Overview 

Locked-In Syndrome (LIS) is a rare and devastating neurological condition where a person loses almost all voluntary movement but remains fully conscious and aware. People with LIS typically experience paralysis of all four limbs (quadriplegia) and are unable to speak  (mutism or anarthria), yet they can usually move their eyes up and down and blink. This condition usually results from damage to the ventral pons, the front part of the brainstem that carries signals from the brain to the body. While the motor pathways are affected, the areas that control alertness and vertical eye movement remain intact.¹

In the past, LIS was most often linked to a blood clot at the base of the brain (basilar artery thrombosis), head injuries, or diseases that damage the protective covering of nerves  (demyelinating disease).  (damage to nerve fibre coverings). However, an increasing number of cases are now caused by medical interventions—so-called iatrogenic causes. These can include complications from anaesthesia, surgery on the brain or spine, radiation treatment, or certain medications. Recognising these risks early is important because many of these complications can be prevented, and prompt action can reduce long-term disability or even save lives.¹

Anaesthesia and locked-in syndrome

Anaesthesia can sometimes lead to complications that increase the risk of locked-in syndrome, mostly when oxygen levels in the body drop too low (hypoxia) or blood pressure falls too much (hypotension). During general anaesthesia, problems such as difficulty inserting a breathing tube (failed intubation), unnoticed pauses in breathing ( apnea), or slow and shallow breathing (hypoventilation) can reduce oxygen supply to the brain. While these events usually affect the outer layers of the brain, the brainstem—especially the pons—can be vulnerable, which may result in LIS.² 

Another possible risk comes from spinal or epidural anaesthesia spreading higher than intended, affecting the brainstem. This can temporarily cause paralysis and breathing difficulties, sometimes mimicking LIS.³ The real concern is delayed recognition, particularly when patients receive medications that temporarily paralyse muscles.

In some cases, patients may experience a “pseudo-locked-in syndrome” (Pseudo-LIS) where they are fully aware but cannot move or speak due to sedation or residual paralysis. This is not true LIS, but it can be frightening and is sometimes mistaken for coma or brain death if careful neurological assessments are not performed.⁴ 

Neurosurgical and spine-related iatrogenic causes

Surgery near the back of the skull or brainstem carries a higher risk of damaging important nerve pathways. Removing lesions such as cavernomas (clusters of abnormal blood vessels), gliomas (brain tissue tumours), or hemangioblastomas (blood vessel tumours) from the pons can accidentally disrupt the pathways that control movement, potentially causing locked-in syndrome. Unfortunately, these outcomes are often permanent, even with careful surgical technique and monitoring.

Neck (cervical spine) surgeries, especially those that fuse or decompress vertebrae near key arteries, can also accidentally damage or block blood flow. These arteries supply the base of the brain, and any injury can reduce blood flow to the pons, increasing the risk of brainstem injury. Even keeping the neck in a poor position during long surgeries may reduce blood supply, making brainstem infarcts more likely.

Rarely, postoperative complications such as bleeding, swelling, or brain tissue shifting (herniation) can press on the brainstem. This is most common after posterior fossa decompression surgery and, if not addressed quickly, can lead to LIS.

Cardiovascular and Endovascular Interventions

An increasing number of locked-in syndrome cases result from heart and large blood vessel procedures. Heart surgeries that use cardiopulmonary bypass —a machine that temporarily takes over the heart and lungs—carry a higher risk of strokes caused by blood clots. Although most strokes affect the main part of the brain, clots can sometimes travel to the posterior circulation, blocking the basilar artery and directly causing LIS.

Other procedures, such as cardiac catheterisation (inserting a thin tube into the heart), carotid stenting(placing a mesh tube in a neck artery), or cerebral angiography (imaging brain blood vessels), can also lead to complications. Air bubbles or clots may block the vertebral arteries, and even small injuries to the artery walls from catheters can cause delayed ischemia (lack of blood flow) that may trigger LIS.⁵

Extracorporeal membrane oxygenation (ECMO), a life-saving support for critically ill patients, also carries risks. It requires blood thinning and large-vessel tube insertion, which can increase the chance of clots. In patients who are heavily sedated or paralysed, LIS may go unnoticed for hours or days unless doctors perform careful neurological checks during planned sedation breaks.

Radiation and device-induced brainstem injury 

Radiation therapy for tumours in the brainstem, cerebellum, or posterior fossa can sometimes cause delayed injury to neural tissue. Although immediate side effects are uncommon, chronic complications such as radiation necrosis—gradual death of brain tissue—may develop months or even years later. If the ventral pons is affected, this damage can lead to locked-in syndrome. These delayed effects can complicate diagnosis because they may mimic tumour recurrence or progression.⁷

In rare instances, locked-in syndrome has occurred due to the misplacement of medical devices. Central lines(tubes inserted into large veins for medication or monitoring) or embolisation coils (tiny coils used to block blood vessels) can accidentally obstruct vertebral arteries. Although these mechanical causes are extremely uncommon, they highlight the critical need for imaging confirmation and precise technique in any procedure involving the neck or upper chest.⁸

Drug-induced locked-in states

Although very rare, some drugs or toxins can create symptoms that resemble locked-in syndrome. For example, botulinum toxin poisoning causes paralysis while leaving awareness intact. Similarly, overdoses of muscle relaxants or sedatives can temporarily mimic the condition, but patients usually recover once the drugs wear off. In a few reported cases,  local anaesthetic toxicity (especially with bupivacaine) has led to short-lived episodes that look like locked-in syndrome during resuscitation.

Chemotherapy agents such as vincristine can lead to peripheral and central neurotoxicity (nerve damage outside or within the brain and spinal cord). Though rare, cases of brainstem toxicity from such drugs have produced LIS-like symptoms.

It is crucial to distinguish these drug-related effects from true structural brainstem injury, because treatment and long-term outlook are very different.

Diagnosis and recognition in iatrogenic settings 

Scans such as MRI or CT are used to look for damage in the brainstem, which is usually the cause of locked-in syndrome. Brain activity tests (EEG) often show normal function, which helps doctors rule out conditions like coma or vegetative states. In some cases, muscle and nerve tests (EMG and nerve conduction studies) are also done to check whether the symptoms are due to problems with the nerves and muscles, such as Guillain-Barré syndrome, rather than the brain.

When LIS is confirmed, prognosis depends on the underlying cause and the speed of recognition. Some cases caused by reversible ischaemia or transient embolic events may see partial recovery. However, outcomes due to surgical trauma or permanent infarction are often chronic, with limited improvement.⁹

FAQs

Can someone with locked-in syndrome think and feel normally?

Yes. People with locked-in syndrome are fully aware and can think, feel, and understand everything around them. The main challenge is that they cannot move or speak, making communication very difficult.

Is locked-in syndrome permanent?

It depends on the cause. In some cases, especially if the damage is limited, people may regain small amounts of movement over time. Others may remain locked-in for the rest of their lives.

How do people with locked-in syndrome communicate?

Most commonly through eye movements, such as blinking or looking in a certain direction. With technology, such as eye-tracking devices and brain–computer interfaces, many people can communicate more effectively.

What support do families need?

Caring for someone with locked-in syndrome is emotionally and physically demanding. Families often benefit from counselling, respite care, and support groups to help them cope and stay connected.

What is the life expectancy for someone with locked-in syndrome?

Life expectancy varies. Some people die shortly after the event that caused the syndrome, while others may live for many years with the right medical care, rehabilitation, and support.

Summary

Locked-in syndrome is a rare and severe condition where a person is fully conscious but unable to move or speak. It usually happens after damage to the brainstem, often from a stroke. Although the body is paralysed, the mind remains active, and eye movements are often the only way to communicate.

Treatment focuses on keeping the person stable, helping them communicate, and supporting their long-term care needs. While the outlook can be very difficult, especially in the early stages, some people do experience small improvements over time. Rehabilitation, technology, and emotional support all play an important role in improving the quality of life for patients and their families.