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- Vinod K GuptaPublished on: 13 April 2016
- Miguel A ReinaPublished on: 13 April 2016
- Published on: 13 April 2016Post-dural puncture headache: pathophysiological mechanisms
- Vinod K Gupta, Physician
Show MoreDear Editor
Reina and co-workers found no difference in morphological features of mounted cadaveric dura mater and arachnoid membranes punctured by disposable 22 gauge Quincke needle with the bevel either in the parallel or in the transverse position.[1]
None of the factors linked to post-dural puncture headache (PDPH) including young age, female sex with lower body mass index, pregnancy or previous PDPH hi...
Show LessDear Editor
Reina and co-workers found no difference in morphological features of mounted cadaveric dura mater and arachnoid membranes punctured by disposable 22 gauge Quincke needle with the bevel either in the parallel or in the transverse position.[1]
None of the factors linked to post-dural puncture headache (PDPH) including young age, female sex with lower body mass index, pregnancy or previous PDPH history[2-4] can be synthesized into a logical hypothesis that predictably explains the particular susceptibility of this sub-population. The concept that size of the dural puncture and PDPH are directly related has evolved the consensus recommendation to use thin, non-traumatic tip needle or the Quincke needle.[4] This recommendation must, however, be balanced against the failure of Tourtellotte et al. to show the relation between smaller needle size and lower frequency of PDPH in their prospective series.[2] Remarkably, Tourtellotte et al. also commented on:
(i) the great variability of PDPH frequency for the same needle size between different authors;
(ii) the lack of conclusive evidence regarding other risk factors; and
(iii) variation in actual frequencies of PDPH in individual series ranging from 0 to 18%.[2] The more recent study of Kuntz et al. confirms that PDPH continues to affect patients and concern neurologists.[3,4]Unpredictable development of PDPH as well as the relative rarity of the headache in spinal anesthesia, obstetric or non-obstetric,[2,4] stimulates lateral thinking. With a “U” shaped or semi-lunar shaped dura- arachnoid lesion (DAL) caused by the Quincke needle,[1] continuous cerebrospinal fluid (CSF) leakage reflects failure of the clean cut edge of the dural flap to effectively seal the DAL. Unlike the dura mater, the inflamed arachnoid membrane can proliferate and is prominently adhesive, which singular tissue properties underlie the frequent development of lumbar spinal arachnoiditis. Whereas simple re-approximation of the cut dural flap to its original position may not stop leakage of CSF, the locally-traumatized and adhesive arachnoid probably seals spontaneously most dural punctures. PDPH might, therefore, be consequential to failure of the arachnoid to seal off the DAL. Quincke needles lessen but do not eliminate the “tent effect” [1] that stretches both the dura mater as well as the arachnoid membrane at the site of the DAL. Due to different biomechanical and tensile properties, rupture of the arachnoid membrane may not always follow the precise anatomical pattern of the dural hole created during lumbar puncture (LP); also partial loss of arachnoid lamina at the site of the DAL is possible. Variable degrees of retraction of the arachnoid membrane at the site of the DAL, as can be seen in the scanning electron microscope pictures presented by Reina et al,[1] may also contribute to prolonged or persistent CSF leakage. If this explanation is truly representative of the biomechanics of the DAL created by LP, use of the same LP needle is unlikely to create identical DAL in different patients; the unpredictability of PDPH in terms of incidence and duration might thus be rationalized.
Low incidence of PDPH in spinal anesthesia 2 intriguingly suggests that spinal anesthesia confers a degree of protection from PDPH. Tourtellotte et al. speculated that the incidence of PDPH might be markedly lessened if patients undergoing diagnostic LP were “treated” like patients undergoing spinal anesthesia.[2] In this context, the clinical circumstances surrounding the LP could also be important. Non-obstetric spinal anesthesia is usually preceded by CT- myelograms (and MRI or both) for evaluating underlying clinical conditions possibly correctable by surgery. Myelography is associated with arachnoiditis.[5] Post-myelography, the subclinically inflamed arachnoid may be primed to seal a subsequent DAL more efficiently. Notably, Tourtellotte et al. found the lowest incidence of PDPH for nonobstetric spinal anesthesia (average frequency was 13%).[2]
Modification of patient-related risk factor(s) to reduce the frequency of PDPH in patients undergoing diagnostic LP has been suggested. 4 No such modifiable factor is, however, currently known. Although the mean CSF values for opening pressure, CSF cell count, and protein concentration were all normal in 44 full-term pregnant women undergoing spinal anesthesia for delivery,[6] pregnancy and the immediate postpartum period are associated with the lowest CSF densities.[7] The less dense the CSF, the greater are the chances of leakage through a DAL. Inducing maximally tolerated dehydration to increase the viscosity of the CSF may possibly reduce susceptibility of women undergoing obstetric spinal anesthesia to develop PDPH. Moreover, dehydration aggravates severity of arachnoiditis induced by aqueous myelography and fluid repletion is recommended before myelography.[8] Paradoxically, dehydration prior to obstetric spinal anesthesia or diagnostic LP may stimulate the arachnoid lamina to seal the DAL more efficiently. Finally, the average frequency of PDPH in obstetric spinal anesthesia was only 18%.[2] Endorphin activity in CSF increases at term pregnancy,[9] indicating development of an adaptive antinociception that possibly reduces incidence of PDPH.
References
1. Reina MA, López A, Badorrey V, De Andrés JA, Martin S. Dura- arachnoid lesions produced by 22 gauge Quincke spinal needles during a lumbar puncture. J Neurol Neurosurg Psychiatry 2004;75:893-7.
2. Tourtellotte WW, Haerer AF, Heller GL, et al. Post-lumbar puncture headaches. Springfield, IL: Charles C. Thomas, 1964.
3. Kuntz KM, Kokmen E, Stevens JC, Miller P, Offord KP, Ho MM. Post- lumbar puncture headaches: experience in 501 consecutive procedures. Neurology 1992; 42: 1884–7.
4. Evans RW, Armon C, Frohman EM, et al. Assessment: prevention of post–lumbar puncture headaches: report of the therapeutics and technology assessment subcommittee of the American Academy of Neurology. Neurology 2000;55:909-14.
5. Eldevik OP, Haughton VM. Risk factors in complications of aqueous myelography. Radiology 1978;128:415-6.
6. Davis LE. Normal laboratory values of CSF during pregnancy. Arch Neurol 1979;36:443.
7. Richardson MG, Wissler RN. Density of lumbar cerebrospinal fluid in pregnant and nonpregnant humans. Anesthesiology 1996;85:326-30.
8. Eldevik OP, Haughton VM. The effect of hydration on the acute and chronic complications of aqueous myelography. An experimental study. Radiology 1978;129:713-4.
9. Lyrenas S, Nyberg F, Willdeck-Lund G, Lindstrom L, Lindberg B, Terenius L. Endorphin activity in cerebrospinal fluid prior to elective cesarean section and in early puerperium. Ups J Med Sci 1987;92:37-45.
Conflict of Interest:
None declared. - Published on: 13 April 2016Post-dural puncture headache: pathophysiological mechanisms.
- Miguel A Reina, MD, Staff
- Other Contributors:
- Virginia Badorrey, Andrés López and José Antonio De Andrés.
Show MoreDear Editor,
We thank Dr. Gupta [1] for his interest in our article [2]. His comments [1] are very interesting when we consider how complex the postdural puncture headache (PDPH) physiopathology can be.
Different and multiple factors contribute in a resulting PDPH, which can justify the differences in the intensity and duration of the headache. Factors such as technique [3-6], doctor’s experience, patien...
Show LessDear Editor,
We thank Dr. Gupta [1] for his interest in our article [2]. His comments [1] are very interesting when we consider how complex the postdural puncture headache (PDPH) physiopathology can be.
Different and multiple factors contribute in a resulting PDPH, which can justify the differences in the intensity and duration of the headache. Factors such as technique [3-6], doctor’s experience, patient’s medical history and the surroundings of the surgical procedure or the neurological diagnosis. The dura-arachnoid lesion (DAL) and the cerebrospinal fluid (CSF) leakage are only isolated influencing factors among the whole involved.
The DAL features, size and later sealing will depend on the needle used, its tip design and its manufacture properties. Needles of the same diameter and tip design made by different manufacturers cannot behave in the same way. We also find from practice that brand new needles can also have its tip damaged or even metallic split edges on its surface [7].
These inadvertent defects are widely evident when the same microscopy technique used to study the DAL lesion is employed. The viscosity and elasticity properties of the dural and arachnoid lamina might not be the same on every patient therefore affecting the final sealing of the lesion.
In general, the arachnoid lesion takes longer to close than the dural lesion. In some patients, it is also possible that a small fragment of the arachnoid lamina can get displaced when performing the puncture, making more difficult its closure and being more likely to result in a PDPH.
The hypothesis based on the arachnoid inflammatory response to the puncture, mentioned by Gupta, can be an accepted hypothesis to explain the arachnoid lesion closure. The same argument can be used to explain the fact that pencil point needles result in less frequency of PDPH than Quincke needles of same diameter although the size of the lesion is similar in both [3].
Whitacre needles result in lesions with more irregular edges when compared to the “C” shaped clean edge lesions caused by Quincke needles. The irregular and torn edges may develop to a local inflammation helping to effectively seal the DAL [3].
When considering the arachnoid and dural lamina lesion, the complete sealing of the arachnoid lesion could be the most important. The dural laminae are very permeable and they are made of collagen and some elastic fibres that provide mechanical support to the dural sac. The arachnoid lamina, on the other hand, is mainly made of arachnoid cells, its mechanical resistance is poor but it behaves as a semi permeable membrane [8-10]. Its sealing would stop the CSF to leak out into the dural sac.
Another aspect to consider is the formation of small cranial subdural haematomas after CSF hypotension following a lumbar puncture [11]. When CSF is lost the encephalon becomes less floating, it is pulled down tractioning the cranial arachnnoid lamina. The exerted traction can result in rupture of the small blood vessels crossing the subdural compartment that leads to small haematoma formation that can be missed on the MRI, although they could be important enough to affect the intensity and duration of the PDPH.
When the needle crosses the dural sac at spinal level, it can also perforate small vessels of the inside of its thickness. Apart from considering the distance between the vessels, puncture site and needle gauge, fortune will play decisive in puncturing the blood vessels. If so, a small haematoma results along the same DAL that will contribute to its closure [12-13]. Changes on the encephalon position during a CSF hypotensive episode will also affect the normal cerebrospinal fluid hydrodynamics. CSF leakage is associated with encephalon prolapse and a reduced size of the subarachnoid cisterns. Under these circumstances, different encephalic areas such as the aqueduct of Sylvius can slightly change their location and modify the tissue distribution. In some patients, these changes might alter the normal CSF circulation. We do not really know if that could modify the headache’s nature.
Another possible factor in relation with the PDPH is the vasodilatation of some encephalic areas secondary to CSF loss (Monroe-Kelly’s theory). The degree of reactive vasodilatation can vary between patients and may depend on previous medical history. Both cerebral MRI and Doppler Ultrasound are non-invasive methods to study the PDPH physiopathology and the effectiveness of its treatment. MRI provides images such as meningeal enhancement with gadolinium captation in all sections, changes on the aqueduct of Sylvius and cerebellar amygdala position, hygromas and subdural haematomas, increased size on the hypophysis, decreased size of the arachnoid cisterns and cerebral ventricles [14].
There is a close relationship between the clinical signs and the radiological features. In fact, these features disappear once the PDPH is resolved. Doppler Ultrasound, on the other hand, provides information on the flow dynamics. Determination of the velocity of the ophthalmic vein flow might be useful in assessing clinical responses to different PDPH treatments [15].
The development of PDPH remains an ongoing problem. The incidence of PDPH is greater after diagnostic lumbar puncture when 20G or 22G needles are used in order to measure CSF pressure and to obtain great volume samples. The incidence is lower after spinal anaesthesia using 25G or 27G needles. In some cases, the arachnoid injection of local anaesthetic agents together with opioid analgesics might contribute as well. Many unresolved questions about PDPH that still need further research.
References
(1). Gupta VK. Post-dural puncture headache: pathophysiological mechanisms. http://jnnp.bmjjournals.com/cgi/eletters/75/6/893#169
(2). Reina MA, Lopez A, Badorrey V, De Andres JA, Martin S. Dura- arachnoid lesions produced by 22 gauge Quincke spinal needles during a lumbar puncture. J Neurol Neurosurg Psychiatry 2004; 75: 893-7.
(3). Reina MA, de Leon-Casasola OA, Lopez A, De Andres J, Martin S, Mora M. An in vitro study of dural lesions produced by 25-gauge Quincke and Whitacre needles evaluated by scanning electron microscopy. Reg Anesth Pain Med 2000; 25: 393-402.
(4). Reina MA, Lopez A, Manzarbeitia F, Amador V, Goxencia I, Olmedilla MC. Skin fragments carried by spinal needles in cadavers. Rev Esp Anestesiol Reanim 1995; 42: 383-5.
(5). Reina MA, Lopez-Garcia A, Dittmann M, de Andres JA, Blazquez MG. Iatrogenic spinal epidermoid tumors. A late complication of spinal puncture. Rev Esp Anestesiol Reanim 1996; 43: 142-6.
(6). Reina MA, Lopez Garcia A, Aguilar JL, Palacios Martin R. Electron microscopic analysis of particles from surgical gloves and their possible introduction into the epidural space during epidural anesthesia. Rev Esp Anestesiol Reanim 1999; 46: 60-6.
(7). López A, Reina MA, Machés F, De Leon Casasola O, De Andrés JA, García Trapero J. Electrón microscopy in quality control of equipment used in regional anesthesia. Tech Reg Anesth Pain Management 2002; 6: 172-179.
(8). Reina MA, Dittmann M, Lopez Garcia A, van Zundert A. New perspectives in the microscopic structure of human dura mater in the dorsolumbar region. Reg Anesth 1997; 22: 161-6.
(9). Reina MA, Lopez-Garcia A, Dittmann M, de Andres JA. Structural analysis of the thickness of human dura mater with scanning electron microscopy. Rev Esp Anestesiol Reanim 1996; 43: 135-7.
(10). Reina MA, Lopez-Garcia A, Dittmann M, de Andres JA. Analysis of the external and internal surface of human dura mater with scanning electron microscopy. Rev Esp Anestesiol Reanim 1996; 43: 130-4.
(11). Reina MA, Lopez A, Benito-Leon J, Pulido P, Maria F. Intracranial and spinal subdural hematoma: a rare complication of epidural and subarachnoid anestesia. Rev Esp Anestesiol Reanim 2004; 51: 28-39.
(12). Reina MA, De Leon Casasola O, Lopez A, De Andres JA, Mora M, Fernandez A. The origin of the spinal subdural space: ultrastructure findings. Anesth Analg 2002; 94: 991-5.
(13). Reina MA, Lopez A, De Andres JA. Origin of spinal subdural hematomas: a postmortem anatomical study. Rev Esp Anestesiol Reanim 2004; 51: 240-6.
(14). Reina MA, Alvarez-Linera J, Lopez A, Benito-Leon J, De Andres JA, Sola RG. Magnetic resonance in dural post-puncture headache in patient with cerebrospinal fluid hypotension. Rev Esp Anestesiol Reanim 2002; 49: 89-100.
(15). Chen CC, Luo CL, Wang SJ, Chen CM, Fuh JL, Lin SH. Colour Doppler imaging for diagnosis of intracranial hypotension. Lancet 1999; 354: 826- 829.
Conflict of Interest:
None declared.