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BAB > Week 7 > Flashcards

Week 7 Flashcards

1
Q

Brain rhythms

A

Electrical activity varies
-region
-behaviour
—disordered

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2
Q

EEG recordings

A

Cortical pyramidal neurones , very large generate biggest electrical signals
Many neurones pick up collected activity, increase level activity bigger signal detected. Neurones doing the same role will be active for similar amount of time
Synchronous activity:
-bigger signal at the more synchronous activity
-pathological or normal patterns

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3
Q

When do neurones fire synchronously

A

Synchronous firing in normal cognition:
-very fast (gamma) oscillations
-produces meaning (perception)

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4
Q

Synchronous firing in sleep

A

EEG allows us to measure the number of neurons that are active and whether they’re active at same time (synchronous) or different times
Height deflection= increase synchronisation
More synchronous activity in sleep

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5
Q

What is sleep

A

State characterised by:
-decrease mobility
-decrease responsiveness to sensory inputs
-decrease cortical excitability
“A readily reversible state of reduced consciousness”

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6
Q

Characteristics of sleep

A

All mammals and birds
-humans- 1/3rd life asleep
Disruption impacts health
It is necessary to

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7
Q

Functions of sleep

A

Evolutionary speculation
Deprivation studies/poor sleepers
-quantity and quality
-impairment of cognitive performance
-decrease mood
-altered physical health

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8
Q

Stages of sleep

A

REM sleep: beta rhythms
-desynchronised EEG activity
-rapid darting eyes
-easily aroused by meaningful stimuli
-when awakened appear alert and attentive
-dreaming
-loss of muscle tone
Awake- beta rhythms
Stage 1 non REM: Theta
Stage 2 non rem sleep:Theta and spindles and K complexes
Stage 3 non rem sleep: Delta
Stage 4 non rem sleep: >50% delta

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9
Q

Hypnogram

A

Key points:
-initially down through stages
-less deep as night progresses
-REM increases in duration

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10
Q

What is the neural basis of wakefulness/sleep

A

Arousal- RAS (reticular activating system). Area of brainstem, lot of nuclei
Is sleep just the absence of wakefulness- no.
Ach and aminergic neurones help thalamus to distribute info to areas of the brain
During wakefulness lots activity Ach and aminergic neurones-> disrupt change in wakefulness
REM- not a high level of aminergic activity. Ach, paralysis
Non REM: decrease Ach and aminergic, increase VLPO (ventral lateral pre optic organ) part of thalamus not active in wakefulness

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11
Q

What induces sleep

A

Multiple factors:
-waking time- adenosine accumulation
-physical activity
-circadian rhythm
—suprachiasmatic nucleus
——retinal input
——neurones “tick”
—protein synthesis/degradation very cyclical
Jet lag
Blind people: due to retinal dysfunction struggle not getting Zettgeber to supreachiasmatic nucleus. Can be problematic. Use alarms to know time of day

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12
Q

Sleep disorders

A

Sleep apnoea
Insomnia
-hunger
-drug related
—withdrawal from hypnotics
—stimulants
Illness

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13
Q

Sleep patterns can be disturbed

A

Depression
-increase REM and enter REM rapidly
Depression affects sleep or vice versa
Schizophrenia, Age, PD, AD

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14
Q

Deep sleep disorders

A

Most prevalent in children
-sleepwalking, bedwetting, night terrors
-self curing

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15
Q

REM sleep (behavioural) disorder

A

Uncommon
Decrease loss of muscle tone
-act out dreams during REM sleep
-limb twitching, taking , yelling, jerking,
-brainstem inhibition abnormal
Precursor to Parkinson’s disease?

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16
Q

Sleep disorders

A

Narcolepsy
-uncontrollable entry into sleep (REM)
-cataplexy
-experimentally, destruction of lateral hypothalamus
—orexin (hypocretin)
—stabilises wakefulness
Decrease orexin containing cells in humans

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17
Q

Sleep as therapy

A

If sleep promotes L/M
-sleep deprivation for decrease traumatic memories
-phobia
—sleep soon after non-traumatic exposure
Deprivation and depression

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18
Q

Functions of the hypothalamus

A

General:
-homeostasis and survival
-motivated behaviours
Integration of somatic and autonomic responses:
-cardiovascular system
-blood composition/volume
-food/water intake
-temperatures control
-circadian rhythms
-reproductive behaviours
-emotional behaviour

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19
Q

Clinical considerations

A

Physical brain injury?
-anatomical location-> rare
Impact of lesions
-diverse symptoms
—nucleus specific
-Progressive changes
-Location
How does hypothalamus control these functions
Influences:
-ANS
-endocrine Integration
-behaviour

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20
Q

Inputs massive integration

A

Sensory inputs:
-internal environment
-receptors within hypothalamus
-viscera via brainstem
-homeostasis
Sensory inputs:
-olfactory/retina
-limbic regions
-hippocampus

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21
Q

Output

A

Pituitary -> hormone
Brain stem -> Ans, coordination of behaviour
Limbic -> emotion
Homeostasis and survival

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22
Q

Structure of the hypothalamus

A

Contains many nuclei
Medial-lateral axis: 3zones
Anterior-posterior axis:
Anterior
-pre optic area
-“set points”
-sleep
-reproductive behaviours
Suprachiasmatic nucleus
Posterior
Tuberal

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23
Q

Structure of the hypothalamus

A

Periventricular zone
SCN
Arcuate nucleus (feeding)
[paraventricular] nucleus
Medial zone:
-paraventricular
-pituitary control
-feeding
-autonomic control
Lateral zone:
-lateral hypothalamic area
-supraoptic nuclei
—release hormones (posterior pituitary)

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24
Q

ANS control

A

Paraventricular nucleus
-brain stem nuclei
—origins of neurons that influence preganglionic SNS/PNS
Evidence:
-stimulations/lesions of hypothalamus
-increase decrease blood pressure and heart rate

25
Q

Endocrine control

A

The hypothalamus is connected
-indirectly to the anterior pituitary
-PVN parvocellular cells
Directly to the posterior pituitary
-PVN and SO magnocellular cells

26
Q

Behavioural control

A

“Motivated”
-wants/likes/needs—> reward

27
Q

Food intake- Role of hypothalamus

A

Glucose and brain. Constraint demand but intermittent supply
Set point disruption ->starvation/obesity
Intake regulation is complex
MS, neurodegenerative disease
Short term regulation
Receptors:
-glucose
-ghrelin
Inputs:
-mechanoreceptors- in gut
-glucose receptors - in hepatic system

28
Q

Food intake- hypothalamic nuclei

A

Long term regulation: fat stores-> leptin->hypothalamus
Arcuate nucleus
-Increase leptin
Paraventricular nucleus
-lesions-> uncontrolled feeding -> obesity
-controls ANS and signals to pituitary
Lateral hypothalamic area
-lesions -> eating ceases-> starvation
Motivation to search for food
-projections widespread
-cortex
—> behaviour
NB- GLP-1 agonists

29
Q

Food intake

A

Feast
- increase leptin
-> hypothalamus
—> pituitary hormones, ANS-> increase metabolic rate
-> decrease feeding behaviour
Increased metabolic rate and decreased feeding behaviour-> normal body weight

30
Q

Temperature control

A

Hypothalamic thermoreceptors
NB Pyrexia - change to set point
-integrated response
Autonomic -vasomotor changes in skin
Endocrine- increase, decrease metabolism
Behavioural- shivering, panting, seek warmth/shade

31
Q

Reproductive behaviour

A

ANS: sexual organs
Endocrine: puberty , reproductive cycling
Behavioural: courtship

32
Q

What is consciousness

A

At its least normal human consciousness consists of a serially time ordered, organised, restricted and reflective awareness of self and the environment. Moreover it is an experience of graded complexity and quantity

33
Q

Arousal level

A

Awareness of the contents of consciousness ( a range of specific functional types of attention, intention, memory, and mood-emotion)
DOC affect both arousal level and awareness of the contents of consciousness

34
Q

What are the neural substrates of consciousness

A

Brainstem nuclei- “ascending reticular activating system”
-basal forebrain
-hypothalamus
-pedunculopontine nucleus
Key neurotransmitters:
-orexin
-adrenergic
-cholinergic

35
Q

What are the neural substrates of consciousness

A

Thalamo-cortical circuits :
-global workspace
-internal and external awareness
Striatum: stimulated by thalamus and frontal cortex , inhibits globus pallidus interna
Globus pallidus interna:
-inhibits thalamus and brain stem nuclei

36
Q

Outcomes in ABI (acquired brain injury) Brain stem death

A

When a person no longer has any brain stem functions and has permanently lost the potential for consciousness and the capacity to breathe

37
Q

Outcomes in ABI: coma

A

Patients have complete failure of the arousal system with:
-no spontaneous eye opening
-and are unable to be awakened by application of vigorous sensory stimulation

38
Q

Unresponsive wakefulness (vegetative state)

A

UW/VS is characterised by:
-the complete absence of behavioural evidence for self or environmental awareness
-there is preserved capacity for spontaneous or stimulus induced arousal evidenced by sleep wake cycles

39
Q

Minimal conscious state

A

In MCS cognitively mediated behaviour occurs inconsistently but is reproducible or sustained long enough to be differentiated from reflexive behaviour
Following simple commands
Gestural or verbal yes/no responses (regardless of accuracy)
Intelligible verbalisation
Purposeful behaviour including movements or affective behaviours:
-appropriate smiling or crying in response to the linguistic or visual content of emotional but not to neural topics or stimuli
-vocalisations or gestures that occur in direct response to the linguistic content of questions
-reaching for objects that demonstrates a clear relationship between object location and direction of reach
-touching or holding objects in a manner that accommodates the size and shape of the object
-pursuit eye movement or sustained fixation that occurs in direct response to moving or salient stimuli
MCS is sub stratified into MCS without language (MCS-) and MCS with language (MCS+)
-may be of prognostic significance

40
Q

How do you define emergence from MCS

A

Characterised by:
Functional communication: accurate yes/no responses
-eg situational orientation questions such as “are you sitting down” and “am i pointing to the ceiling”
Functions object use:
-eg bringing a comb to the head or a pencil to a sheet of paper

41
Q

Akinetic mutism

A

Akinetic mutism AM is a subtype of MCS
Reduced goal directed behaviour is due to severely diminished drive, rather than decreased arousal or direct damage to neural systems
Speech, movement, thought and emotional expression are uniformly reduced
But these responses may be facilitated following exposure to high intensity sensory or personally salient stimuli eg ‘telephone effect’

42
Q

Post traumatic confusional state or delirium

A

Prolonged periods of consciousness
Disorientated
Functional object use
Expressive language
Perseveration
Cognitive impairments

43
Q

Locked in syndrome

A

Locked in syndrome is a de-efferented state characterised by quadriplegia and paralysis of the lower cranial nerves
Patients retain consciousness and can classically communicate by vertical eye movements and eye blinking
Classical LIS: upgaze and blinking only with anarthria and tetra paresis and preserved consciousness
Incomplete LIS: as above but some minimal movement in other limbs noted
Complete LIS: no limb or eye movement but preserved consciousness

44
Q

Cognitive motor dissociation CMD or covert consciousness

A

CMD is characterised by volitional brain activity detected by task-based functional MRI (fMRI) or EEG in patient whose bedside behavioural diagnosis suggests coma, VS/UWS or MCS

45
Q

Assessment of disorders of consciousness

A

Hyper acute
-Glasgow coma score- a change of 2 points on scale is significant
-physical signs
—pupils
—motor responses
—breathing and autonomic responses
Post acute

46
Q

Sites for physical stimulation

A

Finger tip pressure
Trapezius pinch
Supraorbital notch
Features of flexion responses:
Abnormal flexion: slow stereotyped, arm across chest, forearm rotates, thumb clenched, leg extends
Normal function: rapid, variable, arm away from body

47
Q

Hyper acute assessment

A

Physical findings
-pupils
-motor responses
-autonomic/breathing

48
Q

Pupils

A

Structural:
-diencephalic-small reactive
-pretectal- large fixed pupils
-pons- pinpoint
-midbrain- mid position, fixed
-uncal herniation- 3rd n unilateral fixed dilated
Metabolic:
-pin points opiates, antoicholinesterases
-fixed dilated: hypoxic encephalopathy, anticholinergics, botulism

49
Q

Motor findings

A

Hemiplegia
Decorticate
Decerebrate

50
Q

Autonomic features- raised ICP

A

Cushing’s triad
-hypertension
-bradycardia
-respiratory irregularity

51
Q

Autonomic features/breathing

A

Forebrain- increased sensitivity to CO2 regular waxing and waning of respiration (Cheyne stokes)
Midbrain- hyperventilation
Pontine- apneustic prolonged inspiration
Medullary- slowing (rate) and shallowing of respiration (associated nuclei dysfunction eg IX, X, XI)

52
Q

Post acute assessment

A

Diagnosis
Trajectory
Prognosis: futility, meaningful recovery

53
Q

Before saying fixed dilated

A

Terminal brainstem injury
Use magnifying glass to look at pupils

54
Q

Brainstem death

A

Spinal reflexes -seen in 75%
-extension-pronation
-plantar responses
-muscle stretch reflexes
-abdominal reflexes
-“Lazarus sign”-move head, the limbs move

55
Q

Use a scale

A

40% error rate between UW/PVS and MCS if a scale is not used
Scales:
-coma recovery scale- R
-SMART (sensory motor rehabilitation technique)
-WHIM (Wessex head injury matrix)

56
Q

Use a mirror

A

Circa 35% greater response seen with a mirror

57
Q

Pitfalls in ABI consciousness assessment

A

Drugs
Epilepsia partialis continuans
Critical illness neuromyopathy
Late hydrocephalus
Pituitary failure
Type 2 respiratory failure with CO2 narcosis
Hypothermia
Occult spinal injury

58
Q

Importance of diagnosis

A

Prognosis is affected by:
Underlying diagnosis
-traumatic brain injury
-hypoxic ischaemic brain injury
-other brain injury eg infection, vascular
Trajectory

59
Q

Futility

A

Can be reasonably accurately predicted in hypoxic injury- diffuse injuries
Much harder with TBI- focal injuries
Safeguards needed to prevent “self fulfilling prophecy’
Repeated observations will be needed where there are not clear clinical features

BAB (10 decks)

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