Intracranial hypotension (IH) is an uncommon condition due to sustained cerebrospinal fluid (CSF) leakage, resulting in low CSF pressure and volume. The main symptoms include orthostatic headache, nausea and vomiting, vertigo, visual disturbances, auditory aberrations, and seizures. Although its course is often self-limited, IH can sometimes be complicated by subdural fluid collection, subdural hematoma, “brain sagging” resulting in acquired Arnold-Chiari malformation 1 and syringomyelia, severe encephalopathy, prolonged coma, and death. Once clinically suspected, diagnosis may be corroborated, in most cases, by brain magnetic resonance imaging (MRI), typically showing diffuse pachymeningeal gadolinium enhancement, or by measurement of a very low CSF pressure, although normal CSF pressure may be found in some cases. 2 Intracranial hypotension is classically referred to as spontaneous or primary when no obvious cause can be identified 3; in those cases, it is occasionally possible to demonstrate a spinal meningeal tear or diverticulum as the source of the CSF leak. 2,4 Secondary IH has long been known to occur possibly after various interventions whereby a CSF leak is iatrogenically induced, such as diagnostic lumbar puncture, spinal anesthesia, intrathecal chemotherapy, or myelography. 5 It has also been described after brain trauma with skull fracture and after certain neurosurgical procedures, in particular, craniectomy. 6 Finally, chronic IH is a condition that is well known to neurosurgeons when CSF shunting is complicated by overdrainage. 7 We report the case of a patient who suffered from IH-related bilateral subdural hematomas following a routine lumbar diskectomy.
Intracranial hypotension is a rare, and possibly underrecognized, cause of headache in middle age. Occurring spontaneously in the vast majority of cases, it has been occasionally reported after certain neurosurgical procedures involving craniectomy. We report a unique situation in which a patient developed severe postural headache typical of intracranial hypotension, which was complicated by bilateral subdural hematomas, immediately following a routine lumbar diskectomy; the headache resolved spontaneously. We suggest that an intraoperative microscopic dural breach was the site of sustained, but self-limited, cerebrospinal fluid leakage that eventually led to intracranial hypotension.
A 71-year-old healthy man underwent a right L5-S1 diskectomy for a 6-month history of paroxysmal low back pain radiating into the right lower limb in the S1 root distribution. The findings of the neurological examination were normal, and lumbar computed tomography (CT) scan images showed a herniation of the L5-S1 intervertebral disk. The surgical procedure, which typically consists of a laminectomy with removal of disk fragments, was uneventful; in particular, no dural breach was noted microscopically, and immediate postoperative relief of radicular symptoms was obtained.
The day after surgery, the patient noticed a slight diffuse headache while standing up for the first time postoperatively. Over the next 3 weeks, the headache increased dramatically and, because it was consistently relieved when the patient was in the recumbent position, he remained confined to bed most of the time. Various analgesics were ineffective. Additional symptoms included nausea, vomiting, dizziness, tinnitus, neck stiffness, and a brief episode of syncope. He had not at any time suffered any brain trauma.
Upon admission to hospital, the Glasgow Coma Scale was 15, and vital parameters and the results of a neurological examination were normal except for nuchal rigidity and horizontal nystagmus. A brain CT scan revealed bilateral subacute subdural hematomas extending along the frontal, temporal, and parietal regions, more prominent on the right side; the mass effect was minimal. T1-weighted MRI scan images performed with gadolinium injection (Figure 1) showed widespread dural enhancement including along the falx cerebri and the tentorium. A lumbar puncture was not performed in view of the risk of brain herniation.
Treatment with dexamethasone, 9 mg daily, was initiated, and the patient's condition slowly improved. Accordingly, a repeated brain CT scan showed a significant reduction of the size of the hematomas. In order to identify the presumed operative site of the CSF leak responsible for IH, a lumbar MRI was performed 5 weeks after surgery that showed a large collection of CSF around the laminectomy site, but no definite postoperative pseudomeningocele.
Based on the clinical and radiological findings typical of IH, we suspected that, in this case, the pathophysiological mechanism involved an intraoperative microscopic surgical breach in the dura, which passed unnoticed, whereby a period of sustained CSF leakage generated IH and, secondarily, bilateral subdural hematomas. Although not definite, we believe that the causal relationship between surgery and this complication can be rated as highly probable, based upon their close temporal course, the exclusion of any brain trauma, and both clinical and neuroradiological features typical of IH. Difficulty in precisely identifying the location of the CSF leak by lumbar MRI may be related to the prolonged delay between surgery and the examination, to the innocuous nature of the leak itself, or to the technique used, since it has been suggested that radionuclide cisternography or contrast CT myelography might be more sensitive than MRI for this purpose. 2 In addition, since the patient had improved with no specific intervention, it may be inferred that the leak had spontaneously resolved by the time of the lumbar MRI, as suggested by the presence of a large amount of CSF at the site of surgery several weeks later.
Lumbar diskectomy is by far the most common neurosurgical procedure performed worldwide, and the paucity of literature detailing such a complication is surprising, for the following reasons. First, although the risk of an inadvertent dural breach is low during diskectomy, despite the proximity of the dura adjacent to the disk to be removed, a CSF leak does infrequently occur during this procedure. Usually, it is readily identified visually by the neurosurgeon and closed intraoperatively. However, we hypothesize that, just as in our case, the dural breach may be very small, remaining unnoticed during surgery, or the dura may have been intraoperatively weakened and prone to later rupture, which may have resulted in occult CSF leak and IH. Second, the symptoms related to IH may be delayed as long as several weeks after the provoking event, or may remain elusive so that no medical attention is sought, both resulting in nonrecognition of the condition. Finally, as in this case, the self-limited course of IH and the spontaneous resolution of subdural hematomas may also lead to misdiagnosis. It could well be, therefore, that IH and subdural hematomas represent an, as yet, poorly recognized complication of disk herniation repair, and we suggest that any unusual headache, especially if postural, following this type of surgery should alert physicians to the possibility of IH and related complications.