNDROME

Weakness worse in LL

Spincteric abnormalty

Frontal lobe syndromePersonality changes

Intellectual impairmt

Disinhibition

Reappearance of primitive reflexes

ACA STROKE SPARES THE FACE


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Brain stem infarction

Hemiparesis or tetraparesis

Sensory loss

Diplopia

Facial numbness Facial weakness

Nystagmus, vertigo

Dysphagia, dysarthria

Dysarthria, ataxia, hiccups,vomiting

Horner's syndrome

Altered consciousness


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PCA STROKE

The lateral medullary syndrome, also called

posteriorinferior cerebellar artery (PICA)

thrombosis,or Wallenberg's syndrome, is a

common example of brainstem infarction

presenting as acute vertigo with cerebellar

and other signs:


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Weber's syndrome: This is ipsilateral

third nerve paralysis with contralateral

hemiplegia due to an infarct in one sideof the midbrain. Paralysis of upward

gaze may be present

Claude syndrome: ipsilat 3rd nn palsyand contralat ataxia


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INVESTIGATIONS

Neuroimaging : CT, MRI

Carotid doppler US

4-vessel angiography Others

ECG, echo,

FBC, ESR

Urinalysis, FBS

FLP


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MANAGEMENT

Medical emergency

Multidisciplinary

Principles

Prevent or manage complications

Tx stroke primarily

Prevent repeat stroke


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Prevent or manage complications

ABC of resuscitation

Reduce cerebral dema

30 head tilt

Hyperventilation Mannitol: 250-500ml of 20%mannitol, 1-2g/kg

Add lasix

Phenytoin/phenobarb

Hypothermia

Others:urea,glycerol,shunting of csf

hemicraniectomy


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IV N/S 1L 8hrly

Antihypertensives:indications for

antiHTNsives in acute stroke Vit C 100mg TDS, vit E 300mg/day

Physiotx

Speech tx nutritn


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Tx stroke primarily

THROMBOLYSIS :- Intravenous rtPA

[0.9mg/kg to a 90mg max] 10% as a

bolus, then the remainder over 60mins within 3hrs of onset of ischemic

stroke.


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Eligibility criteria for thrombolysis

Eligibility

Age > 18 years

Clinical diagnosis of acute ischaemic stroke Assessedby experienced team

Measurable neurological deficit

Timing of symptom onset well established

CT or MRI and blood test results available

CT or MRI consistent with diagnosis

Treatment could begin within 180 minutes ofsymptom onset


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Exclusion criteria

Symptoms minor or improving rapidly

Haemorrhage on pretreatment CT or MRI

Suspected subarachnoid haemorrhage

Active bleeding from any site

Gastrointestinal or urinary tract haemorrhage in last 21days

Platelet count < 100 x 109/litre

Recent treatment with heparin and activated partial

thromboplastin time above normal Recent treatment with warfarin and INR elevated

Major surgery or trauma in last 14 days

Recent postmyocardial infarction pericarditis


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Neurosurgery,serious head trauma or stroke in last 3

months

History of intracranial haemorrhage (any time)

Known arteriovenous malformation or aneurysm

Recent arterial puncture at non-compressible site

Recent lumbar puncture Blood pressure consistently

> 185 systolic or> 110 diastolic Abnormal blood glucose (< 3 mmol/litre or > 20

mmol/litre)

Suspected or known pregnancy Active pancreatitis

Epileptic,seizure at stroke onset


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ANTIPLATELETAGENT:-Its been foundthat the use of aspirin within 48hrs

of stroke onset reduce both strokerecurrence risk & mortalityminimally.

Clopidogrel,dipyridamole, ticlopidine


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Prevent repeat stroke

Tx all modifiable factors


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DIFFERENTIALS

Cerebral abscess Encephalitis

Cerebral tumors Hypoglycemia

Subdural hematoma Demyelination

SAH Migrainous aura

Todds paralysis Focal seizures

Conversion disorder


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prognosis

About 1/5th of pxs will die within a

month of the event and at least half

of those who survive will be left withphysical disability.


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Conclusion

cerebrovascular diseases (2)

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