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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

Management of mental health disorders in people with MS

Emotional problems in people with MS must be recognised, addressed and treated, rather than dismissed as an inevitable consequence of living with this chronic condition.

Key points

  • An MS diagnosis naturally triggers emotions similar to the stages of grief (denial, anger, bargaining, depression, acceptance); in addition, the unpredictability of MS causes anxiety in many patients.
  • Anxiety, often combined with depression, is linked to a poorer quality of life, cognitive dysfunction, increased risk of suicide, and significant occupational and social problems.
  • Emotional problems in MS are typically exacerbated by fatigue, pain and poor sleep – all of which interfere with therapy and lifestyle adjustments.
  • Emotional changes in MS require treatment, just as physical symptoms do. This should comprise routine screening, targeted drug treatment and structured psychological and behavioural therapies.
  • Motivational coping styles that involve direct problem-solving and active participation in treatment planning (i.e. self-management) help people with MS adjust to their diagnosis.
  • Avoidance coping strategies generally lead to poorer psychological outcomes.
  • The presence of social support is a critical protective factor.

Impact of emotional changes

Emotional disorders have an adverse effect in people with MS, potentially impairing their ability to cope with disability and reducing overall health-related quality of life. Living with MS can also adversely affect relationships, for complex reasons, including both emotional and physical problems associated with the disease. Therefore, such symptoms must be recognised, addressed and treated, rather than dismissed as an inevitable or acceptable consequence of living with a chronic condition such as MS.

Emotional disturbances in people with MS may be reactive, i.e. a natural, adaptive psychological response to being diagnosed with a long-term, unpredictable and potentially disabling disease. Common emotions include grief, sadness, worry, fear, irritability and moodiness. Elisabeth Kübler-Ross in 1969 described five common stages of grief, best known by the acronym DABDA. We have added an extra A, for Anxiety about the future, to include the emotional reaction to a diagnosis of MS. The expands the mnemonic to six stages: DABDAA.

Denial, Anger, Bargaining, Depression, Acceptance, Anxiety

These emotional stages are considered ‘normal’ and an understandable coping mechanism. As with grieving, if they are prolonged, dominant and impact your social and occupational functioning, they are considered abnormal and require intervention. Remaining angry, resentful and depressed for decades will negatively impact your functioning. 

Anxiety and depression in MS

Anxiety affects people with MS with a frequency often matching or exceeding that of depression. The highest prevalence of anxiety is observed in people with MS with low physical disability, defined by an Expanded Disability Status Scale (EDSS) score of less than 3.0. This finding suggests that anxiety is driven less by accumulated physical deficit than by the psychological factors of worry, fear and the inherent unpredictability of MS.

Maladaptive coping strategies are strongly associated with an increased risk of developing mood symptoms. A tendency to use avoidance coping – disengaging from problems rather than confronting them – is a significant predictor of poorer psychological outcomes. Similarly, psychological traits such as low optimism or a less positive attitude can heighten the risk of anxiety.

For a significant subset of patients, MS may first present not to a neurologist, but to a primary care physician, a therapist or a psychiatrist, with symptoms of anxiety or depression. Because the symptoms are psychiatric, the underlying neurological cause is not yet suspected.

Quality of life and daily functioning

Anxiety is a major contributor to the overall disease burden of MS, affecting nearly every aspect of life. Studies show that anxiety, often combined with depression, is linked to a poorer quality of life, cognitive dysfunction, increased risk of suicide, and significant occupational and social problems.

The impact of anxiety on many of the most challenging symptoms of MS – notably fatigue, pain and sleep problems – may be greater even than the effect of depression.  MS symptoms can trigger or worsen anxiety, and the resulting anxiety intensifies the perception and severity of those same symptoms, thus creating a negative feedback loop.

Damaging health behaviours linked to undiagnosed and untreated anxiety can further compromise a patient’s well-being. For example, alcohol and substance abuse, as well as smoking, not only have their own intrinsic health risks but can also interfere with MS management and adherence to treatment. 

Anxiety as a reaction to living with MS

The direct impact of the disease on the brain’s emotional circuits occurs in parallel with the profound psychological and existential challenges of living with MS. Even in the absence of any direct neurological damage to mood-regulating centres, the lived experience of MS itself provides rationale for the development of severe anxiety. 

The unpredictability of the disease and the constant knowledge that a relapse could occur at any time, potentially worsening MS symptoms and existing function, create a state of chronic hypervigilance and worry. This pervasive sense of a loss of control over one’s own body and life is a catalyst for anxiety. Anxiety creates a vicious, self-perpetuating cycle where the physical and psychiatric symptoms mutually reinforce one another.

Anxiety cycle

Multiple stressors

Beyond this overarching uncertainty, living with MS entails a host of stressors.

  • Diagnosis. The diagnostic journey is a period of intense anxiety, often involving a prolonged period of uncertainty as symptoms are investigated. Once diagnosed, patients face a continuous process of adjusting and readjusting to changing abilities.
  • Hidden problems. The invisibility of some of the most burdensome symptoms, such as debilitating fatigue, cognitive fog, or sensory disturbances, can lead to a profound sense of feeling misunderstood, isolated and frustrated.
  • Visible symptoms. Conversely, the emergence of visible symptoms, like a limp or the need for a mobility aid, can bring its own anxieties related to stigma and self-image.
  • Daily life. Financial concerns related to healthcare costs, employment and the ability to continue working, as well as the impact of MS on relationships and potential parenting, may further increase anxiety. 

Existential threat

Profound existential and symbolic threats to a person’s sense of self can further exacerbate anxiety. The sense of loss triggered by a diagnosis of MS – loss of a healthy body, a previously held future and a former identity – is followed by changes in fundamental life roles. This can lead to feelings of inadequacy, guilt and a crisis of identity – perceived as a threat to one’s core self. The constant need to adapt to new limitations can feel like a continuous erosion of the self, and the fear of future disability becomes a fear of further loss of identity.

Addressing this existential dimension of anxiety is crucial for promoting long-term psychological adjustment and overall well-being. Treatment often involves helping individuals grieve their losses, redefine their sense of self and purpose within the context of their illness, and find new sources of meaning and value in their lives. 

Cognitive impairment

The impact of anxiety on cognitive function is well documented. Cognitive impairment, particularly slowed information processing speed, is a common and debilitating feature of MS. Anxiety has a detrimental effect on cognitive domains that are already compromised, such as attention and executive functions. It does this by increasing an individual’s awareness of task-irrelevant, often threat-related, stimuli, which interferes with the goal-oriented cognitive processing required for the task at hand. Thus, the underlying cognitive deficit from MS is compounded by the cognitive interference from anxiety, leading to a greater overall level of impairment than either condition would cause alone. Importantly, therefore, treating a patient’s anxiety can lead to measurable improvements in their cognitive functioning. 

Mood, fatigue, pain and sleep – a vicious cycle

Emotional problems rarely occur in isolation in MS; they are typically part of a clinical syndrome including fatigue, pain and poor sleep. This interconnected symptom cluster reduces health-related quality of life and establishes significant barriers to therapy and lifestyle modification.

Fatigue

Fatigue is one of the most common and disabling symptoms of MS, and it is strongly and consistently correlated with anxiety. This is not a simple correlation but a predictive relationship. Higher levels of anxiety at one point in time can predict the severity of fatigue at a later date. Conversely, higher levels of fatigue can predict the later development or worsening of anxiety.

The severity of depression in highly fatigued people with MS also makes the management of fatigue a high priority in reducing the overall psychiatric burden and allowing patients to engage in psychological interventions such as cognitive behavioural therapy (CBT).

Pain and emotional distress

A two-way relationship also exists between pain and anxiety, where anxiety is associated with higher reported pain intensity and greater interference of pain with daily activities.  The pain symptoms cause distress and anxiety, and the physical and mental state of anxiety (e.g. muscle tension, worry, poor sleep) in turn exacerbates the symptoms. Moderate or severe intensity pain that interferes with work, household activities or enjoyment of life affects about one-third of people with MS.

Sleep

Sleep is probably the most neglected MS-related problem in routine clinical practice; most people with MS have a sleep disorder. Depression, anxiety, pain and many other MS-related symptoms affect sleep quality. Therefore, it is challenging to manage MS-related emotional disorders without addressing sleep quality.

Lifestyle management and adherence

The cyclical nature of this grouping of mood disorder, fatigue, pain and poor sleep creates barriers to effective management. Emotional distress and physical symptoms can hamper efforts to start or maintain a healthy lifestyle. Since modifiable lifestyle factors (e.g. exercise) are associated with reduced pain burden, a vicious cycle is established: the disease causes emotional distress, the emotional distress prevents adherence to healthy behaviours, and the lack of healthy behaviours exacerbates physical symptoms.

Inappropriate laughing and crying

Inappropriate laughing and crying (pseudobulbar affect, PBA) are two neglected symptoms that often go undetected and untreated in people with MS. This doesn’t have to be the case. They are a further sign of significant damage to the brain and yet another reason to diagnose and treat MS early and effectively.

Case study 

When I first met her, she was in her early fifties. She had had MS for over 20 years. Her family now kept her at home, isolated from the wider world. Her behaviour would embarrass them. Why?

She suffered from pathological laughter and occasionally inappropriate crying; her husband and children could not deal with this in public. She was clearly very disabled when I met her; she was unsteady on her feet and had slurred speech and dancing eyes from cerebellar problems. She had gross cognitive impairment. When I introduced myself to her, she burst into tears. Within 2−3 months of starting sertraline, a selective serotonin reuptake inhibitor (SSRI), her husband informed me that her laughing and crying episodes had improved by over 50% and the family were now taking her out regularly. He was very grateful that I had been able to educate them about her symptoms and, more importantly, help her and them as a family deal with this problem.

PBA is diagnosed using standardised scales or questionnaires, which can be self-administered (Center for Neurologic Study-Lability Scale [CNS-LS]). These symptoms respond to tricyclic and SSRI antidepressants and to a combination pill (Nuedexta®; licensed in the USA) that includes dextromethorphan hydrobromide and quinidine sulfate. 

Management of emotional disorders                                                     

Routine screening, targeted drug treatment and structured psychological and behavioural therapies are core components of integrated care in MS. Emotional changes in MS require treatment, just as physical symptoms do.

Screening and education

Routine screening for both anxiety and depression should be part of standard MS care and should be conducted at all scheduled neurological visits. You may be asked to complete different screening questionnaires for depression, anxiety, fatigue and poor sleep. Ideally these should be done before your appointment so that the healthcare professional (HCP) can act on them during the consultation. 

HCPs should educate their patients and their families about potential emotional changes associated with MS, in particular, irritability, crying and mood swings. This education should help reduce the stigma and embarrassment associated with emotional outbursts and enable the patient’s support network to develop coping strategies.

Drug treatment

Drug treatment must be tailored to the specific diagnosis and emotional disorder.

  • Depression and anxiety: The standard use of selective serotonin reuptake inhibitors (SSRIs) and serotonin−norepinephrine reuptake inhibitors (SNRIs) is recommended for the management of clinical depression and anxiety disorders.
  • Irritability: Treatment options for irritability include SSRI antidepressants, which are often needed in addition to CBT. 
  • Pseudobulbar affect (PBA): Low-dose tricyclic or SSRI antidepressants can be effective in the treatment of PBA, but their use is off-label. In the USA, the combination of dextromethorphan hydrobromide and quinidine sulfate has been approved for PBA. In other countries, the combination of these two drugs can be effective in PBA, but again, the use of these two drugs separately is off-label and not recommended.
  • Apathy: Therapeutic strategies, such as cognitive rehabilitation, that enhance cognitive processing speed and executive function are more appropriate for apathy than antidepressants. However, such approaches are hard to access on the UK NHS and are not available in many healthcare systems. There are no licensed medications for apathy, but anecdotal evidence suggests that fampridine and some stimulants may help.
  • Further research: Properly randomised controlled trials are needed to determine the effectiveness of drugs that some patients obtain and use without a prescription. These include cannabis, psychedelics and ketamine, which are currently not licensed for managing anxiety in MS and are not advised.

Psychological and behavioural interventions

Evidence-based structured psychological interventions are as important as drug treatment for the management of anxiety and depression and should be considered a first-line approach in MS. CBT can address maladaptive thought patterns (e.g. catastrophic thinking about the future) and avoidant behaviours common in anxiety. Acceptance and commitment therapy (ACT) focuses on promoting psychological flexibility and acceptance, which is crucial for managing the reactive distress, grief and fear stemming from the unpredictable nature of the disease. Mindfulness, relaxation techniques and structured exercise programs have also been shown to manage anxiety and stress effectively. 

Interventions such as physical activity and social therapies enable some people with MS to process the grief and losses imposed by MS. Simple behavioural strategies, such as taking a break from a conversation when emotions escalate, can also be beneficial. 

Protective factors

Several protective factors can bolster resilience and lower the risk of anxiety. Motivational coping styles that involve direct problem-solving and active participation in treatment planning (i.e. self-management) are associated with better adjustment. One of the most critical protective factors is the presence of social support. Robust practical and emotional help from friends and family, and the knowledge that help is available if needed, significantly reduces the risk of mood symptoms. Finding ways to continue participating in previously enjoyed activities, albeit with new limitations, are key to coping. Interventions aimed at strengthening coping skills, fostering optimism and building social support networks can play a crucial role in preventing and treating anxiety in this population.

The therapeutic challenge

There is substantial symptom overlap between anxiety and depression (e.g. sleep disturbance, fatigue, difficulty concentrating) and between these mood disorders and the primary symptoms of MS. This can make it challenging for HCPs to discern whether a specific symptom, e.g. fatigue, is primarily a neurological symptom of MS, a physical symptom of depression, a consequence of the hyperarousal and poor sleep of anxiety, or a combination of all three. Use of appropriate screening tools can help to ensure that both anxiety and depression are accurately identified and appropriately treated.

Conclusion

MS profoundly affects emotional health across a broad and complex spectrum, manifesting as major depressive disorders, high levels of anxiety, the neurological syndrome of pseudobulbar affect, the cognitive−behavioural syndrome of apathy and, rarely, mania. These emotional changes are driven by primary damage to cortical-subcortical and brainstem circuits, coupled with reactive psychological distress resulting from living with a chronic, unpredictable illness. The current standard of care mandates routine screening, targeted drug treatments and psychological support utilising CBT and ACT. 

Fatigue and insomnia, Sleep disorders

Understanding and managing insomnia in MS

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

Key points

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

Sleep, glorious sleep!

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

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

Causes and impact of insomnia

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

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

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

Approaches to managing insomnia

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

Recording your sleep patterns

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

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

Sleep hygiene

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

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

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

Over-the-counter sleep aids

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

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

Prescription-only sleep aids

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

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

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

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

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

Cognitive approaches to managing insomnia

Cognitive Behavioural Therapy for Insomnia (CBTI)

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

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

Brief behavioural treatment for insomnia

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

eCBTI

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

Complementary and alternative therapies

Sleep restriction

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

Stimulus control

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

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

Relaxation training

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

Cognitive therapy

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

Sleep hygiene education

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

Acceptance and commitment therapy (ACT)

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

Mindfulness

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

Conclusion

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

Diagnosis, Stages of MS

What should I expect during the diagnostic consultation?

The practice of neurology and medicine varies worldwide, so I will explain what to expect if you were to consult me. 

Key points

  • The principles of diagnosing MS are to show the dissemination of lesions in space and time and to exclude alternative diagnoses that mimic MS.
  • Diagnosing MS takes time and should not be rushed; do not be afraid to ask questions.
  • Most patients diagnosed with MS have an emotional response similar to the five stages of grief – Denial, Anger, Bargaining, Depression and Acceptance (DABDA). Additionally, many patients experience Anxiety about the future (DABDA+A).
  • Newly diagnosed patients should avoid overloading themselves with information about MS; much of the online information can be misleading and anxiety-provoking. Guidance is provided below about reliable information sources.
  • Counselling, cognitive behavioural therapy and the support of an MS ‘buddy’ can help patients adjust to a diagnosis of MS, which is a serious condition and should be respected.
  • You should be aware that medical ‘gaslighting’ may happen and know how to deal with it.

Tests to exclude other diagnoses

MS is a clinical diagnosis and a diagnosis of exclusion. Therefore, I would take a detailed medical and neurological history and examine you for neurological signs. Finding signs of involvement in a particular neurological pathway is important for fulfilling the criteria for dissemination in space. MS must involve at least two neuronal pathways. To be confident that no alternative diagnosis could explain your presentation, a full work-up will likely include magnetic resonance imaging (MRI) of the brain and spinal cord, evoked potentials, a lumbar puncture and blood tests. In addition, I would need to show dissemination in time, involving two or more structures separated in time by at least 4 weeks.

The diagnosis of MS is not trivial and should not be rushed. If I doubted the diagnosis, I would wait. The old maxim ‘time is often the best diagnostician’ is as pertinent today as it was in the past. Despite this, the misdiagnosis rate remains stubbornly high. I recommend you read some of the posts that cover the diagnosis of MS in more detail, such as Am I sure that I have MS? and Do I have active MS?

Time to adjust to a diagnosis of MS

You should not expect too much from the initial consultation. The second consultation, once all the diagnostic tests are back, will be the difficult one. Before COVID-19, an MS diagnostic workup in the NHS would take about 6 ̶ 8 weeks. Due to COVID-19-related delays in getting MRI scans and evoked potentials, it currently takes up to 4 months. Occasionally, patients with possible MS are admitted to the hospital because of a disabling attack. This allows us to make a more rapid diagnosis. 

Being diagnosed with MS or any other chronic and potentially disabling disease is distressing. In my experience, patients’ responses are highly variable, including relief about finally getting a diagnosis, surprise, shock, anger or blaming the messenger for the bad news. Some question my judgement and refuse to accept the diagnosis; they may accuse me of being wrong and seek a second, third or fourth opinion. Many are devastated and expect the worst: how long before I need a wheelchair? Rarely patients are uninformed, have little or no idea about MS and ask about the disease. 

Examples of some responses to a diagnosis of MS

I always try and be reassuring and tell patients that MS is now a treatable disease. If we manage their MS actively, we can prevent or at least delay the development of disability for many decades.

Emotional response

I also warn patients about the emotional reaction they will likely have to being diagnosed with MS. The psychological impact of an MS diagnosis and the uncertainty associated with having a potentially disabling disease should never be underestimated. Elisabeth Kübler-Ross in 1969 described five common stages of grief, best known by the acronym DABDA:

Denial, Anger, Bargaining, Depression, Acceptance

We have added an extra A – for Anxiety about the future – to expand this to DABDA+A. People diagnosed with MS may go through these stages in order of the pneumonic, but some will jump around, and others go through some stages many times. Although the Kübler-Ross stages have been criticised in the psychological literature, they provide a valuable framework for discussing a patient’s emotional journey. Being diagnosed with MS is a marathon, not a sprint, and it will take time to come to terms with it.

It is important for healthcare professionals (HCPs) to be there for the journey and to make sure that newly diagnosed patients have access to their MS team and high-quality information about MS. 

Step-wise approach to understanding MS

In the modern era, most patients I diagnose as having MS are aware of the disease and suspect they have MS before I tell them so. I say this because Dr Google, Dr ChatGPT and Dr Bing are only keystrokes away, and their answers are very credible. 

Because of their anxiety, most newly diagnosed patients only take away one thing from the consultation: they have MS.  Almost everything else they hear is forgotten. I encourage patients to record the consultation or bring a partner, friend or family member who can be their backup memory. 

I try to avoid overloading patients with information early on. Instead, I provide links to online resources about having MS. We arrange a follow-up session with the MS nurse specialist in the next 10 ̶ 14 days so that they can ask questions.

Guidance about what information to trust

I counsel patients to stay away from Dr Google, Dr ChatGPT and Dr Bing until they have come to terms with having MS. Much of the MS-related content available on the web is misinformation and disinformation; until you understand the disease, it is difficult to know what information is valid, reliable and helpful and what is quackery. Many patients ignore this advice and overwhelm themselves with information, which can worsen anxiety. 

I don’t introduce recently diagnosed patients to MS-Selfie initially. MS-Selfie is written at too high a level for the average person who is newly diagnosed. If patients want more information, I direct them to the MS Trust, the MS Society and ‘MS Brain Health: time matters’ (for more detail, see Resources and hot topics).  

Counselling, support and respect

Depending on a patient’s response to the diagnosis, we may refer them for counselling, cognitive behavioural therapy and/or mindfulness therapy to help them come to terms with having MS and to help manage their anxiety. Most patients are receptive to these psychological therapies. 

Many people with MS are traumatised by their diagnostic consultation and may experience symptoms of post-traumatic stress disorder from the event. This should not happen in the modern era. In my experience, gestures such as having tissues on hand for a distressed patient or holding their hand are ways that HCPs can demonstrate their empathy.

On rare occasions, particularly for patients who are alone and socially isolated, we may buddy them up with another carefully chosen patient to ask questions and learn about MS. These MS buddies need to be optimistic, able to communicate well and not overwhelm the recently diagnosed patient with information. I work closely with the charity Shift.ms, which does a similar thing. 

In the diagnostic consultation, I avoid too much detail about treating MS and the specific DMTs. These are best discussed at the next visit. With some patients, however, the discussion gets to treatments very quickly. In such cases, I tailor the consultation to the individual’s needs. 

During the diagnostic consultation, I also show patients their MRI scans. Seeing your brain, spinal cord and MS lesions provides an objective way of helping you to visualise the disease. 

Recently diagnosed patients must be given time to ask questions and even to sit in silence. MS is a serious disease, and informing someone about the diagnosis must be done carefully. After more than 30 years as a neurologist, I still find telling my patients they have MS challenging. The patient being diagnosed with MS, as well as the disease, must be respected. 

What if a doctor belittles my concerns?

The term ‘medical gaslighting’ describes a scenario where health professionals dismiss or downplay a patient’s real symptoms, leading to an incorrect diagnosis. Now that we have recognised medical gaslighting as a significant problem in MS, please don’t allow a neurologist to gaslight you. There are things you can do to prevent this. 

  • Keep detailed notes and records. Patient-held notes transform consultations and allow you to become a partner in your healthcare.
  • Ask to record the consultation. Many HCPs don’t like this; just tell them you must listen to the conversation again to ensure you don’t forget things or miss important information. You will be surprised how this changes the HCP’s behaviour. 
  • Ask questions. Then ask some more. And don’t be fobbed off; if you are dissatisfied with the answer, ask the question again. 
  • Take someone with you for support. Having a witness during the consultation has a similar effect to recording the conversation or documenting it with notes. 
  • Focus on your most pressing issues to make the best use of your consultation time. If your HCP is pressed for time, say you understand, but you would like to prioritise the following issues today. This helps you to frame the limits of the consultation and promote a two-way discussion. Also, don’t expect the HCP to have all the answers at their fingertips, but do expect them to come back to you later with the answers.
  • Try and pin down the next steps for your problem; ask what the action points are. For example, if the MRI shows this, how will that change my management? Do I need further investigations? How soon should I switch treatments?

If you still feel that you are being ignored, here are some of your options.

Some courses of action open to you if you experience medical gaslighting.

Abuse, manipulation, gaslighting and delaying a diagnosis are potentially reportable events which HCPs need to know about. Therefore, make your healthcare system aware of the problem rather than suffer in silence.