23. is the phenomena surrounding transection of the
spinal cord that leads to temporary loss or
depression of all or most spinal reflex activity below
the level of a spinal lesion.
the period of spinal shock can last from hours to 6
weeks.
In the acute stage, there will be hypotonic paralysis,
areflexia, loss of sensory function and dysautonomia.
Patient shows retention of the bladder due to the
impaired reflex of emptying the bladder.
In post acute stage, first autonomic reflexes come to
normal.
In the chronic stage, there will be hypertonic
paralysis, hyper-reflexia, spastic-reflex bladder.
Patient at this stage shows incontinence.
29. COMPRESSIVE NONCOMPRESSIVE
Bony changes No bony changes
Root pains No root pains
Upper level of No definite level
sensory loss
present
Zone of
Absent
hyperesthesia may
be present
30. Compressive Non compressive
Usually gradual Usually acute
onset onset
Asymmetrical
involvement of Symmetrical
limbs involvement of
Bladder bowel limbs
disturbance occurs Occurs but late
31. Symptoms Intra medullary Extra medullary
Radicular pain nil common
Funicular pain common Less common
Vertebral pain unusual common
UMN signs late early
LMN signs Prominent and diffuse Unusual /segmental
Sensory involvement Descending Ascending
progression
Sphincter involvement Early Late
Trophic changes Common Unusual
Dissociated sensory loss Yes No
Sacral sensation Spared Lost
32. Inflammation of the spinal cord at a single level. Symptoms
develop rapidly and include limb weakness, sensory
disturbance, bowel and bladder disturbance, back pain, and
radicular pain. Recovery generally begins within 3mo. but is
not always complete.
Causes:
Idiopathic (thought to be autoimmune mechanism)
Infection
Vaccination
Autoimmune disease e.g. SLE, sarcoidosis
MS
Malignancy
Vascular e.g. thrombosis of spinal arteries, vasculitis 2° to
heroin abuse, spinal A-V malformation
33. Investigation
MRI shows swelling of spinal cord
Management
Methylprednisolone injection followed by oral
prednisolone
Good recovery occur in 30% of cases
34. Anterior spinal artery infarction produces paraplegia
or quadriplegia, sensory loss affecting
pain/temperature but sparing
vibration/position sensations (supplied by
posterior spinal arteries), and loss of sphincter
control.
Onset sudden or evolving over minutes or a few
hours.
Associated conditions: aortic atherosclerosis,
dissecting aortic aneurysm, hypotension.
Therapy is directed at the predisposing condition.
35. Paresthesia in hands and feet, early loss of
vibration/position sense, progressive
spastic/ataxic weakness, and areflexia due to
associated peripheral neuropathy; mental
changes and optic atrophy may be present.
Diagnosis is confirmed by a low serum B12
level and a positive Schilling test. Treatment is
vitamin replacement.
36.
37. Isolated progressive paraparesis runs in some
families. Inheritance is variable. Additional
features including cerebellar signs, wasted
hands and optic atrophy are sometimes seen.
The paraparesis is usually mild and progresses
slowly over many years. Some cases have
dystonic features and respond to levodopa.
38. Tubular cavities (syrinxes) form close to the
central canal of the spinal cord. As the syrinx
expands, it compresses nerves within the spinal
cord. Typically presents with wasting and
weakness of hands and arms, and loss of
temperature and pain sensation over trunk and
arms (cape distribution)..
39.
40. Skin care issues (Pressure sores)
DVT
Loss of bladder control & UTI
Loss of bowel control
Loss of sensory function
Loss of motor function
Depression
41. Based on etiology
Compressive – decompressive surgery
ATM – steroids
Supportive care
Physiotherapy