Localization of CNS lesions

1. LOCALIZATION OF CNS LESIONS RABIA SALEEM SAFDAR Postgraduate trainee Pediatrics Unit I 3/30/2012 1

2. APPROACH TO LOCALIZE THE LESION History General physical examination Neurological examination 3/30/2012 2

3. 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 3/30/2012 3

4. 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 3/30/2012 4

5. 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 3/30/2012 5

6. HISTORY Socioeconomic status History of contact of TB History of measels History of travelling 3/30/2012 6

7. • 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 3/30/2012 7

8. General physical examination Involves review of systems Skin Eyes ear nose throat Respiratory Cardivascular Gastrointestinal Musculoskeletal Endocrinology Psychiatric 3/30/2012 8

9. NEUROLOGICAL EXAMINATION Higher mental functions Systemic review ►Cranial Nerve examination ► Sensory system ►Pyramidal System ► Extrapyramidal System ► Cerebellum ► Evaluation of Speech and Language 3/30/2012 9

10. HIGHER MENTAL FUNCTIONS Appearance and behavior Level of Consciousness Orientation with time and space Intelligence level Memory Thought process Primitive reflexes 3/30/2012 10

11. 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. 3/30/2012 11

12. 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. 3/30/2012 12

13. 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 3/30/2012 13

14. Evaluation of a comatose patient Pupil Examination Normal pupils are 3 – 4mm in diameter & equally bilaterally reactive,constrict briskly & symmetrically in response to light 3/30/2012 14

15. PUPIL LESION Slightly smaller but reactive Early stage of thalmic damage Fixed dilated(7mm) pupil ( non- reactive) Oculomotor nerve lesion Fixed midsized pupils(5mm) Mid brain lesion Pinpoint pupils(1-1.5mm) Pontine lesion,opioid overdose Asymmetrical pupils Normal in 20 % of population but reactive.. If one pupil is sluggish to react than the other think mid brain or oculomotor lesion 3/30/2012 15

16. Evaluation of a comatose patient Fundoscopy To see Papilledema : disc margins are blurred,colour of disc is pink and hyperemic,congested veins Optic atrophy : optic disc becomes pale 3/30/2012 16

17. Evaluation of a comatose patient Ocular Movements Check when cervical trauma has been ruled out Pathway tested : Medial longitudinal fasciculus Control centers : FRONTAL EYE FIELD PARAMEDIAN PONTINE RETICULAR FORMATION Tests performed Doll`s eye maneuver( oculocephalic reflex) Caloric test(irrigation with cold water) 3/30/2012 17

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19. 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 3/30/2012 19

20. 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. 3/30/2012 20

21. 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. 3/30/2012 21

22. Cold caloric testing and appropriate responses when the brainstem is intact (top) and when a pontine lesion is present (bottom) is demonstrated. Cold water irrigation— nystagmus to opposite side Warm water irrigation- -- nystagmus to same side COWS----cold opposite,warm same 3/30/2012 22

23. Evaluation of a comatose patient 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 . 3/30/2012 23

24. Decorticate posturing is illustrated on the left. Decerebrate posturing is on the right. 3/30/2012 24

25. Evaluation of a comatose patient 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. 3/30/2012 25

26. GLASGOW COMA SCALE(4-15Y) RESPONSE SCORE EYE OPENING `Spontaneous 4 To Speech 3 To Painful Stimulus 2 None 1 BEST MOTOR RESPONSE Obeys Command 6 Localizes Pain 5 Withdrawl 4 Abnormal Flexion 3 Extensor Repnse 2 None 1 BEST VERBAL RESPONSE Oriented 5 Confused 4 Inaappropriate words 3 Incomprehensible words 2 None 1 3/30/2012 26

27. GLASGOW COMA SCALE(<4y ) RESPONSE SCORE EYE OPENING `Spontaneous 4 To Speech 3 To Painful Stimulus 2 None 1 BEST MOTOR RESPONSE Obeys Command 6 Localizes Pain 5 Withdrawl 4 Abnormal Flexion 3 Extensor Repnse 2 None 1 BEST VERBAL RESPONSE Smiles oriented to sounds,follows objects 5 Crying interactcs 4 Consolable inappropriate 3 Inconsistently consolable Moaning 2 No response 1 3/30/2012 27

28. 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. 3/30/2012 28

29. 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 3/30/2012 29

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32. CRANIAL NERVES 3/30/2012 32

33. CRANIAL NERVES 12 pairs of cranial nerves 3 Types SENSORY I , II, VIII MOTOR III, IV, VI, XI, XII MIXED V,VII,IX,X 3/30/2012 33

34. FUNCTIONS OF CRANIAL NERVES NO NAME FUNCTION I OLFACTORY Smell II OPTIC Sight III OCULOMOTOR Eye movements except lateral rectus and sup.oblique IV TROCHLEAR Superior oblique V TRIGEMINAL Mastication,facial sensations VI ABDUCENT Lateral rectus VII FACIAL Fascial movements taste ant 2/3 rd of tongue VIII VESTIBULOCOCHLEAR Hearing,balance XI GLOSSOPHARYNGEAL Taste from post.1/3 rd of tongue,caritid bodyand baroreceptors,parotid,pharyngeal muscles X VAGUS Taste from epiglottic area,swalloing,palate elevation,abd viscera XI ACESSORY Head turning,shuolder shrugging XII HYPOGLOSSAL Tongue movements 3/30/2012 34

35. NUCLEI OF CRANIAL NERVES CRANIA L 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 3/30/2012 35

36. 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. 3/30/2012 36

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38. 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 3/30/2012 38

39. Direct & consensual light reflexes – Pathway 3/30/2012 39

40. Direct & consensual light reflexes – Pathway 3/30/2012 40

41. 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 3/30/2012 41

42. 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 3/30/2012 42

43. Accommodation reflex 3/30/2012 43

44. WHAT IS THE LESION? WHERE IS THE LESION? Left sided facial palsy, LMN type lesion 3/30/2012 44

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46. SENSORY SYSTEM LOCALIZATION OF LESIONS OF 3/30/2012 46

47. Sensory system Sensory modalities Superficial sensation light touch pain temperature sensibility Deep sensation joint and vibratory sensibility pain from deep muscle and ligamentous structures 3/30/2012 47

48. Sensory system Neuroanatomical pathways Spinothalmic tract Lateral spinothalamic tract(pain, temp) Anterior spinothalamic tract(touch ,pressure) Dorsal column tract ( position,vibration ) 3/30/2012 48

49. Spinal tracts anatomy and function Tract 1 st order neuron Synapse 1 2 nd order neuron Synapse 2 3 rd 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 3/30/2012 49

50. Spinal tracts anatomy and function Tract 1 st order neuron Synapse 1 2 nd order neuron Synapse 2 3 rd order neuron Anterolateral Spinothalmic tract Sensory nerve ending―cell body in dorsal root ganglion—enters spinal cord Ipsilateral grey matter of spinal cord Decussate and ascend contralaterally VPL Of thalmus Sensory cortex 3/30/2012 50

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52. Localization of Sensory lesion Peripheral nerve lesion Isolated nerve palsy( Mononeuropathy ) Mononeuritis multiplex Sensory peripheral neuropath y( polyneuropathy ) Root lesion Spinal cord Brainstem Thalamus Cortex 3/30/2012 52

53. Localization of Sensory lesion 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 ) 3/30/2012 53

54. Sensory distribution of the ulnar nerve . 3/30/2012 54

55. Localization of Sensory lesion Mononeuritis multiplex Combinations of peripheral nerve lesions occur, usually caused by nerve infarcts secondary to vasculitis or diabetic vasculopathy . 3/30/2012 55

56. Localization of Sensory lesion 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). 3/30/2012 56

57. Localization of Sensory lesion 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). 3/30/2012 57

58. Localization of Sensory lesion 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 3/30/2012 58

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61. Localization of Sensory lesion 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. 3/30/2012 61

62. Localization of Sensory lesion Common cord syndromes are: Brown- Séquard syndrome Central cord syndrome (cervical) Complete cord transection 3/30/2012 62

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64. Corticospinal Tract (motor ) Dorsal Column (Joint Position sense light touch) Pyramidal Tract Weaknes Absent Position & Vibration sense 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 3/30/2012 64

65. 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 horn cells involved get flaccid weakness of involved levels. Lesion involved crossing pain and temperature fibers in the anterior commisure 3/30/2012 65

66. Complete cord transection . • loss of all modalities below the level of the lesion 3/30/2012 66

67. 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). 3/30/2012 67

68. Localization of Sensory lesion Brainstem Brainstem 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 . 3/30/2012 68

69. Localization of Sensory lesion 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 ). 3/30/2012 69

70. Localization of Sensory lesion 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 3/30/2012 70

71. 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 SUMMARY Characteristics of sensory system lesions 3/30/2012 71

72. Lesion Findings Medulla 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. 3/30/2012 72

73. PYRAMIDAL TRACT (motor system) LOCALIZATION OF LESIONS OF 3/30/2012 73

74. Pyramidal System Tract 1 st order neuron Synapse 1 2 nd order neuron Synapse 2 D E S C E N D I N G T R A C T 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 LMN leaves Spinal cord Neuro -muscular junction 3/30/2012 74

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76. Pyramidal System Inspection and observation Muscle tone Muscle power Tendon reflexes Co-ordination Gait 3/30/2012 76

77. Pyramidal System Inspection 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 3/30/2012 77

78. Pyramidal System Muscle tone The resistance of a muscle against the passive movement of the joint Assessed by Observing the position of the extremities at rest By pulpating the musle belly Determining the resistance against passive stretch 3/30/2012 78

79. 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. 3/30/2012 79

80. Pyramidal System Muscle power Checked in individual muscles and compared on both sides so that the minor degree of weakness can be recognized Grading 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 No movement 3/30/2012 80

81. 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 3/30/2012 81

82. 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 3/30/2012 82

83. Deep tendon reflexes REFLEX SEGMENTAL INNERVATION NERVE 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 3/30/2012 83

84. Grading of tendon reflexes ABSENT 1 PRESENT (as normal ankle jerk) 2 BRISK 3 VERY BRISK 4 CLONUS 3/30/2012 84

85. Pyramidal System Coordination Finger nose test Heel Knee test 3/30/2012 85

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87. 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 3/30/2012 87

88. 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 . 3/30/2012 88

89. Upper Motor Neuron lesion Cardinal features Weakness or paralysis Spasticity Brisk reflexes Upgoing plantars Loss of superficial abdominal reflexes 3/30/2012 89

90. UMN lesion Sites Motor cortex Internal capsule Brain stem Spinal cord 3/30/2012 90

91. UMN lesion Lesion of motor cortex r esults in monoplegia Specific menifestations are present according to the lobes involved 3/30/2012 91

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95. 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) 3/30/2012 95

96. 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 3/30/2012 96

97. UMN lesion Internal capsule lesion Produces dense hemiplegia and facial nerve palsy of opposite side( uncrossed hemiplagia ) 3/30/2012 97

98. UMN lesion 3/30/2012 98

99. UMN lesion Characteristics 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 extra- pyramidal tracts fibers. 2- Hemi-anesthesia i.e. loss of all sensations from the opposite side of the body due to damage of sensory radiation. 3/30/2012 99

100. 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. 3/30/2012 100

101. 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 3 rd nerve is involved. Lesion is in mid-brain If 6 th and 7 th nerve is involved,lesion is in pons . If 9 th and 10 th nerves are involved, lesion is in medulla 3/30/2012 101

102. 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 3/30/2012 102

103. Lower Motor Neuron lesion Cardinal features Weakness or paralysis Wasting of individual muscles Hypotonia Diminished tendon jerks Downgoing plantars Fasciculations 3/30/2012 103

104. LMN LESION Sites Nuclei of cranial nerves Anterior horn cells Nerve roots Nerves(crania and peripheral) 3/30/2012 104

105. 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 3/30/2012 105

106. THANK yoU 3/30/2012 106