cognitive Neuroscience Flashcards
Cognitive Neuropsychology
Cognitive Neuropsychology is a branch
of cognitive psychology that aims to
understand how the structure and function of
the brain relates to
specific psychological processes
Historical Milestones in Neuropsychology
1913 - William Osler: Defined neuropsychology as the study of biological and psychiatric aspects of mental illness.
1933 - Karl Lashley: Used the term “neuropsychology” at a conference, though he did not provide a formal definition.
1948 - Teuber & Bender: Developed methods to study how traumatic brain injury affects behavior.
1964: Two pivotal** journals **in neuropsychology were established, Neuropsychologia (founded by Hécaen in France) and Cortex (founded by De Renzi in Italy).
Associationism
Jean Baptiste Bouillaud (1825, France)
Jean Baptiste Bouillaud (1825, France)
He tried to confirm through the anatomoclinical correlation method the Gall’s
hypothesis, which postulated the existence
of a specific area in the frontal lobes
specialised in language articulation and
word memory.
In his clinical descriptions, he proposed that
the grey matter was dedicated to intellectual
production and the white matter to verbal
emission.
Associationism
Paul Broca (1861, France)
He reported a post mortem study of
an aphasic patient who was speechless
apart from a single nonsense word: “Tan”.
Broca showed that an area of the left frontal
lobe was damaged. As Tan was unable to
produce speech but could still understand it,
Broca argued that this area might be
specialised for speech production and
that language skills might be localized to
this cortical area.
Lelong, a few weeks later. Lelong, like Tan,
could understand speech but could only
repeat the same 5 words. After examining
his brain, Broca noticed that Lelong had a
lesion in approximately the same area as his
patient Tan. He also noticed that in the more
than 25 patients he examined with aphasia,
they all had lesions to the left frontal lobe but
there was no damage to the right
hemisphere of the brain.
Associationism
Karl Wernike (1874, Germany)
He reported patients with damage further
back in the temporal lobe who could speak
but were unable to understand what was
said to them, providing evidence for two
potentially interconnected language centres.
These clinical descriptions were integrated
into a theory of language organisation
by Lichtheim.
Holistic approach
The early 20th century saw a reaction to the overlyprecise accounts of the diagram making neurologists.
Pierre Marie challenged conclusions against previous
evidence of Broca’s areas in 1906 and Henry
Head attacked the whole field of cerebral localization.
Jackson: “the language is not just words production, but
the expression of a positive thinking”
Lashley (1929): In a series of experiments on rats, Karl
Lashley demonstrated increasingly progressive memory
deficits directly proportional to the extent of the brain
lesion. He suggested that cognitive functions are
distributed and not localized.
functual assymetries with Geschwind and
Levitsky’s (1968)
The modern science of cognitive neuropsychology emerged during the 1960s
stimulated by the insights of the neurologist Norman Geschwind who
demonstrated that the insights of Broca and Wernicke were still clinically
relevant.
research: examining 100 human brains they found
that the posterior and upper portion of the temporal lobe, the part called
planum temporalis, was more developed on the left in 65 cases, and
on the right in 11 cases.
The presence of this anatomical asymmetry, in the Wernicke’s area
indicated as basic for linguistic processes, raised great interest and
allowed for enrichment of this first important result.
Cognitive Revolution”
the growing science of cognitive psychology which had emerged as a
reaction to behaviorism in the mid 20th century.
Psychologists in the mid-1950s acknowledged that the structure of
mental information-processing systems could be investigated in scientifically acceptable ways.
They developed and applied new cognitive processing models to explain experimental data from not only studies of speech and language but also those of selective attention.
Roger Sperry’s Split-Brain Experiments (1959–1968)
Corpus Callosum Research: Sperry studied the corpus callosum, which connects the brain’s hemispheres, by severing it in animals and then in humans to treat epilepsy. He found that the two hemispheres could function independently and that each hemisphere specialized in different functions. His work showed that the left hemisphere was primarily responsible for language interpretation, while the right processed spatial and perceptual information.
Nobel Prize: Sperry received the Nobel Prize in Physiology or Medicine in 1981 for his split-brain research.
Unilateral Spatial Neglect (Jackson and Others)
Definition: After right hemisphere damage, often from a stroke, patients experience deficits in attention and awareness towards the left side (contralesional) of their body or environment. They may not perceive stimuli on the affected side unless it’s pointed out to them.
Patient Experience: Patients may only realize the neglect if it’s explicitly shown to them, such as being asked why their drawing is incomplete. They may comment, “There should be two attention centers.”
Key Point: Neglect is not a sensory deficit but rather a breakdown in attentional processing, causing patients to ignore parts of their own bodies or surroundings.
Anosognosia for Hemiplegia (Babinski Sign)
Patients cannot move the left side of their body and fail to recognize or acknowledge this motor deficit. For example, if asked to clap, they may respond that they did clap. When questioned about the absence of sound, they might rationalize it by saying the therapist was too far away to hear. If further questioned to hold an object, the patient may say they can do it but fail to actually perform the task. If the patient does not recognize this inability, it is considered complete anosognosia for hemiplegia.
Explanation: This condition may be due to damage in the premotor cortex, which normally functions to compare intended motor output with actual movement. Here’s the process:
Movement command is generated in the motor cortex → Lesion in the corticospinal tract causes an interruption → No movement occurs → Damage to the premotor cortex prevents the brain from comparing the intended movement to actual movement, impairing awareness of the deficit.
In studies, stimulating the premotor cortex sometimes leads patients to realize they cannot move, further supporting this role.
Marshall & Newcombe (1966) on
reading and Warrington & Shallice (1969) on memory
The rebirth of neuropsychology was marked by the publishing of two
seminal collaborative papers
Subsequently, work by pioneers such as Elizabeth
Warrington, Brenda Milner, Tim Shallice, Alan
Baddeley and Lawrence Weiskrantz demonstrated that neurological
patients were an important source of data for cognitive
psychologists.
H.M. Case Study (The importance of single cases)
Focus: Research on the neural basis of memory and the distinction between declarative (explicit) and non-declarative (implicit) memory.
Types of Amnesia Observed:
Retrograde Amnesia: Loss of memories prior to the surgery.
Anterograde Amnesia: Inability to form new memories after the surgery.
H.M. experienced retrograde amnesia for up to 11 years but showed gradual recovery. He continued to have anterograde amnesia throughout his life.
The hippocampus was initially thought to be solely responsible for declarative memory. However, research suggests it also plays a role in certain implicit memory processes.
Conclusion: Scientists concluded that while the hippocampus is needed in the creation of new memories, it is not needed in the retrieval of old ones; they are two separate processes.
Telencephalon and Diencephalon:
Structures primarily responsible for higher cognitive functions and executive processes.
COMA
Often results from damage to the brainstem, particularly the reticular formation, which is crucial for maintaining consciousness.
Traumatic Brain Injuries PROTECTION
The meninges (Dura Mater, Arachnoid Mater, Pia Mater) and cerebrospinal fluid (CSF) serve to cushion and protect the brain from impacts against the skull.
Spinal Cord Segments
Cervical: Lesions can lead to tetraplegia (loss of movement in all four limbs).
Thoracic: Lesions can lead to paraplegia (loss of movement in the lower limbs).
Lumbar and Sacral: Control lower body functions and sensations.
Alteration in Body Representation
Importance of Sensory Input
Body representation in the brain relies heavily on sensory input. In cases like somatoparaphrenia, patients lose awareness of certain body parts or their sensations, such as temperature and touch.
Tetraplegia and Body Representation: Loss of sensory feedback and motor control in tetraplegia can lead to changes in body image and representation in the brain. Cognitive assessments for these patients may involve asking them to recognize and describe the function of objects (e.g., a hat, a glove) to evaluate body perception after injury.
The Insula
Functions: The insula processes signals from the body and integrates autonomic functions.
Anterior Insula: Processes primitive bodily information.
Posterior Insula: Processes more refined, somatosensory information.
Historical Note: Originally known as the “heteroceptive cortex” for its role in multisensory integration.
Insula (Posterior Insula): Involved in interoception (perception of internal bodily states like hunger, pain, and heart rate).
The Insular Cortex contributes to the awareness of body sensations and internal states. It’s a primitive part of the brain for body perception.
Homunculus
the distorted scale model of a human drawn or sculpted to reflect the relative space human body parts occupy on the somatosensory cortex (the sensory homunculus) and the motor cortex
Motor and Somatosensory Homunculus: Maps areas in the brain associated with different parts of the body. Although previously thought to contain silent regions, recent studies suggest multisensory integration occurs in the spaces between mapped areas.
Stroke and cerebrovascular deseases
A stroke is a medical emergency that occurs when blood flow to the brain is blocked or there is sudden bleeding in the brain. rapidly developing clinical signs of focal (or global) disturbance of cerebral
function, with symptoms lasting 24 hours or longer, or leading to death, with
no apparent cause other than of vascular origin.”
* Ischemic Stroke
Thrombotic Stroke
Embolic Stroke
* Hemorrhagic Stroke
Intracerebral Hemorrhage (ICH)
Subarachnoid Hemorrhage (SAH)
* Transient Ischemic Attack (TIA)
Transient Ischaemic Attack
focal neurological symptoms attributed to
cerebral ischaemia lasting less than 24 hours, with complete recovery.
schaemic Stroke
In about 85% of cases, stroke is secondary to infarction
Common risk factor
✓ Hypertension
✓ Diabetes
✓ Hypercholesterolemia
✓ Cigarette smoking
✓ Family history
✓ Prior stroke
✓ Cardiac disorders (atrial
fibrillation, valvular abnormalities,
patent foramen ovale, decreased
ejection fraction)
➢ Lacunar Infarction
→ infarction involves a small
volume of the tissue
→ occlusion of a penetrating
artery
→ small vessel disease
➢ Major Infarction
→ infarction involves great
volume of the tissue
→ occlusion of major cerebral
artery
→ Embolic/thrombotic occlusion
Haemorrhagic Stroke
About 10% of acute strokes
➢ They can be traumatic or atraumatic (spontaneous)
➢ It is usually impossible to distinguish between infarction
and intracranial haemorrhage from the history and
examination
➢ Cranial imaging is the only reliable method to distinguish
between infarction and haemorrhage.
Epidural Hematoma
✓ Located in the space between the
Dura and the skull
✓ Traumatic rupture of middle
meningeal artery
Subdural Hematoma
✓ Located in the space between the
Dura and the Arachnoid
✓ Traumatic rupture of the bridging
veins
Subarachnoid Hemorrhage
✓ Located in the CSF-filled space
between the Arachnoid and the Pia
✓ Rupture of an arterial aneurysm in
the subarachnoid space
Haemorrhagic Stroke
Intracerebral or Intraparenchymal Hemorrhage
Haemorrhagic Stroke
Intracerebral or Intraparenchymal Hemorrhage
✓ Located within the brain parenchyma in the cerebral
hemispheres, brainstem, cerebellum, or spinal cord
✓ They can be traumatic or atraumatic (spontaneous)
✓ Atraumatic causes → hypertension, brain tumors, hemorrhagic
conversion of ischemic infarction, vascular malformations, blood
coagulation abnormalities, infections, amyloid angiopathy, and
vasculitis
Deep (typical)
intracerebral Hemorrhage
✓ Hypertension
✓ Involve small penetrating blood vassels
✓ Located in basal ganglia, thalamus and
deep white matter
Lobar (atypical)
intracerebral Hemorrhage
✓ Amyloid angiopathy
✓ Involve greater vassels or vascular
malformations
✓ Located within the cerebral lobes
Alzheimer’s Disease
Structural imaging findings
(CT/MRI)
Marked and disproportionate
medial temporal lobe atrophy
➢ Bilateral hippocampal atrophy
➢ Ventricular enlargement
➢ Generalized cortical atrophy
Alzheimer’s Disease
Functional imaging findings
(SPECT/PET)
and specific symptomatic pharmacological treatments
Symmetrical temporo-parietal
hypometabolism (PET) and
hypoperfusion (SPECT)
Cholinesterase inhibitors
✓ Memantine (NMDA antagonist)
Tumors of the Central Nervous System
Brain tumours include
✓ Primary tumours arising from intracranial structures
✓ Metastases from outside the CNS
➢ Second cause of neurological death
➢ Only definite environmental risk **factor → ionizing radiation
➢ Clinical presentation depends on
✓ Location
✓ Rate of growth
✓ Pathology
➢ Most common symptoms are
✓ *Headache → bi-frontal, worse on one side, not the
worst headache of life
✓ Seizures *→ type and characteristics dependent on
tumour location
✓ Focal deficits → depend on location, usually
subacutely progressive
✓ Cognitive and behavioural symptoms → specific
focal cognitive deficits, depression, paranoid delusions
and personality changes
Infections of Nervous System
High morbidity and mortality
➢ Caused by viruses, bacteria, fungi or protozoa
➢ They may affect the lining of the brain, CSF, brain
parenchyma, spinal cord, nerve roots, peripheral nerve or
muscle
➢ They can be divided into
✓ Meningitis → Pia/Arachnoid Mater and subarachnoid
space
✓ Encephalitis → Brain parenchyma
Meningitis is an inflammation of the membranes, called meninges, that surround the brain and spinal cord. Encephalitis is inflammation of the brain itself.
✓ Focal suppuration or inflammation → Pus-filled (absses) cavity in the brain/spinal cord.
➢ Highly variable presentation
→ from acute fulminating meningitis/encephalitis → death
→ to disease development years after initial infection
➢ Highly variable neurological manifestation
✓ Meningism
✓ Impaired consciousness
✓ Cortical/subcortical dysfunction
✓ Spinal cord, nerve roots, peripheral nerve or muscle
involvement
Demyelinating Diseases
Multiple Sclerosis
https://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/symptoms-causes/syc-20350269
Inflammatory demyelinating disorder of the CNS
Interactions between genes and environmental factors
leading to tissue injury by autoimmune mechanisms
Pathological hallmark → focal plaque or lesion
Wide variety of symptoms → any part of the CNS
Common clinical features
✓ Optic neuritis
✓ Partial spinal cord syndrome (altered sensation,
bladder and bowel disfunction)
✓ Motor involvement → weakness → disease progression
✓ Cognitive impairment → mainly attention, information
processing, memory and executive functions
➢ Diagnosis
✓ Dissemination in time and space (MRI imaging)
✓ Immunological disturbance (lumbar puncture/CSF
analisys)
Parkinson’s Disease
Idiopathic (Idiopathic means arising spontaneously or from an obscure or unknown cause, or peculiar to the individual) neurodegenerative disorder of unknown etiology
loss of pigmented dopaminergic neurons in the substantia nigra
✓ Lewy bodies → cytoplasmic inclusions made up of α-synuclein
➢ Diagnosis is based on clinical features
first part
Parkinson’s Disease
Initially symptoms are unilateral → with disease progression become bilateral
➢ Severity often remains asymmetrical
Cardinal motor features
✓ Resting tremor
✓ Bradykinesia
✓ Cogwheel rigidity
✓ Postural instability
✓ Executive dysfunction
✓ Depression
✓ Anxiety
✓ RBD
Additional non-motor features
✓ Orthostatic hypotension
✓ Constipation
✓ Urinary incontinence
✓ Hyposmia
Epilepsy
Common condition → about 20% of all
neurological consultations
➢ Epilepsy → disorder of brain characterized by an ongoing liability to
recurrent epileptic seizures
➢ Epileptic seizure → transient clinical manifestations that result from an
episode of epileptic neuronal activity
➢ Epileptic neuronal activity → specific dysfunction, characterized by
abnormal synchronization, excessive excitation and/or inadequate inhibition,
that can affect small or large neuronal populations
➢ Clinical manifestations are sudden and usually brief
➢ Symptoms depend on the part of the brain involved and the intensity of the
discharge
✓ Motor
✓ Psychic
✓ Autonomic and sensory phenomenon,
✓ Alteration in consciousness or awareness
The International League Against Epilepsy
(ILAE) classification of epilepsy
Generalized seizures → those that arise from large areas of cortex in both
hemispheres → consciousness is always lost
➢ Partial seizures → those that arise in specific often small loci of cortex in
**one hemisphere
✓ Simple partial seizures → occur without alteration of consciousness
✓ Complex partial seizures → consciousness is impaired or lost
✓ Secondarily generalized seizure **→ partial onset which spreads to
become a generalized attack
Anosognosia for hemiplegia vs. Hemiparesis
Anosognosia for hemiplegia (complete lack of awareness of paralysis) differs from hemiparesis, where patients may still retain some movement.
Hippocampal Sclerosis and Epilepsy:
There is a strong association between hippocampal sclerosis and epilepsy, although it’s unclear if one causes the other. The hippocampus has a variety of cell types, with the right hippocampus involved in spatial memory and the left in language memory. Each side also contains specialized subregions.
Basal Ganglia
Modulates routine motor system outputs.
Inhibition: Inhibits certain behaviors, including risk-taking.
Parkinson’s Disease: Affects basal ganglia (BG) and can lead to pathological risk-taking behavior.
Frontotemporal Dementia (FTD) food preferences
FTD patients may lack sensation in the stomach (e.g., feeling of fullness).
Food flavor perception is linked to stomach sensation.
In neurodegenerative conditions like FTD and Alzheimer’s disease, patients often show memory deficits and may develop new food preferences.
Change in eating behaviour was significantly more common in both of the
Neuroimaging Techniques
Electrophysiology Techniques
EEG and MEG: These techniques measure brain electrical activity with high temporal resolution (ideal for tracking real-time responses) but low spatial resolution (less precise in locating exact brain areas).
EEG: Captures immediate cortical activity, commonly used to study event-related potentials.
MEG: Provides detailed temporal information, observing brain activity that reflects changes in neural currents.
CT/PET: Used to visualize the structure of the brain and map specific lesions.
Lesion Mapping and fMRI: fMRI measures brain activity by observing oxygen levels during tasks, giving insight into the function of gray and white matter.
MRI: Provides structural information about the density of gray and white matter. Structural MRI focuses on anatomy, while functional MRI (fMRI) observes activity in real-time during specific tasks.
Correlation: MRI is used to correlate brain areas with cognitive function or deficits. Brain Stimulation and Neuroplasticity
Brain Stimulation: Brain regions like the cortex can be stimulated to treat a range of conditions. Transcranial Magnetic Stimulation (TMS) has been shown to improve conditions like aphasia (difficulty with language) and drug-resistant depression by stimulating specific brain areas.
Transcranial Direct Current Stimulation (tDCS): This technique uses a low electrical current to modulate brain activity. It’s been used to help with disorders like aphasia and has shown effectiveness in stimulating the frontal lateral area of the brain.
Anosognosia for Hemiplegia: People with this condition are unaware of their own paralysis. This lack of awareness is linked to specific regions in the brain, and cognitive tasks can help assess the extent of this condition.
Behavioral Tasks for spatial neglect
(paper-and-pencil tasks; computerized tasks)
RM’s spontaneous complex graphic productions at the line-cancellation task during the neuropsychological assessment.
Core Assumptions of cognitive neuropsychological approach: The approach is based on three main principles:
The cognitive neuropsychological approach has been based,
since its inception, on the so-called information processing or
flow-chart diagram types of models of the mind, developed
by cognitive psychologists in the 1960s.
Briefly, the mental faculties comprise a number of connected
components, with specific functional properties. For instance,
memory was subdivided into short- and long-term components,
the reading skills into phonological, visual, and semantic
pathways.
* Modularity
* Correspondence between functional and neurological architectures
* Constancy (stability of functional processes)**
Modularity (One of the Three Components)
Fodor’s Modularity Theory:
Modules: Genetically determined, domain-specific, and located in specific neural areas.
Characteristics: Fast, automatic, informationally encapsulated (operate independently), and with limited conscious access.
Examples: Auditory processing, linguistic analysis (syntax, phonology), and visual perception.
Vertical Faculties: Operate like reflexes, handling specialized tasks independently.
Central (Non-Modular) Processes:
Functions like memory, reasoning, and problem-solving are non-modular (not domain-specific and lack specific neural correlates).
Neuropsychologists’ Perspective:
Perceptual Analyzers and Response-Production Systems may also be modular, contrary to Fodor’s view.
Not Always Innate: Some modules may develop over time, rather than being entirely genetically determined.
1. Modularity
Definition: Modules are independent, domain-specific cognitive mechanisms with localized neural structures.
Features: They operate automatically, are informationally encapsulated, and process information independently.
Examples: Auditory processing, linguistic analysis, visual perception.
Distinction: Central processes like reasoning and memory are non-modular and involve horizontal, interconnected functions.
2. Correspondence
Definition: Independent cognitive processes correspond to specific brain areas.
Implication: A lesion in a particular brain area may selectively impair one mental process without affecting others.
Focus: This assumption doesn’t require pinpointing the exact neural mechanisms—only that brain damage can disrupt specific cognitive functions.
3. Constancy (or Transparency)
Definition: After brain damage, cognitive processes are assumed not to reorganize in a way that creates entirely new components or connections.
Patient Strategies: Patients may adopt alternative strategies post-injury, but these strategies should rely on existing components in the normal cognitive system.
Transparency Condition: As long as new strategies are based on intact parts of the normal system, the assumption of constancy holds.
Considerations on the Assumptions
While modularity, correspondence, and constancy provide a framework, interpreting deficits due to brain lesions may not always directly align with the selective impairment of specific cognitive components. Contradictions may arise in neuropsychological observations, suggesting complexity in understanding the effects of brain damage.
Dissociations in Neuropsychology
Purpose: Dissociations help interpret deficits by examining how specific brain lesions affect particular cognitive functions.
Types of Dissociation:
Simple Dissociation:
Description: When a patient performs poorly on Task A (function F1) but normally on Task B (function F2).
Interpretation: Indicates that the damaged brain region is likely responsible for function F1, which is disrupted, while F2 remains intact.
Double Dissociation:
Description: In two patients (or groups), one shows impairment in Task A (F1) but not in Task B (F2), while the other shows the opposite.
Interpretation: Stronger evidence that F1 and F2 rely on distinct brain regions, as each function can be disrupted independently of the other.
its a paradigm
NPS Syndromes: Types of Anatomo-Clinical Relationships
Definition: Different combinations of symptoms and signs linked to specific brain structures or functions, forming distinct types of relationships.
Anatomical Syndrome:
Basis: The cerebral regions or circuits A1, A2, A3, A4..An, in which the functions F1, F2, F3, F4…Fn are localised, are anatomically contiguous.
The conjoint damage of these regions produces the association of symptoms N1, N2, N3, N4..Nn
Example: Damage to a particular area consistently produces a predictable set of symptoms.
Functional Syndrome:
Basis: The symptoms and signs N1, N2, N3, N4…Nn are associated because they are produced by the **impairment of function F. Accordingly, the syndrome is always complete.
Example: A syndrome characterized by memory loss, regardless of the exact brain region affected.
Anatomo-Functional Syndrome:
Basis:The symptoms and signs** N1, N2, N3, N4…Nn are associated because they are produced by the** impairment of function F, localised in the cerebral area R, or in the neural circuit C.**
The anatomo-functional syndrome differs from the anatomical one in that F has a localised neural correlate.
Example: Lesions in a particular area that impair a specific function, showing a clear structure-function relationship.
What is consciousness?
Consciousness is defined as a first-person experience that consists of two major
components: arousal (or wakefulness) and awareness
arousal
refers to the level of alertness and is supported by the function of the
subcortical arousal systems in the brainstem, midbrain and thalamus (Steraide et al.,
1997). Clinically, it is indicated by opening of the eyes.
awereness
refers to the content of consciousness, and it is thought to be supported by
the functional integrity of the cerebral cortex and its subcortical connections.
Awareness can be further reduced to awareness of environment and of self (Posner et
al., 2007). Clinically, awareness of environment is assessed by evaluating command
following and observing non reflex motor behavior, such as eye tracking and localized
responses to pain. Awareness of self, clinically a more ill-defined concept, can be
assessed by the patients’ response to auto referential stimuli, such as the patients’ own
face in the mirror.
Disorders of Consciousness (DoC)
acuate brain injury- coma- lock in state, vegetative state, chronic com and brain death
vegetative state
general: Vegetative State:
Arousal is present, but awareness is not.
Physiological activation, such as reflexive movements and sleep-wake cycles, can be observed.
The brainstem functions, but cortical activity is insufficient for awareness.
Minimally Conscious State (MCS):
Partial awareness: Patients may demonstrate intermittent responsiveness.
Common signs include:
Following commands.
Localizing sounds or objects.
Basic attempts at communication.
Locked-In Syndrome:
Caused by brainstem lesions (e.g., damage to the pons).
Patients have preserved cognitive abilities but are unable to move.
Communication is often limited to eye movements.
Types:
Classic: Eye movements are preserved.
Incomplete: Minimal motor recovery beyond the eyes.
Total: No voluntary movements.
coma
Coma is usually the result of severe, diffuse, bihemispheric lesions of the cortex or
underlying white matter, bilateral thalamic damage, or focal lesions of the paramedian
tegmentum.
The defining clinical feature of coma is the complete loss of spontaneous or stimulusinduced arousal. No sleep–wake cycles are evident on EEG, the eyes remain
continuously closed, and there is no speech or purposeful motor activity, following
commands or sensory stimulation.
Coma is a self-limiting state that typically resolves within 2 weeks and transitions into
either a vegetative state (VS) or a minimally conscious state (MCS)
Vegegative state
The VS is a “state of arousal without awareness”. These patients regain sleep–wake
cycles. However, their motor, auditory and visual functions are restricted to mere
reflexes, and they show no adapted emotional responses.
According to the 1994 Multi-Society Task Force, the criteria for the diagnosis of VS are
the following:
* No evidence of awareness of self or environment and an inability to interact with others;
* No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual,
auditory, tactile or noxious stimuli;
* No evidence of language comprehension or expression;
* Intermittent wakefulness manifested by the presence of sleep–wake cycles;
* Sufficiently preserved hypothalamic and brainstem autonomic functions to permit survival with
medical and nursing care;
* Bowel and bladder incontinence;
* Variably preserved cranial nerve and spinal reflexes
Minimal consciouns state
The minimally conscious state (MCS) was defined as a DOC in 2002 by the Aspen
Workgroup. Patients in MCS manifest at least one of the following:
* Purposeful behavior, including movements or affective behavior contingent to relevant
environment stimuli which are not due to reflexive activity, such as: visual pursuit or
sustained fixation occurring in direct response to moving or salient stimuli, smiling or
crying in response to verbal or visual emotional but not neutral stimuli, reaching for
objects demonstrating a relationship between object location and direction of reach,
touching or holding objects in a manner that accommodates the size and shape of the
object, and vocalizations or gestures occurring in direct response to the linguistic
content of questions;
* Following simple commands:
– Gestural or verbal yes/no response, regardless of accuracy;
– Intelligible verbalization
Locked in syndrome
In the locked-in syndrome (LIS) there is no dissociation between arousal and
awareness. According to the 1995 American Congress of Rehabilitation Medicine
criteria, LIS patients demonstrate:
* Sustained eye opening (bilateral ptosis should be ruled out as a complicating
factor);
* Quadriplegia or quadriparesis;
* Aphonia or hypophonia;
* A primary mode of communication via vertical or lateral eye movements, or blinking
of the upper eyelid to signal yes/no responses;
* Preserved cognitive abilities.
Based on motor capacities, LIS can be divided into three categories:
1. Classic LIS, which is characterized by quadriplegia and anarthria with eye-coded
communication;
2. Incomplete LIS ,which is characterized by remnants of voluntary responsiveness
other than eye movements;
3. Total LIS, which is characterized by complete immobility including all eye
movements, combined with preserved consciousness.
Brain death
Irreversible coma and absence of brain stem reflexes are the major clinical criteria
that are followed by most US hospitals, but these criteria are apparently not
practised in the same way by all institutions. This implies that brain death may be
determined in various ways, a fact that may have consequences in after death
practices, such as organ transplantation.
In 1995, the American Academy of Neurology published the diagnostic guidelines for
brain death, which are:
* Demonstration of coma;
* Evidence for the cause of coma;
* Absence of confounding factors, including hypothermia, drugs, electrolyte and
endocrine disturbances;
* Absence of brainstem reflexes;
* Absent motor responses;
* Positive apnea testing;
* A repeat evaluation in 6 h is advised, but the time period is considered arbitrary;
* Confirmatory laboratory tests are only required when specific components of the
clinical testing cannot be reliably evaluated.
Brain death
Irreversible coma and absence of brain stem reflexes are the major clinical criteria
that are followed by most US hospitals, but these criteria are apparently not
practised in the same way by all institutions. This implies that brain death may be
determined in various ways, a fact that may have consequences in after death
practices, such as organ transplantation.
In 1995, the American Academy of Neurology published the diagnostic guidelines for
brain death, which are:
* Demonstration of coma;
* Evidence for the cause of coma;
* Absence of confounding factors, including hypothermia, drugs, electrolyte and
endocrine disturbances;
* Absence of brainstem reflexes;
* Absent motor responses;
* Positive apnea testing;
* A repeat evaluation in 6 h is advised, but the time period is considered arbitrary;
* Confirmatory laboratory tests are only required when specific components of the
clinical testing cannot be reliably evaluated.
Glasgow Coma Scale
Eye Opening Response
* Spontaneous–open with blinking at baseline 4 points
* To verbal stimuli, command, speech 3 points
* To pain only (not applied to face) 2 points
* No response 1 point
Verbal Response
* Oriented 5 points
* Confused conversation, but able to answer questions 4 points
* Inappropnate words 3 points
* Incomprehensible speech 2 points
* No response 1 point
Motor Response
* Obeys commands for movement 6 points
* Purposeful movement to painful stimulus 5 points
* Withdraws in response to pain 4 points
* Flexion in response to pain (decorticate posturing) 3 points
Extension response in response to pain (decerebrate postunng) 2 points
* No response 1 point
Main issue
Dissociation between the patients’ level of
consciousness and sensorimotor functions
40% of the patients misdiagnosed
neroimaging od DoC
DOC are currently diagnosed with standardized
tools. Diagnosis of DOC still remains a clinical
challenge, due to possible dissociations between
the patients’ consciousness and sensorimotor
functions.
The prognosis of DOC is even more challenging, as
none of the tested measures has shown sufficient
sensitivity
fMRI in DoC
fMRI (Functional Magnetic Resonance Imaging):
Used to detect awareness in vegetative or minimally conscious states.
Example:
A woman unable to move was instructed to imagine walking through her house.
Her brain showed activation similar to healthy individuals during the task.
Challenges:
Standardization is difficult due to brain injuries that distort structure.
No statistical comparisons in early studies as injured brains cannot be normalized to a standard template.Meta-Analysis of fMRI Studies:
Included patients in pharmacological comas or with a history of drug abuse.
Initial findings misclassified vegetative patients as MCS due to underestimated brain activation.
fMRI meta-analysis DoC patients
fMRI meta-analysis
We aimed at formally addressing this issue by meta-analysing the fMRI/PET results available in
the international literature with the Activation Likelihood Estimate (ALE) method
We searched for the brain areas associated with active and passive tasks in DOC patients
classified as UWS (vegetative state) and with MCS. We hypothesised that:
1. active and passive tasks would share brain regions associated with low-level cognitive
processing, e.g. auditory processing, while they should be anatomically segregated at the
level of higher-order-associative cortices;
2. UWS and MCS patients would be characterized by the activation of dissociable neural
networks. In particular, we expect that the dorsal-attentional network, responsible for
externally directed cognitive processes, would be mainly recruited in MCSs;
3. UWS and MCS activations would overlap in regions associated with low-level cognitive
tasks, i.e. with passive tasks mainly; while no signs of shared activations should be found in
brain regions typically activated during active tasks
H1→ The contrast analyses revealed a higher level of activation for the comparison
“active > passive tasks” in the left paracentral lobule (x = -6, y = -24, z = 68; BA 6);
the reversed contrast, namely “passive > active tasks” did not show any significant
effect
H2→ UWS patients activated significant more voxels compared to MCS patients in
the dorsal-attentional network
H3→ overlap the UWS and MCS maps, both with the passive and with the active
maps. The majority of the brain regions reported in the UWS and MCS map
belonged to the ALE map of the passive task, while only 48 out of the 7556 voxels
included in the UWS and MCS map fell within the active task map; these voxels
were located around the left amygdala
Autonomic responses
to emotional stimuli predict
recovery of consciousness DoC
Our study focused on DOC patients in an early stage of the
disorder and combined event-related electrodermal activity
with fMRI markers to address the following two aims (behavioral also included words and non words with emotional meaning)
* to test the possibility of detecting early signs of autonomic
responsiveness to cognitive stimuli in acute DOC patients
(16.6 ± 9.5 days from onset);
* to investigate the prognostic value of such responses
after combination with the voxel-wise measures of
resting-state fMRI low-frequency fluctuations (fALFFs), a
known marker of preserved neurofunctional activity.
Only patients who recovered consciousness (upR) 6 months after their initial
assessment had higher (“normal”) electrodermal-evoked responses for the
emotionally salient words at T0.
➢ The higher the differential electrodermal response, the higher the residual resting
state activity in the PCC region.
➢ A relatively simple (neuro)physiological index, the event-related electrodermal
activity, could be adopted and combined with other behavioural measures to
optimise the prognosis in DOC.
➢ Our behavioural test is an easy-to-use bedside assessment tool that can be
adopted in any clinical centre.
➢ Furthermore, the combination of our measures with the standard clinical scales
may have a substantial impact on both, prognosis and daily care
Design of Autonomic responses
to emotional stimuli predict
recovery of consciousness
T0 (acute stage)
* Coma Recovery Scale
* Skin Conductance
* Resting-state fMRI
T1 (6 months later)
Glasgow Outcome
Scale Extended -
GOSE
Upcoming Responsive
(upR) patients
(GOSE >2)
Upcoming Unresponsive
(upUR) patients
(GOSE <2)
behavioral study in Autonomic responses
to emotional stimuli predict
recovery of consciousness
30 SALIENT WORDS
30 NON-WORDS
Skin conductance was recorded simultaneously and measured with a sensitivity of
0–100 lS, the signal sampled at 500 Sa/s 16-bit, low-pass filtered at 5 Hz
Neuroimaging study in Autonomic responses
to emotional stimuli predict
recovery of consciousness
Resting-state fMRI scan on the same day of the behavioural study
fractional low-frequency fluctuations (fALFF)
a voxel-wise measure of the power of local neuronal activity that can be used to detect
cerebral regions with abnormal or residual normal local functioning.Healthy controls showed a significant difference between words and non-words (F(1,34)=39.2, p<.001)
✓ upR patient’s group median values did not differ from the HC median value (Z=22; p=0.646) suggesting a
normal response.
✓ upUR patient’s group median value was significantly lower than the HC median value (Z=0; p=0.043).
Only patients who recovered consciousness (upR) 6 months after their initial
assessment had higher (“normal”) electrodermal-evoked responses for the
emotionally salient words at T0.
➢ The higher the differential electrodermal response, the higher the residual resting
state activity in the PCC region.
➢ A relatively simple (neuro)physiological index, the event-related electrodermal
activity, could be adopted and combined with other behavioural measures to
optimise the prognosis in DOC.
➢ Our behavioural test is an easy-to-use bedside assessment tool that can be
adopted in any clinical centre.
➢ Furthermore, the combination of our measures with the standard clinical scales
may have a substantial impact on both, prognosis and daily care.
Potential Treatments for Misdiagnosed Vegetative States
Vagal Nerve Stimulation:
Stimulation can increase cortical activity and improve recovery scores.
Raises ethical concerns about informed consent and risk.
Unilateral Spatial Neglect (USN)
Brain-damaged patients with unilateral
visuo-spatial neglect do not orient
toward the contralesional side of
space and may fail to report events
occurring in its peri-personal, personal
and representational components
Frequency:
* present in more than 40% of right brain-injured people
* present in about 20% of left brain-injured (less severe
symptoms)
Etiology:
* cerebrovascular disease
* neoplasm
* head trauma
* degenerative pathology
USN syndrome sectors of space
USN symptoms can dissociate across sensory modalities, sectors of
space (i.e., personal, peri-personal and extra-personal space,
reference frames (egocentric vs allocentric neglect, and tasks.
Finally, not only the type of task but also task demands have been
found to affect neglect severity
Egocentric
(with respect to the observer)
* Allocentric
(with respect to another
extrapersonal event)
* Object-centered
(with respect to a principal axis in
the canonical representation of an
object)
Personal Neglect: assessment
Fluff Test
Comb and Razor Test
Personal Neglect Tests:
Personal neglect, where patients fail to attend to their own contralesional body parts (e.g., pretending to shave or brush their hair), can be assessed with more ecological tasks. These tasks simulate real-world activities to reveal neglect in personal space.
For instance, a 30-second test can measure how many times a patient brushes each side of their hair. Disproportionate brushing on one side indicates neglect of the contralesional side.
Extrapersonal Neglect: assessment
Cancellation task
Line Bisection
Words Reading task (Neglect dyslexia)
Representational Neglect
Representational Neglect (RN):
Refers to neglect in mental imagery or memory-based tasks.
Classic example: The Duomo experiment:
A patient is asked to imagine standing in the Piazza del Duomo and describe stores or landmarks in the square. They initially neglect the stores on the contralesional side (e.g., left side if right hemisphere damaged).
When asked to imagine standing at the opposite end, they describe the stores they previously neglected, now visible on their imagined right side.
Key takeaway: This reveals that representational neglect is not a memory issue. The neglected items are not forgotten but are inaccessible from a specific mental perspective.
In another experiment in Piazza del Popolo, a similar phenomenon was observed, reinforcing the same principles.
Extrapersonal Neglect (EN):
Square test
Maps test
USN syndrome implicit processing
house on fire
USN associated symptoms
Anosognosia: neurological condition in which the patient is unaware of
their neurological deficits.
Somatoparaphrenia: delusional belief concerning the sense of ownership
for the left paralyzed hand, which is attributed to other persons.
Extinction: a failure to report a contralesional (visual or tactile) stimulus
only in the presence of a competing ipsilesional stimulus, when both stimuli
are briefly simultaneously presented
Extinction occurs when a patient can detect a stimulus on the contralesional side (e.g., left side) when it is presented alone, but fails to detect it when simultaneous stimuli are presented to both sides.
Example in Tactile Testing:
A light touch is applied to the left hand alone → the patient says they feel it.
A light touch is applied to the right hand alone → the patient says they feel it.
A light touch is applied to both hands at the same time → the patient reports feeling neither or only the ipsilesional (right) side.
Allochiria: the patient responds to stimuli presented to one side of their
body as if the stimuli had been presented at the opposite side.
USN lesional bases
Grey matter lesions
Parietal cortex
- Classic studies of anatomic-clinical
correlation (Vallar, 1986, 2003; Mort, 2003).
- Neuroimaging studies show activations in the
superior and inferior parietal lobule and less
frequently in the medial temporal cortex during
visuospatial attention tasks (Nobre, 1997,
Corbetta, 2002).
- Primate studies
Temporal cortex (superior temporal gyrus)
- Anatomo-clinical correlation studies
(Karnath, 2001, 2004).
- Primate studies show that in the monkey the
STG is both a center of cortical integration of
sensory integration (Karnath, 2001, 2004)
Frontal cortex (inferior frontal lobe)
- Classical studies of anatomical-clinical
correlation (Heilman and Valenstein,
1972,Vallar, 1986)
- Neuroimaging studies on spatial attention
(Nobre, 1997, Corbetta, 2002) and
extrapersonal space representation (Galati,
2000,Weiss, 2000 and Fink, 2000)
- Primate studies: lesions from the premotor
frontal cortex determine neglect (Watson,
1978)
Subcortical structures
-Anatomic-clinical correlation studies
(Damasio, 1980; Karnath 2002)
-Functional imaging studies (Gitelman, 1999)
USN lesional bases
White matter lesions
Superior Longitudinal Fasciculus
A major white matter tract connecting the frontal, parietal, and temporal regions.
Damage to the SLF has been implicated in neglect, particularly in disrupting communication between brain regions.
However, lesions to the SLF alone do not directly cause neglect but may exacerbate its severity.
Stimulation Studies:
In patients undergoing surgery for tumors, stimulating the SLF produced symptoms of neglect, demonstrating its role in spatial attention.
USN lesional bases
Meta-Analysis Insights:
Neglect is now studied as a disconnection syndrome, involving damage to both gray matter (key regions) and white matter (tracts connecting these regions).
Topological Approach to Neglect
Topological Analysis:
Focuses on the interplay between gray and white matter lesions.
Emphasizes that neglect arises from disruptions in both regional brain networks and their interconnections.
A conjoint approach considers:
Gray Matter Damage: Disrupts specific neural functions (e.g., spatial attention).
White Matter Damage: Disrupts communication between regions, leading to a disconnection syndrome.
Parietal Cortex Stimulation and Neglect
Targeted Electrical Stimulation:
Tiny electrical stimulations were applied to specific areas of the brain during tasks.
Visual Extinction Task:
Stimulation made patients quicker on tasks like line bisection, reducing neglect symptoms (e.g., better spatial awareness during activities like shaving).
Key Finding:
Suggests the parietal cortex—specifically the superior temporal gyrus (STG)—plays a critical role in extrapersonal neglect.
Conclusion:
Neglect is influenced by a balance between hemispheres, with different symptomatology linked to specific regions.
Extrapersonal Neglect: Linked to the STG.
Personal Neglect: Linked to the parietal cortex (P).
USN Cognitive Models for Attention
Attentional Imbalance Theory (Heilman):
Suggests the right hemisphere (RH) supports bilateral attention, while the left hemisphere (LH) is primarily focused on the contralateral side (right space).
In neglect, the RH is unable to compensate for LH hyperactivation, leading to an imbalance favoring the right space.
Representational Theory:
USN is a disorder of mental space
representation, consisting in a left–right
pathological anisometry of the medium for space
representation: the left-side would be more
relaxed and the right-side would be more
contracted/compacted. The contralesional
relaxation of the medium might still sustain
“conscious” representation of contents in space,
albeit with a horizontal size distortion. Beyond a
critical point, the overrelaxed medium no longer
sustains conscious representations. Bisiach’s
theory also foresees that in some individuals, the
disorder affects response level of stimulus
processing (i.e., response bias).
Transformational theory
The brain creates internal models or maps of space that guide our awareness, perception, and interaction with the environment.
In USN, particularly after right hemisphere damage (e.g., in the parietal or temporal lobes), these spatial maps can become distorted or incomplete, especially for the contralateral (usually left) side of space.
More Accepted Theory (Shuman & Corbetta):
Proposes that the left hemisphere becomes hyperactivated as a compensatory process, leading to an attentional imbalance favoring the right side.
Body Representation and Pathological Models
Anorexia Nervosa:
Bodily self-awareness disoders in neuropsychiatric
diseased are charachterized by a dissociation
between the different bodily self components,
suggesting an interruption/distruption of the
multisensory integration mechanism
Involves body size distortion due to a mismatch between:
Interoception (internal body state) and
Exteroception (external perception of the body).
This incongruence results in inaccurate body representation, influenced by somatosensory misrepresentation.
Lock-In Hypothesis:
Suggests body representation is not updated properly in anorexia, leading to a persistent distortion.
Risk Factor for Dementia:
Alterations in body representation are linked to early indicators of dementia.
Pathological Conditions Related to Body Representation
Somatoparaphrenia:
Patients do not recognize their own limb but may attribute it to someone else.
Distinction from Anosognosia:
In anosognosia, patients deny or are unaware of a deficit but do not misattribute their limb.
Finger Agnosia:
Inability to identify or name fingers.
Linked to issues with somatosensory structural descriptions.
Dissociations in Body Awareness:
Patients lose the ability to:
Name body parts, though they can name objects (and vice versa).
Recognize whether a hand is theirs or someone else’s.
Specialized Brain Areas:
Brodmann Area 19:
Involved in visual recognition of body ownership (e.g., distinguishing one’s hands from others’).
Taxonomy of Body Representation
Dyadic Taxonomy (1999):Disruption of body schema
deafferentation
Taxonomy of Body Representation
Dyadic Taxonomy (1999):disruption of body
image
numbsense
The triadic taxonomy
The triadic taxonomy is grounded in the dissociation between apraxia
(disruption of the body schema), autotopagnosia (disruption of the body
structural description), and body-specific aphasia (disruption of the body
semantics)
new taxonomy
new taxonomy
Longo, 2015
Body Representation types:
Action oriented
Non-action
oriented
implicit-explicit perceptual-conceptual
Body Image: subjective experience of the physical structure of our body in
terms of its size, shape and physical composition. (perceptual-explicit)
Body Model: a representation similar to the body image but with large
distortions.(percepual7-implicit7)
Body Superficial Schema: representation that mediates the localization of
tactile sensation onto the skin surface. (implicit-perceptual)
Body Schema: unconscious dynamic knowledge about body posture (implicit perceptual)
Body Structural Description: representation of the knowledge about the
topological organization of the body. (implicit conceptual)
Body Semantic: linguistic representation of the body (explicit conceptual)
Di Vita (2016):
BSA
Bodily self-awareness (BSA)
BSA
Bodily self-awareness (BSA) has been defined as the feeling that
conscious experiences are bound to the **self ** and are experiences of
a unitary entity (Berlucchi & Aglioti, 2010; Blanke, 2012; Salvato et
al., 2019 Blanke, Slater, & Serino, 2015; Legrand, 2006, 2010).
BSA is a multidimensional construct, arising from the integration of
signals coming from the environment (exteroception), viscera
(interoception) and from joints and muscles (proprioception).
BSA entails the feeling and knowing that the body belongs to us
(sense of body ownership), and the sense of agency over our
actions.
BSA also involves the adjustment of physiological parameters (e.g.,
body temperature) to achieve homeostasis.
BSU Illusory paradigms
(healthy individuals)
Illusion paradigms
* Rubber Hand Illusion Mirror-box Illusion
* Mirror-box Illusion
* (MBI) paradigm Full body Illusion
Explorations of the bodily self-awareness components in healthy individuals
Somatoparaphrinia in body self awearness
Somatoparaphrenia (SP) is a disorder in which patients do not recognize or disown a body part (e.g., a limb). This can occur despite the limb being physically present.
Commonly seen after deep subcortical lesions or acute stroke (especially in the first 3-4 days).
Vestibular System Stimulation:
In some cases, cold water injection (3°C) in the vestibular system can temporarily improve recognition of a neglected body part (e.g., left hand) by stimulating sensory areas.
Clinical Example:
A patient might not recognize their left hand despite looking at it, describing it as not belonging to them.
After caloric vestibular stimulation, they may briefly recognize the hand.
Post-30-minute interval, recognition may disappear as the temperature normalizes.
BID
Body Integrity Dysphoria (BID)
an unusual and rare condition characterized by
the persistent and compulsive desire for the
amputation of one or more physically healthy
limbs. Individuals suffering from BID typically
report that their unwanted limb does not belong
to their body and that they would feel “more
complete” after its removal. It has been
characterized in terms of absent ownership
feeling with preserved ownership judgments.
memory of BID
Body Integrity Dysphoria (BID):
BID is characterized by a strong desire to amputate a body part despite no neurological lesion.
Key Features:
High levels of anxiety.
The individual feels the body part does not belong to them.
Obsessional thoughts about amputation are present.
The sense of ownership is altered, but not the physical ability to perform normal motor tasks.
No Brain Lesion: Unlike SP, BID does not have a direct brain lesion.
Onset and Symptoms:
These feelings often begin in adolescence and are not necessarily associated with other psychiatric syndromes.
Individuals might experience obsessive thoughts about amputation and might attempt to pretend the amputation has occurred.
Brain Activation:
Hypoactivation of certain brain regions is observed in some cases, though no clear causal relationship has been found. The exact neurological mechanisms behind SP and BID are still unclear.
Supramarginal Gyrus and Body Ownership:
The Supramarginal Gyrus (SMG) is linked to body ownership.
Reduced gray matter in this area has been associated with distorted body ownership in BID, though the exact connection is still unclear.
Phantom Limb Sensation:
After an amputation, individuals may initially experience phantom limb sensations, where the brain continues to misfire signals as if the missing limb is still there.
Over time, these neurons reorganize, potentially starting to represent other body parts (e.g., the face). This reorganization could lead to the disappearance of the phantom sensation, but the exact timeline for this process can vary.
Attention and Temperature Changes in BID:
In BID, individuals often direct attention to the limb they feel is alien or does not belong to them. Studies have shown that when attention is focused on the limb, there can be bilateral temperature changes (a drop) in the affected limbs.
These changes suggest that somatosensory and pre-motor cortices process body parts in a bilateral manner, reflecting the brain’s representation of the body.
Neural Mechanisms in BID:
Supramarginal Gyrus dysfunction, including gray matter reduction, might contribute to the distorted body ownership that is characteristic of BID.
Brain regions such as the **somatosensory cortex and pre-motor cortex are involved in the bilateral representation of body parts, **which may play a role in BID and how the body is perceived.
Sensory Feedback and Body Ownership:
Sensory stimulation, such as warming the affected limb, can potentially improve body ownership and reinforce the recognition of the limb, especially in disorders like somatoparaphrenia and BID.
Anorexia Nervosa
(AN):
AN is an eating disorder characterised by a restriction of food intake
relative to requirements, intense fear of gaining weight, persistent
behaviours associated with weight reduction and an altered bodily
self-perception (DSM-5TM, 5th ed).
People with AN may exhibit different forms of bodily self-awareness
alterations (for a review, see (Gadsby, 2017)), and their nature is a
current matter of debate.
In AN, bodily self-awareness alterations are so pervasive that they
represent one of the main diagnostic criteria
Anorexi N reasearch findings
Research Findings:
Studies using asynchronous sensory conditions (e.g., mismatched visual and tactile inputs) show that individuals with anorexia nervosa experience unusual sensations, highlighting impaired sensory integration.
Visual information often overrides motor and interoceptive signals, resulting in a persistent, static perception of body size.
Altered interoception can manifest as reduced sensitivity to temperature and pressure.
Interoceptive Processing:
Interoceptive signals, such as those related to hunger or internal body states, may be silenced or misinterpreted. This contrasts with conditions like obesity, where there may be excessive focus on these signals, albeit with difficulty interpreting them accurately.
Neural Mechanisms:
The impairments in sensory integration and interoception are associated with cerebral network disruptions, particularly involving the right hemisphere, which plays a role in body awareness and self-representation.
There may also be a dissociation between visual and interoceptive systems, further contributing to distorted body perception.
Behavioral Implications:
Interoceptive disruptions influence decision-making processes, often leading to heightened risk aversion.
These sensory and interoceptive impairments can reinforce distorted body schemas and perpetuate the condition.
Risk Taking in Anorexia Nervosa
Risk-taking in Anorexia Nervosa
Ballon task with control group, AN, and obese particpants
Patients with AN risk significantly more when the body comes into play!
obese, risk way less, very precarious
Bodily self-awareness arises from the perception of
external and internal signals
❖ It is supported by a cerebral network mainly involving
the right hemisphere
❖ Bodily self-awareness disoders in neuropsychiatric
diseased are charachterized by a dissociation
between the different bodily self components,
suggesting an interruption/distruption of the
multisensory integration mechanism
the lower someone bma the higher the risk taking in the body, interoception comes in
counting hearth bit
body image might be a higher influence for risk tsking
interoception in healthy participants lower risk taking
Types of Dementia
Types of Dementia
Alzheimer’s Disease (AD):
Key Features: Memory loss, inability to learn new information, neurofibrillary tangles, and axonal degeneration.
Social Impacts: Difficulty participating in conversations or following social interactions.
Vascular Dementia:
Symptoms: Fluctuating cognitive and behavioral deficits caused by micro-lesions in the brain’s vascular system.
The brain compensates for damage but exhibits “good” and “bad” days while this happens
Lewy Body Dementia (LBD):
First Symptom: Hallucinations, often occurring early in the disease.
May also include motor symptoms similar to Parkinson’s disease.
Frontotemporal Dementia (FTD):
Characteristics: Behavioral changes, social impairments, and sometimes changes in eating habits or food preferences.
Mixed Dementia:
The most common type, involving a combination of Alzheimer’s disease and vascular dementia features.
dementia
Dementia is a syndrome associated with many neurodegenerative diseases, characterized by a general decline in cognitive abilities that affects a person’s ability to perform everyday activities
1. Dementia defines a complex set of modifications in behaviour; these
modifications are, for the most part “losses”, to which heterogeneous
neuropsychological deficits combine, giving rise to the picture of
cognitive incompetence.
2. The main feature of dementia is its slow, steady deterioration, the
progression of which should be detectable within a 6-12 month
follow-up.
neuroradiological techniques for dementia
Sooner or later, in the course of the
dementing process, the brain shrinks, giving rise
to the macroscopic anatomical picture of the
cerebral atrophy, which can be detected by
neuro- radiological techniques (CT scan or MRI).
onset however, the neuroradiological picture of
the demented patient compared to age-matched
controls may be normal. In some instances,
characteristic neuroradiological abnormalities
might precede the clinical picture of dementia. It
is the case, for example, of the selective atrophy
of the head of the caudate nuclei in the early
stage of Huntington’s chorea.
cachexia
losee in fat in the body, degeneration of bones
Cortical vs. Subcortical Dementia
Cortical Dementias: Impairments in higher cognitive functions, memory, and social interactions (e.g., Alzheimer’s).
Subcortical Dementias: Motor-related symptoms and movement disorders dominate (e.g., Huntington’s disease).
Mild Cognitive Impairment (MCI)
Characteristics:
MCI is a pre-dementia state involving isolated cognitive deficits, such as memory impairment, but without significant impact on daily life.
Differentiation from Depression:
Symptoms of MCI can overlap with depression, leading to diagnostic challenges.
A treatment trial for depression (e.g., 6 months of antidepressants) can help differentiate:
If memory issues persist despite treating depression, dementia is more likely.
Mild cognitive impairment (MCI) is a neurocognitive disorder which
involves cognitive impairments beyond those expected based on an
individual’s age and education but which are not significant enough
to interfere with instrumental activities of daily living
Reversibility:
MCI can sometimes return to normal, especially when caused by reversible factors such as stress or medications.
Additional Considerations
Eating Disorders and Dementia:
Eating disorders in dementia (e.g., FTD) are often behavioral and may involve changes in food preferences or eating habits, not necessarily related to taste or flavor.
Caregiver Burden:
Dementia affects the entire family, requiring substantial caregiving efforts, which can lead to significant physical and emotional strain on caregivers.
Diagnostic Pathway:
Diagnosis typically involves:
General Practitioner (GP) for initial assessment.
Neuropsychological Testing for cognitive evaluation.
Imaging (e.g., MRI) to identify brain atrophy or vascular lesions.
Genetic Testing in specific cases, such as familial Alzheimer’s disease.
Amnesic MCI (aMCI)
is mild cognitive impairment with memory loss as the
predominant symptom; aMCI is frequently seen as a prodromal stage
of Alzheimer’s disease. Studies suggest that these individuals tend to progress
to probable Alzheimer’s disease at a rate of approximately 10% to 15% per
year
Nonamnesic MCI (naMCI)
is mild cognitive impairment in which impairments
in domains other than memory (for example, language, visuospatial, executive)
are more prominent. It may be further divided as nonamnestic single- or
multiple-domain MCI, and these individuals are believed to be more likely to
convert to other dementias (for example, dementia with Lewy bodies).
MCI treatments
Pharmacological
As MCI may represent a prodromal state to clinical Alzheimer’s disease,
treatments proposed for Alzheimer’s disease, such
as antioxidants and cholinesterase inhibitors, could potentially be
useful; however, as of January 2018, there is no evidence to support the
efficacy of cholinesterase inhibitors for the treatment of mild cognitive
impairment. Two drugs used to treat Alzheimer’s disease have been assessed
for their ability to treat MCI or prevent progression to full Alzheimer’s
disease. Rivastigmine failed to stop or slow progression to Alzheimer’s disease
or to improve cognitive function for individuals with mild cognitive impairment;
donepezil showed only minor, short-term benefits and was associated with
significant side effects.
MCI treatments
Current evidence suggests that cognition-based interventions do improve
cognitive performance (i.e. memory, executive function, attention, and speed) in
older adults and people with mild cognitive impairment. Especially, immediate
and delayed verbal recall resulted in higher performance gains from memory
training.
Alzehimer disease
Alzheimer’s disease is a neurodegenerative disease and is the most
common cause of dementia among older people.
There are **two types **of AD: early onset and late onset.
* In early onset AD, symptoms first appear before age 60. Early onset
AD is much less common than late onset. Early onset AD tends to
progress rapidly and can run in families. Several related genes have
been identified.
* Late onset AD, the more common form of the disease, develops in
people age 60 and older. Late onset AD may run in some families, but
the role of genes in the development of the disorder is less clear.
Early AD
The early symptoms of AD can include:
*Language problems, such as trouble finding the name of familiar
objects
*Misplacing items
*Getting lost on familiar routes
*Personality changes and loss of social skills
*Losing interest in things previously enjoyed; flat mood
*Difficulty performing tasks that require some thought, but which used
to come easily (e.g., balancing a checkbook, playing complex games
such as bridge, and learning new information or routines)
Mild AD
As the AD becomes worse, symptoms become more obvious and
interfere with the patient’s ability to take care of himself/herself.
As the AD becomes worse, symptoms become more obvious and
interfere with the patient’s ability to take care of himself/herself.
*Forgetting details about current events
*Forgetting events in your own life history, losing awareness of who you
are
*Change in sleep patterns, often waking up at night
*Difficulty reading or writing
*Poor judgment and loss of ability to recognize danger
*Using the wrong word, mispronouncing words, speaking in confusing
sentences
*Withdrawing from social contact
*Having hallucinations, arguments, striking out, and exhibiting violent
behavior
*Having delusions; experiencing depression and/or agitation
*Difficulty carrying out basic tasks, such as preparing meals, choosing
proper clothing, and driving
Severe AD
People with severe AD can no longer:
*Understand language
*Recognize family members
*Perform the basic activities of daily living, such as eating, dressing,
and bathing
Other symptoms that may occur with AD:
*Incontinence
*Swallowing problems
AD Diagnostic criteria
National Institute on Aging and the Alzheimer’s Association (NIA-AA)v
Probable Alwzehimer disease
This diagnosis is made when there is strong evidence that Alzheimer’s disease is the primary cause of dementia.
Probable Alzheimer’s disease includes all of the following criteria:
- A decline from a previous level of functioning with inability or interference in
carrying out usual daily activities.
- **Loss of two or more cognitive abilities ** such as anterograde amnesia,
aphasia, apraxia, agnosia, or other disturbance in executive functioning. - **Cognitive loss documented ** by mental status examination (MSE) or
neuropsychological tests. - Symptoms not consistent with other cerebrovascular disease, psychiatric
disorders or delirium. - Insidious onset and gradual progression of symptoms.
-** Intact consciousness**
National Institute on Aging and the Alzheimer’s Association (NIA-AA)
Possible Alzheimer’s disease
This diagnosis is used when Alzheimer’s disease is suspected but there is less certainty due to atypical features, co-existing conditions, or incomplete evidence.
The possible Alzheimer’s disease differs from
probable Alzheimer’s disease in terms of onset, course over time and
underlying disorder.
Possible Alzheimer’s disease is diagnosed in the presence of either one of the
following:
In possible AD cognitive impairment is sudden in onset with** insufficient history
or documentation of progressive decline in cognitive abilities.**
The patient has insidious onset of cognitive impairment with gradual
progression over time but in the presence of neurologic, medical condition or
medications that may have notable effect on the cognitive abilities of the
patient.
NIA-AA recommends patients with positive biomarkers (such as Aβ and total
and phosphorylated Tau protein) be diagnosed with Alzheimer’s disease even
in the absence of symptoms.
DSM 5
For major neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if either of the following is present; otherwise,
possible Alzheimer’s disease should be diagnosed
Evidence of a causative Alzheimer’s disease genetic mutation from family history or
genetic testing.
- All three of the following are present:
a)Clear evidence of decline in memory and learning and at least one other
cognitive domain (based on detailed history or serial neuropsychological
testing).
b) Steadily progressive, gradual decline in cognition, without extended
plateaus.
c) No evidence of mixed etiology (i.e., absence of other neurodegenerative
or cerebrovascular disease, or another neurological, mental, or systemic
disease or condition likely contributing to cognitive decline).
Probable and possible AD
DSM 5
For mild neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if there is evidence of a causative
Alzheimer’s disease genetic mutation from either genetic testing or family history.
- Possible Alzheimer’s disease is diagnosed if there is no evidence of a causative
Alzheimer’s disease genetic mutation from either genetic testing or family history, and all
three of the following are present:
a) Clear evidence of decline in memory and learning.
b) Steadily progressive, gradual decline in cognition, without extended
plateaus.
c) No evidence of mixed etiology (i.e., absence of other neurodegenerative
or cerebrovascular disease, or another neurological or systemic disease or
condition likely contributing to cognitive decline)
For a definitive diagnosis of AD, post-mortem
microscopic
histopathological examination of the brain must reveal the deposition of
two types of protein aggregates: **parenchymal deposits of amyloid **(Aβ)
extracellularly as ‘plaques’, and intraneuronal deposits of tau protein
fragments as neurofibrillary ‘tangles’ (NFT), over and above that which
occurs with normal ageing.
Tau deposition may also occur as straight or paired helical filaments
(PHF) surrounding plaques, and argyrophilic neuropil threads, which
are predominantly neuronal dendrites containing tau deposits.
Additionally, at least 80 per cent of cases have congophilic angiopathy,
with cerebrovascular amyloid deposited in small blood vessel walls of
the leptomeninges and cerebral and cerebellar cortex
risk factor for AD
-### Risk Factors for Late-Onset Alzheimer’s Disease (AD)
-
Biological and Demographic:
- Age: Risk increases significantly after 65.
- Sex: Higher risk in females, possibly due to longevity and hormonal factors.
- Genetics: APOE ε4 allele increases risk, though not deterministic.
-
Cognitive and Educational:
- Low Education Levels: Linked to reduced cognitive reserve.
- Cognitive Reserve: High reserve from education, bilingualism, or intellectual engagement lowers risk.
-
Lifestyle and Socioeconomic:
- Lifestyle: Healthy habits (e.g., exercise, diet, non-smoking) protect; poor lifestyle choices impact vascular health and increase risk.
- SES: Low SES reduces access to education and cultural activities, indirectly increasing risk.
- Chronic Stress and Trauma: Associated with AD in vulnerable individuals.
-
Neurological and Medical:
- TBI: History of traumatic brain injury raises risk.
- Chronic Conditions: Severe schizophrenia or anorexia nervosa may contribute through poor brain health.
-
Sleep:
- Sleep Disorders: Poor quality or insufficient sleep impairs beta-amyloid clearance, increasing risk.
- Chronic Sleep Deprivation: Strongly linked to cognitive decline.
-
Occupational and Social:
- Occupation: Limited cognitive stimulation (e.g., some studies on housewives) may increase risk.
- Social Isolation: Reduced cultural and social engagement impacts cognitive reserve.
Protective Factors
- Intellectual and cultural activities, healthy lifestyles, lifelong learning, and social engagement strengthen cognitive reserve and lower AD risk.
This concise list covers key risk and protective factors comprehensively. physiological deficits ⇒ this is
why they get hospitalized
Central Nervous System
Embryological development
Embryological Region Adult Derivatives
Prosencephalon Telencephalon → Cerebral hemispheres, lateral ventricles.
Diencephalon → Thalamus, hypothalamus, retina, third ventricle.
Mesencephalon Midbrain structures: tectum, tegmentum, cerebral aqueduct.
Rhombencephalon Metencephalon → Pons, cerebellum, part of the fourth ventricle.
Myelencephalon → Medulla oblongata, part of the fourth ventricle.
Spinal Cord Spinal cord, central canal.
brodmann areas
. Primary sensory areas → receive signals from the sensory ascending
pathways
✓ V1 → Primary visual cortex (BA17)
✓ S1 → Primary somatosensory cortex (BA1,2,3)
✓ Primary auditory cortex (BA 41-42)
2. Secondary sensory areas → highly connected to the primary areas
3. Motor areas → control voluntary movements-primary motor cortex BA 4
4. Associative areas → mostly in the frontal and temporal cortex
Languages components
LANGUAGE
Language = verbal communication
= is a conventional system based on the use of words according to a complex system of rules
Language < hierarchical units:
1. Phonemes = smallest units of sound without meaning (b-t) (< traits)
2. Morphemes = smallest meaningful units of a word (cat-s)
3. Words
4. Sentences
2 forms: Oral and Written
APHASIA
= disorder of verbal communication due to an acquired brain lesion, involving comprehension/production of verbal messages
5 main characteristics:
1. Acquired lesion = aphasia is not congenital (> 3 years old)
❖ Traumatic or Vascular lesions (stroke)
❖ Progressive: Neoplastic and Degenerative disorders (PPA)
2. Brain lesion = perisylvian regions of the LEFT hemisphere
LH = language-dominant in:
- 95% of right-handers
- 70% of left-handers/mix-handers
3. Deficit of verbal communication = no impairment of communication ability
❖ Use of nonverbal strategies: drawing, miming, pointing, gestures
4. Compromission of 1/more components of the processes of comprehension and production
Linguistics components: Phonology, Morphology, Syntax, Lexicon, Semantics
+ written language [comprehension – reading and production - writing)]
5.** Central processes of linguistic processing** > peripheral processes (articulation, phonation, and perception) intact
❖ Auditory perception deficit = Verbal Deafness (NO: /C-A-T/; YES: cat written)
❖ Motor/Articulatory deficit = Disarthria
karl wernike
❖ CARL WERNICKE – 1874
Discovery of brain area for language comprehension
= posterior third of the 1° temporal convolution of the LH = Wernicke’s area (22)
WERNICKE’S MODEL – CLASSICAL TASSONOMY
A = Auditory images (Wernicke - 22)
M = Motor images (Broca - 44)
A-M = Connection tract (Arcuate Fasciculus)
a = Auditory analysis – A1
m = Articulatory Programming – M1
WERNICKE’S MODEL – CLASSICAL TASSONOMY
Lesion at M:
Motor Aphasia = Broca’s A.
Production deficit
Lesion at A-M:
Conduction Aphasia
Repetition deficit, Inability to translate the auditory structure of a word (A)
into the corresponding articulatory/motor form (M)
❖ Lesion at a: Pure verbal deafness
= no comprehension < no recognition of sounds
❖ Lesion at m: Pure Anarthria
= no production < articulatory disorder
WERNICKE-LICHTEIM MODEL – CLASSICAL TASSONOMY
Lichteim added:
C = Center of concepts = meaning
A = Auditory images (Wernicke - 22)
M = Motor images (Broca - 44)
A-M = Connection tract (white traits)
a = Auditory analysis – A1
m = Articulatory Programming – M1
Neurodegenerative Diseases (NDDs)
➢ Progressive damage to cells and nervous system connections
➢ Caused by a combination of genetic and environmental factors
➢ Progressive loss of selectively vulnerable populations of neurons
➢ Heterogeneous in their clinical presentations and underlying pathophysiology with
overlapping features
➢ No drugs to prevent or cure NDDs
➢ Available treatments aim to control symptoms and possibly slow down the
progression
➢ The two most common neurodegenerative disorders worldwide are
✓ Alzheimer’s Disease (AD)
✓ Parkinson’s Disease (PD)
Alzheimer’s Disease
The most common cause of cognitive decline and is the prototypical cortical dementia
➢ Its prevalence is strongly age-dependent → doubling every 5 years after 60 years old
➢ The most common cause of early onset dementia (< 65 years old)
➢ Histopathological hallmarks
✓ extracellular amyloid plaques
✓ intracellular neurofibrillary tangles
➢ Clinical symptoms start insidiously and gradually progress
➢ Initial and most common symptom → episodic memory impairment
➢ As the pathological process progresses others cognitive deficits appear
✓ Simmetrical and generalized cortical deficits
The anatomo-clinical correlation is a main feature of
classical neuropsychology
The qualitative and nonsystematical psychological analysis of
the patients’ pathological behaviour, often confined to clinical
observation (e.g. Moutier, 1908), was however a main weakness
of the traditional approach.
Clinical observations do not usually take into account relevant
variables, such as sex, age, and education of the patients, which
may affect their normal and pathological behaviour.
WERNICKE-LICHTEIM MODEL – CLASSICAL TASSONOMY
Lesion at C-A:
Transcortical Sensory Aphasia
- Comprehension
+ Repetition/Production (paraphasic)}
is a type of fluent aphasia characterized by impaired comprehension but relatively preserved repetition. It typically arises from damage to specific areas of the brain that disconnect language comprehension centers from other cognitive and linguistic functions.
COGNITIVE MODEL OF ORAL LANGUAGE
. auditoryAnalysis (input) + phonologicalBuffer (output)
= STM systems which remembers simple elements
in order of presentation
2. Conversion system = sub-lexical way
= translation of sounds to phonemes
3. Lexical systems = LTM of words (no meaning)
Four types:
- Phonological Input Lexicon
- Orthographic Input Lexicon
- Phonological Output Lexicon
- Orthographic Output Lexicon
APHASIC DEFICIT
❖ Phonological deficits
❖ Lexical - Semantic deficits
❖ Morpho-syntactic deficits
❖ Automatisms
❖ Articulatory deficits:
- Disarthria = motor speech disorder – weakness of articulatory muscle (< Bilateral lesions at Cerebellum and
Brain stem)
- Anarthria (Apraxia of speech) = motor programming disorder = impairment in the programming of
articulatory movements (< Left Cerebral Cortex, Insula)
PHONOLOGICAL DEFICITS
PHONEMIC PARAPHASIA = omissions, transpositions, additions, or repetitions of phonemes
Examples: “tabe” instead of “table” or “tephelone” instead of “telephone ” or “papple ” for “ apple ”
2. CONDUITES D’APPROACHES = Many attempts with production of phonemic variation of a word with the intent
of approaching the target word (“ta.. tab.. table”)
3. PHONEMIC NEOLOGISM = the word is meaningless due to the many phonemic errors ( “laple” for “ apple ”)
4. NEOLOGISTIC JARGON = production of language containing non-existent words = string of made-up words in
combination with real words that do not make sense together in context
LEXICAL - SEMANTIC DEFICITS
- ANOMIA = difficulty in word-finding
- ANOMIC LATENCIES = patient name something after a long time
- CIRCUMLOCUTIONS = use of an unnecessarily large number of words to name something (i.e., “ you use
it for seeing better” for “glasses”) - SEMANTIC PARAPHASIA = use of words that are related to each other (i.e., “sofa” for “couch”,
“elephant” for “lion”) - VERBAL PARAPHASIA = use of words that are NOT related to each other (i.e., “trousers” for “napkin”)
- PASSE-PARTOUT ELEMENTS = use of generic words to name something (i.e., “thing”, “stuff”..)
- SEMANTIC JARGON = the sentences are meaningless due to many semantic and verbal paraphasias
MORPHO-SYNTACTIC DEFICITS
- AGRAMMATISM = telegraphic speech with simplification of sentence structure:
- Omission of grammatical words (e.g., articles, pronouns…)
- Simplifications of elements (e.g., verbs in the infinitive, singular nouns instead of plural…) - PARAGRAMMATISM = Mild form
- Errors in agreement and in the choice of function words
- Substitutions of grammatical words - Agrammatism
A hallmark of non-fluent aphasia (e.g., Broca’s aphasia), characterized by telegraphic speech and simplified syntax.
Omission of grammatical words:
Intended: “I am going to the store to buy some apples.”
Output: “Go store. Buy apple.”
Simplifications of elements:
Verbs reduced to infinitives:
Intended: “He is running fast.”
Output: “He run fast.”
Singular nouns used instead of plurals:
Intended: “The children are playing.”
Output: “Child play.”
- Paragrammatism
A feature of fluent aphasia (e.g., Wernicke’s aphasia), involving milder grammatical errors.
Errors in agreement:
Intended: “The dogs are barking loudly.”
Output: “The dogs is barking loudly.”
Errors in the choice of function words:
Intended: “I want to go to the beach tomorrow.”
Output: “I want for go at the beach tomorrow.”
Substitution of grammatical words:
Intended: “He went to the park and played soccer.”
Output: “He go in the park for play soccer.”
AUTOMATISMS
- RECURRING UTTERANCES = repetitive verbal behaviours > use of recurrent syllabic fragments (“
tatatata “) - PERSEVERATIONS = repetition of a particular response (such as a word, phrase, or gesture) even when the
question changes - ECHOLALIA = repetition of words said by another person
ASSESSMENT LANGUAGE DISORDER
- SPONTANEOUS SPEECH > qualitative assessment
[Speed; Fluency; Phonological, Lexical-Semantic, Morpho-syntactic errors; Tone of voice; Informative content; Pragmatic rules] - COMPREHENSION
❖ Lexical decision (word vs no-word)
❖ Single word comprehension tasks (choose the right image)
❖ Sentence comprehension tasks (progressive difficulty)
IV. TOKEN TEST
= orders of increasing length and syntactic complexity - LEXICAL RETRIEVAL (Production)
❖ Denomination figure
❖ Definition
❖ Phonemic fluency tasks: F - A – S
❖ Semantic fluency tasks: Colors – Fruits – Animal - REPETITION
❖ Sounds
❖ Syllables
❖ Single words
❖ No-words
❖ Sentences
CLINICAL FORMS OF APHASIA
Classification based on: FLUENT vs NON-FLUENT aphasia
FLUENT APHASIA:
❖ Abundant speech (iperfluent speech - logorrhea)
❖ But meaningless = Anomia, phonemic and semantic
paraphasias, neologism, jargon and paragrammatism
= reduction if the QUALITY of speech
1. WERNICKE’S APHASIA
2. CONDUCTION APHASIA
3. ANOMIC (AMNESTIC) APHASIA
4. TRANSCORTICAL SENSORY APHASIA
NON-FLUENT APHASIA:
NON-FLUENT APHASIA:
❖ Poor speech, short sentences
❖ Agrammatism
❖ Apraxia of speech
= reduction on the QUALITY + QUANTITY of speech
1. BROCA’S APHASIA
2. GLOBAL APHASIA
3. MIXED TRANSCORTICAL APHASIA
4. TRANSCORTICAL MOTOR APHASIA
FLUENT APHASIA
1. WERNICKE’S APHASIA
< Phonological + Lexical + Morpho-syntactic
❖ Main comprehension deficit (oral and written words)
❖ Speech fluent and meaningless: paraphasia, both phonemic and semantics, neologism, jargon
❖ Paragrammatism
❖ Repetition + Denomination deficit
❖ Anosognosia
Lesion:
- Wernicke area (Brodmann area 22)
= posterior portion of the 1° Temporal convolution of the LH
+ Medial Temporal gyrus (Brodmann area 21)
+ Brodmann areas 37,39,40
- CONDUCTION APHASIA
❖ Main repetition deficit
❖ Main phonological deficit: conduites d’approaches + phonemic paraphasia
❖ No deficit: semantic, lexicon or syntax
❖ Comprehension intact
Lesion:
- Supramarginal Gyrus (Brodmann area 40)
- Arcuate fasciculus
Another form: REPETITION APHASIA
= repetition impairment due to deficit of verbal short-term memory
FLUENT APHASIA
3. ANOMIC (AMNESTIC) APHASIA
< Lexical (output)
❖ Main symptom: anomia = difficulty in word finding
Main lexical retrieval deficit > circumlocutions + passe-partout elements
❖ No deficit: phonological, semantic or syntax
❖ Comprehension and repetition intact
Lesion:
- Partial damage of Left Temporo-Parietal areas (Brodmann area 37-39)
- Wernicke area spared
Anomic Aphasia is most frequently observed as a residual effect of more severe aphasias
FLUENT APHASIA
4. TRANSCORTICAL SENSORY APHASIA
< Lexical-semantic
❖ Main comprehension deficit (oral and written language)
❖ Lexical-semantic deficit: anomia + semantic paraphasia
❖ Echolalia
❖ Preserved repetition (but no comprehension of the meaning)
Lesion:
- Extensive lesions at Left Temporo-Parietal areas (Brodmann area 37-39)
- Wernicke area spared
NON-FLUENT APHASIA
1. BROCA’S APHASIA
Main production deficit: telegraphic speech and agrammatism
❖ Phonological, Lexical and Morphological deficits
❖ Apraxia of speech
❖ Comprehension fairly preserved (otherwise = Global Aphasia)
Lesion:
- Broca’s area (Brodmann area 44) = foot of the third frontal gyrus of LH
+ nearly Frontal areas (Brodmann areas 6, 9, 46)
- GLOBAL APHASIA
❖ Severe impairment of all aspects of language
❖ Speech poor and limited to a few stereotyped forms (recurrent syllabic fragments)
❖ Comprehension and repetition also severely impaired
❖ Apraxia of speech
Lesion:
Areas supplied by the left middle cerebral artery:
- Peri-Sylvian cortex
- Pre- and Post - Central gyrus
- Underlying deep hemispheric structures (left F-T-P areas)
NON-FLUENT APHASIA
3. MIXED TRANSCORTICAL APHASIA
(Isolation Aphasia)
❖ Severe comprehension and production deficit
❖ No repetition deficit
❖ Main lexical-semantic deficit
❖ Echolalia
Lesion:
- Cortico-subcortical lesions in the Left Fronto-Temporo-Parietal region
- Broca’s + Wernicke + arcuate fasciculus spared
NON-FLUENT APHASIA
4. TRANSCORTICAL MOTOR APHASIA
❖ Psychomotor (verbal) inertia = absence or severe reduction of spontaneous language
❖ Preserved repetition, comprehension, reading, and writing
❖ Often associated with echolalia + perseverations
Lesion:
- Left premotor frontal areas (Brodmann area 45)
- Broca’s area spared
NEURODEGENERATIVE (LANGUAGE) DISORDERS
PRIMARY PROGRESSIVE APHASIA (PPA)
Diagnosis of PPA:
1. Presence of aphasia, which is the primary cause of difficulties in daily life
2. Aphasia must be the predominant deficit for at least 2 years from onset
+ Mesulam’s 3 criteria:
1. Insidious onset and gradual progression of aphasia
2. Functional consequences impacting daily life
3. Neurodegenerative orig
- LOGOPENIC PPA (LVPPA)
- LOGOPENIC PPA (LVPPA)
Both:
I. Lexical retrieval deficits (anomia) in spontaneous speech
II. Repetition deficit
+ at least 3 of these symptoms:
❖ Phonological errors (in spontaneous speech and naming task)
❖ Sentence comprehension deficits (YES: single-word comprehension)
❖ Verbal short-term memory deficits
❖ Absence of agrammatism and articulatory impairments
❖ Object recognition intact
AGRAMMATIC PPA [nfvPPA]
I. Spontaneous speech is effortful, non-fluent (dysprosodic) with articulatory impairments [Apraxia of speech]
II. Agrammatism
+ at least 2 of these symptoms:
❖ Deficits in syntactically complex sentences comprehension
❖ Intact single words comprehension
❖ Intact object recognition
- SEMANTIC PPA (svPPA/SD)
= Progressive impairment of semantic memory, with NO impairment of episodic memory
Both:
I. Object naming deficits (anomia > semantic paraphasia)
II. Deficit in single-word comprehension
+ at least 3 of these symptoms:
❖ Fluent and syntactically correct speech
❖ Object identification deficits
❖ Surface dyslexia (+ dysgraphia)
❖ Preserved repetition
Memory Overview:
Memory is the cognitive function by which information is encoded, stored,
and retrieved when needed.
Memory is not just a store:
It is a proactive, living function that guides behavior.
Localization:
While some networks and areas are identified, we do not know where memory is “stored.”
Cognitive neuroscientists consider memory as the learning, retention,
reactivation, and reconstruction of the experience-independent internal
representation.
The term of internal representation implies that such a definition of memory
contains two components: the expression of memory at the behavioral or
conscious level, and the underpinning physical neural changes
Memory engram: Arises from the synchronous firing of cells.
Lateralization:
Right Hemisphere (RH): Spatial learning.
Left Temporal Lobe: Story/language memory deficits.
Memory Architecture:
Non-Declarative Memory:
Linked to subcortical structures, especially the basal ganglia.
Short-Term Memory (STM):
Holds 7-9 items temporarily.
Retention of information, not active manipulation.
All information must pass through STM to reach Long-Term Memory (LTM).
Working Memory (WM):
Active manipulation of information; different from STM.
Sensory Feedback:
LTM influences the sensory registration system, creating a feedback loop.
Verbal and Visuo-Spatial Memory
Short-Term Memory (STM):
Verbal STM:
Neural Correlates: Arcuate fasciculus (connects BA 44 and 22).
Damage: Impaired repetition.
Test: Digit Forward Task (assesses verbal STM; normal score ranges help detect deficits).
Visuo-Spatial STM:
Test: Corsi Span Test (patients repeat a sequence by touching the same numbers).
Long-Term Memory (LTM):
Types:
Declarative:
Semantic: Knowledge about facts.
Episodic: Autobiographical memory; relies on networks from the frontal to temporal lobes.
Non-Declarative: Implicit memory, like procedural knowledge.
Debates:
Semantic vs. episodic distinction:
Some evidence suggests overlap, but patient dissociations (e.g., episodic impairment but intact semantic memory) point to differences.
Memory Deficits
Amnesia:
Retrograde: Loss of past memories.
Anterograde: Difficulty forming new memories.
Types:
Korsakoff Syndrome: Due to alcohol abuse; linked to temporal structures.
Frontal Amnesia: Attention deficits impede memory formation.
Diencephalic Amnesia: Damage to limbic structures (e.g., middle temporal lobe).
Transient Global Amnesia: Sudden identity loss (~24 hours).
Psychogenic Amnesia:
Related to PTSD and dissociative syndromes.
Primarily affects autobiographical memory.
Example: A patient lost 12 years of memory after trauma with no detectable brain lesions.
Case Study and Experimentation memory deficits
Psychogenic Amnesia Case:
Patient’s last memory was from 2001 (9/11); forgot 12 years of life.
No lesions detected via MRI/fMRI. Relearned everything gradually.
tDCS Experiment:
Setup:
Stimulation to the left temporal lobe, using true/false questions about memories and emotional measures.
Findings:
False events activated more brain regions than true events.
Reaction times for true events slowed (suggesting implicit recognition).
Vividness linked to visuo-cortical activation
STM
Short-Term Memory (STM):
Holds 7-9 items temporarily.
Retention of information, not active manipulation.
All information must pass through STM to reach Long-Term
Short-term memory (or “primary” or “active memory”) is the capacity for
holding a small amount of information in an active, readily available state
for a short interval. For example, short-term memory holds a phone number
that has just been recited.
The duration of short-term memory (absent rehearsal or active
maintenance) is estimated to be on the order of seconds. The commonly
cited capacity of 7 items, found in Miller’s Law, has been superseded by
4±1 items.
Short-term memory is not the same as working memory, which refers to
structures and processes used for temporarily storing and manipulating
information.
Verbal STM
Verbal STM
Phonological STM: an anatomo- functional model (redrawn from Vallar, Di Betta, &
Silveri, 1997). The dashed lines denote the rehearsal process. The left hemisphere
structures subserving the connection of the processes of phonological analysis and of the
phonological STS with the output buffer may include the arcuate fasciculus (Benson,
Sheremata, Bouchard et al., 1973; Green & Howes, 1977, for review), and white matter
fibre tracts in the insular region (Damasio & Damasio,1980).
Left hemisphere
Phonological store à supramarginal gyrus (parietal lobe)
Rehearsal process à inferior frontal operculum
Arcuate fasciulus, basal ganglia, and cerebellum
Only one patient described with a right hemisphere lesion and MBT deficit.
verb-STM deficits
Span reduction for auditory-verbal materials
- Difficulties in complex sentences comprehension
Important!
* Patient’s performance improves if the material is presented in visual
form.
* The deficit is not attributable to a deficit in phonological analysis.
* The deficit is not attributable to a deficit in language production
visuo-spatial STM
The neural correlates of vsSTM are less clear, but the right parietal
and frontal areas seem to play a crucial role Difficulty in immediate recall of short visual-spatial sequences
The Corsi Span test
Long-term memory
Long-term memory refers to the process that takes information from the
short-term memory store and creates long lasting memories. These
memories can be from an hour ago or several decades ago.
Long-term memory can hold an unlimited amount of information for an
indefinite period of time.
There are two types of long-term memory: procedural and
declarative. Procedural long-term memories are information related to
activities learned through practice and repetition, such as driving a car.
Declarative long-term memories are information about facts, rules,
events, definitions, and experiences that someone can recall when
necessary
Holds data concerning
knowledge about words, facts,
ideas, concepts, algorithms.
Semantic memory may be
described as a mental
thesaurus, which also stores
encyclopaedic facts (e.g.
“where and when Napoleon I
died”), and records that are
not entirely verbal (e.g. the
faces of famous people, the
image of a Ferrari car)
Semantic Episodic
Stores records concerning
events and their spatial and
temporal relationships. It
focuses on one’s life events
that the person has
experienced throughout the
phases of his life.
AMNESIA
Amnesia is a severe and selective deficit of LTM, which involves both
verbal and nonverbal material, and is independent of the modality of
presentation of the stimulus.
The deficit has two main components, with reference to the time
onset of the disease: (1) retrograde amnesia involving events before
the accident; (2) anterograde amnesia involving events at the time
of the accident and following it (see Azam, 1881 and 1893, quoted by
Hacking, 1995,p.l90)
Amnesic syndrome
Long-term episodic memory disorder
* Preserved short-term memory
* Preserved semantic memory
* Preserved implicit memory
* Prevalent deficit of anterograde episodic memory
* Variable deficit of retrograde component
* Absence of widespread cognitive impairment
Amnesic syndrome may be transient or permanent. In the
anterograde form it may affect verbal or visuospatial memory or both
(global amnesia)
Amnesia
Lesion to limbic system structures à middle temporal lobe
Lesion to limbic system structures (temporal lobe)
Lesion to the frontal regions
Lesional correlates
Based on the lesional correlates, one can distinguish between
different type of amnesic syndrome:
Ø Temporal amnesia (e.g. patient HM)
Ø Diencephalic amnesia
Ø Frontal amnesia
The amnesic syndrome can be caused by:
Ø Epilepsy
Ø Encephalitis
Ø Stroke
Ø Dementia
Ø Anoxia
Ø Traumatic brain injury
Transient Global Amnesia
Transient global amnesia appears suddenly and is characterized by
both retrograde and anterograde amnesia.
Diagnostic criteria include duration of less than 24 hours, seizure
must be reported by a reliable observer, prevalent anterograde
amnesia, not accounted for by other neurological conditions such as
epilepsy.
The cause of transient global amnesia are still unknown but vascular
involvement of the limbic system is presumed.
Retrograde amnesia
Retrograde amnesia may involve autobiographical (private)
memories or public memories, or both (clinical dissociations).
The patient of De Renzi et al. (1987a) who suffered a postencephalitic amnesia, exhibited a semantic deficit, anterograde
amnesia, and retrograde amnesia for famous facts; by contrast,
memory for past autobiographical events was preserved (see also
the patients of Grossi, Trojano, Grasso et al., 1988; Kapur et al.,
1989). In the patient of Stuss and Guzman (1988) the retrograde
deficit was more severe for autobiographical events than for famous
facts (see also Tulving, Schacter, & McLachlan, 1988). Also patient
PS, who suffered a paramedian thalamic infarction, had a severe
autobiographical memory deficit, whereas knowledge of famous
people and public events was relatively spared (Hodges & McCarthy,
1993).
Psychogenic amnesia
Psychogenic amnesia or dissociative amnesia is a memory
disorder characterized by sudden retrograde episodic memory loss,
said to occur for a period of time ranging from hours to years to
decades. It occurs in the absence of a brain damage.
More recently, “dissociative amnesia” has been defined as
a dissociative disorder “characterized by retrospectively reported
memory gaps. These gaps involve an inability to recall personal
information, usually of a traumatic or stressful nature.
In a change from the DSM-IV to the DSM-5, dissociative fugue is now
subsumed under dissociative amn
Does anodal tDCS over the left temporal cortex (T3)
restore autobiographical memory in a patient with isolated
retrograde amnesia?
Isolated retrograde amnesia is defined as impaired recollection of experiences
pre-dating brain injury with relatively preserved anterograde learning and memory
(Levine et al., 1998). Autobiographical memory for past events is strongly
involved.
The left middle temporal cortex has recently been reported as a key region for
the autobiographical memory system (Svoboda et al., 2006; Berlingeri et al.,
2014).
Transcranial direct current stimulation (tDCS) is a non-invasive, painless, and
easy to use neuromodulatory technique that can improve performance on a
variety of cognitive tasks in humans (see Bennabi et al., 2014 for a review)
Memory enhancement after tDCS have been explored in neurological diseases
(Boggio et al. 2009; Cotelli et al., 2014). For example, in Alzheimer, Boggio et al.
(2009) reported short-term facilitation effects on visual recognition memory after
temporal anodal tDCS applied 30 min at 2 mA.
Attention: definition
demension and domain
Attention
Definition:
In psychology, attention is the concentration of awareness on a particular phenomenon, excluding other stimuli. It is a complex, multifaceted process allowing individuals to focus on specific experiences, often guided by stimuli in the environment or internal representations (such as long-term memory).
Dimensions of Attention
Intensity:
Involves the reticular formation and governs alertness and vigilance.
Includes:
Alertness: Reacting quickly to simple tasks (e.g., reaction-time tasks).
Sustained Attention: Maintaining focus over longer periods.
Vigilance: Monitoring for signals during extended, simple tasks.
Spatial Attention:
Directing attention to different locations in space.
Example: Shifting visual-spatial attention or reorienting focus.
Selectivity:
Choosing relevant information while suppressing irrelevant stimuli.
Includes:
Selective Attention: Filtering distractions (e.g., identifying apples among strawberries).
Divided Attention: Handling multiple tasks simultaneously.
types of attention
Bottom-Up Attention:
Stimulus-Driven: Automatic response to external factors, such as loud noises or bright lights.
Involuntary: Helps detect potential threats for survival.
Neural Basis: Ventral attention network, involving the superior colliculus and parietal cortex.
Example: Noticing a flashing light without conscious effort.
Top-Down Attention:
Goal-Directed: Conscious focus driven by internal goals and expectations.
Voluntary: Requires effort to prioritize tasks or ignore distractions.
Neural Basis: Dorsal attention network, involving the prefrontal cortex and parietal lobe.
Example: Reading a book in a noisy environment.
Experiments in attention
Purpose:
To study the mechanisms of spatial attention by measuring reaction times to stimuli when attention is directed by valid and invalid cues.
Procedure:
Participants are shown a screen with two target locations (typically represented as boxes or squares on the left and right of the screen).
A central cross acts as the fixation point.
Cues: An arrow is shown that predicts the location where a target will appear (valid or invalid).
Valid Cue: The arrow correctly predicts the target location.
Invalid Cue: The arrow incorrectly predicts the target location.
The target (e.g., a light or object) appears after the cue, and participants must respond as quickly as possible by pressing a key or clicking when they detect the target.
Findings:
Valid Cues: Faster reaction times because attention is directed correctly to the location before the target appears.
Invalid Cues: Slower reaction times, as participants must shift their attention from the cued location to the correct one.
This experiment demonstrates the endogenous (top-down, goal-directed) and exogenous (bottom-up, stimulus-driven) components of attention. It shows how spatial attention can be influenced both by internal cues (endogenous) and automatic shifts based on external stimuli (exogenous).
Key Takeaway:
The difference in reaction times between valid and invalid cues reveals how attention can be manipulated by cues and highlights the brain’s ability to shift focus based on expectations.
Experiment 2: Memory-Based Attention (MBA Task)
Purpose:
To explore how long-term memory (LTM) influences spatial attention and how past experiences (such as learned locations of objects) affect attention deployment.
Procedure:
Learning Phase: Participants are shown scenes with objects in specific locations and asked to memorize the scene (e.g., the locations of objects on a screen).
Test Phase (after a delay, usually 30 minutes):
Participants are cued to direct their attention to a specific location, and targets are presented either in learned locations (valid cues) or in new, unrelated locations (invalid cues).
The task measures how quickly participants can react to targets appearing in learned versus unlearned locations.
Findings:
Faster reaction times are seen for targets appearing in learned locations, indicating that memory plays a role in guiding attention.
This experiment involves memory-based attention, showing that top-down processes are influenced by learned information and experiences stored in LTM.
Neural Mechanisms:
The hippocampus is heavily involved, activating before the visual cortex when participants are focusing on locations they have learned.
However, not all studies find consistent involvement of the hippocampus, likely due to task demands or differences in methodology (e.g., task complexity, explicit vs. implicit memory demands).
Key Takeaway:
Memory-based attention tasks highlight how prior knowledge and experiences can guide attention, allowing us to focus more quickly on familiar or learned locations, with the hippocampus playing a central role in this process.
Experiment 3: Attention in Patients with Hippocampal Damage
Purpose:
To investigate how damage to the hippocampus affects memory-based attention and the brain’s capacity to reorganize and compensate for such damage.
Participants:
Patients with Temporal Lobe Epilepsy (TLE), with either left or right hippocampal damage.
Control Group: Healthy participants without any neurological damage.
Procedure:
Participants perform tasks similar to the MBA task, where they are required to memorize object locations and then respond to targets appearing in either learned or new locations.
The experiment is often combined with MRI imaging to measure brain activity and structural changes, such as gray matter density in the hippocampus.
Findings:
Left hippocampal damage often leads to reorganization in the brain, with the right hippocampus compensating for lost function.
Patients with left hippocampal damage show less correlation between task performance and left hippocampal activity, while right hippocampal activity and gray matter density correlate more strongly with performance, suggesting a compensatory mechanism.
In healthy controls, the left hippocampus is more involved in memory-based attention, but damage to this region does not necessarily lead to a complete loss of function due to brain plasticity.
Key Takeaway:
This experiment provides insight into the brain’s ability to reorganize and compensate for damage, especially in tasks requiring memory-based attention. The findings suggest that the brain can adapt by shifting functions to other regions when necessary, such as the right hippocampus compensating for left hippocampal damage.
Meta-Analyses in attention
if the hippocampus L is important for memory based attention, people with complete damage are not going to have MBA.
results seem to not be involved, but they found people with temporal Lobe the brain has reorganized, MRI, gray matter density, on healthy control, L patients, R patients
healthy participants, the number of neurons in the L hipocamsus, in the R sclerosis there was a correlation with their behavioral performance.
L hippocampus deficit patients reorganized to the R hippocampal so that’s why there was no correlation with the Left hippocampal.
Several meta-analyses have investigated the involvement of the hippocampus and fronto-parietal networks in attention tasks. Key conclusions include:
The fronto-parietal network is consistently implicated in attention, particularly in tasks involving spatial orientation and selectivity.
There is less consensus regarding the role of the hippocampus in attention, as results vary based on task demands and methodology (e.g., explicit vs. implicit memory tasks).
Studies suggest that while the hippocampus plays a role in guiding attention based on long-term memory, its involvement is not always essential, depending on whether the task requires explicit memory retrieval.
Conclusions and Implications
Hippocampus and Attention: While the hippocampus is essential for tasks requiring memory-based attention, especially those relying on learned locations, its role may vary depending on task demands. Brain plasticity enables compensation when hippocampal damage occurs.
Top-Down vs. Bottom-Up Processes: The experiments highlight the interplay between stimulus-driven (bottom-up) and goal-directed (top-down) attention, showing how attention can be both involuntarily captured by external stimuli and deliberately directed by internal goals.
Clinical Implications: The ability of the brain to reorganize after hippocampal damage has implications for treatment and rehabilitation in patients with epilepsy or other brain injuries, suggesting that training and neuroplasticity could be leveraged to improve attention and memory functions.
Executive Functions: Overview and Key Concepts
Executive Functions refer to a set of cognitive processes necessary for controlling behavior and achieving goals. These include attentional control, cognitive inhibition, working memory (WM), cognitive flexibility, decision-making, and reasoning. Executive dysfunctions often result from damage to the frontal lobes and are commonly seen in conditions like traumatic brain injury (TBI) and frontotemporal dementia (FTD).
Working memory: Strongly associated with the frontal lobe, particularly the left hemisphere.
Development: Executive functions emerge in late infancy and continue to develop, peaking around the age of 25.
Historical Case: Phineas Gage
One of the most famous cases illustrating executive dysfunction. After a traumatic injury to his prefrontal cortex, Gage experienced significant changes in personality and behavior, losing cognitive control and becoming impulsive, marking one of the earliest examples of executive function impairment due to frontal lobe damage.
Lobotomies and Frontal Syndrome
Lobotomies: Introduced by Egas Moniz to treat psychiatric patients by severing the white matter in the frontal lobes, leading to severe executive dysfunction.
Frontal Syndrome: Characterized by symptoms like apathy, inertia, and disinhibited behavior (e.g., inappropriate or profane language), often resulting from frontal lobe damage.
Frontal Lobe dissorders
classification
Behavioural disorders
-Motivation
Apathy-Abulia-Anedonia
-Disinhibition
-Impulsivity-Personal
conduct-Social
conduct(sociopathy)
Cognitive disorders
(dysexecutive syndrome)
Distractibility-PerseverationMemory disorders (especially
prospective)-Top-down
attention disorders-Planning
disorders-Disorders of logical
skills(induction, deduction)
Clinical Considerations: Behavioral vs. Cognitive Disorders
In clinical practice, executive dysfunction is classified into behavioral and cognitive disorders:
Behavioral Disorders: Involve deficits in motivation and disinhibition (e.g., impulsive behavior).
Cognitive Disorders: Characterized by issues with distractibility, planning, and memory. These patients often struggle with top-down attention, leading to poor task organization and decision-making.
Testing Executive Functions
Several neuropsychological tests assess executive functions:
Stroop Task: Measures cognitive inhibition by requiring participants to suppress automatic responses.
Gambling Task: Evaluates decision-making under risk and uncertainty.
Wisconsin Card Sorting Test (WCST): Assesses cognitive flexibility and the ability to shift between strategies.
Tower of London: Measures planning and problem-solving abilities.
Somatic Marker Hypothesis
This theory suggests that emotional signals (somatic markers) help guide decision-making by preventing negative outcomes. There is an ongoing debate about the extent to which interoception (awareness of internal bodily states) influences risk-taking decisions.
Somatic Marker Hypothesis
This theory suggests that emotional signals (somatic markers) help guide decision-making by preventing negative outcomes. There is an ongoing debate about the extent to which interoception (awareness of internal bodily states) influences risk-taking decisions.
Frontal Lobe Dysfunction in Criminal Behavior
Neuroimaging studies on criminals have shown that frontal lobe dysfunction is often associated with impaired decision-making and problem-solving:
Orbitofrontal Cortex (OFC): Linked to impulsive and socially inappropriate behavior.
Anterior Cingulate Cortex (ACC): Involved in detecting errors and regulating emotional responses.
Dorsolateral Prefrontal Cortex (DLPFC): Related to impaired planning and problem-solving in criminals. Specific Cases:
A famous case involved a pedophile with no prior criminal history who had a large frontal lobe tumor. When the tumor was removed, his behavior normalized, but the tumor’s regrowth led to a return of the deviant behavior.
Amygdala dysfunction has been linked to deficits in empathy and increased aggressive behavior.
Psychopathy and Organized Crime
Psychopathy does not exist in psychopathy- antisocial behavior.
neuropsychology, studies in criminal behavior. the most robust founding, they have a PROBLEM SOLVING deficit, compared to the normal population.
Studies have shown that people involved in organized crime often exhibit unique cognitive and emotional patterns:
Problem-solving deficits: Criminals tend to have difficulty with decision-making and problem-solving compared to the general population.
Emotional recognition impairments: Criminals, especially in organized crime, are often impaired in recognizing certain emotions, though they may show enhanced recognition of fear as part of their social dominance and intimidation tactics.
Mafia Studies:
Two studies have explored cognitive patterns in individuals from organized crime groups:
Participants were impaired in risk-taking tasks, consistent with the risk-shift phenomenon, where group decisions tend to be riskier than individual decisions.
Lower-level mafia members were found to be better at recognizing fear, which aligns with their role in intimidating others.
The frontal lobe loops
Five parallel and distinct circuits:
1. motor circuit
2. oculomotor circuit
3. dorsolateral prefrontal circuit
4. orbitofrontal circuit
5. anterior cingulate circuit
Typical executive, motivational and personality disorders related to prefrontal
cortical lesions can be determined by dysfunction of the last three circuits.
Dorsolateral loop
Critical for executive
function
* Damage produces
– Inflexibility
– Planning
– Problem-solving
– Goal-directed
behavior
Dorsolateral prefrontal cortext, caudate, globus pallidus, thalamus
Orbitofrontal loop
Involved in social
and emotional
functioning
* Damage produces:
– Disinhibition
– Hyperactivity
– Emotional lability
– Aggressiveness
– Reduce selfawareness
Lateral orbital cortex, caudate, globus pallidus, thalamus
Anterior cingulate loop
Important in
behavioral activation
* Damage results in
– Akinetic mutism
– Abulia
– Impairments in
spontaneous
initiation of behavior
Anterior cincigulate cortex, nucleus accumbes, globus pallidus, thalamus
Frontal syndrome
- apathy
- inertia
- changes in character
- profane behaviour
- uninhibited sexual behavior
- shallowness
- perseverations
- disinhibition
- attentional deficits
The frontal lobe
Lateral Prefrontal Region (8,9,46)
Lesions in this region produce impairment
in a variety of “executive” skills that cut
across domains. Some degree of materialspecificity is present, but relatively weak.
A) Fluency: impaired verbal fluency (left)
or design fluency (right)
B) Memory impairments: defective recency
judgment, metamemory defects, difficulties
in memory monitoring
C) Impaired abstract concept formation
and hypothesis testing
D) Defective planning, motor sequencing
E) Defective cognitive judgement and
estimation
Tranel, 1992The frontal lobe
Frontal Operculum (44,45,47)
A) Left: Broca’s aphasia
B) Right: ‘expressive’ aprosodia
Superior Mesial (mesial 6, 24)
A) Left: akinetic mutism
B) Right: akinetic mutism
Bilateral lesions of mesial SMA (6) and
anterior cingulate (24) produce more
severe form of akinetic mutismThe frontal lobe
Inferior Mesial Region
A) Orbital Region (10, 11)
Lesions in this region produce
disinhibition, altered social conduct,
“acquired sociopathy”, and other
disturbances due to impairment in
fronto-limbic relationships
B) Basal Forebrain (posterior
extension of inferior mesial region,
including diagonal band of Broca,
nucleus accumbens, septal nuclei,
substantia innominata)
Lesions here produce prominent
anterograde amnesia with
confabulation (material specificity
present, but relatively weak)The frontal lobe
Inferior Mesial Region
A) Orbital Region (10, 11)
Lesions in this region produce
disinhibition, altered social conduct,
“acquired sociopathy”, and other
disturbances due to impairment in
fronto-limbic relationships
B) Basal Forebrain (posterior
extension of inferior mesial region,
including diagonal band of Broca,
nucleus accumbens, septal nuclei,
substantia innominata)
Lesions here produce prominent
anterograde amnesia with
confabulation (material specificity
present, but relatively weak)The frontal lobe
Dorsolateral Prefrontal cortex:
Working memory, filtering & interference
control, sustained attention.
Ventromedial and orbitofrontal cortex:
Inhibitory control, planning, social guidance
and decision making
Anterior Cingulate:
An executive attention system that responds
to task difficulty, novelty, error detection and
correction and overcoming habitual
responding
USN symptoms
USN symptoms can dissociate across sensory modalities, sectors of
space (i.e., personal, peri-personal and extra-personal space,
reference frames (egocentric vs allocentric neglect, and tasks. Finally, not only the type of task but also task demands have been
found to affect neglect severity.
Basal ganglia lesions
Hyperkinetic movement disorders
✓ uncontrolled involuntary movements
(jerks and twists)
✓ e.g. Hungtington’s Disease
Hypokinetic movement disorders
✓ Rigidity, slowness and difficulty
initiating movements
✓ e. g. Parkinson’s Disease
Cerebellum
2 main components:
➢ Midline Vermis
➢ Lateral cerebellar hemispheres
❖ Inputs
➢ Motor cortex
➢ Brainstem
➢ Spinal cord
❖ Outputs
➢ Motor cortex via the thalamus
Task: to modulate and refine motor system outputs✓ Ataxia is ipsilateral to lesion
➢ Midline lesions → Truncal Ataxia
➢ Lateral lesions → Appendicular Ataxia
Cerebellar lesion → uncoordinated movement (Ataxia)
Reticular formation
Reticular Formation extends throughout the central portions of the
brainstem, from the medulla to the midbrain
Rostral portion
(upper pons and midbrain)
Level of consciousness
Caudal portion
(medulla and lower pons)
Motor and autonomic functions
