When Do Movement or Coordination Changes Call for a Huntington’s Disease Evaluation?

The phone call came on a Sunday. Maria’s brother had noticed that their father, 52 and never a fidgeter, kept shifting in his chair through the whole football game, fingers tapping a rhythm nobody else could hear. Two weeks earlier he had dropped a full pot of coffee. Their aunt had “gone strange” in her forties and spent her last years in a care home with a diagnosis no one could quite name.

That is the kind of moment that leads a family to ask whether a Huntington’s disease evaluation makes sense: not a dramatic collapse, but a slow accumulation of small changes, a nagging family story and a fear that feels disloyal to say aloud.

The question deserves a clear answer, and the evidence gives one. There are patterns neurologists take seriously, a process that is deliberately careful and a single blood test that can settle the matter. What follows explains each step and, just as importantly, what the results can and cannot tell you.

What a Huntington's disease evaluation actually involves

A Huntington’s disease evaluation is a structured visit, usually with a neurologist who specializes in movement disorders, that looks at three things at once: how you move, how you think and how your mood has changed. Huntington’s disease itself is an inherited condition in which nerve cells in deep brain regions called the basal ganglia gradually break down, and those three domains are where the damage shows first.

The visit opens with a conversation rather than a machine. Expect detailed questions about when the changes started, who noticed them, what medicines you take and, crucially, whether any relative has had unexplained movement problems, early dementia or psychiatric illness. Family trees in Huntington’s are often incomplete, so an adopted parent, an estranged grandfather or a relative who died young are all worth mentioning.

Next comes the neurological examination. The clinician watches you walk, turn, hold your arms out, tap your fingers and follow a moving target with your eyes. Many centers score these observations using the Unified Huntington’s Disease Rating Scale, a standardized checklist that lets the same person be compared with themselves months later. Brief tests of memory, attention and planning follow, along with screening questions about depression, irritability and anxiety.

Imaging and blood work fill in the picture. An MRI may show shrinkage of a basal ganglia structure called the caudate, but the Mayo Clinic notes that scans mainly help rule out other causes rather than confirm the diagnosis. Thyroid, copper and other blood tests exclude conditions that mimic Huntington’s. If the pattern fits, the team then discusses the one test that can confirm it: a genetic blood test for the HTT gene, covered later in this article.

What is the hallmark of Huntington's disease?

Ask a neurologist for the hallmark of Huntington’s disease and you will hear one word: chorea. The term comes from the Greek for “dance,” and it describes involuntary movements that flow unpredictably from one part of the body to another. Early on, chorea can pass for ordinary fidgeting: a shoulder shrug, fingers that drum the table, a foot that will not stay still. People often fold these movements into a deliberate gesture, scratching their head or adjusting their glasses, which is why relatives notice long before the person does.

As the condition progresses, the movements grow larger and harder to disguise. Facial grimacing, writhing of the arms and a lurching, unsteady walk are described by MedlinePlus and Mayo Clinic as typical of the middle stage. Chorea also affects the muscles of speech and swallowing, which is why a change in voice or coughing during meals sometimes belongs on the same list as a twitching hand.

Chorea is not the whole story, though. Huntington’s also produces dystonia, meaning sustained muscle contractions that twist a limb or the neck into an awkward posture, and, later, slowness and stiffness that can resemble Parkinson’s disease. In the juvenile form, which begins before age 20 in a minority of families according to MedlinePlus, rigidity and slowness often dominate and chorea may be minimal.

Clinically, then, chorea is the hallmark. Biologically, the hallmark is different: an expanded stretch of repeating DNA in the HTT gene, present from birth, decades before the first movement. Keeping those two definitions apart matters, because it explains how someone can carry the gene expansion and yet show no chorea for many years.

Early signs of Huntington's disease that are easy to miss

The earliest changes in Huntington’s rarely look like a neurological disease. Cleveland Clinic and Mayo Clinic both describe a period, sometimes lasting years, when subtle shifts in mood and thinking precede any visible movement. A meticulous accountant starts missing deadlines. A patient parent becomes short-tempered. Someone who always planned the family vacation now finds the logistics overwhelming. Because these changes are gradual, families often attribute them to stress, midlife or personality.

Motor changes begin quietly too: clumsiness that was never there before, dropped cups, a new habit of bumping doorframes, handwriting that has grown untidy. Eye movements are a favorite clue for neurologists; difficulty making quick, accurate jumps of gaze from one target to another is one of the earliest measurable signs, even when the limbs still move normally. Restlessness during quiet activities, such as watching television, is another pattern families describe in hindsight.

None of these observations diagnoses anything on its own. Clumsiness, irritability and poor concentration are common in depression, thyroid disease, sleep deprivation and several medication side effects. The point is not to run through a list and tally symptoms; it is to notice a pattern of change from your own baseline that persists over months and has no obvious explanation.

That pattern becomes far more meaningful when a parent or sibling has Huntington’s disease. In that setting, the NHS advises anyone noticing new movement, mood or thinking changes to discuss them with a doctor rather than wait for chorea to become obvious. Without a family history, the same changes still deserve a medical visit; the difference is that Huntington’s will sit further down the list of possibilities and other causes will be checked first.

Who is usually offered a Huntington's disease evaluation, and who is asked to wait

The clearest candidates are adults with new, persistent movement or coordination changes and a known family history. Huntington’s is inherited in an autosomal dominant pattern, meaning a single altered copy of the HTT gene is enough, and each child of an affected parent has a 50 percent chance of inheriting it, as MedlinePlus explains. In that context, a neurologist will usually proceed to a full evaluation without delay.

A second group has symptoms but no family history. This happens more often than people expect. A parent may have died before symptoms appeared, been misdiagnosed with another psychiatric or neurological condition, or not been the biological parent at all. A small number of cases arise when a parent carried a repeat length in the intermediate range that expanded on passing to the child. For these adults, unexplained chorea still warrants an evaluation; the team simply spends more time excluding other causes first.

A third group is at risk but has no symptoms. They may be offered predictive genetic testing, discussed in its own section below, after counseling. This is a choice, not a default, and many people decline.

Who is asked to wait? Children and teenagers without symptoms are generally not tested, because a result would remove their future right to decide for themselves and offers no medical action in the meantime. The exception is a young person with signs suggesting the juvenile form, where a diagnosis guides care now. Adults in the middle of a mental health crisis, a bereavement or a major life upheaval are often asked to pause predictive testing until support is in place. Anyone who has not yet met a genetic counselor is asked to do that first. Waiting, in this setting, is a form of protection rather than a barrier.

What test confirms Huntington's disease? The Huntington's disease genetic test explained

A single blood test confirms Huntington’s disease. It measures the length of a repeating DNA sequence, spelled CAG, inside the HTT gene on chromosome 4. Everyone has this repeat; what matters is how many times it occurs. According to MedlinePlus Genetics, the sequence normally repeats 10 to 35 times. A count of 36 to 39 is associated with reduced penetrance, meaning some people with these lengths develop symptoms and some do not, or do so very late in life. A count of 40 or more is fully penetrant: essentially everyone who lives long enough will develop the disease.

The intermediate range, 27 to 35 repeats, deserves its own explanation because it causes confusion. People in this range do not develop Huntington’s themselves. The repeat can, however, lengthen when passed to a child, particularly through the father, so a result here has implications for future generations even though it is not a diagnosis.

Longer repeats tend to produce earlier onset, which is part of why the juvenile form is usually linked to very large expansions. The correlation is loose, though. Two people with the same count can begin symptoms a decade apart, so the number cannot be used to predict when a person will become unwell.

The test is technically simple and highly accurate, but clinicians treat it carefully. In someone with symptoms and a matching family history, a positive result confirms the diagnosis. In someone with symptoms and no family history, it may be the first anyone knows of Huntington’s in that family, which changes the conversation for siblings and children. For that reason, most centers involve a genetic counselor, a professional trained to explain inherited conditions and their implications, before blood is drawn and again when results are delivered.

Predictive testing for Huntington's when you have no symptoms

Predictive testing means taking the HTT gene test before any symptoms appear, usually because a parent or sibling has been diagnosed. Unlike a diagnostic test, it does not answer “what is wrong with me” but “will this happen to me,” and that is a heavier question. The NHS describes a process built around genetic counseling over several appointments, with time between them to think, rather than a single visit and a phone call.

Those sessions cover more than biology. Counselors explore what a positive result would mean for your relationships, your work, your plans to have children and your mental health, and what a negative result might mean for a sibling who tested positive. Some centers include a psychological assessment, not as a gate but to make sure support is ready. The process is deliberately slow for one reason: a result, once known, cannot be unlearned.

You can stop at any stage, including after the blood has been taken. Results are given in person, and people are encouraged to bring someone with them. A negative result is not always simple either; guilt toward affected siblings is common enough that counselors raise it in advance.

Practical considerations deserve a frank word. In the United States, federal genetic nondiscrimination law protects against health insurance and employment discrimination based on genetic results, but that protection does not extend to life, disability or long-term care insurance, and counselors routinely discuss this. For people planning a family, options include prenatal testing during pregnancy and preimplantation genetic testing combined with IVF. Both are explained neutrally during counseling so that the decision remains yours, made at your own pace, with the option of choosing neither.

What else can look like Huntington's disease?

Chorea is not exclusive to Huntington’s, and a good Huntington’s disease evaluation spends real effort on alternatives. The most common mimic in adults is tardive dyskinesia, a pattern of involuntary facial and limb movements caused by long-term use of medicines that block dopamine, including many antipsychotics and some anti-nausea drugs. A careful medication history, including drugs stopped years ago, is therefore part of every visit.

Metabolic and autoimmune causes come next. An overactive thyroid can produce chorea. Wilson disease, a rare inherited disorder in which copper accumulates in the liver and brain, causes movement and psychiatric changes in young adults and is treatable, which is why copper studies are checked. Lupus and antiphospholipid syndrome occasionally present with chorea. Sydenham chorea follows streptococcal infection, mostly in children. Chorea can also appear with very high blood sugar, during pregnancy or after a stroke affecting the basal ganglia.

Then there are the genetic look-alikes, sometimes grouped as Huntington’s disease-like syndromes. Several inherited conditions, including some spinocerebellar ataxias and a disorder called Huntington disease-like 2, produce a similar triad of movement, cognitive and psychiatric change with a normal HTT result. When the picture fits Huntington’s but the gene test is negative, a neurologist will consider these and may order additional genetic panels.

Finally, ordinary conditions overlap with early symptoms. Essential tremor is rhythmic rather than flowing. Tic disorders involve repetitive, suppressible movements often preceded by an urge. Depression, anxiety, attention disorders and sleep deprivation can each produce the clumsiness, irritability and poor concentration described earlier. Sorting through this list is exactly why a specialist evaluation exists: the goal is not to find Huntington’s but to find the right explanation, whatever it turns out to be.

Diagnostic vs predictive testing: how the pathways compare

People often arrive believing “the Huntington’s test” is one thing. In practice, the same laboratory measurement sits inside two very different clinical pathways, and a third option, monitoring without testing, is legitimate too. The table below summarizes how they differ.

Pathway	Who it is for	Main goal	Typical steps	What a result changes
Diagnostic testing	Adults with movement, cognitive or psychiatric changes suggestive of Huntington’s	Explain current symptoms	Neurological exam, cognitive and mood screening, blood tests and MRI to exclude mimics, then HTT gene test	Confirms or excludes Huntington’s as the cause; opens symptom management and family counseling
Predictive testing	Adults at risk because of a diagnosed relative, with no symptoms	Learn future risk	Genetic counseling over several sessions, optional psychological assessment, reflection period, blood test, results in person	Clarifies whether symptoms will eventually develop; does not indicate when; informs life and family planning
Monitoring without testing	At-risk adults who prefer not to know their gene status	Notice early change while preserving the right not to know	Periodic neurological review, attention to mood and thinking, counseling available at any point	Testing can be revisited if symptoms emerge or preferences change

Two points stand out. First, the diagnostic pathway begins with the person’s symptoms and treats the gene test as confirmation, whereas the predictive pathway begins with the gene and treats symptoms as a future question. Second, neither pathway is faster or “better.” The NHS is explicit that predictive testing is a personal decision and that many at-risk people choose not to take it.

Monitoring without testing is sometimes overlooked. For someone at risk who does not want a definitive answer, a neurologist can still watch for change over time and offer support, without the HTT result ever entering the record. This option keeps the door open in both directions, and clinicians should present it as respectfully as the other two.

What the days and weeks after a Huntington's disease evaluation usually look like

The first evaluation rarely ends with an answer. More often, it ends with a plan: blood tests to collect, an MRI to schedule and a follow-up appointment, sometimes with a genetic counselor before the gene test is even ordered. Laboratory turnaround for the HTT test varies by center, and your team will tell you how long to expect rather than leaving you to guess.

Results appointments are usually done in person. If the result confirms Huntington’s, that visit typically covers what stage the condition appears to be in, which symptoms are causing the most trouble and which specialists to involve. Mayo Clinic describes a multidisciplinary approach that draws on neurology, psychiatry, physical and occupational therapy, speech and language therapy, dietetics and social work, and referrals to several of these often begin within the first weeks.

The emotional weeks matter as much as the clinical ones. Relief at finally having a name, grief for a future that looks different, anger, numbness and a strange clarity can arrive in any order, sometimes in the same afternoon. People who have been through this often say the diagnosis also reframed years of misunderstood behavior in a relative, which brings its own mix of sorrow and forgiveness.

Family conversations follow. A confirmed diagnosis means siblings and children are now known to be at risk, and deciding who to tell, when and how is something genetic counselors help with. Practical steps come gradually: a driving assessment if coordination is affected, a conversation with an employer about adjustments and, when the person is ready, discussion of advance care planning. None of this needs to happen in the first fortnight. A good team paces it to the person and makes clear that the plan belongs to the patient and family, not to the calendar.

How does Huntington's affect daily life?

Huntington’s is described as progressive because its effects widen over years, not months. MedlinePlus reports that people typically live about 15 to 20 years after signs and symptoms begin, and daily life changes in stages across that span. Early on, most people continue working, driving and running a household, though tasks that require juggling several things at once, such as managing finances or organizing a family schedule, become harder. Cleveland Clinic notes that difficulty with planning, prioritizing and flexible thinking is often more disabling in this phase than the movements themselves.

Mood and behavior shape relationships. Irritability, apathy and impulsivity are common and are caused by the disease, not by a failure of character, yet spouses and children frequently experience them as personal. Depression is frequent, and Mayo Clinic emphasizes that it stems from brain changes rather than simply from reacting to the diagnosis, which is why it is treated as a medical problem in its own right.

In the middle stage, chorea and coordination changes affect eating, dressing and walking. Swallowing difficulty raises the risk of choking and of food entering the lungs. Constant movement burns calories, and weight loss becomes a recurring concern; dietitians often recommend higher-calorie foods and adjusted textures. Falls increase, and occupational therapists suggest home changes, from removing loose rugs to installing grab bars.

Later, speech may become hard to understand and full-time care is usually needed. Communication tools, from simple yes-or-no boards to speech devices, help preserve connection. Throughout, the load on caregivers is heavy, and support for them, including respite, is part of good care rather than an optional extra. Daily life with Huntington’s is unquestionably altered, but it remains life, and much of a care team’s work is helping people keep doing what matters to them for as long as possible.

Can you delay Huntington's disease? What treatment can and cannot do

The honest answer is that no treatment has been proven to delay the onset or slow the progression of Huntington’s disease. NINDS and the NHS both state this plainly. Researchers are testing approaches that aim to lower production of the abnormal huntingtin protein, and clinical trials continue, but these remain experimental and should not be described as effective until evidence shows otherwise. Anyone offered an unproven therapy outside a registered trial should ask hard questions.

What treatment can do is manage symptoms, and that is not a small thing. For chorea, one class of medicine, the VMAT2 inhibitors, works by reducing the amount of dopamine released at nerve endings in the basal ganglia; less dopamine signaling means smaller involuntary movements. Certain antipsychotic medicines, which block dopamine receptors, are also used for chorea, particularly when irritability or psychosis coexist. Both classes can cause drowsiness, low mood, restlessness or Parkinson-like stiffness, so the prescribing clinician weighs benefit against risk and adjusts over time. Antidepressants and mood stabilizers address the psychiatric symptoms that so often affect quality of life more than movement does.

Non-drug treatment carries real weight. Physical therapy helps with balance and falls, occupational therapy adapts the home and daily tasks, and speech and language therapy addresses both communication and safe swallowing. Regular physical activity is encouraged by the NHS as generally beneficial for mobility and mood, though it does not alter the disease course.

Decisions about starting, changing or stopping any of these belong with the treating team, who can see the whole picture: which symptoms trouble the person most, what other medicines they take and how they respond over months. What patients and families can do is track what has changed since the last visit and bring that record along; in a condition where progress is measured in years, that diary is often the most useful instrument in the room.

What people often get wrong about Huntington's disease

The first misconception is that Huntington’s begins with chorea. In many people, mood or thinking changes arrive years earlier, so waiting for visible movements before seeking an evaluation can mean years of misattributed depression or “personality change.” The second is that it can skip a generation. It cannot; a child who does not inherit the expanded gene cannot pass it on. What looks like skipping is usually a parent who died before symptoms appeared, a reduced-penetrance repeat that never caused symptoms, or a diagnosis that was missed.

Third, people assume a positive gene test means they are ill now. It does not. Someone with 40 or more CAG repeats carries the genetic basis of the disease, but the diagnosis of Huntington’s disease is made when characteristic motor signs appear on examination. Years or decades can separate the two. Fourth, a negative result in one sibling says nothing about another; each child of an affected parent faces the same 50 percent chance independently.

Fifth, every twitch is not Huntington’s. Fidgeting, restless legs, eyelid flutter and tremor are common and usually benign. The pattern that concerns neurologists is new, persistent, flowing involuntary movement, often alongside cognitive or mood change, in someone whose baseline has shifted.

Sixth, Huntington’s is not only a movement disorder. Mayo Clinic frames it as a condition affecting movement, thinking and mood together, and the psychiatric and cognitive dimensions often matter more to daily function.

Seventh, some believe there is nothing to be done, so why be evaluated. Symptom management, safety planning, swallowing assessment and family counseling all change with a diagnosis, and trial eligibility depends on it too. Finally, the number of repeats is not a countdown clock. Longer repeats trend toward earlier onset across populations, but for an individual the count cannot forecast when symptoms will start, and clinicians avoid using it that way.

Questions to ask your care team

Walking into a Huntington’s disease evaluation with questions written down changes the visit. It slows the conversation, gives you something to hold and signals to the team where your worries actually lie. The list below is a starting point rather than a script; cross out what does not apply and add what keeps you awake at night.

• Based on today’s examination, how likely do you think Huntington’s is compared with other causes of my symptoms?
• Which other conditions are you ruling out, and which tests will do that?
• If you recommend the HTT gene test, will I meet a genetic counselor first, and how will results be given?
• If I test positive, does that mean I have the disease now, or that I will develop it later?
• What should I tell my siblings and children, and can you help me have that conversation?
• Which of my symptoms can be managed, and what are the trade-offs of the options you would consider?
• Who else will be part of my care, and how do I reach them between appointments?
• What changes should prompt me to call before my next scheduled visit?
• Is it safe for me to keep driving or doing my job, and how will we reassess that?
• Are there clinical trials I might be eligible for, and how would I learn more?

Two further habits help. Bring someone with you, because it is hard to absorb detail while processing emotion, and ask for a written summary of the visit. Some people also record the results conversation, with the clinician’s agreement, so they can listen again when the shock has passed.

If you are at risk but have no symptoms, the questions shift. Ask what predictive testing involves, how long the counseling process usually takes at that center, what support is available afterward whatever the result, and whether monitoring without testing is an option you can choose for now.

When to call your doctor

Most of Huntington’s unfolds slowly, and routine concerns can wait for the next scheduled visit. Some situations should not wait. Call your doctor promptly, or seek emergency care, in the following circumstances.

• Choking episodes, coughing or a wet-sounding voice during meals, or a fever with a new cough after choking, which can signal food or liquid entering the lungs.
• A fall with a head injury, loss of consciousness, new confusion or a limb that cannot bear weight.
• Thoughts of suicide or self-harm, in the person with Huntington’s or in a caregiver. Depression in this condition is common and treatable, and in the United States the 988 Suicide and Crisis Lifeline is available by call or text at any hour.
• A sudden, marked worsening of involuntary movements, stiffness, high fever or confusion after starting or changing a medicine.
• Rapid weight loss, inability to keep fluids down, very little urine or other signs of dehydration.
• Severe agitation, aggression or hallucinations that put anyone at risk.
• New symptoms in an at-risk family member that are causing distress, even if they seem minor.

For less urgent changes, a message or call to the care team is still worthwhile: a new tendency to drop things, more frequent stumbles, a change in sleep, a spouse’s observation that mood has shifted. Neurologists rely on this between-visit information, and noticing early means adjustments can be made sooner.

If you have not yet been evaluated and are noticing persistent, unexplained movement or coordination changes, especially with a family history of Huntington’s or of unexplained neurological or psychiatric illness, make an appointment with your primary care clinician and ask about referral to a neurologist. Persistent means weeks to months, not a bad afternoon. Whatever the outcome, the evaluation puts the decision where it belongs: with you and a team that has examined you, rather than with a search engine.

Frequently asked questions

What test confirms Huntington's disease?

A blood test that measures the number of CAG repeats in the HTT gene confirms Huntington’s disease. MedlinePlus Genetics describes 10 to 35 repeats as normal, 36 to 39 as reduced penetrance and 40 or more as fully penetrant. The test is highly accurate, but in someone without symptoms it indicates future risk rather than current disease, which is why genetic counseling accompanies it.

Can you delay Huntington's disease?

No treatment has been proven to delay the onset or slow the progression of Huntington’s disease, according to NINDS and the NHS. Research into therapies that lower the abnormal huntingtin protein is ongoing but remains experimental. Current care focuses on managing chorea, mood changes, swallowing problems and falls through medicines, physical and speech therapy and dietary support, with all decisions made by the treating team.

What is the hallmark of Huntington's disease?

Chorea, the involuntary flowing movement that gives the condition its old name of Huntington’s chorea, is the clinical hallmark. Genetically, the hallmark is an expansion of CAG repeats in the HTT gene, present from birth. Huntington’s also causes dystonia, slowness, cognitive decline and psychiatric changes, and in the juvenile form stiffness may dominate while chorea is minimal, as MedlinePlus notes.

How does Huntington's affect daily life?

Daily life changes gradually across the 15 to 20 years people typically live after symptoms begin, according to MedlinePlus. Early on, planning and multitasking become harder and mood may shift; later, chorea affects eating, dressing and walking, swallowing becomes unsafe and weight loss is common. Full-time care is usually needed in the late stage, and caregiver support is part of good management.

Can I have a Huntington's disease genetic test if I have no symptoms?

Yes, adults with an affected parent or sibling can request predictive testing, but it follows a counseling process rather than a single blood draw. The NHS describes several appointments with a genetic counselor, time to reflect and results given in person. You can stop at any stage, and many at-risk adults choose not to test or to be monitored instead.

What are the early signs of Huntington's disease?

Early Huntington’s often shows as gradual change from a person’s usual self rather than dramatic movement: new clumsiness, restlessness, untidy handwriting, irritability, apathy or trouble organizing tasks. Difficulty with quick eye movements is one of the earliest signs neurologists measure. Because these overlap with depression, thyroid disease and stress, persistent change over months, especially with a family history, is what warrants an evaluation.

Does Huntington's disease chorea always appear first?

No. Cleveland Clinic and Mayo Clinic both describe mood and thinking changes that can precede chorea by years, and in the juvenile form stiffness and slowness may appear instead of chorea. Waiting for obvious involuntary movements before seeking help can delay a Huntington’s disease evaluation, which is why unexplained cognitive or psychiatric change in someone with a family history deserves medical attention.

Can Huntington's disease skip a generation?

It cannot. Huntington’s is autosomal dominant, so a person who does not inherit the expanded HTT gene cannot pass it on, as MedlinePlus explains. Apparent skipping usually reflects a parent who died before symptoms appeared, a reduced-penetrance repeat length that never caused illness, or an earlier diagnosis that was missed or labeled as a different psychiatric or neurological condition.

What does an intermediate CAG repeat result mean?

An intermediate result, 27 to 35 repeats according to MedlinePlus Genetics, means you will not develop Huntington’s disease yourself. The repeat can lengthen when passed to a child, especially through the father, so the result carries implications for future generations. Genetic counselors explain what this means for family planning without it being a diagnosis for you.

Do I need a family history to be evaluated for Huntington's disease?

No. Unexplained chorea or a combination of new movement, cognitive and psychiatric change warrants an evaluation even without a known relative. Family history is often incomplete because of early parental death, misdiagnosis or unknown parentage, and occasionally an intermediate repeat expands into the disease range. Without a family history, the neurologist will simply spend more time excluding other causes before considering the gene test.

References

• MedlinePlus Genetics: Huntington disease
• NHS: Huntington's disease
• Cleveland Clinic: Huntington's disease
• NIH National Institute of Neurological Disorders and Stroke: Huntington's disease

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.