Chapter 40 Postmeningeal Puncture Headache and Spontaneous Intracranial Hypotension

Question 1

Postdural puncture headache (PDPH) caused by

Answer 1

the loss of cerebrospinal fluid (CSF) during the spinal anesthetic placement.

Question 2

Postdural puncture headache (PDPH) symptoms

Answer 2

worse in the recumbent
position and improved when standing. The headache is
characteristically occipital and/or frontal and always bilateral. Symptoms associated with PDPH can include neck
stiffness, nausea, vomiting, photophobia, diplopia, scalp paresthesia, upper and lower limb pain, auditory changes including tinnitus, hypoacousia, and can include mental status
changes

Question 3

Noninfectious arachnoiditis

Answer 3

with associated urinary and fecal incontinence, blindness,
subdural hematomas, intracerebral hemorrhage, and seizures. Headache commonly presents within the first 24 to
48 hr following a dural puncture; however, there have been many reports of headache presenting as much as 7 days later

Question 4

Pathophysiology of the PDPH

Answer 4

an intact skull the sum of the volumes of brain, CSF, and intracranial blood are constant and, therefore, with CSF volume loss, compensatory vasodilatation and venous hypervolemia occur, which may contribute to the headache.

Question 5

PDPHs are not commonly

associated with cervical punctures, why?

Answer 5

The higher the level of lumbar

puncture, the less the hydrostatic pressure at the dural puncture site

Question 6

The uncompensated loss of CSF leads to

Answer 6

a subarachnoid deficit of CSF and often a reduction in the subarachnoid pressure

Question 7

The normal CSF opening pressure in the horizontal position

Answer 7

70 to 180 mm H2O.

Question 8

The direct traction hypothesis states that

Answer 8

the reduction in CSF total
volume, especially in the spinal region, allows the brain to
shift caudally placing traction on the pain-sensitive intracranial structures and causing cerebral vasodilatation that produces the classic headache symptoms

Question 9

Pain-sensitive intracranial structures include

Answer 9

the dura, cranial nerves, and
bridging veins. The ophthalmic branch of the trigeminal
nerve, which refers pain to the frontal region, innervates
the bridging veins and the dura

Question 10

In addition to causing pain,

traction on bridging veins can cause

Answer 10

a tear in the dura, thus

leading to a potential subdural hemorrhage

Question 11

The posterior fossa structures are innervated by

Answer 11

the glossopharyngeal and vagus nerves that refer pain to the

occipital region.

Question 12

Traction of the vagus nerve

Answer 12

stimulate the chemoreceptor regions of the medulla, causing

nausea and vomiting.

Question 13

traction on the upper

three cervical nerves presents as

Answer 13

occipital, cervical, and

shoulder pain and stiffness.

Question 14

traction, or pressure on

the abducens nerve (CN VI)

Answer 14

generate pain, intracranial hypotension can cause nerve palsy with paralysis of the lateral rectus muscle; this can manifest as diplopia.

Question 15

oculomotor nerve (CN III) and
trochlear nerve (CN IV) palsies have been attributed to

Answer 15

intracranial hypotension due to brainstem compression and

ischemia

Question 16

diagnosis of a PDPH

Answer 16

based on the history of a dural puncture or possible dural puncture that worsens within 15 min after sitting or standing and improves within 15 min after lying down, with at least one symptom among neck stiffness, tinnitus, hypacusia, photophobia, and nausea.

Question 17

critical signs and symptoms may indicate concomitant intracranial pathology

Answer 17

The most important of these signs is a changing pattern
of the headache. HA becomes constant or localized unilaterally, or there is new-onset nausea and vomiting. Another critical change is increasing neurologic alterations, which include
sedation, seizures, and new-onset motor and/or sensory
deficits.

Question 18

the differential diagnosis

of PDPH with changing symptomatology should include

Answer 18

intracerebral hemorrhage, infection, eclampsia, and cerebral venous thrombosis.

Question 19

most unintentional dural punctures during epidural anesthesia occur with a

Answer 19

17-gauge Tuohy needle, which is a cutting needle

Question 20

The proposed mechanism behind difference between cutting and blunt tip needles causing PDPH

Answer 20

is that a blunt-tip needle
divides but does not disturb the continuity of the dural
fibers, versus a cutting tip needle, which cuts the dural
fibers.

Question 21

The orientation of the bevel to the dura during dural
puncture has been proposed as a factor affecting the
amount of CSF leakage and the incidence of PDPH.

Answer 21

reduction in the leakage of CSF if the bevel was parallel to

the long axis of the spinal cord

Question 22

Independent risk factors of PDPH

Answer 22

higher incidence
in women versus men, pregnancy, a higher incidence
in the age-group 20 to 50 years, and a higher incidence in patients with lower body mass index.There is also a higher incidence in patients with a headache prior to the dural puncture and a history of prior PDPH.

Question 23

Prevention of PDPH

Answer 23

needle size, needle tip,
and bevel orientation during dural/arachnoid puncture. The smallest needle with a noncutting tip oriented parallel
to the long axis of the spinal cord will reduce the incidence
of PDPH.

Question 24

Treatment options should be balanced with the understanding that

Answer 24

85% of PDPHs last less than 5 days, and, although rare, PDPHs can be associated with significant
morbidity

Question 25

Conservative treatment for PDPH

Answer 25

usually pharmacologic and noninvasive. Recumbent

bed rest relieves the symptoms of PDPH but has no therapeutic benefit. Aggressive hydration is a common therapy

Question 26

Medications reported beneficial in the treatment of PDPH include

Answer 26

methylxanthines, caffeine
and theophylline, sumatriptan, adrenocorticotropic hormone,
and corticosteroids

Question 27

Caffeine

Answer 27

a potent central nervous system stimulant, causes cerebral vasoconstriction. Caffeine is administered as an oral dose of 300 mg or intravenously as 500 mg in 500 to 1000 ml normal saline over 2 hr; the intravenous dose can be repeated over the next 2 to 4 hr

Question 28

Caffeine side effects

Answer 28

seizures, anxiety, and arrhythmias associated with its use

Question 29

Caffeine is contraindicated in patients with a

Answer 29

history of seizure disorder and in patients with pregnancy induced hypertension

Question 30

Epidural treatments for PDPH include

Answer 30

the administration of saline, colloids, fibrin glue, and blood. The gold-standard treatment for PDPH is an epidural blood patch (EBP).

Question 31

contraindications to an EBP

Answer 31

first is patient refusal in general or for a specific reason. In the case of concerns of Jehovah’s
Witnesses about blood transfusions, there are reports of alternative patching materials. Second, the patient’s coagulation
status must be assessed and judged to be within
normal limits to reduce the risk of an epidural hematoma.
Finally, it is not recommended to place an EBP in a septic patient, or through a localized infection or febrile patient due to the obvious concern of introducing bacteria into the epidural space

Question 32

mechanism of EBP

Answer 32

There is an initial early effect,
which occurs within minutes, secondary to compression of
the dura toward the cord and reduction in the intradural
volume. The EBP blood spreads both longitudinally and
circumferentially, thus enveloping the entire dural sac.
The reduction in the spinal intradural volume shifts the
CSF cephalad, thus resuspending the brain and reducing traction. this
intracranial shift in CSF also reduces the intracranial
blood volume and cerebral vasodilatation. A second, more lasting effect is due to
sealing of the dural/arachnoid tear with a gelatinous plug.
This sealing of the dural/arachnoid hole prevents further loss of CSF and allows for regeneration and restoration of the CSF volume. The plug acts as a bridge until permanent repair of the dural/arachnoid hole occurs

Question 33

Risk factors for EBP failure include

Answer 33

placement sooner
than 24 hr after dural puncture, using inadequate volumes
of autologous blood, and performance of the procedure
with residual lidocaine in the epidural space.

Question 34

How much blood to inject in EBP?

Answer 34

Selection of the level of placement should be guided by the observation that 15 ml of blood preferentially spreads cephalad six segments and caudad three segments, or one spinal segment per 1.6 ml of
blood. the ideal target volume
is 20 ml.

Question 35

If the patient complains

of excessive back or leg pain or pressure during injection

Answer 35

less volume can be placed.

Question 36

After the EBP, the patient should remain

Answer 36

supine with the legs slightly elevated

Question 37

Alternative dural patching materials include

Answer 37

epidural fibrin glue and epidural Dextran-40. may be an alternative in patients who are Jehovah’s Witnesses. Alternatives to the epidural blood patch include epidural saline bolus and/or infusions, and surgical exposure and repair of the dural tear.

Question 38

Surgical exposure and repair of a dural tear

Answer 38

a more invasive procedure generally reserved
for severe cases of PDPH that have not responded to
an EBP.

Question 39

Complications after an EBP

Answer 39

The most common
complication is mild low back and radicular pain following
the procedure that resolves spontaneously in a few days and
can be treated with nonsteroidal anti-inflammatory drugs
(NSAIDs). Other possible complications include epidural
hematoma, infection, and arachnoiditis due to unintentional subdural/subarachnoid injection of the blood

Question 40

Spontaneous intracranial hypotension (SIH)

Answer 40

a syndrome with symptoms similar to meningeal puncture headache but the patient has no previous history of meningeal puncture

Question 41

Complications of Spontaneous intracranial hypotension (SIH)

Answer 41

Often self-limiting, it can also result in a life threatening condition such a subdural hematoma.

Question 42

Risk Factors of Spontaneous intracranial hypotension (SIH)

Answer 42

This syndrome is usually suspected in a patient with
postural headache that occurs after a fall, trauma, whiplash,
exercise, or violent coughing

Question 43

Symptoms of Spontaneous intracranial hypotension (SIH)

Answer 43

Symptoms include headache,

nausea and vomiting, blurred vision, tinnitus, vertigo, and photophobia.

Question 44

suspect the presence of Spontaneous intracranial hypotension (SIH)

Answer 44

The triad of postural headache, low CSF pressure on diagnostic lumbar puncture, and meningeal enhancement on the MRI in a patient without any history of dural puncture

Question 45

Etiology of Spontaneous intracranial hypotension (SIH)

Answer 45

leakage of the CSF through a weakness of the spinal meninges such as meningeal diverticulum, or small tears in the root sleeves or perineural cysts (Tarlov cysts).

Question 46

Diagnosis of Spontaneous intracranial hypotension (SIH)

Answer 46

confirmed by low (CSF) pressure on diagnostic lumbar puncture and meningeal enhancement on the magnetic resonance imaging of the
cranium. Diagnostic lumbar puncture usually shows a low CSF pressure (below 60 cm H2O).

Question 47

Characteristic of CSF in Spontaneous intracranial hypotension (SIH)

Answer 47

The CSF protein, and red cell and white cell counts are

usually increased.

Question 48

The MRI of the cranium in SIH

Answer 48

shows meningeal
enhancement, subdural fluid collection, and caudal displacement of the cerebellar tonsils. Meningeal enhancement is usually thickest in patients with low intracranial
pressure and subdural fluid collections are only seen in
patients with meningeal enhancement. The spinal MRI of patients with SIH usually shows epidural or paraspinal
fluid collections and collapse of the dural sac.

Question 49

standard confirmatory

test in the diagnosis of SIH

Answer 49

radionuclide cisternography (RC). The presence of SIH is indirectly proven by the lack of ascent of the injected dye, rapid disappearance of the radioisotope from the CSF (within 4 hr) and the early appearance of the radioisotope in the urinary bladder.

Question 50

What accounts for the appearance of the radioisotope in the urinary bladder in radionuclide cisternography?

Answer 50

The radioisotope is presumed to leak through a meningeal
rent into the epidural space, subsequently taken up by the
epidural vessels and carried into the systemic circulation
and excreted by the kidneys.

Question 51

Disadvantages of Radionuclide Cisternography

Answer 51

inability of RC in demonstrating the site of leak, poor spatial resolution, its invasiveness, and possible radioisotope extravasation through the needle tract, resulting in inaccuracy in its interpretation

Question 52

Radionuclide cisternography ability to demonstrate the site of
leak

Answer 52

A Valsalva maneuver
may improve RC’s ability to demonstrate the site of
leak by increasing the subarachnoid pressure and improving
the chance of the CSF to actively leak and shown on
the RC.

Question 53

Techniques to demonstrate the site of leak.

Answer 53

CT myelography,

magnetic resonance myelography, and radioisotope myelocisternography

Question 54

treatment of choice for SIH

Answer 54

Epidural blood patch (EBP). If one or two EBPs are not effective, then a CT myelography should preferably
be performed before another EBP is performed to delineate
the vertebral level and the side of the CSF leak and
note the presence of multiple leaks. Surgical intervention is warranted if multiple EBPs
are ineffective and the patient’s condition deteriorates

Question 55

Why is EBP is less effective in SIH than in postdural puncture headache?

Answer 55

The lower success rate may be related to the injection of the blood away from the site of the CSF leak, the presence of multiple CSF leaks, and the rare occurrence of CSF leak at the anterior aspect of the dura or the nerve root sleeve. the site of leak can occur anywhere in the spine.