Case presentation : Stroke in the young

1. POST_GRADUATE INTERNS’ CASE MANAGEMENT
CONFERENCE
Spinning Me Softly:
(A Case of Stroke in theYoung)
Presented by:
Allan Joseph O. Santos
Nurol Iman L. Cabugatan
Amer Hussien P. Samporna
Department of Internal Medicine

2. Assalamu Alaycom!

3. OBJECTIVES
At the end of this presentation, we will be able
to answer the following questions:
1. What can be the possible diagnosis in a young adult
patient presenting with dizziness, left sided
weakness and dysarthria?
2. What are the risk factors for stroke in the young?
3. How do you diagnose and manage patients who have
stroke in the young?

4. I. IDENTIFYING DATA
• R.M.
• 35 year old
• Male
• Filipino
• Catholic
• Sampaloc, Manila
• 1st admission
• January 26, 2015

5. II. SOURCE & RELIABILITY
• The patient and his wife were the sources of
information with Good Reliability ( 95% ).

6. III. CHIEF COMPLAINT
Dizziness of
30 minutes duration

7. IV. HISTORY OF PRESENT ILLNESS
• Dizziness : sudden onset
: rotatory
: described as swaying in motion
: not relieved by vomiting
• Vomiting : 3 episodes
: non projectile
: non bilious, non bloody
: ½ cup / episode
8 hours PTA .

8. IV. HISTORY OF PRESENT ILLNESS
• Self medicated : Betahistine (16mg/tab) x 1 dose
: minimal relief
• Fell asleep
8 hours PTA . .

9. IV. HISTORY OF PRESENT ILLNESS
• After waking up : Recurrence of dizziness (same character).
: left sided weakness and numbness.
: slurring of speech.
: inability of right eye to move to the
right.
• Consult OLLH ER : Admission.
30 mins PTA …

10. V. PAST MEDICAL HISTORY
DATE CONSULT COMPLAINT DIAGNOSIS MEDICATIONS
July 2014 OLLH ER
Dizziness and
Vomiting
BPPV
• Betahistine 16mg/tab PRN
• Metoclopramide 10mg/tab
PRN
No Hypertension
No Diabetes
No Asthma
No PTB
No Goiter
No Allergies
No Surgeries

11. ( + ) : Hypertension ( Paternal and Maternal )
: CVD infarct ( Paternal : Uncle )
( Age : 47 y/o )
( - ) : Mental/Psychiatric disorder
: Diabetes mellitus
: Bronchial Asthma
: Malignancy
: Thyroid disease
VI. FAMILY MEDICAL HISTORY

12. • Occupation : Production Technician (Printing Section)
: Garment factory
• Smoker : 25 pack years (25 sticks/day for 20 years)
• Alcoholic beverage Drinker : occasional
: twice a week
: 3 beer bottles/session
• Cannabis use (Age : 16- 24)
VII. PERSONAL & SOCIAL HISTORY

13. VIII. REVIEW OF SYSTEMS
General no weight loss
no fever
no anorexia
no easy fatigability
Skin no jaundice
no bruising
no pruritus
no rashes
no lumps
HEENT no head injury
no trauma
no ear discharge
no nasal discharges
no epistaxis
no mouth sores
no mass
no tinnitus

14. VIII. REVIEW OF SYSTEMS
Neurologic no changes in attention,
no changes in orientation, memory, insight, judgment
no loss of consciousness
no seizures, paralysis
no tremors
no involuntary movements
Respiratory (+) non productive cough
no colds
no hemoptysis
no dyspnea
Cardiovascular no cyanosis
no chest pain
no palpitations

15. VIII. REVIEW OF SYSTEMS
Gastrointestinal no black tarry stools
no abdominal pain / pain in defecation
no rectal bleeding, constipation, diarrhea
no food intolerance
no excessive belching or passing of gas
Musculoskeletal no muscle or joint pain
no swelling, stiffness, redness
no loss of muscle mass.
Genitourinary no polyuria
no nocturia
no urgency
no hematuria
no incontinence.

16. IX. PHYSICAL EXAMINATION
General Survey awake, conscious, coherent, wheelchair borne
not in respiratory distress
Vital Signs BP : 130/80 mmHg
HR : 98 bpm
RR : 20 cpm
Temp : 37.3 o C
O2 Sat : 98 %
Wt : 68 kg
Ht : 166 cm
BMI : 24.67

17. IX. PHYSICAL EXAMINATION
SKIN Skin is brown in color, warm to touch, fair skin turgor, no
lesions.
HEENT Anicteric sclerae, pink palpebral conjunctivae, moist lips
and oral mucosa, no tonsillopharyngeal congestion, no
neck vein distention, no cervical lymphadenopathies. no
palpable masses.
No audible bruit.
RESPIRATORY No fractures, lesions or hematoma, symmetrical chest
expansion, clear breath sounds, no adventitious sound,
no use of accessory muscles for respiration, no
retractions, resonant on percussion. .
CARDIOVASCULAR Adynamic precordium , normal rate, regular rhythm ,
distinct S1 and S2, no murmurs, apex beat at 5th ICS
LMCL. No bruits

18. IX. PHYSICAL EXAMINATION
GASTROINTESTINAL globular abdomen, no visible veins or visible
peristalsis; normoactive bowel sounds.
tympanitic on percussion. No palpable
masses or organomegaly appreciated. No
abdominal bruit noted.
EXTREMITIES no edema, no gross deformity, CRT <2sec.
full and equal pulses, palpable peripheral
pulses

19. NEUROLOGICAL EXAMINATION
Cortical
Frontal Good attention span
(-) Broca’s aphasia
Parietal (-) Right/left disorientation
(-) finger agnosia
Temporal (-) Wernicke’s Aphasia
Occipital Able to identify color and object
MSE Conscious,coherent
Oriented to person, place and time
Able to subtract serial 7’s
Intact immediate, recent and remote memory

20. NEUROLOGICAL EXAMINATION
Sensory 100 % sensation to light touch, pain, pressure
and temperature on the Right upper and lower
extremity.
80 % sensation to light touch, pain, pressure
and temperature on the left upper and lower
extremity.
Motor 5/5 right upper and lower extremities
3/5 left upper and lower extremity
DTR’s +2 on all extremities
(+) babinski, bilateral
Meningeal (-) brudinzki
(-) Kernigs
Cerebellar (+)dysdiadochokinesia, left
(+) dysmetria, left

21. NEUROLOGICAL EXAMINATION
Cranial Nerves
CN I able to smell and identify scent
CN II , III pupils equally and briskly reactive to light , 3-4 mm. On
fundoscopy,(+) red orange reflex (-)hemorrhages,
neovascualrization , AV ratio 2:3.
Near Vision : OS 20/20.
: OD 20/50-1
CN III , IV, VI primary gaze to the left; Right eye cannot move
laterally. Horizontal and vertical nystagmus
CN V V1, V2, V3 : intact sensory and motor
CN VII facial asymmetry, Left
CN VIII intact gross hearing
CN IX , X intact gag reflex; uvula midline ; (+) dysarthria
CN XI good shrug, SCM and trapezius muscle symmetric with
muscle strength of 5/5
CN XII tongue deviated to the left

22. X. SALIENT FEATURES
35 year old, male
dizziness
vomiting
 left sided weakness and numbness
 slurring of speech
Family history of CVD infarct
 25 pack years smoker
 alcoholic beverage drinker
 history of Cannabis use
 CN VI: Lateral rectus palsy, Right
 CN VII: Facial asymmetry, Left
 CN XII: Tongue deviation, Left
 Cerebellar signs:
-dysdiadochokinesia, Left
-dysmetria, Left
-nystagmus
 Bilateral babinski sign

23. Cerebrovascular Accident, Infarct
Pontocerebellar Area , Right
XI. ADMITTING IMPRESSION

24. • Supratentorial vs. Infratentorial
– Supratentorial
• Any structure that is located above the tentorium cerebelli.
(cerebral hemisphere, subcortical)
– Infratentorial
• Any structure that is located below the tentorium cerebelli
(brainstem and cerebellum)
• System of Buffalo, New York,
Where is the lesion?

25. • Supratentorial vs. Infratentorial
– Lesion more likely Supratentorial:
• Dysarthria- 63% of Stroke , ischemic stroke.
Pure dysarthria is more frequently associated
with cortical lesions. (Ionita C. 2004, Neurocritical Care Services at
the Catholic Health System of Buffalo, New York)
• The eyes look toward the brain lesion and away
from the hemiparesis - more likely cerebral
(cortical) in origin (Adams and Victor’s Principles of Neurology 9th
Edition)
Where is the lesion?

26. – More likely Infratentorial
• Dysarthria with additional neurologic signs is
more frequently caused by pontine (brainstem)
involvement. (Ionita C. 2004, Neurocritical Care Services at the Catholic
Health System of Buffalo, New York)
• The eyes look away from the brain lesion and
toward the hemiparesis -more likely a
brainstem lesion (Adams and Victor’s Principles of Neurology 9th
Edition)
Where is the lesion?

27. Where is the lesion?
Signs Upper Motor
Neuron
Lower Motor
Neuron
Atrophy None Severe
Fasciculation None Common
Tone Spastic Flaccid
Distribution
of weakness
Pyramidal/
Regional
Distal/
Segmental
Tendon
reflexes
Hyperactive Hypoactive/
Absent
Babinski’s
sign
Present Absent

28. Where is the lesion?
LEVEL Neurologic Deficits
Pons Right eye cannot move
laterally (abducens nerve )
Facial asymmetry (facial
nerve)
Medulla Tongue deviation left and
dysarthria (hypoglossal
nerve)
Cerebellar
Hemisphere
Dysdiadochokinesia, Left
Dysmetria, Left
CN XII
CN VI
CNVII

29. R.M ,
(+) Acute onset (30 minutes) of dysarthria, dizziness,
left sided weakness, left sided numbness, dysmetria and
dysdiadochokinesia
CVA/STROKE BPPV Multiple
Sclerosis

30. XII. DIFFERENTIAL DIAGNOSES
BENIGN PAROXYSMAL POSITIONAL VERTIGO
-most common disorder of the inner ear’s
vestibular system.
 Dizziness
 Nausea and vomiting
 Horizontal nystagmus
 No sensory deficits
 No motor deficits
Adams and Victors’ Principles of Neurology 9th Edition

31. XII. DIFFERENTIAL DIAGNOSES
MULTIPLE SCLEROSIS
-A chronic condition , inflammatory
demyelinating disease of the CNS.
-Has predilection for the optic nerves and the
spinal cord.
-More commonly in a “relapsing-remitting
pattern”
(initial manifestation improved partially before more
severe symptoms develop subsequently)
(Adams and Victors’ Principles of Neurology, 9th Edition)

32. XII. DIFFERENTIAL DIAGNOSES
MULTIPLE SCLEROSIS
• Sensory loss
• Dysarthria
• Ataxia
• Tremor
• Optic neuritis
• Trigeminal neuralgia
• Diplopia on lateral gaze
• Urinary symptoms
• Constipation
BPPV
• Dizziness
• Nausea and vomiting
• Horizontal nystagmus
• No sensory deficits
• No motor deficits

33. R.M ,
(+) Acute onset (30 minutes) of dysarthria, dizziness,
left sided weakness, left sided numbness, dysmetria and
dysdiadochokinesia
CVA/STROKE BPPV Multiple
Sclerosis

34. At the ER.
CRANIAL CT SCAN
IMPRESSION : Chronic infarct, Right cerebellar hemisphere, suggests delayed contrast
enhanced cranial CT study for further evaluation.
CITICOLINE 1 gm IV
CLOPIDOGREL 75 mg/tab
SULODEXIDE 600 LSU

35. DIFFERENCE of CT SCAN and MRI
CRANIAL CT SCAN
Advantages:
 Widely accessible
 Convenient
 Fast (shorter scanning time)
 Easily rules out hemorrhage
 Less expensive
Disadvantages:
 If done too early, may be
normal
 If seen, lesion not always
specific for stroke
 Radiation exposure
CRANIAL MRI
Advantages:
 Sensitive in detecting ischemia
early (few minutes after stroke
onset)
 Can detect small lesions missed
by CT
Disadvantages:
 Not widely accessible
 Contraindications (braces,
pacemakers,etc)
 Longer scanning time
 May need general anesthesia
 More expensive

36. T1W1

37. T1W1

38. T2W1

39. T2

40. SWI

41. SWI

42. DWI

43. DWI

44. STROKE
Stroke is a neurological impairment
caused by a disruption in blood supply
to a region of the brain.
(American Stroke Association, 2004)

45. STROKE IN THE YOUNG
• Incidence rates under the age of 45(16-45 y.o)
7 to 15 in 100 000 people/year for all stroke
(Ischemic and Hemorrhagic).
• In the Philippines
10.4 to 47 per 100,000 per year
M >F; Infarct more common than hemorrhage.
(Griffiths et.al, 2011, Epidemiology and Etiology of Young Stroke , PGH, Department of Rehabilitation
Medicine)

46. In a study done by Dash et.al, Among 2,634
ischemic stroke patients from January 2005 to
December 2010, 440 patients are age 18-45 years,
5:1 male-to-female ratio. (Risk Factors and Etiology of Ischemic
Strokes in Young Patients: A Tertiary Hospital Study in North India)

47. • In our institution, OLLH, a total of 127 out of
3670 patients were diagnosed to have
Cerebrovascular accident in 2013-2014 alone.
1.5% are Hemorrhagic and 1.93% are Infarct
in origin.
(Annual Census, 2013-2014, OLLH, Department of Internal Medicine)

48. CATEGORIES OF STROKE
Stroke
Ischemic/Infarct
(85%)
Thrombotic
Embolic
Hemorrhagic
(15%)

49. ISCHEMIC/INFARCT
- blockage in blood
vessels in brain.
1. Focal- thrombotic or
embolic occlusion of
major artery.
2. Global-inadequate
cerebral perfusion
(either due to blood
loss, cardiac failure,
etc).
HEMORRHAGE
-ruptured or leaking
blood vessels in the
brain.
1. Parenchymal-into the
brain.
2. Subarachnoid-
surrounding
subarachnoid space.
R.M belongs to this category.
No leaking blood vessels and
no blood seen on CT Scan.

50. STROKE IN GENERAL
• Paralysis
• Numbness
• Sensory deficits
• Aphasia
• Visual field defects
• Diplopia
• Dizziness
• Dysarthria
(Adams and Victor’s Principles of Neurology, 9th Edition)

51. PATHOPHYSIOLOGY
Arterial occlusion
Dec Blood Flow
Energy Failure
Depolarization Glutamate release
Glutamate receptors
Calcium Influx
Activation of
catabolic enzyme
ZERO: necrosis within 4-10min<16-18ml/100mg tissue/min: infarction within hr
CELLULAR
INJURY
<20ml/100mg tissue/min: ischemia w/o infarction

52. CBC 1.26.15
Hemoglobin 168 
Hematocrit 0.48 
WBC 18.29 
Segmenters 0.84 
Stabs 0.03
Lymphocytes 0.13
Monocytes
Platelets 336,000
BLEEDING PARAMETERS RESULT
Prothrombin Time 11.3
Control 11.21 sec
INR 1.01
Protime Activity 98.2 %
APTT 28.2
Control 32.5 sec

53. URINALYSIS RESULT
Color Yellow
Transparency Slightly
Cloudy
Reaction 5.5
Specific
Gravity
1.025
Glucose neg
Albumin neg
Epithelial Cells few
RBC 1-2/hpf
PUS cells 1-2/hpf
Amorphous
Urates
some
Mucus threads many
Bacteria few
CLINICAL CHEMISTRY RESULT
Sodium 148.3
Potassium 4.16
BUN 3.55
Crea 84.0
SGPT 43
Cholesterol 5.86
Triglycerides 0.88
HDL 1.08
LDL 4.38
Uric Acid 0.43

54. FINDINGS : No active parenchymal infiltrates
Heart is not enlarged
Trachea is at midline
CP sulci are intact
IMPRESSION : Normal Chest

55. ECG : Normal sinus rhythm
Non-specific ST-T wave
changes

56. ETIOLOGY OF ISCHEMIC STROKE
THROMBOTIC
ISCHEMIC
STROKE
EMBOLIC
Cardiogenic
Non-cardiogenic
Non-Atherosclerosis Arteriopathy
Non-inflammatory
Infammatory
Hematological Disorder
Viscosity
Coagulopathy

57. EMBOLIC STROKE
A. Cardiogenic
1. Valvular:
- Prosthetic, Endocarditis, MVP
2. Arrhythmia:
-AF, Sick Sinus Syndrome.
3. AMI/LV Aneurysm
4. LV Myxoma
5. Cardiomyopathy
B. Non-Cardiogenic
1. Pulmonary AVM:
- Osler-Weber-Rendu syndrome
2. Pulmonary Embolism
3. DVT/PAOD
ECG : NSR
NSSTTWC

58. THROMBOTIC STROKE
A. NON-ATHEROSCLEROSIS
ARTERIOPATHY
1. Non-inflammatory
a. Moya moya disease
b. Artery dissection
c. Irradiation vasculopathy
d. Fibromuscular dysplasia
e. Fibrinoid vasculopathy
2. Inflammatory
a. LARGE ARTERIES (Temporal arteritis,
Giant cell anteritis, Takayasus Ateritis)
b. MEDIUM (Kawasaki, Polyarteritis Nodosa)
c. SMALL-MEDIUM (Wegener’s
granulomatosis, Microscopic polyangitis)
d. SMALL ARTERIES (IgA vasculitis,
Henoch- Schnolein, Vasculitis related to RA,
Drug-induced vasculitis)

59. NON-INFLAMMATORY
CAROTID and VERTEBRAL ARTERY
DISSECTION
• 2% of all Ischemic strokes.
• 10% of young adult stroke <45 yrs .
• Tear in the intima or media.
• Bleeding within the arterial wall
• Dissects circumferentially and
longitudinally.
ISCHEMIC STROKE due to:
• Embolisation of thrombus formed at the
site of the tear into an intracranial
artery.
• Occlusion of the dissected artery.

60. NON-INFLAMMATORY
Carotid Artery Dissection
 Headache/neck pain
 Horner’s syndrome
 TIA and stroke in carotid
territory
 Cranial nerve palsies
Vertebral Artery Dissection
 Neck pain
 Pain in occipital region and
ears
In TIA and stroke in vertebrobasilar territory, symptoms
usually within hours/ days of dissection but there may be delay
of weeks or even months.
CLINICAL MANIFESTATION

61. NON-INFLAMMATORY
I. Spontaneous
 Genetic connective tissues
disorders (1- 5%)
- Ehlers-Danlos,
- Marfan’s
-Osteogenesis Imperfecta
II. Fibromuscular Dysplasia
 Cystic medial necrosis
 Possibly atheromatous risk
factors
-BP, DM, Smoking, cholesterol
III. Traumatic
 Sports
 Whiplash injury
 Neck manipulation
CAUSES :
Carotid
Duplex Scan
Normal carotid arteries
and vertebral arteries
duplex scan

62. INFLAMMATORY
LARGE ARTERIES
Temporal Arteritis
Takayasus Arteritis
MEDIUM
Kawasaki
Polyarteritis Nodosa
SMALL-MEDIUM
Wegener’s Granulomatosis
Microscopic Polyangitis
SMALL ARTERIES
IgA Vasculitis( Henoch- Schnolein)
Vasculitis related to RA
Drug-induced Vasculitis
Ischaemic stroke in young adults Dr Lillian Choy
Stroke Multidisciplinary Study Day 6 th October
2010
EXAM RESULT
ESR 21.0

63. HEMATOLOGIC DISORDER
1. Viscosity
a. Myelodysplastic Syndrome
-CML
-Polycythemia Vera
-Essential Thrombocythemia
b. Multiple Myeloma
c. Leukemia
2. Coagulopathy
a. Hemoglobin disorder
b. Protein C/S deficiency
c. Antithrombin III deficiency
d.DIC
e. Anti-phospholipid antibody
EXAM RESULT Reference
interval
Anti Thrombin
III
87 % 80 – 120 %
Protein C 116 % 70 – 130 %
Protein S 76 % 60 – 140 %
Remarks Protein C is detected via
chromogenic assay.
Protein S is determined via
functional assay (Clotting method),
which measures physiologically
active Protein S.
Correlation with clinical findings is
required.
CBC 1.26.15
Hemoglobin 168 
Hematocrit 0.48 
WBC 18.29 
Segmenters 0.84 
Stabs 0.03
Lymphocytes 0.13
Monocytes
Platelets 336,000

64. HEMATOLOGIC DISORDER
• Hypercoagulability should be suspected in patients with
ischemic stroke who have the following characteristics:
– Younger than 50 years with no obvious cause of stroke
– History of multiple unexplained strokes
– Previous history of venous thrombosis
– Family history of thrombosis
– Abnormalities on routine screening coagulation tests
HYPERCOAGULABLE STATE

65. HEMATOLOGIC DISORDER
Inherited:
• Factor V Leiden
• Prothrombin gene mutation
• Anti-thrombin deficiency
• Protein C & S deficiencies
• Elevated homocysteine
• Dysfibrinogenemia
• Elevated Factor VIII levels
• Abnormal fibrinolytic system
• Sickle Cell disease
Acquired:
• Antiphospholipid antibody
syndrome
• Supplemental estrogen use
• Cancer
• Medications
• Central venous catheter
• Obesity
• Pregnancy
HYPERCOAGULABLE STATE

66. HEMATOLOGIC DISORDER
HYPERCOAGULABILITY WORK UP
– PT and PTT
– Protein C
– Protein S
– Antithrombin III activity
– Prothrombin gene mutations
– Factor V Leiden gene mutation
– Activated Protein C resistance
– Anticardiolipin antibodies (IgG and
IgM)
– Beta2-glycoprotein I antibodies
(IgG and IgM)
– Lupus anticoagulant tests
• dilute Russell viper venom
time
• dilute activated PTT
• hexagonal phospholipid
– Homocysteine
– Factor VIII activity
– D-dimer
– Lipoprotein (a)
– MTHFR
HYPERCOAGULABLE STATE

67. OTHER CAUSES OF THROMBOTIC
STROKE
Others:
1 .Migraine
2. Pregnancy
3. Trauma
4. Drugs
Cocaine
Heroine
Metamphetamines
5. Genetic
CADASIL

68. Drug Abuse and Stroke
• Should be considered in all
young patients with stroke.
• Cause marked and abrupt
increases in blood pressure
and may precipitate
cerebral vasospasm
• Sympathomimetic drugs:
• Cocaine
• Amphetamines
• Both drugs have been
associated with cerebral
infarction and cerebral
hemorrhage
• Intravenous abuse risk of
stroke through :
• Infective endocarditis
• Cerebral hypoperfusion
Ischaemic stroke in young adults Dr Lillian Choy
Stroke Multidisciplinary Study Day 6 th October
2010

69. CEREBRAL AUTOSOMAL DOMINANT ARTEROPATHY with
SUBCORTICAL INFARCTS and LEUCOENCEPHALOPATHY
(CADASIL)
• Is a systemic disease of the
vasculature whose clinical
effects are confined to the
brain.
• Notch 3 gene mutation.
• 3rd decade-symptom free
• 4th -5th decades- Subcortical
stroke
Features :
• subsequent dementia and
occasionally an associated
depressive illness and/or
seizure disorder
DIAGNOSTICS:
 MRI
MANAGEMENT:
 Supportive
 Modification of vascular risk
factors
 Antiplatelet Therapy
 Anticonvulsant
 Antidepressant
Ischaemic stroke in young adults Dr Lillian Choy
Stroke Multidisciplinary Study Day 6 th October
2010

70. RISK FACTORS FOR STROKE IN THE YOUNG
PERIODICUM BIOLOGORUM VOL. 114, No 3, 347–353, 2012
Risk Factors in Stroke in Young Prevalence
Hypertension, dyslipidemia, diabetes
Smoking
Migraine
Pregnancy and puerperium
Oral contraceptives
Illicit drug-use
45-60%
40-60%
10-35%
5-10%
10-22%
3-12%
Specific diseases
Spontaneous arterial dissection
Fibromuscular dysplasia of carotid and vertebral arteries
VASCULITIS AND CONNECTIVE TISSUE DISORDERS: Churg-Strauss, Wegener’s
vasculitis, polyarteritis nodosa, cryoglobulinemia,inflammatory bowel disease,
sarcoidosis, SLE, APAS
INFECTIVE DISEASES:Syphilis, tuberculous menigitis, acute bacterial meningitis,
varicella-zoster virus, AIDS, hepatitis C
HEMATOLOGIC: Paroxysmal nocturnal hemoglobinuria, TTP, erythrocytosis, leukemia
sickle cell disease
CARDIAC: Patent foramen ovale, atrial septal aneurysm, inter-atrial septum, atrial
fibrillation, cardiomyopathy, valvular disease and endocarditis
40-50%
10-15%
6-10%
4-8%
2-10%
18-30%

71. SMOKING AS STROKE RISK FACTORS
• A meta analysis of 22 studies approximate doubling of
relative risk of cerebral infarction among smokers
versus non-smokers.
• Framing Heart Study
– Relative Risk of heavy smokers (>40 cig/day) twice that of
light smoker (<10 cig/day).
• Studies suggest
– Dose response relationship between pack years of smoking
and carotid-artery intima- media wall thickness
Guidelines for the Prevention, Treatment and Rehabilitation of Brain Attack 5th Edition 2010

72. Plausible Mechanism of Smoking
• Nicotine
– Increases LDL and decreases HDL
– Increases level of thrombin
– Damaged the blood vessel wall
– Increases endothelin (EF-1) constricts blood
vessels
National Institute of Health Public Access, July 2010

73. Diagnostic Testing for Patients With
Stroke
Basic Stroke Evaluation
(Imaging Techniques)
• Cranial Computed Tomography (CT)
• Carotid Ultrasonography ± Transcranial Doppler
• Transthoracic Echocardiography
• ECG Monitoring

74. Blood Tests and Ancillary Procedures
Routine Blood Studies
• CBC with Differential and
Platelet Count
• PT (INR)
• APTT
• Glucose
• Chemistries
• Serology for syphilis
• ESR
PREGNANCY TEST
Blood Test for Hypercoagulable
State
• Anticardiolipin
Antibodies
• Lupus Anticoagulants
• Protein S
• Protein C
• Activated protein C
resistance
• Antithrombin III
Blood Testing for Genetic
– CADASIL
– Fabry disease
– MELAS

75. Comprehensive Stroke Evaluation
• Cranial MRI
• MRA or CTA
• Transesophageal echocardiography (TEE)
• Carotid Duplex Scan
• Prolonged ECG monitoring with Holter

76. DEFINITION OF STROKE SEVERITY
MILD STROKE MODERATE STROKE SEVERE STROKE
Alert patients with any or a
combination of the ff:
1. Mild pure motor weakness
of one side of the body,
defined as: can raise arm
above shoulder, has
clumsy hand, or can
ambulate without
assistance.
2. Pure sensory deficits
3. Slurred but intelligible
speech
4. Vertigo with
incoordination (e.g, gait
disturbance, unsteadiness
or clumsy hand)
5. Visual field defects alone.
Awake patient with significant
motor and/or sensory and/or
language and/or visual deficits
Or
Disoriented, drowsy or light
stupor with purposeful
response to painful stimuli
Deep stupor or comatose
patient with non-purposeful
response, decorticate, or
decerebrate posturing to
painful stimuli
Or
Comatose patient with no
response to painful stimuli
Guidelines for the Prevention, Treatment and Rehabilitation of Stroke by the Stroke Society of the Philippines 5th Edition 2010

77. GUIDELINES FOR MILD STROKE
Management Priorities
Ascertain clinical diagnosis of stroke (history and physical exam are very important)
• Exclude common stroke mimicker
Provide basic emergent supportive care (ABCs of resuscitation)
Monitor neuro-vital signs, BP, MAP, RR, Temp, pupils, O2 saturation
Perform and monitor stroke scales (NIHSS, GCS)
Provide O2 support to maintain O2 saturation >95%
Monitor and manage BP, Treat if MAP >130
Precautions
• Avoid precipitous drops in BP (not >15% of baseline MAP). Do not use rapid acting
sublingual agents; when needed, use easily titratable IV or oral antihypertensive
medications
• Ensure adequate hydration, recommended IVF- 0.9% NaCl

78. Guidelines for Mild Stroke
Emergent Diagnostics
• Complete Blood Count (CBC)
• Blood Sugar (CBG or RBS)
• Electrocardiogram (ECG)
• PT/PTT
• Non-contrast CT scan of the brain or MRI-DWI as soon as possible
• If ICH, compute for hematoma volume

79. GUIDELINES FOR MODERATE STROKE
ISCHEMIC HEMORRHAGIC
NON-CARDIOEMBOLIC
(Thrombotic, Lacunar)
CARDIOEMBOLIC
If within 3 hours of stroke onset,
consider IV recombinant tissue
plasminogen activator (rt-PA)
Selected patients within 3-4.5 hr
time window may benefit with IV
rTPA (see section on thrombolytic
therapy).
Refer to neurologist for evaluation
and decision.
if within 6 hours of stroke onset
and in specialized centers, consider
intra-arterial thrombolysis
Start ASA 160-325mg 24 hr after
rTPA treatment.
If rtPA ineligible, start Aspirin 160-
325mg/day ASAP
Neuroprotection
Early supportive rehabilitation
Consider early decompressive
hemicraniectomy for large
malignant MCA infarction.
If within 3 hours of stroke onset,
condider IV rtPA and refer to neuro
specialist
If within 6 hours of stroke onset
and in specia
(Guidelines for the Prevention, Treatment and Rehabilitation of Stroke, Stroke Society of the Philippines 5th Edition 2010)

80. GUIDELINES FOR MODERATE STROKE
EMERGENT DIAGNOSTICS:
CBC W/ PC
CBG or RBS
PT/PTT
Serum Na and K
ECG
Non-contrast CT scan of brain or MRI-DWI as soon as possible
If ICH, compute for hematoma volume
Guidelines for the Prevention, Treatment and Rehabilitation of Stroke by the Stroke Society of the Philippines 5th Edition 2010

81. Guidelines for Mild Stroke
Early Specific Treatment
CT SCAN
CONFIRMED
ISCHEMIC HEMORRHAGIC
Non-cardioembolic
(Thrombotic Lacunar)
Cardioembolic • Early neurology and/or
neuro surgeon consult for
all ICH is recommended
• Monitor and maintain BP:
target MAP of 110 or SBP
160
• Neuroprotection
• Early rehabilitation once
stable within 72 hours
• Give anti convulsant for
clinical seizures and
proven subclinical or
electrographic seizures,
prophylactic AEDs re
generally not recommend
• Steroids are not
recommended
• Monitor and correct
metabolic parameters
• Correct coagulation/
bleeding abnormalities
• Follow recommendations
for neurosurgical
intervention
• For aneurysmal SAH
• Aspirin 160-325 mg/day.
Start as early as possible
and continue for 14 days
• For secondary prevention,
see under “delayed
management and
treatment”
• Neuroprotection
• Early rehabilitation once
stable within 72 hours
• Consider careful anticoagulant with
IV heparin or SQ low molecular-
weight heparin (LMWH) for those at
high risk for early recurrence (e.g.
AF with thrombus, valvular heart
disease or MI)
OR
• Aspirin 160-325 mg/day (if
anticoagulation is not possible or
contraindicated)
• Neuroptotection
• Early rehabilitation once stable
within 72 hours
• If infective endocarditis is
suspected, give antiobiotics and do
not anticoagulate
Place of
treatment
ADMIT TO HOSPITAL : Acute stroke unit / Regular room

82. EARLY SPECIFIC TREATMENT FOR
ISCHEMIC STROKE
ANTI THROMBOTIC THERAPY IN ACUTE STROKE
DRUG TRIAL DESIGN RESULT
ASPIRIN International stroke
Trial (IST, Lancet 1997; 349:
1569-1581)
19,435 patients with acute
ischemic stroke were
randomized within 48
hours to aspirin 300 mg
day, subcutaneous heparin
5000 units BID or 12,500
units BID, aspirin and
heparin or neither
Aspirin treated patients
had slightly fewer deaths at
14 days , significantly fewer
recurrent ischemic stroke
at 14 days and no excess of
hemorrhagic strokes
For patients receiving
heparin, there were fewer
deaths or recurrent strokes;
however there were more
hemorrhage, mostly in the
higher dose heparin group,
resulting in no net benefits
Chinese acute stroke trial
(CAST, Lancet 1997; 449:
1641-1649)
21,106 patients with acute
ischemic stroke within 48
hours were randomized to
aspirin 160 mg OD or
placebo for upto 4 weeks
Aspirin significantly
reduced the risk of
recurrent stroke or vascular
death

83. EARLY SPECIFIC TREATMENT FOR
ISCHEMIC STROKE
ANTI THROMBOTIC THERAPY IN ACUTE STROKE
DRUG TRIAL DESIGN RESULT
Clopidogrel
– ASA vs Aspirin
Ast assessment of stroke
and TIA to prevent early
recurrence, (FASTER ,
lancet Neurology 2007; 6:
961 – 969)
392 patients with TIAor
minor stroke within 24
hours were randomized
with clopidogrel (300mg
loading dose then
75mg/day plus aspirin 81
mg or aspirin 75 mg alone,
with or without simvastatin
(in factoral design) and
followed for 90 days
The trial was prematurely
terminated because of
failure to recruit patients at
the pre specified
recruitment rate because
of increased use of statins.
Recurrent stroke 90 days
were : clopidogrel-ASA
(7.1%) aspirin alone
(10.1%) absolute risk
reduction of 3.8% P=0.19
LMWH Meta analysis of
randomized cntrolled trials
on low molecular weight
heparins and heparins in
acute ischemic stroke
(stroke 2000; 31: 31 1770-
1778)
Ten trials involving 2885
patients with acute
ischemic stroke low
molecular weight heparin
and heparinoids given with
7 days
The use of LMWH /
heparinoids was associated
with significant reduction
with venous
thromboembolism (DVT
and PE) however, it had no
significant effect on
reducing death and
disability at 6 months

84. PROGNOSIS OF STROKE
• The prognosis and complications of stroke in
young patients are highly dependent on the
underlying cause of stroke, as well as the
amount and location of CNS damage. The 30-
day case fatality is low, particularly in ischemic
stroke (0% to 6%), whereas it ranges from 20%
to 36% for cerebral hemorrhage .
(Gaete, et.a l , Stroke in young adult Prognosis and Complications,2002)

85. SUMMARY

86. FINAL DIAGNOSIS
Acute Cerebrovascular Accident(Infarct),
Pontocerebellar Region, Right

87. References:
• Adams and Victor Principles of Neurology, 9th edition.
• Choy, Lilian.Ischemic Stroke in Young Adults, 2010.
• DeMyer, William Technique of the Neurologic Examination 5th Edition.
• Gaete, et.a l , Stroke in young adult Prognosis and Complications,2002.
• Griffiths et.al, Epidemiology and Etiology of Young Stroke , PGH,
Department of Rehabilitation Medicine.2011.
• Guidelines for the Prevention, Treatment and Rehabilitation of Stroke,
Stroke Society of the Philippines 5th Edition 2010.

88. THANK YOU VERY MUCH.
Wassalam !