Are Tourettes and Epilepsy Related?

Tourette syndrome and epilepsy are distinct neurological conditions, but a growing body of research shows they share meaningful connections. A population-based study found that children with Tourette syndrome face a roughly 18-fold increased risk of developing epilepsy compared to children without the condition. The overlap runs deeper than simple co-occurrence: the two conditions share disrupted brain chemistry, can be confused for each other during diagnosis, and even respond to some of the same treatments. How tightly they are linked, and why, is a question researchers are still working out.

How Often They Occur Together

The strongest statistical evidence for a link comes from a large retrospective study that tracked children with Tourette syndrome over time. Compared to a matched control group, children with Tourette syndrome had an 18-fold higher risk of being diagnosed with epilepsy. That association held even after researchers accounted for other conditions that commonly accompany Tourette syndrome, such as ADHD and obsessive-compulsive disorder, suggesting the connection is not simply a side effect of those comorbidities.¹

That number is striking, and it deserves some context. An 18-fold increase in risk sounds alarming, but epilepsy is relatively uncommon in the general pediatric population. So a large relative increase still translates to a fairly small absolute number of affected children. In a clinical series of eight young patients who had both Tourette syndrome and epilepsy alongside ADHD, the seizures were generally manageable, and seven of the eight were seizure-free after antiepileptic treatment over a seven-year follow-up. The point is not that every child with Tourette syndrome should expect seizures, but that clinicians and parents should be aware the risk exists.

What Brain Scans Reveal About the Overlap

One way researchers have explored the connection is by looking at brain wave patterns in people with Tourette syndrome who have never had a clinical seizure. The results are mixed, which itself tells a story about how subtle the overlap can be.

A study of 30 unmedicated Tourette syndrome patients with no history of seizures found that one in five had abnormal brainwave recordings. About 13% showed epileptiform patterns, the kind of electrical spikes typically associated with seizure disorders, despite never having had a seizure.² A separate study of 38 patients painted a less dramatic picture: about a third had some kind of brainwave abnormality, but true epileptiform activity was rare, turning up in only two patients. Most of the abnormalities in that group showed up in patients who were either taking haloperidol, a medication known to disturb brainwave patterns, or who had other signs of neurological problems.³

The disagreement between these two studies is instructive. The first carefully excluded patients on medication and still found epileptiform activity in a meaningful fraction. The second suggested that much of the abnormal brainwave activity in Tourette patients could be explained by drug effects or additional neurological conditions. The honest reading is that some people with Tourette syndrome do have unusual electrical brain activity that resembles what you see in epilepsy, but it is not universal, and its clinical significance remains debated. Having epileptiform patterns on a brainwave recording does not mean you will develop seizures.

GABA and the Shared Brain Chemistry

If Tourette syndrome and epilepsy overlap, there should be some shared mechanism in the brain to explain it. The leading candidate is a chemical signaling system built around GABA, the brain’s primary inhibitory neurotransmitter. Think of GABA as a braking system. When GABA signaling weakens, brain circuits become more excitable than they should be. That excess excitability is the fundamental problem in epilepsy, and there is increasing evidence it plays a role in Tourette syndrome too.

Postmortem studies of Tourette syndrome patients have revealed changes in the types of brain cells that produce GABA, particularly in brain regions involved in movement control. Certain inhibitory cells are reduced in number in parts of the basal ganglia, and imaging studies of living patients have shown altered GABA receptor activity across multiple brain regions.⁴ These findings point to a tipped balance between excitation and inhibition in the brain. In epilepsy, that imbalance produces seizures. In Tourette syndrome, it may produce tics. The conditions are not identical, but they may share this upstream problem of circuits that are not being properly held in check.

This is also why both conditions tend to emerge during childhood and adolescence. The brain’s inhibitory circuits are still maturing during those years, and disruptions in that maturation process could push a developing nervous system toward tics, seizures, or both. The fact that many children with Tourette syndrome see their tics improve or resolve by adulthood may reflect the eventual catch-up of those inhibitory systems.

When Seizures Look Like Tics

One of the most practically important connections between Tourette syndrome and epilepsy is that they can be mistaken for each other. Certain types of seizures produce movements that look remarkably like tics, and the consequences of a misdiagnosis can be significant.

A case series described three children who were initially diagnosed with tic disorders or Tourette syndrome but turned out to have photosensitive epilepsy. One was a 12-year-old boy whose shoulder shrugs and head jerks had been called Tourette syndrome for three months before video brainwave monitoring revealed that the movements were time-locked to epileptic discharges triggered by flashing light. A 10-year-old girl had been diagnosed with chronic tic disorder based on two years of daily eye blinking and head nodding; she too had epileptic activity triggered by visual stimuli like video games and sunlight. A 14-year-old boy had been treated for tics before monitoring captured his movements as epileptic polyspikes induced by light stimulation.⁵

A similar case involved a patient treated for years for a tic disorder before the correct diagnosis of myoclonic epilepsy was finally made during inpatient brainwave monitoring.⁶ Myoclonic seizures produce sudden, brief, shock-like jerks that can closely resemble the rapid involuntary movements of tics. The difference matters because the treatments are entirely different: tic-suppressing medications do nothing for seizures, and a child with unrecognized epilepsy misses out on anticonvulsant therapy that could eliminate their symptoms.

The lesson from these cases is not that every tic should prompt an epilepsy workup, but that certain features should raise suspicion. Movements that are consistently triggered by light or screens, that do not come with the buildup of inner tension most tic patients describe, or that began suddenly without the typical waxing and waning pattern of tics may warrant a closer look with brainwave monitoring.

Medications That Work Across Both Conditions

The pharmacological overlap between Tourette syndrome and epilepsy is a two-way street. Some anticonvulsant drugs reduce tics, and some medications used for tics can worsen seizure risk.

Topiramate, a drug developed for epilepsy, has shown promise for tic reduction. In a study of patients treated with topiramate for Tourette syndrome, about three-quarters experienced moderate to marked improvement in their tics. The drug was not without drawbacks: roughly a quarter of patients reported cognitive or language problems, and about one in ten experienced mood swings or aggression.⁷ The cognitive side effects in particular are a meaningful trade-off, especially for children and adolescents in school. Still, the fact that an anticonvulsant can suppress tics reinforces the idea that shared brain mechanisms underlie both conditions.

Levetiracetam, another anticonvulsant, has been explored for Tourette syndrome as well, though the evidence is much less convincing. Trials evaluating it have produced conflicting results, and it is considered potentially useful only for select patients rather than a reliable option.⁸

On the other side of the equation, some drugs prescribed for Tourette syndrome can increase seizure risk. Clozapine, an atypical antipsychotic sometimes used for severe cases, carries a recognized seizure risk significant enough that a baseline brainwave recording is recommended before starting the medication, along with ongoing monitoring.⁹ For a patient who already has both conditions, this kind of drug interaction is especially important. A medication that helps tics while lowering the seizure threshold could make the overall picture worse. Clinicians treating patients with both conditions often need to weigh these trade-offs carefully.

Deep Brain Stimulation as a Shared Treatment Target

When medications fail, both Tourette syndrome and epilepsy can be treated with deep brain stimulation, a surgical approach that delivers small electrical pulses to specific brain regions. What is particularly interesting is that researchers have identified at least one brain target that appears to help with both conditions. The centromedian-parafascicular complex of the thalamus, a cluster of cells deep in the brain that acts as a relay station between movement circuits and the cortex, has been used as a stimulation target for both medically resistant Tourette syndrome and drug-resistant generalized seizures.

Deep brain stimulation is reserved for severe, treatment-resistant cases, so the overlap in surgical targets is more relevant to researchers trying to understand the underlying neurology than to most patients. But it offers another clue that these two conditions involve some of the same circuitry. The thalamus helps regulate the flow of signals between deeper brain structures and the cortex, and when that regulation fails, the result can be either uncontrolled movements or uncontrolled electrical discharges, depending on which circuits are most affected.

Could Inflammation Be a Common Trigger

A separate line of research has asked whether inflammation, particularly the immune response triggered by infections, might provoke both tics and seizures in some children. The most discussed framework is PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections) and the broader category PANS (Pediatric Acute-onset Neuropsychiatric Syndrome), in which a child’s immune response to an infection appears to attack brain tissue, producing sudden-onset tics, obsessive-compulsive behavior, or both.

This area of research is genuinely contentious. Among experienced clinicians and researchers, there is substantial disagreement about the role inflammation plays in producing tics and obsessive-compulsive disorder, and the debate extends to best clinical practices for patients who might fit these categories.¹⁰ Some researchers view PANDAS/PANS as a well-supported phenomenon that explains a subset of tic cases; others argue the evidence remains weak and the diagnostic criteria too vague to be clinically useful. The connection to epilepsy in this framework is speculative but plausible: autoimmune encephalitis, in which the immune system attacks the brain, is an established cause of seizures, and if a similar process can produce tics, it could theoretically produce both.

For parents who have seen a child develop tics abruptly after an infection, the PANDAS concept resonates powerfully. The research has not yet settled the question of how common this pathway actually is or how reliably it can be identified. If your child developed tics very suddenly and you suspect an infectious trigger, raising the possibility with a neurologist is reasonable, but be prepared for the reality that expert opinions on this topic vary widely.

Practical Guidance for People Living With Both

If you or your child has Tourette syndrome and you are wondering about epilepsy risk, a few practical points are worth keeping in mind. There is no recommendation for routine epilepsy screening in everyone with Tourette syndrome. The elevated risk, while real, does not translate to a high absolute probability of seizures. Standard clinical judgment applies: if you notice episodes that look different from typical tics, particularly movements that involve loss of awareness, are triggered by flashing lights, or occur in clusters without the usual sense of a building urge to move, bring them up with a neurologist.

If both conditions are present, medication choices deserve extra care. Anticonvulsants with tic-suppressing effects like topiramate can sometimes address both issues with a single drug. Conversely, certain tic medications, including some antipsychotics, can lower the seizure threshold. Make sure every prescribing doctor knows the full diagnostic picture.

Sleep disruption is another area where the two conditions can amplify each other. Both tics and seizures tend to worsen with poor sleep, creating a cycle where one condition aggravates the other. Consistent sleep hygiene is a low-risk intervention that helps both. Screen time before bed, irregular schedules, and stimulant medications taken too late in the day can all undermine sleep quality in ways that are directly relevant to managing either condition.

Functional Neurological Symptoms and the Gray Zone

Beyond classic Tourette syndrome and classic epilepsy, there is a gray zone of conditions that blur the line between the two. Functional movement disorders produce tic-like movements without the neurological markers of either Tourette syndrome or epilepsy. Psychogenic non-epileptic seizures produce events that look like seizures but are not caused by abnormal electrical brain activity. These functional conditions are not rare, and they create diagnostic confusion that is distinct from the seizure-vs-tic problem described earlier.

A study comparing children with psychogenic non-epileptic seizures to those with functional motor disorders found that about a quarter of the seizure group had a family history of epilepsy, compared to just 5% of those with functional movement disorders.¹¹ That finding hints that family history of seizure disorders may predispose some children toward functional neurological symptoms that mimic epilepsy specifically, rather than tics. It also complicates the diagnostic picture further: a child with a tic-like movement might have Tourette syndrome, epilepsy, a functional neurological disorder, or some combination. Getting the right diagnosis often requires the kind of prolonged video brainwave monitoring that caught the misdiagnosed cases described earlier. For families navigating this uncertainty, the most useful step is finding a specialist comfortable with the full spectrum of movement and seizure disorders in children, rather than assuming the first diagnosis is necessarily the final one.