Spastic Paraparesis

Routine for examination of lower limbs:


Inspect (wasting, fasciculations, wheelchair/walking aid, catheter, pes cavus)

Gait and Rhomberg’s test




Sensation (sensory level, joint position sense and vibration)



If time allows and you suspect spastic paraparesis proceed as follows:


Eyes: eye movements (INO, nystagmus), RAPD

Mouth: tongue fasciculations

Hands and arms: small muscle wasting, fasciculations, coordination of upper limbs (past pointing, intention tremor, dysdiadochokinesis), tone, power, reflexes of upper limbs

Back: spinal surgery scars, palpate down spine for tenderness

If spastic paraparesis, cerebellar signs and dorsal column signs consider Friedreich’s ataxia and proceed as per “Station 3 Friedreich’s ataxia”



Present to the examiner:


This patient has a (symmetrical/assymetrical) spastic paraparesis as evidenced by:


Increased tone bilaterally

Pyramidal weakness bilaterally

Increased reflexes

Upgoing plantars and clonus

Spastic scissoring gait


With regards to aetiology:


  1. There was (no) sensory level to suggest cord compression/cord infarction/transverse myelitis
  2. There was (no) dorsal column sensory loss to suggest demyelination/Friedreich’s ataxia/subacute combined degeneration of the cord/taboparesis/cervical myelopathy
  3. There were (no) cerebellar signs to suggest demyelination/Friedreich’s ataxia
  4. There was (no) INO/RAPD to suggest demyelination
  5. There were (no) fasciculations/small hand muscle wasting to suggest motor neuron disease or cervical myelopathy
  6. There were (no) upper motor neuron signs in the upper limbs to suggest cervical myelopathy or bilateral strokes


To complete my examination I would like to:


  • Perform a PR (anal tone, saddle anaesthesia)
  • Examine upper limbs (if not already done) and cranial nerves in full as well as speech and fundoscopy
  • Take a history of back pain, bladder and bowel disturbance, visual problems



Top causes of spastic paraparesis:


  1. Demyelination (multiple sclerosis)
  2. Cord compression
  3. Trauma
  4. Anterior horn cell disease (motor neuron disease)
  5. Cerebral palsy


Spastic paraparesis and sensory level:


  1. Cord compression (due to disc disease/tumour/trauma/infection such as epidural abscess, spinal TB/vascular problem such as haematoma or epidural haemorrhage)
  2. Cord infarction
  3. Transverse myelitis (due to infection, autoimmune, paraneoplastic, sarcoid, neuromyelitis optica)


Spastic paraparesis and dorsal column loss (joint position sense and vibration):


  1. Demyelination (Multiple sclerosis)
  2. Friedreich’s ataxia
  3. Subacute combined degeneration of the cord
  4. Syphilis
  5. Parasagittal meningioma
  6. Cervical myelopathy


Spastic paraparesis and spinothalamic loss (pain and temperature):


  1. Syringomyelia
  2. Anterior spinal artery infarction


Spastic paraparesis and cerebellar signs:


  1. Demyelination (Multiple sclerosis)
  2. Friedreich’s ataxia
  3. Spinocerebellar ataxia
  4. Arnold Chiari Malformation
  5. Syringomyelia


Spastic paraparesis and small hand muscle wasting:


  1. Cervical myelopathy (C5-T1)
  2. Anterior horn cell disease (motor neuron disease)
  3. Syringomyelia


Spastic paraparesis and UMN signs in upper limbs:


  1. Cervical myelopathy (above C5)
  2. Bilateral strokes


Spastic paraparesis and absent ankle jerk:


  1. Motor neuron disease
  2. Friedreich’s ataxia
  3. Subacute combined degeneration of the cord
  4. Syphilis
  5. Cervical myelopathy and peripheral neuropathy of any cause
  6. Conus medullaris


Other causes of spastic paraparesis include:


  1. Hereditary spastic paraparesis
  2. Tropical spastic paraparesis secondary to HTLV-1
  3. Cerebral palsy


Investigations (guided by history and examination):


MRI brain and spine (demyelination, trauma, cord compression)

Visual evoked potentials (if suspect demyelination)

Lumbar puncture (if suspect demyelination)

Bloods: FBC, U+E, LFT, bone profile, CRP, HIV, syphilis, HTLV-1, serum ACE, ESR, ANA, ANCA, antiphospholipid antibodies, immunoglobulins, AQP4 antibodies (NMO), paraneoplastic screen and serum electrophoresis, B12 (SACD of the cord)

Nerve conduction studies and EMG


Management: depends on the underlying cause. For example if it is an acute presentation, arrange an urgent MRI spine and liaise with neurosurgery team if evidence of cord compression.



Multiple Sclerosis


This is a progressive demyelinating disease of the central nervous system (brain and spinal cord)

CNS inflammation is disseminated in time and place

Involvement of spinal cord, cerebellum, brainstem, optic nerve

*does not affect peripheral nerves*

Visual evoked potentials are reduced (slow conduction in optic nerve)

CSF: increased protein, increased lymphocytes, unmatched oligoclonal bands

MRI: active inflammation, hyperintense on T2 (periventricular white matter lesions, corpus callosum, brainstem, cerebellar, spinal cord, optic nerve)

Management: MDT approach, high dose iv steroid acutely, symptom management eg. antispasmodics, disease modifying therapies



Written by Dr Sarah Kennedy


Resources used to write this document are listed in the references section of this webpage.