1) Leprous neuritis is inflammation of the peripheral nerves caused by invasion of lepra bacilli, which leads to nerve function impairment (NFI). It is mediated by Schwann cell invasion and immune/inflammatory reactions.
2) Clinical features include acute/chronic neuritis with sensory, motor, and autonomic NFI. Neuropathic pain is also common. Treatment involves continuing multidrug therapy, anti-inflammatory drugs like corticosteroids, and surgery in severe cases.
3) Preventing leprous neuritis requires early detection/treatment of leprosy and prompt initiation of multidrug therapy, with prophylactic corticosteroids during treatment to reduce reactions. Experimental
5. CLINICAL FEATURES
• Neuritis/neuropathy :
Acute/ subacute/
chronic, demyelinating, nonremitting event
involving cutaneous nerves and larger trunks
• NFI :
sensory, motor & autonomic nerve deficits
due to pathological processes from infection
of nerve
6. NFI
early
Late
Sensory :
Altered heat & cold
sensitivity, hypoesthesia
Sensory :
Hypoesthesia, anesthesia leading to
neuropathic ulcers
Motor :
Mild motor weakness
Motor :
Severe motor weakness progressing to
paralysis
Autonomic :
Decreased sweating
Autonomic :
Severe dryness with fissuring of skin
7. • Silent (Quiscent) neuritis :
progressive sensory or motor impairment
without pain, paraesthesia or tenderness of
nerve & no signs of reaction
• Neuropathic pain :
Pain initiated or caused by a primary lesion or
dysfunction in peripheral or central nervous
system
8. Grading of neuropathic pain
Grade
Degree
Description
0
None
No nerve pain
1
Mild
Complains of nerve pain even when not asked
2
Moderate
Complains severe nerve pain, sleep not disturbed, it is
aggravated by repeated use of the limb
3
Severe
Pain is severe & it interferes with sleep; patient keeps the
limb in rest position & avoids movement
9. Classification of Neuritis
• Acute neuritis : swelling due to nerve abscess
or recent onset rapidly progressing
neurological deficit < 06 mo
• Chronic neuritis : long standing > 06 mo of
gradually progressive neurological deficit with
nerve tenderness or pain
10. • Recurrent neuritis : an episode of neuritis
recurring after a symptom free interval of min
03 mo
• Catastrophic paralysis : sudden paralysis
• Completely destroyed nerves : no residual
nerve function and electrophysiological
studies show no conduction
11. Principles of Therapy
• MDT continuation
• Treating complicating Reactional States
• Prolonged Anti-inflammatory therapy
• Surgery
• Rest / Physical Therapy
• Physiotherapy
13. Corticosteroids
• Anti-inflammatory + Immunosuppressive
• Genomic Action (Nuclear Receptors) – Immediate
Action (Dec Edema / Pro-inflamm CKs)
• Non-Genomic Action (Cystoplamic Receptors) Immunosuppressive Action
• Indicated in ACUTE NEURITIS ; as early as detected
14. WHO regime
Initiate Prednisolone at 40 mg – taper every 02
weeks over 12 weeks (40-30-20-15-10-5-X)
Prolonged Therapy (24 weeks) OR
High-dose Therapy (02 mg/kg)
Favourable Response :
Sensory > Motor NFI (BANDS)
Acute > Chronic > Recurrent Neuritis (AMFES)
15. ADRs (TRIPOD)
• Minor (20%)
Gastric Intolerance / Fungal Inf / Acne
Major (02%)
Peptic Ulcer / Bacterial Sepsis / DM
Immunosuppression may interfere with killing
of Bacilli and reduction in Antigenic Load ;
Concomitant CLOFAZIMINE
16. Clofazimine
• Phenazine derivative
• Dec Granulocyte Chemotaxis / stabilizes
Lysosomes ; binds to Mycobacterial DNA
• Steroid-sparing agent = Anti-inflamm + Antileprosy agent
• ENL / Reduces incidence of T1R
• Slower onset of action
17. REGIME
• 300 mg daily PO X 12 weeks
• 200 mg daily PO for a few months
• 100 mg daily PO continued
ADRs
Cutaneous / Mucosal pigmentation
Gastrointestinal Intolerance
Ichthyosis
18. Thalidomide
• Glutamic Acid derivative
• Anti TNF-A
• Immunomodulatory / Anti-inflamm /
Hypnosedative effects
• FDA-approved for ENL
19. • 100-400 mg daily till pain subsides decrease by 50mg
every 02-04 weeks
• ADRs
Paradoxical Peripheral Neuropathy
50% Reduction in SNAP-a with Normal NCV
Teratogenicity
Proximal Muscle Weakness
Somnolence
Leukopenia
20. AZA
• Immunosuppessive + Anti-inflamm + SSA
• 6-TP (Guanine) ; purine analogue inhibits cell
division , T & B cell function
• 2nd Line Treatment for T1R (ILEP)
• 03 mg/kg/day x 12 weeks with Prednisolone
40mg tapered over 08 weeks
• Pancytopenia / Hepatotoxicity / GI Intolerance
21. CsA
• Immunosuppressant
• Calcineurin Inhibitor Calcium-Calmodulin complex
dec activity of NFAT-1 inhibit IL-2 production
Dec activity of CD4+ T-cells ; Reduction of Anti-Nerve
Growth Factor (NGF) ABs
• Chronic ENL / T1R / Chronic Neuritis
• 5 mg/kg (upto 7.5 mg/kg) tapered over 12 months
• Nephrotoxicity / Hypertension / Dyselectrolemia /
Hypertriglycidemia / Gum Hyperplasia
22. Intraneural Therapy
• Severe Uncontrolled Neuritic Pain
• Isoxsurpine / Tolazoline (VASODILATORS) help
spread Corticosteroids under LA
• Treatment of Claw Hand in 60 yr old over 06
months by Nashed et al
• Intense pain, Nerve fibre damage potential
23. Chr Neuropathic Pain
• Primary lesion / dysfunction of Nerve produces
pain – continuous, burning, Glove-and-Stocking
distt
• Late complication of Hansen’s
• Small fibre neuropathy / Persistent Intraneural
Inflamm
• MDT-completion + Not in Reaction + No NFI
26. EXTRA-NEURAL NEUROLYSIS
Decompression Sx – removes fibrotic bands / ligaments to
open fibro-osseous channels – relives external pressure
INTRA-NEURAL NEUROLYSIS
Longitudnal Incisons in Nerve Sheath Epineurium
INTERFASCICULAR NEUROLYSIS
Individual Nerve Fibres dissected and separated ; risk of
damaging Vasa Nervorum , Fibrosis
NERVE ABSCESS DRAINAGE
Longitudnal incision drain Caseous material
NERVE TRANSPOSITION
Medial Epicondylectomy for Ulnar Nerve
27. General Measures
•
•
•
•
•
•
•
Rest for Acutely inflamed Nerve
Avoidance of trauma
Immobilization with padded splints
Graduated Exercises in Recovery phase
SWD / UST / TENS for added pain control
Hand / Foot Care
Counselling and MDT
28. PREVENTION
• Early Detection of Hansen’s / Reactions
• Prompt initiation of MDT
PROPHYLAXIS
• 20mg/day Prednisolone with 1st 04 months of
MDT lowered risk of T1R
• 300mg/day Clofazimine for 1st 03 months of MDT
lowered incidence of Neuritis
29. EXPERIMENTAL THERAPY
• Drugs and Vaccines blocking Mycobacterial
attachment to Schwann Cell-Axon Unit /
Specific Bacterial Unit causing Nerve tropism
• Neutrotropic Factors (NTFs)
Regulate Schwann Cells to regenerate Axons in PNS
by increasing Impulse Transmission across Axons
blocked by Mycobacterial AGs