Neuropsychology PDF

Introducing neuropsychology Cognitive neurosciences: we study the organiza2on of neurofunc2ons, so the structure and the func2on of the brain, the mind and the mental processes – Through animals – Through Cogni2ve Psychology: studies of the behavioral and func2onal correlates of neurologically healthy subjects in developmental, adult and elderly age – Through Cogni2ve Neuropsychology: studies of the behavioral and func2onal correlates of brain-damaged pa2ents with neuropsychological deﬁcits in developmental, adult and elderly age → cogni2ve neuropsychologists use models to iden2fy “modules” (i.e., processing units) and the way they collaborate to enable psychological processes, such as memory, object recogni2on, or aHen2on to operate Neuropsychology: discipline that studies the cogni2ve, behavioral and emo2onal- mo2va2onal disorders associated with brain lesions or dysfunc2ons – EXPERIMENTAL: inves2ga2on of the (neuro-)func2onal organiza2on of the mind and its neural correlates in rela2on to a cogni2ve (dys)func2on → → it tries to understand impairments to psychological processes in terms of disrup2ons to the informa2on-processing elements involved – CLINICAL: diagnosis and rehabilita2on of these brain disfunc2ons → diagnos2c and prognos2c purposes, pa2ent care and planning, rehabilita2on, forensic (of research) → in focuses on the eﬀects of brain damage/disease on psychological processes, such as memory, language, and aHen2on Neuropsychology is based on the scien2ﬁc method, ﬁts into the ﬁelds of neuroscience and has areas of overlap with psychology, neurology, neuroanatomy, psychiatry, sta2s2cs, basic neurosciences, neural networks, etc. Research methods in neuropsychology: a. the study of single cases (deﬁne a model of normal cogni2ve func2oning) b. the study of groups (large case studies, standardized psychometric procedures, analysis of results using sta2s2cal methods) Who is a neuropsychologist? A neuropsychologist studies the rela2onship between the brain and Behavior: they focus on understanding how brain and/or cerebral altera2ons (e.g., injuries, neurological condi2ons, psychiatric disorders) aﬀect cogni2ve func2ons and behavior → the neuropsychologist can be specialized on children and/or adolescents or adults and elderly – Assessment of cogni2ve func2oning through standardized tests – Diagnosis in collabora2on with other healthcare professionals (trauma2c brain injury, stroke, demen2a, ADHD, learning disorders) – Rehabilita2on: design and implement of treatment plans to help pa2ents regain cogni2ve func2ons and improve daily living skills – Consulta2on, providing guidance to pa2ents and families, helping them understand the impact of neurological issues and oﬀering strategies for coping and support – Research, to further understand brain-behavior rela2onships and to develop new assessment and treatment methods Causes of neuropsychological disorders The central nervous system (CNS) = the brain and the spinal cord (PNS – peripheral nervous system: it’s everything else) THE BRAIN: Cerebrum, the Cerebellum, the Brainstem and the Diencephalon VS the peripheral nervous system (PNS) involves the skeletal nervous system and the autonomic nervous system (ANS) Nerve cells Nerve cells = neurons and nerve ﬁbers Neurons send electrical informa2on via synap2c transmission to other neurons and muscles Ac2ve neurons generate 2ny magne2c ﬁelds Around 86 billion neurons in the human brain, and around 16 billion neurons in the Cerebrum: the number appears to be steady in childhood, but declines in adolescence A SCHEMATIC SYNAPSE: the nerve impulses arrive in the terminal region of the neuron and a series of biochemical mechanisms lead to the ac2on poten2al BIOCHEMICAL MECHANISMS SCHEME: two neurons having ac2on poten2als (APs), converge on a single “receiving” neuron. The ﬁrst releases the excitatory neurotransmiHer (GLU) and the other releases the inhibitory neurotransmiHer (GABA). Depending on the rela2ve inﬂuences of the two compe2ng inputs, the receiving neuron will ﬁre or not The brain > GREY MATTER: neuronal cell bodies, dendrites, and synapses (40% of the brain) > WHITE MATTER: nerve ﬁbers (axons) covered by the myelin (which is white and gives the color to this region: the myelin sheath makes it faster to convey ac2on poten2als) – It allows communica2on from and to gray maHer – It develops throughout the 20’s and peaks in middle age SOMATOSENSATION: Aﬀerent neurons (they carry nerve impulses towards the brain) = Sensory informa2on from the body → towards the dorsal regions of the spinal cord → up to the Somatosensory cortex MOTOR CONTROL: Eﬀerent neurons (they carry impulses away from the brain) = Motor output from the motor cortex → towards the ventral regions of the spinal cord → down to the innervate muscles ¯ DECUSSATION: nerve ﬁbers cross their side at the level of the medulla → brain hemispheres are related to the contralateral part of the body CEREBROSPINAL FLUID The CerebroSpinal Fluid (CSF) is a clear, colorless transcellular ﬂuid that circulates around the CNS FUNCTIONS: 1. NUTRITION: It allows the diﬀusion of nutrients and chemicals from the blood into the space surrounding nerve cells 2. CLEANING: receiving products secreted by the nerve cells themselves 3. PROTECTION: The CSF protects the brain inside the skull and the spinal cord inside the spinal canal THE BLOOD SUPPLY Cerebral arteries to supply oxygenated blood Cerebral veins drain deoxygenated blood from the brain The blood-brain barrier protects the brain 2ssue from harmful elements present in the blood, while s2ll allowing the passage of substances necessary for metabolic func2ons THE CEREBRUM The brain is organized in two hemispheres (lej and right) Delimited by gyrus and sulcus/ﬁssure → the ridges of brain convolu2ons are known as gyri (singular, gyrus), and the valleys between them are called sulci (singular, sulcus) or, if they are especially deep, ﬁssures à sulci are important because they divide the diﬀerent lobes Subdivided in 5 lobes → each divided in specialized areas: Frontal lobe, Occipital lobe, Parietal lobe, Temporal lobe, Insular lobe (according to some there’s a 6th lobe, the Limbic lobe) à Central sulcus = Rolandic sulcus à Lateral ﬁssure = Sylvian ﬁssure Areas are interconnected through the white maHer and create func2onal networks THE CORTEX: the outside vision of the brain BRAIN DEVELOPMENT 1. NEUROGENESIS: neurogenesis involves genera2ng new neurons from neural stem cells, forming the founda2on of cogni2ve abili2es 2. CELL MIGRATION: cell migra2on is the movement of cells to their designated loca2ons in the brain, essen2al for proper brain structure and func2on 3. CELL DIFFERENTIATION: cell diﬀeren2a2on transforms stem cells into specialized neurons and glial cells, crea2ng a diverse neural network 4. CELL MATURATION: cell matura2on involves neural progenitor cells developing into neurons and glial cells, forming the brain’s intricate network 5. SYNAPTOGENESIS: synaptogenesis is the forma2on of synapses between neurons, driven by experiences and s2muli, crucial for learning and brain func2on 6. CELL DEATH AND PRUNING: cell death and pruning eliminate excess neurons and synapses, reﬁning neural circuits for op2mal cogni2ve func2on 7. MYELOGENESIS: myelogenesis forms myelin, insula2ng nerve ﬁbers to speed up signal transmission and enhance brain communica2on BRAIN MATURATION Brain matura2on is related to thinning and pruning à the pre-frontal cortex is the last in matura2on à ajer adolescence we have a progressive reduc2on of neurons but an increase of connec2ons BRAINS ARE DIFFERENT IN STRUCTURE * PYSHIOLOGICAL DIFFERENCES: a. The right frontal region typically projects further forward and is wider than the lej frontal region (the reverse paHern is seen in the occipital lobes) b. The Sylvian ﬁssure extends further back horizontally on the lej side than the right c. The planum temporale is larger on the lej side than on the right d. The two hemispheres are diﬀerent from one another: split-brain studies * LATERALIZATION: The hand we use to write is usually indica2ve of our hemispheric dominance: who’s right-handed usually has a lej-hemispheric dominance for language (i.e., brain region crucial for language lateralized on the lej) → lej hemisphere: it lateralizes language; it has an “analy2cal-sequen2al” processing style (it sees all details) → right hemisphere: it lateralizes visuospa2al skills; it has a more “holis2c-parallel” processing style (it sees the object as a whole) * GENDER: Studies on sex-based diﬀerences in grey maHer have revealed certain paHerns, although the brain’s overall structure is highly individualized, and these ﬁndings reﬂect general trends rather than strict rules > MALES – Bigger in size – Higher grey and white maHer volume compared to females – Bigger amygdala – Higher propor2on of grey maHer in areas related to motor and visuo-spa2al abili2es > FEMALES – Smaller brain → lower white maHer volume but greater grey maHer volume rela2ve to overall brain size compared to men – Bigger hippocampus (hormone diﬀerences) – Bigger corpus callosum: it’s the largest of the 4 nerve tracts bridging the hemispheres (that enables communica2on between the two), in fact we can say that females are less lateralized than males – Higher propor2on of grey maHer in regions associated with emo2onal processing, mul2tasking and verbal communica2on – During ovula2on we are less good in visual processing During motherhood we have a signiﬁcance reduc2on of grey maHer but greater connec2on on white maHer During Menopause we have an altera2on of grey and white maHer in the brain Spa$al reasoning Stronger and more vivid memories of Mental 3D rota$on emo$onal events (long-term memory) Naviga$on by mental maps Naviga$on by landmarks Mechanical tasks Linguis$c abili$es (reading, wri$ng, Movement coordina$on comprehension, speech ﬂuency) Working memory Fine motor coordina$on Perceptual skills History pills Gall and the phrenology – the concept of modularity/localization He was the ﬁrst one to make the hypothesis that a speciﬁc part of the brain is associated to a speciﬁc func2on → he looked at the skull of the brain and hypothesized that, on the basis of the physical size and shape of the skull, one could be able to describe an individual’s personality and other “facul2es” (not true) Anatomo-functional correlations The descrip2on of the func2onal consequences of brain damage/altera2ons allows inferring the func2onal signiﬁcance of each brain region/network E.G: injuries in speciﬁc areas of the brain create highly speciﬁc func2onal symptoms PATIENT “TAN-TAN”: the scien2st Paul Pierre Broca described this pa2ent that was only able to say “Tan-Tan”: in a study post-mortem, he discovered that he had a lesion in a speciﬁc brain area (in the lej inferior frontal gyrus), probably due to epilepsy, syphilis, or a stroke à he understood that a lesion in this part of the brain would cause an expressive aphasia: he couldn’t speak other than uHering, but could comprehend and follow complicated instruc2ons MISTER PHINEAS GAGE: he had a work accident and an iron bar passed through his brain and his personality completely changed, in fact before the surgery he was very shy but later he became very irritable, blasphemy-prone, etc. HENRY GUSTAV MOLAISON: he had epilepsy and was not treatable with a pharmacological treatment, so they decided to make him have a big surgery and remove his hippocampus à he was able to remember everything before the surgery but from that day he couldn’t remember any new informa2on (he remembered informa2on for a maximum of 10-20 seconds): they discovered that hippocampus is a very important region for coding memory ASSUMPTIONS OF THIS CORRELATION Tradi2onally, neuropsychology studies the rela2onship between cogni2ve func2ons and their neurophysiological bases through the inves2ga2on of anatomo-clinical correla2ons Diﬀerent cogni2ve func2ons are localized in speciﬁc brain regions (localiza2on of func2on) → a lesion in a speciﬁc cerebral region determines a deﬁcit in a speciﬁc cogni2ve func2on (and not other func2ons) THUS, we can infer that the speciﬁc brain region is the neural substrate of that speciﬁc cogni2ve func2on and that the brain coordinates mental processes through the collabora2on of mul2ple brain regions (“distributed control networks”) Some injuries in the brain create highly speciﬁc func2onal symptoms: POST-MORTEM CORRELATIONS Nowadays, anatomo-clinical correla2ons are made with more sophis2cated techniques (neuroimaging), but the same logical reasoning is applied LIMITS OF THIS ANATOMO-CLINICAL CORRELATION 1. Diﬀerent types of lesions can be more/less diﬃcult to be circumscribed 2. Diaschisis eﬀects: damage to one brain area can produce, by loss of excita2on, loss of func2on in brain regions adjacent to or remote from, but connected to, the primary site of damage, inducing a dysfunc2on in distant nervous system structures 3. The eﬀect of brain plas2city: the brain compensates to regain func2ons thanks to all kinds of cor2ces = the spontaneous recovery (physiotherapy can help) E.G: phantom limb experience (residual feeling emana2ng from an amputated body region reducing over 2me) → “mirror box” remedy à the func2onal consequences of a brain lesion are due to both the lesion and the brain plas2city processes taking place ajer the lesion itself It is not easy to establish the rela2onship between the lesion and the symptoms Cognitive neuroscientific techniques The enable to study the neural bases of mental processes while the brain is working – Both in pa2ents and healthy people – With mainly non-invasive methodology -> NEUROPHYSIOLOGICAL METHODS: – Electroencephalography (EEG) – Magnetoencephalografy (MEG) -> NEUROIMAGINING: – Magne2c Resonance Imaging (MRI) and func2onal MRI (fMRI) – Positron emission tomography (PET) -> NON-INVASIVE BRAIN STIMULATION (NIBS) – Transcranial Magne2c S2mula2on (TMS) – Transcranial electrical s2mula2on (tES: tDCS/tACS/tRNS) Diﬀerent methods addressing diﬀerent ques2ons: Diﬀerent temporal and spa2al resolu2on Diﬀerent methods addressing diﬀerent ques2ons: Diﬀerent nature of the inference obtained on the rela2onship between brain func2oning and behavioral performance -> Neurophysiological methods: – Electroencephalography (EEG) CorrelaFonal methods – Magnetoencephalografy (MEG) Assessment -> Neuroimaging: – Magne2c Resonance Imaging (MRI) and func2onal MRI (fMRI) – Positron emission tomography (PET) -> Non-invasive brain s2mula2on (NIBS) Causal Inference – Transcranial Magne2c S2mula2on (TMS) Assessment and treatment – Transcranial electrical s2mula2on (tES: tDCS/tACS/tRNS) GENERAL PRINCIPLES APPLIED WHEN DESIGNING NEUROCOGNITIVE STUDIES Similar to those applied in all ﬁelds of experimental psychology The more the beHer (group studies are preferred): many par2cipants and many trials per par2cipants (at least in studies with healthy par2cipants/control groups) Comparisons between at least an experimental and at least a control condi2on are needed (e.g., observa2on of sta2c vs. moving dots to iden2fy V5) Construct validity: Is my behavioral measure the correct opera2onaliza2on of the cogni2ve process that I aim to study? SPECIFIC FOR COGNITIVE NEUROSCIENCE Has my technique the correct spa2al resolu2on to target the speciﬁc brain area of interest? Has my technique the correct temporal resolu2on to capture the process I am interested in? What are the intrinsic limits of my techniques (e.g., contraindica2ons, movement constraints, transportability, costs)? NEUROPHYSIOLOGICAL METHODS – Electroencephalography It records electric ac2vity generated by neurons by using electrodes placed on the scalp The interna2onal 10-20 system is a commonly recognized method to describe and apply the loca2on of scalp electrodes à Clinical use: up to 16 channels; Experimental use: 16, 32, 64, or 128-channel EEGcap Higher frequency and reduced apmpliputed = neuronal desynchroniza2on -> cogni2ve task NEUROPHYSIOLOGICAL METHODS – EVENT RELATED POTENTIALS Event-related poten2als (ERPs) are event-related voltage changes in the ongoing EEG ac2vity à in ERP experimental design, a large number of epochs having as onset a sensory, motor, or cogni2ve s2mula2on are averaged together. - - > sta2s2cal diﬀerences between s2mula2on and rest (or diﬀerent s2mula2ons) à the ERP describes diﬀerent stages of processing with extremely high temporal resolu2on (ms) Experimental group: 13 Parkinson Disease (PD) pa2ents “on” and “oﬀ” dopaminergic medica2on Control group: 13 healthy controls (HC -without dopaminergic medica2on) ERP task: ﬂanker task (see image) Methods: comparison of performances and ERP amplitudes between the groups and between an “on” or “oﬀ” condi2on in PD pa2ents; focus on errors, usually followed by fronto-centrally distributed nega2vi2es (ERPs) à if they make an error, they expect a speciﬁc error (but no diﬀerence at behavioral level with drugs and no drugs pa2ents, but diﬀerence at neurophysiological level) Results: PD pa2ents commiHed more errors than HC, BUT error rates were not signiﬁcantly modulated by dopaminergic medica2on → no diﬀerences at behavioral level PD pa2ents showed reduced Ne/ERN amplitudes rela2ve to HC → diﬀerences at neurophysiological level à if it’s congruent: lej boHom; it’s incongruent: right boHom CRUCIAL ELEMENTS OF EEG AND ERPs – to sum up Components: amplitude and frequency for EEG versus amplitude and latency for ERPs of each wave that represent the sum of the ac2vity of neurons in the area of the brain closest to the recording electrode The topographical distribu2on on the scalp High temporal resolu2on (ms) Low spa2al resolu2on (the problem of source localiza2on: no good localiza2on of where something has happened) PORTABLE DEVICES NEUROPHYSIOLOGICAL METHODS – Magnetoencephalography Same principles of EEG, but EEG is sensi2ve to electrical ﬁelds generated by extracellular currents, whereas MEG primarily detects the magne2c ﬁelds induced by intracellular electrical ac2vity High number of electrodes (60) Magne2c ﬁelds are analyzed to ﬁnd the loca2on of the neuronal sources The resul2ng source loca2ons are superimposed on an MRI image for clinical and experimental purposes MEG has a very high temporal resolu2on (msec) and excellent spa2al resolu2on (mm) IN VIVO BRAIN RECORDING We put records inside the brain à in vivo electrophysiology measures very precisely neuronal ac2vity in the brain as either local ﬁeld poten2als or single units = invasive technique NEUROIMAGINING – Mri and pet scan MRI: Magne2c Resolu2on Imaging PET: Positron Emission Tomography NEUROIMAGINING TECHNIQUES – Positron emission tomography Positron Emission Tomography (PET) is a nuclear imaging test that integrates computed tomography (CT) and a radioac2ve tracer that allows to see how body 2ssues absorb and use diﬀerent chemicals in real 2me (= it assess func2onal brain ac2vity) STEPS: 1. a tracer is injected into your bloodstream 2. the tracer is radiolabeled, meaning it emits gamma rays that are detected by the PET scanner 3. the radioisotopes used in PET to label tracers are 11C, 13N, 150, and 18F (carbon, nitrogen, oxygen and 18F used as a subs2tute for hydrogen) 4. once the tracer is absorbed in the body, subject is posi2oned in the scanner The computer collects the informa2on emiHed by the tracer and displays it on the CT cross- sec2ons: these cross-sec2ons can be added back together to form a 3D image of the brain ++ PET can measure blood ﬂow, blood volume, oxygen usage, 2ssue pH (acidity), glucose (sugar) metabolism, and drug ac2vity, useful for: a. detec2ng the ac2vity of cancer. Because malignant cells grow at a fast rate, they metabolize more sugar than normal cells → how aggressive a tumor is or how its growth is slowed by therapy. b. presurgical evalua2on of seizures a. PET scan from a control subject showing high uptake of 18ﬂuorodopa in the striatum. b. Pa2ent with Parkinson’s disease with motor signs that are mainly conﬁned to the right limbs. 18Fluorodopa uptake is markedly reduced in the lej posterior putamen (the uptake in the area indicated by the arrow is 70% below normal) and reduced to a minor extent in the lej anterior putamen and lej caudate. NEUROIMAGIONING TECHNIQUES – Single-photon emission computerized tomography The single-photon emission computerized tomography (SPECT) is a nuclear imaging scan that integrates computed tomography (CT: X-ray and “slice-by-slice” picture of the en2re brain) and a radioac2ve tracer that allows to see how blood ﬂows to 2ssues and organs STEPS: the same as PET, but diﬀerent tracers and low resolu2on à the radioisotopes typically used in SPECT to label tracers are iodine-123, techne2um-99m, xenon-133, thallium-201, and ﬂuorine-18 ++ a SPECT scan is primarily used to view how blood ﬂows through arteries and veins in the brain à brain injury, presurgical evalua2on of seizures NEUROIMAGINING TECHNIQUES – Magnetic resonance imaging The magne2c resonance imaging (MRI) scan works by using a powerful magnet, radio waves, and a computer to create detailed images: our body is made up of millions of hydrogen atoms (the human body is 80% water), which are magne2c. à when our body is placed in the magne2c ﬁeld, these atoms align with the ﬁeld, a radio wave "knocks down" the atoms and disrupts their polarity, the sensor detects the 2me it takes for the atoms to return to their original alignment = in essence, MRI is structural technique that measures the water content (or ﬂuid characteris2cs) of diﬀerent 2ssues, which is processed by the computer to create a black and white image à the image is highly detailed and can show even the smallest abnormality Functional mri With MRI we are recording Blood Oxygen Level Dependent (BOLD) eﬀect → in func2onal MRI (fMRI), the magne2c ﬁeld is perturbed by radiofrequencies: hemoglobin has diﬀerent magne2c proper2es in its oxygenated and deoxygenated forms Deoxygenated hemoglobin → paramagne2c (= weakly aHracted by externally applied magne2c ﬁelds) Oxygenated hemoglobin → diamagne2c (= repelled by externally applied magne2c ﬁelds) Areas of the brain that are more ac2ve tend to receive higher levels of oxygenated blood which lead to a hemodynamic response, which means that blood releases oxygen to ac2vate neurons at a greater rate than what is actually needed (overcompensa2on) à higher levels of oxygenated blood in a brain area are believed to correspond to a higher neural ac2vity in that cerebral region - - > this change in the rela2ve levels of oxygenated or deoxygenated hemoglobin in blood can be detected on the basis of their diﬀeren2al magne2c suscep2bility BOLD response is slow; each point in the brain is measured every 2/3 seconds (low temporal resolu2on) à the BOLD eﬀect can be measured in each point of the brain (voxel): high spa2al resolu2on - - > more sophis2cated analyses can: – Infer func2onal connec2vity between voxels/brain regions – Apply algorithms to dis2nguish between paHern of ac2va2on (mul2voxel paHern analyses) The obtained results are sta2s2cal maps: this means that they are comparisons between ac2va2on maps in diﬀerent experimental condi2ons NEUROIMAGING TECHNIQUES – Tractography TRACTOGRAPHY = 3D modeling techniques that image brain pathways (tracts) using diﬀusion tensor imaging (DTI) or diﬀusion spectrum imaging (DSI), two variants of MRI à diﬀusion imaging maps the diﬀusion of water molecules in the brain NON-INVASIVE BRAIN STIMULATION (NIBS) – Tms TMS = Transcranial Magne2c S2mula2on = applica2on of a magne2c ﬁeld on the scalp by means of a s2mulator (coil): the 2ssue underneath the coil is subjected to a current ﬂow that generates ac2va2on/inhibi2on à temporary disrup2on of the spontaneous neural ac2vity: it uses strong pulses of magne2za2on that can be focal administered via a hand-held coil, these pulses then increase neuronal excitability → it is beHer suited for the inves2ga2on of superﬁcial brain regions, as concerns have been raised about the safety of the procedure ¯ FARADAY’S PRINCIPLE OF ELECTROMAGNETIC INDUCTION Rapid varia2on in an electrical current can induce a magne2c ﬁeld: > the current ﬂows through the coil for about 1 ms > a large magne2c ﬁeld is produced for about 1 ms This rapid change induces an electrical current in the area under the coil, ac2va2ng neurons and genera2ng a depolariza2on à genera2on of ac2on poten2als = s2mula2on Importance of the neuronal “pre-ac2va2on level” → the amount of depolariza2on in each neuron in response to the TMS pulse depends on the ac2va2on state of the membrane (the higher the stronger). = state-dependency principle Diﬀerent s2mula2on based on: the posi2on of the coil (where on the skull) the orienta2on of the coil (coil inclina2on/angle) frequency: > high frequency TMS (5-20 Hz) = increase of neural excitability > low frequency TMS (1–5 Hz) = decrease of neural excitability TMS protocols diﬀer in the number and frequency of pulses delivered: In single-pulse s2mula2on (spTMS), individual pulses are delivered separately In mul2ple pulse TMS, several pulses are applied with an inter-s2mulus interval of a few milliseconds: either paired pulses TMS (pTMS) or triple pulses TMS (tTMS) In repe22ve TMS, trains of pulses are applied with a ﬁxed frequency (low frequency: 1–5 Hz, or high frequency: 5–20 Hz) Theta-burst s2mula2on consists of applying bursts of several pulses, repeated at a frequency close to 5 Hz (cTBS), or each burst is applied for 2 s and repeated every 10 s for 190 s (intermiHent TBS, iTBS) à in a third variant, intermediate TBS (imTBS), 5 s burst trains are repeated every 15 s EXPERIMENT Subjects: 17 healthy individuals (HC) rTMS trains of two pulses (frequency 10 Hz, dura2on 200 ms, delay 150 ms) over lej and right Extrastriate body area (EBA, black dot) and ventral premotor cortex (vPMc, white dot) Behavioural task: a two-choice matching-to-sample visual discrimina2on task o form discrimina2on task: same ac2on performed by two diﬀerent models o ac2on discrimina2on task: same model performing two diﬀerent ac2ons à s2muli were expected to ac2vate both body part representa2on (EBA) and the related ac2on (vPMc) Results: reac2on 2mes and accuracy o Accuracy: S2mula2on had no eﬀect on accuracy of responses o Reac2on 2mes: EBA rTMS selec2vely impaired the ability to discriminate two diﬀerent forms, vPMc rTMS selec2vely impaired the ability to discriminate two diﬀerent ac2ons o The interference caused by EBA and vPMc s2mula2on was independent of the hemisphere s2mulated à no hemispheric dominance Conclusions: EBA may be crucial for the iden2ﬁca2on of actors, par2cularly when facial cues are unavailable or ambiguous (→actors’ body iden2ty) ++ causa2ve evidence that motor representa2ons are necessary for visuopercep2ve ac2on discrimina2ons and vPMc may represent the observed ac2ons without taking into account the actors’ iden2ty à double dissocia2on paradigm Single-pulse tms Single-pulse TMS and Motor Evoked Poten2als (MEP): the magne2c pulses induced by TMS over the contralateral primary motor cortex (M1) can pass through the scalp and induce a response known as “motor evoked poten2al” (MEP) in the target muscle à this response can be recorded using surface electromyography (EMG) electrodes placed over the muscle of interest - - > the peak-to-peak amplitude of the elicited MEPs is an indica2on of changing cor2cospinal excitability (CSE) -> smaller amplitudes indicate lower excitability, while larger amplitudes suggest higher CSE Repetitive tms Repe22ve TMS (rTMS) for «virtual lesion» paradigms (online/oﬄine rTMS) The problem of localizing the correct target area → neuronaviga2on NON-INVASIVE BRAIN STIMULATION (NIBS) – Transcranial electrical stimulation Transcranial Electrical S2mula2on (tES): techniques aimed to modify the excitability of a target area genera2ng a current ﬂow through the cortex à neuromodula2on Transcranial direct current s2mula2on (tDCS) EXPERIMENTAL PROTOCOLS: On-line, Oﬀ-line, Sham s2mula2on Oﬄine s2mula2on involves a period of pre-s2mula2on in which a task may be completed, followed by a period of s2mula2on and then a post-s2mula2on task (A), or a period of s2mula2on followed by a post-s2mula2on task only (AB) Online s2mula2on involves par2cipants receiving s2mula2on during the task (C) For sham s2mula2on, the task can be applied at any point during the session (D), depending on whether an online or oﬄine protocol is undertaken EXPERIMENT Subjects: Parkinson’s Disease with mild cogni2ve impairment (PD-MCI) versus 20 healthy controls (HC) Aim: Assessing Theory of Mind (ToM), i.e., the ability to understand and predict other people’s behaviors Methods: Anodal tDCS over the medial frontal cortex (MFC) to modulate ToM performance Implica2ons: mPFC has a causal role in TOM → clinical training with anodal tDCS over mPFC to ameliorate TOM in PD-MCI NON-INVASIVE BRAIN STIMULATION (NIBS) – TMS AND TES Non-invasive techniques For assessment and training Safe and regulated techniques Causal inference: if you modify the excitability of a target area, and this s2mula2on or modula2on inﬂuences the behavioral performance, then that speciﬁc area is crucial for that cogni2ve func2on à Importance localizing the correct target area DIRECT ELECTRICAL STIMULATION Direct electrical s2mula2on (DES) is an invasive tool used for example for mapping cogni2ve func2ons while pa2ents are undergoing awake neurosurgery or invasive long-term monitoring to iden2fy epileptogenic 2ssue Summary Each cogni2ve neuroscience technique has its limits and poten2als à It is crucial to integrate them when addressing research ques2ons E.G: combina2on of fMRI + EEG to get both high temporal and spa2al resolu2on E.G: combina2on of fMRI + TMS to obtain good localiza2on and causal inferences Clinical neuropsychology – assessment AIMS Diagnos2c: – discriminate between diﬀerent condi2ons – provide diagnos2c informa2on in cases of nega2ve neuroradiological data (e.g., demen2a, mild trauma) Prognos2c: provide informa2on on the outcomes of certain pathologies (e.g., post- trauma2c coma) Pa2ent care and planning: o inform the pa2ent of his cogni2ve state to understand the altera2ons resul2ng from the disease o inform family members so they can understand and adapt to the condi2on o evaluate the eﬀects of medical therapies on the pa2ent's cogni2ve eﬃciency o evaluate their degree of daily autonomy o evaluate the opportunity of a rehabilita2on interven2on Rehabilita2on: provide the star2ng point for a therapy, planning and managing a therapeu2c program and evaluate its short and long-term eﬀec2veness Medical legal: o diagnos2c: (is it a consequence of…? Is there reason to suspect that brain damage…?) o descrip2on of the pa2ent condi2on: (will it prevent him from working?) For research: single evalua2on during a protocol or pre- and post-treatment 1. Demographic data and cogni2ve-behavioral history: a. obtain informa2on on why and to whom the pa2ent was sent (general prac22oner, hospital, assistance center operators, clinical psychologist, personal request of the pa2ent or family members, for expert/insurance purposes) b. Know the disease onset and its evolu2on c. Know the type of life the pa2ent leads or led before the pathology d. Understanding the premorbid personality e. Know the health of close family members f. Know the outcome of the examina2on of elementary neurological func2ons performed by the neurologist (know of peripheral hearing or vision deﬁcits) g. Know the outcome of the main instrumental inves2ga2ons (e.g., MRI, EEG, PET) and other medical tests (e.g., blood tests and hormonal values) h. Know any premorbid cogni2ve diﬃcul2es (even developmental) 2. Pa2ent interview: o Speech and comprehension skills o Mood tone o AHen2onal skills o Awareness of deﬁcits or illness o Explain the purpose of the exam and what it consists of 3. Administra2on of standardized tests/test baHeries 4. Interview with caregivers/families o Know the pa2ent's family environment o Know how the pa2ent behaves when he/she is at home o Make family members aware of the situa2on and its evolu2on o Provide them with the correct interpreta2on of the pa2ent’s test and behaviors Possible second visit with more ad hoc and ecological tests, to beHer deﬁne the diagnosis Cognitive assessment – test Single test or test baHery (series of tests) → neuro-cogni2ve proﬁle o Proﬁle = cogni2ve areas of strength and weaknesses Tests are standardized (i.e., uniformity of procedure) + norm-referencing process = comparison between the person’s performance and scores generated by age- and/or sex- matched responders First assessment = person’s cogni2ve proﬁle/picture à repea2ng assessment over 2me enable to assess changing in cogni2ve func2oning (recovery or progression) Clinical neuropsychology – treatment Cogni2ve rehabilita2on: assump2on of the plas2c nature of our brain = func2onal reorganiza2on and (re)learning ajer a cerebral lesion à the term “brain plas2city” refers to the property of the brain to vary structure and func2on along development and during adult life, in constant interac2on with the outside world (environment) - - > plas2city concerns the changes in the nervous system organiza2on that underlie various forms of short- and long-term behavioral modiﬁca2on: they include the processes of matura2on, adapta2on to changes in the environment, speciﬁc and unspeciﬁc learning, and the compensa2on Mechanisms -> there can be posi2ve plas2city (resource) or nega2ve plas2city (maladap2ve) Mechanisms of neuroplasticity STRUCTURAL NEUROPLASTICITY FUNCTIONAL NEUROPLASTICITY > Long-term poten2a2on (LTP) is deﬁned as a persistent (= las2ng hours or longer) strengthening of synapses based on recent paHerns of ac2vity > Long-term depression (LTD) is deﬁned as a persistent (= las2ng hours or longer) decrease in synap2c strength depending on speciﬁc s2mula2on Rehabilita2on capitalizes on brain posi2ve plas2city (resource) to reduce the nega2ve eﬀects of a brain damage Cogni2ve remedia2on: based on a restora2ve model that aHempts to reduce or eliminate impaired cogni2on à re-gain the cogni2ve func2on Compensatory techniques: compensate for, or circumvent cogni2ve deﬁcit, with reliance on intact cogni2ve skills and strategies and supports for working around cogni2ve deﬁcits à reduc2on of the disability through: 1. internal self-management strategies, 2. external strategies/environmental modiﬁca2on, 3. errorless learning Visual pathways and agnosia Sensation vs perception SENSATION occurs when sensory receptors detect sensory s/muli: sensory receptors are specialized neurons that respond to speciﬁc types of s/muli → when sensory informa/on is detected by a sensory receptor, sensa/on has occurred E.G: when light that enters the eye causes chemical changes in photoreceptors of the re/na ¯ These cells relay messages (ac/on poten/als) to the CNS TRANSDUCTION = the conversion from sensory s/muli to ac/on poten/als; it represents the ﬁrst step toward percep/on PERCEPTION involves the organiza/on, interpreta/on, and conscious experience of those neural pieces of informa/on → it organizes sensa/ons into complex representa/ons ++ not all sensory s/muli are perceived (and become conscious!): our percep/ons 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 re/na → op/c nerves → op/c chiasm → lateral geniculate nucleus (LGN) of the thalamus → V1 → associa/ve visual cor/ces (V2-V5) Visual pathways carry the informa/on segregated: 1. Spa/ally (re/notopic organiza/on) 2. Qualita/vely (color, shape, movement) → this segrega/on (spa/al versus qualita/ve features) is maintained at the higher levels of the system - - > two pathways, ‘what and where’: they always work in parallel 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 s/muli – OCCIPITAL LOBE V2: important for color discrimina/on – in the cuneus V4: important for object recogni/on – in the fusiform gyrus, temporal lobe, what pathway V3 - V5: important for movement and spa/al percep/on – 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) → s/muli discrimina/on 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 diﬀeren/ate/deﬁne/describe colors) PERIPHERAL ACHROMATOPSIA = cone photoreceptors dystrophy (inherited, present from birth) generates markedly reduced visual acuity, extreme light sensi/vity, and the absence of color discrimina/on → sensory deﬁcit Akinetopsia Cerebral akinetopsia = acquired mo/on blindness → bilateral lesion of V5 → see pa/ent L.M. (Zihl et al., 1983) «perceiving the world in frames», similar to a «strobe lights» situa/on Where and what pathways WHERE: localiza/on in space, guide for movement (vision for ac/on) → dorsal pathway: spa/al loca/on and control of ac/on - - > movement-object coordina/on: from occipital to posterior parietal cortex (dorsal “where” (VISION-FOR-ACTION) WHAT: shape, color, object recogni/on (vision for percep/on) → ventral pathway: characteris/cs of objects - - > object recogni/on: 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 percep/on and recogni/on – The dorsal stream allows objects localiza/on and motor interac/on with objects What and where pathways: a double dissociation – Ventral lesion (visual agnosia) (what pathway): very good motor control and very bad shape percep/on → Visual agnosia (not able to recognize all the object in that picture) or Prosopagnosia (agnosia for faces, not able to recognize faces) – Dorsal lesion (op/c ataxia) (where pathway): very bad motor control very good shape percep/on → Op/c ataxia (not good at reaching or inser/ng something in a hole) or Simultanagnosia (inability to perceive more than a single s/mulus at a /me – rare Limits of double dissociation = double dissocia/on is a way to show that two skills or abili/es are controlled by diﬀerent parts of the brain -> limits: Cerebral lesions are not linear Third pathway for biological movement and social percep/on Intra- and inter-talk between the systems Visual agnosia VENTRAL PATHWAY – WHAT The ventral pathway is based on parvocells Along the inferotemporal cortex visual informa/on becomes integrated (color, shape, texture) Forma/on of object representa/ons, regardless of posi/on, dimension, and luminance AGNOSIA – DEFINITION = from Greek -> ignorance/unknown → it’s a deﬁcit in the ventral stream Deﬁcit of recogni/on in one sensory channel (visual agnosia, tac/le agnosia, auditory agnosia…) Could be category-speciﬁc (objects versus faces) Recogni/on is spared in other sensory modali/es The deﬁcit is independent of sensory impairment (spared sensa/on and processing in primary cor/ces), mental deteriora/on, deﬁcit in aqen/on, memory, or aphasic syndromes THUS, it is a disorder of the cogni/ve processing of s/muli that generates an impaired recogni/on à the subject is not able to recognize and iden/fy a given object, scent, shape, person or en/ty, despite maintaining his/her sensory abili/es APPERCEPTIVE VS ASSOCIATIVE VISUAL AGNOSIA 1. APPERCEPTIVE AGNOSIA: the elementary sensory func/ons (e.g., the recogni/on of color and size) are preserved: inability to integrate elementary sensory data in complex and structured visual percep/ons, dis/nct from the background = inability to put individual parts of a visual s/mulus together to form what psychologists call a percept → inability to copy an image, to describe the details or singular elements of a s/mulus, or to dis/nguish an object from others → unilateral right hemisphere damage: right inferior parietal lobe 2. ASSOCIATIVE AGNOSIA: the pa/ent is not able to iden/ﬁcate a given object, which means that, normally, at a cogni/ve level, the perceived object is compared to the knowledge accumulated by the subject in the seman/c memory, but the pa/ent is not able to recognize the object, to remember its name, nor its correct use = diﬃcul/es of forming links between the percept and stored seman/c informa/on about such items E.G: the examiner shows a glass, the pa/ent perceives the glass, but is not able to recognizes it, remember its name and its use; however, when the examiner asks to the pa/ent to verbally describe what a glass is, the pa/ent answers correctly → the perceptual visual analysis is preserved, but disconnec/on between the perceptual analysis and the seman/c store → usually bilateral damage: crucial area thought to be les hemisphere, more ventral than appercep/ve damage APPERCEPTIVE AGNOSIA o Inability to recognize and name APPERCEPTIVE AGNOSIA objects o Inability to recognize and name o Without sensory deﬁcit objects o Only in the visual modality o Without sensory deﬁcit o Can describe feature of an objects, o Only in the visual modality but cannot recognize the object as a o Can describe feature of an objects, whole but cannot recognize the object as a o Inability to copy by drawing whole o Ability to drawn an object from o Inability to copy by drawing memory o Ability to draw an object from o Perceptual disorder memory o Perceptual disorder Some agnosic pa/ents have category-speciﬁc seman/c deﬁcits E.G: living (visual/perceptual informa/on) versus inanimate objects (func/onal/associa/ve informa/on) Apperceptive visual agnosia Presen/ng a linear drawing instead of the real object, overlapping mul/ple ﬁgures of objects in space, or presen/ng the pa/ent with incomplete, masked or degraded images, unusual perspec/ves, or silhoueqes → more severe recogni/on deﬁcit Pa/ents 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 rela/ng to the visual aspects of the object Usually associated with right occipito-parietal damage Associative visual agnosia The pa/ent: – can discriminate objects but not iden/fy them – can copy drawings – can sort object by category (structural than func/onal matches) – cannot name objects (language is spared) – cannot retrieve the use of an object and all its related func/onal features – may not be able to drawn objects from memory Usually associated with occipito-temporal lesion in the les-hemisphere or bilaterally Cognitive model of visual recognition (Riddoch and Humphrey – 2001) A cogni/ve hierarchical model of object recogni/on and naming: it describes the component process assumed to underpin normal and faulty object recogni/on in diﬀerent steps 1. The ini/al parallel visual processing of objects is along the basic dimensions of color, depth, and form 2. Grouping by collinearity (= iden/ﬁca/on of the edge of the object) 3. Feature binding/mul/ple shape segmenta/on (= combining object features to form shapes, or vice versa) 4. Forma/on of constancy (= recognizing an object as such whether it is near or far away, or even upside-down) 5. Full structural descrip/on 6. Seman/c system stage 7. Category-speciﬁc seman/c problems 8. Name representa/ons (op/cal aphasia) Assessment of visual agnostic patients Review – Assessment steps: Demographic data and cogni/ve-behavioral history Interview with the pa/ent and caregiver(s)/rela/ve(s) Administra/on of standardized tests/test baqeries Copy test Size judgment of geometric ﬁgures (early visual processing) Poppelreuter's Superimposed Figures Test (early visual processing) Coupling of objects in diﬀerent perspec/ves (switching from an observer-based representa/on to an object-based one) Reality decision task (structural descrip/on stored in memory) Figure-ﬁgure associa/on (conceptual knowledge) VOSP (Visual object and space percep/on baqery; Warrington and James, 1991) BORB (Birmingham object recogni/on baqery; Riddoch and Humphreys, 1983) Treatments of visual agnosia Review: Type and extension of the brain lesion Diaschisis eﬀects Assump/on of the plas/c nature of our brain Compensa/ve versus restora/ve approches Based on the deﬁcit level: Single ﬁgure/leqere/silhouqe recogni/on Figure in 2D and 3D Presenta/on in diﬀerent prospec/ves Real versus unreal objects Categoriza/on tasks (grouping and matching) for structural and/or seman/c 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: aser verbal descrip/on -> no memory deﬁcit → osen associated to prosopagnosia and achromatopsia COLOR AGNOSIA = a special case of visual agnosia: deﬁcit in color naming and/or color-object associa/on → in the absence of achromatopsia, amnesia for colors or aphasia for colors Prosopoagnosia Prosopagnosia, or face blindness, is a cogni/ve disorder of face percep/on in which it is impaired the ability to recognize visually-presented faces of known/famous people, including one's own face (self-recogni/on) – Faces are recognizable in other modali/es or by "feature-by-feature" recogni/on strategies involving secondary clues (e.g., glasses, hat, clothing, walking paqern, hair color, mustache, skin color, body shape, voice). – Facial parts, other aspects of visual processing (e.g., object discrimina/on), intellectual func/oning (e.g., decision-making), or memory abili/es 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 cor/ces (lingual and fusiformgyri- the Fusiform Face Area [FFA]) CONGENITAL PROSOPAGNOSIA Developmental prosopagnosia or congenital prosopagnosia is a face-recogni/on deﬁcit evident since childhood and that is lifelong, that cannot be aqributed to acquired brain damage and in the presence of intact visual and intellectual func/ons prevalence of 2.5% probably related to gene/c 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 percep/on 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 emo/on Possibility of facial recogni/on 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 percep/on processes and the seman/c informa/on humans hold about people in their memories Damage in right anterior temporal regions may play a cri/cal role in associa/ve prosopagnosia Pa/ents are able to tell whether photos of people's faces are the same or diﬀerent and derive the age and sex from a face (sugges/ng they can make sense of some face informa/on) Diﬃculty in iden/fying the person or provide any informa/on about them such as their name, occupa/on, or when they were last encountered PROSOPOAGNOSIA – MODEL NEURAL CORRELATES Grey maqer 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 recogni/on of faces can be accompanied by an unconscious recogni/on of them ¯ TWO–ROUTE MODEL OF FACE RECOGNITION (BAUER, 1984) The ventral route (iden/ﬁca/on detector) would be responsible for overt recogni/on and the more dorsal one (signiﬁcance detector) for covert recogni/on → prosopagnosia would consist in a deﬁcit of the ventral pathway ASSESSMENT Review – Assessment steps: Demographic data and cogni/ve-behavioral history Interview with the pa/ent and caregiver(s)/rela/ve(s) Administra/on of standardized tests/test baqeries Matching Faces Task (Benton Facial Recogni/on Test) = evalua/on of perceptual processing → same perspec/ve TREATMENT Review: Type and extension of the brain lesion Diaschisis eﬀects Assump/on of the plas/c nature of our brain Compensa/ve versus restora/ve approaches – analysis of visual features – face matching – face discrimina/on – photo-name associa/on – categoriza/on of faces (presenta/on of faces belonging to the same occupa/onal category, recogni/on of the category they belong to and therefore recogni/on) – memoriza/on techniques (associa/on of salient feature, name occupa/on for learning of unfamiliar faces; verbaliza/on of relevant aspects of the person during the presenta/on of the familiar face) – caricature presenta/ons – seman/c associa/ons Capgras delusion In 1923 Capgras and collaborators described a psychiatric symptom in which the pa/ent 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 pa/ents = the pa/ent holds a delusion that a friend, spouse, parent, another close family member, or pet has been replaced by an iden/cal impostor, despite recogni/on of familiarity of their behavior and appearance → not a deﬁcit in percep/on or recogni/on of faces, but disconnec/on with the emo/onal recogni/on, it is resistant to logical-ra/onal explana/ons - - > the delusion most commonly occurs in individuals with schizophrenia or neurological pa/ents aser brain injury or neurodegenera/ve diseases, as demen/a with Lewy bodies and other forms of demen/a PROSOPAGNOSIA VS CAPGRAS DELUSION à 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 recogni/on → Prosopagnosia ‘B’ damage: loss of the aﬀec/ve response and the autonomic reac/on to a face + conﬂict in the integra/ve device → Capgras delusion ‘C’ damage: loss of diﬀeren/al skin conductance responses for familiar and unfamiliar faces → not delusions (fronto-ventromedial lesioned subjects) 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 pa/ents with adequate hearing (as measured by standard audiometry) !! Please note: typically refers to nonverbal sounds (vs. pure word deafness) ++ dis/nc/on between appercep/ve and associa/ve agnosia, but very few cases described in scien/ﬁc literature TACTILE (SOMATOSENSORY) AGNOSIA = inability to recognize objects from touch i.e., integrate/iden/fy tac/le representa/ons of items → in pa/ents with adequate somatosensorial sensa/ons indica/ng no elementary somatosensory loss E.G: no damage to the aﬀerent pathways ++ dis/nc/on between appercep/ve and associa/ve agnosia, but very few cases described in scien/ﬁc literature Dorsal pathway Spa/al percep/on leads to the ability to form and manipulate an internal representa/on of the outside world, and in some cases, to locate oneself in it: – Localizing points in space – Depth percep/on – Line orienta/on and geometric rela/on (= judging angles or orienta/on of lines) – Mo/on – Mental rota/on – Construc/onal skills – Route ﬁnding – Spa/al memory: higher-level processing, cri/cally dependent on visual percep/on and visual experience Spa/al processing is subserved by the dorsal or “where” stream, that terminates in the parietal lobes → damage to this stream aﬀects the percep/on of objects in space, detec/on of mo/on, and mental rota/on - - > this stream interacts with other cor/cal regions to mediate spa/al construc/onal skills, route ﬁnding, and spa/al memory; the hippocampus is also a crucial structure in route ﬁnding Most of spa/al processes are related to the right hemisphere, except for mo/on (bilateral V5 and surrounding areas), though the les one s/ll makes important contribu/ons NEVERTHELESS, the les hemisphere can make important contribu/ons to the overall processing through the employment of complementary processing styles, detectable especially aser brain injury Dis/nct movement-processing can be aﬀected -> possible presence of double dissocia/on Strict rela/onship with other cogni/ve func/ons, especially memory, aqen/on and working memory Affordances Indicate the ac/on possibili/es oﬀered by objects, independent of the visual features that allow their recogni/on (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 coordina/on and accuracy of visually-guided movements (command or copy): pa/ents can execute body-oriented movements normally, compensa/ng for defec/ve visual control by using somatosensory cues (e.g., using touch) → not related to motor, sensory, visual acuity, or visual ﬁeld deﬁcits → object recogni/on is usually spared → diﬃcult in reach for objects or imitate movements → in the dorsal stream Balint-holmes syndrome It includes: – Op/c ataxia – Simultanagnosia: not able to perceive more than one object at the /me – Oculomotor apraxia: paralysis of the eye ﬁxa/on with inability to look voluntary into the peripheral visual ﬁeld. Diﬃculty in visual scanning and maintain ﬁxa/on on an object – Almost always associated with anosognosia: the pa/ent 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 dis/nguish the single objects – dorsal form: you cannot put together the whole scene and understand its complexity à they lose the Navon eﬀect, so global features are perceived more quickly than local features Gerstmann’s syndrome = another syndrome that includes visuo-percep/ve deﬁcits → associated with a lesion in the les angular gyrus (inferior parietal lobe) in the dominant hemisphere (if this happens on the right we have an other syndrome) → e/ology: stroke, tumors, mul/ple sclerosis → deﬁned by these concurrent deﬁcits: – Finger agnosia – Agraphia (some/mes + alexia) – Acalculia – Les/right disorienta/on → there is not a cure for Gerstmann’s Syndrome (only symptoma/c and suppor/ve treatment) - - > some/mes, symptoms diminish over /me → 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 percep/on Intra- and inter-talk between the systems Language and aphasia Communication and language Animals use several modali/es to communicate (e.g., sounds or gestures) Communica/on in humans is highly related to verbal language Language is not a synonym of communica/on: only humans communicate through arbitrary/conven/onal symbols, which are diﬀerent between popula/ons and in constant evolu/on à language includes the whole set of these conven/onal signals and the rules to combine them The complexity and sophis/ca/on of human language suggests that extensive regions of the brain must be dedicated to dealing with it What is language? Any communica/ve act through language implies: – a sender (encoding of a message in a linguis/c sequence) – a receiver (decoding of the message = understanding of the meaning) → language produc/on and language comprehension Hemispheric dominance The two cerebral hemispheres (leG and right) do not necessarily par/cipate equally in each cogni/ve func/on As for manual preference, the dominance of the leG hemisphere for language is gene/cally programmed (= you use one more than the other) → the concept of dominance does not imply that one hemisphere governs the other, nor that one hemisphere presides exclusively over single integra/ve func/ons Thus, perysilvian lesions that cause aphasia are usually located in the leG hemisphere in almost all right-handed people and approximately 70% of leG- handed or ambidextrous people → in a small % of right-handed people (between 1% and 5%), aphasia may be due to a right hemispheric lesion The right hemisphere – Understands words and short sentences – Deciphers wriPen language – Weak capacity for retaining the auditory message – Does not have access to the expressive faculty – It is also responsible for knowledge of social concepts and interpreta/on of prosody (emo/onal aspects of language), so it’s associated with “higher-level” language tasks → pa/ents with right hemisphere disorders may lose the ability to comprehend and show emo/on (e.g., empathy and embarrassment), interpret sarcasm, and manipulate prosody - - > metalinguis/c features mapped onto the linguis/c message Diﬀerent aspects of language are related to diﬀerent areas: > Seeing words: occipital area (visual cortex) > Hearing words: perisylvian area > Speaking words: frontal area Aphasic syndromes Definitions > Aphasia: general term meaning disrup/on/loss of language func/on(s) > Syndrome: a number of symptoms co-occurring (occurring together) and characterizing a par/cular disease; the mechanis/c reason for their co-occurrence is not always fully understood; but of the e/ology (= set of causes of a disease or condi/on) APHASIC SYNDROME refers to a disorder in language produc/on and/or comprehension (which can be diﬀerently aﬀected) following a brain lesion, in pa/ents with fully acquired language skills → the deﬁcits cannot be due to the inability to produce linguis/c sounds (deﬁcits in the phono- ar/culatory apparatus), perceive linguis/c sounds (deafness) or mental confusion / disorienta/on / delusion - - > e/ology: 40% following a stroke condi/on, but it can be present also in degenera/ve disorders (e.g., Alzheimer’s and Pick’s diseases), or related to brain inﬂamma/on, tumor or head injury Broca’s aphasia Pa/ent “Tan-Tan” had impaired language produc/on but spared comprehension: pa/ents have diﬃcul/es in producing a coherent speech as they seem to have problems in ﬁnding the words they want to use; some words are omiPed (telegraphic speech); some have comprehension diﬃcul/es → aGer his death he discovered, through the autopsy, that he had a lesion in the leG inferior frontal gyrus - - > conclusions: language produc/on is localized in the leG inferior frontal gyrus (sylvian ﬁssure, frontal area) ++ usually aware of the problem Wernicke’s aphasia Described a pa/ent with ‘opposite’ symptoms as compared to Broca’s – Fluent speech – Many sound errors – Use of seman/cally inappropriate words: non-words, made-up words, paraphasias (words that are seman/cally related but nevertheless inappropriate → this speech is called “word salad” because it tends to include random words and phrases thrown together – Impaired comprehension – Usually not aware of the problem Wernicke hypothesized a damage in the “storehouse of auditory word forms” and, by analyzing the autopsy of a pa/ent showing similar symptoms, he supposed that this storehouse could be located in the posterior part of the superior temporal gyrus (STG) ¯ Wernicke (1877) Der aphasische Symptomenkomplex: the ﬁrst theore/cal model on language neurophysiology in which it was said that… – The brain is organized in projec/on pathways and associa/ve areas – The whole leG peri-sylvian region is responsible for language → they were right in a way, the problem was that they didn’t understand that it was a network of regions, not just a speciﬁc one The Wernicke’s arc (1874): Wernicke added the following to what Broca had said language depends on a system, including: A storehouse (long-term store) of auditory images of words → lesion in Superior Temporal gyrus = Wernicke’s aphasia A storehouse of motor images of words → lesion in Inferior Frontal gyrus = Broca’s aphasia à these 2 systems are connected through an anatomical structure/pathway → the arcuate fasciculus WERNICKE-LICHTHEIM MODEL (1885): Localiza/onist model Speech input -> auditory analysis of this input à it arrives in region A (Wernicke area): now 2 diﬀerent pathways 1. Comprehend the linguis/c message → then go to M (Broca area) and produce speech 2. Repeat what we heard: from A to M (Arcuate fasciculus) → and ﬁnally ar/culatory planning and speech output *M = Motor center -> storehouse for motor representa/on of words *A = Auditory center -> storehouse for auditory representa/on of words *B = concept center -> conceptual representa/ons (B from German “Begriﬀe”, which means “concepts”) thanks to this model we can understand diﬀerent aphasic syndromes ß Subcortical sensory aphasia/subcortical motor aphasia = related to sensory and motor aspects, so you’re not able to hear sounds or ar/culate speeches with your muscles ++ related to gray maPer Broca’s aphasia = deﬁcit in produc/on and ar/cula/on (related to gray maPer: inferior frontal gyrus) → speech is: – slow – eﬀormul – non-ﬂuent – very simple gramma/cal structure → speech programming deﬁcit: loss of the ability to execute speech movements (no facial or vocal muscle paralysis) → we have a Telegraphic and Agramma/c speech → pa/ents: – may have similar “agramma/cal” problems when wri/ng – may be able to use well-prac/ced expressions (“It never rains but it pours!”) and to sing a well-known song – usually have preserved comprehension – may read aloud in a rela/vely unaﬀected way → disorder not related to the “mechanics” of moving the muscles that are concerned with speech Wernicke’s aphasia Opposite paPern of symptoms to Broca’s aphasia = deﬁcit in comprehension, repe//on, naming and meaningful output (related to gray maPer: superior temporal gyrus) → speech is ﬂuent speech, but with liPle or no meaning (word salad) → we can observe: – produc/on of neologism and non-words – seman/c paraphasias – paragramma/sm – anosognosia: they’re not aware of their problem because they are not aware of what they are producing Agrammatism (Broca) vs Paragrammatism (Wernicke) > AGRAMMATISM = refers to the widespread omission of func/on words (ar/cles, preposi/ons, auxiliary verbs) and inﬂec/ons (e.g., adding “-ed” or “ing” to a verb to change its tense, adding “s” to a noun to make it plural, using correct pronouns) coupled with a reten/on of content words (nouns and non-conjugated verbs) → eﬀormul and telegraphic speech E.G: when asked to describe a picture of children playing in the park, the aﬀected individual responds with, "trees..children..run.” > PARAGRAMMATISM = refers to the inability to form gramma/cally correct sentences à well-constructed sentences with errors in gramma/cal morphemes and subs/tu/on of lexical items Transcortical motor aphasia Similar to Broca’s = aphasia but with preserved repe//on and spontaneous speech is absent ++ presence of echolalia (to repeat things aloud) ++ white maPer disconnec/ons Transcortical sensory aphasia Similar to Wernicke’s = impaired comprehension, preserved repe//on and spontaneous speech ++ presence of echolalia (to repeat things aloud) ++ white maPer disconnec/ons Conduction aphasia = preserved comprehension, impaired repe//on (especially of novel or unusual words) ++ white maPer disconnec/ons à the frequency of phonological errors in conduc/on aphasic pa/ents depends on the posterior extension of the lesion, i.e., how much it aﬀects: – the posterior part of the superior temporal gyrus (BA 22) and the neighbor posterior parietal cortex (supramarginal gyrus, BA 40) – or the white maPer connec/ng it to frontal regions (arcuate fasciculus) Anomic aphasia = disturbance in the produc/on of single words, most marked for common nouns, intact comprehension and repe//on à disturbances of concepts and/or the sound paPerns of words à inferior parietal lobe or connec/ons between parietal lobe and temporal lobe; can follow many lesions Global aphasia = major disturbance in all language func/ons: it aﬀects both produc/on and comprehension of language à disrup/on of all language processing components à large por/on of the perisylvian associa/on cortex Isolation of the language zone = disturbance of both spontaneous speech (sparse, hal/ng speech) and comprehension, with some preserva/on of repe//on; echolalia common à disconnec/on between concepts and both representa/ons of word sounds and the speech produc/on mechanism à cortex just outside the perisylvian associa/on cortex Summary Limits of the “classical” aphasic syndromes classification 1. Most aphasic pa/ents show deﬁcits in both language comprehension and language produc/on, while the model implies a dichotomy à par/ally replaced by the classiﬁca/on in ﬂuent vs. non-ﬂuent aphasia forms 2. The associa/on between symptoms and lesions is not so reliable à the brain regions involved in language are much more than those iden/ﬁed by the classical Wernicke-Lichtheim model 3. The classiﬁca/on does not consider the analysis of deﬁcits in the diﬀerent areas of linguis/cs (phonological, morphological, lexical, syntac/c level) à allows a bePer classiﬁca/on of symptoms and their co-occurrence 4. The model does not explain the paPern of dissocia/ons found in aphasic pa/ents, e.g., dissocia/ons between deﬁcits in diﬀerent gramma/cal classes (e.g., nouns and verbs) or lexical categories 5. The model does not allow explaining the behavior of some aphasic pa/ents in tasks like reading and wri/ng or repe//on of non-words 6. The model does not provide the possibility of processing non-lexical sequences (non- words) ¯ Non-words Non-word = a sequence of lePers or sounds that is not accepted as a word by speakers of a speciﬁc language, used especially in (neuro)psychological or linguis/c experiments Fluent vs non-fluent aphasia This classiﬁca/on maintains the dichotomy between anterior vs. posterior lesions leading (most likely) to diﬀerent types of disturbances (ﬂuent vs. non- ﬂuent aphasia), but the diﬀerence between the two does not regard produc/on vs. comprehension: they are characterized by a qualita/vely diﬀerent speech à this classiﬁca/on focuses on the quality of the speech > FLUENT APHASIA No ar/culatory deﬁcits nor eﬀormul speech; no agramma/sm (but paragramma/sm) Smooth and abundant speech, long sentences but possible phonological errors, neologisms (phonological deﬁcits) and seman/c errors and anomie (seman/co-lexical deﬁcits) More frequent in the elderly à see Wernicke’s aphasia, conduc/on aphasia > NON-FLUENT APHASIA Possible presence of ar/culatory deﬁcits and agramma/sm Short sentences, reduced speech More frequent in young subjects à see Broca’s aphasia, global aphasia Psycholinguistic perspective LINGUISTICS: The scien/ﬁc study of language and its manifesta/ons à language is hierarchically organized: 1. Phone0cs studies how humans produce and perceive sounds (phone/c tracts) 2. Phonology studies how languages/dialects systema/cally organize their sounds in words 3. Morphology describes the rules applied to combine phonemes in words 4. Syntax describes the rules applied to combine words in sentences 5. Seman0cs describes the associa/on between words and meaning (damage: temporal pole) 6. Grammar describes the rules to combine units in hierarchical structures 7. Pragma0cs studies the language in a context, how it is used in social interac/ons Psycholinguistics It’s the study of the psychological/cogni/ve processes at the basis of language – it studies the interrela/on between linguis/c factors and psychological aspects; – it concerns the mechanisms by which language is processed and represented in the mind and the brain (neurolinguis/cs) à psycholinguis/cs and neurolinguis/cs study the psychological and neurobiological factors that enable humans to acquire, use, comprehend, and produce language à analysis of symptoms of aphasic pa/ents based on diﬀerent levels of analysis (phonological units, words, sentence, discourse) Language is hierarchically organized – Phonological units are the dis/nc/ve units that allow the iden/ﬁca/on of words, and are composed by phone/c tracts (= how sounds are produced by the phono-ar/culatory apparatus and perceived by the auditory one) – Morphemes are the elementary units of words conveying informa/on – Some morphemes combine to create words (e.g., preﬁx [sub-, pre-, an/-]) – Words combine to create sentences Phonetics and phonology PHONETICS studies how humans produce and perceive sounds (units = phone/c tracts) à the physical features of verbal communica/on Ar/culatory phone/cs = how speech sounds are produced Auditory phone/cs = classiﬁca/on of speech sounds based on how they are perceived à phone/c tracts (= how sounds are produced by the phono-ar/culatory apparatus and perceived by the auditory one PHONOLOGY studies the rules used to systema/cally organize sounds in words. à phonological units allow the iden/ﬁca/on of words, and are composed by phone/c traits Classification of language sounds (glossary) VOWELS AND CONSONANTS Vowels = speech sounds produced by an open conﬁgura/on of the vocal tract, with vibra/on of the vocal cords but without audible fric/on (no obstacles in the ﬂux of air), see a, e, i, o, u, y Consonants = speech sounds ar/culated with complete or par/al closure (obstruc/on) of the vocal tract à Consonants are either voiced (sonant) or voiceless (surd) o Voiced consonants are pronounced with the same vocal murmur (vibra/on of the vocal cords) that is heard in vowels e.g., b, d, g, l, r, m, n, z o Voiceless consonants are produced without a vibra/on of the vocal cords and lack this murmur e.g., p, t, c (k, q), f, h, s, x à Consonants can be also classiﬁed depending on the place of ar/cula/on = where in the vocal tract the obstruc/on of the consonant occurs, and which speech organs are involved E.G: bilabial consonants involve both lips, velar consonants involve the tongue against soG palate Disorders of phonological processing PHONOLOGICAL SELECTION ERRORS (PRODUCTION) = result in the produc/on of incorrect phonemic sequences, easily recognizable when they cons/tute neologisms à crucial features: They include the speciﬁc sounds of the pa/ent’s language à phoneme percep/on is categorical (Liberman, 1967): o We can primarily dis/nguish (and systema/cally produce) the speech sounds that we have learnt through linguis/c development (mother tongue) o Once these categorical boundaries are learnt, they cannot be forgoPen The neologisms follow the same phonemic rules of the pa/ent’s language (e.g., no sequences of consonants) PHONOLOGICAL PROCESSING ERRORS In aphasic pa/ents, a phonological deﬁcit is characterized by the presence of phonemic paraphasias (subs/tu/ons, omissions, addi/ons and transposi/ons of phone/c units) even mul/ple that some/mes make the target words unrecognizable (phoneEc neologisms) à oGen the pa/ent tries to correct the phonemic errors produced by means of spontaneous correc/ons, some/mes repeated in trials (conduites d’approche) - - > in some cases the phonemic errors can result in words that actually exist and thus simulate a lexical rather than phonological subs/tu/on Phonemic paraphasia refers to the subs/tu/on of a word with a word or a nonword that preserves at least half of the segments and/or number of syllables of the intended word à some examples of phonemic paraphasias: An/cipatory errors: a syllable from later in the word replaces a syllable from earlier in the word →"papple" for apple or "lelephone" for telephone Paradigma/c errors: based on similarity in how the sounds are formed →"marmer" for barber → lips-related consonants Subs/tu/on errors: involve a clear phonological subs/tu/on →"ragon" for wagon Epenthe/c errors are the inser/on of a segment into the target → "plants" for pants Metathe/cal errors: the full exchange of segments →"deks" for desk DISORDERS OF PHONOLOGICAL PROCESSING Phonological decoding (comprehension) When listening to spoken words – Frequency eﬀect: higher frequency phonemes and phonological sequences are more easily iden/ﬁed – Lexical status: real VS non-words → people make more errors when listening to non-words than words and tend to interpret acous/cally ambiguous phonemes in the form that is seman/cally congruent Morpho-syntactic aspects of language Morphemes are the elementary units of words conveying informa/on à some morphemes combine to create words (e.g., preﬁx [sub-, pre-, an/-]) Words combine to create sentences Sentences convey rela/onships between the meaning of words → Morpho-syntac/c aspects are the set of the proposi/onal content of a sentence → Studies in this domain aim to explain why pa/ents make morphological, syntac/c, or morphosyntac/c errors in language produc/on and comprehension MORPHOLOGY: describes the rules applied to combine phonemes in words – Describes the class of each word (noun, pronoun, verb, adjec/ve, preposi/on…) – Describes how to conjugate verbs and create deriva/ons – (deriva/on = the forma/on of a word by changing the form of the base or by adding aﬃxes/suﬃxes to it, e.g., “hope” to “hopeful”) SYNTAX: describes the rules applied to combine words in sentences – Describes the order of the words, how to organize subordinates (dependent) – Describes how to use func/onal words (closed class words)*, e.g., pronouns (you, them), modal verbs (could, must), determiners (a, the), preposi/ons (of, in), and conjunc/ons (and, but) MORPHO-SYNTAX: describes the rela/onship between morphology and syntax, e.g., rules applied to achieve agreement between nouns and verbs (singular/plural) The guy cooks Sentences convey rela/onships between the meaning of words à proposi/onal content of a sentence à SYNTACTIC STRUCTURES: describe how individual words can be arbitrarily combined to convey proposi/onal content → express one of several equally likely rela/ons E.G: approximately 85% of aphasic pa/ents have troubles in understanding/use the syntac/c structure to convey/determine sentence meaning (Caplan et al., 1985) E.G: pa/ents with Broca’s aphasia show more errors in understanding sentences with reversable roles (where seman/cs cannot ‘help’) → the syntac/c structure is the only source of informa/on SYNTACTIC STRUCTURES Are studied by linguis/cs as syntac/c trees (Noam Chomsky, 1928-alive) à rules to describe how meaning can be derived from syntac/c structures → iden/ﬁca/on of thema/c roles = who does what → crucial for understanding co-reference (pronouns, reﬂexives), passive sentences… They divide each sentence in diﬀerent types of morphemes: depending of the complexity and structure of the three, we will have diﬀerent types of trees * S = sentence * NP = noun phrase * VP = verb phrase * N = noun * V = verb DISORDERS OF SYNTACTIC PRODUCTION = sentence produc/on is a process including three major stages à aphasic disturbances can aﬀect: 1. The produc/on of gramma/cal vocabulary elements → agramma/sm and paragramma/sm 2. The ability to generate syntac/c forms → impoverishment of syntac/c structures in spontaneous speech (simpliﬁca/on) 3. The ability to assign thema/c roles (severely aﬀected pa/ents) NEUROANATOMY OF SYNTACTIC PROCESSING PREMISE: deﬁcits in syntac/c comprehension and produc/on oGen co-occur in agramma/c pa/ents, but they can also dissociate, and the severity of the deﬁcit does not correlate à they do not appear to depend on a single func/onal impairment (ONLY) Syntac/c processing involves the whole leG perisylvian associa/ve cortex – Inferior frontal gyrus (BA 45, 44) (Broca) – Angular gyrus (BA 39) (integra/ve cortex) – Supramarginal gyrus (BA 40) (integra/ve cortex) – Superior temporal gyrus (BA 22) (Wernicke) à distributed func/on with distributed sub-func/ons EXPERIMENT Despite much research on agramma/sm, the lesion correlates of paragramma/sm are s/ll unknown Subjects: 53 right-handed pa/ents with aphasia following chronic leG-hemisphere stroke Task: retelling the Cinderella story Methods: lesion-symptom mapping was used to inves/gate the degree to which the lesion correlates of agramma/sm and paragramma/sm overlap or dissociate à four expert raters assessed videos - - > consensus discussion determined each subject’s classiﬁca/on with respect to gramma/cal deﬁcits as Agramma/c, Paragramma/c, both, or No Gramma/cal Deﬁcit à each subject’s lesion was manually drawn on a high-resolu/on MRI and lesion-symptom mapping analyses were performed (covariates: lesion volume and speech rate) Results: damage to Broca’s area was signiﬁcantly associated with agramma/sm but not paragramma/sm, while damage to the leG posterior superior and middle temporal gyri was signiﬁcantly associated with paragramma/sm but not agramma/sm → DOUBLE DISSOCIATION paradigm à picture both at clinical, structural and func/onal level: DISORDERS OF LEXICO-SEMANTIC PROCESSING Lexical seman/cs is the branch of linguis/cs which is concerned with the systema/c study of word meanings à lexicon refers to the store of language labels associated with concepts - - > seman/c lexicons are made up of lexical entries: lexical entries are seman/c (not orthographic) and are interconnected with seman/c rela/ons NEVERTHELESS, deﬁcits in the seman/c system or in the lexical retrieval (lexicon) lead to similar behaviors (e.g., anomia – not being able to retrieve speciﬁc labels) - - > the organiza/on of lexicon has been studied by psycholinguis/cs using computa0onal modelling – they are ar/ﬁcial systems mimicking the behavior of pa/ents and healthy subjects – they provide hypotheses on the organiza/on of both the cogni/ve and the neural systems (‘ar/ﬁcial’ neural networks) *Lexicon labels are diﬀerent from conceptual and seman/c ones It allows us to: – Phonological input lexicon (Ellis & Young, 1988) translates acous/c to seman/c representa/ons = understanding of the meaning of words – Phonological output lexicon (Ellis & Young, 1988) translates a concept into a spoken word – Lexicon = connec/ons between domains (coherent with a distributed view of linguis/c representa/ons in the brain) OTHER LEXICO-SEMANTIC EFFECTS > WORD FREQUENCY Even in the lexical-seman/c domain, frequency plays a role à more frequent words have more connec/ons (more features in common) with other words (more resistant = less prone to errors) > AGE OF ACQUISITION Words that are acquired earlier in development are more resistant = less prone to errors (in the absence of a neurological disorders) à during early learning, connec/on strength changes are large à then they become smaller as the knowledge accumulates (simula/ons through computa/onal modelling) LEXICO-SEMANTIC ERRORS Among the deﬁcits at the seman/c-lexical level: Anomia = a diﬃculty in retrieving words Anomic latency = in the case of a simple delay in recalling a target word à the words not recalled can some/mes be replaced by circumlocu/ons Error in the choice of words, for which there are subs/tu/ons with terms of similar meaning (seman0c paraphasias; for example: “glass” for “boPle”) or with words without a rela/on of meaning (verbal paraphasias; for example: “tablecloth” for “telephone”) PARAPHASIAS = confusions of words or the replacement of one word by another real word; length of the word is not oGen preserved à some examples: – Categorial: same category → /ger for lion, car for van. – Associa/ve: replace the target word with one that is related to the target but is not of the same category → foot with shoe – Superordinate: replace a speciﬁc target word with a more generalized group to which the target word involves → pear with fruit – Subordinate: replace the target word with one that is more speciﬁc → rose for ﬂower Aphasic patients – sum of frequent symptoms Verbal stereotypy = nonproposi/onal uPerance characterized by repe//on of a syllable, word, or phrase (e.g., “ba-ba-ba,” “yep,” “bloody hell,” “wait a minute”), typically used in high frequencies and as emo/onal exclama/ons Phonemic paraphasias = subs/tu/ons, omissions, addi/ons and transposi/ons of phonemes in a word Phone0c neologisms Conduites d’approche = eﬀort to correct the phonemic errors produced by repeated spontaneous correc/ons à PHONETICS Anomia = deﬁcit at the seman/c-lexical level, diﬃculty in retrieving words Anomic latency = simple delay in recalling a target word Circumlocu0ons = a descrip/on of the word in place of the target word à LEXICO-SEMANTIC LEVEL Seman0c paraphasias = subs/tu/ons of the target word with another seman/cally related Verbal paraphasias = subs/tu/ons of the target word with another not seman/cally related à SEMATIC LEVEL Agramma0sm VS Paragramma0sm à MORPHO-SYNTACTIS LEVEL Double dissociation: category-specific deficits NATURAL OBJECTS (dog, tree, strawberry, …) → leG inferior temporal lesions VS ARTIFICIAL OBJECTS (comb, scissors, iron, …) → leG parietal lesions = we may not be able to name natural objects, but ar/ﬁcial objects because they are related to diﬀerent brain regions à 2 hypotheses: 1. Separate organiza/on at lexical output level (Hart, Berndt and Caramazza, 1985) 2. Diﬀerent organiza/on of conceptual knowledges (Warrington and Shallice, 1984) → natural objects have visual representa/ons (leG occipito-temporal cortex), ar/ﬁcial objects have func/onal representa/on (leG parietal cortex) ¯ in a similar way ¯ NOUN → lesions in intermediate part of the second temporal gyrus VS VERBS → leG premotor frontal lesions for non-ﬂuent aphasia; leG posterior temporal and inferior parietal lesions for ﬂuent aphasia à 2 hypotheses: 1. Noun and verbs have diﬀerent rela/ve weight of perceptual features (Bird, Howard and Franklin, 2000) à verbs have less sensory informa/on 2. Based on a peripheral lexical level, where lexical labels are represented separately (Caramazza and colleague, 2002) à diﬀerent places where we represent nouns and verbs How to test a patient with language impairments General medical history and history of language – leG-handed or right-handed – bilingual – reading and wri/ng – evolu/on of the linguis/c disorder Spontaneous speech (during the clinical interview) = the general ability to interact and communicate is tested while asking the pa/ent to provide details related to pathology, disturbances, family situa/on, habits… à it allows evalua/ng – the speech content: is it informa/ve? – the pragma/cs: is language appropriate to the situa/on? – comprehension: does the pa/ent understand my ques/ons? During spontaneous speech it is also possible to iden/fy: – ar/culatory disturbances – phonological, lexical/seman/c, morphological, syntac/c errors – persevera/ons and automa/sms (e.g., repe//on of brief lexical idiosyncra/c sequences or even meaningless syllables) Systema/c evalua/on of language abili/es in the diﬀerent areas (phonological, lexical/seman/c, morphological, syntac/c errors) à can be done at very diﬀerent degrees of precision/detail International language batteries NEUROLINGUISTIC APPROACH – Boston Diagnos/c Aphasia Examina/on (BDAE) [Goodglass e Kaplan, 1972, 1982] – Aachener Aphasie Test (AAT) [Huber e coll, 1983] – Western Aphasia BaPery (WAB) [Kertesz, 1982] PSYCHOLINGUISTIC APPROACH – Psycholinguis/c Assessment (PALPA) [Kay e coll, 1992] PRAGMATIC APPROACH – Communica/ve abili/es of daily living (CADL) [Holland, 1980] How to test a patient with language impairments SystemaEc evaluaEon of language abiliEes in the diﬀerent areas (phonological, lexical/semanEc, morphological, syntacEc errors) à can be done at very diﬀerent degrees of precision/detail Object naming or object picture test to assess lexical retrieval ability à possible presence of anomia, anomic latency, circumlocu/ons à generally, the non-retrieved word is not lost at all; it is not accessible to the pa/ent at that moment, but it can be facilitated through more automa/c sentences or expressions, or be found on other occasions RepeEEon tasks → phonemic paraphasias, phonemic neologisms and conduites d'approche à to test repe//on ability, s/muli of diﬀerent length and complexity are used: star/ng with bisyllabic words with a simple structure (alterna/on consonant- vowel) and con/nues with progressively longer and more complex words Oral comprehension 1. Execu/on of verbal orders: it is best to avoid the most obvious ones, which are part of a medical examina/on and can get randomly correct answers (e.g. "Open your mouth"); it is more appropriate to give "ar/ﬁcial" orders (e.g. "Knock the table three /mes"), to be sure that the pa/ent has actually recognized and understood the command 2. Recogni/on of objects: the pa/ent is presented with a series of common objects; the examiner names one and asks the pa/ent to indicate it (e.g. "What is the key?", "What is the pen?") 3. Repe//on of words and phrases, said by the examiner Other related syndromes – Alexia – Agraphia – Acalculia Treatment Please note: in the diﬀerent phases of stroke and related aphasia disorder (acute versus chronic), a diﬀerent therapeu/c approach is suitable due to the diﬀerent neurophysiological mechanisms underpinning each phase à diﬀerent disorder -> diﬀerent treatment plan (if the pa/ent is the same) 1. Behavioral protocols for Speech and Language therapies a. PHONOMOTOR TREATMENT: aims to boost word retrieval through the training of phonological skills à mul/modal approach: use of mirror, mouth pictures, wriPen representa/ons, etc. - - > training starts with single phonemes and gradually progresses to phoneme sequences in nonwords and real words b. SEMANTIC FEATURE ANALYSIS: lexical retrieval is supported by strengthening seman/c networks à use of feature analysis charts that provide informa/on regarding use, loca/on, physical proper/es, and associa/on concepts to generate seman/c features of target concepts c. VERB NETWORK STRENGTHENING TREATMENT: lexical retrieval, sentence produc/on and discourse are facilitated by working on verbs, which have a central role in seman/cs and syntax d. SOUND PRODUCTION TREATMENT: ar/culatory–kinema/c treatment à incorrectly produced sounds (i.e., monosyllabic and polysyllabic words, phrases, sentences) are prac/ced hierarchically through modeling, repe//on, minimal pair contrast, orthographic cuing, integral s/mula/on (i.e., “watch me, listen to me, say it with me”), and ar/culatory placement instruc/ons e. TREATMENT OF UNDERLYING FORMS: based on genera/ve syntax and targets deﬁcits exhibited at the sentence level in people with agramma/c aphasia by training the produc/on of gramma/cally complex sentences à use of wriPen cards that have the components of simple ac/ve declara/ve sentences (e.g., subject, verb) and a picture illustra/ng the ac/on - - > aGer iden/fying the verb, pa/ents are trained to reorder sentence components to produce more complex sentences f. CONSTRAINT-INDUCED LANGUAGE THERAPY: a treatment approach for expressive language diﬃcul/es à forced use of spoken language and restraint of all other communica/on modali/es (e.g., hand gesturing) à it is an intensive approach necessita/ng massed prac/ce g. MELODIC INTONATION THERAPY: ﬁrst developed to recruit right hemispheric brain regions related to the awareness of melody and rhythm to improve expressive language in individuals with non-ﬂuent aphasia à based on (i) rhythmic tapping of the leG hand that accompanies the produc/on of syllables, and (ii) exaggera/on of the natural prosody of speech 2. Computerized aphasia therapies derived via computers, smartphones, or tablets à allows for long-term and low-cost therapy op/ons 3. NIBS: Non-invasive brain sEmulaEon a. Upregulate neural ac/vity in perilesional brain areas of the aﬀected hemisphere through excitatory s/mula/on protocols (i.e., high frequency rTMS or anodal tDCS) à perilesional regions of the leG hemisphere are recruited to subserve the reorganiza/on and gain of language b. Downregulate neural ac/vity in contralesional brain regions through inhibitory s/mula/on protocols (i.e., low frequency rTMS or cathodal tDCS) à based on the “interhemispheric compe//on model”: there exists a mutual and balanced inhibi/on between the brain hemispheres - - > stroke-induced damage to one hemisphere disrupts this balance leading to reduced inhibi/on from the aﬀected to the unaﬀected hemisphere; the unaﬀected hemisphere, in turn, increases its inhibitory signals to the aﬀected hemisphere -> this ac/va/on in the unaﬀected right language brain regions is deleterious to recovery (maladap/ve plas/city) THUS, by downregula/ng contralesional homologous brain regions via inhibitory protocols, language recovery can be induced à Please remember: rTMS can be delivered alone, tDCS should be always associated to a behavioral speech and language therapy Reading and writing Reading and writing abilities Neuropsychology tries to explain: – the processes involved in reading and wri7ng in healthy subjects – reading (dyslexia, alexia) and wri7ng (agraphia) deﬁcits in pa7ents > Reading = the conversion of a sequence of graphemes (printed leCers) into a sequence of sounds (phonemes) à Reading aloud tasks > Wri7ng = the conversion of a sequence of sounds (phonemes) into a sequence of graphemes (printed leCers) à Dicta7on exercises Reading and writing neural correlates Reading and writing cognitive correlates We can dis*nguish between: Peripheral stages = processing of percep7ve features (visual aspect of the s7mulus) or selec7on of motor paCern (non-linguis7c processes) E.G: analysis of single leCers while reading, actual movement planning while wri7ng Central stages = based on lexico-seman7c knowledge and grapheme-phoneme conversion mechanisms à enabling the spelling of words = iden7ﬁca7on of the correct sequence of leCers that cons7tute each word Reading Writing Peripheral deﬁcits include: Peripheral deﬁcits include: – Neglect dyslexia – Impairments of the graphemic buﬀer – ACen7onal dyslexia – Apraxic agraphia – Pure alexia (with or without ideomotor apraxia) (non-linguis7c deﬁcits) – Spa7al agraphia

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