Children can get ALS, but it is exceptionally rare. The condition is called juvenile ALS, defined as symptom onset before age 25, and it accounts for a very small percentage of all ALS cases. The vast majority of people diagnosed with ALS are between 58 and 69 years old. When ALS does appear in young people, it tends to look different from the adult form in important ways, including its causes, how it progresses, and which symptoms appear first.
What Juvenile ALS Looks Like
In adults, ALS often begins with weakness in the hands or trouble speaking. In children and teens, the earliest signs are more commonly related to stiffness and movement problems in the legs. A child might develop a stiff or awkward way of walking, begin walking on their toes, or have increasing difficulty with coordination. Muscle weakness typically starts in the feet or lower legs and works its way upward over time.
Other early symptoms can include tightness in the facial muscles, slurred speech, and difficulty swallowing. Some forms of juvenile ALS have been documented with symptom onset as early as 22 months old, though onset during the school-age years or teenage years is more typical. One reported case involved a child who began developing gait problems and leg stiffness at age 7. Two siblings in another case showed distal wasting and abnormally brisk reflexes at ages 11 and 12.
Why It Happens in Young People
Most adult ALS cases are “sporadic,” meaning they appear without any family history or identifiable genetic cause. Juvenile ALS is the opposite. It is far more frequently tied to inherited gene mutations, even in cases where no one else in the family has been diagnosed.
Several specific genes are involved. Mutations in genes called ALS2, SETX, and SPG11 tend to cause a slowly progressive form that can span decades. These are the more common genetic culprits in juvenile cases. However, mutations in two other genes, SOD1 and FUS, can cause a much more aggressive form. A review of published cases found that among juvenile patients with no family history who carried identified mutations, the majority had FUS mutations, particularly one specific mutation (p.P525L) associated with rapid progression and shorter survival. This means that even without a known family history of ALS, a genetic cause may still be driving the disease in a young person.
How Progression Differs From Adult ALS
One of the most important distinctions is that juvenile ALS does not always follow the rapid, fatal course that defines adult ALS. The trajectory depends heavily on which gene is involved.
Forms caused by ALS2 or SETX mutations often progress very slowly over many years. Some patients live for decades after diagnosis, and these forms have been described as nonfatal in medical literature. This is a stark contrast to adult-onset ALS, where most patients survive two to five years after diagnosis.
The aggressive forms, particularly those linked to FUS and some SOD1 mutations, are a different story. These can progress quickly even in teenagers, resembling or outpacing the speed of adult ALS. Researchers have emphasized that both SOD1 and FUS mutations should be screened in any young ALS patient with rapid progression, regardless of whether there is a family history.
How Juvenile ALS Is Diagnosed
Diagnosing ALS in a child is significantly harder than in an adult because several other childhood conditions cause similar symptoms. The most common motor neuron disease in children is spinal muscular atrophy (SMA), which has a well-established genetic test and is typically the first condition neurologists rule out. Hereditary spastic paraplegia and juvenile primary lateral sclerosis also mimic juvenile ALS closely, as both cause leg stiffness and speech difficulties without the muscle wasting that distinguishes ALS.
The diagnostic process generally involves nerve conduction studies and a needle EMG test, which measures electrical activity in muscles. Doctors look for a specific combination of signs: evidence that nerve connections to muscles are actively breaking down (called ongoing denervation) alongside signs that the remaining nerves have been compensating over time (seen as unusually large electrical signals from surviving nerve cells). MRI imaging helps rule out structural problems in the brain or spinal cord. Newer tools, including blood tests that measure levels of a protein released by damaged nerve cells, are increasingly used to support the diagnosis.
Because ALS in children is so uncommon and overlaps with several other conditions, families often go through a long diagnostic process. Genetic testing plays a larger role than it does in adult ALS, since the juvenile form is so frequently linked to identifiable mutations.
What Parents Should Watch For
The chances of a child developing ALS are extremely low. Most children with muscle weakness, clumsiness, or gait changes have far more common and less serious explanations. That said, certain patterns are worth bringing to a pediatric neurologist’s attention: progressive weakness in the hands or feet that gets worse over months, increasing stiffness in the legs that affects walking, new onset of toe-walking in a child who previously walked normally, or slurred speech that develops gradually without an obvious cause.
The key word is “progressive.” Many childhood conditions cause temporary weakness or coordination problems. ALS, whether juvenile or adult, is defined by steady, ongoing decline in motor function. If symptoms plateau or fluctuate, a different diagnosis is far more likely.