This document discusses the diagnosis and management of inflammatory diabetic neuropathies. It presents two case studies and analyzes the findings. It then covers topics such as the classification of diabetic neuropathies by anatomy and etiology. Specific inflammatory neuropathies discussed in detail include diabetic lumbosacral radiculoplexus neuropathy, diabetic cervical radiculoplexus neuropathy, and diabetic chronic inflammatory demyelinating polyradiculoneuropathy. Diagnostic tests and their findings are summarized. Treatment options emphasized include immunotherapy with corticosteroids which may improve pain and physical therapy. The conclusion stresses the importance of recognizing these inflammatory neuropathies due to their different management and prognosis compared to more common diabetic neuropathies.

1. Diagnosis and Managing
inflammatory diabetic neuropathies
Rahbar, M. MD

2. Case 1
• A 70 Y/O diabetic male with weakness and atrophy of right
upper since 6 months ago
• Acute onset and stable from the onset
• ↓reduced sensation and DTR: both sides, uppers>lowers,
right >Left
• MMT 1-2/5 in RU, 3-4/5 LU; lowers 5/5
• ROM; normal
• EMG and NCV studies of upper limbs
– Moderate neuropathy
– Severe C8-T1 (active denervation) and moderate, mainly, chronic
C5 to C7 radiculopathy
• Cervical MRI : moderate mid cervical spondylosis
• Lab Data, unremarkable except for BS

3. Nerve conduction Studies (NCS): Lowers

4. Nerve conduction Studies (NCS): Uppers

5. Case 2
• A 65 y/o female with sudden onset left lower weakness
since one weeks ago (WB)
• EMG report bilateral mild L5 and S1 root irritation?
• Lumbar MRI, mild spondylosis
• Brain, cervical and thoracic MRI, unremarkable
• Pelvic US, unremarkable
• No Hx DM but lab date, ↑FBS×2, (125-135 mg/dl)
• ↓Sensation in involved side
• MMT 1-3/5 in right and 4-5/5 in left; DTR ↓ or abolished in lowers

6. Case 2
• SNAPs, unobtainable
• Motor NVS, low amplitude with lower limit NCV, f-waves
and h-responses were unobtainable
• Femoral nerve CMAP; L, unobtainable and R, low
amplitude
• EMG, ↓recruitment with ↑firing rate; paraspinal, some
polyphasic MUPS with ↓recruitment

7. Synthesis of the examination findings
• Anatomical
– One lesion
– Multiple lesions
– A diffuse process?
• Syndromal or entity
– radiculopathy, neuropathy, plexopathy, MMN with CB, MND,
UML
• Aetiological (←anatomical or syndromal synthesis)
– discopathy/spondylosis, metabolic and toxic, vascular?

8. Anatomical Diabetic neuropathy classification
• Symmetrical length dependent
• Focal
– Median or ulnar neuropathy
• Multifocal
– Radiculoplexus neuropathies (affect roots, plexus and
individual nerves)

9. Etiology classification
• Metabolic complications
– Most diabetic neuropathies
• Diabetic polyneuropathy
• Compression/entrapment neuropathies
• Inflammatory
– Diabetic radiculoplexus neuropathy (microvasculitis)
• Diabetic lumbosacral radiculoplexus neuropathy
• Diabetic cervical radiculoplexus neuropathy
• Diabetic thoracic radiculopathy
• Painless diabetic motor neuropathy
– Non-diabetic radiculoplexus neuropathy
– Diabetic chronic inflammatory demyelinating polyradiculoneuropathy

10. →

11. Diabetic lumbosacral radiculoplexus neuropathy
• Well known of the inflammatory diabetic neuropathies
• Several different names in the literature
– Diabetic polyradiculopathy, diabetic amyotrophy, diabetic
mononeuritis multiplex and proximal diabetic neuropathy
• The differing names are reflective of historical controversy over the primary
site of nerve injury in these patients
• Common patterns
– Nerve damage at multiple levels
• Nerve roots, lumbar and/or sacral plexus, and peripheral nerve
(radiculoplexus neuropathy)
– Occurred In 1% of both insulin-dependent and noninsulin-dependent
diabetic patients

12. Common patterns
• Tends to occur in patients with shorter duration of diabetes
– Most patients with DLRPN do not have diabetic retinopathy or
nephropathy
• Presentation hallmarks
– Prominent pain component, marked asymmetric weakness, and
subacute presentation
• Classically begin focally with pain → weakness of a lower limb (lumbosacral)
• →bilateral with a median time to bilaterality of 3 months and involve the upper
limbs (cervical) or the trunk (thoracic)
• Occasionally painless

13. Nerve conduction
studies/electromyography
• Axonal-predominant neurogenic process in the lower extremities
– Asymmetric pattern
– Neurogenic findings more diffuse than the clinical presentation
• Outside the lumbosacral distribution
– Cervical radiculoplexus neuropathies
• Reduced sensory nerve action potentials
• Fibrillation potentials in lumbosacral paraspinal muscles
– Confirming the anatomical localization of root
• Cerebrospinal fluid protein
– Elevated with a normal cell count.
• Nerve pathology
– Microvasculitis, ischemic injury and axonal degeneration
– Secondary demyelinating changes due to underlying axonal atrophy

14. Diabetic cervical radiculoplexus neuropathy
• Upper extremity involvement in isolation, or is the
predominant neuropathic feature
– Unilateral or bilateral
• Usually pain followed by weakness
• More common in Type 2 diabetic patients
• Nerve conduction studies/EMG
– Axonal process
• ↑CSF proteins
• Nerve biopsies
– Ischemic injury, inflammation, and microvasculitis

15. CIDP
• Classical CIDP
– Symmetrical, motor predominant, proximal and distal weakness
neuropathy
• Diabetic CIDP as a controversial issue
– A coincidental occurrence
– Some diabetic radiculoplexus neuropathy misdiagnosed
“diabetic CIDP”
• Frequent coexistence of electrophysiological findings of axonal loss
and demyelination in diabetic polyneuropathy
– in some cases over interpreted as CIDP

16. Diabetic CIDP
• No pathophysiological association between the two conditions
– Some forms of radiculoplexus neuropathy such as the painless,
motor and lower limb predominant neuropathy
• CIDP in diabetic patients
– More axonal electrophysiological features than patients with CIDP
alone
• Partially secondary to coexisting diabetic polyneuropathy
– The first line treatments for CIDP
• Corticosteroids, intravenous immunoglobulins, and/or plasma exchange
– Immunotherapy responsive in most diabetic patients
• Less benefit than in idiopathic CIDP
• Greater axonal loss and/or an underlying diabetic polyneuropathy

17. Therapy
• Symptomatic therapy
– Pain control measures
– Physical therapy
– Gait assistive devices (when necessary)
• Immunotherapy
– Corticosteroids
– Improve pain
– Earlier treatment may result in a better and quicker response

18. Conclusion & future perspective
• Very important to recognize
– Their management and prognosis different from the more
common diabetic neuropathies
– Radiculoplexus neuropathies have inflammatory
pathophysiology due to microvasculitis from ischemic injury
– In most cases, appear to be monophasic
• Supportive therapies and pain control are important
• Immunotherapy