m


 It is over more than 100 years since the

description of our entity Post -dural puncture
headache (PDPH).
 PDPH typically begins within two days (following
spinal anaesthesia procedure) but may be delayed
for as long as two weeks and resolves
spontaneously within a few days.
 PDPH is a dull, permanent, non-throbbing pain of
the Fronto/Occipital region with involvement of the
neck and shoulders.
 The intensity ranges from mild to excruciating with
worst in upright position or during cough or
straining.
 There may be assosciated nausea,
photophobia,tinnitus,diplopia,cranial nerve palsy
and rarely cortical vein thrombosis,subarachnoid
hemorrhage or subdural hematoma.
 PDPH is postulated to be a consequence of one of
two non-mutually exclusive mechanisms, both
involving CSF leaking through a needle-induced
dural hole.

 One hypothesis is that the decrease in CSF

results in an increase blood volume from
vasodilation secondary to the Monro±Kellie
doctrine because the sum of the volumes of the
brain matter, CSF, and blood must remain the
same.
 The second hypothesis is that the decrease in
CSF volume results in sagging of the brain in the
cranial vault when the patient assumes the upright
position, which pulls on the falx cerebri, cerebral
blood vessels, and tentorium, resulting in
excruciating positional head pain.
1. Young age.
2. Female gender.
3. Pregnancy and labour.
4. Size of the needle.
5. Direction of the cutting needle bevel when
puncturing the dura.
 Proper diagnosis in the treatment of PDPH as
there is a strong possibility for misdiagnosis.

 Other possibilities such as

meningitis,subarachnoid hemorrhage has to be
ruled out as they do present with more or less
similar clinical features.
  Once diagnosis is established 24 hrs of
conservative therapy is recommended as there
occurs spontaneous resolution.
1. Bed rest in supine position.
2. Proper hydration.
3. Pharmacological agents -
paracetamol,caffeine,mild opiates.
4. Invasive treatment ± Epidural Blood Patch and
epidural administration of saline.
 ãhen EBP is used in patients suffering from
moderate to severe or prolonged PDPH, two
mechanisms likely bring about this effect.
 Formation of a plug in the dural defect, which
stops the loss of CSF.
 Simultaneous reduction in the volume of the
subarachnoid space through expansionof the
epidural space, which eliminates the relative CSF
deficiency.
 COMLICATIONS ± infection and aggrevation of
the headache.
 It is a structural analogue of gamma aminobutyric
acid.
 First use was as an antiepileptic as gabapentin
 Mechanism of action:
 Pregabalin binds to the alpha-2-delta subunit
of the N-type calcium channels, and modulates
calcium influx at nerve terminals.
 Henceforth reduces the release of several
neurotransmitters, including glutamate, noradrenaline,
serotonin, dopamine, and substance P.
  PHARMACOKINETICS
1. Bioavailability exceeds 90% irrespective of dose.
2. Half-life is 5.5-6.7 hours.
3. It is renally excreted of which 98% remains
unchanged in urine.
4. Does not undergo hepatic metabolism and is not
bound to plasma proteins.
5. Absorption of pregabalin is not saturable
(contrary to gabapentin),resulting in a linear
pharmacokinetics.
  THEREPEUTIC USES:
1. As an anti-epileptic
2. As an analgesic
(i). in neuropathic pain
(ii). has been recently found to be effective in
hyperalgesia.
(iii).an effective preop oral dose of pregabalin has found to
effective in post op pain relief and reduction in intra op
requirement of opiods.
 3. The exact mechanism of action of pregabalin is
not well understood but clinical experience and
has demonstrated its analgesic efficacy and safety
in PDPH.