S8 Higher cortical function Flashcards

1
Q

describe the fine structure of the cortex

A

most inputs are from the thalamus and other cortical areas
most outputs are from pyramidal cells and project to widespread areas
information is processed in the complex synaptic network found between inputs and outputs

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2
Q

what is the frontal lobe responsible for ?

A

motor control (pre-central gyrus)
Expression of speech (usually left hemisphere)
Behavioural regulation
Cognition - higher thought e.g mental arithmetic
Eye movements thought corticonuclear projections
Continence - at the medial part of FL as this is where motor homunculus of genitalia reside

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3
Q

what is the parietal lobe responsible for ?

A

sensory (postcentral gyrus)
Comprehension of speech (usually left hemisphere)
Body image (usually right) - if this is affected, they fail to recognise that the left half of the world exists eg can’t see half the TV (hemispatial neglect)
awareness of the external environment (attention)
calculation and writing
visual pathways (superior optic radiations ) project through white matter

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4
Q

what is the temporal lobe responsible for ?

A
Hearing
Olfaction
Memory
Emotion
Visual pathways projecting through white matter (inferior optic radiations)
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5
Q

what is cerebral dominance ?

A
idea that certain functions are overrepresented in one hemisphere over the other
Sequential processing (left hemisphere) : language, mathematics so trouble speaking may be a left hemisphere lesion 
'Whole picture' processing (right hemisphere) : Body image, visuospatial awareness, emotion and music
Left hemisphere is dominant in 95% of people
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6
Q

describe the language pathways in the brain

A

primarily in left hemisphere
Broca’s area (inferior lateral frontal lobe) - production of speech
Wernicke’s area (superior temporal lobe) - interpretation of language
they are connected to each other via the arcuate fasciculus, white matter pathway and flow of info is W–> B

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7
Q

describe the pathway for repeating a heard word

A

Auditory cortex in temporal lobe is where we first hear sound
Axons go from Auditory cortex to WA which works out what these patterns of impluse mean
WA projects along the arcuate fasciculus to BA which communicates with the motor cortex, driving the muscles to produce speech

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8
Q

describe the pathway for speaking a written word

A

from visual cortex in occipital lobe, information is projected to WA, then via arcuate fasciculus to BA which instructs the motor cortex to contract muscles for speech

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9
Q

describe the pathway for speaking a thought

A

input of thought from all over the cortex projects to WA then via arcuate fasciculus to BA, which instructs the motor cortex to contract muscles for speech

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10
Q

what is wernickes aphasia ?

A

Fluent speech ( BA working fine) but doesn’t make sense as a patient cannot understand what has been asked due to WA

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11
Q

what is broca’s aphasia

A

patient can understand what has been said as WA is fine but cannot speak fluently due to BA

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12
Q

describe how memory is stored in the brain

A

two types ; declarative - for explicit memories and facts, stored in cerebral cortex non-declarative - for implicit memories, motor skills and emotions stored in the cerebellum
memories are thought to be stored in a relatively distributed fashion throughout the brain
consolidation is the change from short to long term memory
the hippocampus is crucial for consolidating declarative memories. It strengthens synapses within the cortex, makes it release more transmitters and forms more receptors on postsynaptic neurones

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13
Q

define arousal

A

emotional state associated with a goal or avoidance of something noxious

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14
Q

define consciousness

A

awareness of the external world and internal states

consciousness involves the cerebral cortex and reticular formation (+ feedback loop)

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15
Q

describe reticular formation

A

a population of specialised interneurons in the brainstem
sends excitatory axons up the cortex
has numerous excitatory inputs which regulate the level of arousal ; sensory system and cortex
has widespread outputs (ascending fibres)
Thalamus (sensory gating ) - third output, sends excitatory projections up to cortex via glutamate
Hypothalamus - Second output, sends excitatory projections up to the cortex via histamine
Basal forebrain nuclei - first relay station, sends excitatory projections up to cortex via ACh
Spinal cord (muscle tone)
reticular activating system is responsible for arousal

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16
Q

what is glasgow coma scaled used for ?

A

looks at eye movements, motor response and verbal response - lower score indicates more severe damage

17
Q

what is an electroencephalogram

A

measures activity of neurones in the cortex

deprived of sensory input and neurones in the brain tend to fire synchronously

18
Q

describe the stages of sleep with regards to the EEG ?

A

during the night, you pass through 6 cycles of sleep, progressing from an awake state down to stage 4 and then going from stage 4 rapidly up into REM sleep. Going down through the 4 stages, the EEG shows decreasing frequency and increasing amplitude as neuronal populations in the cortex become synchronous
Awake - beta waves eyes open 50Hz
eyes closed - when brain is deprived of input, waves go into synchrony , alpha waves 10 Hz
Stage 1 (sleep) - theta waves, 5Hz
S 2/3 - background of theta waves with sleep spindles within it and K - complex’s
S4 - delta waves, 1 Hz
REM sleep - similar to beta waves and this is when we dream

19
Q

what is the neural mechanism of sleep

A

involves deactivating the reticular activating system and thus cortex and inhibiting the thalamus. The + feedback loop between RAS and cortex is inhibited leading to the decreased cortical activity. Inhibition of the positive feedback loop is assisted by the removal of sensory inputs (e.g turning off lights before sleep)

20
Q

describe the paradox of REM sleep

A

initiated by neurones in the pons
the eeg activity is similar during arousal (beta waves) but difficult to rouse due to strong inhibition of thalamus.
Muscle tone is lost due to descending inhibition of LMNS by glycinergic fibres arising from the reticular formation and running down the reticulospinal tracts
eye movements are preserved.
autonomic effects are seen including penile erection and loss of thermoregulation

21
Q

what are the functions of sleep

A

energy conservation
memory consolidation
clearance of extracellular debris

22
Q

what are some disorders of sleep

A

insomnia, narcolepsy ( cant regulate sleep-wake cycles; becomes sleepy during the day), sleep apnoea (difficulty breathing)

23
Q

what are some disorders of consciousness ?

A

Brain death - cortical and brainstem damage
Coma - cortical and brainstem damage. Unarousable and unresponsive to stimuli. No sleep-wake cycle detectable
PVS - widespread cortical damage like coma but with some spontaneous eye opening. Sleep - wake cycle detectable
Locked in syndrome - basilar/ pontine artery occlusion. eye movements can be preserved but all other somatic motor functions lost from the pons down

24
Q

how can pathogens gain entry to the CNS

A

via direct spread (e.g middle ear infections), blood-borne infections (e.g sepsis) or iatrogernic (e.g surgery)

25
Q

what is meningitis

A

inflammation of the leptomeninges (pia and arachnoid, not dura meter)
presents with headache, neck stiffness and a fever
causative organisms (from 0-30 years) : E. coli, H. influenza, N . meningitides, S. pneumoniae
Chronic meningitis can occur, caused by M Tuberculosis, there is granulomatous inflammation, fibrosis of the meninges and nerve entrapment
Complications: death, cerebral infarctions and cerebral abscesses

26
Q

what is encephalitis ?

A

viral inflammation of the brain parenchyma
pathogen causes the entire brain tissue to swell causing a neuronal cell death
causative organisms : HSC, polio and rabies

27
Q

describe prion diseases of the brain

A

result of mutated prion proteins (PrP)
prion proteins are normal constituents of neuronal synapses
Mutation to the PrPs occurs by sporadic, familial or ingested mutations
Mutated PrPs which interact with normal PrPs undergo post-translational conformational changes causing aggregations of PrPs
PrPs aggregate and causing neuronal death and holes in the grey matter
produce spongiform encephalopathies and can be seen in vCJD (Variant Creutzfeldt-Jakob disease)

28
Q

what is dementia

A

alzheimers, vascular, lewy body and picks disease
Alzheimers : get loss of cortical neurones and increased neuronal damage causing :
Neurofibrillary tangles : tau which normally stabilises microtubules becomes hyperphosphorylated
Senile plaques : amyloid deposition in vessels (can lead to downs syndrome)

29
Q

what is the normal range of ICP

A

normal ICP 0-10 mmhg
usually icp maintained by reducing blood or CSF volume
cerebral blood flow maintained below ICP of 60mmhg

30
Q

describe the clinical significance of raised ICP

A

can get from expanding lesions, SOL (e.g tumours haematomas), this shall compress and damage tissue around the lesion, displace midline structures and cause herniation
cushings reflex occurs in response to RICP which results in increased BP, reduced HR and irregular respiration

31
Q

what is herniation

A

protrusion of an organ through wall that normally contains

3 types subfalcine uncal and tonsillar

32
Q

what is subfalcine herniation

A

herniation the same side as the mass. cingulate gyrus pushed under the free edge of falx cerebri. Get ischaemia in the medial parts of the parietal and frontal lobe and to the corpus callosum due to resultant compression of the anterior cerebral artery leading to infarction

33
Q

what is uncal herniation

A

uncus herniates through the tentorial notch. Damage to oculomotor nerve on the same side. Occlusion of blood flow in posterior cerebral and superior cerebellar arteries. Fatal because of secondary haemorrhage into the brainstem - duret haemorrhage

34
Q

what is tonsillar herniation

A

cerebellar tonsils pushed into the foramen magnum compressing the brainstem

35
Q

describe tumours affecting the neurosystem

A

benign tumours are commonly meningeal origin (meningioma)
Malignant tumours are commonly astrocyte origin (astrocytoma)
most tumours are metastasis from another area of the body

36
Q

describe stroke with regards to neuropathology

A

disturbance of CNS function due to vascular disease
can either be cerebral infarction or cerebral haemorrhage
risk factors: hypertension, hyperlipidaemia and diabetes mellitus
pathogenesis : usually from an embolism, can also be from thrombosis

37
Q

what types of infarct can affect the neurosystem

A

regional or lacuna (associated with hypertension, affects basal ganglia )

38
Q

describe cerebral haemorrhages

A

spontaneous, can be intracerebral or subarachnoid
intracerebral : associated with hypertensice vessel damage causes SOL –> RICP
subarachnoid haemorrhage : from rupture of berry aneurysm, occurs at branching points in circle of willis, get sudden headache and loss of consciousness