LATERAL COMPRESSIVE LESION (contd) Long tract damage - complete cord lesion motor deficit: the speed of cord compression affects the clinical picture. Slowly growing lesions present with difficulty in walking; the legs may 'jump' at night. Examination reveals u.m.n. signs often with an asymmetric distribution. Rapidly progressive lesions produce 'spinal shock' - the limbs are flaccid, power and reflexes diminished or absent and plantar responses are absent or extensor.
sensory deficit: involves all modalities and occurs up to the level of the lesion.
bladder: patient first notices difficulty in initiating micturition. Retention follows, associated with incontinence as automatic emptying occurs. Constipation is only noticed after a few days. Some patients develop priapism (painful erection).
CENTRAL CORD LESION
/•Impairment of all sensory modalities up to the level of the lesion.
Power and reflexes diminished or absent
'CAPE' sensory deficit
'CAPE' sensory deficit
Segmental damage: A central lesion initially damages the second sensory neuron crossing to the lateral spinothalamic tract; pain and temperature sensations are impaired in the distribution of the involved segment. As the lesion expands, anterior horn cells are also involved and a l.m.n. weakness occurs.
Long tract effects: further lesion expansion damages the spinothalamic tract and corticospinal tracts, the most medially situated fibres being involved first. With lesion in the cervical region, the sensory deficit to pain and temperature extends downwards in a 'cape'-like distribution. As the sacral fibres lie peripherally in the lateral spinothalamic tract, sacral sparing can occur, even with a large lesion. Involvement of the corticospinal tracts produces u.m.n. signs and symptoms in the limbs below the level of the lesion. The bladder is usually involved late.
In the cervical cord, sympathetic involvement may produce a unilateral or bilateral Horner's syndrome.
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