S8: cerebral cortex and consciousness Flashcards
Describe the cerebral cortex
Arranged as 6 layers containing cell bodies and dendrites
Outputs: axons of pyramidal neurones
-projection fibres: going down to brainstem and cord
-commissural fibres: going between hemispheres
-association fibres: connect nearby regions of cortex in the same hemisphere
Inputs: thalamus and other cortical areas (reticular formation – maintains consciousness)
Describe the functions of the frontal lobe, with effects of damage
Motor – can result in contralateral weakness
Expression of speech – expressive dysphasia
Behaviour regulation – impulsive & disinhibited behaviours
Cognition – difficulty with tasks such as complex problem solving
Eye movements – conjugate gaze & other eye movement disturbances
Continence – urinary incontinence
Describe the functions of the parietal lobe, with effects of damage
Sensory – contralateral anaesthesia affecting all modalities
Comprehension of speech – receptive dysphasia
Body image and awareness of external environment – neglect
Calculation and writing – affect calculation ability
(NB: contralateral inferior homonymous quadrantanopia as superior optic radiations are in parietal lobe)
Describe the functions of the temporal lobe, with effects of damage
Hearing – number of complex effects on hearing
Olfaction – number of complex effects on smell
Memory – amnesia, trigger memories leading to déjà vu
Emotion – may be related to pathogenesis of some psychiatric disorders
(NB: contralateral superior homonymous quadrantanopia as inferior optic radiations are in temporal lobe)
Describe cerebral ‘dominance’
Left hemisphere – language & mathematical/logical functions
Right hemisphere – body image, visuospatial awareness, emotion & musical ability
Allows us to predict the effects of lobe lesions
Corpus callosum allows the two hemispheres to communicate with one another – destruction can cause alien hand syndrome & subtle effects on language processing
Describe Broca’s area
In the infero-lateral frontal lobe
Sits near to mouth/pharynx of PMC
Responsible for the production of speech
Damage can cause staccato speech, where the patient still understands what is being said to them
Describe Wernicke’s area
At the parieto-temporal junction
Sits near to primary auditory cortex
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
What happens in large middle cerebral artery infarcts?
Can cause a dense/global aphasia where both areas are destroyed leading to virtually no verbal language function
What is the arcuate fasciculus?
Connects Broca’s and Wernicke’s areas
Damage can cause the inability to repeat heard words
Compare declarative and nondeclarative memories
Declarative – factual information, tends to be stored in cerebral cortex
Nondeclarative – motor skills, emotion, tends to be stored in subcortical structures and cerebellum
Compare short term and long term memory
Short term memory – stored for seconds to minutes as reverberation or echo in cortical circuits
Long term memory – stored for very long periods in the cerebral cortex, cerebellum etc. following consolidation
List factors influencing consolidation
Emotional context
Rehearsal
Association
Describe the function of the hippocampus
Helps to consolidate declarative memories
Sits deep in the temporal lobe
Has multimodal inputs from many brain systems
Facilitates consolidation of memories in the cortex via its output pathways (fornix -> mammillary bodies -> thalamus -> cortex)
Describe long term potentiation
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
Define consciousness and arousal
Consciousness: related to awareness of external environment and internal states
Arousal: related concept which is associated with goal-seeking behaviour and avoidance of noxious stimuli
Describe the role of the cerebral cortex and reticular formation in consciousness
Cerebral cortex – the site where conscious thoughts arise (receives many inputs, including from the reticular formation)
Reticular formation – the circuitry that keeps the cortex ‘awake’ (receives many inputs, including from the cortex and sensory systems)
Cortex and reticular formation are connected by reciprocal excitatory projections, forming a positive feedback loop
Describe the outputs from the reticular formation to the cortex
Occurs via three major relay nuclei
Reticular formation sends cholinergic projections to these relays:
1) Basal forebrain nuclei send excitatory cholinergic fibres to cortex
2) Hypothalamus sends excitatory histaminergic fibres to the cortex
3) Thalamus sends excitatory glutamatergic fibres to the cortex
Reticular formation sends projections down the cord for muscle tone
What is the GCS?
Clinical assessment of consciousness Three components, looking for best response in each: 1) Eye opening 2) Motor response 3) Verbal response
Describe the difference between the flexor and extensor response to pain
Flexor response to pain – lesion above the level of the red nuclei, response is still ‘semi-physiological’
Extensor response to pain – lesion below the level of the red nuclei, response is not physiological at all
What is an electroencephalogram?
Measures the combined activity of thousands of neurones in a particular region of cortex
Good for detecting neuronal synchrony -> phenomenon which occurs commonly in the brain during both physiological and pathological processes such as sleep and epilepsy & evidence of normal cerebral function
List functions of sleep
Energy conservation/repair
Memory consolidation
Clearance of extracellular debris
‘resetting’ of the CNS
Outline the stages of sleep on an EEG
Stage 1 sleep – background of alpha + interspersed theta waves
Stage 2/3 sleep – background of theta + interspersed sleep spindles and k-complexes:
-sleep spindles: high frequency bursts arising from the thalamus
-k-complexes: emergency of ‘intrinsic rate’ of the cortex
Stage 4 sleep – delta waves
REM sleep – dreaming occurs in this stage, so like EEG in conscious patient
Outline the neural mechanism of non-REM sleep
Deactivation of the reticular activating system & inhibition of the thalamus
Deactivation is facilitated by removal of sensory inputs -> fewer positive influences on positive feedback loop
Describe REM sleep
Initiated by neurones in the pons, difficult to rouse due to strong thalamic inhibition
Decreased muscle tone due to glycinergic inhibition of LMN
Eye movements & other CN functions can be preserved
Autonomic effects are seen
Essential for life – long term deprivation leads to death
Describe common sleep disorders
Insomnia – commonly caused by underlying psychiatric disorder
Narcolepsy – rare disorder, some cases are caused by mutations in the orexin gene
Sleep apnoea – often caused by excess neck fat leading to compression of airways during sleep and frequent waking
List causes of raised ICP
Haematoma/haemorrhages Tumours Space occupying lesions Cerebral oedema Infections
What is a subfalcine herniation?
Ipsilateral cingulate gyrus down and under the falx cerebri
Ischaemia of medial parts of frontal and parietal lobes and corpus callosum because compression of the anterior cerebral artery
Describe trans-tentorial herniation
Uncus/medial part of the parahippocampal gyrus through the tentorial notch:
-damage to CN 3 on ipsilateral side
-occlusion of the blood flow in posterior cerebral and superior cerebellar arteries resulting in ischaemia
COMMON mode of death
What is a tonsillar herniation?
Cerebellar tonsils pushed into foramen magnum
Compresses the brainstem
Describe extradural haemorrhage
Damage to the middle meningeal artery
Accumulation between dura mater and skull
Commonly associated with trauma: skull fractures, scalp bruises
Presents: lucid interval then signs (drowsiness and neurological deficits)
Describe subdural haematoma
Shearing of bridging veins
Accumulation between the dura mater and arachnoid mater
Acute: traumatic, rapid blood accumulation
Chronic: elderly and chronic alcoholics
Describe subarachnoid haemorrhage
Shearing of meningeal blood vessels
Traumatic: basal skulls fractures, contusions
Spontaneous: ruptured berry aneurysm, amyloid angiopathy, vertebral artery dissection, arteriovenous malformations
Symptoms: sudden onset headache, rapid neurological deterioration, sudden collapse
Describe strokes
Sudden event producing a disturbance of CNS function due to vascular disease
Two different types: ischaemic & haemorrhagic
Risk factors: hyperlipidaemia, hypertension, diabetes mellitus etc
Describe ischaemic stroke
Obstruction of blood supply leads to ischaemia
If there’s collateral blood supply then some overlap and limits damage
Watershed areas – areas that lie at most distal portion of artery territory -> wedge shaped necrosis (seen after hypotensive episode)
Describe embolic occlusion causing stroke
Most common
Cardiac mural thrombus, atherosclerosis
Middle cerebral artery – most affected (direct extension of internal carotid artery)
Emboli lodge in branches and areas where there’s underlying atherosclerosis
Describe thrombotic occlusion causing stroke
Superimposed thrombi overlying atherosclerotic plaque
Common sites – carotid bifurcation, origin of MCA, basilar artery
Fragments can fall off and embolise to distal sites
Lacunar infarcts – small penetrating arteries occluded resulting in small mm infarcts
Describe spontaneous intracerebral haemorrhage
Commonly caused by: hypertension, cerebral amyloid angiopathy, arteriovenous and cavernous malformations, tumours
Common sites affected: basal ganglia, thalamus, pons and cerebellum
Complications: silent to accumulation of haemorrhage resulting in raised ICP, midline shift and compression of adjacent brain parenchyma
Describe cerebral amyloid angiopathy
Advancing age
Amyloid deposition in the walls of small and medium sized meningeal and cortical vessels
Rigid and inflexible and weakens wall
Risk of haemorrhage
Different distribution to hypertensive ICH
Describe arteriovenous and cavernous malformations
Arteriovenous malformations – most common 10-30 years male, subarachnoid vessels to brain/vessels within the brain, wormlike vascular channels
Cavernous malformations – loose vascular channels, distended, thin walled, in cerebellum & pons
List examples of CNS tumours and symptoms
Primary: gliomas, parenchymal, meningeal, neuronal & poorly differentiated
Secondary: metastatic
Symptoms: seizures, headaches, focal neurological deficits, raised ICP
Describe meningitis
Inflammation of leptomeninges
Types: acute pyogenic, aseptic, chronic & carcinomastosis
Symptoms: headache, photophobia, irritability, altered consciousness, stiff neck, focal neurological impairment
Investigations: CT scans, lumbar puncture
Complications: cerebral oedema, cerebral infarction, cerebral abscess/empyema etc
Describe encephalitis
Infection of brain parenchyma
Viral > bacterial
Neurones death by viruses (inclusion bodies)
Examples: temporal lobe – HZV, spinal cord MN – polio, brainstem – rabies
Describe prion diseases
Abnormal cellular protein accumulates
Leads to cell injury: neurone cell death, synapse loss, microvascuolations, lack of inflammation
Sporadic, familial & iatrogenic
Types: Creutzfeldt-Jakob disease, scrapies, mad cow disease
Compare Creutzfeldt-Jakob and variant Creutzfeldt-Jakob disease
Creutzfeldt-Jakob disease - > 70 years, rapidly progressive dementing illness, cerebellar ataxia & global dementia, definitive diagnosis made on post mortem examination
Variant Creutzfeldt-Jakob disease – young adults, slower progression, starts with behavioural issues, prolonged incubation period
Describe Alzheimer’s disease
Sporadic, earlier onset if familial
Amyloid beta plaques and neurofibrillary tangles
Neuronal damage -> loss of neurones, cortical atrophy & shrunken brain
Sign and symptoms: impaired intellectual function, impaired memory, altered mood and behaviour, disorientated
Describe Huntington’s disease
Autosomal dominant
Hyperkinesia – involuntary jerky movements
CAG trinucleate repeat expansion
Mutant protein broken down to intranuclear aggregates of Huntington protein
Cell injury and death, gliosis
