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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.

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.