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Localization in Neurology- 2
Specific lesions & syndromes
Lesion- CNS
 Upper motor neuron
 Weakness
 Disuse atrophy
 Spasticity
 Reflexes
 Extensor plantar
 NCV- normal
 No denervation
potentials in EMG
 Lower motor neuron
 Weakness
 Wasting-marked & early
 Flaccidity
 Loss of reflexes
 Fasciculations
 NCV- abnormal
 Denervation potentials
in EMG
Lesion- brain
 UMN
 Spasticity
 UL-flexor, LL-extensor
 Paralysis of voluntary
movements
 No involuntary move.
 Exaggerated DTR
 Plantar-extensor
 EPS
 Rigidity
 All-flexor>extensor
 Mildly decreased
voluntary movements
 Involuntary movements
 Normal DTR
 Plantar-flexor
Localization in spinal cord
 Uppermost sensory level
 Pain over a vertebra
 Radicular pain
 Band-like sensation
 Isolated flaccidity/atrophy/areflexia
& distal UMN signs
Lesion- spinal cord
 Extramedullary
 Radicular pain
 Localised vertebral t’ness
 Brown-Sequard hemicord
syndrome
 Early UMN signs
 Ascending sensory symp.
 Sharp sensory level
 Marked sacral sensory loss
 Early CSF abnormalities
 Intramedullary
 Poorly localised burning pain
 Dissociated loss of pain, with
spared joint position sense
 Late UMN signs
 Commom coexistence of
LMN+UMN signs
 Descending sensory symp.
 Sacral sparing
 Normal/minimally altered
CSF
Lesion- lower spinal cord
 Cauda equina
 Pain common, projected
to perineum/thigh
 LMN type paraparesis
 Asymmetric
 Saddle anaesthesia
 Late bladder & bowel
involvement
 Conus medullaris
 Pain less prominent
 Absent anal reflex
 More symmetrical
 B/L saddle anesthesia
 Early bladder & bowel
involvement and
impotence
MCA infarct
 Embolic
 Contralateral hemiplegia &/or
hemianaesthesia
 Dominant hemisphere- aphasia
 Non-dominant hemisphere-
agnosia & apraxia
Basilar artery infarct
 Mostly embolic
 Bilateral long tract signs-
sensory & motor
 With cranial nerve- V-VIII- symptoms
 With cerebellar dysfunction
Medullary syndromes
 Lateral
 Trigeminal sensory nucleus & spinothalamic tracts affected
 Causing I/L face & C/L body loss of pain & temperature
sensation
 Ataxia, nystagmus, vertigo, dysphagia, hoarseness
 Horner’s syndrome- ptosis, miosis, I/L anhidrosis
 Medial
 Hypoglossal nerve, medullary pyramids & medial leminiscus
affected
 Causing I/L tongue deviation, C/L hemiplegia & C/L loss of
touch/position/vibration sensation
Bulbar palsy
 B/L LMN defect of IX-XII cranial nerves
 Dysphagia (liquid>solid), nasal regurgitation,
slurred speech
 Nasal speech, wasted tongue with fasciculation,
absent gag reflex
 Pseudobulbar palsy-
 B/L UMN defect of IX-XII cranial nerves
 Dysphagia, dysarthria, emotional lability
 Slow indistinct speech, spastic tongue, brisk jaw jerk
 Frontal release signs
Craniovertebral junction anomaly
 Neck/shoulder pain
 Short, webbed neck with ROM
 Vertigo, drop attacks, syncope- due to
vertebrobasilar ischemia
 Upper cord compression- spastic paresis,
posterior column defects ± Lhermitte sign
 Brain compression- nystagmus, hoarseness,
dysarthria, dysphagia, ataxia
Spinal cord
 Transverse myelitis
 Upper sensory level for all sensations,
LMN signs at the level of lesion, flaccid paralysis
(spinal shock)UMN signs distally, B/B involved
 Anterior spinal artery syndrome
 Upper sensory level for pain/temperature,
sparing of posterior columns, UMN signs distally
 Brown-Sequard syndrome
 I/L spastic paralysis & loss of joint/position sense,
C/L loss of pain/temperature sensation
Motor neuron disease
 Selectively affect motor neurons, that
control voluntary muscle activity
 Types-
 Amyotrophic lateral sclerosis- UMN+LMN
 Primary lateral sclerosis- UMN
 Progressive muscular atrophy- LMN
 Bulbar palsy- bulbar LMN
 Pseudobulbar palsy- bulbar UMN
Inflammatory demyelinating polyneuropathy
 Acute- AIDP
 Symmetric ascending weakness, cranial n. may be
involved, areflexia, myalgia
 With or without dysesthesias, loss of position sense
more common & severe than loss of pain/temp.
 Autonomic dysfunction- orthostatic hypotension
 Chronic- CIDP- >8 weeks
In the end
 Neuromuscular junction-
 Symmetrical proximal muscle weakness,
with bulbar involvement
 Fatigable, variable
 Sensory, reflexes, bladder-bowel- normal
 Myopathy-
 Symmetrical proximal muscle weakness, bulbar
spared
 Progressive, waddling gait
 Sensory, reflexes, bladder-bowel- normal

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Localization in neurology 2

  • 1. Localization in Neurology- 2 Specific lesions & syndromes
  • 2. Lesion- CNS  Upper motor neuron  Weakness  Disuse atrophy  Spasticity  Reflexes  Extensor plantar  NCV- normal  No denervation potentials in EMG  Lower motor neuron  Weakness  Wasting-marked & early  Flaccidity  Loss of reflexes  Fasciculations  NCV- abnormal  Denervation potentials in EMG
  • 3. Lesion- brain  UMN  Spasticity  UL-flexor, LL-extensor  Paralysis of voluntary movements  No involuntary move.  Exaggerated DTR  Plantar-extensor  EPS  Rigidity  All-flexor>extensor  Mildly decreased voluntary movements  Involuntary movements  Normal DTR  Plantar-flexor
  • 4. Localization in spinal cord  Uppermost sensory level  Pain over a vertebra  Radicular pain  Band-like sensation  Isolated flaccidity/atrophy/areflexia & distal UMN signs
  • 5. Lesion- spinal cord  Extramedullary  Radicular pain  Localised vertebral t’ness  Brown-Sequard hemicord syndrome  Early UMN signs  Ascending sensory symp.  Sharp sensory level  Marked sacral sensory loss  Early CSF abnormalities  Intramedullary  Poorly localised burning pain  Dissociated loss of pain, with spared joint position sense  Late UMN signs  Commom coexistence of LMN+UMN signs  Descending sensory symp.  Sacral sparing  Normal/minimally altered CSF
  • 6. Lesion- lower spinal cord  Cauda equina  Pain common, projected to perineum/thigh  LMN type paraparesis  Asymmetric  Saddle anaesthesia  Late bladder & bowel involvement  Conus medullaris  Pain less prominent  Absent anal reflex  More symmetrical  B/L saddle anesthesia  Early bladder & bowel involvement and impotence
  • 7. MCA infarct  Embolic  Contralateral hemiplegia &/or hemianaesthesia  Dominant hemisphere- aphasia  Non-dominant hemisphere- agnosia & apraxia
  • 8. Basilar artery infarct  Mostly embolic  Bilateral long tract signs- sensory & motor  With cranial nerve- V-VIII- symptoms  With cerebellar dysfunction
  • 9. Medullary syndromes  Lateral  Trigeminal sensory nucleus & spinothalamic tracts affected  Causing I/L face & C/L body loss of pain & temperature sensation  Ataxia, nystagmus, vertigo, dysphagia, hoarseness  Horner’s syndrome- ptosis, miosis, I/L anhidrosis  Medial  Hypoglossal nerve, medullary pyramids & medial leminiscus affected  Causing I/L tongue deviation, C/L hemiplegia & C/L loss of touch/position/vibration sensation
  • 10. Bulbar palsy  B/L LMN defect of IX-XII cranial nerves  Dysphagia (liquid>solid), nasal regurgitation, slurred speech  Nasal speech, wasted tongue with fasciculation, absent gag reflex  Pseudobulbar palsy-  B/L UMN defect of IX-XII cranial nerves  Dysphagia, dysarthria, emotional lability  Slow indistinct speech, spastic tongue, brisk jaw jerk  Frontal release signs
  • 11. Craniovertebral junction anomaly  Neck/shoulder pain  Short, webbed neck with ROM  Vertigo, drop attacks, syncope- due to vertebrobasilar ischemia  Upper cord compression- spastic paresis, posterior column defects ± Lhermitte sign  Brain compression- nystagmus, hoarseness, dysarthria, dysphagia, ataxia
  • 12. Spinal cord  Transverse myelitis  Upper sensory level for all sensations, LMN signs at the level of lesion, flaccid paralysis (spinal shock)UMN signs distally, B/B involved  Anterior spinal artery syndrome  Upper sensory level for pain/temperature, sparing of posterior columns, UMN signs distally  Brown-Sequard syndrome  I/L spastic paralysis & loss of joint/position sense, C/L loss of pain/temperature sensation
  • 13. Motor neuron disease  Selectively affect motor neurons, that control voluntary muscle activity  Types-  Amyotrophic lateral sclerosis- UMN+LMN  Primary lateral sclerosis- UMN  Progressive muscular atrophy- LMN  Bulbar palsy- bulbar LMN  Pseudobulbar palsy- bulbar UMN
  • 14. Inflammatory demyelinating polyneuropathy  Acute- AIDP  Symmetric ascending weakness, cranial n. may be involved, areflexia, myalgia  With or without dysesthesias, loss of position sense more common & severe than loss of pain/temp.  Autonomic dysfunction- orthostatic hypotension  Chronic- CIDP- >8 weeks
  • 15. In the end  Neuromuscular junction-  Symmetrical proximal muscle weakness, with bulbar involvement  Fatigable, variable  Sensory, reflexes, bladder-bowel- normal  Myopathy-  Symmetrical proximal muscle weakness, bulbar spared  Progressive, waddling gait  Sensory, reflexes, bladder-bowel- normal