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Sem 5 > NS 11: Higher functions of the brain > Flashcards

NS 11: Higher functions of the brain Flashcards

1
Q

define amnesia

A

inability to remember (due to pathology)

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2
Q

what is anterograde amnesia?

A

inability to form new memories following an accident, as some fault in consolidation of new experience into long term memory. Often assoc. with temporal lobe damage, part. hippocampal gyrus.

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3
Q

what is retrograde amnesia?

A

inability to recall events that occurred before some precipitating event e.g. car crash. Failure of LT memory. These memories distributed throughout cerebral cortex so condition may follow generalised lesions e.g. Alzheimer’s disease.

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4
Q

what are the cortical association areas?

A

parts of cerebral cortex that do not have a primary motor or sensory role, but instead are involved in higher order processing of sensory info necessary for perception and movement initiation.
information brought together from different modalities

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5
Q

what might a focal lesion in the supplementary motor area result in?

A

motor apraxia= inability to perform a purposive movement even though no paralysis exists, as area involved in motor planning, organising complex movements, thinking about the movement.
motor apraxia may also occur with premotor or parietal association area lesions.

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6
Q

how is SA of cerebral cortex increased?

A

convoluted structure

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7
Q

the cerebral cortex can be divided into 6 layers structurally, what are the functions of these?

A

layers 1-3= output to other cortical assoc areas, so send info across brain-either along same hemisphere or acrosss.
4th= receives input from motor and sensory cortices, thalamus and brainstem
5 and 6= output to hippocampus, basal ganglia, cerebellum and thalamus

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8
Q

functions of association areas of frontal lobes?

A

intelligence-higher intellect, understanding, language, personality, social conduct, mood

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9
Q

functions of association areas of dominant parietal lobe- angular gyrus*?

A

language- names of objects, calculation-mathematics

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10
Q

functions of association areas of non-dominant parietal lobe?

A

visiospatial functions e.g. spaces and shapes

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11
Q

disorders associated with lesions of parietal association areas?

A

asterognosis-can’t recognise objects on tactile stimulation, and the neglect syndrome

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12
Q

what happens in neglect syndrome?

A

patient fails to recognise contralateral body side and its surroundings e.g. damage in right hemisphere parietal association area will cause patient to not bathe left sidde of body, will not eat food on left side of food tray as doesn’t exist in mind of patient.

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13
Q

functions of association areas of temporal lobe?

A

memory, language

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14
Q

functions of association areas of occipital lobe?

A

vision

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15
Q

will aphasia be fluent or non fluent if damage to wernicke’s area?

A

fluent- *input, receptive dysphasia, problem with language understanding and formulation, but not word production.

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16
Q

symptoms/signs of frontal lobe lesions?

A

CL paralysis/paresis: lower face, U and L limbs, Babinski response= M1 area
motor apraxia- can’t perform purposeful movements despite no muscle paralysis- premotor area and SMA damage
nonfluent expressive dysphasia- Broca’s area
poor concentration, easily distracted, personality changes
perseveration- repetition of a particular response, unable to change how you do something so can’t learn new tasks

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17
Q

symptoms/signs of parietal lobe lesions?

A

CL anaesthesia- damage S1
tactile and visual agnosia, visual disorientation, neglect of CL self and surroundings
attention defecits

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18
Q

symptoms/signs of temporal lobe lesions?

A

decrease in hearing and ability to localise sounds, both CL
fluent aphasia, receptive- Wernicke’s area
memory impairment of past events= retrograde
prosopagnosia= can’t recognise faces
antergrade amnesia
anosmia= recognition defecits

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19
Q

symptoms/signs of occipital lobe lesions?

A

CL homonymous hemianopia

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20
Q

appearance on CT of cerebral cortex in patient with Alzheimer’s?

A

significant atrophy

global lesion*

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21
Q

what is the dominant hemisphere?

A

the hemisphere that contains centers for language comprehension and production, usually the left (95% of people.)

22
Q

what does lateralisation of function refer to?

A

higher functions e.g. analytical thinking, language comprehension and production of emotional thinking are centered more in 1 cerebral hemisphere than the other.

23
Q

functions centered in dominant cerebral hemisphere (usually left)?

A 
Language: spoken/heard
written/read
gestured/seen
Maths
Logic
Motor skills 
(handedness)

so hemisphere processes info. in sequence e.g. language

24
Q

functions centered in non dominant cerebral hemisphere (usually right)?

A 
Emotion of language
Music/art- drawing and composing
Visiospatial
Body awareness
recognition of faces

hemisphere looks at the whole picture e.g. spatial awareness

25
Q

pathway for speaking a heard word?

A

primary auditory area- hear word
wernicke’s area via arcuate fasciculus- interpret word
broca’s area- word production
motor cortex- stimulate muscle of speech

26
Q

overall anatomical location in cerebral cortex where language is mainly represented?

A

cortical areas bordering the lateral fissure of the dominant hemisphere
=Broca and Wernicke areas

27
Q

pathway for speaking a written word?

A

visual input, then from visual association areas to left angular gyrus where objects recognised and named
Wernicke’s area- words put into sentences, to Broca’s area via arcuate fasciculus
broca’s- motor programs from here projected to motor cortex- elicits speech.

28
Q

characterisitcs of wernicke’s aphasia?

A

receptive/sensory aphasia
fluent- word production normal, but use of words defective, speak jargon
patient cannot comprehend language- whether heard, read or spoken- and cannot write (agraphia).
loss of mathematical skills

29
Q

what is a conduction aphasia?

A

lesion interrupts association fibres in arcuate and superior longitudinal fasciculi that allows wernicke area to project into broca area.
speech deficiency similar to receptive aphasia but as comprehension intact, patient makes repeated attempts to say the right words.
also impairment in naming objects and pictures.

30
Q

characteristics of broca’s aphasia?

A

expressive/motor
nonfluent- slow and prolonged output of words, poor articulation
poorly constructed sentences, disjointed speech
can’t get words out but can understand what is being said

may still be able to sing as music production associated with non-dominant hemisphere.

31
Q

what is global aphasia?

A

loss of language almost complete
combines defecits seen in broca, wernicke and conduction
accompanied by paralysis of right lower facial muscles and right UL
results from massive lesion caused by occlusion of middle cerebral artery

32
Q

what is declarative memory?

A

key facts- concerned with naming objects, remembering events, recognition of places
assessed consciously, rapidly learned but also rapidly forgotten

33
Q

regions of cerebral cortex associated with declarative memory?

A

hippocampus and widespread regions of cerebral cortex

34
Q

what is procedural memory?

A

being able to perform motor skills e.g. riding a bike, learnt and perfected by practice
memories difficult to form but once formed are long lasting and can be performed without conscious recollection.

35
Q

brain areas associated with procedural memory?

A

basal ganglia, cerebellum, pre-motor cortex

36
Q

what factors contribute to ST memories becoming LT memories?

A

emotion
rehearsal
association
automatic memory

physical changes occur in synaptic connections- brain plasticity

37
Q

how does memory formation take place?

A

senses to cortical sensory areas, to amygdala nd hippocampus, to diencephalon, basal forebrain and pre-frontal cortex, which also connect with cortical sensory areas

amygdala= part of limbic system
pre-frontal cortex= can link diff parts of same memory together e.g. what you heard, saw, smelt, so remember all parts of event together.

38
Q

NT essential for long term potentiation of memories?

A

glutamate- acts on NMDA receptors

LT potentiation= allows formation of memories

39
Q

what is long term depression in terms of memories?

A

weakening of infrequently used synapses

40
Q

type of amnesia that occurs with destruction of hippocampus?

A

anterograde amnesia= inability to form new memories

hippocampus= necessary for LT potentiaition- this also requires excitatory NT glutamate- acting on NMDA receptors.

41
Q

type of amnesia that occurs in Alzheimer’s?

A

retrograde= can’t retrieve old memories

42
Q

type of amnesia that occurs with TIAs?

A

transient global

43
Q

various causes of amnesia?

A 
vitamin B deficiency
alcohol
vascular interruption
tumours
trauma
infections
electric convulsive therapy- used in tment of depression
44
Q

why is taste classified as a higher order function?

A

** dependent on multiple sense e.g. olfaction and sight of food

45
Q

what is the Wada test?

A

can determine which cerebral hemisphere is dominant
Here the patient raises both arms and begins to count. A short acing barbiturate is then injected into one of the carotid arteries. If the injection is made into the carotid artery on the same side as the dominant hemisphere the opposite arm will fall and the counting will stop. If made into the carotid on the other side the contralateral arm will drop but the counting continue. ( as counting mediated by dominant side?*)

46
Q

define senile dementia

A

a clinical syndrome characterised by loss of memory, coupled with cognitive defecit e.g. language, problem solving and impaired social and occupational functioning.

47
Q

Alzheimer’s disease is a form of senile dementia, where neurones are damaged directly, What happens in this disease?

A

= most prevalent form of irreversible senile dementia.
cause=unknown.
disorder can only be confirmed at autopsy by presence of light microscopic changes in brain= abnormal protein deposits, and degeneration of neurones. Amyloid senile plaques form in neuropil and walls of cerebral b.vessels. Neurofibrillary tangles in cytoskeleton of neurones cause cell death, and then remain in EC space afterwards. Amyloid protein= toxic to surrounding structures.
senile plaques most common in temporal and posterior parietal lobes.
thinning of gyri and widening of sulci, plus neuronal death with protein deposits, produces significant brain atrophy.
in prefrontal, posterior parietal and temporal lobes, pyramidal neurones selectively degenerate causing alterations in mood, sleeping patterns, awareness of ext environment and memory.
supra-normal degeneration of cholinergic neurones in basal nucleus of Meynert and noradrenergic neurones in locus ceruleus may contribute to memory impairment and impaired attention. in amygdala, underlie behaviour changes.

48
Q

2nd leading cause of dementia in elderly?

A

cerebrovascular disease

49
Q

how does vascular dementia occur?

A

due to multiple infarcts, with many individuals having underlying hypertensive disorders, which cumulatively result in memory impairment and behavioural abnormalities.
uneven distribution of defecits.
other than hypertension, may be caused by DM, smoking, alcohol and cardiac arrhythmias.

50
Q

subcortical origins of irreversible dementia?

A

Parkinson or Huntington disorders

51
Q

3rd commonest cause of dementia, after alzheimer’s and vascular disease?

A

Lewy body dementia= lewy bodies seen in brainstem and neocortex.
typically fluctuating cognitive impairment, detailed visual hallucinations, and parkinsonism.

Sem 5 (35 decks)

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