Chronic Low Back Pain with Lower Extremity Weakness: A Case for Conversion Disorder
Jamie Zeman, DC1, Lindsey Rae, DC2
1 Chiropractic Resident, VA Finger Lakes Healthcare System
Published: August 2020
Journal of the International Academy of Neuromusculoskeletal Medicine
August 2020, Volume 17, Issue 1
The original article copyright belongs to the original publisher. This review is available from: http://ianmmedicine.org ©2020 Zeman/Rae and the International Academy of Neuromusculoskeletal Medicine. This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
The purpose of presenting this case is to describe the management of an adult male patient with chronic low back pain and right lower extremity weakness with differential diagnosis including lumbar radiculopathy vs conversion disorder. The authors will describe the patient’s presentation as well as their treatment approach, review possible etiologies, and propose mechanisms to explain treatment response. They will also describe the research, however limited, regarding manual therapies for management of conversion disorder.
A 46-year-old male Army veteran presented with low back pain and right lower extremity weakness of approximately 15 years’ duration. The patient’s primary care physician had made a diagnosis of chronic low back pain, lumbar radiculopathy and right foot drop. He had a limited response to conservative care. Advanced testing included lumbar MRI and EMG, neither of which supported a diagnosis of lumbar radiculopathy.
Management and Outcome
Treatment included manual spinal manipulative therapy, manual flexion/distraction, and home care recommendations of lumbar stretches and cutaneous stimulation. Outcome measures included the PROMIS Pain Interference Short Form 6b and VAS. Repeat examination at the 6th follow-up appointment revealed improved right lower extremity strength and increased sensation to pinprick. Functional improvement included patient-reported improved ease of ambulation.
A male patient with chronic low back pain and right lower extremity weakness responded favorably to conservative treatment of lumbar flexion/distraction technique, spinal manipulation, and home recommendations of lumbar stretches and cutaneous stimulation. Given the chronicity of the complaint and the failure of advanced imaging and electrodiagnostic studies to produce correlative findings, it is unclear whether recovery was the result of lumbar radiculopathy responding to manual therapy or a functional neurologic disorder responding to non-specific therapeutic effects.
chronic low back pain, chiropractic, flexion-distraction, spinal manipulation, lumbar radiculopathy, foot drop, conversion disorder, functional neurologic symptoms disorder
Proximal neuropathies with clinical presentation of foot drop can include a lesion of the L5 nerve root, lumbar plexus, or the sciatic nerve. Foot drop is a term used to describe weakness of the dorsiflexor muscles of the foot, especially tibialis anterior. The innervation of the tibialis anterior begins in the anterior horn cells of the lower spinal cord. Axons travel in the L4 and L5 spinal roots, join to form the sciatic nerve, and travel within the common peroneal nerve before terminating as the deep peroneal nerve which supplies the tibialis anterior, extensors of the toes, and fibularis tertius for foot eversion. The deep peroneal nerve also supplies sensation to the skin over the anterolateral aspect of the lower leg to the dorsum of the toes. The medial terminal branch of the deep peroneal nerve provides cutaneous innervation to the web space between the first two toes. Foot drop is commonly associated with peripheral nerve entrapment at the neck of the fibula, however it can also be a result of anterior horn cell disease, L5 radiculopathy, and sciatic nerve disorders. Distal vs proximal nerve involvement is distinguished by testing of the flexors of the hip, knee, and plantar flexion, as foot drop will likely only affect foot eversion and dorsiflexion. Impingement of the common peroneal nerve may cause variable presentations in sensory or muscle activation of the distal leg. 1, 2
Lumbar radiculopathy is often caused by protrusion of the disc material into the neuroforamen leading to nerve root irritation and impingement. 3 Lumbar radiculopathy may or may not present with symptoms of low back pain radiating into the lower extremity. The affected nerve root can cause pain, weakness, or loss of sensation in a myotomal or dermatomal pattern in the lower extremity. Any lesion to the lumbar roots or plexus may also present as weakness in the lower extremity with weakness in dorsiflexion typically being the most apparent associated weakness. A thorough clinical history is needed when generating a differential diagnosis and identifying potential confounders. 2. 3
According to the North American Spine Society (NASS) the diagnosis of lumbar radiculopathy caused by disc herniation is most supported by positive findings from manual muscle testing, sensory testing, supine straight leg raise, Lasegue sign, and crossed Lasegue sign.4 Other research found dermatomal radiation, positive Valsalva’s maneuver, and positive straight leg raising to be predictors for signs of lumbar radiculopathy (not specific to disc herniation) on needle electromyographic testing (EMG). 5 Specific spinal level of involvement is difficult to determine from clinical presentation as research has demonstrated variability of dermatomal distributions and radicular patterns.3,6
Additional evaluation or testing is indicated when the etiology of muscle weakness and loss of sensation is unclear. The most recent NASS guidelines on advanced studies for suspected lumbar radiculopathy recommend magnetic resonance imaging (MRI) and computed tomography (CT) of lumbar spine first. Further imaging may include lumbar radiographs or extremity CT or MRI to rule out insidious pathology such as soft tissue masses and bone lesions. Electrodiagnostic testing may be appropriate if there is suspicion of nerve root compression.4 Nerve conduction and EMG studies are useful in determining nerve level of involvement and degree of axonal atrophy if present. In differential diagnosis of foot drop, a pathology of the common fibular nerve will show conduction and EMG abnormalities specific to that nerve. Any involvement of the biceps femoris or tibialis posterior indicates more proximal lesions. This type of testing can also help predict recovery, as those who show little axonal damage typically recover within weeks, where those with demyelinating damage may take months to years to recover. 2
When advanced imaging and testing does not correlate well with symptomatology, conversion disorder (CD), also known as functional neurologic symptoms disorder (FND), may warrant consideration. Conversion disorder is a psychiatric disorder in which symptoms and signs affecting voluntary motor or sensory function cannot be explained by pathoanatomical conditions. Conversion disorder symptoms include blindness, paralysis, dystonia, seizures, anesthesia, difficulty walking, hallucinations, dementia, swallowing deficits, motor tics, among other neurologic symptoms. The term conversion disorder was coined by Sigmund Freud, who hypothesized that the symptoms not well explained by medical etiology were due to somatic manifestation of unconscious or repressed psychologic conflict.7 Guidelines for diagnosis listed in DSM 5 include “(1) one or more symptoms of altered voluntary motor or sensory function; (2) clinical findings showing incompatibility between the symptom/s and recognized neurological or medical conditions; (3) these symptoms or deficits are not better explained by another medical or mental health disorder; and (4) the symptom/s cause clinically significant distress or impairment in social, occupational, or other important areas of functioning that warrants medical attention.“ 8 Due to the rarity and variability in presentation of CD, an estimated 2 to 22/100,000 cases per year, evidence based guidelines on diagnosis and treatment are limited.
The onset of symptoms related to CD typically correlate with a certain stressor or trauma. The physical presentation will have no underlying pathoanatomical cause and the affected individual cannot control the symptoms. The patient may exhibit a general lack of concern over the physical symptoms. Differential diagnosis for CD includes myasthenia gravis, multiple sclerosis, polymyositis, stroke, lupus, and spinal cord injury. Anesthesia associated with CD typically occurs in the extremities and will have very precise and sharp boundaries. In cases of weakness, paralysis, or paraplegia, deep tendon reflexes are normal, rather than decreased, and Babinski sign is absent. The symptoms may correlate with half of the body or a single limb and does not follow anatomical patterns. Dystonia presents as an inverted foot or clenched fist of adult onset with a fixed posture .7
Treatment for CD is individualized to symptoms, targeting both psychosocial and physical symptoms. Confronting patients about the psychological nature of their condition is a delicate process and trying to explain the etiology to the patient without first developing strong patient rapport may only exacerbate symptoms. It is advised against giving the diagnosis at initial encounter.7 Laying the groundwork for discussion of psychosocial factors involves providing examples of stress-related physical symptoms such as high blood pressure in times of stress or tachycardia when nervous. Evidence for treatment strongly supports cognitive behavioral therapy (CBT). Other psychotherapies, physical therapy, occupational therapy, and speech therapies are utilized to address return to function and quality of life.9, 10
A 46 year old veteran was referred to the chiropractic clinic with primary complaints of chronic low back pain with a long history of weakness in the right leg. The patient was a part time student during active treatment. Comorbidities included gastroesophageal reflux disease, chronic obstructive lung disease, depression, and tobacco use.
Complicating factors included bilateral knee pain related to history of parachuting while in the Army Airborne unit approximately 30 years ago. The veteran’s career in the service ended when his primary parachute failed to open, and his spare parachute opened late. He recalls a hard landing on his feet and then losing consciousness from the fall. He reports no lingering injuries related to this incident, aside from knee pain.
The patient related his onset of low back pain to a fall over 20 years ago. Mechanism of injury was a slip and fall on wet bathroom tiles, where he landed with his low back contacting the edge of the bathtub. The onset of pain was sudden and severe. He could not ambulate due to pain at the time of injury and was transported by friends to emergent care. After serious pathology was ruled out the patient was treated with narcotic pain medication, which he continued for about 15 years. He described being on long term opioids for chronic pain as a “blurry time” and seemed to lose perception of time and memory eluding to struggles with opioid addiction. He expressed difficulty with his ability to recall specific details of the history of symptoms. The following history is the best representation gathered from subjective history and extensive chart review through VA and DoD databases. He denied referral of pain from the low back to the lower extremities during or shortly following initial injury.
The symptoms of weakness and numbness in the right lower extremity came on gradually, over 10 years ago, without inciting event or injury. He recalls the symptoms occurring periodically at first, presenting as gradual right foot drop, then overall right lower extremity weakness. The symptoms of leg weakness had been present and constant for at least 5 years. At initial evaluation with this author the patient described weakness – especially with ankle, knee, and hip motion – as well as numbness over the entire right lateral thigh, leg, and dorsum and lateral aspect of the foot. The patient was unable to recall any specific positional changes, activity, or medications which improved or exacerbated right lower extremity numbness and weakness. He denied any painful referral into the right lower extremity. Low back symptoms were primarily located in a band-like distribution across the lumbosacral and sacroiliac region extending to the lateral iliac crests. Low back pain presented as constant pain of mild-moderate intensity, with periods of exacerbations. Quality of low back pain was dull, achy, and stiff. Symptoms were more pronounced in the morning and improved with light activity. Pain did not limit any activity. During severe episodes of pain patient experienced a burning sensation in the gluteal musculature and proximal posterior thighs bilaterally. Pain medications included Ibuprofen (3x800mg), Tramadol (2x50mg), and Cyclobenzaprine (2x5mg) daily as needed for pain management. Patient denied any symptoms of urinary incontinence or retention, constipation, bowel incontinence, or saddle anesthesia. Patient denied any history of cancer, unexpected weight loss, stroke, or progressive headaches. No personal history or family history of inflammatory arthropathies.
Previous treatments had included chiropractic care for a 6-month period with biweekly treatments as supportive care consisting of spinal manipulation; his last treatment was approximately one month before his consultation to the VA chiropractic clinic. Previous manual spinal manipulation had resulted in 2-3 week patient-reported improved symptoms. Occasionally following chiropractic treatments the patient had experienced short term (<1 day) painless paresthesia described as “static” affecting the lateral right thigh and leg. He had seen numerous providers over the years for progression of low back and right leg complaint and expressed difficulty recalling what specialties he had consulted. He did not recall any past treatments improving leg sensation or strength. He did not recall a surgical consultation, but eludes to completing a nerve conduction test, the results of which are noted within the chart review section.
A neurology consultation from approximately 8 years ago indicated the patient presented with right knee pain and leg numbness which did not fit a neuroanatomical distribution. Reflexes were normal and symmetric at that time. A repeat nerve conduction study (NCS) and EMG also completed at that time indicated improvement of testing from a year earlier and was, in fact, completely normal despite patient presentation. No further workup was done at that time. There was no treatment or change in symptoms following that consultation.
Based on chart review it had been at least 10 years since patient had met with a mental health provider regarding depression. It is unclear what type of psychotherapy patient had participated in.
Review of Testing
Lumbar and thoracic MRIs from one year prior to chiropractic consultation revealed mild degenerative disc changes, worst at L5-S1, with mild foraminal lumbar stenosis. Findings included a small disc protrusion and annular fissure at L5-S1, where the disc margin abuts the descending S1 roots, left greater than right. There was no evidence of significant thoracic spine degenerative disc changes or stenosis. No modic changes seen. No significant facet arthropathy or stenosis.
A Cervical MRI from approximately 8 years ago was essentially normal.
Per neurology consultation chart review, NCS and EMG from 8 years prior did not demonstrate electrophysiologic evidence of a right lumbar radiculopathy. These findings were improved when compared to NCS 1 year prior which had indicated asymmetry between the left and right peroneal motor F-wave responses, though still within normal limits. The interpreting clinician noted that the results of the prior test may have been a result of incomplete effort, as opposed to neuroanatomical pathology.
Physical examination showed a well-nourished 68.5in, 169.5lb male. Gait was steady with the use of cane, right rigid knee brace, and right AFO brace. Sagittal and coronal spinal curves were essentially normal. The patient transitioned with some difficulty due to right leg weakness, but no signs of apparent discomfort. The writer questioned that there may have been very subtle flexion/decorticate posturing of the extremities. Soft tissue palpation revealed flaccidity of the right hamstrings, right tensor fascia lata, right gluteal, right calf, and right quadriceps. Muscular hypertonicity was noted in the lumbar paraspinals bilaterally.
Lumbar range of motion was mildly-moderately limited in extension and mildly limited in right rotation with mild increase in focal low back pain. No change in leg sensation with lumbar range of motion. Seated and supine straight leg raise was negative for lower extremity symptoms at 80 degrees. Supine knee to chest, posterior shear, and FABER was essentially negative for change in lumbar or extremity symptoms. Sacral thrust and Yeoman’s provoked local low back pain. No orthopedic testing produced any changes to right leg symptoms.
Motor strength of myotomes of the left lower extremity (L1-S1) was graded 5/5. Right hip flexion was graded 4/5, right hip adduction 4+/5, right hip abduction 3/5, right knee flexion 3/5, right knee extension 4/5, right ankle dorsiflexion 0/5, right ankle plantar flexion 4/5, and right great toe extension 4/5.
Reflexes at Patellar and Achilles tendons graded 2+ bilaterally. Sensation on the left lower extremity was intact to pinprick. Sensory testing of the right lower extremity revealed complete lack of sensation to pinprick over the lateral half of LE and dorsum of the foot, exam tested from the proximal-thigh extending distally. During palpation over clothing at the proximal thigh, patient reported decreased sensation to light touch over the right trochanter and lateral gluteal region when compared to the left. Babinski reflex was absent bilaterally. Rapid ankle dorsiflexion revealed one beat clonus on the right, no clonus on the left. Vibration sensation was intact bilaterally at the distal phalanx of the great toe. Upper extremity neurological evaluation revealed motor strength graded 5/5 C5-T1 bilaterally. Hoffman’s sign absent bilaterally.
The patient presentation lead to differential diagnosis of chronic mechanical low back pain, lumbar radiculopathy, right foot drop, and conversion disorder. The lack of clinical correlation between MRI, electrodiagnostic testing, and presentation was confounding. There seemed to be no clear anatomical explanation for anesthesia or weakness or the right lower extremity. The patient relocated multiple times over the past several years and indicated poor compliance with respect to attendance of medical appointments. This, in addition to a history of opioid abuse, complicated his history and the progression of his medical condition. From the patient history it appeared that initial diagnosis was right foot drop, which over a period of years evolved into lumbar radiculopathy. The patient was seeking treatment of low back pain only during this consultation with no expectation that treatment would change chronic lower extremity symptoms, which was also discussed in the report of findings and consent.
According to NASS guidelines for the conservative treatment of low back pain and/or lumbar radiculopathy, spinal manipulation is an option for symptomatic relief, however there is insufficient evidence regarding treatment effect of spinal manipulation and traction/distraction. 4 Research is favorable for spinal manipulation on improving acute radicular symptoms, however there is very limited evidence on the effect of spinal manipulation for chronic radicular symptoms. 11 The patient had responded favorably to spinal manipulation in the past for low back symptoms and was seeking to continue this treatment modality. Chiropractic treatment in our clinic consisted of spinal manipulation, flexion/distraction therapy to the lumbar spine, and therapeutic exercises for stretching the lumbar musculature. Patient education included discussion of hurt vs harm, mind-body relaxation, and overall wellness at multiple appointments. Initial treatment frequency was weekly for 4 weeks, then every 2-3 weeks for supportive care. The patient was also given the option for physical therapy referral, which he declined.
The veteran had been treated a total of 14 times over a time period of 6 months. The patient responded favorably to care, with unexpected changes in lower extremity symptoms. Within 4 visits the patient noticed “pins and needles” intermittently following treatment in the area of the right lower extremity which was previously described as “numb” to all light touch. At the 6th treatment the patient explained that anytime the skin in this region was contacted he would feel a combination of tingling and burning in the area which he described as hypersensitive to touch. A re-examination was completed at the 6th appointment. At the re-examination motor strength of right ankle dorsiflexion improved to 2+/5, and right great toe extension improved to 4+/5. All other myotomes tested essentially the same. Deep tendon reflexes were still essentially normal. No clonus noted on rapid ankle dorsiflexion, as noted at initial exam. The patient was instructed to stimulate the hypersensitive area by massaging it with a hairbrush several times daily. At eight treatments the burning sensation had resolved, and while the entire right extremity was reported to feel less sensitive than the right, it was no longer completely “numb” to light stimulation as at consultation. Over this progression of treatments, the patient also began to report that he could initiate some dorsiflexion of the right foot, but foot would become “stuck” in that position. The patient was referred to physical therapy to attempt to capitalize on current progress. Following 14 visits it was also noted that the patient did not feel the need to refill his cyclobenzaprine or tramadol prescriptions.
Outcomes Measures of Visual Analog Scale and Patient Reported Outcomes Measurement Information System (PROMIS®) Pain Interference Score were recorded at consultation and at the 6th and 12th follow up appointments.12 Results are recorded in Table 1.
The initial diagnosis and presentation several years ago was right foot drop. The patient presentation with symptoms of lack of sensation and weakness in areas outside of the deep peroneal nerve supply indicate foot drop is not a complete diagnosis in this case. The chart review and previous advanced testing did not correlate well with patient presentation. Confounding factors that did not support a typical lumbar radiculopathy included the distal to proximal progression of symptoms, no history of pain in the affected extremity, and normal deep tendon reflexes. It should be reiterated that both previous EMG and NCV studies were essentially normal. 5 In the history and examination, there were no signs suggesting of a demyelinating disorder such as multiple sclerosis, Parkinson disease, stroke, Gullian-Barre, etc. There were no other abnormalities in the review of systems, no suspicion of autoimmune diseases, and the patient did not present with weakness or numbness in any other extremity. The distribution of anesthesia was also confounding as it seemed to include several dermatomes with a very clear border of symptoms. Though evidence has shown that radicular symptoms do not commonly follow a dermatomal pattern related to level of nerve root involvement, this can also describe findings of CD. 6
Due to the chronicity of right lower extremity weakness and anesthesia, the improvement over the course of manual therapy alone was somewhat unexpected. The reported anesthesia had been present and constant for at least 5 years, and questionably episodic for about 10 years prior to that. The pathoanatomical theory for decrease in sensation and muscle strength is mechanical compression and associated chemical and inflammatory response. Nerve fiber deformation and demyelination can lead to numbness and paresthesia. There is limited research on axonal regeneration, but one retrospective study indicated patients continued to experience improving symptoms even at 1 year following decompression surgery. 13 The theoretical mechanism of action of lumbar flexion/distraction in combination with spinal manipulation may explain improvement of radicular type symptoms, if this were a case of radiculopathy. Previous studies have supported that distraction of the lumbar spine can temporarily decompress lower lumbar disk spaces and facet joints and theoretically reduce disc protrusion. 14
Based on the presentation of this case, conversion disorder does warrant consideration. Some authors have suggested a correlation between chronic pain, PTSD, anxiety, and depression with CD. 9,7 There is also question of a higher incidence of CD in veterans, however research in this area is very limited. 10 The writer questions association between opioid use and the presentation of this veteran’s complaints, however no related literature was found concerning incidence of CD and opioid use at the time of this report. During the course of care the veteran’s primary care team was considering referral to spine surgery. Given the presence of medically unexplained symptoms an early diagnosis of conversion disorder may help to avoid unnecessary medical interventions. Treatment for conversion disorder typically involves complementary and alternative medicine and an integrative approach to treatment. 10 Based on this patient’s presentation a psychology referral may have been a more appropriate option than surgical consultation. The treating provider was unfamiliar with conversion disorder at the start of this veteran’s treatment plan, which delayed co-management with mental health providers.
There is very limited research on chiropractic treatment and conversion disorder; only one article mentioning both chiropractic and conversion disorder was found through a PubMed search at the time of this case study’s submission. The case report reviewed chiropractic treatment of an 11-year-old girl referred by her psychologist for the treatment of extremity tremors attributed to conversion disorder. She experienced complete resolution of symptoms after 12 treatments of spinal manipulation over the course of 5 weeks. 15 While this study does not correlate well with our patient presentation, it is another example of conversion disorder managed with chiropractic treatment. One possible explanation may be the role of context and non-specific therapeutic effects of the chiropractic encounter which may include provider relationship, treatment features (including therapeutic touch) and environment.16 A PubMed search for conversion disorder and/or radiculopathy/foot drop found one article presenting a case of a 24 year old male with sudden insidious unilateral foot drop and ascending numbness in the left leg not well explained by examination or history. Symptoms had been present for 3 weeks at the time of advanced testing including NCV, EMG, and brain CT. Curiously the patient had experienced a recent increase in stress not long before onset of symptoms due to the death of his brother from a motor accident in which his brother’s limbs were severed. Presentation of symptoms prompted multidisciplinary treatment with a psychiatrist, physiatrist, and physiotherapist which included gait training, CBT, and venlafaxine (serotonin norepinephrine reuptake inhibitor). The patient experienced complete resolution of symptoms after 6 days of intensive therapy. 17 This case is rather thought-provoking as the presentation is very similar, including the reported distal to proximal onset of symptoms. An inventory of psychosocial stressors at the time of the veteran’s onset of symptoms in this case study would have been interesting for comparison.
This report is meant to raise awareness of a rare condition that may present with musculoskeletal complaints and mimic other common conditions. The authors do not claim to definitively diagnosis or treat conversion disorder.
It is still unknown as to whether it was the manual/mechanical approach to treatment or the non-specific therapeutic effects of treatment including informal patient education which resulted in changes in lower extremity symptoms. Since symptoms have been present for so long, it is difficult to determine how much effect of the current lower extremity weakness has been due to the reliance of AFO and lack of muscle activation. In the absence of clear pathoanatomic etiology of unilateral lower extremity weakness, conversion disorder may be an appropriate diagnosis. Early diagnosis and treatment may save the patient unnecessary testing and interventions.
Written informed consent was obtained from the patient for publication of this report. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
The authors declare that they have no competing interests.
JZ organized the information and drafted the bulk of the manuscript. LR contributed to manuscript preparation.
We would like to thank Paul Dougherty for his assistance in editing this manuscript for submission. There were no sources of funding.
1. Sourkes M, Stewart JD. Common peroneal neuropathy: a study of selective motor and sensory involvement. Neurology. 1991;41:1029–33.
2. Stewart JD. Foot drop: where, why and what to do? Practical Neurology. 2008;8:158-169.
3. Kortelainen P, Puranen J, Koivisto E, Lahde S. Symptoms and signs of sciatica and their relation to the localization of the lumbar disc herniation. Spine. 1985;10(1):88-92.
4. Kreiner DS, et al. An evidence-based clinical guideline for the diagnosis and treatment of lumbar disc herniation with radiculopathy. The Spine Journal. 2014;14(1):180-191.
5. Coster S, de Bruijn SFTM & Tavy DLJ. Diagnostic value of history, physical, examination and needle electromyography in diagnosing lumbosacral radiculopathy. J Neurol. 2010:257-332. https://doi.org/10.1007/s00415-009-5316-y.
6. Murphy DR, Hurwitz EL, Gerrard JK, Clary R. Pain patterns and descriptions in patients with radicular pain: Does the pain necessarily follow a specific dermatome? Chiropractic and Osteopathy. 2009: 7-9. doi:10.1186/1746-1340-17-9.
7. Ali S, Jabeen S, Pate RJ, Marwah S, Chinala S, Milankumar N, Rida S. Conversion disorder – mind versus body: a review. Innov Clin Neruosci. 2015;12(5-6):27-33.
8. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. Fifth ed. Arlington: American Psychiatric Association, 2013.
9. National Organization for Rare Disorders. Functional Neurologic Disorder [Internet]. Rare disease information; 2018. Available from: https://rarediseases.org/rare-diseases/fnd/
10. Tsui P, Deptula A, Yuan DY. Conversion disorder, functional neurological symptoms disorder, and chronic pain: comorbidity, assessment, and treatment. Curr Pain Headache Rep. 2017;21;6: 29. doi: 10.1007/s11916-017-0627-7.
11. Leininger B, Bronfort G, Evans R, Reiter T. Spinal manipulation or mobilization for radiculopathy: a systematic review. Phys Med Rehabil Clin N Am. 2011;22(1):105-125.
12. Amtmann DA, Cook K.F, Jensen MP, Chen WH, Choi SW, Revicki D, Cella D, Rothrock N, Keefe F, Callahan L, Lai JS. Development of a PROMIS item bank to measure pain interference. Pain. 2010;150(1):173-82.
13. Huang P, Sengupta DK. How fast pain, numbness, and paresthesia resolves after lumber nerve root decompression: a retrospective study of patient’s self-reported computerized pain drawing. Spine. 2014;39(8):529-536. doi: 10.1097/BRS.0000000000000240.
14. Gay RE, Bronfort G, Evans RL. Distraction manipulation of the lumbar spine: a review of the literature. J Manipulative Physiol Ther. 2005;28(4):266-73.
15. Alcantara J, Adamek R. The chiropractic care of a child with extremity tremors concomitant with a medical diagnosis of conversion disorder. Complementary Therapies in Clinical Practice. 2012;18(2):89-93.
16. Newell D, Lothe LR, Raven TJL. Contextually Aided Recovery (CARe): a scientific theory for innate healing. Chiropr Man Therap, 2017; 13(26):6.
17. Ayaz SB, Matee S, Malik R, Ahmad K. Conversion disorder; an usual etiology of unilateral foot drop. Acta Neurol Taiwan. 2015;24(2):47-51.