Postdural Puncture Headache

Etiology

Causes of PDPH include dural puncture during a lumbar puncture (LP), diagnostic myelography, a subarachnoid (spinal) block, or following unintentional dural puncture from epidural anesthesia or injection for pain. Similar low-CSF pressure (intracranial hypotension) symptoms can also occur spontaneously or following craniotomy, placement of ventricular shunts, brain/spinal trauma, or spinal surgery. Risk factors for PDPH include dehydration, systemic illness, prior headaches, use of a large caliber or cutting needle, female gender, pregnancy, younger age, the use of a cutting or larger bore spinal needle, or inexperienced proceduralist.[4][5]

Epidemiology

PDPH is more common in women, younger ages (20 to 40 years), those with prior headaches (especially prior PDPH), and low body mass index. PDPH is uncommon in the elderly, likely because of brain atrophy. Other risk factors include caliber of the needle, use of a cutting needle, especially if inserted or rotated perpendicular to the long axis of the dural fibers, whereas use of a small caliber pencil-tipped needle decreases the risk, as does reinsertion of the stylet. The experience of the physician, the number of punctures, and removal of large amounts of CSF fluid may or may not be related to PDPH incidence. Positioning during (sitting versus decubitus) or after (bedrest or upright) the LP is unrelated to PDPH.

Incidence has been estimated to be quite variable in the literature, but may be approximately 10% to 40% of LP procedures, but can be as low as 2% when small gauge (less than or equal to 24 gauge) non-cutting needles are used. Symptoms of PDPH typically occur within 48 to 72 hours of LP but can be delayed for months afterward.[6][7]

Pathophysiology

PDPH occurs with low cerebrospinal fluid volume from a leak at the site of the dural puncture that exceeds spinal fluid production resulting in low CSF pressure (intracranial hypotension). Traction precipitates symptoms on pain-sensitive structures such as the meninges, blood vessels (especially veins and sagittal or transverse sinuses), cranial nerves, and upper cervical nerves. Sagging of the brain downward in the upright position contributes to orthostatic symptoms. Magnetic resonance imaging (MRI) studies have demonstrated evidence of vascular dilation (engorgement of venous sinuses, enhancement of meningeal layers and enlargement of the vascular pituitary gland) to compensate for the diminished volume of CSF. Since physical maneuvers which increase intracranial venous volume (such as coughing, laughing, Valsalva maneuver or internal jugular compression) worsen a headache suggesting that PDPH symptoms are at least in part due to the compensatory central venous dilation.[8][9]

History and Physical

Symptoms of PDPH include bilateral frontal or an occipital headache worse in the upright position, improved supine, associated with nausea, dizziness, neck pain, visual changes and occasionally tinnitus, hearing loss or radicular symptoms into the arms. Symptoms, especially headache, may also be worse with coughing and Valsalva maneuver, even in the supine position.

Physical examination is usually unremarkable, and the typical patient should not exhibit fever, meningismus, altered mentation or focal neurologic findings. In unusual cases, focal findings might include nystagmus, horizontal diplopia, facial numbness or palsy. Palsy of cranial nerve VI (Abducens) is an uncommon finding that may cause diplopia.  A firm continuous pressure in the abdomen may temporarily improve headache symptoms by indirectly increasing CSF pressure. Pressure on the jugular vein can worsen the headache symptoms. 

Evaluation

Diagnosis of PDPH is clinical, and laboratory studies or imaging are typically not necessary. Severe or persistent cases, especially those which no longer are alleviated with recumbent positioning should prompt neuroimaging to exclude subdural hematoma or cerebral or venous thrombosis.

Lumbar puncture in patients suspected of PDPH is discouraged (since this would likely exacerbate symptoms) but would demonstrate low to even negative (less than zero) CSF opening pressure. CSF may reveal white and red blood cells, elevated protein levels or xanthochromia.

In patients with long-standing PDPH or intracranial hypotension, MRI with gadolinium enhancement may demonstrate descent of the cerebellar tonsils (similar to a Chiari type 1 malformation), effacement of the basilar cisterns, thickening of the meninges, subdural fluid accumulation, venous sinus engorgement and an enlarged pituitary gland. These changes are reversible with treatment. Effacement of the basilar cisterns can also be seen on computerized tomography (CT) brain imaging and could be confused with subarachnoid hemorrhage. CT myelography or MRI of the spine can reveal the location and extent of CSF leak.[10][11]

Treatment / Management

Initial symptom management with simple analgesics, oral or intravenous hydration, and avoidance of the upright position may often be effective. PDPH symptoms can resolve spontaneously within one to two weeks in over two-thirds of patients. In many cases, symptoms are severe and persistent and require intervention.  

There is some evidence to support the use of oral or intravenous caffeine (300 mg to 500 mg in one L of intravenous fluid over one hour) for PDPH, although effects may be transient with high failure and recurrence rates.

Specific treatment of the dural leak may not be required in all cases since spontaneous resolution typically occurs within days to weeks. However, prolonged symptoms and complications have been reported when treatment is not pursued.

The idea of using blood to patch a hole in the dura was described in 1960 by Dr. James Gorley, a surgeon from Pennsylvania.  He described placing small volumes of blood outside the dura to treat PDPH, with very good results.  This later became the concept for the epidural blood patch.

Definitive treatment with an epidural blood patch is recommended when symptoms persist after conservative treatment. For post partum mothers recovering from childbirth and with a high degree of responsibility for caring for their child, a PDPH can be quite disabling.  Many physicians will treat early with an epidural blood patch in these situations.  For this procedure, 10 ml to 30 ml of autologous venous blood is injected by an anesthesiologist into the epidural space at the level of the prior procedure.  This is thought to create a "patch" over the dural puncture and decrease CSF leak, or simply increase the intracranial pressure.  Success rates are higher than 75% to 90%, especially if repeated but can rarely be complicated by back pain, meningeal irritation, radiculopathy, bulbar neuropathy, meningeal infection, hematoma or cauda equina syndrome.

A two to three-day continuous epidural saline infusion may be less effective and have fewer adverse effects than blood patch, but require an indwelling epidural catheter, bedrest, and hospitalization.  This is rarely done.

Multiple experimental treatments have been suggested, including oral or parenteral steroids, intramuscular adrenocorticotrophic hormone (ACTH), oral gabapentin, methylxanthines (through vasoconstriction and decreased central venous volume), such as IV aminophylline (5 mg/kg to 6 mg/kg over 20 min) or oral theophylline (300 mg every six to eight hours), and sumatriptan or other triptans. Several cases have reported the successful use of local injection of cyanoacrylate adhesive or fibrin glue for refractory cases.  Due to high success rates and low complication rates of the epidural blood patch, it remains the gold standard of therapy for PDPH. [12][13][14]

Frovatriptan use for 5 days before LP seems to reduce the incidence of post-LP headaches in some studies. sumatriptan did not show benefit when used for just 1 day before the LP.

Differential Diagnosis

• Caffeine withdrawal

• Intracranial pathology

• Meningitis

• Migraines

• Pneumocephalus

• Sinus related Preeclampsia

Complications

Rarely, prolonged or severe cases can result in cerebral venous thrombosis, subdural hematoma from traction on dural veins, seizures, hypopituitarism, syringomyelia, herniation, coma, and death.