1) A 60-year-old man presented with sudden onset right-sided hemiplegia upon waking. 2) On examination, he had right-sided weakness and sensory loss consistent with involvement of the left middle cerebral artery territory. 3) Brain imaging revealed an acute ischemic stroke in the left middle cerebral artery distribution, likely due to thrombotic occlusion of that vessel.

2. OUTLINE
 Brief anatomy and physiology of brain lobes and
their blood supply
 Different terminology
 Causes of hemiplegia:
 Stroke in details
 Approach to a patient presenting with hemiplegia
 History taking
 Physical examination
 Investigation
 A case: brain storming

4. Brain
blood
supply
ICA
Vertebr
al.a
•Hypophyseal.
a
•Ophthalmic. a
•Antrerior
choroidal.a
•Supply:optic tract,
coridal plexus, internal
capsule, globus pallidus
•ACA
•Supply medial aspect
of frontal and parital
lobe
•Upper lateral part of
cortex of both lobes
•MCA
•Supply the whole
lateral surface of
parietal, temporal ,and
frontal lobe
Anterior and
posterior
spinal. a
•Supply spinal
cord•Ant & post
inferior
cerebellar.a
•Sperior
cerebellar. a
•Supply
cerebellum
•PCA
•Occipital lobe
•Inferomedial
aspect of temporal
Basil
ar. a

5. BLOODSUPPLYOF BRAIN

7. Anterior Limb -Frontopontine fibres, Thalamocortical fibres to frontal lobe
Genu - Corticonuclear/ corticobulbar fibres and Corticospinal fibres to head and
neck
Posterior Limb - Corticospinal fibres to trunk, upper and lower limbs,
corticorubral fibres, temporopontine, parietopontine and occipitopontine fibres,
thalamocortical fibres to temporal, parietal and occipital lobes
Retrolentiform part -Optic radiations from lateral geniculate body (thalamus) to
Visual cortex in occipital lobe
Sublentiform part -Auditory radiations from Medial geniculate body (thalamus) to

9. DIFFERENTTERMIMOLOGIES
 Paresis: partial or incomplete paralysis
 Plegia: complete paralysis
 Monoplegia is a paralysis of a single limb, usually an arm
 Hemiplegia: total paralysis of the arm, leg, and trunk on the
same side of the body.
 Paraplegia: an impairment in motor or sensory function of the
lower extremities.
 Triplegia : is paralysis of three limbs.
 Quadriplegia : is paralysis of all limbs, paraplegia is similar
but does not affect the arms

10. Causes of hemiplegia
• cerebral hemorrhage
• strokeVascular
• encephalitis, meningitis, brain abscessInfective
• glioma-meningiomaNeoplastic
• disseminated sclerosis, lesions to the internal
capsule
Demyelination
• Cerebral palsyCongenital
• Brown-Séquard syndrome
Spinal cord
diseases
traumatic

12. Definitions
 Stroke:
 Clinical syndrome of rapid onset of focal deficits of
brain function lasting more than 24 hours or leading
to death
 Transient Ischemic attack (TIA):
 Clinical syndrome of rapid onset of focal deficits of
brain function which resolves within 24 hours
 Amaurosis fugax

13. DefinitioNS
 Progressive Stroke:
 A stroke in which the focal neurological deficits
worsen with time
 Also called stroke in evolution
 Completed Stroke:
 A stroke in which the focal neurological deficits
persist and do not worsen with time

14. Epidemiology
 Third most common cause of death after cancer
and ischeamic heart disease
 Most common cause of severe physical
disability
 Incidence and prevalence of stroke is on the rise
due to increasing adoption of unhealthy lifestyle
& an increasing life expectancy

15. StrokeRiskFactors
 Fixed
 Age
 Gender (Male>Female)
 Race (Afro-
Caribbean>Asian>Euro
pean)
 Heredity
 Previous vascular event
eg. MI, peripheral
embolism
 High fibrinogen
 Modifiable
 Hypertension
 Heart disease (Atrial
fibrillation, endocarditis)
 Diabetes mellitus
 Hyperlipidaemia
 Smoking
 Excess alcohol
consumption
 Oral contraceptives

16. Typesof Stroke
Ischemic
Hemorrhagic

17. IschemicStroke
 80% of strokes
 Arterial occlusion of an intracranial vessel leads
to hypoperfusion of the brain region it supplies
 three etiological types:
 Thrombotic
 Embolic
 Systemic hypoperfusion

18. Etiologyof ischemicstroke
 Thrombotic
 Lacunar stroke 20%
 Large vessel
thrombosis
 Hypercoagulable
disorders
 Embolic
 Artery to artery
 Carotid bifurcation
 Aortic arch
 Cardioembolic
 Atrial fibrillation
 Myocardial infarction
 Mural thrombus
 Bacterial endocarditis
 Mitral stenosis
 Paradoxical embolus

19. ATP depletion
Hypoperfusion
Failure of Na+/K+ ATPase membrane ionic pump
Calcium entryGlutamate release
Activation of lipid peroxidases, proteases & NO synthase
Destruction of intracellular organelles, cell
membrane & release of free radicals
Free fatty acid release
Activation of pro-coagulant
pathways
Liquefactive
necrosis
Thrombus/embolus
Membrane depolarization & cytotoxic cellular
edema

20. Hemorrhagic Stroke
 Four types:
 Epidural
 Subdural
 Subarachnoid √
 Intraparenchymal √
 Higher mortality rates
when compared to
ischemic stroke

21. Intracerebral Hemorrhage
• Result of chronic hypertension
• Small arteries are damaged due to hypertension
• In advanced stages vessel wall is disrupted and
leads to leakage
• Other causes: amyloid angiopathy, anticoagulant
therapy, cavernous hemangioma, cocaine,
amphetamines

22. SubarachnoidHemorrhage
 Most common cause is rupture of saccular or Berry
aneurysms
 Other causes include arteriovenous malformations,
angiomas, mycotic aneurysmal rupture etc.
 Associated with extremely severe headache

25. History taking
 The history and physical examination should be used to
distinguish between other disorders in the differential
diagnosis of brain ischemia .
 As examples, seizures, syncope, migraine, and
hypoglycemia can mimic acute ischemia.
 It is important to ask the patient or a relative whether the
patient takes insulin or oral hypoglycemic agents, has a
history of a seizure disorder or drug overdose or
abuse, medications on admission, recent trauma, or
hysteria.
 The history is also important in separating ischemia
from hemorrhage and distinguishing between subtypes
of ischemia and hemorrhage.

26. History taking in hemiplegia
 When did the event started?
 What is the total duration of the illness? If
multiple, ask about each episodes.
 What according to the patient or relatives were
the initial presenting symptoms?
 What was the exact mode of onset: was it abrupt,
sudden, sub-acute, or gradual?
 When was the maximum deficit noted: in the
beginning or later.
 Time course of the initial symptoms? Static or
progress
 Any associated symptoms: CVS,RS,or GIT?

27. assessing the CNS
function?
 Was there any loss of consciousness/ in the beginning or later;did he
recover from it? And for how long he stays unconsciousness?
 What is the emotional status of the patient; memory and
intellegance?
 Is speech affect and if so in what way? Motor, sensory, conductive
aphasia?
 Which of the cranial nerve is affected and what are the symptoms
related?
 What is the degree of motor weakness?
 Are you able to wear your cloths? put button of your clothes? eat?
Open the door?
 Are you able to stand? Walk? Move your limbs?

28. 1- Is the patient having
neurological problem?
 Yes or no?
 Is it a medical condition simulating
hemiplegia?
 Post icteal Todd’s paralysis, or episode of MS
 If yes, what are the neurological deficits:
 Hemiplegia, UMN facial weakness, hemianesthesia,
homonymous hemianopia
 Dysphasia in right hemiplegia and dysarthria in a
left hemiplegia
 Crossed hemiplegia
 Cervical cord lesion

29. 2-Which are the CNS
structures involved?
 Cerebral cortex
 Pyramidal tract
 Extra-pyramidal tract
 Cerebellum
 Brain stem nuclei
 Cranial nerve

30. 3- Is it a UMN lesion or a
LMN lesion?
UMN Disease LMN Disease
Suprasegmental Segmental
1. Weakness of the functional group of muscles
(depending on the site of lesion).
1. Weakness in one or more muscles, depending the
segmental involvement.
2. Spastic paralysis. 2. Flaccid paralysis.
3. Hypertonia. 3. Hypotonia (may be atonia if the destruction is
complete).
4. Hyperreflxia (Exaggerated Deep Tendon
Reflexes “DTRs”).
4. Deep Tendon Reflexes (DTRs) are lost in sever
cases (decreased otherwise).
5. Positive Babinski’s sign (Extensor plantar reflex:
dorsiflexion of foot). Triple Flexion: dorsiflexion of foot,
leg and thigh).
5. Babinski’s sign is absent.
6. Disuse atrophy. 6. Neurogenic atrophy (denervation atrophy) about
70% - 80%.
7. Nerve conduction is normal. 7. Nerve conduction is abnormal.
8. No fibrillations or fasciculations. 8. Fibrillations and fasciculations may be present.
9. Clonus is present. 9. No clonus seen.
10. Bilateral movements such as eyes, jaws, pharynx,
larynx and neck are little affected or not at all.

31. 4- in which way the speech
is effected?

32. 5- is there a UMN or LMN
facial paralysis?
 UMN facial paralysis:
 Upper half of face is spared
 Lower half affected
 no Bell’s phenomena
 Taste not affected
 LMN facial paralysis:
 Entire half of the face affected
 Bell’s phenomena present
 Taste affected

33. 6- what is the site of
localization of lesion?
• Partial deficit, speech involvement, cortical
sensory, focal sezure
• Brain lobs deficit
cortex
• Full hemiplegia
Sub-cortical
lesion
• Dense hemiplegia, sparing of speech
• Absence of speech deficit and sizuresInternal capsule
• Hemiparalysis, hemianopia, hemisensory
loss, and emerging hyperpathiaThalamic lesion
• Crossed hemiplegiaBrain stem

34. 7- is it an ischemic stroke or
Hemorrhagic stroke??
Ischemic stroke Hemorrhagic stroke
•Start suddenly
•Over seconds or
minutes
•Most cases do not
progress (Complete
stroke)
•Classically detected by
patient in the morning
when waking up
•May or may not be
preceded by episodes of
TIAs
•Mainly in HTN patients
•55-75 years of age
• smooth onset
•Over minutes or hours
•Steady progress despite
treatment
•Signs of increase ICT
•Usually associated with
severe headache and
vomiting

35. 8-IF IT ISCHEMIC WHICH
ARTERY INVOLVED??
carotid
• Contralateral weakness
• Contralateral numbness
• Dysphasia
• dysarthria
• ipsilatera;l mono-ocular
• Contralateral
homonymous
vertebral
• Bilateral or shifting
weakness
• Bilateral or shifting
numbness
• diplopia
• Dysarthria
• Inco-ordination of upper
limbs
• Ataxia/ imbalance/
disequilibrium
• Visual loss in both
homonymous fields

36. 9- is it internal carotid artery
syndrome?
 Often asymptomatic
 Due to collaterals circulations
 Ext. carotid and ophthalmic anastamosis
• Warning
symptoms:
•Episode of
confusion
•Speech
dysfunction
•Amouriosis fugax
(transient mono-
ocular blindness)
•Fleeting
parasthesia
•Neurological deficits:
•Same as that of
MCA territory infract
•Contralateral
Hemiplegia
•Contralateral
sensory symptoms
•Local carotid
examination:
•Feeble carotide
pulsation
•Feeble temporal. a
pulsation
•Cervical bruit over
carotid
•Carotid doppler
angiography

37. 10- which cerebral artery
syndrome?
MCA
• Contra-lateral weakness face, UL, & LL
• Contralateral hemisensory loss
• Broca’s, wernecke’s, conduction, global aphasia
• contralateral homonymous hemianopia
ACA
• Contralateral paralysis of leg and foot
• Sensory loss in the contralateral leg and foot
• Gait apraxia
PCA
• Thalamic syndrome: hemiplagia ,and hemisensory loss, followed
with searing pain (thalamic hyperpathia)
• Up regulation of threshold for pain
• The pain aggrevated by: heat, cold, emotion of listening to music,

38. 11
-

39. Physical Examination
 Level of consciousness, mental status, speech, &
gait.
 Cranial nerves, motor function, sensory function,
and superficial and deep tendon reflexes.
 Special reference:
 Optic fundus: papilledema
 Signs of meningeal irritation: Kernig's Signs, and
Brudzinski's Sign
 Signs of head injury

40. Level f consciousness

41. Mental status

42. MOTOR FUNCTION
 BODY POSTURE
 INSPECTION- MUSCLE BULK
 TONE
 POWER
 REFLEXES
 CO-ORDINATION

43. SENSORY FUNCTION
 Pain and temperature
 Pressure and touch
 Proprioception, vibration, and fine touch

44. Examination of a stroke
patient
Skin:
• Xanthalasma
• rash(arteritis,
splinter
hemorrhage)
• color and
temperature
changes
Eye:
• Diabetic changes
• retinal emboli
• HTN changes
CVS:
• Heart rhythme
(AF)
• BP (HTN
,hypoBP)
• JVP(HF,
hypovolemia)
• Murmurs
• Peripheral pulse &
bruits
RS:
• Signs of
pulmonary
embolism
• Signs of
respiratory
infection
Abdomen:
• Palpable bladder
(urinary retention)

45. Investigation
 All patients with suspected stroke should have the
following studies immediately upon admission to the
emergency department:
 Noncontrast brain CT or brain MRI
 Electrocardiogram
 Complete blood count including platelets
 Cardiac enzymes and troponin
 Electrolytes, urea nitrogen, creatinine
 Serum glucose
 Prothrombin time and international normalized ratio
(INR)
 Partial thromboplastin time
 Oxygen saturation
 Lipid profile

46. Investigations
•For diagnosing ischemic
stroke in the emergency
setting:
•CT scans (without
contrast):
•Sensitivity: 16%
•Specificity: 96%
•MRI scan:
•Sensitivity: 83%
•specificity :98%
•For diagnosing hemorrhagic
stroke in the emergency setting:
•CT scans (without
contrast):
•Sensitivity: 89%
•Specificity: 100%
•MRI scan:
•Sensitivity: 81%
•specificity :100%
•For detecting chronic hemorrhages, MRI scan is more sensitive

47. Case1
 A right handed 60 years old man was admitted with
weakness involving the right side of the body. He
woke up from sleep unable to move his right arm or
leg. The family noted that he had right sided facial
drooping. He was also noted to have difficulty
speaking.
 No fever, headache, vomiting, seizure or loss of
consciousness. He denied any chest pain or
palpitation.
 He have an episode of weakness affecting his right
arm that resolved within a few hours a few months
prior to this episode.
 Past HX of DM and HTN for 6 years. Also diagnosed
with IHD previously. On medication
 No history of smoking or alcohol consumption.

48. case1
 On examination:
 Alert oriented and attentive
 Vitals: BP(180/100), RR (22), temp(36.8), O2
saturation (98%)
 He have:
 Expressive aphasia
 Right sided UMN seventh cranial nerve palsy
 Homonymous hemianopsia
 Dense right sided hemiplagia and hemianesthesia.
 Irrigulare heart sound. No murmur
 Destended urinary bladder

49. Case 1
 What is the cause of his symptoms?
 What are the risk factors?
 What type of stroke he have?
 Which are the CNS structures involved?
 Which cerebral artery most likely involved?
 What investigation you will order?