Akinetic mutismis amedicalcondition wherepatientstend neither to move (akinesia) nor speak (mutism). It is the most extremedisorder of diminished motivation.Akinetic mutism was first described in 1941 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 can speak in whisperedmonosyllables.[1][3]Patients often show visual fixation on their examiner, move their eyes in response to anauditorystimulus, or move after often repeated commands.[1][2]Patients with akinetic mutism are notparalyzed,but lack thewillto move.[1]Many patients describe that as soon as they "will" or attempt a movement, a "counter-will" or "resistance" rises up to meet them.[4]
| Akinetic mutism | |
|---|---|
| Specialty | Neurology,Psychiatry |
Types
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Akinetic mutism varies across all patients. Its form, intensity, and clinical features correspond more closely to its functional anatomy rather than to its pathology. However, akinetic mutism most often appears in two different forms: frontal and mesencephalic.[2]
Frontal akinetic mutism
editAkinetic mutism can occur in the frontal region of the brain and occurs because of bilateralfrontal lobedamage. Akinetic mutism as a result of frontal lobe damage is clinically characterized ashyperpathic.[5]It occurs in patients with bilateral circulatory disturbances in the supply area of theanterior cerebral artery.[2]
Mesencephalic akinetic mutism
editAkinetic mutism can also occur as a result of damage to themesencephalicregion of the brain. Mesencephalic akinetic mutism is clinically categorized assomnolentorapatheticakinetic mutism.[5]It is characterized byvertical gaze palsyandophthalmoplegia.This state of akinetic mutism varies in intensity, but it is distinguished by drowsiness, lack of motivation, hyper-somnolence, and reduction in spontaneous verbal and motor actions.[2][5]
Symptoms and signs
editCauses
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Akinetic mutism can be caused by a variety of things. It often occurs after brain injury or as a symptom of other diseases.
Frontal lobe damage
editAkinetic mutism is often the result of severefrontal lobeinjury in which the pattern of inhibitory control is one of increasing passivity and gradually decreasing speech and motion.[citation needed]
Thalamic stroke
editMany cases of akinetic mutism occur after a thalamic stroke.[3]Thethalamushelps regulate consciousness and alertness.[citation needed]
Ablation of cingulate gyrus
editAnother cause of both akinesia and mutism isablationof thecingulate gyrus.Destruction of the cingulate gyrus has been used in the treatment ofpsychosis.Such lesions result in akinesia, mutism,apathy,and indifference to painful stimuli.[7]Theanterior cingulate cortexis thought to supply a "global energizing factor" that stimulates decision making.[8]When the anterior cingulate cortex is damaged, it can result in akinetic mutism.[citation needed]
Other
editAkinetic mutism is a symptom during the final stages ofCreutzfeldt–Jakob disease(a rare degenerativebraindisease) and can help diagnose patients with this disease.[2][9]It can also occur in a stroke that affects bothanterior cerebral arteryterritories.[citation needed]Another cause isneurotoxicitydue to exposure to certain drugs such astacrolimusandcyclosporine.
Other causes of akinetic mutism are as follows:
- Respiratory arrestandcerebral hypoxia[6]
- Acute cases ofencephalitis lethargica[3]
- Meningitis[3]
- Hydrocephalus[3]
- Trauma[3]
- Tumors[3]
- Aneurysms[3]
- Olfactory groovemeningioma
- Cyst in third ventricle[1]
- Toxical lesions and infections ofcentral nervous system[10]
- Delayed post-hypoxic leukoencephalopathy(DPHL)[6]
- Creutzfeldt–Jakob disease(mesencephalic form)[2]
Diagnosis
editAkinetic mutism can be misdiagnosed asdepression,delirium,orlocked-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.[citation needed]
Treatment
editMagnesium sulfate
editTreatments using intravenousmagnesium sulfatehave 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 500 mg of magnesium every eight hours, and improvement was seen after 24 hours. She became more verbal and attentive, and treatment was increased to 1000 mg every eight hours as conditions continued to improve.[11]
Cyst puncture
editAs seen 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
editSymptoms of akinetic mutism suggest a possible presynaptic deficit in thenigrostriatal pathway,which transmits dopamine. Some patients with akinetic mutism have shown to improve withlevodopaordopamineagonist therapy,[12]or by repleting dopamine in the motivational circuit withstimulants,antidepressants,oragonistssuch asbromocriptineoramantadine.[6]
Other treatments includeamantadine,carbidopa-levodopa,donepezil,memantine,and oralmagnesium oxide.[6][11]
History
editFourteen-year-old Elsie Nicks was the first patient to be diagnosed with akinetic mutism byHugh Cairnsin 1941. She suffered from severe headaches her entire life and was eventually givenmorphineto 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 rightlateral ventriclewas 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 two more times over the next seven months and was eventually removed. After eight months of rehabilitation, Elsie no longer experienced headaches or akinetic mutism symptoms.[1]
See also
editReferences
edit- ^abcdefghijCairns, H; R. C. Oldfield; J.B. Pennybacker; D. Whitteridge (1941)."Akinetic mutism with an epidermoid cyst of the 3rd ventricle".Brain.64(4): 273–290.doi:10.1093/brain/64.4.273.
- ^abcdefgOtto, Anke; Inga Zerr; Maria Lantsch (1998)."Akinetic mutism as a classification criterion for the diagnosis of Creutzfeldt–Jakob Disease".Journal of Neurology, Neurosurgery, and Psychiatry.64(4): 524–528.doi:10.1136/jnnp.64.4.524.PMC2170038.PMID9576547.
- ^abcdefghijkNagaratnam, Nages; Kujan Nagaratnam; Kevin Ng; Patrick Diu (2004). "Akinetic mutism following stroke".Journal of Clinical Neuroscience.11(1): 25–30.doi:10.1016/j.jocn.2003.04.002.PMID14642361.S2CID36669323.
- ^Sacks, Oliver (1973).Awakenings.United States: Vintage Books. p. 7.
- ^abcNagaratnam, Nages; Catriona McNeil; J.S. Gilhotra (1999). "Akinetic mutism and mixed transcortical aphasia following left thalamo-mesencephalic infarction".Journal of the Neurological Sciences.163(1): 70–73.doi:10.1016/s0022-510x(98)00329-3.PMID10223414.S2CID26188424.
- ^abcdefYarns, Brandon; Davin Quinn (2013)."Telephone Effect in Akinetic Mutism From Traumatic Brain Injury".Psychosomatics.54(6): 1–2.doi:10.1016/j.psym.2013.06.006.PMID23932533.
- ^Fix JD.Neuroanatomy.4th ed.
- ^Struss, DT; Alexander MP; Shallice T; Picton TW; Binns MA; Macdonald R; Borowiec A; Katz DI. (2005). "Multiple frontal systems controlling response speed".Neuropsychologia.43(3): 396–417.doi:10.1016/j.neuropsychologia.2004.06.010.PMID15707616.S2CID9821228.
- ^Vachalová, Ivana; Viola Gindl; Josef G. Heckmann (August 2013). "Acute inferior homonymous quandrantanopia in a 71-year-old woman".Journal of Clinical Neuroscience.21(4): 683–685.doi:10.1016/j.jocn.2013.05.015.PMID24210803.S2CID22692004.
- ^Kotchoubey, Boris; Manfred Schneck; Simone Lang; Niels Birbaumer (2003). "Event-related brain potentials in a patient with akinetic mutism".Clinical Neurophysiology.33(1): 23–30.doi:10.1016/S0987-7053(03)00003-0.PMID12711129.S2CID18789359.
- ^abRozen, 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.PMID22672948.
- ^Yang, Chun-Pai; Huang, Shih; Lin, Lu; Kao, Hsieh; Huang, Lee Tsai (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(7): 602–606.doi:10.1016/j.clineuro.2007.04.012.PMID17543443.S2CID24185020.