Final

Question 1

What are the three main sources of CNS protection?

Answer 1

Skull, Meninges, CSF

Question 2

What are the three main arteries supplying the cerebral cortex?

Answer 2

Middle cerebral artery, anterior cerebral artery, and posterior cerebral artery.

Question 3

What area does the middle cerebral artery serve?

Answer 3

Inferior division supplies the temporal lobe and superior provides lateral sides of the brain.

Question 4

What areas does the anterior cerebral artery supply?

Answer 4

Supplies medial surface of the brain and some of the prefrontal cortex.

Question 5

What areas does the posterior cerebral artery supply?

Answer 5

Supplies mostly the occipital lobe.

Question 6

List the four threshold for loss of brain function due to hypoxia and/or ischemia.

Answer 6

Ischemia and/or hypoxia:
- 10 seconds of brain ischemia = loss of consciousness
- 20 seconds of ischemia = electrical activity ceases
Low flow and/or reduced oxygen
- Flow <20ml/100g/min is insufficient for electrical signaling but cells may survive
- Flow <10ml/100g/min for more than a few minutes, or a few minutes of total ischemia = irreversible brain damage.

Question 7

Name the main imagery techniques for evaluation of adults with speech, language, and cognitive-communication disorders.

Answer 7

(Conventional) Angiography
Computer Assisted Tomography (CT)
Magnetic Resonance Imaging
Magnetic Resonance Angiography
Positron Emission Tomography
Electroencephalography

Question 8

Describe angiography (conventional). Provide one benefit and one limitation.

Answer 8

Provides structural images of the blood vessels over time.
Benefit: Evaluates blood vessels without radiation
Limitation: Injection site may bleed or bruise

Question 9

Describe computer-assisted tomography.

Answer 9

Structural images collected via multi-angle X-ray.
Benefit: Scan is short and extremely fast, shows acute blood
Limitation: Radiation exposure, not as clear as other methods

Question 10

Describe MRI.

Answer 10

Structural images collected via exposing brain to magnetic fields.
Benefit: no radiation exposure, allows for multiplanar and 3 dimensional evaluation, good resolution and a clear image
Limitation: Expensive, long wait for scheduling, picture quality susceptible to patient movement (may require sedation)

Question 11

Describe MRA.

Answer 11

Structural images of blood vessels at one moment in time.
Benefit: gives benefits of an angio and an MRI, high resolution
Limitation: Expensive

Question 12

Describe PET.

Answer 12

Radiation emitted by radioisotopes injected into artery; can measure metabolism.
Benefit: Functional image of where glucose is metabolized- shows where things may be going wrong
Limitation: Radiation exposure, most expensive, can’t see anatomy, poor resolution

Question 13

Describe ECT.

Answer 13

Measures brain electrical activity.
Benefit: Shows a functional image, maps out brain activity
Limitation: Can’t see anatomy

Question 14

Differentiate TBI and ABI.

Answer 14

TBI: a disruption in the normal function of the brain that can be caused by a bump, blow, or jolt to the head or a penetrating head injury. Damage is via applied force such as gravity or missiles.
ABI: acquired damage to the brain, such as a stroke, diffuse hypoxic-ischemic injury, diffuse toxic-metabolic injury

Question 15

Describe the Glasgow coma scale and its link to TBI severity.

Answer 15

The GCS is a rating scale that classifies TBI severity by mild, moderate or severe based on the presentation at the hospital. The scale looks at three abilities: eye opening, motor response, and verbal response. This provides a score from 3 to 15, with 14-15 being mild, 8-13 being moderate, and below 8 being severe.

Question 16

Order the different levels of consciousness, from most severe to least.

Answer 16

Brain death
Coma
Vegetative state
Minimally conscious
Post-traumatic amnesia

Question 17

Describe brain death.

Answer 17

Unarousable, no purposeful responses, brainstem reflexes absent

Question 18

Describe a coma. How do you differentiate this from brain damage?

Answer 18

Unarousable unconsciousness, no purposeful response to stimulation, abnomal sleep-wake cycles (typically fixed patterns on EEG), brainstem reflexes present
Differentiated by brainstem reflexes are present.

Question 19

Describe vegetative state. How do you differentiate this from a coma?

Answer 19

Can be persistent or transient, no purposeful response, brainstem reflexes and automatic behaviours may be present, sleep wake cycles are present but abnormal, outcome depend on time and etiology.
Differentiated by presence of sleep wake cycles (vegetative functions are present), eyes are open.

Question 20

Describe a minimally conscious state. How do you differentiate this from a vegetative state?

Answer 20

Inconsistent meaningful behaviour in a patient who otherwise appears to be in vegetative state.
Differentiated by inconsistent meaningful behaviours.

Question 21

Constrast delirium and locked in syndrome.

Answer 21

Delirium: Hallucinations and anterograde amnesia associated with autonomic dysfunction (hyperthermia)
- Common form is delirium tremens (DT)
- Sleep wake cycles are atypical
- Transient medical condition
Locked-in Syndrome: quadriparesis and lower facial paralysis due to stroke of the pons (Brainstem stroke)
- Cranial nerve function above level of the pons intact
- No altered consciousness (cognitive functions are intact)

Question 22

Define a cognitive communication disorder.

Answer 22

Term used to describe a set of communication features that result from underlying deficits in cognition.

• Difficulties can include issues with hearing, listening, understanding, speaking, reading, writing, conversational interaction, and social communication
• May result of underlying deficits with cognition such as attention, orientation, memory, organization, information processing, reasoning, problem solving, executive functions, or self-regulation.

Question 23

Define dementia.

Answer 23

Dementia is a syndrome of acquired and persistent declines in several thinking abilities. It is an umbrella term that can be caused by a variety of conditions, including AD, vascular dementia, Lewy Body dementia, PD, and a mixture of conditions. The behaviours you can see include memory problems, problems with words and speaking, problems with seeing objects in space, problems with planning and organizing, problems with making appropriate decisions, and problem with paying attention to one thing at a time.

Question 24

List the major characteristics of AD.

Answer 24

AD is an abnormal process occurring in the brain, caused by plaques, tangles, inflammation, and nerve cell death in the brain. The plaques and tangles are primarily in the frontal and temporal lobes, hippocampus and the adjacent areas.

Question 25

List the major characteristics of vascular dementia.

Answer 25

VD is caused by multiple infarcts and commonly co-occurs with AD. It shows with heterogenous cognitive and motor signs depending upon the site of the lesion but generally shows a stepwise decline with abrupt changes in mental state. You may see aphasia, comprehension or executive functioning deficits, or depression.

Question 26

List the major characteristics of Lewy Body disease.

Answer 26

The neuropathology of LBD is distributed in the frontal and temploral lobes and the basal ganglia, characterized by protein deposits, called Lewy Bodies, in the cell bodies. It presents with cognitive dysfunction, fluctuating attention, visual hallucinations and/or sensitivity to neurolipids, motor and autonomic dysfunction, and acting out dreams and/or other sleep disturbances. Possible significant memory loss, likely difficulties in planning and problem solving, difficulties with sense of direction or spatial awareness, possible language problems and fluctuating cognition abilities

Question 27

List the major characteristics of frontotemporal dementia.

Answer 27

FD is characterized by pick bodies in the cortex and later atrophy of frontal and temporal lobes. It is more common in women then men and presents general around age 50. The behavioural variant results in poor decision making, emotional blunting, hyperorality, compulsion to explore environment, changes in dietary preference and sexual behaviour, auditory and visual agnosia, repetitive behaviours, socially inappropriate behaviour, general loss of interest or motivation, loss of empathy, compulsiveness, changes in executive functioning. Langauge variant results in progressive reduction in verbal output, both language expression and comprehension with verbs are often most affected

Question 28

Describe the stages of language decline and communication decline in AD-type dementia.

Answer 28

Early – Forget what was heard or read, word retrival problems are often some of the first complaints
Over time – discourse fragmented or impoverished, decreased coherence, tangentiality, perseverations, decreased ablity to formulate ideas and express them orally or written. Eventually you see impaired comprehension because of impaired working memory and learning but phonology and syntax are mostly preserved until relatively late.

Question 29

What are the clinical signs of TBI?

Answer 29

Any period or loss of or decreased consciousness
Any loss of memory of events immediately before or after injury
Neurologic deficits such as muscle weakness, loss of balance, vision disruption, change in speech or language
Any alteration in mental state (confusion, disorientation, concentration)

Question 30

Describe post-traumatic amnesia.

Answer 30

No new declarative memories after the incident

No clear timeline of recovery

Question 31

Summarize the main steps of neurotransmission.

Answer 31

1. Neuron at rest has negative intracellular fluid (ICF) relative to extracellular fluid (ICF) (This difference is about -65mV)
2. Inputs from other neurons changes this electrical potential in either a positive or negative direction.
3. If the sum of inputs is to change the ICF to -35mV, voltage-gated Na+ channels in the neuron cell membrane open and Na+ flows into the cell.
4. The ICF then becomes more positive and when the ICF charge reaches about +35mV (about 1 msec), voltage-gated Na+ channels close and voltage-gated K+ channels open > K+ flows out of the cell > ICF becomes more negative and “overshoots” the resting potential > K+ channels close > cell returns to -65mV resting potential and voltage-gated Na+ channels open again
5. The initial change in electrical potential in the neuron is propagated down the axon, and ultimately causes release of neurotransmitters into the synapse. 6. Neurotransmitters in turn act to change the membrane potential of the postsynaptic neuron via either binding at a postsynaptic receptor (e.g., an ion channel) or making other changes in the postsynaptic neuron.

Question 32

Give examples of steps in neurotransmission where drugs can exert their effects.

Answer 32

Drugs can act anywhere in the series of events described above, including blocking Na+ or K+ channels (or keeping them open), blocking or competing with neurotransmitters at postsynaptic binding sites, acting as neurotransmitters at postsynaptic binding sites, blocking reuptake of neurotransmitters into the presynaptic neuron, and blocking breakdown of neurotransmitters in the ECF.

Question 33

What are the main comprehension communication characteristics for RDH?

Answer 33

Difficulty with abstract language, figurative language, and ambiguous communication E.g., sarcasm, jokes, idioms, irony, and everyday inferencing
Difficulty making inferences and understanding the global meanings of discourse such as topic, gist, and big picture
Impaired comprehension of extralinguistic features (pragmatics)

Question 34

What are the main expression communication characteristics for RDH?

Answer 34

Lack of verbal organization
Difficulty with sequencing and problem solving
Focus on irrelevant, small details that may not relate to the big picture of the conversation
More words and less information
Difficulty responding to abrupt changes in stimuli
May be egocentric in conversation contributions
Reduced back-channeling

Question 35

What are the main social communication characteristics for RDH?

Answer 35

Flat affect → reduced intonation
Reduced eye contact
Poor turn-taking
Decreased conversation initiation
Reduced knowledge of social violations and social cues and may not be aware of social boundaries 
Difficulty understanding emotions in tone of voice, facial expressions, body language  
Difficulty with Theory of Mind
Impaired application of shared knowledge

Question 36

What are some other communication characteristics for RDH?

Answer 36

Anosognosia
Impaired recall and recognition of non-verbal episodic memory
Limitations in spatial and verbal working memory
Reduced reasoning and judgement
Unilateral (body, visual, spacial, and object) neglect (in writing, reading, and social contexts)
Poor executive functions
Reduced inhibition

Question 37

Discuss some macrolevel difficulties you might see with RHD.

Answer 37

Macrostructure level deficits: typically more words with less information, may be tangential, and may be associated with confabulations.

Question 38

Discuss some microlevel difficulties you might see with RHD.

Answer 38

Microstructure level deficits: impairments in understanding lexical ambiguity, errors in comprehension of connotative meanings (lion=regal) but not denotative meanings (animal with mane), impairments in generating alternative meanings regardless of metaphor, and errors in elaborative inferencing

Question 39

What are some strengths of individuals with RHD?

Answer 39

Syntax and semantics: able to structure sentences and paragraphs
Perform well with discourse tasks when drawing inferences is not required or low (context is provided)

Question 40

Compare RHD and aphasia. * = shared with CCD.

Answer 40

RHD: difficulty communicating, compromised pragmatics, insufficient organization, discourse cohesion, poor topic management, and egocentric/inappropriate topic choices, difficulties with turn-taking and social cues, impaired macrostructure, difficulties with implied or figurative language, breakdowns with more complex, abstract communication, lack of awareness of difficulties, reasoning and judgement, verbose with flat affect, difficulty identifying main idea
Aphasia: difficulty speaking, impaired phonological, lexical semantic, and morphosyntactic processing, issues with syntactic organization, impaired microstructure (omitting content words), understanding figurative language literally or missing subtleties, shore fragmented phrases and difficulties understanding utterances, lack of awareness (fluent), hard time following fast speech, anomia and accurate lexical retrieval difficulties.
Similarities: difficulties dealing with complex stimuli

Question 41

Compare RHD with cognitive communication disorders.

Answer 41

Similarities: pragmatic and discourse difficulties are primarily a product of other cognitive deficits like ToM, social cognition, attention and working memory, limited working memory
CCD: difficulties in pracmatics and discourse deficits beyond lexical-semantic and morphosyntactic levels, anomia is really common

Question 42

Describe some difficulties someone with RHD may have in conversation.

Answer 42

In conversation, the impaired comprehension of intent may lead to reduced requests for information, interest in the effect of an utterance on a conversation partner, ability to weigh plausibility, sensitivity to extralinguistic information, indirect speech acts that signal non-literal meaning, and internal motivations of communication partner, use of conventions signaling turn-taking and topic initiation, topic maintenance, and back-channeling.

Question 43

How might communication participation be impacted by RHD?

Answer 43

Initiate a conversation without informing the listener
Be excessively verbose and tangential, despite listener feedback
Fail to take the listener’s perspective about what’s important in everyday conversations
Attempt few conversational repairs

Question 44

Compare dementia with age-related cogntive changes in adults with intellectual disabilities.

Answer 44

Differences: initial presentation of dementia in DS may be a change in something other than declarative learning (memory) Eg. executive functions, cannot use a typical dementia screening due to change from baseline, must reflect a change over time
Similarlities: similar to AD where declarative learning is impaired more than non-declarative with a progressive decline over time

Question 45

General a communication intervention principle based on cognitive characteristics of dementia.

Answer 45

Principle: Rely on non-declarative learning for people with dementia, using conditioned reflexes, skills and habits, and emotional associations that remain and can be learned.
Focus on those positive experiences at all times - you will bring about positive emotions
Eg. Spaced retrieval work
Routines are important and therapy should follow a similar schedule.