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LOCALIZATION OF LESION
   Inability to move a part – Paralysis

   Interruption of motor pathways between
    cerebral cortex and muscles

   Divided into UMN and LMN

   Both limbs on one side of body affected –
    Hemiplegia
FEATURES OF UMN LESIONS
 Weakness
 Distal muscle groups affected

 Axial movements, extraocular, upper facial,
  pharyngeal and jaw muscles are spared
 Hypertonia

 Deep reflex exaggerated

 Loss of abdominal reflex

 Extensor plantar

 No muscle wasting
COMPLAINTS OF UMN LESION
 Stiffness of legs
 Tendency to trip over

 Unable to walk on rough ground

 Difficulty to climb steps

 Dragging of foot
FEATURES OF LMN LESION
 Weakness
 Hypotonia

 Loss of tendon reflex

 Fasciculation of muscle

 Contracture of muscle

 Trophic changes
UMN                               LMN

Voluntary activity lost, reflex   Both voluntary and reflex
activity present                  activity lost

Spastic paralysis due to          Flaccid paralysis due to
hypertonia, clasp knife           hypotonia
rigidity and ankle clonus
present
Deep reflexes are                 Both superficial and deep
exaggerated due to                reflexes absent
increase in muscle tone.
Some of the superficial
reflexes are lost and some
altered
Muscle atrophy occur slowly Rapid muscular atrophy


Reaction of degeneration          Reaction of degeneration
absent                            present
HOW TO LOCALIZE UMN LESIONS
cortex
   Paralysis on opposite side, extent depends on area
    involved. Unequal weakness of limbs

   Seizure +

   Aphasia + (if dominant hemisphere is involved)

   Loss of cortical sensation

   No movement disorder

   No visual field defect [except in occipital lobe
    involvement]
SUBCORTICAL / THALAMUS
   Paralysis on opposite side

   Unequal weakness of limb

   Loss of primary sensation

   Homonymous visual field defect

   No seizure/ no aphasia

   Movement disorder[BG – chorea, parkinsonism,
    hemibalallismus]
INTERNAL CAPSULE
   Dense hemiplegia and UMN facial palsy

Lesion extending posterior
 Hemianesthesia



   Homonymous hemianopia
MID BRAIN
   Crossed hemiplegia

   Weber syndrome [3rd nerve palsy]

   Benedicts syndrome [3rd nerve, red nucleus,
    cerebellar ataxia]
PONS
   Crossed hemipelgia

   Millard Gubler syndrome [6th and 7th nerve palsy]

   Lesion in basis pontis can cause ataxic hemiparesis
    [ weakness + cerebellar on same side]
MEDULLA
   Crossed hemiplegia

   Jackson syndrome [ 12th nerve palsy]

   Involvement of medial lemniscus leads to loss of
    sensation

   Cruciate hemiplegia
SPINAL CORD
   Brown sequard syndrome [hemiplegia on the side
    of involvement without face] lesion above C5

   Effects below the level – UMN type motor loss and
    sensory loss

   At the level – LMN type

   Above the level – Hyperaesthesia
SPINAL CORD LESION
HOW TO LOCALIZE LMN LESION
Presenting       Anterior horn   Peripheral    Neuromuscula Muscle
features         cell disease    nerve         r junction   disease
                                               disease
Distribution     Asymmetric      Symmetric     Extra ocular,   Symmetric
                 limb/ bulbar    and distal    bulbar and      proximal or
                                               proximal limb   distal limb
                                               muscles         muscles
Muscle           Marked and      Moderate      None            Early stage –
atrophy          early                                         slight
                                                               Late – marked
Sensory          None            Parasthesia   None            None
involvement


Characteristic   Fasciculation   Combined      Diurnal         Usually
features         and cramps      sensory and   fluctuation     proximal
                                 motor                         involvement
Reflex           Variable        Decreased     Normal          Decreased
EXTRA PYRAMIDAL SYSTEM
 Difficulty to initiate movements
 Hypertonia – rigidity [cog wheel]

 No loss of power of muscles and wasting

 Bradykinesia or akinesia

 Involuntary movement

 Plantar response – Flexor
CEREBELLAR LESION
 Ataxia
 Nystagmus

 Dysarthria

 Intension tremor

 Hypotonia

 Dysdiadocokinesis

 Plantar response – Flexor

 Paralysis is not a feature of cerebellar disease

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Localization of lesion in hemiplegia

  • 2. Inability to move a part – Paralysis  Interruption of motor pathways between cerebral cortex and muscles  Divided into UMN and LMN  Both limbs on one side of body affected – Hemiplegia
  • 3. FEATURES OF UMN LESIONS  Weakness  Distal muscle groups affected  Axial movements, extraocular, upper facial, pharyngeal and jaw muscles are spared  Hypertonia  Deep reflex exaggerated  Loss of abdominal reflex  Extensor plantar  No muscle wasting
  • 4. COMPLAINTS OF UMN LESION  Stiffness of legs  Tendency to trip over  Unable to walk on rough ground  Difficulty to climb steps  Dragging of foot
  • 5. FEATURES OF LMN LESION  Weakness  Hypotonia  Loss of tendon reflex  Fasciculation of muscle  Contracture of muscle  Trophic changes
  • 6. UMN LMN Voluntary activity lost, reflex Both voluntary and reflex activity present activity lost Spastic paralysis due to Flaccid paralysis due to hypertonia, clasp knife hypotonia rigidity and ankle clonus present Deep reflexes are Both superficial and deep exaggerated due to reflexes absent increase in muscle tone. Some of the superficial reflexes are lost and some altered Muscle atrophy occur slowly Rapid muscular atrophy Reaction of degeneration Reaction of degeneration absent present
  • 7. HOW TO LOCALIZE UMN LESIONS cortex  Paralysis on opposite side, extent depends on area involved. Unequal weakness of limbs  Seizure +  Aphasia + (if dominant hemisphere is involved)  Loss of cortical sensation  No movement disorder  No visual field defect [except in occipital lobe involvement]
  • 8. SUBCORTICAL / THALAMUS  Paralysis on opposite side  Unequal weakness of limb  Loss of primary sensation  Homonymous visual field defect  No seizure/ no aphasia  Movement disorder[BG – chorea, parkinsonism, hemibalallismus]
  • 9. INTERNAL CAPSULE  Dense hemiplegia and UMN facial palsy Lesion extending posterior  Hemianesthesia  Homonymous hemianopia
  • 10. MID BRAIN  Crossed hemiplegia  Weber syndrome [3rd nerve palsy]  Benedicts syndrome [3rd nerve, red nucleus, cerebellar ataxia]
  • 11. PONS  Crossed hemipelgia  Millard Gubler syndrome [6th and 7th nerve palsy]  Lesion in basis pontis can cause ataxic hemiparesis [ weakness + cerebellar on same side]
  • 12. MEDULLA  Crossed hemiplegia  Jackson syndrome [ 12th nerve palsy]  Involvement of medial lemniscus leads to loss of sensation  Cruciate hemiplegia
  • 13. SPINAL CORD  Brown sequard syndrome [hemiplegia on the side of involvement without face] lesion above C5  Effects below the level – UMN type motor loss and sensory loss  At the level – LMN type  Above the level – Hyperaesthesia
  • 15. HOW TO LOCALIZE LMN LESION Presenting Anterior horn Peripheral Neuromuscula Muscle features cell disease nerve r junction disease disease Distribution Asymmetric Symmetric Extra ocular, Symmetric limb/ bulbar and distal bulbar and proximal or proximal limb distal limb muscles muscles Muscle Marked and Moderate None Early stage – atrophy early slight Late – marked Sensory None Parasthesia None None involvement Characteristic Fasciculation Combined Diurnal Usually features and cramps sensory and fluctuation proximal motor involvement Reflex Variable Decreased Normal Decreased
  • 16. EXTRA PYRAMIDAL SYSTEM  Difficulty to initiate movements  Hypertonia – rigidity [cog wheel]  No loss of power of muscles and wasting  Bradykinesia or akinesia  Involuntary movement  Plantar response – Flexor
  • 17. CEREBELLAR LESION  Ataxia  Nystagmus  Dysarthria  Intension tremor  Hypotonia  Dysdiadocokinesis  Plantar response – Flexor  Paralysis is not a feature of cerebellar disease