PARAPLEGIA By Dr Bashir Ahmed Dar Associate professor Medicine Chinkipora sopore kashmir
Causes of flaccid paralysis • Anterior horn cellspoliomylitis • Nerve rootradiculitis,polyradicul opathy,tabes dorsalis,cauda equina • Peripheral nerves-GB syndrome,peripheral neuropathy
• Myoneural junctionmyasthenia gravis,lambert eaton syndrome,periodic paralysis • Muscles - myopathy
• 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.
Causes of spastic paraplegia Compressive • Extramedullary • Intradural - -meningioma,neurofibr oma,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
Intramedullary • • • •
syringomyelia, haematomyelia, intramedullary tumor eg, ependymoma, glioma
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
What is spastic paraplegia • Involvement of spinal cord and cerebrum produce spastic UMN paraplegia. • Has two types • Paraplegia in flexion and paraplegia in extension.
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
• Sacral sparing-absent • Bowel bladder disturbances– early • Vertebral tenderness may be present • CSF changes –froins syndrome common
• Present • Late • Absent • Rare
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
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
• 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
Cord compression at multiple sites • Arachnoiditis( tubercular there is patchy involvement) • Neurofibromatosis • Multiple sclerosis • Secondary deposits • Cervical spondylitis
Paraplegia without sensory loss • • • • •
Hereditory spastic paraplegia Lathyrism GB syndrome Amyotropic lateral sclerosis fluorosis
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.
Difference between conus medularis and cauda equina syndrome • The conus medularis is Signs in conus terminal portion at medullaris while which cord ends and planter are flexor or cauda equina is bunch not elicitable with of roots.therefore the asymmetrical LMN main distinction paralysis in cauda between the two is the equina syndrome. plantars extensor and symmetrical LMN
• Conus leison • Bilateral symmetrical of both lower limbs • No root pains
• Cauda equina leion • Asymmetrical involvement of both lower limbs • Severe root pains • Asymetrical sensory loss
• Bilateral saddle anaesthesia
• Bulbocavernous s1-s2, and anal reflex are absent • Bladder bowel disturbances common • Planters extensors
• Depending upon root invlvement • Relatively spared • Normal or not elecitable
Episodic weakness causes • Mysthenia gravis • Hyperthyroidism • Periodic paralysis( hyperkalaemia or hypokalaemia)
Investigations • Routine blood tests • Urine test,also for culture and sensitivity • Bllod chemistry eg blood urea,creatinine,electrol ytes • X ray chest • Lymph node biopsy
• CSF examination • CT scan,MRI • CT –Myelography meniscus sign intradural,brush sign extradural,expansion sign in syringomyelia
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
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,
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.