Locked-In syndrome

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Locked-In syndrome is a condition in which a patient is aware and awake, but cannot move or communicate due to complete paralysis of nearly all voluntary muscles in the body. It is the result of a brain stem lesion in which the ventral part of the pons is damaged. It results in quadriplegia and inability to speak in otherwise cognitively intact individuals. Those with Locked-In syndrome may be able to communicate with others by coding messages by blinking or moving their eyes, which are often not affected by the paralysis.

Locked-in syndrome is also known as Cerebromedullospinal Disconnection, De-Efferented State, Pseudocoma, and ventral pontine syndrome. Unlike persistent vegetative state, in which the upper portions of the brain are damaged and the lower portions are spared, locked-in syndrome is caused by damage to specific portions of the lower brain and brainstem with no damage to the upper brain.

Patients who have Locked-In Syndrome are conscious and aware with no loss of cognitive function. They retain proprioception and sensation throughout their body. Some patients may have the ability to move certain facial muscles, most often some or all of the extraocular eye muscles. The majority of locked-in syndrome patients do not regain motor control, but devices are available to help patients communicate.

Parisian journalist Jean-Dominique Bauby had a stroke in 1995, and when he awoke 20 days later he found that his body had all but stopped working: he could only control his left eyelid. By blinking his eye he dictated a letter at a time and in this way he wrote The Diving Bell and the Butterfly.

1 Causes
2 Treatment
3 Long Term Recovery
4 References

[edit] Causes

Locked-In syndrome may result for a number of reasons, including:

Traumatic brain injury
Diseases of the circulatory system
Medication overdose
Damage to nerve cells, particularly destruction of the myelin sheath, caused by disease.

[edit] Treatment

There is no standard treatment for Locked-In syndrome, nor is there a cure. Stimulation of muscle reflexes with electrodes (Neuromuscular stimulation) has been known to help patients regain some muscle function. Other courses of treatment are often symptomatic. New direct brain interface mechanisms may provide future remedies.