Localization of CNS lesions

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LOCALIZATION OF CNS LESIONS

RABIA SALEEM SAFDARPostgraduate trainee

Pediatrics Unit I

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APPROACH TO LOCALIZE THE LESION

History General physical examination Neurological examination

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HISTORY Biodata of Patient(name,age,sex,address) Chief complaint Quality of symptoms Mode of onset Course since onset Frequency of symptoms Severity of symptoms Precipitating factors if any Ameliorating factors like medications Pevious diagnostic evaluation

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HISTORY Prior medical history Natal perinatal and postnatal history Developmental milestones Immunization Trauma Surgery previously done Previously or present medications used Any bleeding disorder Previous history of any neurological problem Previous infection especially involving CNS

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HISTORY Family History Family tree Consanguinty Relatives having similar problems Age and state of health of living relatives Age and cuase of death of deceased relatives

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HISTORY Socioeconomic status

History of contact of TB

History of measels

History of travelling

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• Smell• Visual defect• Diplopia• Ptosis• Hearing disturbance• Vertigo, Lightheadedness• Swallowing difficulty• Speech disturbance• Sleep disturbance

• Involuntary movement• Weakness• Gait disturbance• Incoordination• Muscle atrophy• Tremor• Muscle Cramps• Bladder/bowel control• Weight change

• Pain• Numbness• Paresthesia/ aneasthesia• Headache• Seizure/syncope• Memory• Behavior/Mood change• Aphasia

SYSTEMIC INQUIRY RELEVANT TO CNS

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General physical examination

Involves review of systems Skin Eyes ear nose throat Respiratory Cardivascular Gastrointestinal Musculoskeletal Endocrinology Psychiatric

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NEUROLOGICAL EXAMINATION Higher mental functions Systemic review►Cranial Nerve examination

► Sensory system►Pyramidal System

► Extrapyramidal System ► Cerebellum ► Evaluation of Speech and Language

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HIGHER MENTAL FUNCTIONS Appearance and behavior Level of Consciousness Orientation with time and space Intelligence level Memory Thought process Primitive reflexes

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HIGHER MENTAL FUNCTION

Level of Consciousness Level of consciousness implies awareness of surroundings. Consciousness is dependent on the normal functioning of the

reticular activating system, which originates in the pons and projects to the cortex of bilateral hemispheres via the thalamus.

The reticular activating system activates the cortex when one awakens and inhibits the cortex when in sleep.

The hypothalamus is also important in maintaining level of alertness.

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HIGHER MENTAL FUNCTION

Level of Consciousness During brain herniation,compression of the reticular

activating system may produce profound coma

Metabolic abnormalities such as hyperglycemia or drugs may produce coma by impairing neuronal function diffusely within the brain.

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Evaluation of a comatose patient

Evaluation of a comatose patient requires examination of four steps

Pupils and Fundoscopy Ocular movements Motor response to pain Pattern of breathing

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Pupil Examination

Normal pupils are 3 – 4mm in diameter & equally bilaterally reactive,constrict briskly & symmetricallyin response to light

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PUPIL LESIONSlightly smaller but reactive Early stage of thalmic damageFixed dilated(7mm) pupil ( non- reactive)

Oculomotor nerve lesion

Fixed midsized pupils(5mm) Mid brain lesionPinpoint pupils(1-1.5mm) Pontine lesion,opioid overdoseAsymmetrical pupils Normal in 20 % of population

but reactive..If one pupil is sluggish to react than the other think mid brain or oculomotor lesion

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FundoscopyTo see Papilledema:disc margins are blurred,colour of disc

is pink and hyperemic,congested veins

Optic atrophy: optic disc becomes pale

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Ocular MovementsCheck when cervical trauma has been ruled out

Pathway tested: Medial longitudinal fasciculusControl centers : FRONTAL EYE FIELD PARAMEDIAN PONTINE RETICULAR FORMATIONTests performed1. Doll`s eye maneuver(oculocephalic reflex)2. Caloric test(irrigation with cold water)

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LESION SYMPTOMS

RIGHT ABDUCENT Right eye cannot look right

RIGHT PPRF(paramedian pontine reticular formation)

Neither eye can look right

LEFT MEDIAL LONGITUDIONAL FASCICULUS

Internuclear ophthalmoplegia left eye cannot look right,Right eye has nystagmus

LEFT FRONTAL EYE FIELD

Neither eye can look right but slow drift towards left

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A patient has the appearance shown in the diagram below on attempted gaze to the right. All other ocular movements are normal. Where is the lesion?

The abducens nerve innervates the lateral rectus muscle and mediates lateral gaze. The inability to abduct the right eye suggests a lesion in the right abducens nerve.

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A patient has the appearance shown in the diagram below on attempted gaze to the left (A) or right (B). Convergence is normal. Where is the lesion?

BILATERAL MEDIAL LONGITUDIONAL FASCICULUS :The patient can abduct both eyes (lateral gaze is normal), but cannot adduct both eyes (medial gaze is impaired on voluntary eye movements). However, both oculomotor nuclei and nerves are intact since convergence is normal. Thus the lesion is in the medial longitudinal fasciculus (MLF), and information from the abducens nucleus is not reaching the oculomotor nucleus to mediate the medial component of voluntary conjugate gaze.

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Cold caloric testing andappropriate responses when the brainstem isintact (top) and when a pontine lesion is present(bottom) is demonstrated.

Cold water irrigation—nystagmus to opposite sideWarm water irrigation--- nystagmus to same sideCOWS----cold opposite,warm same

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Motor response to pain

Look for lateralizing signs such as asymmetry of movement either spontaneously or to painful stimulation

Decorticate posturing is characterized by tonic flexion of the arms and extension of the legs and implies a lesion at the level of the midbrain

Decerebrate posturing is manifest as tonic adduction and extension of the arms and legs and suggests a lesion at the level of the pons.

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Decorticate posturing isillustrated on the left. Decerebrate posturingis on the right.

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Respiratory patterns Cheyne-Stokes respiration:respiratory pattern of metabolic

disease.

Central neurogenic hyperventilation:manifest as rapid shallow breathing, indicates midbrain dysfunction.

Cluster or apneustic breathing:suggests pontine injury.

Ataxic, shallow breathing: results from medullary lesion.

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GLASGOW COMA SCALE(4-15Y)RESPONSE SCORE

EYE OPENING`Spontaneous 4To Speech 3To Painful Stimulus 2None 1

BEST MOTOR RESPONSEObeys Command 6 Localizes Pain 5Withdrawl 4Abnormal Flexion 3Extensor Repnse 2None 1

BEST VERBAL RESPONSEOriented 5Confused 4Inaappropriate words 3Incomprehensible words 2None 1

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GLASGOW COMA SCALE(<4y)RESPONSE SCORE

EYE OPENING`Spontaneous 4To Speech 3To Painful Stimulus 2None 1

BEST MOTOR RESPONSEObeys Command 6 Localizes Pain 5Withdrawl 4Abnormal Flexion 3Extensor Repnse 2None 1

BEST VERBAL RESPONSESmiles oriented to sounds,follows objects 5Crying interactcs 4

Consolable inappropriate 3 Inconsistently consolable Moaning 2

No response 1

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HIGHER MENTAL FUNCTIONS

Primitive reflexes

Primitive reflexes are automatic stereotypic movements directed from the brainstem and require no cortical involvement (thought).

Must be abated in order for proper neurological organization of the brain to develop.

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HIGHER MENTAL FUNCTIONS

Causes of retained Primitive Reflexes Children born via cesarean section Trauma Toxicity exposure Anesthetics Early walkers Head injuries Excessive falls Chronic ear infections

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CRANIAL NERVES

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CRANIAL NERVES 12 pairs of cranial nerves

3 Types

SENSORY I , II, VIII MOTOR III, IV, VI, XI, XII MIXED V,VII,IX,X

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FUNCTIONS OF CRANIAL NERVESNO NAME FUNCTION

I OLFACTORY SmellII OPTIC SightIII OCULOMOTOR Eye movements except lateral rectus and

sup.obliqueIV TROCHLEAR Superior obliqueV TRIGEMINAL Mastication,facial sensationsVI ABDUCENT Lateral rectusVII FACIAL Fascial movements taste ant 2/3rd of tongueVIII VESTIBULOCOCHLEAR Hearing,balance

XI GLOSSOPHARYNGEAL Taste from post.1/3rd of tongue,caritid bodyand baroreceptors,parotid,pharyngeal muscles

X VAGUS Taste from epiglottic area,swalloing,palate elevation,abd viscera

XI ACESSORY Head turning,shuolder shruggingXII HYPOGLOSSAL Tongue movements

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NUCLEI OF CRANIAL NERVES

CRANIAL NERVE NUCLEI LOCATION

I and II Directly goes to cerebral cortex

III,IV midbrain

V,VI,VII and VIII pons

IX,X,XI,XII medulla

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You are testing the blink reflex on your patient. When you touch a piece of cotton to the right eye, both eyelids close in a blink. When you touch the left eye, neither eye closes. Which of the following cranial nerves is involved in a lesion?

Left trigeminal. The trigeminal nerve (CN 5) is the afferent arm of the blink reflex (corneal reflex) and the facial nerve (CN 7) is the efferent arm. If there is a lesion of left CN 5, sensation of touching the cornea will not be conveyed centrally, and neither eye will blink.

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Reflexes Afferent Efferent

Corneal V (i) VII

Jaw jerk V (iii) sensory V (iii) motor

Gag IX IX , X

pupillary II III

CRANIAL NERVE REFLEXES

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Direct & consensual light reflexes – Pathway

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Direct & consensual light reflexes – Pathway

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CRANIAL NERVES

Cornea or Conjunctiva ↓ Ophthalmic branch of the TGN ↓ Main sensory ganglion of the TGN ↓Internuncial neurons connect with the motor nucleus of the facial nerve on Both

sides (Through the medial longitudinal fasciculus) ↓ Facial nerve ↓ Orbicularis oculi of both sides ↓ Closure of the eyelids

Corneal reflex : Light touching of the cornea or conjunctive results in blinking of the eye lids

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CRANIAL NERVES Accommodation reflex

When the eyes are directed from a distant object to a near object:

Medial recti contracts (Brings convergence) Lens thickens to increase the refractory power by

contracting ciliary muscles Pupils constrict to restrict light waves to the thickest

central part of the lens

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Accommodation reflex

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WHAT IS THE LESION?WHERE IS THE LESION?

Left sided facial palsy, LMN type lesion

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SENSORY SYSTEMLOCALIZATION OF LESIONS OF

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Sensory system Sensory modalities Superficial sensation light touch pain temperature sensibility Deep sensation joint and vibratory sensibility pain from deep muscle and ligamentous structures

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Sensory system Neuroanatomical pathways Spinothalmic tract

Lateral spinothalamic tract(pain, temp) Anterior spinothalamic tract(touch ,pressure)

Dorsal column tract(position,vibration)

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Spinal tracts anatomy and function

Tract 1st order neuron

Synapse 1 2nd order neuron Synapse 2 3rd order neuron

Dorsal column

Sensory nerve ending―cell body in dorsal root ganglion―ascend ipsi -lateral in spinal cord

Ipsilateral nucleus cuneatus n gracilis

Decussate in medulla―ascend contralaterally in medial leminiscus

VPL of thalmus

Sensory cortex

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Spinal tracts anatomy and function

Tract 1st order neuron

Synapse 1 2nd order neuron

Synapse 2

3rd order neuron

AnterolateralSpinothalmictract

Sensory nerve ending―cell body in dorsal root ganglion—enters spinal cord

Ipsilateral grey matter of spinal cord

Decussate and ascend contralaterally

VPLOf thalmus

Sensory cortex

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Localization of Sensory lesion

Peripheral nerve lesion Isolated nerve palsy(Mononeuropathy) Mononeuritis multiplex Sensory peripheral neuropathy(polyneuropathy) Root lesion Spinal cord Brainstem Thalamus Cortex

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Isolated nerve palsy(Mononeuropathy)

Sensory loss is in the distribution of that nerve invoved.

Example Ulnar nerve lesion(sensory loss is over the medial

one and a half fingers both anteriorly and posteriorly)

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Sensory distribution of the ulnar nerve .

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Mononeuritis multiplex

Combinations of peripheral nerve lesions occur, usually caused by nerve infarcts

secondary to vasculitis or diabetic vasculopathy.

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Sensory peripheral neuropathy Disease affecting peripheral nerves may affect the

Schwann cell myelin sheath (demyelinating neuropathy) or the nerve axons (axonal neuropathy).

Peripheral neuropathy characteristically symmetrical and greater distally than proximally(gloove and stocking pattern).

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Sensory peripheral neuropathy

In any peripheral nerve or root lesion the sensory or motor arc of the deep tendon reflex can be interrupted leading to diminished or absent deep tendon reflexes.

Distal reflexes (ankle) are diminished more than proximal reflexes (biceps).

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Root lesion(Rediculopathy)The location of common root paresthesias are C-5 shoulder region; C-6 thumb; C7 middle finger; C-8 5th finger; L-4 knee L-5great toe S-1 medial sole of the foot

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SYMPTOMS OF NERVE ROOT LESION

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Spinal cord Ascending and descending pathways are interrupted

sensation is usually diminished distal to the lesion Localizing signs would be Localized root pain Sensory loss below the level of the lesion, An absent root reflex at the level of the lesion Increased reflexes below this level.

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Common cord syndromes are: Brown-Séquard syndrome Central cord syndrome (cervical) Complete cord transection

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CorticospinalTract(motor)

Dorsal Column(Joint Positionsense lighttouch)

Pyramidal TractWeaknes

Absent Position& Vibrationsense

Absent pain& temperature

Brown-Séquard syndrome • ipsilateral plegia below the lesion• ipsilateral proprioception and light touch loss below the lesion• contralateral pain and temperature loss below the lesion

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Central cord syndrome (cervical)• shawl distribution pain and temperature loss• sparing of light touch and proprioception• lower motor neuron weakness of the affected cord levels (anterior horn cell involvement)

Shawl distribution pain &temperature loss if anterior horncells involved get flaccidweakness of involvedlevels.

Lesion involved crossing pain andtemperature fibers in theanterior commisure

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Complete cord transection. • loss of all modalities below the level of the lesion

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Neurological examination revealed: ---paralysis and increased DTRs of left leg ---loss of vibration and proprioception of left leg ---loss of pain and temperature sensation in the right leg Where is the lesion?

This is an example of the Brown-Sequard syndrome (hemisection of the spinal cord). Tracts involved in a lesion of the left spinal cord involve (1) the left corticospinal tract, which will synapse with lower motor neurons in the left limbs; (2) the left dorsal column containing primary sensory neurons for vibration and proprioception from the left limbs; and (3) the left spinothalamic tract containing secondary sensory neurons for pain and temperature sensation coming from the right limbs (the pain/temperature neurons cross at the level of entry in the anterior commissure after synapsing in the dorsal horn).

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BrainstemBrainstem lesions at the level of the medulla has: Ipsilateral loss of pain and temperature of the face Contralateral loss on the body. Light touch and proprioceptive loss is contralateral Above this level all sensory modality findings are

contralateral to the side of the lesion because all pathways have crossed.

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Thalamus

Thalamic lesions produce contralateral loss of all sensory modalities in the face,extremities and trunk.

Stimulation may be perceived as uncomfortable and painful(dysesthesia).

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Cortical lesions

Lesions of the cerebral cortex cause diminution of all sensory modalities on the contra lateral side of the body.

In addition, higher integrative sensory functions are impaired causing defects in stereo gnosis, two-point discrimination etc

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Lesion FINDINGS

Peripheral nerve All sensory modalities are affected.The borders are sharply demarcated.There may be hyperesthesia, discomfort and pain

Root All sensory modalities are affected.Sensory loss is vague but in a dermatomal distribution.Pain is present and may radiate in the dermatome distribution.

Spinal cord There is sensory dissociation.A unilateral lesion produces ipsilateral loss of light touch and proprioception and contralateral loss of pain and temperature

SUMMARYCharacteristics of sensory system lesions

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Lesion FindingsMedulla There is sensory dissociation.

Pain and temperature are lost on the ipsilateral side of the face and contralateral side of the body.Light touch and proprioception are lost on the contralateral side of the body.

Upper brainstem There is sensory dissociation.All sensory modalities are now crossed and on the same side.Unilateral lesions cause contralateral loss of sensory modalities

Thalamus Sensory dissociation is no longer present.Ipsilateral lesions produce contralateral loss of all modalities.

Cerebral cortex Sensory dissociation is absent.Ipsilateral lesions produce contralateral loss of all modalities.Discriminative sensory functions are lost.

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PYRAMIDAL TRACT(MOTOR SYSTEM)

LOCALIZATION OF LESIONS OF

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Pyramidal SystemTract 1st order

neuronSynapse 1 2nd order

neuronSynapse 2 D

ESCENDINGTRACT

Lateral Corticospinal tract

UMN:Cell body in motor cortex descend s ipsilaterally through internal capsule until decussate at pyramid and descends contralaterally

Cell body of anterior horn of spinal cord

LMNleaves Spinal cord

Neuro-muscular junction

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Pyramidal System Inspection and observation Muscle tone Muscle power Tendon reflexes Co-ordination Gait

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Pyramidal SystemInspection and observation Size and bulk of muscle Any obvious wasting Visible fasciculations Position of the limb General body posture Scar marks or lacerations Ulceration Swelling Hip: Internaly rotated in anterior dislocation of hip Externaly rotation-posterior dislocation of hip

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Pyramidal System Muscle tone The resistance of a muscle against the passive

movement of the jointAssessed by Observing the position of the extremities at rest By pulpating the musle belly Determining the resistance against passive stretch

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Pyramidal System Hypertonia Spasticity: consists of an increase in tone that affects different

muscle groups to different extent. Rigidity: consists of increased resistance to passive movement

that is independent of direction of movement i-e it effects the flexors as well as extensors equally.

Hypotonia : defined as reduced resistance to the passive movement-the distal portion of the limb is easily waved when limb is shaken to and fro.

Paratonia: it seems to be rigidity when the examiner moves the limb rapidly but normal tone when the limb is moved slowly.

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Pyramidal System

Muscle power Checked in individual muscles and compared on both sides so that

the minor degree of weakness can be recognizedGrading of muscle power according to MEDICAL RESEARCH COUNCIL

Grade Muscle power

5 Normal power

4 Active movement against resistance and gravity

3 Active movement against gravity not resistance

2 Active movement possible only with gravity eliminated

1 Flicker or trace of movements

0 No movement

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Pyramidal System Tendon Reflexes Superfial reflexes Planter reflex Abdominal reflex Anal reflex Cremasteric reflex Deep tendon reflexes Knee jerk Ankle jerk Biceps jerk Supinator jerk Triceps jerk

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SUPERFICIAL REFLEXES

REFLEX HOW EXCITED

CLINICAL RESULT

LEVEL OF CORD

PLANTAR REFLEX Scrathing laterally on sole of foot

Flexion of big toe(downward movement)

L5 ,S1

SCAPULAR REFLEX Scrathing skin in intrascapular region

Contraction of scapular muscles

C 5 to T 1

ABDOMINAL REFLEX

Scrathing on abdominal wall below costal margin and in iliac fossa

Contraction of abdominal muscles

T 7 to T 12

ANAL REFLEX Scratching near anus Contraction of anal sphincter

S3, S4

CREMESTERIC REFLEX

Stoking skin at upper and inner thigh

Upward movement of testes

L1,L2

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Deep tendon reflexesREFLEX SEGMENTAL

INNERVATIONNERVE

KNEE REFLEX L3,L4 Femoral

BICEPS JERK C 5,C 6 Musculocutaneous

BRACHIORADIALIS JERK

C 5, C6 Radial

TRICEPS JERK C 7,C8 Radial

ANKLE JERK S 1,S 2 Tibial

JAW JERK Pons Mandibular branch of trigeminal nerve

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Grading of tendon reflexes

0 ABSENT1 PRESENT (as normal ankle jerk)

2 BRISK

3 VERY BRISK

4 CLONUS

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Pyramidal System

Coordination

Finger nose test

Heel Knee test

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GAIT Gait Disturbances in Pyramidal Tract Lesions

HEMIPLEGIC GAIT:Patient does not lift his leg off the ground so that toes remain in contact with ground.Leg swings forward and outward in a circular fashion(ONLY ONE LEG INVOVED)

SPASTIC GAIT (Scissor Like Gait) Patient don’t lift his feet from the ground UMN paraplegia

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Comparison and Contrast b/w UML and LMN lesion

SIGN UMN lesion LMN lesion

Weakness Present Present

Atrophy Absent Present

Fasciculations Absent Present

Reflexes Brisk Dimished

Tone Increase Decrease

Babinski Upgoing Downgoing

Spastic paralysis Present Absent

UMN lesions may ipsilateral or contralateral while LMN lesions are usually ipsilateral.

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Upper Motor Neuron lesion

Cardinal features Weakness or paralysis Spasticity Brisk reflexes Upgoing plantars Loss of superficial abdominal reflexes

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UMN lesionSites Motor cortex Internal capsule Brain stem Spinal cord

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UMN lesion

Lesion of motor cortex results in monoplegia

Specific menifestations are present according to the lobes involved

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LOBES IMPORTANT REGIONS

DEFICIT AFTER LESION

FRONTAL LOBE Primary motor cortex

Contralateral spastic paresis(area of homonculus affected),premotor:apraxia

Frontal eye field Eye deviation to ipsilateral side

Broca`s area Expressive aphasia

Prefrontal cortex Frontal lobe syndrome:poor judement,difficulty in concentrating,inappropriate social behaviour

PARIETAL LOBE Primary somatosensory

Contralateral hemihypesthesia

Superior parietal lobule

Contralateral asteriognosis,apraxia

Inferior parietal lobule

Contralateral hemianopia, rt n lft confusion (dominant)alexia,dyscalculia,unilateral neglect(non- dominant)

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LOBES IMPORTANT REGION DEFICIT AFTER LESION

TEMPORAL Primary auditory cortex Deafness :bilateral damage

Wernick s area Receptive aphasia

Hippocampus Bilateral lesion leads to poor short term and long term memory

Olfactory bulb Ipsilateral anosmia

Mayer loop Contralateral upper quadrantanopia

OOCIPITAL Primary visual cortex Cortical blindness with macular sparing

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UMN lesionInternal capsule lesion

Produces dense hemiplegia and facial nerve palsy of opposite side(uncrossed hemiplagia)

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UMN lesion

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UMN lesionCharacteristics of internal capsule lesion:

1- Hemi-plegia i.e. paralysis of the muscles present in the opposite side of the body due to damage of pyramidal and extrapyramidal tracts fibers.

2- Hemi-anesthesia i.e. loss of all sensations from the opposite side of the body due to damage of sensory radiation.

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UMN lesion

3- Hemi-anopia i.e. loss of vision in the opposite halves of visual fields of both eyes. So, lesion in the right internal capsule leads to loss of vision in the left halves of visual fields of both eyes. It is due to damage of optic radiation.

4- Decrease hearing; it is due to damage of auditory radiation. No deafness because each ear is bilaterally represented in the cerebral cortex.

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UMN lesion Brain stem lesion produces crossed hemiplegia i-e

cranial nerve is affected on one side and the hemiplegia of the opposite side

If 3rd nerve is involved. Lesion is in mid-brain If 6th and 7th nerve is involved,lesion is in pons. If 9th and 10th nerves are involved, lesion is in medulla

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UMN lesion Spinal cord

Whenever there is a lesion of spinal cord ,there will be UMN signs below the level of lesion

Upper limb involved ---- above C 5 Absent abdominal reflexes----- above T 8 Specific sensory level is always present

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Lower Motor Neuron lesion

Cardinal features

Weakness or paralysis Wasting of individual muscles Hypotonia Diminished tendon jerks Downgoing plantars Fasciculations

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LMN LESION Sites

Nuclei of cranial nerves Anterior horn cells Nerve roots Nerves(crania and peripheral)

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LMN LESION Cranial nerves: Produces paralysis of muscles supplied

by the cranial nerves and LMN type of lesion of cranial nerve

Anterior horn cell : paraparesis or quadriparisis

Root: muscle supplied by root is paralysed

Single peripheral nerve :muscle supplied by that nerve is paralysed

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THANK YOU

Localization of CNS lesions

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