Difference between revisions of "Bilateral Parietal Lobe Dysfunction"

 
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'''Balint’s syndrome''' (Chechlacz 2018) Patients have characteristic lesions in bilateral parietal or parieto-occipital lobes (typically part of superior parietal lobule and angular gyrus)
 
'''Balint’s syndrome''' (Chechlacz 2018) Patients have characteristic lesions in bilateral parietal or parieto-occipital lobes (typically part of superior parietal lobule and angular gyrus)
 
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* May occur from invasive tumors, global cerebral hypoperfusion affecting watershed areas between middle and posterior cerebral arteries, neurodegenerative disease (PCA), or traumatic injury. Patients experience a chaotic world around them, as unreachable objects appear and disappear out of mind; may bump into objects and have difficulty eating/drinking due to difficulties reaching for food.
May occur from invasive tumors, global cerebral hypoperfusion affecting watershed areas between middle and posterior cerebral arteries, neurodegenerative disease (PCA), or traumatic injury. Patients experience a chaotic world around them, as unreachable objects appear and disappear out of mind; may bump into objects and have difficulty eating/drinking due to difficulties reaching for food.
 
  
 
Comprises of three main symptoms:
 
Comprises of three main symptoms:
 
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* Simultanagnosia – a lost ability to comprehend more than one object in a scene. Dorsal simultanagnosia: resulting from impaired spatial awareness of more than one object, as seen in Balint’s syndrome. Ventral simultanagnosia: damage to left temporo-occipital regions (left posterior ventral cortex) resulting in alexia and impaired reporting of multiple letters
Simultanagnosia – a lost ability to comprehend more than one object in a scene. Dorsal simultanagnosia: resulting from impaired spatial awareness of more than one object, as seen in Balint’s syndrome. Ventral simultanagnosia: damage to left temporo-occipital regions (left posterior ventral cortex) resulting in alexia and impaired reporting of multiple letters
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* Oculomotor apraxia – difficulty with voluntary shifting of gaze direction without evidence of paralysis. Eye movements guided by sound or touch may remain intact
 
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* Optic ataxia – inability to point to or grasp objects under visual guidance
Oculomotor apraxia – difficulty with voluntary shifting of gaze direction without evidence of paralysis. Eye movements guided by sound or touch may remain intact
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** No difficulty when guided by sound or touch
 
 
Optic ataxia – inability to point to or grasp objects under visual guidance
 
o No difficulty when guided by sound or touch
 
  
  

Latest revision as of 09:35, 13 June 2021

Balint’s syndrome (Chechlacz 2018) Patients have characteristic lesions in bilateral parietal or parieto-occipital lobes (typically part of superior parietal lobule and angular gyrus)

  • May occur from invasive tumors, global cerebral hypoperfusion affecting watershed areas between middle and posterior cerebral arteries, neurodegenerative disease (PCA), or traumatic injury. Patients experience a chaotic world around them, as unreachable objects appear and disappear out of mind; may bump into objects and have difficulty eating/drinking due to difficulties reaching for food.

Comprises of three main symptoms:

  • Simultanagnosia – a lost ability to comprehend more than one object in a scene. Dorsal simultanagnosia: resulting from impaired spatial awareness of more than one object, as seen in Balint’s syndrome. Ventral simultanagnosia: damage to left temporo-occipital regions (left posterior ventral cortex) resulting in alexia and impaired reporting of multiple letters
  • Oculomotor apraxia – difficulty with voluntary shifting of gaze direction without evidence of paralysis. Eye movements guided by sound or touch may remain intact
  • Optic ataxia – inability to point to or grasp objects under visual guidance
    • No difficulty when guided by sound or touch


References

Chechlacz, M. Bilateral parietal dysfunctions and disconnections in simultanagnosia and Bálint syndrome. in Handbook of Clinical Neurology vol. 151 249–267 (Elsevier, 2018). https://pubmed.ncbi.nlm.nih.gov/29519461/