Abstract
There is, at least in Scandinavia, a growing use of epidural steroid injections for back pain and sciatica, and potential side-effects may be underestimated. The characteristic magnetic resonance imaging (MRI) signs of intracranial hypotension are not sufficiently widely recognized by practising radiologists.
Case report
A 38-year-old woman was admitted due to acute left-sided sciatica. Computed tomography (CT) of the lumbar spine demonstrated a disc herniation squeezing the left L5 spinal nerve root. She underwent physiotherapy, but due to persistent pain was treated with three epidural injections of a local anaesthetic and a steroid. Two weeks after the third injection she started intensive physical training, and the day after a heavy bicycle exercise she experienced severe headache and nausea as well as tinnitus. The headache persisted for weeks; it was alleviated when lying down and exacerbated when resuming an upright position. After 1 month a CT scan of the cranium including the sinuses was undertaken with no abnormal findings. Four months after the headache had first appeared, an MRI was carried out. The radiologist described a pituitary enlargement suggesting a macro adenoma, with marked enhancement in the pineal stalk as well as in the entire pituitary gland (Fig. 1). A neurologist was unable to demonstrate abnormal clinical findings. Since there were no abnormalities concerning pituitary hormones and computerized visual fields were normal, it was decided to await further developments.
(a) Sagittal view of non-contrast T1-weighted magnetic resonance (MR) demonstrates pituitary enlargement raising the optic chiasm slightly upwards, as well as caudal displacement of cerebellar tonsils and crowding of the prepontine cistern. (b) Sagittal view of post-contrast T1-weighted MR demonstrates diffuse enhancement and pachymeningeal thickening, and homogeneous enhancement of the pituitary gland due to hyperaemia. Note contrast enhancement along the clivus.
One year later, MRI demonstrated an entirely normal pituitary gland (Fig. 2), and the headache had disappeared. When retrospectively scrutinizing the MRI series, it became obvious that the first series demonstrated a diffuse pachymeningeal enhancement and protrusion of the cerebellar tonsils through the foramen magnum in addition to the pituitary enlargement. One year later, all these findings had disappeared. A retrospective diagnosis of intracranial hypotension was obvious, and we hypothesize that this may be related to the combination of repeated epidural injections with steroids and heavy physical training.
(a) Sagittal view of non-contrast T1-weighted magnetic resonance (MR) of the same patient 1 year later. The size of the pituitary gland is within normal limits, and there is no longer caudal displacement of the cerebellar tonsils. The prepontine cistern has resumed its normal size. (b) Sagittal view of post-contrast T1-weighted MR of the same patient 1 year later. Note absence of the exaggerated contrast enhancement along the pachymeninges including along the clivus.
Discussion
The cardinal clinical manifestation of (spontaneous) intracranial hypotension is orthostatic headache relieved by recumbence. Additional symptoms may be neck pain, nausea, diplopia, distorted hearing, visual blurring, and low back pain (1). Our patient complained of typical orthostatic headache associated with nausea; however, the diagnosis was nevertheless not initially recognized. A common complication of intracranial hypotension is the appearance of a subdural haematoma, presumably due to sagging of the brain stretching veins bridging the arachnoidea to the dural sinuses. The headache is probably due to traction or distortion of various intracranial pain-sensitive structures; however, dilation of cerebral veins and sinuses may also play a role.
A low cerebrospinal fluid (CSF) opening pressure, sometimes even negative, secures the diagnosis. However, the pressure may exceptionally be within normal limits (2). The leucocyte count as well as the amount of protein in the CSF may be normal or slightly elevated. In the present case the CSF was not examined since the condition was not suspected.
During recent years MRI has been increasingly used to confirm or reveal the diagnosis of spontaneous intracranial hypotension. The characteristic findings are diffuse bilateral and non-nodular pachymeningeal enhancement along with ‘sagging’ of the brain manifested by descent of the cerebellar tonsils (3, 4). Both of these signs were clearly demonstrated in our patient (Fig. 1), although overlooked by the examining radiologist. However, pituitary enlargement mimicking an adenoma or hyperplasia may also be an MRI feature of intracranial hypotension (5, 6), sometimes confusing the diagnosis, as in the present case.
Most cases of spontaneous intracranial hypotension are probably caused by leakage of CSF into the extra-arachnoid space in the spine, most often the thoracic part (7, 8). As with the patient reported here, a CSF leak was not substantiated since the condition was not suspected, but it is reasonable to presume that repeated epidural injections employing, inter alia, a steroid may have caused local weakening of meninges, resulting in a tear and formation of a fistula in conjunction with heavy exercise. Whether this presumed leak was related to the combination of an attenuated dura due to repeated steroid injections and over-exertion initiating the leakage remains speculative, but to us this seems an intriguing possibility. We are aware of only one previous report of intracranial hypotension following epidural steroid injection, and the patient previously reported was injected in the cervical region (9).