There are a number of headache syndromes that mimic chronic migraine but require different management. One group of headaches may be characterized by low cerebrospinal pressure. The defining clinical symptom of intracranial hypotension headaches is improvement when lying flat; the flat posture reduces cerebrospinal fluid outflow, possibly increases CSF production, and relieves gravitational traction on the meninges. Causes of intracranial hypotension include headache following lumbar puncture (post-LP headache), spontaneous intracranial hypotension, spinal fluid leaks, and likely a number of other mechanisms that are currently poorly understood. Diagnosis is by history of postural sensitivity, and diagnostic lumbar puncture. Careful measurement of CSF pressure is mandatory, as straining or breath holding may spuriously raise cerebrospinal fluid pressure. An MRI obtained with gadolinium enhancement can show typical meningeal enhancement but this must be looked for specifically, and will likely be missed on a non-contrasted MRI.
There are emerging surgical procedures to intervene in these types of headaches. However, there are some simple measures that may help, both in diagnosis and, in some cases, may be sufficiently effective treatment. These include caffeine administration in high doses, and the administration of ACTH or similar analogues; both of these agents increase CSF production.
Two interesting articles from the literature follow. They refer to post-LP headache, but the mechanism of treatment may be applicable to all headache caused by intracranial hypotension. Both caffeine administration and the use of ACTH are simple to administer and carry little risk.
Reg Anesth. 1997 Sep-Oct;22(5):432-4.
Adrenocorticotropic hormone infusion as a novel treatment for postdural puncture headache.
Kshatri AM, Foster PA.
Department of Anesthesia, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, USA.
Abstract
BACKGROUND AND OBJECTIVES: In two patients, one scheduled for epidural anesthesia and the other for placement of a spinal catheter for operative procedures, severe postdural puncture headache developed and was refractory to conservative therapy.
METHODS: The first patient had several unintentional dural punctures, and the second underwent a planned dural puncture with an 18-gauge needle for insertion of a 20-gauge catheter. When neither patient responded to conservative therapy following development of postdural puncture headache, an infusion of adrenocorticotropic hormone (ACTH) was given prior to consideration of epidural blood patching.
RESULTS: Both patients obtained complete and permanent relief from their headaches.
CONCLUSION: A single treatment with ACTH may offer an alternative therapy in the treatment of postdural puncture headache.
PMID: 9338904 [PubMed - indexed for MEDLINE]
Publication Types, MeSH Terms, Substances
LinkOut - more resources
Use of Intravenous Tetracosactin in the Treatment of Postdural Puncture Headache: Our Experience in Forty Cases
Luz Cánovas, MD PhD, Carmen Barros, Ana Gómez, Marcos Castro and Andrés Castro
Department of Anesthesiology, Complejo Hospitalario Orense, Spain
To the Editor:
Adrenocorticotropic hormone (ACTH) for treatment of Postdural Puncture Headache (PDPH) has been briefly mentioned in literature (1–4). We present the use of tetracosactin in 40 patients suffering PDPH.
All patients presented with severe headache in the occipital region that worsened in the upright position, associated in most cases with nausea and vomiting (5). Tetracosactin, which contains the first 24 amino acids of the natural ACTH sequence and has the same physiological properties, was administered. Saline solution 1.5 U/kg in 250 mL was administered over 30 min (2,3). Pain intensity was evaluated after 6, 24, and 72 h post-therapy. After 6 h, 38 patients of the study presented complete pain relief, which remained in further controls.
The ACTH-induced production of aldosterone causes an increase in the intravascular volume and may determine the closure of the orifice by others means: dural edema or by physical opposition of the dural orifice margins (6).
It has been speculated with the possibility of ACTH increasing CSF production, through a sodium active transport mechanism, and a possible increase in the production of β endorphins in the central nervous system with a subsequent increase in pain threshold (1,4).
We believe that IV ACTH is an effective alternative to conservative therapy in PDPH.
References
↵ Collier B. Treatment for PDPH. Br J Anaesth 1994; 72: 366–7. FREE Full Text
↵ Foster P. ACTH treatment for post lumbar puncture headache. Br J Anaesth 1994; 72: 429.
↵ Kshatri A, Foster P. Adrenocorticotropic hormone infusion as a novel treatment for postdural puncture headache. Reg Anesth 1997; 22: 432–4. Medline
↵ Carter B, Pasupuleti R. Use of intravenous cosyntropin in the treatment of postdural puncture headache. Anesthesiology 2000; 92: 272–4. Medline
↵ Liu S. Why are postdural puncture headaches still a problem? Reg Anesth Pain Med 2000; 25: 393–402. CrossRefMedline
↵ Baysinger C, Menk E, Horte E, Middaugh R. The successful treatment of dural puncture headache after failed epidural blood patch. Anesth Analg 1986; 65: 1242–4. FREE Full Text
