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Transverse myelitis

A subtype of myelitis (inflammation of the spinal cord) characterized by rapid paralysis


and sensory changes below the level of the affected segment. Sometimes associated
with a band-like sensation across the trunk. Causes include infections (e.g., herpes
zoster), autoimmune disorders, and vascular malformations.

Causes:
 Multiple sclerosis, most common
 Neuromyelitis optica 
 Infections 
 Autoimmune (like SLE and antiphospholipid syndrome) or postinfectious
inflammation (like mycoplasmal infections, Lyme disease, syphilis, TB, or viral
meningoencephalitis).
 Vasculitis 
Certain drugs, like amphetamines, IV heroin, or antiparasitic or antifungal drugs.
Symptoms and Signs:
 Pain in the neck, back, or head may occur.

 A bandlike tightness around the chest or

abdomen 
 Weakness 
 Tingling 
 Numbness of the feet and legs 
 Difficulty voiding

 Deficits may progress over several more days to a complete transverse


sensorimotor myelopathy, causing: 
1. paraplegia, 
2. loss of sensation below the lesion, 
3. urinary retention, and 
4. fecal incontinence.
 Occasionally, position and vibration sensation are spared, at least initially.

 The syndrome occasionally recurs in patients with multiple sclerosis, SLE, or


antiphospholipid syndrome.
Diagnosis of acute transverse myelitis is suggested by transverse sensorimotor
myelopathy with segmental deficits. 
Guillain-Barré syndrome can be distinguished because it does not localize to a
specific spinal segment.
 MRI and CSF analysis:
 MRI typically shows cord swelling if transverse myelitis is present and can
help exclude other treatable causes of spinal cord dysfunction (eg, spinal
cord compression).
 CSF usually contains monocytes, protein content is slightly increased, and
IgG index is elevated (normal, ≤ 0.85).
 A test for a marker for neuromyelitis optica IgG (NMO-IgG)—which is an
autoantibody that targets the astrocyte water channel protein aquaporin-
4— is highly specific and helps distinguish neuromyelitis optica from
multiple sclerosis.
 Other tests to identify treatable causes:
 Chest x-ray 
 PPD 
 Serologic tests for mycoplasma, Lyme disease, and HIV 
 ESR 
 Antinuclear antibodies 
 CSF and blood Venereal Disease Research Laboratory (VDRL) tests
Brain MRI is done; multiple sclerosis develops in 50% of patients who have multiple
.periventricular T2 bright lesions and in 5% who do not have them
Paraplegia

https://www.slideshare.net/NaveenKumar577/paraplegia-36885508
Brown-Séquard syndrome
 Definition: hemisection of the spinal cord (often in the cervical cord) 
Etiology
 Unilateral compression commonly through trauma (e.g., often penetrating
injuries, or crush injury)
 Less commonly: disc herniation, spinal epidural hematoma, spinal
epidural abscess (rare) or tumor, multiple sclerosis, complication
of decompression sickness  [1

Clinical features 

 Ipsilateral
o Loss of all sensations at the level of the lesion
o Loss of proprioception, vibration, and tactile (fine touch)
discrimination below the level of the lesion due to an
interrupted posterior column
o Segmental flaccid paresis at the level of the lesion due to the affection
of lower motor neurons at the level of the lesion
o Spastic paralysis below the level of the lesion
o Ipsilateral Babinski sign 
 due to the affection of upper motor neuron axons in the lateral
corticospinal tracts 

o In lesions above T1, Horner syndrome occurs due to damage


to ipsilateral sympathetic fibers (the oculosympathetic pathway).
 Contralateral: loss of pain, temperature, and non-discriminative touch (crude
touch) sensation one or two levels below lesion due to an
interrupted spinothalamic tract

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