Nontraumatic Disorders of the Spinal Cord Flashcards
Spinal cord syndromes
Causes of posterior cord syndrome
- Multiple sclerosis or demyelination
- Cervical spondylotic myelopathy
- Spinal cord tumors
- Atlantoaxial subluxation
- Friedreich ataxia
- Subacute combined degeneration
Causes of myelitis
Acute idiopathic transverse myelitis treatment
For patients with acute idiopathic TM, we suggest high-dose intravenous glucocorticoid treatment
For patients with acute TM complicated by motor impairment, we suggest additional treatment with plasma exchange
Our preferred regimen is five treatments, every other day for 10 days
Evaluation of suspected transverse myelitis
https://www.uptodate.com/contents/image?imageKey=NEURO%2F88920&topicKey=NEURO%2F14088&search=myelitis&rank=2~150&source=see_link
Diagnostic criteria for transverse myelitis
https://www.uptodate.com/contents/image?imageKey=NEURO%2F88914&topicKey=NEURO%2F14088&search=myelitis&rank=2~150&source=see_link
Potential medical work-up for suspected acute transverse myelitis
https://www.uptodate.com/contents/image?imageKey=NEURO%2F65585&topicKey=NEURO%2F14088&search=myelitis&rank=2~150&source=see_link
Elsberg syndrome
acute lumbosacral radiculitis featuring cauda equina syndrome with myelitis
Acute urinary retention with loss of sacral sensation due to lumbosacral radiculitis secondary to severe primary HSV infection.
This complication is transient but usually requires catheterization until clinical improvement ensues
Causes of acute flaccid paralysis
https://www.uptodate.com/contents/image?imageKey=NEURO%2F71165&topicKey=NEURO%2F126102&search=myelitis&rank=3~150&source=see_link
Spinal epidural abscess pathogenesis and most common pathogen
can occur from direct spread (vertebral osteomyelitis, local surgical or anesthetic procedures) or hematogenous spread from a distant infection (bacterial endocarditis, genitourinary infection)
approximately one-third of patients with SEA have no identifiable source for the infection
Staphylococcus aureus causes more than 50% of cases
classic diagnostic triad for spinal epidual abscess and treatment
The classic diagnostic triad for SEA consists of fever, back pain, and neurologic deficits.
** However, only a small proportion of patients have all three components at presentation
Treatment may include fluoroscopic or ultrasound guided, drainage, and any necessary stabilization of the spine.
Systemic antibiotics are given for up to 2 months
Spinal epidural abscess imaging
Abscesses visualized by MRI usually demonstrate fluid-equivalent signal intensity on T2-weighted images with rim enhancement and a hypointense center
Syringomyelia etiology
Syringomyelia most commonly occurs in the setting of the Chiari malformation type I
Other causes of syringomyelia are:
●Other congenital malformations (eg, Klippel-Feil syndrome, and tethered spinal cord)
●Postinfectious
●Postinflammatory (transverse myelitis and multiple sclerosis)
●Spinal neoplasms (especially ependymoma and hemangioblastoma)
●Post-traumatic
Syringomyelia diagnosis and management
The syrinx follows CSF signal characteristics on all MRI sequences:
T1: hypointense
T2: hyperintense, although there may be hypointense regions representing flow or pulsation artifact
Surgical decompression with fenestration and/or shunt placement is recommended for patients with neurologic deterioration or intractable central pain
Syringomyelia clinical findings
A symptomatic central cord lesion typically encroaches on the medial aspect of the CSTs or on the anterior horn gray matter, producing weakness that is more prominent in the arms than the legs.
Fibers mediating the deep tendon reflexes are interrupted as they pass from the dorsal to the ventral horn, thus causing tendon reflex loss at the level of the spinal cord lesion.
There are usually no bladder symptoms, but urinary retention may occur.
Loss of pain and temperature sensation in the distribution of one or several adjacent dermatomes at the site of the spinal cord lesion is caused by disruption of crossing spinothalamic fibers in the ventral commissure!!
Dermatomes above and below the level of the lesion have relatively normal pain and temperature sensation, creating the so-called “suspended sensory level.”
Vibration and proprioception are often spared.
Syringobulbia causes dysphagia, nystagmus, pharyngeal and palatal weakness, asymmetric weakness and atrophy of the tongue, and sensory loss in the distribution of the trigeminal nerve
Spinal cord arteriovenous shunts clinical findings and diagnosis
The most common initial symptoms are radicular pain, sensory disturbance, leg weakness, and bladder dysfunction.
Seventy-five percent of patients have a slowly progressive myelopathy caused by cord compression from an AVM, and 10% have a sudden onset of cord compression due to hemorrhage or spinal cord infarction.
Weakness and numbness may increase after ambulation.
MRI and magnetic resonance angiography can identify the lesions, but angiography is the gold standard
T1
* signal voids from high-velocity flow
* dilated perimedullary vessels indent/scallop the cord
T2
* signal voids from high-velocity flow
* increased cord signal due to cytotoxic edema or myelomalacia
Spinal cord vascular supply
Which part is more vulnerable to infarctions
Three major vessels arising from the vertebral arteries in the neck supply the spinal cord.
There is one anterior spinal artery (ASA) and a pair of posterior spinal arteries (PSAs).
The ASA supplies the anterior two-thirds of the spinal cord.
Along its course, the ASA and PSAs are augmented by radicular arteries.
The thoracic spinal cord is particularly dependent on radicular contributions (τμηματικές μυελικές αρτηρίες) and may be the most vulnerable to infarction
The most prominent thoracic radicular artery is the artery of Adamkiewicz, also known as the artery of the lumbar enlargement.
The artery of Adamkiewicz contributes to the ASA between the T9 to T12 level in 75 percent of individuals, but may be found above and below this level
Causes of spinal cord infarction
https://www.uptodate.com/contents/image?imageKey=NEURO%2F57862&topicKey=NEURO%2F1125&search=spinal%20cord%20infarct&rank=3~98&source=see_link
classic neurologic finding in vitamin B12 deficiency
other findings
subacute combined degeneration of the dorsal (posterior) and lateral columns (white matter) of the spinal cord due to demyelination
areflexia, sensory ataxia, paraparesis, and extensor plantar responses!
Cervical radiculopathy: which nerve root is most often affected
C7 nerve root is most often affected (60%), followed by C6 (25%)
Lumbar radiculopathy: which nerve root is most often affected
L5 is the most commonly compressed
nerve root, followed closely by S1
Approach to acute cervical radiculopathy
https://www.uptodate.com/contents/image?imageKey=NEURO%2F109708&topicKey=NEURO%2F5271&search=radiculopathy&rank=4~150&source=see_link
Approach to acute lumbosacral radiculopathy
https://www.uptodate.com/contents/image?imageKey=NEURO%2F101562&topicKey=NEURO%2F5262&search=radiculopathy&rank=1~150&source=see_link
Most common cause of acquired spastic paraparesis in middle and older adulthood
Cervical spondylotic myelopathy
Cervical spondylotic myelopathy clinical findings
Patients frequently have difficulties with balance, especially spasticity, and radicular symptoms.
Bladder incontinence is uncommon, but urinary frequency is common when spasticity is present.
On examination, lower motor neuron signs are
present at the level of the lesion, and upper motor neuron signs are present below the lesion.
Signs and symptoms differentiating between conus medullaris and cauda equina syndrome
Cauda equina syndrome etiology and clinical findings
The cauda equina syndrome is caused by an intraspinal lesion caudal to the conus that injures two or more of the 18 nerve roots constituting the cauda equina within the lumbar spinal canal
Potential etiologies include developmental abnormalities such as neural tube defects, infectious or inflammatory conditions, or mass lesions such as tumors.
The cauda equina syndrome is typically associated with marked neurologic disability. The clinical presentation is dominated by bilateral leg weakness in multiple root distributions (L3-S1) and may be associated with perineal sensory symptoms as well as bowel, bladder, and sexual dysfunction due to involvement of the S2-4 spinal nerve roots
loss of reflexes!!
Copper deficiency myeloneuropathy: risk factors and clinical findings
Gastric surgery is the most common cause of acquired copper deficiency.
Other causes include excessive zinc ingestion, dietary copper deficiency, malabsorption syndromes, and chelation therapy in Wilson disease.
Neurologic manifestations – The most common neurologic manifestation of acquired copper deficiency is that of a myeloneuropathy. Patients typically present with a subacute onset of a gait disturbance. Examination reveals long tract signs with spasticity in the legs and Babinski response, along with impaired vibration and position sense and a positive Romberg sign
Hematologic manifestations – The hematologic hallmark of copper deficiency is anemia and leukopenia; these are present in most, but not all, patients with associated neurologic deficits
Nitrous oxide toxicity
Neurologic toxicity is well documented in patients who misuse N2O, and due to its effects on vitamin B12.
Neurological findings include sensorimotor polyneuropathy, ataxia, and psychosis
The clinical effects are commonly from a myelopathy involving the cervical spine similar to the subacute combined degeneration syndrome associated with pernicious anemia
Neurotoxicity is potentially reversible with vitamin B12 (cyanocobalamin) supplementation and abstinence from N2O
