Midbrain Ischemia Presenting as Vertical Gaze Palsy: Value of Diffusion-Weighted Magnetic Resonance Imaging

Seifert, Thomas; Enzinger, C; Ropele, Stefan; Storch, Maria K.; Fazekas, Franz

doi:10.1159/000078601

Cited by 8 publications

(8 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This seems likely because it is well known that supranuclear oculomotor disturbances are caused by paramedian midbrain lesions. 30 Furthermore, because multisystem involvement is a typical feature of mitochondrial diseases, 31 this novel phenotype may reflect a mitochondrial dysfunction that contributes to the underlying pathogenesis of SPG7-HSP. Paraplegin, which is localized to inner mitochondrial membrane, is a mitochondrial metalloprotease belonging to the AAA protein superfamily (adenosine triphosphatase associated with diverse cellular activities).…”

Section: Mutation Analysismentioning

confidence: 99%

A novel form of autosomal recessive hereditary spastic paraplegia caused by a new SPG7 mutation

Warnecke

Duning²,

Schwan³

et al. 2007

Neurology

View full text Add to dashboard Cite

The new SPG7 gene mutation leads to a novel complicated autosomal recessive hereditary spastic paraparesis phenotype that widens the spectrum of different brain systems that are optionally affected in hereditary spastic paraplegia (HSP). In this novel phenotype, spastic paraparesis is related to cerebral damage of corticospinal tracts. Impairment of attention and executive functions is due to white matter loss in frontal lobes. Furthermore, supranuclear palsy is caused by white matter damage in the midbrain. This multisystem affection, which was detected by the use of diffusion tensor imaging, may reflect a mitochondrial dysfunction that contributes to the underlying pathogenesis of SPG7-HSP.

show abstract

Section: Mutation Analysismentioning

confidence: 99%

A novel form of autosomal recessive hereditary spastic paraplegia caused by a new SPG7 mutation

Warnecke

Duning²,

Schwan³

et al. 2007

Neurology

View full text Add to dashboard Cite

show abstract

“…Similarly, damage to NSP nuclei like the pulvinar leads to spatial neglect in humans (Karnath et al, 2002;Ward et al, 2002). Ischemia in the area supplied by the thalamo-subthalamic paramedian artery when extending to the paramedian tha-lamus (ventral posterior nuclei, dorsomedial, centromedian and central medial nuclei) shows itself clinically as impaired consciousness, hypersomnia, aphasia, amnesia and hemineglect (Seifert et al, 2004). These three above-described classes of empirical facts show that the thalamus is in a position to hold the prime role in modulating the state and level of consciousness.…”

Section: Empirical Results Supporting the Role Of Thalamus In Consciomentioning

confidence: 99%

Dendritic integration theory: A thalamo-cortical theory of state and content of consciousness

2020

View full text Add to dashboard Cite

The idea that the thalamo-cortical system is the crucial constituent of the neurobiological mechanisms of consciousness has a long history. For the last few decades, however, consciousness research has to a large extent overlooked the interplay between the cortex and thalamus. Here we revive an integrated view of the neurobiology of consciousness by presenting and discussing several recent major findings about the role of the thalamocortical interactions in consciousness. Based on these findings we propose a specific cellular mechanism how thalamic nuclei modulate the integration of different processing streams within single cortical pyramidal neurons. This theory is inspired by recent work done in rodents, but it integrates decades of work conducted on various species. We illustrate how this new view readily explains various properties and experimental phenomena associated with conscious experience. We discuss the implications of this idea and some of the experiments that need to be done in order to test it. Our view bridges two long-standing perspectives on the neural mechanisms of consciousness and proposes that cortical and thalamo-cortical processing interact at the level of single pyramidal cells.

show abstract

“…There were not many reported cases of upward and downward gaze palsy due to a unilateral rostral and dorsal midbrain lesion [1][2][3][4][5][6][7][8][9][10]. Therefore, the neural structures and pathways underlying vertical gaze control are yet not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Upward and Downward Gaze Palsy, Convergence Palsy, Concomitant Skew Deviation and Bilateral Light-Near Dissociation Due to a Unilateral Rostral and Dorsal Midbrain Infarction

2015

View full text Add to dashboard Cite

A 48-year-old man with atrial septal defect abruptly developed upward and downward gaze palsy with a loss of vertical oculocephalic reflex and smooth pursuit, convergence palsy, concomitant skew deviation with left-sided hypotropia, and bilateral light-near dissociation. Cranial magnetic resonance imaging demonstrated a localized infarction in the left-sided rostral and dorsal midbrain. Neuro-ophthalmologic findings suggested that the left-sided rostral interstitial nucleus of the medial longitudinal fasciculus, left-sided interstitial nucleus of Cajal, and posterior commissure might be involved. There were not convergence retraction nystagmus, and eyelids retraction and lag, probably because the nucleus of the posterior commissure might be spared.

show abstract

Midbrain Ischemia Presenting as Vertical Gaze Palsy: Value of Diffusion-Weighted Magnetic Resonance Imaging

Cited by 8 publications

References 19 publications

A novel form of autosomal recessive hereditary spastic paraplegia caused by a new SPG7 mutation

A novel form of autosomal recessive hereditary spastic paraplegia caused by a new SPG7 mutation

Dendritic integration theory: A thalamo-cortical theory of state and content of consciousness

Upward and Downward Gaze Palsy, Convergence Palsy, Concomitant Skew Deviation and Bilateral Light-Near Dissociation Due to a Unilateral Rostral and Dorsal Midbrain Infarction

Contact Info

Product

Resources

About