Clinical and Experimental Aspects of Akinetic Mutism

Fm, Skultety

doi:10.1001/archneur.1968.00480010019001

Cited by 47 publications

(10 citation statements)

References 31 publications

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“…In 5 patients a picture of akinetic mutism has been described (Case 1 in [38]; Cases 1 and 2 in 1591; Patients 17 and 28 of our series). In all these cases, the infarct was thalamopeduncular and bilateral and extended into the lateral tegmental formations, in keeping with observations made in humans by Krayenbuhl et a1 [34] and Skultety [63].…”

Section: Clinicoanatornical Correlations Patterns Of Initiation and Csupporting

confidence: 89%

Paramedian thalamic and midbrain infarcts: Clinical and neuropathological study

Castaigne¹,

Lhermitte

Buge

et al. 1981

Annals of Neurology

535

240

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The clinical and neuropathological findings in 28 cases of paramedian thalamic and midbrain infarcts are reported. The 4 instances of unilateral paramedian thalamic infarct were characterized by mood and behavioral changes, limitation of the infarct to the center of the anatomical paramedian territory, and symmetrical configuration of the paramedian thalamic arteries. Basilar artery occlusion was found in 1 patient. The 5 cases of bilateral paramedian thalamic infarcts were characterized by disturbances of consciousness and behavior, extension of the infarct (to the mammillothalamic tracts in 4 cases, the red nuclei in 3, and the hypothalamus in 2), and a variable paramedian thalamic arterial pattern. The arterial pattern was symmetrical in 2 cases, asymmetrical in 1, and unilateral in 1. The basilar artery was occluded in 1 case, the basilar communicating and posterior cerebral arteries in 1, and a third patient had occlusion involving an aneurysm of the basilar artery. The 19 patients with paramedian thalamopeduncular infarcts had marked disturbances of consciousness (hypersomnia, deep coma, akinetic mutism) associated with ocular motility changes. Later, abnormal movements--always delayed--and memory disturbances were observed in some. Thalamic changes were restricted to beh paramedian territory in only 3 cases. The arterial pattern was symmetrical in 5. The basilar and posterior cerebral arteries were occluded in 4 patients each. Paramedian infarcts were rarely found as isolated lesions and were always bilateral when there was only one arterial pedicle. The paramedian thalamic pedicle can supply the polar thalamic territory.

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Section: Clinicoanatornical Correlations Patterns Of Initiation and Csupporting

confidence: 89%

Paramedian thalamic and midbrain infarcts: Clinical and neuropathological study

Castaigne¹,

Lhermitte

Buge

et al. 1981

Annals of Neurology

535

240

View full text Add to dashboard Cite

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“…These three patients and the ligation cases of Poppen (1939), Dandy (1945), and Skultety (1968) suggest that neuroanatomical structures which receive their vascular supply from the anterior cerebral artery can produce akinetic mutism when bilaterally damaged. Though there is some individual variation, the anterior cerebral artery usually supplies the cingulate cortex via its callosal branches, the medial surface of the frontal lobe via frontopolar and other branches, the medial portion of the head of the caudate nucleus, the septal nucleus and the parolfactory area through perforating branches, and the medial caudate, medial putamen, and portions of the internal capsule via the recurrent branch of Heubner (Alexander, 1942;Gillilan, 1968).…”

Section: Discussionmentioning

confidence: 86%

“…In fact, the great variety of neuroanatomical areas which have been proposed as a site for the production of akinetic mutism has caused some workers to despair. In speaking of akinetic mutism, Skultety (1968) concluded: 'The syndrome has been reported with lesions of the third ventricle, thalamus, basal ganglia, midbrain, anterior cingulate gyrus, and also associated with basilar artery occlusion, central pontine myelinolysis, and obstructive hydrocephalus. From this, it would appear that the syndrome has little localizing value.'…”

Section: Discussionmentioning

confidence: 99%

“…Poppen (1939) and Dandy (1946) each reported a case of akinetic mutism after operative sacrifice of both anterior cerebral arteries. Skultety (1968) described a patient who developed akinetic mutism after the clipping of the right anterior cerebral artery during the removal of a falx meningioma with apparent postoperative thrombosis in the left anterior cerebral artery. This communication describes three cases of akinetic mutism associated with spontaneous bilateral anterior cerebral artery occlusion and discusses the neuroanatomical substrate which may underlie the appearance of this syndrome.…”

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confidence: 99%

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Akinetic mutism and bilateral anterior cerebral artery occlusion

Freemon

1971

Journal of Neurology, Neurosurgery & Psychiatry

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A 68 year old retired depressed white male was admitted to the surgical service because of a self-inflicted minor gunshot wound to the chest. The only significant past history was a myocardial infarction 13 years previously. After successful treatment of his chest wound the patient was transferred to the psychiatric service because of continued suicidal thoughts and statements. One morning a week later he awoke feeling unusually 'groggy' as he told his room-mate. On his way to the bathroom the patient fell and could not arise. When he was examined his eyes were open but he could not speak or follow commands. The doll's head manoeuvre showed extraocular movements to be full. Pupils were equal and reactive to light. Gag reflex was present as were corneal reflexes. A slight plastic rigidity was present in all limbs. The only move-.r K.1 ment elicitable was a slight withdrawal of each limb to deep pain stimulation. However, if the patient's arm was held over his face and allowed to drop, it usually fell in such a way as to miss his face. Tendon reflexes were bilaterally symmetrical and hyperactive, particularly in the lower extremities with sustained clonus at both ankles. Bilateral Babinski signs were present, as were snout and grasp reflexes. The patient would look at the examiner and would follow him with his eyes. Several attempts to communicate with the patient using eye movements or eye blinks as signals were entirely unsuccessful. Within an hour after the insult, an electroencephalogram was performed which showed low voltage 2-2i Hz generalized activity. A lumbar puncture showed an opening pressure of 140 mm CSF and a closing pressure of 120 mm CSF; glucose was 77 mg and protein 45 mg/100 ml. There were no cells in the CSF and there was no xanthochromia. The next morning the patient had lost his superficial appearance of alertness. His eyes were closed and his musculature was flaccid unless he was stimulated at which time he became rigidly opisthotonic with extension of legs and arms, with flexion at the wrists. He had CheyneStokes respiration with an apnoeic period of 20 seconds. At this time the pupils remained equal and reactive, extraocular movements were intact as estimated by the doll's head manoeuvre, and caloric examination showed conjugate tonic deviation of the eyes toward the side of the cold water. The patient died 10 days later.NEUROPATHOLOGICAL FINDINGS External examination revealed bilateral softening from the frontal pole to the inferior occipital region with slight clouding and thickening of the overlying meninges. Coronal sections showed severe infarction on the left, involving the entire frontoparietal and temporal cortex extending through subcortical white matter to the basal ganglia, including the head of the caudate nucleus but sparing the thalamus.

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“…Otras estructuras neuroanatómicas cuya lesión provoca MA se sitúan en el diencéfalo, principalmente algunos núcleos talámicos, y en el mesencefálo, quizás por afectación del sistema reticular activador ascendente (Cairns, 1952;Caravanna, Bertero, Caravanna, Strigaro y Monaco, 2009;Cravioto, Silberman y Feigin, 1960;Kemper y Romanul, 1967;Ross y Stewart, 1981;Skultety, 1968;Wijdicks y Crandford, 2005). Ambas formas dan lugar al denominado MA diencéfalo-mesencefálico que se caracteriza por un menor grado de vigilancia que en el mutismo frontal.…”

Section: Fisiopatología De Las Lesiones En El Mutismo Acinéticounclassified

Mutismo Acinético: revisión, propuesta de un protocolo neuropsicológico para el diagnóstico diferencial y su aplicación a un caso.

Rodríguez-Bailón¹,

Triviño-Mosquera

Ruiz-Pérez³

et al. 2012

analesps

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Resumen: El mutismo acinético es considerado como una alteración del estado motivacional de la persona, por la cual el paciente es incapaz de iniciar respuestas verbales o motoras de carácter voluntario, aún teniendo preservadas las funciones sensoriomotoras y de vigilancia. La lesión, que puede ser vascular, infecciosa, tóxica o degenerativa, incide sobre dos circuitos que podrían estar funcionalmente relacionados: el cortex frontal medial con afectación del cíngulo anterior, o el daño en regiones talámicas y mesencefálicas relacionadas con la formación reticular activadora ascendente. El diagnóstico de mutismo acinético resulta a veces difícil de establecer, y suele confundirse con algunos tipos de afasias o estados de alteración de la conciencia, que tienen un abordaje clínico y un pronóstico notablemente diferentes. Con el objetivo de llevar a cabo un buen diagnóstico diferencial proponemos un protocolo clínico con una evaluación neuropsicológica breve de las funciones que pudieran estar diferencialmente afectadas en todos esos síndromes, como atención, praxias y lenguaje. Exponemos un caso de mutismo evaluado con este protocolo para demostrar su especificidad a la hora de distinguirlo de otras afecciones o síndromes. Palabras clave: mutismo acinético; córtex cingulado anterior; evaluación neuropsicológica; neuropsicología; síndrome frontal.Title: Akinetic Mutism: a review, proposal of neuropsychological protocol to establish a differential diagnosis and its application to a case. Abstract: Akinetic mutism is considered as a disturbance of a person´s motivational state, therefore the patient is unable to initiate verbal or motor responses, although they continue to maintain sensorimotor and vigilant functions. The lesion can be vascular or it can be caused by infections, cerebral degeneration and toxicity. Lesions can influence the functions of two cerebral circuits: the Frontal medial cortex affecting to cingulated cortex, or it can damage the thalamic and mesencephalic regions related to the ascending reticular activating system. It is difficult to diagnose Akinetic Mutism since it can be confused with some types of aphasia and altered states of consciousness, which require different interventions. In order to complete a clinical protocol we recommend a brief neuropsychological evaluation of functions such as attention, praxis and language, all of which could be affected by the syndromes previously named. We expound a case of akinetic mutism evaluated with this protocol in order to show its specificity distinguishing akinetic mustism from other syndromes. Key words: akinetic mutism; anterior cingulate cortex; neuropsychological assesment; neuropsychology; frontal syndrome. Introducción y objetivosEl mutismo acinético (MA) se configura como un síndrome difícil de diagnosticar que, a menudo, se confunde con otras alteraciones neuropsicológicas tales como afasia motora, trastornos atencionales, estados de mínima conciencia o síndrome de cautiverio, entre otros.Nuestro trabajo tiene un doble objetivo. En prime...

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Clinical and Experimental Aspects of Akinetic Mutism

Cited by 47 publications

References 31 publications

Paramedian thalamic and midbrain infarcts: Clinical and neuropathological study

Paramedian thalamic and midbrain infarcts: Clinical and neuropathological study

Akinetic mutism and bilateral anterior cerebral artery occlusion

Mutismo Acinético: revisión, propuesta de un protocolo neuropsicológico para el diagnóstico diferencial y su aplicación a un caso.

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