Paraplegia By Dr Bashir Ahmed Dar Associate Professor of Medicine Chinkipora sopore Kashmir

PARAPLEGIA By Dr Bashir Ahmed Dar Associate professor Medicine Chinkipora sopore kashmir

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

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,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

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 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.

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

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,electrolytes
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
3 rd ,4 th 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.

Paraplegia By Dr Bashir Ahmed Dar Associate Professor of Medicine Chinkipora sopore Kashmir

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