Lower Back Pain Diagnosis and Imaging

Lower Back Pain

• Do not perform imaging for lower back pain within the first 6 weeks unless red flags are present (severe or progressive neurologic deficits or serious underlying conditions)
• If there is a concern for a vertebral compression fracture, a plain lumbar spine x-ray should be done immediately after evaluation

Peripheral Neuropathy

• Can be particularly devastating in older adults, causing gait impairment from sensory and motor deficits, leading to a propensity to fall
• Prevalence up to 10% in older adults, 30%-60% in patients >60 years with diabetes mellitus
• Common causes:
  • Medications, alcohol abuse, and nutritional deficiencies
  • Renal disease (uremia)
  • Monoclonal gammopathy (e.g., multiple myeloma)
  • Neoplasia
• Diagnosis:
  • History geared towards identifying possible causes and risk factors
  • Neurologic examination to establish evidence of length-dependent loss of sensory and/or motor function
  • Electromyography and nerve conduction studies to help classify the neuropathy
  • Refer acute, atypical, rapidly progressive, or severe forms of neuropathy to a neurologist with expertise in neuromuscular medicine
• Treatment:
  • Depends on underlying cause
  • Optimizing glucose control can lessen the severity of diabetic neuropathy
  • Treating neuropathic pain:
    • Tricyclic antidepressants (off-label)
    • Gabapentin or pregabalin (FDA-approved for post-herpetic neuralgia; pregabalin also approved for diabetic neuropathy)
    • Duloxetine (FDA-approved)
    • Tapentadol (FDA-approved)
    • Tramadol and opioids (all off-label) (SOE=B)
    • Topical agents (e.g., capsaicin cream, lidocicine patch) (SOE=B)

Radiculopathy

• Cause: compression of spinal root as it exits spinal cord
• In older adults, may result from:
  • Herniated discs
  • Osteophyte formation
• Symptoms:
  • Pain may radiate down neck, back, arm, or leg
  • Neurologic examination may reveal:
    • Motor and sensory defects
    • Diminution of reflexes in distribution of spinal root(s)
• Diagnosis:
  • MRI with contrast and lumbar puncture with cytology may help make the diagnosis
  • Acute inflammatory demyelinating polyradiculoneuropathy (AIDP), also termed Guillain-Barré syndrome, is an acute, immune-mediated form of polyradiculopathy
  • Chronic inflammatory demyelinating polyneuropathy is a chronic form of AIDP and requires long-term immunotherapy
  • Patients with diabetes may present with diabetic amyotrophy, a lumbosacral polyradiculitis and plexopathy

Myopathy

• Characterized by proximal muscle weakness, wasting, and diminished or absent reflexes
• Can be accompanied by increases in muscle enzymes, myopathic pattern on electromyogram, and abnormal muscle biopsy
• Polymyositis: disorder of skeletal muscle
  • Muscle biopsy shows signs of lymphocytic infiltration, and usually also myocyte degeneration and regeneration
  • Prednisone is the treatment of choice but should be used with caution in older adults
• Thyroid-related myopathies:
  • Weakness and wasting are greatest in the pelvic girdle muscles and, to some extent, the muscles of the shoulder region
  • Reflexes can be normal, and diagnosis is based on the distribution of muscle weakness
  • Improves with successful treatment of the underlying endocrine disorder, such as hypothyroidism

Motor Neuron Disease (Amyotrophic Lateral Sclerosis)

• Progressive, fatal neurodegenerative condition involving both upper and lower motor neuron cell bodies
• Symptoms:
  • Progressive weakness and wasting of skeletal muscles
  • Often in combination with bulbar palsy and respiratory failure
  • Common symptoms: gait disturbance, falls, foot drop, weakness in grip, dysphagia, dysarthria
• Electromyography demonstrates findings consistent with diffuse denervation and poor recruitment of motor units
• Differential diagnosis:
  • Lesions at the level of the foramen magnum
  • Combination of cervical myelopathy associated with cervical and lumbar polyradiculopathies
  • Motor-predominant peripheral polyneuropathy
• Average survival 2-3 years, with the presence of bulbar weakness carrying a poorer prognosis
• Treatment is mostly supportive, with riluzole having modest effects on survival, time to tracheostomy (SOE=A)

Myelopathy (Spinal Cord Dysfunction)

• Intrinsic lesions can result from spinal cord tumors, vascular events (infarcts or hemorrhages), or trauma
• Extrinsic lesions are more prevalent, such as:
  • Cervical spondylosis
  • Disc prolapse or herniation
  • Vertebral body subluxation due to rheumatoid arthritis
  • Meningioma or spinal metastases
• MRI can be helpful for diagnosis, but abnormal findings are common in older adults
• Decompressive surgery is recommended for persistent pain or progressive neurologic deficit

Multiple Sclerosis

• Most common cause of disability in young adults

• Recurrent, occasionally progressive, inflammatory demyelination of white matter of brain and spinal cord

• Multiple varied neuro symptoms and signs

• Autoimmune attack on myelin: brain and spinal cord

• Cause unknown

• Genetic susceptibility

• Human herpes virus 6

• Latent infection in CNS

• Vitamin D Deficiency

• Symptoms:

  • Unilateral vision loss
  • Diplopia (days to weeks)
  • Hemiparesis (slow insidious)
  • Fatigue, mobility, cognitive dysfunction, bowel and bladder, depression and mood disorders

• Diagnosis:

  • History
  • MRI [supports the diagnosis]
  • Cerebral spinal fluid

• Differential diagnoses:

  • Acute disseminated encephalomyelitis
  • Syringomyelopathy
  • Foramen magnum lesion
  • Progressive multifocal leukoencephalopathy
  • Pernicious anemia
  • Spinal cord tumor
  • Vasculitis
  • CNS infections
  • Neuro syphilis
  • Lyme disease
  • Hereditary ataxia

• Diagnostic criteria:

  • Two attacks, two areas of CNS involved
  • Neuro signs at least two separate areas of involvement
  • Best fit

• Subtypes:

  • Relapsing Remitting (RR)
  • Secondary progressive (SP)
  • Progressive relapsing (PR)
  • Primary progressive (PP)

• Management:

  • Disabling symptoms
  • Acute attacks—therapies to reduce inflammation and shorten duration
  • Long-term treatment
    • Five therapies approved
    • Reduce attacks
    • Prevent new lesions in brain
    • Slow disability

• Nonpharmacologic treatment:

  • Aggressive rehab after acute events
  • 80% of patients use complementary or alternative medicine
  • Yoga
  • Cannabis extracts

• Pharmacology:

  • Symptomatic treatments
  • Disease-modifying agents
    • Have the potential to change the long-term sequelae of disease progression
    • Very expensive, long-term medications
    • Many side effects
    • Poor adherence very common
    • Interferon type medications
    • Other immune modulators### Guillain-Barré Syndrome (GBS)

• Approximately 15% of patients experience residual weakness after 3 years.

• The International Guillain-Barré Syndrome Outcome Study (IGOS) is an internationally collaborated prospective trial aiming to examine outcomes of GBS based on clinical and biological determinants and predictors.

Myasthenia Gravis

• Normally, impulses travel along the nerve to the ending, releasing acetylcholine, which binds to acetylcholine receptors, generating muscle contraction.
• In Myasthenia Gravis (MG), a person's own antibodies block, alter, or destroy acetylcholine receptors, preventing muscle contraction.
• MG is a disease of skeletal muscle acetylcholine receptors, where acetylcholine is unable to bind to receptors on the postsynaptic membrane to transmit nerve impulses to muscle fibers.
• The thymus is believed to be the site of antibody production in MG.
• 80% of MG patients have thymus hyperplasia or thymus tumor.
• 80-90% of MG patients have auto-antibodies directed at acetylcholine receptor sites.