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Paraplegia is paralysis or weakness (paraparesis) of both lower limbs. It may be

due to:
- Pyramidal (U.M.N.) lesion resulting in spastic paraplegia.
- Lower motor neurone (L.M.N.) lesion resulting in flaccid paraplegia.

Spastic Paraplegia

It is paralysis or weakness of both lower-limbs due to bilateral pyramidal
tract lesion, most commonly in the spinal cord (spinal paraplegia), and less
commonly in the brain stem or the cerebral parasagittal region (cerebral
paraplegia). Spinal paraplegia may be: 1. Focal: paraplegia with sensory level.
2. Systemic.
3. Disseminated.

Causes of Spinal Paraplegia:

I- Focal causes:
A. Compression:
1. Vertebral:
- Fracture or fracture-dislocation of the vertebra, Disc prolapse and
spondylosis, Pott's disease, Neoplastic diseases: Primary or metastatic and
Deformity of the vertebral column as kyphoscoliosis.
2. Meningeal (extramedullary):
- Extradural e.g. leukaemic deposits.
- Dural e.g. meningioma.
- Intradural e.g. neurofibroma.
3. Cord (intramedullary): Syringomyelia .
B. Inflammatory: Transverse myelitis - Myelomeningitis - Myeloradiculitis.
C. Vascular: Anterior spinal artery occlusion.
II. Systemic causes:
A systemic disease in neurology is a disease which affects one or more systems
selectively and is usually bilateral and symmetrical. When a systemic disease affects the
pyramidal tracts, either alone or with other tracts, paraplegia will result.
A. Heridofamilial:
1. Hereditary spastic paraplegia.
2. Hereditary ataxias e.g. Friedreich's or Marie's ataxia.
B. Symptomatic:
1. Pellagral lateral sclerosis.
2. Subacute combined degeneration.
C. Idiopathic: motor neurone disease.
III. Disseminated cause: Disseminated Sclerosis (D.S.)

Causes of Cerebral Paraplegia:

A. Causes in the Parasagittal Region: (area of cortical presentation of L.L.)
1. Traumatic e.g. depressed fracture of the vault of the skull, Subdural
2. Vascular e.g. superior sagittal sinus thrombosis.
3. Inflammatory e.g. encephalitis, meningio-encephalitis.
4. Neoplastic e.g. parasagittal meningioma.
5. Degenerative e.g. cerebral palsy.
B. Causes in the Brain Stem:
Syringobulbia and midline tumors. These lesions arise in the midline and
involve the innermost fibers which are those of the lower limbs.
Clinical Picture of Focal Paraplegia
A. At the level of the lesion:
1. Vertebral manifestations: only present if the cause is vertebral.
- Localized pain or tenderness.

- Localized deformity or swelling.

2. Radicular manifestations: only present in extra-medullary causes.

a) Posterior root affection:
- Early pain in the back referred to the distribution of the affected root and
described as girdle pain; it is exaggerated by coughing, sneezing and straining.
- Later, there is hypoesthesia or anesthesia in the dermatome supplied by
the affected root.
b) Anterior root affection: localized L.M.N. weakness in the muscles supplied
by the affected root.
N.B: As the lesion in paraplegia is below the cervical segments (which supply
the muscles of the arm), the L.M.N. affection at the level of the lesion is not
clinically evident; this is due to the difficulty in eliciting wasting and the

difficulty of testing for tone and deep reflexes in the trunk and abdominal
muscles. If the lesion involves the cervical segments, there is quadriplegia
with evident signs of L.M.N.L. in the upper limbs.
B. Below the level of the lesion: (cord manifestations):
1. Motor Manifestations: They depend on whether the cause of the lesion is
acute or gradual.
a) If the cause is acute (inflammation, vascular or traumatic), the paraplegia
passes through 2 stages:
Stage of flaccidity due to neuronal shock:
Immediately following the lesion, there is sudden paralysis of the lower
limbs, associated with complete loss of tone and absence of reflexes. This stage
lasts from 2 to 6 weeks.
Stage of spasticity due to recovery from the neuronal shock:
On recovery from the shock stage, the full picture of U.M.N.L. will be established
including: hypertonia, hyper-reflexia, positive Babinski sign & may be clonus.
b) If the cause is gradual (e.g. neoplastic):
atoryThe shock stage is absent and there will be gradual progressive weakness
of LL with hypertonia and hyper-reflexia.
- The weakness affects distal more than the proximal muscles and the flexor
more than the extensors.
- The hypertonia and hyper-reflexia affect the extensor group of muscles
(antigravity) more than the flexor group (progravity). The paraplegia in this stage is
described as (paraplegia in extension)
- With further progression of the lesion, the extrapyramidal fibers in the cord will be
affected. The hypertonia and hyper-reflexia will be more in the flexor group of
muscles than in the extensors. In this stage the paraplegia is described as
(paraplegia in flexion).
This last stage may be associated with the mass reflex where there is spontaneous

urination, defecation and sweating on scratching the skin over the medial side of
the thigh.
N.B: Piere Marie Foix test is done by firm passive plantar flexing of the toes
and foot. This will result in spontaneous "withdrawal reflex" i.e. spontaneous
flexion of the hip, knee and dorsiflexion of the ankle if the paraplegia is passing
from extension to flexion.

1. Cause
2. Hypertonia
3. Position of L.L.
4. Deep reflexes
5. Clonus
6. Mass reflex
7. Bladder

Paraplegia in extension

Paraplegia in flexion

Pyramidal lesion
More in extensors

Pyramidal and extrapyramidal

More in flexors
Less exaggerated
May be present
Automatic bladder

2. Sensory of Manifestations:
a) If the cause of the lesion is extramedullary, encroachment on the ascending
tracts at the site of lesion results in sensory level below which, all types of
sensations are diminished. There is early loss of sensation in the saddle area (S
3, 4, 5), as the sacral fibres lie in the outermost part of the spinothalamic tracts in the
b) If the cause of the lesion is intramedullary, there will be a jacket
sensory loss (hyposthetic area with normal sensations above and below it). The

sensory loss is of a dissociated nature i.e. pain and temperature sensations are
lost but touch and deep sensations are preserved; this is due to the interruption of
the crossing fibers carrying pain and temperature by the midline lesion, while touch
and deep sensation fibers ascend in the posterior column without decussation. The
sensations over the saddle area are preserved (sacral spare), as the sacral fibers lie
far from the midline lesion.
Arrangement of fibers within the spinothalamic tract

3. Sphincteric Manifestations:
a. In acute lesions: There is
retention of urine in the shock stage,
followed by precipitancy of micturition.
b. In gradual lesions: There is
precipitancy of micturition which




bladder when complete transaction

of the cord occurs.
* These





extramedullary lesions and early in





pyramidal fibres controlling the bladder centre lie medially in the cord.
Management of Paraplegia
I. General:
- Frequent change of the patient's posture to guard against bedsores.
- Care of the skin by frequent washing with alcohol followed by talc powder. In
case of urinary incontinence, frequent change of bed-sheets.
- Care of the bladder: If there is retention, use parasympathomimetic drugs. If this
fails, use a catheter to evacuate the bladder.

II. Physiotherapy
III. Symptomatic Treatment:
Analgesics and sedatives for pain, Muscle relaxants for the spasticity, Vitamins
and tonics.

IV. Specific Treatment: (treatment of the cause)

1. Antituberculous drugs in Pott's disease.
2. Deep Xray in case of intramedullary tumors.
3. Surgical eradication in case of extramedullary tumors.
Differentiation between extramedullary & intramedullary lesions






Painful due to posterior



root irritation

Absent or late


1. Motor

Usually asymmetrical

Usually symmetrical

2. Sensory

- Sensory level.
- All types of sensations are
diminished below the level
including pain, temp, and
- Early loss of sensation in
the saddle area.

- Jacket sensory loss.

- Dissociated sensory loss
i.e. loss of pain and temp,
with preservation of touch.

Possible vertebral lesion


Clinical Picture

Plain x-Ray

- Late loss of sensation in the

saddle area (sacral spare)

Modified from: Elwan H: Principles of Neurology.University book center, Cairo, Egypt, 2007.