There can be variation in the licensing of
different medicines containing the same drug.
Tablet
▶Febuxostat (Non-proprietary)
Febuxostat 80 mg Febuxostat 80mg tablets | 28 tablet P
£24.36 DT = £5.64
Febuxostat 120 mg Febuxostat 120mg tablets | 28 tablet P
£24.36 DT = £24.36
▶Adenuric (A. Menarini Farmaceutica Internazionale SRL)
Febuxostat 80 mg Adenuric 80mg tablets | 28 tablet P £24.36
DT = £5.64
Febuxostat 120 mg Adenuric 120mg tablets | 28 tablet P
£24.36 DT = £24.36
Neuromuscular disorders
Neuromuscular disorders
Drugs that enhance neuromuscular transmission
Anticholinesterases are used as first-line treatment in ocular
myasthenia gravis and as an adjunct to immunosuppressant
therapy for generalised myasthenia gravis.
Corticosteroids are used when anticholinesterases do not
control symptoms completely. A second-line
immunosuppressant such as azathioprine p. 881 is
frequently used to reduce the dose of corticosteroid.
Plasmapheresis or infusion of intravenous
immunoglobulin [unlicensed indication] may induce
temporary remission in severe relapses, particularly where
bulbar or respiratory function is compromised or before
thymectomy.
Anticholinesterases
Anticholinesterase drugs enhance neuromuscular
transmission in voluntary and involuntary muscle in
myasthenia gravis. Excessive dosage of these drugs can
impair neuromuscular transmission and precipitate
cholinergic crises by causing a depolarising block. This may
be difficult to distinguish from a worsening myasthenic
state.
Musculoskeletal system
Muscarinic side-effects of anticholinesterases include
increased sweating, increased salivary and gastric secretions,
increased gastro-intestinal and uterine motility, and
bradycardia. These parasympathomimetic effects are
antagonised by atropine sulfate p. 1404.
Neostigmine p. 1188 produces a therapeutic effect for up
to 4 hours. Its pronounced muscarinic action is a
disadvantage, and simultaneous administration of an
antimuscarinic drug such as atropine sulfate or
propantheline bromide p. 93 may be required to prevent
colic, excessive salivation, or diarrhoea. In severe disease
neostigmine can be given every 2 hours. The maximum that
most patients can tolerate is 180 mg daily.
Pyridostigmine bromide p. 1188 is less powerful and
slower in action than neostigmine but it has a longer
duration of action. It is preferable to neostigmine because of
its smoother action and the need for less frequent dosage. It
is particularly preferred in patients whose muscles are weak
on waking. It has a comparatively mild gastrointestinal effect
but an antimuscarinic drug may still be required.
Neostigmine is also used to reverse the actions of the non-
depolarising neuromuscular blocking drugs.
Immunosuppressant therapy
Corticosteroids are established as treatment for myasthenia
gravis; although they are commonly given on alternate days
there is little evidence of benefit over daily administration.
Corticosteroid treatment is usually initiated under in-patient
supervision and all patients should receive osteoporosis
prophylaxis.
In generalised myasthenia gravis prednisolone p. 716 is
given. About 10% of patients experience a transient but very
serious worsening of symptoms in the first 2–3 weeks,
especially if the corticosteroid is started at a high dose.
Smaller doses of corticosteroid are usually required in ocular
myasthenia. Once clinical remission has occurred (usually
after 2–6 months), the dose of prednisolone should be
reduced slowly to the minimum effective dose.
In generalised myasthenia gravis azathioprine is usually
started at the same time as the corticosteroid and it allows a
lower maintenance dose of the corticosteroid to be used.
Ciclosporin p. 883, methotrexate p. 963, or mycophenolate
mofetil p. 891 can be used in patients unresponsive or
intolerant to other treatments [unlicensed indications].
Acetylcholine-release enhancers
Amifampridine p. 1188 is licensed for the symptomatic
treatment of Lambert-Eaton myasthenic syndrome (LEMS), a
rare disorder of neuromuscular transmission.
Fampridine p. 895 is licensed for the improvement of
walking in patients with Multiple sclerosis p. 893 who have a
walking disability.
Skeletal muscle relaxants
The drugs described are used for the relief of chronic muscle
spasm or spasticity associated with Multiple sclerosis p. 893
or other neurological damage; they are not indicated for
spasm associated with minor injuries. Baclofen, diazepam,
and tizanidine act principally on the central nervous system.
Dantrolene has a peripheral site of action; cannabis extract
has both a central and a peripheral action. Skeletal muscle
relaxants differ in action from the muscle relaxants used in
anaesthesia, which block transmission at the neuromuscular
junction.
The underlying cause of spasticity should be treated and
any aggravating factors (e.g. pressure sores, infection)
remedied. Skeletal muscle relaxants are effective in most
forms of spasticity except the rare alpha variety. The major
disadvantage of treatment with these drugs is that reduction
in muscle tone can cause a loss of splinting action of the
spastic leg and trunk muscles and sometimes lead to an
increase in disability.
Baclofen p. 1190 inhibits transmission at spinal level and
Musculoskeletal system
also depresses the central nervous system. The dose should
be increased slowly to avoid the major side-effects of
sedation and muscular hypotonia (other adverse events are
uncommon).
Dantrolene sodium p. 1417 acts directly on skeletal muscle
and produces fewer central adverse effects making it a drug
of choice. The dose should be increased slowly.
Diazepam p. 360 can also be used. Sedation and
occasionally extensor hypotonus are disadvantages. Other
benzodiazepines also have muscle-relaxant properties.
Muscle-relaxant doses of benzodiazepines are similar to
anxiolytic doses.
Tizanidine p. 1192 is an alpha2-adrenoceptor agonist
indicated for spasticity associated with Multiple sclerosis
p. 893 or spinal cord injury.
g Cannabis extract p. 1190 can be trialled as an adjunct
treatment for moderate to severe spasticity in multiple
sclerosis if other pharmacological treatments are not
effective. Treatment must be initiated and supervised by a
specialist. For further information see Multiple sclerosis
p. 893. h
Other muscle relaxants
The clinical efficacy of methocarbamol p. 1191 and
meprobamate p. 363 as muscle relaxants is not well
established, although they have been included in compound
analgesic preparations.
NEUROPROTECTIVE DRUGS
PDF pages 1207, 1208
