Spinal cord disorders

Acute Transverse Myelitis
Blockage of the Spinal Cord’s Blood Supply
Cervical Spondylosis
Compression of the Spinal Cord
Hereditary Spastic Paraparesis
Subacute Combined Degeneration
Syrinx of the Spinal Cord and Brain Stem

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Amr Hassan, M.D.
Associate professor of Neurology - Cairo
University

SPINAL CORD
DISORDERS

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12. Spinal cord disrders
Definitions:
Spinal Tetraplegia (quadriplegia): It is paralysis of both
upper and lower-limbs due to bilateral pyramidal tract
lesion in the cervical region of the spinal cord.
Spinal Paraplegia: It is paralysis of both lower limbs due
to bilateral pyramidal tract lesion in the thoracic region of
the spinal cord.

14. 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 as osteosarcoma or haemangioma.
• Metastatic from a Iry carcinoma of the thyroid,
breast, lung, stomach, kidney & prostate.
- Deformity of the vertebral column as kyphoscoliosis.

15. CAUSES OF SPINAL PARAPLEGIA:
1) FOCAL CAUSES :
A. Compression:
2. Meningeal (extramedullary):
- Extradural e.g., leukaemic deposits.
- Dural e.g., meningioma, pachymeningitis hypertrophica of
syphilis.
- Intradural e.g., neurofibroma, cystic arachnoiditis.
3. Cord (intramedullary):
- Syringomyelia - Glioma or Ependymoma of the cord.
B. Inflammatory:
- Transverse myelitis - Myelomeningitis - Myeloradiculitis.
C. Vascular: Anterior spinal artery occlusion.

16. CAUSES OF SPINAL PARAPLEGIA:

ll. 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. Subacutc combined degeneration.

C. Degenerative: Motor Neurone Disease.

17. CAUSES OF SPINAL PARAPLEGIA:
III. Disseminated causes :
Multiple Sclerosis. (acute transverse myelitis in
R.R.M.S. or progressive myelopathy in P.P.M.S.).
Neuromyelitis optica ( Devic’s disease).

18. CLINICAL PICTURE OF FOCAL PARAPLEGIA

Clinical picture of focal paraplegia
At the level of the lesion:

Vertebral manifestations: only present if the cause is vertebral.
Localised pain or tenderness.
Localised deformity or swelling.

Radicular manifestations: only present in extra-medullary causes.

Motor manifestations (Anterior root affection): localised L.M.N.
weakness in the muscles supplied by the affected root.
Sensory manifestations (Posterior root affection): Early pain in the
back Later there is hyposthesia or anaesthesia in the dermatome
supplied by the affected root.

19. Below the level of the lesion:
The motor manifestations : They depend on whether the cause of the lesion is acute
or gradual.
If the cause is acute: (inflammatory,vascular or traumatic).

The paraplegia passes by 2 stages:

Stage of flaccidity due to neuronal shock:
This stage lasts from 2 to 6 weeks.
Spinal shock is a state of transient physiologic (rather than anatomic) reflex depression
of cord function below the level of injury, with associated loss of all sensorimotor
functions.
Immediately following the lesion there is sudden paralysis of the lower limbs,
associated with complete loss of tone and absence of reflexes (flaccid paralysis).

Stage of spasticity due to recovery from the neuronal shock:
On recovery from the shock stage, the fullblown picture of U.M.N.L. will be established
including: hypertonia, hyperreflexia, positive Babinski sign & may be clonus.
CLINICAL PICTURE OF FOCAL PARAPLEGIA

20. If the cause is gradual (e.g. neoplastic):
The shock stage is absent, and there will be gradual progressive weakness of the
lower limbs with hypertonia and hyperreflexia.

The weakness is distal more than proximal & affecting flexors more than the
extensors.
The hypertonia and hyperreflexia 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 fibres in the cord will
be affected. The hypertonia and hyperreflexia 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, defaecation and sweating on scratching the skin over
the medial side of the thigh associated with reflex erection and ejaculation on
squeezing the glans penis.
CLINICAL PICTURE OF FOCAL PARAPLEGIA

21. 2) The sensory manifestations :
If the cause of the lesion is extramedullary:
Compression on the ascending tracts at the site of lesion results in
a sensory level below which all types of sensations are
diminished or lost.
There is early loss of sensation in the saddle area (S 3, 4, 5), as the
sacral fibers lie in the outermost part of the spinothalamic tracts
in the cord.
If the cause of the lesion is intramedullary:
Dissociated sensory loss: i.e., Pain and temp sensations are lost but
touch and deep sensations are preserved; this is due to the interruption
of the crossing fibers carrying pain and temp, by the midline lesion,
while touch and deep sensation fibers ascend in the posterior column
without decussation.
Jacket sensory loss: A hyposthetic area with normal sensations
above and below it. Findings with intramedullary lesion restricted to
region of central canal. Loss of pain and temperature perception is
noted in the dermatomes supplied by the affected segments.
Sacral spare :The sensations over the saddle area are preserved, as the
sacral fibers lie far from the midline lesion.
CLINICAL PICTURE OF FOCAL PARAPLEGIA

22. C T L S S L T C
Extramedullary compression causes sensory level
with involvement of the sacral area

23. C T L S S L T C
Intramedullary compression causes sacral
spare

24. Intramedullary
lesion cause:
Jacket sensory loss

26. 3) Sphincteric manifestations :
In acute lesions retention of urine in the shock stage,
followed by precipitancy of micturition.
In gradual lesions: precipitancy of micturition which may
terminate in automatic bladder when complete transaction
of the cord occurs.
These changes start late in extramedullary lesions and early
in intramedullary lesions as the pyramidal fibres
controlling the bladder centre lie medially in the cord.
CLINICAL PICTURE OF FOCAL PARAPLEGIA

27. Sphincter manifestations

Sphincter manifestations
Acute-----retention with
overflow
Precipitancy
Automatic bladder
Mass reflex
NB :early in
intramedullary and late in
extramedullary

28. Sphincter manifestations

Sphincter manifestations
Acute-----retention with
overflow
Precipitancy
Automatic bladder
Mass reflex
NB :early in
intramedullary and late in
extramedullary

29. Intramedullary lesion cause
early sphincteric involvement

30. Intramedullary lesion cause
early sphincteric involvement
Extra
medullary
lesion

31. Investiations

Spinal cord imaging: Imaging of the cervical region in case of tetraplegia and
dorsal region in case of paraplegia can be helpful in detection of focal causes
e.g. tumor, fracture vertebra … etc.
Plain X ray
CT spine
MRI Spine

Diagnosis of myelopathy:
MRI Cervical spine shows an intramedullary cervical lesion


Laboratory studies: According the cause e.g. serum level of Vitamin B12 in
subacute combined degeneration of the cord, viral serology, tumor markers
..etc.
Other investigations: Tailored according the cause e.g. Tuberculin test in Pott’s
disease, evoked potential in M.S….etc.

33. Management
General measures:
Frequent change of the patient's posture to guard against bedsores and hypostatic pneumonia.
Care of the skin.
Care of the bladder:catheterization to evacuate the bladder in case of urine retention.
Prophylactic anticoagulants and elastic stocking to guard against D.V.T.

Physiotherapy:
Massage to increase the blood supply to the paralysed muscles.
Passive exercises to guard against fibrosis and stiffness.
Active exercises to strengthen the muscles.
Positioning: The paralysed limb is put in a position slightly opposite to the hypertonia.

Specific Treatment: Treatment of the cause e.g. surgical excision of tumors, surgical decompression and
stabilization in traumatic causes, steroids in M.S., Antituberculous treatment in Pott’s disease.

34. Causes of cerebral paraplegia:
Causes in the parasagittal region: (area of cortical presentation of
L.L.)
Traumatic e.g. Depressed fracture of the vault of the skull or
Subdural haematoma.
Vascular e.g. superior sagittal sinus thrombosis.
Inflammatory e.g. encephalitis, meningio-encephalitis.
Neoplastic e.g. parasagittal meningioma.
Diplegic cerebral palsy.
Causes in the brain stem:
Syringobulbia.
Midline brain stem tumours: These lesions arise in the midline and
involve the innermost pyramidal fibres which are those of the
lower limbs.

35. Where is the lesion?
Parasagittal
Brain stem
Spinal
Systemic involvement

Dissemination

36. Clinical manifestations
A-Clinical picture at the level of the lesion
Cerebral (headache, papillodema, confusion)
Spinal (vertebarl manifestations, radicular involvement,
LMNL)
Systemic (associated ataxia, retinal disease, skin disease)
Disseminated lesions (optic neuritis, ataxia)

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