Diagnostic Imaging of Pain

Richard F. Cody Jr

Asako Miyakoshi

Kenneth R. Maravilla

Pain is one of the most common indications for clinical imaging examinations. Pain could be an indicator of imminent tissue damage, such as ischemia, direct injury, malignancy, inflammation, and infection. It could also be due to peripheral or central nervous system diseases. Imaging protocols are tailored based on acuteness, character, and location of the pain and the working diagnosis. In case of acute pain, life-threatening and surgical emergency can be in the differential. Therefore, often imaging for acute pain is to confirm or exclude the presumed ominous diagnosis in doubt, such as acute fracture and associated tissue damage, intracranial hemorrhage, aortic dissection, pneumothorax, pneumoperitoneum, etc., based on history, labs, and physical exam findings. Even when the presumed urgent diagnosis is excluded, imaging exams are often useful in delineating the cause of pain.

For patients with recurrent or persistent pain whose diagnosis remains obscure after routine imaging workup, it might be challenging to make a diagnosis or find the cause of pain. Specialized imaging techniques such as magnetic resonance (MR) neurogram, discogram, and imaging-guided injection should be chosen depending on the careful review of the clinical scenarios. American College of Radiology (ACR) Appropriateness Criteria are a useful resource when the next imaging tool is uncertain. It consists of evidence-based guidelines to assist decision making for specific clinical conditions. In some institutions, it is incorporated into electronic medical records and ordering systems.

A comprehensive discussion of radiographs, computed tomography (CT), magnetic resonance imaging (MRI), ultrasound, and radionuclide examinations (such as bone scan) for evaluation of pain should include almost all radiologic subspecialties. This is beyond the scope of this chapter and can be found in most general diagnostic imaging textbooks.

This chapter is dedicated to the evaluation of pain related to the nervous system and reviews the imaging approach to several regional pain syndromes. It discusses imaging techniques that can be used to select surgical candidates among patients with back pain, tic douloureux, and peripheral nerve entrapment syndromes. Techniques and indications for MRI of the cranial nerves and posterior fossa vasculature, and high-resolution MRI of the brachial plexus and peripheral nerves are also discussed.

Headache

Headache is a common symptom. The lifetime prevalence of any form of headache is 93% in men and 99% in women.¹ Unless acute findings such as hemorrhage, tumor, and meningoencephalitis are of clinical concern, choosing the patient who should have a cranial imaging study can be challenging (see Chapter 62). The diagnostic yield of neuroimaging examinations in patients with headache and a normal neurologic examination, or in patients with typical migraine, is low (Table 19.1).² For example, in adult and pediatric patients with known migraine and no change in symptoms, routine neuroimaging is discouraged.³

TABLE 19.1 Neuroimaging Yield in Headache

	Percentage of Patients with Underlying Condition
Headache Type	Tumor	AVM	Hydrocephalus	Aneurysm	SAH	Infarct
Normal exam	0.8	0.2	0.3	0.1	0.2	1.2
Migraine	0.3	0.07	—	0.7	—	—
AVM, arteriovenous malformation; SAH, subarachnoid hemorrhage.
Adapted from Evans RW. Diagnostic testing for the evaluation of headaches. Neurol Clin 1996;14(1):1-26. Copyright © 1996 Elsevier. With permission.

Specific clinical features associated with significant intracranial abnormality, however, should prompt neuroimaging. Acute onset of an extremely severe headache (often described as “thunderclap” or “sudden worst headache of life”) should be treated as an emergency, due to increased positive predictive value for subarachnoid hemorrhage (SAH) from intracranial aneurysms in adults, and arteriovenous malformation (AVM) or other vascular malformations in children.²^,⁴^,⁵^,⁶^,⁷ Other imaging-appropriate clinical scenarios include worsening subacute headache, headache associated with focal neurologic signs or cognitive impairment (in patients without a history of migraine), new headache in patients older than age 50 years, and headache in immunocompromised patients or patients with known malignancy.²^,⁴^,⁵^,⁸ Patients over the age of 65 years with new onset of pathologic headache have a 15% incidence of serious intracranial disease, including temporal arteritis, tumor, and infarct. In contrast, patients younger than age 65 years (other than the acute SAH subset) have only a 1.5% incidence of detectable underlying pathology.⁹

ACUTE HEADACHE

Sudden onset of severe headache—especially if associated with neurologic abnormality or depressed sensorium—suggests possible acute SAH from an aneurysm or other vascular malformation. The devastating consequences of untreated, ruptured aneurysm require prompt exclusion of SAH in this setting: Patients who survive their initial hemorrhage have a 50% chance of a fatal rehemorrhage within 1 year, with the highest risk in the immediate postbleed period.¹⁰^,¹¹ Rapid diagnosis with high sensitivity is best made by CT demonstration of hyperdense blood in the subarachnoid space.¹²

If SAH is found on initial noncontrast head CT, subsequent magnetic resonance angiography (MRA), computed tomography angiography (CTA), or catheter angiogram is directed at detecting and localizing an aneurysm (Fig. 19.1) or AVM (Fig. 19.2). Venous sinus thrombosis (Figs. 19.3 and 19.4),¹³^,¹⁴ benign perimesencephalic SAH,¹⁵ and arterial dissection (Fig. 19.5)¹⁶^,¹⁷ may also result in SAH in the absence of an aneurysm or vascular malformation on CTA. In addition, migraine, and bacterial meningitis (in the proper clinical setting, e.g., stiff neck and fever) can also present as severe acute headache but without presence of SAH on acute CT.

FIGURE 19.1 Subarachnoid hemorrhage caused by ruptured terminal internal carotid artery aneurysm. A: Nonenhanced computed tomography shows hyperdense aneurysm (arrow) and blood within interhemispheric and sylvian fissures (arrowheads). The ventricles are mildly enlarged and clot is present within the third ventricle. B: Left internal carotid artery arteriogram shows a 2-cm aneurysm arising from the termination of the internal carotid artery. C: A second, unruptured aneurysm is seen at the junction of the left anterior cerebral artery and the anterior communicating artery (arrow).

FIGURE 19.2 Arteriovenous malformation. A 39-year-old man with several days’ headache. A: Noncontrast computed tomography shows enlarged, slightly hyperdense vessels in the sylvian fissure (arrow). B: Hyperdense, dilated veins at the parietal vertex (arrow). C: Computed tomographic angiography shows the arteriovenous malformation nidus (arrow), as well as dilated feeding arteries and peripheral draining veins.

FIGURE 19.3 Venous sinus thrombosis with cortical infarct. A 26-year-old postpartum woman with headache and left hemiparesis. A: Axial fluid attenuation inversion recovery (FLAIR) image at level of centrum semiovale shows increased signal in precentral gyrus, indicating cortical infarct. B: Nonenhanced computed tomography shows high attenuation in vein of Galen and straight sinus (arrow). C: Magnetic resonance venogram shows absence of flow through straight sinus (arrow) with patent sagittal and transverse sinuses.

As noted earlier, imaging the patient with suspected SAH should begin with nonenhanced CT. Cisterns and sulci must be carefully examined for hyperdense acute blood, which can be subtle if the amount of hemorrhage is small, or if the study is performed more than 24 hours after the bleed occurred. Nonenhanced CT has a sensitivity of 98%¹⁸ for detection of acute SAH within 12 hours of onset (in fact, 100% on emergency CTs has been reported).¹⁹ CT sensitivity for detection of SAH is reduced as the time interval from hemorrhage increases.²

A lumbar puncture (LP) may be considered in the possible—but uncommon—scenario of a patient for whom there is a bona fide high clinical index of suspicion for acute SAH and a negative head CT.¹⁸^,²⁰ Detection of xanthochromic cerebrospinal fluid (CSF) on LP remains the “gold standard” for sensitivity in detecting SAH in this setting.²¹^,²² In patients for whom an LP is truly indicated to assess for occult SAH, care must be taken for pristine technique: ideally a one-pass, atraumatic tap, with small caliber (25G or 22G) spinal needle. No xanthochromia and red blood cell count <2000 × 10⁶/L reasonably excludes aneurysmal SAH.²³

In the absence of SAH, nonenhanced CT can detect signs of other pathologies, including increased density within a thrombosed dural venous sinus, venous infarction, and edema associated with intracranial mass lesions. If subtle abnormalities are found on nonenhanced CT, further imaging evaluation may include contrast-enhanced CT or (preferably) MRI. In the absence of SAH, MRI is a more sensitive technique to evaluate the patient for other causes of headache, including dural venous sinus occlusion, infarct, mass lesion, or intracranial infection.
If SAH is detected, CTA and/or catheter angiography with digital subtraction angiography (DSA) is generally used to further evaluate the location and features of an aneurysm, pial AVM, dural arteriovenous fistula (DAVF), or other vascular malformation. Dural venous sinus thrombosis is better evaluated by computed tomography venogram (CTV) rather than magnetic resonance venogram (MRV) with contrast MRA/MRI because MRI and MRV may be affected by flow artifact resulting in false-positive appearance.

FIGURE 19.4 Venous sinus thrombosis with bilateral thalamic infarcts in a 24-year-old woman with 4 days of headache followed by several hours of nausea and depressed consciousness. Nonenhanced computed tomography shows low attenuation changes in both thalami, with increased attenuation in the internal cerebral veins (arrow) and straight sinus (arrowhead).

FIGURE 19.5 Internal carotid artery dissection in a 37-year-old man with headache and left pupillary constriction. A: Computed tomographic angiography at skull base shows decreased caliber of left internal carotid artery (white arrow) at the skull base. Intramural hematoma surrounds the narrowed lumen (black arrow). Normal right internal carotid artery (arrowhead). B: Left internal carotid arteriogram shows smooth narrowing of distal cervical internal carotid with near complete occlusion at the skull base (arrows).

Computed Tomography Angiography and Magnetic Resonance Angiography

MRA and CTA are useful for rapid, noninvasive diagnosis of intracranial vascular lesions. CTA is a dynamic technique in which thin-slice, contiguous images are rapidly obtained during the first pass of an intravenous bolus injection of iodinated contrast. Through proper timing, the images are acquired as the bolus of contrast fills the intracranial arteries and provides high-resolution images of the intracranial vessels. This provides a sensitive, rapid, and relatively noninvasive means to detect aneurysms, AVMs and arteritis, which can be seen as vessel wall irregularities.

Using state-of-the-art multidetector CT, axial images covering the entire cerebral vasculature can be acquired in a few seconds. Using rapid computer processing, multiplanar and three-dimensional (3D) reconstructions can be created to display the enhanced blood vessels in a manner analogous to the projection images from catheter angiography. When indicated, CTA can be easily performed immediately following the initial noncontrast CT while the patient is still on the CT table. MRA is a possible alternative technique, but it is more time-consuming and may not be suitable in the setting of acute intracranial hemorrhage, when the patient may be unable to hold still and requires close monitoring. Whereas conventional MRA visualizes flow-related signal within the vascular lumen, CTA depicts the surrounding structures with better spatial resolution, such
as vascular calcification, plaque formation, and extrinsic compression. The quality of CTA in detecting aneurysms is comparable to DSA. However, DSA is still considered by many to be the “gold standard” for aneurysm assessment and may be superior to CTA for surgical treatment planning.²⁴^,²⁵^,²⁶^,²⁷^,²⁸^,²⁹

CTA or MRA can provide rapid diagnosis or exclusion of aneurysms and AVMs in the patient with severe acute onset headache. These images are also used to clarify subtle findings in patients with questionable abnormalities on noncontrast CT. For example, carotid or vertebral artery dissection can be detected by imaging the upper cervical vasculature with the earlier described imaging techniques (see Fig. 19.5).³⁰^,³¹ Supplemental MRI with axial fat-saturated T1-weighted sequences in addition to MRA is also highly sensitive for detection of small, focal mural thrombus seen in carotid or vertebral dissections.³²^,³³

CHRONIC HEADACHE

Image findings are unrevealing in most cases of uncomplicated chronic headache. Intracranial lesions often present with headache but usually are associated with other neurologic signs or symptoms.³⁴ When headaches are caused by underlying pathologic disorders, the differential diagnosis is broad. Serious primary conditions include intraparenchymal, dural, or skull base tumors³⁵; unruptured aneurysms³⁶^,³⁷; abscesses; arterial dissection³⁸^,³⁹; venous sinus thrombosis; vasculitis⁴⁰; and AVMs.⁴¹ A normal CT or MRI without intravenous contrast excludes most intracranial masses to reassure the clinician and justify continued clinical observation and symptomatic treatment. If the clinical evaluation points toward neoplasm, abscess, or a vascular process, then contrast-enhanced CT or, preferably, contrast-enhanced MRI is appropriate next study. As already discussed, if there is a high clinical index of suspicion for vasculitis, CTA or MRA is useful technique to explore further.⁴² So-called “black-blood” postcontrast MRA is a newer highly specialized MRI technique that may be used to better assess vessel wall abnormalities, such as vessel wall enhancement that occur in cases of inflammatory vasculitis or prior hemorrhage (Figs. 19.6 and 19.7).⁴³^,⁴⁴

FIGURE 19.6 Vasculitis. Young patient who presented with aphasia and bilateral middle cerebral artery (MCA) territory infarcts. Cerebrospinal fluid analysis indicated the presence of anti-varicella zoster virus (anti-VZV) antibodies, confirming a diagnosis of VZV vasculitis. Three-dimensional reconstruction of the posterior circulation from time-of-flight (TOF) magnetic resonance angiography (MRA) (A) shows high-grade stenosis of the right P2 posterior cerebral artery (short arrow). There were additional stenoses involving the inferior division of the bilateral M1 MCA and bilateral A2 anterior cerebral artery (not shown). On T1 postcontrast intracranial vessel wall imaging (IVWI) (B), there is a circumferential enhancing lesion involving the stenotic segment (long arrow), compatible with inflammatory vasculopathy. On follow-up IVWI and TOF MRA performed 2 months (C and D) and 4 months (E and F) later, there is progressive improved luminal patency (short arrow, C and E) and diminished wall enhancement (long arrow, D and F), which corresponded with clinical improvement. (Reprinted from Mossa-Basha M, Alexander M, Gaddikeri S, et al. Vessel wall imaging for intracranial vascular disease evaluation. J Neurointerv Surg 2016;8[11]:1154-1159, with permission from BMJ Publishing Group Ltd.)

Noncontrast CT scanning of the craniofacial region is the study of choice for the imaging evaluation of acute and chronic inflammatory diseases of the sinonasal cavities. Conventional plain film radiography is no longer utilized for this purpose due to its low sensitivity and specificity.

Acute sinusitis is a common cause of headache or facial pain. Sinus CT is performed as a rapid, high-resolution, thin-section CT examination targeted to include the paranasal sinuses.
Because the information is primarily related to bone detail, these scans can be acquired with lower radiation dose levels. The axial thin-section, high-resolution data can be reformatted into coronal, sagittal, or any other desired imaging plane. CT has the additional advantage of enabling evaluation of the middle ear and mastoid air cells. Possible findings include observation of air-fluid levels that are associated with acute sinusitis. An additional finding suggestive of acute inflammatory sinusitis in the appropriate clinical setting is the presence of “frothy” material within one or more sinus cavities. Findings of mucosal thickening and subtle bony wall thickening reflect changes associated with chronic sinusitis and osteitis. When surgery is indicated for repetitive, recurrent, or intractable chronic sinusitis, thin-section, 3D CT technique with multiplanar viewing also assists in operative planning for endoscopic sinus surgery (Fig. 19.8).⁴⁵

FIGURE 19.7 Black-blood magnetic resonance imaging to identify probable source of hemorrhage. Fifty-six-year-old female presenting with thunderclap headache. Axial noncontrast computed tomography (CT) head (A) shows diffuse basal cistern subarachnoid hemorrhage. On 3D time-of-flight (TOF) magnetic resonance angiography (MRA) (B and E), there is a left supraclinoid internal carotid artery (ICA) aneurysm (B, short white arrow) and basilar tip aneurysm (E, long white arrow). There is no corresponding enhancement of the left supraclinoid aneurysm (short white arrows) on T1 pre-(C) and postcontrast (D) intracranial vessel wall imaging (IVWI), whereas the basilar tip aneurysm (F, arrowhead; G, thick arrow) shows circumferential wall enhancement when comparing T1 pre- (F) and postcontrast (G) IVWI. The basilar tip aneurysm was emergently treated endovascularly (curved arrow) as seen on coronal T1 postcontrast IVWI (H). (Reprinted from Alexander MD, Yuan C, Rutman A, et al. High-resolution intracranial vessel wall imaging: imaging beyond the lumen. J Neurol Neurosurg Psychiatry 2016;87[6]:589-597, with permission from BMJ Publishing Group Ltd.)

INTRACRANIAL HYPOTENSION

The syndrome of intracranial hypotension is often characterized by positional headache. Presenting signs and symptoms are variable and may include nausea/vomiting and visual, auditory, or vestibular disturbances. CSF hypotension can be caused by development of a CSF leak due to head or spinal trauma or secondary to skull base surgery. It can also develop spontaneously, likely arising from dural thinning/erosion from adjacent inflammation or infection.⁴⁶ Intracranial hypotension may also result from slow, persistent CSF leakage following a spinal puncture or from a spontaneous dural defect, or from overshunting of CSF after placement of a ventriculoperitoneal shunt.⁴⁷^,⁴⁸

Findings associated with CSF hypotension are best demonstrated on cranial MRI with gadolinium enhancement. This demonstrates a “pachymeningeal” pattern of smooth, continuous, enhanced dural thickening. In some cases, this may be associated with small subdural effusions and/or downward vertical displacement of the brainstem and cerebellar tonsils (Fig. 19.9).
These are generally reversible and disappear with resolution of CSF hypotension after successful treatment by blood patch, epidural saline injection, or surgical repair of the defect.⁴⁹^,⁵⁰^,⁵¹ Headache with MR findings of diffuse enhanced dural thickening, not explained by prior surgery or infection, should prompt a diligent search for possible site of an occult CSF leak. This can be done with MRI using a heavily fluid-weighted 3D sequence such as Constructive Interference in Steady State (CISS, Siemens trade name), Balanced Fast Field Echo (BFFE, Philips) or Fast Imaging Employing STeady-state Acquisition (FIESTA, GE) to provide an MR cisternogram or MR myelogram type of image.⁵²^,⁵³^,⁵⁴^,⁵⁵

FIGURE 19.8 Chronic sinusitis. Coronal, nonenhanced screening sinus computed tomography through the face shows opacification of the left maxillary sinus caused by chronic inflammation (long arrow). The ostiomeatal unit (short arrow) and uncinate process (arrowhead) are clearly demonstrated on the opposite side.

FIGURE 19.9 Cerebrospinal fluid hypotension caused by overshunting. A 54-year-old woman with ventriculoperitoneal shunt. Diffuse dural thickening and enhancement (arrow) caused by shunt valve with insufficient resistance. Similar findings may be seen in patients with postlumbar puncture, dural tears, or posttraumatic cerebrospinal fluid leaks.

INTRACRANIAL HYPERTENSION (PSEUDOTUMOR CEREBRI)

On the other hand, increased intracranial pressure could cause moderate to severe headache, vision change, nausea, and vomiting. Papilledema can be seen on funduscopic evaluation, which eventually leads to loss of vision if left untreated. After excluding secondary intracranial hypertension such as mass lesion, dural venous sinus thrombosis, systemic diseases, and medication, idiopathic intracranial hypertension should be considered. It is more common among overweight females. Increased intracranial pressure is confirmed by measuring opening pressure during LP. On imaging, prominent CSF in tortuous optic sheaths, empty sella turcica, and slit-like ventricles are supportive findings.

Facial Pain

Intractable trigeminal neuralgia (tic douloureux) can be caused from irritation of the nerve from a vascular loop that contacts the cisternal portion of the fifth cranial nerve near its exit from the pons.⁵⁶ The vessels most responsible for this often arise from a branch of the superior, anterior-inferior, or posterior-inferior cerebellar arteries (see Chapter 67). Surgical intervention with placement of a small Teflon prosthetic “pad” or “spacer,” to separate the offending vessel from the root entry zone of the cranial nerve, is often effective in relieving symptoms.⁵⁷ Diagnosis of vascular loops in the prepontine cistern and cerebellopontine angle was difficult before the development of high-resolution MRI. Thin-section heavily fluid-weighted steady-state, free precession, gradient echo techniques (BFFE, CISS, FIESTA) provide a cisternogram image of the basal cisterns that outline the cranial nerves and vessels in the area. This technique can effectively display the offending vascular loop in relation to the cranial nerve. The diagnosis of vascular loop syndrome is made by demonstration of a blood vessel contiguous with, or actually distorting, a cranial nerve close to its origin from the brainstem at the root entry zone in correlation with the appropriate clinical symptoms. This portion of the nerve lacks a full nerve sheath and thus is sensitive to irritation from pulsations from the contacting artery. The diagnosis must be based on appropriate correlation with clinical symptoms because up to 49% of asymptomatic patients may show similar vascular imaging findings.⁵⁸ These MR studies not only aid in identification of surgical candidates but also serve as a roadmap for surgical treatment planning (Fig. 19.10).⁵⁸^,⁵⁹^,⁶⁰^,⁶¹^,⁶²^,⁶³

Other structural causes of trigeminal nerve dysfunction include mass lesions near the trigeminal nerve such as meningioma, schwannoma, arachnoid cyst, cholesteatoma, and epidermoid cyst.⁶⁴^,⁶⁵ These can be diagnosed by conventional cranial MRI and CT studies.

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