CNS - Clinical Evaluation of Hemiplegia

8/7/2019 CNS - Clinical Evaluation of Hemiplegia

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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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Documents

CNS - Clinical Evaluation of Hemiplegia