The locked-in syndrome (pseudocoma) describes patients who are awake and conscious but selectively deefferented, i.e., have no means of producing speech, limb or facial movements. People with such brainstem lesions often remain comatose for some days or weeks, needing artificial respiration and then gradually wake up, but remaining paralyzed and voiceless, superficially resembling patients in a vegetative state or akinetic mutism. In acute locked-in syndrome (LIS), eye-coded communication and evaluation of cognitive and emotional functioning is very limited because vigilance is fluctuating and eye movements may be inconsistent, very small, and easily exhausted.
Those with locked-in syndrome may be able to communicate with others through coded messages by blinking or moving their eyes, which are often not affected by the paralysis. The symptoms are similar to those of sleep paralysis. Patients who have locked-in syndrome are conscious and aware, with no loss of cognitive function. They can sometimes retain proprioception and sensation throughout their bodies. Some patients may have the ability to move certain facial muscles, and most often some or all of the extra-ocular eye muscles.
Causes Of locked-in syndrome
Possible causes of locked-in syndrome include:
- Snakebite cases – More frequently from a krait bite and other neurotoxic venoms, as they cannot, usually, cross the blood–brain barrier
- Amyotrophic lateral sclerosis (aka Lou Gehrig’s disease)
- Brainstem stroke
- Diseases of the circulatory system
- Medication overdose [examples needed], or central pontine myelinolysis secondary to rapid correction of hyponatremia
- Multiple sclerosis
- Damage to nerve cells, particularly destruction of the myelin sheath, caused by disease or central pontine myelinolysis secondary to rapid correction of hyponatremia
- A stroke or brain hemorrhage, usually of the basilar artery
- Traumatic brain injury
Curare poisoning mimics a total locked-in syndrome by causing paralysis of all voluntarily controlled skeletal muscles. The respiratory muscles are also paralyzed, but the victim can be kept alive by artificial respiration, such as mouth-to-mouth resuscitation. In a study of 29 army volunteers who were paralyzed with curare, artificial respiration managed to keep an oxygen saturation of always above 85%, a level at which there is no evidence of altered state of consciousness. Spontaneous breathing is resumed after the end of the duration of action of curare, which is generally between 30 minutes and eight hours, depending on the variant of the toxin and dosage.
Neither a standard treatment nor a cure is available. Stimulation of muscle reflexes with electrodes (NMES) has been known to help patients regain some muscle function. Other courses of treatment are often symptomatic. Assistive computer interface technologies, such as Dasher, or OptiKey, combined with eye tracking, may be used to help patients communicate.