Brain & Behavior - Week 7

Front 1

What are the 3 cardinal symptoms of DLB? What are the treatments?

Back 1

Dementia with Lewy Bodies:
- fluctuations in alertness
- visual hallucinations
- parkinsonism
Tx: Cholinesterase inhibitors
** v. sensitive to antipsychotic drugs **

Front 2

What happens in REM sleep? What happens in the disorder?
Tx?

Back 2

REM sleep - body is paralyzed except for eyes, but in disorder the person is not paralyzed and they act out their dreams.
Tx: Small dose of clonazepam
** often preceeds DLB **

Front 3

What lesion will cause a semantic dementia?
What are the 4 signs? (hint: both + and -)

Back 3

Bilateral temporal pole and inferolateral cortex.
+: fluent grammatical speech and repition relatively good.
-: semantic paraphasias (word or phenom substitutions), loose meaning of objects

Front 4

What is spatial acalculia?

Back 4

when a person has trouble with math for spatial and not comprehension reasons (e.g. writes #s in the wrong place!)

Front 5

What is motor neglect?
Lesions in what 3 areas could cause this?

Back 5

A reluctance to use a limb in the absence of a discernable weakness.
Lesions:
- striatum
- lateral thalamus
- frontoparietal cortex

Front 6

What does it mean if someone has aprosodia?
What is it caused by?

Back 6

They have lost the ability to encode (motor) or decode (sensory) emotional intonnations of speech, without losing the ability to experience emotions.
Caused frontal hemisphere lesions (usually R)

Front 7

A parietal lesion on which side will not cause neglect?

Back 7

A lesion on the L will not usually cause neglect b/c the right parietal lobe is dominant and can attend to both sides

Front 8

What is the problem that results from MS inflamation recovery?

Back 8

When the axonal demyelination is repaired the body ends up making more nodes of Ranvier and this slows conduction

Front 9

What are the 4 classical presentations for MS (ie pt traits)

Back 9

White
Woman (2:1males)
From temperate climate
between 15-50yrs

Front 10

What is the name given to the first attack seen in MS patients?
What are the 3 most common initial symptoms?

Back 10

Clinically Isolated Syndrome (onset = days, lasts weeks and may have full or imcomplete recovery)
Symptoms:
-upper limb sensory
- optic neuritis
- acute weakness

Front 11

When diagnosing MS when would you use a cranial MRI? When would you use a spinal? Why?

Back 11

Cranial is the most sensitive so start here. However in older pts (>50yrs old) there can be lesions that are part of aging. Therefore use a spinal MRI for these pts. Spinal lesions are NOT part of aging. 75% of pts will have an abnormal spinal MRI

Front 12

What 5 findings would make you think a person probably does NOT have MS?

Back 12

1. wrong demographic (age/race)
2. Lesions attributable to a single lesion
3. No cardinal symptoms (optic neuritis, sensory & bladder symptoms) even after ++ yrs!
4. Steadily progressing without remission (primary progressive form is ++ rare!
5. CSF/MRI remains normal for ++ years

Front 13

What are prognostically bad signs in MS? (there's 5)

Back 13

1. Male gender and older age of onset
2. High relapse rate, incomplete recovery
3. increased lesion burden on initial MRI
4. Insidious onset of motor symptoms
5. early cerebellar involvement
6

Front 14

What 2 things can current MS treatment do? What 2 things can it NOT do?

Back 14

MS treatment CAN:
1. Hasten recovery from attacks with steroids
2. Several drugs will prevent the attacks

MS treatment CANNOT:
1. Prevent the onset of the progressive phase
2. Halt the progression of the disease

Front 15

What is the definition of a coma?
Obtunded? Stupor?

Back 15

State of deep unresponsiveness where pt lays with eyes closed and cannot be aroused to respond appropriately to stimuli even when vigorous. No goal directed movement.
Obtunded = reduced alertness, only aroused with minimal stimulation
Stupor = reduced alertness, only aroused with vigorous stimulation

Front 16

What is the difference between arousal and awareness?
What is the level of each in a vegetative state?

Back 16

Arousal is a level of consciousness that comes from brainstem. Awareness is the content of consciousness and comes from the cerebral cortex.
Vegetative = high arousal and low awareness (no content in consciousness)

Front 17

What NT arousal system projects to the thalamus?

What 5 NT systems project to the cortex?

Back 17

The cholinergic system projects to the thalamus, making it receptive.
Cortical projections:
Monominergic, cholinergic, histaminergic, orexinergic and thalamic

Front 18

To produce a coma or stupor, 1 of what 3 areas must be damaged?

Back 18

1. Both cerebral hemispheres

Ascending arousal system:
2. paramedian region of the upper brainstem*
3. diencephalon*
* on both sides of the brain!

Front 19

A lesion where will produce Locked-in Syndrome? What are the 4 deficits that arise and what specifically was damaged to produce each one?
What 3 functions remain intact?

Back 19

A lesion at the base of the pons:
1. Quadraparesis -- CST
2. Loss of lateral gaze -- (PPRF, CN6)
3. Facial paresis (CN7)
4. Anarthria (CN X, XII)
Intact: awareness (normal cognition), vertical eye movements (riMLF) and vision

Front 20

What are 3 types of herniations that can happen?

Back 20

1. Subfalcine - cingulate gyrus goes under the falx
2. Uncal - the uncus of the temporal lobe goes under the tentorium
3. Tranforaminal - the cerebellar tonsils go thru the F.magnum

Front 21

How do cold calorics work? (ie what happens when cold water is instilled?)

Back 21

Cold water creates a convection current causing an imbalance of vestibular tone between the 2 ears = illusion of rotation. The horizontal canals control the M&LR via the VOR pway.

Front 22

What happens in a normal conscious person when cold water is instilled into their R ear?

Back 22

Cold water in R ear will cause fast jerk nustagmus towards L but slow deviation to R. (COWS mnemonic refers to fast phase (nystagmus) only!)

Front 23

During cold calorics, what does it mean if there are no nystagmus movements? What about no ocular movements at all?

Back 23

Absent nystagmus means there is cerebral damage, (b/c the fast phase is our conscious attemp to overcome the loss of fixation that we perceive when we are rotating)
A loss of any movement means that in addition to cerebral damage, there has been Bstem reflex damage (the slow drift is actually reflexive movement)

Front 24

What sign would identify a pt with structural rather than metabolic causes of coma?

Back 24

Asymmetric occulomotor function

Front 25

In a right lateral pontine lesion, what would happen when cold water was instilled into the R ear? How about the L ear?

Back 25

Front 26

In a left paramedian pontine lesion (that included the MLF), what would happen when cold water was instilled into the R ear? How about the L ear?

Back 26

Eyes on L have water in R ear! (can only look laterally in unaffected eye!)

Front 27

What is the name of an MLF lesion? What type of gaze would be produced during cold calorics of the R eye? L eye?

Back 27

Front 28

Following a R CN3 palsy, what type of gaze would be produced during cold calorics of the R eye? L eye?

Back 28

Front 29

A right uncal herniation will always cause what symptom? It will also produce hemiparesis, the side of the hemiparesis depends on what?

Back 29

Uncal herniation will cause decreased LOC and an ipsilateral CN3 palsy.
If the hemiparesis is:
- Ipsilateral then the cerebral peduncle (opposite side of lesion) is pressing against the tentorial edge.
- Contralateral then the uncus on the same side as the lesion is compressing the cerebral peduncle

Front 30

Damage to what would create these pupils?

Back 30

Destruction of parasympathetic fibers to pupillary constrictors!
Damage to CN3 - uncal?

Front 31

A lesion where (and destroying what) would create this type of pupils?

Back 31

Note how they are midposition and fixed. Lesion in midbrain has destroyed the EW nucleus. Pupils will not respond to light

Front 32

A lesion where (and destroying what) would create this type of pupils?

Back 32

Descending sympathetic tract through the pons is severed therefore no pupillary dilation.

Front 33

Define the following terms:
- sleep onset latency
- REM latency
- sleep efficiency

Back 33

- sleep onset latency: time from lights out to sleep

- REM latency: time from sleep onset to REM sleep (short in depressed ppl)

- sleep efficiency: time asleep/time in bed (high when ppl sleep deprived!)

Front 34

Why are benzo's not a good sleep-aid?

How long is the circadian day?

Back 34

B/c they reduce the restorative, slow wave sleep

24.18hrs

Front 35

What is forced desynchronization used for?

Back 35

Keep ppl awake when they should be asleep, if physiological processes still happen then it is d/t circadian rhythms and not sleeping!

Front 36

What regulates the circadian clock?

Back 36

The suprachiasmic nuclei that get input from the retina (transplantation will flip internal clock!)
Afferents - retinohypothalmic, lateral geniculate & raphe nuclei
Efferents - paraventricular nuclei, thalamus, hypothalamus
** has a strong influence over other organs but independent molecular clocks exist

Front 37

What are the 3 key elements in a sleep history?

Back 37

1. Problems/habits initiating sleep?
2. During sleep - wake up? alarm clock?
3. During day - was sleep restorative? morning h/a? (alarm bell b/c marker of CO2 retention d/t severe obstruction)

Front 38

Insomnia is a v. common disorder of increased arousal and sleep initiation problems. If a person is complaining of this what must you rule out?
What are the 4 treatments?

Back 38

Must r/o restless legs. If there’s maintenance probs then do a sleep study.
Tx: sleep log & hygiene, stimulus control, sleep restriction & learned relaxation response.

Front 39

Sleep apnea is a disorder of breathing in sleep causing excessive sleepiness. What makes it worse (3)?
What is it associated with (5)?
What are the 3 main symptoms?

Back 39

Sleep apnea: worse with position, sedatives and alcohol.
Risk: 17” neck, obesity, ENT disorders, Neuromuscular disorders, HoTh.
Symptoms: excessive daytime sleepiness, pseudo-depression, morning h/a (CO2 buildup and polycythemia. Should have <5 resp disturbances events / hr of sleep

Front 40

What is restless leg syndrome?
What are the causes (4)?
What are the 3 treatments?
What can cause an augmentation?

Back 40

RLS = sensation that produces periodic limb movement (relieves sensation). Begins or worsens at rest & in evening.
Causes: central or periph nervous system problems, prego’s, EtOH, Fe deficiency
underlying cause (Eg. Give Fe), dopamine agonists 1hr before bed, opiods in exceptional circumstances,
** sinemet may cause augmentation!

Front 41

How do you diagnose narcolepsy? (ie what is the test?)

Back 41

dx made with 2 sleep onset REM periods in 4-5 naps (“multiple sleep latency test”). Test done after a normal sleep period.

Front 42

What 4 things are associated with narcolepsy?

Back 42

1. excessive daytime sleepiness,
2. hypnagogic hallucinations,
3. cataplexy (sudden and transient episode of loss of muscle tone, often triggered by emotions),
4. sleep paralysis.

Front 43

What 3 things are used to treat narcolepsy?

Back 43

Alerting agents (Ritalin),
Anticataplectics (GHB, SSRIs, Anticholinergics, Ritalin),
Strategic napping

Front 44

What is the definition of neurologically determined death?

Back 44

The irreversible loss of the capacity for consciousness combined with the irreversible loss of all brainstem functions including capacity to breathe.

Front 45

What are the 2 ways of testing for extraocular eye movements when determining brain death?

Back 45

1. Doll's eyes - with HOB at 30deg, turn pt's head from side to side, any movement of eyes = NOT brain dead
2. Cold calorics: 120cc of cold water into both ears. Again, ANY eye movement excludes brain death

Front 46

What are the 3 physiologic changes that accompany brain death?

Back 46

1. Central diabetes insipidus
2. Vasodilation (loss of sympathetics) with subsequen Hothermia
3. Endocrine deficiencies (hypothyroid, hOadrenalism, etc)

Front 47

In what 4 ways is brain death different from a persistent vegetative state?

Back 47

1. PSV's will spontaneously ventilate
2. PVS's will maintain cardioV stability
3. PVS pts have sleep/wake cycles
4. PVS lasts months to years, brain death occurs over hours

Front 48

What parameters do you keep up for donor maintenance?

Back 48

1. Appropriate hydration and BP
2. Lytes and urine output
3. Blood gases
4. Body temperature

Front 49

What are the 6 elements of a language exam?

Back 49

1. Spontaneous speech
2. Comprehension
3. Naming
4. Repetition
5. Writing
6. Reading

Front 50

What are the 5 components of spontaneous speech?

Back 50

1. Fluency and Effort
2. Paraphasias (Verbal = word substitutions & Literal = sound substitutions)
3. Word finding
4. Articulation
5. Prosody

Front 51

What are the 4 components of Auditory comprehension?

Back 51

1. Single words: "point to the ____"
2. Phrases: "point to the ___describe object___"
3. Whole body commands: "stand up, walk to the door, turn around and come back
4. Syntax: small grammatical parts of speech "of, before, uder", test by asking "do you eat a banna before you peel it?"

Front 52

What is a good basic screen of reading skills?

Back 52

Show the following sentece:
"Point to the second word in this sentence"
If they get it right it's a reasonable screen. If not look at the error... if they pointed to "second" it could be a frontal lobe problem

Front 53

What is a good way to test writing? What is a bad way of testing writing skills?

Back 53

Writing one's name is usually the last thing to go therefore don't use this as a test. Instead, have the pt look at a picture and write about what they see.

Front 54

What are the 4 non-fluent aphasias?

Back 54

1. Broca's
2. Transcortical motor
3. Global
4. Mixed transcortical

Front 55

What are the 4 fluent aphasias?

Back 55

1. Wernicke's
2. Conduction
3. Anomic
4. Transcortical sensory

Front 56

Are conduction aphasias fluent or non-fluent? What is the problem with their speech? Where is the lesion?

Back 56

Fluent! But frequent paraphasia (substitution) errors (poor naming) and poor repitition.
Lesion in the arcuate fibers that connect W to B

Front 57

Is Wernicke's aphasia fluent or non-fluent? What is the problem with their speech? Where is the lesion?

Back 57

Fluent!
Speech is perceived but the language content is incorrect = poor comprehension, with poor repitition and poor naming.
Damage to the superior temporal lobe (1st temporal lesion)

Front 58

Is Broca's aphasia fluent or non-fluent? What is the problem with their speech? Where is the lesion?

Back 58

Non-fluent!
Speech is difficult to initiate, labored and halting. Despite good comprehension, naming and repetition are poor.
Posterior inferior frontal (B's area)

Front 59

Are Global aphasias fluent or non-fluent? What is the problem with their speech? Where is the lesion?

Back 59

Non-fluent!
Poor globally!! (ie poor repetition, naming and comprehension)
Lesion involved frontal, temporal and parietal lobes (including W and B)

Front 60

Are Transcortical sensory aphasias fluent or non-fluent? What is the problem with their speech? Where is the lesion?

Back 60

Fluent - poor comprehension, but have fluent, grammatical speech.
Good repetition but poor naming.
Lesion to temporo-parietao-occipital junction (sparing W's)

Front 61

What does the perisylvian region do?

Back 61

Connects Wernicke's area to Broca's. Also serves as repetition pathway.

Front 62

Are Transcortical MOTOR aphasias fluent or non-fluent? What is the problem with their speech? Where is the lesion?

Back 62

Non-fluent halting speech d/t damage to the frontal lobe.
Good comprehension & repetition, but poor naming).
Able to repeat words b/c arcuate fasciculus is intact (Preserved repetition is a defining quality of all transcortical aphasias).

Front 63

Are mixed transcortical aphasias fluent or non-fluent? What is the problem with their speech? Where is the lesion?

Back 63

Non-fluent with poor comprehension. Good repetition and poor naming (as always!)
"People who suffer mixed transcortical aphasia struggle greatly to produce propositional language or to understand what is being said to them, yet they can repeat long, complex utterances or finish a song once they hear the first part."
Lesion = ant & post association cortex while sparing perisylvian language region.

Front 64

Is anomic aphasia fluent or not? What is the problem and what type of lesion causes this?

Back 64

Fluent speech.
Repetition and comprehension are intact - only problem is naming. Person will ++ word search!
Lesion = temporo-parietal

Front 65

What type of lesion will produce alexia without agraphia?

Back 65

Unilateral lesion in an occipital area. Visual information from one side must get the angular gyrus for processing (ie to be "read"). Midline occipital lesions will prevent information from both sides from getting to AG. Can write but not read!!

Front 66

What are the 5 bedside tests for frontal lobe functioning?

Back 66

1. Initiation of mental activities - ask for words or things beggining with a certain letter
2. Distractability & inattention - serial 7s/3s; color-word test
3. Inability to shift set (perseverence) - drawing multiple loops, pt can't stop at 3. GO-No-GO
4. Perceptual pull - ask pt to draw 10 to 11 - will put had at 10 b/c v.concrete thinkers. Boston naming test - can't correctly name things b/c drawn to most salient features
5. Theory of Mind - no awareness of content of other ppl's mind (can't estimate what they would know)

Front 67

What are the 3 delusions that are characteristic of frontal lobe damage?

Back 67

1. Reduplicative paramnesia - belief that a familiar person or place has been duplicated. (pt aware of how bizarre this is)
2. Capgras - same as above except for people only - not places!
3. Impaired self-awareness: seeing a stranger who stands behind mirrors does everything you do and follows you around

Front 68

What are 5 of the 7 personality changes associated with frontal lobe damage?

Back 68

1. Aparthy
2. Disinhibition
3. Change in social conduct (ie shoplifting)
4. Inappropriate jocularity
5. Poor hygiene
6. Rudeness
7. Poor insight

Front 69

What does "aura" mean?

Back 69

Aura - a seizure with preserved consciousness, acts as a warning and preceded the "larger" sz. Can be any sensory modality

Front 70

For a TONIC-CLONIC generalized sz describe:
-sz itself
- aura
- duration
- Loss OC?
- Post-ictal confusion?
-

Back 70

- Tonic clonic: initial general msk tone causes pt to fall, followed by apnea +/- incontinence, and the rhythmic contractions of all msks
- aura: No
- duration 1-2mins
- Loss OC? Yes
- Post-ictal confusion? Yes

Front 71

For an Absense generalized sz describe:
-sz itself
- aura
- duration
- Loss OC?
- Post-ictal confusion?

Back 71

Absense: brief unresponsiveness, may have only minor blinking/twitching or mouth movements
- aura: NO
- duration 5-10sec
- Loss OC? Yes
- Post-ictal confusion? No

Front 72

For a simple partial sz describe:
-sz itself
- aura
- duration
- Loss OC?
- Post-ictal confusion?

Back 72

Simple partial occurs in one part of the brain, can produce jerking of one part of the body or an odd sensation
- aura: Yes (Sz can be just the aura)
- duration: 5-10sec
- Loss OC? No
- Post-ictal confusion? No
** Can secondarily generalize

Front 73

For a complex partial sz describe:
-sz itself
- aura
- duration
- Loss OC?
- Post-ictal confusion?

Back 73

Complex partial involves only one part of the brain and a loss of awareness. Produces automatisms like hand gestures, picking at clothes, grimacing, etc
- aura: Yes
- duration: 5sec - 5min
- Loss OC? Yes
- Post-ictal confusion? Yes
** Can also secondarily generalize

Front 74

What is the difference between an absence Sz and a complex partial with regards to:
- age of onset
- aura
- post-ictal confusion

Back 74

- age of onset: A = childhood, CP = any age
- aura: A = no CP = yes
- post-ictal confusion: A = no, CP = yes
CP tends to produce more complex movements

Front 75

Define epilepsy.
What is the cause in most people?

Back 75

Epilepsy is a chronic disease of recurrent unprovoked seizures. Person could have a lesion in their brain, but the Sz itself is unprovoked (2/3 are idiopathic!)