Ataxia in Children: What It Is and When It's Urgent

If your child has suddenly become unsteady

A child who has newly become wobbly, is stumbling, cannot walk normally, or has suddenly become clumsy needs medical assessment today — not tomorrow, and not “let us see how they are in the morning.”

Call 911 or go to an emergency department immediately if there is also: headache, especially with vomiting; drowsiness, confusion or difficulty waking; neck stiffness or fever; weakness, numbness or difficulty speaking; any possibility your child has taken medication, alcohol or another substance; or a recent head injury.

Take any medication bottles or containers with you if ingestion is possible. In the United States you can also call Poison Control on 1-800-222-1222.¹³

Quick answer. Ataxia means impaired coordination and balance. The distinction that decides everything is how fast it appeared. Ataxia that developed over hours or days in a previously well child is a medical emergency — across 1,167 children studied, the causes included poisoning in 14.1% and tumors in 7.3%.² Ataxia that has always been there, and is stable, is not an emergency; it is a condition managed with therapy and support. A sudden worsening in a child with known chronic ataxia is treated as a new emergency.

Key Takeaways

Speed of onset is the triage question. Hours to days in a previously well child means today. Long-standing and stable means an appointment.
Postinfectious cerebellitis is the most common cause of acute ataxia at 38.0%² — but it is a diagnosis of exclusion, not an assumption to make at home.
About one in seven cases is poisoning or medication ingestion, and about one in fourteen is a tumor.² In one emergency-department series brain tumors ran higher still, at 11.2%.¹ Those numbers are why sudden ataxia is never watched at home.
Five causes account for roughly three quarters of cases,² which is why an emergency department can work through this efficiently once your child is in front of them.
Most children with postinfectious cerebellar ataxia recover completely, typically within two to four weeks.⁵
A change in a child with known ataxia is a new event. Do not attribute a sudden worsening to the existing diagnosis.
Chronic ataxia is managed, not cured, and physical, occupational and speech therapy carry most of the functional load.
Fatigue makes coordination measurably worse. Pacing is a real intervention, not a soft one.

What ataxia looks like

Ataxia is a description of a pattern, not a diagnosis in itself. It means the parts of the nervous system that coordinate movement are not working smoothly — most often the cerebellum, but also the sensory pathways that tell the brain where the body is in space.⁷

Where you see it	What you might notice
Walking	Wide-based stance; staggering; veering; cannot walk heel-to-toe; looks “drunk”
Limbs	Reaching past or short of a target; tremor that worsens as the hand approaches; clumsiness with buttons, cups, cutlery
Speech	Slurred, slowed, or oddly variable in volume and rhythm — sometimes described as scanning speech
Eyes	Jerky movements; difficulty following a moving object smoothly; overshooting when looking to a target
Trunk	Difficulty sitting steadily; swaying when still; needing hands to prop
In young children	Often shows first as sudden refusal to walk, unusual clinginess, wanting to be carried, or falling much more than usual

What ataxia is not. Ataxia is not general clumsiness. Many children are clumsy, and developmental coordination disorder is common and quite different — it develops gradually, is present across a child’s history, and does not appear over a weekend. Ataxia is also distinct from low muscle tone and from vestibular disorders, although these can look similar and sometimes co-occur.

The distinction that decides everything

	Acute ataxia	Chronic or progressive ataxia
Onset	Hours to days, in a previously well child	Months to years, or present from early life
What it means	Something has changed. Medical emergency.	An ongoing condition
Where you go	Emergency department, today	Pediatric neurology, by appointment
Typical causes	Infection, ingestion, inflammation, tumor, stroke, injury	Genetic, structural, metabolic, cerebral palsy
First priority	Rule out the time-sensitive causes	Establish a diagnosis and build a support plan

The rest of this page follows that split.

Acute ataxia — a medical emergency

Acute ataxia means unsteadiness that developed over hours or days in a child who was previously fine. It is a recognized presentation to pediatric emergency departments, though an uncommon one — in a multicenter Italian study of 509 children with a mean age of 5.8 years, acute ataxia accounted for 0.021% of all emergency attendances.¹

Uncommon, but consequential. A systematic review pooled eleven studies covering 1,167 children and estimated the frequency of each cause using Bayesian methods.²

Cause	Expected value	95% credible interval
Postinfectious cerebellitis	38.0%	35.3–40.8%
Drug intoxication or poisoning	14.1%	12.1–16.1%
CNS infection or inflammation	8.1%	6.6–9.8%
Neoplasm (tumor)	7.3%	5.9–8.8%
Peripheral neuropathies, including Guillain-Barré	6.6%	5.3–8.1%

Together these accounted for 74.1% of cases.²

Read those numbers as a parent and the case for urgency writes itself. The most common cause is benign and self-limiting. But roughly one in seven children presenting this way has been poisoned or has taken medication, and roughly one in fourteen has a tumor — and in the Italian emergency-department series, tumors ran higher still at 11.2%.^1,2 There is no way to distinguish these at home, and two of them are time-sensitive.

Postinfectious cerebellitis — the most common, and still not a home diagnosis

Also called acute post-infectious cerebellar ataxia. It is an immune response following a viral illness, most typically in children under six. In one national center series it accounted for 50.5% of acute ataxia, within a group where 86.9% of cases were immune-associated.⁴

The reassuring part: most children recover completely in two to four weeks.⁵

The part that matters: this is a diagnosis of exclusion. It is what is left after the other things have been ruled out — not something to conclude at home because your child had a cold last week. The whole point of the emergency assessment is to arrive at this diagnosis safely rather than assume it.

Ingestion and poisoning — the one to declare immediately

At 14.1% of cases this is the second most common cause, and the one where your information changes everything.²

Young children explore by mouth and are efficient at finding things. Common culprits include sedating antihistamines, sleep medications, anticonvulsants, benzodiazepines, alcohol including hand sanitizer and mouthwash, and cannabis edibles, which look like candy.

What to do: say it out loud, early, and without embarrassment. Clinicians are not judging you; they are trying to narrow a differential fast. Bring every container from the house your child could conceivably have reached, including a grandparent’s pill organizer or a visitor’s handbag. Call Poison Control on 1-800-222-1222 on the way.¹³

Neoplasm — and the reason “wait and see” fails

Around one in fourteen children presenting with acute ataxia has a tumor.² Posterior fossa tumors sit near the cerebellum and can present with unsteadiness, often alongside early-morning headache, vomiting classically on waking, head tilt, or double vision.

This is not a reason to panic when your child is wobbly — most of the time it is not this. It is a complete answer to the question “can we see how they are in the morning?”

CNS infection and inflammation

Includes meningitis, encephalitis, acute cerebellitis and acute disseminated encephalomyelitis. Acute cerebellitis deserves separate mention: once used interchangeably with postinfectious ataxia, it has a distinctly worse course, shows abnormalities on brain MRI, and can lead to rapid posterior fossa swelling. Some of these children need urgent neurosurgical treatment, and structural cerebellar changes can still be visible on follow-up imaging.³ Fever, neck stiffness, altered consciousness or seizures alongside ataxia move this up the list sharply.

Guillain-Barré syndrome and its variants

Around 6.6% of cases.² Guillain-Barré typically causes ascending weakness, but the Miller Fisher variant presents with the triad of ataxia, absent reflexes and abnormal eye movements, and can look cerebellar at first glance. Loss of reflexes is the distinguishing exam finding, which is one reason a proper neurological examination matters.

Opsoclonus-myoclonus syndrome — rare, and a true emergency

Uncommon, but important enough to belong here. It presents with severe ataxia, opsoclonus — chaotic, darting eye movements, sometimes called dancing eyes — and sudden muscle jerks. It may be misdiagnosed as a benign postinfectious cause at first, and it is frequently paraneoplastic, often associated with neuroblastoma.¹⁴ The eye movements are the tell. If your child’s eyes are moving in a chaotic, rapid, non-rhythmic way, say so explicitly.

Stroke, head injury and episodic causes

Stroke occurs in children, is under-recognized and is often diagnosed late, partly because clinicians and parents do not expect it. Sudden ataxia with facial droop, one-sided weakness, speech difficulty or severe sudden headache warrants emergency assessment without delay.

Ataxia after a head injury — even a seemingly minor one, and even hours later — needs assessment. Post-traumatic ataxia can reflect concussion, but also bleeding or a posterior fossa injury.

Migraine variants and benign paroxysmal vertigo of childhood cause recurrent, self-limiting ataxia in some children. These are legitimate diagnoses, but ones a neurologist makes over time after other causes are excluded — not conclusions to reach during a first episode.

Red flags — what makes it more urgent

Any of these alongside unsteadiness means emergency department, now

Headache, especially with vomiting or on waking
Drowsiness, confusion or difficulty waking
Fever or neck stiffness
Weakness, numbness or facial droop
Difficulty speaking or swallowing
Chaotic, darting eye movements
Any possibility of ingestion — medication, alcohol, cannabis, anything
Recent head injury
A seizure
Rapid worsening over hours
A child who is unusually still, floppy, or not themselves
Loss of reflexes, if you have been told this

A study of 88 children found that headache, loss of consciousness and visual dysfunction appeared exclusively in the group with clinically urgent neurological pathology, and that hyporeflexia and dysmetria carried higher risk. Older age and longer symptom duration were also associated with the urgent group.⁶ That is useful to a clinician; it is not a filter for a parent. If it is new, it gets assessed.

What happens at the hospital

Knowing the sequence removes some of the fear.

History and examination, which do most of the work. Expect detailed questions about exactly when it started, how fast it developed, recent illness, medication access at home and anywhere your child has visited, head injury, and whether anything similar has happened before. The examination looks at gait, coordination, reflexes, eye movements and mental status.
Toxicology screening, where ingestion is possible. Standard panels do not catch everything, which is why the containers matter.
Neuroimaging, sometimes. Many causes are imaging-negative, including acute cerebellar ataxia itself. MRI is the ideal study and is better for posterior fossa tumors; CT is acceptable when the priority is quickly excluding a surgical emergency.⁵ Not every child needs a scan, and a clinician deciding against one is not necessarily cutting corners.

Chronic and progressive ataxia

Chronic ataxia has been present a long time and is relatively stable. Progressive ataxia worsens gradually over months or years. Both are managed rather than urgently investigated — with one absolute exception, below.

Category	Examples	Typical onset
Cerebral palsy	Ataxic cerebral palsy	Present from early life; recognized in infancy or toddlerhood
Inherited ataxias	Friedreich ataxia; ataxia-telangiectasia; spinocerebellar ataxias	Childhood to adolescence, varying by condition
Structural	Cerebellar malformations, including Joubert syndrome and Dandy-Walker	Present from birth
Metabolic	Mitochondrial conditions, including Leigh syndrome	Infancy to childhood
Episodic	Episodic ataxias; migraine variants	Childhood, in attacks
Acquired	After brain injury, tumor treatment or severe infection	Follows the causing event

Friedreich ataxia

The most common inherited ataxia. It is autosomal recessive, caused in most cases by a GAA trinucleotide repeat expansion in the frataxin gene, with a prevalence of roughly 1 in 40,000. Onset is before age 25, most typically around 10 to 15 years.⁸

It affects more than balance: the picture includes progressive gait ataxia with loss of proprioception and vibration sense, absent deep tendon reflexes, cerebellar dysarthria, scoliosis and hypertrophic cardiomyopathy.⁹ Earlier onset is associated with faster progression, and children are the most severely affected group.¹⁰

What has changed. Omaveloxolone (Skyclarys) is the first FDA-approved treatment for Friedreich ataxia, indicated for adults and adolescents aged 16 and older.¹¹ In its pivotal trial the difference from placebo at 48 weeks was −2.40 points on the modified Friedreich Ataxia Rating Scale in the pre-specified full analysis set, which excludes patients with severe pes cavus; across everyone randomized it was −1.93.¹¹ For younger children it is not approved, but a global phase 3 trial in children aged 2 to under 16 is under way.¹² If your child has Friedreich ataxia and is under 16, that is worth raising with your neurologist.

Ataxia-telangiectasia

A rare inherited condition combining progressive ataxia, usually appearing in toddlerhood as a child begins walking, with telangiectasias — small dilated blood vessels, often first seen in the whites of the eyes — immune deficiency with recurrent infections, and increased cancer risk. It matters to identify because the immune and cancer surveillance implications change management substantially.

Ataxic cerebral palsy

One of the recognized types of cerebral palsy, in which the dominant features are difficulty with balance and coordination rather than stiffness or involuntary movements. It is the least common subtype. Onset is by definition early and the picture is non-progressive, though function changes as a child grows.

Episodic ataxia

A group of genetic conditions causing recurrent attacks of ataxia lasting minutes to hours, often with normal function in between. Triggers can include stress, exertion, illness or caffeine. Some subtypes respond well to specific medication, which makes getting the diagnosis genuinely worthwhile rather than academic.

A change in an existing pattern is a new event

A child with known chronic ataxia who suddenly gets worse should be assessed as if this were acute ataxia. Do not attribute a sudden change to the existing condition. Children with chronic neurological conditions get infections, ingest things, sustain head injuries and develop new problems at least as often as anyone else — and are more likely to have those things attributed to their diagnosis and missed.

Getting a diagnosis for chronic ataxia

Expect a detailed developmental and family history; neurological examination; MRI of the brain, looking at cerebellar structure; blood tests including metabolic studies; and increasingly genetic testing — often a targeted ataxia panel first, sometimes exome or genome sequencing.

A cause is not always found, and that can be a legitimate outcome after appropriate investigation rather than a failure. Even without a name the functional picture can be described and supported, and genetic re-analysis some years later sometimes yields an answer that was not available at the time.

Our therapy guides cover what happens after a diagnosis, and the cost and insurance guides cover how families typically fund ongoing therapy.

Therapy and rehabilitation

Where ataxia is ongoing, the goal is function, safety and participation — not eliminating the ataxia.

Physical therapy carries most of the load: balance and postural control, gait training, core and proximal stability, strategies for safe transfers and falls, and equipment where it helps. Task-specific practice and intensity matter.
Occupational therapy for fine motor tasks, handwriting or typing alternatives, dressing and self-care, seating and positioning, and school adaptations. Weighting and stabilizing strategies are sometimes used to dampen tremor for specific tasks.
Speech-language therapy where speech is affected or where swallowing is involved. Swallowing safety deserves specific attention in progressive conditions.
Equipment and orthotics — walkers, wheelchairs for distance, adapted seating, bathroom equipment. Mobility equipment expands a child’s world rather than shrinking it; the framing that using a wheelchair is giving up costs children participation and independence.
Fatigue management. Coordination measurably worsens with fatigue, so a child who looks fine at nine in the morning and is falling at three is not being difficult. Pacing, rest scheduling and reducing unnecessary effort earlier in the day are genuine interventions.

A note on expectations. In non-progressive ataxia, function typically improves with therapy and growth. In progressive conditions, therapy focuses on maintaining function and adapting as things change — real work with real value, even when the underlying condition is advancing.

School, safety and daily life

At school, useful accommodations include extra time between classes or leaving early to avoid crowded corridors, a second set of books to avoid carrying, seating near the door and away from traffic, typing instead of handwriting, adapted PE rather than exclusion from it, a supervised place to eat if swallowing is affected, and permission to use an elevator. These belong in an IEP or 504 plan — our guide to IEPs and 504 plans covers how each is written, and our resources for teachers include material you can share with school staff.

At home, the highest-yield changes are unglamorous: remove loose rugs, add grab rails and non-slip surfaces in the bathroom, improve lighting on stairs and at night, use a shower seat, and use cups and cutlery designed for reduced coordination.

Socially and emotionally, ataxia is visible, and children notice. Falls in front of peers, being last, and being excluded from PE all carry a cost adults sometimes underestimate. Ask your child directly what bothers them — the answer is often not what you would assume, and it is frequently something fixable.

Frequently Asked Questions

My child suddenly became wobbly. What should I do?

Seek medical assessment today. Sudden-onset unsteadiness in a previously well child needs urgent investigation: across 1,167 children, causes included drug intoxication or poisoning in 14.1% and tumor in 7.3%.² Go to an emergency department if there is also headache, vomiting, drowsiness, fever, weakness, chaotic eye movements or any possibility of ingestion — and call Poison Control on 1-800-222-1222 if a substance may be involved.

What causes ataxia in children?

For acute ataxia, a systematic review of 1,167 children found the most common causes were postinfectious cerebellitis (38.0%), drug intoxication or poisoning (14.1%), CNS infection or inflammation (8.1%), neoplasm (7.3%) and peripheral neuropathies including Guillain-Barré syndrome (6.6%) — together 74.1% of cases.² Chronic causes include cerebral palsy, inherited ataxias such as Friedreich ataxia, structural differences in the cerebellum, and metabolic conditions.

How long does post-infectious cerebellar ataxia last in children?

Most children recover completely in two to four weeks.⁵ It is the most common cause of acute ataxia. But it is a diagnosis of exclusion — what remains after other causes have been ruled out, not something to assume at home because your child had a cold last week.

Could my child’s unsteadiness be a brain tumor?

Possible but not likely. Neoplasm accounted for 7.3% of acute ataxia cases across 1,167 children,² and the Italian emergency-department series put brain tumors second at 11.2%.¹ That is low enough not to panic and high enough that sudden ataxia is never watched at home. Posterior fossa tumors may present with unsteadiness alongside early-morning headache, vomiting on waking, head tilt or double vision.

Can medication cause ataxia in a child?

Yes. Some medications cause unsteadiness as a side effect, and accidental ingestion of adult medication is a leading cause of acute ataxia in young children at around 14% of cases.² Mention any possible access when seeking help, bring the containers, and call Poison Control on 1-800-222-1222.

What is opsoclonus-myoclonus syndrome?

A rare but urgent cause of ataxia featuring severe unsteadiness, chaotic darting eye movements sometimes called “dancing eyes”, and sudden muscle jerks. It may be misdiagnosed as a benign postinfectious cause at first, and it is frequently paraneoplastic, often associated with neuroblastoma.¹⁴ If your child’s eyes are moving chaotically, say so explicitly to the clinician.

Will my child need an MRI for ataxia?

Not necessarily. Many causes of acute ataxia are imaging-negative, including acute cerebellar ataxia itself. MRI is the ideal study and is better for posterior fossa tumors, but CT is acceptable when the priority is quickly excluding a surgical emergency.⁵ A clinician deciding against imaging on the basis of history and examination is not necessarily cutting corners.

Is ataxia the same as clumsiness?

No. Many children are clumsy, and developmental coordination disorder is common — it develops gradually and is present across a child’s history. Ataxia describes a specific pattern of impaired coordination and balance, and sudden onset is a medical emergency in a way that general clumsiness is not.

What is ataxic cerebral palsy?

One of the recognized types of cerebral palsy, in which the main features are difficulty with balance and coordination rather than stiffness or involuntary movements. It is the least common subtype, present from early life, and non-progressive — though function changes as a child grows.

Is there a treatment for Friedreich ataxia?

Yes, for older children and adults. Omaveloxolone (Skyclarys) is the first FDA-approved treatment, indicated for Friedreich’s ataxia in adults and adolescents aged 16 and older.¹¹ In its pivotal trial the difference from placebo at 48 weeks was −2.40 points on the modified Friedreich Ataxia Rating Scale in the pre-specified full analysis set, and −1.93 across everyone randomized.¹¹ For younger children it is not approved, but a global phase 3 trial in children aged 2 to under 16 is under way.¹² Worth raising with your neurologist.

Can a child have ataxia without it being an emergency?

Yes. Chronic ataxia that has been present a long time and is stable is not an emergency and is managed with therapy and support. The emergency is a change: ataxia that is new, or a sudden worsening in a child whose ataxia was previously steady. The distinction is how quickly it appeared, not how severe it looks.

My child has known ataxia and has suddenly gotten worse. Is that just the condition?

Treat it as a new emergency and get it assessed. Children with chronic neurological conditions get infections, ingest things and sustain head injuries as often as anyone else — and are more likely to have those events attributed to their existing diagnosis and missed.

Will therapy make my child’s ataxia go away?

Generally no, and that is not the goal. Therapy targets function, safety and participation. In non-progressive ataxia function usually improves with therapy and growth; in progressive conditions therapy maintains function and adapts as things change.

Why is my child’s balance worse in the afternoon?

Fatigue measurably worsens coordination. A child who is steady in the morning and falling by mid-afternoon is not being difficult. Pacing, scheduled rest and reducing effort earlier in the day are genuine interventions worth building into the school day.

Sources

Garone G, Reale A, Vanacore N, et al. Acute ataxia in paediatric emergency departments: a multicentre Italian study. Archives of Disease in Childhood. 2019;104(8):768–774. PMID 30948362. A retrospective review of children aged 1 to 18 attending 11 pediatric emergency departments over eight years. 509 patients, mean age 5.8 years, accounting for 0.021% of all emergency attendances. The most common cause was acute postinfectious cerebellar ataxia at 33.6%; brain tumors were second at 11.2%, followed by migraine-related disorders at 9%.
Etiologies of Acute Ataxia in Children: A Systematic Review of 1167 Subjects. Journal of Child Neurology. 2026. PMID 41325013. Eleven studies totalling 1,167 children, with expected values and 95% credible intervals estimated by Bayesian methods. Postinfectious cerebellitis 38.0% (35.3–40.8%); drug intoxication or poisoning 14.1% (12.1–16.1%); central nervous system infection or inflammation 8.1% (6.6–9.8%); neoplasm 7.3% (5.9–8.8%); peripheral neuropathies including Guillain-Barré syndrome 6.6% (5.3–8.1%) — together accounting for 74.1% of cases.
Acute cerebellitis in children: a variable clinical entity. Journal of Child Neurology. 2018;33(10):675–684. PMID 29888646. “Acute cerebellar ataxia is the most common cause of acute ataxia in children and it usually runs a self-limiting and ultimately benign clinical course. A small proportion of children have evidence of inflammatory swelling in the cerebellum. Many of these children suffer more severe and potentially life-threatening forms of cerebellar ataxia and may need more intensive treatments including urgent neurosurgical treatments... Many children with acute cerebellitis have long-term neurological sequela and evidence of structural cerebellar changes on follow-up imaging.”
Etiologies and clinical characteristics of acute ataxia in a single national children’s medical center. Brain and Development. 2024. PMID 38000948. 99 children, median onset 55 months. 86.9% had immune-associated acute ataxia, of which acute postinfectious cerebellar ataxia was the most common diagnosis at 50.5%, followed by CNS demyelinating disease at 18.2% and Guillain-Barré syndrome at 9.1%.
Acute Cerebellar Ataxia. StatPearls. Most children with postinfectious acute cerebellar ataxia recover completely, typically within two to four weeks. Many causes of acute ataxia are imaging-negative, including acute cerebellar ataxia itself; MRI is the ideal study and is better for posterior fossa tumors, while CT is acceptable where the priority is quickly excluding a surgical emergency.
Taşdelen A, et al. Evaluation of Acute Ataxia in the Pediatric Emergency Department: Etiologies and Red Flags. Pediatric Neurology. 2023. PMID 36462247. 88 children, median age 5; 37 (42%) had clinically urgent neurological pathology. In that group median age and symptom duration were significantly higher. Hyporeflexia or areflexia and dysmetria were associated with higher risk, and headache, loss of consciousness and visual dysfunction appeared exclusively in the urgent group.
National Institute of Neurological Disorders and Stroke. Ataxia. Background on ataxia as a sign rather than a diagnosis, and on the cerebellar and sensory pathways involved.
Friedreich Ataxia. GeneReviews. The most common inherited ataxia; autosomal recessive, in most cases a GAA trinucleotide repeat expansion in the frataxin (FXN) gene. Prevalence roughly 1 in 40,000. Onset before age 25, most typically between 10 and 15 years.
Friedreich Ataxia. NINDS. The clinical picture: progressive gait ataxia with loss of proprioception and vibration sense, absent deep tendon reflexes, cerebellar dysarthria, scoliosis and hypertrophic cardiomyopathy.
Patel M, et al. Progression of Friedreich ataxia by age of onset. Earlier onset is associated with faster progression, with children among the most severely affected.
Lynch DR, Chin MP, Delatycki MB, et al. Safety and Efficacy of Omaveloxolone in Friedreich Ataxia (MOXIe Study). Annals of Neurology. 2021;89(2):212–225. In the pre-specified full analysis set, mFARS change from baseline was −1.55 ± 0.69 on omaveloxolone against +0.85 ± 0.64 on placebo — a difference of −2.40 ± 0.96 (P = 0.014) at week 48. That set excludes patients with severe pes cavus; across the all-randomized population of 103 the difference was −1.93. The FDA label indicates SKYCLARYS (omaveloxolone) “for the treatment of Friedreich’s ataxia in adults and adolescents aged 16 years and older”, and states that safety and effectiveness have been established in pediatric patients aged 16 and older.
BRAVE: a study of omaveloxolone in children with Friedreich ataxia. ClinicalTrials.gov. A global phase 3 trial in children aged 2 to under 16, randomized against placebo. Worth raising with a neurologist for a child below the approved age.
Poison Help. Poison Control centers in the United States are reachable 24 hours a day on 1-800-222-1222.
Opsoclonus-myoclonus syndrome associated with neuroblastoma: insights into antitumor immunity. Pediatric Blood & Cancer. 2022;69(11):e29949. PMID 36094353. “Opsoclonus-myoclonus syndrome (OMS) is a rare neurological disorder. Half of these cases occur in children with neuroblastoma.”

Medical disclaimer. This page is for general educational purposes and does not constitute medical advice, diagnosis, or treatment. It is not a substitute for evaluation by a qualified clinician who knows your child. If your child has newly become unsteady, seek medical assessment today rather than waiting.