Mutism (complete silence)

Mutism refers to the most severe disorders of speech initiation and is manifested by the loss of the ability to vocalize in general, that is, complete silence.

Lighter forms of speech initiation disorders are manifested only by a delay (delay) in the initiation of speech (for example, in Parkinson's disease). Delayed initiation of speech (delayed speech responses) is characteristic of general mental retardation (deep stunning; abulia; severe depression) or with selective inhibition of speech activity (large prefrontal tumors; atrophic processes in the Broca area; other states of “speech hypokinesia” that manifest themselves as prolonged latent period of speech responses, maladjustment, concise style of responses).

Syndromic differential diagnosis of true mutism should be carried out with another, outwardly similar, syndrome - anarthria. Most patients with mutism have a violation of laryngeal functions without disturbing the facial, oral muscles or muscles of the tongue.

Mutism can also have a purely psychogenic (conversion) origin. Finally, mutism can be part of complex behavioral disorders, such as negativity or catatonia for schizophrenia. True mutism (“akinesia of speech”, “akinesia of the tongue”) is characteristic of akinetic mutism or severe akinetic forms (rarely) of Parkinson's disease, especially at the time of increased akinesia (“akinetic attack”, “freezing”, “motor block.” Mutism, like psychomotor phenomenon, described in many neurological diseases, characterized by very different localization (often bilateral) brain damage.

Mutism often accompanies or is associated with its genesis with such different syndromes as akinesia (speech), aphasia (speech apraxia), abulia, apathy, aphemia, anarthria, and may or may not be accompanied by other neurological disorders.

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Causes and clinical forms of mutism

1. Akinetic mutism of different localization. "Front" and "back" syndromes of akinetic mutism, hyperkinetic mutism.
2. Mutism in the picture is the syndrome of a "locked up" person.
3. Other forms of mutism in brain diseases:
   • Damage to Brock's cortical speech area (in the acute stage of motor aphasia)
   • Damage to the additional motor area
   • Damage to the deep sections of the left frontal lobe
   • Damage to putamen
   • Bilateral damage to the pale ball
   • Bilateral thalamic damage (for example, with thalamotomy)
   • Cerebellar mutism
   • Mutism with severe pseudobulbar palsy
4. Bilateral paralysis of the pharynx or vocal cords ("peripheral mutism")
5. Psychogenic mutism
6. Psychotic Mutism.

Akinetic mutism is a condition characterized by complete akinesia and mutism, that is, a loss of ability for any movements, including speech. There is no motor response even to severe pain stimuli. But the visual indicative reaction is preserved; possible fixation of the gaze and tracking function. Despite the aspiration and total immobility, the patient is not in a true coma (“awake coma”); he looks you in the eyes and this persistently looking look as if promises speech; he watches a moving object, but no stimulus can get a motor response.

Akinetic mutism is described in a third ventricular tumor, traumatic, anoxic or vascular lesions affecting the frontal cortex, both hemispheres, the cingulate gyrus (especially when the anterior cingulate gyrus is involved on both sides - the so-called “akinetic mutism anterior syndrome”), thalamus.

Bilateral midline (paramedian) injuries in the mesodiencephalic region, especially with the involvement of peri-gray gray matter (the mesencephalon reticular formation - the so-called “akinetic back syndrome”), can cause prolonged akinetic mutism in humans. Akinetic mutism is also described in patients with AIDS, a neuroleptic malignant syndrome.

As a reversible state, akinetic mutism occurs when leaving a severe comatose state of a different nature, in particular after an acute traumatic brain injury. In this situation, there is also the so-called hyperkinetic mutism, a condition characterized by motor arousal and mutism, which culminates in the ordering of motor behavior and the recovery of speech activity.

The syndrome of a “locked person” is manifested by quadriplegia, “mutism” (its real cause is anarthria) and intact consciousness, in which the ability to communicate is usually limited to vertical eye movements and eyelid movements (blinking). Most cases of locked man syndrome are caused by occlusion of the basilar artery, which leads to a cerebral infarction in the area of the ventral parts of the pons. Other possible causes: hemorrhage, abscess, demyelination in the ventral part of the bridge and the medulla oblongata, which interrupts the cortico-spinal paths to the extremities and the cortico-nuclear pathways to the lower cranial nerves (de-efferentation syndrome). The syndrome is also described in alcoholic nutritional encephalopathy. CT confirms the location of the lesion. This is also indicated by abnormal auditory stem potentials. EEG is usually normal.

Damage to Brock's cortical speech area may be accompanied by a deep inhibition of speech activity, which is manifested by mutism, which precedes the manifestation of signs of motor aphasia. Thus, the acute phase of the stroke, which led to speech apraxia (motor aphasia), is manifested in the beginning by a more extensive inhibition of expressive speech with the suppression of any voice (not only speech) activity.

Damage to the additional motor area in the medial premotor part of the superior frontal gyrus is often mentioned as the cause of mutism. Most of the cases described point to left-side injuries, but some observations refer to mutism for right-side injuries to this area. Usually, global akinesia first develops, then (after days and weeks) it is replaced by contralateral akinesia and mutism. Small unilateral damage can cause only transient mutism; extensive prefrontal damage, especially the exciting cingulate gyrus, leads to prolonged mutism.

Damage to the deep sections of the left frontal lobe, adjacent directly to the anterior horn of the lateral ventricle, also sometimes cause transient mutism. When recovering, signs of transcortical motor aphasia may be observed.

Transient mutism can also be observed with injuries of putamen (bilateral or only left-sided). The recovery period is characterized by reduced spontaneous speech activity and some extrapyramidal symptoms (hypophony, hypokinetic articulation). Separate messages are devoted to bilateral damage to the pale ball, which manifest similar symptoms of mutism with general akinesia and apathy.

Damage to the anterior parts of the thalamus (especially bilateral and left-sided) can cause mutism and, usually, global akinesia (thalamic tumors, hemorrhage into it, stereotactic thalamotomy, bilateral or, sometimes, left-sided).

Acute bilateral damage to both cerebral hemispheres can rarely lead to mutism (cerebellar mutism). This mutism on average lasts 1-3 months (up to 20 weeks); his recovery goes through a stage of dysarthria. Oral apraxia is often detected. The syndrome is described in the removal of cerebellar tumors in children.

Finally, mutism can occur with severe pseudobulbar palsy due to diffuse bilateral hemispheric lesions, as well as with bilateral paralysis of the pharyngeal muscles and vocal cords (“peripheral mutism”), for example, in Charcot's disease.

Neuroleptics usually cause hypokinesia or akinesia with a decrease in speech activity, but complete mutism is usually not observed here. Malignant neuroleptic syndrome may in the early stages include the symptoms of akinetic mutism.

Psychogenic mutism is usually observed in the picture of polysyndromic hysteria and is accompanied in such cases by other demonstrative motor (multiple movement disorders), sensitive, vegetative (including paroxysmal) and emotional-personal psychogenic disorders that facilitate diagnosis.

Psychotic mutism is usually manifested by the lack of spontaneous and reciprocal speech with the inherent ability to speak and understand the speech addressed to the patient. Psychotic mutism is observed in the picture of massive psychopathological (depressive stupor; catatonia; negativism) and behavioral disorders of the psychotic (often schizophrenia) range.

[2], [3], [4], [5], [6], [7],

Diagnostic tests for mutism

MRI of the brain, the study of cerebrospinal fluid, USDG of the main arteries of the head, consultation of a neuropsychologist and, if necessary, a psychiatrist and an ENT specialist (phoniatrist).

[8], [9]