Spontaneous Cerebrospinal Fluid Leak Following Pilates
Spontaneous Cerebrospinal Fluid Leak Following Pilates
The hallmark symptom of intracranial hypotension is an orthostatic headache that is worse when in the upright position and resolves or improves when lying flat. Other symptoms include diplopia, hearing loss, vertigo and meningism.
The most characteristic findings on MRI of the head is pachymeningeal enhancement with downward displacement of the brain, which can be mistaken for a Chiari type I malformation. Subdural hematomas are common in patients with SIH and are usually bilateral but without mass effect. Since the most common cause of SIH is a spontaneous spinal CSF leak, patients should undergo spinal imaging to try and identify a dural tear. CT or MRI myelography are the preferred spinal imaging technique as they provide accurate localization of the tear compared to MRI. Localization of the tear is useful when considering the use of an epidural blood patch; the treatment of choice in patients who have failed conservative management (bed rest, NSAIDs and caffeinated drinks). Since our patient responded to conservative measures, she did not require an epidural blood patch. There was, therefore, no requirement to determine the exact location of the dural tear using myelography. Clinical improvement usually precedes resolution of the abnormalities documented on neuroimaging of the head although the time between symptomatic and MRI resolution is variable.
The underlying cause of spontaneous CSF leaks remains unknown but there is an association with connective tissue disorders. Up to 20% of patients have subtle sketetal abnormalities such as those seen in Marfan syndrome (tall stature, joint hypermobility and arachnodactyly) with no other stigmata of the disease. In some of these patients there is abnormal expression of fibrillin metabolism. It has also been reported that in patients with an underlying dural weakness a small traumatic event may be enough to produce a spontaneous CSF leak. In our patient, there was no evidence of a connective tissue disease and we feel that a trivial traumatic event during her pilates class resulted in the development of a dural tear. A retrospective study of 30 patients with CSF hypovolemia describes one case of spontaneous intracranial hypotension following a yoga class. However, there has been no previous documentation in the literature of 'pilates reformer' classes being associated with a spontaneous spinal CSF leak and, to our knowledge, this is the first case.
Discussion
The hallmark symptom of intracranial hypotension is an orthostatic headache that is worse when in the upright position and resolves or improves when lying flat. Other symptoms include diplopia, hearing loss, vertigo and meningism.
The most characteristic findings on MRI of the head is pachymeningeal enhancement with downward displacement of the brain, which can be mistaken for a Chiari type I malformation. Subdural hematomas are common in patients with SIH and are usually bilateral but without mass effect. Since the most common cause of SIH is a spontaneous spinal CSF leak, patients should undergo spinal imaging to try and identify a dural tear. CT or MRI myelography are the preferred spinal imaging technique as they provide accurate localization of the tear compared to MRI. Localization of the tear is useful when considering the use of an epidural blood patch; the treatment of choice in patients who have failed conservative management (bed rest, NSAIDs and caffeinated drinks). Since our patient responded to conservative measures, she did not require an epidural blood patch. There was, therefore, no requirement to determine the exact location of the dural tear using myelography. Clinical improvement usually precedes resolution of the abnormalities documented on neuroimaging of the head although the time between symptomatic and MRI resolution is variable.
The underlying cause of spontaneous CSF leaks remains unknown but there is an association with connective tissue disorders. Up to 20% of patients have subtle sketetal abnormalities such as those seen in Marfan syndrome (tall stature, joint hypermobility and arachnodactyly) with no other stigmata of the disease. In some of these patients there is abnormal expression of fibrillin metabolism. It has also been reported that in patients with an underlying dural weakness a small traumatic event may be enough to produce a spontaneous CSF leak. In our patient, there was no evidence of a connective tissue disease and we feel that a trivial traumatic event during her pilates class resulted in the development of a dural tear. A retrospective study of 30 patients with CSF hypovolemia describes one case of spontaneous intracranial hypotension following a yoga class. However, there has been no previous documentation in the literature of 'pilates reformer' classes being associated with a spontaneous spinal CSF leak and, to our knowledge, this is the first case.
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