Substance use among individuals with functional neurological disorder (FND) appears to be at least as common as, and in many settings higher than, in the general population, but precise prevalence rates vary widely across studies due to differences in diagnostic criteria, populations, and assessment methods. Clinical cohorts from neurology and psychiatry services often show elevated rates of alcohol, benzodiazepines, and prescription opioid use, as well as tobacco and cannabis, particularly in patients with chronic symptoms and multiple comorbidities. In many tertiary FND clinics, a meaningful minority of patients report hazardous or dependent patterns of use, though this is likely an underestimation because routine screening is inconsistent and self-report can be influenced by stigma and fear of judgment.
Patterns of substance use are shaped by the high burden of associated conditions in FND, including chronic pain, insomnia, anxiety, depression, and post-traumatic stress. Alcohol is frequently used as a self-management strategy for emotional dysregulation, social anxiety, intrusive memories, or difficulty winding down at night. Benzodiazepines tend to be prescribed initially for acute anxiety, panic, or non-epileptic seizures, but long-term use is common and can lead to physiological dependence, cognitive slowing, and worsening functional symptoms, especially in older adults. Opioids are often introduced for persistent pain syndromes, musculoskeletal problems, or headaches that co-occur with FND, and prolonged prescribing increases the risk of tolerance, opioid use disorder, overdose, and hyperalgesia.
Comparative studies suggest that patients with FND share many substance use patterns seen in other populations with complex somatic symptom presentations, such as chronic pain or functional gastrointestinal disorders. Tobacco use is frequently reported and may be linked to higher levels of stress, socioeconomic adversity, and coexisting mood or anxiety disorders. Cannabis use varies by jurisdiction and availability, but in some regions it is commonly used to manage pain, sleep, and anxiety, with mixed impact on symptom severity and daily functioning. Illicit stimulant and sedative use appears less prevalent than alcohol or prescription medications but may be underrecognized, particularly in younger adults and those with prior trauma or unstable housing.
Psychiatric comorbidity is an important factor when interpreting epidemiological data. Many individuals with FND meet criteria for one or more anxiety disorders, depressive disorders, or trauma-related conditions, all of which independently increase vulnerability to substance use problems. Historical and current trauma, including interpersonal violence and childhood adversity, are consistently associated with both FND and substance misuse. In some cohorts, the presence of post-traumatic stress disorder or borderline personality traits is associated with heavier alcohol or drug consumption, more frequent crisis presentations, and greater difficulties engaging with structured care.
Health care utilization patterns also shape the epidemiology of substance use in FND. Patients commonly present to emergency departments with acute episodes of functional weakness, seizure-like events, or gait disturbances, where sedative medications such as benzodiazepines or short-acting opioids may be administered in attempts to terminate episodes or manage distress and pain. Repeated exposure in crisis settings can inadvertently reinforce reliance on these medications and contribute to ongoing use after discharge. Over time, this may blur the distinction between medically initiated and patient-initiated substance use and complicate efforts to evaluate the true prevalence of independent substance use disorders.
Socioeconomic factors play a significant role, with higher substance-related risk observed among individuals facing unemployment, housing instability, limited social support, or barriers to accessing coordinated physical and mental health care. In many health systems, people with FND experience diagnostic delays, fragmented treatment pathways, and inconsistent follow-up. These systemic gaps may increase vulnerability to self-medication with alcohol or drugs as people attempt to cope with disabling symptoms and perceived lack of effective medical responses. Geographic differences in prescribing practices, availability of specialist services, and local drug markets further contribute to regional variability in observed prevalence.
From an epidemiological standpoint, medication-related harms deserve particular attention. Long-term benzodiazepine use is frequently documented in older FND cohorts, especially among those with chronic anxiety, insomnia, or long-standing non-epileptic attacks. Such use is associated with increased falls, cognitive impairment, and paradoxical agitation, which can exacerbate disability and complicate assessment of functional symptoms. Similarly, chronic opioid prescribing for comorbid pain conditions in FND is linked with worse functional outcomes, higher rates of hospitalization, and increased likelihood of co-prescription with other sedatives, raising concerns about accidental overdose and cardiorespiratory complications.
Existing studies are limited by sample selection, often focusing on patients referred to specialized neurology or psychogenic non-epileptic seizure clinics rather than community populations. As a result, prevalence estimates for substance use and substance use disorders may be skewed toward more severe or complex cases. Cross-sectional designs also make it difficult to disentangle whether substance use precedes FND symptoms, emerges as a response to chronic disability and psychosocial stress, or both. Longitudinal data are sparse, but available evidence indicates that substance use often persists over time in the absence of targeted interventions, even when some aspects of functional symptoms improve.
Cultural attitudes toward mental health, addiction, and medically unexplained symptoms influence disclosure and reporting. In some cultural contexts, strong stigma attached to both psychiatric diagnoses and alcohol or drug use leads to underreporting, whereas in others, normalization of heavy drinking or cannabis use may obscure recognition of risky patterns. Gender norms may also shape observed epidemiology, with women more likely to present with FND and men, in many societies, reporting higher levels of certain substance use, yet women may experience more rapid progression from initial use to harm and encounter additional barriers to treatment.
Available data indicate that people with FND are a clinically important group in which substance use, medication dependence, and related harms are common enough to warrant routine, structured assessment in both neurological and psychiatric settings. Recognizing these epidemiological patterns supports early identification of risk, informs service planning, and highlights the need for integrated approaches that address functional symptoms alongside substance-related behaviors rather than treating them as separate or secondary concerns.
Neurobiological intersections between FND and substance use
Neurobiological models linking functional neurological disorder and substance use converge on several shared systems: stress-response circuitry, networks for emotion regulation and interoception, motor control pathways, and higher-order predictive processes in the brain. While the precise mechanisms are still being elucidated, it is increasingly understood that FND symptoms reflect altered functioning within normal neural networks rather than structural damage. Many of these same networks are sensitive to the acute and chronic effects of alcohol, benzodiazepines, opioids, and other substances, creating multiple points at which substance exposure can amplify, mask, or otherwise modify functional symptoms.
A key intersection involves the hypothalamic–pituitary–adrenal (HPA) axis and broader stress systems. Many individuals with FND show evidence of heightened autonomic arousal, altered cortisol patterns, or increased sensitivity to stress, often in the context of prior trauma or chronic adversity. Psychoactive substances can acutely dampen or heighten stress responses, but with repeated use, they tend to destabilize stress-regulating systems. Alcohol and benzodiazepines may initially feel calming by enhancing GABAergic inhibition and dampening limbic activity, yet chronic exposure can lead to compensatory changes that reset stress circuits toward hyper-reactivity. During withdrawal or between doses, this can manifest as increased anxiety, irritability, autonomic surges, and sleep disruption, all of which can serve as triggers or exacerbating factors for functional seizures, tremors, or weakness.
Corticostriatal and corticolimbic networks that integrate motivation, reward, and movement are also heavily implicated in both FND and substance use. Neuroimaging studies in FND highlight abnormal connectivity and activation patterns between the anterior cingulate cortex, supplementary motor area, insula, and basal ganglia during voluntary movement attempts and symptom provocation. In parallel, these regions are central to the reinforcing and habit-forming effects of substances. Repeated activation of reward circuits by alcohol, opioids, or stimulants strengthens learned associations between internal states (such as distress or fatigue), environmental cues, and substance-seeking behaviors. In someone with FND, who may already have difficulty distinguishing between voluntary and involuntary actions or between bodily signals of emotion and illness, these altered learning processes can contribute to both symptom maintenance and the emergence of compulsive substance use patterns.
Interoception—the brain’s perception and interpretation of internal bodily sensations—is another shared domain. FND has been linked to both heightened and distorted interoceptive awareness, with patients often reporting intense physical sensations of fear, pain, or fatigue that feel overwhelming or inexplicable. Substances that modulate bodily sensations, such as cannabis, alcohol, or opioids, may temporarily reduce unpleasant sensations or alter the emotional salience attached to them. Over time, however, these agents can disrupt the reliability of internal signals by changing pain thresholds, altering cardiorespiratory responses, and affecting gastrointestinal and vestibular function. This can further destabilize interoceptive processing and contribute to the perception that the body is unpredictable or uncontrollable, reinforcing the cognitive and emotional conditions under which functional symptoms flourish.
Predictive processing frameworks offer a useful lens for understanding how FND and substance use may interact at the level of brain computation. In this view, the brain continually generates predictions about sensory input and updates them based on incoming signals. FND has been conceptualized as a failure to appropriately update or weight predictions about bodily states and motor intentions, such that top-down expectations override bottom-up evidence. Substances can acutely alter the precision or salience assigned to both predictions and sensory inputs. For example, during intoxication, sensory noise may be increased or certain cues may become overly salient, while during withdrawal, interoceptive signals associated with craving, anxiety, and discomfort may be over-weighted. Individuals who have learned, often implicitly, that bodily sensations are dangerous or uncontrollable may be especially vulnerable to interpreting these substance-related changes as signs of neurological catastrophe, thereby precipitating or worsening functional episodes.
Neurotransmitter systems modulated by commonly used substances overlap with those implicated in FND. GABA and glutamate balance is critical for motor inhibition, seizure thresholds, and sensory gating. Benzodiazepines potentiate GABA-A receptor activity, which can transiently suppress hyperexcitability and reduce subjective anxiety. However, chronic exposure leads to receptor adaptations that reduce GABAergic efficacy and increase glutamatergic tone. This shift raises the risk of rebound anxiety, tremor, and seizure-like phenomena on dose reduction or missed doses. In someone with non-epileptic attacks, such neuroadaptations can blur the clinical picture, as benzodiazepine withdrawal may mimic epileptic seizures or intensify functional events, complicating diagnosis and management.
Similarly, opioids exert powerful effects on pain pathways and reward circuits. Repeated opioid exposure can induce hyperalgesia, where modest nociceptive input produces exaggerated pain. Many individuals with FND already experience pain amplification related to central sensitization and altered attention to bodily signals. Opioid-induced hyperalgesia can therefore magnify pain-related distress and disability, feeding into cycles of symptom focus, avoidance of movement, and fear of exacerbation that are central to FND maintenance. At the same time, the reinforcing properties of opioids on mesolimbic dopamine pathways increase the likelihood that patients will persist with or escalate opioid use even when functional outcomes are worsening.
The role of sleep and circadian regulation provides another neurobiological bridge. Disturbed sleep is extremely common in FND and can exacerbate vulnerability to functional symptoms through effects on attention, emotion regulation, and pain processing. Substances used for self-medication—especially alcohol, sedating antihistamines, and short-acting hypnotics—may help with sleep onset but typically reduce slow-wave and REM sleep quality, fragment the night, and impair next-day cognitive function. Chronic poor sleep amplifies limbic reactivity, decreases prefrontal control, and impairs the capacity to use cognitive strategies taught in FND therapies. It also lowers thresholds for craving and increases relapse risk in those with emerging substance use disorders, creating a mutually reinforcing loop between sleep disruption, functional symptoms, and substance use.
Autonomic nervous system dysregulation is a frequent finding in FND, manifesting as orthostatic intolerance, tachycardia, gastrointestinal upset, and sweating. Many psychoactive substances exert potent acute effects on autonomic tone. Nicotine and stimulants increase sympathetic drive, while alcohol and some sedatives transiently enhance parasympathetic activity before rebound sympathetic activation. With chronic use, these fluctuations can entrench a pattern of autonomic instability. Patients may interpret palpitations, dizziness, or shortness of breath related to substance effects as signs of impending collapse or seizure-like episodes, particularly if they have limited psychoeducation about both FND and substance use. This misinterpretation fuels anxiety, heightens bodily vigilance, and strengthens the association between distress and functional symptom onset.
Neuroplasticity and learning processes relevant to recovery from FND are also shaped by substance exposure. Effective FND interventions rely on the brain’s capacity to form new associations between movement and safety, re-map symptom-related cues, and build confidence in voluntary control. Chronic substance use can impair synaptic plasticity, attention, and working memory, making it harder to engage consistently in physiotherapy, cognitive-behavioral strategies, or exposure-based approaches. For instance, heavy alcohol use reduces hippocampal volume and disrupts memory consolidation, which can blunt the impact of psychoeducation and skill-building sessions. Sedating medications may dampen arousal to a level that interferes with active participation in therapy, while withdrawal states can produce irritability and distractibility that undermine therapeutic alliance.
Genetic and epigenetic factors likely influence the shared vulnerabilities that predispose some individuals to develop both FND and problematic substance use. Polymorphisms affecting serotonergic, dopaminergic, and stress-response genes have been implicated in a range of conditions characterized by heightened emotional reactivity, impulsivity, or sensitivity to trauma. Epigenetic modifications resulting from early adversity can alter the expression of genes involved in HPA axis regulation, immune function, and synaptic plasticity. These changes may prime individuals to react more strongly to stress, perceive bodily sensations as more threatening, and experience greater reward or relief from substances. While specific genetic markers for FND remain under investigation, the overlapping risk architecture with mood, anxiety, and addiction disorders suggests that shared biological predispositions are likely.
Another level of intersection lies in how the brain prioritizes and allocates attention. FND is associated with biases toward symptom-related cues and away from external tasks, often in the context of limited attentional capacity under stress. Substances, by altering arousal and attentional focus, can acutely shift these biases. For example, stimulants can narrow attention and increase scanning for threat or bodily sensations, while alcohol may reduce top-down monitoring and increase reliance on automatic, habitual responses. Over time, substance-related cues themselves become highly salient, capturing attention and driving behavior even when they conflict with long-term goals. When combined, these attentional distortions can make it harder for patients to implement strategies that redirect focus away from symptoms and toward functional activities.
Neuroinflammatory and immune pathways provide an additional, emerging area of overlap. Chronic alcohol use, certain illicit drugs, and even long-term high-dose opioids can promote low-grade neuroinflammation, affecting microglial activation and cytokine signaling. Although research on immune markers in FND is still limited, some findings suggest alterations in inflammatory profiles in subsets of patients, particularly those with significant comorbid stress and pain. Neuroinflammation can impact mood, fatigue, and cognitive clarity, which are key determinants of how people interpret and cope with bodily sensations. It may also influence pain processing and motor function via effects on glial–neuronal interactions, potentially creating a biological context in which both functional symptoms and substance-related harms are more likely to emerge and persist.
The neurobiology of habit formation and extinction is central to understanding why both FND symptoms and substance use can become entrenched, and why change often requires structured, repetitive interventions. Habits are encoded through corticostriatal loops that gradually shift control from deliberate, goal-directed systems to more automatic, cue-driven processes. Functional movement patterns, such as learned non-use of an affected limb or automatic generation of seizure-like events in response to specific triggers, share many features with other well-established habits. Substance use behaviors, likewise, become increasingly automatic over time. Interventions that aim to reshape these patterns—such as graded exposure to feared movements, behavioral activation, or contingency management for substance use—rely on intact learning mechanisms in these same circuits. Understanding the overlapping neural substrates of habit allows clinicians to appreciate why addressing substance use is not only a parallel goal but often a prerequisite for successful FND rehabilitation, as ongoing substance exposure may repeatedly reinforce old patterns and interfere with the acquisition of healthier ones.
Clinical assessment of substance use in FND care
Assessment of substance use in the context of functional neurological disorder requires a deliberate, structured, and nonjudgmental approach that begins at first contact and continues throughout care. Rather than treating alcohol, benzodiazepines, opioids, nicotine, or illicit drugs as peripheral issues, clinicians should view them as potentially important contributors to symptom expression, treatment engagement, and overall safety. This means building routine screening into neurological, rehabilitation, and mental health assessments, while recognizing that many patients will initially minimize or omit disclosure due to shame, fear of being dismissed, or prior experiences of stigma in medical settings.
Establishing a collaborative tone is central to eliciting accurate information. Clinicians can frame questions about substance use as part of understanding how the person has tried to cope with distressing symptoms, emphasizing curiosity rather than blame. For example, asking “What kinds of things do you use to help you get through bad days or nights?” can feel less confrontational than directly inquiring about “drugs” or “addiction.” Normalizing the conversation by saying that many people with chronic pain, sleep problems, or seizure-like episodes experiment with alcohol or medications to manage symptoms helps patients feel less singled out and more willing to share relevant details.
Routine use of brief, validated screening tools improves detection and provides a common language for multidisciplinary teams. Instruments such as the Alcohol Use Disorders Identification Test (AUDIT or AUDIT-C), the Drug Abuse Screening Test (DAST-10), or the Tobacco, Alcohol, Prescription medication, and other Substance use (TAPS) tool can be incorporated into intake questionnaires or electronic health records. These screens should be supplemented by open-ended clinical interviewing that clarifies patterns of use, context, and perceived benefits and harms. For prescribed medications with dependence potential, such as benzodiazepines, Z-drugs, or opioids, specific questions about dose, frequency, source of prescriptions, early refill requests, and use outside prescribed parameters are essential.
A detailed history should map the temporal relationship between substance use and the onset and course of functional symptoms. Clinicians can explore whether FND symptoms emerged before any regular substance use, appeared during a period of escalation, or followed episodes of intoxication, withdrawal, or medication changes. Distinguishing symptoms that occur predominantly during withdrawal (for example, tremor, anxiety, insomnia, or seizure-like events after reducing benzodiazepines or alcohol) from those that are present at baseline helps clarify diagnostic formulations and guides risk management. Asking patients to describe a typical day, including timing of substance use relative to symptom flares, can reveal patterns that might not emerge from more abstract questioning.
Assessment should systematically cover different substance categories, as focusing on one (such as alcohol) may miss significant problems with others. Inquiry can follow a structured sequence: alcohol; prescribed sedatives and anxiolytics; prescribed and non-prescribed opioids; cannabis; stimulants including cocaine, amphetamines, and prescribed ADHD medications; over-the-counter agents like antihistamines or codeine-containing products; and nicotine and vaping. For each, clinicians should document age of first use, heaviest lifetime use, past attempts to cut down, periods of abstinence, and any history of withdrawal, overdose, or treatment for substance use disorders. Particular attention is needed when patients report abrupt discontinuation of long-term benzodiazepines or high-dose alcohol, due to the risk of withdrawal seizures, delirium, or worsening functional episodes.
Evaluating the functions that substance use serves is as important as quantifying the amount. Many individuals with FND use alcohol or medications to manage panic, social anxiety, ruminative thoughts, nightmares, or the anticipation of functional seizures. Others rely on opioids or cannabis to reduce pain that they experience as disabling and inadequately controlled by other means. Some may use stimulants to counter fatigue or cognitive slowing, particularly if sedating medications have been prescribed for sleep or mood. Understanding these functions—self-soothing, numbing, energy regulation, social facilitation—provides essential information for treatment planning and for identifying healthier alternatives that can be integrated into the FND care pathway.
Risk assessment must include both immediate safety and longer-term harms. Immediate concerns encompass acute intoxication that could impair participation in examinations or therapies, concurrent use of multiple sedatives (such as opioids and benzodiazepines) that raises overdose risk, and the possibility of alcohol or benzodiazepine withdrawal in hospitalized patients. Longer-term risks involve cognitive impairment, falls, interference with neuroplastic rehabilitation, and the potential for escalating use in response to unrelieved pain or distress. Clinicians should routinely ask about driving, operating machinery, caring for dependents, and any episodes of blackouts, injuries, or emergency visits related to substance use.
Physical examination and basic investigations can provide corroborating evidence and detect medical complications. Signs such as tremor, autonomic instability, pupillary changes, track marks, hepatomegaly, or unexplained bruising may point toward substance-related issues. Laboratory tests may include liver enzymes, complete blood count, renal function, and, when indicated, toxicology screens or serum drug levels. In the context of FND, examination findings may be complex, with overlapping functional and substance-related components; documenting which signs fluctuate with attention or distraction versus those that show consistent physiological patterns can help differentiate these contributions.
Assessment of mental health comorbidity is inseparable from evaluating substance use in FND. Screening for depression, anxiety disorders, post-traumatic stress disorder, and personality difficulties helps clarify the emotional drivers of substance use and informs choice of psychological and pharmacological interventions. Trauma-informed interviewing is particularly important, as early interpersonal trauma is common in both FND and substance use disorders and may influence current coping strategies and relational dynamics with clinicians. When asking about trauma, clinicians should link the inquiry to understanding present difficulties and ensure that supports are in place before exploring highly distressing experiences in depth.
In emergency and acute care settings, rapid yet careful assessment is often needed when patients present with seizure-like episodes or sudden functional weakness. Clinicians should inquire about recent substance intake, missed doses, or attempts to self-discontinue medications, as well as any new prescriptions or dose changes. Where feasible, collateral information from family, caregivers, or paramedics can clarify whether benzodiazepines, alcohol, or other sedatives were administered pre-hospital or upon arrival, and whether these interventions appeared to modify symptom patterns. Documenting these details prevents misinterpretation of response to sedatives as evidence for or against epileptic seizures and supports safer subsequent prescribing decisions.
Medication reconciliation is a crucial step, especially for those receiving prescriptions from multiple providers. Clinicians should review electronic records, pharmacy dispensing histories where available, and any medication lists brought by the patient. Discrepancies between reported and documented prescriptions can signal unrecognized dependence, doctor-shopping, or misunderstanding of dosing instructions. In patients taking chronic opioids, benzodiazepines, or muscle relaxants, it is important to establish the total daily dose in morphine or diazepam equivalents, assess for polypharmacy with other central nervous system depressants, and consider whether current regimens are consistent with evidence-based guidelines for pain and anxiety management.
Cultural, social, and gender factors shape how substance use is experienced and disclosed, and these influences should be explicitly considered during assessment. In some communities, heavy alcohol consumption may be normalized and not spontaneously identified as problematic by patients, whereas in others, modest use may be heavily stigmatized and underreported. Women, who are more frequently represented in FND clinics, may face specific barriers to talking about alcohol or drug use due to caregiving roles, fear of child protection involvement, or cultural expectations of abstinence. Clinicians can mitigate these barriers by explicitly acknowledging them, assuring confidentiality within legal limits, and clarifying that the goal of asking is to improve safety and tailor treatment, not to judge or punish.
Because FND care is typically multidisciplinary, assessment of substance use should be shared and coordinated across team members rather than occurring in isolation. Neurologists, psychiatrists, psychologists, physiotherapists, occupational therapists, and nurses can each contribute perspectives based on their interactions with the patient. For instance, a physiotherapist may notice fluctuating performance that seems related to days when the patient reports heavier alcohol use or missed doses of prescribed medications, while a psychologist may learn about cannabis use during sessions on anxiety or sleep. Regular team meetings where observations about substance use and functional symptoms are discussed support coherent care plans and reduce the risk of mixed messages about the acceptability of ongoing use.
Clear documentation is vital for continuity and safety. Clinicians should record not only quantities and frequencies but also the patient’s own narrative about why they use substances, what they perceive as helpful or harmful, and their level of readiness for change. Using frameworks such as the stages of change (precontemplation, contemplation, preparation, action, maintenance) can help situate current motivation and guide the pace and style of interventions. It is helpful to distinguish between patients who are firmly unwilling to consider change, those who are ambivalent but open to discussion, and those actively seeking support to reduce or stop use, as each group requires a different engagement strategy.
Assessment is also the stage at which realistic expectations about FND treatment can be discussed in relation to substance use. Clinicians can explain that many rehabilitation and psychological approaches rely on stable attention, emotional regulation, and consistent participation, all of which can be undermined by heavy substance use or frequent intoxication and withdrawal cycles. Framing substance use as a modifiable factor that may be limiting the effectiveness of FND therapies helps patients see the practical relevance of addressing it. At the same time, it is important to avoid implying that FND is solely caused by substance use or that recovery is contingent on immediate abstinence; such messages can reinforce shame and disengagement.
When problematic use is identified, preliminary conversations about options for change can begin within FND services, even if specialized addiction treatment will be needed later. Clinicians can provide brief interventions that highlight the link between substance use and current goals, such as reducing seizure-like episodes or improving mobility, and can collaboratively explore tapering and alternatives for symptom management. For example, discussing gradual benzodiazepine reduction alongside non-pharmacological strategies for anxiety, sleep, and functional episodes allows patients to envision a pathway that does not rely solely on medication removal. Early involvement of addiction specialists or liaison psychiatry may be warranted in complex cases, but the initial engagement often occurs in the FND clinic, underscoring the importance of clinicians’ confidence and skill in this area.
Ongoing reassessment is essential, as patterns of substance use can evolve in response to changes in symptoms, social circumstances, or treatment phases. New stressors, such as loss of employment, relationship breakdown, or flare-ups of pain, may lead to increased reliance on alcohol or medications even among patients who initially reported minimal use. Regular check-ins about coping strategies, sleep, pain, and mood provide opportunities to revisit substance use without singling it out or creating a sense of surveillance. By embedding these inquiries into routine follow-up, clinicians signal that substance use is a legitimate and expected topic within FND care, thereby supporting earlier identification of emerging risk and more timely, collaborative intervention.
Integrated treatment strategies for co-occurring FND and substance use
Integrated treatment for co-occurring functional neurological disorder and substance use rests on the principle that both conditions are best addressed together rather than sequentially. Parallel care pathways that treat substance use in isolation from functional symptoms often fail because each problem affects the course of the other. A coordinated approach aims to stabilize the person’s relationship with substances, optimize participation in FND-specific therapies, and reduce overall disability. This requires shared formulations, joint goal-setting, and clear communication across neurology, rehabilitation, and addiction or mental health services.
Developing a shared biopsychosocial formulation is a critical early step. Clinicians and patient work together to map how functional symptoms, emotional distress, substance use, and contextual stressors interact over time. Visual tools such as timelines or simple diagrams can illustrate cycles in which pain, sleep disturbance, or seizure-like episodes lead to increased alcohol, benzodiazepines, or opioids, which then disrupt sleep, worsen mood, and reduce capacity to engage in therapy. Articulating these loops in concrete terms shifts the conversation from blame to problem-solving and helps identify leverage points for change, such as sleep routines, activity pacing, or specific triggers for craving and functional episodes.
Motivational interviewing (MI) provides a foundation for engaging people ambivalent about changing substance use. In FND settings, MI can be tailored to emphasize functional goals: walking further without a wheelchair, reducing frequency of non-epileptic attacks, returning to part-time work, or resuming caregiving roles. Rather than arguing for abstinence, clinicians elicit the person’s own reasons for wanting better control over their body and daily life, and gently explore how current substance use patterns may help in the short term but interfere with these aims over time. Reflective listening, affirmations of effort, and curiosity about past successes in coping support a collaborative tone that reduces defensiveness and increases readiness for change.
Behavioral strategies targeting both substance use and FND can be integrated into a single plan. For example, activity scheduling and graded exposure to avoided situations may be designed to simultaneously reduce functional avoidance (such as fear of going out due to seizure-like events) and substance-related cues (such as drinking when alone at home). Patients can be guided to identify “high-risk” times of day when symptoms and craving coincide—late evenings when pain is worst, or mornings after poor sleep—and to develop alternative routines for those windows, including brief relaxation exercises, distraction activities, or contacting supportive others. Linking each strategy to specific symptom and substance triggers makes the plan more concrete and easier to implement.
Cognitive-behavioral interventions for FND can be modified to address substance-related beliefs and expectations. Many patients hold the view that alcohol or sedative medications are the only effective way to calm their nervous system or prevent seizures. Clinicians can collaboratively test these assumptions by setting up behavioral experiments, such as comparing functional episode frequency on days when non-pharmacological coping is used before turning to substances versus days when substances are used immediately. Reviewing the results in a structured way helps patients see that other strategies can produce partial or sometimes substantial relief, thereby reducing perceived reliance on substances as the sole safety tool.
Rehabilitation therapies, particularly physiotherapy and occupational therapy, play a central role in integrated care. These interventions focus on retraining normal movement patterns, reducing fear of bodily sensations, and rebuilding daily routines. When substance use is present, therapists may need to adjust session timing to periods of minimal intoxication or withdrawal, and to monitor for fluctuations in concentration, balance, and fatigue that might increase injury risk. Treatment plans can include explicit goals related to attending sessions sober, tracking how symptoms feel during and after therapy on days with and without substance use, and practicing grounding or breathing techniques when craving or anxiety arises during movement exercises.
Pharmacological management within integrated treatment is often complex, especially when prescribed medications like benzodiazepines or opioids have become entrenched. Collaborative tapering and alternatives approaches are central. Tapers should be individualized, slow, and clearly explained, with dose reductions small enough to minimize withdrawal symptoms that could mimic or exacerbate functional events. Written schedules, pill organizers, and frequent check-ins help maintain adherence. At each stage, clinicians introduce and reinforce non-pharmacological strategies for anxiety, sleep, and pain, so that patients feel they are gaining tools rather than simply losing medications.
When tapering sedatives or opioids, cross-specialty collaboration is crucial to prevent fragmented prescribing. Ideally, one clinician or team assumes responsibility for coordinating the plan, while others agree not to offer ad hoc refills that undermine progress. Electronic prescribing alerts, shared care plans, and direct communication between neurologists, primary care providers, psychiatrists, and pain specialists reduce the risk of mixed messages. Emergency departments and urgent care clinicians can be informed about the agreed tapering schedule and recommended non-opioid, non-benzodiazepine strategies for acute symptom flares, thereby supporting consistency even during crises.
Alternative pharmacologic options may be indicated for some patients, but they should be used judiciously. For anxiety and mood symptoms driving both FND and substance use, antidepressants, particularly SSRIs or SNRIs, may provide a safer long-term base than chronic benzodiazepines. For pain, non-opioid regimens combining anticonvulsants, certain antidepressants, and topical agents can be considered, alongside clear education that medications alone are unlikely to fully resolve complex pain within FND. Sleep management can incorporate low-dose sedating antidepressants, melatonin, or carefully monitored off-label agents, always coupled with behavioral sleep interventions. The guiding principle is to minimize medications with high dependence potential and to frame any pharmacologic additions as part of a broader rehabilitation-focused plan.
Addressing alcohol or illicit drug use often requires formal addiction treatment components adapted for people with FND. Outpatient programs can integrate psychoeducation about functional symptoms into standard relapse prevention curricula, helping patients recognize how spikes in anxiety, dissociation, or motor symptoms may function as relapse triggers. Conversely, FND clinics can borrow core elements from addiction work, such as functional analysis of use episodes, craving management techniques, and contingency planning for high-risk situations. Where withdrawal management is necessary, inpatient or medically supervised detoxification may be arranged with careful monitoring for both substance-related and functional symptoms, as well as prevention of unnecessary escalation of sedative prescribing in response to non-epileptic events.
Trauma-focused interventions may be highly relevant, particularly for individuals whose substance use and FND are both linked to interpersonal violence or early adversity. Timing is critical: intensive trauma processing while substance use is unstable or functional symptoms are extremely volatile can increase distress and destabilization. A phased approach that emphasizes safety, stabilization, and skills-building first is often preferable. Once the person has basic emotion regulation tools, some degree of symptom control, and a more predictable pattern of substance use or early remission, evidence-based trauma therapies such as EMDR or trauma-focused CBT can be introduced in collaboration with FND and addiction teams.
Family and caregiver involvement can strengthen integrated treatment when handled thoughtfully. Psychoeducation sessions with relatives can clarify the nature of FND, the role of substance use in symptom escalation or dampening, and practical ways to support both rehabilitation and change in substance use. Caregivers may need guidance on avoiding unintentional reinforcement, such as repeatedly offering sedative medications at the first sign of distress or providing alcohol to prevent conflict. Joint sessions can help negotiate boundaries around substances in the home, safety planning for crises, and how to respond to functional episodes without escalating medical or substance-related interventions.
Addressing social determinants of health is also part of an integrated strategy. Instability in housing, employment, or income can undermine progress in both FND rehabilitation and substance use change. Social workers and case managers can assist with disability benefits, vocational rehabilitation, and access to community resources, thereby reducing baseline stress and the perceived need for substances as coping tools. Where possible, linking patients to peer support groups—whether FND-focused, recovery-focused, or both—can provide validation and practical ideas from others facing similar challenges, reducing isolation and enhancing hope.
Monitoring and outcome evaluation are essential to guide ongoing adjustments in treatment. Clinicians can track not only traditional addiction outcomes (days of use, quantity, cravings) but also FND-specific measures such as attack frequency, mobility, self-care capacity, and quality of life. Graphing these indicators over time allows patients and teams to see how changes in substance use relate to functional improvements or setbacks. This shared data can reinforce motivation when reductions in substance use coincide with better symptom control and may prompt review of the plan when new patterns emerge, such as substitution of one substance for another or increased reliance on over-the-counter sedatives.
For some individuals, full abstinence is neither immediately achievable nor clearly necessary for functional gains. Harm reduction approaches can be pragmatically integrated, focusing on reducing the most dangerous aspects of use while still pursuing FND rehabilitation. Examples include encouraging use of lower-alcohol beverages, setting limits on daily intake, spacing doses further apart, avoiding mixing alcohol with prescribed sedatives, using clean injecting equipment, or establishing “no-use” periods around key activities such as physiotherapy sessions or childcare. Clinicians can explicitly link these harm reduction steps to goals like decreasing seizure-like episodes during the day or improving balance to prevent falls.
Relapse in substance use or worsening of functional symptoms should be anticipated rather than viewed as treatment failure. Integrated plans include advance crisis strategies that specify what the patient and clinicians will do if substance use escalates, attacks intensify, or suicidality emerges. This may involve predefined thresholds for contacting services, temporary increase in appointment frequency, or short-term adjustment of medications without restarting long-term sedatives. Reviewing relapses through a nonjudgmental, problem-solving lens—what was happening in life, how symptoms and emotions were managed, what could be done differently next time—supports learning and resilience rather than shame and disengagement.
Throughout integrated treatment, a consistent message is that the person’s symptoms are real and modifiable, and that substance use is understood as an attempt to cope rather than a moral failing. Aligning all team members around this stance reduces the risk of invalidating or contradictory interactions and promotes trust. Over time, as individuals experience gains in functional capacity, improved mood, and more stable relationships with substances, they often become more willing to further reduce or stop use and to take increasingly active roles in their own rehabilitation, reinforcing a virtuous cycle that supports longer-term recovery across both domains.
Ethical and systemic considerations in managing substance use within FND services
Ethical and systemic questions emerge immediately when addressing substance use within services for functional neurological disorder, because patients are simultaneously vulnerable to both overmedicalization and therapeutic neglect. Clinicians must navigate the tension between respecting autonomy and protecting patients from iatrogenic harm, particularly when long-term prescribing of benzodiazepines or opioids has become entrenched. Decisions about continuing, tapering, or refusing to initiate such medications cannot be driven solely by individual clinician preference; they should be anchored in transparent, evidence-informed policies that acknowledge the specific dynamics of FND and co-occurring substance use while guarding against stigma and blame.
A central ethical concern is nonmaleficence in prescribing. Many people with FND arrive in specialist care after years of escalating pharmacotherapy that has provided limited benefit and significant side effects. Continuing potentially harmful regimens without critical review can reinforce dependence and diminish opportunities for rehabilitation. At the same time, abrupt discontinuation or rigid “no-sedative” rules may trigger withdrawal, exacerbate distress, and damage therapeutic relationships. Ethically sound practice involves careful risk–benefit analysis, shared decision-making, and stepped changes that prioritize safety. This often includes gradual tapering and alternatives for symptom management, explained in language that emphasizes partnership and concern for long-term wellbeing rather than punishment for prior prescribing or patient behavior.
Respect for patient autonomy requires more than simply offering choices; it depends on ensuring that patients have accurate, comprehensible information about how substances may interact with FND symptoms, mood, and cognition. Many individuals have never been told that chronic high-dose benzodiazepines can worsen anxiety over time, interfere with the retraining of movement, and increase fall risk, or that opioids may amplify pain via hyperalgesia and sap energy needed for rehabilitation. Providing balanced psychoeducation about these mechanisms, while acknowledging perceived short-term benefits, supports truly informed consent. Autonomy is further enhanced when patients are invited to articulate their goals, values, and tolerances for different risks, and when care plans are framed as experiments that can be adjusted based on observed outcomes.
Justice and equitable access to care are recurring systemic challenges. People with FND frequently experience diagnostic overshadowing, where new physical complaints or safety concerns are prematurely attributed to functional symptoms or substance use without adequate assessment. Conversely, some health systems marginalize FND by labeling it “non-organic,” resulting in limited access to neurological or rehabilitation resources compared with other chronic conditions. When substance use is present, these biases can compound each other, leading to exclusion from programs that have zero-tolerance policies on intoxication, or to refusal of services such as inpatient rehabilitation or pain management. Ethically, services should strive to design pathways that explicitly include, rather than exclude, individuals with both FND and substance-related difficulties, recognizing them as a group with substantial unmet need.
Stigma is a major ethical and systemic issue at the intersection of FND and substance use. Many patients report prior experiences of being dismissed as “faking,” “drug seeking,” or “psychosomatic,” which undermine trust and discourage honest disclosure of alcohol or drug use. Clinicians may unconsciously adopt pejorative attitudes, particularly when confronted with recurrent crises or perceived nonadherence. Addressing this requires deliberate cultivation of a trauma-informed, nonjudgmental culture within services. Training should emphasize that functional symptoms are genuine expressions of brain–body dysfunction, that substance use often reflects attempts to cope with overwhelming experiences, and that both are strongly shaped by social context. Clinical supervision and reflective practice groups can help staff notice and challenge stigmatizing language or behaviors that might otherwise become normalized.
Confidentiality and information-sharing present further ethical considerations, especially within multidisciplinary teams and across service boundaries. FND care often involves neurologists, psychiatrists, psychologists, therapists, and social workers; addiction services and primary care may also be involved when substance use is significant. Patients may worry that disclosing heavy drinking or non-prescribed substances will lead to loss of medications, legal problems, or child protection involvement. Clear communication about how information will be used, what must be shared for safety, and what remains confidential is essential. Consent processes can include explicit discussion about sharing substance-related information with other treating clinicians to coordinate care, with an emphasis on how this reduces duplication, conflicting advice, and the risk of unsafe prescribing.
Safety-related thresholds sometimes necessitate overriding patient preferences, creating ethical tension. For example, continued co-prescription of opioids and benzodiazepines at high doses, in the context of recurrent overdose or severe respiratory disease, may pose an unacceptable level of risk. In such situations, clinicians may ethically decline to continue current regimens while offering structured alternatives. Documenting the rationale, engaging in repeated dialogue, and providing practical support (such as facilitated referral to addiction services, or monitored tapers) help maintain respect even when clear boundaries are set. Services should avoid unilateral, unexplained discontinuation, which can push patients toward unregulated sources and undermine any remaining trust in healthcare.
Systemic prescribing cultures exert a powerful influence on individual decisions. In some settings, emergency departments routinely administer benzodiazepines to terminate non-epileptic attacks or sedate distressed patients with FND. While often well-intentioned, this practice can inadvertently reinforce functional episodes, increase expectations of pharmacologic rescue, and contribute to later dependence. Service-level guidelines that discourage sedative use for non-epileptic events, and instead promote behavioral de-escalation and clear psychoeducation, can shift norms. Implementing such guidelines is an ethical responsibility at the organizational level, not solely a matter of individual clinician preference. Regular audit and feedback on prescribing patterns, including tracking high-dose or long-term sedatives in FND populations, support accountability and quality improvement.
Resource allocation also raises ethical questions. Integrated pathways that combine FND rehabilitation with substance use treatment require time, staffing, and cross-service coordination that may not be readily available. Health systems frequently fund separate silos—neurology, mental health, addiction, pain—each with its own criteria and outcome measures. Patients with overlapping needs may fall between these silos or be deemed “too complex” for standard programs. Ethically, planners should recognize the high cumulative morbidity and healthcare utilization associated with co-occurring FND and substance use, and prioritize development of collaborative models such as shared clinics, liaison roles, or joint care protocols. These investments can reduce emergency presentations, unplanned admissions, and unnecessary investigations, aligning ethical commitments with system efficiency.
Eligibility criteria for services must be scrutinized for unintended discrimination. Rules that exclude anyone with active substance use from group therapy, day programs, or residential rehabilitation may be justified on safety grounds in some contexts, but they often lack nuance and fail to differentiate between levels of risk. A more ethically coherent approach is to define specific safety requirements—such as no intoxication on arrival, or agreement to medication supervision—while allowing people with ongoing, but managed, substance use to participate. Where exclusion is necessary, services should have clear pathways to help patients stabilize substance use and re-enter FND programs, rather than creating a one-way exit with no realistic route back.
Clinician competence is another systemic concern. Many neurologists and rehabilitation professionals report limited training in assessing and managing substance use, while addiction specialists may be unfamiliar with FND presentations and wary of “functional” diagnoses. This skills gap can lead to mutual avoidance, with each side expecting the other to take the lead. Ethically, institutions have a responsibility to provide interdisciplinary education that builds basic competence in both domains. Joint case conferences, shared workshops, and co-authored protocols can help professionals learn from each other, reduce misconceptions, and develop more coherent, ethically grounded approaches for patients with overlapping conditions.
Legal and regulatory frameworks shape how services manage substance use within FND care. Prescribing regulations, controlled substance monitoring programs, and professional guidelines on long-term benzodiazepine or opioid use may constrain certain options while leaving others ambiguous. Clinicians must balance adherence to these regulations with individualized care, ensuring that patients understand the external constraints on prescribing decisions rather than experiencing them as purely personal refusals. When legal concerns arise—for example, about fitness to drive in the context of seizure-like episodes and heavy alcohol use—clinicians should explain their reporting obligations, explore ways to mitigate the impact (such as temporary restrictions, planning alternative transport), and offer advocacy around related social or occupational consequences where appropriate.
The principle of beneficence implies a proactive approach to building hope and agency, which has ethical weight in a group often exposed to pessimistic or invalidating messages. Systemically, services should avoid deterministic narratives that suggest people with FND and substance use are unlikely to improve or are “too complex” for mainstream care. Instead, communication—both in clinical encounters and in written materials—can emphasize that symptoms are real and modifiable, that substance-related harms are reducible even when abstinence is not immediately attainable, and that meaningful functional gains are possible. Such messaging respects patients’ dignity and supports their capacity to engage with challenging changes in behavior, including reductions in substances that have long been central to coping.
Ethical practice also extends to how research and quality-improvement efforts are conducted. People with FND and substance use are often excluded from clinical trials for both functional disorders and addiction, limiting the evidence base that informs care and perpetuating uncertainty regarding effective interventions. Investigators and ethics committees should scrutinize exclusion criteria that automatically remove participants with “unstable” substance use or “psychogenic” symptoms, considering whether adaptations—such as additional supports, flexible scheduling, or stratified analyses—could allow safe inclusion. Involving patients with lived experience on advisory panels can help identify research priorities, ensure that outcome measures reflect what matters to them, and guard against designs that inadvertently reinforce stigma.
Systemic approaches must attend to broader social and cultural determinants that shape both FND and substance use. Poverty, discrimination, gender-based violence, and limited access to stable housing or employment are not simply background factors; they influence symptom onset, coping patterns, and the feasibility of recommended changes. Ethically, FND services should build partnerships with community agencies, social care, and advocacy groups to address these determinants as part of routine care. This may include facilitating legal advice for benefits or housing, linking patients to culturally specific support networks, and adapting interventions to be feasible in low-resource contexts. Recognizing and responding to these systemic influences affirms that responsibility for change does not rest solely on the individual patient, but is shared across health systems and the societies in which they operate.
