Session 11: Higher Functions of the Brain Flashcards
What are the association areas of the brain?
The association areas make up 70 to 80% of the surface of the cortex. These regions, the parietal-temporal-occipital (or parietal-occipitotemporal) association area, the prefrontal association area and the limbic association area, receive, integrate and analyse signals from multiple cortical and subcortical regions and their output produces the complex ‘human’ behaviours, which make up our individuality – the cortical association areas are where information from different modalities are brought together for processing.
Describe the cortex
Inputs to layer IV from (information going up):
- Motor and sensory cortices, thalamus and brain
Outputs (informing going down)
- From layers V and VI to hippocampus, basal ganglia, cerebellum and thalamus
- From layers I, II and III to other cortical association areas (information going deeper to the brain)
The cortex is a very dense network of neurones (~2-3 mm shrinks due to atrophy or Alzheimer’s)
Describe the functions of the frontal lobe and possible manifestations of frontal lobe lesions
Frontal Lobe: higher intellect, personality, mood, social conduct, interpretation of meaning and language (dominant hemisphere). Damage to the frontal lobe can be diverse but can cause personality and behavioural changes as well as inability to solve problems. Examples include mood changes, inappropriate social conduction, perseveration (and associated inflexibility - cannot process new ideas). Perseveration is the repetition of a particular response, such as a word, phase, or gesture despite the absence of cessation of a stimulus and symptoms include “lacking ability to transition or switch ideas appropriately with the social context, as evidenced by the repetition of words or gestures after they have ceased to be socially relevant or appropriate”.
Describe the functions of the parietal and temporal lobes + possible manifestations of lesions
Parietal Lobe: language, calculation (dominant hemisphere) and visiospatial functions (non-dominant hemisphere – music, emotions etc). Parietal lobe lesions can cause attention deficits (associated with contralateral neglect syndrome e.g. right hemisphere damage leads to contralateral neglect – only eats half the food on the plate etc) – not aware of deficit.
Temporal lobe: memory and language. Temporal lobe lesions will produce recognition deficits (such as agnosia and prosopagnosia (‘facial blindness’). Other agnosias can be auditory (not able to differentiate between different sounds e.g. difference between phone and car horn).
Describe the function of the occipital lobe and problems global lesions could create
Occipital lobe: vision
Any global lesions can cause more severe problems – cognitive deficits, as seen in dementia e.g. in Alzheimer’s, cerebrovascular disease.
Memory and thought tend to go first and deficit progresses, inappropriate social conduct and emotions (overreacting, reacting more negatively than expected) occur.
Key questions to ask in assessment include “Who am I? Where am I? What year is it? Who is the Prime Minister?”
Describe the limbic association area
The limbic association area attaches emotional connotations to our sensory input and consequent behaviour. It rewards appropriate behaviours with pleasure sensations and negative sensations to inappropriate behaviours. These reward/punishment centres of the limbic system are closely associated with the ability to learn.
Association of the cortex connect cortical tissue strips to the rest of the brain. They can be short-range connections (such as arcuate fibres) or long-range connections (such as occipito-frontal connections, which include superior longitudinal fasciculus or the arcuate fasciculus).
Describe what is meant by dominant and non-dominant hemispehres
Individuals can be described as having a dominant and non-dominant hemisphere, whereby certain functions are carried out using onside of the brain and others on the other side, known by a process ‘lateralisation’.
The dominant hemisphere (normally the left hemisphere) will involve the language (spoken/heard, written/read, and gestured/seen), maths, logic and motor skills (handedness), whereas the non-dominant hemisphere will involve emotion, music/art, visiospatial and body awareness. So in a stroke for example that affected the dominant hemisphere, patient may not be able to understand sign language etc.
The dominant hemisphere is the left hemisphere in up to 95% of people.
However, connections are made between the two hemispheres, allowing information to travel from one side to the other. These connections are achieved mainly through the corpus callosum (band of connective tissue), as well as the anterior and midbrain commissures; any lesions to the corpus callosum can mean individuals can elicit a response from their dominant hemisphere (e.g. action from a written word) without the non-dominant (body awareness) knowing why.
To summarise: the left hemisphere processes information in sequence (e.g. language) and the right hemisphere looks at the whole picture (e.g. spatial awareness)
Describe lateralisation of language and the two pathways that arise
Language is also lateralised. The input into this system is via Wernicke’s area (found on the temporal lobe) which acts in the interpretation of written and spoken words, whilst the output comes from Broca’s area (found on the frontal lobe), which acts in the formulation of the language components (i.e. putting words into a sequence of order), sending information to motor cortex (which deals with moving lips or hands etc).
As a consequence of these two areas, two pathways develop for speaking; one for speaking a heard word and one for speaking a written word
- Pathway for speaking a heard word: Primary Auditory Area => Wernicke’s Area sends fibres (via arcuate fasciculus) to => Broca’s Area => Motor Cortex
- Pathway for speaking a written word: Primary Visual Cortex, via angular gyrus to => Wernicke’s Area, via arcuate fasciculus => Broca’s Area => Motor Cortex
NB: lesions that affect the angular gyrus are associated with alexia and agraphia (can’t read nor write).
Describe the difference between Wernicke’s and Broca’s aphasias. What other possible aphasias are there?
Any damage to Wernicke’s area can result in a Wernicke’s Aphasia (which is a receptive/sensory/central aphasia); when this affects the dominant side, (damage to the non-dominant side will be less severe), individuals have a disorder of comprehension, producing a fluent yet unintelligible speech (producing jargon aphasia). There may also be associated loss of mathematical skills (loss of ability to interpet symbols).
Any damage to Broca’s area can result in a Broca’s Aphasia (which is an expressive or motor aphasia); when this affects the dominant side, individuals present with poorly constructed sentences and disjointed speech, yet their comprehension is fine. Interestingly people can still sing very well (motor output is from a different part of the brain).
Other types of aphasia that can develop are conduction aphasia (difficulty in repetition), nominal/amnesic aphasia (cannot remember names) or a global/total aphasia (damage to both Wernicke’s and Broca’s Areas – rapidly leads to demntia as cannot interpret anything in the world around you).
Dementia describes the disruption of behaviour consequent upon the degradation of these areas by a wide variety of disease processes including vCJD (Variant Creutzfeldt-Jakob disease).
Summarise the parieto-occipitotemporal, pre-frontal and limbic assoication areas
The parieto-occipitotemporal areas integrate the visual, proprioceptive and auditory inputs necessary to an understanding of our relationship to the immediate surroundings. Other areas, particularly Wernicke’s area, is essential to the comprehension of the meaning of spoken or written words, so that if damaged here a patient may remain fluent but make up words or speak with a great tangle of words (receptive dysphasia).
The pre-frontal association area is concerned with integrating complex sensory and motor associations allowing us to consider the consequences of an action or plan for the future. Within the pre-frontal cortex the specialised Broca’s area is necessary for the translation of thoughts into words, damage here and the patient’s speech becomes slow and laboured.
The limbic association area attaches emotional connotations to our sensory input and consequent behaviour. It rewards appropriate behaviours with pleasurable sensations, but dumps embarrassment and guilt upon any socially inept behaviour. The reward/punishment centres in the limbic system are closely associated with our ability to learn.
Where are memories stored? What are the two types? Which structures are involved in which?
Memories are stored throughout the cortex e.g. visual memories in visual cortex, auditory memories in auditory cortex.
Memory underlies our ability to learn new information.
Psychologists classify memory into procedural memory, involved in the performance of motor skills, riding a bicycle for example, which are learnt and perfected by practice, and declarative memory, concerned with the naming of objects, recognition of places, remembering events etc.
For procedural memories, the cerebellum, basal ganglia and the pre-motor cortex are involved. Such memories are difficult to form, but once formed are long-lasting and can be performed without conscious recollection.
Declarative memories, which are assessed continuously, are rapidly learned but also rapidly forgotten, depend upon connections between the hippocampus and widespread regions of the cerebral cortex.
How may declarative memories also be classified?
Declarative memory may also be classified according to the time frame over which it persists.
Immediate memory: the ability to hold an experience in mind for a few seconds provides us with our sense of the present.
Short term memory describes the ability to hold an experience for a few minutes or hours. Short term memory can be considered to be our ‘working memory’ – allowing us to retain information until a task has been performed e.g. memorising a phone number, then forgetting it as soon as your call is finshed.
Finally information may be storied in a long-term memory to be retrieved days, months, years later. It’s not affected by other mental activity.
What does the process to form and retrieve a memory require?
The ability to form and retrieve a memory involves several distinct processes.
Memories are produced as a result of synaptic changes that occur, producing a concept of “neuronal plasticity”.
Repetition and consolidation, the process by which immediate experiences are converted first into short term then into long-term memories, appears to depend upon physical changes in synaptic connections.
The act of remembering refers to the process whereby information is retrieved from long-term storage into consciousness (declarative memory) or is expressed as motor skill (procedural memory).
Memories will be committed if there is emotion involved, rehearsal/repetition, association or simply just an “automatic memory”.
Which areas are involved in memory formation?
Memories form via synaptic links between the cortical sensory areas (inputting into the region), amygdala and hippocampus (where long term memory occurs and structural changes develop), and the diencephalon, thalamus, hypothalamus basal forebrain and the prefrontal cortex (interprets and organises the memory for storage – allows us to find memory again – the prefrontal cortex is like an indexing system).
What is meant by long-term potentiation?
The formation of memories has been described to be based around the concept of ‘long-term potentiation (LTP)’. LTP is a long-lasting enhancement in signal transmission between two neurones that results from stimulating them synchronously; LTP makes a memory stronger by allowing circuits to adapt to allow more presynaptic messengers to be present – there is up-regulation of the synapse such as more vesicles, more neurotransmitters etc. Glutamate (NMDA receptors) are involved.
The opposite of LTP is long-term depression, where there is a weakening of infrequently used synapses, causing gradual loss of memory (synaptic connections diminish)
Age and memory
- Memory function reaches peak at 25
- At 40+ brain cells die at a rate of 10,000 a day
- At 85+ 50% of individuals have Alzheimer’s disease
Recap higher functions of the cortex
Cerebral hemispheres are responsible for cognition and higher mental function (memory, reasoning, language, social skills, vision etc)
- Left hemisphere – language
- Right hemisphere – special awareness
Occipital Lobe: visual cortex and visual processing (macula has large representation in the visual cortex – so some forms of visual field loss can occur without involving the macular (‘macular sparing’))
Temporal lobe: involved in language, recognition of faces and objects, emotional response (e.g. stranger vs close family) and memory
- Left Temporal Lobe: dominant in 9 out of 10 and contains Wernicke’s area.
- Overactivity can lead to temporal lobe epilepsy. The seizures involve sensory changes e.g. unusual smell that is not there (olfactory illusion) or a memory disturbance.
- Characteristic aura – gustatory or olfactory hallucination
- Incredibly heightened emotions e.g. fear
- Seizures may lead to temporal lobe damage => problems with memory
Frontal Lobe:
- Broca’s area (left) – expressive, non-fluent aphasia if damaged
- Motor cortex
- Executive function
Parietal Lobe: sensation and perception, ‘multimedia’ understanding of bodily self and surroundings => can test 2 point discrimination (fine and tough), joint position sense, fine touch and temperature. Lips have a lot of sensitivity – large representation in the cortex.
Describe the changes seen in damage done to the anterior frontal lobes
Withdrawn
Apathetic
Abulic (lack of will or initiative and can be seen as a disorder of diminished motivation – more extreme than apathy)
Euphoric (without feeling so)
Inappropriate
Amoral
Loss of social rules
Loss of empathy
NB: olfactory groove meningiomas grow along the nerves that run between the brain and the nose => tumours cause loss of smell. If they grow large enough, olfactory groove meningiomas can also compress the nerves to the eyes, causing visual symptoms. They can grow to large size prior to being diagnosed due to changes in the sense of smell and mental status changes being difficult to recognise.
What is Dementia? Describe its progression
Dementia is described as progressive decline of cognitive function (impairment of intellect, reason and personality without impairment of consciousness), usually affecting the cortex as a whole (though can sometimes be patchy). Memory becomes affected and intellect gradually falls, with associated loss of emotional control, deterioration of social behaviour and loss of motivation. It is an acquired loss of cognitive ability sufficiently severe to interfere with daily function and quality of life.
Markers of Dementia
- Progressive deterioration: memory, intellect, behaviour, personality, speech
- Other physical difficulties e.g. slowness of movement
Clinical Course of Onset of Dementia: the rate of progression depends upon the primary cause of tissue degeneration
Describe Chronic Dementia. What abnormal proteins accumulate in dementia?
Vascular damage of brain tissue:
- Underpined by diseases of the vascular system
- Neuronal death is secondary to the vascular disease
Neurodegenerative
- Accumulation of abnormal proteins
- Neuronal cell death
Commonest Chronic Dementias are: Alzheimer’s disease, Dementia with Lewy bodies and Fronto-temporal Dementia.
Dementia is a substantial cause of morbidity with 10% of over 65s affected and 20% of over 80s affected. There are numerous causes for dementia, the most common of which are Alzheimer’s Disease, Dementia with Lewy Bodies and vascular dementia.
Describe Alzheimer’s
Commonest cause of dementia, accounting for 65% of dementia cases – and is present in 47% over age 85. 2:1 female predominance
It is seen as an exaggerated ageing process and presents with a progressive memory loss, various aphasias, apraxia, agnosia, behavioural changes (e.g. agitation, aggression or wander) or depression.
The course is progressive over several years, with death resulting in an extreme state of cognitive decline. Prognosis is 5 years (but variable between 10 and 20 years).
It presents with neurofibrillary tangles and senile plaques. The neurofibrillary tangles are intracellular twisted filaments of the Tau protein; the Tau protein normally binds to and stabilises the microtubules in the cell yet in AD, they become hyperphosphorylated and very stable, producing the neurofibrillatory tangles. The senile plaques are foci of enlarged axons, synaptic terminals and dendrites, with amyloid deposition in the vessels in the centre of the plaque; the amyloid proteins appear to form as a result of upregulation of amyloid precursor protein and mutation to the enzymes which normally break down the amyloid proteins (both genes found on Chromosome 21).
Describe DLB
DLB occurs for 4-10%of dementia cases, M=F and is characterised by fluctuation in cognition, especially in attention and alertness; memory loss may not occur in the early stages. There are Cortical Lewy Bodies seen at autopsy (similar to those seen in Parkinson’s Disease), which are a hallmark of DLB. It is a synucleinopathy.
Associated with Parkinsonism (particularly if lewy bodies in basal ganglia).
Lewy bodies may begin in the basal ganglia or the cortex but progresses to the other site as the disease progresses
Prominent visual hallucinations
Delusions and paranoia
Fluctuates in severity from day to day
REM sleep behaviour disorder (no muscle atonia so act out very violent dreams – can injure themselves or sleeping partner)
Sensitive to haloperidol (antipsychotic) – problem in misdiagnosis, causes them to become rigid and can lead to death.
As it progresses, it starts to resemble AD with worsening movement difficulties, problems with speech and swallowing, challenging behaviour.
Prognosis – eight years after the first symptoms
DLB usually has a much more rapid onset of symptoms than AD.
What is meant by Le Fort’s Fractures?
Head trauma can vary from a simple fracture of the nose to a condition, which causes a patient to die overnight in ITU.
Three common fractures, caused for example by a fist tight, are fractures of the nose, of the zygomatic arch and of the mandible.
Each of these fractures needs prompt treatment and can give rise to a sensory deficit.
More serious fractures involving the whole face arise from road traffic accidents. The facial bones fracture in 3 different patterns depending upon the severity of the trauma. These are called Le Fort’s Fractures
- Le Fort I (horizontal maxillary fracture): a fracture of the maxilla just above the teeth which remain in the detached portion of the bone
- Le Fort II – the body of the maxilla is separated from the facial skeleton with a horizontal fracture through the nose and vertical fractures from the floor of the orbit
- Le Fort III: a horizontal fracture through the top of the nose, the sphenoid bone and the fronto-zygomatic sutures and zygomatic arches. The maxilla and other bones of the face are entirely separated from the cranium.
