© 2007 World Institute of Pain, 1530-7085/07/$15.00Pain Practice, Volume 7, Issue 1, 2007 47–52

Blackwell Publishing IncMalden, USAPPRPain Practice1530-70852007 World Institute of Pain? 2007714752Original ArticleIntracranial Hypotension Following Motor Vehicle AccidentHUNTOON AND WATSON

Address correspondence and reprint requests to: Marc A. Huntoon,MD, Department of Anesthesiology, Mayo Clinic College of Medicine, 200First Street SW, Rochester, MN 55905, U.S.A. Tel: +1 507-284-9700; Fax:+1 507-284-0120; E-mail: huntoon.marc@mayo.edu.

CASE STUDIES FROM THE MAYO CLINICSection Editor: Marc A. Huntoon, MD

Intracranial Hypotension Following Motor Vehicle Accident:

An Overlooked Cause of Post-Traumatic Head and Neck Pain?

Marc A. Huntoon, MD*; James C. Watson, MD†

Departments of *Anesthesiology and †Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota, U.S.A.

� Abstract: Motor vehicle accidents result in many patientswith chronic head and neck pain, some of which meet thecriteria for a “whiplash syndrome.” The cervical zygapophy-sial joint synovium, muscular, and ligamentous strains andother anatomical sites are often implicated in the pathophys-iology of these cases. Some patients have a characteristicconstellation of vague neurological symptoms, often includ-ing headache, posterior neck discomfort, dizziness, nausea,and sometimes visual changes. Recently presented researchhas noted that some patients who have a whiplash-associ-ated disorder have imaging findings consistent with a low-pressure cerebrospinal fluid leak. Some of these patientsrespond favorably to high-volume epidural blood patch. Thefollowing case presentation focuses on the differential diag-nosis of a post-traumatic headache syndrome, specific imag-ing findings, and treatment strategies. �

Key Words: whiplash, cerebrospinal fluid leak, headache,cervical zygapophysial joint pain, epidural blood patch

INTRODUCTION

According to the Quebec Classification of Whiplash-Associated Disorders (WAD), the following definitionwas advocated: “Whiplash is an acceleration–decelera-tion mechanism of energy transfer to the neck. It mayresult from rear-end or side impact motor vehicle colli-sions, but can also occur during diving or other mis-haps. The impact may result in bony or soft-tissueinjuries (whiplash injury), which in turn may lead to avariety of clinical manifestations (Whiplash-AssociatedDisorders).”1 The task force further proposed a gradedsystem of classification of these disorders to aid in futureepidemiological and clinical studies. In the classification,patients are graded according to the following scale:Grade 0 patients have no physical signs and no neckcomplaints; Grade 1 patients present with neck com-plaints of pain and stiffness, but without physical signs;Grade 2 patients have neck complaints and signs ofmusculoskeletal injury such as point tenderness ordecreased range of motion; Grade 3 patients have neckcomplaints associated with concomitant neurologicalsigns, such as weakness, sensory loss, or reflex changes;and Grade 4 patients have an objective fracture ordislocation evident on imaging and examination. Allpatients in any grade may manifest additional symptoms

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including headache, memory loss, dizziness, tinnitus,deafness, dysphagia, and temporomandibular jointpain. Patients with Grade 2 musculoskeletal findings arethought to have had neck muscular or ligament sprainsand potentially bleeding or injury of cervical facet cap-sules. Those patients with Grade 3 neurological signsare thought to have a multitude of possible differentialdiagnoses, including cervical intervertebral disc hernia-tions, mechanical injuries to nervous structures, orsecondary irritation by bleeding or inflammation. Inpatients presenting with WAD with neurological signs,various synonyms are used, such as cervicobrachialgia,cervicogenic headache, cervicalgia, or headaches of cer-vical origin.1

A previous study of healthy volunteers examined cer-vical spine motion using cineradiography. The subjectsexperienced a controlled rate (1.1 m/s) 10° descent in astandard car seat, without head restraint, mounted ona sled rail system that was crashed into a paddeddamper. In one example, at impact, the C5 inferiorarticular facet moved inferiorly toward the C6 superiorfacet surface and produced impingement, as opposed tothe normal gliding motion of extension. With significantconcentrated bending forces in the lower cervicalmotion segment, the authors proposed that the zygapo-physial synovial joint surface (fold) might be injuredduring this impingement causing neck pain (facet syn-ovial fold impingement syndrome).2 Lord et al.3 hadexamined the prevalence of cervical zygapophysial jointpain in patients with greater than 3-month-durationneck pain symptoms after a whiplash injury. Patientswere subjected to controlled random order, double-blinded local anesthetic, and saline sham blocks todetermine which whiplash patients responded to cervi-cal zygapophysial joint blockade. In the Lord et al.study, headache as the major symptom was used toscreen patients for third occipital nerve blocks and dif-ferentiate from those patients with neck pain predomi-nance. Those patients either had no headache or hadneck pain greater than headache, thus received blocksof the medial branches of the cervical dorsal rami atlevels below C2/3. Patients with headache as their mostdominant symptom responded 50% of the time to thirdoccipital nerve block, indicating the C2/3 zygapophysialjoint as a pain generator. History and symptoms thusare important in the proper work-up and selection oftreatment(s) for patients with WAD or other postmotorvehicle accident head and neck pain syndromes. Differ-entiating which symptom predominates, that is, head orneck pain, may be an aid to choosing proper therapy.

CASE REPORT

A 60-year-old white female nurse was involved in amotor vehicle accident in which she was a front-seatpassenger in a collision with a large deer. By 24 hoursafter the collision, she manifested a severe occipitalheadache. The patient initially treated herself conserva-tively with acetaminophen and ibuprofen. After outsidephysician evaluations, she presented approximately3 weeks later to the Mayo Clinic Neurology departmentwith ongoing headache and diplopia (characterized bydivergence insufficiency), and now minimal upper cer-vical discomfort. Symptoms were markedly positionalin character with near-resolution of symptoms whilesupine, but increasing headache intensity while stand-ing, and highest intensity in the sitting position. She hada sensation of “fullness” in her ears. The patient’s pastmedical history was one of generally good health,although she had been treated for primary biliary cir-rhosis (proven by liver biopsy), hereditary hemachroma-tosis, and asthma. Medications included: Ursodiol750 mg orally every morning and 500 mg at night;Prilosec 20 mg orally every day; ibuprofen 400 mg threetimes daily, aspirin 325 mg orally each day; acetami-nophen 1000 mg twice daily; Advair 100/50 as neededevery morning; calcium 1000 mg each day; andalbuterol inhaler 2 puffs every 6 h as needed for herasthma. A review of systems was negative for chronicspinal or head pain. The patient remembered only min-imal head movement at the time of the impact, no lossof consciousness, and did not strike her head on thewindshield or dashboard. Physical examination demon-strated a pulse of 76, blood pressure of 166/80 mm Hg,and an initial numerical rating pain scale of 5/10. Sheappeared to be in no distress and was well-developed,well-nourished with a weight of 82 kg and height of172.4 cm. Pupils were equal and approximately 4 mm.Extraocular movements were intact. Her neck wassupple without point tenderness or decreased range ofmotion. There were no meningeal tension signs. Her gaitwas normal and no weakness, sensory loss, or otherneurological changes were evident. Prior to arrival atMayo Clinic, the patient had been evaluated with mag-netic resonance imaging (MRI) at an outside facility.The MRI was evaluated by Neurology and Radiologynoting “brain sag,” and diffuse continuous non-nodularpachymeningeal enhancement without leptomeningealenhancement. Cervical MRI demonstrated markedengorgement of cervical epidural venous plexus, andevidence of marked extradural cerebrospinal fluid (CSF)

Intracranial Hypotension Following Motor Vehicle Accident • 49

below the sixth cervical level, consistent with a nonlo-calized dural leak. The patient had not been imagedbelow the cervical level. She was diagnosed with anintracranial hypotension/dural CSF leak syndrome. Shewas empirically scheduled with the Pain Medicine inter-ventional suite for lumbar epidural blood patch, andadvised to report back earlier if symptoms worsened. Ifshe did not respond to lumbar blood patch, the planwas to proceed first with low cervical epidural bloodpatch, followed by myelography with computed tomog-raphy (CT) and neurosurgical referral to more preciselydefine the location of the leak. Three days later, thepatient received a fluoroscopically guided epiduralblood patch via an L5/S1 interlaminar midline ap-proach. A total of 16 mL of 20 mL total withdrawnsterile autologous blood was slowly and incrementallyinjected until significant lower back pressure limitedadditional injection volume. One week after the injec-tion the patient had noted dramatic improvement in herpositional occipital headache and she was advised tofollow up as needed thereafter.

DISCUSSION

Although our patient did not have a “whiplash syn-drome” in the classic sense (because she had a front–end collision), she suffered a post-traumatic extraduralleak with multiple manifestations of ongoing loss of CSFvolume. Patients with WAD often have long-term com-plaints of neck pain, but occasionally also have symp-toms that could be related to an underlying neurologicaldisorder such as headache, visual and auditory changes,dizziness, and nausea. Most recent research has focusedon the cervical zygapophysial joints, but some patientstreated with joint injections and radiofrequency neuro-tomies do not receive benefit. Because of the nonspecificnature of many of these complaints, and frequent asso-ciated psychological findings, patients are often assumedto be seeking compensation or to have significant painamplification because of psychological distress. A recentevaluation of patients who received radiofrequencymedial branch neurotomies for cervical whiplash syn-drome contradicts these assumptions. Patients in thestudy demonstrated improvements in visual analog painscores of both litigant and nonlitigant patients at 1 year(nonlitigants 2.9 points vs. 4.0 points in litigants,P = 0.05). Thus, the evidence did not support litigantsas malingering or receiving other secondary gainsrelative to their whiplash syndrome.4 Additionally, inanother randomized placebo-controlled double-blindstudy of whiplash patients receiving radiofrequency

neurotomies of cervical medial branches, both prepro-cedural and postprocedural psychological assessmentswere conducted with the Symptom Checklist-90-Revised (SCL-90-R). Criteria used by the psychologistsfor definite resolution of psychological distress includednormalization of previously elevated subscales, orreturn to normal of somatization scales and at leastseven of the eight other subscales. In this study, allpatients who had relief of their pain manifested resolu-tion of psychological distress. Conversely, all but onepatient with ongoing pain continued to display psycho-logical distress.5

A recent abstract discussed the use of epidural bloodpatch therapy for chronic WAD. The authors studied 66chronic WAD patients with symptoms of 3 months orgreater. Patients were evaluated with radioisotope (RI)cisternography to discern the presence or absence ofCSF leaks. Interestingly, 37 of the 66 patients hadabnormal RI cisternograms suggesting that a dural tearmight be present in some of these patients and thelumbar spine was the most common area involved. Theauthors also noted improvement in symptoms of head-ache, dizziness, visual impairment, and nausea aftertreatment with high-volume epidural blood patches.6

MRI IMAGING

Our patient displayed many of the classic findings asso-ciated with CSF depletion. Mokri has recently outlinedthe classic MRI findings of low cerebrospinal pressure/volume headaches in an excellent review.7

Based on the Monro-Kellie hypothesis, in a situationwhere the patient has an intact skull, assuming brainmatter volume is constant, a loss of volume (from anextradural leak in the spine) in the cranial vault mustbe compensated by volume from elsewhere. This com-pensation can be in the form of subdural fluid collec-tions, or an increase in venous blood. Thus, whenevaluating the head MRI, the cerebral ventricles willoften appear smaller, and the brain may be noted to sagor descend within the cranial vault, with cerebellar ton-sillar crowding in the posterior fossa manifesting aChiari-1-like appearance (Figure 1). One should see evi-dence of pachymeningeal enhancement with gadoliniumcontrast administration. The enhancement of the pachy-meninges will be linear and non-nodular, as well astypically bilateral and uninterrupted (Figure 2). Thepachymeninges do not have a blood–brain barrier, whileleptomeninges do, thus venous hyperemia may be seenin the pachymeninges. Further, one may see dilation ofthe cerebral venous sinuses (Figure 2), and flattening or

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Figure 1. Sagittal T1 MRI head. Left: normal. Right (case): there is evidence of cerebellar tonsillar descent and crowding in theforamen magnum (arrow) and obliteration of the prepontine subarachnoid cistern (dashed arrow) characteristic of “brain-sag.”

Figure 2. Coronal T1 + gadolinium contrast MRI head. Left (case): diffuse, continuous, non-nodular pachymeningeal enhancement(multiple short arrows) is apparent. Note that there is no leptomeningeal (arachnoid and pia) enhancement within the sulci. Thereis engorgement of the venous sinuses (superior sagittal sinus demonstrated—long thin dashed arrow) and the ventricular system isvery small. Right: (a case of chronic basilar predominant meningitis related to sarcoidosis): note the nodular and patchy characterof the enhancement surrounding the brainstem and scattered in several sulci (multiple thick arrows).

Intracranial Hypotension Following Motor Vehicle Accident • 51

inferior displacement of the optic chiasm and promi-nence/engorgement of the pituitary gland.

In the spine MRI, there may be evidence of extradu-ral fluid collections (Figures 3 and 4) and swelling of theepidural venous plexus. MRI is not sufficient to find theactual site of leak, as the spinal fluid spread commonlyextends to cover several levels.7

CONCLUSION

This case is an excellent example of a post-traumaticCSF leak occurring in association with new-onset posi-tional headache, diplopia, and auditory complaints. Theexact area of CSF leak was not clear, as the patientimproved with an empiric lumbar epidural blood patch,and did not require further definitive investigations suchas CT myelogram or RI cisternogram. When patientscomplain of neck pain with little or no associated head-ache or neurological signs, the source of pain may likelybe in the cervical facet joints, or cervical muscles andligaments. While the exact incidence of CSF leaks inWAD is unknown, and is likely low, it appears that MRIevaluation with gadolinium contrast administrationshould at least be considered in the differential diagnosisof headache-predominant postwhiplash patients.

Key Points

• Multiple studies have demonstrated that the zyg-apophysial joints may be implicated as pain gen-erators in postwhiplash injured patients withpredominately neck pain, and approximately50% of patients have pain relief after selectiveblockade of cervical medial branches below C2/3.

• Patients with predominately headache symptomspost whiplash also have a prevalence of approx-imately 50% of C2/3 zygapophysial joint pain.

• Radiofrequency neurotomy of the third occipitalnerve for occipital headache symptoms is effec-tive in many patients, and may reverse signs ofpsychological distress in WAD patients.

• Patients who manifest post-traumatic headachesymptoms as their major symptom, especiallyin association with other neurological signs orsymptoms, should be considered for MRI evalu-ation with contrast.

• MRI imaging is an excellent screening tool forthe diagnosis of low cerebrospinal pressure/volume headaches, and will display characteristicsigns including pachymeningeal enhancementwith gadolinium, cerebellar descent or brain sag,

Figure 3. Sagittal T2 fast recovery, fast spinecho (FRFSE) cervicalspine MRI. Demonstrates (arrows top to bottom) extradural cere-brospinal fluid (CSF) (top arrow) lying anterior to the dura (sec-ond/middle arrow) with normal intrathecal/subarachnoid CSF(third arrow) lying anterior to the spinal cord. The location ofthe CSF leak cannot be determined from this image.

Figure 4. Axial T2 fast spinecho (FSE) cervical spine MRI. Demon-strates extradural CSF (vertical oriented arrow) surrounding cir-cumferentially the intact dura (horizontally oriented dashedarrow). Again normal intrathecal CSF lies between the dura andspinal cord.

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subdural fluid collections, and venous sinusengorgement. Spine MRI will also show signs, insome cases, of extradural fluid collections or epi-dural venous enlargement.

• Patients may respond well to epidural bloodpatch therapy if signs of CSF leak or cerebralvolume changes are apparent on MRI.

• Further research should consider the actual prev-alence of low CSF pressure and spinal extraduralfluid leaks in refractory cases of WAD or post-traumatic headache syndromes.

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2. Kaneoka K, OnoK, Inami S, Hayashi K. Motionanalysis of cervical vertebrae during whiplash loading. Spine.1999;24:763–770.

3. Lord SM, Barnsley L, Wallis BJ, Bogduk N. Chroniccervical zygapophysial joint pain after whiplash: a placebo-controlled prevalence study. Spine. 1996;21:1737–1744.

4. Sapir DA, Gorup JM. Radiofrequency medial branchneurotomy in litigant and non-litigant patients with cervicalwhiplash. Spine. 2001;26:E268–E273.

5. Wallis BJ, Lord SM, Bogduk N. Resolution of psy-chological distress of whiplash patients following treatmentby radiofrequency neurotomy: a randomized, double-blind,placebo-controlled trial. Pain. 1997;73:15–22.

6. Ishikawa S, Yokoyama M, Moriyama E, et al. Epi-dural blood patch therapy for chronic whiplash associateddisorder. IARS Abstracts. http://www.abstractsonline.org/viewer/viewAbstractPrintFriendly.asp? Accessed December 7,2006.

7. Mokri B. Spontaneous low cerebrospinal pressure/volume headaches. Curr Neurol Neurosci Rep. 2004;4:117–124.