Two Stroke Patients Laughed Hard but Felt No Joy, a Clue That the Brain Can Split Laughter From Mirth

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“Even though it looked like laughing, it didn’t feel like laughing at all,” one of them told his doctors.

That line, from a case series published in Frontiers in Psychiatry on Sept. 4, turns the report into more than a safety warning. MedicalDaily first covered the cases as a possible side effect of repetitive transcranial magnetic stimulation, or rTMS. Read closely, they also reveal a strange split: the body carrying out a laugh while the mind supplies none of the joy behind it.

Neurologists Shusheng Jiao and Xiuhong Xu of Bethune International Peace Hospital in Shijiazhuang described two right-handed men, ages 48 and 42, who had ischemic strokes on the right side of the brain in July 2024. Both received low-frequency rTMS, a noninvasive treatment that uses magnetic pulses to alter brain activity, at one pulse per second over the hand area of the left primary motor cortex, the region that drives voluntary movement, in daily 20-minute sessions.

The older man began laughing during his third session, in bursts lasting 5 to 40 seconds. The younger man felt a brief urge to laugh during his fourth session and found it easier to laugh for several hours afterward, but he did not tell the medical team. During his fifth session, uncontrollable episodes of 5 to 30 seconds began. In both men, moving the coil forward to the left prefrontal cortex stopped the laughter, and returning it to the motor cortex brought it right back.

Neither man described anything like amusement. The first called the laughter completely involuntary and “not funny at all,” and said he felt embarrassed and confused. The second said it “came out of nowhere” and that he “had no control over it.” Both went through a short period of low mood and restlessness after their episodes.

The authors place their findings within two brain systems thought to produce laughter: an emotional network anchored in deep structures such as the amygdala, hypothalamus, and anterior cingulate, and a volitional network that includes the motor cortices. In these two men, the outward act of laughing appeared to fire without the feeling that usually comes with it.

In 1998, neurosurgeon Itzhak Fried and colleagues reported in Nature that electrically stimulating the anterior supplementary motor area, a region involved in starting speech, made a 16-year-old epilepsy patient laugh. Her laughter came with a sense of merriment, but she seemed to laugh first and find a reason afterward, crediting something different as funny each time.

In 2019, an Emory University team reported that stimulating the cingulum bundle, a white-matter tract, produced smiling, laughter, and reports of happiness and relaxation in three epilepsy patients. In one, the calming effect allowed the patient to come off intravenous sedation during awake brain surgery while still completing language testing.

The stroke cases sit at the opposite end: the machinery of laughter, apparently stripped of its emotional content. The primary motor cortex is not traditionally considered a core part of the brain’s laughter network, the authors acknowledged. They proposed that in brains made more excitable by a recent stroke, repeated stimulation may have spread along connections to premotor, prefrontal, and cingulate regions linked to limbic areas. That idea remains a hypothesis, and neither patient underwent functional brain imaging to test it.

Laughter without feeling may sound familiar to families of stroke survivors. A more common condition, pseudobulbar affect, or PBA, causes sudden outbursts of laughing or crying that do not match a person’s mood. The Cleveland Clinicsays researchers estimate that 2 million to 7 million people in the U.S. have PBA, which can follow stroke, traumatic brain injury, ALS, multiple sclerosis, and other neurological conditions. Drawing on earlier studies, a 2015 review of stroke-associated PBA put its prevalence among stroke patients at roughly 11% to 34%, with figures varying by diagnostic scale. The FDA has approved a combination of dextromethorphan and quinidine, sold as Nuedexta, to treat it.

The new episodes looked different. They appeared only during stimulation, tracked the position of the coil, and stopped when treatment ended. Jiao and Xu classified them as ictal laughter, meaning laughter driven by seizure-like electrical activity, similar to gelastic, or “laughing,” seizures.

A one-hour EEG recorded right after the first man’s third session showed scattered sharp waves over the right anterior temporal region and both sides of the frontal lobes. The authors described this as suggestive of cortical irritability but not definitive evidence of epileptic discharges. The second man declined EEG testing.

Doctors stopped rTMS in both men, and the laughter did not return during their hospital stays. Both had made near-complete recoveries three months later.

Seven months after his first admission, the older man was readmitted with recurrent left-sided weakness, and clinicians tried the same rTMS protocol again. Within five minutes, he reported a strong urge to laugh. Stimulation was stopped immediately, and no full laughing episode followed.

The authors describe theirs as the first report of rTMS-induced ictal laughter in stroke patients. Seizures are uncommon with this kind of stimulation, with an estimated incidence below 0.1% for low-frequency protocols in research the authors cite. Still, they warn that inappropriate laughter, a lowered laughter threshold, or an urge to laugh may signal an impending seizure-like event, and that stimulation should be halted right away.

The report has clear limits. It involves just two patients, no sham comparison, no EEG captured during an episode, and manual rather than image-guided coil placement. The authors could not rule out that stimulation unmasked an existing seizure tendency.

People receiving rTMS who notice unexpected sensations should tell their care team promptly, and anyone with frequent, uncontrollable laughing or crying after a stroke should ask a clinician whether PBA or another condition may be involved.

Did the two stroke patients feel happy when they laughed?

No. Both described the laughter as involuntary and humorless, and both felt low and restless afterward. One said that even though it looked like laughing, it did not feel like laughing at all.

What does this suggest about how the brain produces laughter?

The cases fit the idea that laughter involves at least two systems, one that produces the physical act and one that supplies the emotion. In these men, stimulation over a motor region appeared to trigger the physical act alone, though that interpretation rests on two patients and was not tested with brain imaging.

It appears to be different. PBA is a relatively common post-stroke condition with spontaneous outbursts, while these episodes occurred only during stimulation and were classified by the authors as seizure-like.

Seizures with low-frequency rTMS are uncommon, with an estimated incidence below 0.1%. This two-patient report suggests people in the early weeks and months after a stroke may warrant closer monitoring.

What should someone receiving rTMS do if they feel an urge to laugh?

Tell the care team right away. The authors recommend stopping stimulation immediately if laughter, a lowered laughter threshold, or an urge to laugh appears.