MRI FINDINGS IN LUMBAR PUNCTURE HEADACHESYNDROME: ABNORMAL DURAL-MENINGEALAND DURAL VENOUS SINUS ENHANCEMENT

ROHIT BAKSHI, MD, LASZLO L. MECHTLER, MD,SAADAT KAMRAN, MD, EUGENE GOSY, MD,VERNICE E. BATES, MD, PETER R. KINKEL, MD,AND WILLIAM R. KINKEL, MD

Intracranial hypotension (IH) is a treatable cause of ened by sitting or standing. Symptoms may be persis-tent and may include other disabling features such aspersistent headaches. Persistent cerebrospinal fluid

(CSF) leak at a lumbar puncture (LP) site may cause nausea, tinnitus, and blurred vision; therefore, promptdiagnosis and treatment of LPHA is desirable. TheIH. We present postcontrast MRI of a patient with

post-lumbar-puncture headache (LPHA) showing ab- diagnosis of LPHA may not always be clear, particu-larly when the subsequent headache is similar to thenormal, intense, diffuse, symmetric, contiguous du-

ral-meningeal (pachymeningeal) enhancement of the headache that prompted the LP. A noninvasivemethod of confirming the diagnosis of LPHA wouldsupratentorial and infratentorial intracranial dura,

including convexities, interhemispheric fissure, ten- therefore be welcome.We present a patient with a headache syndrometorium, and falx. MRI also showed abnormal dural

venous sinus enhancement, a new finding in LPHA, following LP that was cured by an epidural bloodpatch. Pretreatment MRI showed marked intense ab-suggesting compensatory venous expansion. Thus,normal dural gadolinium enhancement resemblingIH and venodilatation may play a role in the devel-findings previously described in other headache syn-opment of LPHA. Elsevier Science Inc., 1999dromes associated with persistent leakage of cerebro-

KEY WORDS: spinal fluid (CSF). In addition, we present the newfinding of abnormal dural venous sinus enhance-Intracranial hypotension; Lumbar puncture; Meningeal

enhancement; MRI; Venous enhancement ment in LPHA, suggesting compensatory venousexpansion.

INTRODUCTIONCASE REPORT

Post-lumbar puncture headache (LPHA) may be ef-A 26-year-old woman presented to our center withfectively treated by various pharmacologic and inter-one day of severe headaches. The pain was bilateral,ventional means. The headache usually begins 48throbbing, and maximal at the vertex, radiating to thehours after lumbar puncture (LP) and is usually pos-neck and low back. The headache was unrelated totural. The pain is relieved upon reclining and wors-body or head position. She complained of similarchronic headaches previously that were not as severe

From the University at Buffalo (SUNY) School of Medicine and as the current headache. She had no nausea, visualBiomedical Sciences, Buffalo, NY, Departments of Neurology,

disturbances, or photophobia. A noncontrast headNeuroimaging, Lucy Dent Imaging Center, Buffalo, NY, and KaleidaHealth-Millard Fillmore Gates Circle Hospital, Buffalo, NY. CT scan was normal (not shown). A lumbar puncture

Address correspondence to: Rohit Bakshi, MD, Neuroscience demonstrated clear CSF with a normal opening pres-Center E-2, 100 High St., Buffalo, NY 14203; e-mail: rbakshi@buffalo.

sure, no cells, normal protein and glucose, and unre-eduReceived December 2, 1998; accepted February 23, 1999. markable routine cultures. She was treated with oral

CLINICAL IMAGING 1999;23:73–76 Elsevier Science Inc., 1999. All rights reserved. 0899-7071/99/$–see front matter655 Avenue of the Americas, New York, NY 10010 PII S0899-7071(99)00109-6

74 BAKSHI ET AL. CLINICAL IMAGING VOL. 23, NO. 2

FIGURE 1. Postcontrast CSE T1WI (Picker 1.5T) (A-axial; B-coronal). Abnormal, diffuse, symmetric, contiguous dural-meningeal (pachymeningeal) enhancement is noted. The enhancement involves much of the supratentorial and infratento-rial intracranial dural mater, including the convexities, interhemispheric fissure, tentorium, and falx. Abnormal leptomen-ingeal enhancement is absent, helping to exclude a subarachnoid inflammatory condition, such as leptomeningitis. Intenseenhancement and expansion of the superior sagittal sinus is also noted (arrows). The noncontrast MRI is unremarkable (notshown). Subsequent to this scan, an epidural blood patch cured the patient’s severe positional headaches.

analgesics and discharged from the emergency room. shown), revealing no venous thrombosis or subduralhygromas. Coronal images suggested mild inferiorTen days after LP, she presented to our outpatient

center complaining of recurrent headaches that had displacement of the cerebellar tonsils (not shown),although sagittal images were not obtained. Subse-begun 24 hours after the LP. The new headaches dif-

fered from her prior headaches, with associated nau- quent to this scan, these new headaches were curedin minutes by an epidural blood patch (performed atsea and worsening of pain upon sitting up and stand-

ing. These headaches were more generalized and the previous lumbar puncture site using 10 cc of au-tologous blood). During the next three years she con-much more severe than the previous ones. A brain

MRI scan (Figure 1), performed two weeks after LP, tinued to have rare bilateral headaches, diagnosed astension/migraine headaches, requiring intermittentshowed abnormal, diffuse, symmetric, contiguous

pachymeningeal enhancement of the supratentorial use of nonsteroidal anti-inflammatory medication.The severe positional generalized headaches did notand infratentorial intracranial dural mater, including

the convexities, interhemispheric fissure, tentorium, return. A repeat MRI scan was not performed.and falx. Abnormal leptomeningeal enhancementwas absent, helping to exclude a subarachnoid in-

DISCUSSIONflammatory condition. Intense enhancement andThe differential diagnosis of abnormal diffuse pachy-expansion of the superior sagittal sinus was also

noted. The noncontrast MRI was unremarkable (not meningeal enhancement includes infectious/inflam-

75MARCH/APRIL 1999 POST-LUMBAR-PUNCTURE HEADACHE

matory, neoplastic, and postoperative causes [1], each LPHA [5,7], in each of which abnormal dural en-hancement similar to the current case was noted. Inof which were excluded in this case by CSF data andone case, resolution of the abnormal dural enhance-longitudinal follow-up. The most likely cause of thement correlated with headache improvement [7].diffuse dural enhancement noted in our case was per-However, the current case is the first description ofsistent CSF leakage with intracranial hypotension (IH).abnormal venous expansion in LPHA. Taken together,Intracranial hypotension is an increasingly recognizedthese observations suggest that abnormal diffuse MRIneurologic syndrome, characterized by postural, bilat-dural-meningeal and venous sinus enhancement mayeral headaches that occur or worsen shortly afterbe helpful in identifying patients with LPHA, andassuming the upright position, and disappear ormay implicate IH, venous dilatation, or both, in theimprove after resuming the recumbent position [2].pathophysiology of LPHA [13]. However, repeat MRIAdditional symptoms may include nausea, vomiting,was not performed in our patient to confirm post treat-dizziness, photophobia, and changes in hearing. Thement resolution of the abnormal venous enhancement.syndrome of IH may be due to a variety of etiologies,Thus, our hypothesis regarding the association of ve-including spinal arachnoid cyst, LP, spinal anesthe-nous expansion and LPHA and potential pathophys-sia, cranial trauma/surgery, overdraining ventriculariologic relationship between the two requires furthershunts, or idiopathic/spontaneous mechanisms [3–9].study. Furthermore, the specificity and sensitivity ofMRI is emerging as a valuable method of recognizingthese MRI findings in the diagnosis of LPHA is notIH [3–8]. In agreement with our case, on postcontrastestablished and clinical correlation is essential.images, abnormal, intense, diffuse, symmetric, con-

We conclude that MRI may show characteristictiguous dural-meningeal (pachymeningeal) enhance-findings in LPHA related to IH due to a persistentment is commonly noted in IH. This enhancementCSF leak at the LP site. We hypothesize that theseusually involves much of the supratentorial and in-characteristic postcontrast MRI findings include bothfratentorial intracranial dural mater, including thedural meningeal and venous sinus enhancement.convexities, interhemispheric fissure, tentorium, andThis abnormal enhancement in LPHA is similar tofalx cerebri. However, abnormal leptomeningeal en-other forms of IH, and is consistent with the hypothe-hancement is normally absent. In more acute statessis that IH or venous dilatation is the cause of LPHA.of IH, abnormal enhancement and expansion of theIdentifying these characteristic MRI findings in thedural venous sinuses may also be noted, as they wereappropriate clinical setting may lead to better recog-in our case. This expansion of the dural venous si-nition and prompt treatment of LPHA, eliminatingnuses and pachymeningeal enhancement most likelythe need for further testing.relates to venous engorgement in response to low

CSF volume. This compensatory dural, venous, and,venular dilatation most likely acts to maintain ade-

We thank Evelyn Calderon, Kim Marie Malicki, James Pierotti,quate intracranial volume in the response to persis-Jennifer Ruske, Dolly Sadjak, Janice Tokarczyk, Joan Schurr, andtent CSF leakage [10].the MRI technologists for technical assistance and the staff of the

Our patient developed these abnormal MRI find- Kideney Health Sciences Library. Images of this case were pre-ings in the setting of LPHA, suggesting that IH may sented by the coauthors in a book chapter [13] and are used with

permission from the publisher.play a role in the pathophysiology of LPHA. Whetheror not IH, reduced CSF volume, or both, is the causeof LPHA has been debated [11]. Very large reduc-tions in intracranial CSF volume correlate with REFERENCESLPHA [12]. However, persistent leakage of CSF ap-

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