This is the most frequently occurring demyelinating neuromuscular disorder. It’s a chronic progressive disease characterized by repeated exacerbations and partial remissions. It is characterized by the formation of plaques within the brain and spinal cord. These plaques cause demyelination around the axons, resulting in weakness and spasticity as well as sensory dysfunction.Upper motor neurone lesions, cerebellar lesions and sensory deficits are common.

Anaesthetic considerations.

• General anaesthesia does not exacerbate MS. Non-depolarizing neuromuscular blocking agents may be used in normal doses. Caution should be exercised when using depolarizing neuromuscular blocking agents if the patient is debilitated. With the use of Suxamethonium, there is a risk of hyperkalemia

Regional blockade.

• Local anaesthetics may exacerbate the symptoms due to the increased sensitivity of demyelinated axons to local anaesthetic toxicity. New lesions may develop coincidentally at the time of regional blockade and subsequent symptoms may be difficult to differentiate from nerve injury or may be blamed on the block. Complications have been reported with spinal anesthesia (Weak myelin sheath and direct neurotoxicity from LAs have been suggested as reason for this). Epidural may be relatively safer in this regard. (In epidural technique, there will be a lower concentration of LA in white matter). Therefore in general, regional blockade may be relatively contraindicated.

Temperature maintenance is important as symptoms can deteriorate with an increase in temperature, as demyelinated axons are also more sensitive to heat.

Most often, postop exacerbation, if it occurs, is due to fever and infections

We should explain the chance of exacerbation of symptoms before any form of regional anesthesia

TREATMENT

• The treatment of MS includes treating acute attacks to limit sequelae, prophylactic medications to  reduce rate of progression, and symptomatic/supportive therapy

• Acute attacks are treated with high-dose corticosteroids, i.v. methylprednisolone 500–1000 mg every day divided every 6 or 12 hours; tapered over 7–10 days.

• Prophylactic medications include the disease-modifying drugs interferon β and glatiramer acetate. Side effects include local infections, fatigue, depression, and anxiety. Regular CBC, LFT, and electrolyte checks are needed.

• For progressive disease, immunomodulatory drugs such as methotrexate, cyclosporine, cyclophosphamide, azathioprine, total lymphoid irradiation, mitoxantrone (risk of cardiotoxicity), mycophenolate mofetil, or interferon-β may be employed

• Symptomatic therapies include antidepressants for depression, anticholinergics for hyperreflexic bladder, alpha-blockers or cholinergics/catherization for flaccid bladder, amantadine for fatigue, antispasticity drugs (baclofen, tinzanidine, dantrolene, benzodiazepines) for muscle spasticity, AEDs for tremor, clonus, and pain, and sildenafil for sexual dysfunction. More invasive methods, for example, botulinum toxin injections for focal spasticity or bladder augmentation for spastic bladder may be required in more severe cases

• Supportive care includes physical/occupational therapy, coping strategies or lifestyle modifications, cognitive-behavioral therapy, and emotional support.

• In more severe cases, ambulatory aids or wheelchairs and other home-assist devices and caregiver support may be necessary