Remember: In cases of suspected CES, per-rectal examination is essential to document any loss of anal tone.
Useful Selected Questions to Ask/Facts to Establish?
- Mode of onset and rate of progression (e.g. sudden onset implying a possible vascular (or ischaemic) aetiology versus gradual).
- Any evidence of weakness in upper limbs? (Useful for localisation as upper limb involvement points towards a lesion in cervical spine or brainstem or hemisphere; hemisphere lesions usually lead to contralateral weakness affecting face, arms and legs variably depending on the site of the lesion, whereas a cord lesion usually produces bilateral weakness with possible evidence of LMN signs at the level of the lesion and UMN signs below the level of the lesion with a sensory level).
- Presence of any associated pain with or without the history of malignancy? [(Pain is often the first symptom in patients with spinal extradural metastases (SEM) and can be radicular or referred, often worse with recumbency (at night) and with movement and can be bilateral in the thoracic region (radicular); presence of low back pain, bilateral sciatica, unilateral or bilateral weakness of dorsiflexion (foot drop) or plantarflexion may indicate the presence of CES; weakness may not be associated with any pain (e.g. in diabetes mellitus)].
Remember: Do not ignore bilateral radicular thoracic pain worse with recumbency in a patient, particularly with a known history of previous malignancy as they may have SEM requiring urgent attention. Common malignancies involving spine are lymphoma, lung, breast, prostate and those from GI tract.
- Any associated sensory loss (e.g. present in the setting of a cortical lesion, spinal cord lesion (look for a sensory level) and radiculopathy (involvement of nerve root) and in peripheral neuropathy; absent in diseases like motor neurone disease, neuromuscular junction problems, for example myasthenia gravis and primary muscle diseases).
Remember: Saddle anaesthesia (in the region of anus, perineum, lower genitals, buttocks and posterior superior thighs) is a common sensory abnormality associated with CES.
- Any evidence (from history or examination) of bowel and bladder involvement [e.g. urinary retention followed by overflow incontinence (preceded by hesitancy and other non-specific urinary complaints) is an important finding associated with CES; faecal incontinence may also occur in CES; finally SEM compressing thoracic or cervical spine can also present with these symptoms including impotence].
- Evidence of spasticity versus flaccidity (spasticity with hyperreflexia implies an UMN lesion, therefore the lesion is in the spinal cord, brainstem or hemisphere; any lesion resulting in CES will cause a flaccid and areflexic weakness with this LMN pattern of weakness being seen in any peripheral cause from the anterior horn cell to the root, to the plexus and to the nerves).
- Establish whether patient is on anticoagulation therapy (e.g. warfarin leading to a spinal extradural haematoma with UMN signs).
- Any evidence of sepsis (raised inflammatory markers and temperature) with a recent history of staphylococcal infection suggests an extradural spinal abscess with associated back pain and tenderness on palpation.
Differential Diagnoses (Table 9.1)
Table 9.1 Differential diagnoses for weak legs with points to note.
| Clinical presentations/conditions | Points to note |
| Spastic paraparesis (Chapters 18 and 26) | Autoimmune conditions like MS, transverse myelitis; degenerative cervical or thoracic spinal stenosis; herniated intervertebral discs (cervical/thoracic); neoplastic process like extradural metastases, intradural extramedullary lesions, for example meningioma/neurofibroma, intradural intramedullary cord tumours, for example ependymoma and astrocytoma; subacute combined degeneration of the cord (SACD) due to vitamin B12 deficiency; infectious, for example spinal epidural abscess, tropical spastic paraparesis HTLV-1 infection; amyotrophic lateral sclerosis (ALS); spinal epidural haematoma (usually due to anticoagulation or trauma). Note: Trauma or cord infarction can cause spinal shock leading to acute cord syndrome presenting with flaccid weakness evolving to spastic paraparesis over days/weeks |
| Flaccid paraparesis (Chapter 24) | Peripheral neuropathies like Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) (diagnosed clinically and with nerve conduction studies); tabes dorsalis associated with syphilis (occurs >15 years after infection due to damage to cauda equina and dorsal root ganglia); acquired muscle disease, for example polymyositis (normal sensation and initially persevered reflexes with raised creatine kinase) |
| SACD | Due to vitamin B12 deficiency (dietary or pernicious anaemia); subacute presentation with degeneration of dorsal column and corticospinal tracts; loss of joint position sense causing sensory ataxia and unsteadiness; progressive spasticity and paraplegia; visual disturbances with or without optic atrophy. |
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