The article on Suicidal ideation and suicide in MSprompted many responses from newsletter readers. Their comments provide a deep and arguably multifaceted look at how people with MS view suicidal ideation, mental health and assisted dying. I have summarised the key arguments below.
Suicide: a rational decision or a mental health disorder?
A significant thread throughout the comments is the belief that contemplating suicide is a logical, rational response to the relentless physical decline caused by MS, rather than a psychiatric illness.
Conversely, there is pushback against dismissing the clinical reality of mental health disorders in MS.
Arguments for and against assisted suicide
Those advocating for the right to assisted dying focus primarily on bodily autonomy and the prevention of extreme suffering.
Arguments against legalising assisted dying focus on fears of systemic healthcare degradation, coercion and procedural concerns.
Defining the role of the healthcare system
The medical literature focuses entirely on preventing suicide by identifying and treating underlying distress, rather than providing policies to guide people with MS toward assisted suicide. Most articles state that suicide in MS is not inevitable and emphasise aggressive treatment of the drivers of suicidal ideation.
However, the patient community, or at least part of it, has highlighted a desperate need for policies that allow for open, non-judgmental dialogue about end-of-life fears without people with MS immediately losing their autonomy. Therefore, learnings and policies could be implemented to identify and support these individuals.
Policies for systematic screening and identification
To accurately identify who is experiencing suicidal ideation, healthcare professionals (HCPs) must stop relying on people with MS to volunteer this information spontaneously.
Mandatory routine screening. Clinics must embed a validated screening tool, such as the Patient Health Questionnaire-9 (PHQ-9), into routine MS reviews.
Targeted screening at critical junctures. Screenings should occur at least annually and, crucially, at major transition points. These include diagnosis, relapses, major disability milestones (like losing the ability to walk or drive), or when transitioning to secondary progressive MS.
Structured follow-up questions. If someone with MS screens positive for suicidal ideation, policies must dictate specific follow-up questions to assess imminent risk. Clinicians must ask whether the individual has a plan, access to the means, or has made any preparations for suicide.
Immediate action protocols. The presence of a plan, access to means, or preparatory behaviour must trigger an urgent, ideally same-day, psychiatric referral.
Policies for intervention and support
Once identified, the healthcare system must have pathways to address the physical, psychological and social drivers of the patient’s distress.
Aggressive treatment of comorbidities. Depression is not just a ‘normal’ reaction to having MS. Clinic policies should encourage the proactive use of antidepressant drug treatments, talking therapies, mindfulness and cognitive behavioural therapy, which have a good evidence base in MS.
Holistic symptom management. Physical symptoms directly drive suicidal ideation; therefore, treating pain, fatigue, sleep disturbances and intimate issues (bladder, bowel or sexual dysfunction) must be viewed as an active suicide prevention strategy.
Mandatory safety planning. For at-risk people with MS, HCPs must collaboratively develop a written safety plan (such as the Stanley-Brown Safety Plan) that outlines warning signs, coping strategies and crisis contacts.
Embedded mental health professionals. At a systemic level, it should be a minimum standard – not a luxury – to have a clinical psychologist or neuropsychologist embedded directly within the MS care service.
Policies for managing ‘rational’ end-of-life discussions
While the clinical framework aims to prevent suicide, some people with MS may advocate for policies that allow them to discuss the realities of severe disability safely.
Destigmatising the conversation. HCPs should be trained to initiate calm, kind and reassuring discussions about general mental health shortly after a diagnosis of MS. They should normalise the fact that people with MS may experience fears about mortality or even abstract thoughts of suicide when facing severe disability.
Protecting patient ‘agency’. Policies should ensure that when people with MS express fears about their future or end-of-life scenarios, the medical system does not immediately ‘swoop in’ with aggressive interventions that strip them of their voice.
Facilitating frank discussions. MS support services should facilitate open discussions about life in the later stages of MS, including the associated problems, rather than treating it as a taboo subject. The latter must not be rose-tinted, but realistic.
Implementing these policies requires significant investment and a shift in how chronic illness is managed, ensuring mental health is treated with the same urgency as physical health.
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:
‘Have you had thoughts that life isn’t worth living, or that you’d be better off dead?’
‘Have you had thoughts of harming yourself?’
‘Have you thought about how you might do it?’ (plan)
‘Do you have access to the means?’ (access)
‘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 atiasp.info/crisis-centres-helplines/
You are not alone, and help is available.
References
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.
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.
Many people with MS are traumatised by how their MS was diagnosed. It doesn’t have to be this way, and there are things you can do to relieve the symptoms.
Key points
Despite advances in knowledge about MS, a diagnosis of the disease can be traumatic, especially if it is communicated in an insensitive, abrupt way.
More than one in 20 people with MS have a confirmed diagnosis of post-traumatic stress disorder (PTSD) relating to their diagnostic experience.
Symptoms of PTSD include flashbacks of the trauma, panic attacks or racing pulse when remembering it, nightmares and difficulty sleeping.
Interventions such as cognitive behavioural therapy (CBT), mindfulness and psychotherapy remain the mainstay of treatment for PTSD.
Public perceptions about MS
Jacqueline du Pré, the celebrated British cellist, tragically died from MS in 1987 at the age of 42. Her death was extensively covered on TV and in the newspapers, and this publicity most likely helped to shape the general public’s view of MS in the late ‘80s and ‘90s: MS was a disease that struck when you were young and invariably caused disability and early death. Back then, most people in the general population knew little about MS. Their perceptions were potentially coloured by advertising such as that from the MS charities, showing young people with MS in wheelchairs – a campaign intended to prompt donations for research.
Fortunately, things have changed and the modern approach to fund raising by MS charities is more positive, thoughtful and sensitive. In addition, most people who turn out to have MS already suspect their diagnosis because they have asked ‘Dr Google’ or their favourite AI large language model. Despite this, many people with MS are traumatised from the diagnosis and subsequently meet the diagnostic criteria for post-traumatic stress disorder (PTSD) specifically related to their MS diagnosis and outlook.
Symptoms of post-traumatic stress
The following symptoms are associated with PTSD.
Poor concentration
Flashbacks or vivid memories of the trauma as if it was recurring
Intrusive thoughts of the traumatic event
Avoidance of people and places, to reduce symptoms
Nightmares, thoughts or memories of the trauma while asleep
Anxiety
Panic attacks or racing pulse, excessive sweating, shaking or chills when remembering the trauma
Depression
Hyper-alertness in situations that remind you of the traumatic event
Difficulty sleeping; struggling to get to sleep or to stay asleep
Anger as a result of the traumatic experience
Anhedonia or loss of enjoyment of things you found pleasurable before the event
A feeling of detachment from friends and family, or those closest to you
Change in life goals you had before the trauma.
Case study
A patient of mine, now in her late 60s, was diagnosed with MS in the early 1990s. She has benign MS and has done very well. Apart from mild gait unsteadiness, back pain and a weak right leg that causes a slight limp when she is tired, she is fully functional. She was treated with interferon-beta for 14 years; her only ‘MS medication’ currently is a low dose of gabapentin at night, which helps to dull the back pain so that she can get a good night’s sleep.
Despite having a good prognosis, she suffers from PTSD in relation to how her MS was diagnosed all those years ago. The private neurologist she consulted was not an MS expert and he had not prepared her for the diagnosis. During her diagnostic appointment, he simply walked up to a backlight X-ray displaying her MRI scans and announced, with his back to her, that she had a lot of white blobs on her MRI, which confirmed his suspicions that she had MS. He then turned around and said he would write to her GP with the details. And that was the end of the consultation; no time for questions, no information on MS, its treatment or prognosis.
My patient recalls walking out of the consultation with a cold panic enveloping her. On catching the tube home, she encountered a poster from an MS charity of a young person leaning forward in a wheelchair, with a zip down their spine. The implication was that damage to the spinal cord from MS had caused the disability. To this day, she gets regular and intrusive flashbacks of these experiences. The flashbacks are associated with feelings of anxiety or panic, palpitations, hyperventilation, hot flushes, sweating and a feeling of doom. They can come on spontaneously, but they typically happen before a hospital appointment and particularly when she has an MRI scan. In fact, MRI is such a problem that she now refuses to have repeat scans. The white blobs have become monsters that she imagines are expanding and suffocating her.
Her GP has diagnosed PTSD and prescribed a selective serotonin reuptake inhibitor (SSRI). This helped to reduce the frequency and intensity of the flashbacks. However, it caused weight gain, so she stopped taking it. She has subsequently found cognitive behavioural therapy (CBT) and mindfulness or meditation helpful, though not a cure.
My patient above may be an extreme example, but asking the relevant questions reveals that about one-quarter of people with MS have symptoms of PTSD, and more than one in 20 have a confirmed diagnosis of PTSD. Why, then, are healthcare professionals in general so bad at communicating the diagnosis of MS? What can they do to improve the experience?
Personal reflection
After sustaining multiple life-threatening injuries in a pedestrian road traffic accident in 2020, I have flashbacks about the accident. These are not intrusive and are typically triggered by crossing the road, approaching a traffic intersection or hearing a motorcycle in the distance. These flashbacks are fleeting and are not associated with any systemic symptoms. I, therefore, suspect flashbacks are a normal phenomenon for people who have just suffered a traumatic experience. However, experiencing them for myself has provided a context and a deeper understanding of how traumatic it can be to be diagnosed with MS or indeed with any chronic disabling disease.
Management of post-traumatic stress disorder
Neuropsychological interventions such as CBT, mindfulness and psychotherapy remain the mainstay of treatment for PTSD. Some people find that exposure therapy (being reminded of the trauma) helps to reduce the frequency of flashbacks and the severity of anxiety and panic attacks. Exposure therapy is becoming high tech, with immersive virtual reality scenarios.
Medications that can help with PTSD include SSRIs and other classes of antidepressants. Some people find psychedelics helpful, for example psilocybin and MDMA (commonly known as magic mushrooms and ecstasy, respectively); these are being studied in PTSD. Alternative treatments such as yoga and acupuncture may help. Exercise when done regularly is also useful.
If you have symptoms of PTSD that are troubling you, please seek advice from your healthcare professional.
Shift.ms
George Pepper, a co-founder of a social network for people with MS, describes his diagnostic experience as very poor, with no support offered to people like him. This prompted him to set up Shift.ms, to create an online resource centre and supportive community to help people, particularly young people, come to terms with the diagnosis of MS. The Shift.ms YouTube movie ‘Gallop’ is almost autobiographical and captures some of George’s experiences before and during the diagnostic phase of MS. I would highly recommend watching the video.
This MS-related group of symptoms is probably neglected in routine MS neurological practice and may fall through the cracks.
Key points
Dissociative states in people with MS may arise for different reasons: organic (resulting from damage to the temporal and parietal lobes), psychogenic (following psychological trauma) or iatrogenic (induced by drug treatments).
Such states range from transient feelings of unreality to recurring episodes of depersonalisation and/or derealisation. Other presentations may also occur.
Depersonalisation feels like being detached from one’s own body or thoughts, feeling like an ‘outside observer’ of one’s life.
Derealisation feels like being detached from the external world, which may appear foggy, dreamlike, lifeless or two-dimensional.
In MS, dissociation often has a physical (organic) basis in the brain. This article explores the specific effects of damage to each of the four lobes of the human brain.
Managing dissociative states in MS requires a dual approach: biological (treating the underlying MS disease) and psychological.
To differentiate between physical and psychological causes, doctors must consider the possibility of an MS relapse, an infection or the effects of an MS-related treatment. Checks for balance, hearing and psychological screening are also needed.
Causes and range of dissociative states
People with MS have an elevated risk of experiencing dissociative phenomena that give rise to alterations of consciousness, self-perception and reality testing (being able to assess what is real versus what is imagined). These dissociative states − ranging from transient feelings of unreality to chronic depersonalisation−derealisation disorder (DPDR) and non-epileptic seizures − are often undiagnosed. They may arise for different reasons.
Organic dissociation results from damage(lesions)to the temporal and parietal lobes, which can disrupt neural networks responsible for ‘embodied self-awareness’ (the constant experience of oneself through physical sensations, emotions and bodily signals).
Psychogenic dissociative states can occur in people with MS following the psychological trauma of diagnosis and the high prevalence of comorbid post-traumatic stress disorder (PTSD).
Iatrogenic dissociative states can be induced by drug treatments, particularly high-dose corticosteroids and psychoactive symptomatic treatments.
Dissociation is typically characterised by disruption in the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control and behaviour. The most frequently reported dissociative symptoms in the MS population fall under the spectrum of depersonalisation−derealisation.
Depersonalisation (the fragmentation of self)
Depersonalisation is characterised by a persistent or recurring feeling of being detached from one’s own body or thoughts. People with MS describe this as feeling like an ‘outside observer’ of their life, like watching oneself in a movie, or like a ‘robot’ with no control over their speech or actions. In MS, depersonalisation is associated with damage to the parietal lobe or the spinal cord – areas that help the brain detect body position and movement (proprioception). People with damage to these areas may feel as though a limb does not belong to them. This is not a delusion, because the person may see their limb move and intellectually know it is theirs. Rather, it is a sensory problem with the ‘body schema’ (the brain’s internal map of your body), that no longer matches your physical body.
Derealisation (the distortion of the world)
Derealisation involves a feeling of being detached from your surroundings. The external world may appear foggy, dreamlike, lifeless, colourless or artificially two-dimensional. Objects may appear distorted in size or shape; sounds may seem muted or distant. Derealisation is often worsened by sensory problems in people with MS (affecting sight, sound, touch, taste, smell or movement). Optic neuritis, a common early sign of MS, causes visual blurring, reduced colour intensity and visual field defects (gaps); see Colour vision and Driving at night. When the brain receives unclear visual input, it struggles to construct a vivid, real-feeling model of the environment, which can lead to a secondary sense of derealisation.
Problems with balance (vestibular dysfunction, leading to vertigo, dizziness and gait instability) are often associated with derealisation; conflicting signals from the eyes and inner ear can cause people with MS to feel disoriented.
Non-epileptic seizures
Non-epileptic seizures, also referred to as dissociative seizures, resemble epileptic seizures − involving convulsive movements, apparent loss of consciousness and stiffening of the body. However, they are not caused by abnormal electrical activity in the brain (usually visible on an electroencephalogram) but are psychological, most likely a mechanism for managing distress or trauma. Care is needed to determine the correct cause in each individual because people with MS are actually at increased risk for epilepsy due to brain lesions. Studies of magnetic resonance imaging (MRI) scans suggest that damage in the right brain hemisphere or the frontal lobes may increase the risk of non-epileptic seizures.
Dissociative amnesia and brain fog
Dissociative amnesia is the inability to recall important personal information, far beyond ordinary forgetting. It is usually related to stress or trauma. In MS, this poses a diagnostic challenge because many patients already experience cognitive dysfunction that affects processing speed and working memory. A study differentiating organic (‘true’) memory loss from dissociative amnesia in MS found that people who reported memory problems often had high levels of dissociation and anxiety but did not show major problems on formal memory testing.1 This implies that the ‘memory loss’ experienced by many people with MS may be an attention problem due to a mild dissociative state or emotional overload, rather than a result of permanent damage to memory structures in the brain.
Dissociative identity disorder
While rare, cases of dissociative identity disorder (DID) have been reported in people with MS. DID is characterised by the presence of two or more distinct personality states. Affected individuals typically have experienced childhood trauma, which makes them more prone to develop dissociation. A diagnosis of MS acts as a further stressor that challenges their sense of identity. Other symptoms of DID may include physical weakness and sensory loss, which can mimic an MS relapse and lead to misdiagnosis.
Underlying disease processes in MS
In the general psychiatric population, dissociative disorders are usually regarded as psychological in origin. In MS, however, dissociation often has a physical basis in the brain. MS damages myelin (the protective covering of nerve fibres), severs nerve connections and affects grey matter, all of which disrupts communication between different brain regions. When these connections are broken, the brain cannot integrate sensation, emotion and thought into a conscious experience.
Structure of the brain, showing the left and right cerebral hemispheres (left) and the four lobes (frontal, parietal, temporal and occipital; right) in each cerebral hemisphere. Each individual lobe has particular key roles; however, they do not function in isolation but as part of a wider system of neural networks. From Gemini Pro.
Temporal lobe
The temporal lobes play a central role in processing memory and emotions as well as in combining auditory and visual information. MS-related damage in these areas is associated with psychiatric symptoms, including psychosis and dissociation. The temporal lobe also houses the limbic system, comprising the amygdala (which processes emotion) and the hippocampus (which supports memory). If there is damage to the white matter pathways between the limbic system and the frontal cortex (a region known as the uncinate fasciculus) or to sensory regions, the emotional content of experiences can be lost. For example, when a person with MS sees a familiar object or person, the visual cortex sends information to the limbic system, thus activating the appropriate emotional response (e.g. warmth, recognition). If MS disrupts this connection, the person may recognise the object but feel no emotional familiarity. This mismatch, i.e. recognition without feeling, is central to derealisation and to the jamais vu phenomenon (the strange feeling that something familiar is suddenly unfamiliar or new) that is often reported in temporal lobe disorders.
A sagittal (longitudinal) view of the human brain showing the interconnected network of the limbic system, a key regulator of emotion, memory and spatial navigation. From Gemini Pro 3.0.
Temporal lobe epilepsy
MS lesions in the temporal lobe can sometimes trigger epileptic activity. Even in the absence of full-blown convulsions, abnormal electrical activity there can cause ‘dreamy states,’ profound déjà vu or feelings of unreality similar to the warning phase (aura) of temporal lobe epilepsy. Symptoms of depersonalisation disorder overlap with those experienced in temporal lobe epilepsy, particularly unusual body experiences and memory distortions.
Parietal lobe
The parietal lobe combines sensory information from different sources to form a single perception (cognition) and helps the brain build a map of the body and the world around us. The brain constantly updates this map, or ‘body schema’, using signals from the spinal cord. MS lesions in the parietal lobe or spinal cord can interrupt this information and deprive the brain of body map data.
When the brain ceases to receive reliable input from a limb, because of MS-related damage, it may ‘dissociate’ that body part from its self-image. This can manifest as:
asomatognosia (the inability to recognise a part of one’s own body)
somatoparaphrenia (the delusion that a limb belongs to someone else)
depersonalisation (see above).
Temporoparietal junction
The temporoparietal junction, where the temporal and parietal lobes meet, is a hub for integrating balance, visual and somatosensory signals to locate the ‘self’ in space. Electrical stimulation of this area can cause out-of-body experiences. In MS, lesions affecting the temporoparietal junction or the balance pathways in the brainstem can trigger dissociative events (for example, a feeling of floating above one’s body or viewing oneself from outside. These episodes are often linked to balance problems, suggesting that the brain is trying to make sense of conflicting signals.
Occipital lobe
The occipital lobe is the main visual processing centre of the brain. Damage in this region or in visual pathways can lead to complex visual distortions that trigger derealisation. ‘Alice in Wonderland Syndrome’ is a perceptual distortion in which objects appear much smaller (micropsia) or much larger (macropsia) than they really are. When damage from MS affects the visual association areas, vision may appear two-dimensional, with the world looking ‘flat’ or like a painted backdrop. This loss of depth perception contributes to the feeling of living in a movie or a simulation.
Clinico-radiological paradox
The clinico-radiological paradox refers to the discrepancy between the number and volume of MS lesions seen on MRI and a patient’s level of physical disability. Some people with MS have extensive brain lesions but relatively normal movement and minimal disability scores. While these patients may appear physically ‘fine’, lesions in high-level areas of the cortex (frontal, parietal and temporal lobes) can disrupt cognitive and emotional networks. Such individuals may be at high risk for subjective dissociation − feeling fragmented or cognitively detached − while objective observers (and disability scales) fail to register any deficit. These hidden symptoms can worsen the patient’s sense of isolation and unreality.
Trauma-related causes
Receiving a diagnosis of MS
While localised MS lesions create the ‘hardware failure’ in the brain that enables dissociation, psychological factors often provide the ‘software trigger’. Receiving a diagnosis of MS may be considered a medical trauma, often involving invasive procedures (lumbar punctures), frightening MRI experiences (claustrophobia) and hospitalisations. These repeated exposures to threat and a feeling of helplessness and vulnerability can induce a state of chronic hyperarousal and subsequent dissociation, consistent with the dissociative subtype of PTSD. Many people with MS meet the diagnostic criteria for PTSD specifically related to their MS diagnosis and outlook (please see, How common is post-traumatic stress disorder in people with MS?). Developing an ongoing, incurable and potentially disabling neurological condition can shatter one’s expectations for the future. By detaching from the reality of their diagnosis, people with MS may attempt to shield themselves from overwhelming anxiety and grief. Dissociation serves as an adaptive defence mechanism – a ‘mental flight’ when physical flight is impossible. This sounds dramatic, but it may explain why some people with MS develop dissociative disorders.
Childhood trauma
Research has demonstrated a potential relationship between childhood trauma, dissociation and the development of MS. Severe stress, neglect or abuse in childhood permanently dysregulates the hypothalamic−pituitary−adrenal axis (a system that is crucial for the body’s stress management). It consists of three organs that each release hormones to eventually raise cortisol levels in the body. This results in a chronic proinflammatory state and altered cortisol responses, which may increase biological susceptibility to developing MS later in life. Large-scale cohort studies indicate that women who experienced childhood abuse are significantly more likely to develop MS in the future.2
Treatment-related causes
The management of MS involves disease-modifying therapies (DMTs) and corticosteroids for acute relapse management. Many of these agents have significant neuropsychiatric side effects that can mimic, induce or exacerbate dissociative states.
Corticosteroids. High doses of the intravenous corticosteroid methylprednisolone (e.g. 1000 mg daily for 3−5 days) are the standard of care for speeding up the recovery from acute MS relapses. It is known to cause acute psychiatric adverse effects in many patients (dependent on the corticosteroid dose).Symptoms often begin with insomnia and euphoria but can progress to severe mood lability, anxiety and frank dissociation and delirium. Patients may experience a ‘steroid high’ followed by a crash into depression; some develop acute psychosis with hallucinations and confusion. Corticosteroids enhance dopamine activity. They may cause acute, reversible reductions in hippocampal volume. Their effect on the brain presumably decouples the patient from reality, leading to a temporary dissociative or psychotic state that resolves upon tapering the steroid dosage.
Interferon-beta has a longstanding association with depression and anxiety. Interferons are cytokines that induce a proinflammatory response similar to ‘sickness behaviour,’ which includes social withdrawal, fatigue and anhedonia (inability to feel pleasure in activities that are usually considered to be pleasurable). They may also decrease serotonin levels in the brain.While direct dissociation is less common, the severe anxiety and depression induced by interferons presumably lower the threshold for the onset of stress-induced depersonalisation.
Natalizumab is a highly effective monoclonal antibody, but it carries specific risks. The ‘wearing off’ effect in the week preceding the next infusion can be characterised by intensifying fatigue, cognitive fog and mood instability, which may manifest as a feeling of detachment or unreality.The most severe risk associated with natalizumab is progressive multifocal leukoencephalopathy; this causes extensive, rapid demyelination that can lead to confusion, personality changes and cognitive decline. These symptoms can be misinterpreted as psychiatric dissociation or dementia in the early stages.
Fingolimod, an S1P modulator, has been associated with posterior reversible encephalopathy syndrome. This condition involves swelling in the posterior brain regions (parietal/occipital lobes) caused by leakage of fluid from capillaries. It presents with acute confusion, visual changes, headaches and altered consciousness − a constellation of symptoms that could mimic derealisation and dissociation.
Symptomatic treatments. Abrupt withdrawal of baclofen and tizanidine, which are used for spasticity, can cause severe delirium, hallucinations and dissociation. Similarly, gabapentin and pregabalin, which are often used in people with MS to manage neuropathic pain, can cause sedation and cognitive clouding (‘zombie-like’ feeling) that contribute to depersonalisation.
Diagnosis
When someone with MS develops dissociative symptoms, doctors must first rule out physical (organic) causes before assuming the problem is purely psychological. A diagnostic algorithm should do the following.
1. Rule out an MS relapse Any new onset of psychiatric or dissociative symptoms warrants an MRI scan with gadolinium. New lesions in the temporal, parietal or frontal lobes can directly cause these symptoms.
2. Rule out infection Urinary tract infections are extremely common in MS and are the leading cause of acute confusional states (delirium) that can mimic dissociation. A urinalysis and a workup for other infections are mandatory.
3. Review medication Assess for recent steroid use, cumulative damage from anticholinergic drugs (e.g. for bladder dysfunction) or withdrawal from muscle relaxants (baclofen and tizanidine).
4. Check balance and hearing ‘Neuro-otological examination’ is a specialised assessment for dizziness, vertigo, hearing loss and balance disorders. Checking for nystagmus (uncontrollable eye movements) helps to diagnose balance disorders. Treating vertigo may resolve the derealisation.
5. Carry out psychological screening Your health professional can use the Dissociative Experiences Scale (DES-II) or the Dissociative Disorders Interview Schedule to quantify symptom severity. People with MS generally score in the normal range on DES-II unless they have comorbid DID or PTSD.
Differentiating organic from psychiatric dissociation is difficult. It may require referral to a neuropsychiatrist. MS-related brain fog or cognitive impairment with an organic basis is characterised by slowed processing speed, word-finding difficulties and fatigue. Patients try to engage but fail. In comparison, psychiatric dissociation is characterised by a subjective sense of detachment (‘I am not here’). Patients may have preserved processing speed but feel emotionally disconnected. As noted above, MS cog-fog often contains a dissociative component driven by anxiety. Treating the anxiety usually clears the ‘cog-fog’ more effectively than cognitive rehabilitation alone.
Management
Managing dissociative states in MS requires a dual approach: biological (i.e. treating the underlying MS disease) and psychological.
Drug treatments
The primary prevention of organic dissociation involves preventing new lesion formation. High-efficacy DMTs are the best way to preserve brain volume and connectivity. Psychotropics such as selective serotonin reuptake inhibitors (e.g. fluoxetine, sertraline) can help manage the anxiety and depression that underlie DPDR. They may also help with MS-related fatigue. Antipsychotics (e.g. quetiapine, olanzapine) may be rarely indicated for managing steroid-induced psychosis or organic paranoia related to temporal lobe lesions. Lamotrigine and other anticonvulsants (e.g. carbamazepine and oxcarbazepine) can be used to treat both seizures and depersonalisation; they are particularly beneficial in patients with temporal lobe pathology.
Psychological interventions
Cognitive behavioural therapy is the gold standard for treating DPDR. It helps patients reframe the terrifying sensation of ‘going crazy’ or ‘disappearing’ as a harmless (albeit distressing) symptom of anxiety or the disease. This reduces the catastrophic thinking that perpetuates the dissociation.
Eye movement desensitisation and reprocessing (EMDR) can be effective for MS-related PTSD (medical trauma) or childhood trauma. However, standard EMDR can be overwhelming for patients with dissociation. Modified (e.g. ‘titrated’) EMDR protocols can prevent flooding the patient with traumatic memories before they have stabilisation skills. EMDR is available via some UK NHS psychiatric services.
Grounding and mindfulness techniques (e.g. holding an ice cube, describing the environment) anchor the patient in the present moment and help them to manage acute episodes of derealisation. Mindfulness-based stress reduction has shown efficacy in improving the quality of life and reducing depressive symptoms in people with MS.
Vestibular rehabilitation therapy (VRT) is a specialised, exercise-based physical therapy designed to reduce vertigo, dizziness and imbalance. It should be offered to people with MS where derealisation is driven by vertigo. VRT helps the brain compensate for inner-ear deficits through personalised exercises that focus on gaze stabilisation, balance training and habituation. Physical therapy to improve balance and gaze stability can directly reduce the feeling of unreality.
Conclusions
To self-manage dissociative states effectively, individuals with MS can proactively apply several key principles highlighted above. During acute episodes of derealisation or dissociation, employing practical grounding and mindfulness techniques – such as holding an ice cube or actively describing the immediate environment – can serve as vital tools to anchor oneself in the present moment. Furthermore, individuals can apply cognitive behavioural principles by ‘reframing’ their experiences. Recognising that terrifying feelings of ‘disappearing’ or ‘going crazy’ are often harmless symptoms of anxiety or the disease itself can help reduce the catastrophic thinking that perpetuates dissociation.
Effective self-management also involves staying vigilant about physical triggers (e.g. monitoring for signs of urinary tract infections or medication side effects) and pursuing targeted physical interventions, such as vestibular rehabilitation exercises, if feelings of unreality are driven by dizziness and balance issues. By combining these practical coping strategies with a clear understanding of the biological and psychological origins of their symptoms, individuals with MS can regain a sense of control and significantly reduce the impact of dissociative states on their daily lives.
References
Bruce J, et al. Self-reported memory problems in multiple sclerosis: influence of psychiatric status and normative dissociative experiences. Arch Clin Neuropsychol 2010;25:39–48.
Rehan ST, et al. Association of adverse childhood experiences with adulthood multiple sclerosis: A systematic review of observational studies. Brain Behav 2023;13:e3024.
Emotional problems in people with MS must be recognised, addressed and treated, rather than dismissed as an inevitable consequence of living with this chronic condition.
Key points
An MS diagnosis naturally triggers emotions similar to the stages of grief (denial, anger, bargaining, depression, acceptance); in addition, the unpredictability of MS causes anxiety in many patients.
Anxiety, often combined with depression, is linked to a poorer quality of life, cognitive dysfunction, increased risk of suicide, and significant occupational and social problems.
Emotional problems in MS are typically exacerbated by fatigue, pain and poor sleep – all of which interfere with therapy and lifestyle adjustments.
Emotional changes in MS require treatment, just as physical symptoms do. This should comprise routine screening, targeted drug treatment and structured psychological and behavioural therapies.
Motivational coping styles that involve direct problem-solving and active participation in treatment planning (i.e. self-management) help people with MS adjust to their diagnosis.
Avoidance coping strategies generally lead to poorer psychological outcomes.
The presence of social support is a critical protective factor.
Impact of emotional changes
Emotional disorders have an adverse effect in people with MS, potentially impairing their ability to cope with disability and reducing overall health-related quality of life. Living with MS can also adversely affect relationships, for complex reasons, including both emotional and physical problems associated with the disease. Therefore, such symptoms must be recognised, addressed and treated, rather than dismissed as an inevitable or acceptable consequence of living with a chronic condition such as MS.
Emotional disturbances in people with MS may be reactive, i.e. a natural, adaptive psychological response to being diagnosed with a long-term, unpredictable and potentially disabling disease. Common emotions include grief, sadness, worry, fear, irritability and moodiness. Elisabeth Kübler-Ross in 1969 described five common stages of grief, best known by the acronym DABDA. We have added an extra A, for Anxiety about the future, to include the emotional reaction to a diagnosis of MS. The expands the mnemonic to six stages: DABDAA.
These emotional stages are considered ‘normal’ and an understandable coping mechanism. As with grieving, if they are prolonged, dominant and impact your social and occupational functioning, they are considered abnormal and require intervention. Remaining angry, resentful and depressed for decades will negatively impact your functioning.
Anxiety and depression in MS
Anxiety affects people with MS with a frequency often matching or exceeding that of depression. The highest prevalence of anxiety is observed in people with MS with low physical disability, defined by an Expanded Disability Status Scale (EDSS) score of less than 3.0. This finding suggests that anxiety is driven less by accumulated physical deficit than by the psychological factors of worry, fear and the inherent unpredictability of MS.
Maladaptive coping strategies are strongly associated with an increased risk of developing mood symptoms. A tendency to use avoidance coping – disengaging from problems rather than confronting them – is a significant predictor of poorer psychological outcomes. Similarly, psychological traits such as low optimism or a less positive attitude can heighten the risk of anxiety.
For a significant subset of patients, MS may first present not to a neurologist, but to a primary care physician, a therapist or a psychiatrist, with symptoms of anxiety or depression. Because the symptoms are psychiatric, the underlying neurological cause is not yet suspected.
Quality of life and daily functioning
Anxiety is a major contributor to the overall disease burden of MS, affecting nearly every aspect of life. Studies show that anxiety, often combined with depression, is linked to a poorer quality of life, cognitive dysfunction, increased risk of suicide, and significant occupational and social problems.
The impact of anxiety on many of the most challenging symptoms of MS – notably fatigue, pain and sleep problems – may be greater even than the effect of depression. MS symptoms can trigger or worsen anxiety, and the resulting anxiety intensifies the perception and severity of those same symptoms, thus creating a negative feedback loop.
Damaging health behaviours linked to undiagnosed and untreated anxiety can further compromise a patient’s well-being. For example, alcohol and substance abuse, as well as smoking, not only have their own intrinsic health risks but can also interfere with MS management and adherence to treatment.
Anxiety as a reaction to living with MS
The direct impact of the disease on the brain’s emotional circuits occurs in parallel with the profound psychological and existential challenges of living with MS. Even in the absence of any direct neurological damage to mood-regulating centres, the lived experience of MS itself provides rationale for the development of severe anxiety.
The unpredictability of the disease and the constant knowledge that a relapse could occur at any time, potentially worsening MS symptoms and existing function, create a state of chronic hypervigilance and worry. This pervasive sense of a loss of control over one’s own body and life is a catalyst for anxiety. Anxiety creates a vicious, self-perpetuating cycle where the physical and psychiatric symptoms mutually reinforce one another.
Multiple stressors
Beyond this overarching uncertainty, living with MS entails a host of stressors.
Diagnosis. The diagnostic journey is a period of intense anxiety, often involving a prolonged period of uncertainty as symptoms are investigated.Once diagnosed, patients face a continuous process of adjusting and readjusting to changing abilities.
Hidden problems. The invisibility of some of the most burdensome symptoms, such as debilitating fatigue, cognitive fog, or sensory disturbances, can lead to a profound sense of feeling misunderstood, isolated and frustrated.
Visible symptoms. Conversely, the emergence of visible symptoms, like a limp or the need for a mobility aid, can bring its own anxieties related to stigma and self-image.
Daily life. Financial concerns related to healthcare costs, employment and the ability to continue working, as well as the impact of MS on relationships and potential parenting, may further increase anxiety.
Existential threat
Profound existential and symbolic threats to a person’s sense of self can further exacerbate anxiety. The sense of loss triggered by a diagnosis of MS – loss of a healthy body, a previously held future and a former identity – is followed by changes in fundamental life roles. This can lead to feelings of inadequacy, guilt and a crisis of identity – perceived as a threat to one’s core self.The constant need to adapt to new limitations can feel like a continuous erosion of the self, and the fear of future disability becomes a fear of further loss of identity.
Addressing this existential dimension of anxiety is crucial for promoting long-term psychological adjustment and overall well-being. Treatment often involves helping individuals grieve their losses, redefine their sense of self and purpose within the context of their illness, and find new sources of meaning and value in their lives.
Cognitive impairment
The impact of anxiety on cognitive function is well documented. Cognitive impairment, particularly slowed information processing speed, is a common and debilitating feature of MS. Anxiety has a detrimental effect on cognitive domains that are already compromised, such as attention and executive functions. It does this by increasing an individual’s awareness of task-irrelevant, often threat-related, stimuli, which interferes with the goal-oriented cognitive processing required for the task at hand. Thus, the underlying cognitive deficit from MS is compounded by the cognitive interference from anxiety, leading to a greater overall level of impairment than either condition would cause alone. Importantly, therefore, treating a patient’s anxiety can lead to measurable improvements in their cognitive functioning.
Mood, fatigue, pain and sleep – a vicious cycle
Emotional problems rarely occur in isolation in MS; they are typically part of a clinical syndrome including fatigue, pain and poor sleep. This interconnected symptom cluster reduces health-related quality of life and establishes significant barriers to therapy and lifestyle modification.
Fatigue
Fatigue is one of the most common and disabling symptoms of MS, and it is strongly and consistently correlated with anxiety. This is not a simple correlation but a predictive relationship. Higher levels of anxiety at one point in time can predict the severity of fatigue at a later date. Conversely, higher levels of fatigue can predict the later development or worsening of anxiety.
The severity of depression in highly fatigued people with MS also makes the management of fatigue a high priority in reducing the overall psychiatric burden and allowing patients to engage in psychological interventions such as cognitive behavioural therapy (CBT).
Pain and emotional distress
A two-way relationship also exists between pain and anxiety, where anxiety is associated with higher reported pain intensity and greater interference of pain with daily activities. The pain symptoms cause distress and anxiety, and the physical and mental state of anxiety (e.g. muscle tension, worry, poor sleep) in turn exacerbates the symptoms. Moderate or severe intensity pain that interferes with work, household activities or enjoyment of life affects about one-third of people with MS.
Sleep
Sleep is probably the most neglected MS-related problem in routine clinical practice; most people with MS have a sleep disorder. Depression, anxiety, pain and many other MS-related symptoms affect sleep quality. Therefore, it is challenging to manage MS-related emotional disorders without addressing sleep quality.
Lifestyle management and adherence
The cyclical nature of this grouping of mood disorder, fatigue, pain and poor sleep creates barriers to effective management. Emotional distress and physical symptoms can hamper efforts to start or maintain a healthy lifestyle.Since modifiable lifestyle factors (e.g. exercise) are associated with reduced pain burden, a vicious cycle is established: the disease causes emotional distress, the emotional distress prevents adherence to healthy behaviours, and the lack of healthy behaviours exacerbates physical symptoms.
Inappropriate laughing and crying
Inappropriate laughing and crying (pseudobulbar affect, PBA) are two neglected symptoms that often go undetected and untreated in people with MS. This doesn’t have to be the case. They are a further sign of significant damage to the brain and yet another reason to diagnose and treat MS early and effectively.
Case study
When I first met her, she was in her early fifties. She had had MS for over 20 years. Her family now kept her at home, isolated from the wider world. Her behaviour would embarrass them. Why?
She suffered from pathological laughter and occasionally inappropriate crying; her husband and children could not deal with this in public. She was clearly very disabled when I met her; she was unsteady on her feet and had slurred speech and dancing eyes from cerebellar problems. She had gross cognitive impairment. When I introduced myself to her, she burst into tears. Within 2−3 months of starting sertraline, a selective serotonin reuptake inhibitor (SSRI), her husband informed me that her laughing and crying episodes had improved by over 50% and the family were now taking her out regularly. He was very grateful that I had been able to educate them about her symptoms and, more importantly, help her and them as a family deal with this problem.
PBA is diagnosed using standardised scales or questionnaires, which can be self-administered (Center for Neurologic Study-Lability Scale [CNS-LS]). These symptoms respond to tricyclic and SSRI antidepressants and to a combination pill (Nuedexta®; licensed in the USA) that includes dextromethorphan hydrobromide and quinidine sulfate.
Management of emotional disorders
Routine screening, targeted drug treatment and structured psychological and behavioural therapies are core components of integrated care in MS. Emotional changes in MS require treatment, just as physical symptoms do.
Screening and education
Routine screening for both anxiety and depression should be part of standard MS care and should be conducted at all scheduled neurological visits. You may be asked to complete different screening questionnaires for depression, anxiety, fatigue and poor sleep. Ideally these should be done before your appointment so that the healthcare professional (HCP) can act on them during the consultation.
HCPs should educate their patients and their families about potential emotional changes associated with MS, in particular, irritability, crying and mood swings. This education should help reduce the stigma and embarrassment associated with emotional outbursts and enable the patient’s support network to develop coping strategies.
Drug treatment
Drug treatment must be tailored to the specific diagnosis and emotional disorder.
Depression and anxiety: The standard use of selective serotonin reuptake inhibitors (SSRIs) and serotonin−norepinephrine reuptake inhibitors (SNRIs) is recommended for the management of clinical depression and anxiety disorders.
Irritability: Treatment options for irritability include SSRI antidepressants, which are often needed in addition to CBT.
Pseudobulbar affect (PBA): Low-dose tricyclic or SSRI antidepressants can be effective in the treatment of PBA, but their use is off-label. In the USA, the combination of dextromethorphan hydrobromide and quinidine sulfate has been approved for PBA. In other countries, the combination of these two drugs can be effective in PBA, but again, the use of these two drugs separately is off-label and not recommended.
Apathy: Therapeutic strategies, such as cognitive rehabilitation, that enhance cognitive processing speed and executive function are more appropriate for apathy than antidepressants. However, such approaches are hard to access on the UK NHS and are not available in many healthcare systems. There are no licensed medications for apathy, but anecdotal evidence suggests that fampridine and some stimulants may help.
Further research: Properly randomised controlled trials are needed to determine the effectiveness of drugs that some patients obtain and use without a prescription. These include cannabis, psychedelics and ketamine, which are currently not licensed for managing anxiety in MS and are not advised.
Psychological and behavioural interventions
Evidence-based structured psychological interventions are as important as drug treatment for the management of anxiety and depression and should be considered a first-line approach in MS. CBT can address maladaptive thought patterns (e.g. catastrophic thinking about the future) and avoidant behaviours common in anxiety. Acceptance and commitment therapy (ACT) focuses on promoting psychological flexibility and acceptance, which is crucial for managing the reactive distress, grief and fear stemming from the unpredictable nature of the disease. Mindfulness, relaxation techniques and structured exercise programs have also been shown to manage anxiety and stress effectively.
Interventions such as physical activity and social therapies enable some people with MS to process the grief and losses imposed by MS. Simple behavioural strategies, such as taking a break from a conversation when emotions escalate, can also be beneficial.
Protective factors
Several protective factors can bolster resilience and lower the risk of anxiety. Motivational coping styles that involve direct problem-solving and active participation in treatment planning (i.e. self-management) are associated with better adjustment.One of the most critical protective factors is the presence of social support. Robust practical and emotional help from friends and family, and the knowledge that help is available if needed, significantly reduces the risk of mood symptoms.Finding ways to continue participating in previously enjoyed activities, albeit with new limitations, are key to coping. Interventions aimed at strengthening coping skills, fostering optimism and building social support networks can play a crucial role in preventing and treating anxiety in this population.
The therapeutic challenge
There is substantial symptom overlap between anxiety and depression (e.g. sleep disturbance, fatigue, difficulty concentrating) and between these mood disorders and the primary symptoms of MS.This can make it challenging for HCPs to discern whether a specific symptom, e.g. fatigue, is primarily a neurological symptom of MS, a physical symptom of depression, a consequence of the hyperarousal and poor sleep of anxiety, or a combination of all three. Use of appropriate screening tools can help to ensure that both anxiety and depression are accurately identified and appropriately treated.
Conclusion
MS profoundly affects emotional health across a broad and complex spectrum, manifesting as major depressive disorders, high levels of anxiety, the neurological syndrome of pseudobulbar affect, the cognitive−behavioural syndrome of apathy and, rarely, mania. These emotional changes are driven by primary damage to cortical-subcortical and brainstem circuits, coupled with reactive psychological distress resulting from living with a chronic, unpredictable illness. The current standard of care mandates routine screening, targeted drug treatments and psychological support utilising CBT and ACT.
Sexual dysfunction is a common symptom in men with MS, with a prevalence that surpasses that seen in the general population and other chronic disease states. Despite sexual dysfunction being one of the most frequently overlooked and under-addressed MS symptoms, it seldom gets documented and treated in men with MS.
Key points
Many men with MS experience some form of sexual difficulty; however, this important aspect of overall well-being is underdiagnosed and undertreated.
Such difficulties usually result from a combination of neurological, psychological, social and cognitive factors.
Primary dysfunction, caused by damage to the network of signals between the brain, spinal cord and peripheral nerves, can affect the ability to achieve an erection, orgasm or ejaculation; it may also adversely affect libido, sexual desire and genital sensation.
Secondary dysfunction results from other MS-related symptoms, including fatigue, spasticity, pain, weakness, bladder dysfunction and bowel dysfunction. Many of the medications used to manage such symptoms may cause or worsen sexual difficulties.
Tertiary dysfunction refers to the psychological, emotional and interpersonal challenges of living with MS: depression, anxiety, low self-esteem and impaired body image are among the factors that impact sexual desire and confidence.
Management of male sexual dysfunction requires a coordinated, multidisciplinary and personalised approach that involves the MS team, a urologist, physiotherapist, occupational therapist and a psychologist or sex therapist.
A wide range of medications, interventions and lifestyle modifications are available that can help couples affected by MS to adapt to the current reality and build a new, satisfying form of intimacy.
An overlooked and distressing symptom
Sexual dysfunction is a common symptom in men with MS, with a prevalence that surpasses that seen in the general population and other chronic disease states. Most studies report that 50–90% of men living with MS will experience some form of sexual difficulty during their disease course. Despite this, sexual dysfunction is one of the most frequently overlooked and under-addressed MS symptoms, and it seldom gets documented and treated in men with MS. This is a clinical paradox, an example of a ‘conspiracy of silence’ where both parties in the clinical encounter overlook a significant issue affecting quality of life.
The main reasons why sexual dysfunction in men with MS is under-recognised, underdiagnosed and undertreated are the taboos of discussing it in the clinic, both from the patient and the HCP perspective. Surveys reveal that the primary barriers to discussing sexual health on the part of HCPs include:
time constraints during appointments
the major problem that the issue is ‘outside of my role’
lack of professional training
perceived patient discomfort.
Concurrently, patients are often reluctant to initiate these conversations owing to embarrassment, shame or a deeply held belief that sexuality is somehow incompatible with having a disability. This disconnect between the reality of the patient experience and the focus of the clinical consultation means that a treatable condition that causes significant distress is often left to fester, impacting mental health and relationships.
Far from being a peripheral concern, sexual function and sexual health are essential components of overall well-being. In men with MS, the onset of sexual dysfunction often precipitates a decline in quality of life, negatively affecting mood, self-esteem and intimate relationships. The distress frequently extends beyond the individual, impacting partners and contributing to marital conflict. The enquiry below illustrates the distress experienced by one man who contacted me for advice; his experience is not uncommon, unfortunately.
Case example
I am a 30-year-old man with relapsing MS. I was diagnosed during my first year of University, aged 18. I presented with transverse myelitis, weakness of both legs and urinary retention. I have been on natalizumab for 12 years and have done very well. However, I have sexual problems with difficulty getting and maintaining an erection. This is affecting my relationship with my wife. Whenever I bring this up with my MS nurse or neurologist, I get dismissed. My GP has given me Viagra, which helps, but its effects are unpredictable, and it often lets me down. I have gotten to the point where I now avoid sexual activity. What advice can you give to help me and others like me?
A complex range of causes
The underlying causes (aetiology) of sexual dysfunction in men with MS are usually complex, variable and dynamic. Some men with MS experience sexual dysfunction as part of a relapse, and they recover with time. However, sexual dysfunction in men with MS usually results from a combination of neurological, psychological, social and cognitive factors. It is therefore vital to approach it from three different perspectives.
Primary dysfunction arises directly from MS lesions within the central nervous system that disrupt the neural pathways governing sexual response.
Secondary dysfunction is the consequence of other MS symptoms, such as fatigue, pain, spasticity, or bladder and bowel issues, which create physical barriers to sexual activity.
Tertiary dysfunction encompasses the psychosocial, emotional and cultural issues that stem from living with a chronic illness, including depression, altered body image and changes in relationships.
Clinical presentations of male sexual dysfunction
Erectile dysfunction
This is the most commonly and widely studied sexual problem in men with MS. Defined as the consistent inability to achieve or maintain a penile erection sufficient for satisfactory sexual performance, erectile dysfunction (ED) affects a large majority of men with MS who report sexual issues, with some estimates as high as 80%. Across the entire male MS population, approximately 70% experience erectile problems at some point after an MS diagnosis.
Ejaculatory and orgasmic dysfunction
While ED receives the most attention, disorders of ejaculation and orgasm are also common and can be even more distressing for patients owing to a lack of effective treatments. Studies estimate that 35–50% of men with MS experience problems with ejaculation. The Male Sexual Health Questionnaire is used as a screen for dysejaculation. Ejaculatory disorders manifest as:
delayed ejaculation or anejaculation: difficulty or complete inability, respectively, to ejaculate despite adequate stimulation
premature ejaculation: climaxing too rapidly for sexual satisfaction
anorgasmia: the failure to reach orgasm
altered orgasmic sensation: a less intense or less pleasurable orgasmic experience.
Disorders of libido or sexual desire
A diminished or absent interest in sex is another crucial component of sexual dysfunction in men with MS. Though less rigorously studied than ED, one report suggests that reduced libido affects approximately 40% of men with MS. Loss of libido is particularly complex, often arising from a combination of damage to the brain’s centres that impact desire, the secondary effect of fatigue, and tertiary psychological factors like depression and anxiety.
Altered genital sensation
The direct neurological impact of MS can manifest as abnormal sensations in the genital area, including numbness (decreased sensation), paraesthesias (e.g. pins and needles) or dysaesthesias (unpleasant or painful sensations, such as burning). These sensory disturbances can fundamentally alter the experience of sexual touch, making it less pleasurable or even painful, thereby directly interfering with arousal and orgasm.
The focus on ED in both MS research and clinical practice is driven in part by the availability of effective pharmacological treatments for this issue; this creates an incomplete picture of the patient’s experience. A management plan that successfully restores erectile function, for example, but fails to address a co-existing inability to ejaculate or a profound lack of sexual desire will ultimately fail to improve the patient’s overall sexual satisfaction and quality of life. A thorough clinical evaluation that assesses all phases of the sexual response cycle is therefore needed.
Functional changes underlying male sexual dysfunction in MS
Primary dysfunction
Normal human sexual function is a complex process that requires the integration of signals between the brain, spinal cord and peripheral nerves. MS damages this network in several ways, causing primary sexual dysfunction.
Cerebral and brainstem lesions
MS lesions in the brain and brainstem affect libido, arousal and orgasm.
Libido and arousal: Sexual desire is not merely a hormonal process; it originates in the brain. Lesions in higher cortical areas, particularly the limbic system (the brain’s emotional centre) and the hypothalamus, can diminish libido and impair the capacity to process sensory or psychological cues as erotic.MRI studies have correlated dysfunction in arousal and erection with lesions in specific brain regions, including the frontal lobe, prefrontal cortex, temporal lobe, insula and hippocampus.
Orgasm: Orgasm is also vulnerable to cerebral damage, and orgasmic dysfunction is associated with lesions in the pons (part of the brainstem), left temporal lobe and right occipital areas.
Spinal cord lesions
The spinal cord relays neuronal signals from the brain to the genitals and transmits sensory information back up to the brain. Lesions along the spinal tracts are the leading cause of ED and ejaculatory disorders.
Erectile function: Penile erection is a neurovascular phenomenon mediated by two distinct pathways, both of which can be compromised by MS. A psychogenic erection, initiated by erotic thoughts or sensory stimuli processed by the brain, depends on intact nerve signals travelling down the spinal cord to the pelvic organs. A reflexogenic erection, triggered by direct physical touch to the genitals, relies on a reflex arc located in the sacral segments of the spinal cord (S2−S4). MS lesions can disrupt these pathways individually or in combination. Consequently, depending on the specific location of the spinal damage, a man might be able to achieve an erection from direct touch but not from psychological arousal, or vice versa.
Ejaculation: Ejaculation is a far more complex reflex than erection, involving the coordinated contraction of multiple pelvic muscles and requiring precise, intact communication between the brain and the entire length of the spinal cord. This complexity makes it exceptionally vulnerable to disruption by MS lesions, which helps explain why ejaculatory problems in MS are so common and difficult to treat.
Autonomic and hormonal factors
The autonomic nervous system, which controls involuntary bodily functions, plays a pivotal role in regulating erection and ejaculation. MS can cause autonomic dysfunction, further contributing to these problems. Additionally, emerging evidence suggests that chronic inflammation associated with MS, as well as hypothalamic lesions, can disrupt the hypothalamic-pituitary-gonadal axis. This can lead to altered levels of sex hormones, such as testosterone, and has even been linked to impaired sperm quality.
Secondary dysfunction
Secondary sexual dysfunction arises from other MS-related symptoms and the side effects of medications used to treat these symptoms.
Fatigue: Fatigue is one of the most common and disabling MS-associated symptoms that directly undermines sexual function by reducing the physical energy and motivation required for intimacy.When daily life is already exhausting, sexual activity can feel like an insurmountable task.
Spasticity, pain and weakness: Spasticity, chronic pain, and muscle weakness can make movement difficult and some sexual positions uncomfortable or impossible. Painful muscle spasms can be triggered by the movements of sexual activity, leading to a conditioned avoidance of sex.
Bladder dysfunction and bowel dysfunction: The fear of urinary or faecal incontinence during sexual activity is a potent psychological deterrent. With more than 50% of people with MS experiencing bladder and bowel issues, this is a widespread concern.The anxiety and embarrassment associated with a potential accident can cause individuals and their partners to avoid physical intimacy altogether.
Side effects of medication: Many of the medications prescribed to manage the symptoms of MS can, ironically, cause or exacerbate sexual dysfunction. Antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants, are well known for causing decreased libido, ED and anorgasmia. Similarly, medications for spasticity, neuropathic pain and urinary frequency can also interfere with sexual responses.
Tertiary dysfunction
Tertiary dysfunction refers to the complex web of psychological, emotional and interpersonal challenges that arise from living with a chronic, unpredictable illness like MS. These factors can be just as debilitating to a person’s sexual health as any physical symptom.
Depression and anxiety: There is a strong, two-way, destructive relationship between MS, depression and sexual dysfunction. Depression affects 30–50% of individuals with MS, and it is an independent predictor of sexual dysfunction.The experience of sexual failure can, in turn, trigger or worsen feelings of depression, despair and isolation, creating a vicious cycle that is difficult to break.
Body image and self-esteem: The physical changes brought on by MS – such as a limp, the need for a cane or wheelchair, weight gain from steroids or inactivity, or tremors – can profoundly damage a man’s body image and sense of masculinity. This may lead to feelings of being ‘flawed’, ‘broken’ or ‘unattractive’ that erode self-esteem and sexual confidence.
Relationship dynamics and role changes: MS does not just affect the individual; it impacts the entire relationship. Performance anxiety and fear of rejection can lead to avoidance of intimacy.A particularly challenging dynamic arises when an intimate partner must assume significant caregiving responsibilities. This ‘role reversal’ can blur the lines between lover and caregiver, disrupting the emotional foundation of the sexual relationship.The partner’s own sexual satisfaction and quality of life are also frequently diminished, highlighting the two-way nature of sexual dysfunction.
Management of male sexual dysfunction in MS
A single treatment approach towards sexual dysfunction in MS often fails because it is a multifactorial problem that requires a coordinated, multidisciplinary approach. This includes the MS team, a urologist, a physiotherapist, an occupational therapist and a psychologist or sex therapist. Failure to implement an interdisciplinary approach is usually because the MS team is reluctant to initiate the conversation about sexual health or lacks knowledge.
Before any medication or therapy is initiated, it is essential to break the ‘conspiracy of silence’ and create a safe, confidential environment for open communication between the patient, their partner and the healthcare provider. For the MS HCP, this involves routinely and proactively asking about sexual health as part of a holistic review of systems, often alongside questions about bladder and bowel function. For the patient, having ‘permission’ to discuss these sensitive issues can be profoundly therapeutic, reducing shame and ‘validating’ their experience as a legitimate medical concern.
Management of primary sexual dysfunction
Pharmacotherapy for erectile dysfunction
Oral phosphodiesterase-5 (PDE-5) inhibitors: Medications such as sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra) and avanafil (Spedra) are the first-line pharmacological treatments for ED in men with MS. Vardenafil is generally not available on the NHS, and avanafil is prescribed via specialist sexual dysfunction clinics. Sildenafil (Viagra) has a short half-life and needs to be taken before intercourse is planned. In comparison, tadalafil (Cialis) has a long half-life and is called the weekend Viagra. Some men with MS find that combining the two drugs is synergistic. Please note that they come in different doses, so you will need to titrate the dose to find the one that works best for you. These drugs do not create an erection spontaneously; they work by enhancing the natural erectile process, increasing penile blood flow in response to sexual arousal.Clinical trials have demonstrated their efficacy, but they may be effective in only about 50% of men with MS (a lower rate than in the general population), likely due to the underlying neurological deficits.These drugs are contraindicated in men taking nitrate medications for heart conditions.
Injectable and intraurethral medications: For men who do not respond to or cannot take oral PDE-5 inhibitors, these locally administered medications are highly effective second-line options. Alprostadil, a synthetic prostaglandin, can be injected directly into the erectile tissue of the penis (intracavernosal injection) or inserted as a small suppository into the urethra.These methods induce an erection directly and are often successful when oral agents are not.
Management of ejaculatory and orgasmic disorders
This remains an area of unmet clinical need, as there are currently no medications specifically approved or consistently effective for treating delayed ejaculation or failure to reach orgasm (anorgasmia) in MS. Some antidepressants (e.g. SSRIs) may be used ‘off-label’ to treat premature ejaculation thanks to their side effect of delaying orgasm. For delayed ejaculation or anorgasmia, the focus shifts to enhancing stimulation through manual or oral techniques or with the use of assistive devices like penile vibrators.
Addressing low libido and sensory changes
A review of the patient’s current medications is needed because many drugs, especially SSRIs, can suppress libido. Switching to an alternative antidepressant with a more favourable sexual side effect profile, such as bupropion or certain SNRIs (serotonin and norepinephrine reuptake inhibitors), may be beneficial. If blood tests reveal low testosterone levels, hormone replacement therapy may be considered to improve desire and energy. For altered genital sensation, the goal is to compensate for the diminished nerve signals by increasing the intensity and focus of stimulation using vibrators, different types of touch, or other sexual aids.
Management of secondary sexual dysfunction
Fatigue: Energy conservation is paramount. This involves planning sexual activity for times of day when energy is highest (often the morning), taking a nap beforehand, and collaborating with a partner to find less physically demanding sexual positions, such as spooning.
Spasticity: Proactive management can prevent painful muscle spasms from disrupting intimacy. This may include gentle stretching or massage before sex, taking an antispasticity medication like baclofen approximately 30–60 minutes before sexual activity, and/or experimenting with positions that minimise muscle tightness and discomfort.
Bladder and bowel issues: Careful planning can alleviate the anxiety surrounding potential incontinence. Strategies include restricting fluid intake for a few hours before sex, ensuring the bladder and bowel are emptied immediately beforehand and using intermittent self-catheterisation if needed. Using a condom can also provide a sense of security against urinary leakage.
Cognitive changes: For individuals whose concentration is affected by MS, creating an environment conducive to focusing is helpful. This means minimising external distractions, such as television or phones, and maximising sensual stimuli, including lighting, music and scent, to help maintain focus on the intimate experience.
Psychological counselling and sex therapy are the cornerstone of a holistic management plan and include cognitive behavioural therapy (CBT). CBT can be effective for challenging and reframing the unhelpful thoughts and beliefs that fuel performance anxiety and negative body image. Couples counselling provides a structured forum to improve communication, openly discuss fears and frustrations, and collaboratively explore the changes MS has brought to the relationship, including the sensitive shift from partner to caregiver.
Sensate focus and body mapping are specific sex therapy techniques that are particularly valuable for couples affected by MS. These exercises involve non-demand, non-goal-oriented sensual touching, shifting the focus away from intercourse and orgasm and toward the rediscovery of pleasure. This is especially important when genital sensation has been altered, as it helps couples identify new erogenous zones and broaden their definition of intimacy.
Rehabilitation and lifestyle interventions
These approaches focus on improving physical function and overall health to support sexual well-being.
Pelvic floor exercises are crucial for maintaining erectile rigidity and for the muscular contractions associated with ejaculation. A specialised physiotherapist can design an exercise programme (for example, Kegel exercises) to strengthen these muscles, potentially improving erectile and ejaculatory control. While much of the research into pelvic floor training has focused on women, the principles are also directly applicable to men.
General health has a direct impact on sexual function. Lifestyle modifications such as adopting a heart and brain-healthy diet, engaging in regular physical activity as tolerated, maintaining a healthy weight and quitting smoking can all improve vascular health.
Assistive devices for erectile dysfunction
For men with ED that is refractory to medication, mechanical aids are an important and effective option. Vacuum constriction devices consist of a plastic cylinder placed over the penis, a hand-held pump that creates a vacuum to draw blood into the penis, and a constriction band that is slipped onto the base of the penis to trap the blood and maintain the erection for up to 30 minutes.
Vacuum constriction device operated by a hand-held pump.
Penile prostheses or penile implants are a surgical solution for severe, intractable ED. A device is surgically implanted into the penis that allows the man to create a rigid erection mechanically. This uses saline to inflate the cylinder that is implanted in the penis. The saline can be pumped from a reservoir into the prosthesis or erectile cylinder to mimic an erection. The saline can then be pumped from the cylinder back into the reservoir to cause detumescence. This is typically considered a third-line treatment when all other options have failed.
Penile implant for severe erectile dysfunction
Education, education, education ….
Providing clear, accurate information to the patient and their partner about how MS can affect sexual function helps to demystify the problem, correct common misconceptions (e.g. that sexual activity will worsen the disease), and empower the couple to explore solutions collaboratively.
A management plan for male sexual dysfunction needs to be personalised to address specific primary, secondary and tertiary factors. The goal is often not just to restore previous sexual function but to help the man with MS to adapt to a new reality, encouraging him and his partner to build a new, satisfying form of intimacy.
This calls for improved clinical education of MS healthcare professionals, the integration of standardised screening tools into routine care, and a fundamental shift in clinical culture toward a more holistic model of well-being that values sexual health as a core component of MS management.
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.
I suggest you start with a simple self-help guide to improve your sleep hygiene.
Ensure you spend an appropriate amount of time asleep, at least 6 hours in bed. Some people need more than this to feel refreshed.
Limit daytime naps to 30 minutes. Please note that napping does not make up for inadequate nighttime sleep.
Avoid stimulants such as caffeine, modafinil and nicotine close to bedtime.
Only drink alcohol in moderation. Alcohol is known to help you fall asleep faster, but too much disrupts sleep.
Exercise helps improve sleep quality. As little as 10 minutes of aerobic exercise daily can enhance the quality of sleep.
Don’t eat before going to bed. Heavy foods and fizzy drinks can trigger indigestion or heartburn/reflux that disrupts sleep.
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.
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.
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.
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.
Fatigue in MS is common, but it is often not investigated or managed properly. This post highlights the complexity of MS-related fatigue and explains why and how to manage it holistically.
Key points
The different mechanisms underlying MS-related fatigue are explained.
The MS disease process, the burden of living with MS, and other factors such as drug side effects, comorbidities and lifestyle choices may all contribute to fatigue in MS.
Practical guidance is provided on managing many aspects of MS-related fatigue, using a holistic and systematic approach.
Not all fatigue is MS-related; it is important to ascertain if your fatigue could be due to another disease process.
Fatigue is one of the most disabling of all the symptoms of MS. It is the symptom that over 50% of people with MS would most like to be rid of. MS-related fatigue has several underlying mechanisms.
Fatigue caused by MS disease processes
Inflammation in the brain
Inflammatory mediators or cytokines associated with MS – in particular, interleukin-1 (IL-1) and TNF-alpha – trigger ‘sickness behaviour’. This is the response to inflammation that forces us to rest and sleep so that our body can recover. Sickness behaviour is also the body’s response to a viral infection such as flu; in fact, many people with MS describe their fatigue as being like the fatigue they experience with flu.
Sickness behaviour from an evolutionary perspective is well conserved and occurs in most animals. This type of fatigue needs to be managed by switching off ongoing inflammation in the brain. Many people with MS who take a highly effective DMT report feeling much better and free from fatigue and/or brain fog. This is why recent-onset fatigue that cannot be explained by other factors (see below) may indicate MS disease activity. At present, fatigue on its own does not constitute a relapse.
Many patients with MS who have had COVID-19 tell me that MS-related cog-fog and fatigue feel like the cog-fog and fatigue of COVID-19 and long-COVID. As many as one in four people with long-COVID experience cog-fog, which includes problems in attention, language fluency, processing speed, executive function, and memory: these are the same problems that affect people with MS.
Cog-fog related to MS and to COVID-19 could be linked to the same inflammatory mechanisms. This syndrome of systemic inflammation causing profound fatigue and cog-fog is not new. Some people with MS who have a systemic infection take weeks or months to return to normal; some patients with more advanced MS never return to their original baseline. This is why, as part of the holistic management of MS, we need to treat and prevent systemic infections as best we can.
The overlap between COVID-19 and MS-related cog-fog raises the question whether both are due to viral infections. There is some evidence of recent Epstein-Barr virus (EBV) reactivation in patients with long-COVID,1 suggesting that the EBV rather than the SARS-CoV-2 may be causing long-COVID symptoms. This is important because chronic EBV infection has been associated with chronic fatigue syndrome. It has also been suggested that chemo-brain is due to similar mechanisms, i.e. chemotherapy triggers CNS inflammation, which causes cog-fog.
Neural plasticity
When parts of the brain are damaged by MS, other areas are co-opted to help take over, or supplement, the function of the damaged area. In other words, people with MS use more brain power than people without MS to complete the same task. This usually manifests as mental fatigue and is why people with MS have difficulty concentrating for prolonged periods and multitasking. At present we have no specific treatment for this type of fatigue, but some patients find amantadine or modafinil helpful. There is also some emerging evidence that fampridine may help with cognitive fatigue. However, preventing damage in the first place should prevent this type of fatigue.
Exercise-related conduction block
Damage to axons that conduct electrical impulses is the reason why people with MS notice their legs getting weaker or another neurological symptom getting worse with exercise. We think this is due to demyelinated or remyelinated axons failing to conduct electrical impulses when they become exhausted. Exercise-induced fatigue is probably the same as temperature-related fatigue; a rise in body temperature also causes vulnerable axons to block and stop conducting. To deal with this type of fatigue we need therapies to promote remyelination and to increase conduction. These types of fatigue are treated by rest, cooling and possibly drugs such as fampridine that improve conduction. At the heart of this type of fatigue is localised energy failure.
Fatigue from living with MS symptoms
Temperature sensitivity
Many people with MS are temperature sensitive. Typically, high temperatures worsen fatigue, but low temperatures also affect some patients. Many people with MS manipulate their behaviour to avoid hot or cold environments. Some find it helpful to use cooling suits, but these are costly and are not covered by NHS funding. Cold or ice baths, swimming and air conditioning can all help with temperature-related fatigue.
Case example
One of my patients had a walk-in butcher’s fridge installed in her house, and she spends 30 minutes there 4 ̶ 5 times a day to manage her fatigue. She is a wheelchair user, and she sits in her wheelchair in the fridge.
Menstrual and menopausal fatigue
Menstrual (or catamenial) fatigue is a form of temperature-related fatigue that occurs in women during the second half of the menstrual cycle when their body temperature increases. It responds to paracetamol and to non-steroidal anti-inflammatory drugs such as ibuprofen and naproxen. Fatigue is a common symptom of menopause too; some women with MS who are menopausal and have fatigue find hormone replacement therapy helpful.
Whether or not men go through a ‘menopause’ is a moot point. Testosterone levels do drop with age, however, and some male patients find that testosterone replacement therapy helps their MS-related fatigue. In the UK, the indications for testosterone replacement therapy are very well defined and do not include MS-related fatigue, so most people with MS who want to try this therapy need to pay for a private prescription.
Bladder problems
Intermittent waking due to bladder problems may result in fatigue from disrupted sleep. Bladder problems may also contribute to insomnia, with the affected individual needing to visit the bathroom frequently and unable to relax into sleep. For detailed guidance on managing bladder problems, particularly at night, please see the bladder and bowel section of the website, particularly the article on nocturia.
Insomnia due to pain and discomfort
Other disease-related factors that contribute to fatigue include insomnia from pain, discomfort of being unable to turn in bed and restless legs syndrome (RLS). RLS is common in people with MS, affects sleep quality and is associated with poor cognition. For detailed guidance on managing these MS symptoms, please see the post entitled Sleep disrupted by pain and discomfort.
A case scenario
“A 28-year-old woman with early relapsing ̶ remitting MS, on glatiramer acetate, and little overt neurological impairment suffers from severe fatigue, which is worse during the latter half of her menstrual cycle. She has recently split up with her long-term partner because of the impact her symptoms have had on her relationship. She has also had to stop working as a bank clerk because of her fatigue.”
Prof G’s response This patient needs to be examined and will need an MRI and a lumbar puncture to measure her spinal fluid neurofilament levels. If she has evident inflammatory disease activity, her DMT will need to be switched. She needs a full medical assessment, which includes a screen for comorbidities.
The patient complains of cognitive fatigue and, despite not having much physical disability, she was found to have a high brain MS lesion load and noticeable brain volume loss. A formal neuropsychological assessment to establish if she has cognitive impairment would allow her to be referred to a cognitive rehabilitation programme; this can target specific areas to help her cope with her cognitive deficits.
To combat fatigue during her menstrual cycle, this patient did well on naproxen, which is longer acting than ibuprofen and paracetamol. Naproxen only needs to be taken during the second half of her cycle. She was screened for poor sleep hygiene, and she volunteered intermittent early morning waking due to bladder problems and anxiety. Both would need to be addressed as part of her fatigue management programme.
It was clear that the patient had both depression and anxiety, which were related to the impact of MS on her occupational and social functioning. This must be managed with cognitive behavioural therapy (CBT), mindfulness and an exercise programme. If this approach is not helpful, then I would suggest the judicious use of an antidepressant and, failing this, a referral to a psychiatrist and/or psychologist.
Fatigue resulting from other factors
Comorbidities and other diseases
Comorbidities and other diseases related to MS can cause fatigue and should be screened for. These include infections (see above). In people with more advanced MS, the urinary tract is most often affected, but other sites of infection include the sinuses, teeth, lungs, skin (intertrigo and pressure sores) and bowels.
Fatigue is common with thyroid disease; an underactive thyroid gland (hypothyroidism) and an overactive gland (hyperthyroidism, or thyrotoxicosis) cause fatigue. Diabetes, other endocrine (hormonal) problems, anaemia and heart, kidney, liver or lung diseases all cause fatigue.
Side effects of drugs
Fatigue is a common side effect of many medications, particularly drugs that cause sedation and some DMTs. Flu-like side effects from interferon-beta, for example, may make fatigue worse. Anticholinergics and antispasticity drugs are sedating, blunt cognition and may worsen MS-related fatigue. If you have fatigue, therefore, it is important to review your medications. MS is associated with polypharmacy, but some of the medications that cause or exacerbate fatigue can be reduced in dose, stopped or potentially replaced with alternatives that don’t exacerbate fatigue.
Lack of sleep and/or sleep disorders
Poor sleep means you feel tired in the morning. Most people with MS have poor sleep hygiene and almost half have an actual sleep disorder. A clue to this is how you feel in the morning and whether you have excessive daytime sleepiness. If you wake up in the morning and don’t feel refreshed and/or you fall asleep frequently during the day, you need a formal sleep assessment. You can complete the Epworth Sleepiness Scale online to see if you have a problem.
Depression and anxiety
Fatigue is a common symptom of depression and anxiety. Of the many online screening tools for depression and anxiety, the best one to use if you have MS is probably the Hospital Anxiety and Depression Scale (HADS).
Obesity
Being overweight requires additional energy to perform physical tasks, and obesity itself causes fatigue. Recently an association has been found between obesity and depression. Obesity also predisposes you to sleep disorders; obese people with MS are more likely to have obstructive sleep apnoea. For all these reasons you should engage with lifestyle and wellness programmes to manage obesity and fatigue.
Deconditioning
Deconditioning is simply the term we use for being unfit. If you are unfit, performing a demanding physical task makes you tired. Deconditioning is treated with exercise, which paradoxically can reduce fatigue. Patients may claim that exercising makes their fatigue worse. Yes, that does happen, but if you persevere and get fitter your fatigue often improves. The important thing is to start a graded exercise programme and build up slowly. Exercise does some incredible things to the brain, many of which explain why it is effective at treating not only fatigue but also depression and anxiety. Exercise is a form of ‘disease-modifying therapy’ and hence everyone with MS should be participating in an exercise programme.
Poor nutrition and ‘food coma’
Some people with MS are anorexic and eat very poorly; as a result, they have little energy. Although this is quite rare, I have had a few such patients over the years. Similarly, overnutrition may have the same effect. Some of the hormones your gut produces cause you to feel tired and want to sleep; this is the so-called siesta effect (also referred to as food coma or postprandial hypersomnolence). Reducing the size of your meals and changing your eating behaviour may improve this. Postprandial hypersomnolence has two components.
A state of perceived low energy related to activation of the parasympathetic nervous system (which is part of the autonomic nervous system) in response to expansion of the stomach and duodenum from a meal. In general, the parasympathetic nervous system slows everything down.
A specific state of sleepiness triggered by the hormone cholecystokinin that helps digest food and regulate appetite. It is released in response to eating and to changes in the firing and activation of specific brain regions. The coupling, or interaction, of digestion and the brain is referred to as ‘neurohormonal modulation of sleep’ and it underlies the reflexes responsible for postprandial hypersomnolence. There is therefore a well-studied biological reason why we feel sleepy after eating a meal.
Managing food coma – practical tips
The first patient who alerted me to the problem of food coma in MS was so affected by postprandial hypersomnolence that she now eats only one meal a day, late in the evening. She can then ‘crash’ and go to sleep about an hour after eating. She needs to be functional during the day but cannot do her professional work if she eats anything substantial during working hours because of her overwhelming desire to sleep. She has tried caffeine, modafinil and amantadine to counteract postprandial hypersomnolence, but all these substances had only a small effect.
Other patients reporting postprandial hypersomnolence derive some benefit from the judicious use of stimulants. You can start by self-medicating with caffeine, but this may have the drawback of worsening your bladder function. Please note, however, that it is not advisable to take stimulants later than about 3 pm or 4 pm because they have a long half-life and can cause insomnia.
Some patients find carbohydrate-rich foods particularly potent at inducing ‘food coma’. Indeed, glucose-induced insulin secretion is one of the drivers of this behavioural response. This may be why people who fast or eat very low-carbohydrate or ketogenic diets describe heightened alertness and an ability to concentrate for long periods. Another option is to reduce your meal size: instead of large meals, try eating multiple small snacks during the day.
Exercise has helped some patients deal with postprandial hypersomnolence. I am not sure exactly how exercise works – possibly by lowering glucose and insulin levels and improving insulin sensitivity. The latter will reduce hyperinsulinaemia, which not only causes postprandial hypersomnolence but is an important driver and component of metabolic syndrome and obesity.
Postprandial hypersomnolence will be worse if you already suffer from a sleep disorder and excessive daytime sleepiness. Most people with MS have a sleep disorder, so there is little point in focusing on postprandial hypersomnolence and ignoring the elephant in the room.
Using your energy effectively
One strategy to manage MS-related fatigue is to imagine your energy levels as a battery, i.e. you have only so much energy in the day. People with MS have smaller batteries than people without MS and therefore need to plan their day and activities to maximise their use of energy. For example, if you do something tiring in the morning, you should rest in the afternoon to conserve energy for evening activities. Similarly, if you find some activities very tiring, such as taking a hot shower or bath, plan to do this in the evening before bed.
Conclusion
It is apparent from this discussion that fatigue in MS is more complex than we realise. So be careful, or at least wary, if your neurologist simply wants to reach for the prescription pad to get you out of the consultation room. Any MS-related symptoms that can affect sleep need to be managed accordingly. Like other MS-related problems, a holistic and systematic approach is needed to manage and treat MS-related fatigue correctly. Not all fatigue is MS-related. This is why it is important to take a step backwards and ask yourself if your fatigue could be due to another disease process.
Reference
Gold JE et al. Investigation of long COVID prevalence and its relationship to Epstein-Barr virus reactivation. Pathogens 2021;10:763.
The practice of neurology and medicine varies worldwide, so I will explain what to expect if you were to consult me.
Key points
The principles of diagnosing MS are to show the dissemination of lesions in space and time and to exclude alternative diagnoses that mimic MS.
Diagnosing MS takes time and should not be rushed; do not be afraid to ask questions.
Most patients diagnosed with MS have an emotional response similar to the five stages of grief – Denial, Anger, Bargaining, Depression and Acceptance (DABDA). Additionally, many patients experience Anxiety about the future (DABDA+A).
Newly diagnosed patients should avoid overloading themselves with information about MS; much of the online information can be misleading and anxiety-provoking. Guidance is provided below about reliable information sources.
Counselling, cognitive behavioural therapy and the support of an MS ‘buddy’ can help patients adjust to a diagnosis of MS, which is a serious condition and should be respected.
You should be aware that medical ‘gaslighting’ may happen and know how to deal with it.
Tests to exclude other diagnoses
MS is a clinical diagnosis and a diagnosis of exclusion. Therefore, I would take a detailed medical and neurological history and examine you for neurological signs. Finding signs of involvement in a particular neurological pathway is important for fulfilling the criteria for dissemination in space. MS must involve at least two neuronal pathways. To be confident that no alternative diagnosis could explain your presentation, a full work-up will likely include magnetic resonance imaging (MRI) of the brain and spinal cord, evoked potentials, a lumbar puncture and blood tests. In addition, I would need to show dissemination in time, involving two or more structures separated in time by at least 4 weeks.
The diagnosis of MS is not trivial and should not be rushed. If I doubted the diagnosis, I would wait. The old maxim ‘time is often the best diagnostician’ is as pertinent today as it was in the past. Despite this, the misdiagnosis rate remains stubbornly high. I recommend you read some of the posts that cover the diagnosis of MS in more detail, such as Am I sure that I have MS? and Do I have active MS?
Time to adjust to a diagnosis of MS
You should not expect too much from the initial consultation. The second consultation, once all the diagnostic tests are back, will be the difficult one. Before COVID-19, an MS diagnostic workup in the NHS would take about 6 ̶ 8 weeks. Due to COVID-19-related delays in getting MRI scans and evoked potentials, it currently takes up to 4 months. Occasionally, patients with possible MS are admitted to the hospital because of a disabling attack. This allows us to make a more rapid diagnosis.
Being diagnosed with MS or any other chronic and potentially disabling disease is distressing. In my experience, patients’ responses are highly variable, including relief about finally getting a diagnosis, surprise, shock, anger or blaming the messenger for the bad news. Some question my judgement and refuse to accept the diagnosis; they may accuse me of being wrong and seek a second, third or fourth opinion. Many are devastated and expect the worst: how long before I need a wheelchair? Rarely patients are uninformed, have little or no idea about MS and ask about the disease.
Examples of some responses to a diagnosis of MS
I always try and be reassuring and tell patients that MS is now a treatable disease. If we manage their MS actively, we can prevent or at least delay the development of disability for many decades.
Emotional response
I also warn patients about the emotional reaction they will likely have to being diagnosed with MS. The psychological impact of an MS diagnosis and the uncertainty associated with having a potentially disabling disease should never be underestimated. Elisabeth Kübler-Ross in 1969 described five common stages of grief, best known by the acronym DABDA:
Denial,Anger,Bargaining, Depression,Acceptance
We have added an extra A – for Anxiety about the future – to expand this to DABDA+A. People diagnosed with MS may go through these stages in order of the pneumonic, but some will jump around, and others go through some stages many times. Although the Kübler-Ross stages have been criticised in the psychological literature, they provide a valuable framework for discussing a patient’s emotional journey. Being diagnosed with MS is a marathon, not a sprint, and it will take time to come to terms with it.
It is important for healthcare professionals (HCPs) to be there for the journey and to make sure that newly diagnosed patients have access to their MS team and high-quality information about MS.
Step-wise approach to understanding MS
In the modern era, most patients I diagnose as having MS are aware of the disease and suspect they have MS before I tell them so. I say this because Dr Google, Dr ChatGPT and Dr Bing are only keystrokes away, and their answers are very credible.
Because of their anxiety, most newly diagnosed patients only take away one thing from the consultation: they have MS. Almost everything else they hear is forgotten. I encourage patients to record the consultation or bring a partner, friend or family member who can be their backup memory.
I try to avoid overloading patients with information early on. Instead, I provide links to online resources about having MS. We arrange a follow-up session with the MS nurse specialist in the next 10 ̶ 14 days so that they can ask questions.
Guidance about what information to trust
I counsel patients to stay away from Dr Google, Dr ChatGPT and Dr Bing until they have come to terms with having MS. Much of the MS-related content available on the web is misinformation and disinformation; until you understand the disease, it is difficult to know what information is valid, reliable and helpful and what is quackery. Many patients ignore this advice and overwhelm themselves with information, which can worsen anxiety.
I don’t introduce recently diagnosed patients to MS-Selfie initially. MS-Selfie is written at too high a level for the average person who is newly diagnosed. If patients want more information, I direct them to the MS Trust, the MS Society and ‘MS Brain Health: time matters’ (for more detail, see Resources and hot topics).
Counselling, support and respect
Depending on a patient’s response to the diagnosis, we may refer them for counselling, cognitive behavioural therapy and/or mindfulness therapy to help them come to terms with having MS and to help manage their anxiety. Most patients are receptive to these psychological therapies.
Many people with MS are traumatised by their diagnostic consultation and may experience symptoms of post-traumatic stress disorder from the event. This should not happen in the modern era. In my experience, gestures such as having tissues on hand for a distressed patient or holding their hand are ways that HCPs can demonstrate their empathy.
On rare occasions, particularly for patients who are alone and socially isolated, we may buddy them up with another carefully chosen patient to ask questions and learn about MS. These MS buddies need to be optimistic, able to communicate well and not overwhelm the recently diagnosed patient with information. I work closely with the charity Shift.ms, which does a similar thing.
In the diagnostic consultation, I avoid too much detail about treating MS and the specific DMTs. These are best discussed at the next visit. With some patients, however, the discussion gets to treatments very quickly. In such cases, I tailor the consultation to the individual’s needs.
During the diagnostic consultation, I also show patients their MRI scans. Seeing your brain, spinal cord and MS lesions provides an objective way of helping you to visualise the disease.
Recently diagnosed patients must be given time to ask questions and even to sit in silence. MS is a serious disease, and informing someone about the diagnosis must be done carefully. After more than 30 years as a neurologist, I still find telling my patients they have MS challenging. The patient being diagnosed with MS, as well as the disease, must be respected.
What if a doctor belittles my concerns?
The term ‘medical gaslighting’ describes a scenario where health professionals dismiss or downplay a patient’s real symptoms, leading to an incorrect diagnosis. Now that we have recognised medical gaslighting as a significant problem in MS, please don’t allow a neurologist to gaslight you. There are things you can do to prevent this.
Keep detailed notes and records. Patient-held notes transform consultations and allow you to become a partner in your healthcare.
Ask to record the consultation. Many HCPs don’t like this; just tell them you must listen to the conversation again to ensure you don’t forget things or miss important information. You will be surprised how this changes the HCP’s behaviour.
Ask questions. Then ask some more. And don’t be fobbed off; if you are dissatisfied with the answer, ask the question again.
Take someone with you for support. Having a witness during the consultation has a similar effect to recording the conversation or documenting it with notes.
Focus on your most pressing issues to make the best use of your consultation time. If your HCP is pressed for time, say you understand, but you would like to prioritise the following issues today. This helps you to frame the limits of the consultation and promote a two-way discussion. Also, don’t expect the HCP to have all the answers at their fingertips, but do expect them to come back to you later with the answers.
Try and pin down the next steps for your problem; ask what the action points are. For example, if the MRI shows this, how will that change my management? Do I need further investigations? How soon should I switch treatments?
If you still feel that you are being ignored, here are some of your options.
Some courses of action open to you if you experience medical gaslighting.
Abuse, manipulation, gaslighting and delaying a diagnosis are potentially reportable events which HCPs need to know about. Therefore, make your healthcare system aware of the problem rather than suffer in silence.
