Neurology-A Head to Toe Discipline. A Primer to 'be able to' decipher 3 questions: Where, What and Why is the Lesion-Fostering Neurophilia

1. CLINICAL LOCALIZATION
IN NEUROLOGY
Dr.B.P.SHELLEY, MBBS, MD, DM , FRCP Edin

2. Correlative clinical neurology, imaging findings and surgical results run hand in glove.
There are, however, at times we do face discordance/unexplainable clinical
parameters or radiological features.
OCCAM'S RAZOR
Suppose there exist two explanations for an occurrence. In this case, the simpler
one is usually better. Another way of saying it is that the more assumptions you
have to make, the more unlikely an explanation is. Occam's razor applies
especially in the philosophy of science, but also more generally.
HICKAM’S DICTUM
HICKAM'S DICTUM IS a counterargument to the use of Occam's razor in the medical
profession. The principle is commonly stated: "Patients can have as many
diseases as they damn well please". The principle is attributed to John Hickam,
MD.
CLINICAL RATIONALISM-WISDOM
Clinical medicine sometimes is not like mathematics

5. Ann Indian Acad Neurol 2018;21:9-18.
Arch Med Health Sci 2017;5:1-8.
Dr. Ralph Jozefowicz

6. PRINCIPLES OF NEUROLOGICAL DIAGNOSIS
• Symptom profile and symptom analysis - HISTORY
• Grouping of signs ( by EXAMINATION) and symptoms –
SYNDROMIC FORMULATION & PATTERN RECOGNITION
• Mode of ONSET and COURSE
• Anatomic Localization – WHERE IS THE LESION?
• Pathology – WHAT IS THE LESION?
• Aetiology – WHY IS THE LESION?
• Investigations
• Final Diagnosis

7. GENERAL PRINCIPLES: NEUROLOGICAL
LOCALISATION
 Observe each symptom carefully, and consider its significance.
 Then put the several symptoms together and consider the
meaning of their combination especially whether there is any
one part of the nervous system at which disease might cause
them all
 Lastly, consider the way they came on as indicating the nature
of the lesion, comparing this with the evidence of their seat and
remembering also that their character may in itself tell you
something of their probable nature. When described in the
abstract, this may seem a lengthy process. It may even seem a
formidable process . As a rule it is neither”
Sir William Gowers

8. PROBLEM SOLVING IN NEUROLOGY
 Symptom recognition, symptom cluster & symptom analysis
 Pattern Recognition
 Logical Analysis-Inductive reasoning; based on neuroanatomy,
neurological disorders knowledge database (clinical pattern, temporal
profile, etiology, and neuropathology
 Longitudinal (vertical extent) vs. Transverse localization (horizontal
extent)
 Unilateral; Bilateral; Symmetrical; Asymmetrical; Multifocal; Diffuse
 To define the level of the lesion: CNS vs. PNS
– Supratentorial : cerebral hemispheres
– Infratentorial : brainstem, cerebellum
– Spinal : spinal cord, nerve roots
– Multiple levels (multifocal)

9. PROBLEM SOLVING-PATHOLOGY
WHAT IS THE LESION?
• Define the most likely pathology:
– Infective
– Vascular : Acute
– Inflammatory : Subacute
– Neoplastic : Focal and chronic
– Heredofamial Degenerative : Diffuse and chronic
– Traumatic
– Toxic-metabolic-Physical agents (radiation etc)
– Demyelinating
– Dysmyelinating
– Post infective/Para-infective
– Endocrine

10. LOGICAL REASONING : THE BASICS
• Define Level of the lesion:
– Supratentorial : cerebral hemispheres (lobology)
– Infratentorial : brainstem, cerebellum
– Spinal : spinal cord, nerve roots
– Multiple levels (multifocal- encephalomyeloradiculopathy
(TB, CHIKC, CMV,HSV,EBV,ADEM; metastasis,
neurofirbromatosis)

11. STEPS IN THE DIAGNOSIS OF NEUROLOGIC
DISEASE
• History
• Neurologic examination
• Anatomic diagnosis [where-localisation, regional, point, vertical,
horizontal]
• Pathologic diagnosis [what]
• Etiologic diagnosis [why]

12. NERVOUS SYSTEM
Nervous System
CNS PNS
Brain Spinal
cord
Peripheral
nerves
Nerve
ganglia
Cr N (12) Sp N (31) Splanchnic N

13. REGIONS FOR
NEUROLOGICAL
LOCALIZATION
UMN
LMN

14. Supratentorial Level
Motor deficits with neighborhood lobology signs
– Weakness and/ or loss of sensation on the same side of
the face and body (Uncrossed weakness & COPS)
– Contralateral to lesion
– Seizures, MMSE abnormal; Behavioural alterations,
Psychiatric disturbances; Lobe functions-abnormal;
Altered level/content of consciousness

15. Supratentorial Level
Lobology Signs
– Visual field defect
– Olfactory symptoms
– Language disturbance (aphasia)
– Memory deficit
– Attention deficit ( amnesia)
– Affect and emotional disturbance
– Impaired performance of learned motor skills
– Seizures

16. Infratentorial Level
– Weakness and /or cranial nerve deficits on the side of
lesion (ipsilateral to lesion)
– Long tracts signs on the opposite side of the body
(contralateral to lesion)
– Crossed hemiplegia (at brainstem-pons-ipsilateral LMN
VII and contralateral hemiplegia & COPS)
– Above pons- Uncrossed hemiplegia (UMN VII and
hemiplegia on the same side, contralateral to lesion)

17. Infratentorial Level
• Segmental: Ipsilateral to lesion
– Weakness of upper and lower face muscles
– Double vision (Diplopia)
– Difficulty with articulation (Dysarthria)
– Difficulty swallowing (Dysphagia)
– Incoordination (Ataxia)

18. Spinal level
– Weakness or sensory loss in both sides of the body but
not the face (cranial nerves spared-below FM)
– Upper motor neuron weakness in:
• Quadriparesis or paraparesis
• Monoparesis(leg) or hemiparesis
– Sensory loss with sensory level (myelopathic level)
– Sphincteric involvement
– Brown Sequard, Transverse myelopathy
– Red Flag: Cortical paraplegia; Pseudospinal stroke

19. PATTERN RECOGNITION
• Mode of presentation: acute, subacute, chronic
• Temporal profile: intermittent, paroxysmal, partially/completely
reversible, residual neurological disability, remitting-relapsing,
recurrent, progressive, progressive with intermittent relapses
• UMN vs. LMN
• Aetiology
• Upper motor neuron weakness
– In the upper limbs-Extensors weaker than flexors
– In the lower limbs-Flexors weaker than extensors
– Muscle stretch reflexes are brisk- Hyperreflexia

20. Divisions of the Neuraxis
• Cortical Brain
• Subcortical Brain
• Brainstem
• Cerebellum
• Spinal Cord
• Root
• Peripheral Nerve
• Neuromuscular
Junction
• Muscle

21. PATTERN RECONITION-PARKINSONISM
• Bradykinesia
• Tremor at rest
• “Cogwheel rigidity”
• Postural instability
• Shuffling gait
• Monotonous speech, hypophonia
• Stooped posture

22. PATTERN RECONITION-PERIPHERAL
NEUROPATHY
• Motor Weakness predominantly distal
– Hypotonia
• Glove and stocking sensory loss
• Diminished reflexes-Hyporeflexia
• Pan-sensory modalities affected (large vs. small fiber
neuropathy)
• Exceptions: Proximal neuropathies: Guillain- Barre syndrome,
CIDP, Porphyric neuropathy, GB mimics, Diabetic proximal
neuropathy (PDN)

23. PATTERN RECONITION-MYOPATHY
• Proximal greater than distal muscle weakness
• Neck muscles often affected
• Sensations are intact; Pure motor presentation
• Muscle stretch reflexes are normal (Ankle DTRs last to be lost)
• Presence of pseudohypertrophy
• Duchenne muscular dystrophy, polymyositis
• HIMET acronym
• Exceptions: Distal myopathies: Welander; Miyoshi, Nonaka,
Udd, Markesberg-Griggs, Laing distal myopathy

24. PATTERN RECONITION-RADICULOPATHY
• Proximal (upper lumbar roots) as well as distal weakness (lower
lumbo-sacral roots) innervated by a common nerve root
• Vertebral pain (extradural compression)
• Radicular pain (sensory root)
• Dermatomal sensory loss
• Segmental reflex alteration:
– C5,6: Biceps and brachioradialis
– C7: Triceps jerk
– L3,4: Knee jerk
– S1: Ankle jerk

25. PATTERN RECONITION-PARTIAL MYELOPATHY
(Brown Sequard syndrome)
• At the level of the lesion: Segmental Lower motor neuron
weakness
• Upper motor neuron weakness, hyperreflexia and Babinski sign
ipsilateral to the lesion
• Dissociated sensory loss:
– Vibration and proprioception- ipsilateral
– Pain and temperature-Contralateral
– Sensory level

26. SYSTEMIC
EXAMINATION CLUES

27. MENTAL STATUS EXAMINATION
• Level of consciousness
• Speech
• Vocabulary
• Orientation
• Knowledge of current events
• Judgment
• Emotional response
• Memory
• Object recognition
• Calculation

28. BRIEF MENTAL FUNCTION – CORTICAL LOCALISATION
MMSE
• Orientation
• Registration
• Attention & Calculation
• Recall [Memory]
• Language

29. MMSE
Domain Test
Orientation Year,season,date,day,month /
state,country,state/city,hospital,ward
Registration
[STM]
3 common objects [Glass,pen,watch]
Attention
Calculation
Spell ‘WORLD’ backwards 100-7/40-7 serial 5 steps
5 minute Recall 3 objects repeated above
Language Naming:2 objects;Repetition;Ideational apraxia-3
stage command;Read & Obey; Write a sentence;
Copy intersecting pentagons
Localization 5 minute recall – Memory; Left medial temporal)
Naming/Repetition/Read/Writing – Left language
areas. Calculation / Ideational apraxia – Left parietal
Constructional praxis – Parietal (Rt>Lt parietal)

31. LOBE LOCALIZATION

32. FRONTAL LOBE
• Anosmia – orbitofrontal
• Motor deficit – contralateral hemiplegia [hands,tongue,lips,foot]
• Language (Lt frontal) – Broca’s motor aphasia
• Kennedy Foster syndrome
• Apathy,Depressed (Left)
• Frontal bladder deficits
• Primitive release reflexes – Prefrontal lobe
• Paratonic rigidity (Geganhalten)
• Cognitive deficits – Dorsolateral frontal
• Abulia / Akinetic mute state
• Behavioural disinhibition
• Pseudopsychopathic behaviour Rt Orbitofrontal
• No sensory deficits, No visual field deficits

33. FRONTAL LOBOLOGY – PHINEAS GAGE
1868
Phineas Gage, the science of brain localization; phrenology-functional
specialization-anatomical correlation-’modularity of the mind’

34. Neurological stamp
Phineas Gage and the science of brain localization
Commemorating the 150th anniversary of the event; the first
day cover shows Dr John Martin Harlow
J Neurol Neurosurg Psychiatry 2001;71:761

35. TEMPORAL LOBE
• Medial temporal – Hippocampus, Taste & Smell (Uncus;Insula)
• Lateral temporal – Wernicke’s aphasia
• Auditory cortex (Heschl transverse gyri) – auditory hallucinations
• Wernicke aphasia – Sensory aphasia Left STG
• Visual field deficits – Upper homonymous quadrantanopia
• Memory deficits – Medial temporal [Rt- visual memory / Lt- verbal
memory]
• Temporo occipital – Visual hallucinations
• Korsakoff amnesic defect – memory deficits in chronic alcoholics
• Kluver-Bucy syndrome [Bilateral temporal]

36. PARIETAL LOBE
• Wernicke’s aphasia – Left angular and supramarginal gyrus
• Homonymous hemianopia ( inferior quadrantanopia)
• Cortical sensory loss – 2 point discrimination; stereognosis;
tactile localisation; graphesthesia
• Gerstmann syndrome Lt parietal – Lt/Rt confusion, acalculia,
agraphia, finger agnosia
• Hemi Neglect rt parietal
• Ideational / Ideomotor apraxia Lt parietal
• Dressing apraxia Rt parietal
• Topographical disorientation Rt parietal
• Anosognosia Rt parietal
• Constructional apraxia Rt>Lt parietal

37. OCCIPITAL LOBE
• Visual field defects – Homonymous hemianopia
• Visual hallucinations
• Cortical blindness [Bilat]
• Visual agnosia – Object agnosia [Lt]; Simultanagnosia [Bilat],
Colour anomia [Lt] ; Alexia [Lt]

38. DESTRUCTIVE LESIONS

39. CORTICAL ‘IRRITATIVE’
SIGNS

41. LOBOLOGY - LOCALIZATION

42. CEREBRAL CORTICAL REPRESENTATION – BODY
SCHEMA

43. MOTOR / SENSORY CORTICAL
REPRESENTATION

44. CORTICAL vs SUBCORTICAL

45. SUBCORTICAL - BASAL GANGLIA
Internal
capsule

46. Motor pathway – UMN and LMN
Internal capsule localization – 3 Hs
•Hemiplegia – dense (UL= LL)
•Hemianesthesia
•Hemianopia

47. PATTERN OF MOTOR WEAKNESS
• Cortical Paraplegia
• UL>LL = Cortical Watershed zone stroke (Man in a Barrel)
• LL>UL = Subcortical Watershed zone stroke (Pseudospinal stroke)
• Mute + bilateral UMN VII + Pseudobulbar Palsy = Opercular Syndrome
• Faciobrachial weakness = Anterior Limb IC (Heubner’s artery)
• Crossed hemiplegia; UL>LL weakness = Cruciate hemiplegia
(Medullary pyramidal decussation to upper cervical cord C23 level)
• Stroke picture, somnolent mutism, agitated delirium with hallucinations
= Top of Basilar Syndrome (“hidden eye signs”)
• Stroke, Horner’s syndrome, Anterior neck pain (carotidynia) = Carotid
dissection
• Ipsilateral cranial nerve involvement + contralateral pyramidal signs =
Brain stem lesions
• COPS: Cortical lesion= head deviated Opposite to plegia / Pontine
lesion = head/eye deviated to Same side of plegia

48. PERISYLVIAN LANGUAGE AREAS
Broca
area
Wernicke
area
Arcuate fibers

49. Brain stem Localization – Crossed syndromes
Midbrain
syndrome
Pontine
syndrome
Medullary
syndrome

50. III,IV
V,VI,VII
IX,X,XI,XII
Cerebellar signs

51. BRAINSTEM LOCALIZATION
Weber syndrome (Base of Midbrain) Ipsilateral III + Contralateral
hemiplegia
Claude syndrome Ipsilateral III + Contralateral
cerebellar ataxia/red nucleus
tremor
Benedikt syndrome Ipsilateral III + Contralateral long
tract signs (CST,Cerebellar,Tremor)
Millard Gubler syndrome (Base of
Pons)
Ipsilateral VI and VII + Contralateral
hemiplegia
Wallenberg syndrome (Lateral Medulla) Ipsilateral V,IX,X,ataxia,face pain
loss + contralateral spinothalamic
loss
Medial medullary syndrome Ipsilateral XII + contralateral
hemiplegia

52. MOTOR WEAKNESS PATTERN
• CORTICAL
Monoparesis, body regions that have maximal cortical
representation is most affected + Cortical signs
• SUBCORTICAL
Monoparesis
• INTERNAL CAPSULE
Hemiplegia, Hemianesthesia, Homonymous hemianopia
• BRAINSTEM
Ipsilateral cranial nerve signs + Contralateral hemiplegia

53. MOTOR TRACT SOMATOTOPIC LAMINATIONS

54. CST LAMINATIONS

55. UMN vs LMN

56. 1st Step - UMNL vs. LMNL
Cerebral cortex to spinal cord
(excluding AHC)
 UMN distribution of motor
weakness (Pyramidal
weakness)
 Spasticity
 DTRs – hyper reflexic
 Absent superficial reflexes
 Normal muscle bulk
 Paralysis of movement
 Plantar response – Babinski
sign positive
 No fasciculation
AHC level to muscle
 LMN distribution of weakness
 Hypotonia
 DTRs – areflexic / hyporeflexic
 Plantar response – No
Babinski sign
 Paralysis of muscle
 Muscle bulk – wasting /
atrophy (3 weeks) [Parietal
wasting]
 Focal / Segmental myotomal
muscle weakness
 Fasciculation present

57. MOTOR CORTEX REPRESENTATION
Pyramidal distribution of motor weakness

59. CEREBRAL LOCALIZATION
Site How to localise
Cerebral cortex [Cortical] [Grey
matter]
Lobe functions / Lobe function tests
[Aphasia,apraxia,agnosia,behavioural
& personality changes,h/o
seizures,MMSE alterations]
Motor weakness - monoparesis
Subcortical [White matter] Hemiplegia,Hemianesthesia,Hemiano
piaDenser weakness
pattern,movement disorders [Basal
ganglia],No seizures,No cognitive
deficits usually
Diencephalon Thalamic syndrome,Asc RAS –
altered level of consciousness
Brain stem The company of cranial nerve deficits
Ipsilateral cranial nerve +
contralateral long tract signs
[Crossed signs]

60. MOTOR WEAKNESS LOCALIZATION
Monoparesis + Cortical signs
Monoparesis;No cortical signs
3 H’s
Ipsilat III + Contralateral H
Ipsilat VI/VII + Contralateral H
Ipsilat V,IX,X,XII + Contra
Long tract signs
Only weakness, No Cr N signs

61. LMN LESIONS
• Anterior Horn Cells (AHC)
• Roots – Radiculopathy
• Plexus – Plexopathy
• Peripheral Nerves – Neuropathy
• NMJ
• Muscle - Myopathy

62. CLUES FOR LMN LOCALIZATION
Type/Site of Lesion Diagnostic Features
Anterior Horn Cell Focal/Segmental LMN type of
weakness; Pure Motor signs;
Fasciculations
Roots Root pains; Localization according to
root affected [Motor & Sensory signs]
Plexus No root pains; Plexus anatomy &
localization [Mainly motor signs]
Peripheral Nerves Motor + Sensory signs
Neuromuscular Junction Pure motor signs; Fatigability; Diurnal
variation
Muscle Pure motor signs

63. RADICULOPATHY
• Motor signs – DTRs – hypo/areflexic
Biceps – C5
Triceps – C7
Supinator – C6
Knee – L4
Ankle – S1
• Sensory signs – Dermatomal loss

65. SENSORY LOCALIZATION
CN V Face T4: Nipple
C2-3: Neck T10: Umbilicus
C4: Shoulder L1: Inguinal
C6: Thumb L3: Knee
C7: M. finger L5: Ant. Leg and foot
C8: L. finger S1: Heel

66. NEUROPATHY MYOPATHY
Distal Symmetrical Motor; Glove &
Stocking sensory signs
Pure Motor; No Sensory
Symmetrical Proximal weakness;
Selective muscle involved with
hypertrophy/pseudohypertrophy
DTRs – Hyporeflexic; Distal Ankle
jerks – lost first/early
DTRs – Normal; Proportional to
muscle bulk/weakness;Ankle jerks –
preserved till late/last to be lost
Proximal Neuropathy
AIDP/GB Syndrome
Diabetic Amotrophy
Porphyric Neuropathy
Distal Myopathy - Genetic
Extensor Digitorum Brevis (EDB) -
wasted
EDB - preserved
JPS/Vibration Sense - affected JPS/Vibration Sense – Normal

67. AUTONOMIC NERVOUS
SYSTEM

70. VISUAL FIELD
DEFECTS

72. EOM SO4 / LR6 /OM3

73. ADD ABD
SR/IQ
IR/SQ
SR
IR
IQ
SQ
MR LR

74. SUPRANUCLEAR
GAZE PALSY
NUCLEAR /
INFRANUCLEAR
PALSY

75. LEFT GAZE PALSY
LEFT INO

77. PUPIL EXAMINATION

78. LIGHT REFLEX
PATHWAY

79. Upper half of face – bilateral
cortical representation

81. UMN VII PALSY

82. LMN VII PALSY

83. EMOTIONAL FACIAL PARESIS
• Emotional facial paresis (EFP) is characterized by impaired activation
of face muscles with emotion [smiling; mimetic smile)] but normal
voluntary activation.
• Volitional facial paresis affects facial movements with voluntary effort,
sparing activation on emotion.
• Volitional facial paresis (VFP) refers to weakness of facial muscles on
voluntary effort while emotional movements are preserved.
• Separate pathways for volitional and emotional facial muscle control
• Sites EFP: frontal lobe white matter, SMA, striatocapsular territory,
anterolateral thalamus, insula, posterior thalamus, subthalamus,
hypothalamus, operculum, mesial temporal lobe and insula, dorsal
midbrain
• Sites for VFP: involvement of motor cortex/descending pyramidal
tract/corticobulbar pathways; sparing BG, frontal & temporal
• Aetiology: stroke, lacunar infarcts, tumours, demyelinating lesions,
hematoma, ICA dissection

84. Emotional Facial Palsy
(EFP)
(A) Symmetric voluntary
activation (showing the teeth)
(B) right EFP while smiling
(C) MRI showing left
striatocapsular infarction
A B
C

85. Hge infarct-lat
thalamus,BG, insula;
Rt ICA thrombus
Left frontal WM
edema; sparing
thalamus & BG
Hematoma- left posterior
SITES/AETIOLOGY-EFP

86. (A) “Showing the teeth” demonstrates symmetric innervation on volition. (B) Smiling discloses left
emotional facial paresis. Right Horner’s syndrome is demonstrated by the small palpebral fissure.
(C) Contrastenhanced T1-weighted MRI. Section at the upper pontine level documenting
involvement of the cerebellum and the right dorsal pontine tegmentum. For C and D, right is on the
right-hand side. (D) Drawing of the upper pontine level. The hatched area corresponds to the area
involved as shown in C. This area is quite distinct from the corticobulbar tract mediating voluntary
facial innervation
EFP OF PONTINE
ORIGIN

87. VOLUNTARY FACIAL PARESIS
(A) VFP (showing the teeth), (B) symmetric activation with emotion
(laughing). (C) MRI after intravenous gadolinium (0.1 mmol lkg body
weight) showing enhancement of the right cortex.
A B C

88. MYELOPATHY
Sensory level
Motor level
Reflex level
Vibration level

89. Cervical – Add 1
T1-T6 – Add 2
T789 – Add 3
T10 – L1L2
T11 – L3L4
T12 – L5
L1- Sacral segments

90. Conus Medullaris Cauda Equina
Spontaneous pain Bilateral;Symmetric
S234 (Perineum/Thighs)
Radicular
pain;Unilateral;Asymme
tric at S234
Sensory deficit Saddle
area,Bilateral,Symmetrical,
Dissociative
Saddle,Unilateral,Asym
metric,No
dissociation,All
sensations affected
Motor loss Symmetric,Less marked Asymmetric,Marked
Reflex loss Ankle lost Knee/Ankle lost
Sphincters Early and marked Late and less marked
Trophic changes Common Less marked
Sexual functions Erection impaired Less impaired
Onset Sudden and Bilateral Gradual and Unilateral

91. REFLEX LEVEL LOCALIZATION - MYELOPATHY

92. Motor Eye Field Area
CO PS
CO Cortical – Eyes
deviated to opposite to
side of weakness
PS Brainstem – Eyes
deviated to same side of
weakness

93. POSTURING - LOCALIZATION

98. NEUROLOGICAL
EXAMINATION

99. The Holmesian logician: Sherlock Holmes’ “Science of Deduction and Analysis”
Cognitive heuristics, Thinking and Deducing Logical Proofs