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Spinal cord disorders

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Amr Hassan, M.D. Associate professor of Neurology - Cairo University SPINAL CORD DISORDERS
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Page 1: Spinal cord disorders

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

University

SPINAL CORD

DISORDERS

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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.

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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.

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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.

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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.

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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).

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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.

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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

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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

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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

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C T L S S L T C

Extramedullary compression causes sensory level with involvement of the sacral area

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C T L S S L T C

Intramedullary compression causes sacral spare

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Intramedullary lesion cause:

Jacket sensory loss

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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

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Sphincter manifestations

Sphincter manifestations Acute-----retention with

overflow

Precipitancy

Automatic bladder

Mass reflex

NB :early in intramedullary and late in extramedullary

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Sphincter manifestations

Sphincter manifestations Acute-----retention with

overflow

Precipitancy

Automatic bladder

Mass reflex

NB :early in intramedullary and late in extramedullary

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Intramedullary lesion cause early sphincteric involvement

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Intramedullary lesion cause early sphincteric involvement

Extra medullary

lesion

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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.

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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.

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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.

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Where is the lesion? Parasagittal

Brain stem

Spinal

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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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