Medicine – Spastic Paraparesis

Spastic paraparesis means weakness of both lower limbs caused by an upper motor neurone lesion, usually affecting the corticospinal tracts in the spinal cord or, less commonly, bilateral cerebral motor pathways. The legs are weak and stiff, with increased tone and other pyramidal signs.

An asterisk (*) signifies a common cause.

1. Increased Tone

The characteristic motor abnormality is spasticity, meaning increased muscle tone that is velocity-dependent.

On examination, the legs may feel stiff when moved passively.

The increase in tone is usually more marked in the antigravity muscle groups.

2. Clonus

Clonus is a series of rhythmic involuntary muscle contractions triggered by sudden stretching of a muscle.

It is a sign of an upper motor neurone lesion.

A common example is:

Ankle clonus.

Sustained clonus strongly supports significant corticospinal tract dysfunction.

3. Weakness

Patients have weakness affecting both lower limbs.

The pattern depends on the level and severity of the lesion, but the weakness is usually accompanied by:

Spasticity.

Hyperreflexia.

Extensor plantar responses.

The legs may become stiff and difficult to move despite relatively preserved muscle bulk early in the disease.

4. Extensor Plantar Responses

An extensor plantar response, or positive Babinski sign, is an important pyramidal sign.

When the lateral sole is stimulated, the great toe extends upward and the other toes may fan.

Therefore:

Spastic paraparesis + extensor plantars → corticospinal tract involvement.

5. Hyperreflexia

Although not explicitly listed in the original notes, brisk deep tendon reflexes are usually expected in a pure upper motor neurone spastic paraparesis.

Typical findings include:

Brisk knee jerks.

Brisk ankle jerks.

Clonus.

However, reflexes may be reduced if a condition also damages peripheral nerves, such as subacute combined degeneration or Friedreich ataxia.

6. Atrophy and Contractures

Muscle wasting is not usually a prominent early feature of a pure upper motor neurone lesion.

However, chronic severe weakness and immobility may cause:

Disuse atrophy.

Muscle shortening.

Joint contractures.

Therefore, atrophy and contractures are generally late secondary changes, rather than primary features of corticospinal tract disease.

7. Gait

Patients may develop a characteristic spastic gait.

Features may include:

Stiff-legged walking.

Reduced knee flexion.

Scissoring of the legs in severe bilateral spasticity.

Difficulty lifting the feet.

Slow, effortful walking.

The exact gait varies with the underlying cause.

8. Multiple Sclerosis*

Multiple sclerosis is an important cause of spastic paraparesis, especially in younger adults.

Demyelinating plaques involving the spinal cord corticospinal tracts may produce:

Bilateral leg weakness.

Spasticity.

Hyperreflexia.

Extensor plantar responses.

Other MS manifestations may coexist, such as optic neuritis, sensory symptoms, bladder dysfunction, diplopia, or ataxia.

9. Cerebral Palsy*

Cerebral palsy can produce chronic spastic paraparesis when bilateral motor pathways controlling the lower limbs are affected.

A classic form is spastic diplegia, in which:

Both legs are more affected than the arms.

The patient may have:

Increased tone.

Scissoring gait.

Contractures.

Delayed motor development.

This is a non-progressive brain injury, although the musculoskeletal consequences can change over time.

10. Spinal Cord Compression*

Spinal cord compression is one of the most important causes of acquired spastic paraparesis.

Compression damages the corticospinal tracts and may also affect sensory and autonomic pathways.

Clinical features may include:

Back or neck pain.

Spastic leg weakness.

Sensory level.

Bladder or bowel dysfunction.

Hyperreflexia and extensor plantars.

Depending on the cause and progression, spinal cord compression may require urgent investigation.

11. Cervical or Thoracic Spondylosis

Spondylosis refers to degenerative changes of the spine.

When these changes narrow the spinal canal and compress the spinal cord, they may produce degenerative cervical myelopathy or, less commonly, thoracic cord compression.

The patient may develop:

Spastic leg weakness.

Gait difficulty.

Hand clumsiness if the cervical cord is involved.

Brisk reflexes.

Extensor plantar responses.

12. Neoplasia

Tumours can cause spastic paraparesis through compression or infiltration of the spinal cord.

Possible causes include:

Metastatic vertebral disease.

Epidural tumour.

Primary spinal tumour.

Intramedullary tumour.

A history of cancer together with new back pain and progressive leg weakness should raise concern for metastatic spinal cord compression.

13. Disc Prolapse

A large intervertebral disc prolapse may compress the spinal cord if it occurs at a level where the spinal cord is present, particularly in the cervical or thoracic spine.

This can produce:

Spastic paraparesis below the lesion.

By contrast, a lumbar disc prolapse below the conus more commonly compresses nerve roots and causes cauda equina or radicular LMN signs rather than spastic paraparesis.

14. Motor Neurone Disease

Motor neurone disease, particularly amyotrophic lateral sclerosis, can cause a mixture of upper and lower motor neurone findings.

If corticospinal tract involvement is prominent in the lower limbs, the patient may develop:

Spastic paraparesis.

However, additional findings such as:

Muscle wasting.

Fasciculations.

Bulbar weakness.

may suggest combined LMN involvement.

15. Spinal Cord Infarction

Spinal cord infarction may cause sudden or rapidly developing bilateral leg weakness.

The clinical pattern depends on which vascular territory is affected.

Anterior spinal artery infarction may produce:

Motor weakness.

Loss of pain and temperature below the lesion.

with relative preservation of:

Vibration and proprioception, at least initially.

Spasticity may develop after the acute spinal shock phase.

16. Vasculitis

Systemic or central nervous system vasculitis can damage the spinal cord through inflammatory vascular injury and ischaemia.

This may produce a myelopathy with:

Spastic paraparesis.

Sensory abnormalities.

Sphincter dysfunction.

Other systemic inflammatory features may provide clues to the diagnosis.

17. Myelitis

Myelitis means inflammation of the spinal cord.

A common clinical syndrome is transverse myelitis.

Patients may develop:

Bilateral weakness.

Sensory level.

Bladder or bowel dysfunction.

Initially reduced reflexes in spinal shock, followed later by spasticity and hyperreflexia.

Causes include autoimmune disease, infection, demyelinating disease, and idiopathic inflammatory myelopathy.

18. Subacute Combined Degeneration

Subacute combined degeneration due to vitamin B12 deficiency affects the:

Dorsal columns.

Corticospinal tracts.

Peripheral nerves.

It can therefore produce:

Spastic paraparesis.

Sensory ataxia.

Loss of vibration and proprioception.

Peripheral neuropathy.

Extensor plantar responses.

Reflexes may paradoxically be reduced because of simultaneous peripheral nerve damage.

19. Friedreich Ataxia

Friedreich ataxia can also produce pyramidal tract involvement and spastic weakness of the legs.

However, the clinical picture is mixed and usually includes:

Progressive ataxia.

Peripheral sensory neuropathy.

Pes cavus.

Kyphoscoliosis.

Absent tendon reflexes.

Extensor plantar responses.

Cardiomyopathy.

Therefore, it is not a simple pure spastic paraparesis.

20. Syringomyelia

Syringomyelia is formation of a fluid-filled cavity, or syrinx, within the spinal cord.

Classically, it causes:

Loss of pain and temperature in a cape-like distribution.

Preserved vibration and proprioception early.

Lower motor neurone weakness at the level of the lesion.

If the syrinx expands and damages corticospinal tracts, it can eventually produce:

Spastic weakness of the legs below the lesion.

21. Syphilis

Neurosyphilis can affect the spinal cord in several ways.

The classic form tabes dorsalis primarily damages the dorsal columns and dorsal roots, producing sensory ataxia and reduced reflexes rather than a typical spastic paraparesis.

However, other syphilitic forms, such as meningovascular or meningomyelitic disease, can involve corticospinal pathways and cause spastic weakness.

Therefore, syphilis is a less common and more context-dependent cause.

22. Spastic Paraparesis – Note Form

Definition: bilateral lower-limb weakness with upper motor neurone signs.

Tone: increased.

Reflexes: usually brisk.

Clonus: may be present.

Plantar responses: extensor.

Weakness: both legs.

Atrophy: usually secondary to chronic disuse rather than an early primary feature.

Contractures: may develop in chronic severe spasticity.

*Common demyelinating cause: ** multiple sclerosis.

*Common developmental cause: ** cerebral palsy, especially spastic diplegia.

*Common structural cause: ** spinal cord compression.

Cord compression causes: spondylosis, tumour and disc prolapse.

Other causes: motor neurone disease, spinal cord infarction, vasculitis, myelitis, subacute combined degeneration, Friedreich ataxia, syringomyelia and neurosyphilis.

23. Useful Localisation Clues

Spastic paraparesis + sensory level → spinal cord lesion likely.

Spastic paraparesis + bladder dysfunction → spinal cord disease particularly important.

Spastic paraparesis + optic neuritis/other disseminated neurological episodes → consider MS.

Spastic paraparesis + loss of vibration/proprioception + neuropathy → consider vitamin B12 deficiency.

Spastic paraparesis + ataxia + pes cavus + cardiomyopathy → consider Friedreich ataxia.

Spastic paraparesis + cape-like pain/temperature loss → consider syringomyelia.

Key Clinical Pattern

Think of spastic paraparesis as:

Bilateral leg weakness + increased tone + hyperreflexia/clonus + extensor plantar responses.

The major categories are:

Demyelinating → MS.

Developmental → cerebral palsy.

Compressive → spondylosis, tumour, disc disease.

Inflammatory/vascular → myelitis, vasculitis, spinal cord infarction.

Metabolic/hereditary → B12 deficiency, Friedreich ataxia.

A particularly important clinical rule is:

Spastic paraparesis with a sensory level or new bladder/bowel dysfunction should prompt urgent consideration of spinal cord compression or another myelopathy.