Balint-Holmes Syndrome & Organization of Parietal Lobe Flashcards
Bálint-Holmes Syndrome
- Spatial restriction of attention/ simultagnosia:
- Psychic paralysis of gaze/ ocular apraxia /oculomotor apraxia
- Optic ataxia
Bálint-Holmes Syndrome Location of damage
Bilateral and nearly symmetric lesions:
• Posterior parietal lobe, upper temporal lobe, and occipital lobe
Bálint-Holmes Syndrome Causes of Damage
- Cerebrovascular disease (as in Bálint’s original case)
- Tumour
- Trauma
- Prion disorders (e.g. Creutzfeldt-Jakob disease) and viral infections (e.g. HIV).
- Neurodegenerative conditions (Parkinson’s, Alzheimer’s disease) might be the most common cause
Bálint-Holmes Syndrome Symptoms/Deficits (in first patient)
• Left hemineglect syndrome
- Could shift attention and “see” things on the left following a verbal instruction
• Apperceptive agnosia
• Visual disorientation
Bálint-Holmes Syndrome Symptoms/Deficits
- Defect in reading and writing
- Fail to recognize position and distances between objects
- Unable to grasp or point accurately to objects
Spatial disorder of attention/ simultagnosia
Inability to report all items and relations in a complex visual scene
Ocular/oculomotor apraxia
inability to disengage/shift gaze (could be also attention) from fixated objects (visual grasp)
- With effort (e.g., on verbal command), Balint’s patient could “disengage” attention from the right visual field and “shift” attention to the left
- Wandering gaze until the target is located
- In some patients, the eyes can move to a non-visual target (e.g., source of sound) spontaneously.
Optic Ataxia
Inability to reach and grasp targets under visual
guidance (greatest deficit in peripheral visual field):
• Greatest deficit in peripheral visual field
• Lack of coordination between visual input and motor
output
- “Hand effect” -> misreaching with one hand into any
visual field (usually tested for the dominant hand)
- “Field effect” -> difficulty reaching in the contralesional
field with any hand
Isolated Optic Ataxia
- Happens rarely
- Can be produced by localized discrete unilateral lesions
- Intact visual fields and stereoscopic vision
- Normal oculomotor control
- Normal proprioception
- Normal motor abilities except for misreaching
Optic Ataxia: location of damage
Large bilateral posterior lesions involving multiple functional areas
Optic Ataxia: deficits
Deficits in reaching:
- Dysmetria under visual guidance (overshooting or undershooting of the target)
- No deficit when reaching is aided by non-visual (proprioceptive or auditory) cues to reach a target
- Reaching which is not under visual guidance remains normal (bring food to mouth normally)
Hypotheses explaining reaching deficits in optic ataxia
- Errors in reaching are due to disruption of an online
correction mechanism (test using “jumping targets”)
- Optic ataxia patients do not show automatic adjustment
of movements
- Largest impairment in the peripheral vision - Failure to convert the location of the visual stimulus,
coded in eye coordinates into the appropriate action in
motor (muscle) coordinates (deficient coordinate
transformation)
Posterior Parietal Cortex: Area LIP
- > motor plan for eye movements (saccadic eye movements)
- > attention processing
Posterior Parietal Cortex: Area AIP
grasping movements
Parietal Reach Region (PRR)
- > includes areas MIP, V6A (& other areas near parieto-occipital fissure)
- > reach-related activity
- > plan of reaching movements
