Back Pain and Diabetic Peripheral Neuropathy
Given the fact that 50% of people with diabetes will present with peripheral neuropathy,¹ clinicians should consider diabetes as an etiology for the presenting symptom of back pain – including any region of the spine, whether cervical, thoracic, lumbar, or sacral. Of course, clinicians must be certain that diabetes is indeed present in the patient. This means testing for abnormal values of:
Fasting blood glucose (FBT)
HgA1c-Hemoglobin A1c, or,
2-hour glucose tolerance test (2H-GTT)
The pain may be due to diabetic-related acute ischemic neural infarction, as well as axonal loss and/or demyelination stemming from evolving micro-ischemia of the perineural arterioles that nourish the various nerve roots involved. These pathological findings, in turn, may be related to the hyperglycemic state and insulin deficiency, usually type 2 diabetes mellitus. Such patients are usually older than 50 years, with associated significant weight loss. The precise pathophysiology is less certain.
An inflammatory, immune-mediated vascular radiculoplexopathy is the current probable etiology,²⁻⁵ with most researchers supporting an immune vasculopathy as the cause of this condition. Hence, studies indicate a favorable result when using immunomodulating agents.⁶
The course is usually monophasic and recovery to some degree over many months may be expected. Nonetheless, neuro sequelae may persist.
Nerve Root Pain and Diabetes
More common nerve root presentations of diabetic spine pain include:
Thoraco-abdominal polyradiculopathy: This disorder is seen in 15% insulin-dependent diabetes and in 13% non-insulin-dependent diabetes.⁷
Lumbosacral plexopathy, also known as diabetic amyotrophy or Bruns-Garland syndrome: Prevalence of diabetic lumbosacral plexopathy in individuals with diabetes is 0.08%, but it shows up more in those with type 2 diabetes (1.1%) compared to those with type 1 diabetes (0.3%).⁸ Prevalence is consistent across ethnicity/race and gender, and rarely occurs in adolescents ages 13 to 16 years.⁹ Generally, about 60% of patients recover within 12 to 24 months, however, some remaining weakness, stiffness, and pain may persist, with some patients occasionally relapsing.¹⁰
Neuropathic Pain in Diabetes: Symptoms and Clinical Presentations
Subjective Complaints
Since diabetes is considered a systemic metabolic illness, the presenting symptomology – which may be widespread beyond the spine – and physical examination must further establish that a neuropathic pain state is evident.
Initial symptoms may present acutely (eg, pain due to neural infarction), or be more insidious, (eg, gradual evolution of nerve pathology such as localized numbness, tingling, pain – usually burning – and motor dysfunction along the path of the impaired nerve root(s) – dermatomal or belt-like. These symptoms may be contiguous. Not all symptoms are required at any given time for diagnosis but any grouping is acceptable.
Generally, there is no history of trauma and the pain and symptom severity are variable. When the onset is acute, the pain will be more severe and less so when the onset is gradual. The pain descriptors are usually burning, aching, sharp, shooting, and cramping. The symptom distribution is localized to the affected nerve roots of the spine but can also be lateralized. There is usually little to no relief with over-the-counter analgesics.
Objective Findings
To facilitate and expedite the examination, have the patient complete a pain-symptom body style chart(see Figure 1), which should reveal at a glance the strong probability of the presence of a diabetic radicular neuropathic pain state (ie, either thoraco-abdominal polyradiculopathy or lumbosacral plexopathy). The patient will typically mark lines of pain that emanate from the spine’s involved nerve roots and follow the related dermatome. They can be unilateral or bilateral in distribution.
Diagnosing Thoraco-Abdominal Radiculopathy
To determine thoraco-abdominal radiculopathy via physical exam, at a minimum, a safety pin and reflex hammer should be utilized, with a queen square type is recommended for ease of use (see Figure 2).
Start with inspection of the patient’s spine, looking for soft-tissue asymmetries (ie, bulging of the affected thoracic or abdominal wall) that may be indicative of muscle atrophy of those muscle groups innervated by the affected nerve root(s).
Cervical region (Roots C1-C8)
C3, C4, trapezius
C5, rhomboid
C5, C6, supraspinatus, infraspinatus muscles
Thoracic region (Roots T1-T12)
Intercostal muscles
Then do the same for the patient’s anterior chest and abdominal wall.
There may be altered sensation in the affected roots as well. This may be in the form of decreased sensation, or increased pain sensitivity to touch or pin prick, or even allodynia (eg, painful sensation to a non-noxious stimulus, light touch evoked severe pain). The dermatome will facilitate isolating and identifying the affected nerve roots involved.
Diagnosing Lumbosacral Plexopathy
For suspicion of a lumbosacral plexopathy, inspect the muscle groups of both lower extremities for focal atrophy and altered sensation:
Lumbosacral region (Roots L1-L5 & S1-S4)
L1, Abdominal internal obliques
L2-4, Iliopsoas (hip flexor), Adductor longus (hip adductor)
L5, Tibialis anterior, Extensor hallucis longus, Extensor digitorum brevis Gastrocnemius, lateral head, Ankle dorsiflexion muscles
S1, Gastrocnemius, medial head
The neurological exam must be extended to include motor and sensory testing of the lower extremities to correlate any atrophy related weakness. Also test the deep tendon reflexes:
Knee jerks (patellar): Roots L3, L4
Ankle jerks (Achilles): Root S1
These may be asymmetric if their corresponding nerve roots are part of the affected region.
Differential Diagnoses: Diabetic Back Pain
Overlapping Conditions
When considering the assessment and differential diagnosis, keep in mind that multiple contributing factors may be present and be responsible for the subjective and objective findings (eg, spinal segmental lesions, herniated nucleus pulposus). Clinicians should also consider:
Shingles – Herpes zoster prodrome
Forme fruste Herpes zoster
Forme fruste_indicates an incomplete phenotypic expression of a condition (eg, shingles without the rash or_zoster sine herpete wherein typical skin lesions and blisters are absent but pain is present)
Post-herpetic neuralgia (PHN)
Spinal metastases
Myocardial infarction
Acute cholecystitis
Acute appendicitis
Diverticulitis
Laboratory Tests
The differential diagnoses will direct additional testing. As there can be other causes for neuropathy (eg, anemia, B12 deficiency, hypothyroidism, and connective tissue disorders,) the specialist may order the following testing:
Fasting plasma glucose
Hemoglobin A1c
Complete blood count
Complete metabolic panel (electrolytes and liver function panel)
Vitamin B-12 and folate levels
Thyroid function tests
Erythrocyte sedimentation rate
C-reactive protein
Serum protein electrophoresis with immunofixation electrophoresis
Antinuclear antibody
Anti-SSA and SSB antibodies
Rheumatoid factor
Paraneoplastic antibodies
Rapid plasma reagin
Genetic screens
Hematology screen (for anemia)
Sequential multiple analysis-7 (renal function and electrolyte imbalances)/complete metabolic panel (CMP)
Neurodiagnostics
Electrodiagnostic testing should include paraspinal EMG (may reveal denervation) in both thoraco-abdominal polyradiculopathy and lumbosacral plexopathy. The addition of nerve conduction velocity and EMG testing for both lower extremities may also be revealing, demonstrating a widespread polyneuropathy.
Imaging
Recommended radiologics and imaging modalities that may further clarify the differential diagnosis are x-rays: thoracic and lumbosacral series and CT and MRI: thoracic, lumbar, and Technetium 99 nuclear bone scan.
Specialty Consultation
Specialty consultation may be necessary regarding additional advanced diagnostics and treatment.
Education
The examiner should engage the patient and support system with a clear education of the preliminary diagnoses and how they relate to the presenting problems and proposed treatment.
Diabetic-Related Back Pain Treatment Approaches
Treatment for diabetic-related back pain will always be dependent upon the degree of diagnostic certainty at the first visit and refined at follow-up visits. Initially, treatment may target symptoms only, such as optimization of blood glucose, analgesics, anti-neuropathic adjuvants, tricyclic antidepressants, SNRIs, anti-epileptic adjuvants, gabapentin, duloxetine, pregabalin, or opioids.
Treatment might also include local anesthetic differential neural blockade, followed by XL-NMA (cross-link neural matrix antinociception) injection of high density (20 mg/ml, gel particles/ml, 100K, particle size, 0.28-0.50 mm), cross-linked hyaluronic acid at the same levels.
More advanced treatment approaches may include immunomodulating agents such as intravenous human immunoglobulin (IVIg),¹¹⁻¹³ pulsed methylprednisolone,¹⁴˒¹⁵ plasma exchange¹⁶˒¹⁷ or cyclophosphamide.¹⁸
Physical therapy will assist to improve functional mobility in the patient, such as for transfers and ambulation, while the use of assistive devices and exercise and range-of-motion stretches can maintain and improve lower extremity motor function.
Given the clinical considerations herein, the patient with diabetic back pain will likely need to be managed in a multidisciplinary manner.
Practical Takeaways for Managing Back Pain due to Diabetes
Back pain due to diabetes requires a high index of suspicion. Clinicians should not assume that a patient presentation of back pain is due to the more accustomed causes. Taking a deliberate history and performing a pain-focused examination, as indicated herein, can help to rule diabetic etiology in or out as a possible cause for the pain.
Remember, back pain in the diabetic individual should remind you of early shingles of the thoracic, abdominal wall, or of the lower extremities, only without the rash. Once identified and supported by the various diagnostic modalities as noted above, treatment can be straight forward.