Lumbar Puncture Headache: A Review
Neil H. Raskin, M.D.
University of California School of Medicine- San Francisco, San Francisco, CA 94143-0114. Accepted for Publication: January 5, 1990. SYNOPSIS
August Bier, the father of spinal anesthesia, suffered and reported the first lumbar puncture (LP) headache. On August 24, 1898 his assistant, a Dr. Hildebrandt, attempted to administer a spinal anesthetic to Dr. Bier; it was never completed because the syringe did not fit the already implanted spinal needle.1 Bier himself suggested that continued leakage of cerebrospinal fluid (CSF) through the dural puncture site was the cause of headache, a theory that has been embraced by the medical community; however, the mechanism is probably more complex. Nearly 50 years ago, J. Lawrence Pool, using an endoscopic technique to visualize the surface of the spinal cord and the cauda equina, frequently observed large collections of epidural fluid two to four days following lumbar puncture in patients without headache.2 Evidence that will be presented below suggests that CSF volume alterations may be the signal closest to the headache mechanism. (Headache 30:197-200, 1990) THE CLINICAL SYNDROME
Headache following lumbar puncture usually begins within 48 hours, but may be delayed for up to 12 days. The headache is decidedly positional, beginning when the patient sits or stands upright and relieved upon reclining or with abdominal compression. The longer the patient is upright, the longer the latency before head pain subsides. It is worsened by head shaking and jugular vein compression. Frontal headache occurs about as often as occipital or diffuse headache3 (Table 1). The pain is usually reported as a dull ache but may be throbbing. Nausea and stiff neck are common accompaniments; blurred vision, "spots" before the eyes, photophobia, tinnitus, vertigo and diminished hearing also occur on occasion.4 The symptoms persist for an average of four days but occasionally persist for weeks to months. Subdural hematoma or hygroma may rarely attend this syndrome.5 Tourtellote et al.,6 in their extensive review of the world literature, found the incidence of LP headache to be 30 percent; others have found the incidence to be closer to 15 percent.4 It occurs much less often among children under the age of 13 years7 and adults beyond the seventh decade (Table 2). Women are Table 1 Lumbar Puncture Headache: Location and Accompanying Symptoms Among 118 Patients Headache Location Frequency (%) Occipital 25 Frontal 22 Occipitofrontal 25 Accompanying symptoms Nuchal stiffness and pain 57 Low back pain 35 Nausea 22 Blurred vision 10 Tinnitus 5 Vomiting 2
(Modified from Abouleish E, de la Vega S, Blendinger I, Tio T-O: Long-term follow-up of epidural blood patch. Anesth Analg 54:459-463, 1975.) Table 2 Relationship of Age to Incidence of Post-Lumbar-Puncture Headache Postural No. Lumbar Headaches Age (yrs.) Punctures No. (%) 10-19 537 51 10 20-29 1,994 321 16 30-39 1,833 261 14 40-49 1,759 192 11 50-59 1,736 133 8 60-69 1,094 45 4 70-79 297 7 2 80-89 27 1 3
(Data from Vandam LD, Dripps RD: Long-term follow-up of patients who received 10,098 spinal anesthetics. JAMA 161:586-591, 1956.) affected twice as often as men. Factors that have been alleged to decrease the incidence of headache include (1) lying supine following the procedure, (2) lying prone following the procedure, (3) use of small diameter needles, (4) removing the LP needle when the patient is prone and with the head down, and (5) adequate hydration.6 However, other than small needle diameter, the contribution of which has been clearly established,8 all the other aforementioned factors have been challenged by empirical data showing no benefit.9,10,11,12
PATHOPHYSIOLOGY
The role of psychological factors in the development of LP headache appears to be minimal. Van-dam and Dripps4 administered spinal anesthetics to 100 patients who were first anesthetized with general anesthetics. Although none of these patients knew that a lumbar puncture had been performed, the incidence of typical postural headache following the procedure was the same as in patients who were aware of the procedure. Following lumbar puncture, the loss of CSF volume decreases the brain's supportive cushion, so that when a patient is upright there is probably dilatation and tension placed on the brain's anchoring structures, the pain-sensitive dural sinuses, resulting in pain. The putative role of the sudden decrease in CSF volume may have been previously underestimated. Fay13 found that upon reducing CSF volume, three populations of patients could be identified with varying "thresholds" of headache provocation (Figure 1). It seems plausible to posit that patients who develop LP headache are the low threshold group. Continued leakage of CSF appears to be common following LP whether or not headache develops.2 Cerebrospinal fluid hypotension often but inconsistently attends LP headache. Marshall14 performed a second lumbar puncture 24 hours after the first on 43 patients whether or not headache had developed; six reported positional headache and on the second LP had opening pressures of 150, 105, 60, 35, 0 and 0 mm H2O. Among those without headache, seven had pressures of 50 mm H2O or less, one had 0 and one 5 mm H2O. Similarly, Kunkle, Ray and Wolff15 showed that LP headache was independent of pressure considerations, within the lumbar subarachnoid space or intracranially. They suggested that headache was related to a change in the normal pressure differential between the inside and outside of intracranial venous structures, resulting in venous dilatation. Venous dilatation following CSF removal is known to occur in cats.16Jugular compression increases the severity of LP headache15 by causing further venous dilatation despite
its tendency to increase intracranial pressure; this phenomenon affirms the conclusion that headache is not caused by intracranial hypotension per se. A decrease in CSF volume also leads to labyrinthine alterations which may lead to impaired hearing or tinnitus that on occasion occur in this syndrome. Audiograms have been restored to normal in such patients after intrathecal infusions of normal saline.4 TREATMENT
Whereas LP headaches usually subside over a few days and do not require aggressive therapy, occasional patients become bedbound, and for them effective therapy is available. The mechanism through which these treatments act raise interesting questions about the pathophysiology of the syndrome. Epidural Saline. The first specific approach to the LP headache problem was the injection of saline epidurally, with the unlikely aim of increasing pressure within the epidural space in order to compress the dural sac and reduce the leakage of CSF. Rice and Dabbs17 gave large volume (30 ml) single bolus injections and stopped headache abruptly in eight out of eleven patients, but in four, headache returned. It was later shown that 20 ml of saline injected into the lumbar epidural space resulted in an immediate rise in epidural space pressure of 650 mm H2O and an elevation in subarachnoid space pressure of 850 mm H2O. These pressure increments lasted from three to ten minutes.18 The larger the volume of saline, the higher the pressures, and the faster the injection, the steeper but more transient the peak. Because the rise in pressure is short-lived and is greater within the subarachnoid space than outside it, its beneficial effect is unlikely to be explained in terms of stopping CSF leakage. From the practical point of view, epidural saline infusion remains a useful strategy when other methods fail; an infusion rate of 20 ml per hour continued for 48 to 72 hours is a commonly used successful regimen.19,20 Epidural Blood Patch. Based on his observation that headache seemed to follow traumatic bloody lumbar punctures less often than atraumatic spinal taps, Gormley21 introduced the epidural injection of autologous blood, which has become the most predictable and rapidly effective measure for terminating LP headache.22 Over 95 percent success rates have been reported in several series,1,23 but occasionally two or more blood patches are necessary. After 12 ml of blood is injected epidurally, the blood spreads bidirectionally over nine spinal segments, six upward and three downward,24 so that if sealing the puncture site is its mechanism, it is not essential for the blood to be injected at the original LP locus. Since the spread of epidurally injected blood is more cephalad than caudad, injecting at a lower puncture site is appropriate if the original site cannot be used or in the instance of multiple punctures. Curiously, blood patches fail most of the time when performed
within 24 hours of the LP, but rarely fail when done at least two to three days later.25,26 This observation alone raises doubt that the mechanism for the success of blood patching is simply obstruction of the dural hole. The most common complication of blood patches is back pain at the injection site, which occurs in as many as one-third of patients; although usually transient, it may persist for months.3 Less common complications include radicular pain and paresthesia and lumbosacral meningismus.27,28 Mechanism of Epidural Blood and Saline Injections. Epidural injections of blood have been believed to form a gelatinous tamponade over the dural hole that prevents CSF leakage and allows the dural rent to undergo normal healing. Fibroblastic activity begins 48 hours after blood patching, collagen deposition begins at two weeks, and scar formation is complete within three months.29 However, following a successful blood patch, patients are immediately headache-free and remain so. It is inconceivable that the tensile strength of the bloody tamponade is sufficient for this effect. Alternatively, a sudden increment in CSF pressure is the common denominator of both epidural blood and saline injections, suggesting that the latter may serve as a signal that deactivates the LP headache mechanism, possibly by antagonizing adenosine receptors (v.i.). Moreover, compression of the dural sac per se may have consequences that are presently unknown. Dura mater is richly innervated with adrenergic, cholinergic and peptidergic fibers25 which may bear importantly on the mechanism of this syndrome. The author has seen three patients who were successfully treated with epidural blood patches for LP headache but then sustained a recurrence four to six months later and were again successfully blood-patched. A further recurrence some months later was not successfully patched and, despite failure to find a CSF leak with intrathecal radioisotope and metrizamide studies, all three were explored surgically; no CSF leakage could be identified at operation. In this circumstance, the surgeon applies a pad of fat to the lumbar dural sac and glues it in place. All three patients were headache-free thereafter; the follow-up period is now four to six years. The putative role of dural sac compression by blood, saline or a fat pad is posited. Caffeine. In a controlled, double-blind prospective study, Sechzer and Abel31 showed that intravenous caffeine sodium benzoate was dramatically effective in 75 percent of patients after a single 500 mg dose. A second dose was given within two hours if headache persisted, with additional benefit ensuing, raising the total success rate to 85 percent. Theophylline, closely related to caffeine pharmacologically, is also effective when taken orally (300 mg three times daily) for LP headache.32 Both caffeine and theophylline produce intracerebral arterial constriction probably via blockade of brain adenosine receptors,33 resulting in decreased cerebral blood flow and decreased CSF pressure.34 Decreased venous tone could result from such vascular effects, thus explaining these drugs' actions in LP headache, but it is worth examining further the biologic role of adenosine. Adenosine dilates vessels in the cerebral circulation and has a variety of actions on central neurons. It inhibits the release of almost all neurotransmitters, whether excitatory or inhibitory.35,36 Adenosine receptors are activated by hypercapnia and participate in the mechanism leading to the resultant increased cerebral blood flow.33 Since there is little reason to believe that caffeine's actions in LP headache are through closure of a dural hole, one may speculate that a sudden decrease in CSF volume such as occurs following lumbar puncture, activates adenosine receptors thus producing venous and arterial dilatation and the resulting syndrome of LP headache. Could a sudden increment in CSF pressure that results from an epidural injection of blood or saline serve as a signal to deactivate adenosine receptors? (Figure 2). PRACTICAL CONSIDERATIONS
Although one effort at substantiation has failed,9 Easton's37 suggestion that the incidence of LP headache can be reduced by removing the needle when the patient is prone with the foot of the examining table raised approximately 25 cm makes good sense. In this position there is negative hydrostatic pressure in the lumbar subarachnoid space, so that when the needle is withdrawn, there should be inversion of the puncture site perimeter rather than eversion, lessening the probability of an enduring aperture. Maintaining the patient in this position for 60 minutes affords time for sealing the dural hole. Easton has rarely seen LP headache after adopting this technique; nor has the author. Smith, Perkin and Rose38 tested this observation in a prospective, single-blind trial and found that Easton's method yielded substantially fewer headaches; the difference was significant by chi-squared test but not when the Yates' correction was applied. It is the author's view that this issue remains open and, unless conclusive negative data appear, will continue to use this method. Should headache become a problem, caffeine
sodium benzoate, 500 mg, is given intravenously over two to three minutes and the patient remains supine for 20 minutes; if headache persists, the process is repeated. If caffeine fails, epidural blood injection follows. REFERENCES
1.
Ostheimer GW: Headache in the postpartum period, in Marx GF (ed): Clinical Management of Mother and Newborn. New York, Springer-Verlag, 1979, pp 27-41.
2.
Pool JL: Myeloscopy: intraspinal endoscopy. Surgery 11:169-182, 1942.
3.
Abouleish E, de la Vega S, Blendinger I, Tio T-O: Long-term follow-up of epidural blood patch. Anesth Analg 54:459-463, 1975.
4.
Vandam LD, Dripps RD: Long-term follow-up of patients who received 10,098 spinal anesthetics. JAMA 161:586-591, 1956.
5.
Newrick P, Read D: Subdural hematoma as a complication of spinal anesthetic. Br Med J 285:341-342, 1982.
6.
Tourtellotte WW, Haerer AF, Heller GL, Somers JE: Post-Lumbar Puncture Headaches. Springfield, IL, Charles C Thomas, 1964.
7.
Bolder PM: Postlumbar puncture headache in pediatric oncology patients. Anesthesiology 65:696-698, 1986.
8.
Tourtellotte WW, Henderson WG, Tucker RP, et al: A randomized double-blind clinical trial comparing the 22 versus 26 gauge needle in the production of the post-lumbar puncture syndrome in normal individuals. Headache 12:73-78, 1972.
9.
Hilton-Jones D, Harad RA, Gill MW, Warlow CP: Failure of postural manoeuvres to prevent lumbar puncture headache. J Neurol Neurosurg Psychiatry 45:743-746, 1982.
10.
Carbaat PAT, van Crevel H: Lumbar puncture headache: controlled study on the preventive affect of 24 hours' bed rest. Lancet ii:1133-1135, 1981.
11.
Dieterich M, Brandt T: Incidence of post-lumbar puncture headache is independent of daily fluid intake. Eur Arch Psychiatr Neurol Sci 237:194-196, 1988.
12.
Vilming ST, Schrader H, Monstad I: Post-lumbar-puncture headache: the significance of body posture. Cephalalgia 8:75-78, 1988.
13.
Fay T: A new test for the diagnosis of certain headaches: the cephalalgiogram. Dis Nerv System 1:312-315, 1940.
14.
Marshall J: Lumbar-puncture headache. J Neurol Neurosurg Psychiatry 13:71-74, 1950.
15.
Kunkle EC, Ray BS, Wolff HG: Experimental studies on headache: analysis of the headache associated with changes in intracranial pressure. Arch Neurol Psychiatry 49:323-358, 1943.
16.
Forbes HS, Nason GI: The cerebral circulation. Arch Neurol Psychiatry 34:533-547, 1935.
17.
Rice GG, Dabbs CH: The use of peridural and subarachnoid injections of saline solutions in the treatment of severe postspinal headache. Anesthesiology 11:17-23, 1950.
18.
Usubiaga JE, Usubiaga LE, Brea LM, Goyena R: Effect of saline injections on epidural and subarachnoid space pressures and relation to postspinal anesthesia headache. Anesth Analg 46:293-296, 1967.
19.
Baysinger CL, Menk EJ, Harte E, Middaugh R: The successful treatment of dural puncture headache after failed epidural blood patch. Anesth Analg 65:1242-1244, 1986.
20.
Bart AJ, Wheeler AS: Comparison of epidural saline placement and epidural blood placement in the treatment of post-lumbar puncture headache. Anesthesiology 48:221-223, 1978.
21.
Gormley JB: Treatment of postspinal headache. Anesthesiology 21:565-566, 1960.
22.
OIsen KS: Epidural blood patch in the treatment of post-lumbar puncture headache. Pain 30:293-301, 1987.
23.
Crawford JS: Experiences with epidural blood patch. Anaesthesia 35:513-515, 1980.
24.
Szeinfeld M, Ihmeidan IH, Moser MM, Machado R, Klose KJ, Serafini AN: Epidural blood patch: evaluation of the volume and spread of blood injected into the epidural space. Anesthesiology 64:820-822, 1986.
25.
Berrettini WH, Simmons-Alling S, Nurnberger Jl: Epidural blood patch does not prevent headache after lumbar puncture. Lancet i:856-857, 1987.
26.
Loeser EA, Hill GE, Bennett GM, Sederberg JE: Time vs. success rate for epidural blood patch. Anesthesiology 49:147-148, 1978.
27.
Wilkinson HA: Lumbosacral meningismus complicating subdural injection of blood patch. J Neurosurg 52:849-851, 1980.
28.
Cornwall RD, Dolan WM: Radicular back pain following lumbar epidural blood patch. Anesthesiology 43:692-693, 1975.
29.
DiGiovanni AJ, Galbert MW, Wahle WM: Epidural injection of autologous blood for post-lumbar puncture headache. Anesth Analg 51:226-232, 1972.
30.
Edvinsson L, Uddman R: Adrenergic, cholinergic and peptidergic nerve fibres in dura matter-involvement in headache? Cephalalgia 1:175-179, 1981.
31.
Sechzer PH, Abel L: Post-spinal anesthesia headache treated with caffeine. Curr Ther Res 24:307-312, 1978.
32.
Feuerstein TJ, Zeides A: Theophylline relieves headache following lumbar puncture. KIin Wochenschr 64:216-218, 1986.
33.
PhiIlis JW, DeLong RE: An involvement of adenosine in cerebral blood flow regulation during hypercapnia. Gen Pharmacol 18:133-139, 1987.
34.
Mathew RJ, Wilson WH: Caffeine induced changes in cerebral circulation. Stroke 16:814-817, 1985.
35.
Snyder SH, Sklar P: Behavioral and molecular actions of caffeine: focus on adenosine. J Psychiat Res 18:91-106, 1984.
36.
Chin JH: Adenosine receptors in brain: neuromodulation and role in epilepsy. Ann Neurol 26:695-698, 1989.
37.
Easton JD: Headache after lumbar puncture. Lancet i:974-975, 1979.
38.
Smith FR, Perkin GD, Rose FC: Posture and headache after lumbar puncture. Lancet i:1245, 1980.
Neil H. Raskin, M.D.
University of California School of Medicine- San Francisco, San Francisco, CA 94143-0114. Accepted for Publication: January 5, 1990. SYNOPSIS
August Bier, the father of spinal anesthesia, suffered and reported the first lumbar puncture (LP) headache. On August 24, 1898 his assistant, a Dr. Hildebrandt, attempted to administer a spinal anesthetic to Dr. Bier; it was never completed because the syringe did not fit the already implanted spinal needle.1 Bier himself suggested that continued leakage of cerebrospinal fluid (CSF) through the dural puncture site was the cause of headache, a theory that has been embraced by the medical community; however, the mechanism is probably more complex. Nearly 50 years ago, J. Lawrence Pool, using an endoscopic technique to visualize the surface of the spinal cord and the cauda equina, frequently observed large collections of epidural fluid two to four days following lumbar puncture in patients without headache.2 Evidence that will be presented below suggests that CSF volume alterations may be the signal closest to the headache mechanism. (Headache 30:197-200, 1990) THE CLINICAL SYNDROME
Headache following lumbar puncture usually begins within 48 hours, but may be delayed for up to 12 days. The headache is decidedly positional, beginning when the patient sits or stands upright and relieved upon reclining or with abdominal compression. The longer the patient is upright, the longer the latency before head pain subsides. It is worsened by head shaking and jugular vein compression. Frontal headache occurs about as often as occipital or diffuse headache3 (Table 1). The pain is usually reported as a dull ache but may be throbbing. Nausea and stiff neck are common accompaniments; blurred vision, "spots" before the eyes, photophobia, tinnitus, vertigo and diminished hearing also occur on occasion.4 The symptoms persist for an average of four days but occasionally persist for weeks to months. Subdural hematoma or hygroma may rarely attend this syndrome.5 Tourtellote et al.,6 in their extensive review of the world literature, found the incidence of LP headache to be 30 percent; others have found the incidence to be closer to 15 percent.4 It occurs much less often among children under the age of 13 years7 and adults beyond the seventh decade (Table 2). Women are Table 1 Lumbar Puncture Headache: Location and Accompanying Symptoms Among 118 Patients Headache Location Frequency (%) Occipital 25 Frontal 22 Occipitofrontal 25 Accompanying symptoms Nuchal stiffness and pain 57 Low back pain 35 Nausea 22 Blurred vision 10 Tinnitus 5 Vomiting 2
(Modified from Abouleish E, de la Vega S, Blendinger I, Tio T-O: Long-term follow-up of epidural blood patch. Anesth Analg 54:459-463, 1975.) Table 2 Relationship of Age to Incidence of Post-Lumbar-Puncture Headache Postural No. Lumbar Headaches Age (yrs.) Punctures No. (%) 10-19 537 51 10 20-29 1,994 321 16 30-39 1,833 261 14 40-49 1,759 192 11 50-59 1,736 133 8 60-69 1,094 45 4 70-79 297 7 2 80-89 27 1 3
(Data from Vandam LD, Dripps RD: Long-term follow-up of patients who received 10,098 spinal anesthetics. JAMA 161:586-591, 1956.) affected twice as often as men. Factors that have been alleged to decrease the incidence of headache include (1) lying supine following the procedure, (2) lying prone following the procedure, (3) use of small diameter needles, (4) removing the LP needle when the patient is prone and with the head down, and (5) adequate hydration.6 However, other than small needle diameter, the contribution of which has been clearly established,8 all the other aforementioned factors have been challenged by empirical data showing no benefit.9,10,11,12
PATHOPHYSIOLOGY
The role of psychological factors in the development of LP headache appears to be minimal. Van-dam and Dripps4 administered spinal anesthetics to 100 patients who were first anesthetized with general anesthetics. Although none of these patients knew that a lumbar puncture had been performed, the incidence of typical postural headache following the procedure was the same as in patients who were aware of the procedure. Following lumbar puncture, the loss of CSF volume decreases the brain's supportive cushion, so that when a patient is upright there is probably dilatation and tension placed on the brain's anchoring structures, the pain-sensitive dural sinuses, resulting in pain. The putative role of the sudden decrease in CSF volume may have been previously underestimated. Fay13 found that upon reducing CSF volume, three populations of patients could be identified with varying "thresholds" of headache provocation (Figure 1). It seems plausible to posit that patients who develop LP headache are the low threshold group. Continued leakage of CSF appears to be common following LP whether or not headache develops.2 Cerebrospinal fluid hypotension often but inconsistently attends LP headache. Marshall14 performed a second lumbar puncture 24 hours after the first on 43 patients whether or not headache had developed; six reported positional headache and on the second LP had opening pressures of 150, 105, 60, 35, 0 and 0 mm H2O. Among those without headache, seven had pressures of 50 mm H2O or less, one had 0 and one 5 mm H2O. Similarly, Kunkle, Ray and Wolff15 showed that LP headache was independent of pressure considerations, within the lumbar subarachnoid space or intracranially. They suggested that headache was related to a change in the normal pressure differential between the inside and outside of intracranial venous structures, resulting in venous dilatation. Venous dilatation following CSF removal is known to occur in cats.16Jugular compression increases the severity of LP headache15 by causing further venous dilatation despite
its tendency to increase intracranial pressure; this phenomenon affirms the conclusion that headache is not caused by intracranial hypotension per se. A decrease in CSF volume also leads to labyrinthine alterations which may lead to impaired hearing or tinnitus that on occasion occur in this syndrome. Audiograms have been restored to normal in such patients after intrathecal infusions of normal saline.4 TREATMENT
Whereas LP headaches usually subside over a few days and do not require aggressive therapy, occasional patients become bedbound, and for them effective therapy is available. The mechanism through which these treatments act raise interesting questions about the pathophysiology of the syndrome. Epidural Saline. The first specific approach to the LP headache problem was the injection of saline epidurally, with the unlikely aim of increasing pressure within the epidural space in order to compress the dural sac and reduce the leakage of CSF. Rice and Dabbs17 gave large volume (30 ml) single bolus injections and stopped headache abruptly in eight out of eleven patients, but in four, headache returned. It was later shown that 20 ml of saline injected into the lumbar epidural space resulted in an immediate rise in epidural space pressure of 650 mm H2O and an elevation in subarachnoid space pressure of 850 mm H2O. These pressure increments lasted from three to ten minutes.18 The larger the volume of saline, the higher the pressures, and the faster the injection, the steeper but more transient the peak. Because the rise in pressure is short-lived and is greater within the subarachnoid space than outside it, its beneficial effect is unlikely to be explained in terms of stopping CSF leakage. From the practical point of view, epidural saline infusion remains a useful strategy when other methods fail; an infusion rate of 20 ml per hour continued for 48 to 72 hours is a commonly used successful regimen.19,20 Epidural Blood Patch. Based on his observation that headache seemed to follow traumatic bloody lumbar punctures less often than atraumatic spinal taps, Gormley21 introduced the epidural injection of autologous blood, which has become the most predictable and rapidly effective measure for terminating LP headache.22 Over 95 percent success rates have been reported in several series,1,23 but occasionally two or more blood patches are necessary. After 12 ml of blood is injected epidurally, the blood spreads bidirectionally over nine spinal segments, six upward and three downward,24 so that if sealing the puncture site is its mechanism, it is not essential for the blood to be injected at the original LP locus. Since the spread of epidurally injected blood is more cephalad than caudad, injecting at a lower puncture site is appropriate if the original site cannot be used or in the instance of multiple punctures. Curiously, blood patches fail most of the time when performed
within 24 hours of the LP, but rarely fail when done at least two to three days later.25,26 This observation alone raises doubt that the mechanism for the success of blood patching is simply obstruction of the dural hole. The most common complication of blood patches is back pain at the injection site, which occurs in as many as one-third of patients; although usually transient, it may persist for months.3 Less common complications include radicular pain and paresthesia and lumbosacral meningismus.27,28 Mechanism of Epidural Blood and Saline Injections. Epidural injections of blood have been believed to form a gelatinous tamponade over the dural hole that prevents CSF leakage and allows the dural rent to undergo normal healing. Fibroblastic activity begins 48 hours after blood patching, collagen deposition begins at two weeks, and scar formation is complete within three months.29 However, following a successful blood patch, patients are immediately headache-free and remain so. It is inconceivable that the tensile strength of the bloody tamponade is sufficient for this effect. Alternatively, a sudden increment in CSF pressure is the common denominator of both epidural blood and saline injections, suggesting that the latter may serve as a signal that deactivates the LP headache mechanism, possibly by antagonizing adenosine receptors (v.i.). Moreover, compression of the dural sac per se may have consequences that are presently unknown. Dura mater is richly innervated with adrenergic, cholinergic and peptidergic fibers25 which may bear importantly on the mechanism of this syndrome. The author has seen three patients who were successfully treated with epidural blood patches for LP headache but then sustained a recurrence four to six months later and were again successfully blood-patched. A further recurrence some months later was not successfully patched and, despite failure to find a CSF leak with intrathecal radioisotope and metrizamide studies, all three were explored surgically; no CSF leakage could be identified at operation. In this circumstance, the surgeon applies a pad of fat to the lumbar dural sac and glues it in place. All three patients were headache-free thereafter; the follow-up period is now four to six years. The putative role of dural sac compression by blood, saline or a fat pad is posited. Caffeine. In a controlled, double-blind prospective study, Sechzer and Abel31 showed that intravenous caffeine sodium benzoate was dramatically effective in 75 percent of patients after a single 500 mg dose. A second dose was given within two hours if headache persisted, with additional benefit ensuing, raising the total success rate to 85 percent. Theophylline, closely related to caffeine pharmacologically, is also effective when taken orally (300 mg three times daily) for LP headache.32 Both caffeine and theophylline produce intracerebral arterial constriction probably via blockade of brain adenosine receptors,33 resulting in decreased cerebral blood flow and decreased CSF pressure.34 Decreased venous tone could result from such vascular effects, thus explaining these drugs' actions in LP headache, but it is worth examining further the biologic role of adenosine. Adenosine dilates vessels in the cerebral circulation and has a variety of actions on central neurons. It inhibits the release of almost all neurotransmitters, whether excitatory or inhibitory.35,36 Adenosine receptors are activated by hypercapnia and participate in the mechanism leading to the resultant increased cerebral blood flow.33 Since there is little reason to believe that caffeine's actions in LP headache are through closure of a dural hole, one may speculate that a sudden decrease in CSF volume such as occurs following lumbar puncture, activates adenosine receptors thus producing venous and arterial dilatation and the resulting syndrome of LP headache. Could a sudden increment in CSF pressure that results from an epidural injection of blood or saline serve as a signal to deactivate adenosine receptors? (Figure 2). PRACTICAL CONSIDERATIONS
Although one effort at substantiation has failed,9 Easton's37 suggestion that the incidence of LP headache can be reduced by removing the needle when the patient is prone with the foot of the examining table raised approximately 25 cm makes good sense. In this position there is negative hydrostatic pressure in the lumbar subarachnoid space, so that when the needle is withdrawn, there should be inversion of the puncture site perimeter rather than eversion, lessening the probability of an enduring aperture. Maintaining the patient in this position for 60 minutes affords time for sealing the dural hole. Easton has rarely seen LP headache after adopting this technique; nor has the author. Smith, Perkin and Rose38 tested this observation in a prospective, single-blind trial and found that Easton's method yielded substantially fewer headaches; the difference was significant by chi-squared test but not when the Yates' correction was applied. It is the author's view that this issue remains open and, unless conclusive negative data appear, will continue to use this method. Should headache become a problem, caffeine
sodium benzoate, 500 mg, is given intravenously over two to three minutes and the patient remains supine for 20 minutes; if headache persists, the process is repeated. If caffeine fails, epidural blood injection follows. REFERENCES
1.
Ostheimer GW: Headache in the postpartum period, in Marx GF (ed): Clinical Management of Mother and Newborn. New York, Springer-Verlag, 1979, pp 27-41.
2.
Pool JL: Myeloscopy: intraspinal endoscopy. Surgery 11:169-182, 1942.
3.
Abouleish E, de la Vega S, Blendinger I, Tio T-O: Long-term follow-up of epidural blood patch. Anesth Analg 54:459-463, 1975.
4.
Vandam LD, Dripps RD: Long-term follow-up of patients who received 10,098 spinal anesthetics. JAMA 161:586-591, 1956.
5.
Newrick P, Read D: Subdural hematoma as a complication of spinal anesthetic. Br Med J 285:341-342, 1982.
6.
Tourtellotte WW, Haerer AF, Heller GL, Somers JE: Post-Lumbar Puncture Headaches. Springfield, IL, Charles C Thomas, 1964.
7.
Bolder PM: Postlumbar puncture headache in pediatric oncology patients. Anesthesiology 65:696-698, 1986.
8.
Tourtellotte WW, Henderson WG, Tucker RP, et al: A randomized double-blind clinical trial comparing the 22 versus 26 gauge needle in the production of the post-lumbar puncture syndrome in normal individuals. Headache 12:73-78, 1972.
9.
Hilton-Jones D, Harad RA, Gill MW, Warlow CP: Failure of postural manoeuvres to prevent lumbar puncture headache. J Neurol Neurosurg Psychiatry 45:743-746, 1982.
10.
Carbaat PAT, van Crevel H: Lumbar puncture headache: controlled study on the preventive affect of 24 hours' bed rest. Lancet ii:1133-1135, 1981.
11.
Dieterich M, Brandt T: Incidence of post-lumbar puncture headache is independent of daily fluid intake. Eur Arch Psychiatr Neurol Sci 237:194-196, 1988.
12.
Vilming ST, Schrader H, Monstad I: Post-lumbar-puncture headache: the significance of body posture. Cephalalgia 8:75-78, 1988.
13.
Fay T: A new test for the diagnosis of certain headaches: the cephalalgiogram. Dis Nerv System 1:312-315, 1940.
14.
Marshall J: Lumbar-puncture headache. J Neurol Neurosurg Psychiatry 13:71-74, 1950.
15.
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