Introduction & Background: Only 12 years ago the first report on pachymeningeal gadolinium enhance-men in low-pressure headaches appeared in the lit-erasure. Intracranial hypotension is a result of low CSF volume caused by either spontaneous or postoperative leakage. The syndrome has been reported to occur after head trauma, a tear in a spinal nerve root sheath, per neural cyst, or spinal arachnoids diverticulum. Iatrogenic causes include lumbar puncture or overtraining ventricular or spinal shunts. Spontaneous intracranial hypotension is thought to result from rupture of a spinal arachnoids membrane that allows CSF passage into the subdural or epidural space. It is typically not attributable to a major traumatic event or prior diagnostic or therapeutic intervention; however, intracranial hypotension may be associated with a history of minor trauma such as sports activities or severe coughing. Diffuse pachymeningeal enhancement is thought to reflect the Monroe-Kellie rule, which describes the inverse relationship of CSF volume and intracranial blood volume within the rigid confines of the skull. This reflex mechanism protects nervous tissue by maintaining a constant buffer (i.e., blood or CSF) subjacent to its bony covering. Though this principle was described for intracranial processes and helps to explain the reason for intracranial pachymeningeal enhancement, it can also be applied to the bony spinal canal. Explaining pachymeningeal enhancement in the spine becomes more difficult because the hyper vascular outer dural layer covering the brain does not extend to cover the spine, and the single layer of durra that does cover the spine is relatively vascular. Perhaps reports of pachymeningeal enhancement along the spinal canal in intracranial hypotension more accurately reflect prominent epidural venous engorgement. In all cases of intracranial hypotension reported in the literature, patients presented with headaches. These headaches are typically generalized and pulsating, and often resolve with recumbence. Other clinical features may include nausea or emesis, diploid, neck pain, disturbance in hearing, vertigo, photophobia, and visual deficits. CSF pressures have reportedly been low, normal, or even high. CSF examination may be normal, or may reveal xanthocromia, lymphocytic pleocytosis, or increased protein possibly secondary to dural venous engorgement. With few exceptions, intracranial MR imaging of intracranial hypotension reveals diffuse pachymeningeal enhancement. Subdural fluid collections and brain descent, as measured by inferior displacement of the tier relative to the incisures line, may also be seen. Pachymeningeal enhancement is characteristically thick, smooth, and uninterrupted. The enhancement is thought to result from accumulation of gadolinium-based contrast material in engorged Dural veins and in the interstitial of the durra. More et al reported subdural fluid collections that were mostly bilateral and without mass effect in 69% of patients with intracranial hypotension. The authors also described imaging evidence of brain or brain-stem descent in 62% of patients in their series. Ventricular size in subjects with intracranial hypotension is usually small (1), but can reverse after treatment of the CSF leakage. In the relatively few reports in the literature of spinal imaging findings of intracranial hypotension, MR images showed extramural fluid collections and pachymeningeal enhancement (1, 4 “6). MR images may also depict the site of CSF leakage in the spine (1). Herein, we described a case of intracranial hypotension with symmetric bulky epidural enhancement seen along the ANTEROLATERAL borders of the cervical spine. This enhancement was compatible with engorged epidural venous structures based on their characteristic location in the ANTEROLATERAL spinal canal and sparing of the midline. Renowned et al (6) described a single case of intracranial hypotension with epidural venous engorgement in the region of the caudal equine, and Rabin et al (4) described another case of intracranial hypotension with prominent flow voids within the ventral epidural space near the midline of the upper thoracic spine adjacent to a ventral extramural fluid collection. Treatment of intracranial hypotension varies, depending on its origin and type. If intracranial hypotension is the result of a shunt procedure or surgery, then treatment is usually surgical. Spontaneous intracranial hypotension is often treated first with conservative management, and if this is not effective, an epidural blood patch is used. Surgical correction may be required when all other measures have failed, especially if a Dural tear or other meningeal defect has been demonstrated. In addition to the correction of meningeal defects, surgical drainage of subdural hematomas, a frequent complication of ICH, also may be necessary.