Lyrics · 完整歌詞
The clinical effects of a spinal cord lesion become clearer
when the major ascending
and descending pathways are related to the levels at which they cross.
The lateral corticospinal tract has already decussated in the medullary pyramids,
so within the cord it serves the same side.
The dorsal columns, carrying proprioception and vibration,
also cross in the medulla and are ipsilateral.
The spinothalamic tract carries pain and temperature and crosses within one
or two segments of entry,
so within the cord it is contralateral.
Within the corticospinal tract the arm fibres lie medially
and the leg fibres laterally.
A central contusion from hyperextension in a degenerate neck therefore weakens the
arms more than the legs.
Brown-Séquard hemisection removes ipsilateral power and proprioception and contralateral pain
and temperature from one or two segments below.
Anterior cord infarction removes power and pain
but spares the posteriorly supplied dorsal columns.
Syringomyelia cuts the crossing spinothalamic fibres centrally,
producing a cape of dissociated sensory loss with preserved touch.
Jefferson is a C1 burst from axial loading,
type II odontoid fractures are the commonest and least likely to unite,
and Hangman is bilateral C2 pars fracture from hyperextension.
The clinical effects of a spinal cord lesion become clearer
when the major ascending
and descending pathways are related to the levels at which they cross.
Acute care begins with airway, breathing, circulation and immobilisation,
then CT for bone and MRI for cord oedema, haematoma and ligament.
Neurogenic shock is haemodynamic:
injury above T6 severs sympathetic outflow while the vagus persists,
producing hypotension with bradycardia and warm skin.
Vasopressors, not fluid alone,
maintain a mean arterial pressure of 85 to 90 mmHg for seven days.
Spinal shock is reflex: every reflex below the lesion vanishes,
and the returning bulbocavernosus reflex marks its end.
High-dose methylprednisolone is no longer standard care;
at most it is an option within eight hours
and is never given for penetrating injury.
Chronic injury above T6 breeds autonomic dysreflexia.
A noxious stimulus below the lesion, most often a distended bladder,
drives unopposed sympathetic discharge
and a systolic rise of 20 to 40 mmHg or more.
Above the lesion the vagus slows the heart and the face flushes.
Treatment is to sit the patient up,
loosen clothing and remove the trigger,
giving nifedipine only if the systolic pressure remains at 150 mmHg
or above.
Voluntary anal contraction excludes ASIA grade A,
and grade C becomes D
when at least half the key muscles reach grade three.
Urinary infection is the commonest complication,
and heterotopic ossification is never excised while alkaline phosphatase remains raised.
Reflex erection depends on S2 to S4
and psychogenic erection on T11 to L2.
Below the conus at L1 to L2 the roots form the cauda equina.
Asymmetric saddle anaesthesia,
absent ankle reflexes
and urinary retention demand decompression within 24 to 48 hours.
An upper trunk plexus injury at C5 to C6 produces the waiter's
tip posture of Erb palsy.
A lower trunk injury at C8 to T1 produces a claw hand with Horner
syndrome,
because T1 carries the sympathetic fibres to the eye.
The clinical effects of a spinal cord lesion become clearer
when the major ascending
and descending pathways are related to the levels at which they cross.