When double vision is not a squint: thyroid eye disease and orbital fractures

Two people describe the same symptom to me in the same week. A woman in her fifties says her eyes have started crossing. A man in his thirties says he sees two of everything when he looks up, ever since he took an elbow to the face at football. Both of them use the word squint, and both have been told by someone that it is probably nothing.

They do not have the same problem. One has a muscle that has become stiff, the other has a muscle that is physically trapped, and neither is the condition most people picture when they hear the word squint. That word belongs mostly to childhood, and it describes something quite different.

What is the difference between a squint and double vision?

A squint is a description of where the eyes point. Double vision is a description of what you see. They overlap, but they are not the same thing, and the difference matters more than it sounds.

In childhood squint, the eye muscles usually work perfectly well. The problem is one of aiming and control: the two eyes are not directed at the same point, so the brain receives two slightly different pictures. A young brain solves this by quietly ignoring one of them, which is why many children with a visible squint do not complain of seeing double at all. That suppression is also the reason a childhood squint needs attention early, because the ignored eye can fail to develop properly. My colleague Dr Chan Li Yen, who is a paediatric ophthalmologist, writes about how to spot that drift in a child, and if you are here about a child rather than yourself, hers is the more useful piece.

An adult brain cannot do that trick. When the eyes stop working as a pair in adulthood, you see two images, and you notice immediately. So new double vision in an adult is almost never the childhood condition arriving late. It is usually something mechanical.

Why would an eye get stuck?

Because the eye sits inside a closed bony box with very little spare room, and anything that swells or traps its contents restricts how it can move. The eye is turned by six small muscles, each a strap running from the back of the socket to the surface of the eyeball. Those straps work by contracting to pull the eye one way while the opposite muscle relaxes and lengthens to allow it. That second half is the part people forget. An eye cannot look up unless the muscle underneath it is willing to stretch.

So when a muscle becomes stiff, or scarred, or physically caught on something, the eye stops travelling in the direction away from that muscle. Doctors call this a restrictive pattern, and it produces a very particular kind of double vision: one that changes depending on which way you look. That is the single most useful clue you can bring me, and it is one you can notice yourself before you ever reach a clinic.

How does thyroid eye disease cause double vision?

By inflaming the eye muscles until they thicken and then scar, which leaves them short and stiff rather than weak. In thyroid eye disease the immune system targets the tissues inside the socket, and the muscles are among the first things affected. They swell during the active phase and, if the inflammation runs long enough, some of that swelling is replaced by fibrous tissue that does not stretch again.

The muscle most often involved is the inferior rectus, the one that sits underneath the eye and pulls it down. When that muscle will not lengthen, the eye cannot rotate upward properly, so the double vision is at its worst looking up and often disappears looking down. Patients tell me they are fine reading and terrible on an escalator. The medial rectus, on the inner side, is the next most commonly affected, which makes looking outward difficult.

Not everyone with thyroid eye disease develops this. Most do not. But it is common enough that any adult with new double vision gets their thyroid considered, and any patient of mine with thyroid eye disease gets their eye movements measured at every visit, so that a change is caught as a change rather than discovered late. This is the part of the condition I have spent the most time on: during my fellowship I worked on a fourteen year review of patients treated with a steroid sparing drug for exactly this problem, looking at whether we could control the inflammation while bringing steroid doses down.

What happens when the socket is fractured?

A blow to the eye can crack the thin bone of the socket floor, and tissue from inside the orbit can drop through the crack and become trapped. The floor of the eye socket is roughly as thick as a fingernail in places, and it sits directly above the sinus. When something strikes the eye hard, that thin bone can give way, which actually protects the eyeball itself. The problem is what follows.

Fat, and sometimes a portion of the inferior rectus muscle, can herniate down into the space below and catch there. The eye is then tethered. Looking up becomes restricted, painful, or impossible, and the double vision is worst in exactly that direction. In younger patients the bone is springier and can snap back like a trapdoor, closing on the tissue and gripping it firmly. That version deserves particular respect, because a tightly trapped muscle can trigger nausea and a slowing of the pulse, and it should be assessed the same day rather than left to settle.

Not every orbital fracture needs an operation. Many settle as the bruising resolves and the double vision fades with it. The decision rests on whether tissue is genuinely trapped, how much the eye has sunk back, and whether the movement is recovering on its own over the first week or two. I have written more broadly about what happens inside the orbit and why that compartment behaves the way it does.

How do you work out which one it is?

By measuring the misalignment in different directions of gaze, and then by testing whether the eye is truly stuck rather than simply weak. The first part is straightforward. If the misalignment is much the same wherever you look, the pattern points toward a problem of control, which is the childhood type. If it changes markedly with direction, and there is one direction the eye plainly will not travel, that points to a mechanical restriction.

The second part is a test where the eye is gently moved with an instrument after numbing drops, to feel whether it will rotate passively. A muscle that is merely weak will still allow the eye to be moved. A muscle that is scarred or trapped will not, and you can feel the difference. Alongside that we look at the lids and the position of the eye, ask about thyroid symptoms and any injury, and image the socket when the story or the examination calls for it.

The reason I go through all of this rather than reaching for a scan first is that a scan shows anatomy, not function. A fracture on a scan does not prove the muscle is trapped, and a normal looking muscle can still be stiff. The examination decides, and the scan supports it.

What can be done about it?

Quite a lot, but the timing is as important as the technique. For thyroid eye disease, surgery to realign the eyes is normally deferred until the inflammation has been settled for several months, because operating while the tissues are still changing gives a result that will not hold. That waiting period is difficult for patients, and it is worth saying plainly that it is not neglect. While waiting, prisms fitted to glasses can help some people, particularly when the misalignment is modest and steady, though they work less well when the deviation shifts a great deal between directions of gaze.

When the time is right, the operation usually involves releasing or repositioning the stiff muscle so the eye can travel again. The honest part of that conversation is that a scarred muscle is less predictable than a healthy one, and more than one procedure is sometimes needed to get comfortable single vision in the positions that matter most, which are straight ahead and reading. If a fracture has trapped tissue, the repair is different in nature: the tissue is freed and the floor is supported so it cannot drop again.

Where thyroid eye disease is the cause, the eye surgery is only one part. It sits within a sequence that starts with settling the inflammation, alongside your endocrinologist managing the gland itself, and the surgical steps follow a fixed order for reasons I explain in the orbit and thyroid section.

When should I get double vision looked at?

Whenever it is new. That is the short answer, and I would rather see someone whose double vision turns out to be a minor and settling problem than miss the person whose is not. Cover one eye. If the doubling disappears when either eye is covered, the two eyes are not working as a pair, and that deserves assessment.

Some presentations should not wait for a routine appointment: double vision that arrives suddenly, particularly with a headache, a drooping lid or a pupil that has changed size, and double vision after a blow to the face where looking up makes you feel sick. Those belong in an emergency eye service today. Everything else belongs in a proper assessment soon, with someone who will measure it rather than glance at it. If your concern is a child rather than an adult, the route is different again and starts with a paediatric ophthalmologist, and the eyelid side of childhood eye problems is something I cover separately in my piece on droopy eyelids in children. And if what actually prompted this search was that your eyes simply look tired or changed, the causes are broader than this article, and I have mapped them in what actually makes eyes look tired.