Session 8 Flashcards
Describe the fine structure of the cerebral cortex
Arranged as 6 layers containing cell bodies and dendrites (i.e. cortex is grey mater)
Most outputs from the cortex are the axons of pyramidal neurones (e.g. upper motor neurones in the primary motor cortex are pyramidal neurones)
Outputs can be projection fibres going down to brainstem and cord (e.g. upper motor neurones)
Outputs can be commissural fibres going between hemispheres (e.g. corpus callosum)
Outputs can be association fibres connecting nearby regions of cortex in the same hemisphere (e.g. arcuate fasciculus)
Most inputs are from thalamus and other cortical areas - An important population of inputs arise from the reticular formation, maintaining cortical activation (consciousness)
Interneurones connect inputs and outputs in a complex way, giving rise to behaviour, emotion, memory etc.
What are the frontal lobe functions and how might these be affected with cortical damage?
Frontal lobe functions, with effects of cortical damage
o Motor
- Primary motor cortex and associated areas are here
- Frontal lobe damage can result in contralateral weakness
o Expression of speech (usually left hemisphere)
- Broca’s area is here
- Damage to left frontal lobe can result in expressive dysphasia
o Behavioural regulation / judgement
- Prefrontal cortex etc. is here
- Damage to frontal lobes can lead to (usually) impulsive, disinhibited behaviours e.g. sexual inappropriateness, aggression
o Cognition
- Prefrontal cortex etc.
- Frontal lobe damage (particularly the right) can cause difficulty with tasks such as complex problem solving, including calculation
o Eye movements
- Contain the frontal eye fields
- Damage can cause problems with conjugate gaze and other eye movement disturbances (however, diplopia without other cortical features would suggest brainstem/cranial nerve problem)
o Continence
- Contain cortical areas responsible for maintenance of continence (e.g. paracentral lobules)
- Damage can cause urinary incontinence
What are the functions of the parietal lobe and the effects of cortical damage there?
o Sensory
- Contains primary sensory cortex and associated areas
- Damage might result in contralateral anaesthesia affecting all modalities (modalities converge at the cortex)
o Comprehension of speech
- Contains part of Wernicke’s area
- Damage to left parietal lobe can cause a receptive dysphasia
o Body image and awareness of external environment
- Seems to be involved with acknowledgement that things (including the body) exist
- Damage to right parietal lobe can lead to neglect.
o Calculation and writing
- Works with frontal lobe to perform these tasks
Damage to left parietal lobe can affect calculation ability (but maybe also frontal lobe)
o Although not a cortical function, remember that the superior optic radiation projects through the parietal lobe
- Damage here can cause a contralateral inferior homonymous quadrantanopia
What are the functions of the temporal lobe and what would be the effects of cortical damage?
o Hearing
Primary auditory cortex sits on superior surface of temporal lobe, near to Wernicke’s area
Damage can lead to a number of complex effects on hearing which are not the remit of
the unit. Auditory hallucinations may be a feature of temporal lobe lesions
o Olfaction
Primary olfactory cortex sits on the inferomedial aspect of the temporal lobe
Damage can lead to a number of complex effects on smell which are not the remit of the unit.
Olfactory hallucinations may be a feature of temporal lobe lesions
o Memory
The hippocampus is a crucial structure for consolidating declarative memories
Damage may lead to amnesia (but remember that there are two hippocampi, one in each temporal lobe). Also, some pathologies such as temporal lobe epilepsy can trigger memories, leading to a feeling of deja vu
o Emotion
Temporal lobes contain a number of limbic system structures such as the hippocampus and amygdala
Effects of lesions are complex, but may be related to pathogenesis of some psychiatric disorders
o Although not a cortical function, remember that the inferior optic radiation projects through the temporal lobe
Damage here can cause a contralateral superior homonymous quadrantanopia
What is cerebral dominance?
o Some functions are represented more prominently in one hemisphere
In 95% of people, the left hemisphere is dominant for language and mathematical/logical functions
In 95% of people the right hemisphere is dominant for body image, visuospatial awareness, emotion and musical ability
o Knowledge of cerebral dominance allows us to predict the effects of lobe lesions (e.g. a dysphasia is likely to have arisen from left hemisphere damage)
o The corpus callosum allows the two hemispheres to communicate with one another, meaning we can be thought of as an ‘average’ of the two hemispheres
Destruction of the corpus callosum can cause some interesting deficits such as alien hand syndrome and subtle effects on language processing
What is Broca’s area and what does it do?
In the infero-lateral frontal lobe
Sits near to mouth/pharynx area of primary motor cortex
Responsible for the production of speech
Damage can cause staccato speech, where the patient still understands what is being said to them (Broca’s / expressive dysphasia)
What is Wernicke’s area and what does it do?
At the parieto-temporal junction
Sits near to primary auditory cortex in temporal lobe
Responsible for the comprehension of speech
Damage can cause fluent, nonsensical speech where the patient does not appear to understand what is being said to them (Broca’s / receptive dysphasia)
How can middle cerebral artery infarcts affect verbal language fucntion?
Large middle cerebral artery infarcts can cause am dense / global aphasia where both areas are destroyed leading to virtually no verbal language function
How are Broca’s and Wernicke’s areas connected?
Broca’s and Wernicke’s areas are connected by the arcuate fasciculus
Damage to this white matter pathway can cause the inability to repeat heard words
What are the types of memory and how is memory stored in the brain?
o Memories are believed to be stored across wide areas of the brain
o Types of memory:
Declarative / explicit
Factual information
Tends to be stored in cerebral cortex
Nondeclarative / implicit
Motor skills
Emotion
Tends to be stored in subcortical structures (e.g. basal ganglia) and cerebellum
Short term memory
Stored for seconds to minutes as a ‘reverberation’ or ‘echo’ in cortical circuits
Long term memory
Stored for very long periods in the cerebral cortex, cerebellum etc. (up to a lifetime) following consolidation
What is memory consolidation?
Converting short term memories into long term memories
Factors influencing consolidation:
o Emotional context (if an event has strong emotional content, then it tends to be remembered better)
o Rehearsal (you are all familiar with this idea)
o Association (if you can associate a piece of knowledge with something you already know it tends to be more easily remembered)
The hippocampus helps to consolidate declarative memories
The hippocampus sits deep in the temporal lobe (in fact, it is the rolled medial edge of the temporal lobe)
It has multimodal inputs from many brain systems (making it good at associating stimuli) It has a role as an ‘oscillator’, facilitating consolidation of memories in the cortex via its output pathways (primarily the fornix⇒ mammillary bodies⇒ thalamus⇒cortex)
Long term potentiation (LTP) is the key molecular mechanism of memory consolidation
What is long term potentiation (LTP) of memories?
Long term potentiation (LTP) is the key molecular mechanism of memory consolidation
Causes changes in glutamate receptors in synapses leading to synaptic strengthening
New physical connections can also form between neurones to further strengthen connections (axonal sprouting)
What is consciousness?
o A very slippery concept
o Related to awareness of external environment and internal states
o Arousal is a related concept which is associated with goal-seeking behaviour and avoidance of noxious stimuli
What are the two neural components required for consciousness?
Consciousness requires two neural components to be functioning normally, and connected to each other
o Cerebral cortex – the site where conscious thoughts arise -Receives many inputs, including from the reticular formation
o Reticular formation (particularly the reticular activating system in the brainstem) – the circuitry that keeps the cortex ‘awake’ - Receives many inputs, including from the cortex and sensory systems
o Cortex and reticular formation are connected by reciprocal excitatory projections, forming a positive feedback loop - Positive feedback loops are seen when there is a binary outcome (e.g. sleep/awake, ovulating/not ovulating etc)
Describe outputs from the reticular formation to the cortex
o Occurs via three major relay nuclei
o Reticular formation sends cholinergic (excitatory) projections to these relays
- Basal forebrain nuclei send excitatory cholinergic fibres to cortex (think sedative side effects of anticholinergics)
- The hypothalamus sends excitatory histaminergic fibres to the cortex (think sedative side-effects of sedating antihistamines)
- The thalamus sends excitatory glutamatergic fibres to the cortex
o The reticular formation also sends projections down the cord, responsible for maintaining muscle tone
How is consciousness assessed clinically?
Glasgow Coma Scale
Four components, looking for best response in each
• Eye opening
o Spontaneous eye opening (4) suggests normal cortical and brainstem function
o Response to speech (3) suggests slightly diminished cortical function but still functioning brainstem
o Response to pain (2) suggests impaired cortical function but brainstem preserved so that reflex opening can occur
o No response (1) suggests severe damage to brainstem +/- cortex
• Motor response
o Obeys commands (6) suggests normal function with working connections from auditory system to brainstem/cord
o Localises to stimuli (5) suggests diminished higher cortical function but still connections working from sensory to motor cortex
o Withdraws to pain (4) suggests that there is still a ‘physiological’ reflex response to stimuli
o Flexor response to pain (3) suggests a lesion above the level of the red nuclei. This response is still ‘semiphysiological’
o Extensor response to pain (2) suggests a lesion below the red nuclei. This response is not physiological at all
o No response to pain (1) suggests severe damage to brainstem +/- cortex
• Verbal response
o Oriented in time/place (5) suggests normal cortical function
o Confused conversation (4) suggests diminished higher cortical function but language centres are still functioning adequately
o Inappropriate words (3) suggests language centres have been damaged
o Incomprehensible sounds (2) suggests cortical damage with brainstem mediated groans
o No response (1) suggests severe damage to brainstem +/- cortex
What is an electroencephalogram
o Measures the combined activity of thousands of neurones in a particular region of cortex
o High temporal resolution, low spatial resolution
o Good for detecting neuronal synchrony (a phenomenon which occurs commonly in the brain during both physiological and pathological processes such as sleep and epilepsy), and evidence of normal cerebral function
What are the functions of sleep?
Generally unknown
Energy conservation / repair?
Memory consolidation?
Clearance of extracellular debris?
‘Resetting’ of the CNS?
What are the stages of sleep?
4 major stages + rapid eye movement (REM) sleep
Typically pass through around 6 cycles of sleep per night
Stages are characterised by typical EEG pattersn
• Awake with eyes open
o Beta waves – irregular, 50Hz
• Awake with eyes closed
o Alpha waves – regular, 10Hz
• Stage 1 sleep
o Background of alpha + interspersed theta waves (theta at around 5Hz, regular)
• Stages 2/3 sleep
o Background of theta + interspersed sleep spindles and k-complexes:
- Sleep spindles are high frequency bursts arising from the thalamus
- K-complexes represent the emergence of the ‘intrinsic rate’ of the cortex
• Stage 4 sleep
o Delta waves – regular, 1Hz
- Related to k-complexes seen in stages 2/3
• REM sleep
o EEG similar to beta waves
o Dreaming occurs in this stage, so similar to the EEG in a conscious patient
Describe the neural mechanism of non-REM sleep?
Complex
Deactivation of the reticular activating system (and hence cortex) + inhibition of the thalamus
This deactivation is facilitated by removal of sensory inputs (fewer positive influences on positive feedback loop)
Describe the neural mechanism of REM sleep
Initiated by neurones in the pons (i.e. initiation appears to be an active process)
Similar EEG to when awake with eyes open (beta waves), but difficult to rouse due to strong thalamic inhibition
Decreased muscle tone due to glycinergic inhibition of lower motor neurones
Eye movements and some other cranial nerve functions can be preserved (e.g. teeth grinding)
Autonomic effects are seen (e.g. penile erection, loss of thermoregulation)
Essential for life – long term deprivation leads to death
What is insomnia?
Habitual sleeplessness; inability to sleep.
Commonly caused by underlying psychiatric disorder as opposed to ‘primary’ insomnia
What is narcolepsy?
Condition characterized by an extreme tendency to fall asleep whenever in relaxing surroundings.
- Rare disorder
- Some cases are caused by mutations in the orexin gene. Orexin is a peptide transmitter involved in sleep
What is sleep apnoea ?
Potentially serious sleep disorder in which breathing repeatedly stops and starts.
- Common condition, often caused by excess neck fat leading to compression of airways during sleep and frequent waking
- Causes excessive daytime sleepiness
