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CLINICAL EVALUATIO
HEMIPLEGIA
Dr. S. Aswini Kumar. MD
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Anatomy of Brain
Fore brain
receiving sensory information fromvarious sensory inputs of body
processing the information received andcorrelating them with prior ones
thinking, perceiving, producing andunderstanding language
controlling motor function and autonomicfunctions
Mid brain:
auditory and visual responses
Hind brain
balancing equilibrium and co-ordination
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Physiology of brain3
Frontal lobe: Provides executive control over much of the brain's higher fu
Consciousness, self-awareness, judgment, initiation, motivation
Planning, sequencing, word formation, control over emotional responses
Parietal lobe: Perceives, analyzes, and assembles touch information from
Integrates visual, auditory, and touch information to formulate complete impre
Left - letters come together to form words and where words are put together in
Right - recognizing shapes, being aware of one's body in space
Temporal lobe: Hearing, memory acquisition, perception, and categorizat
Comprehension of language, listening, reading; music
Occipital lobe: Dedicated entirely to vision
In terms of detection, identification, and interpretation of objects.
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Handedness & Contra-laterality of brain co
90% of general population-right handed
10% left handed
Handedness
By birth not by training
Test by natural skill; not learned skills
Throwing stones, kicking football
Determination of hemispherical dominance Right handed
99% left dominant hemisphere
Left handed
70% of left handed left dominanthemisphere
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Blood supply of brain5
Carotid system Internal carotid
Middle cerebral M1 M2
Ophthalmicartery
Anteriorcerebral
A1Anterior
communicating
Anteriorchoroidal
Vertebralsystem
Basilar
Posteriorcerebral
Ant inferiorcerebellar
Post inferiorcerebellar
Posteriorcommunicating
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The Circle of Willis6
Named after Thomas Willis (16211673)
Anterior cerebral artery (left and right)
Anterior communicating artery
Internal carotid artery (left and right)
Posterior cerebral artery (left and right)
Posterior communicating artery (left and right)
Physiologic significance
In event of narrowed or blocked vessel
preserve the cerebral perfusion
avoid the symptoms of ischemia
Considerable anatomic variation exists
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The internal capsule7
Anterior limb:
lenticulostriate branches of middlecerebral artery (superior half)
recurrent artery of Heubner off ofthe anterior cerebral artery (inferior half)
Genu:
lenticulostriate branches of middlecerebral artery
Posterior limb:
lenticulostriate branches of middlecerebral artery (superior half)
anterior choroidal artery off ofthe internal carotid artery (inferior half)
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Corticospinal tract8
Originates from pyramidal cells in layer Vof the cerebral cortex
Axons that travel down through the brain
stem and spinal cord - upper motor neurons
Long axons to the motor cranial nerve nuclei
mainly of the contralateral side of the
midbrain (cortico-mesencephalic tract)
pons (cortico-pontine tract)
medulla oblongata (cortico-bulbar tract)
spinal cord (corticospinal tract)
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Pathophysiology of ischemic stroke9
loss of bloodsupply to part of
the brain
initiatesthe ischemic
cascade
the brain becomeslow in energy
re
produces less ATPbut releases lactic
acid
Lactic acidpotentially
destroy cells sinceit is an acid
disrupts thenormal acid-base
balance in thebrain
le
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Ischemic penumbra and clinical signific10
A central area of irreversible infarction
the point of maximum insult called core
Surrounding area of potentially reversible
Called as ischemic penumbra.
It has two different segments
Inner area of diffusion abnormality
Outer area of perfusion abnormality
Hypoxia of the cells near the location of theoriginal insult
Target for revascularization if given within 60minutes
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History taking in Hemiplegia11
When did the event start? When was he last found to be in a normal What is the total duration of the illness? If multiple, of each episode?
What according to the patient or relatives were the initial presenting
What was the exact mode of onset; was it abrupt, sudden, sub-acute
When was the maximum deficit noted; was it in the beginning or later
What was the progress of the initial symptoms; static, progressing or
What were the associated symptoms; in CNS as well as CVS, RES and
What investigations he has under gone so far and what are the ones
What treatment the patient has received so far and what the ones pl
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History specific for assessing the CNS f12
Was there any loss of consciousness in the beginning/later; did he rec Is he able to co-operate in interview and the physical examination?
What is the emotional state of the patient; memory and intelligence?
Is speech affected and if so in what way? Motor, sensory or conductiv
Which of the cranial nerves are affected and what are the symptoms
What is the degree of motor weakness, wasting, flaccidity or stiffness
Are all the modalities of sensations normally appreciated or are they
Is the patient able to stand with/without support; swaying while stand
Any symptoms of increased intra-cranial tension like headache or vom
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Precise and complete neurological exam13
Confirms the presence of a stroke syndrome, distinguishes stroke from Evaluation of level of consciousness and mental status, speech and ga
Cranial nerves, motor function, sensory function, superficial, deep tend
Special reference to
Optic fundus - papilledema
III sign of uncal herniation
VI sign of increased ICT
Signs of meningeal irritation
Signs of head injury
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1. Is the patient having neurological pr14
Yes or No?
Or is it only hysterical or malingering?
Is it a medical condition simulating hemiplegia?
Post ictal Todds paralysis, episode of multiple sclerosis? ADEM?
If Yes what are the neurological deficits
Hemiplegia, UMN Facial weakness, hemianesthesia, homonymous hemiano
Dysphasia in a right hemiplegia and dysarthria in a left hemiplegia
Faciobrachial monoplegia
Crossed hemiplegia
Cervical cord lesion?
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3. Is there UMN or LMN facial paralysis16
Inspect the face at rest for voluntary & mimetic movements Examine symmetry of eye blinking and speech motion
Ask to raise eyebrows (frontalis)
Close eyes (orbicularis oculi)
Bells phenomenon (Superior rectus)
Show teeth (orbicularis oris)
Blow out cheeks (buccinator)
Scrunch up nose (nasalis)
Retract chin (platysma)
UM
Upper ha
Low
No B
T
LM Entire half
Bells phe
Other signs
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4. In what way speech is affected?17
First test spontaneous speech? What the patient asks for in the morning Bro
For tea/food/going to toilet
Now test the comprehension Whether he understands the meaning of words
Give some simple commands lift up the unaffected arm show the tongue
Test for intactness of conduction pathway Conductive aphasia
Whether the patient is able to repeat what the examiner says. Use a phrase
Test for naming intactness of the arcuate bundle Anomic aphasia Show an object like a pen and ask to name it; not merely to handle it or even use it
Try whether the patient can read aloud? Pure word blindness
Give a news paper and ask the patient to read aloud from it
Try whether a patient can understand spoken language? Pure word deafnes
inability to comprehend the meaning of speech, but still being able to hear, speak, read, and w
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5. What is the site of localization of les18
Cortex
Partial deficit, speech involvement, quadrantinopia, cortical sensory, focal
Sub-cortical region
Denser lesion, Full hemiplegia,
Internal capsule
Dense hemiplegia, sparing of speech, absence of speech defects and seiz
Thalamic
Hemiparalysis, hemianopia, hemisensory loss and emerging hyperpathia
Brain stem
Crossed hemiplegia - Nuclear type of cranial nerve lesions + contralatera
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6. What is the possible pathology of the les19
Is it an
ischemic infarct
embolic infarct
hemorrhagic infarct
hemorrhagic transformation of an ischemic infarct
hemorrhage
Is there evidence of significant or dangerous cerebral edema?
Its it a demyelination
Acute Disseminated Encephalomyelitis or Episode of MS
Is it a space occupying lesion: cerebral abscess cerebral tumor, cerebr
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7. Is it an ischemic stroke?20
Blood supply to part of the brain is decreased, leading to dysfunction
Cerebral atherosclerosis (producing flow limiting stenosis of a cerebral ves
Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
Embolism (obstruction due to an embolus from elsewhere in the body)
Systemic hypoperfusion (general decrease in blood supply, e.g. in shock)
Venous thrombosis (infarcts are more likely to undergo hemorrhagic transfo
Clinical features Start suddenly, over seconds to minutes, and in most cases do not progress
Classically detected by the patient in the morning when waking up
May or may not be preceded by episodes of transient ischemic attakcs
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8. Is it a TIA/evolving stroke/completed21
Transient Ischemic Attacks
Acute focal non-convulsive neurological dysfunction caused by reversible ischemia rec
Evolving stroke
Deficit occurs in a progressive or step wise fashion culminating in major deficit
In carotid territory within 24 hours and in vertebrobasilar territory within 72 hours
Completed stroke
The deficit is prolonged and permanent causing demonstrable parenchymal damage
Most completed strokes reach the maximum neurological deficits within an hour of on
Reversible Ischemic Neurological deficit
The neurological deficit lasts beyond 24 hours but resolves within 3 weeks
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9. Is it in carotid artery/vertebrobasilar
Contralateral weakness
Contralateral numbness
Dysphasia
Dysarthria Ipsilateral mono-ocular
Contralateral homonymous
Combination of above
Bilateral or shifting wea
Bilateral/shifting numb
Diplopia
Dysarthria Inco-ordination of uppe
Ataxia/imbalance/dise
Visual loss in both homo
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Carotid Vertebral
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10. Is it an Internal carotid artery syndr
Often asymptomatic
Reason collateral circulation
Ext. carotid ophthalmic anastamosis
Superficial/deep cervical
Opposite carotid anterior segment
Warning symptoms
Episodes of confusion
Speech dysfunction
Amourosis fugax
Fleeting paresthesia
Neurological deficits
Minimal neurological
Same as that of MCA
Contralateral hemiple
Contralateral sensory
Local examination of c
Feeble carotid pulsat
Feeble temporal arte
Cervical bruit over ca
Carotid doppler angi
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11. Is it a Middle cerebral artery syndro
Largest branch and continuation of ICA
Most common site of ischemic stroke
Clinical picture depends on site of occlusion:
Stem, Superior, Inferior or LS
Contralateral weakness Face UL LL
Contralateral hemisensory loss
Brocas, Wernecke, conduction, global aphasia
Contralateral homonymous hemianopia or Qopia
Paresis of conjugate gaze to opposite
Gerstmanns syndrome (dominant parietal)
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12. Is it a Anterior cerebral artery synd25
Areas supplied by the ACA include:
Medial surface of the frontal lobe
Anterior 4/5th of corpus callosum, parietal lobes
Anterior 1/2 internal capsule and basal ganglia
1 of lateral surface of frontal and parietal lobe
If stroke occurs prior to ACoA (A1)
well tolerated due to collateral circulation
If stroke occurs distal to the ACoA (A2)
Paralysis of the contralateral foot and leg
Sensory loss in the contralateral foot and leg, Gait apraxia
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13. Is it a Anterior choroidal artery synd26
Supply blood to structures which include
internal capsule & crus cerebri
lateral geniculate body
globus pallidus, tail of caudate nucleus
Neurological deficits:
Contralateral Hemiplegia Contralateral hemihypesthesia
Homonymous hemianopia
These arise from ischemic damage to the posterior limb of the interna
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14. Is it a Posterior cerebral artery synd27
Thalamic syndrome of Djerine-Roussy Hemi-sensory loss along with hemiplegia Followed by an agonizing or searing pain
Also termed as thalamic hyperpathia
Other features: Persistent pain
Aggravated by heat and cold
Even by emotions of listening to music Responds poorly to analgesics.
Up regulation of threshold for pain Once pain threshold is overcome
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15. Is it a crossed hemiplegia?28
Weber Syndrome
Ipsilateral III + Contrlateral HP
Benedicts Syndrome
Ipsilateral III +
Contralateral hemiplegia and tremor
Millard Gubler Syndrome
Ipsilateral VI + VII + Contralateral Hemiplegia Raymond Foville
Ipsilateral VI + VII
Medial Medullary Syndrome
Ipsilateral XII +Contralateral Hemiplegia
Weber
Millard
Gubler
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16. Is it cerebral embolism?29
1. Cardiac sources various sites
Aortic root
Native aortic valve
Prosthetic aortic valve
Left ventricular chamber
Native mitral valve
Prosthetic mitral valve
Left atrial chamber
Pulmonary veins
2. Non-cardiac source
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17. Is it a cardiac source of cerebral em30
Aortic root aneurysm with thrombus
Aortic valve Endocarditis acute/subacute
Aortic Prosthetic valve Tissue/mechanical
Left ventricular mural thrombus
Left ventricular aneurysm with thrombus
Mitral valve stenosis-rheumatic in origin
Mitral valve endocarditis
Mitral valve prolapse
Atrial fibrillation
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18. Is it a non-cardiac source of emboli31
Pulmonary venous thrombosis
Suppurative lung abscess, bronchiectasis
Bronchogenic carcinoma secondaries
Air embolism
Fat embolism
Amniotic fluid embolism
Paradoxical embolism PFO
Tetralogy of Fallot, Eisenmenger syndrome
Carotid artery cerebral artery embolism
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19. Is it a Hemorrhagic stroke?32
Severe essential hypertension
55-75 years of age
Smooth onset over minutes or hours
steady progress in spite of treatment
Features of increased ICT
Types:
Epidural/ Subdural Intra-parenchymal
Intra-ventricular
Sub-arachnoid
Thalamic hemorrhage
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20. Is it a Young stroke?
Embolic stroke
Carotid artery dissection
Procoagulant states: SLE, TTP, DIC
Polycythemia
B Thalassemia
Sickle Cell disease
Protein S deficiency Protein C deficiency
Factor V Leiden mutation
Hyperhomocystinemia
Antiphospholipid antibodies
Vasculitis
PAN, Waegners,Taka
Primary CNS Vasculiti
Secondary to Mening
Subarachnoid Hemorrh
Miscellaneous
Oral contraceptives
Eclampsia of pregnan
Cocaine and ampheta
Fibromuscular dysplas
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21. Is it a stroke mimic?
Post ictal Todds paralysis
Transient and follows aseizure
Brain infections
Fever, headache and papilledema
Brain tumors
Progressive headache, papilledema
Demyelinating Disease (ADEM, MS)
Recurrent episodes, distant lesions
Hemi-parkinsonism
Rigidity rather than spasticity
Hypertensive Encephal
Accelerated hyperten
Subdural hematoma
Waxing-waning neuro
Conversion disorder
Stress situation underl
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Summary
Basic Sciences
Applied anatomy
Functional components
Handedness
Hemispherical dominance
Blood supply
Circle of Willis
Internal Capsule
Corticospinal tract
Pathophysiology
Neurological Assessme
TIA, RIND, Evolved/co
Carotid/vertebrobasi
Localization: Cortical/
Arterial territory: MC
Thalamic/crossed hem
Type: Ischemic, embol
Cardiac/non-cardiac
Location of hemorrhag
Young stroke/cerebra
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