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Cerebrovascular Diseases

Important Points:
  1. Stroke – Abrupt onset of a non convulsive and focal neurologic deficit, and signs and symptoms last for >24 hours.
  2. Completed Stroke – Rapid in onset with persistent neurological deficit which does not progress beyond 96 hours.
  3. Evolving Stroke – There is gradual step –wise development of neurological deficit, not accounted by cerebral edema.
  4. Stroke In Progression – Same as evolving stroke.
  5. Transient Ischemic Attack (TIA) – The focal neurological deficit resolves completely within 24 hours. Q
  6. Reversible Ischemic Neurological Deficit (RIND)– Neurological deficit completely resolves within one week Q
  7. Crescendo TIA – The occurrence of increasing number and frequency of TIA.
  8. Stuttering Hemiplegia – Internal carotid artery lesions which are characterized by repeated episodes of TIA followed by fully evolved stroke.
  9. Cryptogenic Stroke – Stroke for which no cause is apparent.

Causes of Stroke (Ref. Hari. 18th ed., Pg- 3276)


Young Stroke – Stroke in age group < 40years.


Important causes





Conn. tissue diseases

LA thrombus

Sickle cell anemia





Paradoxical embolism



Infective endocarditis



Marantic endocarditis

Multiple myeloma


Dilated cardiomyopathy

Protein C/S deficiency


Miscellaneous causes

  1. Pregnancy
  2. Drugs – Cocaine, Amphetamine
  3. Oral contraceptives
  4. Infections – TB, Mucormycosis
  5. Nephrotic syndrome

Note: Most common cause of stroke in young women in India among OCP users is Cortical vein thrombosis.

Table 370-5 Risk of Stroke Following TIA: The Abcd2 (Ref. Hari. 18th ed., Pg- 3280)



Clinical Factor


1. Age ≥ 60 years


2. SBP >140 mm Hg or DBP >90 mm Hg


3. Clinical symptoms  


    Unilateral weakness


    Speech disturbance without weakness


4. TIA Duration    


    >60 minutes


    10–59 minutes


5. Diabetes (oral medications or insulin)


Total Score 7
More the ABCD2 Score more is the likely of 3-Month Rate of Stroke (%)


Pathophysiology –

  1. Cerebral infarction (85%)
    1. Thrombotic (25%)
      1. Lacunar Lipohyalinosis
      2. Large vessel Atherosclerosis
    2. Embolic (75%) (FAQ)
      1. Cardioembolic Cardiac lesions
      2. Artery – artery Atherosclerosis
Important Point:

Embolism is the most common of CVA

Recent Advances- Watershed Stroke (LQ 2012)

  1. A watershed stroke is defined as an ischemia, or blood flow blockage, that is localized to the border zones between the territories of two major arteries in the brain. The term “watershed” refers to those areas of the brain that receive dual blood supply from the branching ends of two large arteries.
  2. Watershed locations are those border-zone regions in the brain supplied by the major cerebral arteries where blood supply is decreased.
  3. Watershed strokes are localized to two primary regions of the brain, and are termed cortical watersheds (CWS) and internal watersheds (IWS).
    1. watershed strokes (CWS), or outer brain infarcts, are located between the cortical territories of the anterior cerebral artery (ACA),middle cerebral artery (MCA), and posterior cerebral artery (PCA).
    2. Internal watershed strokes (IWS), or subcortical brain infarcts, are located in the white matter along and slightly above the lateral ventricle, between the deep and the superficial arterial systems of the MCA, or between the superficial systems of the MCA and ACA.
  1. Cerebral haemorrhage (15%)
    1. Intraparenchymal (10%) HT, AVM
    2. Subdural (<1%) Trauma
    3. Epidural (<1%) Trauma
    4. Subarachnoid (1 to 2%) Trauma (M/C cause) Ruptured aneurysm
Important Point:

Most common site of hemorrhagic CVA is Intracerebral hemorrhage.

PPA used for weight loss can cause haemorrhagic stroke


Hypertension is the most important cause of intracerebral hemorrhage

Important Points:

In order of frequency of occurrence of location of aneurysm

  1. Anterior communicating – Ant. Cerebral junction (29%)
  2. Post communicating – Internal carotid junction (28%)
  3. Middle cerebral bifurcation (18%)
  4. Intracranial carotid bifurcation (8%)
  5. Vertebrobasilar or basilar bifurcation (3%)

Lacunar infarction (small vessel stroke)

  1. The term lacunar infarction refers to infarction following atherothrombotic or lipohyalinotic occlusion of small arteries (30 to 300 μm)  in the brain. Occlusion of such small penetrating arteries are now termed as small vessel strokes.
  2. Each of these vessels can occlude by
    1. Atherothrombotic disease at its origin
    2. Development of lipohyalinotic thickening
  3. Thrombosis of the vessels cause small infarcts referred to as lacunes.
  4. Hypertension and age are the principal risk factors.

Important Points:- Distinct clinical syndromes associated with lacunar infarcts.

  1. Pure motor hemiparesis
    1. Most common lacunar syndrome
    2. Results from infarction of contralateral internal capsule (may also be seen with infarcts in corona radiata and pons)
    3. The face, arm and leg are equally affected
    4. There is no sensory loss, homonymous hemianopia, Aphasia or hemineglect
  1. Pure sensory stroke
    1. Infarction almost always involves the thalamus
    2. Sensory loss is present throughout the contralateral side,
    3. Sensation is usually decreased for all sensory modalities, and no other neurologic deficits are present.
    4. Patient often complains of abnormal spontaneous sensation, such as "pins-and-needles" or skin tightness.
  1. Sensorimotor stroke
    1. Infarcts involve both internal capsule and thalamus
  1. Ataxic hemiparesis
    1. Contralateral weakness and limb ataxia
    2. Weakness and ataxia present on the same side with the ataxia usually more severe than the weakness.
    3. Most commonly occurs in the pons, the internal capsule or the corona radiata
  1. Dysarthria Clumsiness syndrome
    1. Prominent dysarthria and ataxia of the upper limb
    2. Facial weakness, dysphagia and varying degrees of weakness in the arm and leg
    3. Associated with infarction in the internal capsule or the pons.


Important Points:

Blood supply to specific brain areas –

  1. ThalamusQ – Branches of post communicating, basilar & PCA.
  2. Mid brainQ – Post. cerebral, superior cerebellar, basilar.
  3. PonsQ – Basilar, Ant, Inf, & superior cerebellar.
  4. MedullaQ – Vertebral, ant & post spinal, Post. inf cerebellar, basilar.
  5. CerebellumQ – Superior cerebellar, ant inferior cerebellar, Post. inf cerebellar
  6. Internal capsuleQ – Superior half → Lenticulostriate branches of MCA.
    Inferior half → Ant. limb – ACA through Heubner artery
    Post. limb  Ant. 1/3 Post. communicating
                  → Post. 2/3 Ant. choroidal.


Important Points:
  1. Most common site is in the territory of middle cerebral artery.
  2. Most common site of atherosclerosis that leads to stroke → origin of internal carotid artery with in 2 cm & post. wall.                                                     
  3. Most common site – Putamen

Hypertensive Hemorrhage

  1. Intraparenchymal (Hypertensive)
    1. Basal ganglia (Putamen) M/C site (LQ 2012) 
    2. Thalamus
    3. Cerebellum
    4. Pons.
  2. Subarachnoid Junction of anterior communicating artery with ant cerebral artery.
    (Most common cause of SAH is trauma (FAQ)
    The focal neurological signs vary according to the site of the hemorrhage

Intraparenchymal bleed

  1. Basal ganglia: (Putamen)
    1. Arteries involved - Medial & lateral striate branches of Middle cerebral artery
    2. Manifestations
      1. Contralateral hemiparesis is the sentinel sign
      2. When haemorrhage is large, signs of brainstem compression may appear
  2. Thalamus
    1. Arteries involved - Perforating branches of posterior cerebral artery
    2. Manifestations
      1. Hemisensory loss involving all modalities
      2. Contralateral pain syndrome during recovery period (Dejerine -Roussy syndrome) (LQ 2012)
      3. Several typical ocular disturbances:
        1. Down & inward deviation of eyes
        2. Unequal pupils with loss of light reflex
        3. Skew deviation with eye opp. hemorrhage deviated down and medially
        4. I/L Horner’s syndrome
        5. Absence of convergence
        6. Paralysis of vertical gaze
        7. Retraction nystagmus
  3. Pons
    1. Arteries involved: Basilar artery
    2. Manifestations (3 P’s = Pin Point Pupil, hyperpyrexia, quadriparesis)
      1. Quadriplegia               
      2. Deep coma         
      3. Decerebrate rigidity    
      4. Pinpoint pupil that react to light
      5. Hyperventilation
      6. Hypertension              
      7. Hyperhidrosis             
      8. Hyperpyremia
      9. Impairment of reflex eye movement on head turning (doll's head or oculocephalic maneuver)
  4. Cerebellum
    1. Arteries involved:
      1. Superior cerebellar       
      2. Ant. inferior cerebellar         
      3. Post. Inferior cerebellar
    2. Manifestations
      1. Occipital headache        
      2. Vomiting      
      3. Gait ataxia  
      4. Dizziness or vertigo     
      5. Dysarthria
      6. Dysphagia
      7. Stupor & coma if brainstem compression occurs
      8. Ocular changes
        1. Paresis of conjugate gaze
        2. Forced deviation of eyes to opposite side
        3. I/L 6th nerve palsy

Lesion in Individual artery

  1. Anterior cerebral artery
It is one of the terminal branch of internal carotid artery. It supplies the entire medial surface of cerebral hemispheres including a strip of cortex for about 2 cm along the superolateral surface.
Recurrent artery of Heubner Q is an important branch and its involvement causes faciobrachial monoplegia.

Occlusion of anterior cerebral artery


It is usually well tolerated because of collateral flow, esp in case of occlusion of proximal segment.


If both A2 Segments arise from a single anterior cerebral stem, the occlusion affects both hemisphere. 

Sign & Symptoms

Structures involved

a. Paralysis of opposite foot & leg

Motor leg area

b. Cortical sensory loss over foot & leg

Sensory area for foot & leg

c. Urinary incontinence

Sensorimotor area in paracentral lobule

d. Abulia, slowness

Cingulate gyrus & medial inferior portion of frontal, parietal & temporal

e. Gait ataxia

Frontal cortex near leg motor area

f. Paraparesis

B/L motor leg area due to occlusion of single origin of A2 Seg.

  1. Middle cerebral artery – 
    It supplies the lateral surface of cerebrum.
    1. Frontal pole & strip of cortex which is supplied by ACA
    2. Lower temporal and occipital pole which is supplied by PCA.
      In the sylvian fissure it divides into superior & Inf. division.

Occlusion of middle cerebral artery



Signs & Symptoms

Structures involved

1. Paralysis of contralateral Face, arm, leg (Hemiplegia) (LQ 2012)

1. Somatic motor area for face, arm, Leg (Descending Fibers)

2. Sensory loss of face, arm, leg

2. Somatic sensory area

3. Motor aphasia (Broca’s aphasia) (sup div of MCA)

3. Motor speech area of left frontal lobe

4. Gerstmann syndrome (Acalculia, agraphia, finger anomia & right – left confusion)

4. Dominant parietal cortex.

5. Anosognosia, hemineglect, dressing apraxia, constructional apraxia, spatial agnosia (L)

5. Non dominant parietal cortex.

6. Homonymous hemianopia

6. Optic radiations deep to second temporal convolution

7. Paralysis of conjugate gaze to opposite side

7. Frontal eye field.

8. Sensory (Wernicke’s aphasia)

8. Sensory speech area of dominant hemisphere (temporal) (Inf. div. of MCA).


Extra Edge: Jackson’s Sign: (LQ 2012)


Jackson’s Sign In hemiparesis during quiet respiration the movement of the paralyzed side of the chest may be greater than that of the opposite side. However, the paralyzed side moves less under forced respiration.

  1. Posterior cerebral arteryQ
Posterior cerebral arteryQ– It supplies the medial surface of temporal and occipital lobes and their tentorial surface. It also supplies cerebellum, medulla, pons, mid brain Subthalamus and thalamus.

Occlusion of posterior cerebral artery

Peripheral territory



Symptoms & signs

Structures involved

1. Homonymous hemianopia with macular Sparing

→ Calcarine cortex/optic radiation.

2. Colour blindness, Anton’s syndrome

→ B/L occipital lobe with involvement of some cortical blindness (Preserved pupillary reflex)

3. Balint's syndrome

→ Bilateral visual association area lesions.


Extra Edge: Balint’s syndrome - A disorder of the orderly visual scanning of the environment, usually resulting from infarctions secondary to low flow in the "watershed" between the distal PCA and MCA territories, as occurs after cardiac arrest. Patients may experience persistence of a visual image for several minutes despite gazing at another scene (palinopsia) or an inability to synthesize the whole of an image (asimultanagnosia). (Ref. Hari. 18th ed., Pg- 3287)

Central territory



Symptoms & signs

Structures involved

1. Thalamic syndrome – Sensory loss of modalities, spontaneous pain & paresthesia, choreoathetosis, intention tremor

→ Postero ventral nucleus of thalamus.

2. Benedict syndrome – C/L cerebellar ataxia with ipsilateral III nerve palsy

Red nucleus and III nerve.

3. Nothnagel syndrome – Ipsilateral cerebellar signs

Superior cerebellar peduncle

4. Claude’s = Nothnagel + Benedict syndrome


5. Weber’s syndrome – contralateral Hemiplegia with ipsilateral III nerve palsy

Pyramidal tract with III nerve.

Lateral medullary syndrome – It is due to occlusion of

  1. Post. inf. cerebellar artery (PICA)
    It is also known as Wallenberg’s syndrome.

Anterior Choroidal Artery (AIPG 2011)

  1. This artery arises from the internal carotid artery
  2. It supplies the posterior limb of the internal capsule and the white matter posterolateral to it, through which pass some of the geniculocalcarine fibers.
  3. The complete syndrome of anterior choroidal artery occlusion consists of:
    1. Contralateral hemiplegia,
    2. Hemianesthesia (hypesthesia),
    3. Homonymous hemianopia.
  4. However, because this territory is also supplied by penetrating vessels of the proximal MCA and the posterior communicating and posterior choroidal arteries, minimal deficits may occur, and patients frequently recover substantially.

Extra Edge: Blood supply of internal capsule:

  1. ANT LIMB =  ACA (medial striate a) + MCA (lateral striate a)
  2. GENU =  ICA (Ant Choroidal a)
  3. POST LIMB =  ICA (Ant Choroidal a) + MCA (lateral striate a)

Basilar artery syndrome
CADASIL (cerebral Autosomal dominant arteriopathy with subcortical infarcts & leukoencephalopathy) (Ref. Hari. 18th ed., Pg-3279
  1. It is a monogenic stroke syndrome.
  2. It is an inherited disorder that presents as small-vessel strokes, progressive dementia, and extensive symmetric white matter changes visualized by MRI.
  3. Approximately 40% of patients have migraine with aura, often manifest as transient motor or sensory deficits.
  4. Onset is usually in the fourth or fifth decade of life.
  5. This autosomal dominant condition is caused by one of several mutations in Notch-3, a member of a highly conserved gene family characterized by epidermal growth factor repeats in its extracellular domain.
  6. Other monogenic ischemic stroke syndromes are
    1. Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL)
    2. Hereditary endotheliopathy, retinopathy, nephropathy, and stroke (HERNS).
    3. Fabry's disease also produces both large-vessel arteriopathy and small-vessel infarcts by an unknown mechanism.
Important Points:

Subclavian Steal Syndrome –

  1. This occur due to stenosis or occlusion of subclavian artery proximal to the origin of the vertebral artery.
  2. The increased metabolic demand of left or right arm musculature during exercise is met by retrograde blood flow down the vertebral artery and this results in symptoms of brain stem ischemia.

Investigations –

  1. CT Scans
    1. Infarcts are detected after 24 – 48 hours.Q      
    2. Fail to detect small ischemic stroke in the posterior fossa. Also fail to show small cortical infarcts
    3. Better than MRI in detecting early hemorrhage.Q

CT Scan

  1. Infarct upto 12 hrs. CT may be normal in cerebral infarct.
  2. Then low attenuations occur in 24-36 hrs, ischemic tissue swells producing a mass effect by 2nd to 3rd day Subsides by 7th day.
  3. After 7 days infarcted tissue is invaded by phagocytic glial cell which increases attenuation. So plain CT looks near normal.
  4. Same time infarcted area is also invaded by New Blood vessel which show an area of enhancement after iodinated contract media. Enhancement is maximum in 2nd week.

  1. MRI
    1. It can detect infarct in all locations of brain.
    2. FLAIR (Fluid attenuated inversion recovery)Q
    3. MRI with fat saturation – used to visualize extra & intracranial arterial dissection.Q
  2. Cerebral Angiography –  It is the ‘gold standard’ for identifying and quantifying atherosclerotic stenosis, aneurysm, Q  vasospasm, intraluminal thrombi, fibromuscular dysplasia, A – V fistula, vasculitis and collateral channels of blood flow.
  3. Ultrasound techniques –
    1. Doppler ultrasound assessment of flow velocity (it is the best screening test for ICA stenosis).
    2. Transcranial Doppler assessment of middle, anterior and posterior cerebral artery & vertebrobasilar flow.
  4. PET (Positron emission tomography) - Can quantify cerebral blood flow.
  5. SPECT (single photon emission tomography)

MANAGEMENT – (Ref. Hari. 18th ed., Pg- 3271)


Main goal is to prevent or reverse brain injury.


Note. The only thrombolytic agent approved for the treatment of acute ischemic stroke is: Tissue Plasminogen activator (Ref. Hari. 18th ed., Pg-3272, table 370.1)

Medical support

  1. BP should be maintained using fluids, vasopressors.
    1. If BP >185/110 β1 – blocker esmolol
    2. Deep vein thrombosis Heparin     
    3. Cerebral edema – Peaks on 2nd or 3rd day I.V. Mannitol
  2. Thrombolysis – Agent used is Recombinant Tissue Plasminogen Activator (rt PA)​
    1. Clinical diagnosis of stroke
    2. CT shows no hemorrhage or significant edema
    3. Symptoms duration 3hours.
    4. Age 18years .
  3. Anticoagulation – Agent used is heparin
    Antiplatelet agents –
    1. Aspirin
    2. Ticlopidine   
    3. Clopidogrel  
    4. Glycoprotein IIb/IIIa inhibitors
  4. Neuroprotective agents –
    Prolongation of tolerance of brain to ischemic long enough to allow other measures to be employed to mitigate ischemic. Agents used are:
    1. Hypothermia            
    2. Drugs blocking excitatory amino acid pathways.  

Pentoxifylline, helps blood flow, has been used to treat venous leg ulcers. It is indicated for the treatment of leg pain caused chronic occlusive arterial disease of the limbs.

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