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At least 19 recordsLinked to original sources
PubMed1998

[Significance of single photon emission computed tomography and akinetic mutism].

Akinetic mutism is a reactive status with permanent opening of the eyes. The accountable lesions are always bilateral. The injured cerebral structures include the frontal gyri, the thalami or the mesencephalic areas. In one case of a 44-year-old patient, magnetic resonance imaging and computed tomography were not contributive. Tc99m brain SPECT imaging was performed and displayed bilateral frontal hypoactivity. This case suggests that this technique could be helpful for diagnosis when clinical features and radiological pattern are opposite.

Adult↗
PubMed1996

[Akinetic mutism with right hemiplegia caused by infarction in the territory of the left anterior cerebral artery].

A 65 years old woman with chronic high blood pressure and diabetes mellitus presented with a mutism akinetic of sudden onset and a right total hemiplegia with a Babinski sign secondary to a left anterior cerebral artery infarction. She had had six months earlier a transient gait disturbance. At that time, the CT scan showed lacunar infarcts of the head of both caudate nuclei. Neuropathological examination revealed that the left infarction of the anterior cerebral artery involved the superior frontal gyrus, the supplementary motor area, the cingulate gyrus and the corpus callosum. There were also multiple lacunes of the head of both caudate nuclei, anterior limb of the internal capsules, white matter, basal ganglia and thalami. The mutism akinetic was thought to be the result of a bilateral disruption of a functional loop including on each side, the supplementary motor area, the cingulate gyrus, the subcallosal tract and the head of the caudate nucleus. On the right side, the lesion of the caudate nucleus could have interrupted this loop normally involved in the induction of voluntary movements and in the communication with the external surroundings.

Aged↗
PubMed2004

Subarachnoid haemorrhage and akinetic mutism.

Two rare cases of akinetic mutism induced by aneurysmal subarachnoid haemorrhage are reported. The literature is reviewed, the possible pathophysiological mechanism of akinetic mutism is considered and the association between these two conditions is explored with an attempt to address the roles of medical treatment and surgery and to discuss prognosis.

Adult↗
PubMed1995

[Akinetic mutism--a review of the literature].

Cairns and coworkers (1941) introduced the term "akinetic mutism" to denote a syndrome characterised by lack of responsiveness in the presence of apparently preserved vigilance. The present paper reviews clinical data as well as results of animal experimentation to outline the functional-neuroanatomic basis of this constellation. The clinical literature following the original publication of Cairns et al. (1941) reported syndromes of "akinetic mutism" in bilateral mesodiencephalic or frontal lesions of various aetiology. At least two pathomechanisms of akinetic mutism can be differentiated: (a) reduced "arousal" of cortical functions due to lesions at or rostral to the mesodiencephalic junction; (b) impaired activation of the motor system following bilateral damage to the frontal lobes. Since perceptual and cognitive functions are disturbed as well in mesodiencephalic akinetic mutism, the latter notion does not seem to be adequate. The terms "apallic syndrome" or "vegetative state" are rather more appropriate in these instances. The label "akinetic mutism" can then be restricted to a pathophysiologically distinct syndrome, i.e. reduced motor activation following bilateral frontal damage.

Akinetic Mutism↗
PubMed2001

BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction.

INTRODUCTION: Akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA) territory is reported rarely, however, often leading to akinetic mutism. CASE REPORT: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. Electroencephalography, 24h after admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and polymorphic delta activity. DISCUSSION: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs. However, BIPLEDs may occur in bilateral ACA territory infarction.

Aged↗
PubMed1997

Role of cavum septum pellucidum in akinetic mutism of hydrocephalic children.

Two children 9 and 13 years of age with histories of aqueductal stenosis developed akinetic mutism after multiple shunt revisions. The girl had spontaneous relief of her akinetic mutism 1 month later, after parenteral antibiotics and multiple shunt revisions. The akinetic mutism of the boy was resistant to antiparkinsonian therapy before megadosage of bromocriptine (120 mg/day). Both children had a prominent cavum septum pellucidum (CSP), which has rarely been involved in the pathogenesis of akinetic mutism. Because of the rapid shrinkage of the girl's CSP after shunt revision, but not that of the boy even after stereotactic fenestration of the wall of his CSP, their eventual outcomes were different. Wide CSP (WCSP) may play an important role in the occurrence of akinetic mutism in hydrocephalic patients.

Adolescent↗
PubMed1990

Cyclosporin-associated akinetic mutism and extrapyramidal syndrome after liver transplantation.

Three patients developed akinetic mutism on the third day after the introduction of intravenous cyclosporin A, given for immunosuppression after liver transplantation. One patient in addition developed a florid orofacial dyskinesia, which resolved completely, as did the akinetic mutism, after withdrawal of cyclosporin. In these patients the time course of the akinetic mutism and extrapyramidal syndrome, which developed in the absence of any other identifiable cause, suggests cyclosporin A was the precipitating factor. Subsequently, two of the patients showed signs of pseudobulbar palsy with abnormalities in the pons on MRI scanning, suggesting central pontine myelinolysis (CPM). None of the patients had experienced significant fluctuations in serum sodium or other risk factors for central pontine myelinolysis and the exact relationship to the earlier cyclosporin related mutism was not clear.

Adult↗
PubMed1999

Akinetic mutism after fourth ventricle choroid plexus papilloma: treatment with a dopamine agonist.

BACKGROUND: Akinetic mutism is a behavioral state wherein a patient seems to be awake but does not move or speak. Several patients are reported to have developed mutism after posterior fossa surgery. We present a patient who developed akinetic mutism after total excision of a choroid plexus papilloma of the fourth ventricle, and who was treated with bromocriptine. CASE DESCRIPTION: An 18-year-old woman was admitted with akinetic mutism, which had developed 6 days after posterior fossa surgery. She had had no neurologic deficit in the first 5 days after surgery and could communicate with her family. Despite antioedematous therapy and daily lumbar punctures to drain cerebrospinal fluid, there was no clinical improvement after she entered the akinetic mute state. Brain magnetic resonance revealed ventriculomegaly; brain single photon emission computed tomography revealed bilateral reduction of perfusion in the frontal region. Because daily lumbar drainage did not result in clinical improvement, shunt placement was not considered. Bromocriptine therapy was begun at a dose of 2x2.5 mg; 24 hours later, the patient started to speak and move her upper extremities. Further improvement occurred over the following week when the dose was increased to 3x2.5 mg. Bromocriptine was replaced with a placebo to determine whether the neurologic improvement was caused by the medicine. The patient's neurologic status deteriorated progressively; therefore, bromocriptine was restarted and she was discharged from the hospital. During the 6 months of follow-up, the patient has remained in good health. CONCLUSIONS: The etiology of akinetic mutism is not clear. Monoaminergic pathways, particularly dopaminergic cell groups, are most probably involved in this syndrome, because bromocriptine has a dramatic effect on these patients, as demonstrated in our case.

Adolescent↗
PubMed2004

Akinetic mutism following stroke.

This is an appraisal of the varied clinical presentation and the neural substrate for akinetic mutism following stroke. The diagnosis is important as akinetic mutism is often misdiagnosed as depression, delirium and locked-in-syndrome. This is a descriptive study of eight selected patients with akinetic mutism following infarction/haemorrhage in different regions of the brain with characteristic syndromes. They involved the critical areas namely, the frontal (cingulate gyrus, supplementary motor area and dorso-lateral border zone), basal ganglia (caudate, putamen), the mesencephalon and thalamus. The disorders of speech and communication took different forms. The speech disorder included verbal inertia, hypophonia, perseveration, softened and at times slurred. The linguistic disturbances were fluent, non-fluent, anomia and transcortical (motor, mixed) aphasias. The findings were related to what is known about the neuroanatomic location of the lesions and the role of the frontal-subcortical circuitry in relation to behaviour. Akinetic mutism could be explained by damage to the frontal lobe and or interruption of the complex frontal subcortical circuits.

Adult↗
PubMedDate not supplied

Akinetic mutism due to diphenylhydantoin toxicity.

Akinetic mutism (AM) is a rare, specific, unconscious state. An AM patient seems to be awake, lacks mental activity, is unable to speak, and does not respond to any environmental stimulus. Cyclical sleep and awake states are maintained, and incontinence is present. Various factors such as tumor, vascular events, drug use and radiotherapy are responsible for the development of AM. A 12-year-old epileptic patient displayed AM and diphenylhydantoin toxicity (DPH). She seemed awake, was unable to speak or to understand, and had no movements with either spontaneous or noxious stimuli. Her serum DPH level was greater than 40 micrograms/ml. Magnetic resonance imaging (MRI) showed mild cerebellar atrophy. All known causes of AM were excluded. The AM state in this patient was considered to be due to toxic DPH levels. She regained her motor and mental activity within two months after carbamazepine was administered to replace DPH. She was symptom-free when examined at the two-year follow-up. No similar adverse effect of DPH has been reported to date.

Akinetic Mutism↗
PubMed1993

Development of akinetic mutism and hyperphagia after left thalamic and right hypothalamic lesions.

A case of childhood post-traumatic akinetic mutism is presented. The patient showed a hyperphagic condition while recovering from akinetic mutism. He had lesions in the left interlaminal nucleus of the thalamus, right globus pallidus, and right dorsomedial nucleus of the hypothalamus. Laboratory data indicated slightly disturbed hypothalamic functions. In general, akinetic mutism can be seen with bilateral destructive lesions, while hyperphagia may occur after destruction of dorsomedial hypothalamic nucleus, but it is very rare. This is the first reported case of akinetic mutism caused by a unilateral lesion.

Akinetic Mutism↗
PubMed1998

Akinetic mutism as a classification criterion for the diagnosis of Creutzfeldt-Jakob disease.

OBJECTIVES: Among the classification criteria for the diagnosis of Creutzfeldt-Jakob disease, akinetic mutism is described as a symptom which helps to establish the diagnosis as possible or probable. Akinetic mutism has been anatomically divided into two forms--the mesencephalic form and the frontal form. The aim of this study was to delimit the symptom of akinetic mutism in patients with Creutzfeldt-Jakob disease from the complex of symptoms of an apallic syndrome and to assign it to the individual forms. METHODS: Between April and December 1996, 25 akinetic and mute patients with Creutzfeldt-Jakob disease were consecutively examined. The patients were classified according to the definition of akinetic mutism by Cairns and secondly in accordance with the features constituting the complete picture of an appalic syndrome (defined by Gerstenbrand). RESULTS: From 25 patients with definite Creutzfeldt-Jakob disease, 24 patients showed impoverishment of speech and, after a mean duration of four (range 1.1-11.2) months, almost complete absence of voluntary movements and speech. Seven patients were classified as being mute and akinetic and assigned to the mesencephalic form whereas 13 patients were classified as apallic. One patient was mute without being akinetic and four patients were comatose. CONCLUSION: Diffuse brain damage underlies akinetic mutism in patients with Creutzfeldt-Jakob disease. The term can be used as a classification criterion for the diagnosis of Creutzfeldt-Jakob disease; however, it should be applied very carefully and delimited clearly from the apallic syndrome.

Adult↗
PubMed1975

[Akinetic mutism and bicingular softening. 3 anatomo-clinical cases].

The authors describe three pathological cases of akinetic mutism with, as a common basic lesion, bilateral infarction of the cingulate gyrus secondary to aneurysm of the anterior communicating artery (case n degrees 1), to a huge olfactory meningioma (case n degrees 2), both operated on, and to atheromatous occlusion of the anterior cerebral arterial system (case n degrees 3). These three cases enable a variety of "anterior and waking" akinetic mutism to be described which is unusual enough to be compared with other mesencephalic and diencephalic aspects of this syndrome. It is in fact an akinetic mutism characterized by: a certain dissociation in its non-response to various stimuli, a particularly marked appearance of wakefulness when day-time alertness is considered, conservation of the waking-sleeping rhythm, perception and reaction unpredictable and paradoxical in both degree and quality, complete absence of any spontaneous verbal communication in contrast to relative break-down of solicited communication which is infrequent, uncertain and unresponsive to the usual methods of stimulation, without any possibility of a code. In addition, there is a remarkable mimic and segmental general akinesia, resistant to the usual nociceptive stimuli, but sensitive to slight excitation of the manual and oral zones. Besides this special akinetic mutism, there are variously systematised signs, mostly asymmetrical, indicating lesion of the cortico-sub-cortical frontal structures bordering on the gyrus cinguli. This unusual behaviour pattern corresponds in these three cases to extensive anterior bilateral ischemic lesions of the cingulate gyrus regularly associated with bilateral infarctions confined to the medial aspect of F1 in the superficial territory of the two anterior cerebral arteries, to possible neurosurgical changes (ablation of the right frontal pole) and to compressive or ischaemic lesions of the gyrus rectus. These exclusively cortico-sub-cortical associated lesions are in contrast with the remarkably intact caudate nuclei, the pallidal, thalamic, hypothalamic and septal formations and the anterior pillars of the fornix. These findings compared with the results of experimental research carried out by M. Kennard, help, if help is needed, to resolve the apparent contradictions between the effects of therapeutic cingulectomies or cingulotomies and the scanty pathological data already available in cerebral vascular pathology.

Adult↗
PubMed1987

[Akinetic mutism from recurrent hydrocephalus: successful treatment with levodopa, bromocriptine and trihexyphenidyl].

A case of akinetic mutism was reported with reference to a marked improvement by levodopa, bromocriptine and trihexyphenidyl. A 39-year-old male, first seen on February 2, 1981, had an occipitalgia, accompanied by nausea and vomiting. For several months before this consultation, the patient had suffered from asthenopia. Brain CT scan and cerebral angiogram demonstrated internal hydrocephalus due to aqueduct stenosis of unknown etiology. After a ventriculoperitoneal shunt operation on February 20, 1981, he completely recovered. Two years and a half after the shunt insertion he had no difficulty in his daily life. He reentered the hospital on December 21, 1983, because of personality change, mental deterioration and bradykinesia. Brain CT scan showed recurrent hydrocephalus resulting from shunt blockage. Following the shunt revision, hydrocephalus was resolved. Nevertheless, the patient did not return to his previous state. And he became bed-ridden, incontinent of urine, and unable to take fluids or foods, following which he went into a state of akinetic mutism. Other neurological findings were as follows: upward gaze palsy, impaired convergence, convergence nystagmus, plastic rigidity of neck and all four limbs, and diffuse hyperreflexia with right Babinski's sign. Abnormal involuntary movement was not seen. On March 27, 1984, levodopa therapy was instituted and on April 2, trihexyphenidyl was combined with levodopa. Shortly after administration of levodopa and trihexyphenidyl, akinetic mutism began to improve, but upward gaze palsy was not affected. He began to speak and could walk unassisted by the end of July.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Event-related brain potentials in a patient with akinetic mutism.

The clinical pattern of complete akinetic mutism (AM) was observed in a patient with a bilateral infarction of the anterior cerebral arteries extending to the rostral cingulate cortex and the supplementary motor areas. Since the patient was unable to produce any overt response, event-related brain potentials (ERPs) were used to obtain information about cortical processing of stimuli. Oddball tasks with simple acoustical stimuli and semantic categories were used. Verbal processing was further assessed by comparing event-related potentials to words compatible versus incompatible to the semantic context. Although the pattern of cortical responses was abnormal, differential responses were clearly obtained to semantically different word classes. Thus, the hypothesis about cortical non-responsivity of AM patients, drawn from several previous reports, was not supported. An ERP examination in AM patients can deliver information about their mental state, provided that the stimuli and tasks possess a wide range of informational complexity and motivational value.

Akinetic Mutism↗