Classically cord lesions present with following signs

Classically cord lesions present with following signs

Bilateral neurological motor and sensory deficit in limbs +/-definite sensory deficit +/-sphincter dysfunction, either all of these or any of these in various combinations.
However it’s not essential to find a classical picture.

Motor deficit; usually bilateral hyper-reflexic hyper tonic & with up going planters. Can be unilateral in case of hemicord lesions on the same side of the deficit. More prominent in anterior &/or lateral cord lesions. Motor signs may not be prominent or may be absent in posterior cord lesions. If only lower limbs are affected lesions are probably in thoracic cord. If upper & lower limbs are also affected then probably cervical cord. Lower motor type deficit in lower limbs is rarely seen in Lumbar spinal cord damage.

Sensory deficit: sensory level traditionally mentioned in books isn’t always found. However if found its useful to localise the level. Sensory loss with reduced ankle jerks mean associated peripheral neuropathy. However sensory loss with increased ankle jerks usually mean cord lesions. Sensory loss below knee with reduced ankle jerks is peripheral neuropathy. Sensory loss below L1 with reduced ankle jerks is cauda equina syndrome. Sensory loss including L1 or above means Spinal cord lesions. Inguinal ligaments is T12, umbilicus is T10, costal margin is T6, nipple is T4, axilla is T1, medial upper arm is C8, index finger is C7, lateral upper arm is C6, shoulder area is C5, neck is C3-4, back of neck is C2.
Sensory deficits are more prominent in posterior or lateral cord lesions & may be absent in anterior cord lesions. Hemicord lesion will cause position/vibration loss on same side ( same for motor loss) but contra lateral pain & touch loss.
Central cord lesions affect spinothalamic of upper body & position vibration of lower body first. Opposite is true for lesions compressing the cord from outside.

Cortical lesions causing unilateral motor & sensory loss on the same side while hemicord lesions will cause motor on one side & spinothalamic on opposite side.

Sphincter involvement : fibres from frontal lobe to sacral cord runs close to the central cord, so the lesions from central part of cord will affect the sphincters earlier while lesions compressing from outside may not involve sphincters or involve later. Sphincter involvement can be there at cord lesions at any level. Cauda equina syndrome also involves sacral roots & hence sphincter dysfunction. However peripheral neuropathy almost never involves sphincter & same is the case with Guillian Barre syndrome.

Hemicord: motor & position vibration sensations on same side of lesion while pain temperature on opposite side.

Syringomyelia: pain temperature of upper limbs first with wasting of hands , later with spastic lower limb weakness.

Transverse Myelitis: usually gives classical cord lesion of sensory level,sphincter involvement & spastic limb weakness.

Cauda Equina: patchy sensory loss below L1, sphincter involvement & flaccid lower limb patchy weakness.

Compressive lesions usually give patchy / incomplete cord signs depending on anterior/posterior location & also arising from within the cord or compressing from outside.

Multiple levels of cord compression may give multiple sensory / motor levels & incomplete cord signs.

Cord compression combined with Lower motor neuron lesions ( absent ankle jerks with up going planters) may be seen in diseases affecting cord & dorsal root ganglion/peripheral nerves e.g. Neuropathy+ cord compression, neurosyphilis, B12 deficiency causing subacute combined degeneration, meningoradiculopathy, multiple disc prloapses,spinocerebellar ataxia etc etc.

MRI spine is the test of choice but it is not 100% exclusive for some pathologies which are usually not very common.