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
Educational resource from ReLiva Physiotherapy, for patients suffering from frozen shoulder or adhesive capsulitis. Has details on stages of frozen shoulder, home remedy tips and physiotherapy treatment and exercises. Not a medical advice.
Educational resource from ReLiva Physiotherapy, for patients suffering from frozen shoulder or adhesive capsulitis. Has details on stages of frozen shoulder, home remedy tips and physiotherapy treatment and exercises. Not a medical advice.
A brief account on major toxidrome and an explanation about how the clinical features occur. anticholinergic, cholinergic, sympathomimetic, opiate, sedative toxidrome and serotonin syndrome and neuroleptic malignant syndrome are explained with the management.
ANAESTHESIA MANAGEMENT IN PATIENTS OF NEUROMUSCULAR DISORDERS.pptxSumit Tyagi
Comprehensive ppt covering myasthenia graves in details along with other neuromuscular disorders.
brief and complete solution for presentation needs of DNB/MD students in anaesthesia department.full coverage of myasthenia graves with light on all other neuromuscular disease.illustrative diagram of NMJ.Tabular list of drugs exacerbating myasthenia graves and increasing the duration of action of the muscular relaxants
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