Paraplegia approach

1. APPROACH TO PARAPLEGIA
PRESENTER- DR.JAYKRAT CHAUDHARY

2. • Paralysis or the suffix “-plegia”- indicates weakness so severe that a
muscle cannot be contracted at all.
• whereas paresis refers to partial weakness.

3. • Weakness- reduction in the power that can be exerted by one or
more muscles.
• fatigability- inability to sustain the performance of an activity that
should be normal for a person of the same age, sex, and size.
• severe proprioceptive sensory loss- prevents adequate feedback
information about the direction and power of movements
• Bradykinesia-in which increased time is required for full power to be
exerted
• Apraxia- a disorder of planning and initiating a skilled or learned
movement unrelated to a significant motor or sensory deficit.

4. PARAPLEGIA
• Originates from Greek language
• Para + plēssein means ‘strike at side’
• Partial or complete weakness of lower half of the body with
involvement of both the legs that is usually due to injury or disease of
spinal cord in thoracic and lumbar region
• Impairment in motor function of the lower extremities
• With or without involvement of sensory system
• Paraplegia - Complete weakness
• Paraparesis - Partial weakness

5. CLASSIFICATION
Paraplegia is classified into
• Spastic paraplegia –umn type
• Flaccid paraplegia.-lmn type

6. SIGNS THAT DISTINGUISH THE ORIGIN OF
WEAKNESS
• Sign umn lmn
• Atrophy none severe
• Fasciculation none common
• Tone spastic decreased
• Distribution of weakness pyramidal/regional distal/segmental
• Muscle stretch reflexes hyperactive hypoactive/absent
• Babinski sign present absent

7. UMN/LMN

10. PARAPLEGIA IN EXTENSION PARAPLEGIA IN FLEXION

11. SPASTIC[UMN] PARAPLEGIA
• PURE MOTOR-
1.LATHYRISM-Due to kesari dal consumption containing neurotoxin
BOAA Or ODAP.
• ONSET-gradual
• FAMILY HISTORY
• TREATMENT – SUPPORTIVE CARE

12. 2.HEREDITARY SPASTIC PARAPLEGIA-
Mode of inheritance-AD,AR,X-linked recessive.
Onset-gradual
Age of presentation-dual-early childhood ,adulthood
3.AMYOTROPHIC LATERAL SCLEROSIS[MND]
Onset-gradual
Limb onset/bulbar onset

13. 4.ERB’S SPASTIC PARAPLEGIA-syphilitic meningomyelitis with
primary optic atrophy.
Onset-gradual
P/H/O-GENITAL ULCER
INVESTIGATION-SERUM VDRL/CSF VDRL

14. 5.CEREBRAL CAUSE
• Traumatic
Depressed fracture of the vault of the skull , Subdural hematoma,
bullet injury to paracentral lobule
• Vascular
Superior sagittal sinus thrombosis ,unpaired aca thrombosis
• Inflammatory - Encephalitis , Meningo-encephalitis- leading to acute
hydrocephalus
• Neoplastic - Parasagittal meningioma
• Degenerative - Cerebral diplegia

15. SENSORY-MOTOR
• Spinal cause

16. • Compressive myelopathy

17. Non compressive myelopathy
1.Vascular – thrombosis of anterior spinal artery
Onset- sudden
Joint ,position sense and vibration spared

18. • INFLAMMATORY-Acute transverse myelitis
• Onset- acute to sub acute
• Follows a viral illness or post-vaccinal
• Partial or complete sensory loss in all modalities with a definite upper
level.
• Early bowel and bladder involvement.
• Girdle constriction at the level of lesion with zone of hyperesthesia
just above it.mid thoracic region is the most common site.

19. • DEMYELINATING-
1. MULTIPLE SCLEROSIS-
• ONSET – gradual
• Weakness-waxing and weaning
• Diagnosis-MRI of brain and spine-shows lesion and plaques
• CSF examination-oligoclonal band of igG
• Visual and sensory evoked potential

20. 2.NEUROMYELITIS OPTICA OR DEVIC’S DISEASE-optic neuritis + acute
myelitis
• Anti-AQP4 igG Ab
• Anti-MOG igG Ab
3.SACD-
ONSET- gradual
investigation-vit B12 level

21. Friedreich ataxia- genetic disease
• Autosomal recessive mode of inheritance
TROPICAL SPASTIC PARAPLEGIA-
HTLV-1 associated
Onset-gradual
• RADIATION MYELOPATHY
• PARANEOPLASTIC MYELITIS
• ANTIPHOSPHOLIPID ANTIBODY SYNDROME

22. FLACCID [LMN] PARAPLEGIA
• PURE MOTOR-
• 1.G B. SYNDROME-ACUTE INFECTIVE POLYRADICULONEUROPATHY
• Areflexic atonic ascending motor paralysis
• onset-sub acute
• Ascending paralysis
• In 50% have b/l VII nerve palsy
• Bowel and bladder – absent
• CSF study- Albumino-cytological dissociation

23. 2.Acute poliomyelitis-CNS involvement occur in 4-5% cases
• 3 to 4 % had non paralytic poliomyelitis – aseptic meningitis
• <1% had paralytic poliomyelitis
• Acute asymmetric flaccid paralysis and muscle atrophy
• Polio virus affect the motor neuron in the anterior horn cell of spinal
cord.
3.Progressive muscular atrophy- type of motor neuron disease
It affect on LMN.

24. •PURE SENSORY-
• TABES DORSALIS-
• Occur in late stage of neurosyphilis
• Demyelination and degeneration
Of dorsal column of spinal cord
• charcot joint
• decreased or absent DTR
• shooting nerve root pain
• sensory ataxia
• impaired proprioception

25. • SENSORY MOTOR-
1.UMN LESION IN SPINAL SHOCK-ATM
SPINAL INJURY
2.NERVE ROOTS- cauda equina syndrome

27. 3.PERIPHERAL NERVE-LUMBAR PLEXUS INJURY[POSAS
ABSCESS,HEMATOMA]
5.NM JUNCTION-MYASTHENIA GRAVIS
LAMBERT EATON SYNDROME
PERIODIC PARALYSIS
6.MUSCLES- MYOPATHY

28. CAUSE OF PARAPLEGIA ACCORDING TO
ONSET OF ILLNESS
• acute[minutes to hour]
Trauma - Fracture dislocation of vertebrae
Vascular - Thrombosis of ASA Endarteritis/Hematomyelia
• Sub acute[hours to days]
Infection-epidural abscess
Transverse Myelitis
• chronic[weeks to month]
Neoplastic- meningioma/ependymoma/glioma/astrocytoma

29. COMPRESSIVE VS NON COMPRESSIVE
MYELOPATHY
• Features compressive Non compressive
•
UPPER LEVEL OF SENSORY LOSS + -

30. EXTRAMEDULLARY VS INTRAMEDULLARY
COMPRESSIVE MYELOPATHY

32. EXTRAMEDULLARY MYELOPATHY

33. LOCALIZATION OF LESION
spinal cord segment related to vertebrae

34. • D7 lesion -Abdominal reflexes lost in all four quadrants • Cremasteric
reflexes B/L lost • Plantar B/L extensor
• D10 lesion - Abdominal reflexes lost in lower 2 quadrants •
Cremasteric reflexes B/L lost • Plantar B/L extensor
• L1 lesion -Abdominal reflexes present in all four quadrants •
Cremasteric reflexes B/L lost • Plantar B/L extensor

35. CHANGES IN DEEP TENDON REFLEXES

36. TONE OF MUSCLE
• DECREASE AT THE LEVEL OF LESION
• INCREASE BELOW THE LEVEL OF LESION
• HYPOTONIA AND AREFLEXIA S/O SPINAL SHOCK

37. SENSORY LOSS IN VARIOUS SPINAL CORD
LESION

38. BROWN SEQUARD SYNDROME[hemisection
of spinal cord]
• Loss of pain, temp C/L to the hemisection- interruption of crossed
spinothalamic tract
• I/L loss of proprioception – interruption of ascending fibers of
posterior column

39. • I/L spastic weakness due to interruption of descending corticospinal
tract
• Segmental LMN signs and sensory changes at the level of lesion due
to damage of the roots and anterior horn cells at the level of lesion

40. THANKYOU