Letters to the Editor

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We read with interest the recent paper of Bezov et alregarding greater occipital nerve block in the managementof postdural puncture headache (PDPH).1 Among varioustherapeutic strategies employed to relieve this debilitatingheadache recently, several case reports have been publishedwhereby bilateral greater occipital nerve blocks have beenproposed as an alternative technique to the epidural bloodpatch.1-3 It has also been advocated as a second step afterconservative measures have failed.1 Furthermore, it hasbeen reported to be successful in providing complete head-ache relief in 68.4% of cases after 1 to 2 blocks, and 31.6%after 4 attempts.2

We appreciate that symptom relief is very important fornursing mothers, but in doing so, are we missing something?

PDPH has been a vexing problem to anesthetists sincethe first reports of August Bier in 1898. Headache is thoughtto be primarily due to loss of cerebrospinal fluid (CSF) withresultant intracranial hypotension. There occurs downwardtraction on pain-sensitive structures of the brain along withcompensatory vasodilatation of cerebral blood vessels.4 It ismore accurate to call the clinical spectrum of symptomsthat follow dural puncture, the postdural puncture syn-

drome, rather than PDPH, which falsely implies the head-ache as the only manifestation.5

Neglected dural leak may lead to a chronic headache,or even more seriously, it may lead to a number of neuro-logical complications, such as cranial nerve palsy. Rarely itmay lead to subdural hematoma and peripartum seizures.6

Focusing on headache as the primary treatment targetfails to address the primary pathophysiology of unabatedCSF leak. Unresolved headaches following a lumbar punc-ture should prompt further investigation.7 If the headacheresolves and the pathology persists, investigations could bedelayed with dire consequences. So targeting the headachealong with the underlying pathology represents a rationalapproach.

Application of an epidural blood patch may, therefore,be a safe way to not only treat typical postlumbar punctureheadache but also to prevent subdural hematoma afterlumbar puncture.6

To understand this rather complicated issue, we coulduse the analogy of compartmental syndrome in the lowerlimb where a nerve block can mask the pain, which canresult in even a worse outcome. Likewise, the cases wherePDPH was not relieved by hydration, simple analgesia,and other conservative therapeutic techniques are prob-ably the cases where more serious sequelae can occurdue to a persistent CSF leak, and an early bloodpatch probably acts as a safeguard against such seriouscomplications.

Faisal Rasool, MBBS, FCARCSI, FRCAUniversity Hospitals Leicester – Anaesthesia,

Leicester, UKKausik Dasgupta, MBBS, MD, FRCA

University Hospitals Leicester – Anaesthesia,Leicester, UK

REFERENCES

1. Bezov D, Ashina S, Lipton R. Post-dural puncture head-ache: Part II – Prevention, management, and prognosis.Headache. 2010;50:1482-1498.

2. Naja Z, Al-Tannir M, El-Rajab M, Ziade F, Baraka A. Nervestimulator-guided occipital nerve blockade for postduralpuncture headache. Pain Pract. 2009;9:51-58.

3. Matute E, Bonilla S, Girones A, Planas A. Bilateral greateroccipital nerve block for post-dural puncture headache.Anaesthesia. 2008;63:557-558.

4. Hannerz J, Ericson K, Bro Skejo HP. MR imaging withgadolinium in patients with and without post-lumbar punc-ture headache. Acta Radiol. 1999;40:135-141.

Conflict of Interest: The authors report no conflict of interest.

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5. Kuczkowski KM. Post-dural puncture headache in obstetricpatient: An old problem – New solutions. Minerva Anest-esiol. 2004;70:823-830.

6. Vos PE, de Boer WA, Wurzer JA, van Gjin J. Subduralhematoma after lumbar puncture: Two case reports andreview of the literature. Clin Neurol Neurosurg. 1991;93:127-132.

7. Gaucher DJ Jr, Perez JA Jr. Subdural hematomafollowing lumbar puncture. Arch Intern Med. 2002;162:1904-1905.

Posterior Reversible EncephalopathySyndrome: A Syndrome Not Present inthe ICHD-IIhead_2142 826..828

Posterior reversible encephalopathy syndrome(PRES), originally named “reversible posterior leukoen-cephalopathy syndrome,”1 describes a syndrome character-ized by neuroimaging findings of reversible vasogenicedema without infarction. It is evidenced by seizures,encephalopathy, visual symptoms, and headache.2

The term PRES was later adopted to replace “revers-ible posterior leukoencephalopathy syndrome” as a resultof the widespread employment of magnetic resonanceimaging (MRI) and, in particular, as a result of the studyingof the brain with diffusion weight imaging in routine exami-nation. Consequently, lesions were found to be rarely iso-lated to the posterior parieto-occipital white matter, ofteninvolving the cortex, and less frequently frontal lobes, basalganglia, and brainstem.3

This important syndrome could be secondary to manydiseases: preeclampsia and eclampsia, impaired renal func-tion, abrupt arterial hypertension, transplantation, sepsis,and exposure to immunosuppressants. It is described inan autoimmune disease setting (ie, systemic lupus erythe-matosus, Wegener’s granulomatosis, systemic sclerosis,polyarteritis nodosa). The distinctive role of autoimmunedisease in the pathophysiology of PRES is often associatedwith concurrent hypertension, renal disease, or with the useof immunosuppressants.3

Published literature on PRES is scant, and generallyrestricted to case reports and imaging studies. Publicationsdealing with clinical phenotypes are few.This limited body ofwork, however, suggests the symptoms, in decreasing order,are: seizures, disturbed vision, headache, altered mentalfunction, nausea and vomiting, and brainstem symptoms.1

Headache is among the pivotal clinical features. It ispresent in about 50% of cases, but specific research on thistopic is lacking, and its clinical features are reported withlittle detail.

In the second edition of the International Classifica-tion of Headache Disorders (ICHD-II), the only referenceto this syndrome is within point 1.5.3 – regarding the differ-ential diagnosis with persistent aura without infarction:“Exclude posterior leukoencephalopathy by diffusion MRIamong other things.4”

In chapter 6 of the ICHD-II, where PRES could beinserted, specifically at point 6.7.3, we find a syndrome:Headache attributed to benign (or reversible) angiopathy of

the central nervous system.

This syndrome, which can be due to causes different toPRES, appears to be rarer than PRES, and it is character-ized by a headache with thunderclap-like characteristics. Itpresents a different pathogenetic mechanism, generallywith a benign prognosis, and could be considered amongdifferential diagnoses with PRES.5

The purpose of this correspondence is not to outlinethe specific PRES classification criteria, incorporating clini-cal and neuroimaging parameters. A precise classificationcould be outlined only after both a comprehensive exami-nation of the existing literature and specific research onthe topic. We were prompted to write after a recent obser-vation in our clinic of PRES in a puerpera with migraine-like headache as an isolated clinical symptom. We wish tohighlight that PRES is not specifically considered in theICHD-II. We also recommend its promotion to possibleinsertion in the ICHD-II appendix after proper studiesdefining the associated clinical headache features.

Ferdinando Maggioni, MD; Sara Pompanin, MD;Giuseppe Maggioni; Giorgio Zanchin, MD

Department of Neurosciences, University of Padua,Padua, Italy

REFERENCES

1. Roth C, Ferbert A. The posterior reversible encephalopathysyndrome: What’s certain, what’s new? Pract Neurol.2011;11:136-141.

2. Hinchey J, Chaves C, Appignani B, et al. A reversible pos-terior leukoencephalopathy syndrome. N Engl J Med.1996;334:494-500.

3. Fugate JE, Claassen DO, Cloft HJ, Kallmes DF, Kozak OS,Rabinstein AA. Posterior reversible encephalopathy syn-drome: Associated clinical and radiologic findings. MayoClin Proc. 2010;85:427-432.Conflict of Interest: The authors report no conflict of interest.

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4. Headache Classification Subcommittee of the InternationalHeadache Society. The international classification of head-ache disorders: 2nd edition. Cephalalgia. 2004;24(Suppl.1):9-160.

5. Ducros A, Bousser MG. Reversible cerebral vasoconstric-tion syndrome. Pract Neurol. 2009;9:256-267.

Are the ICHD-II Criteria forHemicrania Continua Too Restrictive?head_2144 827..829

We read with great interest the recent discussion of ourpaper by Drs. Taylor, Kaniecki, and Landy.1 We agree thatthe current International Classification of Headache Disor-ders 2nd Edition (ICHD-II) criteria for hemicrania con-tinua (HC) are too strict. Twenty-nine of our patientssuffered from unilateral headaches which were unclassifi-able according to ICHD-II. None of these had an underly-ing causative extra- or intracranial lesion. In 17 patients(59%) headache was paroxysmal, and in 12 (41%) it wascontinuous. Details of the latter subgroup follow.

Criterion A (headache for >3 months) was met in 2 ofthe 12 patients. Criterion B ((1) unilateral pain withoutside-shift; (2) daily and continuous; (3) moderate intensitywith exacerbations) was fulfilled in all 12 patients. CriterionC (at least 1 ipsilateral autonomic feature during exacerba-tions) was met in 5 patients; and criterion D (absoluteresponse to 75 mg of indomethacin b.i.d.) in 3. Two patientsmet all criteria except A, and both of these exhibited anabsolute response to indomethacin (D). Six patients failedto meet 2 criteria, namely A and D in 3, C and D in 2 and A,and C in 1. Only the last benefited from an absoluteresponse to indomethacin. The remaining 4 patients did not

fulfill 3 of the criteria A–D, and none of these demonstratedan absolute response to indomethacin.

Revising the ICHD-II criteria for HC would increasethe number of HC diagnoses in our 12 patient subgroup to6. Relaxing criterion A to a duration of 2 weeks instead of 3months would have allowed us to diagnose HC in 2 patients.Revision of criteria C and D to require either the presenceof autonomic symptoms or complete response toindomethacin, but not necessarily both would have allowedthe diagnosis of HC in an additional 4 patients.

Our patient series supports previously published data2

highlighting the poor sensitivity of the current ICHD-IIcriteria of HC. Even though our sample size is small, thedata suggest that relaxation of criteria A, C, and D mayincrease the sensitivity of the ICHD-II scheme. Of course, itis likely that increased sensitivity would come at the cost ofdecreased specificity.3

Acknowledgments: The authors thank Stephen L.

McClellan, MD, PhD, for proofreading the manuscript.

Stefan Seidel, MD; Christian Wöber, MDDepartment of Neurology, Medical University of Vienna,

Vienna, Austria

REFERENCES

1. Seidel S, Lieba-Samal D, Vigl M, Wober C. Clinical featuresof unilateral headaches beyond migraine and cluster head-ache and their response to indomethacin. Wien KlinWochenschr. 2011;123:536-541.

2. Cittadini E, Goadsby PJ. Hemicrania continua: A clinicalstudy of 39 patients with diagnostic implications. Brain.2010;133:1973-1986.

3. Shultz EK. Analytical goals and clinical interpretation oflaboratory procedures. In: Burtis CA, Ashwood ER, eds.Tietz Textbook of Clinical Chemistry. Philadelphia, PA: WBSaunders Co.; 1994:496-498.Conflict of Interest: The authors report no conflict of interest.

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