Type OneAVM

Type one AVM occurs predominantly in the lower thoracic and upper lumbar regions of adult males in the fifth through seventh decades and represents about 60-80% of AVM diagnoses. In this condition an intradural-extramedullary fistula develops. The fistula drains into the vertebral venous outflow system. Symptoms develop secondary to increased venous pressure, which results in venous stasis within the spinal cord. These changes lead to increased intramedullary pressure and congestion. Cord edema and decreased perfusion develop into cord ischemia and, eventually, irreversible cord damage may develop.

Clinical presentation. The most common presentation of type one AVM is that of slowly evolving myelopathy. Over the course of months or years, patients develop increasing motor deficits such as paraparesis and sensory loss. Subsequently disturbances in micturition may occur as well. It is believed that the myelopathy develops secondary to sustained increased venous pressure, which results in venous engorgement and spinal cord ischemia. Physical examination reveals myelopathic findings: a combination of upper and lower motor neuron signs. At times, the symptoms are aggravated by exercise and may be accompanied by low back pain. In rare instances, when thrombosis or hemorrhaging occurs, sudden deterioration may evolve with progressive neurological loss.

Imaging studies. Plain radiographs remain normal throughout the course of the disease and are therefore not helpful. CT may detect an enlarged spinal cord. Post-contrast administration there may be enhancement of pial veins along the cord surface. It is difficult to diagnose this condition solely on CT. MRI, however, is much more sensitive than CT. On T1WI the cord appears hypointense. The most sensitive, pervasive, but nonspecific MRI finding is increased cord signal on T2WI. This finding, however, may be also observed following an infection, inflammatory conditions, demyelinating diseases, vasculitis, or cord neoplasms. The increased cord signal will disappear following embolization or resection of the fistula. The coronal venous plexus may enhance as well. Multiple flow voids may be found on the cord surface. These correspond with dilated pial veins, which are usually seen on the dorsum of the cord and are found in only half of the patients. At times, it is difficult to differentiate between flow voids and cerebro-spinal fluid pulsation artifacts, thus rendering this finding less reliable. Another common finding on MRI is the associated mass effect or cord swelling. This usually appears over several cord segments and may raise the suspicion that the patient is suffering from a spinal cord tumor (Figures 13-4A and 13-4B). It is felt that the mass effect corroborates the presence of venous hypertension and cord edema. Following contrast administration multiple serpentine veins may be seen on the cord surface with occasional patchy enhancement within the cord. None of the MRI findings is pathognomonic of AVM. The combination of several findings, however, raises the suspicion for AVM, at which point an angiographic study should be ordered. This allows direct visualization of the coronal venous plexus (Figure 13-5). A reliable finding attesting to the presence of venous hypertensive myelopathy is peripheral cord hypointensity on T2WI. This finding, which has been recently described, is probably caused by sluggish blood flow containing deoxy-hemoglobin within the distended capillary system.

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