Cognition: Final Exam

What are the **3** primary roles of the **left hemisphere**?

Language

Details (Speech)

Control of the right side of the body

What are the **5** main contributions of the **right hemisphere**?

Language comprehension

Prosody

Pragmatic aspects of communication

Visual-perceptual skills

Awareness (And attention)

Explain the role of the **left hemisphere** by describing it “as a basket of fruit”.

This hemisphere sees the image as discrete individual parts; it sees a basket of individual fruits because this hemisphere is a serial processor.

Explain the role of the **right hemisphere** by describing it “as a face”.

This hemisphere synthesizes the information and sees it as a whole because this hemisphere is a parallel processor.

Define **Anosognosia**:

Reduced awareness of acquired deficits/impairments.

Define **Anosodiaphoria**:

Reduced emotional reaction or concern for a deficit (Might be aware of the deficits).

Define **Left Homonymous Hemianopia**:

This is a field cut. The individual may know that objects are on the other side and that they need to turn their head. They are open to the idea that there is more that they can see.

Define **Left Unilateral Neglect**:

Not a vision problem; **unable to perceive the left side**. They lost the right side’s impulse to look at the entirety of the scene. The person only looks to the right because the left hemisphere tells them that is all there is to see. They do not believe they are missing anything and are unable to compensate if not trained.

The Theory of Left Neglect

An injury in the right parietal lobe results in our left brain to only telling us to look to the right; due to the damage, our right brain is no longer able to tell us to look everywhere.

Types of **WHAT** neglect:

1. Egocentric
2. Object Centered

Define **Egocentric Neglect**:

Neglect down the middle of your own perspective; not necessarily always right down the middle.

Define **Object Centered Neglect**:

Neglect on the object itself.

Types of **WHERE** neglect:

1. Personal Neglect
2. Peri-Personal Neglect
3. Extra-Personal Neglect

Define **Personal Neglect**:

Failure to attend to left side of their body.

Define **Peri-Personal Neglect**:

Neglect of things in arms reach on left. Impacts paper/pencil, eating, etc.

Define **Extra-Personal Neglect**:

Beyond arms reach.

The spouse of someone with a recent dx of RHD says, “*Yes, I already know that she doesn’t see to the left*”. How should you respond to someone who doesn’t understand neglect to be anything more than a visual problem?

You may be quite right in thinking her vision has changed since this stoke.  And, it may have indeed changed. But there is something unique about the region of the brain, the right side, that she injured.  **This is something that goes deeper than vision**. Her right side, the injured side, has specific jobs to do and they are frequently centered around the idea of perception of the world around us. If we were to injure that side, we would lose or diminish this awareness of the scope of the world. If we weaken the right side, we then begin to overly rely on the left. Our left side of our brain is great for communicating, but not so good at telling us about the world around us.  In fact, it only tells us to look to the right.  **To the left brain, the world only exists on the right.  It’s not just that the left thinks it is best to look to the right, but rather that the right side is all there is to be seen**. So even if Ed had absolutely perfect vision, his left brain would tell him to align his perfect eyes to the right because it knows of no other place to look.   

Describe **Normal Pressure Hydrocephalus** (NPH):

Reversible dementia

Accumulation of excess cerebral spinal fluid (CSF) in the brain’s ventricles.

**Results in**: Unsteady gait, loss of bladder control (Later in disease), cognitive dysfunction (Slowing processing speed, diminished working memory, executive functioning).

Significant improvement in executive function after shunt surgery.

Describe **Frontotemporal Dementia** (FTD):

Includes bvFTD and PPA.

**Behavioral Variant Frontotemporal Dementia** (bvFTD): Profound behavioral changes

**Primary Progressive Aphasia** (PPA): Gradual onset. Must be the initial and primary symptom for at least two years and must be the prominent symptom throughout the course of the disease. Visuospatial, episodic memory, or behavioral problems are not compatible with a diagnosis of PPA. Deficits cannot be attributable to CVA, trauma, tumor, or psychiatric factors. **PPA diagnosis requires**: No history of stroke, trauma, tumor; progression (Worsening) of skills; 2 years of symptoms.

Describe **Vascular Dementia**:

“*Multi-Infarct*” Dementia.

Inadequate blood flow, sudden or accumulating cognitive changes from stroke(s).

Occurs over time as “silent” strokes accumulate.

Second most common, can co-occur with other dementias.

Symptoms vary (Dependent upon location of vascular changes).

Average life expectancy is 3 years following onset.

Risk factors are the same for heart disease and stroke.

Higher risk of developing depression than other disorders.

Describe **Dementia with Lewy Bodies** (LBD):

3rd most common dementia behind Alzheimer’s and vascular.

Presence of Lewy bodies in brain.

“Over-lap” in symptoms with Parkinson’s disease.

Cognitive deficits ***then*** movement deficits; **top-down progression**.

**Changes in**: Reasoning, increased confusion, decreased attention, visual hallucinations, delusions, difficulty interpreting visual information, memory loss is significant, but less than Alzheimer’s disease.

Rapid eye movement sleep disorder (“Dream-Enacting Behavior”).

Disruption of autonomic system.

*Consideration for Therapy*: Emphasize auditory information over visual.

Describe **Parkinson’s Disease Dementia** (PDD):

50-80% will eventually develop PDD.

Diagnosed in people with __at least one year__ history of PD.

Movement deficits ***then*** cognitive; **bottom-up progression**.

The onset of PDD is characterized by insidious onset and slow progressive decline, with a predominant deterioration in executive functions.

*Cognitive changes involve*: Diminished sustained and alternating attention, slower processing speeds, reduced executive function in area of feedback, reduced memory, and potential language and visuospatial deficits as disease progresses.

Cueing strategies are beneficial due to decline in executive functioning.

Describe **Chronic Traumatic Encephalopathy** (CTE):

Growing evidence that repeated blows to the head, concussive, or sub-concussive, are at increased risk of developing CTE.

Not new, “punch-drunk” syndrome. CTE related onset and severity was linked to number of rounds fought not number of times knocked out.

**Symptoms**: Memory loss, confusion, personality changes, erratic behavior.

Diminished executive function for attention and organization diminished motor skills.

Likely related to accumulation of abnormal protein, **Tau**, in brain.

No definitive test other than autopsy.

No treatment, no cure, only prevent repeated head trauma.

Describe **Korsakoff’s Syndrome** (KS):

Caused by lack of **thiamine** (Vitamin B1).

Commonly in alcoholics, but also within eating disorders, effects of chemotherapy.

KS is considered to be the chronic form of Wernicke’s Encephalopathy (Acute Stage).

__Three key presentations of KS__:


1. Confabulation (Rambling, does not make sense).
2. Absent to poor acquisition of new information (Poor consolidation).
3. Ataxic gait.

**Alzheimer’s Dementia** and **Ethics**: SLP role throughout disease progression

SLP’s who serve this population should be: Specifically educated and appropriately trained to do so.

Most common dementia-associated diseases are progressive in nature, and, SLP’s have an ethical responsibility to provide appropriate services that will benefit the individual and maximize cognitive-communication functioning at **all stages** of the disease process.

Collaborate with many other disciplines in caring for individuals with dementia.

Alzheimer’s Dementia **Progression**:

**Stage 1**: Asymptomatic changes in hippocampus.

**Stage 2**: Symptomatic; changes throughout limbic system.

**Stage 3**: Profound changes across all brain lobes, especially frontal and temporal.

Mild Cognitive Impairment (MCI): **Diagnosis**

Self-reporting of memory problems with corroboration from an informant.

Measurable memory impairment on standardized testing, outside the range for healthy older adults.

No impairment of reasoning, general thinking skills, or ability to perform daily activities.

Mild Cognitive Impairment (MCI): **Classifications**

**Amnestic MCI**: Related to __memory deficits__.

**Non-Amnestic MCI**: Related to __other cognitive functions__.

Mild Cognitive Impairment (MCI): **Characteristics**

Mild, but measurable changes in cognition.

Preclinical condition.

Suggestive of increased risk for developing dementia, “Transitional stage”.

MCI is diagnosed following mild symptoms, when patient is yet unimpaired.

Progression of **memory loss** in Alzheimer’s Dementia:

1. Working memory
2. Declarative memory/Episodic
3. Declarative memory/Semantic
4. Procedural memory

Alzheimer’s Dementia’s impact on **executive functioning** (EF):

Patients often display a decline in: Planning, self-motivation, goal setting, cognitive flexibility, and decision making.

Alzheimer’s Dementia’s impact on **communication**:

Early stages: Decreased confrontational **naming** and generative naming AND **poor discourse performance** (“Empty speech”, increased wordiness, tangential utterances, sentence fragments, decreased relevant ideas, decreased orientation to time/place, frequent repetitions).

Define **Traumatic Brain Injury** (TBI):

Alteration in brain function, or other evidence of brain pathology, caused by an external force (Falls, assaults, MVA, sports injuries).

Define **Acquired Brain Injury** (ABI):

An injury to the brain, which is not hereditary, congenital, degenerative, or induced by birth trauma (Stroke, near drowning, aneurysm, tumor, infectious disease, anoxic injury).

TBI’s possible impacts on **communication**:

Mutism is common early

Possible aphasia

Dysarthria (Noted in 33% of TBI)

Cognitive-communication deficits (100% poor topic maintenance, cohesion, reduced comprehension of discourse, abstraction)

In what ways do TBI/ABI patients struggle with **executive functioning**?

Struggle to set reasonable goals, plan/organize their behavior to reach the goals, inhibit behaviors that are incompatible with reaching goals, monitor performance, revise plans.

**Intervention for TBI**: Encoding and Consolidation Compensations

Written strategy examples: Memory notebooks, diaries, appointment calendars, day planners.

Teach that verbally presented information needs to be written down immediately.

Approaches will need to be modified as the disease progresses.

**Intervention for TBI**: Spaced Retrieval

Memory training procedure

Systematic recall of facts/procedures (Staff names, room number, swallowing precautions) over successively longer intervals and the retention of information over longer time periods.

It utilizes procedural memory skills, in this case the procedural memory component of priming.

Instead of mass practice, practice is distributed.

Often relies on preserved reading abilities.

Important to pair the “learned fact” to an execution of that information.

Might require periodic “booster sessions”.

**Intervention for TBI**: Errorless Learning

Clinicians use cues and instructional strategies that minimize the opportunity of the patient making errors.

Errorless learning appears to be more efficient and accurate than effortful learning.

Errorless learning can be utilized in combination with other learning strategies.