higher function deficits resulted from lesions of white matter or the association cortices
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Disconnection Syndromes (DS). Higher function deficits resulted from lesions of white matter or the association cortices ‘Functional’ disorders such as schizophrenia, autism, dyslexia Founded on: Anatomy, post-mortem dissections, monkeys. More recently: DTI, Tractography. - PowerPoint PPT PresentationTRANSCRIPT
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Higher function deficits resulted from lesions of white matter or the association cortices
‘Functional’ disorders such as schizophrenia, autism, dyslexia
Founded on: Anatomy, post-mortem dissections, monkeys.
More recently: DTI, Tractography
Disconnection Syndromes (DS)
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‘The Classical associationist era’ Paradigm based on two central tenets:
1) Localization of function in discrete cortical areas
2) Connections between areas through white matter association pathways
DS before Geschwind
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Franz Joseph Gall (1758-1828): White matter Grey matter Phrenology (England)
DS before Geschwind
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Theodor Meynert (1833-1892): White matter fibers:
1) Projection fibers
2) Commissural fibers
3) Association fibers
DS before Geschwind
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Karl Wernicke (1848-1904): The father of Disconnection theory ‘fundamental psychic elements’ /
‘memory images’
“… mediated by means of their manifold connections via the association fibres” (Wernicke, 1885)
DS before Geschwind
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Karl Wernicke (1848-1904): Higher functions arise through associative
connections,
Disorders of higher function from their breakdown
Critisizm: No cortical specialization other than motor/sensory
Theoretical framework explained classical DS
DS before Geschwind
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Motor component (Broca) Sensory component (Wernicke) Lesions:
Broca Pure motor aphasia Wernicke Pure sensory aphasia Arcuate Fasciculus Conduction aphasia
Conduction Aphasia
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Lesions:
Cortical (Visual cortex)
Apperceptive agnosia
Trans-Cortical (associative
fiber connections) Associative agnosia
Visual Agnosia
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Hugo Liepmann (1863-1925)
Higher movement disorders Spontaneous movements Planned gestures
Disconnection of visual, auditory and somatosensory areas from motor area
The apraxias
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Left hemisphere dominant for complexmovements control
Lesions: Left parietal lobe bilateral apraxia
Anterior portion of corpus callosum Unilateral apraxia (left)
Left motor area (not shown)
bilateral apraxia + right paresis
The apraxias
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Jules Déjérine (1849-1917)
Left angular gyrus = visual verbal centre
Lesions: Left angular gyrus Alexia + Agraphia Left central white matter occipital lesion
Pure alexia
Pure Alexia
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Déjérine model suggested Higher functions located in cortex An area specialized for higher visual function outside
the visual cortex
Wernicke’s opposition to higher functional centers
The early 20th century (holistic, anti-localizationist)
1965 (localization theory, DS)
The fall of the classical era
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Flechsig’s rule Include sensory and motor cortices and
interhempispheric connections Association cortex acted as an obligatory relay
station
Phylogenetic perspective Higher-order association area in the parietal lobe Connections that did not depend on the limbic
system
Geschwind’s neo-associationism
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The role of the angular gyrus: Déjérine visual memories of letters and words Geschwind forming multimodality associations
Geschwind focused on DS caused by lesions of association cortex (parietal lobe)
“…A ‘disconnexion lesion’ will be a large lesion either of association cortex or of the white matter leading from association cortex” (Geschwind, 1965)
Geschwind’s neo-associationism
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Failure of a stimulus to evoke memories/affective response
Disconnections between limbic lobe and - Somatosensory cortex pain asymbolia Auditory cortex verbal learning impairment etc. Visual system (indirect connections) no
symptoms
Disconnections between sensory areas and limbic cortex
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Modality-specific language deficits
Disconnections can be direct or indirect (through the angular gyrus)
Four syndromes: Tactile aphasia/Anomia Pure word deafness Pure alexia Modality-specific agnosia
Disconnections between sensory areas and Wernicke’s area
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Left hemisphere disconnections:
Hand motor cortex from posterior sensory areas Apraxia
Broca’s area from Wernicke’s Conduction aphasia
Disconnections between sensory areas and motor cortex
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Geschwind contribution:1. Association cortex as an obligatory relay2. Hierarchies of associations within the IPL3. Importance of IPL in phylogeny and ontogeny of
language
Two research paths: Damasio (CT, PET, SPET) Mesulam (Tracing neural connections, computation
theory etc.)
DS After Geschwind
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Functional subdivision of the association cortex
‘Extended territories’ composed of specialized cortical subregions serving different but related functions
Parallel, bidirectional, distributed processing
Contemporary neuroanatomical basis of higher brain functions
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Two key elements underlie higher function deficits:1. Loss of specialized cortical function2. Damage to connecting pathways
Recent techniques enable research of disorders caused by hyperconnection and cortical hyperfunction
Contemporary neuroanatomical basis of higher brain functions
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Territories composed of specialized subregions Intra-territorial connections (U-shaped) Inter-territorial connection (Long)
Hodotopic framework of clinicopathological correlations
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Topological mechanism (Topos = place) Prosopagnosia, face hallucinations
Hodological mechanism (Hodos = road / path) Conduction aphasia, autism
Hodotopic framework of clinicopathological correlations
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Hodotopic framework of clinicopathological correlations
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Direct (Long segment) Indirect (Anterior, Posterior)
Pure hodological mechanism: Long segment Conduction
aphasia Long, anterior, posterior
Global aphasia
Language network disorders
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Direct (Long segment) Indirect (Anterior, Posterior)
Pure topological mechanism: Anterior portions of
Geschwind’s Non-fluent aphasia
All of Geschwind’s Mixed trans-cortical
aphasia All of Geschwind’s + deep white
matter Global aphasia
Language network disorders
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Direct (Long segment) Indirect (Anterior, Posterior)
Hyperfunction: Indirect Semantically based
sympthoms
Direct Excessive repetition ( e.g. echolalia)
Language network disorders
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Med. Frontal Med. Parietal (DMPF, yellow) Motor SPL (DLFP, green) Motor IPL (VLFP, red)
Lesions: SPL Depends on which praxic
subfunctions are affected
SPL + White matter Additional abnormalities
Praxis network disorders
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Indirect (U-shaped occipito-temporal, red) Direct (Inferior longitudinal fasciculus, green)
Lesions: Direct specific deficits related
to the cortical specializations lost
Indirect + medial white matter Visual hypo-emotionality/
Visual amnesia
Visual network disorders
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Direct (Inferior longitudinal fasciculus, green) Indirect (U-shaped occipito-temporal, red)
Hyperfunction: Indirect Visual hallucinations
Hyperconnectivity: Indirect / Direct Unclear
( Synaesthesia? Phobia)?
Visual network disorders