headache after spinal tap

[ForumGal]

>

Hi Shannon -- this time waiting worked. Next time I'll offer him hypericum.
I'm assuming he's going to get spinal taps for his eyes again. One person
sent a constitutional suggestion, but I don't think he'll go for such treatment,
plus it really was an accute, evidently a common result of a tap. And here's
hoping this message doesn't appear on the list twice, as many of my messages
have been doing lately (sorry). Best, Margaret

[Sheri Nakken]

At 08:34 AM 02/16/2004 EST, you wrote:
hypericum.
treatment,
here's

I'm sceptical that any of the routine suggestions given (of remedies) would
necessarily be helpful. It isn't about the puncture wound.
I think that you have to take the whole case in order to find the right
remedy - what is unique about this person's headache and accompnaying symptoms

Here's an article that explains from the medical perspective what they
think is going on, but really not extremely helpful for us.
Again, it doesn't help us to prescribe homeopathically based on what
allopathy 'thinks' is going on physiologically.

But at least you will see there are mechanisms that are going on in the
body that are contributing to the headache and giving hypericum or ledum
routinely for a puncture would is probably not going to help much unless
that remedy matches the symptom picture.

http://cumc.columbia.edu/news/review/ar ... _0003.html

P&S Medical Review: Mar 1994, Vol.1, No.2
Post-Lumbar Puncture Headache

William Fearon
Class of 1994
Columbia University
College of Physicians and Surgeons, New York, NY

Introduction

HEADACHE following lumbar puncture was first described in 1898 by Dr.
August Bier who stated, after his assistant Dr. Hildebrandt attempted to
deliver a spinal anesthetic to him, `All these symptoms [pressure in the
head and dizziness] disappeared as soon as I lay down horizontally, but
they returned when I arose.'[1] Post-lumbar puncture headache (PLPH) is
easily diagnosed by its postural nature and distinct history. Its exact
pathophysiology is unclear but stems from persistent leakage of
cerebrospinal fluid (CSF) from the puncture site. Typically self-limited in
nature, the occasional persistence of PLPH has encouraged development of a
variety of prophylaxes and treatments. This review will describe clinical
characteristics of the syndrome, discuss theories of pathogenesis and
detail common management.

Clinical Characteristics

PLPH can arise after any invasion of the subarachnoid space via dural
puncture, including spinal anesthesia, lumbar myelography, diagnostic
lumbar puncture (LP), and coincidental dural tap during epidural
anesthesia. The reported incidence of PLPH ranges from 15 percent to 30
percent.[2,3] A review of the literature from 1891 to 1964 revealed a 32
percent incidence after diagnostic LP and an incidence of 18 percent in
obstetric and 13 percent in non- obstetric patients after spinal
anesthesia.[4] The incidence was less in the latter two groups when smaller
needles were used, when anesthesiologists performed the procedure, and when
fluid was injected, not removed.[4] PLPH occurs more often in young adults,
who are affected four times more often than patients aged 60 to 69
years.[5] The lower incidence among older people has been suggested to
arise from a decrease in elasticity of pain-sensitive structures secondary
to atherosclerosis, or from age-related mechanical changes in the epidural
space.[6] Young women experience PLPH about twice as often as young men,
but several papers reporting this finding have not addressed age and sex as
independent risk factors. [4, 5]

The onset of PLPH is usually within 24 to 48 hours after dural puncture but
may be delayed as long as 12 days. Symptoms are usually self-limited. With
conservative management 50 percent of headaches resolve spontaneously
within four days, 75 percent within seven days, and 95 percent within six
weeks.[6] The longest reported PLPH lasted 19 months.[8] Early onset of
headache after LP correlates with a worse prognosis.

PLPH is typically described as dull or throbbing, frontal or occipital in
origin and radiating to other areas of the head. Its most unique, often
diagnostic characteristic is its postural nature; standing exacerbates the
headache, while lying down partly or totally alleviates it. Headshaking,
coughing and jugular compression worsen the symptoms. Associated complaints
may include nuchal pain and stiffness, low back pain, diplopia, tinnitus,
nausea and vomiting.

Pathogenesis

The exact pathophysiology of PLPH remains unclear. Bier first suggested
that persistent leakage of CSF greater than its production by the choroid
plexus causes a net decrease in CSF volume and intracranial pressure. When
a patient stands up after LP, the resulting downward shift of the brain
stretches pain- sensitive structures and results in a headache.[1] The work
of Sciarra and Carter in 1952 at the Neurological Institute supported
Bier's hypothesis. They performed LPs on 102 patients, half of whom had 10
to 12 mL of CSF removed, half of whom had no fluid removed. The
investigators found no significant difference in incidence of PLPH between
the two groups and concluded that whether or not CSF was removed during LP
did not influence the subsequent development of PLPH.[9] Persistence of the
dural hole and loss of CSF through the defect has been verified by direct
observation at autopsies[10] and laminectomies,[11] by myeloscopy[12] and
by radioisotope myelography.[13] The postural nature of PLPH lends support
to this theory; in an upright position, CSF leakage and CSF hypotension are
increased by gravity, further decreasing the brain's supportive cushion and
exacerbating symptoms. More recently, Grant, et al. used magnetic resonance
imaging to demonstrate that 19 of 20 patients had decreased CSF volume 24
hours post LP; 11 of the 20 complained of headache. These results suggest a
relationship between intracranial CSF volume loss and development of
PLPH.[14]

Other evidence points to different factors. Marshall performed LPs on 43
patients and twenty-four hours later repeated LPs on all 43 patients,
whether or not a patient had developed PLPH.[15] In the 6 patients who had
developed PLPH, repeat LP demonstrated opening pressures of 150, 105, 60,
35, 0, and 0 mm H20. Seven patients who had not developed PLPH all had
opening pressures less than 50 mm H20. Marshall's results demonstrated no
significant association between CSF pressure at repeat LP and presence of
PLPH.

Some have postulated that development of PLPH may be more dependent upon
creation of an intra- and extra-luminal pressure differential in
intracranial vessels and not upon CSF hypotension per se.[16] In fact,
jugular compression has been noted to exacerbate PLPH, despite increasing
CSF pressure.[16] The common factor in both jugular compression and CSF
removal appears to be the differential that results between intravascular
pressure and surrounding intracranial pressure. Pressure changes are
speculated to cause traction on pain-sensitive anchoring structures and
consequently PLPH.[5]

The possible importance of vascular status is demonstrated by the fact that
caffeine administration has been shown to relieve PLPH.[18] Caffeine causes
cerebral vasoconstriction by blocking adenosine receptors, which dilate
vessels when activated. Less cerebral blood flow decreases the amount of
blood in the brain and may lessen the traction on pain sensitive supporting
structures, relieving PLPH. Adenosine receptors may therefore play an
important role in the syndrome's pathogenesis. The decrease in CSF volume
secondary to persistent CSF leakage after LP may activate the adenosine
receptors directly, causing cerebral vasodilatation, stretching pain
sensitive cerebral structures and resulting in PLPH.

Psychological factors have been suggested as important in the pathogenesis
of PLPH. Daniels and Sallie explicitly warned a subgroup of their patients
about the possibility of PLPH and found a 46 percent incidence of PLPH in
this subgroup compared to a 6 percent incidence in those who did not
receive such notification.[19] Vandam and Dripps, however, delivered spinal
anesthesia to 100 patients already under general anesthesia without their
knowledge.[6] These investigators found the same incidence of PLPH in these
patients as in those with previous knowledge of the procedure, suggesting
that psychological factors play little role in development of this
syndrome. Thus, the role of psychological factors in the development of
PLPH is unclear and requires further study.

In an attempt to explain why not all patients develop PLPH after dural
puncture, Gobel, et al. used mechanical pressure stimuli to induce pain
prior to LP.[20] He classified patients into three groups with varying pain
thresholds: sensitive, medium- sensitive, and insensitive. The percentage
of those patients `sensitive' to the mechanical pressure stimuli developed
PLPH at a significantly higher rate than those categorized as
`insensitive'. These findings suggest that some patients may be at greater
inherent risk of developing PLPH.

In another study Gobel, et al. used transcranial dopplers to demonstrate
that patients who develop PLPH have a significantly higher systolic flow
velocity in the right middle cerebral artery prior to LP.[21] There was
significant decrease in flow velocity in the right middle cerebral artery
after LP only in those patients who had developed PLPH. Although no inverse
relation between flow velocity and vessel diameter was proved, one may be
inferred. Therefore, Gobel's findings not only offer a predictor for which
patients are most susceptible to PLPH, but also support the theory that
dilatation of intracranial vessels plays a role in onset of PLPH.

Persistent leakage of CSF is the initiating abnormality in the pathogenesis
of PLPH. Whether and exactly how CSF hypotension, cerebral vasodilatation
or both cause traction on cerebral pain- sensitive supporting structures
and contribute to PLPH development remains to be further clarified, as does
any role of psychological factors.

Management

Prevention of this syndrome is controversial. Bed rest for several hours
after LP has been the standard prophylactic measure since Sicard first
suggested it in 1902.[4] Brocker added support to this recommendation in
1958 when he found a less than 0.5 percent incidence of PLPH in patients
who remained supine for three hours after LP, compared to a 36 percent
incidence in those who did not.[22]

More recently, however, some have suggested that bed rest after LP may only
delay symptoms or decrease the severity of PLPH but not prevent it.[3] In a
study of 300 patients, Vilming, et al. found no significant difference in
incidence of PLPH among patients who ambulated immediately after LP and
those who remained supine.[23] In addition, patients who ambulated and
developed PLPH were found to have fewer associated symptoms, such as
nausea, compared to those who remained supine and developed PLPH. Further
evidence against prophylactic bedrest comes from Thornberry, et al. who, in
a prospective randomized trial of 80 obstetric patients, found that early
ambulation actually decreases the incidence and intensity of PLPH.[22]
Prophylactic bedrest after LP is now less favored and early ambulation is
recommended by some.[5, 22]

Introduction of the needle with its bevel parallel to the dura's
longitudinal fibers is another prophylactic measure that may reduce the
incidence of PLPH.[25] This method of insertion separates the fibers rather
than cutting them, facilitating closure of the hole upon needle withdrawal.
Dittman, et al. studied the effect of the bevel's position relative to
dural fibers and found that although the shape of the hole is different,
the size is unaffected.[26] The authors also discovered that dural
thickness ranges between 0.5 mm to 2.0 mm and that holes in thicker areas
tend to close more rapidly than holes in thinner areas. Fortuitous puncture
of a thicker area might be expected to decrease the incidence of PLPH,
which may explain the wide range reported.

During insertion the angle of the needle in relation to the thecal sac may
also affect the incidence of PLPH. By inserting the needle at a narrow
angle (more tangentially) the dura and arachnoid are punctured at different
points along the course of the thecal sac. This leaves an unmolested area
between the two holes which may become apposed upon needle withdrawal and
prevent CSF leakage. Other prophylaxes such as removing the needle when the
patient is prone with the patient's head down, providing adequate hydration
(orally or intravenously), and using antidiuretics have been suggested, but
never proved to decrease incidence of PLPH.

The use of an epidural blood patch (EBP) is well recognized for treatment
of PLPH and has been suggested for prophylactic use. An EBP is performed by
removing 10 to 20 mL of the patient's blood from a peripheral vein then
slowly injecting it into the lumbar epidural space. It is not necessary to
inject the blood at the exact spot of the LP because it will migrate a few
spinal segments superiorly and inferiorly. After injection the patient
remains supine for 6 hours. Berrettini, et al., however, found prophylactic
EBP ineffective.[27] In their study the small amount of blood injected
(only 3 mL) and the large needle used (20 gauge) may have skewed the
results. In addition, CSF leakage is greatest during the first 24 hours
post-LP and interferes with blood clotting. Heide and Deiner in 1990
demonstrated a 22 percent incidence of PLPH in patients with a prophylactic
EBP versus a 45 percent incidence in those without.[28] They used a 22
gauge needle, injected 4 to 8 mL of blood and more carefully evaluated the
time course and severity of patients' complaints. EBP may be an effective
means of prophylaxis against PLPH, depending on the exact protocol,
however, it is much less effective than therapeutic EBP (discussed below)
and may be unnecessary in a typically mild, self-limited syndrome.

Recently, a device which delivers absorbable collagen through an introducer
sheath to promote hemostasis at an arterial puncture site has been
studied.[29] This method of sealing a puncture has not been reported as a
means of prophylaxis against PLPH.

The only measure clearly and repeatedly shown to decrease the incidence of
PLPH is the use of smaller gauge needles; incidence of PLPH decreases as
needle size decreases.[30] The smaller needle creates a smaller hole which
closes more rapidly resulting in less leakage of CSF. Many investigators
have recently found that use of a blunt ended needle results in a
significantly lower incidence of PLPH compared to a sharp ended needle.[31]
A sharp needle cuts the dural fibers while a blunt needle merely pushes
them aside, allowing the hole to reseal more easily upon needle withdrawal.

Although the PLPH syndrome typically resolves spontaneously, multiple
methods of treatment have been tested with a range of outcomes. Initially,
bed rest in the horizontal position and adequate hydration, are
recommended. The former may decrease the amount of CSF leakage by
eliminating the effects of gravity, while the later is thought to maintain
a ready supply of fluid for the production of CSF. Several authors disagree
with the later hypothesis, feeling that forced fluid intake is useless and
has no effect on CSF production.[1, 5]

Simple analgesics and caffeine may ameliorate symptoms.[5] Intravenous
administration of 500 mg of caffeine sodium benzoate has been shown to
relieve 75 percent of PLPHs. A second dose of 500 mg can be given to those
25 percent unaffected by the first, and 10 percent more will be relieved of
PLPH.[18] Presumably caffeine has an inhibitory interaction with the
adenosine receptors.

In the past abdominal binders and epidural saline infusions (20 mL per hour
for 48 to 72 hours) were suggested for persistent PLPH.[32] Both methods
purport to slow or stop CSF leakage by building a favorable pressure
differential between the epidural and subarachnoid spaces. It has been
shown, however, that epidural saline injections actually increase both
epidural and subarachnoid pressures so that the subarachnoid pressure
remains greater than epidural pressure.[33] If true, another mechanism must
be responsible for relief provided by this treatment. The increase in
epidural pressure, although not leading to a pressure differential, may be
enough to invert the edges of the dural puncture, making the hole smaller,
lessening CSF leakage and aiding in ultimate closure.[4] It is also
possible that the increase in epidural and subarachnoid pressures causes
inactivation of adenosine receptors, leading to vasoconstriction and relief
of PLPH.[4] Abdominal binders and epidural saline infusions are
infrequently utilized modes of treatment because of their uncomfortable,
unwieldy natures.

The role of an EBP in treatment of a PLPH was first suggested by Gormley
who observed a decreased incidence of PLPH after traumatic LPs and
hypothesized that the blood must somehow prevent PLPH.[34] He performed the
first EBP in 1960; subsequently it has been shown to have a 90 to 95
percent success rate.[32] Headache typically improves within a few hours
after EBP and resolves completely by the next day. EBP most likely leads to
clot formation and plugging of the dural hole thereby stopping CSF leakage.
However this mechanism explains only the longterm effects of the EBP. The
mechanism responsible for the immediate relief provided by an EBP might be
similar to one suggested for saline infusions, namely, inhibition of
adenosine receptors. The side effects of EBPs include transient
paresthesias, residual back stiffness in approximately 15 percent which
usually resolves within days, but may last longer; acute aseptic meningitis
after unintentional subarachnoid injection; and rarely, subdural
hematoma.[4] If the first EBP fails, a second one may be attempted, often
with success.

Alternatives to EBP in persistent cases include epidural Dextran 40
patching and surgical closure of the dural rent. Use of a Dextran 40 patch
instead of blood has not been extensively studied but was shown to have a
greater than 70 percent success rate in a series of 56 patients.[35] It may
prove to be an important option for specific patients such as Jehovah's
Witnesses who refuse blood products, but it does have the added risk of
causing an allergic reaction. Surgical closure of the dural rent is rarely
attempted but has relieved PLPH refractory to standard treatment.

Conclusion

After LP, headache associated with sitting or standing and relieved by
reclining is a common occurrence in young adults. The pathophysiology of
PLPH is related to persistent leakage of CSF, causing downward shift of the
brain and traction on its pain- sensitive structures. Dilatation of
intracranial vessels has also been implicated in its pathogenesis. Use of
smaller gauge needles has been demonstrated to decrease the incidence of
PLPH. Since PLPH is usually self-limited, conservative treatment such as
bedrest, hydration, and analgesia are tried first. If persistent, PLPH may
be alleviated with caffeine or EBP. The pathophysiology and treatment of
PLPH remain controversial. Recent advances in imaging techniques and
rigorous prospective studies should clarify much of this controversy.

References

Brownridge P. The management of headache in accidental dural puncture in
obstetric patients. Anesthesia and Intensive Care 1983;11:4-15.

Flaatten H, Rodt SA.,Vannes J, et al. Postdural puncture headache using 26-
or 29-gauge needles in young patients (abstract). Reg Anaesth 1988;11:5.

Carbaat PAT, van Crevel H. Lumbar puncture headache: Controlled study on
the preventive effect of 24 hour bed rest. Lancet 1981;1:1133-5.

Fernandez E. Headaches associated with low spinal fluid pressure. Headache
1990;30:122-8.

Fishman, R.`Examination of the cerebrospinal fluid: techniques and
complications.' in Cerebrospinal fluid in the diseases of the nervous
system, 2d ed. Philadelphia: W.B. Saunders Company, 1992.

Drippps RD, Vandam LD. Long-term follow-up of patients who received 10,098
spinal anesthetics. JAMA 1954;156:1486-91.

Raymond JR, Raymond PA. Post-lumbar puncture headache. Western Journal of
Medicine 1988;148:551-4.

Niall CT, Globerson JA, de Rosayro MA. Epidural blood patch for postdural
puncture headache: It's never too late. Anesthesia and Analgesia
1986;65:895-6.

Sciarra, D, Carter C. Lumbar puncture headache. JAMA 1952;148:841- 42.

Thorson G. Neurologic complications after spinal anesthesia. Acta Chir
Scand Suppl. 1947;121:34.

Brown BA, Jones OW. Prolonged headache following spinal puncture. Response
to surgical treatment. J Neurosurgery 1962;19:349-50.

Pool JL. Myeloscopy: intraspinal endoscopy. Surgery 1942;11:169-82.

Lieberman LM, Tourtellotte WW, Newkirk TA. Prolonged post lumbar puncture
cerebrospinal fluid leakage from the lumbar subarachnoid space demonstrated
by radioisotope myelography. Neurology 1971;21:925-29.

Grant R, Condon B, Hart I, Teasdale GM. Changes in intracranial CSF volume
after lumbar puncture and their relationship to post-L.P. headache. J
Neurol Neurosurg Psychiatry 1991;54:440-2.

Marshall J. Lumbar puncture headache. J Neurol Neurosurg Psychiatry
1950;13:71-4.

Kunkle EC, Ray BS, Wolff HG. Experimental studies on headache: analysis of
the headache associated with changes in intracranial pressure. Arch Neurol
Psychiatry1943;49:323-58.

Forbes HS, Nason GI. The cerebral circulation. Arch Neurol Psychiatry
1935;34:533-47.

Sechzer PH, Abel L. Post-spinal anesthesia headache treated with caffeine.
Part II: Intracranial vascular distention, a key factor. Curr Ther Res
1979;26:440-8.

Daniels AM, Sallie R. Headache, lumbar puncture, and expectation. Lancet
1981;i:1003.

Gobel H, Schenkl S. Post-lumbar puncture headache: the relation between
experimental suprathreshold pain sensitivity and a quasi- experimental
clinical pain syndrome. Pain 1990;40:267-78.

Gobel H, Klostermann H, Lindner V, Schenkl S. Changes in cerebral
haemodynamics in cases of post-lumbar puncture headache: a prospective
transcranial doppler ultrasound study. Cephalgia 1990;10:117-22.

Brocker RG. Technique to avoid spinal-tap headache. JAMA 1958;168:261-3.

Vilming ST, Schrader H, Monstad I. Post-lumbar puncture headache: the
significance of body posture. A controlled study of 300 patients. Cephalgia
1988;8:75-8.

Thornberry EA, Thomas TA. Posture and post-spinal headache. A controlled
trial in 80 obstetric patients. BR J Anaesth 1988;60:195-7.

Mihic Dn. Post-spinal headache and relationship of needle bevel to
longitudinal dural fibers. Reg Anaesth 1985;10:76-81.

Dittman M, Schafer HG, Ulrich J, Bond-Taylor W. Anatomical re- evaluation
of lumbar dura mater with regard to post-spinal headache. Effect of dural
puncture. Anaesthesia 1988;43:635-7.

Berrettini WH, Nurnberger JI. Epidural blood patch does not prevent
headache after lumbar puncture. Lancet 1987;i:856-7.

Heide W, Deiner HC. Epidural blood patch reduces the incidence of post
lumbar puncture headache. Headache 1990;30:280-1.

Sanborn TA, Gibbs HH, Brinker JA, Knopf WD, Kosinski EJ, Roubin GS. A
multicenter randomized trial comparing a percutaneous collagen hemostasis
device with conventional manual compression after diagnostic angiography
and angioplasty. J Am Coll Cardiol 1993;22:1273-9.

Tourtellotte WW. 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 1972;12:73-8.

Braune HJ, Huffman G. A prospective double-blind clinical trial, comparing
the sharp Quincke needle (22G) with an `atraumatic' needle (22G) in the
induction of PLPH. Acta Neurol Scand 1992;86:50-4.

Raskin NH. Lumbar puncture headache: a review. Headache 1990;30:197-200.

Usubiaga JE, Usubiaga LE, Brea LM, Goyena R. Effect of saline injections on
epidural and subarachnoid space pressures and relation to post-spinal
anesthesia headache. Anesth Analg 1967;46:293-6.

Gormley JB. Treatment of postspinal headache. Anesthesiology 1960;21:565-6.

Aldrete JA, Barrios-Alarcon J, Tapia D, Penas M, Lavine L. Treatment of
post-spinal headache with epidural Dextran 40. Anesthesiology 1987;67:A221.
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[ForumGal]

In a message dated 2/16/04 11:10:20 PM, minutus@yahoogroups.com writes:



Hi all,
I've pulled another "rem" possibility, above, from the piece Sheri Nakken
sent on PLPH. I had forgotten that coffee was also suggested by other folks
on the list. This is a remedy Robert can REALLY relate to -- he's a big
coffee fan. I'll tell him about it. Best, Margaret

[Robyn]

Just to mention that DeGroote in his Physical Examination and observation
in Homeopathy under Hypericum has headache after lumbar puncture. Out of
the whole list of Clinical observations, this is the only one highlghted.

Robyn

"Never forget that you are unique, like everyone else"
----------
In a message dated 2/16/04 11:10:20 PM, minutus@yahoogroups.com writes:

>

Hi all,
I've pulled another "rem" possibility, above, from the piece Sheri
Nakken
sent on PLPH. I had forgotten that coffee was also suggested by other
folks
on the list. This is a remedy Robert can REALLY relate to -- he's a big
coffee fan. I'll tell him about it. Best, Margaret

[Jayant Joshi]

Dear members,
Most of the persons receiving spinal anaesthesia suffer from spinal headaches esp. women undergoing LSCS. I 've treated many of them with ledum Pal 1M & Natr.Sulph 200 1 dse each with 80% women getting relief. U can try these drugs.
RJJ

ForumGal@aol.com wrote:

>

Hi Shannon -- this time waiting worked. Next time I'll offer him hypericum.
I'm assuming he's going to get spinal taps for his eyes again. One person
sent a constitutional suggestion, but I don't think he'll go for such treatment,
plus it really was an accute, evidently a common result of a tap. And here's
hoping this message doesn't appear on the list twice, as many of my messages
have been doing lately (sorry). Best, Margaret
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