Week 7 Flashcards
Brain rhythms
Electrical activity varies
-region
-behaviour
—disordered
EEG recordings
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
When do neurones fire synchronously
Synchronous firing in normal cognition:
-very fast (gamma) oscillations
-produces meaning (perception)
Synchronous firing in sleep
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
What is sleep
State characterised by:
-decrease mobility
-decrease responsiveness to sensory inputs
-decrease cortical excitability
“A readily reversible state of reduced consciousness”
Characteristics of sleep
All mammals and birds
-humans- 1/3rd life asleep
Disruption impacts health
It is necessary to
Functions of sleep
Evolutionary speculation
Deprivation studies/poor sleepers
-quantity and quality
-impairment of cognitive performance
-decrease mood
-altered physical health
Stages of sleep
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
Hypnogram
Key points:
-initially down through stages
-less deep as night progresses
-REM increases in duration
What is the neural basis of wakefulness/sleep
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
What induces sleep
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
Sleep disorders
Sleep apnoea
Insomnia
-hunger
-drug related
—withdrawal from hypnotics
—stimulants
Illness
Sleep patterns can be disturbed
Depression
-increase REM and enter REM rapidly
Depression affects sleep or vice versa
Schizophrenia, Age, PD, AD
Deep sleep disorders
Most prevalent in children
-sleepwalking, bedwetting, night terrors
-self curing
REM sleep (behavioural) disorder
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?
Sleep disorders
Narcolepsy
-uncontrollable entry into sleep (REM)
-cataplexy
-experimentally, destruction of lateral hypothalamus
—orexin (hypocretin)
—stabilises wakefulness
Decrease orexin containing cells in humans
Sleep as therapy
If sleep promotes L/M
-sleep deprivation for decrease traumatic memories
-phobia
—sleep soon after non-traumatic exposure
Deprivation and depression
Functions of the hypothalamus
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
Clinical considerations
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
Inputs massive integration
Sensory inputs:
-internal environment
-receptors within hypothalamus
-viscera via brainstem
-homeostasis
Sensory inputs:
-olfactory/retina
-limbic regions
-hippocampus
Output
Pituitary -> hormone
Brain stem -> Ans, coordination of behaviour
Limbic -> emotion
Homeostasis and survival
Structure of the hypothalamus
Contains many nuclei
Medial-lateral axis: 3zones
Anterior-posterior axis:
Anterior
-pre optic area
-“set points”
-sleep
-reproductive behaviours
Suprachiasmatic nucleus
Posterior
Tuberal
Structure of the hypothalamus
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)
ANS control
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
Endocrine control
The hypothalamus is connected
-indirectly to the anterior pituitary
-PVN parvocellular cells
Directly to the posterior pituitary
-PVN and SO magnocellular cells
Behavioural control
“Motivated”
-wants/likes/needs—> reward
Food intake- Role of hypothalamus
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
Food intake- hypothalamic nuclei
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
Food intake
Feast
- increase leptin
-> hypothalamus
—> pituitary hormones, ANS-> increase metabolic rate
-> decrease feeding behaviour
Increased metabolic rate and decreased feeding behaviour-> normal body weight
Temperature control
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
Reproductive behaviour
ANS: sexual organs
Endocrine: puberty , reproductive cycling
Behavioural: courtship
What is consciousness
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
Arousal level
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
What are the neural substrates of consciousness
Brainstem nuclei- “ascending reticular activating system”
-basal forebrain
-hypothalamus
-pedunculopontine nucleus
Key neurotransmitters:
-orexin
-adrenergic
-cholinergic
What are the neural substrates of consciousness
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
Outcomes in ABI (acquired brain injury) Brain stem death
When a person no longer has any brain stem functions and has permanently lost the potential for consciousness and the capacity to breathe
Outcomes in ABI: coma
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
Unresponsive wakefulness (vegetative state)
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
Minimal conscious state
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
How do you define emergence from MCS
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
Akinetic mutism
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’
Post traumatic confusional state or delirium
Prolonged periods of consciousness
Disorientated
Functional object use
Expressive language
Perseveration
Cognitive impairments
Locked in syndrome
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
Cognitive motor dissociation CMD or covert consciousness
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
Assessment of disorders of consciousness
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
Sites for physical stimulation
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
Hyper acute assessment
Physical findings
-pupils
-motor responses
-autonomic/breathing
Pupils
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
Motor findings
Hemiplegia
Decorticate
Decerebrate
Autonomic features- raised ICP
Cushing’s triad
-hypertension
-bradycardia
-respiratory irregularity
Autonomic features/breathing
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)
Post acute assessment
Diagnosis
Trajectory
Prognosis: futility, meaningful recovery
Before saying fixed dilated
Terminal brainstem injury
Use magnifying glass to look at pupils
Brainstem death
Spinal reflexes -seen in 75%
-extension-pronation
-plantar responses
-muscle stretch reflexes
-abdominal reflexes
-“Lazarus sign”-move head, the limbs move
Use a scale
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)
Use a mirror
Circa 35% greater response seen with a mirror
Pitfalls in ABI consciousness assessment
Drugs
Epilepsia partialis continuans
Critical illness neuromyopathy
Late hydrocephalus
Pituitary failure
Type 2 respiratory failure with CO2 narcosis
Hypothermia
Occult spinal injury
Importance of diagnosis
Prognosis is affected by:
Underlying diagnosis
-traumatic brain injury
-hypoxic ischaemic brain injury
-other brain injury eg infection, vascular
Trajectory
Futility
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
