Tag Archives: frontal lobe

Cognition and mental health

Suicidal ideation and suicide in MS

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

Key points

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

The problem we avoid talking about …

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

How common are suicidal ideation and suicide in MS?

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

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

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

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

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

Regional and temporal patterns

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

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

Limitations of study data

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

Who is at risk of suicidal ideation among people with MS

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

1. Psychiatric comorbidity: depression and anxiety

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

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

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

2. Disease-related factors

Several disease features align with suicidal ideation across studies.

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

3. Sociodemographic factors

The evidence here is more mixed.

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

4. Social and existential factors

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

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

Screening for suicidal ideation in the clinic

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

The Patient Health Questionnaire-9 (PHQ-9)

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

The Beck Scale for Suicide Ideation (BSI)

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

The Beck Depression Inventory-II (BDI-II)

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

The Hospital Anxiety and Depression Scale (HADS)

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

What should you be asked if a screen is positive?

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

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

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

Suicide prevention: what can we do?

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

At the clinical level

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

At the patient and family level

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

At the system level

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

The bottom line

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

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

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

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

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

You are not alone, and help is available.

References

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

Cognition and mental health

Dissociative states and MS

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

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.

sagittal

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

  1. 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.
  2. Rehan ST, et al. Association of adverse childhood experiences with adulthood multiple sclerosis: A systematic review of observational studies. Brain Behav 2023;13:e3024.
Cognition and mental health

MS and bipolar disorder: understanding the link

The association between multiple sclerosis (MS) and depression is well-established. Are people with MS also at risk of developing bipolar disorder?

Key points

  • Bipolar disorder is significantly more common in people with MS than in the general population.
  • This is not merely a byproduct of the stress of chronic illness; it also has to do with changes in the brain, caused by MS, that affect mood as well as physical function.
  • Mood symptoms may be caused by MS lesions, disease-related inflammation, or medications (steroids in particular).
  • Differentiating ‘primary’ (organic) mania from ‘secondary’ (MS-related) mania is crucial to ensure the correct diagnosis and treatment.
  • Key features that distinguish MS-related mania from organic mania include:
    • Late onset, often after age 35–40 years, or onset associated with MS disease progression
    • Weak or absent family history of bipolar disorder
    • Lack of response to standard treatments for bipolar disorder
  • Treatment for people with MS who experience bipolar disorder is available and effective. With coordinated care, they can successfully manage their symptoms.

MS affects movement, sensation and other bodily functions, but it also impacts the brain systems involved in thinking, emotions and behaviour. Here, I discuss the relationship between MS and bipolar disorder, a mental health condition that causes episodes of unusually high mood (mania or hypomania) and low mood (depression). Bipolar disorder has received less attention than depression in people with MS, despite its substantial effect on quality of life, treatment adherence and prognosis.

For some people with MS, symptoms of bipolar disorder appear for the first time as their disease develops. In others, existing mood symptoms may be made worse by inflammation, brain lesions or medications used to treat MS. This article explains why bipolar symptoms occur in MS, how they may present, how they can be recognised early and how they can be effectively managed.

How common is bipolar disorder in MS?

Research consistently shows that bipolar disorder is more common in people with MS than in the general population. In the general population, bipolar disorder affects roughly 1–2.4% of people. In MS, studies report current and lifetime prevalence rates of about 3% and 8%, respectively. This means people with MS have approximately double or even treble the usual risk.

Importantly, this increased risk is not simply because people with MS interact with healthcare systems more frequently than the general population, which increases the likelihood of mental health conditions being detected (we call this the ‘admission rate’ bias). Nor is it merely a byproduct of the stress of chronic illness (which might explain depression). Large studies that compare people with MS to similar individuals without MS still show a higher rate of bipolar disorder in the MS group. This suggests the association is real and probably related to changes in the brain caused by MS.

What factors cause MS-related mania?

Researchers believe there are three main mechanisms that drive cognitive and behavioural changes in MS; they can occur alone or together.

  • MS lesions that affect mood-regulating circuits
  • inflammation and immune changes
  • treatment-related factors.

Understanding these mechanisms allows clinicians to distinguish MS-related mania from ‘primary’ (organic) psychiatric illness and to deliver appropriate management.

MS lesions that affect mood-regulating circuits

This mechanism disrupts the ‘hardware’ that controls mood. MS causes inflammation and lesions (scarring) in the brain. Areas that are especially important for controlling emotions and behaviour include:

  • the right orbitofrontal cortex (OFC) – involved in regulating social behaviour, judgement and impulse control
  • the temporal lobes – important for memory and emotional processing
  • the white-matter pathways that connect these regions with deeper emotional and reward centres such as the amygdala and thalamus.

If MS lesions interfere with these circuits, the balance between emotional impulses and rational control can be disrupted. This may lead to behaviours that are characteristic of mania, including disinhibition (reduced ‘internal brakes’), uncontrolled emotions, euphoria (unusually elevated mood) and impulsivity. This pattern is sometimes called secondary mania (mania caused directly by a brain condition such as MS).

There is evidence that right-sided frontal or temporal injury leads to mania-like behaviours in other conditions (e.g. stroke, traumatic brain injury, tumours).

Understanding right- and left-sided brain functions

Consistent with literature on secondary mania from stroke or tumours, MS-associated mania is most often associated with right-sided brain lesions. The right hemisphere is dominant for processing negative emotions and withdrawal behaviours, while the left hemisphere processes positive emotions and approach behaviours. A lesion in the right hemisphere may impair the processing of negative emotions, leading to an unopposed ‘positive’ or euphoric affect (‘highs’) driven by the intact left hemisphere.

Inflammation and immune changes

During MS relapses or periods of immune activation, inflammatory molecules disrupt how brain cells communicate (think of it as a disruption to the brain’s ‘software’). One important system involved is the kynurenine pathway, which controls how the body uses tryptophan (an amino acid essential for the creation of compounds such as serotonin and melatonin).

Inflammation increases the activity of an enzyme called indoleamine 2,3-dioxygenase. This shifts tryptophan away from serotonin production towards production of quinolinic acid, a substance that overly stimulates nerve cells through NMDA receptors (N-methyl-D-aspartate receptors). This ‘excitatory overload’ can lead to symptoms like those seen in primary mania, such as agitation, mood instability, sleep disturbance and racing thoughts.

Kynurenic pathway - MS-Selfie gg1

The kynurenine pathway in inflammation-induced pathology of the central nervous system. Activation of IDO in peripheral immune cells (e.g. macrophages) or in the brain leads to production of kynurenine. This is converted to kynurenic acid in astrocytes and to quinolinic acid in microglia. Kynurenic acid can block the release of glutamate and dopamine, contributing to cognitive dysfunction. Quinolinic acid, by contrast, can increase glutamate release, which contributes to neurodegeneration. Figure modified from Haroon et al.

3-HAO, 3-hydroxy-anthranilic acid oxygenase; IDO, indoleamine-2,3-dioxygenase; KAT II, kynurenine aminotransferase II; KMO, kynurenine-3-monooxygenase; NMDA, N-methyl-D-aspartate.

This pathway is one of the clearest biochemical links between MS inflammation and bipolar-type symptoms.

Treatment-related factors

Some medications used in MS influence mood and may contribute to manic symptoms.

Steroids

High-dose intravenous methylprednisolone, typically 1000 mg/day for 3–5 days, is the most common cause of drug-induced mania in MS. Up to 12% of people treated with corticosteroids experience symptoms of mania, and nearly 65% of those with psychiatric side effects present with a mix of mania and psychosis.

A history of prior steroid-induced mood changes, female sex, older age and higher steroid doses increase risk. Steroid-induced mania typically appears 3 − 4 days after starting treatment (median 11 days in some studies) and may involve:

  • severe insomnia
  • pressured speech
  • irritability or agitation
  • grandiosity
  • psychosis in severe cases.

Symptoms usually resolve when the dose is tapered (within roughly 3 weeks), but they can persist longer in individuals with underlying bipolar disorder. I therefore try to avoid treating MS relapses with steroids. However, this is not always possible.

Other agents that may cause mania

  • Amantadine, used for fatigue, can trigger mania in susceptible individuals.
  • Modafinil and methylphenidate, also used for fatigue, have been linked to sudden switching between manic and depressive symptoms.
  • Cannabinoids may destabilise mood or cognition.
  • Interferons more commonly cause depression than mania, but irritability, aggression and mania have been reported. The risk of new psychiatric symptoms is low, and patients with stable mood disorders can usually tolerate interferons with careful monitoring.
  • Fingolimod is linked to mood changes; severe rebound inflammatory activity after discontinuation could theoretically trigger mania.

Diagnosis of MS-related mania

Distinguishing between primary bipolar disorder, secondary MS-related mania and steroid-induced mania can be difficult. Accurate diagnosis is essential for effective management, as treatment for one form may exacerbate another. Below are some of the ‘atypical’ features of MS-related mania that deviate from classic bipolar disorder.

Late onset of symptoms

Primary bipolar disorder usually begins in adolescence or early adulthood. In contrast, secondary mania associated with MS can appear later, often after age 35–40 or during disease progression. A manic or psychotic episode may sometimes be the first manifestation of MS, occurring months or years before a neurological diagnosis.

Mania coinciding with an MS relapse

A sudden change in mood, sleep or behaviour that coincides with new neurological symptoms (e.g. numbness, vision changes, weakness) may indicate that inflammation or new lesions are affecting mood circuits. There may also be evidence of disease progression from MRI scans.

Weak family history

Primary bipolar disorder often runs in families; the absence of a family history suggests a secondary cause (i.e. MS-related pathology).

Disproportionate cognitive decline

Impulse control and executive functions, such as planning, organising and paying attention, are impaired – possibly reflecting frontal lobe involvement.

Mania as an MS relapse

A minority of patients present with isolated psychiatric symptoms (mania, psychosis, delirium) as the only manifestation of a relapse. MRI often reveals new frontal or temporal lesions, even when motor or sensory signs are absent.

Lack of response to standard treatments

Failure to respond to standard mood stabilisers, or paradoxical worsening with antidepressants, warrants a re-evaluation for organic causes.

Genetic considerations

Is the risk solely environmental (inflammation/lesions), or do MS and bipolar disorder share a genetic root? The Major Histocompatibility Complex (MHC) on chromosome 6 is the primary genetic risk factor for MS (specifically the HLA-DRB1*15:01 allele). Interestingly, Genome-Wide Association Studies have suggested that the MHC region is also involved in bipolar disorder and schizophrenia.
There is some evidence that, in certain familial clusters, a gene located near the HLA locus (possibly involving the HLA-DR2 antigen) could confer susceptibility to both autoimmune demyelination and bipolar disorder. Other studies have indicated the opposite: that specific MS risk alleles in the HLA region are associated with decreased schizophrenia risk. The results are therefore mixed; some haplotypes may increase the risk of severe mental illness, while others appear protective against it. It is likely that environmental factors (inflammation, lesion burden) play a greater role than genetics in most cases.

Is the risk solely environmental (inflammation/lesions), or do MS and bipolar disorder share a genetic root? The Major Histocompatibility Complex (MHC) on chromosome 6 is the primary genetic risk factor for MS (specifically the HLA-DRB1*15:01 allele). Interestingly, Genome-Wide Association Studies have suggested that the MHC region is also involved in bipolar disorder and schizophrenia.

There is some evidence that, in certain familial clusters, a gene located near the HLA locus (possibly involving the HLA-DR2 antigen) could confer susceptibility to both autoimmune demyelination and bipolar disorder. Other studies have indicated the opposite: that specific MS risk alleles in the HLA region are associated with decreased schizophrenia risk. The results are therefore mixed; some haplotypes may increase the risk of severe mental illness, while others appear protective against it. It is likely that environmental factors (inflammation, lesion burden) play a greater role than genetics in most cases.

Management

Treatment of MS-related mania depends on the cause.

Steroid-induced mania

If steroids triggered the symptoms, the steroids should be tapered or discontinued if safe.
Short-term antipsychotic medications, such as quetiapine, olanzapine or risperidone, can help stabilise mania symptoms. Quetiapine has the added benefit of aiding sleep, which is commonly disrupted in people with MS. Use of low-dose benzodiazepines during the steroid course can help to reduce the insomnia that often precedes or triggers mania.

Mania caused by MS inflammation

If mania is part of an organic, MS relapse, treating the inflammation is important. High-dose steroids may then be necessary, even though they can in other circumstances cause mania.
This crucial distinction underscores the need for close coordination between neurology and psychiatry.

Mood swings

Lithium is still the gold standard mood stabiliser and is generally safe for psychiatric management in MS. The anticonvulsants valproate, lamotrigine and carbamazepine are useful alternatives in people with MS; they treat both the mania and other MS-related comorbidities, such as neuropathic pain and trigeminal neuralgia.

Managing future steroid treatment

People with a known history of bipolar disorder or steroid-induced instability may benefit from:

  • starting a low-dose mood stabiliser (e.g. lithium) before the steroid course
  • adding an antipsychotic temporarily (e.g. olanzapine)
  • using sleep support (e.g. low-dose benzodiazepines) to prevent insomnia (a common trigger for mania).

Long-term management

Any MS patient presenting with new-onset mania requires a comprehensive workup, including MRI (to check for new frontal/temporal lesions) and a review of recent medication changes, rather than a direct referral to psychiatry. Ongoing coordination between neurologists and psychiatrists is, however, essential. A neurologist might misinterpret mania as ‘euphoria’ related to frontal lobe damage (pseudobulbar affect), while a psychiatrist might miss the neurological signs of an MS relapse that is driving the mood change. Screening tools (e.g. Mood Disorder Questionnaire) may help identify individuals at higher risk but should not replace clinical judgement.

Recognising the distinguishing features of MS-related mania allows clinicians to intervene promptly, reduce misdiagnosis and optimise care. With integrated neurological and psychiatric management, most people with MS experiencing bipolar symptoms can achieve stable, effective control of their mood and maintain a high quality of life.

Reference

Haroon, E et al. Psychoneuroimmunology meets neuropsychopharmacology: translational implications of the impact of inflammation on behavior. Neuropsychopharmacology Rev; 2011:1–26.

Cognition and mental health

Mental ill-health in MS: prevalence and causes

It is now well established that the burden of MS extends far beyond the purely neurological problems to include mental health.

Key points

  • Many patients with MS experience both anxiety and depression.
  • Other emotional and behavioural changes associated with MS include cognitive changes, apathy, inappropriate laughing and crying, euphoria, mania and bipolar disorder.
  • Physical symptoms like fatigue, sleep disturbances, concentration difficulties, numbness, tingling and dizziness may occur both in MS and in anxiety states, complicating diagnosis.
  • Unless severe anxiety symptoms are formally diagnosed as an anxiety disorder, individuals miss out on targeted treatments.
  • There is growing evidence that MS-related emotional changes are not necessarily a psychological consequence of living with a disability.
    • They may have a biological origin related to structural damage in the brain, caused by the MS disease process.
    • Brain imaging techniques that measure activity reveal how these brain networks function in real time.
  • Emotional changes sometimes occur as a side effect of medications used in the management of MS, including steroids used to treat MS relapses..

Background and introduction

Multiple sclerosis (MS) is a chronic, inflammatory and neurodegenerative disease of the central nervous system (CNS) that is typically defined by its physical manifestations, such as motor weakness, sensory disturbances and fatigue. However, the burden of MS extends far beyond the purely neurological problems to include cognitive changes and mental health disorders such as anxiety, depression, apathy, mania and uncontrolled laughter and crying.

Anxiety and depression in people with MS

Among the most prevalent mental health problems in MS is anxiety, a condition that for many years was overshadowed by the clinical and research focus on depression. Anxiety is not a secondary issue but a core component of the disease experience for many people with MS. Anxiety and depression in MS are closely related, with many patients experiencing both simultaneously. Indeed, the presence of depression in people with MS is a strong predictor of the future development of anxiety, and vice versa. Both conditions share common underlying psychological risk factors such as avoidant coping styles and low optimism as well as unhealthy behaviours like smoking or lack of exercise.

Many large-scale studies have shown that anxiety is more prevalent in the MS population than in the general population. Two meta-analyses published in 2017 and 2023 assessed more than 50 published studies; based on pooled results, they estimated that 22% and 36%, respectively, of people with MS experienced anxiety.1,2 The prevalence rates for depressive disorders in people with MS are about 20−30%. Further research, utilising the UK MS Register, suggests that more than half (54%) of the 4000 patients recorded in the database have experienced clinically significant anxiety and 47% have experienced depression.3

MH anxiety

The proportions of people with different levels of anxiety (normal, mild, moderate or severe) and who have a depression score of 8 or above (N = 1961). Data from UK MS Register.3

MH depression

The proportions of people with different levels of depression (normal, mild, moderate or severe) and who have an anxiety score of 8 or above (N = 2268).  Data from UK MS Register.3

By contrast, the lifetime prevalence of any anxiety disorder in the general population in the USA is around 29% (though the prevalence at a specific point in time is lower). Anxiety is also significantly more prevalent in MS than in many other chronic neurological conditions, suggesting a relationship that may be specific to the pathophysiology or lived experience of MS.

Psychiatric symptoms versus psychiatric disorders

A critical nuance in understanding the epidemiology of anxiety in MS lies in the distinction between clinically significant anxiety symptoms and formally diagnosed anxiety disorders. The two are related but not interchangeable, and the disparity between their prevalence rates reveals a crucial aspect of the clinical challenge. The 2017 meta-analysis that found a 22% prevalence for anxiety disorders also found a substantially higher (34%) prevalence of clinically significant anxiety symptoms. This discrepancy indicates that for every ten patients who meet the formal diagnostic criteria for a specific anxiety disorder, such as generalised anxiety disorder (GAD) or panic disorder, there are approximately 15 patients who experience a level of anxiety that is severe enough to cause distress and impair functioning but is not formally identified and diagnosed in a clinical setting. The result is that these individuals miss out on targeted interventions such as specific psychotherapies or drug treatment that they might otherwise receive.

This large population of symptomatic but undiagnosed individuals may exist for several reasons. First, there is considerable symptom overlap between anxiety and MS itself. Physical symptoms like fatigue, sleep disturbances, concentration difficulties, numbness, tingling and dizziness can be manifestations of either MS or an anxiety state, creating a diagnostic challenge for clinicians and confusion for people with MS. Second, both patients and clinicians may view anxiety as an ’understandable’ or ’normal’ psychological reaction to living with a chronic, unpredictable illness, rather than as a distinct, treatable clinical entity. Finally, the historical research emphasis on depression may have led to less routine screening for anxiety in clinical practice. As an MSologist, it is also essential to differentiate formal depressive disorders from clinically significant depressive symptoms, which are much commoner than disorders.

Among those who do meet the criteria for a formal disorder, GAD appears to be the most prevalent, followed by panic disorder and obsessive-compulsive disorder. Recognising the full spectrum of anxiety, from subclinical symptoms to formal disorders, is essential for developing effective screening protocols and ensuring that all people with MS experiencing anxiety receive appropriate care (see article on management of mental ill-health in MS).

Other emotional and behavioural changes

MS impairs neuropsychiatric function (the interplay between neurological and psychological functioning) in a similar manner to its effects on other neurological functions. Living with MS can result in personality changes and subsequent relationship problems.

Cognitive changes

Cognitive impairment (i.e. dysfunction), particularly slowed information processing speed, is a common, well-documented and debilitating feature of MS. Anxiety has a demonstrably detrimental effect on cognitive domains that are often already compromised in MS, such as attention and executive functions.

Apathy

Apathy, characterised by profound loss of interest, blunted affect and reduced motivation, is also common in MS, particularly advanced MS. It is often misdiagnosed as depression. Apathy is not merely a component of low mood but is linked to executive dysfunction. Predictors identified include depressive symptoms, poor global quality of life, and poor attention and information processing speeds, probably due to MS lesions in the frontal lobe.

Inappropriate laughing and crying

Pathological laughing and crying, also known as pseudobulbar affect (PBA), are common but under-recognised and undertreated symptoms of MS that can be highly distressing and embarrassing for the patient and their relatives. The sudden, involuntary and explosive expressions of laughter or crying characteristic of PBA are often disproportionate or unrelated to the individual’s underlying emotional state.PBA is also associated with cognitive and mood problems, though the sudden and disproportionate emotional reactivity differentiates it from depression. The clinical presentation is due to frontal lobe or brainstem damage resulting from MS, which disrupts motor control pathways for emotional expression.  

Rare affective changes

Euphoria and mania are relatively uncommon in people with MS but are often triggered by high-dose steroids used to treat MS relapses.

Bipolar disorder is significantly more common in people with MS than in the general population; please see the separate post/chapter on this. The diagnosis must be made and treated by psychiatrists and involves lifelong therapy. 

The biological basis of mental illness in MS

MS-related emotional and mood changes are not necessarily a consequence of disability; they are often intrinsic to the MS disease process. This was recognised by the French neurologist Charcot, who, in 1877, noted pathological laughing, weeping, euphoria and depression in his patients who had MS.

Anxiety as a manifestation of MS pathology

While the psychological stress of living with a chronic illness contributes to anxiety in MS, there is growing evidence that anxiety is not solely a reactive or psychological phenomenon. The same autoimmune attack that damages myelin and axons, leading to physical disability, also targets and disrupts the complex neural circuits responsible for mood regulation, threat perception and emotional processing. 

Neuroinflammation and demyelination (damage to nerve insulation) are directly implicated in the development of anxiety and other psychiatric disorders. MS lesions are not confined to areas of the brain responsible for motor and sensory function but also occur within the networks that govern emotion and mood.

Structural and functional brain changes

Research has shown that people with MS can develop gradual grey matter loss in brain regions involved in emotion and motivation, particularly the limbic system and the basal ganglia. The limbic system includes the hippocampus, amygdala and cingulate cortex, and it plays a central role in processing emotions. Changes in the shape of the hippocampus have also been observed.

MH limbic system

Primary components of the limbic system. Modified from Encyclopaedia Britannica Inc.

These structural changes are thought to contribute to the development of mood and anxiety problems in MS. When MS-related inflammation, demyelination (damage to nerve insulation) or atrophy affects these areas, the brain’s ability to regulate fear and emotional responses can be disrupted. This creates a biological vulnerability to anxiety. From a structural perspective, therefore, anxiety in MS can be viewed as a direct consequence of neurological damage, in the same way that damage to the optic nerve causes visual impairment, or damage to the spinal cord leads to motor weakness.

In people with MS, depressive symptoms are consistently correlated with the volume of lesions in the brain and the degree of damage to connections between the cortex and subcortex. Neuroimaging studies show an association between depression and damage in the frontal and temporal areas of the cortex. In contrast, PBA is associated with lesions in the brainstem.

Brain imaging techniques that measure activity, such as functional MRI (fMRI), help to explain how these structural changes translate into anxiety symptoms. Rather than only showing where structural damage exists, fMRI studies reveal how brain networks function in real time. One key process identified in anxious people with MS is ‘fear overgeneralisation’. This occurs when the brain reacts to safe or neutral situations as if they were dangerous. For example, an individual learns to associate a specific signal (e.g. a picture of a circle) with a negative outcome (e.g. a mild electric shock). Anxious individuals tend to ’overgeneralise’ this fear, responding with fear to a similar but harmless signal (e.g. an oval), thus expanding their perception of danger in everyday life.

fMRI studies show that this process mainly involves the hippocampus (which is responsible for comparing incoming new experiences with ‘learned’ memories of danger) and the anterior insula (which plays a key role in generating the physical and emotional feeling of fear). In MS patients with anxiety, the physical pathways connecting these two regions are often disrupted, so that accurate information from the hippocampus is less effectively communicated to the anterior insula. As a result, the anterior insula may generate strong fear responses even when a situation is only mildly threatening or even safe.

fMRI studies have also revealed that many MS patients exhibit greater brain responses or increased recruitment of key emotional regions (e.g. prefrontal cortex and amygdala) compared to healthy controls. This likely reflects compensatory mechanisms the brain deploys to limit the clinical expression of emotional symptoms. The damaged MS brain tries to cope.

Neurological versus psychological causes

MS can trigger primary psychopathology as a result of demyelination and damage to specific functional circuits within the brain, as described above. It can be challenging to differentiate primary organic issues from reactive psychological problems, which is why people with MS may be referred for psychiatric assessments. 

I have, however, also seen patients in whom the initial symptoms were psychiatric, e.g. depression or (rarely) mania, but who were later found to have MS. The link between MS-related CNS damage and emotional symptoms is based on lesion location and lesion burden. For example, MS patients with lesions affecting the functional parts of the brain (rather than the connecting structures) exhibit a higher burden of emotional symptoms than those with lesions confined to the spinal cord. Our emotions are part of brain function in a similar way to motor function. Therefore, it is not surprising that MS impacts emotions. 

Lesion location and emotional symptoms

The evidence for a direct correlation between lesion location and anxiety is inconsistent. Some researchers suggest that, unlike depression, anxiety in MS may be driven more by psychosocial pressures and the psychological reaction to the illness rather than by focal brain damage. This discrepancy does not necessarily invalidate the biological basis of anxiety in MS. It may be that anxiety is related to more diffuse or subtle pathological changes, such as microstructural damage in white matter tracts or widespread neuroinflammation, that are not easily captured by conventional MRI lesion analysis. It is also possible that the broad distribution of the brain’s anxiety circuits means that damage to any number of different locations could produce a similar clinical outcome, making it difficult to pinpoint a single ’anxiety-causing’ lesion location. 

Other contributing factors

Emotional changes may occur as a side effect of medications used in the management of MS, including certain disease-modifying therapies. People with MS are also susceptible to the effects of the menopause, seasonal affective disorder and comorbidities associated with depression and anxiety, such as alcohol and other substance misuse disorders. It is advisable, therefore, to have a complete assessment before having a mood disorder labelled as being due to MS. 

Anxiety in MS may also be caused by high-dose corticosteroids, which are the standard treatment for MS relapses. Steroids have significant neuropsychiatric side effects, including anxiety, mania, insomnia and psychosis. For someone with MS already dealing with the stress of a relapse, the addition of steroid-induced anxiety can be particularly distressing.

‘Prodromal’ MS and psychiatric symptoms

Psychiatric comorbidities, such as anxiety and depression, have historically been viewed as consequences that follow the diagnosis of MS. Recent research, however, points to the existence of an ‘MS prodrome’, during which anxiety and depression occur years before the first classical neurological event.4 Increased rates of anxiety are a significant feature of this prodromal phase, suggesting that anxiety and/or depression may be early signs of MS, not merely a consequence. This body of recent research supports the idea that psychiatric symptoms in MS have a biological origin. This is most likely driven by the same low-level, diffuse neuroinflammatory and neurodegenerative processes that are smouldering away in the CNS long before the first eloquent MS lesion.

References

  1. Boeschoten, RE et al. Prevalence of depression and anxiety in multiple sclerosis: A systematic review and meta-analysis. J Neurol Sci 2017;372:331−341.
  2. Zhang X et al. The prevalence and risk factors of anxiety in multiple sclerosis: A systematic review and meta-analysis. Front Neurosci 2023;17:1120541.
  3. Jones KH, et al. A large-scale study of anxiety and depression in people with multiple sclerosis: a survey via the web portal of the UK MS Register. PLoS ONE 2012;7:e41910.
  4. Ruiz-Algueró, M et al. Health care use before multiple sclerosis symptom onset. JAMA Netw Open 2025;8:e2524635.
Bladder and bowel, Intimate issues

Male sexual dysfunction in multiple sclerosis

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.

  1. Primary dysfunction arises directly from MS lesions within the central nervous system that disrupt the neural pathways governing sexual response.
  2. 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.
  3. 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.