S8: cerebral cortex and consciousness

Question 1

Describe the cerebral cortex

Answer 1

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)

Question 2

Describe the functions of the frontal lobe, with effects of damage

Answer 2

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

Question 3

Describe the functions of the parietal lobe, with effects of damage

Answer 3

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)

Question 4

Describe the functions of the temporal lobe, with effects of damage

Answer 4

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)

Question 5

Describe cerebral ‘dominance’

Answer 5

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

Question 6

Describe Broca’s area

Answer 6

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

Question 7

Describe Wernicke’s area

Answer 7

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

Question 8

What happens in large middle cerebral artery infarcts?

Answer 8

Can cause a dense/global aphasia where both areas are destroyed leading to virtually no verbal language function

Question 9

What is the arcuate fasciculus?

Answer 9

Connects Broca’s and Wernicke’s areas

Damage can cause the inability to repeat heard words

Question 10

Compare declarative and nondeclarative memories

Answer 10

Declarative – factual information, tends to be stored in cerebral cortex
Nondeclarative – motor skills, emotion, tends to be stored in subcortical structures and cerebellum

Question 11

Compare short term and long term memory

Answer 11

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

Question 12

List factors influencing consolidation

Answer 12

Emotional context
Rehearsal
Association

Question 13

Describe the function of the hippocampus

Answer 13

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)

Question 14

Describe long term potentiation

Answer 14

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

Question 15

Define consciousness and arousal

Answer 15

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

Question 16

Describe the role of the cerebral cortex and reticular formation in consciousness

Answer 16

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

Question 17

Describe the outputs from the reticular formation to the cortex

Answer 17

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

Question 18

What is the GCS?

Answer 18

Clinical assessment of consciousness 
Three components, looking for best response in each:
1) Eye opening 
2) Motor response 
3) Verbal response

Question 19

Describe the difference between the flexor and extensor response to pain

Answer 19

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

Question 20

What is an electroencephalogram?

Answer 20

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

Question 21

List functions of sleep

Answer 21

Energy conservation/repair
Memory consolidation
Clearance of extracellular debris
‘resetting’ of the CNS

Question 22

Outline the stages of sleep on an EEG

Answer 22

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

Question 23

Outline the neural mechanism of non-REM sleep

Answer 23

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

Question 24

Describe REM sleep

Answer 24

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

Question 25

Describe common sleep disorders

Answer 25

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

Question 26

List causes of raised ICP

Answer 26

Haematoma/haemorrhages 
Tumours 
Space occupying lesions 
Cerebral oedema 
Infections

Question 27

What is a subfalcine herniation?

Answer 27

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

Question 28

Describe trans-tentorial herniation

Answer 28

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

Question 29

What is a tonsillar herniation?

Answer 29

Cerebellar tonsils pushed into foramen magnum

Compresses the brainstem

Question 30

Describe extradural haemorrhage

Answer 30

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)

Question 31

Describe subdural haematoma

Answer 31

Shearing of bridging veins
Accumulation between the dura mater and arachnoid mater
Acute: traumatic, rapid blood accumulation
Chronic: elderly and chronic alcoholics

Question 32

Describe subarachnoid haemorrhage

Answer 32

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

Question 33

Describe strokes

Answer 33

Sudden event producing a disturbance of CNS function due to vascular disease
Two different types: ischaemic & haemorrhagic
Risk factors: hyperlipidaemia, hypertension, diabetes mellitus etc

Question 34

Describe ischaemic stroke

Answer 34

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)

Question 35

Describe embolic occlusion causing stroke

Answer 35

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

Question 36

Describe thrombotic occlusion causing stroke

Answer 36

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

Question 37

Describe spontaneous intracerebral haemorrhage

Answer 37

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

Question 38

Describe cerebral amyloid angiopathy

Answer 38

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

Question 39

Describe arteriovenous and cavernous malformations

Answer 39

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

Question 40

List examples of CNS tumours and symptoms

Answer 40

Primary: gliomas, parenchymal, meningeal, neuronal & poorly differentiated
Secondary: metastatic
Symptoms: seizures, headaches, focal neurological deficits, raised ICP

Question 41

Describe meningitis

Answer 41

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

Question 42

Describe encephalitis

Answer 42

Infection of brain parenchyma
Viral > bacterial
Neurones death by viruses (inclusion bodies)
Examples: temporal lobe – HZV, spinal cord MN – polio, brainstem – rabies

Question 43

Describe prion diseases

Answer 43

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

Question 44

Compare Creutzfeldt-Jakob and variant Creutzfeldt-Jakob disease

Answer 44

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

Question 45

Describe Alzheimer’s disease

Answer 45

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

Question 46

Describe Huntington’s disease

Answer 46

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