1) Stroke is defined as a sudden loss of brain function due to a disruption in blood flow to the brain. The two main types are ischemic (caused by blockage) and hemorrhagic (caused by bleeding). 2) Risk factors for stroke include hypertension, heart disease, diabetes, smoking, high cholesterol, previous TIA, family history, and age. 3) Ischemic strokes are caused by thrombosis or embolism and block blood vessels leading to "infarction" of brain tissue. Hemorrhagic strokes are caused by bleeding, usually from hypertension, aneurysms, or vascular malformations.

1. STROKE SYNDROME
Dr.Shyam Sunder Sharma
PM&R Department
SMS Medical College
Jaipur

2. STROKE SYNDROME
CONTENTS
Definition
Epidemiology
Risk factors
Patho physiology
Basic anatomy of Brain
Blood supply of Brain
Types of Stroke
Syndromes

3. Definitions
Stroke is defined as a nontraumatic brain injury caused by
occlusion or rupture of cerebral blood vessels that results in
sudden neurologic deficit characterized by loss of motor
control, altered sensation, cognitive or language
impairment,disequilibrium, or coma
The more modern term cerebrovascular accident (CVA) which
excludes nonvascular conditions that can present with stroke like
symptoms, such as seizure, syncope, hypoxemia, traumatic brain
injury, or brain tumor

6. RISKFACTORS
Nonmodifiable Risk Factors:
• Age—the single most important risk factor for stroke
worldwide
• After age 55, incidence increases for both males and
females
• Sex (male > female)
• Race (African Americans > whites > Asians)
• Family history of stroke

7. Modifiable (Treatable) Risk Factors:
• Hypertension
• History of TIA: ~ 5% of patients with TIA will develop a
completed stroke within 1 month if untreated;
14%
within 1 year
• Heart disease:
– Congestive heart failure (CHF) , coronary
artery disease (CAD), Valvular heart disease,
arrhythmias increase risk of embolic stroke, Atrial
fibrillation
• Diabetes: two fold increase in risk. Good blood
sugar control has not been shown to alter the
risk of stroke
• Cigarette smoking

8. • cocaine use, < 2 drinks/day relative risk
0.51; > 7 drinks/day relative risk 2.96
• High-dose estrogens (birth control pills)
• Systemic diseases associated with hypercoagulable
states
• Elevated RBC count, hematocrit, fibrinogen
• Protein S and C deficiencies
• Sickle-cell anemia
• Hyperlipidemia
• Migraine headaches
• Sleep apnea

9. Stroke Pathophysiology
• Normal cerebral auto regulation maintains a cerebral
perfusion rate of 50 mL/100 g cerebral tissue/min,
which remains constant regardless of acute
changes in systemic mean arterial pressure
• During cerebrovascular compromise, normal neural
activity can be sustained with a CBF as low as
20mL/100 g/min, but a rate below 10 mL/100
g/min results in cellular death
• CBF range between 10 and 20mL/100 g/min, the
basic cellular functions are supported but the
sodium– potassium pump fails, rendering the
neural cells “electrically silent”

10. Basicanatomy of brain

12. BASICNEUROANATOMICALREVIEWOFTHEMAJOR
VESSELSINVOLVEDINSTROKE

13. INTERNALCAPSULE

14. Blood supply of different areasofbrain

15. TYPESOFSTROKE
• ischemic stroke-
Thrombotic
Embolic
Lacunar
• hemorrhagic
stroke-
Intracerebral
Subarachnoid

18. ISCHEMICSTROKES(88%)
1)Thrombotic (large artery thrombosis):
• 35% of all strokes Usually occurs during sleep (patient often
awakens unaware of deficits)
• May have “stuttering,” intermittent progression of neurologic
deficits, or be slowly progressive (over 24–48 hours)
• Neurologic deficit varies according to cerebral territory affected
• Perfusion failure distal to site of severe stenosis or occlusion of
major vessels

19. 2)Embolic:
30% of all strokes
• Immediate onset of neurologic deficits
• Usually occurs during working hours
• Seizures may occur at onset of stroke
• Most commonly due to cardiac source: mural thrombi
and platelet aggregates
• cardiac thrombus caused by atrial fibrillation,
rheumatic heart disease (eg, mitral stenosis), post-
MI, and vegetations on heart valves in bacterial or
marantic endocarditis or prosthetic heart valves

20. 3)Lacunar:
• 20% of all strokes
• Onset may be abrupt or gradual
• Lacunes are small infarcts (less than 15 mm) seen in the
putamen, pons, thalamus, caudate, and internal capsule
Causes: occlusive arteriolar or small artery disease (occlusion of
deep penetrating branches of large vessels)
• Occlusion occurs in small arteries of 50–200 mm in diameter
• Strong correlation with hypertension (up to 81%); also
associated with microatheroma, microembolism, or rarely
arteritis
• CT shows lesion in about 2/3 of cases (MRI more sensitive)

21. Lacunarstroke

22. Neuroanatomic Locations of Ischemic Stroke (Adams,1997)
INTERNAL CAROTID
ARTERY (ICA):
• The most variable syndrome.
Occlusion occurs most frequently in
the first part of the ICA immediately
beyond the carotid bifurcation
• ICA occlusions are often
asymptomatic(30–40%
cases)
• Cerebral infarction: variable
presentation with complete ICA
occlusion; from no symptoms (if good
collateral circulation exists) to severe

24. MIDDLE CEREBRAL ARTERY (MCA)
•Occlusion occurs at stem of middle cerebral artery or at one of
the 2 main divisions (superior or inferior) of the artery in the
Sylvian sulcus

25. •Superior Division of the MCA:
• The superior division of MCA supplies rolandic
and prerolandic areas
• Most common cause of occlusion of superior
division of MCA is an embolus
• Sensory and motor deficits on contralateral face and
arm > leg
• Head and eyes deviated toward side of infarct
• With left side lesion (dominant hemisphere)—
global aphasia initially, then turns into Broca’s
aphasia (motor speech disorder)
• Right side lesion (nondominant hemisphere)—
deficits on spatial perception,
hemineglect,constructional apraxia, dressing
apraxia– Muscle tone usually decreased initially
and gradually increases over days or weeks to

26. • Inferior Division of the MCA
• – The inferior division of the MCA is the blood supply to the
lateral temporal and inferior parietal lobes
• With lesion on either side—superior quadrantanopia or
homonymous hemianopsia
• Left side lesion → Wernicke’s aphasia
• Right side lesion → left visual neglect

28. ANTERIOR CEREBRAL ARTERY (ACA)
• Contralateral weakness and sensory loss, affecting
mainly distal contralateral leg (foot/leg more affected
than thigh)
• Mild or no involvement of upper extremity
• Head and eyes may be deviated toward side of
lesion acutely
• Urinary incontinence
• contralateral grasp reflex
• paratonic rigidity
• motor aphasia if left side is affected
• Disturbances in gait and stance = gait apraxia

29. POSTERIOR CEREBRAL ARTERY (PCA):
• Clinical presentation:
• Visual field cuts (when bilateral, may have denial of cortical
blindness = Anton syndrome)
• prosopagnosia (can’t read faces)
• Palinopsia (abnormal recurring visual imagery)
• Alexia (can’t read)
• Trans cortical sensory aphasia (loss of power to comprehend
written or
spoken words; patient can repeat)
• Structures supplied by the interpeduncular branches of the PCA
include the oculomotor cranial nerve (CN3) and trochlear (CN4)
nuclei and nerves
• Clinical syndromes caused by the occlusion of these branches
include
Weber syndrome

30. Brain Stem Stroke Syndromes

34. Weber Syndrome (Base of Midbrain):
• Obstruction of interpeduncular branches of
posterior cerebral artery or posterior choroidal
artery or both

36. Millard-Gubler Syndrome (Base of
Pons):
• Obstruction of circumferential
branches of basilar artery.
• Ipsilateral abducens (CN6) and facial
(CN7) palsies
Sign & symptom:
• Contralateral hemiplegia
• Inspilateral sixth nerve pulsy
• Inspilatral facial weakness

40. HEMORRHAGIC STROKES
• 12% of all strokes
• secondary to hypertension, ruptured aneurysm,
arteriovenous
• malformation (AVM), blood dyscrasias/bleeding
disorders, anticoagulants, bleeding into tumor

41. I Hypertensive Intracerebral Hemorrhage (ICH)
• Linked to chronic HTN (> 1/3 occur in
normotensives)
Symptoms
• – Sudden onset of headache (HA) and/or LOC
• – Vomiting at onset in 22–44%.
• – Seizures occur in 10% of cases (first few
days after onset).
• – Nuchal rigidity is common

42. Cont.
• Locations : putamen, thalamus, pons, cerebellum, and
cerebrum:
• 1. Putamen (internal capsule ):
• Hemiplegia
• Vomiting in ~ 50%
• headache
• With smaller hemorrhages: Headache leading to aphasia,
hemiplegia, eyes deviate away from paretic limbs

43. 2. Thalamus:
.Hemiplegia by compression of adjacent internal
capsule
.Contralateral sensory deficits
.Aphasia present with lesions of the dominant side
.Contralateral hemineglect with involvement on the
nondominant side. Ocular disturbances with
extension of hemorrhage into subthalamus
3. Pons:
.Deep coma results in a few minutes
.Total paralysis, small pupils (1 mm) that react to
light
. Decerebrate rigidity → death occurs in few hours

44. 4. Cerebellum: develops over several hours.
• Coma/LOC unusual vomiting
• Occipital headache
• Vertigo
• Inability to sit, stand, or walk,
• Eyes deviate to opposite side (ipsilateral CN6
palsy);
• Dysarthria,
• Dysphagia

45. II. Subarachnoid Hemorrhage (SAH)
• Typically due to a ruptured saccular arterial
aneurysm
• Arterial dilations found at bifurcations of larger
arteries at the base of the brain (Circle of Willis or
major branches
• 90–95% of saccular aneurysms occur on the
anterior part of the Circle of Willis
• Peak age for rupture = fifth and sixth decade

46. Clinical Presentations of SAH:
• severe Headace classically described as “worst
Headache of my life”
• Sudden, transient LOC in 20–45% at onset
• Seizures: 4% at onset/25% overall
Compression of adjacent structures such as the
oculomotor nerve (CN3)
• Signs of CN3 involvement:
• Deviation of ipsilateral eye to lateral side (lateral
or divergent strabismus) because of unopposed
action of lateral rectus muscle
• Ptosis,mydriasis (dilated pupil) and paralysis of
accommodation due to interruption
ofparasympathetic fibers in CN3

47. • Risk of rebleeding within one month 30%; 2.2% per
year during first decade
• Mortality from rebleeding in the early weeks after
initial event: 50–60%
• Vasospasm: common complication occurring in ~
25% of cases; caused by the presence of blood
breakdown products (vasoactive amines)

48. III. Vascular Malformations/AVMs
A vascular malformation in the brain consisting of a
tangled mass of dilated vessels that forms an
abnormal communication between the arterial and
venous systems is known as an arteriovenous
malformation (AVM).
Bleeding May be:
• parenchymal (41%)
• Subarachnoid (23%)
• Intraventricular (17%) hemorrhage