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CONTINUING
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Multiple sclerosis
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Multiple sclerosis: managing

a complex neurological disease
NS769 Embrey N (2014) Multiple sclerosis: managing a complex neurological disease.
Nursing Standard. 29, 11, 49-58. Date of submission: May 31 2014; date of acceptance: September 1 2014.

Aims and intended learning outcomes

Abstract
This article aims to improve nurses knowledge
This article describes the complex neurological condition multiple sclerosis of the management of multiple sclerosis (MS),
(MS) and its management. It outlines the pathophysiology and symptoms, a complex neurological condition. After
the importance of timely access to specialist services for treatment of reading this article and completing the time out
symptoms, and relapse and disease management. New and emerging activities you should be able to:
therapies for the management of MS, the role of the multidisciplinary Explain the pathophysiology of MS.
team, the importance of holistic assessment and the role of the MS Discuss the signs, symptoms and
specialist nurse are discussed. Self-management of MS is integral to management of MS.
managing this life-limiting long-term condition. While there is no cure for Describe the treatment options available.
MS, new and oral disease-modifying therapies providing better efficacy Promote self-management of the condition
in stabilising the disease have recently been introduced, reducing relapse and multidisciplinary working.
frequency and disease activity, and delaying the progression of disability.

Author
Nikki Embrey, clinical nurse specialist (multiple sclerosis), North Midland
MS Service, University Hospital of North Staffordshire, Stoke on Trent.
Correspondence to: nikki.embrey@uhns.nhs.uk
Keywords
Central nervous system, multiple sclerosis, neurological condition,
relapse, self-management, symptom management, chronic disease,
relapsing-remitting conditions, patient-centered care, self-care
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To write a CPD article: please email gwen.clarke@rcnpublishing.co.uk
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Introduction
In 2010, an estimated 126,669 people in the
UK had MS, with 6,003 new cases diagnosed
in the same year (Mackenzie et al 2014).
This study recognised an increasing population
of people who are living longer with MS and
the implications this has for MS services.
MS is a common chronic neurological
condition causing disability in young adults
(MacLurg et al 2005). It is a central nervous
system (CNS) disorder involving the brain
and spinal cord, demyelination of nerves and
impairment of nerve conduction.
MS often affects those aged 20-40 and
affects three times more women than men.
The condition is occasionally diagnosed in
young children and those over 65 years of age.
There are varying courses of the condition,
the most common being acute, inflammatory
episodes (relapses), followed by periods of
remission. However, this is often superimposed
on a background of progressive disability,
reduced functionality and neurological
impairment. MS may exist subclinically.

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CPD neurology

The trigger for the initial symptoms and
how the condition develops are not
understood fully. MS symptoms are variable,
and the disease is unpredictable; for some,
life expectancy is unaffected, while others
may experience years of disability or
early death.
While the cause of MS is still not known,
and a cure has not been found, the management
of MS has improved significantly. Since the
introduction of disease-modifying treatments
(DMTs) under the risk-sharing scheme
(Department of Health (DH) 2002) there has
been an increase in MS services, in particular
access to specialist nurses and an increasing
understanding and responsiveness towards
patient management. The revised National
Institute for Health and Care Excellence (NICE)
(2014a) MS guidelines have now been published.
Pathophysiology
MS is a complex condition (Dutta and
Trapp 2006). It is an inflammatory,
demyelinating disease of the white matter
of the CNS that develops in a genetically
susceptible individual after exposure to
non-specific environmental factors (MS Trust
2011). Mechanisms for breakdown of the
blood-brain barrier (BBB) are incompletely
understood in MS, although immune
cells are thought to infiltrate the brain,
leading to inflammation and demyelination
(Minagar and Alexander 2003). Following
myelin breakdown (Figure 1), axonal and
glial injury, nerve conduction is blocked,
resulting in nerve pathways malfunctioning
(Goodkin et al 1998). Frequent relapses
lead to an overgrowth of astrocytes, which
results in scarring (plaques) (Zajicek
et al 2007). Magnetic resonance imaging
(MRI) studies suggest subtle focal tissue
alterations may precede the appearance of
an active MS plaque (Lassmann et al 2007).
Lesions appear mainly in a periventricular
distribution, with clusters around the
ventricles, but thecortex can also be affected,
with diffuse injury of the normal-appearing
white matter (Lassmann et al 2007).
Oligodendrocyte destruction also results in
loss of the myelin sheath, which leads to the
variable symptoms of MS, depending on the
areas affected.
Complete time out activity 1
Cause
The cause of MS remains unknown; however,
the evidence points towards a complex
interaction with genetic and environmental

FIGURE 1
Structure of neurones

Myelinated neurone

Cell body

Myelin Nerve fibre (axon)

Passage of messages along the axon

Demyelinated neurone
1 Consider the process
Damaged myelin
of demyelination and
(demyelination)
the cells responsible
for creating myelin that
are targeted in MS.
What is the function of
PETER LAMB

myelin and the effect

of its breakdown Passage of distorted messages along the axon
on an individual?

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factors. These are thought to provoke the A lumbar puncture and analysis of
immune system to produce an autoimmune cerebrospinal fluid (CSF) can provide
response, which attacks the cells that supporting evidence of a diagnosis of MS.
form myelin. With time, axonal loss and A positive result is usually indicated by elevated
neurodegeneration lead to accumulative levels of immunoglobulin G antibodies,
disability. Degeneration is thought to begin protein, and oligoclonal bands
early in the subclinical phase. Various factors which indicate the breakdown of myelin
may influence progression, such as familial in the CSF and not present in the serum
risk, gender, diet, levels of vitamin D3 and sample taken at the same time. Other tests
ultraviolet-B (UVB) exposure, month and include neurophysiological tests, visual
place of birth, smoking, migration and evoked potentials, and measuring the speed
Epstein-Barr serology (MS Trust 2011). of impulses from the cortex along the optic
pathways, which are often delayed in MS.
Vasculitis and immunology screening will rule
Diagnosis out conditions with similar symptoms. Unless
Diagnosis is made by a neurologist, the patient has typically relapsing-remitting
however a team of specialist healthcare MS, it is difficult to interpret the type of MS at
professionals, including nurses, will be diagnosis. Criteria by which MS is diagnosed
involved. Common initial symptoms are indicated in Table 2. 2 Consider the
of MS include: Complete time out activities 3 and 4 findings on an MRI scan
Visual disturbances such as pain in and that might suggest
around the eyes, blurred vision and altered a person with MS is
colour perception, as a result of optic Management in the early stage of
nerve inflammation. MS nurses co-ordinate patient care from demyelination and
Sensory disturbances such as diagnosis; general nurses also care for people compare them with
numbness, paraesthesia or weakness, with MS in primary and secondary care the findings on an MRI
as a result of inflammation along the spine settings. Management of patients with MS of someone with more
(transverse myelitis). follows three pathways: advanced demyelination.
Balance problems, vertigo and Symptom management.
diplopia, as a result of brainstem or Relapse management. 3 A patient newly
cerebellar inflammation. Disease management using DMTs. diagnosed with MS
Neurologists undertake a detailed history and asks you about the
neurological examination, gather evidence Symptom management condition. Think about
of previous episodes or neurological damage, The most common symptom of MS how you would respond
and request investigations such as MRI to involving visual pathways is optic neuritis, in a way that the
help support a clinical diagnosis of MS. which presents as acute, unilateral eye pain, patient understands.
Table 1 lists the different MRI techniques accentuated by ocular movements, followed by Suggested reading:
used. T1-weighted images show hypo-intensities variable visual loss (scotoma) of mainly central Multiple Sclerosis
indicating areas of permanent nerve damage. vision. It is rare for bilateral simultaneous optic Trust (2011)
T1 images enhanced with gadolinium neuritis to occur in MS. If optic neuritis occurs Multiple Sclerosis
contrast show current disease activity bilaterally, the impairment is asymmetrical, Information for
where the BBB is disrupted and show active and usually more severe in one eye. More often, Health and Social
inflammation areas of new or enlarging the lesion of the optic nerve is retrobulbar Care Professionals.
lesions. T2-weighted images indicate the (the area of inflammation is between the back www.mstrust.org.
disease burden of lesions the load of old of the eye and the brain). As well as visual uk/downloads/
and new lesions. acuity and pain, the patient may present ms-info-health-
Complete time out activity 2 with desaturation of colour. Treatment professionals.pdf
MS Society
TABLE 1 information What
Magnetic resonance imaging techniques used in diagnosis is MS? tinyurl.
T1-weighted images T2-weighted images Gadolinium-enhanced images com/k258cte,
and Causes of MS
Provide better Reveal inflammatory lesions Highlight blood-brain barrier disruption;
www.mssociety.
correlation between demyelination, gliosis, enhancing the images will reveal
disability and black axonal loss, new or active lesions that are currently active or org.uk/what-is-ms/
holes of irreversible and old lesions, remyelination, inflammatory. information-about-
axonal loss. and overall burden of disease. ms/causes

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CPD neurology

for optic neuritis is high-dose steroids (see duloxetine, gabapentin or pregabalin is

section on relapse). recommended as initial treatment for
Internuclear ophthalmoplegia refers to neuropathic pain (NICE 2013). If the initial
abnormal horizontal ocular movements, treatment is not effective or not tolerated,
with lost or delayed adduction and one of the other three drugs should be offered,
horizontal nystagmus of the abducting eye, and then switched again if the second and
and is caused by a lesion in the brainstem. third drugs are not effective or not tolerated.
When present bilaterally, it is usually coupled Capsaicin creamshould be considered for
with vertical nystagmus on upwards gaze. localised neuropathic pain if the patient is
A bilateral internuclear ophthalmoplegia avoiding or unable to tolerate oral treatments
is most suggestive of MS. Treatment for (NICE 2013). Cannabis sativa extract,
internuclear ophthalmoplegia is high-dose capsaicin patch, lacosamide, lamotrigine,
steroids. Nystagmus is characterised by rapid, levetiracetam, morphine, oxcarbazepine,
small-amplitude, pendular oscillations of topiramate, tramadol (long-term use)
the eyes in the primary position. Patients
frequently complain of oscillopsia oscillation FIGURE 2
of objects in the field of vision, which impairs Magnetic resonance imaging scan of a female
visual performance. with multiple sclerosis
Sensory symptoms occur in almost all
patients during the course of the disease,
reflecting spinothalamic or posterior column
lesions, and are variable. Examination
shows disruption to the sense of vibration,
pin-prick, hot and cold, or joint position.
Pain can be persistent or paroxysmal, often
having an effect on quality of life, and its
management is complex.
Assessment of pain is important and
involving a pain specialist to manage the
patients pain is indicated in some cases.
Primary pain is a direct result of nerve

SCIENCE PHOTO LIBRARY

damage; secondary or nociceptive pain is a
consequence of musculoskeletal problems,
and is often related to posture complications;
and neuropathic pain manifests as dysaesthesia
or paraesthesia. A choice of amitriptyline,

4 Which of the TABLE 2

following is most 2010 revised McDonald criteria for diagnosis of multiple sclerosis
suggestive of a Attacks Lesions Additional criteria for diagnosis
clinical diagnosis
2 attacks or more 2 lesions or more None. Clinical evidence alone will suffice.
of MS and why?
Two occurrences 2 attacks or more 1 lesion Dissemination in space on magnetic resonance imaging
of optic neuritis (MRI), or await further clinical attack implicating a
one year apart. different central nervous system (CNS) site.
Progressive 1 attack 2 lesions Dissemination in time on MRI, or await further clinical
weakness of the legs attack implicating a different CNS site.
over one year. 1 attack 1 lesion Dissemination in space and time on MRI, or await
Temporary loss of further clinical attack implicating a different CNS site.
feeling in the hands, 0 attack (progression One year of disease progression (retrospective or
which occurs again from onset) prospective) and at least two out of three criteria:
six months later. Dissemination in space in the brain.
An episode of optic Dissemination in space in the spinal cord based on
neuritis, followed six 2 or more T2 lesions.
months later by right Positive cerebrospinal fluid.
arm weakness. (Adapted from MS Trust 2011, Polman et al 2011)

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and venlafaxine should not be used unless
advised by a specialist.
Pain specialists, neurosurgeons and
the multidisciplinary team, including
neuro-psychologists, may need to be
involved in the management of pain in MS.
Pharmacological and non-pharmacological
treatments including complementary and
alternative treatments have been extensively
reviewed in the recent MS guidelines (NICE
2014a). The guidelines provide evidence-based
statements, following review of available
MS research studies linked to pain in MS.
Lhermittes phenomenon is a sudden transient
sensory shock-like symptom radiating down
the spine triggered by flexing the head
forward, as a result of posterior column
involvement. Trigeminal neuralgia is more
common in people with MS than the general
population (Zvartau-Hind et al 2000).
Initial treatment of trigeminal neuralgia is
carbamazepine, with specialist referral
for further treatment (NICE 2013).
Paraparesis, or paraplegia, occurs as a result
of lesions in the descending motor tracts of
the spinal cord. Spasticity is common with
extensor spasms of the legs and sometimes
the trunk. Neurological examination may
show exaggerated deep tendon reflexes,
sustained clonus or extensor plantar responses.
Paraparesis is caused by damage to the upper
motor neurones, accompanied by lower-limb
weakness, and may be exaggerated by
infection, constipation and other problems.
A multidisciplinary team approach, including
physiotherapy and occupational therapy,
is advocated. MS guidelines indicate baclofen
and gabapentin to be used as first-line
treatment options; tizanidine and dantrolene
to be used as second-line treatment options;
and benzodiazepines as third-line options
(NICE 2014a). Nabiximols or fampridine
are not recommended but intrathecal
baclofen was found to result in inhibition of
spinal reflexes, reducing spasms, clonus and
pain (NICE 2014a).
Uhthoffs phenomenon occurs with a rise
in body temperature, causing slowed nerve
conduction and increased neurological
symptoms, from visual (sensory) disturbance
to central motor function loss (Humm
et al 2004). Nurses can provide advice on
using cooling suits, avoiding hot climates and
keeping hydrated.
Attacks of motor or sensory phenomena
(paroxysmal symptoms) can occur as a
result of demyelinating lesions. Lesions
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within the brainstem may cause paroxysmal
diplopia, facial paraesthesia, trigeminal
neuralgia, ataxia, and dysarthria. Motor
system involvement results in painful tonic
contractions of muscles.
Co-ordination is affected if there is
demyelination to cerebellar pathways
affecting gait, standing and sitting balance,
causing intention tremor and ataxia.
Examination typically reveals dysmetria
and dysdiadochokinesia. Intention tremor
(action tremor) can affect the upper
body, head, walking and sitting balance,
and trunk. Cerebellar signs are usually
mixed with pyramidal (corticospinal) tract
signs. Tremor affects 25-60% of patients,
can be severely disabling and embarrassing
for patients, and is difficult to manage
(Koch et al 2007). Various pharmacological
and non-pharmacological treatments were
discussed by Koch et al (2007), including
gabapentin, but cannabinoids appear
ineffective. It was found to be important to
involve the multidisciplinary team, particularly
physiotherapy and orthotics, and limb cooling
achieved functional improvement. Tremor
reduction using stereotactic thalamotomy
or stimulation guidance is outlined in
Interventional Procedure Guidance No.
188 (NICE 2006).
Bowel, bladder and sexual dysfunction
are common in patients with MS. Urinary
urgency and/or frequency should be treated
with anticholinergic (antimuscarinic)
medications if a post-void assessment is
normal (NICE 2012), and continence nurse
advisers should be consulted. Urinary tract
infections are common and may increase
the extent of bladder dysfunction. Further
information can be found in the UK
consensus on bladder management (Fowler
et al 2009). Constipation is common,
and faecal incontinence is rare. Contributory
factors include lack of exercise; poor diet and
fluid intake; medications; decreased rectal
sensation; and sphincter dysfunction. Sexual
dysfunction is reported in men with erectile
dysfunction and women with reduced vaginal
sensation; and fatigue and medications can
also affect libido. Assessment of bowel,
bladder and sexual dysfunction is vital in the
clinical setting to provide optimal care and
advice, and assess the effects symptoms may
have on relationships. Ward (2005) provided
practical suggestions for the management
of sexual dysfunction, recognising the
importance of the nurses role in raising
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CPD neurology
such issues with patients and providing
education and support.
Fatigue is the most common symptom
experienced by people living with MS.
In a survey of 2,265 people with MS, 88%
reported moderate to high levels of fatigue,
which had an effect on activities of daily living
(Hemmett et al 2004). Disrupted sleep as a
result of pain, spasms, irritable legs, bladder
overactivity and medications is a contributory
factor. There appears to be a correlation
between fatigue and disturbed sleep in MS
patients. Self-management strategies support
patients to manage disabling symptoms by
understanding underlying causes, exercising,
and conserving energy. Amantadine
is recommended by NICE (2014a),
as are mindfulness training, cognitive
behavioural therapies (CBT) and fatigue
management programmes.
At least half of people with MS experience
depression, and a quarter have anxiety
disorders (Siegert and Abernethy 2005).
It is not known whether depression in MS
patients reflects a comorbid association with
bipolar illness, or is an effect of frontal or
subcortical white matter disease (Korostil and
Feinstein 2007). Several approaches may be
taken to treat depression, including self-help,
counselling, interpersonal therapies, talking
therapies, CBT, pharmacological therapies,
use of antidepressants, or a combination of
therapies (NICE 2009). The rate of suicide
in people with MS was 7.5 times higher than
for the age-matched general population
(Sadovnick et al 1991).
Formal psychometric testing shows
approximately half of all people with MS
experience some inefficiency in concentration
or other mental tasks (MS Trust 2011),
and cognitive impairment may be present
early in the condition. Frequent abnormalities
relate to abstract conceptualisation, short-term
memory, attention, and speed of information
processing. Psychological assessment of
underlying problems may help, however
5 Think about treatment proves difficult.
the silent or hidden Complete time out activity 5
symptoms associated
with MS and the Relapse management
difficulties they present Confavreux et al (2000) defined MS relapse
for the individual. as occurrence or re-occurrence of worsening
Access the NICE symptoms of neurological dysfunction,
(2014a) guidelines to lasting more than 24 hours, stabilising
confirm options for and/or resolving either partially or completely,
symptom management. and not fatigue or fever-related. Symptoms
occurring within one month after the initial
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symptoms were considered part of the same
relapse. Relapses are also called attacks,
episodes, flare-ups and acute exacerbations.
Infection should always be excluded as a
possible underlying cause for worsening
symptoms (pseudo or super-imposed relapse).
Relapses are spontaneous events, but may
be worsened by stress, anxiety and fatigue.
Relapse is rare during pregnancy, especially
during the third trimester, but the risk of
relapse increases post-partum before returning
to the pre-pregnancy rate at three months
(Confavreux et al 1998).
High-dose steroids reduce inflammation
and speed recovery, but should only be
prescribed following assessment (NICE
2014a). The recommended treatment regimen
involves methylprednisolone 0.5g orally for
five consecutive days (NICE 2014a). However,
in severe relapse, those who have not responded
to oral glucocorticoids or those who require
monitoring with diabetes or mental health
problems, intravenous (IV) methylprednisolone
500mg-1g should be administered daily for
three to five days (NICE 2014a).
Disease management using
disease-modifying treatments
The emergence of DMTs in the 1990s changed
the management of MS, and resulted in
the development of the MS specialist nurse
role and establishment of the risk-sharing
scheme to enable access to DMTs for people
with MS (DH 2002). The scheme allowed
suitably eligible patients, assessed using
the Association of British Neurologists
(ABN) (2009) guidelines, to be treated using
DMTs. Data are being collected from more
than 5,000 patients registered in the study,
which ends in 2015. This data will provide
evidence of benefits and risks of conventional
treatment. The ABN guidelines are designed
to support and represent a national consensus
concerning appropriate use of currently
approved therapies.
Interferon beta 1b the first available
licensed DMT for treatment of MS
and interferon beta 1a, reduce the frequency
and severity of relapses for patients with
relapsing-remittingMS (RRMS) (Box 1);
however, some patients continue to have
accruing disability. While the body produces
several types of interferons (cytokines)
naturally, interferon beta 1b and 1a were found
to modulate T cell and B cell activity and reduce
the permeability of the BBB to inflammatory
cells (Dhib-Jalbut and Marks 2010).
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 Glatiramer acetate reduced the relapse
rate by about one third over two years in
patients with RRMS (Johnson et al 1995).
The drug is a synthetic combination of four
amino acids, resembling myelin basic protein,
has a diverse mechanism of action and
immune-modulatory and neuro-protective
consequences (Aharoni 2013).
Natalizumab is the first licensed treatment
given by infusion for highly active RRMS
or rapidly evolving severe MS two or more
disabling relapses in one year and one or
more gadolinium-enhancing lesions, or a
significant increase in T2 lesion load compared
with previous MRI. It acts by preventing the
migration of immune cells across the BBB,
preventing inflammation and the destruction
of myelin (Steinman 2005). Natalizumab
is the most efficacious MS therapy, reducing
relapse by around two thirds, with a 92%
reduction in lesions on gadolinium-enhanced
MRI, and evidence suggesting it slows
progression of disability and improves
quality of life (Polman et al 2006). Progressive
multifocal leukoencephalopathy is a rare
side effect that can cause death or
severe disability.
Natalizumab and interferon beta 1a
(subcutaneous injection) were shown to be
superior to all other conventional treatments
for preventing relapses in RRMS in the
short term, compared with a placebo, with a
moderate protective effect against disability
progression (Filippini et al 2013).
Complete time out activity 6
Oral therapies
Fingolimod was the first licensed, oral,
second-line treatment for patients with
RRMS where first-line treatment failed.
It acts by binding to receptors on the
surface of lymphocytes, and has unique
immunoregulatory properties, preventing
immune cells from exiting the lymphoid
tissue and reaching the inflammatory tissue.
A 50% reduction in relapse rate was reported
(Ingwersen et al 2012). Research suggests
fingolimod may stimulate re-myelination
(Jackson et al 2011). It is contraindicated in
patients with previous immunodeficiency,
a risk of opportunistic infections, severe active
infections, hepatitis, severe liver impairment,
malignancies and hypersensitivities. Side effects
include a rare bradyarrhythmia, which requires
careful monitoring post initiation of treatment
for six hours. Fingolimod has not been studied
in patients with underlying cardiac problems
or those on beta blockers. It causes a significant
reduction in lymphocyte count and infections
require monitoring.
Teriflunomide is an approved treatment
for MS (NICE 2014b) as an alternative to
conventional treatments for patients with
active RRMS and eligible to be used as a
first-line therapy (NICE 2014b). It reduced
numbers of B cells and T cells, and helps to
protect against relapses by limiting the increase
in lymphocytes and reducing the inflammation
that leads to demyelination. Teriflunomide has
immunomodulatory and anti-inflammatory
actions and studies show that the relapse rate

BOX 1
Types of multiple sclerosis (MS)
Relapsing remittingMS (RRMS) is characterised by clearly defined relapses with full recovery or with
sequelae and residual deficit. This type of MS accounts for approximately 85-90% of MS cases at onset
(MS Trust 2011). However, many will eventually enter a secondary progressive phase.
Secondary progressive MS(SPMS) occurs in around 65% of people with RRMS (MS Trust 2011).
SPMS is characterised by an initial relapsing course, followed by progression with or without relapse,
minor remissions and plateaus. Some studies suggest SPMS develops in most patients with RRMS,
causing greater neurological disability (MS Trust 2011).
Primary progressive MS is diagnosed in 10-15% of people with MS (MS Trust 2011). This type of MS
is characterised by disease progression from initial onset, occasional plateaus and temporary minor
improvements. Patients experience a steady decline in function from initial symptoms and never have
acute attacks. These patients have a more even sex distribution, tend to have a later age of onset,
and may have a worse prognosis for disability compared to patients with RRMS. 6 A patient asks
Benign MS may exist, but can only be diagnosed if the patient remains completely able in all functional for advice on the side
neurologic systems for at least 15 years after onset. Some patients never experience a second relapse. effects of natalizumab.
Although the exact frequency of this benign form of disease is unknown, many will never come to Describe how you would
medical attention. Among patients in a population-based cohort study who had MS for ten or more provide a response that
years, about 17% had minimal or no disability (Pittock et al 2004). is positive, realistic
Progressive relapsingMS is characterised by progressive disease from onset, with clear acute relapses, and based on research
with or without full recovery. Progression continues during periods between disease relapses. evidence.

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CPD neurology
is reduced by a similar percentage to beta
interferons relapse rate. It has disability data
showing reduction in disability progression.
Side effects include influenza, infections,
paraesthesia, diarrhoea, nausea, elevated
liver enzymes (alanine transaminase (ALT))
and hair thinning. Teriflunomide can take
eight months to two years to exit the system,
and pregnancy is not advised until the drug has
been eliminated from the blood; an accelerated
elimination procedure is recommended to
rapidly achieve a safe plasma concentration
level. The drug requires twice-weekly blood
monitoring in the initial phase of treatment.
Dimethyl fumarate is an approved therapy for
RRMS (NICE 2014c). It reduces inflammation
caused by the MS immune response and
has neuroprotective properties. One study
compared it to a placebo, showing a significant
reduction in the relapse rate of 48-53% and a
reduction of disability progression of 34-38%.
A second study compared it to glatiramer
acetate, which showed similar statistically
significant results a 44-51% reduction in
relapses and a reduced disability progression
of 21-24% after two years (Gold et al 2012).
It decreases the number of new and enhancing
lesions on MRI after two years. Side effects
include flushing, feeling hot, diarrhoea,
nausea, abdominal pain and headache.
Blood monitoring is similar to that required
for interferons.
Alemtuzumab is a novel therapy using
annual infusion for three to five days and is
recommended for people with active RRMS
(NICE 2014d). Alemtuzumab works by
binding and destroying white blood cells,
preventing immune cells from entering
the brain and attacking myelin. The most
recent data indicate a significantly reduced
relapse rate and a reduction in worsening
disability when compared to standard MS
therapies. Side effects include infusion site
reactions, insomnia, fatigue, infections and,
less commonly, autoimmune thyroid problems
and immune thrombocytopenia.
Future therapies may include laquinomod,
7 Consider the level an oral immunomodulatory therapy that
of information available has undergone phase 3 trials; daclizumab,
to patients to help them a monoclonal antibody being compared
make a decision about with beta interferons in phase 3 trials;
the use of a particular and ocrelizumab, a monoclonal antibody being
therapy. What therapy studied in patients with primary progressive
would you recommend MS (PPMS). Stem cells may have the potential
to someone diagnosed to restore lost function in nerve cells as a
with RRMS? result of MS, but research is still in the early
stages. Cannabis studies have shown evidence
56 november 12from
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of anti-inflammatory properties, promotion
of re-myelination and neuroprotection (MS
Trust 2011), with the CUPID trial evaluating
if tetrahydrocannabinol can slow disability
progression in PPMS; tetrahydrocannabinol
use in secondary progressive MS has failed to
demonstrate effects (Zajicek et al 2013).
Complete time out activity 7
Role of the specialist nurse
MS specialist nurse numbers have increased
steadily, with many co-ordinating DMT
risk-sharing schemes, collating data and
educating patients about realistic treatment
expectations. Newer therapies demand closer
monitoring of the patient; side effect profiles
are increased; and more treatment options are
available, making the care of these patients
more complex. To ensure concordance
with oral therapies, good decision making
by the MS nurse is essential (Ward-Abel
et al 2014). Specialist nurses have an integral
role in the management of patients with MS
they add value to patient care while generating
efficiencies for organisations through new and
innovative ways of working (Royal College of
Nursing (RCN) 2010). Benefits generated by
specialist nurses include reduced waiting times;
avoidance of unnecessary hospital admission
and/or re-admission; reduced post-operative
hospital stay times; freed-up consultant
appointments; delivery of community services
at the point of need; reduced treatment
drop-out rates; provision of education
to health and social care professionals;
introduction of innovative service delivery
frameworks; and direct specialist advice
given to patients and their families (RCN
2010). Further work is being undertaken to
evaluate the MS specialist nurses role (Mynors
et al 2012). The MS Society and MS Trust
support nurses, and have developed strong
partnerships to improve care and services for
everyone affected by MS.
Self-management
Self-management is still a relatively new
concept for enabling patients to manage
the life-changing diagnosis of MS. Factors
important to self-management of MS
include the patients knowledge and skills
relating to their condition; confidence to
enable action; improved self-efficacy; use of
available resources; working in partnership
with the multidisciplinary team; and skills in
NURSING STANDARD
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only. No other usesPUBLISHING
without permission.
problem-solving, setting goals, monitoring and
decision making (Embrey 2005, 2006). Nurse
specialists readily promote self-management
programmes similar to the Expert Patient
Programme (DH 2001), which aims to
involve patients in the treatment process and
share responsibility for disease management
with health and social care professionals,
to ensure better control of their quality of
life. Self-management programmes can be
designed to reduce severity of symptoms or
improve confidence, resourcefulness and
self-efficacy (DH 2001). The overall goal of
self-management is to help people to help
themselves, with the premise that the better
their self-management, the better their
symptom control and quality of life; however,
the focus must be on patient activity rather
than on basic education (Barlow et al 2002).
A nurses role, whether on the ward or in
the community, is to encourage optimal
medication management, increase adherence,
and promote persistence, which results in
fewer relapses and the ability of patients to 8 Consider the
manage their own health (Stokl et al 2010). support the MS Society
Complete time out activity 8 and MS Trust can offer
patients and nurses.
You may wish to access
Conclusion their websites at: www.
While there is still much to learn about MS, mssociety.org.uk and
treatments have improved significantly. www.mstrust.org.uk
In particular, treatments for those with

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CPD neurology

RRMS appear to improve relapse rates, professionals to provide optimum care,

9 Now that you have
completed the article,
you might like to write
a reflective account.
Guidelines to help you are
on page 62.
reduce disease activity and delay progression.
The nurses role in providing individuals with
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them self-manage their condition is pivotal
to effective management of this condition.
All members of the multidisciplinary team
have a role in supporting those affected
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signposting patients to quality services
and enabling them to live independently.
In a time of developments in treatment
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supporting decision making in the future
and in educating patients, carers and
healthcare professionals NS
Complete time out activity 9

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