User:Crowen4/Akinetic mutism
Akinetic mutism is a medical term describing patients tending neither to move (akinesia) nor speak (mutism). Akinetic mutism was first described in 1941 by Cairns et al. as a mental state where patients lack the ability to move or speak[1] . However, their eyes may follow their observer or be diverted by sound[1] . Patients lack most motor functions such as speech, facial expressions, and gestures, but demonstrate apparent alertness[2]. They exhibit reduced activity and slowness, and speak in whispered monosyllables [1] [3]. Patients often show visual fixation on their examiner, move their eyes in response to an auditory stimulus, or move after often repeated commands[1] [2] . Patients with akinetic mutism are not paralyzed, but lack the will to move[1] . Many patients describe as soon as they ‘will’ or attempt a movement, a ‘counter-will’ or ‘resistance’ rises up to meet them[4] .
Description
Akinetic mutism varies across all patients; its form and clinical features correspond more closely to its functional anatomy rather than its pathology. However, akinetic mutism most often appears in two different forms: frontal and mesencephalic [2].
Frontal akinetic mutism
Hyperpathic akinetic mutism occurs in the frontal region of the brain and follows bilateral frontal damage. It occurs in patients with bilateral circulatory disturbances in the supply area of the anterior cerebral artery [2].
Mesencephalic akinetic mutism
Somnolent or apathetic akinetic mutism occurs in the mecencephalic region of the brain. It is characterized by vertical gaze palsy and ophthalmoplegia. Patients appear drowsy and lack motivation[2].
Causes
Akinetic mutism can be caused by a variety of things. It often occurs after brain injury or as a symptom of other diseases. Akinetic mutism occurs approximately four months after the appearance of symptoms[2] .
Frontal lobe damage
Akinetic mutism is often the result of severe frontal lobe injury in which the pattern of inhibitory control is one of increasing passivity and gradually decreasing speech and motion.
Ablation of cingulate gyrus
Another cause of both akinesia and mutism is ablation of the cingulate gyrus. Destruction of the cingulate gyrus has been used in the treatment of psychosis. Such lesions result in akinesia, mutism, apathy, and indifference to painful stimuli.[5] The Anterior cingulate cortex is thought to supply a "global energizing factor" that stimulates decision making.[6] When the Anterior cingulate cortex is damaged it will create akinetic mutism.
Other causes
- Another example of a cause of this disorder is an olfactory groove meningioma. It is also seen in the final stages of Creutzfeldt-Jakob Disease (a rare degenerative brain disease), and in acute cases of encephalitis lethargica. It can also occur in a stroke that affects both anterior cerebral artery territories. Another cause is neurotoxicity due to drugs such as Tacrolimus and Cyclosporine.
Other causes of akinetic mutism are as follows:
- Thalamic stroke [7]
- Respiratory arrest and Cerebral hypoxia [8]
- Encephalitis, meningitis, hydrocephalus, trauma, tumors, aneurysms [3]
- Cyst in third ventricle [1]
- Toxical lesions and infections of central nervous system [9]
- Delayed post-hypoxic leukoencephalopathy (DPHL) [8]
- Creutzfeldt-Jakob Disease (mesencephalic form) [2]
Treatments
Akinetic mutism can be misdiagnosed as depression, delirium, or locked-in syndrome, all of which are common following a stroke[3]. Patients with depression can experience apathy, slurring of speech, and body movements similar to akinetic mutism. Similarly to akinetic mutism, patients with locked-in syndrome experience paralysis and can only communicate with their eyes[3] . Correct diagnosis is important to ensure proper treatment. A variety of treatments for akinetic mutism have been documented, but treatments vary between patients and cases.
Magnesium sulfate
Treatments using intravenous magnesium sulfate have shown to reduce the symptoms of akinetic mutism. In one case, a 59 year old woman was administered intravenous magnesium sulfate in an attempt to resolve her akinetic mutism. The patient was given 500mg of magnesium every eight hours, and improvement was seen after 24 hours. She became more verbal and attentive, and treatment was increased to 1000mg every eight hours as conditions continued to improve [10]. Other treatments include amantadine, carbidopa-levodopa, donepezil, memantine, and oral magnesium oxide [8][10].
Cyst Puncture
As seen below in the case of Elsie Nicks, the puncture or removal of a cyst causing akinetic mutism can relieve symptoms almost immediately. However, if the cyst fills up again, the symptoms can reappear[1] .
Dopamine agonist therapy
Symptoms of akinetic mutism suggest a possible presynaptic deficit in the nigrostriatal pathway, which transmits dopamine. Some patients with akinetic mutism have shown to improve with levodopa or dopamine agonist therapy [11].
Cases
Elsie Nicks
14 year old Elsie Nicks was the first patient to be diagnosed with akinetic mutism by Cairns in 1941. She suffered from severe headaches her entire life and was eventually given morphia to help with treatment. She began to enter a state of akinetic mutism, experiencing apathy and loss of speech and motor control. A cyst on her right lateral ventricle was tapped, and as soon as the needle advanced toward the cyst, she let out a loud noise and was able to state her name, age, and address. After her cyst was emptied, she regained her alertness and intelligence, and she had no recollection of her time spent in the hospital. The cyst was drained 2 more times over the next seven months and was eventually removed. After 8 months of rehabilitation, Elsie no longer experienced headaches or akinetic mutism symptoms[1].
Telephone Effect
One study shows the results of the Telephone Effect. In this instance, a man with akinetic mutism was unable to speak and answer questions from his observer. If his observer stepped outside and called the man on the telephone, the man would pick up and answer any questions he was asked. If the observer returned to the room, the man was once again unable to answer any questions, returning to his state of mutism[8] .
OJ
54 year old patient, OJ, had a thalamic stroke causing frontal lobe dysfunction and somnolent akinetic mutism. He became drowsy, his speech was reduced to mutism, and experience behavioral changes such as apathy, slowness, lack of spontaneity, and disinhibition. Over the course of three months, his symptoms worsened until his verbal and motor movements were almost completely reduced. There is no mention of treatment for OJ[7] .
46 year old Man
One case describes a 46 year old male admitted to the hospital with fever and meningism. An MRI showed he suffered from a thalamic stroke. His eyes remained open, but he could not comprehend or follow instructions, perform voluntary movements, or feed himself. However, he showed unceasing grasping and unrestrainable manipulation of whatever object (such as clothes, chairs, tubes, etc.) that the examiner placed in his personal space. He did not respond to any pharmacological interventions such as dopamine, amantadine, and acetyl-choline-esterase inhibitors. This case also does not mention any successful treatments (carota) [12].
References
- ^ a b c d e f g h Cairns, H (1941). "AKINETIC MUTISM WITH AN EPIDERMOID CYST OF THE 3RD VENTRICLE". Brain. 64 (4): 273–290. doi:10.1093/brain/64.4.273.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b c d e f g Otto, Anke (1998). "Akinetic mutism as a classification criterion for the diagnosis of Creutzfeldt-Jakob Disease". Journal of Neurology, Neurosurgery, and Psychiatry. 64: 524–528. doi:10.1136/jnnp.64.4.524.
{{cite journal}}:|access-date=requires|url=(help); Check date values in:|accessdate=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b c d Nagaratnam, Nages (2004). "Akinetic mutism following stroke". Journal of Clinical Neuroscience. 11 (1): 25–30. doi:10.1016/j.jocn.2003.04.002.
{{cite journal}}:|access-date=requires|url=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Sacks, Oliver (1973). Awakenings. United States: Vintage Books. p. 7.
- ^ Fix JD. Neuroanatomy. 4th ed.
- ^ Struss DT et al.,2005, Multiple frontal systems controlling response speed, Neuropshichologia, 43: 396-417
- ^ a b Nagaratnam, Nages (1999). "Akinetic mutism and mixed transcortical aphasia following left thalamo-mesencephalic infarction". Journal of the Neurological Sciences. 163: 70–73.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b c d Yarns, Brandon (2013). "Telephone Effect in Akinetic Mutism From Traumatic Brain Injury". Psychosomatics: 1–2.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Kotchoubey, Boris (2003). "Event-related brain potentials in a patient with akinetic mutism". Clinical Neurophysiology. 33: 23–30. doi:10.1016/S0987-7053(03)00003-0.
{{cite journal}}:|access-date=requires|url=(help); Check date values in:|accessdate=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b Rozen, Todd (2012). "Rapid resolution of akinetic mutism in delayed post-hypoxic leukoencephalopathy with intravenous magnesium sulfate". Neurorehabilitation. 30 (4): 329–332. doi:10.3233/nre-2012-0763. PMID 22672948.
- ^ Yang, Chun-Pai (2007). "Diminution of basal ganglia dopaminergic function may play an important role in the generation of akinetic mutism in a patient with anterior cerebral arterial infarct". Clinical Neurology and Neurosurgery. 109: 602–606. doi:10.1016/j.clineuro.2007.04.012.
{{cite journal}}:|access-date=requires|url=(help); Check date values in:|accessdate=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Carota, Antonio (2013). "Akinetic mutism and utilization behavior after bilateral thalamo-polar artery stroke". Acta Neurol Belg. doi:10.1007/s13760-013-0213-7.
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