Tract or Funicular Pain

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Funicular or tract pain refers to pain arising from dysfunction or irritation of the longitudinal spinal cord tracts (funiculi) rather than nerve root (radicular) or musculoskeletal structures. It is essentially a central (spinal cord) pain syndrome caused by lesions of the intraspinal sensory pathways (spinothalamic tracts or dorsal columns). Clinically, funicular pain is characteristically diffuse, often burning or stabbing, and does not follow dermatomal distributions. Patients may describe unusual sensations such as a cold, aching dysesthesia in an extremity. A classic example is , an electric shock-like sensation down the spine or limbs with neck flexion, seen in cervical cord demyelination.

Historical Overview

The concept of “funicular” or “tract” pain has been recognized for over a century, initially in the context of false-localizing signs in neurology. Collier (1904) described instances where intracranial tumors produced remote neurological signs. By the mid-20th century, reports had emerged of high spinal cord lesions causing lower extremity pain mimicking sciatica​.

Scott (1956) reported cord tumors causing “sciatica” in the legs, and Langfitt & Elliott described cervical cord compression presenting as back and leg pain. These early descriptions established that cord compression can produce pain referred to distant regions, defying usual anatomical localization. The term “funicular pain” (from the Latin funiculus, meaning cord) emphasizes its origin in the spinal cord tracts. In more recent decades, funicular pain has been noted in conditions like cervical spondylotic myelopathy, intramedullary spinal tumors, multiple sclerosis, and subacute combined degeneration, albeit often under-recognized. Growing awareness of this phenomenon has prompted its inclusion in modern pain syndrome texts as a distinct entity, given its unique mechanisms and diagnostic challenges.

Clinical Significance

Funicular pain is important to recognize because it often presents without the classic signs of myelopathy or radiculopathy, leading to misdiagnosis. Patients may undergo unnecessary workups or surgeries at the wrong spinal level. For example, a patient with cervical cord compression might only report leg pain, causing clinicians to focus on the lumbar spine in error. Inclusion of funicular pain in pain textbooks alerts clinicians to this pitfall. Early identification is crucial: timely treatment of the underlying cord lesion (e.g. decompression of a cervical stenosis) can resolve the pain and prevent neurological disability, whereas missed diagnoses can lead to persistent pain and cord damage. For musculoskeletal physicians, neurologists, and pain specialists, understanding funicular pain broadens the differential for limb or truncal pain syndromes and improves patient outcomes by directing attention to possible central lesions.

Epidemiology

Funicular pain is relatively rare and not well quantified in population studies, largely because it is a manifestation of underlying conditions rather than a primary diagnosis. It most often arises in the setting of cervical spondylotic myelopathy (CSM) or other spinal cord lesions. Degenerative cervical myelopathy itself is fairly common in older adults (estimated incidence ~4 per 100,000 per year), but only a small fraction of CSM patients (likely <5%) present predominantly with funicular (tract) pain. A recent systematic review identified 10 reported cases of cervical cord compression presenting as sciatica-like leg pain. Adding several newer case series, fewer than 20 well-documented cases exist in literature, though this is probably an underestimate as awareness grows. In a case series by Secer et al. (2022), four patients with CSM had primary low back or leg pain due to tract involvement. Similarly, Han et al. (2024) reported four cases of CSM misdiagnosed as lumbar disease before cord compression was recognized.

Demographically, funicular pain due to degenerative myelopathy tends to occur in middle-aged and older adults. The systematic review found a mean age of ~53 years (range 34–75) among reported cases. Both men and women can be affected; slight male predominance has been noted in CSM cases (consistent with CSM’s male-to-female ratio of ~3:1​

Risk Factors

The primary “risk factor” for funicular pain is having a lesion that affects central nociceptive pathways without immediately causing overt motor deficits. Cervical spondylosis with cord compression is a prime example – especially multi-level spondylosis or ossification causing tight spinal canals. Notably, many reported patients had coexisting lumbar degenerative changes, which can confound the clinical picture. Thus, patients with known lumbar spine disease may be at risk of misdiagnosed funicular pain if they also develop an upper spinal cord lesion.

Other risk conditions include intramedullary processes like multiple sclerosis (MS) and B12 deficiency (subacute combined degeneration); these preferentially damage dorsal columns or spinothalamic tracts, often producing dysesthetic pain in limbs. For instance, dysesthetic extremity pain occurs in up to 12–28% of MS patients, which is essentially a form of funicular pain due to demyelination of central sensory pathways. Spinal cord tumors (ependymomas, astrocytomas) are another risk context – funicular pain may precede other signs, especially with slow-growing intramedullary tumors

Pathophysiology

Cross-section of the spinal cord illustrating the dorsal (posterior), lateral, and ventral (anterior) funiculi (white matter columns). Lesions in these funiculi – particularly the lateral funiculus housing the spinothalamic pain pathways – can cause funicular pain referred to regions below the lesion.

Anatomy

To understand funicular pain, one must recall the organization of the spinal cord white matter. The white matter is subdivided into three regions on each side: the dorsal (posterior) funiculus, the lateral funiculus, and the ventral (anterior) funiculus.Each funiculus contains specific ascending and descending tracts.

• The dorsal funiculus (posterior columns) carries the gracile and cuneate fasciculi – responsible for vibration sense, proprioception, and fine touch.
• The lateral funiculus contains the lateral corticospinal tract (motor) and important sensory tracts, notably the lateral spinothalamic tract which transmits pain and temperature from the opposite side of the body.
• The ventral funiculus contains the anterior corticospinal tract and the anterior spinothalamic tract (carrying crude touch).

These funiculi are longitudinal cables of axons, so lesions affecting them can cause symptoms below the level of injury. Funicular pain specifically implicates the ascending sensory tracts in these columns. For example, a lesion in the cervical lateral funiculus impacting the spinothalamic tract may be perceived as pain in the leg, because those lateral funicular fibers originate from lumbar levels (the somatotopy of the spinothalamic tract has sacral fibers most lateral)

Mechanisms

Funicular pain is fundamentally a type of central neuropathic pain arising from a spinal cord lesion. Several mechanisms have been proposed:

• Irritation of the Spinothalamic Tract: The most cited mechanism in compressive lesions is mechanical distortion or irritation of ascending spinothalamic tract neurons. Compression of the cord (by a cervical osteophyte, herniated disc, tumor, etc.) can cause ectopic impulses or hyperactivity in these nociceptive pathways, which the brain interprets as pain in the corresponding body part. Chan et al. described funicular leg pain as “a referred pain due to irritation of the ascending spinothalamic tract”. Notably, because these tracts cross and ascend several levels, a cervical lesion can produce leg pain, a classic false-localizing phenomenon. The pain is often diffuse and non-dermatomal because spinothalamic tract fibers represent broad regions, not the focused distribution of a single nerve root.
• Dorsal Column Involvement: Lesions of the dorsal columns (posterior funiculi) can produce paraesthetic pain syndromes as well. Demyelination (as in MS) or B12 deficiency affecting the posterior columns often leads to Lhermitte’s sign and diffuse tingling or “electric” pains in the limbs. These are also funicular pains, although dorsal column-mediated. In subacute combined degeneration (Vitamin B12 deficiency), for example, patients can experience aching or burning in the legs alongside the classic gait ataxia, due to dorsal (and lateral) column degeneration (historically termed “posterior lateral sclerosis” or funicular myelosis). Thus, any long tract – dorsal or lateral – carrying sensory information when disrupted can result in neuropathic pain below the lesion.
• Central Sensitization and Neuroinflammation: Beyond direct mechanical irritation, chronic spinal cord injury (SCI) and compression can induce central sensitisation. Animal studies show that cord injury leads to hyperexcitability of dorsal horn neurons, reduced inhibitory neurotransmitters (like GABA) in the cord, and activation of microglia and astrocytes releasing pro-inflammatory cytokines. These changes can sustain neuropathic pain even in the absence of ongoing compression. For instance, chronic CSM might cause permanent changes in neural circuitry such that pain persists as cord “phantom pain.” Patients often describe burning, shooting, or unpleasant sensations typical of neuropathic pain. The fact that some patients have residual dysesthesia (like a persistent “cold feeling” in a limb) even after surgical decompression supports a component of central sensitization or irreversible tract injury.
• Ischemia of Spinal Tracts: Compressive myelopathy can compromise microcirculation in the cord. Ischemia of lateral columns might preferentially affect the metabolically active pain fibers and lead to their dysfunction, analogous to the central pain that follows spinal cord infarction. Vascular mechanisms are supported by dynamic factors: neck extension in cervical stenosis can transiently worsen cord compression and blood flow, triggering leg pain (as seen in some patients whose thigh pain was provoked by cervical extension). This suggests a positional ischemia or stretch of the funiculi eliciting pain.

Funicular pain arises when pathological processes within the spinal cord’s white matter – whether compression, inflammation, demyelination, or ischemia – cause abnormal activation of pain pathways. Unlike peripheral neuropathic pain, which is due to nerve damage, funicular pain is due to central pathway disturbance, often producing poorly localized, persistent pain. It is frequently accompanied by other signs of cord involvement (hyperreflexia, sensory level), but remarkably can occur in isolation as a heralding symptom. This central origin also means that typical peripheral provocation tests (like straight leg raise for sciatica) are negative, which is an important diagnostic clue.

Clinical Features

Patients with funicular pain often present with an odd constellation of symptoms that can be mistaken for musculoskeletal or radicular pain. Key features include:

• Diffuse, Non-Dermatomal Pain: The pain is typically described as diffuse and deep, not confined to a single dermatome or peripheral nerve territory. For example, a patient might have an aching or burning pain that spans the buttock, posterior thigh, and calf in a non-specific pattern, or a girdle-like pain around the trunk. They may have difficulty localizing it (“somewhere in the leg” or “deep in the back”). This contrasts with radicular pain, which extends down a narrow band.
• Quality of Pain: Funicular pain is often a dysaesthetic pain – patients use descriptors like burning, tingling, cold, throbbing, or knife-like. A classic description is a “cold, unpleasant sensation” in an extremity. Some patients report it as a deep ache or a crushing sensation. Importantly, it is usually continuous or chronic rather than purely intermittent. In cases of cord compression, it may fluctuate with posture (for instance, worse on neck extension or prolonged walking, as in neurogenic claudication). Unlike acute radicular pain that can be lancinating, funicular pain tends to be persistent and nagging.
• Provoking/Relieving Factors: Because funicular pain originates in the cord, mechanical maneuvers that affect the cord can provoke it. Neck flexion causing Lhermitte’s shock-like pain is one example. In cervical stenosis, extending the neck (which further narrows the canal) may reproduce leg pain. Some patients note that Valsalva or coughing (which elevates CSF pressure) transiently exacerbates the pain, again pointing to an intrathecal source. Notably, straight leg raise test is usually normal, distinguishing it from sciatica due to nerve root compression. Root tension signs (SLR or Spurling’s test for cervical root) are typically negative in pure funicular pain, since the nerve roots themselves are not the source. Often, no position fully relieves the pain, though some patients find partial relief in positions that decompress the cord (e.g., cervical flexion or lying down if spinal canal stenosis is the cause).
• Associated Neurologic Signs: A crucial aspect is that objective neurologic deficits may be subtle or absent, especially early on. Patients with cord compression presenting as funicular pain might lack the classic upper motor neuron signs initially. However, a careful exam often reveals clues: brisk reflexes in the legs, an upgoing plantar (Babinski sign), subtle gait disturbance, or a sensory level to pinprick. Han et al. reported that all four of their misdiagnosed CSM patients had some abnormal neurologic signs (e.g. hyperreflexia, Babinski or Hoffmann’s sign) on re-examination. In other cases, the only sign might be an unexplained sensory change (like diminished pain sensation below a certain spinal level) or mild weakness. If the dorsal columns are involved, loss of vibration sense or a positive Romberg test might be present. Absence of clear neurologic signs, however, does not exclude cord pathology – about 20% of cervical myelopathy patients show no obvious myelopathic signs on initial exam​. This is why funicular pain can be so misleading.

Differential Diagnosis

Given its atypical presentation, funicular pain must be distinguished from several other conditions:

Radiculopathy (Nerve Root Pain): This is the most common confusion. Radicular pain (e.g. sciatica) radiates in a band down the limb, is often sharp or shooting, and typically exacerbates with maneuvers stretching the nerve root (such as straight-leg raise for lumbar roots, or Spurling’s maneuver for cervical roots). In contrast, funicular pain is non-dermatomal and not worsened by root stretch. Radiculopathy usually comes with other root signs: numbness or paresthesias in the nerve distribution, reduced reflexes, or motor weakness in muscles innervated by that root. Funicular pain lacks these specific root findings, though it may coexist with normal strength and sensation in dermatomes. For example, a patient with L5 radiculopathy will have pain down the lateral leg, foot drop or toe extensor weakness, and a diminished reflex at the medial hamstring – none of which would be explained by a high cord lesion causing tract pain. Another distinguishing feature is chronicity: radicular pain from disc herniation might be acute/subacute with a precipitating event, whereas funicular pain (especially from myelopathy) tends to be insidious and chronic (months to years).

Referred Visceral or Myofascial Pain: Diffuse “non-anatomical” pain can also be due to referred pain from visceral organs or myofascial trigger points. For instance, diaphragmatic irritation can cause shoulder/trapezial pain (Kehr’s sign), or pelvic organ pathology can refer pain to the low back. These referred pains are usually dull and aching. However, they do not typically present as isolated limb dysesthesias or mimic claudication, and neurological exam is normal. A distinguishing point is that funicular pain often has a neuralgic quality (tingling, shock-like, band-like) that referred visceral pain lacks. Myofascial pain syndromes can cause diffuse back or neck pain but are aggravated by muscle use and palpation of trigger points, whereas funicular pain is not directly reproducible by local palpation. Clinical context (e.g. risk factors for pancreatic or pelvic disease) and appropriate organ-specific tests (ultrasound, etc.) would guide this differential.

Peripheral Polyneuropathy: If a patient has burning or dysesthetic pain in the feet or hands bilaterally, one might consider a peripheral neuropathy (like diabetic neuropathy). However, funicular pain from a cord lesion typically has a “level” – symptoms begin at a certain trunk or limb level and spare areas above. Peripheral neuropathies usually have a stocking-glove distribution and often involve distal weakness or loss of reflexes. Additionally, neuropathy wouldn’t usually present as isolated thigh or trunk pain without distal extremity involvement, nor would it be position-dependent. Normal nerve conduction studies and the presence of any myelopathic signs (brisk reflexes, etc.) would point away from peripheral neuropathy and toward a central cause.

Spinal Cord Tumors: Intramedullary tumors (like ependymomas, astrocytomas) can cause funicular pain, while extramedullary (e.g. meningiomas) more often cause radicular pain by root compression. In the differential, one must consider a spinal cord neoplasm if funicular pain is prominent. Clues favoring a tumor would be a very gradual onset over years, often with a cape or hemicape distribution of sensory change, and sometimes segmental lower motor neuron signs at the level of the tumor (if it involves the anterior horn or exiting root at that level). For example, a high thoracic cord tumor might present as “band-like” abdominal pain (pseudo-visceral pain) or leg pain​. Scott’s 1956 cases of upper cord tumors manifested solely as leg pain mimicking sciatica. Over time, these often progress to more obvious signs (weakness, sphincter disturbance). Differentiating tumor from degenerative stenosis may require imaging since both can present with tract pain. MRI with contrast is critical here – a tumor will enhance or have an obvious mass effect distinct from degenerative changes.

Multiple Sclerosis and Transverse Myelitis: In younger patients with funicular-type pain (especially Lhermitte’s sign or patchy limb dysesthesias), demyelinating disease is a consideration. MS classically causes Lhermitte’s phenomenon (a type of funicular pain) and can produce chronic neuropathic pain in limbs. Usually, there are other signs of MS (optic neuritis history, patchy deficits, brain lesions on MRI). Subacute transverse myelitis can cause band-like trunk pain at the onset, often with rapid development of paralysis or sensory level – distinguishing it by its acute, severe course. However, a partial myelitis might initially manifest as isolated tract pain (e.g. a longitudinally extensive dorsal column lesion in neuromyelitis optica could present as diffuse torso pain). The presence of inflammatory markers, MRI findings of cord lesions, and patient age help differentiate these from compressive causes.

Lumbar Spinal Stenosis (Neurogenic Claudication): A particularly challenging differential is an older patient with leg pain on walking. Neurogenic claudication from lumbar canal stenosis causes leg pain, often bilateral, brought on by walking and relieved by rest or lumbar flexion. Funicular pain due to cervical compression can also present as leg pain on exertion (as in the case of intermittent claudication from cervical myelopathy). In such cases, termed “funicular claudication,” the cervical cord lesion causes leg pain with activity, possibly related to increased cord activity or slight cord motion during gait. Distinguishing these relies on careful exam: lumbar stenosis claudication often has lower extremity positional relief (leaning forward), absent if the cause is cervical. Moreover, lumbar stenosis might have diminished reflexes or segmental weakness, whereas cervical myelopathy can have brisk reflexes and Babinski. Imaging is usually needed; notably, some patients have both lumbar and cervical pathology (tandem stenosis). In Chan et al.’s reports, patients indeed had coexistent lumbar degenerative changes, muddying the picture. A key point is that cervical cord compression should be suspected in any “sciatica” or claudication case that has unexplained upper motor neuron signs (hyperreflexia, Babinski) or an atypical pain pattern.

Essentially funicular pain is a diagnosis of exclusion that requires a high index of suspicion. When a patient presents with limb or truncal pain that is diffuse, atypical, or accompanied by subtle cord signs, one must consider a spinal cord origin. Distinguishing funicular pain from radicular pain is particularly crucial: funicular (tract) pain is central, diffuse, constant, and often “weird” in quality; radicular pain is peripheral, shooting, dermatomal, and provoked by nerve stretch. The differential diagnosis can be narrowed by thorough neurologic examination and targeted investigations as outlined below.

Diagnosis

Evaluating funicular pain requires looking beyond the apparent site of pain and assessing the spinal cord integrity. The diagnostic approach to funicular pain is to prove or exclude a central lesion. Start with MRI of the entire spinal axis as needed. Use electrodiagnostics to rule out peripheral causes. Consider invasive tests or blocks if uncertainty persists. The clinician must keep an open mind – if initial tests are negative yet suspicion remains high (e.g., pain pattern and exam strongly suggest cord involvement), repeat imaging or second-look studies may be warranted. In some cases, the true diagnosis only becomes clear retrospectively when the patient responds to treatment targeting the spinal cord (e.g., surgical decompression). Thus, maintaining a high suspicion and thoroughly evaluating the neuraxis is essential when facing unexplained limb pain that could be funicular.

Imaging – MRI as First-Line: Magnetic resonance imaging (MRI) of the spinal cord is the cornerstone for diagnosing the cause of funicular pain. The key is to image the entire relevant neuraxis, not just the region where pain is felt. For example, in a patient with isolated “leg” pain but suspected funicular syndrome, cervical and thoracic spine MRI should be obtained (in addition to lumbar if needed). T2-weighted MRI can reveal spinal cord compression, intrinsic cord lesions (tumors, demyelination), or other pathologies. In Chan et al.’s cases, MRI showed significant cervical cord compression at C4–5 and C5–6 in a patient whose primary complaint was leg pain​. If an intramedullary lesion like MS plaque is suspected, MRI with gadolinium contrast helps to identify active inflammation or tumor enhancement. Whole-spine MRI is advisable if the level is unclear, since false localizing pain can come from anywhere above the affected region.

For degenerative causes, MRI often shows cervical spondylotic myelopathy changes: cord compression by disc-osteophyte complexes or ligamentum flavum infolding, sometimes with high T2 signal in the cord (myelomalacia) indicating chronic injury. Interestingly, some cases of funicular pain have minimal MRI changes other than cord crowding, making the diagnosis challenging. In such cases, additional dynamic imaging may be needed.

Dynamic Myelography / CT Myelogram: When static MRI is inconclusive or if positional factors are suspected, a myelogram with the neck in different positions can be informative. Kozaki et al. (2020) demonstrated the value of post-myelogram dynamic CT: in their patient, cervical extension during myelography markedly narrowed the subarachnoid space at C4–6 and reproduced the thigh pain. Flexion vs. extension imaging showed that extension caused ventrolateral cord compression (likely impinging the spinothalamic tract), correlating with symptom provocation. Such dynamic studies can uncover intermittent cord impingement that MRI in neutral might miss. However, myelography is invasive, requiring lumbar puncture and intrathecal contrast. Adverse effects (headache, nausea, arachnoiditis) are not uncommon. Therefore, myelography is used selectively – for example, in patients who cannot have MRI or when dynamic instability is strongly suspected. CT myelogram can better delineate bony spurs or ossified ligaments compressing the cord. In older cases (e.g., Scott 1956), myelography was key to diagnosing cord tumors presenting as leg pain. Today, MRI has largely superseded myelography, but dynamic myelography remains an option if standard imaging is equivocal.

Neurophysiological Studies: Electrophysiologic tests can help differentiate a cord lesion from peripheral nerve problems. Electromyography (EMG) and nerve conduction studies (NCS) of the lower limbs are often performed in the workup of leg pain. In funicular pain due to cord compression, EMG/NCS will typically not show a radiculopathy or peripheral neuropathy, but may show signs of myelopathic process. For example, EMG might reveal diffuse denervation below a certain spinal level (due to corticospinal tract involvement causing disuse changes) or normal peripheral study despite patient’s symptoms. Kozaki’s case had EMG changes suggestive of neurogenic process below C5, supporting an upper motor neuron lesion rather than a lumbosacral radiculopathy. Another useful modality is somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs). These can detect conduction delays in the dorsal columns or corticospinal tracts, respectively, even if the patient has minimal deficits. In cord compression cases with funicular pain, SSEPs from the legs may be prolonged, indicating dorsal column dysfunction, or MEPs may be delayed, indicating corticospinal involvement – subtle evidence of myelopathy. Spinal cord evoked potentials (SCEPs) are another research tool mentioned in case reports. While not routine, these tests can strengthen the case for a cord lesion when MRI findings are borderline.

Diagnostic Blocks: A novel diagnostic approach described in the literature is the use of cervical epidural or nerve root blocks to localize the source of pain. Chan et al. (2011) reported using a C5–6 interlaminar epidural steroid injection in a patient with leg pain and both cervical and lumbar stenoses; the cervical epidural completely relieved the leg pain (whereas an earlier lumbar root block had failed)​. This suggested the cervical cord compression was the true origin (by temporarily reducing inflammation/compression at that level)​. In a second case, a selective C4–5 nerve root block with epidural spread abolished the leg pain transiently, guiding surgeons to decompress the cervical spine. The principle is that if anesthetizing or relieving pressure at a suspected cord level stops the distal pain, it confirms a funicular origin. However, such blocks carry risks (spinal cord infarct, nerve injury, infection) and should be done with caution. They are generally reserved for difficult diagnostic dilemmas, and even then, an informed multidisciplinary discussion is needed. It’s also worth noting that a cervical epidural steroid injection might have non-specific pain-modulating effects, so interpretation must be careful to avoid false reassurance​. In practice, if imaging clearly shows cord compression, diagnostic blocks are usually unnecessary and one would proceed to definitive treatment.

Laboratory and Other Tests: These are guided by differential considerations. If an inflammatory myelopathy is in question, spinal fluid analysis via lumbar puncture (for oligoclonal bands, infectious workup) may be indicated – though typically funicular pain by itself would not prompt a tap unless MS or transverse myelitis is suspected. Vitamin B12 levels should be checked if dorsal column signs or risk factors for deficiency are present, since B12 deficiency myelopathy can cause funicular symptoms. Similarly, tests for syphilis (tabes dorsalis historically causes lightning pains in legs) or other etiologies might be done in select cases. In a cancer patient with new unexplained limb pain, imaging for spinal metastasis (including MRI of the spine) is critical, as epidural spinal cord compression from tumor can produce funicular-type pain (often described as a band of pain at the level of compression, or radicular pain with cord signs).

Management

Management of funicular pain revolves around two parallel goals: treating the underlying lesion causing the tract dysfunction, and alleviating the pain (and other symptoms) through medical or interventional pain management. A multidisciplinary approach is often required, especially when pain persists after addressing the cause.

In practice, for a patient with confirmed cervical funicular pain from CSM, a reasonable management plan would be: proceed with surgical decompression (e.g., ACDF or laminectomy). While awaiting surgery or if surgery is delayed, treat pain with gabapentin (titrating up to ~1800 mg/day as tolerated) and/or amitriptyline 25 mg at night, plus physiotherapy for conditioning. If pain is severe, a short course of oral steroids or a cervical epidural steroid injection could be considered for temporary relief. After surgery, continue neuropathic pain meds if needed; many patients can taper off if pain resolves, but if residual dysesthesia remains, maintain the medications. Monitor for improvement in neurologic function and pain over 3–6 months.

Treating the Underlying Cause

Since funicular pain is a symptom of a pathology (e.g., cord compression, demyelination, etc.), definitive management targets that pathology:

Spinal Cord Compression (Degenerative): If a patient is found to have significant cervical or thoracic cord compression corresponding to the funicular pain, surgical decompression is usually indicated. Evidence and consensus in degenerative cervical myelopathy support surgery for moderate to severe cord compression or progressive symptoms​. In the context of funicular pain, even if myelopathic signs are mild, the pain itself can be an indication for surgery because it implies cord tract irritation. Numerous case reports document dramatic pain relief after decompressive surgery: Chan’s patients experienced “significant pain relief” after cervical laminectomy or corpectomy, and in the Han et al. series, all cases had full resolution of sciatica-like pain following anterior cervical decompressions. Surgical options include anterior cervical discectomy and fusion (ACDF) for disc osteophyte complexes, cervical corpectomy for multi-level stenosis, or laminoplasty/laminectomy with or without fusion for posterior element compression. The choice depends on the pathology location and surgeon expertise. One interesting point: because funicular pain can be a relatively early manifestation of myelopathy, surgical outcomes are often good in terms of pain relief, as the tract has not been irreversibly damaged yet. Indeed, funicular pain often reverses quickly post-op, as seen in reports. Intraoperative findings sometimes even confirm the mechanism (e.g., a tight osteophyte impinging the anterolateral cord). If multiple levels are involved (cervical and lumbar), typically the more critical compression (cord level) is addressed first. Careful surgical planning is needed to avoid under-treating (e.g., if tandem stenosis, both regions might ultimately need surgery).

Intramedullary Lesions: For intrinsic cord tumors causing funicular pain, neurosurgical resection or debulking is the definitive treatment. Early neurosurgical referral is warranted if imaging shows an intramedullary mass. Resection of tumors like ependymomas often results in pain improvement, though recovery depends on tumor type and extent. For demyelinating lesions (MS), disease-specific therapy is indicated – high-dose corticosteroids for an acute myelitis or disease-modifying therapies for relapsing MS to prevent future lesions. In B12 deficiency, aggressive B12 repletion can halt progression and sometimes improve symptoms if instituted early. Similarly, if funicular pain were due to radiation myelopathy or other less common causes, treat those causes (though many are irreversible). In summary, targeted therapy (surgical, medical, or nutritional) for the causative lesion is paramount and often yields the best chance of pain resolution.

Spinal Cord Ischemia or Infarct: If funicular pain stems from vascular issues (e.g., an arterio-venous malformation or infarction), management might involve endovascular treatment of AVMs or supportive care for infarcts. Unfortunately, established infarct-related cord pain is often permanent, requiring symptom management (discussed below).

Pain Management

Neuropathic pain from the spinal cord can be challenging to control. A combination of pharmacological, rehabilitative, and interventional strategies is used, analogous to treating central pain syndromes like post-SCI pain or MS-related pain:

Pharmacological Treatments: First-line medications are those for neuropathic pain, such as anticonvulsants and antidepressants. Gabapentinoids (gabapentin, pregabalin) are commonly used and have shown efficacy in spinal cord injury neuropathic pain. Guidelines (e.g., the CanPain SCI clinical practice guideline) recommend gabapentin or pregabalin as first-line for neuropathic pain in SCI. Pregabalin has Class I evidence for reducing central neuropathic pain in SCI at doses up to 600 mg/day. Typical dosing would start low (e.g., gabapentin 300 mg at night or pregabalin 75 mg BID) and titrate upward to effect. Tricyclic antidepressants (TCAs) like amitriptyline or nortriptyline, and serotonin-norepinephrine reuptake inhibitors (SNRIs) like duloxetine, are also evidence-based options for neuropathic pain. Duloxetine 60–120 mg daily can be helpful (not available in New Zealand), especially if comorbid depression or anxiety exist. TCAs (25–75 mg at night) may improve pain and sleep, but their anticholinergic side effects require caution in older patients. In MS-related central pain, these same classes are used, with moderate success rates. Topical agents (like lidocaine or capsaicin creams) have limited utility in funicular pain given the poorly localized nature, but could be tried if there is a focal area of allodynia on the skin. For severe cases, tramadol or other moderate opioids can be considered as second-line add-on therapy. Tramadol has dual action (weak μ-opioid agonist and SNRI activity) that can help neuropathic pain; doses of 50–100 mg up to QID might be used, carefully monitoring for dependence or side effects. Strong opioids are generally less effective for central pain and carry high risk, so they are not preferred long-term solutions. In refractory cases, baclofen (a muscle relaxant and GABA_B agonist) can sometimes help, especially if there is spinal cord spasticity contributing to discomfort. Baclofen may also modulate central pain via spinal inhibitory pathways; typical dosing is 5–20 mg TID as tolerated. In some spinal cord injury patients, baclofen pumps (intrathecal baclofen) are used for spasticity and may have ancillary benefit on central pain. Corticosteroids have a role if an acute inflammatory lesion is present (e.g., an MS relapse or acute compressive injury with cord edema). High-dose IV methylprednisolone might reduce cord swelling and possibly pain in those scenarios. However, in chronic degenerative cases, steroids are not routinely used except as part of epidural injections or short-term trials.

Physical and Rehabilitation Therapy: While pain from a cord lesion is not “mechanical,” patients often benefit from physical therapy to address secondary issues. Gentle exercise and gait training can improve function, which indirectly can enhance pain coping. For example, after cervical decompression, rehabilitation helps maximize neurologic recovery, which may lessen residual pain. Assistive devices (canes, walkers) and orthotics may be needed if there is any weakness or balance issue, to prevent falls – important because falls in myelopathy patients can worsen cord injury. Transcutaneous electrical nerve stimulation (TENS) is sometimes tried for neuropathic pain, though evidence for central pain is limited; some patients subjectively find it distracts from the dysesthetic sensations. Psychological support and pain coping strategies are vital in chronic cases. Central pain can be distressing and unrelenting, leading to depression or anxiety. Cognitive-behavioral therapy techniques, meditation, or biofeedback might help patients manage the pain better. In an interdisciplinary pain program, these modalities are often combined with medical management.

Interventional Pain Procedures: For refractory funicular pain not relieved by the above measures (especially if the causative lesion has been treated or is untreatable), interventional neuromodulation can be considered. One option is spinal cord stimulation (SCS), which involves epidural electrode placement typically in the dorsal epidural space. SCS is well established for peripheral neuropathic pain (like failed back surgery syndrome), and there is experience using it in spinal cord injury pain and postlaminectomy cord pain. By delivering electrical pulses, SCS can produce paresthesias that override pain signals (gate control theory) and also induce neuromodulatory neurotransmitter changes. Reports suggest SCS can improve central neuropathic pain in some patients, particularly if at-level (segmental) spinal pain is present. The target level for SCS paddle placement would depend on pain distribution; e.g., mid-thoracic leads for leg pain. SCS success in pure central pain is variable, but given a low risk profile, a trial of stimulation can be offered if resources allow. Another modality is intrathecal drug delivery systems (pain pumps). These can administer medications like morphine, baclofen, or ziconotide directly into the CSF at spinal levels, achieving higher local concentrations with fewer systemic effects. Intrathecal clonidine or baclofen might modulate spinal pain circuits. Intrathecal ziconotide (a calcium channel blocker peptide) is FDA-approved for refractory pain including central pain, though its use requires specialist oversight due to psychiatric side effects. Transcranial magnetic stimulation (TMS) and other noninvasive neuromodulation have been explored for central pain. Repetitive TMS of the motor cortex has shown analgesic effects in spinal cord injury pain in research trials. The analgesia from TMS is thought to stem from activating descending inhibitory pathways that modulate dorsal horn activity. While not yet standard, some tertiary pain centers offer TMS sessions to patients with central neuropathic pain as an adjunct. Similarly, transcranial direct current stimulation (tDCS) and deep brain stimulation (for very severe cases) are in the realm of experimental or last-resort therapies.

Management of Co-morbidities: In a patient with funicular pain due to myelopathy, addressing co-morbid factors can improve outcomes. For example, optimizing diabetic control in a diabetic with compressive myelopathy may improve microvascular health of the cord. Avoiding medications that worsen myelopathy (like nitrous oxide anesthesia in B12-deficient patients, which can precipitate cord damage) is important. Bone health should be optimized (vitamin D, calcium) if long-term disability is expected to prevent fractures. In those who undergo surgery, good perioperative care (physical therapy, DVT prophylaxis, etc.) ensures better recovery and less pain.

Discussion

Despite increased recognition, funicular pain remains a somewhat elusive diagnosis with several controversies and gaps in understanding.

One debate revolves around the pathophysiology: While spinothalamic tract irritation is a leading theory, the precise mechanism of pain generation in cord lesions is not fully clarified. Why do some cord compressions produce excruciating tract pain, whereas others (even severe ones) produce numbness or no pain at all? The variability suggests involvement of individual differences in anatomy and neurochemistry. It’s hypothesized that partial injuries or compressions that leave dorsal horn neurons hyper-excitable (but not destroyed) are likelier to cause pain than complete transections (which cause anesthesia). Further research into spinal cord pain pathways – perhaps identifying biomarkers (imaging or molecular) for tract irritation – is needed. For instance, advancements in neuroimaging like functional MRI of the spinal cord or DTI could shed light on which tracts are activated during funicular pain episodes, helping confirm the pathologic substrate. Some recent works using diffusion tensor tractography show promise in correlating microstructural damage with symptoms in CSM. Ongoing studies are exploring whether DTI metrics can predict which patients with cervical stenosis develop tract pain versus those who remain asymptomatic.

Another area of discussion is the diagnostic approach. There is no standardized guideline on diagnosing funicular pain; clinicians often rely on anecdotal strategies. The use of diagnostic nerve blocks to confirm the level of lesion (as done by Chan et al.) is intriguing but not widely validated. Future prospective studies could evaluate the sensitivity and specificity of, say, cervical epidural blocks in diagnosing cervical-origin leg pain. Moreover, the role of neurophysiological tests (SSEP, MEP) in asymptomatic or minimally symptomatic cord compression could be studied: can these tests predict pain development or recovery? Some literature indicates evoked potentials can uncover subclinical cord dysfunction, but their correlation with pain specifically is not established.

From a therapeutic angle, when to intervene surgically in cases of tract pain is a point of debate. In traditional teaching, surgery for CSM is often advised when objective myelopathy is present. But in funicular pain cases, patients might have severe pain with little myelopathy. Should we operate based on pain alone? Many spinal surgeons would proceed if imaging shows significant cord compression and other causes are ruled out – as the risk of neurological decline exists and pain relief is likely. However, there is no high-level evidence (like a trial) addressing surgery for “pain-predominant” myelopathy. Collecting data on outcomes of such patients would be valuable. The general trend in recent reports is that earlier decompression leads to better pain and neurologic outcomes, so leaning toward treatment is reasonable, but each case should be individualized.

A controversy in management is how to handle patients in whom no clear compressive lesion is found (e.g., they have signs of cord dysfunction and pain, but MRI is normal or shows only mild bulging). These might represent cases of microscopic cord injury or inflammation. One could argue for an empirical trial of therapy (e.g., immunotherapy if suspect inflammatory cause, or careful observation with serial imaging). The lack of clarity can be frustrating for both patient and clinician. Future research might identify molecular markers in CSF or blood indicating spinal cord pathology even when imaging is unrevealing, potentially guiding earlier treatment.

In terms of future therapies, neuroregeneration and neuroprotection in the spinal cord are ultimate goals. For example, if a drug could prevent or reverse demyelination in early CSM, it might stop funicular pain without surgery. Experimental treatments like remyelinating agents or anti-inflammatory biologics for degenerative myelopathy are being explored at the preclinical level. Likewise, microglial inhibitors or modulators (e.g., minocycline, which has been trialed in central pain) could become adjuvants to limit central sensitization in cord injury pain. Neuromodulation technologies are rapidly advancing: high-frequency SCS (10 kHz stimulation without paresthesia) and dorsal root ganglion (DRG) stimulation are new modalities that might be tested for central pain. While DRG stimulation is typically for peripheral focal pain, one could envision stimulating DRGs at a certain level to modulate central pain signaling.

Another aspect is rehabilitative technology: robotic gait training or functional electrical stimulation for paralyzed muscles in SCI might indirectly reduce neuropathic pain by promoting neural plasticity. Brain-computer interfaces and neurofeedback are cutting-edge methods that, in the future, could allow patients to self-modulate their pain by harnessing neuroplastic changes.

From a clinical trials perspective, funicular pain as an entity is hard to study due to its low incidence. However, it overlaps with central neuropathic pain from SCI and MS, which have larger patient populations for trials. So advances in those fields likely will carry over to funicular pain management. For instance, any new medication proven to help SCI pain (such as cannabinoids, which are being studied for central pain) would likely be tried in funicular pain patients as well.

Education and awareness are also future directions: increasing training for clinicians to recognize that leg pain can come from a neck problem, or back pain from a cord tumor (the concept of false localizing sign). Tools like clinical checklists or algorithms (e.g., “Red flags for funicular pain” including bilateral symptoms, non-dermatomal distribution, subtle UMN signs) could be developed to prompt early MRI of the spine in appropriate cases.

Conclusion

Funicular pain is a distinct pain syndrome generated by pathology of the spinal cord’s long tracts. It presents a diagnostic challenge by masquerading as more common peripheral pain conditions, yet it carries significant clinical implications. Early recognition – by noting features like diffuse, non-dermatomal pain and subtle myelopathic signs – is critical to avoid missed or delayed diagnosis. The neuroanatomy of the dorsal, lateral, and ventral funiculi provides the key to understanding how a lesion in one region of the cord can produce remote pain. While relatively rare, funicular pain appears in a variety of settings, from cervical spondylotic myelopathy and intramedullary tumors to demyelinating diseases. A thorough workup with appropriate imaging of the entire spinal axis and neurophysiologic testing can confirm the diagnosis and pinpoint the cause. Treatment should be directed at the underlying lesion whenever possible – often leading to marked relief, as seen when decompressing a compressed cord or resecting a tumor – and supplemented with neuropathic pain management strategies to improve the patient’s comfort and function. For the advanced practitioner, awareness of funicular pain expands the differential diagnosis for limb and axial pain syndromes and underscores the importance of a comprehensive neurologic assessment in all pain patients. Ongoing research into spinal cord pain mechanisms and emerging interventions holds promise to further enhance care for patients with this challenging pain syndrome. In essence, funicular pain reminds us that the spinal cord can “speak” in the language of pain, and we must listen carefully for its subtle cues.

Reading

Funicular pain - Chan 2011.pdf - 348 KB (f)

Funicular pain - Reeves 1968.pdf - 1,017 KB (f)

Funicular pain - Ito 1998.pdf - 1.58 MB (f)