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Higher function deficits resulted from lesions of white matter or the association cortices

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.

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Higher function deficits resulted from lesions of white matter or the association cortices

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  1. 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

  2. DS before Geschwind • ‘The Classical associationist era’ • Paradigm based on two central tenets: • Localization of function in discrete cortical areas • Connections between areas through white matter association pathways

  3. DS before Geschwind • Franz Joseph Gall (1758-1828): • White matter • Grey matter • Phrenology (England)

  4. DS before Geschwind • Theodor Meynert (1833-1892): • White matter fibers: • Projection fibers • Commissural fibers • Association fibers

  5. DS before Geschwind • 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)

  6. DS before Geschwind • 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

  7. Conduction Aphasia • Motor component (Broca) • Sensory component (Wernicke) • Lesions: • Broca Pure motor aphasia • Wernicke  Pure sensory aphasia • Arcuate Fasciculus  Conduction aphasia

  8. Visual Agnosia • Lesions: • Cortical (Visual cortex) Apperceptiveagnosia • Trans-Cortical (associative fiber connections) Associative agnosia

  9. The apraxias • Hugo Liepmann (1863-1925) • Higher movement disorders • Spontaneous movements  • Planned gestures  • Disconnection of visual, auditory and somatosensoryareas from motor area

  10. The apraxias • Left hemisphere dominant for complex movements control • Lesions: • Left parietal lobe  bilateral apraxia • Anterior portion of corpus callosum Unilateral apraxia (left) • Left motor area (not shown)  bilateral apraxia + right paresis

  11. Pure Alexia • Jules Déjérine (1849-1917) • Left angular gyrus= visual verbal centre • Lesions: • Left angular gyrus Alexia + Agraphia • Left central white matter occipital lesion  Pure alexia

  12. The fall of the classical era • 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)

  13. Geschwind’s neo-associationism • 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

  14. Geschwind’s neo-associationism • 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)

  15. Disconnections between sensory areas and limbic cortex • 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

  16. Disconnections between sensory areas and Wernicke’s area • 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

  17. Disconnections between sensory areas and motor cortex • Left hemisphere disconnections: • Hand motor cortex from posterior sensory areas  Apraxia • Broca’s area from Wernicke’s Conduction aphasia

  18. DS After Geschwind • Geschwind contribution: • Association cortex as an obligatory relay • Hierarchies of associations within the IPL • Importance of IPL in phylogeny and ontogeny of language • Two research paths: • Damasio (CT, PET, SPET) • Mesulam (Tracing neural connections, computation theory etc.)

  19. Contemporary neuroanatomical basis of higher brain functions • Functional subdivision of the association cortex • ‘Extended territories’ composed of specialized cortical subregions serving different but related functions • Parallel, bidirectional, distributed processing

  20. Contemporary neuroanatomical basis of higher brain functions • Two key elements underlie higher function deficits: • Loss of specialized cortical function • Damage to connecting pathways • Recent techniques enable research of disorders caused by hyperconnectionand cortical hyperfunction

  21. Hodotopic framework of clinicopathological correlations • Territories composed of specialized subregions • Intra-territorial connections (U-shaped) • Inter-territorial connection (Long)

  22. Hodotopic framework of clinicopathological correlations • Topological mechanism (Topos = place) • Prosopagnosia, face hallucinations • Hodological mechanism (Hodos = road / path) • Conduction aphasia, autism

  23. Hodotopic framework of clinicopathological correlations

  24. Language network disorders • Direct (Long segment) • Indirect (Anterior, Posterior) • Pure hodological mechanism: • Long segment  Conduction aphasia • Long, anterior, posterior  Global aphasia

  25. Language network disorders • 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

  26. Language network disorders • Direct (Long segment) • Indirect (Anterior, Posterior) • Hyperfunction: • Indirect Semantically based sympthoms • Direct  Excessive repetition (e.g. echolalia)

  27. Praxis network disorders • 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

  28. Visual network disorders • 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

  29. Visual network disorders • Direct (Inferior longitudinal fasciculus, green) • Indirect (U-shaped occipito-temporal, red) • Hyperfunction: • Indirect Visual hallucinations • Hyperconnectivity: • Indirect / Direct Unclear (Synaesthesia? Phobia?)

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