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Mri findings in lumbar puncture headache syndrome
MRI FINDINGS IN LUMBAR PUNCTURE HEADACHE SYNDROME: ABNORMAL DURAL-MENINGEAL AND 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 persistent headaches. Persistent cerebrospinal fluid (CSF) leak at a lumbar puncture (LP) site may cause IH. We present postcontrast MRI of a patient with post-lumbar-puncture headache (LPHA) showing abnormal, intense, diffuse, symmetric, contiguous dural-meningeal (pachymeningeal) enhancement of the supratentorial and infratentorial intracranial dura, including convexities, interhemispheric fissure, tentorium, and falx. MRI also showed abnormal dural venous sinus enhancement, a new finding in LPHA, suggesting compensatory venous expansion. Thus, IH and venodilatation may play a role in the development of LPHA. Elsevier Science Inc., 1999 KEY WORDS:
Intracranial hypotension; Lumbar puncture; Meningeal enhancement; MRI; Venous enhancement
INTRODUCTION Post-lumbar puncture headache (LPHA) may be effectively treated by various pharmacologic and interventional means. The headache usually begins 48 hours after lumbar puncture (LP) and is usually postural. The pain is relieved upon reclining and worsFrom the University at Buffalo (SUNY) School of Medicine and Biomedical Sciences, Buffalo, NY, Departments of Neurology, Neuroimaging, Lucy Dent Imaging Center, Buffalo, NY, and Kaleida Health-Millard Fillmore Gates Circle Hospital, Buffalo, NY. Address correspondence to: Rohit Bakshi, MD, Neuroscience Center E-2, 100 High St., Buffalo, NY 14203; e-mail: rbakshi@buffalo. edu Received December 2, 1998; accepted February 23, 1999. CLINICAL IMAGING 1999;23:73–76 Elsevier Science Inc., 1999. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
ened by sitting or standing. Symptoms may be persistent and may include other disabling features such as nausea, tinnitus, and blurred vision; therefore, prompt diagnosis and treatment of LPHA is desirable. The diagnosis of LPHA may not always be clear, particularly when the subsequent headache is similar to the headache that prompted the LP. A noninvasive method of confirming the diagnosis of LPHA would therefore be welcome. We present a patient with a headache syndrome following LP that was cured by an epidural blood patch. Pretreatment MRI showed marked intense abnormal dural gadolinium enhancement resembling findings previously described in other headache syndromes associated with persistent leakage of cerebrospinal fluid (CSF). In addition, we present the new finding of abnormal dural venous sinus enhancement in LPHA, suggesting compensatory venous expansion. CASE REPORT A 26-year-old woman presented to our center with one day of severe headaches. The pain was bilateral, throbbing, and maximal at the vertex, radiating to the neck and low back. The headache was unrelated to body or head position. She complained of similar chronic headaches previously that were not as severe as the current headache. She had no nausea, visual disturbances, or photophobia. A noncontrast head CT scan was normal (not shown). A lumbar puncture demonstrated clear CSF with a normal opening pressure, no cells, normal protein and glucose, and unremarkable routine cultures. She was treated with oral 0899-7071/99/$–see front matter PII S0899-7071(99)00109-6
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FIGURE 1. Postcontrast CSE T1WI (Picker 1.5T) (A-axial; B-coronal). Abnormal, diffuse, symmetric, contiguous duralmeningeal (pachymeningeal) enhancement is noted. The enhancement involves much of the supratentorial and infratentorial intracranial dural mater, including the convexities, interhemispheric fissure, tentorium, and falx. Abnormal leptomeningeal enhancement is absent, helping to exclude a subarachnoid inflammatory condition, such as leptomeningitis. Intense enhancement and expansion of the superior sagittal sinus is also noted (arrows). The noncontrast MRI is unremarkable (not shown). Subsequent to this scan, an epidural blood patch cured the patient’s severe positional headaches.
analgesics and discharged from the emergency room. Ten days after LP, she presented to our outpatient center complaining of recurrent headaches that had begun 24 hours after the LP. The new headaches differed from her prior headaches, with associated nausea and worsening of pain upon sitting up and standing. These headaches were more generalized and much more severe than the previous ones. A brain MRI scan (Figure 1), performed two weeks after LP, showed abnormal, diffuse, symmetric, contiguous pachymeningeal enhancement of the supratentorial and infratentorial intracranial dural mater, including the convexities, interhemispheric fissure, tentorium, and falx. Abnormal leptomeningeal enhancement was absent, helping to exclude a subarachnoid inflammatory condition. Intense enhancement and expansion of the superior sagittal sinus was also noted. The noncontrast MRI was unremarkable (not
shown), revealing no venous thrombosis or subdural hygromas. Coronal images suggested mild inferior displacement of the cerebellar tonsils (not shown), although sagittal images were not obtained. Subsequent to this scan, these new headaches were cured in minutes by an epidural blood patch (performed at the previous lumbar puncture site using 10 cc of autologous blood). During the next three years she continued to have rare bilateral headaches, diagnosed as tension/migraine headaches, requiring intermittent use of nonsteroidal anti-inflammatory medication. The severe positional generalized headaches did not return. A repeat MRI scan was not performed. DISCUSSION The differential diagnosis of abnormal diffuse pachymeningeal enhancement includes infectious/inflam-
MARCH/APRIL 1999
matory, neoplastic, and postoperative causes [1], each of which were excluded in this case by CSF data and longitudinal follow-up. The most likely cause of the diffuse dural enhancement noted in our case was persistent CSF leakage with intracranial hypotension (IH). Intracranial hypotension is an increasingly recognized neurologic syndrome, characterized by postural, bilateral headaches that occur or worsen shortly after assuming the upright position, and disappear or improve after resuming the recumbent position [2]. Additional symptoms may include nausea, vomiting, dizziness, photophobia, and changes in hearing. The syndrome of IH may be due to a variety of etiologies, including spinal arachnoid cyst, LP, spinal anesthesia, cranial trauma/surgery, overdraining ventricular shunts, or idiopathic/spontaneous mechanisms [3–9]. MRI is emerging as a valuable method of recognizing IH [3–8]. In agreement with our case, on postcontrast images, abnormal, intense, diffuse, symmetric, contiguous dural-meningeal (pachymeningeal) enhancement is commonly noted in IH. This enhancement usually involves much of the supratentorial and infratentorial intracranial dural mater, including the convexities, interhemispheric fissure, tentorium, and falx cerebri. However, abnormal leptomeningeal enhancement is normally absent. In more acute states of IH, abnormal enhancement and expansion of the dural venous sinuses may also be noted, as they were in our case. This expansion of the dural venous sinuses and pachymeningeal enhancement most likely relates to venous engorgement in response to low CSF volume. This compensatory dural, venous, and, venular dilatation most likely acts to maintain adequate intracranial volume in the response to persistent CSF leakage [10]. Our patient developed these abnormal MRI findings in the setting of LPHA, suggesting that IH may play a role in the pathophysiology of LPHA. Whether or not IH, reduced CSF volume, or both, is the cause of LPHA has been debated [11]. Very large reductions in intracranial CSF volume correlate with LPHA [12]. However, persistent leakage of CSF appears to occur in patients after LP whether or not LPHA develops [11]. Furthermore, the finding of low CSF pressure is neither sensitive nor specific for LPHA [11]. It could be argued therefore that the abnormal enhancement noted in our case was an incidental result of the LP, but unrelated to the patient’s LPHA. However, a group of investigators recently showed that uncomplicated LP alone is unlikely to cause abnormal meningeal enhancement on MRI [1]; abnormal enhancement occurred in only 1% of cases. Only a few previously published case reports have shown abnormal MRI findings in patients with
POST-LUMBAR-PUNCTURE HEADACHE
75
LPHA [5,7], in each of which abnormal dural enhancement similar to the current case was noted. In one case, resolution of the abnormal dural enhancement correlated with headache improvement [7]. However, the current case is the first description of abnormal venous expansion in LPHA. Taken together, these observations suggest that abnormal diffuse MRI dural-meningeal and venous sinus enhancement may be helpful in identifying patients with LPHA, and may implicate IH, venous dilatation, or both, in the pathophysiology of LPHA [13]. However, repeat MRI was not performed in our patient to confirm post treatment resolution of the abnormal venous enhancement. Thus, our hypothesis regarding the association of venous expansion and LPHA and potential pathophysiologic relationship between the two requires further study. Furthermore, the specificity and sensitivity of these MRI findings in the diagnosis of LPHA is not established and clinical correlation is essential. We conclude that MRI may show characteristic findings in LPHA related to IH due to a persistent CSF leak at the LP site. We hypothesize that these characteristic postcontrast MRI findings include both dural meningeal and venous sinus enhancement. This abnormal enhancement in LPHA is similar to other forms of IH, and is consistent with the hypothesis that IH or venous dilatation is the cause of LPHA. Identifying these characteristic MRI findings in the appropriate clinical setting may lead to better recognition and prompt treatment of LPHA, eliminating the need for further testing.
We thank Evelyn Calderon, Kim Marie Malicki, James Pierotti, Jennifer Ruske, Dolly Sadjak, Janice Tokarczyk, Joan Schurr, and the MRI technologists for technical assistance and the staff of the Kideney Health Sciences Library. Images of this case were presented by the coauthors in a book chapter [13] and are used with permission from the publisher.
REFERENCES 1. Mittl RL, Yousem DM. Frequency of unexplained meningeal enhancement in the brain after lumbar puncture. AJNR 1994;15:633–638. 2. Rando TA, Fishman RA. Spontaneous intracranial hypotension: report of two cases and review of the literature. Neurology 1992;42:481–487. 3. Mokri B, Parisi JE, Scheithauer BW, Piepgras DG, Miller GM. Meningeal biopsy in intracranial hypotension: meningeal enhancement on MRI. Neurology 1995;45:1801–1807. 4. Good DC, Ghobrial M. Pathologic changes associated with intracranial hypotension and meningeal enhancement on MRI. Neurology 1993;43:2698–2700. 5. Pannullo SC, Reich JB, Krol G, Deck MDF, Posner JB. MRI changes in intracranial hypotension. Neurology 1993;43:929– 926.
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6. Hochman MS, Naidich TP, Kobetz SA, Fernandez-Maitin A. Spontaneous intracranial hypotension with pachymeningeal enhancement on MRI. Neurology 1992;42:1628–1630. 7. Bourekas EC, Lewin JS, Lanzieri CF. Postcontrast meningeal MR enhancement secondary to intracranial hypotension caused by lumbar puncture. J Comput Assist Tomogr 1995;19:299–301. 8. Mokri B, Krueger BR, Miller GM, Piepgras DG. Meningeal gadolinium enhancement in low-pressure headaches. J Neuroimaging 1993;3:11–15. 9. Marcelis J, Silberstein SD. Spontaneous low cerebrospinal fluid pressure headache. Headache 1990;30:192–196.
CLINICAL IMAGING VOL. 23, NO. 2
10. Fishman RA, Dillon WP. Dural enhancement and cerebral displacement secondary to intracranial hypotension. Neurology 1993;43:609–611. 11. Raskin NH. Lumbar puncture headache: a review. Headache 1990;30:197–200. 12. Grant R, Condon B, Hart I, Teasdale GM. Changes in intracranial CSF volume after lumbar puncture and their relationship to post-LP headache. J Neurol Neurosurg Psychiatry 1991;54:440–442. 13. Bakshi R, Lindsay BD, Kinkel PR. Brain magnetic resonance imaging in clinical neurology. In: Joynt RJ, Griggs RC (eds): Clinical Neurology. Philadelphia: Lippincott, Williams & Wilkins, 1999;1(4A):1–203.
Intracranial hypotension (IH) is a treatable cause of persistent headaches. Persistent cerebrospinal fluid (CSF) leak at a lumbar puncture (LP) site may cause IH. We present postcontrast MRI of a patient with post-lumbar-puncture headache (LPHA) showing abnormal, intense, diffuse, symmetric, contiguous dural-meningeal (pachymeningeal) enhancement of the supratentorial and infratentorial intracranial dura, including convexities, interhemispheric fissure, tentorium, and falx. MRI also showed abnormal dural venous sinus enhancement, a new finding in LPHA, suggesting compensatory venous expansion. Thus, IH and venodilatation may play a role in the development of LPHA. Elsevier Science Inc., 1999 KEY WORDS:
Intracranial hypotension; Lumbar puncture; Meningeal enhancement; MRI; Venous enhancement
INTRODUCTION Post-lumbar puncture headache (LPHA) may be effectively treated by various pharmacologic and interventional means. The headache usually begins 48 hours after lumbar puncture (LP) and is usually postural. The pain is relieved upon reclining and worsFrom the University at Buffalo (SUNY) School of Medicine and Biomedical Sciences, Buffalo, NY, Departments of Neurology, Neuroimaging, Lucy Dent Imaging Center, Buffalo, NY, and Kaleida Health-Millard Fillmore Gates Circle Hospital, Buffalo, NY. Address correspondence to: Rohit Bakshi, MD, Neuroscience Center E-2, 100 High St., Buffalo, NY 14203; e-mail: rbakshi@buffalo. edu Received December 2, 1998; accepted February 23, 1999. CLINICAL IMAGING 1999;23:73–76 Elsevier Science Inc., 1999. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
ened by sitting or standing. Symptoms may be persistent and may include other disabling features such as nausea, tinnitus, and blurred vision; therefore, prompt diagnosis and treatment of LPHA is desirable. The diagnosis of LPHA may not always be clear, particularly when the subsequent headache is similar to the headache that prompted the LP. A noninvasive method of confirming the diagnosis of LPHA would therefore be welcome. We present a patient with a headache syndrome following LP that was cured by an epidural blood patch. Pretreatment MRI showed marked intense abnormal dural gadolinium enhancement resembling findings previously described in other headache syndromes associated with persistent leakage of cerebrospinal fluid (CSF). In addition, we present the new finding of abnormal dural venous sinus enhancement in LPHA, suggesting compensatory venous expansion. CASE REPORT A 26-year-old woman presented to our center with one day of severe headaches. The pain was bilateral, throbbing, and maximal at the vertex, radiating to the neck and low back. The headache was unrelated to body or head position. She complained of similar chronic headaches previously that were not as severe as the current headache. She had no nausea, visual disturbances, or photophobia. A noncontrast head CT scan was normal (not shown). A lumbar puncture demonstrated clear CSF with a normal opening pressure, no cells, normal protein and glucose, and unremarkable routine cultures. She was treated with oral 0899-7071/99/$–see front matter 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 duralmeningeal (pachymeningeal) enhancement is noted. The enhancement involves much of the supratentorial and infratentorial intracranial dural mater, including the convexities, interhemispheric fissure, tentorium, and falx. Abnormal leptomeningeal enhancement is absent, helping to exclude a subarachnoid inflammatory condition, such as leptomeningitis. Intense enhancement and expansion of the superior sagittal sinus is also noted (arrows). The noncontrast MRI is unremarkable (not shown). Subsequent to this scan, an epidural blood patch cured the patient’s severe positional headaches.
analgesics and discharged from the emergency room. Ten days after LP, she presented to our outpatient center complaining of recurrent headaches that had begun 24 hours after the LP. The new headaches differed from her prior headaches, with associated nausea and worsening of pain upon sitting up and standing. These headaches were more generalized and much more severe than the previous ones. A brain MRI scan (Figure 1), performed two weeks after LP, showed abnormal, diffuse, symmetric, contiguous pachymeningeal enhancement of the supratentorial and infratentorial intracranial dural mater, including the convexities, interhemispheric fissure, tentorium, and falx. Abnormal leptomeningeal enhancement was absent, helping to exclude a subarachnoid inflammatory condition. Intense enhancement and expansion of the superior sagittal sinus was also noted. The noncontrast MRI was unremarkable (not
shown), revealing no venous thrombosis or subdural hygromas. Coronal images suggested mild inferior displacement of the cerebellar tonsils (not shown), although sagittal images were not obtained. Subsequent to this scan, these new headaches were cured in minutes by an epidural blood patch (performed at the previous lumbar puncture site using 10 cc of autologous blood). During the next three years she continued to have rare bilateral headaches, diagnosed as tension/migraine headaches, requiring intermittent use of nonsteroidal anti-inflammatory medication. The severe positional generalized headaches did not return. A repeat MRI scan was not performed. DISCUSSION The differential diagnosis of abnormal diffuse pachymeningeal enhancement includes infectious/inflam-
MARCH/APRIL 1999
matory, neoplastic, and postoperative causes [1], each of which were excluded in this case by CSF data and longitudinal follow-up. The most likely cause of the diffuse dural enhancement noted in our case was persistent CSF leakage with intracranial hypotension (IH). Intracranial hypotension is an increasingly recognized neurologic syndrome, characterized by postural, bilateral headaches that occur or worsen shortly after assuming the upright position, and disappear or improve after resuming the recumbent position [2]. Additional symptoms may include nausea, vomiting, dizziness, photophobia, and changes in hearing. The syndrome of IH may be due to a variety of etiologies, including spinal arachnoid cyst, LP, spinal anesthesia, cranial trauma/surgery, overdraining ventricular shunts, or idiopathic/spontaneous mechanisms [3–9]. MRI is emerging as a valuable method of recognizing IH [3–8]. In agreement with our case, on postcontrast images, abnormal, intense, diffuse, symmetric, contiguous dural-meningeal (pachymeningeal) enhancement is commonly noted in IH. This enhancement usually involves much of the supratentorial and infratentorial intracranial dural mater, including the convexities, interhemispheric fissure, tentorium, and falx cerebri. However, abnormal leptomeningeal enhancement is normally absent. In more acute states of IH, abnormal enhancement and expansion of the dural venous sinuses may also be noted, as they were in our case. This expansion of the dural venous sinuses and pachymeningeal enhancement most likely relates to venous engorgement in response to low CSF volume. This compensatory dural, venous, and, venular dilatation most likely acts to maintain adequate intracranial volume in the response to persistent CSF leakage [10]. Our patient developed these abnormal MRI findings in the setting of LPHA, suggesting that IH may play a role in the pathophysiology of LPHA. Whether or not IH, reduced CSF volume, or both, is the cause of LPHA has been debated [11]. Very large reductions in intracranial CSF volume correlate with LPHA [12]. However, persistent leakage of CSF appears to occur in patients after LP whether or not LPHA develops [11]. Furthermore, the finding of low CSF pressure is neither sensitive nor specific for LPHA [11]. It could be argued therefore that the abnormal enhancement noted in our case was an incidental result of the LP, but unrelated to the patient’s LPHA. However, a group of investigators recently showed that uncomplicated LP alone is unlikely to cause abnormal meningeal enhancement on MRI [1]; abnormal enhancement occurred in only 1% of cases. Only a few previously published case reports have shown abnormal MRI findings in patients with
POST-LUMBAR-PUNCTURE HEADACHE
75
LPHA [5,7], in each of which abnormal dural enhancement similar to the current case was noted. In one case, resolution of the abnormal dural enhancement correlated with headache improvement [7]. However, the current case is the first description of abnormal venous expansion in LPHA. Taken together, these observations suggest that abnormal diffuse MRI dural-meningeal and venous sinus enhancement may be helpful in identifying patients with LPHA, and may implicate IH, venous dilatation, or both, in the pathophysiology of LPHA [13]. However, repeat MRI was not performed in our patient to confirm post treatment resolution of the abnormal venous enhancement. Thus, our hypothesis regarding the association of venous expansion and LPHA and potential pathophysiologic relationship between the two requires further study. Furthermore, the specificity and sensitivity of these MRI findings in the diagnosis of LPHA is not established and clinical correlation is essential. We conclude that MRI may show characteristic findings in LPHA related to IH due to a persistent CSF leak at the LP site. We hypothesize that these characteristic postcontrast MRI findings include both dural meningeal and venous sinus enhancement. This abnormal enhancement in LPHA is similar to other forms of IH, and is consistent with the hypothesis that IH or venous dilatation is the cause of LPHA. Identifying these characteristic MRI findings in the appropriate clinical setting may lead to better recognition and prompt treatment of LPHA, eliminating the need for further testing.
We thank Evelyn Calderon, Kim Marie Malicki, James Pierotti, Jennifer Ruske, Dolly Sadjak, Janice Tokarczyk, Joan Schurr, and the MRI technologists for technical assistance and the staff of the Kideney Health Sciences Library. Images of this case were presented by the coauthors in a book chapter [13] and are used with permission from the publisher.
REFERENCES 1. Mittl RL, Yousem DM. Frequency of unexplained meningeal enhancement in the brain after lumbar puncture. AJNR 1994;15:633–638. 2. Rando TA, Fishman RA. Spontaneous intracranial hypotension: report of two cases and review of the literature. Neurology 1992;42:481–487. 3. Mokri B, Parisi JE, Scheithauer BW, Piepgras DG, Miller GM. Meningeal biopsy in intracranial hypotension: meningeal enhancement on MRI. Neurology 1995;45:1801–1807. 4. Good DC, Ghobrial M. Pathologic changes associated with intracranial hypotension and meningeal enhancement on MRI. Neurology 1993;43:2698–2700. 5. Pannullo SC, Reich JB, Krol G, Deck MDF, Posner JB. MRI changes in intracranial hypotension. Neurology 1993;43:929– 926.
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6. Hochman MS, Naidich TP, Kobetz SA, Fernandez-Maitin A. Spontaneous intracranial hypotension with pachymeningeal enhancement on MRI. Neurology 1992;42:1628–1630. 7. Bourekas EC, Lewin JS, Lanzieri CF. Postcontrast meningeal MR enhancement secondary to intracranial hypotension caused by lumbar puncture. J Comput Assist Tomogr 1995;19:299–301. 8. Mokri B, Krueger BR, Miller GM, Piepgras DG. Meningeal gadolinium enhancement in low-pressure headaches. J Neuroimaging 1993;3:11–15. 9. Marcelis J, Silberstein SD. Spontaneous low cerebrospinal fluid pressure headache. Headache 1990;30:192–196.
CLINICAL IMAGING VOL. 23, NO. 2
10. Fishman RA, Dillon WP. Dural enhancement and cerebral displacement secondary to intracranial hypotension. Neurology 1993;43:609–611. 11. Raskin NH. Lumbar puncture headache: a review. Headache 1990;30:197–200. 12. Grant R, Condon B, Hart I, Teasdale GM. Changes in intracranial CSF volume after lumbar puncture and their relationship to post-LP headache. J Neurol Neurosurg Psychiatry 1991;54:440–442. 13. Bakshi R, Lindsay BD, Kinkel PR. Brain magnetic resonance imaging in clinical neurology. In: Joynt RJ, Griggs RC (eds): Clinical Neurology. Philadelphia: Lippincott, Williams & Wilkins, 1999;1(4A):1–203.