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.
2
Q
What causes the symptoms of dementia?
A
progressive neurodegeneration that damages the brain.
3
Q
How does dementia differ from delirium in terms of consciousness?
A
Unlike delirium, dementia does not affect consciousness, which remains intact
4
Q
Does dementia worsen over time?
A
Yes
5
Q
What kinds of personality and behavioral changes are associated with dementia?
A
increased irritability, apathy, or agitation.
6
Q
List at least five cognitive functions commonly affected by dementia.
A
Memory, thinking, orientation, calculation, learning capacity, language, and judgment.
7
Q
How does dementia impact language abilities?
A
can cause difficulties in understanding and producing language.
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.
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.
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
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.
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.
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.
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.
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.
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
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.
18
Q
Which subtype of dementia is the most common?
A
Alzheimer’s disease
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)
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.
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
22
Q
What behavioral changes are commonly observed in individuals with Alzheimer’s disease?
A
Wandering, confusion, and sometimes agitation or aggression
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.
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
25
Which stage of dementia requires 24/7 care, and why?
Severe cognitive impairment requires 24/7 care due to the individual’s inability to perform basic functions such as swallowing and communicating.
26
What is the role of tau protein in normal neurons?
Tau protein helps stabilize microtubules within neurons.
27
What happens to tau protein in Alzheimer’s disease?
tau protein becomes hyperphosphorylated, forming paired helical filaments that aggregate into neurofibrillary tangles
28
How do neurofibrillary tangles disrupt neuron function?
They disrupt intracellular transport, impairing the neuron's ability to move nutrients and other essential molecules
29
What causes the formation of amyloid plaques in Alzheimer’s disease?
The amyloid precursor protein is abnormally cleaved into beta-amyloid, which aggregates to form extracellular plaques.
30
What are the effects of amyloid plaques on the brain?
They trigger inflammation, neuronal cell death, and reduced synaptic transmission.
31
What are the combined effects of neurofibrillary tangles and amyloid plaques on the brain?
They lead to neuron loss, brain atrophy, diminished neurotransmission, and reduced connectivity between brain regions.
32
What imaging feature is typically observed in the later stages of dementia due to neuron loss?
Widespread brain shrinkage.
33
What happens to the brain's ventricles as a result of brain matter loss in dementia?
The ventricles enlarge as brain matter dies
34
Which brain region is primarily responsible for memory formation and is most affected in Alzheimer’s disease?
The hippocampus, and its shrinkage leads to memory loss.
35
Name two genetic risk factors strongly associated with Alzheimer’s disease.
The APOE4 allele and APP mutations, which affect beta-amyloid processing.
36
What are two key environmental risk factors for Alzheimer’s disease?
Low education and poor diet.
37
Name three medications used to slow the progression of Alzheimer’s disease
- Donepezil
- Memantine
- Rivastigmine:
38
how do donepezil work
An acetylcholinesterase inhibitor that boosts acetylcholine, enhancing memory and cognition.
39
how does memantine work
An NMDA receptor antagonist that prevents excitotoxic damage to neurons.
40
how does rivastigmine work
Another acetylcholinesterase inhibitor with similar effects as Donepezil.
41
What causes vascular dementia?
caused by vascular events such as ischemic or hemorrhagic strokes that lead to brain damage
42
How does vascular dementia typically progress?
It follows a “staircase” progression, with sudden deteriorations followed by periods of relative stability or improvement.
43
What are common personality changes observed in vascular dementia?
Changes in behavior and emotion are typical personality changes in vascular dementia
44
What does "labile mood" mean in the context of vascular dementia?
Labile mood refers to sudden mood swings, such as laughing and crying in quick succession.
45
What is unique about the insight of patients with vascular dementia compared to other dementias?
Patients with vascular dementia often retain insight and are aware of their cognitive deficits
46
What are the two main types of vascular events that cause brain damage in vascular dementia?
- Ischemic events: Blocked blood flow leading to oxygen deprivation.
- Hemorrhagic events: Bleeding into brain tissue.
47
How do ischemic and hemorrhagic events contribute to the cognitive decline in vascular dementia?
Both types of events damage brain tissue, disrupt neural pathways, and impair the brain’s ability to function effectively.
48
What is the primary focus of medication and treatment for vascular dementia?
The primary focus is on preventing further vascular damage
49
Name four strategies used to prevent additional vascular damage in vascular dementia.
- Blood pressure control
- Anticoagulation for atrial fibrillation (AF)
- Cholesterol-lowering therapies
- Lifestyle modifications
50
What causes frontotemporal dementia (FTD)?
FTD is caused by progressive atrophy of the frontal and/or temporal lobes
51
What are the key characteristics of the behavioral variant of FTD (bvFTD)?
- Profound personality changes: impulsivity, loss of social norms, and apathy.
- Loss of insight and working memory deficits.
52
Which cognitive skills are typically preserved in FTD, making it harder to detect via standard tests?
Memory, praxis, perception, and spatial skills are typically preserved
53
Which brain region is associated with personality changes in FTD, and why?
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.
54
What symptoms result from temporal lobe atrophy in FTD?
Temporal lobe atrophy leads to deficits in language and emotional regulation
55
What causes Lewy Body Dementia (LBD)?
LBD is caused by the abnormal accumulation of alpha-synuclein proteins, forming Lewy bodies within neurons.
56
What are the primary consequences of Lewy body accumulation?
Neuronal death and dopamine dysfunction, which impair movement and contribute to cognitive decline
57
What are the key cognitive symptoms of LBD?
Progressive cognitive decline with fluctuating attention.
58
How do motor symptoms in LBD overlap with another neurodegenerative disorder?
LBD motor features overlap with Parkinson’s disease, including difficulty with movement.
59
What type of hallucinations are commonly seen in LBD?
vivid, and detailed visual hallucinations
60
What sleep disturbance is characteristic of LBD?
REM sleep disturbance, such as acting out dreams.
61
What are Lewy bodies, and where are they commonly found in LBD?
Lewy bodies are aggregates of alpha-synuclein proteins, commonly found in the substantia nigra, cortex, and limbic system.
62
How does acetylcholine dysfunction manifest in LBD?
Cholinergic deficits contribute to cognitive and psychiatric symptoms.
63
What causes Creutzfeldt-Jakob Disease (CJD)?
CJD is caused by prions, which are abnormally folded proteins that induce other proteins to misfold, leading to brain tissue destruction.
64
How quickly does dementia progress in CJD?
Dementia progresses rapidly, over weeks to months.
65
List five key symptoms of CJD.
Memory loss
Personality changes
Hallucinations
Myoclonus (sudden jerking)
Coma and eventual death
66
What is the defining characteristic of prion proteins in CJD?
Prion proteins are insoluble and abnormally folded, spreading misfolding to other proteins.
67
How do prions cause disease at the molecular level?
Misfolded prions induce normal prions to misfold, spreading the disease.
68
What treatment options exist for prion diseases?
There is no treatment for prion diseases
69
Name the four licensed pharmacological agents for dementia treatment.
Donepezil
Rivastigmine
Memantine
Galantamine
70
Which medications are classified as cholinesterase inhibitors?
Donepezil, Rivastigmine, and Galantamine.
71
What is the mechanism of action of cholinesterase inhibitors?
They inhibit acetylcholinesterase, increasing acetylcholine levels in the brain
72
For which types of dementia are cholinesterase inhibitors primarily used?
Alzheimer’s disease and sometimes Lewy Body Dementia.
73
What are common adverse effects of cholinesterase inhibitors?
Nausea, diarrhea, insomnia, muscle cramps, and bradycardia.
74
What is the mechanism of action of memantine?
Memantine blocks excessive NMDA receptor activation by glutamate, reducing excitotoxicity and neuronal death
75
In which stages of Alzheimer’s disease is memantine typically used?
Moderate to severe Alzheimer’s disease
76
What are common adverse effects of memantine?
Dizziness, headaches, constipation, and confusion
77
Why is it important to assess Activities of Daily Living (ADL) functioning over time?
Declining ADL functioning can indicate progressive cognitive impairment, a hallmark of dementia
78
Which imaging modalities are typically used to assess structural brain changes in dementia?
MRI or CT scans.
79
What are specific radiological findings in dementia subtypes?
- Hippocampal atrophy: Alzheimer’s disease.
- White matter hyperintensities: Vascular dementia.
- Enlarged ventricles or sulci: General signs of brain atrophy.
80
What are the main stages of memory processing?
1. input
2. sensory memory
3. short-term memory
4. long-term memory
5. retrival
6. forgetting
81
Describe what input and sensory memory is
- Input: Information enters the brain.
- Sensory Memory: Briefly holds sensory information.
82
Describe what short and long-term memory is
- Short-Term Memory: Temporarily stores information in use.
- Long-Term Memory: Stores information permanently through encoding
83
Describe what retrieval and forgetting is
- Retrieval: Accessing stored information for conscious thought.
- Forgetting: Loss of information due to interference, decay, or retrieval failure.
84
How does information transfer from short-term to long-term memory?
Through practice, repetition, and encoding, with emotional responses strengthening this transfer
85
What is encoding in memory formation?
Encoding converts sensory input into a format that can be stored and retrieved later.
86
What is retrieval, and why is it important?
Retrieval brings stored long-term memory back into short-term memory. It is crucial for conscious thought and decision-making
87
What are the three primary reasons for forgetting?
- Interference: New information conflicts with old information.
- Decay: Memory weakens over time without use.
- Failure to Retrieve: Inability to access stored information.
88
What are the two main categories of memory?
- Declarative (Explicit & Conscious)
- Non-Declarative (Implicit & Unconscious)
89
What is episodic memory? Provide an example.
- Episodic memory is the memory of personal experiences and specific events
- Example: Recalling your high school graduation day
90
What is semantic memory? Provide an example.
- 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
Which brain structure plays a key role in declarative memory?
The mammillary brain
92
What type of memory is referred to as "flashbulb memory"?
Vivid, detailed memories of emotionally charged events
93
What is procedural memory, and provide an example.
Procedural memory is the memory for skills and actions.
Example: Riding a bike or typing on a keyboard
94
What does the perceptual representation system relate to, and give an example
It relates to memory of object features.
Example: Recognizing the shape of a football.
95
What is classical conditioning, and provide an example.
Classical conditioning is learning through association
Example: Feeling hungry when hearing a dinner bell
96
What is non-associative learning, and provide an example
Non-associative learning involves changes in response to repeated stimuli.
Example: Habituating to a loud sound over time
97
What is the visuospatial sketchpad? Provide an example.
The visuospatial sketchpad holds visual and spatial information.
Example: Remembering the layout of a map.
98
What is the role of the episodic buffer?
It integrates information from multiple sources into a coherent episode
99
What does the phonological loop process?
It processes verbal and auditory information
100
What is the function of visual semantics?
It links visual input to meaning
101
How does the episodic long-term memory function in working memory?
It connects working memory to personal experiences
102
What is the role of the language system in the central executive?
It processes spoken and written language.
103
What is amnesia?
Amnesia is the complete or partial loss of memory, which may be caused by injury, disease, drugs, or traumatic experiences
104
What is retrograde amnesia? Provide an example
Retrograde amnesia is the inability to recall memories formed before an injury.
Example: Forgetting the details of a car accident before the crash
105
What is anterograde amnesia? Provide an example.
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
What does Ribot's Law state about memory disruption?
The most recently acquired memories are the most vulnerable to disruption from brain damage.
107
Why are recent memories more vulnerable than older ones?
Recent memories are still being consolidated and are vulnerable.
Older memories are more securely encoded and stored across the brain.
108
Provide an example illustrating Ribot’s Law.
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
How does Korsakoff syndrome relate to memory retention?
Patients with Korsakoff syndrome struggle to recall recent memories but can often access older memories.
110
How does dementia progression affect memory?
Early stages affect short-term memory first, while severe dementia disrupts older memories.
111
What condition did Patient HM have before surgery?
Refractory temporal lobe epilepsy.
112
What surgical procedure was performed on Patient HM?
Bilateral medial temporal lobectomy, including the removal of the hippocampus.
113
What was the primary outcome of the surgery?
- Success: Significant improvement in epilepsy.
- Side Effects: Severe memory impairments, including anterograde amnesia
114
What type of amnesia did Patient HM exhibit? Provide an example
Anterograde amnesia—he could not form new long-term memories.
115
What conclusion was drawn from Patient HM’s case?
The medial temporal lobe is crucial for encoding and consolidating new memories.
116
What is memory consolidation?
The process where new memories move from temporary storage to long-term storage, strengthening memory traces and making them resistant to forgetting.
117
Describe the two stages of memory consolidation
- 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
How does sleep contribute to memory consolidation?
During sleep, the brain replays and integrates new information, facilitating its storage in the neocortex.
119
What impact does sleep deprivation have on consolidation?
Sleep deprivation disrupts consolidation, weakening the ability to store new memories.
120
What is semantic dementia?
A progressive loss of conceptual knowledge, often associated with temporal lobe atrophy
121
Which temporal lobe is commonly affected in semantic dementia, and why?
The left temporal lobe, as it is language dominant
122
What aspect of memory remains intact in early stages of semantic dementia?
Episodic memory, such as daily routines and autobiographical information
123
What is confabulation
creation of false or erroneous memories arising in neurological conditions
124
What are the common causes of confabulation
- Wernicke’s Korsakoff Syndrome
- Traumatic Brain Injury (TBI)
125
What are the 2 types of confabulation
- Spontaneous Confabulation: occurs without any external prompting, often due to frontal lobe damage.
- Provoked Confabulation: triggered by questions or tasks requiring memory recall
126
What is explicit (declarative) memory? Provide an example
Explicit memory involves consciously recalling information.
Example: Remembering the capital of France or someone’s birthday
127
What is implicit (non-declarative) memory? Provide an example.
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
How does the brain respond to learning?
Learning involves adaptive changes in synaptic connectivity, strengthening or weakening connections based on the importance, relevance, or recency of the information.
129
Which brain regions are associated with different types of memory?
Basal ganglia: Implicit memory.
Cortex: Long-term explicit memory.
Amygdala: Emotional memory.
130
What happens to synaptic connections when we learn new and important information?
Synaptic connections are strengthened, making it easier to remember the information.
131
What is a cell assembly?
A group of neurons that form a network of connections and become activated together in response to a stimulus.
132
What is reverberating activity in the context of a cell assembly?
Reverberating activity occurs when neurons keep sending signals back and forth to each other even after the stimulus is gone.
133
How does reverberating activity affect memory?
The more reverberating activity occurs, the stronger the connections between neurons become, reinforcing the memory.
134
How can partial activation of a cell assembly trigger a full memory?
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
What is Hebb’s Rule?
- "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
How does Hebb’s Rule relate to learning and memory?
Learning and memory result from changes in synaptic strength, where repeated synchronous firing strengthens neuronal connections, while asynchronous firing weakens them.
137
What happens to neurons that fire together repeatedly?
Their synaptic connections are strengthened
138
What happens to neurons that fire out of sync?
Their connections weaken
139
What is long-term potentiation (LTP)?
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
What is the significance of the hippocampus in studying LTP?
The hippocampus’s distinct shape and anatomy allow easy identification and recording of specific pathways electrophysiologically.
141
How does high-frequency stimulation (HFS) affect synaptic strength in LTP?
- Single HFS: Causes an increase in excitatory postsynaptic potential (EPSP) that lasts for hours.
- Multiple HFS: Extends this effect, lasting days to months.
142
Which pathway in the hippocampus is particularly associated with memory processing and LTP?
the perforant pathway.
143
What happens when glutamate is released in an inactive cell during LTP?
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
How does depolarization affect an active cell during LTP?
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
What is the role of AMPA and NMDA receptors in an active cell during LTP?
- AMPA receptors allow Na⁺ influx.
- NMDA receptors allow both Na⁺ and Ca²⁺ influx, provided the Mg²⁺ block is removed by depolarization.
146
What does Ca²⁺ influx through NMDA receptors activate during LTP?
It activates protein kinase C (PKC) and Ca²⁺/calmodulin-dependent kinase II (CaMKII)
147
What are the effects of CaMKII activation on AMPA receptors?
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
What makes CaMKII unique in maintaining LTP?
- 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
Why is CaMKII referred to as a "molecular switch"?
Because its self-sustained activity maintains increased synaptic excitability for extended periods (minutes to hours) without further Ca²⁺ input.
150
Why is protein synthesis important for the late phase of LTP?
Protein synthesis strengthens synaptic connections and solidifies changes necessary for long-term memory storage, preventing the fade of LTP.
151
What are the three stages of memory formation?
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
What happens if protein synthesis inhibitors are introduced during consolidation?
Memory consolidation is disrupted, and the information cannot be remembered later.
153
What activates CREB
CREB is activated through phosphorylation by enzymes such as protein kinase A and CaMKII
154
What is CREB role in memory
its role is to initiate the transcription of genes necessary for protein synthesis, converting short-term memory into long-term memory.
155
What is long-term depression (LTD)?
LTD is a process that weakens synaptic connections, leading to a decrease in synaptic strength
156
What type of stimulation induces LTD?
Low-frequency stimulation causes LTD by reducing EPSP amplitude.
157
How does LTD work on a molecular level?
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
How does Ca²⁺ signaling differ in LTP and LTD?
- 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
What happens if NMDA receptors are blocked
it blocks LTP and impairs spatial learning
160
What effect does alcohol have on memory
- amnesia and blackouts
- impairs short-term memory
161
How does alcohol result in amnesia
blocks NMDA receptors
162
What is the effect of benzodiazepines on memory
- anterograde amnesia
- impairs ability to form new memories post-administration
163
How does benzodiazpines result in anterograde amnesia
- indirectly enhance GABA receptors
- sedative and anxiolytic effects
164
What is the role of scopolamine
- muscarinic receptor antagonist blocks Ach receptors
- disrupts theta waves and impairs spatial learning
165
Explain how nerve regeneration is possible in the PNS
- 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
Can nerve regenerate in the CNS
no
167
Why can't nerve regenerate in the CNS
- oligodendrocytes produce inhibitory factors that prevent the regeneration of neurons in the CNS
168
Why is adult neurogenesis helpful in memory
- helps create "space" for new memories.
- preventing older memories from becoming confused with newer ones.
169
What is the hierarchical organisation of sensory systems
1. receptors
2. thalamic relay nuclei
3. primary sensory cortex
4. secondary sensory cortex
5. association cortex
170
What is the role of receptors in sensory systems
detect sensory information from the environment
171
What is the role of the thalamic relay nuclei in sensory systems
act as a relay station (direct sensory signals to specific regions of cerebral cortex)
172
What is the role of primary sensory cortex
responsible for basic level of processing
173
What is the role of secondary sensory cortex in sensory systems
further processes sensory information from primary sensory cortex
174
What is the role of the association cortex in sensory systems
integrates sensory information for decision-making & interpretation
175
What are unimodal association areas
Process information from 1 sensory modality (visual association only processes visual information)
176
What are multimodal association areas
- Integrates information from many sensory modalities (>1 modalities)
- language comprehension (hearing + seeing mouth movements)
177
What is the posterior association area
Perception (involves visual information) to help orient ourselves in environment
178
What is the temporal association area
- Connects emotion and memory inputs --> creates associations between sensory information and past experiences & emotions
- Example: recognise familiar faces or smells w/ stored memories
179
What is the prefrontal association area
- Governs executive functions (ex: planning, decision-making) by integrating sensory inputs, memories and goals
- Example: using sight and sound to navigate busy traffic
180
What is prosopagnosia and cause
- inability to recognise faces
- damage to temporal lobe
181
What is visual agnosia and cause
- difficulty recognising objects visually despite perfect vision
- damage to occipital-temporal regions
182
What is anosognosia and cause
- denial of one"s own illness or deficits
- damage to the parietal lobe
183
How does information converge from unimodal to multimodal areas
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
What is meant by the processing is reversed in the motor system
It begins with higher-level motor areas plan the overall behaviour and sequence, while the primary motor cortex enacts specific movements.
185
What is the role of the premotor cortex
- generates motor programs
- prepares movement and organises which muscles and sequences will be needed
186
What is the role of the primary motor cortex
- neurons in this area fire to control fine details of movement
187
What is the role of Broca's area
involved in articulating speech
188
What happens if there is damage to Broca's area
- Broca's aphasia
- speech is fragmented but comprehension remains intact
189
What is the role of Wernicke's area
Supports fluent speech production and comprehension
190
What happens if there is damage to the Wernicke's area
- Wernicke's aphasia
- fluent but often nonsensical speech and poor comprehension
191
What is the purpose of the Wada procedure
temporarily deactivates one hemisphere to determine which side of the brain is dominant for language
