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Historical Background
Lumbar puncture was introduced into clinical practice in early
1890s by Wynter and Quicke for the treatment of infectious meningitis
and hydrocephalus. Their initial report included a description of what
was most probably a PDPH.
1
However, it was the introduction of spinal
anesthesia by Bier in 1898, followed by rapid expansion of its use over
the next 2 years, that led to widespread recognition of the problem.
2
An
early report noted a headache rate of 50%, an incidence that is probably
accurate given the large bore needles in use at the time; the short
reported duration of 24 hours probably reects lack of adequate follow-
up.
3
The association between low cerebrospinal uid (CSF) pressure
and PDPH was noted in early work by Sicard
4
and Hosemann,
5
and the
work of Ingvar
6
demonstrated a persistent leak in cadavers with dural
puncture, which suggested that altered CSF hydrodynamics was the
most probable cause of the headache. The report of a persistent hole in
the arachnoid and dura by MacRoberts,
7
and the work by Heldt
8
that
INTERNATIONAL ANESTHESIOLOGY CLINICS
Volume 52, Number 3, 1839
r
2014, Lippincott Williams & Wilkins
18
|
www.anesthesiaclinics.com
REPRINTS: CURTIS L. BAYSINGER, MD, DEPARTMENT OF ANESTHESIOLOGY, VANDERBILT UNIVERSITY SCHOOL OF
MEDICINE, 4202 VUH VUMC, 1211 MEDICAL CENTER DR., NASHVILLE, TN 37232-7580. E-MAIL: CURTIS.L.
BAYSINGER@VANDERBILT.EDU
CSF leakage was common after meningeal puncture, added corroborat-
ing evidence to the theory. Although the relationship between headache
and low CSF pressure created by drainage of CSF was shown in the
1930s and 1940s by Masserman
9
and Kunkle et al,
10
it was the work of
Dripps and Vandam in the 1950s showing the direct relationship
between needle size (and thus the amount of CSF leaked) and the
incidence of PDPH that established low intracranial pressure as the
presumed root cause of the pain in PDPH.
Pathophysiology of PDPH
Persistent CSF leak is currently not disputed as the cause of
persistently low CSF pressure and reductions in CSF volume in patients
with PDPH.
11
CSF leak has been demonstrated with numerous
radionuclide studies, during epiduroscopy, and at surgery.
12
Loss of
CSF through the meningeal hole has been demonstrated to be greater
than human CSF production in patients with PDPH
13
and most often
occurs with cutting needles of 25G or larger.
14
Although the dura has been classically held as the most important layer
that is violated when CSF leak occurs,
15
it is the combination of the
arachnoid and dural layers that retain CSF.
16
The dura consists of multiple
layers of collagen and elastic bers that do not have a particular
orientation,
17
whereas the arachnoid is a 5- to 6-cell-thick layer with an
orientation along the longitudinal line of the spinal axis.
16
Thus, it may be
damage to the arachnoid/dura combination that causes the persistent CSF
leak, not the dura per se, and it is the arachnoids longitudinal orientation
that may explain the clinical observation that PDPH is more likely when
orienting a cutting spinal needle perpendicular to the axis of the spine.
18,19
The mechanism by which persistent CSF leak, low CSF pressure,
and the reduction in CSF volume create the headache associated with
PDPH is not clear.
1,12,20
The theory of low CSF pressure leading to
downward pull on pain-sensitive structures in the upright position is
supported by radiographic studies showing downward displacement of
intracranial structures and tension placed on meninges and blood
vessels known to contain stretch pain sensors.
20,21
Cranial nerve
entrapment by the sagging of the pons in patients with cranial nerve
palsies and PDPH has been demonstrated.
20,22
These symptoms are
relieved when the patient assumes the supine position.
20,22
In an
alternate theory, CSF loss leads to vasodilation as a consequence of the
Monroe-Kellie doctrine.
11
As the volume of CSF content is constant, the
decrease in CSF volume is accompanied by an increase in blood volume
and intracranial vessel stretching. This theory is supported by ultra-
sound and radiographic studies showing increases in intracranial blood
ow in patients with PDPH.
22,23
Pain bers within the arterial system
Accidental Dural Puncture and Postdural Puncture Headache 19
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may be signicant contributors along with those in venous structures. A
recent study that demonstrated a signicant correlation between a
decrease in the puslatility index of the cerebral circulation and the
severity of PDPH also suggests that arterial vessels are a signicant
source for pain.
24
Finally, increased hypersensitivity to substance P, low
levels of which are associated with a substantially increased risk for
PDPH, may be an important contributor to headache.
25
Further research into the mechanisms that underlie pain expression
is required. Not all patients with signicant meningeal rents get a
headache, which may be explained by random variations in lumbar
dural thickness; individuals with an ADP in an area of thicker dura may
be less likely to get PDPH because of less CSF leakage.
12
In addition, not
all patients with headaches have decreased CSF pressure, and the link
between the rate of CSF leak and headache severity is not well
established.
1
Conclusions
ADP with subsequent PDPH is a signicant source of patient
morbidity. A better understanding of how CSF leak causes headache and
why some patients develop PDPH after ADP while others do not is
needed. Although the association of greater risk for PDPH with patient
demographics and needle size is well established, studies of factors that
might reduce the risk for ADP and thus PDPH have only recently been
undertaken. At present there is no effective way to prevent PDPH after
ADP, although small trials involving neuraxial opioid and systemic
cosyntropin use and the observation that vaginal delivery is associated
with a higher incidence of PDPH than cesarean delivery need further
investigation. Intrathecal catheter use after ADP probably does not
reduce PDPH. EBP therapy is effective compared with conservative
measures. The surveys of obstetric anesthesia providers that show that
many institutions do not track patients with ADP, do not have
standardized protocols for ADP and PDPH management, and fail to
follow-up patients after EBP are worrisome.
32 Baysinger
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The author has no conict of interest to disclose.
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