Visual Pathways and Agnosia PDF

**Visual pathways and agnosia** **Sensation vs perception** **SENSATION** occurs when sensory receptors detect sensory stimuli: sensory receptors are specialized neurons that respond to specific types of stimuli → when sensory information is detected by a sensory receptor, sensation has occurred...

**Visual pathways and agnosia** **Sensation vs perception** **SENSATION** occurs when sensory receptors detect sensory stimuli: sensory receptors are specialized neurons that respond to specific types of stimuli → when sensory information is detected by a sensory receptor, sensation has occurred E.G: when light that enters the eye causes chemical changes in photoreceptors of the retina ↓ These cells relay messages (action potentials) to the CNS TRANSDUCTION = the conversion from sensory stimuli to action potentials; it represents the first step toward perception **PERCEPTION** involves the organization, interpretation, and conscious experience of those neural pieces of information → it organizes sensations into complex representations ++ not all sensory stimuli are perceived (and become conscious!): our perceptions are affected by various factors, including beliefs, values, prejudices, and previous experiences **Visual pathways** Up to half of the cerebral cortex is directly or indirectly involved in visual processing Visual pathways = ganglion cells of the retina → optic nerves → optic chiasm → lateral geniculate nucleus (LGN) of the thalamus → V1 → associative visual cortices (V2-V5)  Visual pathways carry the information segregated: 1. Spatially (retinotopic organization) 2. Qualitatively (color, shape, movement) → this segregation (spatial versus qualitative features) is maintained at the higher levels of the system \- - \> two pathways, 'what and where': they always work in parallel Immagine che contiene Cervello, disegno, schizzo, arte Descrizione generata automaticamente **WHERE** **PATHWAY**: it starts from V1 and ends in the parietal lobe **WHAT PATHWAY**: starts from V1 and ends in temporal lobe **V1**: maps and processes visual stimuli -- OCCIPITAL LOBE **V2**: important for color discrimination -- in the cuneus **V4**: important for object recognition -- in the fusiform gyrus, temporal lobe, what pathway **V3** - **V5**: important for movement and spatial perception -- in the where pathway E.G: If we have a lesion in V4, we will have achromatopsia VS If we have a lesion in V5, we will have akinetopsia **Achromatopsia** **CEREBRAL ACHROMATOPSIA** = acquired color blindness → bilateral lesion of V4 (physical trauma, hemorrhage or tumor) → stimuli discrimination based on their luminosity is preserved perceptual deficit, different from other higher-level deficits (as color anomia (inability to name colors) or color agnosia (inability to differentiate/define/describe colors) **PERIPHERAL ACHROMATOPSIA** = cone photoreceptors dystrophy (inherited, present from birth) generates markedly reduced visual acuity, extreme light sensitivity, and the absence of color discrimination → sensory deficit **Akinetopsia** Cerebral akinetopsia = acquired motion blindness → bilateral lesion of V5 → see patient L.M. (Zihl et al., 1983) «perceiving the world in frames», similar to a «strobe lights» situation **Where and what pathways** WHERE: localization in space, guide for movement (vision for action) → dorsal pathway: spatial location and control of action \- - \> movement-object coordination: from occipital to posterior parietal cortex (dorsal "where" (VISION-FOR-ACTION) WHAT: shape, color, object recognition (vision for perception) → ventral pathway: characteristics of objects \- - \> object recognition: from occipital to inferior temporal cortex (ventral "what" (VISION-FOR-PERCEPTION) Differences between the systems mainly regard the behavioral responses they evoke: - The ventral stream allows objects conscious perception and recognition - The dorsal stream allows objects localization and motor interaction with objects  **What and where pathways: a double dissociation** - Ventral lesion (visual agnosia) (what pathway): very good motor control and very bad shape perception → Visual agnosia (not able to recognize all the object in that picture) or Prosopagnosia (agnosia for faces, not able to recognize faces) - Dorsal lesion (optic ataxia) (where pathway): very bad motor control very good shape perception → Optic ataxia (not good at reaching or inserting something in a hole) or Simultanagnosia (inability to perceive more than a single stimulus at a time -- rare **Limits of double dissociation** = double dissociation is a way to show that two skills or abilities are controlled by different parts of the brain -\> limits: - Cerebral lesions are not linear - Third pathway for biological movement and social perception - Intra- and inter-talk between the systems **Visual agnosia** **VENTRAL PATHWAY -- WHAT** - The ventral pathway is based on parvocells - Along the inferotemporal cortex visual information becomes integrated (color, shape, texture) - Formation of object representations, regardless of position, dimension, and luminance **AGNOSIA -- DEFINITION** = from Greek -\> ignorance/unknown → it's a deficit in the ventral stream - Deficit of recognition in one sensory channel (visual agnosia, tactile agnosia, auditory agnosia...) - Could be category-specific (objects versus faces) - Recognition is spared in other sensory modalities - The deficit is independent of sensory impairment (spared sensation and processing in primary cortices), mental deterioration, deficit in attention, memory, or aphasic syndromes - THUS, it is a disorder of the cognitive processing of stimuli that generates an impaired recognition the subject is not able to recognize and identify a given object, scent, shape, person or entity, despite maintaining his/her sensory abilities **APPERCEPTIVE VS ASSOCIATIVE VISUAL AGNOSIA** 1. [APPERCEPTIVE AGNOSIA]: the elementary sensory functions (e.g., the recognition of color and size) are preserved: inability to integrate elementary sensory data in complex and structured visual perceptions, distinct from the background = inability to put individual parts of a visual stimulus together to form what psychologists call a percept → inability to copy an image, to describe the details or singular elements of a stimulus, or to distinguish an object from others → unilateral right hemisphere damage: right inferior parietal lobe 2. [ASSOCIATIVE AGNOSIA]: the patient is not able to identificate a given object, which means that, normally, at a cognitive level, the perceived object is compared to the knowledge accumulated by the subject in the semantic memory, but the patient is not able to recognize the object, to remember its name, nor its correct use = difficulties of forming links between the percept and stored semantic information about such items **APPERCEPTIVE AGNOSIA** - Inability to recognize and name objects - Without sensory deficit - Only in the visual modality - Can describe feature of an objects, but cannot recognize the object as a whole - Inability to copy by drawing - Ability to drawn an object from memory - Perceptual disorder **APPERCEPTIVE** **AGNOSIA** - Inability to recognize and name objects - Without sensory deficit - Only in the visual modality - Can describe feature of an objects, but cannot recognize the object as a whole - Inability to copy by drawing - Ability to draw an object from memory - Perceptual disorder Some agnosic patients have category-specific semantic deficits E.G: living (visual/perceptual information) versus inanimate objects (functional/associative information) **Apperceptive visual agnosia** Presenting a linear drawing instead of the real object, overlapping multiple figures of objects in space, or presenting the patient with incomplete, masked or degraded images, unusual perspectives, or silhouettes → more severe recognition deficit Patients are unable to follow the contours of objects with fingers, to make a copy of a drawing, since they cannot form a well-structured percept BUT, drawing from memory is generally possible → integrity of the knowledge relating to the visual aspects of the object  Usually associated with right occipito-parietal damage **Associative visual agnosia** The patient: - can discriminate objects but not identify them - can copy drawings - can sort object by category (structural than functional matches) - cannot name objects (language is spared) - cannot retrieve the use of an object and all its related functional features - may not be able to drawn objects from memory Usually associated with occipito-temporal lesion in the left-hemisphere or bilaterally **Cognitive model of visual recognition (Riddoch and Humphrey -- 2001)** A cognitive hierarchical model of object recognition and naming: it describes the component process assumed to underpin normal and faulty object recognition in different steps 1. The initial parallel visual processing of objects is along the basic dimensions of color, depth, and form 2. Grouping by collinearity (= identification of the edge of the object) 3. Feature binding/multiple shape segmentation (= combining object features to form shapes, or vice versa) 4. Formation of constancy (= recognizing an object as such whether it is near or far away, or even upside-down) 5. Full structural description 6. Semantic system stage 7. Category-specific semantic problems 8. Name representations (optical aphasia) **Assessment of visual agnostic patients** Review -- Assessment steps: - Demographic data and cognitive-behavioral history - Interview with the patient and caregiver(s)/relative(s) - - - Size judgment of geometric figures (early visual processing) - Poppelreuter\'s Superimposed Figures Test (early visual processing) - Coupling of objects in different perspectives (switching from an observer-based representation to an object-based one) - Reality decision task (structural description stored in memory) - Figure-figure association (conceptual knowledge) - VOSP (Visual object and space perception battery; Warrington and James, 1991) - BORB (Birmingham object recognition battery; Riddoch and Humphreys, 1983) **Treatments of visual agnosia** Review: - Type and extension of the brain lesion - Diaschisis effects - Assumption of the plastic nature of our brain - Compensative versus restorative approches Based on the deficit level: - Single figure/lettere/silhoutte recognition - Figure in 2D and 3D - Presentation in different prospectives - Real versus unreal objects - Categorization tasks (grouping and matching) for structural and/or semantic features **Other forms of visual agnosia** **PLACE AGNOSIA (TOPOGRAPHIC AGNOSIA)** = a special case of visual agnosia: the inability to recognize places, which yet can be retrieved E.G: after verbal description -\> no memory deficit → often associated to prosopagnosia and achromatopsia **COLOR AGNOSIA** = a special case of visual agnosia: deficit in color naming and/or color-object association → in the absence of achromatopsia, amnesia for colors or aphasia for colors **Prosopoagnosia** Prosopagnosia, or face blindness, is a cognitive disorder of face perception in which it is impaired the ability to recognize visually-presented faces of known/famous people, including one\'s own face (self-recognition) - Faces are recognizable in other modalities or by \"feature-by-feature\" recognition strategies involving secondary clues (e.g., glasses, hat, clothing, walking pattern, hair color, mustache, skin color, body shape, voice). - Facial parts, other aspects of visual processing (e.g., object discrimination), intellectual functioning (e.g., decision-making), or memory abilities are intact → studies have shown that 1 in 50 people have some form of prosopagnosia, with developmental being the most common \- - \> usually associated to a right or bilateral lesion in occipito-temporal inferior cortices (lingual and fusiformgyri- the Fusiform Face Area \[FFA\]) **CONGENITAL PROSOPAGNOSIA** Developmental prosopagnosia or congenital prosopagnosia is a face-recognition deficit evident since childhood and that is lifelong, that cannot be attributed to acquired brain damage and in the presence of intact visual and intellectual functions - prevalence of 2.5% - probably related to genetic factors - individuals never adequately develop the ability to recognize faces **ACQUIRED PROSOPAGNOSIA -- APPERCEPTIVE AND ASSOCIATIVE** *[APPERCEPTIVE PROSOPAGNOSIA]* is related to earliest processes in the face perception system - Damage in right occipital temporal regions, especially in the fusiform gyrus - People with this disorder cannot make any sense of faces and are unable to make same--different judgments when they are presented with pictures of different faces - Unable to recognize both familiar and unfamiliar faces - Difficulty in recognizing facial emotion - Possibility of facial recognition based on non-face clues, such as clothing, hairstyle, - skin color, or voice *[ASSOCIATIVE PROSOPAGNOSIA]* has spared perceptual processes but impaired links between early face perception processes and the semantic information humans hold about people in their memories - Damage in right anterior temporal regions may play a critical role in associative prosopagnosia - Patients are able to tell whether photos of people\'s faces are the same or different and derive the age and sex from a face (suggesting they can make sense of some face information) - Difficulty in identifying the person or provide any information about them such as their name, occupation, or when they were last encountered **PROSOPOAGNOSIA -- MODEL** **NEURAL CORRELATES** Grey matter involvement: Occipital Face Area (OFA), the Fusiform Face Area (FFA), the Anterior Temporal cortex (AT), as well as the Inferior Longitudinal Fasciculus  **ACQUIRED PROSOPAGNOSIA -- OVERT VS COVERT** Behavioral (eye movements) and electrophysiological (ERP) studies have shown that the absence of conscious recognition of faces can be accompanied by an unconscious recognition of them ↓ TWO--ROUTE MODEL OF FACE RECOGNITION (BAUER, 1984) The ventral route (identification detector) would be responsible for overt recognition and the more dorsal one (significance detector) for covert recognition → prosopagnosia would consist in a deficit of the ventral pathway **ASSESSMENT** [Review -- Assessment steps:] - Demographic data and cognitive-behavioral history - Interview with the patient and caregiver(s)/relative(s) - Administration of standardized tests/test batteries *Matching Faces Task* (Benton Facial Recognition Test) = evaluation of perceptual processing → same perspective **TREATMENT** [Review:] - Type and extension of the brain lesion - Diaschisis effects - Assumption of the plastic nature of our brain - Compensative versus restorative approaches - analysis of visual features - face matching - face discrimination - photo-name association - categorization of faces (presentation of faces belonging to the same occupational category, recognition of the category they belong to and therefore recognition) - memorization techniques (association of salient feature, name occupation for learning of unfamiliar faces; verbalization of relevant aspects of the person during the presentation of the familiar face) - caricature presentations - semantic associations **Capgras delusion** In 1923 Capgras and collaborators described a psychiatric symptom in which the patient believes that the most significant (familiar) people have been replaced by lookalikes (impostors, robots or aliens); since the 1980s, the Capgras delusion has been reported in neurological patients = the patient holds a delusion that a friend, spouse, parent, another close family member, or pet has been replaced by an identical impostor, despite recognition of familiarity of their behavior and appearance → not a deficit in perception or recognition of faces, but disconnection with the emotional recognition, it is resistant to logical-rational explanations \- - \> the delusion most commonly occurs in individuals with schizophrenia or neurological patients after brain injury or neurodegenerative diseases, as dementia with Lewy bodies and other forms of dementia **PROSOPAGNOSIA VS CAPGRAS DELUSION** Immagine che contiene testo, schermata, Carattere, diagramma Descrizione generata automaticamente  they're the opposite, one is the mirror of the other **REVIEW OF THE OVERT AND COVERT FACE RECOGNITION MODEL** 'A' damage: loss of overt face recognition → Prosopagnosia 'B' damage: loss of the affective response and the autonomic reaction to a face + conflict in the integrative device → Capgras delusion 'C' damage: loss of differential skin conductance responses for familiar and unfamiliar faces → not delusions (fronto-ventromedial lesioned subjects) Immagine che contiene testo, schermata, Carattere, diagramma Descrizione generata automaticamente **Agnosia in other sensory channels** **AUDITORY AGNOSIA** = the inability to recognize sounds E.G: associate a sound to the object/event that usually produces it → in patients with adequate hearing (as measured by standard audiometry) !! Please note: typically refers to nonverbal sounds (vs. pure word deafness) ++ distinction between apperceptive and associative agnosia, but very few cases described in scientific literature **TACTILE (SOMATOSENSORY) AGNOSIA** = inability to recognize objects from touch i.e., integrate/identify tactile representations of items → in patients with adequate somatosensorial sensations indicating no elementary somatosensory loss E.G: no damage to the afferent pathways ++ distinction between apperceptive and associative agnosia, but very few cases described in scientific literature **Dorsal pathway** Spatial perception leads to the ability to [form] and [manipulate] an internal representation of the outside world, and in some cases, to locate oneself in it: - Localizing points in space - Depth perception - Line orientation and geometric relation (= judging angles or orientation of lines) - Motion - Mental rotation - Constructional skills - Route finding - Spatial memory: higher-level processing, critically dependent on visual perception and visual experience - Spatial processing is subserved by the dorsal or "where" stream, that terminates in the parietal lobes → damage to this stream affects the perception of objects in space, detection of motion, and mental rotation \- - \> this stream interacts with other cortical regions to mediate spatial constructional skills, route finding, and spatial memory; the hippocampus is also a crucial structure in route finding - Most of spatial processes are related to the right hemisphere, except for motion (bilateral V5 and surrounding areas), though the left one still makes important contributions NEVERTHELESS, the left hemisphere can make important contributions to the overall processing through the employment of complementary processing styles, detectable especially after brain injury - Distinct movement-processing can be affected -\> possible presence of double dissociation - Strict relationship with other cognitive functions, especially memory, attention and working memory **Affordances** Indicate the action possibilities offered by objects, independent of the visual features that allow their recognition (color, texture...) E.G: an orange and a tennis ball look very different but they afford the same movements **Optic ataxia** From Greek, "optos" means of the eye, and "taxis" means without order = disorder of coordination and accuracy of visually-guided movements (command or copy): patients can execute body-oriented movements normally, compensating for defective visual control by using somatosensory cues (e.g., using touch) → not related to motor, sensory, visual acuity, or visual field deficits → object recognition is usually spared → difficult in reach for objects or imitate movements → in the dorsal stream **Balint-holmes syndrome** It includes: - Optic ataxia - Simultanagnosia: not able to perceive more than one object at the time - Oculomotor apraxia: paralysis of the eye fixation with inability to look voluntary into the peripheral visual field. Difficulty in visual scanning and maintain fixation on an object - Almost always associated with anosognosia: the patient is not aware of his/her deficits → following a bilateral occipito-parietal lesion **Simultagnosia** = ability to perceive single elements in a complex scene, but not the whole image - ventral form: you are not able to distinguish the single objects - dorsal form: you cannot put together the whole scene and understand its complexity **Gerstmann's syndrome** = another syndrome that includes visuo-perceptive deficits → associated with a lesion in the [left angular gyrus] (inferior parietal lobe) in the dominant hemisphere (if this happens on the right we have an other syndrome) → etiology: stroke, tumors, multiple sclerosis → defined by these concurrent deficits: - Finger agnosia - Agraphia (sometimes + alexia) - Acalculia - Left/right disorientation → there is not a cure for Gerstmann's Syndrome (only symptomatic and supportive treatment) \- - \> sometimes, symptoms diminish over time → lesions of the right angular gyrus (inferior parietal lobe) lead to hemineglect syndrome **What and where -- limits of double dissociation** Limits: - Cerebral lesions are not linear - Third way for biological movement and social perception - Intra- and inter-talk between the systems