Differential Dx/Cognition Flashcards
1
Q
Red Flag EMERGENCY situations to identify on subjective exam include:
- Loss of ___, or difficult to ___
- Extreme ___ (not consistent with premorbid diagnosis)
- Uncontrolled ___
- ___ stiffness with fever
- [Slow / rapid] onset of [diffuse / focal ] neuro signs
- Severe ___ with other neurologic signs (c/f subarachnoid hemorrhage)
- Non-responsive ___ ___
A
Red Flag EMERGENCY situations to identify on subjective exam include:
- Loss of CONSCIOUSNESS, or difficult to AROUSE
- Extreme CONFUSION (not consistent with premorbid diagnosis)
- Uncontrolled SEIZURES
- NECK stiffness with fever
- RAPID onset of FOCAL neuro signs (e.g. sudden onset double vision, slurred speech, etc)
- Severe HEADACHE (“worst headache of my life”) with other neurologic signs (c/f subarachnoid hemorrhage)
- Non-responsive AUTONOMIC DYSREFLEXIA (emergent! individual could have a large stroke as a result)
2
Q
Non-emergent situations to note on subjective exam, but warrant referral:
- __ and __ dysfunction
- Neurologic signs inconsistent with ___
- Change in ___ status
- Report of symptoms of ___
- Signs/symptoms of systemic illness (e.g. __ or __)
A
Non-emergent situations to note on subjective exam, but warrant referral:
- BOWEL and BLADDER (and sexual) dysfunction
- Neurologic signs INCONSISTENT with DIAGNOSIS: e.g. progressive neuro signs in a non-progressive diagnosis; bulbar or other CN changes; significant changes in personality or cognition - E.g. with UTI in pt with PD; Evidence of motor neuron dz (fascinations, atrophy, weakness) not previously diagnosed)
- Change in AUTONOMIC status
- Report of symptoms of TRANSIENT ISCHEMIC ATTACK (TIA)
- Signs/symptoms of systemic illness (e.g. FEVER or DIAPHORESIS)
These all warrant an email or phone call to MD, but not an emergency!
3
Q
Localizing symptoms, e.g. with weakness
A
Start with - is it CNS vs PNS?
Then…
UMN: Cortex, brainstem, spinal cord - the whole motor pathway
LMN: Motor CN & nuclei, anterior horn cells in the spinal cord (note, these are special because they’re the start of the LMN even though they technically sit in the CNS!), spinal peripheral n, nerve root, NM junction, or th muscle itself!
CNS: might see sensory pattern: cortical, brianstem, spinal cord; BG, Cb, cortical association areas
Other brainstem signs (e.g. arousal, visceral function)
Other spinal cord issues (e.g. autonomic control of bowel, bladder, and sexual dysfxn)
PNS: sensory - CNs that provide sensation or special sensation. Peripheral nerves and nerve roots also provide sensation from the body. Autonomic component: may be noticing autonomic signs/symptoms!
4
Q
Central motor patterns - distinguishing between UMN/LMN lesions
- Weakness?
- Atrophy?
- Fasciculations?
- Reflex changes?
- Tone?
A
Central motor patterns - distinguishing between UMN/LMN lesions LMN: - +Weakness - Profound ATROPHY - +Fasciculations (e.g. w/ALS) - DECREASED Reflexes - DECREASED tone
UMN:
- +Weakness
- No atrophy (except in chronic conditions d/t disuse)
- NO fasciculations
- Increased (except in setting of spinal shock right after an acute lesion, see initial hypo or a-reflexia)
- Increased TONE (except in acute lesions)
5
Q
General patterns of weakness - localize lesion location and common patterns of weakness
- Cortex (hemisphere)
- Brainstem
- Spinal Cord Injury
- Polyneuropathy
- Neuromuscular junction
- Myopathy
A
General patterns of weakness - localize lesion location and common patterns of weakness
- Cortex (hemisphere): contralateral face and body
- Brainstem: IPSILATERAL face, CONTRALATERAL body (because a lesion that involves the facial NUCLEUS/nerve will affect face on same side, but if it hits motor tracts there, you’ll catch contralateral body! But definitely depends on where lesion is in the brainstem)
- Spinal Cord Injury: at and below level of the lesion
- Polyneuropathy: distal > proximal (e.g. weakness in “stocking-glove” pattern)
- Neuromuscular junction: Patchy weakness (e.g. shoulders, face), face is a common location for weakness (e.g. with Myastheina gravis - think about the mm you use a lot that are at a higher risk for fatigue, that is a common neuromusc junction pattern!)
- Myopathy: Proximal > distal (depends on the type of myopathy)
Structures:
UMN: Cortex, brainstem, spinal cord - the whole motor pathway
LMN: Motor CN & nuclei, anterior horn cells in the spinal cord (note, these are special because they’re the start of the LMN even though they technically sit in the CNS!), spinal peripheral n, nerve root, NM junction, or the muscle itself!
6
Q
Distinguish CNS vs PNS sensation loss patterns
A
CNS sensation patterns:
- Follows the homunculus: body regions are together, so sensation loss tends to follow similar areas!
- Selective loss of certain modalities (e.g. pain and temp)
- Loss of higher-order perceptual functions (e.g. stereognosis, graphesthesia, extinction)
PNS sensation loss:
- Follows peripheral nerve distribution
- Follows dermatomes (spinal nerve roots)
- Patterns like “stocking glove” loss (e.g. polyneuropathy)
7
Q
Common cerebellar patterns
A
Cb patterns:
- Dysmetria, dysdiadochokinesia, hyper/hypometria
- Nystagmus
- Dysarthria
- Ataxia (usually Cb, but sometimes sensory!)
8
Q
Common basal ganglia patterns
A
BG patterns
- Bradykinesia, hypokinesia
- Athetosis / chorea
- Tremor
- Dystonia
9
Q
___ is an inability to perform skilled tasks that cannot be explained by weakness, sensory loss, or ataxia.
A
APRAXIA is an inability to perform skilled tasks that cannot be explained by weakness, sensory loss, or ataxia.
10
Q
___ is a disorder of higher-order perception, includes astereognosis, agraphesthesia.
A
AGNOSIA is a disorder of higher-order perception, includes astereognosis, agraphesthesia.
11
Q
Brainstem dysfunction might result in…
A
Brainstem dysfunction might result in impaired…
- Visceral control
- Consciousness/alertness
- Sleep regulation
- Autonomic
12
Q
Spinal cord dysfunction may result in
A
Spinal cord dysfunction may result in:
- Bowel and bladder dysfunction
- Sexual dysfunction
13
Q
Classifying etiology/pathogenesis of a lesion - helpful pneumonic is “TIM VaDeTuCoNe” - what does it stand for?
A
Classifying etiology/pathogenesis of a lesion - helpful pneumonic is "TIM VaDeTuCoNe:" Trauma Inflammation/ Infection Metabolic Vascular Degenerative Tumor Congenital Neurogenic/Psychogenic
14
Q
What is Tabes Dorsalis?
- What is impacted?
- Cause?
- Symptoms? Sensation changes? DTRs? Balance?
A
What is Tabes Dorsalis?
- What is impacted? DEMYELINATION OF THE POSTERIOR COLUMNS OF THE SPINAL CORD (IMPACTS TRAVELING DCML TRACT), CAUSED BY SYPHILIS
- Symptoms?
- –Lightning-like back and leg pain
- – ABSENT position and vibratiory sense
- – ABSENT DTRs
- –+Rhomberg
- –SENSORY ATAXIA
15
Q
Pain is as a complex, multi-system [input / output] to the brain. It is produced by the brain when the brain perceives ___. Not all pain is bad! It helps for survival.
A
Pain is a complex, multi-system OUTPUT of the brain! It is produced by the brain when the brain perceives DANGER, but not all pain is bad! It helps for survival.
16
Q
____ are sensory receptors that transduce and encode damage or potential tissue damaging stimuli. Specifically, they are a ___ nerve ending which convert ___, ___, and ___ energy into electrical signals and carry it to the CNS. They are located in [what parts of the body? (6)]. They can become sensitized, which results in [central / peripheral / both] changes.
A
NOCICEPTORS are sensory receptors that transduce and encode damage or potential tissue damaging stimuli. Specifically, they are a FREE nerve ending which convert MECHANICAL, THERMAL, and CHEMICAL energy into electrical signals and carry it to the CNS. They are located in skin (cutaneous), muscles, joints, tendon, intervertebral discs, VISCERA, and around nervi nervorum of peripheral nerves. There are also “silent” nociceptors! Nociceptors can become sensitized, which results in BOTH CENTRAL AND PERIPHERAL changes.
17
Q
Cutaneous nociceptors respond to [one / many] noxious stimulus: ___, ___, or __
A
Cutaneous nociceptors respond to ONE noxious stimulus: MECHANICAL, HOT, or COLD
18
Q
Polymodal nociceptors respond to [one / many] stimuli (e.g. __, __, or __)
A
Polymodal nociceptors respond to many stimuli (e.g. MECHANICAL, CHEMICAL, or THERMAL)
19
Q
Role of Nociceptors:
- A nociceptor is a sensory receptor that encodes __stimuli and carries it to the __.
- With acute tissue damage, there are __ changes along with tissue __ which activates nociceptors. Once ___ goes away, the pain should go away! But if it doesn’t, we have a chronic pain problem due to impaired ____.
- In persistent or chronic pain, continued input changes the nociceptor’s ___ and CNS inputs, which maintains the ongoing pain.
- Ongoing nociceptor activity stimulates ___ responses, such as ___ nervous system and ___ modulation pathways.
A
Role of Nociceptors:
- A nociceptor is a sensory receptor that encodes NOXIOUS stimuli and carries it to the CNS.
- With acute tissue damage, there are INFLAMMATORY changes along with tissue INJURY which activates nociceptors. Once INFLAMMATION goes away, the pain should go away! But if it doesn’t, we have a chronic pain problem due to impaired CNS processing.
- In persistent or chronic pain, continued input changes the nociceptor’s SENSITIVITY and CNS inputs, which maintains the ongoing pain.
- Ongoing nociceptor activity stimulates ___ responses, such as SYMPATHETIC nervous system and BRAINSTEM modulation pathways.
20
Q
Pain that persists after an injury is termed ___ pain. This is also known as ___ pain or ___ ___. This is a is a [PNS/CNS] [output / input]. It is [disproportionate / proportionate ] to tissue injury, [stays local to the site of injury / may move around from 1 side to another], and may produce abnormal __ and __. This happens because the CNS undergoes ___ ___ post-injury, especially if nociceptors continue to fire - can be maladaptive if left untreated! Long and short, the underlying pathology [is / may not be] the primary problem.
A
Pain that persists after an injury is termed PERSISTENT PAIN. This is also known as CENTRAL pain or CENTRAL SENSITIZATION. This is a CNS OUTPUT. It is DISPROPORTIONATE to tissue injury, may MOVE from one side to another, may produce ABNORMAL SENSATION and MOTOR DYSFUNCTION. After an injury, the CNS undergoes PLASTIC REORGANIZATION particularly if the nociceptors continue to fire - this can be maladaptive if left untreated!
The underlying pathology MAY NOT BE the problem.
21
Q
In central sensitization, we see [central / peripheral / sympathetic ] involvement. Centrally, the multiple areas of the brain are involved and become ___, meaning they fire in response to sub-threshold (i.e. non-painful) stimuli. Specific areas within the brain involved with pain include the ___, ___, ___, and ___. Additional areas involved in the brainstem include the ___ [white / grey] matter and the __. Also involves [volitional / reflexive ] responses within the spinal cord; ascending [facilitatory / nociceptive / inhibitory] pathways; and descending [facilitatory / nociceptive / inhibitory]
A
In central sensitization, we see peripheral damage as well as involvement of both the CNS and sympathetic nervous system. Centrally, the multiple areas of the brain are involved and become SENSITIZED, meaning they fire in response to sub-threshold (i.e. non-painful, e.g. to soft touch) stimuli. Specific areas within the brain involved with pain include the THALAMUS, AMYGDALA, ANTERIOR CINGULATE CORTEX, and PREFRONTAL CORTEX. Additional areas involved in the brainstem include the PERIAQUEDUCTAL GREY MATTER and the SUPERIOR COLLICULUS. Also involves REFLEXIVE responses within the spinal cord; ascending NOCICEPTIVE pathways; and descending FACILITATORY AND INHIBITORY pathways
22
Q
In peripheral sensitization, we see increased spontaneous response, [increased / decreased] threshold firing, [increased/decreased] responsiveness to the same noxious stimuli, resulting in an increase or spreading of symptoms. This is directly responsible for increased input to the ___ via the ___. In the context of an acute injury, this is [unexpected / expected] - explain the pathophysiology: ____. With an acute injury, continuous pain input into the CNS causes ____ and this [is expected/ should be avoided] - so, manage pain, avoid ___, and promote gentle mobility!
A
In peripheral sensitization, we see increased spontaneous response, DECREASED threshold firing, INCREASED responsiveness to the same noxious stimuli, resulting in an increase or spreading of symptoms. This is directly responsible for increased input to the CNS via the SPINAL CORD. In the context of an acute injury, this is EXPECTED!
With an injury inflammatory cytokines are released and are sensitizing the peripheral nociceptors, which is expected during the acute healing process. But! With an acute injury, continuous pain input into the CNS causes HYPERSENSITIVTY and this SHOULD BE AVOIDED - so manage pain, avoid IMMOBILIZATION, and promote gentle mobility!
23
Q
What types of neurons exist in the dorsal horn to respond to various types of sensory inputs? Which ones respond to pain/noxious stim?
A
Dorsal horn includes:
High threshold neurons
Low threshold neurons
Wide dynamic range neurons
*Both HIGH threshold and WDR neurons respond to noxious stim! (NOT low threshold neurons)
24
Q
How does central sensitization change the firing of neurons in the dorsal horn of the spinal cord?
A
High threshold and wide dynamic range neurons (both of which respond to noxious stim normally) continue to fire together after an injury. If pain persists, it is often due to the WIDE DYNAMIC RANGE NEURONS interpreting a non-painful stimulus as a PAINFUL stimulus.
25
High threshold neurons in the dorsal horn respond to __ stimuli.
Low threshold neurons in the dorsal horn respond to __ stimuli.
Wide dynamic range neurons in the dorsal horn respond to __ stimuli.
High threshold neurons in the dorsal horn respond to NOXIOUS stimuli.
Low threshold neurons in the dorsal horn respond to INNOCUOUS (i.e. NOT noxious) stimuli.
Wide dynamic range neurons in the dorsal horn respond to both NOXIOUS and NON-NOXIOUS stimuli.
26
In central sensitization, we see increased responsiveness to [what types of?] stimuli. Symptoms [stay local / spread beyond the injured area aka the ___ ___]. The firing threshold [is decreased / is increased / stays the same]. These patients typically have [bouts of pain / constant pain even at rest]. Patients often report unusual sensations including __, __, or ___ sensations. What changes do we see on inspection of the limb itself?
In central sensitization, we see increased responsiveness to BOTH NOXIOUS and NON-NOXIOUS stimuli. Symptoms SPREAD BEYOND THE INJURED AREA (aka the RECEPTIVE FIELD), commonly in the limbs - pain area is often larger than primary injury, may not be located near primary injury. The firing threshold IS DECREASED. These patients typically have CONSTANT pain even at REST. Patients often report unusual sensations including BURNING, SHOOTING, or TEARING sensations. Pain area is often larger than the primary injury and may not be located near the primary injury. We see increased EDEMA as well as a change in COLOR and/or TEMPERATURE, as well as occasionally unusual movements (e.g. restless leg syndrome).
27
Increased response or specifically a PAINFUL response) to innocuous stimulus following injury is called ___. This can also result in motor dysfunction, including abnormal __, ___, and ___. Increased CNS receptors activity post injury further intensifies CNS input = ___.
Increased response (or specifically a PAINFUL response) to innocuous stimulus following injury is called ALLODYNIA. This can also result in motor dysfunction, including abnormal MOVEMENTS (e.g. restless leg syndrome), TREMORS, and local DYSTONIA. Increased CNS receptor activity post injury further intensifies CNS input = HYPERALGESIA.
28
Central sensitization causes changes in the body map, which at the brain level is the ___. When brain areas normally devoted to specific body parts/functions start to overlap, we call this ___. In the motor cortex, this may make it more difficult to __ and move that body part. In the sensory cortex, the limb might feel too __ to move, perhaps as a protective strategy. This may result in body perception disturbances, including __, __, lack of ___, dysfunction in ___ ___ ___, ___ of the limb, or a desire to __. Research shows that with increased body perception disturbance, it correlates with increased ___ and impaired ___ (e.g. 2-pt discrimination).
Central sensitization causes changes in the body map, which at the brain level is the HOMUNCULUS. When brain areas normally devoted to specific body parts/functions start to overlap, we call this SMUDGING. In the motor cortex, this may make it more difficult to ISOLATE and move that body part. In the sensory cortex, the limb might feel too SENSITIVE to move, perhaps as a protective strategy. This may result in body perception disturbances, including DISLIKE ("I don't like this limb"), DISTORTED perception, lack of OWNERSHIP ("that's not my hand"), dysfunction in TWO-POINT DISCRIMINATION, DENIAL of the limb, or a desire to AMPUTATE. Research shows that with increased body perception disturbance, it correlates with increased PAIN and impaired TACTILE ACUITY (e.g. 2-pt discrimination).
29
Syndromes associated with central sensitization includes... (4)
Examples of central sensitization...
- Complex Regional Pain Syndrome (CRPS), including Shoulder-Hand Syndrome
- Phantom limb pain
- Neuropathic pain, shingles, pain following SCI (interestingly, most pain is below level of injury, despite perhaps absent sensation there!), and diabetes
30
The amygdala is one area that is impacted in central sensitization. It responds to __, __, __, and __.
The amygdala is one area that is impacted in central sensitization. It responds to THREAT, FEAR, STRESS, ANGER.
Give pt control back: "Those are just my sensitive nerves! I don't need to give those my attention!"
31
Techniques to help "calm the brain down" in the setting of central sensitization. Pt needs to be given confidence that they are in control of their mind, understand that movement and pain doesn't mean harm, need strategies to stay in control and decrease abnormal response. Mindfulness helps! It helps to decrease __, __, __, __, __ an d__.
Techniques to help "calm the brain down" in the setting of central sensitization. Pt needs to be given confidence that they are in control of their mind, understand that movement and pain doesn't mean harm, need strategies to stay in control and decrease abnormal response. Mindfulness helps! It helps to decrease PAIN, SYMPTOM SEVERITY, DEPRESSION, ANXIETY, ATTENTION and CRAVINGS.
32
Fear of movements = __ __. Goal of PT interventions is to reduce their fear of movement and catastrophizing. Educate pt that pain doesn't mean that they can't move! Neuroscience education reduces __, __, __, and improves __. This must be individualized based on pt's education level, learning preferences, and complexity of pain. Must include paced education, movement pacing, graded exposure, pt goal setting, and HEP.
Fear of movements = FEAR AVOIDANCE Goal of PT interventions is to reduce their fear of movement and catastrophizing. Educate pt that pain doesn't mean that they can't move!
Neuroscience education reduces PAIN, DISABILITY, CATASTROPHIZATION, and IMPROVES MOVEMENT. Must be individualized based on pt's education level, learning preferences, and complexity of pain. Must include paced education, movement pacing, graded exposure, pt goal setting, and HEP.
33
Per Loeser's research, pain is stated as 4 concepts: ...
Nociception
Pain recognition at the cortical level
Pt perceived suffering
Pain behaviors
Pain is an interaction of the biological, psychological, and sociocultural variables
"When do you see yourself getting better? What do you hope to do?"
34
Individuals with CRPS often have persistent __, __ disturbances, and dysfunctional MOVEMENT that are not immediately identified. The longer symptoms persist, the more _ __ occurs. Needs a biopsychosocial approach and early intervention.
Individuals with CRPS often have persistent PAIN, SENSORY disturbances, and dysfunctional MOVEMENT that are not immediately identified. The longer symptoms persist, the more CORTICAL REORGANIZATION occurs. Needs a biopsychosocial approach and early intervention.
35
Diagnosis of CRPS 1 (aka ___) requires 2 to 4 of the below criteria:
- ____ event or period of ___
- Pain is ____ and includes either __ or __
- ___ or changes in blood flow to the ___, or ___ activity
- Diagnosis is excluded by the existence of conditions that would account for pain
Diagnosis of CRPS 1 (aka previously called REFLEX SYMPATHETIC DYSTROPHY) requires 2 to 4 of the below criteria:
- NOXIOUS event or period of IMMOBILIZATION
- Pain is DISPROPORTIONATE and includes either ALLODYNIA or HYPERALGESIA
- EDEMA or changes in blood flow to the SKIN, or SUDOMOTOR activity
- Diagnosis is excluded by the existence of conditions that would account for pain
36
Diagnosis of CRPS II aka ___ requires all three of the following to be present:
- Continuing pain and ___. Could also be __ after a nerve injury, though is not limited to an injured nerve
- ___ or changes in blood flow to the ___, or ___ activity in the region of pain
- Diagnosis is excluded by the existence of conditions that would account for pain
Diagnosis of CRPS II aka CAUSALGIA requires all three of the following to be present:
- Continuing pain and ALLODYNIA. Could also be HYPERALGESIA after a nerve injury, though is not limited to an injured nerve
- EDEMA or changes in blood flow to the SKIN, or SUDOMOTOR activity in the region of pain
- Diagnosis is excluded by the existence of conditions that would account for pain
37
Cognitive impairments include an interrelationship between executive function, working memory, and attention. Specifically, the overlap between executive processes and attention includes [what aspects of attention], and all three overlap to contriubte to [what 3 aspects of memory?]
Cognitive impairments include an interrelationship between executive function, working memory, and attention. Specifically, the overlap between executive processes and attention includes SELECTIVE ATTENTION, DIVIDED ATTENTION, ALTERNATING ATTENTION, and TASK PERSISTENCE, and all three overlap to contribute to WORKING MEMORY, PROSPECTIVE MEMORY, and AWARENESS.
38
Executive functions are those that drive and self-regulate behavior. Specifically, they allow us to:
- Make __
- Evaluate __
- __ and __ actions
- Manage __ or __ situations
- Evaluate progress toward __
- ___ behavior if necessary
Executive functions are those that drive and self-regulate behavior. Specifically, they allow us to:
- Make DECISIONS
- Evaluate RISK
- PLAN and PRIORITIZE actions
- Manage NEW or NOVEL situations
- Evaluate progress toward GOALS
- CHANGE behavior if necessary
39
What areas of the brain are involved in the processing of executive function?
- Frontoparietal attention network (Dorsolateral prefrontal cortex, inferior frontal sulcus, middle frontal gyrus, infraparietal sulcus)
- Lateral prefrontal cortex
- Anterior cingulate
- Brodmann area 10
40
What disorders may affect executive function / frontal lobe function?
```
Frontotemporal dementia
Alzheimer's dz
Progressive supranuclear palsy
Corticobasal degeneration
Vascular dz
Parkinson's dz
Infectious or inflammatory diseases of the CNS
TBI
Psychiatric disorders
Creutzfeldt-Jakob Disease
Wilson's Disease
Huntington's Disease
```
41
Dysexecutive syndrome is associated with dysfunction to which cortical area? Specifically, we see problems with what activities?
Dysexecutive syndrome is associated with damage to the DORSOLATERAL frontal cortex.
We see problems with planning, strategy development, problem solving despite distractions, and cognitive persistence, as well as emotion, and behavior regulation. Involves integrating sensory info & making decisions! Trouble developing a plan (evaluating options, not thought out), not good at evaluating performance/integrating feedback/ recognizing errors
42
Disinhibition is associated with dysfunction to which cortical area? There are connections between the ___ frontal cortex to the __ and the __ region. Main issues include... (5)
Disinhibition (and attention/ distractibility!) = ORBITOFRONTAL cortex damage. Connections between the INFERIOR PREFRONTAL CORTEX to the AMYGDALA and the TEMPORAL region. Main issues include...
- DISINHIBITION
- EMOTIONAL LABILITY
- DECREASED JUDGEMENT
- DISTRACTABILITY
- PERSEVERATION
Might be restless, impulsive, socially inappropraite (immaturity, lacking self-control, inappropriate cheerfulness or optimism), denial of deficits, and behaviors, as well as attentional signs (distractability, impulsive responses), difficulty shifting (disengaged, perseveration), slow processing of info
43
Apathy is associated with dysfunction to which cortical area?
Apathy = MEDIAL prefrontal lobe damage. Also have connections to the amygdala.
Decreased affect, initiative; motor and verbal production decreased; "pseudo-depression"
44
The Barco-Crosson Hierarchy of Awareness starts with ___ awareness - they are aware of their impairments. The second level is ___ awareness, which involves knowing that there is a problem as it is happening (e.g. noting a problem with your memory while you're doing a certain task). The top of the pyramid is ___ awareness; this requires the first 2 types of awareness to be present to then ___ a problem because of deficits you know you have.
The Barco-Crosson Hierarchy of Awareness starts with INTELLECTUAL awareness - they are aware of their impairments. The second level is EMERGENT awareness, which involves knowing that there is a problem AS IT IS HAPPENING (e.g. noting a problem with your memory while you're doing a certain task). The top of the pyramid is ANTICIPATORY awareness; this requires the first 2 types of awareness to be present to then ANTICIPATE a problem because of deficits you know you have.
45
Agnosia is the inability to interpret __ and hence to ___ things, typically as a result of brain damage. The ___ is a good outcome measure to assess a pt's insight into their deficits. Denial of deficits is called __.
Agnosia is the inability to interpret SENSATIONS and hence to RECOGNIZE things, typically as a result of brain damage. The FUNCTIONAL SELF-ASSESSMENT SCALE is a good outcome measure to assess a pt's insight into their deficits - pt and a caregiver or therapist complete it, looks at pt's perceived independence with functional mobility & ADLs, often done in rehab setting. Denial of deficits is called ANOSAGNOSIA.
46
Memory can be subdivided into two primary types: __ and __.
Memory can be subdivided into two primary types: DECLARATIVE and NON-DECLARATIVE.
47
Declarative memory helps you recall facts/concepts (i.e. [episodic / semantic] memory - examples?) and events [i.e. [episodic / semantic] memory - examples?). What parts of the brain do these occur in? How long are they stored?
Within episodic memory, we can also store __ associations after a single trial; episodic memory is [fixed / flexible] and can be [difficult to apply / readily applied] to novel contexts.
Declarative memory helps you recall facts/concepts (i.e. [SEMANTIC memory; e.g. states and their capitals; parts of the brain) and events [i.e. EPISODIC memory; e.g. what you had for lunch or did on vacation).
Episoidic = MEDIAL TEMPORAL LOBES, ANTERIOR THALAMIC nucleus, mamillary body, fornix, and PREFRONTAL CORTEX
Semantic = INFEROLATERAL temporal lobes
BOTH types are stored anywhere from MINUTES to YEARS
Within episodic memory, we can also store ARBITRARY associations after a single trial (e.g. links to smells/things you hear that is reminiscent of a time/place); episodic memory is flexible and can be READILY applied to novel contexts. Storage/recall is based on relative importance of the event!
48
Non-declarative memory includes 4 categories:
Generally, it is acquired across [single / multiple ] trials (except in the case of __) and tends to be [flexible and able to adapt to varied situations / inflexible and bound the learning situation]
Non-declarative memory includes 4 categories:
- Procedural: skills and habits
- Priming and Perceptual Learning
- Simple Classical Conditioning (includes both emotional and skeletal responses)
- Nonassociate Learning
Generally, it is acquired across MULTIPLE trials (except in the case of PRIMING) and tends to be INFLEXIBLE AND BOUND TO THE LEARNING SITUATION, not readily accessed by response systems that were not involved in the original learning. Tends to be learned by practice and doing! (e.g. learning to do a layup, drive stick shift)
*With practice, even someone who cannot remember things (declaratively) can still learn a skill via non-declarative pathways!!
49
What type of memory is associated with the following brain areas:
- Medial Temporal Lobe/Diencephalon?
- Striatum?
- Neocortex?
- Amygdala?
- Cerebellum?
- Reflex pathways?
What type of memory is associated with the following brain areas:
- Medial Temporal Lobe/Diencephalon = DECLARATIVE (facts/events)
- Striatum = PROCEDURAL (skills and habits)
- Neocortex = PRIMING and PERCEPTUAL learning
- Amygdala = EMOTIONAL Responses associated w/ Simple classical conditioning
- Cerebellum = SKELETAL responses associated w/simple classical conditioning
- Reflex pathways = NONASSOCIATE learning
50
Examples of disorders which disrupt episodic memory...
```
Dementias
Encephalitis
Korsakoff's syndrome
Concussion
TBI
Seizure
Hypoxic-ischemic injury
Cardiopulmonary bypass
Medication side-effects
Vit B12 deficiency
MS
```
51
Semantic memory is closely tied to your ability to formulate and understand ___, which makes sense given primary brain location in the ___!
Semantic memory is closely tied to your ability to formulate and understand LANGUAGE, which makes sense given primary brain location in the INFEROLATERAL TEMPORAL LOBE!
52
Examples of disorders which may disrupt semantic memory...
Dementias
Encephalitis
Concussion
TBI
53
Post traumatic amnesia is a state of __ which occurs after a brain injury which impacts their ability to remember [old / ongoing] events. Can also impact the time just prior to the injury and still be considered post-traumatic amnesia. Often can indicate the __ of injury, may be assessed by neuropsych or SLP.
Post traumatic amnesia is a state of CONFUSION which occurs after a brain injury which impacts their ability to remember ONGOING events. Can also impact the time just prior to the injury and still be considered post-traumatic amnesia. Often can indicate the SEVERITY of injury, may be assessed by neuropsych or SLP.
54
Retrograde amnesia describes the period [before/after] point of brain injury, vs anterograde amnesia describes the period [before/after] point of brain injury.
Retrograde amnesia describes the period BEFORE point of brain injury, vs anterograde amnesia describes the period AFTER point of brain injury (inability to remember ongoing events). Memories are PRESERVED before the onset of the retrograde amnesia.
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# Define source memory.
Define prospective memory.
Source memory = recall of where you obtained X information, remembering that you passed X info along to X person (may see impaired source memory w/person who repeats same story/info to a person over and over again)
Prospective memory = trying to remember to do something in the future
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Disorders which disrupt procedural memory (and may benefit from a declarative cue to accomplish a task!)... (6)
Disorders which disrupt procedural memory (and may benefit from a declarative cue to accomplish a task!)
- Parkinson's Dz
- Huntington's Dz
- Progressive supranuclear palsy
- Olivopontocerebellar degeneration
- Depression
- OCD
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Both explicit and implicit memory systems are used together with learning. These two systems are dissociated: you can have damage (or intactness) of one but not the other. SO! Use knowledge of the affected brain areas, psych results, and observation to determine the best strategies for teaching! Procedural tasks can be described explicitly (though this may not help learning).
Both explicit and implicit memory systems are used together with learning. These two systems are dissociated: you can have damage (or intactness) of one but not the other. SO! Use knowledge of the affected brain areas, psych results, and observation to determine the best strategies for teaching! Procedural tasks can be described explicitly (though this may not help learning).
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The __, __, and ___ are three tests that screen for declarative memory impairment.
The MINI MENTAL STATUS EXAM (MMSE), MONTREAL COGNITIVE ASSESSMENT (MoCA) and ST. LOUIS UNIVERSITY MENTAL STATUS EXAM (SLUMS) are three tests that screen for declarative memory impairment.
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The __ and __ are tests that can be used as serial assessments of cognition (declarative memory) in the acute/inpatient settings. Originally used in __ population, but can be used more broadly.
The orientation log (O-log) and Cognitive Log (Cog-log) can be used as serial assessments in the acute/inpatient settings. Originally used in BRAIN INJURY, but can be used more broadly.
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Tests of [implicit / explicit] memory include the dot clearing task, which is an example of ___ . When you see a word (40 words presented on screen in 2 seconds), you have a tendency to remember that word more than a word you haven't seen. Then, you're shown 60 words (30 are pulled from the original set, and 30 words are new). Brain is ___ to recognize a word you have seen recently more so than a word you have not seen previously.
Tests of IMPLICIT memory include the dot clearing task, which is an example of PRIMING. When you see a word (40 words presented on screen in 2 seconds), you have a tendency to remember that word more than a word you haven't seen. Then, you're shown 60 words (30 are pulled from the original set, and 30 words are new). Assessed your reaction time of "when you knew the word" and response time of "when you type word in" and if they'r correct. Brain is PRIMED to recognize a word you have seen recently more so than a word you have not seen previously.
*Not a lot of tasks which assess implicit motor memory, except in research settings!
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With a declarative memory impairment, first consider if this will improve or degrade with time? Strategies to manage impairment will shift over time if things improve or worsen. Use [rehabilitative/compensatory] strategies.
These will work best with [mild / moderate / severe] injuries and if the person is motivated to learn new strategies, is [aware / unaware] of their deficits, and can ___ when new strategies make sense. If injury is more [mild
/ severe], you need a lot of ___; procedural elements [help / do not help]. Difficult to get consistent use of devices/supports unless you can make them ___ which taps into their __ learning.
With a declarative memory impairment, first consider if this will improve or degrade with time? Strategies to manage impairment will shift over time if things improve or worsen. Use COMPENSATORY strategies (e.g. a memory notebook, written cues/schedule). These will work best with MILD TO MODERATE injuries and if the person is motivated to learn new strategies, is AWARE of their deficits, and can PROBLEM-SOLVE when new strategies make sense. If injury is more SEVERE, you need a lot of REPETITION; procedural elements HELP. A familiar environment is SO helpful; new environments may make their cognitive impairment seem worse. Difficult to get consistent use of devices/supports unless you can make them HABITUAL which taps into their PROCEDURAL learning. Sometimes building in supports (such as cues) can be more flexible than trying to make something a habit. Examples include imagery, paging/reminder system, self-instructional strategies, memory notebooks, etc.
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With procedural learning, we are effectively trying to form a ___. Best to do [blocked / random] practice in conditions which are [most / least] similar to actual context. Procedural learning [cannot / may / always] occur(s) without declarative memory of skill development. Explicit instruction/verbal cues can [improve / interfere with] procedural learning! Internal vs external cues are best for procedural learning?
With procedural learning, we are effectively trying to form a HABIT. Best to do BLOCKED practice in conditions which are MOST similar to actual context. Procedural learning MAY occur without declarative memory of skill development. Explicit instruction/verbal cues can INTERFERE WITH procedural learning! EXTERNAL POINT OF REFERENCE is better than internal for procedural learning.
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Attentional networks in the brain are anatomically [focused / widespread]. ___ is a key neurotransmitter in attention.
Attentional networks in the brain are anatomically WIDESPREAD. DOPAMINE is a key neurotransmitter in attention.
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Attention demands involve both automatic and controlled processing. [Automatic / Controlled] processing is fast, not attention demanding, occurs parallel in nature to other more active processes, and is not "volitional" (i.e. you can't turn it off) and involves the processing of often unavoidable stim. E.g. at a cocktail party you are tuning out all kinds of stim, but then you hear your name (has meaning to you!) you turn your active attention to it in a volitional way.
Attention demands involve both automatic and controlled processing. AUTOMATIC
processing is fast, not attention demanding, occurs parallel in nature to other more active processes, and is not "volitional" (i.e. you can't turn it off) and involves the processing of often unavoidable stim. E.g. at a cocktail party you are tuning out all kinds of stim, but then you hear your name (has meaning to you!) you turn your active attention to it in a volitional way.
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Attention demands involve both automatic and controlled processing. [Automatic / Controlled] processing is slow, attention demanding, serial in nature, and strongly "volitional"
Attention demands involve both automatic and controlled processing. CONTROLLED processing is slow, attention demanding, serial in nature (meaning you need to focus on 1 thing and not something else in order to be successful), and strongly "volitional." E.g. reading an article, trying to understand a concept that is new to you. When people say "you can't multitask," they tend to be referring to this - when really you might be switching back and forth between two "spotlighted" tasks.
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Types of attention:
- ___ attention = vigilence
- ___ attention - requires inhibition, filtering out background noise
- ___ attention = switching from one task to another (which impacts performance of both tasks!)
- ___ attention = performing at least two tasks at one
Recall, attention requires executive control to be able to focus!
Types of attention:
- SUSTAINED attention = vigilence
- FOCUSED attention - requires inhibition, e.g filtering out background noise
- ALTERNATING attention = switching from one task to another (which impacts performance of both tasks!). In a patient case, may see perseveration as an extreme.
- DIVIDED attention = performing at least two tasks at one, doing a motor and cognitive task concurrently
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Selective attention, divided attention, alternating attention, and task persistence all require an overlap of both attentional processes and ___. Things like working memory, prospective memory, and awareness require attentional processes, ___ function, and ___ processes!
Selective attention, divided attention, alternating attention, and task persistence all require an overlap of both attentional processes and EXECUTIVE FUNCTION (prefrontal cortex). Things like working memory, prospective memory, and awareness require attentional processes, EXECUTIVE function, and MEMORY processes!
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Working memory is a function of your central executive function. It relies on the visualspatial sketchpad which processes ___ (e.g. the "map" of how to get somewhere), the episodic buffer which processes ___ (e.g. related to events) and the phonological loop which processes ___ (e.g. your locker number is 819, the combination for the lock is 8-20-12). But really, instead of working memory, this is more reflective of working __. The ___ [brain area] is important in this.
Working memory is a function of your central executive function. It relies on the visualspatial sketchpad which processes VISUAL SEMANTICS (e.g. the "map" of how to get somewhere), the episodic buffer which processes EPISODIC LTM (e.g. related to events that have happened to you, the "YouTube of your life") and the phonological loop which processes LANGUAGE AND AUDITORY INFO (e.g. understanding the language and meaning of it, e.g. your locker number is 819, the combination for the lock is 8-20-12). But really, instead of working memory, this is more reflective of working ATTENTION! PREFRONTAL CORTEX is important in this.
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Dual task processing occurs in the [part of the brain]. Dual tasking looks at primary task and expects that when you add a secondary task, you'll see some [improvement/detriment] in performance due to a __ issue.
Dual task processing occurs in the DORSOLATERAL PREFRONTAL CORTEX (specifically the inferior frontal sulcus : middle frontal gyrus: intraparietal suclus) all part of the fronto-parietal attention network. Dual tasking looks at primary task and expects that when you add a secondary task, you'll see some DETRIMENT in performance due to a RESOURCE CAPACITY issue.
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Dual task problems arise in what patient populations?
```
Alzheimers
TBI
CVA
PD
MS
```
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What factors contribute to dual task abilities?
Examination of dual task performance (rather than just looking at cognitive or motor performance alone) helps to predict risk for ___.
```
Attention deficits
Executive function impairments
mobility impairments (balance impairment may require more attention to maintain stability which takes away from reserves!)
Memory deficits
Depressive symptoms
Anxiety
```
Examination of dual task performance (rather than just looking at cognitive or motor performance alone) helps to predict risk for FALLS. Odds ratio for falling was 5.3 when older adults stopped walking when talking
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When assessing dual tasking, consider the individual and the demand that the task will impose! E.g. for someone who is dysarthric, what will be the impact of a spoken task?
When assessing dual tasking, consider the individual and the demand that the task will impose! E.g. for someone who is dysarthric a spoken task will be much more attention demanding than an alternate task (e.g. a manual task/carrying water - this might be harder for someone w/ataxia!). Also consider age/experience, educational level, cognitive impairments etc.
Make sure to assess single task first, then determine dual task cost when doing them together! May see speed-accuracy trade-off.
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Examples of postural dual tasks...
Vary your walking parameters! (self-selected vs faster walking; narrowed BOS; turns; avoidign obstacles; agility tasks)
Concurrent manual tasks (e.g. carry cup of water or a tray; manipulating objects; reaching for targets; functional activities like texting or dialing a phone)
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Examples of cognitive dual tasks...
Reaction time tasks
Rote tasks (alphabet, counting)
Serial, repetitive tasks (subtractions, n-back)
Working memory tasks (digit span, list recall)
Discrimination tasks (Stroop - e.g. word "red" spelled in blue ink and needing to verbalize the color of the ink, clock test)
Fluency tasks ("name as many words that start with the letter..." - F, A, S are used most common; categories)
Visual search/identification (obstacle avoidance, VR applications; number of X that you see in this hall)
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Increased risk for falls in older adults is associated with:
- Discrepancy between TUG and TUG-cog of >___ seconds
- TUG-cog >___ sec
Increased risk for falls in older adults is associated with:
- Discrepancy between TUG and TUG-cog of >4.5 seconds
- TUG-cog >15 sec
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How to train/improve attention?
- [acute / post-acute] training is best supported
- Training should include teaching ___ strategies
- Provide feedback and education about the types of attention and conditions which might be challenging
- [Consistent/varied] conditions/complexity
- Practice of [simple/more complex] functional tasks
- Focus on [clinic setting /real-life conditions] to encourage generalization
- Start [complex/simple] where difficulty occurs then increase difficulty once meeting a pre-set level of accuracy
How to train/improve attention?
- POST-ACUTE training is best supported (in acute setting, various medication effects and/or medical instability impacts their ability to attend)
- Training should include teaching SELF-REGULATION / SELF-TALK strategies
- Provide feedback and education about the types of attention and conditions which might be challenging
- VARIOUS conditions/complexity
- Practice of MORE COMPLEX functional tasks
- Focus on REAL-LIFE CONDITIONS to encourage generalization
- Start SIMPLE where difficulty occurs then increase difficulty once meeting a pre-set level of accuracy
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Describe the following theories which may explain dual task performance
- Fixed attentional capacity
- Bottleneck theory
Describe the following theories which may explain dual task performance
- Fixed attentional capacity: You have a CERTAIN AMOUNT OF ATTENTION that you can allocate to things for a motor or cognitive task. Interference occurs with increased demands/difficulty of either of those - make sure the level of challenge adequately challenges resources, but not too much!
- Bottleneck theory: You are only able to really process ONE thing at a time. With training, you can move through from 1 item to the next (serial processing) more quickly
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Relationships between cognition and gait
Changes in cognition and gait speed over time?
Any relationship between gait speed and cognition in normal adults vs those with cog impairment/dementia?
- BOTH cognitive scores and gait decline over time
- SLOW gait speed precedes cognitive decline, and a faster baseline gait speed is associated w/ less cognitive decline across all cognitive scores
...BUT in those w/mild cognitive impairment or dementia, baseline COGNITION is not associated with changes in gait speed
- Faster gait speed is associated with better MEMORY, EXEC FXN, and GLOBAL COGNITION
Long story short: gait speed may be useful to measure as a risk factor for cognitive decline!
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Relationship between executive function and falls?
***Executive function deficits have been associated with falls, decr gait speed, gait performance (including incr gait variability), and freezing of gait in Parkinson's dz!
Relationship between poor executive fxn and increased fall risk!
- --> Association btwn poor exec fxn and declines in gait speed
- --> Impaired exec fxn associated w/more serious falling patterns
* ***---> Decreased exec fxn = increased gait variability (in pts w/dementia) = higher fall risk
Stride time variability (reflects 1 of the final pathways that the central system regulates - could demarkate frontal cortical dysfunction in those w/ or w/out dementia!) is a relevant marker of gait stability and fall risk
---> increased variability in gait = increased fall risk
Exec fxn (e.g. frontal assess battery, clock test, verbal fluency, stroop interference) and attention correlated w/gait fxn in AD and PD, as well as w/falls in older adults
Freezing of gait in PD is associated w/exec dysfxn and visuospatial measures
Gait stability correlates w/visuospatial measures in older adults
Some studies show relationship btwn memory and gait speed in combination w/exec dysfxn
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An individual with dementia /cognitive dysfunction is more likely to walk ___ and with greater gait ___. Additionally, we can assume an individual with Alzheimer's has impaired executive function, which we know is associated with __.
An individual with dementia /cognitive dysfunction is more likely to walk SLOWLY (DECREASED GAIT SPEED) and with greater gait VARIABILITY. Additionally, we can assume an individual with Alzheimer's has impaired executive function, which we know is associated with MORE SERIOUS FALLS.
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To assess the impact of cognitive function on gait, we want to assess ___! Describe the two major tests to do this.
To assess the impact of cognitive function on gait, we want to assess DUAL TASKING!
If pt has relatively intact gait (0.95 m/s or faster) and has dual task cost of >=18%, predicts falls! (we don't know the cutoff with slower gait speeds). PD and AD might have larger dual task cost.
Describe the two major tests to do this.
(1) Walking While Talking Test
Description: A test of dual task demands. Assesses time taken to walk a set distance (40ft in Verghese study)
- Walk
- Walk while reciting alphabet (simple dual task)
- Walk while reciting every other letter of the alphabet (Complex)
Cutoffs:
>=20 sec for WWT simple = HIGH sensitivity for identifying fallers (89%), modest specificity (46%) to r/o falls
>=33 sec for WWT complex = HIGH sensitivity for identifying falls (95.6%), modest specificity to r/o fall (38.5%)
(2) TUG + TUG Cog
- Do TUG
- Assess secondary task: while in sitting, have pt count backward by 3s (or find another appropriately challenging but doable cognitive task)
- Next have pt do TUG and simultaneously count backward by 3s
- Record time to complete and errors made on cognitive task
Calculate Dual-Task Cost (i.e. interference):
(TUG Cog time - TUG time) / TUG time = Dual task cost (%)
- Be sure to think about how dual-task interference applies to BOTH the cognitive and the motor task!
- --> Mutual interference: both motor and cog tasks decline in dual-task condition. Means pt has INADEQUATE attentional resources, and now demands are exceeding total capacity.
- --> Motor interference with no cognitive interference: only MOTOR task declines in dual task condition. This also suggests INADEQUATE attentional resources, but now the cognitive performance is prioritized - there is capacity sharing with primary allocation of capacity to the cognitive task
- --> Motor interference w/cognitive benefit: cognitive task performance actually improves relative to single task conditions! Could be considered a less severe form of dual-task interference - dual task decline in gait occurred not d/t insufficent resources, but because the resources were OVER allocated to the cog task.
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Key concepts in training balance/mobility in clients with dementia?
- Do DUAL TASK TRAINING to reduce fall risk!!! (in older adults, pts w/dementia, and PD)
- ---> Older adults prioritize the motor component of the dual task to a lesser extent than younger adults, which increases fall risk in dual task conditions. You can train them to focus more on mobility and less on cognitive task (and/or well as compensate: teaching them not to dual task)
- --> Dual task performance gets worse as cognitive impairment gets worse
- Cognitive pharmacological therapy: cholinesterase inhibitors and memantine
- Exercise: High intensity resistance and functional exercise program (e.g. sit to stand, walking altering speed), IMPROVED temporal and spatial characteristics (but nto for step width or step variability) of gait for older adults with mild to moderate dementia
- Group exercise program with dual task training improves gait but not vascular health in older adults without dementia
- Fall prevention: classic multifactorial intervention is NOT as effective in those w/cognitive deficits! May be that the underlying mechanisms for falls differ, and/or a failure to address cognitive deficits adequately. Improving attention and executive function can be a complementary way to treat mobility decline and fall risk.
- --> Cognitive remediation alone improved gait velocity both during walking and walking w/dual task! Dual task performance only improves in study groups who had variable priority instructions (i.e. prioritize walking, vs prioritize cog task)
SO train dual task in individuals with dementia to improve dual tasks!! Does best if you progressively increase the complexity of the task AND if you vary the focus of attention during training
Falls are TWICE as common in people with cognitive dysfunction as in cognitively intact older adults!!
Music and/or rhythmic auditory cuing at a comfy tempo resulted in DECLINE in gait in a single session in alzheimers individuals - (specifically decline in spatial gait parameters, maybe d/t impaired exec fxn)
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Exercise and cognitive function
Does physical activity improve cognitive function? Parameters?
Groot et al 2016. (meta analysis)
Physical activity DOES improve cognitive function
- both in pts with and without AD
- Needs aerobic activity - Aerobic alone or a combo Aerobic + non aerobic works! (but non-aerobic alone doesn't do it)
- Low frequency (<150 min/wk) or high frequency (>150 min/wk) both work, but low frequency is actually better than high frequency!
Coelho FG et al 2013:
Multimodal exercise (includes motor + cog tasks simultaneously) intervention improves frontal cognitive functions and gait in Alzheimer's dz!
(1 hr session 3x/wk, 16 wks vs just "daily activities" in control group)
BUT Young et al 2015 Cochrane Review:
NO evidence that aerobic physical activities (even if they improve cardiorespiratory fitness) have any cognitive benefit in cognitively HEALTHY adults (though physical activity is inversely related to dementia, particularly w/walking programs)
- There IS a relationship that individuals who exercise more have a reduced risk of cognitive decline, but RCT studies don't show this as consistently
- Maybe not all types of exercise impact cognition (or specific types of exercise impact specific cognitive domains)
- But exercise improves cardiovascular health, and improved cardiovascular health decreases risk for developing dementia
BUT in individuals who alredy have mild cognitive impairment, high levels of participation in physical leisure activities are associated with reduced risk of dementia! Exercise plays a protective role in this population.
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Dementia is defined as aN [acquired / inborn] intellectual impairment produced by brain dysfunction. It comprises at least one of the following spheres of mental activity...
Dementia is [common/ uncommon] involving as many as __% of those >65yo, and __% of those >85yo.
Dementia is defined as an ACQUIRED intellectual impairment produced by brain dysfunction.
It comprises at least one of the following spheres of mental activity...
- Language
- Memory
- Visuospatial skills
- Emotion
- Cognition (abstraction, calculation, judgement, and executive function)
Dementia is COMMON involving as many as 10% of those >65yo, and 50% of those >85yo (1/3 families will have a parent affected!)
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Causes of dementia...
Neurodegenerative disorders
- Alzheimer's Dementia (43% of all cases, most common)
- Down syndrome
- Parkinson's
- Dementia w/Lewy Bodies (LBD)
- Huntington's dz
- Frontotemporal dementia (including Pick's)
Cerebrovascular Disorders
- Vascular dementia (20%, 2nd most common!) - d/t strokes, or multiple infarcts
- Vasculitis
- Subarachnoid hemorrhage
Toxic/Metabolic Encephalopathies
- Endocrine disorders: Thyroid, parathyroid, pituitary, and adrenal disorders
- Drugs (illegal OR even prescribed drugs!)
- EtOH
- Industrial agents
- Heavy metals
- Carbon monoxide
Prior Associated Disorders
- Creutzfeld-Jakob dz
Neurogenetic Disorders
- Spinocerebellar ataxias
- Myotonic dystrophy
- Wilson disease
Infectious Disorders
- Meningitis (e.g. TB)
- Encephalitis
- Neurosyphilis
Miscellaneous
- Post-traumatic dementia
- Demyelinating MS
- Neoplasm
- Hydrocephalus
- Depression
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Be sure to seek out reversible or treatable causes of dementia! These include... (8)
- Depression (most common): 4.5%
- --> Leads to changes in cognitive processing and can be mistaken for dementia in the elderly!
- --> Geriatric Depression Scale can discriminate the pattern of depressive symptoms from general characteristics of the elderly population; 30?s, takes up to 30 mins; has a short form with 15 items takes 5-7 mins
- --> Patient Health Questionnaire (PHQ-2 and PHW-9) are commonly used and validated screening tools; PHQ2 has high sensitivity but lower Sp, but PHQ-9 has lower Sn but higher Sp...so do PHQ-2 first! If that's +for depression (whereas a negative would more definitively rule out), do the PHQ-9 too (which if +, can more definitively rule IN).
- Overuse of certain meds or misuse
- Normal pressure hydrocephalus (1.6%)
- Metabolic including B12 deficiency (1.5%)
- Hypothyroidism
- Neoplasm (1.5%)
- Infections (0.6%)
- AIDS
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In acute illness, any cognitive change could be due not to dementia but perhaps to ___ (which is NOT a type of dementia!)
This is defined as a transient disorder with a relatively [ rapid / slow] onset, a course that typically [ remains constant / fluctuates] and a [long / short] duration, typically ___.
Essential features of this include:
- Reduced ability to maintain __ to external stimuli and appropriately shift to new external stimuli
- ____ thinking, as manifested by __, __, or __ speech
Underlying causes should be treated.
In acute illness, any cognitive change could be due not to dementia but perhaps to DELIRIUM (which is NOT a type of dementia!)
Delirium is defined as a transient disorder with a relatively RAPID onset, a course that typically FLUCTUATES and a BRIEF duration, typically HOURS TO WEEKS (most often DAYS).
Essential features of this include:
- Reduced ability to MAINTAIN ATTENTION to external stimuli and appropriately SHIFT ATTENTION to new external stimuli
- DISORGANIZED thinking, as manifested by RAMBLING, IRRELEVANT, or INCOHERENT speech
Underlying causes should be treated.
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In more insidious cognition change, physicians will first want to rule out __, __, or ___ side effects/misuse. If that workup is unrevealing, will refer for further w/u.
In more insidious cognition change, physicians will first want to rule out DEPRESSION, B12 DEFICIENCY, or MEDICATION SIDE EFFECTS/MISUSE. If that workup is unrevealing, will refer for further w/u.
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How do delirium, dementia, and depression differ?
Rate of onset?
Level of consciousness?
Mood?
Duration?
Cognitive Features?
Sleep/wake cycles?
Psychomotor changes?
Associated features?
DEMENTIA
- Insidious onset, often slower
- Impaired consciousness only very LATE in dz, not earlier
- Stable mood
- Duration is long term
- Reduced short > long term memory
- Reversed day/night cycle
- Late onset psychomotor changes
DELIRIUM
- ACUTE onset
- Highly variable, often impaired consciousness
- Variable mood w/consciousness
- SHORT duration (hours to weeks; often in the range of days)
- SHORT attention span
- Hour to hour variation in sleep/wake cycles
- MARKED psychomotor changes
- Often in the setting of stressful event, medical conditions, post-anesthesia, or related to medications
DEPRESSION
- Acute onset
- Unusual consciousness
- Depressed mood with diurnal variation
- Short duration (weeks)
- Reduced short and long term memory
- Hypersomnia or insomnia
- Look at past history when diagnosing
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A ___ deficiency can lead to pernicious anemia.
Symptoms include __, __, __, and __.
Dietary deficiency can lead to this - what foods are critical to maintaining these levels? What dieting groups are most at risk and may need to take supplements?
Other than lacking this in the diet, an absorption problem could also lead to deficiencies. What is an example of a condition that leads to inability to absorb this? How does this condition come about (typical predisposing features/PMHx)? How is it fixed?
A VITAMIN B12 deficiency can lead to pernicious anemia.
Symptoms include CONFUSION, PERIPHERAL NEUROPATHY (often leads to balance problems!), WEAKNESS, and DEPRESSION.
Most doctors now routinely screen for all elderly patients for this problem.
Dietary deficiency can lead to low B12 levels, specifically diets low in MEAT, POULTRY, SEAFOOD, DAIRY PRODUCTS, and EGGS.
VEGANS and VEGETARIANS will need B12 supplements?
If there's a B12 deficiency but they ARE getting adequate levels in their diet, it likely means they have pernicious anemia secondary to an ABSORPTION problem, e.g. ATROPHIC GASTRITIS (which is asymptomatic in and of itself!). This absorption problem may be secondary to SURGERY to stomach or small intestine (e.g. hiatal hernia repair, gastric bypass surgery) , abnormal bacterial growth in the small intenstine, or an intestinal dz (e.g. Crohn's dz, celiac dz). Since they can't absorb B12 in the GI tract, they need B12 SHOTS.
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Mild cognitive impairment is a syndrome defined as cognitive decline greater than expected for that person's __ and ___, but [does / does not] interfere notably with activities of daily life.
In adults >65yo, prevalence ranges fro 3-19%!
Prognosis?
Any findings on imaging?
Mild cognitive impairment is a syndrome defined as cognitive decline greater than expected for that person's AGE and EDUCATIONAL LEVEL, but DOES NOT interfere notably with activities of daily life.
In adults >65yo, prevalence ranges fro 3-19%!
Prognosis? SOME people with MCI seem stable or return to normal over time, but >50% progress to dementia within 5 YEARS
MCI with:
- ATROPHIC LESIONS show widespread involvement of several cognitive domains over time
- --> Higher rate of conversion to dementia after 2 years with atrophic MCI, compared to vascular MCI
- --> Atrophic MCI typically converts to degenerative forms of dementia (e.g. Alzheimer's , Lewy Body Dementia)
- VASCULAR LESIONS show slight decline limited to EXECUTIVE FXNS
- --> Vascular MCI converts more often to vascular forms of dementia (post-CVA)
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Impacts of mild cognitive impairment on gait?
- Is gait imapcted?
- What cognitive domains are important to maintain a normal gait pattern in the presence of a cogntive load?
- Gait impairments (frontal, parkinsonian, and hemiparetic gait) were TWICE as common among pts with amnestic MCI (ie with memory problem, than non-amnestic ie no memory problem)
- Pts with MCI and gait abnormalities were MORE disabled than those with MCI without gait deficits
ATTENTION, EXECUTIVE FUNCTION, and WORKING MEMORY are important to maintain a normal gait pattern (e.g. to maintain velocity) in the presence of a cognitive load (e.g. dual task). This happens even early on (not during simple walking, but YES with dual task!)
(to flip it around, slowing gait speed during dual task is associated with poor performance in attention, executive fxn, and working memory)
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Alzheimer's disease accounts for __% of all dementia cases. It is more common in [ M / W ] and in those who have [any genetic influences? ] [ any PMHx influences?]
Pathophysiology?
Onset of memory and cognitive problems is [fast / slow] and insidious, typically between the ages of __-__ (most common >__yo). Intellectual decline eventually results in ability to perform ADLs and lasting changes in personality.
Clinical features of Alzheimer's include... (5)
Alzheimer's disease accounts for 43% of all dementia cases. It is more common in WOMEN and in those who have a 1ST DEGREE RELATIVE WITH THE DZ or in those with a HISTORY OF HEAD TRAUMA.
Onset of memory and cognitive problems is SLOW and insidious, typically between the ages of 40-90 (most common >65 yo). Intellectual decline eventually results in ability to perform ADLs and lasting changes in personality.
Clinical features of Alzheimer's include...
- MEMORY LOSS
- APRAXIA
- VISUOSPATIAL impairment
- CONCRETENESS
- PRESERVED MOTOR FXN in the early stages
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Pathophysiology of Alzheimer's dz?
Pathophysiology of AD?
- Amyloid plaques and neurofibrillary tangles which first form in the HIPPOCAMPUS. Unknown if these are the cause of AD vs are a byproduct of the AD process.
- --> Plaques consist largely of the protein fragment beta-amyloid.
- --> Tangles are made up of tau, a protein usually involved in maintaining the internal structure of the nerve cell
- --> Excess phosphorylation (which normally helps to modify Tau proteins) appears to contribute to tangle formation and prevent the protein from doing its job
- --> Oxidative stress caused by free radicals is also regarded as characteristic of AD
- --> Brain inflammation is typical
- --> Many pts w/AD show signs of cerebrovascular dz, particularly when older
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Medications to treat Alzheimer's and other dementias
Primary goal of meds is to [cure / slow] disease process
Big categories of meds:
- ___ inhibitors (e.g. __, __, and __) , which prevent the breakdown of ACh which is important for __ and __. These delay worsening of symptoms for ___-__ months for ~50% of people. Generally these are well tolerated, but side effects may include __, __, loss of __, and increased frequency of __.
- ___ receptor agonist (e.g. __), which regulates the activity of glutamate which is also involved with __ and __. This delays worsening of symptoms for some people temporarily, similar to other category above. Can cause side effects such as __, __, __, and __.
Medications to treat Alzheimer's and other dementias
Primary goal of meds is to SLOW disease process
Big categories of meds:
- CHOLINESTERASE inhibitors (e.g. ARICEPT, EXELON, and RAZADYNE) , which prevent the breakdown of ACETYLCHOLINE which is important for LEARNING and MEMORY. These delay worsening of symptoms for 6-12 months for ~50% of people. Generally these are well tolerated, but side effects may include NAUSEA, VOMITING, loss of APPETITE, and increased frequency of BOWEL MOVEMENTS.
- NMDA receptor agonist (e.g. MEMANTINE / NAMENDA), which regulates the activity of GLUTAMATE which is also involved with LEARNING and MEMORY. This delays worsening of symptoms for some people temporarily, similar to Cholinesterase inhibitors as above. Can cause side effects such as HA, CONSTIPATION, CONFUSION, and DIZZINESS.
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Describe clinical features of the stages of Alzheimer's Disease
Early AD:
Intermediate AD:
Late AD:
Describe clinical features of the stages of Alzheimer's Disease
Early AD:
- Problems retaining NEW Information
- Forgetfulness
- Social withdrawal: may stop participating in activities and hobbies they formerly loved
- Moody
- Disoriented to time
- Poor judgement
Intermediate AD:
- Behavioral and personality changes
- Parkinsonism and psychotic symptoms are most evident
- Begin to see changes in gait (e.g. shuffling), wandering starts, and confusion of day/night
- Late in this stage, may be excessive wandering behavior and they forget how to eat. Weight loss is a problem.
- Client starts to require care in this stage
Late AD:
- Loss of most functional abilities
- Incontinent
- Lose ability to walk, become at risk for contracture and decubiti development
- Anorexia
- Illogical
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Changes in balance and gait in Alzheimer's dz
Even with very mild AD, we see: (relative to controls)
- Impaired tandem stance times with eyes open and closed
- Longer TUG times
- Slower gait speed (comfy pace)
- Higher dual task cost for gait speed, with gradual decline in gait speed and step length during both single and dual tasking in AD
- See temporal and spatial disturbances, as well as instability in single limb stance during gait
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Vascular dementia is more common in [M / F], and is the second most common form of dementia. Symptoms often come on after a __ or other ___ event. Also called multi-__ dementia.
Clinical course: Typically progresses [gradually / in a stepwise manner]
Clinical features?
Vascular dementia is more common in MEN, and is the second most common form of dementia. Symptoms often come on after an MI or other CARDIO- or CEREBROVASCULAR event (and in the context of other cardiac risk factors) Also called multi-INFARCT dementia.
Clinical course: Typically progresses IN A STEPWISE MANNER likely correlated with infarcts/loss of perfusion.
Clinical features?
Depends on what areas of the brain the lesions occur in. Fronto-subcortical areas are more at risk for perfusion problems, so we often see APATHY and DEPRESSION in vascular dementia (less so in AD).
---> SUBCORTICAL vascular dementia relates to SMALL vessel dz and hypoperfusion, resulting in focal and diffuse ischemic white matter lesions, often in the frontal subcortical neuronal networks. Dominant pattern tends to be behavioral alterations and dysexecutive syndrome. May be associated w/gait and balance alteration, and apathy.
- Early gait disturbances
- Early and frequent falls
- Early personality changes
- May also see depression and emotional incontinence
Comparing to AD, pts with vascular dementia are...
- Less likely to be agitated or psychotic (as in AD)
- CAN occur concurrently with AD = "Mixed dementia"
- Harder to diagnose! And most individuals w/AD have some vascular contribution
EFFECTIVE EARLY treatment of HTN can protect against cognitive decline!!
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Lewy Body Dementia - how is it different from AD?
| Typical symptoms?
Lewy Body Dementia: presence of dementia with relative SPARING OF MEMORY.
Typical symptoms =
- Gait and balance disorders
- Prominent hallucinations (primary symptom in 33% of cases!) and delusions
- Sensitivity to antipsychotics (these pts have a bad reaction to these due to the extrapyramidal syndrome features that are present with LBD; which is bad considering often present initially w/hallucinations/ delusions and are initially seen in IP psych departments)
- Fluctuations in attention
LBD patients are MORE impaired on attention tests compared to AD Patients
Commonly see FLUCTUATIONS in cognition (particularly late in dz; which we don't see as much in AD)
Neuropsychiatric problems/ symptoms are COMMON - so these pts are often seen in psychiatric centers
- Depressive symptoms are more common in LBD than AD
Pts with LBD show MORE rapid motor deterioration than those w/AD
Cannot differentiate AD vs LD based on cognitive tests alone
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You CAN differentiate between dementia types based on motor performance!
Individuals with [ AD / PD / LBD] show greater deficits in gait, balance, and hand dexterity than those with [ AD / PD / LBD]. Performance on the ____ [outcome measure] is able to differentiate between groups too!
You CAN differentiate between dementia types based on motor performance!
Individuals with LEWY BODY DEMENTIA show greater deficits in gait, balance, and hand dexterity than those with AD or PD. Performance on the TINETTI MOBILITY TEST is able to differentiate between LBD, AD, and PD groups as well as between PD dementia and LBD dementia groups!
Individuals with the same dz stage with LBD walked SLOWER, had SHORTER STRIDE lengths, demonstrated poorer BALANCE on Tinetti and Berg, and had poorer performance on DUAL TASK and FIGURE of EIGHT walking compared to PD and AD groups!
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Frontotemporal dementias (FTD) encompass a group of disorders with a common, basic degenerative pattern like that seen w/frontal lobe degeneration. Includes __ disease.
We see mild to moderate __ lobe atrophy.
Mean age of onset is __-__yo. Duration of dz is __-__ years.
Symptoms compared to individuals w/alzheimer's?
Frontotemporal dementias (FTD) encompass a group of disorders with a common, basic degenerative pattern like that seen w/frontal lobe degeneration. Includes PICK disease.
We see mild to moderate FRONTAL lobe atrophy.
Mean age of onset is 45-70yo. Duration of dz is 3-17 YEARS
Symptoms:
- FTD pts are LESS disoriented and have MORE difficulty problem solving compared to AD
- Short term memory is relatively spared
- Relatively preserved ability to negotiate environment
- Speech is involved EARLY (similar to AD)
- EARLY changes in personality and behavior
- --> Hypochondriasis, schizophrenia, OCD, and things like anxiety and depression can be so severe that they can end up in a psych ER or treated for these problems LONG before dx of dementia is made
- Disinhibition is common
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Rate of decline in the various dementias?
FTD: fastest decline
LBD: generally progresses faster than AD, though one study said it had the rate of decline is the same as other types of dementia
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Normal pressure hydrocephalus is a syndrome of [acute / chronic] dilation of the ___ with normal __ pressure.
Clinical symptoms include:
Typical medical management and anticipated improvements (gait? cognition?)
Normal pressure hydrocephalus is a syndrome of CHRONIC VENTRICULAR dilation with normal CSF pressure.
Clinical symptoms include:
- DEMENTIA (widespread cognitive dysfxn with a predominance of visuospatial deficits; executive function and verbal memory are less affected)
- GAIT DYSFXN
- URINARY INCONTINENCE
* There's a dissociation btwn gait and cog dysfxn in NPH suggesting DIFFERENT pathophysiology yielding both symptoms!
Typical medical management and anticipated improvements:
Gait dysfunction typically responds to SURGICAL SHUNTING, but COGNITION does NOT always improve after surgery
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Alcohol (EtOH) related dementias
Talk to me a little about Wernicke-Korsakoff syndrome
- Deficiency of what? Why and what's EtOH's role in this?
- Symptoms? (acute vs chronic)
- Prognosis? What's the acute vs chronic form called?
Associated with brain atrophy with sulcal widening and ventricular dilation
Can be accompanied by other alcohol-related diseases, such as peripheral neuropathy and Cb atrophy
Spectrum of dementias include: (related to damage to liver which causes damage to brain)
- Marchiafava-Bignami
- Acquired hepatocerebral degeneration
- *** Wernicke-Korsakoff syndrome
- --> WERNICKE'S (WE) is an ACUTE neuropsych disorder caused by thiamine/Vit B1 deficiency.
- ---> Associated with AMS, ataxia, and opthalmoplegia.
- ---> Increased incidence of WE among alcoholics is due to inadequate nutritional intake together w/EtOH inhibitory effects on thiamine absorption.
- ---> Wernicke's is life-threatening
KORSAKOFF"s syndrome is a persistent neuropsychiatric syndrome associated w/amnesia (memory problems) and disorientation
- Caused by combined effects of thiamine deficiency + excessive EtOH consumption
* *Korsakoff = CHRONIC Wernicke's (*K-orsakoff = K-ronic), but not as life threatening as Wernicke's
- Korsakoff's has difficulty forming memory and implementing executive functions
- Ataxia and incoordination
OTHER FACTS:
- EtOH use often leads to peripheral neuropathy and associated motor and balance disorders
-EtOH use is high in elderly; be sure to ask older adults about EtOH intake!
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How are dementias diagnosed?
Generally based on SYMPTOMS, though labwork helps to diagnose a few forms (e.g. B12 deficiencies)
Imaging may be helpful, but benefits remain controversial. Generally, want to pursue imaging with less common dementia presentations:
- Onset <60yo
- Focal signs/symptoms
- Presence of early onset gait disturbances
In AD, use of imaging does NOT change care or outcomes
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Impact of PT on hospital LOS with frail, older adults including those with dementia
Older, frail adults (including those w/dementia) who were hospitalized showed a shorter LOS (7 days, vs 13 days - a 6-day difference!!) than those w/infrequent PT!
High frequency PT predicts (even after adjusting for age, illness severity, gender comorbidity, fraility):
- Functional improvement
- Shorter LOS
- Likelihood of being discharged without a formal care package
Hartley P et al 2016
