Your Federal Quarterly Tax Payments are due April 15th Get Help Now >>




        By Ajala Abayomi M.
 Introduction
 Burden of CVD
 Classification
 Risk factors
 Pathophysiology
 Making a diagnosis
 Other investigations
 Treatment
 Prevention
 Prognosis
 Conclusion
 To the public stroke means weakness on
  one side, often with loss of speech.
 Hippocrates referred to this phenomenon
  of sudden paralysis as ‘Apoplexy’- meaning
  struck by violence.
 Other cultures see it as a way of dying,
  spiritual attacks, witch theory / step-mum
  theory, offended the gods /godesses.
 Stroke is defined as the clinical
  syndrome of rapid onset of cerebral
  deficit (usually focal) lasting more than 24
  hours or leading to death, with no
  apparent cause other than a vascular one.
 Transient ischemic attack (TIA). This
  means a focal deficit, such as a weak limb,
  aphasia or loss of vision lasting from a few
  seconds to 24 hours.
 In TIA there is complete recovery & the
  attack is usually sudden.
 Completed stroke means the deficit
  has become maximal, usually within 6
 Stroke-in-evolution describes
  progression during the first 24 hours.
 Minor stroke-Patients recover without
  significant deficit, usually within a week.
 Reversible Ischemic Neurological
  Deficit (RIND) a focal brain ischemia in
  which the deficit improves over a
  maximum of 72 hours deficits may not
  completely resolve in all cases
Burden of CVD
 Stroke is a common neurological problem
 15 million cases yearly (2/3rd developing
 5.5 million deaths yearly;
 Approximately 50% of survivors have a
  residual neurologic deficit and greater than
  25% require chronic care.
 The incidence of cerebrovascular diseases
  increases with age, and the number of stroke
  cases is projected to increase as the elderly
  population grows, with a doubling in stroke
  deaths in the United States by 2030.
 A major cause of mortality-
  1/3rd die, 1/3rd recover, 1/3rd remain
 1/3rd of all stroke cases are misdiagnosed.
 There is a male preponderance (3:1)
 Frequency in hospital populations- 0.9-4%
  of admissions and 0.5-45% of neurological
 The major risk factors in Nigeria are
  hypertension, diabetes and
   Based on Aetiology
    (1) Ischemic (2) Hemorrhagic
    Ischemic can be Thrombotic or Embolic
    Hemorrhagic can be Subarachnoid or
    Intracerebral hemorrhages

   Based on site of affectation
    ◦ Anterior Cerebral Artery syndrome
    ◦ Middle Cerebral Artery syndrome
    ◦ Posterior Cerebral Artery syndrome
                          Acute Stroke

      Ischemic (80%)             Hemorrhagic (20%)

Thrombotic                                       Subarachnoid H.
                                     Intracerebral & Cerebellar H
                 Embolic (30%)
Lacunar (20%)                    Subdural & Extradural
Large vessel (30%)               H. and Hematoma

   Artery-artery        Cardioembolic
                                  AF, IHD,VHD,
Risk factors/aetiology of CVD
    Modifiable risk factors
     ◦ Hypertension
     ◦ Diabetes Mellitus
     ◦ Hyperlipidaemia
     ◦ Cardiogenic causes-
      Atrial fibrillation, Mural thrombus, Myocardial
      infarction, Dilated cardiomyopathy, Valvular lesions
      like-Mitral stenosis, Mechanical valve, Bacterial
      endocarditis, Paradoxical embolus- Atrial septal defect,
      Patent foramen ovale, Atrial septal aneurysm
◦ Hematologic causes
 Sickle cell anemia, B thalassemia, polycythemia vera,
 protein C and S deficiency, antithrombin III deficiency,
 DIC,Thrombotic thrombocytopenic purpura

◦ Vasculitis
 PAN, Wegner’s, Takayasu, Giant cell arteritis

◦ Drugs
 Cocaine, Amphetamine, Phenylpropanolamine,

◦ Metastatic brain tumor
 Choriocarcinoma, melanoma, renal cell carcinoma, thyroid
 Ca, atrial myxoma
      Alcohol, Cigarette, Aneurysms, Obesity, OCP’s, Physical
      inactivity, Low socioeconomic status, Moyamoya dx

      CADASIL (Cerebral Autosomal Dominant Arteriopathy
      with Subcortical Infarcts and Leukoencephalopathy) is an
      inherited disorder that presents as small-vessel strokes,
      progressive dementia, and extensive symmetric white
      matter changes visualized by MRI.
   Non modifiable risk factors
    ◦ Age (> 55 for males, > 65 for females)
    ◦ Sex (Male sex, postmenopausal female)
    ◦ Family history (Of stroke or previous history of
    ◦ Ethnicity/Race- black race, , stroke belt in US
                For Ischemic CVD
    Acute occlusion of an intracranial vessel causes
     reduction in blood flow to the brain region it
    Atherosclerosis and subsequent plaque formation,
     thrombus formation, platelet aggregation,
     hypercoagulable states, cardiac emboli from
     thrombotic centers on atrial or ventricular wall or
     valves, they all cause narrowing of blood vessels.
    The magnitude of flow reduction is a function of
     collateral blood flow and this depends on individual
     vascular anatomy and the site of occlusion.
 CBF of <10ml/100g/min leads to infarction.
  CBF of 10-20ml/100g/min will cause
  ischemia and not infarction unless
  prolonged for hours or days.
  CBF of >20ml/100g/min will not cause any
  significant damage.
 If blood flow is restored prior to a
  significant amount of cell death, the patient
  may experience only transient symptoms i.e.
  a TIA.
  For Hemorrhagic CVD
            Intracerebral Hemorrhages
 Hypertension, trauma, and cerebral amyloid
  angiopathy cause the majority of these
 Chronic hypertension produces a small vessel
  vasculopathy characterized by lipohyalinosis,
  fibrinoid necrosis, and development of
  Charcot-Bouchard aneurysms
 Rupture of microaneurysms (Charcot-
  Bouchard aneurysms, 0.8-1.0 mm diameter)
  and degeneration of small deep penetrating
  arteries are the principal pathology.
 Basal ganglia, pons, cerebellum and subcortical
  white matter usually affected
  Subarachnoid Hemorrhages
 Excluding head trauma, the most common
  cause of SAH is rupture of a saccular
  (berry) aneurysm. Others, AVM, vasculitis
 About 2% of adults harbor intracranial
 Hypertension, OCP’s, cigarette smoking,
  alcohol etc leads to rupture.
 On rupture, there is cerebral tissue death
  either by the mass effect of the
  hemorrhage or direct Cytotoxic effect of
 Complications of SAH can cause death
  faster – rebleeding, seizures, vasospasm,
Making a diagnosis
 Clinical presentation
 Is it a stroke or a TIA
 What part of the brain or hemisphere is
 Is it Ischemic or Hemorrhagic
 What Vessel in the brain is affected
 Physical examination and neuro exam
 If not stroke what else can it be
    Clinical Presentation
 Weakness of one side of the body or total
  paralysis (Hemiparesis or Hemiplegia)
 Speech abnormality (Motor or sensory
  aphasia, dysarthria)
 Visual impairment
 Severe headache( Worst Headache of my life) &
 Loss of consciousness
         Is it a TIA or a Stroke
 The patient experiences a temporary focal
  neurological deficit such as slurred speech,
  aphasia, amaurosis fugax ( sudden
  monocular blindness), or weakness or paralysis
  of a limb.
 Onset is rapid; usually onset is less than 5
  minutes duration usually 2-15 minutes;
  can last up to 24 hours
 Consciousness is usually preserved in TIA.
 Symptoms (vary depending on the CNS
  anatomy involved)
   Sensation of swelling or numbness of the
    hand, arm, or one side of the face or tongue
    (Hemisensory loss)
   Loss of strength in an arm, hand or leg
   Hemianopic visual loss
   Difficulties in speaking or reading (aphasia)
   No neurological deficit remains after
    the attack
   One episode in a lifetime to > 20 in one day
   May be the only warning of an impending
      Part of the brain affected
       Left (Dominant) Hemisphere Stroke:
                  Common Pattern
 Aphasia
 Right Hemiparesis
 Right-sided sensory loss
 Right visual field defect
 Poor right conjugate gaze
 Dysarthria
 Difficulty reading, writing, or calculating
 Right (Non-dominant) Hemisphere Stroke:
               Common Pattern
 Defect of left visual field
 Extinction of left-sided stimuli
 Left Hemiparesis
 Left-sided sensory loss
 Poor left conjugate gaze
 Dysarthria
 Spatial disorientation
    Brain Stem Stroke: Common Pattern

 Hemiparesis or tetraparesis
 Sensory loss
 Diplopia
 Facial numbness
 Facial weakness (lower motor neurone)
 Nystagmus, vertigo
 Dysphagia, Dysarthria
 Ataxia, hiccups, vomiting
 Horner's syndrome
 Altered consciousness
 Crossed signs
Hemorrhagic or Ischemic
                Ischemic    Hemorrhagic
    Loss of        -ve         +ve
  Headache        -ve            +ve
   Vomiting       -ve            +ve
 Previous TIA     +ve             -ve
Gradual Onset     +ve      -ve (Sudden and
   Activity        -ve           +ve
    HBP         -ve/mild   Moderate/ Severe
 Bloody CSF       -ve            +ve
Siriraj stroke score
  +2 x ( headache +ve = 1, -ve = 0)
  +2 x (vomiting +ve = 1, -ve = 0)
  +2.5 x (coma; semicoma =2;
     stupor; drowsy = 1; alert = 0)
  + DBP x 0.1
  -3 x Atheroma markers (DM, Angina
  pectoris, Intermittent claudication)
 Total >+1= haemorrhage,
  < -1 = infarction
 Between –1 and +1 = CT scan for
What arterial territory is involved?
        Middle Cerebral Artery Syndrome
   Paralysis of the contralateral face, arm, and leg;
   Sensory impairment over the same area
   Motor aphasia and sensory aphasia
   Central aphasia, word deafness, anomia, jargon
    speech, sensory agraphia, Gerstmann syndrome
    (acalculia, alexia, finger agnosia, right-left confusion)
   Conduction aphasia
   Homonymous hemianopia (often homonymous
    inferior quadrantanopia)
   Paralysis of conjugate gaze to the opposite side
         Non dominant hemisphere (MCA)
   Apractognosia of the nondominant hemisphere,
    anosognosia, hemiasomatognosia, unilateral
    neglect, agnosia for the left half of external space,
    dressing “apraxia,”
   Constructional apraxia, distortion of visual
    coordinates, inaccurate localization in the half
    field, impaired ability to judge distance, upside-
    down reading, visual illusions (e.g., it may appear
    that another person walks through a table):
   Loss of topographic memory is usually due to a
    nondominant lesion, occasionally to a dominant
      Anterior Cerebral Artery Syndrome

 Paralysis of opposite foot and leg
 A lesser degree of paresis of opposite arm
 Cortical sensory loss over toes, foot, and leg
 Urinary incontinence
 Contralateral grasp reflex, sucking reflex,
  gegenhalten (paratonic rigidity)
 Abulia (akinetic mutism), slowness, delay,
  intermittent interruption, lack of spontaneity,
  whispering, reflex distraction to sights and
 Impairment of gait and stance (gait apraxia)
 Dyspraxia of left limbs, tactile aphasia in left
Anterior Cerebral Artery   Middle Cerebral Artery
         Posterior Cerebral Artery Syndrome
   Homonymous hemianopia (often upper quadrantic):
   Cortical blindness, awareness or denial of blindness
    (Anton’s syndrome), color blindness, prosopagnosia
    (inability to recognize familiar faces), photophobia
   Failure to see to-and-fro movements, inability to
    perceive objects not centrally located, apraxia of
    ocular movements, inability to count or enumerate
    objects, tendency to run into things that the patient
    sees and tries to avoid
   Memory defect
   Complex hallucination
   Sensory loss (all modalities), spontaneous pain
    and dysesthesias, choreoathetosis, intention
    tremor, spasms of hand, mild hemiparesis:
   Claude’s syndrome: Crossed cerebellar ataxia
    with ipsilateral third nerve palsy
   Weber’s syndrome: third nerve palsy and
    contralateral hemiparesis (cerebral peduncle)
   Contralateral hemiplegia.
    Paralysis or paresis of vertical eye movement,
    skew deviation, sluggish pupillary responses to
    light, slight miosis and ptosis (retraction
    nystagmus and “tucking” of the eyelids may be
   Contralateral rhythmic, ataxic action tremor;
    rhythmic postural or “holding” tremor (rubral
          GPE and Neuro Exam
                       General Physical
   Px may be unconscious or lying in bed
   Weakness on one side of the body as evident by
    facial asymmetry (flattening of the nasolabial fold on
    one side compared to the other, mild asymmetry of
    the palpebral fissures or of the face as the patient
    smiles), deviation of the leg. Hemiplegic gait
   The drawing shows facial weakness on the left side
    due to a stroke. The right side
     of the mouth is drawn up
    towards the normal side.
 Hemiplegic Gait-
  The shoulder is adducted; the elbow is flexed; the
  forearm is pronated, and the wrist and fingers are flexed.
  In severe cases, the hand may be clenched; the knee is
  held in extension and the ankle is plantar flexed, making
  the paralyzed leg functionally longer than the other. The
  patient therefore has to circumduct the affected leg to
  ambulate. Patient's shoe may be worn more on the
  affected side.
 Problems with memory, thinking, attention, or learning
 Speech
 Muscle tone (flaccidity later spasticity), power ( ) and
 Sensory loss over affected side of the body
 Cranial nerves (Almost all CN can be affected but 7
If not stroke what else can it be
 •   Subdural haematoma
 •   Cerebral tumour
 •   Head injury
 •   Todd’s Palsy
 •   Focal encephalitis
 •   Cerebral abscess
 •   Hypoglycaemia
 •   Hypertensive encephalopathy.
 •   Metabolic encephalopathy.etc.
 CT, MRI, CT imaging will demonstrate
  hemorrhage immediately, Infarctions are
  usually detectable at 1 week although 50%
  may not be detected
 Functional MRI;DWI&PWI.
 Dynamic perfusion CT
 Digital subtraction angiography: the gold
  standard for neurovascular evaluation
  prior to carotid endarterectomy.
             Other Investigations
 HB/Wbc, PCV/Platelet count/ PT/PTTK
 ESR, glucose, cholesterol, urea,
 Urinalysis; Microalbuminuria predicts
  hemorrhagic transformation in infarction–
  endothelial dysfunction
 Various test for hypercoagulable states.
 Serum level of homocysteine, C-R protein,
  IL-6, IL-8 &TNF & Troponin I.
 Skull X-ray
 Lumbar puncture (Exclude raised ICP)
 HbSS screening;
 ECG / Chest X-ray
 Carotid USS / duplex & CT angiography-
  atherosclerotic vessel & aneurysms.
 Transcranial doppler-non-invasive -
  intracranial arterial stenosis.
 Echocardiography
 A medical emergency
 Multydisplinary approach, Neurologist,
  Neurosurgeon , Anesthesiologist,
  Physiotherapist , Speech therapist

   Emergency mgt
   Treat the aetiology and prevent/treat complications
   Rehabilitation- Physical and speech therapy
   ABCD of resuscitation,
   May require airway support and ventilatory
   Maintain adequate tissue oxygenation
   Nurse 300 head up,
   Volume status: Correct for hypovolaemia and
    keep electrolytes in the normal range. give N/S
    not dextrose.
   Urgent CT/MRI.

                    If Ischemic
Thrombolytic- Streptokinase, Urokinase, Alteplase,
Anticoagulant: LMW heparin,
Antiplatelet therapy: Aspirin
Give antioxidant
                 If Hemorrhagic
   Avoid anticoagulants and antiplatelet drugs
    including salicylates, nonsteroidal anti-
    inflammatory drugs, ticlopidine, heparin and
   Avoid rapid reduction of intracranial pressure.
   Close monitoring for signs of increased pressure
    on the brain, such as restlessness, confusion,
    difficulty following commands, projectile vomiting
    and headache. Other measures will be taken to
    keep you from straining from excessive coughing,
    vomiting, or lifting, or straining to pass stool or
    change position.
   Keep BP low, but avoid a rapid reduction.
                 CPP= MAP-ICP
   Cranial decompression- Hemicraniotomy
   An aneurysm can be “clipped” by a neurosurgeon
    or “coiled” by a neurointerventional radiologist
   Endarterectomy for Internal artery stenosis
   Treat any aetiologic factor- DM, HPT, Heart
   Do not give antihypertensive for 48hrs or more,
    except persistent DBP>110, Malignant or HT
   Fever: treat and look for source of fever.
   Hypoglycemia/hyperglycemia: Keep under control.
    Hyperglycemia may worsen the ischemic injury.
   DVT Prophylaxis: This is a must as stroke patients
    have a high risk for DVT! It is important to use
    either sc heparin 5,000 IU q. 8 or 12 hrs. or sc
    enoxaparin 30 mg q. 12 hrs. plus early ambulation!
        Mgt of CNS complications
 Cerebral oedema
    24hrs(Hemorrhagic), 1-5days(ischemic)
    Tx- Mannitol, with Frusemide to prevent
     rebound raised intracranial pressure,
     decompressive craniotomy.
   Hemorrhagic transformation
    ◦ Occurs in Large infarction, MLS, age
    ◦ Tx decompress ICP, Haematoma evacuation.
   Acute Hydrocephalous
    ◦ May follow Hemorrhagic CVD
    ◦ Tx-Shunt(VP), Oedema, Evacuate haematoma
 Cerebral oedema
 Seizures
 Hydrocephalus
 Hemorrhagic transformation
 Fever
 Hyperglycemia
 Cardiac arrhythmias
 Bedsores, DVT, Pulmonary embolism,
 Depression
 Vasospasm
 Bleeding
            Prevention of CVD
   Treatment of hypertension (of vital importance)
   Cessation of smoking
   Active exercise lifestyle (recommend 30-60 min
    exercise, four to six times per week)
   Moderate alcohol consumption
   Statin therapy reduces cerebrovascular disease by
    up to a third even in people with a low
    cholesterol level
   Anticoagulation in atrial fibrillation
   Weight reduction in obesity
   Proper treatment of diabetes
   Treating polycythemia
   Surgery for carotid stenosis
 Advanced age, location of hemorrhage
  within the posterior fossa, depressed level
  of consciousness at initial presentation all
  worsen prognosis.
 Nearly 50% mortality for hemorrhagic
 About 25% mortality for ischemic
 Recurrence of stroke
 1/3 permanent disability and institutional
 Brain though 2% of body weight
  requires15% of cardiac output & 20% of
  total body oxygen.
 Neurons - Predominantly aerobic, few
  minutes of ischemia - irreversible injury.
 Our main aim as Doctors should be
  emergency mgt to save the ischemic
  penumbra so as to prevent disability and
  death of our patient.
           THANK YOU

To top