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
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 cordAnt
& post inferior cerebellar.a Sperior cerebellar. a Supply
cerebellum PCA Occipital lobe Inferomedial aspect of temporal Basil
ar. a
BLOODSUPPLYOF BRAIN
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
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
Causes of hemiplegia cerebral hemorrhage strokeVascular
encephalitis, meningitis, brain abscessInfective
glioma-meningiomaNeoplastic disseminated sclerosis, lesions to the
internal capsule Demyelination Cerebral palsyCongenital
Brown-Squard syndrome Spinal cord diseases traumatic
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
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
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
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
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
Hemorrhagic Stroke Four types: Epidural Subdural Subarachnoid
Intraparenchymal Higher mortality rates when compared to ischemic
stroke
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
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
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.
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?
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?
1- Is the patient having neurological problem? Yes or no? Is it
a medical condition simulating hemiplegia? Post icteal Todds
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
2-Which are the CNS structures involved? Cerebral cortex
Pyramidal tract Extra-pyramidal tract Cerebellum Brain stem nuclei
Cranial nerve
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
Babinskis sign (Extensor plantar reflex: dorsiflexion of foot).
Triple Flexion: dorsiflexion of foot, leg and thigh). 5. Babinskis
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.
4- in which way the speech is effected?
5- is there a UMN or LMN facial paralysis? UMN facial
paralysis: Upper half of face is spared Lower half affected no
Bells phenomena Taste not affected LMN facial paralysis: Entire
half of the face affected Bells phenomena present Taste
affected
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
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
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
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
10- which cerebral artery syndrome? MCA Contra-lateral weakness
face, UL, & LL Contralateral hemisensory loss Brocas,
werneckes, 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,
11 -
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
Level f consciousness
Mental status
MOTOR FUNCTION BODY POSTURE INSPECTION- MUSCLE BULK TONE POWER
REFLEXES CO-ORDINATION
SENSORY FUNCTION Pain and temperature Pressure and touch
Proprioception, vibration, and fine touch
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)
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
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
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.
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
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?
