Akinetic mutism

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Akinetic mutism

Specialty Psychiatry

Akinetic mutism is a medical term describing patients tending neither to move

(akinesia) nor speak (mutism). 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 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 that as soon as
they 'will' or attempt a movement, a 'counter-will' or 'resistance' rises up to meet
them.[4]

Contents

 1Types
o 1.1Frontal akinetic mutism
o 1.2Mesencephalic akinetic mutism
 2Symptoms
 3Causes
o 3.1Frontal lobe damage
o 3.2Thalamic stroke
o 3.3Ablation of cingulate gyrus
o 3.4Other
 4Diagnosis
 5Treatment
o 5.1Magnesium sulfate
o 5.2Cyst puncture
o 5.3Dopamine agonist therapy
 6History
 7See also
 8References
 9External links

Types[edit]
Frontal akinetic mutism can occur after a frontal lobe injury

The mesencephalic form of akinetic mutism occurs in the midbrain (4)

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[edit]
Akinetic mutism can occur in the frontal region of the brain and occurs because
of bilateral frontal lobe damage. Akinetic mutism as a result of frontal lobe
damage is clinically characterized as hyperpathic.[5] It occurs in patients with
bilateral circulatory disturbances in the supply area of the anterior cerebral artery.
[2]

Mesencephalic akinetic mutism[edit]

Akinetic mutism can also occur as a result of damage to
the mesencephalic region of the brain. Mesencephalic akinetic mutism is
clinically categorized as somnolent or apathetic akinetic mutism.[5] It is
characterized by vertical gaze palsy and ophthalmoplegia. 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[edit]

Lack of motor function (but not paralysis)[1]

Lack of speech [1]

Apathy[6]

Slowness[6]

Disinhibition[3]

Causes[edit]

Many cases of akinetic mutism have occurred after a thalamic stroke.

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[edit]
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.
Thalamic stroke[edit]
Many cases of akinetic mutism occur after a thalamic stroke.
[3]
 The thalamus helps regulate consciousness and alertness.
Ablation of cingulate gyrus[edit]
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.[7] The anterior cingulate cortex is 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.
Other[edit]
Akinetic mutism is a symptom during the final stages of Creutzfeldt–Jakob
disease (a rare degenerative brain disease) and can help diagnose patients with
this disease.[2][9] It can also occur in a stroke that affects both anterior cerebral
artery territories. Another cause is neurotoxicity due to exposure to certain drugs
such as tacrolimus and cyclosporine.
Other causes of akinetic mutism are as follows:

Respiratory arrest and cerebral hypoxia [6]

Acute cases of encephalitis lethargica[3]

Meningitis[3]

Hydrocephalus[3]

Trauma[3]

Tumors[3]

Aneurysms [3]

Olfactory groove meningioma

Cyst in third ventricle [1]

Toxical lesions and infections of central nervous system [10]

Delayed post-hypoxic leukoencephalopathy (DPHL) [6]

Creutzfeldt–Jakob disease (mesencephalic form) [2]

Diagnosis[edit]
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.

Treatment[edit]
Magnesium sulfate[edit]
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 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[edit]
As 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[edit]
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,[12] or
by repleting dopamine in the motivational circuit with stimulants, antidepressants,
or agonists such as bromocriptine or amantadine.[6]
Other treatments include amantadine, carbidopa-
levodopa, donepezil, memantine, and oral magnesium oxide.[6][11]

History [edit]
Fourteen-year-old Elsie Nicks was the first patient to be diagnosed with akinetic
mutism by Hugh Cairns in 1941. She suffered from severe headaches her entire
life and was eventually given morphine 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 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[edit]
 Selective mutism
 Locked-in syndrome
 Athymhormic syndrome
 Catatonia
 Aboulia

References[edit]
1. ^ Jump up to:a b c d e f g h i j Cairns, 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.
2. ^ Jump up to:a b c d e f g Otto, 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.  PMC 2170038. PMID 9576547.
3. ^ Jump up to:a b c d e f g h i j k Nagaratnam, 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.  PMID  14642361.
4. ^ Sacks, Oliver (1973).  Awakenings. United States: Vintage Books. p. 7.
5. ^ Jump up to:a b c Nagaratnam, 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.  PMID  10223414.
6. ^ Jump up to:a b c d e f Yarns, 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.  PMID  23932533.
7. ^ Fix JD. Neuroanatomy. 4th ed.
8. ^ 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. PMID 15707616.
9. ^ 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. PMID 24210803.
10. ^ 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. PMID 12711129.
11. ^ Jump up to: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.
12. ^ 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. PMID 17543443.