Tag Archives: social

Cognition and mental health

Suicidal ideation and suicide in MS

Mental health problems and suicide are the underbelly of MS, the elephant in the consulting room. I have attempted to discuss these topics in a way that is not too dark, based on data from a 2026 systematic review. Please be aware, however, that the content may still be upsetting.

Key points

  • The suicide rate among people with MS is roughly twice that of the general population.
  • Several biological, psychological and social factors contribute to suicide risk:
    • depression and anxiety: a biological basis for these comorbidities exists in MS
    • MS disease-related factors: increased disability, disease duration and progression; life-changing symptoms
    • socio-demographic factors: age, male sex, living alone, education level
    • social and existential factors: loneliness, social exclusion and low perceived social support; loss of purpose and meaning; financial strain; fear of stigma.
  • Thoughts of ending one’s life – ‘suicidal ideation’ – precede suicide attempts; effective screening tools exist, are quick to complete and can identify patients at risk of suicide.
  • Systematic screening is not optional but should be part of the basic standard of care.
  • Suicide prevention in MS requires participation by the clinic, the patient (and their family) and the health system.
  • If you or someone you know is having thoughts of suicide, please reach out for help. Support groups are available.

The problem we avoid talking about …

MS is a chronic, unpredictable and often disabling neurological condition. People with MS know this, and as a result they carry a psychological burden that is usually overlooked in a 15-minute annual outpatient appointment. Mental health problems and suicide are the elephant in the MS consulting room. They sit quietly alongside the disability progression conversation, the drug treatment switch discussion, and the “How are things at home?” question that healthcare professionals (HCPs) often forget to ask.

How common are suicidal ideation and suicide in MS?

Suicidal ideation – thoughts of ending one’s life, with or without a plan – is the single most important precursor to suicide attempts, and death by suicide among people with MS is far more common than most HCPs appreciate. A landmark Canadian study in 1991 found that suicide was the third most common cause of death reported in MS clinics.1 The proportion of deaths due to suicide among people with MS (15%) was 7.5 times the proportion in an age-matched general population (2%).

More recent work suggests that the suicide rate among people with MS is roughly twice that of the general population.2 A 2026 systematic review and meta-analysis of suicidal ideation in MS draws on 18 studies and more than 8,000 people with MS to provide a picture of how common it is, what drives it and where the gaps are in MS care.2 From these combined data, the authors estimate that one in five people (20%) in an MS clinic waiting room has considered suicide. This is higher than the 13% figure from a 2020 meta-analysis,3 and the authors suggest two plausible explanations:

  • an expanding evidence base that now includes more diverse settings
  • a real rise in suicidal ideation rates – perhaps linked to the COVID-19 pandemic, growing geopolitical instability and reduced stigma around reporting mental health symptoms.

Individual study prevalence ranged dramatically, from 8% in a Canadian cohort to 36% in an Iranian cohort. This is probably telling us something important about how context, culture, income level and healthcare infrastructure shape suicide risk.

In most high-income countries, lifetime suicidal ideation prevalence in the general population is around 9–10%. The recent 20% figure in people with MS2 is therefore roughly double that seen in the background population – a finding echoed by many independent studies.

Regional and temporal patterns

In the 2026 review, subgroup analysis based on country income level reported a pooled suicidal ideation prevalence of 17% among the 14 high-income countries compared with 32% in the countries with ‘upper-middle’ incomes (three studies from Iran and one from Brazil).2 This aligns with what we know about mental health inequities more broadly – poverty, housing insecurity, financial strain, limited access to psychiatric services, and stigma all worsen outcomes in lower-resource settings. (Please note, the ‘upper-middle income’ data in this review came from just two countries; therefore, we should be cautious about extrapolating to sub-Saharan Africa, South Asia or Latin America as a whole.)

Suicidal ideation prevalence figures published between 19911 and 20262 from many studies conducted across different regions of the world vary widely and may appear inconsistent. The 2026 figure of 20% still means, however, that roughly one in five people with MS has active suicidal thoughts, and global crises in the last five years may be masking an underlying deterioration that will only become visible in the next generation of studies.

Limitations of study data

The 2026 review has limitations that need to be acknowledged. Study methodologies vary widely: suicidal ideation is measured with different instruments and at different time points; diagnostic criteria for MS are inconsistently reported; variability between studies is high. The ‘20% prevalence’ figure from 2026 is therefore an estimate with uncertainty. What is not uncertain is that suicidal ideation is substantially more common in MS than in the general population, and that it is driven by modifiable factors and hence is preventable. 

Who is at risk of suicidal ideation among people with MS

No single risk factor predicts suicidal ideation in isolation. Suicide is the final common pathway of several biological, psychological and social factors. Consistent drivers can be grouped into four domains.2

1. Psychiatric comorbidity: depression and anxiety

Depression and anxiety are the most consistently reported risk factors for suicidal ideation in MS.2 Depression affects up to 50% of people with MS at some point, far exceeding the 14–21% figure in the general population. This matters because depression in MS is both more common and more severe than in the general population, and it is driven by a mixture of:

  • neuroinflammation and hormonal factors (depression in MS is not simply a ‘reaction’ to having MS – it has a biological basis)
  • lesion location, particularly in limbic and frontal lobe/cortex pathways
  • disease-modifying therapy (DMT) side effects (particularly with interferon therapy)
  • the psychological burden of uncertainty, disability and loss of role.

Anxiety, which is often under-recognised and under-treated in MS, frequently coexists with depression and independently elevates suicidal ideation risk.

2. Disease-related factors

Several disease features align with suicidal ideation across studies.

  • Greater disability – measured both by clinician-rated EDSS (Expanded Disability Status Scale) scores and by self-reported physical impairment. The latter may be a stronger predictor than EDSS scores, because it captures the subjective experience of living with impairment.
  • Longer disease duration – though this relationship is complex. Study results vary, suggesting that some patients adapt psychologically over time, probably depending how well they adjust to living with MS.
  • Progressive MS – higher suicidal ideation rates are found in people with more advanced MS when compared with the earlier relapsing–remitting phase. Many HCPs and healthcare systems think that once someone with MS becomes disabled, the disease is not modifiable. I hope landmark studies like ocrelizumab in PPMS (O’HAND study), siponimod in SPMS (EXPAND study) and tolebrutinib in non-relapsing SPMS (HERCULES study) change this perspective. 
  • Specific symptoms – fatigue, sleep disturbance, spasms, bladder and bowel difficulties, and speech and swallowing problems also correlate with suicidal ideation. Together, these symptoms erode quality of life.

3. Sociodemographic factors

The evidence here is more mixed.

  • Age – findings are inconsistent. Some studies identify older patients (≥ 65 years) as higher risk; others find younger people with MS more vulnerable. Both extremes carry risk for different reasons; younger recently diagnosed patients face a challenge to their identity and loss of envisioned future; older patients face accumulated disability and social isolation.
  • Male sex – some (but not all) studies find men at higher risk, consistent with general population data on completed suicide.
  • Unmarried status and living alone are both associated with increased suicidal ideation in multiple studies.
  • Education level – most studies suggest that higher educational attainment is protective (better health literacy, coping strategies, economic resources); one Iranian study found the opposite, perhaps reflecting unmet expectations or awareness of prognosis.

4. Social and existential factors

This domain is the easiest to miss in a busy MS clinic but most important to address.

  • Low perceived social support, from family, friends and significant others, is a consistent risk factor.
  • Loneliness and social exclusion – ‘feeling socially excluded’ strongly correlates with suicidal ideation.
  • Hopelessness and loss of purpose – perceived loss of control, loss of masculinity/femininity and failure to achieve an expected role contribute psychologically to suicidal ideation.
  • Challenges to faith or spiritual meaning – having a sense of purpose, comfort in faith, and church membership can all be helpful and protective (in those for whom they are important).  
  • Financial strain and anticipated stigma are particularly important in lower-resource settings.

Screening for suicidal ideation in the clinic

If 20% of people with MS experience suicidal ideation but only a small fraction volunteer it spontaneously, systematic screening is not optional but should be part of the basic standard of care. Effective screening tools exist, and they are quick to complete.

The Patient Health Questionnaire-9 (PHQ-9)

The PHQ-9 is the most practical and widely validated mental health tool for neurological conditions, including MS; it is particularly suited to detecting suicidal ideation. Item 9 of this 9-item self-report depression screen specifically asks about thoughts of self-harm or being better off dead. It takes under 3 minutes to complete and can be done in the waiting room or electronically before the clinic. Scores above 10 indicate clinically significant depression warranting action. A positive response to item 9 should trigger a suicide risk assessment. It could be argued that every MS clinic should administer the PHQ-9 at least annually, and at every unscheduled visit where there has been a relapse, a significant disability progression, a DMT change or a major life event.

The Beck Scale for Suicide Ideation (BSI)

The BSI is a 20-item instrument designed specifically for suicide risk. It is more detailed than the PHQ-9 and is better suited to psychiatric follow-up than to first-line screening.

The Beck Depression Inventory-II (BDI-II)

The BDI-II is a broader 21-item depression measure that includes a suicide item. This is often used in research settings but takes longer to complete than the PHQ-9 in a clinic.

The Hospital Anxiety and Depression Scale (HADS)

The HADS is my favoured option that captures both anxiety and depression domains. It does not, however, include a direct suicide item, so a ‘positive’ (i.e. high: 11−21) HADS score should always prompt a follow-up suicide-specific question.

What should you be asked if a screen is positive?

Clinicians often feel awkward asking directly about suicide. Evidence is unambiguous that asking about suicide does not increase the risk. A graded approach works well:

  1. ‘Have you had thoughts that life isn’t worth living, or that you’d be better off dead?’
  2. ‘Have you had thoughts of harming yourself?’
  3. ‘Have you thought about how you might do it?’ (plan)
  4. ‘Do you have access to the means?’ (access)
  5. ‘Have you taken any steps or made any preparations?’ (intent)

Presence of a plan, access to means, or preparatory behaviour indicates a high imminent risk and demands urgent psychiatric referral – ideally, the same day.

Suicide prevention: what can we do?

Suicide prevention in MS operates at three levels: the clinic, the patient and the system.

At the clinical level

  • Screen systematically. A good MS service should embed PHQ-9 into routine MS review and not rely on patients volunteering suicidal ideation. If I were setting up an MS clinic now, I would include PHQ-9 in routine screening and add it to the annual questionnaire that patients must complete before each clinic visit. 
  • Treat depression and anxiety aggressively. Depression and anxiety are the dominant modifiable risk factors. Selective serotonin reuptake inhibitors (SSRIs: sertraline, citalopram, escitalopram) are first-line, well-tolerated drugs and have no meaningful interaction with current DMTs. Cognitive behavioural therapy (CBT) – including web-based models – has a good evidence base in MS. We should reject the dogma that ‘of course they’re depressed, they have MS’ as a reason not to proactively manage depression.
  • Address symptom burden. Fatigue, pain, sleep disturbance, bladder dysfunction and spasticity are not just quality-of-life issues – they are suicide risk factors that need to be treated. Please make sure that your MS care team provides relevant support. 
  • Be alert at transition points. Diagnosis, relapse, disability milestones (losing the ability to walk, work or drive), DMT failure, and being labelled as having secondary progressive MS are all periods of elevated risk. 
  • Assess social support explicitly. Who do you live with? Who helps you? Who would you call at 3 am? Treat loneliness and social isolation as vital potential danger signs.
  • Restrict means where appropriate. Safe storage of medications, particularly in patients with large quantities of prescribed opioids, benzodiazepines or anticholinergics, can save lives. This conversation needs to be had with the patient, their partner and their family. 
  • Document and communicate risk. A named crisis contact, a safety plan, and timely communication with the GP or primary care physician should be standard practice.

At the patient and family level

  • Psychoeducation. Many people with MS don’t know that depression is a common and treatable part of MS – they assume sadness and hopelessness are inevitable. Naming and confronting depression and suicidal ideation helps.
  • Normalise help-seeking. The stigma of psychiatric care in MS remains real. Framing mental health as part of MS care, not something separate, reduces that barrier.
  • Involve family. Family members are often the first to notice a change – withdrawal, giving away possessions, changes in sleep. They need to be taught about what to watch for.
  • Build purpose and connection. Peer support groups (e.g. MS Society, Shift.ms, MS Trust, MS International Federation resources, National MS Society [US]), vocational rehabilitation, social prescribing, church attendance, volunteering and hobbies all buffer against hopelessness. Having a purpose in life and being productive reduce the likelihood of suicidal ideation.
  • Safety planning. A written safety plan – warning signs, coping strategies, people to call, reasons for living, means restriction – is a simple but evidence-based self-administered intervention. The Stanley-Brown Safety Plan is freely available online.

At the system level

  • Integrate mental health into MS services. A neuropsychologist or clinical psychologist embedded in an MS service should not be a luxury; it is the minimum standard for a condition where one in two patients develops depression. That said, most NHS MS clinics don’t employ a neuropsychologist, and referring people with MS for assessment and management takes time.
  • Address inequity. The doubled suicidal ideation prevalence in upper-middle-income countries2 is not inevitable. It reflects under-resourced mental health services, stigma, and financial barriers to care – all modifiable at a policy level.
  • Research under-represented populations. The Bazmi review2 of 14 high-income and three upper-middle-income countries openly discusses its limitations: it includes no data from low-income countries and none from most of Asia, Africa or Latin America, beyond a single Brazilian study. MS care cannot be evidence-based at a global level if the evidence is dominated by findings from high-income countries. More research is needed. 

The bottom line

If you are an HCP and are reading this, please remember that roughly one in five of your MS patients has had thoughts of suicide. Most of them have not told you. The dominant drivers – depression, anxiety, disability, symptom burden, loneliness, hopelessness – are either treatable or modifiable, and the screening tools are simple, brief and validated. Although suicidal ideation is common in people with MS, it is driven by modifiable factors and hence is preventable. Suicide in MS is not inevitable. It is, however, easy to miss. Every person with MS deserves a clinician who asks directly, listens without flinching, and acts on what they hear.

If you or someone you know is having thoughts of suicide, please reach out for help.

In the UK, Samaritans are available 24/7 on 116 123.

In the US, the 988 Suicide and Crisis Lifeline is available by call or text.

In other countries, the International Association for Suicide Prevention (IASP) maintains a directory of crisis services at iasp.info/crisis-centres-helplines/

You are not alone, and help is available.

References

  1. Sadovnick AD, et al. Cause of death in patients attending multiple sclerosis clinics. Neurology 1991;41:1193. doi.org/10.1212/WNL.41.8.1193.
  2. Bazmi E, et al. Global prevalence and risk factors of suicidal ideation in multiple sclerosis: a systematic review and meta-analysis. Health Sci Rep 2026;9:e72331. doi: 10.1002/hsr2.72331.
  3. Kouchaki E, et al. Prevalence of suicidal ideation in multiple sclerosis patients: meta‐analysis of international studies. Soc Work Pub Health 2020;35:655–63.

Fatigue and insomnia, Sleep disorders

Understanding and managing insomnia in MS

Insomnia is the most common sleep disorder I encounter in my MS practice. It often goes untreated because people with MS accept it as part of living with the disease or because healthcare professionals (HCPs) prioritise other MS-related problems.

Key points

  • Insomnia is more common in people with MS than in the general population and is associated with poor mental health and other medical problems.
  • Factors that contribute to insomnia include anxiety, frequent visits to the bathroom, pain, leg spasms, restless legs, inability to roll over in bed, menopausal symptoms (hot flushes and night sweats) and poor sleep hygiene; they need to be managed appropriately.
  • Several online tools and questionnaires exist that can help you assess the nature and severity of insomnia.
  • Sleep aids (drugs) available over the counter or on prescription may be helpful.
  • Cognitive and digital approaches to insomnia management also have a role but are not widely available or suitable for everyone.
  • Complementary and alternative therapies are a valuable aid to self-management of insomnia.

Sleep, glorious sleep!

Sleep is the most essential performance-enhancing agent we know. You know what it is like if you wake in the morning and have had a good night’s sleep; you feel energised, your mood is good and you are ready to face the day. In contrast, when you wake from a night of tossing and turning, or not being able to turn, legs jerking, getting up several times to go to the toilet, maybe with a hangover from too much alcohol the night before, then you are irritable, your mood is low and it is challenging to get through the day. 

Most studies on sleep in MS show that over 70% of people with MS have a sleep disorder. In an MS-Selfie survey on sleep, a minority (33%) of 173 respondents described their sleep as good, very good or excellent, with 49% formally diagnosed with one or more sleep disorder and over 80% not having undergone formal sleep studies. Insomnia is the most common sleep disorder I encounter in my MS practice. Insomnia is defined as difficulty initiating or maintaining sleep, which can be a symptom or a disorder. If a disorder, insomnia is associated with a feeling of distress about poor sleep, and it disrupts social or occupational functioning.

Causes and impact of insomnia

In the general population, ~10% of adults have insomnia disorder and another 15 ̶ 20% report occasional insomnia, i.e. the symptom. In comparison, 40 ̶ 50% of people with MS have insomnia. Insomnia is more common in women than in men and is associated with poor mental health and other medical problems. Common MS-associated symptoms linked to insomnia (and resulting in fatigue) include pain, lack of bladder control, spasticity, restless legs, periodic limb movements and discomfort from being unable to turn in bed; other factors that contribute to insomnia – not just in people with MS but also more widely –  include alcohol and stimulant misuse, menopausal symptoms, poor sleep hygiene (daytime napping), deconditioning (lack of exercise), anxiety and depression. All these problems can interfere with sleep initiation, maintenance or perception in people with MS.

Insomnia can be episodic (with symptoms lasting 1 ̶ 3 months) or situational (of short duration, in response to a specific event of circumstance) and tends to follow a persistent course. Episodic insomnia refers to insomnia for a defined period, for example lasting several months linked to anxiety. In comparison, situational insomnia refers to insomnia triggered by a specific stimulus or event, such as sleeping away from home or after alcohol consumption. Chronic insomnia can cause depression and is associated in the general population with the development of hypertension and dementia. Insomnia assessment, diagnosis and management require a careful history to document its course, concomitant comorbidities and potential contributing factors. 

Several studies show that approximately 40% of people with MS have obstructive sleep apnoea and that it is not necessarily associated with obesity and a large neck. Sleep apnoea in MS may be due to brain stem pathology from MS affecting pharyngeal (throat) muscle function. If you know or think you are a snorer and you have periods when you stop breathing, you can download one of the many smartphone sleep apps that can assess this.

Approaches to managing insomnia

Any MS-related symptoms that can affect sleep need to be managed appropriately. How can you treat insomnia if your sleep is interrupted by anxiety-related rumination, nocturia, pain, leg spasms, restless legs, inability to roll over in bed, menopausal symptoms of hot flushes and night sweats and poor sleep hygiene? 

Recording your sleep patterns

A 24-hour history of sleep ̶ wake behaviours can help to identify additional behavioural and environmental factors for intervention. Patient-reported outcome measures (PROMS) and sleep diaries provide valuable information about the nature and severity of insomnia. They can help screen for other sleep disorders and monitor treatment progress.

A sleep diary should collect information on your sleep cycle (bedtime, arising time, napping) and estimates of your sleep ̶ wake characteristics, i.e. sleep latency (how long it takes to fall asleep), number and duration of awakenings, and an estimated overall sleep time. Useful PROMS include the Insomnia Severity Index, the Pittsburgh Sleep Quality Index, the STOP-BANG Sleep Apnea Questionnaire (for evaluating the risk of sleep apnoea) and the Restless Legs Syndrome Rating Scale. 

Sleep hygiene

I suggest you start with a simple self-help guide to improve your sleep hygiene.

  1. Ensure you spend an appropriate amount of time asleep, at least 6 hours in bed. Some people need more than this to feel refreshed. 
  2. Limit daytime naps to 30 minutes. Please note that napping does not make up for inadequate nighttime sleep. 
  3. Avoid stimulants such as caffeine, modafinil and nicotine close to bedtime. 
  4. Only drink alcohol in moderation. Alcohol is known to help you fall asleep faster, but too much disrupts sleep.
  5. Exercise helps improve sleep quality. As little as 10 minutes of aerobic exercise daily can enhance the quality of sleep. 
  6. Don’t eat before going to bed. Heavy foods and fizzy drinks can trigger indigestion or heartburn/reflux that disrupts sleep.
  7. Ensure you get adequate exposure to natural light; exposure to sunlight during the day and darkness at night help to maintain a regular sleep ̶ wake cycle. 
  8. Establish a regular relaxing bedtime routine, which helps the body recognise it is bedtime. This could include taking a shower or bath or reading. However, avoid reading or watching emotionally upsetting content before attempting to sleep.
  9. Make sure that your sleep environment is pleasant. Your mattress and pillows should be comfortable. The bedroom should be cool for optimal sleep (16 ̶ 20°C). The bright light from lamps, smartphones and television screens can make it difficult to fall asleep, so turn those lights off or adjust them when possible. Use the blue filter mode on your smartphone and other devices to reduce the inhibition of melatonin from light. Consider using blackout curtains, eyeshades, earplugs, white noise machines and other devices to make the bedroom more relaxing.
  10. If you have pain, nocturia, restless legs, sleep apnoea or other causes of discomfort, get these adequately managed via your HCP.

If these self-help measures fail, other current treatment options include prescription-only and over-the-counter (OTC) medications, cognitive behavioural therapy for insomnia (CBTI) and complementary and alternative therapies. 

Over-the-counter sleep aids

Over-the-counter sedatives tend to be first-generation antihistamines with potent centrally acting anticholinergic effects that impair cognitive function and long-term brain health. I recommend you avoid them (see newsletter entitled ‘Your anticholinergic burden’). 

Some people with MS self-medicate with OTC melatonin, cannabidiol (CBD) or tetrahydrocannabinol (THC) preparations. Melatonin has a U-shaped dose ̶ response curve for some individuals; therefore, lower doses may be better than higher doses. In general, I cannot recommend the use of CBD or THC for insomnia. CBD is a drug and is associated with liver toxicity; it may also interact with your other medications. However, if you do decide to buy CBD and/or THC, please use a reputable supplier and pharmaceutical-grade products. Medicinal cannabis cannot be prescribed on the NHS but can be obtained via private clinics. Many patients purchase it online; as a doctor, I cannot recommend buying it this way. 

Prescription-only sleep aids

If you raise the issue of insomnia with your HCP, they may reach for the prescription pad. Before accepting a sedative, please be aware of its limitations and ensure you have optimised all the above guidance. Sedatives are only a short-term solution; they work well for about 4 ̶ 5 days before you develop tachyphylaxis and need higher doses. Tachyphylaxis refers to the rapidly diminishing response to successive doses of a drug, rendering it less and less effective. Once you develop tachyphylaxis and stop taking sedatives, you may experience rebound insomnia. Benzodiazepines (e.g. diazepam) are addictive and doctors generally avoid prescribing them for insomnia. However, they still have a role when insomnia is part of acute anxiety. The sedatives most often used are the so-called Z-drugs (zolpidem, zopiclone, zaleplon and eszopiclone). Zopiclone and eszopiclone have a longer half-life than the other two drugs (5 ̶ 6 hours). In comparison, zolpidem and zaleplon act for a much shorter period (1 ̶ 3 hours). 

The older, tricyclic antidepressants, such as amitriptyline, are commonly used as sedatives. I have largely stopped prescribing them unless there is another reason for using a tricyclic, e.g. to help with pain management (please read my newsletter ‘Amitriptyline: the neurologist‘s dirty little secret’. I mostly use duloxetine in my clinical practice for pain management. It is not as sedating as tricyclic antidepressants, but some patients find it helps with sleep. Duloxetine is a serotonin ̶ noradrenaline reuptake inhibitor and has fewer anticholinergic side effects than tricyclics.

Antispasticity agents such as baclofen and gabapentinoids (gabapentin and pregabalin) also help sleep, but they should only be used for insomnia if you have spasticity or, in the case of the gabapentinoids, spasticity and/or pain that needs to be managed.  

Psychiatrists and some neurologists use sedating antipsychotics to help with insomnia. Sadly, as a neurologist, I have seen too many severe adverse events resulting from the liberal use of antipsychotics as sedatives. There needs to be a good reason for prescribing an antipsychotic, and insomnia in isolation is not one of them; however, there is a role for them in patients with cognitive issues or significant psychiatric problems. The older generation antipsychotics (e.g. haloperidol) have now been replaced by safer drugs such as quetiapine and olanzapine.

A new class of sedatives is now available in some countries; these are the dual orexin receptor antagonists suvorexant, lemborexant and daridorexant. Daridorexant is NICE approved for use by the NHS; it is recommended for treating insomnia in adults with symptoms lasting for 3 nights or more per week for at least 3 months and whose daytime functioning is considerably affected, but only if CBTI has been tried and not worked, or if CBTI is not available or is unsuitable.

Cognitive approaches to managing insomnia

Cognitive Behavioural Therapy for Insomnia (CBTI)

Only some patients receive CBTI, owing to a lack of adequately trained therapists. CBTI aims to change the behaviour and psychological factors that contribute to insomnia (e.g. anxieties and unhelpful beliefs about sleep). At the core of CBTI are behavioural and sleep-scheduling strategies (sleep restriction and stimulus control instructions), relaxation methods, psychological and/or cognitive interventions to change unhelpful beliefs or excessive worrying about insomnia, and sleep hygiene education. 

CBTI is focused on sleep and oriented toward problem-solving. A psychologist typically guides the process over roughly six consultations. Several variants in the methods for implementing CBTI include shorter formats, group therapy, using other providers such as counsellors and specialist nurses, and the use of telehealth digital platforms, including smartphone applications. 

Brief behavioural treatment for insomnia

This abbreviated version of CBTI emphasises behavioural components and is typically implemented in fewer sessions. It involves education about sleep regulation, factors that promote or interfere with sleep, and a tailored behavioural prescription based on stimulus control and sleep restriction therapy.

eCBTI

Digital CBTI (eCBTI) is becoming increasingly popular. The Sleepio application, which is recommended and covered by the NHS, has a positive effect on several sleep outcomes and is said to be as effective as medication. NICE recommends Sleepio as a cost-saving option for treating insomnia and insomnia symptoms in primary care for people who would otherwise be offered sleep hygiene or sleeping pills. A medical assessment should be done before referral to Sleepio for people who may be at higher risk of other sleep disorder conditions, such as during pregnancy or in people with comorbidities.

Complementary and alternative therapies

Sleep restriction

Limit the time you spend in bed to match your sleep time as closely as possible. After the initial restriction, the sleep window can be gradually adjusted upward or downward on a weekly basis as a function of sleep efficiency (time asleep÷time spent in bed×100) until an appropriate sleep duration is established.

Stimulus control

You need to follow a set of instructions designed to reinforce the association between bedtime and bedroom stimuli with sleep and to re-establish a consistent sleep ̶ wake schedule.

  • Go to bed only when you feel sleepy.
  • Get out of bed when you are unable to sleep.
  • Use the bed and bedroom for sleep and sex only; do not use your bed for reading, watching television, etc.
  • Try and get up at the same time every morning.
  • Avoid napping.

Relaxation training

Try using different procedures such as progressive muscle relaxation and imagery training to reduce arousal, muscle tension and intrusive thoughts that interfere with sleep. Relaxation procedures need to be practised daily over a few weeks. 

Cognitive therapy

This is a psychological approach to revising many common misconceptions about sleep and reframing unhelpful beliefs about insomnia and its daytime consequences. This method also reduces excessive worrying about sleep difficulties and their daytime consequences. Additional cognitive strategies include paradoxical intention (willingly trying to stay awake rather than trying to fall asleep) to alleviate the performance anxiety triggered by attempting to force sleep.

Sleep hygiene education

These general guidelines include advice about a healthy diet, exercise, substance use, and optimising environmental factors such as light level, noise and excessive temperature that may promote or interfere with sleep (see above). 

Acceptance and commitment therapy (ACT)

ACT is a form of psychotherapy that aims to educate people to stay focused on the present moment and accept life experiences, thoughts, and feelings (even negative ones) without trying to change them. ACT uses different methods and processes (e.g. acceptance, defusion, mindfulness, and committed action) to increase psychological flexibility.

Mindfulness

This meditation method involves observing one’s thoughts and feelings and letting go of the need to change or ruminate. Originally designed to reduce stress and anxiety, mindfulness has been adapted for the management of insomnia and can be included as one component of ACT.

Conclusion

Poor sleep, be it due to a comorbid sleep disorder, MS-related symptoms or poor sleep hygiene, is a very common problem in people with MS. It contributes to daytime fatigue and hypersomnolence and impacts physical and cognitive function. As a result, poor sleep reduces quality of life and can exacerbate other MS-related problems such as poor cognition, anxiety and depression. It is essential that poor sleep is documented, investigated appropriately and treated accordingly to improve the functioning and quality of life of people with MS.

Pregnancy and childbirth, Women's health

Concerns about parenting

Being disabled or unemployed because of MS does not mean you cannot be a good parent. Here I cover some of these practical considerations as well as the steps you can take to reduce the potential risk of your child developing MS.

Can I be a good parent if I become disabled from my MS?

This is difficult to answer and depends on how disabled you are, the nature of your disabilities and whether you have support. For example, some patients who are wheelchair users, or close to being wheelchair users, when they give birth manage to nurse and look after their children. On the other hand, some patients with cerebellar problems find it very difficult to bathe, change and feed their babies due to poor coordination and tremor. If you have advanced MS, the decision to start or extend your family needs to be discussed with your partner. If necessary, ask an occupational therapist to assess you and discuss all the issues relevant to you becoming a parent. Disability per se is not a reason not to have children, but it does raise important issues that need careful consideration. The decision to have children needs to be taken by you and not by your HCP.

If I become disabled or unemployed because of MS, will I be able to support my children?

This is another difficult question, and the answer depends on your circumstances. In the modern era having children and supporting them is expensive, but most high-income countries have social safety nets to protect you and your family in times of adversity. We now have effective DMTs that prevent or delay disability, so deciding to have children is easier than it was in the pre-DMT era.

What is the risk of my children getting MS?

MS is not a genetic disease in the Mendelian sense that you pass on to your children with a well-defined inheritance pattern. However, there are genetic factors that increase your risk of getting MS. In high-prevalence countries such as the UK, the lifetime chances of a woman developing MS is about 1 in 375 ̶ 400; for a man, it is close to 1 in 750 ̶ 800. However, for a daughter whose mother has MS, the risk is close to 1 in 40, and for a son, it is lower than 1 in 80. In some studies, the latter risk is no higher than the background rate. If the father has MS, the risk of his daughter developing MS is about half the risk of mother ̶ daughter pairing, i.e. 1 in 70. For a son of a father with MS, the risk is likely lower than this, but the results across studies are inconsistent.  

Can I prevent my children from getting MS?

Based on the known and modifiable risk factors for MS, you should try and keep your children vitamin D replete. To do this, you will likely need to supplement your children’s vitamin D intake as follows:

  • for children less than 2 years of age, 600 IU per day
  • for children 2 ̶ 10 years of age 2,000 IU per day
  • for children above 10 years of age, 4,000 IU vitamin D3 per day (the same dose we recommend for adults).

Other modifiable risk factors are childhood and adolescent obesity and smoking. We estimate that about 15 ̶ 20% of new or incident new cases could potentially be prevented by eliminating obesity and smoking in the general population. I must stress that these suggested interventions are based on studies that show associations between the risk factors and MS but may not necessarily be cause and effect. I should also point out that most people with all the risk factors for MS will not get the disease. This implies that the development of MS involves other random factors, or bad luck, that can’t necessarily be modified.

The issues raised above show you how complex the management of MS has become, which is why there is a push for people with MS to be managed in specialist MS units.

References

Krysko KM et al. Treatment of women with multiple sclerosis planning pregnancy. Curr Treat Options Neurol 2021;23:11.

Other articles in this series on Pregnancy and childbirth
Planning for pregnancy
Managing MS during pregnancy
Preparing to give birth
Breastfeeding if you are on a DMT

DMTs, Treatment strategy

How immunosuppressed am I?

Do you understand the difference between short-term intermittent and long-term continuous immunosuppression? Here we address another of the key questions to consider before deciding on a specific disease-modifying therapy (DMT).

Key points

  • Immunosuppressive disease-modifying therapies (DMTs) reduce the immune system’s effectiveness.
  • It is important to weigh up the benefits and risks of short-term versus continuous immunosuppression.
  • Non-selective DMTs suppress the adaptive and innate immune systems; selective DMTs do not affect the innate immune system and are thus associated with a low risk of bacterial infections.
  • The implications of immunosuppression need to be considered within the context of other health and lifestyle factors.

Which DMTs cause immunosuppression?

A useful way of thinking about DMTs is based on whether they are immunosuppressive. Broadly speaking, an immunosuppressive is any DMT that reduces the immune system’s activation or effectiveness. 

From a regulatory perspective, for a drug to be classified as immunosuppressive, it should: 

  • cause significant lymphopaenia or leukopenia (reduced white cell counts)
  • be associated with opportunistic infections (infections that don’t occur in people with a normal, healthy immune system)
  • reduce antibody and/or T-cell responses to vaccines 
  • increase the risk of secondary malignancies. 

Based on the above criteria, the interferon-beta preparations and glatiramer acetate are immunomodulatory rather than immunosuppressive. Teriflunomide is also an immunomodulatory therapy with the potential, albeit small, to cause immunosuppression. In real life, however, very few people with MS treated with teriflunomide develop significant lymphopaenia or leukopenia; if they do, we tend to stop the drug. The other licensed DMTs are immunosuppressive to a greater or lesser degree. 

Short-term versus continuous immunosuppression

The duration and intensity of immunosuppression further determine the risks. Short-term or intermittent immunosuppression associated with an immune reconstitution therapy (IRT) front-loads the risks, which decrease substantially once the immune system has reconstituted itself. In comparison, long-term continuous or persistent immunosuppression, which occurs with most maintenance DMTs, accumulates problems over time, particularly opportunistic infections and secondary malignancies.

Live vaccines are, in general, contraindicated in patients on continuous immunosuppressive therapies. However, someone with MS on an IRT who has reconstituted their immune system can tolerate and respond to live vaccines. The benefits of administering live vaccines always need to be balanced against the risks of the vaccine.

The main characteristics of continuous persistent and short-term (intermittent) immunosuppression. Modified from Giovannoni, Curr Opin Neurol.1
AHSCT, autologous haematopoietic stem cell transplantation; PML, progressive multifocal leukoencephalopathy.

Selective versus non-selective immunosuppression

Immunosuppression that accompanies DMTs may be selective or non-selective. Non-selective therapies deplete and/or suppress both the adaptive immune system (T cells and B cells) and the innate immune system (monocytes, neutrophils and natural killer [NK] cells). Alemtuzumab, AHSCT (autologous haematopoietic stem cell transplantation) and mitoxantrone are non-selective and are therefore associated with acute bacterial infections such as listeriosis, nocardiosis and cytomegalovirus reactivation. In comparison, anti-CD20 agents (ocrelizumab and ofatumumab) and cladribine are selective, do not affect the innate immune system and are therefore associated with a low risk of acute bacterial infections. 

How immunosuppressed are you_MET vs IRT_2 Dec 2024

Classification of disease-modifying therapies for relapsing forms of MS. Modified from Giovannoni, Curr Opin Neurol.1
AHSCT, autologous haematopoietic stem cell transplantation.

Other considerations

Please note that the implications of immunosuppression are not black and white but interact with other factors such as:

These factors have been highlighted during the COVID-19 pandemic, particularly in relation to the risk of severe COVID-19 and the variations in vaccine responses among people with MS (including waning of the immune response).

It is important to realise that we can derisk (reduce the risk of) some complications associated with long-term immunosuppression and the use of DMTs. Please see the post entitled How can I reduce my chances of adverse events on specific DMTs?

References

  1. Giovannoni G. Disease-modifying treatments for early and advanced multiple sclerosis: a new treatment paradigm. Curr Opin Neurol 2018;31:233 ̶ 43.
Diagnosis

Am I sure that I have MS?

The multiple sclerosis misdiagnosis rate is around 5% and this has major implications for individuals and the treatment of MS.

Key points

  • A wrong diagnosis of MS may have financial, social and psychological consequences for the individuals concerned, affecting major life decisions.
  • Some MS treatments have life-threatening complications and should only be prescribed for people with a clear diagnosis of MS.
  • Some of the diseases that mimic MS can be made worse by disease-modifying treatments for MS.
  • Diagnostic criteria for MS have evolved and now take account of clinical, electrical, laboratory and magnetic resonance imaging findings.

A case study

She had been diagnosed with multiple sclerosis 8 years ago and had been taking interferon-beta since her diagnosis. I told her that I didn’t think she had MS and that her diagnosis was almost certainly complicated migraine with aura. The lesions on her magnetic resonance imaging (MRI) scan were non-specific white matter lesions and not inflammatory. Her neurological examination, spinal fluid analysis and evoked potentials (EPs) were normal. What clinched the non-MS diagnosis for me was the history of neurological events, which were too short-lived and migratory to be MS attacks. The final piece of the jigsaw was that a special MRI sequence showed none of her white matter lesions had a central vein, which told me that none of her white matter lesions was an MS lesion.  Her anger was palpable. She was angry because she had decided not to start a family and had changed her career because of the fear of becoming disabled in the future and not being able to work or look after a child.  This case illustrates why I always try to review the diagnosis of patients referred to me with MS and why it is important to answer this question before starting a disease-modifying therapy (DMT).   

Making a diagnosis of MS

Unfortunately, there is no single test to diagnose MS. Rather, MS is diagnosed by combining a set of clinical and MRI findings, electrical or neurophysiological investigations and laboratory tests. If these tests fulfil a set of so-called MS diagnostic criteria, the healthcare professional (HCP) or neurologist makes a diagnosis of MS. 

The underlying principles of diagnosing MS are to show the dissemination of lesions in space and time and exclude possible mimics of MS. The diagnostic criteria have evolved over time from 1) being based purely on clinical attacks,1 to 2) include electrical and spinal fluid tests as well as clinical attacks,2 and 3) to add on the use of MRI to help confirm dissemination in time and space.3–6  

Dissemination in time 

This means that two attacks or MS lesions must occur at least 30 days apart or that oligoclonal bands (OCBs) of immunoglobulins can be detected in the spinal fluid.

Dissemination in space 

This requires MS lesions to occur in different locations, for example, the optic nerve and the spinal cord. 

Electrical tests

The electrical or neurophysiological tests are called evoked potential (EPs) and test electrical conduction in a particular pathway. They can show lesions in nerve pathways that are not evident on the neurological examination or seen on MRI. The EPs can also show slow electrical conduction, which is one of the hallmarks of diseases that affect myelin, the insulation around nerves that is responsible for speeding up the electrical conduction of nerve impulses.

Laboratory tests

The laboratory tests are typically done to exclude other diseases that can mimic MS. Examining the spinal fluid for the presence of OCBs is useful in helping to make an MS diagnosis. OCBs are the fingerprint of a specific type of immune activation within the central nervous system (CNS). The OCB fingerprint is relatively specific for the diagnosis of MS in the correct clinical context. (OCBs are also found in CNS infections and other autoimmune diseases, but these are relatively easy to differentiate from MS.)

Please be aware that you may have MS according to the latest diagnostic criteria when you could not be diagnosed with MS using past criteria.

Why is a correct diagnosis important?

Neurologists get the diagnosis wrong in approximately 5% of people with MS. In other words, one in 20 people who have a diagnosis of MS in life does not have MS when their brain is studied post mortem. This data is based on a large study in a region of Denmark.7 More recently, a study from a specialist MS centre in the United States reported a misdiagnosis rate of approximately 15% in patients with presumed MS referred to their centre for treatment.8 

Why is getting the diagnosis of MS correct so important? Firstly, some MS treatments have life-threatening complications; you don’t want to expose people without MS to these complications. More concerning is that some of the diseases that mimic MS can be made worse by MS DMTs. Finally, a diagnosis of MS has many psychological, social, financial and economic implications. Even if you turn out to have ‘benign disease’, just having a diagnosis of MS, has implications for your life choices and may impact your ability to get insurance cover, to name obvious examples. I, therefore, advise you to make sure you have MS and not an MS mimic.

Common MS mimics

References

  1. Schumacher GA, et al. Problems of experimental trials of therapy in multiple sclerosis: Report by the Panel on the Evaluation of Experimental Trials of Therapy in Multiple Sclerosis. Ann N Y Acad Sci 1965;122:552–68.
  2. Poser CM, et al. New diagnostic criteria for multiple sclerosis: guidelines for research protocols. Ann Neurol 1983;13:227–31.
  3. McDonald WI, et al. Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis. Ann Neurol 2001;50:121–7.
  4. Polman CH, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the “McDonald Criteria”. Ann Neurol 2005;58:840–6.
  5. Polman CH, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol 2011;69:292–302.
  6. Thompson AJ, et al. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol 2018;17:162–73.
  7. Engell T. A clinico-pathoanatomical study of multiple sclerosis diagnosis. Acta Neurol Scand 1988;78:39–44.
  8. Kaisey M, et al. Incidence of multiple sclerosis misdiagnosis in referrals to two academic centers. Mult Scler Relat Disord 2019;30:51–6.