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Principles of Med Neuroscience > L.2.5 > Flashcards

L.2.5 Flashcards

1
Q

What is dementia, and how is it classified (disease or syndrome)?

A
  • Dementia is a syndrome
  • It results from progressive damage to the brain, leading to a decline in multiple higher cognitive functions.
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2
Q

What causes the symptoms of dementia?

A

progressive neurodegeneration that damages the brain.

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3
Q

How does dementia differ from delirium in terms of consciousness?

A

Unlike delirium, dementia does not affect consciousness, which remains intact

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4
Q

Does dementia worsen over time?

A

Yes

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5
Q

What kinds of personality and behavioral changes are associated with dementia?

A

increased irritability, apathy, or agitation.

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6
Q

List at least five cognitive functions commonly affected by dementia.

A

Memory, thinking, orientation, calculation, learning capacity, language, and judgment.

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7
Q

How does dementia impact language abilities?

A

can cause difficulties in understanding and producing language.

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8
Q

What is the term for difficulty in coordinating body movements in dementia, and give an example?

A

Praxis; an example is having trouble buttoning a shirt.

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9
Q

How is memory specifically impacted by dementia?

A

Memory issues in dementia may include forgetting recent events, names, or how to perform familiar tasks.

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10
Q

What does “perception” refer to in the context of dementia, and what are some difficulties associated with it?

A

Perception involves recognizing objects and sounds, and difficulties might include not recognizing a familiar face or misinterpreting common sounds

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11
Q

How can one differentiate between normal aging and dementia in terms of cognitive decline?

A

Normal aging involves occasional forgetfulness, while dementia includes severe and progressive impairments in memory and other cognitive domains, significantly affecting daily life.

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12
Q

What specific changes in judgment might be seen in someone with dementia?

A

Impaired judgment in dementia could lead to unsafe decision-making, such as crossing a busy street without looking or giving away large sums of money to strangers.

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13
Q

What are the three stages of cognitive impairment in the progression of dementia?

A

Mild cognitive impairment, moderate cognitive impairment, and severe cognitive impairment.

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14
Q

What are the key features of mild cognitive impairment (MCI)?

A

Slight memory or cognitive challenges while managing everyday tasks remains possible. MCI is not necessarily indicative of dementia.

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15
Q

How does moderate cognitive impairment differ from mild cognitive impairment?

A

individuals struggle to manage their affairs and daily activities, often exhibit erratic or volatile behavior, and cannot live alone.

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16
Q

What are the hallmark features of severe cognitive impairment?

A

Loss of independence, being bedridden, non-verbal communication, inability to swallow, and requiring 24/7 care

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17
Q

Name at least five main subtypes of dementia.

A

Alzheimer’s disease, vascular dementia, frontotemporal dementia, Lewy body dementia, Creutzfeldt-Jakob disease (CJD) dementia, and alcoholic dementia.

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18
Q

Which subtype of dementia is the most common?

A

Alzheimer’s disease

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19
Q

What are some key features of Alzheimer’s disease?

A

Memory loss, dysphasia (language difficulties), dyspraxia (movement coordination impairment), anosmia (loss of smell)

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20
Q

Define dysphasia and provide an example of how it manifests in Alzheimer’s disease

A

Dysphasia is a language difficulty, such as trouble finding the right words to express thoughts.

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21
Q

What is dyspraxia, and how does it present in Alzheimer’s patients?

A

Dyspraxia is an impairment in coordinating movement despite physical ability, such as difficulty buttoning a shirt

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22
Q

What behavioral changes are commonly observed in individuals with Alzheimer’s disease?

A

Wandering, confusion, and sometimes agitation or aggression

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23
Q

What is anosmia, and how might it be relevant to Alzheimer’s disease?

A

Anosmia is the loss of smell, which is a common symptom in Alzheimer’s disease.

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24
Q

How does vascular dementia differ from Alzheimer’s disease in terms of progression?

A

Vascular dementia often progresses in a stepwise pattern due to successive strokes or brain injury, whereas Alzheimer’s progresses more steadily

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25
Q

Which stage of dementia requires 24/7 care, and why?

A

Severe cognitive impairment requires 24/7 care due to the individual’s inability to perform basic functions such as swallowing and communicating.

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26
Q

What is the role of tau protein in normal neurons?

A

Tau protein helps stabilize microtubules within neurons.

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27
Q

What happens to tau protein in Alzheimer’s disease?

A

tau protein becomes hyperphosphorylated, forming paired helical filaments that aggregate into neurofibrillary tangles

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28
Q

How do neurofibrillary tangles disrupt neuron function?

A

They disrupt intracellular transport, impairing the neuron’s ability to move nutrients and other essential molecules

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29
Q

What causes the formation of amyloid plaques in Alzheimer’s disease?

A

The amyloid precursor protein is abnormally cleaved into beta-amyloid, which aggregates to form extracellular plaques.

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30
Q

What are the effects of amyloid plaques on the brain?

A

They trigger inflammation, neuronal cell death, and reduced synaptic transmission.

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31
Q

What are the combined effects of neurofibrillary tangles and amyloid plaques on the brain?

A

They lead to neuron loss, brain atrophy, diminished neurotransmission, and reduced connectivity between brain regions.

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32
Q

What imaging feature is typically observed in the later stages of dementia due to neuron loss?

A

Widespread brain shrinkage.

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33
Q

What happens to the brain’s ventricles as a result of brain matter loss in dementia?

A

The ventricles enlarge as brain matter dies

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34
Q

Which brain region is primarily responsible for memory formation and is most affected in Alzheimer’s disease?

A

The hippocampus, and its shrinkage leads to memory loss.

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35
Q

Name two genetic risk factors strongly associated with Alzheimer’s disease.

A

The APOE4 allele and APP mutations, which affect beta-amyloid processing.

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36
Q

What are two key environmental risk factors for Alzheimer’s disease?

A

Low education and poor diet.

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37
Q

Name three medications used to slow the progression of Alzheimer’s disease

A
  • Donepezil
  • Memantine
  • Rivastigmine:
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38
Q

how do donepezil work

A

An acetylcholinesterase inhibitor that boosts acetylcholine, enhancing memory and cognition.

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39
Q

how does memantine work

A

An NMDA receptor antagonist that prevents excitotoxic damage to neurons.

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40
Q

how does rivastigmine work

A

Another acetylcholinesterase inhibitor with similar effects as Donepezil.

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41
Q

What causes vascular dementia?

A

caused by vascular events such as ischemic or hemorrhagic strokes that lead to brain damage

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42
Q

How does vascular dementia typically progress?

A

It follows a “staircase” progression, with sudden deteriorations followed by periods of relative stability or improvement.

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43
Q

What are common personality changes observed in vascular dementia?

A

Changes in behavior and emotion are typical personality changes in vascular dementia

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44
Q

What does “labile mood” mean in the context of vascular dementia?

A

Labile mood refers to sudden mood swings, such as laughing and crying in quick succession.

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45
Q

What is unique about the insight of patients with vascular dementia compared to other dementias?

A

Patients with vascular dementia often retain insight and are aware of their cognitive deficits

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46
Q

What are the two main types of vascular events that cause brain damage in vascular dementia?

A
  • Ischemic events: Blocked blood flow leading to oxygen deprivation.
  • Hemorrhagic events: Bleeding into brain tissue.
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47
Q

How do ischemic and hemorrhagic events contribute to the cognitive decline in vascular dementia?

A

Both types of events damage brain tissue, disrupt neural pathways, and impair the brain’s ability to function effectively.

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48
Q

What is the primary focus of medication and treatment for vascular dementia?

A

The primary focus is on preventing further vascular damage

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49
Q

Name four strategies used to prevent additional vascular damage in vascular dementia.

A
  • Blood pressure control
  • Anticoagulation for atrial fibrillation (AF)
  • Cholesterol-lowering therapies
  • Lifestyle modifications
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50
Q

What causes frontotemporal dementia (FTD)?

A

FTD is caused by progressive atrophy of the frontal and/or temporal lobes

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51
Q

What are the key characteristics of the behavioral variant of FTD (bvFTD)?

A
  • Profound personality changes: impulsivity, loss of social norms, and apathy.
  • Loss of insight and working memory deficits.
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52
Q

Which cognitive skills are typically preserved in FTD, making it harder to detect via standard tests?

A

Memory, praxis, perception, and spatial skills are typically preserved

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53
Q

Which brain region is associated with personality changes in FTD, and why?

A

The frontal lobe is associated with personality changes due to the loss of control over primitive instincts. This is supported by the Phineas Gage case study.

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54
Q

What symptoms result from temporal lobe atrophy in FTD?

A

Temporal lobe atrophy leads to deficits in language and emotional regulation

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55
Q

What causes Lewy Body Dementia (LBD)?

A

LBD is caused by the abnormal accumulation of alpha-synuclein proteins, forming Lewy bodies within neurons.

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56
Q

What are the primary consequences of Lewy body accumulation?

A

Neuronal death and dopamine dysfunction, which impair movement and contribute to cognitive decline

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57
Q

What are the key cognitive symptoms of LBD?

A

Progressive cognitive decline with fluctuating attention.

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58
Q

How do motor symptoms in LBD overlap with another neurodegenerative disorder?

A

LBD motor features overlap with Parkinson’s disease, including difficulty with movement.

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59
Q

What type of hallucinations are commonly seen in LBD?

A

vivid, and detailed visual hallucinations

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60
Q

What sleep disturbance is characteristic of LBD?

A

REM sleep disturbance, such as acting out dreams.

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61
Q

What are Lewy bodies, and where are they commonly found in LBD?

A

Lewy bodies are aggregates of alpha-synuclein proteins, commonly found in the substantia nigra, cortex, and limbic system.

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62
Q

How does acetylcholine dysfunction manifest in LBD?

A

Cholinergic deficits contribute to cognitive and psychiatric symptoms.

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63
Q

What causes Creutzfeldt-Jakob Disease (CJD)?

A

CJD is caused by prions, which are abnormally folded proteins that induce other proteins to misfold, leading to brain tissue destruction.

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64
Q

How quickly does dementia progress in CJD?

A

Dementia progresses rapidly, over weeks to months.

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65
Q

List five key symptoms of CJD.

A

Memory loss
Personality changes
Hallucinations
Myoclonus (sudden jerking)
Coma and eventual death

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66
Q

What is the defining characteristic of prion proteins in CJD?

A

Prion proteins are insoluble and abnormally folded, spreading misfolding to other proteins.

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67
Q

How do prions cause disease at the molecular level?

A

Misfolded prions induce normal prions to misfold, spreading the disease.

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68
Q

What treatment options exist for prion diseases?

A

There is no treatment for prion diseases

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69
Q

Name the four licensed pharmacological agents for dementia treatment.

A

Donepezil
Rivastigmine
Memantine
Galantamine

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70
Q

Which medications are classified as cholinesterase inhibitors?

A

Donepezil, Rivastigmine, and Galantamine.

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71
Q

What is the mechanism of action of cholinesterase inhibitors?

A

They inhibit acetylcholinesterase, increasing acetylcholine levels in the brain

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72
Q

For which types of dementia are cholinesterase inhibitors primarily used?

A

Alzheimer’s disease and sometimes Lewy Body Dementia.

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73
Q

What are common adverse effects of cholinesterase inhibitors?

A

Nausea, diarrhea, insomnia, muscle cramps, and bradycardia.

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74
Q

What is the mechanism of action of memantine?

A

Memantine blocks excessive NMDA receptor activation by glutamate, reducing excitotoxicity and neuronal death

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75
Q

In which stages of Alzheimer’s disease is memantine typically used?

A

Moderate to severe Alzheimer’s disease

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76
Q

What are common adverse effects of memantine?

A

Dizziness, headaches, constipation, and confusion

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77
Q

Why is it important to assess Activities of Daily Living (ADL) functioning over time?

A

Declining ADL functioning can indicate progressive cognitive impairment, a hallmark of dementia

78
Q

Which imaging modalities are typically used to assess structural brain changes in dementia?

A

MRI or CT scans.

79
Q

What are specific radiological findings in dementia subtypes?

A
  • Hippocampal atrophy: Alzheimer’s disease.
  • White matter hyperintensities: Vascular dementia.
  • Enlarged ventricles or sulci: General signs of brain atrophy.
80
Q

What are the main stages of memory processing?

A
  1. input
  2. sensory memory
  3. short-term memory
  4. long-term memory
  5. retrival
  6. forgetting
81
Q

Describe what input and sensory memory is

A
  • Input: Information enters the brain.
  • Sensory Memory: Briefly holds sensory information.
82
Q

Describe what short and long-term memory is

A
  • Short-Term Memory: Temporarily stores information in use.
  • Long-Term Memory: Stores information permanently through encoding
83
Q

Describe what retrieval and forgetting is

A
  • Retrieval: Accessing stored information for conscious thought.
  • Forgetting: Loss of information due to interference, decay, or retrieval failure.
84
Q

How does information transfer from short-term to long-term memory?

A

Through practice, repetition, and encoding, with emotional responses strengthening this transfer

85
Q

What is encoding in memory formation?

A

Encoding converts sensory input into a format that can be stored and retrieved later.

86
Q

What is retrieval, and why is it important?

A

Retrieval brings stored long-term memory back into short-term memory. It is crucial for conscious thought and decision-making

87
Q

What are the three primary reasons for forgetting?

A
  • Interference: New information conflicts with old information.
  • Decay: Memory weakens over time without use.
  • Failure to Retrieve: Inability to access stored information.
88
Q

What are the two main categories of memory?

A
  • Declarative (Explicit & Conscious)
  • Non-Declarative (Implicit & Unconscious)
89
Q

What is episodic memory? Provide an example.

A
  • Episodic memory is the memory of personal experiences and specific events
  • Example: Recalling your high school graduation day
90
Q

What is semantic memory? Provide an example.

A
  • Semantic memory is general knowledge and facts about the world.
  • Example: Knowing Paris is the capital of France, even if you’ve never visited
91
Q

Which brain structure plays a key role in declarative memory?

A

The mammillary brain

92
Q

What type of memory is referred to as “flashbulb memory”?

A

Vivid, detailed memories of emotionally charged events

93
Q

What is procedural memory, and provide an example.

A

Procedural memory is the memory for skills and actions.
Example: Riding a bike or typing on a keyboard

94
Q

What does the perceptual representation system relate to, and give an example

A

It relates to memory of object features.
Example: Recognizing the shape of a football.

95
Q

What is classical conditioning, and provide an example.

A

Classical conditioning is learning through association
Example: Feeling hungry when hearing a dinner bell

96
Q

What is non-associative learning, and provide an example

A

Non-associative learning involves changes in response to repeated stimuli.
Example: Habituating to a loud sound over time

97
Q

What is the visuospatial sketchpad? Provide an example.

A

The visuospatial sketchpad holds visual and spatial information.
Example: Remembering the layout of a map.

98
Q

What is the role of the episodic buffer?

A

It integrates information from multiple sources into a coherent episode

99
Q

What does the phonological loop process?

A

It processes verbal and auditory information

100
Q

What is the function of visual semantics?

A

It links visual input to meaning

101
Q

How does the episodic long-term memory function in working memory?

A

It connects working memory to personal experiences

102
Q

What is the role of the language system in the central executive?

A

It processes spoken and written language.

103
Q

What is amnesia?

A

Amnesia is the complete or partial loss of memory, which may be caused by injury, disease, drugs, or traumatic experiences

104
Q

What is retrograde amnesia? Provide an example

A

Retrograde amnesia is the inability to recall memories formed before an injury.
Example: Forgetting the details of a car accident before the crash

105
Q

What is anterograde amnesia? Provide an example.

A

Anterograde amnesia is the inability to form new memories after the onset of an injury.
Example: Being unable to remember meeting someone new post-injury.

106
Q

What does Ribot’s Law state about memory disruption?

A

The most recently acquired memories are the most vulnerable to disruption from brain damage.

107
Q

Why are recent memories more vulnerable than older ones?

A

Recent memories are still being consolidated and are vulnerable.
Older memories are more securely encoded and stored across the brain.

108
Q

Provide an example illustrating Ribot’s Law.

A

After being knocked unconscious, a person might lose memories from the past two weeks but retain older memories, like their wedding day or childhood events.

109
Q

How does Korsakoff syndrome relate to memory retention?

A

Patients with Korsakoff syndrome struggle to recall recent memories but can often access older memories.

110
Q

How does dementia progression affect memory?

A

Early stages affect short-term memory first, while severe dementia disrupts older memories.

111
Q

What condition did Patient HM have before surgery?

A

Refractory temporal lobe epilepsy.

112
Q

What surgical procedure was performed on Patient HM?

A

Bilateral medial temporal lobectomy, including the removal of the hippocampus.

113
Q

What was the primary outcome of the surgery?

A
  • Success: Significant improvement in epilepsy.
  • Side Effects: Severe memory impairments, including anterograde amnesia
114
Q

What type of amnesia did Patient HM exhibit? Provide an example

A

Anterograde amnesia—he could not form new long-term memories.

115
Q

What conclusion was drawn from Patient HM’s case?

A

The medial temporal lobe is crucial for encoding and consolidating new memories.

116
Q

What is memory consolidation?

A

The process where new memories move from temporary storage to long-term storage, strengthening memory traces and making them resistant to forgetting.

117
Q

Describe the two stages of memory consolidation

A
  • Initial Encoding: New memories are processed by the sensory cortex and temporarily stored in the hippocampus.
  • Consolidation: Processed information is transferred to the neocortex for permanent storage.
118
Q

How does sleep contribute to memory consolidation?

A

During sleep, the brain replays and integrates new information, facilitating its storage in the neocortex.

119
Q

What impact does sleep deprivation have on consolidation?

A

Sleep deprivation disrupts consolidation, weakening the ability to store new memories.

120
Q

What is semantic dementia?

A

A progressive loss of conceptual knowledge, often associated with temporal lobe atrophy

121
Q

Which temporal lobe is commonly affected in semantic dementia, and why?

A

The left temporal lobe, as it is language dominant

122
Q

What aspect of memory remains intact in early stages of semantic dementia?

A

Episodic memory, such as daily routines and autobiographical information

123
Q

What is confabulation

A

creation of false or erroneous memories arising in neurological conditions

124
Q

What are the common causes of confabulation

A
  • Wernicke’s Korsakoff Syndrome
  • Traumatic Brain Injury (TBI)
125
Q

What are the 2 types of confabulation

A
  • Spontaneous Confabulation: occurs without any external prompting, often due to frontal lobe damage.
  • Provoked Confabulation: triggered by questions or tasks requiring memory recall
126
Q

What is explicit (declarative) memory? Provide an example

A

Explicit memory involves consciously recalling information.
Example: Remembering the capital of France or someone’s birthday

127
Q

What is implicit (non-declarative) memory? Provide an example.

A

Implicit memory involves unconscious memories related to skills and automatic responses that don’t require active thinking.
Example: Riding a bike or driving a car

128
Q

How does the brain respond to learning?

A

Learning involves adaptive changes in synaptic connectivity, strengthening or weakening connections based on the importance, relevance, or recency of the information.

129
Q

Which brain regions are associated with different types of memory?

A

Basal ganglia: Implicit memory.
Cortex: Long-term explicit memory.
Amygdala: Emotional memory.

130
Q

What happens to synaptic connections when we learn new and important information?

A

Synaptic connections are strengthened, making it easier to remember the information.

131
Q

What is a cell assembly?

A

A group of neurons that form a network of connections and become activated together in response to a stimulus.

132
Q

What is reverberating activity in the context of a cell assembly?

A

Reverberating activity occurs when neurons keep sending signals back and forth to each other even after the stimulus is gone.

133
Q

How does reverberating activity affect memory?

A

The more reverberating activity occurs, the stronger the connections between neurons become, reinforcing the memory.

134
Q

How can partial activation of a cell assembly trigger a full memory?

A

Once connections in a cell assembly are well-established, even partial activation (e.g., seeing a friend’s hairstyle) can trigger the entire memory of the associated stimulus (e.g., their face)

135
Q

What is Hebb’s Rule?

A
  • “Neurons that fire together, wire together” — connections between neurons are strengthened when they fire together.
  • Conversely, “Neurons that fire out of sync, lose their link,” weakening their connections
136
Q

How does Hebb’s Rule relate to learning and memory?

A

Learning and memory result from changes in synaptic strength, where repeated synchronous firing strengthens neuronal connections, while asynchronous firing weakens them.

137
Q

What happens to neurons that fire together repeatedly?

A

Their synaptic connections are strengthened

138
Q

What happens to neurons that fire out of sync?

A

Their connections weaken

139
Q

What is long-term potentiation (LTP)?

A

A process where high-frequency stimulation (HFS) of synaptic pathways leads to a long-lasting increase in synaptic strength, crucial for memory and learning

140
Q

What is the significance of the hippocampus in studying LTP?

A

The hippocampus’s distinct shape and anatomy allow easy identification and recording of specific pathways electrophysiologically.

141
Q

How does high-frequency stimulation (HFS) affect synaptic strength in LTP?

A
  • Single HFS: Causes an increase in excitatory postsynaptic potential (EPSP) that lasts for hours.
  • Multiple HFS: Extends this effect, lasting days to months.
142
Q

Which pathway in the hippocampus is particularly associated with memory processing and LTP?

A

the perforant pathway.

143
Q

What happens when glutamate is released in an inactive cell during LTP?

A
  1. Glutamate binds to AMPA receptors, causing a small excitatory postsynaptic potential (EPSP).
  2. NMDA receptors remain inactive because their ion channels are blocked by Mg²⁺.
144
Q

How does depolarization affect an active cell during LTP?

A
  1. AMPA receptors open, allowing Na⁺ influx and depolarization of the cell.
  2. Depolarization expels Mg²⁺ from NMDA receptors, enabling Na⁺ and Ca²⁺ influx.
145
Q

What is the role of AMPA and NMDA receptors in an active cell during LTP?

A
  • AMPA receptors allow Na⁺ influx.
  • NMDA receptors allow both Na⁺ and Ca²⁺ influx, provided the Mg²⁺ block is removed by depolarization.
146
Q

What does Ca²⁺ influx through NMDA receptors activate during LTP?

A

It activates protein kinase C (PKC) and Ca²⁺/calmodulin-dependent kinase II (CaMKII)

147
Q

What are the effects of CaMKII activation on AMPA receptors?

A
  1. Phosphorylation of AMPA receptors increases their sensitivity to glutamate.
  2. Insertion of new AMPA receptors increases the number of active receptors, strengthening the synaptic response.
148
Q

What makes CaMKII unique in maintaining LTP?

A
  • CaMKII can self-phosphorylate, becoming constitutively active (remains active without additional Ca²⁺ input).
  • This allows it to sustain synaptic strengthening even after the initial stimulus stops.
149
Q

Why is CaMKII referred to as a “molecular switch”?

A

Because its self-sustained activity maintains increased synaptic excitability for extended periods (minutes to hours) without further Ca²⁺ input.

150
Q

Why is protein synthesis important for the late phase of LTP?

A

Protein synthesis strengthens synaptic connections and solidifies changes necessary for long-term memory storage, preventing the fade of LTP.

151
Q

What are the three stages of memory formation?

A
  1. Acquisition (training): Initial learning.
  2. Consolidation: Processing and storing memory for long-term retention.
  3. Recall (testing): Retrieving memory to test the strength of consolidation.
152
Q

What happens if protein synthesis inhibitors are introduced during consolidation?

A

Memory consolidation is disrupted, and the information cannot be remembered later.

153
Q

What activates CREB

A

CREB is activated through phosphorylation by enzymes such as protein kinase A and CaMKII

154
Q

What is CREB role in memory

A

its role is to initiate the transcription of genes necessary for protein synthesis, converting short-term memory into long-term memory.

155
Q

What is long-term depression (LTD)?

A

LTD is a process that weakens synaptic connections, leading to a decrease in synaptic strength

156
Q

What type of stimulation induces LTD?

A

Low-frequency stimulation causes LTD by reducing EPSP amplitude.

157
Q

How does LTD work on a molecular level?

A
  1. LTD is dependent on NMDA receptor activation.
  2. Prolonged, low-level increases in Ca²⁺ activate phosphatases.
  3. Phosphatases dephosphorylate AMPA receptors.
  4. Dephosphorylation leads to the removal of AMPA receptors from the postsynaptic membrane, weakening the synapse
158
Q

How does Ca²⁺ signaling differ in LTP and LTD?

A
  • High levels of Ca²⁺ activate kinases, leading to AMPA receptor phosphorylation and insertion, strengthening the synapse
  • Low levels of Ca²⁺ activate phosphatases, leading to AMPA receptor dephosphorylation and removal, weakening the synapse.
159
Q

What happens if NMDA receptors are blocked

A

it blocks LTP and impairs spatial learning

160
Q

What effect does alcohol have on memory

A
  • amnesia and blackouts
  • impairs short-term memory
161
Q

How does alcohol result in amnesia

A

blocks NMDA receptors

162
Q

What is the effect of benzodiazepines on memory

A
  • anterograde amnesia
  • impairs ability to form new memories post-administration
163
Q

How does benzodiazpines result in anterograde amnesia

A
  • indirectly enhance GABA receptors
  • sedative and anxiolytic effects
164
Q

What is the role of scopolamine

A
  • muscarinic receptor antagonist blocks Ach receptors
  • disrupts theta waves and impairs spatial learning
165
Q

Explain how nerve regeneration is possible in the PNS

A
  • after injury schwann cells help promote the repair and regeneration of damaged nerves
  • macrophage clear debris from damaged nerve
  • parent neuron switches to a growth state
166
Q

Can nerve regenerate in the CNS

A

no

167
Q

Why can’t nerve regenerate in the CNS

A
  • oligodendrocytes produce inhibitory factors that prevent the regeneration of neurons in the CNS
168
Q

Why is adult neurogenesis helpful in memory

A
  • helps create “space” for new memories.
  • preventing older memories from becoming confused with newer ones.
169
Q

What is the hierarchical organisation of sensory systems

A
  1. receptors
  2. thalamic relay nuclei
  3. primary sensory cortex
  4. secondary sensory cortex
  5. association cortex
170
Q

What is the role of receptors in sensory systems

A

detect sensory information from the environment

171
Q

What is the role of the thalamic relay nuclei in sensory systems

A

act as a relay station (direct sensory signals to specific regions of cerebral cortex)

172
Q

What is the role of primary sensory cortex

A

responsible for basic level of processing

173
Q

What is the role of secondary sensory cortex in sensory systems

A

further processes sensory information from primary sensory cortex

174
Q

What is the role of the association cortex in sensory systems

A

integrates sensory information for decision-making & interpretation

175
Q

What are unimodal association areas

A

Process information from 1 sensory modality (visual association only processes visual information)

176
Q

What are multimodal association areas

A
  • Integrates information from many sensory modalities (>1 modalities)
  • language comprehension (hearing + seeing mouth movements)
177
Q

What is the posterior association area

A

Perception (involves visual information) to help orient ourselves in environment

178
Q

What is the temporal association area

A
  • Connects emotion and memory inputs –> creates associations between sensory information and past experiences & emotions
  • Example: recognise familiar faces or smells w/ stored memories
179
Q

What is the prefrontal association area

A
  • Governs executive functions (ex: planning, decision-making) by integrating sensory inputs, memories and goals
  • Example: using sight and sound to navigate busy traffic
180
Q

What is prosopagnosia and cause

A
  • inability to recognise faces
  • damage to temporal lobe
181
Q

What is visual agnosia and cause

A
  • difficulty recognising objects visually despite perfect vision
  • damage to occipital-temporal regions
182
Q

What is anosognosia and cause

A
  • denial of one”s own illness or deficits
  • damage to the parietal lobe
183
Q

How does information converge from unimodal to multimodal areas

A
  1. Information from individual senses (ex: sight, sound) processes in unimodal areas
  2. It integrates in multimodal association areas
  3. It allows complex perception and understanding across sensory modalities
184
Q

What is meant by the processing is reversed in the motor system

A

It begins with higher-level motor areas plan the overall behaviour and sequence, while the primary motor cortex enacts specific movements.

185
Q

What is the role of the premotor cortex

A
  • generates motor programs
  • prepares movement and organises which muscles and sequences will be needed
186
Q

What is the role of the primary motor cortex

A
  • neurons in this area fire to control fine details of movement
187
Q

What is the role of Broca’s area

A

involved in articulating speech

188
Q

What happens if there is damage to Broca’s area

A
  • Broca’s aphasia
  • speech is fragmented but comprehension remains intact
189
Q

What is the role of Wernicke’s area

A

Supports fluent speech production and comprehension

190
Q

What happens if there is damage to the Wernicke’s area

A
  • Wernicke’s aphasia
  • fluent but often nonsensical speech and poor comprehension
191
Q

What is the purpose of the Wada procedure

A

temporarily deactivates one hemisphere to determine which side of the brain is dominant for language

Principles of Med Neuroscience (12 decks)

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