Stuttering without callosal apraxia resulting from infarction in the anterior corpus callosum

Kakishita, Koji; Sekiguchi, Eri; Maeshima, Shinichiro; Okada, Hideo; Okita, Ryuji; Ozaki, Fuminori; Moriwaki, Hiroshi

doi:10.1007/s00415-004-0424-1

Cited by 8 publications

(2 citation statements)

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“…In addition to this case, there have been five cases of infarct of the corpus callosum that caused stuttering. All five involved the body to some extent and three involved the splenium 19. Three of the five developed a callosal apraxia, though that was not the case with our patient.…”

Section: Discussioncontrasting

confidence: 64%

Acquired stuttering due to recurrent anaplastic astrocytoma

Peters

Turner

2013

BMJ Case Reports

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Acquired (neurogenic) stuttering is a rare phenomenon seen after cerebral infarction or brain injury. Aetiology of this symptom is unclear, but recent evidence supports that it is a disturbance in the left hemispheric neural network involving the interplay between the cortex and basal ganglia. We present the case of a patient who develops acquired stuttering after a recurrence of a right temporoparietal anaplastic astrocytoma (WHO grade III). We also review other cases of acquired stuttering and known anatomical correlates.

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Section: Discussioncontrasting

confidence: 64%

Acquired stuttering due to recurrent anaplastic astrocytoma

Peters

Turner

2013

BMJ Case Reports

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“…Although less frequently, right hemisphere lesions have also been associated with neurogenic stuttering following stroke, including the temporal [Ardilla and Lopez, 1986] and frontal lobes [Balasubramanian et al, 2003], the basal ganglia [Tani and Sakai, 2011] and the thalamus [Abe et al, 1993]. In addition, cases have been reported with involvement of the supplementary motor area [Ackermann et al, 1996;Van Borsel et al, 1998], corpus callosum [Hamano et al, 2005;Kakishita et al, 2004], cerebellum [Grant et al, 1999;Tani and Sakai, 2010], and brainstem [Abe et al, 1993;Balasubramanian et al, 2003]. These case-based observations clearly represent a bewildering array of possible lesion sites reported to be associated with the onset of neurogenic stuttering following stroke.…”

Section: Introductionmentioning

confidence: 99%

A crucial role for the cortico-striato-cortical loop in the pathogenesis of stroke-related neurogenic stuttering

Theys

Nil

Thijs³

et al. 2012

Hum. Brain Mapp

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Neurogenic stuttering is an acquired speech disorder characterized by the occurrence of stuttering-like dysfluencies following brain damage. Because the onset of stuttering in these patients is associated with brain lesions, this condition provides a unique opportunity to study the neural processes underlying speech dysfluencies. Lesion localizations of 20 stroke subjects with neurogenic stuttering and 17 control subjects were compared using voxel-based lesion symptom mapping. The results showed nine left-hemisphere areas associated with the presence of neurogenic stuttering. These areas were largely overlapping with the cortico-basal ganglia-cortical network comprising the inferior frontal cortex, superior temporal cortex, intraparietal cortex, basal ganglia, and their white matter interconnections through the superior longitudinal fasciculus and internal capsule. These results indicated that stroke-induced neurogenic stuttering is not associated with neural dysfunction in one specific brain area but can occur following one or more lesion throughout the cortico-basal ganglia-cortical network. It is suggested that the onset of neurogenic stuttering in stroke subjects results from a disintegration of neural functions necessary for fluent speech.

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