Approximately 6 million people in the United States (U.S.) live with some form of paraly. Paralysis is a medical condition experienced when an individual strength and control over a group of muscles in a part of the body. Moreover, paralysis might occur when signals transmitted between the brain and muscle through the nerve cells are blocked. The nerve cells are essential in ensuring the movement of muscles in the body. Locked-in syndrome is a form of paralysis. It is a neurological-related illness characterized by a patient’s inability to control voluntary muscles’ movement in all parts of the body. Despite the patient being conscious and able to control the eye’s movement, they are paralyzed and mute. Smith and Delargy (2005) categorize locked-in syndrome into three types: classic, incomplete, and complete. Individuals with the classic locked-in syndrome remain conscious, and the ability to move their eyes vertically. Patients with incomplete locked-in syndrome can partially move their arms, retain vertical eye movements, and make feeble sounds. The complete locked-in syndrome occurs when an individual is unable to move any muscles of the body. Therefore, this paper investigates the causes and effects of locked-in syndrome and recommends possible therapies.

Locked-in syndrome is a neurological disorder that occurs when the transmission of signals is inhibited between the brain and the muscles. The brain serves as a vital organ in enabling muscle movement. Kratochwil et al. (2017) point out the pons as a significant part of the brain that helps transfer nervous system signals between the various brain and spinal cord sections. The pons links the cerebral cortex with the medulla oblongata. It helps in communication and coordination in the brain—for example, the pons help relay sensory information and trigger sleep and arousal. The pontine nuclei make up about two-thirds of the human pons. The pontine nuclei comprise neurons that relay signals between the cerebral cortex and cerebellum—damaging the pons results in neurological-related issues such as the occurrence of locked-in syndrome.

The occurrence of locked-in syndrome is associated with various factors that damage the brain, especially the pons (Smith and Delargy, 2005). Common causes might include traumatic brain injury, tumors, demyelinating disorders, and stroke. Traumatic brain injuries trigger locked-in syndrome when the pons is damaged because of physical injuries on the head. Serious head injuries damage the connection between the medulla oblongata, cerebellum, and cerebrum, inhibiting the transfer of signals between the brain and muscles (Smith and Delargy, 2005). Therefore, individuals suffering from severe head injuries are susceptible to locked-in syndrome.

Locked-in syndrome is associated with the occurrence of demyelinating diseases. These diseases affect the transmission of signals from the brain through the nervous system. Kratochwil et al. (2017) identify myelin as a vital layer on the nerves that assist in the rapid movement of signals from the body to the rest of the body organs. However, demyelinating disorders damage the nerve’s protective layer, myelin sheaths (Kratochwil et al., 2017). The destruction of the nerve layer results in the formation of scar tissues on the nerve. Therefore, the transmission of signals between the brain and other muscles in the body is affected. Demyelinating disorders might lead to loss of vision, weak and stiff muscles, and sensory changes.

Locked-in syndrome is associated with the occurrence of stroke in the brain. This condition occurs when blood is blocked from reaching the brain leading to a limited supply of oxygen to the brain cells (Smith and Delargy, 2005). Inhibited supply of oxygen causes the brain cells to die, which results in cerebrovascular illnesses such as stroke. Head injuries and other underlying conditions might result in clogged or a ruptured artery, causing an ischemic or hemorrhagic stroke. Therefore, pontine stroke causes locked-in syndrome as the body experiences limited functioning of the brain.


LIS is caused by lesions that may affect the caudal ventral midbrain or ventral pons, while the cerebrum’s integrity remains uncompromised. The third cranial nerve nucleus lies ventromedial in the midbrain close to the cerebral aqueduct. Tracts project anteriorly, beginning from the nucleus to innervate eye muscles. The pupil’s reflexes, facilitated by parasympathetic traveling on the third cranial distally, may remain uncompromised/conserved in ischemia episodes (Das et al., 2020). Ventromedial midbrain lesions will affect this neve, causing complete LIS. Cranial nerves 4 and 6, which regulate the eyes’ abduction through lateral rectus muscles and the eye’s downward movement through superior oblique muscles, respectively, may be altered by lesions in the ventral pons.

The lesions that cause LIS may include masses, demyelinating disorders, infection traumas, and vascular lesions. Vascular complication presenting in the form of ischemic or hemorrhagic stroke is the most pertinent cause. Individuals exposed to this risk often have a history of hypertension (Das et al., 2020). Traumatic brain injury is the second most prominent cause of LIS. LIS from traumatic brain injuries has been reported from penetrating or blunt trauma, resulting in a thrombotic occlusion or tear of the vertebrobasilar artery. Most posttraumatic cases of LIS are characterized by direct physical damage.

Corticobulbar tracts that pass through the pons and midbrain contain upper motor neurons for the 5th, 7th, 9th, 10th, 11th, and 12th cranial nerves. The pontine respiratory group found in the pons tegmentum could be altered in sizable lesions resulting in respiratory distress and apnea signs. Such lesions do not damage the reticular activating system that lies dorsally and controls wakefulness. Therefore, this function remains uncompromised in persons having LIS.

The spinothalamic and corticospinal tracts mediate the truncal and limb sensory and motor functions. The two tracts travel through the ventral pons and the midbrain crus cerebri. Consequently, their function would be affected by any midbrain lesions. The basilar artery, which feeds from two vertebral arteries, supplies the ventral pons (Das et al., 2020). Any anomalies in these arteries can lead to the development of signs of LIS. However, the signs may differ from one case to another because of the causative agent’s nature, which complicated the diagnosis.

Conservation of Eye Movement

Although lateral and medial gaze palsies are common, LIS patients retain control of the upper eyelids and vertical eye movement. In LIS, the mid-brain tectum is spared, allowing patients to communicate using eye movements (Aziz, 2020). Apart from eye movement, hearing may be preserved with varying degrees of visual difficulties. 

In conclusion, locked-in syndrome is an impairing condition that results in significant loss of functioning. The primary treatment method involves the reversal or removal of the causative agent. Initial acute management should focus on securing patients’ airways for adequate oxygen saturation and stabilizing cardiac stability and blood pressure. Care is then directed at addressing the precipitating agent. In the event of a hemorrhagic or ischemic stroke, sift stroke protocol should be employed. Das et al. (2020) assert that prompt thrombolytic therapy may expedite recovery in cases related to ischemia. Removal of precipitating masses should be initiated in mass lesions and tumors. LIS treatment from central myelinolysis focuses on the provision of supportive measures. Close monitoring of respiratory status and gradual sodium abnormalities correction is imperative. Inflammatory neuropathies may also be treated similarly.


Aziz, M., 2020. Locked-in-Syndrome (aka. pseudocoma). Available at: https://houstonmedicalclerkship.com/wp-content/uploads/2020/10/Locked-in-syndrome-presentation.pdf [Accessed 24 March 2021]

Cleveland Clinic, 2021. Paralysis [Online] Available at:  <https://my.clevelandclinic.org/health/diseases/15345-paralysis> [Accessed 24 March 2021].

Das, J.M., Anosike, K. and Asuncion, R.M.D., 2020. Locked-in Syndrome. StatPearls

Kratochwil, C. F., Maheshwari, U., & Rijli, F. M., 2017. The long journey of pontine nuclei neurons: From Rhombic Lip to Cortico-Ponto-Cerebellar Circuitry. Frontiers In Neural Circuits [online] 11, 33. <Available at https://doi.org/10.3389/fncir.2017.00033> [24 March 2021]

Smith, E. and Delargy, M., 2005. Locked-in syndrome.’ BMJ [online], 330(7488), pp.406-409. Available at < https://sci-hub.do/10.1136/bmj.330.7488.406> [24 March 2021]

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