Paraplegia By Dr Bashir Ahmed Dar Associate Professor of Medicine Chinkipora sopore Kashmir
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Transcript of Paraplegia By Dr Bashir Ahmed Dar Associate Professor of Medicine Chinkipora sopore Kashmir
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PARAPLEGIA
ByDr Bashir Ahmed Dar
Associate professor Medicine
Chinkipora sopore kashmir
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Causes of flaccid paralysis
• Anterior horn cells-poliomylitis
• Nerve root- radiculitis,polyradiculopathy,tabes dorsalis,cauda equina
• Peripheral nerves-GB syndrome,peripheral neuropathy
• Myoneural junction- myasthenia gravis,lambert eaton syndrome,periodic paralysis
• Muscles - myopathy
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• Flaccid paralysis means lower motor neuron paralysis resulting from the disease of anterior horn cells,radicles,peripheral nerves and muscles
• Acute onset of UMN type of paralysis may present flaccid instead of spastic paralysis due to shock.
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Causes of spastic paraplegia Compressive
• Extramedullary• Intradural - --
meningioma,neurofibroma,arachnoiditis
• Extradural--- potts disease(caries spine)
• Vertebral neoplasms eg, metastasis,myloma
• Pachymeningitis• Prolapsed IVD• Epidural abcess or
haemorrage• Fracture dislocation of
vertebra ,pagets disease,osteoporosis
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Intramedullary
• syringomyelia,
• haematomyelia,
• intramedullary tumor eg,
• ependymoma, glioma
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What is Cerebral Paraplegia
• The lower limbs and bladder (micturition centre)are represented in paracentral lobule, leisions in this area produce paraplegia with bladder disturbance-eg retension urine and cortical type of sensory loss.may b associated with headache,vomiting and fits.
• Causes are
• cerebral diplegia
• superior sagital sinus thrombosis
• Parasagital meningioma
• Thrombosis of unpaired anterior cerebral artery
• Gunshot injury of this area
• Internal hydrocephalus
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What is spastic paraplegia
• Involvement of spinal cord and cerebrum produce spastic UMN paraplegia.
• Has two types
• Paraplegia in flexion and paraplegia in extension.
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Differences
• Etramedullary • Root pain---common• UMN signs –early• Sensory deficit—
contralateral loss of pain and temp with ipsilateral loss of proprioception
• Intramedullary • Rare • Late • Dissociated sensory
loss
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• Sacral sparing-absent• Bowel bladder
disturbances– early• Vertebral tenderness
may be present• CSF changes –froins
syndrome common
• Present
• Late • Absent
• Rare
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Non compressive causes
• MND –amyotropic lateral sclerosis
• MS• Acute transverse
myelitis• Subacute combined
degeneration of cord vit 12 def.
• Lathyrism• Syringomyelia• Hereditory spastic
paraplegia• Tropical spastic
paraplegia• Radiation myelopathy
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Differences between compressive and non compressive paraplegia
• (compressive)• Boney changes• Root pains• Upper level of sensory
loss present • Zone of
hyperaesthesia may be present
• (non compressive)• No boney changes• No root pains• No definite level
• Absent
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• Usually gradual onset• Asymetrical
involvement of limbs• Commonest cause is
caries• Bladder bowel
disturbance occurs
• Usually acute onset• Symmetrical
involvement of limbs• Commonest cause
MND• Occours but late
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Cord compression at multiple sites
• Arachnoiditis( tubercular there is patchy involvement)
• Neurofibromatosis
• Multiple sclerosis
• Secondary deposits
• Cervical spondylitis
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Paraplegia without sensory loss
• Hereditory spastic paraplegia
• Lathyrism
• GB syndrome
• Amyotropic lateral sclerosis
• fluorosis
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Paraplegia with loss of deep tendon jerks
• In paraplegia the tendon jerks are brisk.they can only become absent when pt is either in spinal shock or there is involvement of affrent or efferent side of reflex
• eg , in• Neural shock(spinal)• Radiculitis- the jerk whose
root is involved will be absent
• Peripheral neuropathy-bilat ankle jerks will be absent
• Reflex activity may be absent in presence of severe infection due to supression.
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Difference between conus medularis and cauda equina syndrome
• The conus medularis is terminal portion at which cord ends and cauda equina is bunch of roots.therefore the main distinction between the two is the plantars extensor and symmetrical LMN
Signs in conus medullaris while planter are flexor or not elicitable with asymmetrical LMN paralysis in cauda equina syndrome.
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• Conus leison• Bilateral symmetrical
of both lower limbs
• No root pains
• Bilateral saddle anaesthesia
• Cauda equina leion• Asymmetrical
involvement of both lower limbs
• Severe root pains
• Asymetrical sensory loss
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• Bulbocavernous s1-s2, and anal reflex are absent
• Bladder bowel disturbances common
• Planters extensors
• Depending upon root invlvement
• Relatively spared• Normal or not
elecitable
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Episodic weakness causes
• Mysthenia gravis
• Hyperthyroidism
• Periodic paralysis( hyperkalaemia or hypokalaemia)
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Investigations
• Routine blood tests• Urine test,also for
culture and sensitivity• Bllod chemistry eg
blood urea,creatinine,electrolytes
• X ray chest• Lymph node biopsy
• CSF examination• CT scan,MRI• CT –Myelography
meniscus sign intradural,brush sign extradural,expansion sign in syringomyelia
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Tropical spastic paraplegia
• Females• 3rd ,4th decade• Associated with
HTLV-1 infection• This is UMN spastic
paraplegia without sensory disturbance.
• Bladder disturbances• And is non
compressive progressive myelopathy
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Features of paraplegia
• Pain over spine or along roots
• Sensory loss below ,and hyperasthesia at the level
• Motor weakness• Urgency or hesitency
leading to retension of urine
• Involvement of spinothalamic and dorsal column tract.
• Loss of deep tendon reflexex at level due to root if
• All reflexes below level lost
• Tone increased,
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Lathyrism
• It is due to khesari dal(lathyrus sativus)
• May involve families in locality
• The causative factor is BOAA, a neurotoxin.due to spasticity they pass through one stick stage,scissor gait,then
• Two stick stage then crawling.