History
See the list below:
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Pain is the most commonly reported symptom. Pain may be localized or diffuse and commonly is reported as a dull ache or a burning or stabbing sensation.
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Other symptoms include increased weakness, numbness, increased spasticity, and hyperhidrosis (increased sweating).
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Symptoms often are aggravated by postural change or the effects of the Valsalva maneuver.
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Decreased reflex micturition, progressive orthostasis, autonomic dysreflexia, and relatively painless joint deformity or swelling (Charcot joint) also may be reported. Syringomyelia is the most common cause of Charcot joint in the upper extremity. [14]
Physical
See the list below:
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Spasticity often is increased compared to findings noted in prior examinations. Deep tendon reflex changes (either increased or decreased) may be noted compared with findings from prior examinations.
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Ascending sensory level and sensory dissociation (selective loss of pain and temperature sensation) are very sensitive indicators for detecting progressive PTS. Numbness may involve the face if the syrinx has ascended into the brainstem. (See image below.)
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Progressive weakness and wasting can occur but may be a late finding.
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Other signs may include a complete or partial Horner syndrome or other evidence of dysautonomia (eg, labile blood pressure, hyperhidrosis).
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Signs may be unilateral because ascension of syrinxes often occurs unilaterally.
Causes
Traumatic SCI with tethering of the spinal cord to the dura results in impaired CSF circulation. Incomplete spinal canal decompression may predispose the person to tethering and CSF obstruction. These factors are thought to cause syrinx development.
Research supports the concept that chronic mechanical stress to the spinal cord increases the risk for development of syringomyelia. Spinal instrumentation without decompression is also associated with earlier onset of syringomyelia.
A study by Asan indicated that syringomyelia is a typical later result of a spinal concussion sustained through vertical forces, as based on magnetic resonance imaging (MRI) performed more than 6 months postconcussion. [15]
A study by Yeo et al found that compared with healthy controls, patients with PTS demonstrated significantly lower peak cranial and caudal CSF flow velocities in the spinal subarachnoid space above and below the syrinx, with a significantly shorter caudal flow duration found. The investigators suggested that an association exists between syrinx formation and changes in the CSF flow’s timing. [16]
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This illustration shows a T1-weighted, cervical magnetic resonance imaging (MRI) scan of multiple syrinx cavities (arrows). Note the lowest thin cavity extending into the thoracic spinal cord.
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This T2-weighted magnetic resonance imaging (MRI) scan (same patient as above) delineates the syrinx cavity. Note the spinal cord edema extending rostrally from the upper limit of the cavity.
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T2-weighted magnetic resonance imaging (MRI) scan (same patient as above) after patient underwent expansile duraplasty. Note dramatic reduction in size of the main syrinx cavity (white).
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T2-weighted sagittal image of large, multiloculated cervical syrinx extending into brainstem. Patient had preserved functional status.
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T1-weighted magnetic resonance imaging (MRI) scan of a slender syrinx (arrow) extending from the C5 vertebral level. This syrinx extends beyond the image to an area of spinal cord disruption at the T3 vertebral level.
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Same patient as in image above, with the magnetic resonance imaging (MRI) scan slightly farther down the cervicothoracic region of the spine
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T2 proton density magnetic resonance imaging (MRI) scan demonstrating syrinx cavity (arrow) extending from approximately C6-C7 to T2. The syrinx cavity is 9 mm at its widest dimension. The spinal cord is reduced to a thin membrane at this level and is atrophic below.
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T1-weighted image demonstrating a large, multiloculated cervical syrinx cavity. This is a recurrent syrinx, having come back despite an attempt at drainage utilizing expansile duraplasty.