mystery of yawning
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La parakinésie brachiale oscitante
Yawning: its cycle, its role
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Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
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15 janvier 2012
J Clin Neurosci.
2011;18(12):1738-40
A child with mutism after bilateral thalamic infarction.
 
Pluchon C, Jaafari N, Loiseau-Corvez MN, Parizel A, Vandermarcq P, Hankard R, Gil
 
Service de Neurologie, Unité de Neuropsychologie et Rééducation du Langage, Centre Hospitalier Universitaire (CHU) de Poitiers, France.

Chat-logomini

 
The occurence of mutism after thalamic lesions has rarely been observed before adulthood. We report a 6.5-year-old girl who presented with sudden mutism with a decreased level of alertness. Her MRI revealed a T2-fluid attenuated inversion recovery hyperintensity in both thalami, which suggested bithalamic infarction in the territory of the thalamo-perforating arteries and, more specifically, the para-median territories. Mutism was followed by a deficit of speech initiation with slow and slurred speech. Her speech returned to normal at 3 months after the onset of symptoms. Thus mutism could be the equivalent of akinetic mutism limited to the speech sphere.
 
1. Introduction
 
 
Thalamic lesions, including paramedian thalamic infarction, may cause akinetic mutism (AM),' -3 a neurological disorder in which the patient in unable to speak (mutism) and move (akinesia). AM was described in 1941 by Cairns et al. in a patient with an epidermoid cyst in the third ventricle - the patient became more alert and responsive after several evacuations of the cyst, but he could not speak.4 Following this landmark case, the term "akinetic mutism" has been used to describe a syndrome characterized by marked reduction of nearly all motor functions, including facial expression, gestures, and speech output, but with some degree of alertness. The critical areas involved are the frontal lobe (cingulate gyrus, supplementary motor area, and the dorso-lateral border zones), basal ganglia (caudate and putamen), and the mesencephalus and thalamus. Moreover, thalamic lesions may cause aphasia, particularly after infarction of the tubero-thalamic artery and/or the territory of the paramedian thalamo-perforating artery.''6 These aphasias may cause a reduction in speech, wordfinding deficits, paraphasias, hypophonia, and dysarthria, but never mutism only. In children, thalamic lesions may cause aphasia"' or AM.9 A strictly isolated mutism has rarely been documented. We have found only one patient, 17 years of age, who presented with complete mutism with acute confusion after bithalamic infarction following a deep cerebral vein thrombosis.'() Here we report mutism after paramedian bilateral thalamic infarctions in a young child, and discuss the significance of this mutism.
 
2. Case report
 
A 6.5-year-old girl without any significant medical history presented at Centre Hospitalier Universitaire (CHU), Poitiers, France, after acute onset of paramedian bilateral thalamic infarction. Her family, birth history, and developmental milestones were unremarkable. Six hours before her admission, she was restless and had elementary auditory hallucinations before falling asleep, and once asleep, she could not be woken by her mother.
 
On admission she was afebrile, in a sleep-like state, with a regular heart rate of 84 beats per minute, and blood pressure of 108/ 58 mm Hg. Neurologic evaluation showed that she woke only with painful stimuli. She was completely mute and did not answer any questions. When she was awake she could comply with simple instructions (for example, sitting on her bed and raising an arm). She had normal symmetric mobility in her limbs with brisk deep tendon reflexes, normal pupillary reactions and normal fundoscopy. Her eye movements were normal. She had urinary incontinence. When she was awake, she swallowed slowly without choking. Her ear, nose and throat evaluation was normal.
 
Her cerebrospinal fluid and routine hematological and biochemical tests were normal, and were negative for blood alcohol and urine toxicology. Her coagulation tests, which included fibrinogen, prothrombin, antithrombin III, protein C, protein S, factors V, VIII, and IX were normal. Test activated protein-C resistance was normal. Tests for the human immunodeficiency virus, hepatitis B, and the Epstein-Barr virus were negative. She tested negative for a collagen-related disease or a vasculitis syndrome (that is, lupus anticoagulant, rheumatoid factor, anticardiolipin antibodies, antineutrophilic cytoplasmic antibodies, lupus erythematosus [LE] cell and antinuclear factors). Two days later, periods of sleep-mess were alternated with alertness, and although she could comply with commands, she remained completely mute.
 
A brain MRI on admission showed an area of hyperintensity on T2-weighted and fast fluid-attenuated inversion recovery images consistent with infarction and/or edema in the thalami. Two days after admission, magnetic resonance angiography showed no vessel abnormality. Arteriography performed 3 days after admission showed that Percherons" artery was normal, and vascularised both thalami well.
 
An echocardiogram, using colour Doppler flow, revealed a small patent foramen ovale with a left to right shunt. Thus, a paradoxical embolism from a subclinical venous thrombosis was presumed to have occurred, causing a cerebral infarction. A non-surgical transcatheter closure of the patent foramen ovale was planned. After a few days of sodium enoxaparin, she was started on low dose acetyl salicylate.
 
Fifteen days later, an electroencephalogram demonstrated major polymorphic delta waves and sharp waves predominantly in the bilateral frontal derivations. Neurologic evaluation showed a moderate right hemiparesis with right central facial paresis. We observed fluctuations in vigilance, and yawning, with intermittent chewing movements. However, when the vigilance was normal, the patient was completely mute - no sound was emitted spontaneously. She could understand and comply with instructions (for example, correctly pointing to her forehead, nose, and her mother's mouth). She was able to identify simple words correctly written with doctor's oral commands. Her mutism progressively receded towards defective speech initiation with a reduction of spontaneous speech. One month later, she obtained a score of 50/100 (normal, average score of 51 for the same-age population) on a battery of vocabulary tests for children (picture denomination) by Chevrie-Muller et al. 12 Three months later, she showed significant recovery: her speech was fluent and her verbal expression was normal.
 
3. Discussion
 
Stroke affecting the thalamus may cause aphasia, 5,6 or AM like stroke also affecting the cingulate gyrus, the basal ganglia
and mesencephalon.3 To our knowledge, this is the first report of a young child presenting with mutism only (without other symptoms). Kothare et al.1° have reported mutism in a 17year-old girl after a hemorrhagic thalamic infarction secondary to deep cerebral vein thrombosis. After the mutism had resolved, there was a deficit of sustained attention and changing capabilities. Garg and De Myer reported three children with infarction of the thalamo-perforating artery, who all presented, as in our patient, with lethargy, which receded in 3 or 4 days, but none suffered from mutism.
 
Although our patient was not confused, as were Kothare et al's patients,1° she did experience disturbances in vigilance. These changes in vigilance led us to confirm that she became mute immediately after the stroke. The mutism subsequently gave way to a speech initiation deficit, with slow and slurred speech. Her speech then became normal. What was the significance of the mutism? It was not initially a transcortical motor aphasia since repetition was impossible. When she recovered from mutism, there was only a slowing of speech. Thus, it could not be considered aphasia. We concluded that her mutism could be considered equivalent to AM limited to speech. This observation, as also demonstrated by Garg and DeMyer,7 correlates with the relatively good prognosis of thalamic infarction in children.