Mutism (complete silence)

Mutism is one of the most severe disorders of speech initiation and is characterized by the loss of the ability to vocalize at all, that is, complete silence.

Milder forms of speech initiation disorder are manifested only by a delay in speech initiation (for example, in Parkinson's disease). Delayed speech initiation (delay in speech responses) is characteristic of states of general mental inhibition (deep stupor; abulia; severe depression) or with selective suppression of speech activity (large tumors of the prefrontal localization; atrophic processes in the Broca area; other states of "speech hypokinesia" manifested by a long latent period of speech responses, laconic style of responses).

Syndromic differential diagnosis of true mutism should be made with another, outwardly similar syndrome - anarthria. Most patients with mutism have laryngeal dysfunction without impairment of facial, oral or tongue muscles.

Mutism may also have a purely psychogenic (conversion) origin. Finally, mutism may be a component of complex behavioral disorders, such as negativism or catatonia in schizophrenia. True mutism ("speech akinesia", "language akinesia") is characteristic of akinetic mutism or severe akinetic forms (rare) of Parkinson's disease, especially at the moment of increased akinesia ("akinetic attack", "freezing", "motor block". Mutism, as a psychomotor phenomenon, has been described in many neurological diseases characterized by very different localization (usually bilateral) of brain damage.

Mutism is often accompanied or associated by 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. "Anterior" and "posterior" syndromes of akinetic mutism, hyperkinetic mutism.
2. Mutism in the picture is the syndrome of a "locked-in" person.
3. Other forms of mutism in brain diseases:
   • Damage to the cortical speech area of Broca (in the acute stage of motor aphasia)
   • Supplementary motor area lesions
   • Damage to the deep parts of the left frontal lobe
   • Damage to the putamen
   • Bilateral lesions of the globus pallidus
   • Bilateral thalamic lesions (eg, thalamotomy)
   • Cerebellar mutism
   • Mutism in 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, i.e. loss of the ability to make any movements, including speech. There is no motor response even to strong painful stimuli. But the visual orientation reaction is preserved; fixation of the gaze and the tracking function are possible. Despite the aspontaneity and complete immobility, the patient is not in a true coma ("awake coma"); he looks you in the eyes and this stubbornly directed gaze seems to promise speech; he follows a moving object, but no stimulus can elicit a motor response.

Akinetic mutism has been described in cases of tumors of the third ventricle, traumatic, anoxic, or vascular lesions affecting the frontal cortex, both hemispheres, cingulate gyrus (especially with involvement of the anterior cingulate gyrus on both sides - the so-called "anterior akinetic mutism syndrome"), and thalamus.

Bilateral midline (paramedian) lesions in the mesodiencephalic region, especially with involvement of the periaqueductal gray matter (reticular formation of the mesencephalon - the so-called "posterior syndrome of akinetic mutism") can be the cause of prolonged akinetic mutism in humans. Akinetic mutism has also been described in patients with AIDS, malignant neuroleptic syndrome.

As a reversible condition, akinetic mutism occurs when recovering from severe comatose states of various origins, in particular after acute craniocerebral trauma. In this situation, so-called hyperkinetic mutism also occurs - a condition characterized by motor excitation and mutism, which ends with the regulation of motor behavior and the restoration of speech activity.

Locked-in syndrome is characterized by quadriplegia, "mutism" (its real cause is anarthria), and intact consciousness, with communication usually limited to vertical eye movements and eyelid movements (blinking). Most cases of locked-in syndrome are caused by basilar artery occlusion, resulting in brainstem infarction in the ventral pons. Other possible causes include hemorrhage, abscess, and demyelination in the ventral pons and medulla oblongata, interrupting the corticospinal tracts to the limbs and the corticonuclear tracts to the lower cranial nerves (de-efferentation syndrome). The syndrome has also been described in alcoholic nutritional encephalopathy. CT confirms the location of the lesion, as do abnormal brainstem auditory potentials. EEG is usually normal.

Damage to the cortical speech area of Broca can be accompanied by profound inhibition of speech activity, which manifests itself as mutism, which precedes the manifestation of signs of motor aphasia. Thus, the acute phase of a stroke that has led to speech apraxia (motor aphasia) initially manifests itself as more extensive inhibition of expressive speech with the suppression of any vocal (not only speech) activity.

Damage to the supplementary motor area in the medial premotor part of the superior frontal gyrus is often cited as a cause of mutism. Most reported cases involve left-sided lesions, but anecdotal reports of mutism have been reported with right-sided lesions. Typically, global akinesia develops first, then (after days or weeks) contralateral akinesia and mutism. Small unilateral lesions may cause only transient mutism; extensive prefrontal lesions, especially those involving the cingulate gyrus, result in permanent mutism.

Damage to the deep portions of the left frontal lobe, immediately adjacent to the anterior horn of the lateral ventricle, also sometimes causes transient mutism. During recovery, signs of transcortical motor aphasia may be observed.

Transient mutism may also be observed with damage to the putamen (bilateral or only left-sided). The recovery period is characterized by decreased spontaneous speech activity and some extrapyramidal symptoms (hypophony, hypokinetic articulation). Some reports are devoted to bilateral damage to the globus pallidus, which manifests itself with similar symptoms of mutism with general akinesia and apathy.

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

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

Finally, mutism can be observed in severe pseudobulbar paralysis caused by diffuse bilateral hemispheric lesions, as well as in bilateral paralysis of the pharyngeal muscles and vocal cords (“peripheral mutism”), for example, in Charcot's disease.

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

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

Psychotic mutism usually manifests itself as a lack of spontaneous and responsive speech with the preserved ability to speak and understand 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 (usually schizophrenia) circle.

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Diagnostic tests for mutism

MRI of the brain, examination of cerebrospinal fluid, ultrasound Doppler imaging of the main arteries of the head, consultation with a neuropsychologist and, if necessary, a psychiatrist and ENT doctor (phoniatrist).

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