lesson 6: sensory (hyper)sensitivity - insights from clinical and general populations

acquired brain injury

any damage in the brain that happens after birth

stroke

blood supply to the brain is cut off

traumatic brain injury

result of a physical impact on the head (ex car crash)

brain tumor

a tumor that grows in the brain

sensory hypersensitivity

shift on the continuum of sensitivity after injury

sensory hypersensitivity: underlying mechanisms

1. Broken filter?

2. Slower processing?

3. Lowered threshold?

4. Hospitalization?

5. Brain damage?

broken filter

o   Impaired selective attention

o   After brain injury this filtering mechanism often works ineffectively, as a result these people pay attention to irrelevant info, overloading the brain with irrelevant info and therefore creating this feeling of sensory overwhelm

attentional filter

allows us to concentrate on one thing while filtering out other irrelevant stimuli (thoughts, background noice …)

slower processing

Process info more slowly, leading them to feel overwhelmed more quickly with their fast pace sensory environment

lowered threshold

o Sensory threshold level

o   After brain injury this threshold can be lowered and therefore people start to notice a lot more sensory stimuli, contributing to the sense of sensory hypersensitivity

sensory threshold level

the point at which the stimulus is intense enough/long enough for us to consciously notice it → there’s a lot of stimuli that we really don’t notice, because they do not reach this threshold level (sounds that aren’t loud enough)

hospitalization

o   People with a brain injury are often hospitalized, which can last for months, taking them away from sensory rich daily life to a less rich environment of a hospital

o   Can this play a role?

brain damage

Sensory hypersensitivity related to brain damage?

speed of visual processing

how much performance improved as the display ration of the red letter improved, beyond an individual threshold

fast visual processing

Sharp improvement in performance with only a small increase in the ration

slower visual processing

More gradual improvement across a larger increase in the ration

Stroke patients with visual hypersensitivity

reduced attentional filter + lower sensory threshold compared to the others

Emotional interpretation/significance of stimuli

whether a stimulus is perceived as dangerous or annoying

structural brain damage

to certain regions or white matter tracks is also 1 of the underlying mechanisms of post-stroke sensory hypersensitivity

Sensory processing sensitivity (SPS)/highly sensitive personality

-        Personality or temperament trait

-        20-30% of the population scores high

-        Measurable with questionnaires

SPS as continuum

o The more sensitive individuals are compared to orchids → only flourish well in optimal circumstances (perfect amount of light, water, temperature…)

o People who are less sensitive are compared to dandelions → quality of their functioning is less affected by the quality of the environment

o Tulips are in between

high sensitive/orchids

• Show a pos outcome when encountering a pos environment (a lot of support results in higher well-being)

• When they are in neg environments (ex. a maltreating environment), it also has a bigger effect (depression or anxiety)

low sensitive/dandelions

their functioning is much less effected by the quality of their environment

mind-wandering network

for daydreaming…

default mode network

attention switch network

for alertness when hearing your name …

salience network

interoceptive awareness

people with higher SPS notice their bodily symptoms more easily (hunger, thirst, heartbeat …), they are more distracted by them and have a higher emotional awareness (they know the link between bodily signals and their emotions, ex feeling stress in your stomach → they listen more to these signals, but trust them less)

predictors of fluctuation in overstimulation

• Levels of overstimulation based on internal and external triggers (momentary observations)

• fatigue

• pos and neg mood

hypersensitivity

-        Continuum of sensitivity

-        Specific sensitivities are observed in clinical/subclinical conditions

-        In autism spectrum disorder (both hypo- and hypersensitivity)

-        In chronic pain

-        After stroke

-        In the general population

chronic pain

-        Pain that persists or recurs for longer than 3 months

-        Such pain often becomes the sole or predominant clinical problem in some patients

-        As such it may warrant specific diagnostic evaluation, therapy and rehabilitation

-        Chronic pain is a frequent condition, affecting an estimated 20% of people worldwide

-        It’s multifactorial: biological, psychological and social factors contribute to the pain syndrome

clinical picture chronic pain

people with chronic pain often describe everyday sensory events as too bright, too loud, too rough, too string or simply too aversive, this extends beyond pain intensity itself

Multi-modal evaluation of sensory sensitivity (MESSY)

developed for people who had a stroke

7 subscales of sensitivity

1.     Multisensory

2.     Visual

3.     Autitory

4.     Tactile

5.     Smell and taste

6.     Environmental temperature

7.     Motion

Self-reported pain

o   Pain-intensity

o   Pain frequency

o   Pain comparison to others

Demographic variables: age, sex, BMI, education level, marital status, ethnicity and clinical diagnoses

causes of sensory hypersensitivity in pain

1. altered central gain

2. hypervigilance

3. descending pain modulation links light to pain

4. sensory modulation disorder

central sensitization

refers to changes into the nociceptive system

this term had been created for the nociceptive pathway, so you need to find a link between the nociceptive pathway and other sensory modalities

altered central gain

you can refer to whatever increased sensitivity you might have (biological, by different sensory stimuli)

pregabalin

drug used in chronic pain

suggests that this would reduce the increased activity against the placebo

generalized hypervigilance theory

-        Has been criticized

-        Hypervigilance is a term that was used specifically for increased attention to certain body parts or certain S

-        Here the criticism: no specific test for attention, they just inferred that there is increased attention, but just because there is an increased response → link that had a jump in it

rostroventral medulla

has ON and OFF cells

ON cells

neurons that react when the S appears → respond after heat onset

OFF cells

when the S disappears → stop responding after heat onset

ON and OFF cells

These are the cells typically coding a nociceptive S, but after sensitization (that is one of the situations that would occur in patients with chronic pain), you see that the firing for light S changes too → same mechanisms that happen in humans

descending modulation

-        The neurobiological pathways are different (one is for coding ascending information and the other one is for coding the descending information), the interpretation is also slightly different

-        Not per se pain modulatory system, but failure of inhibition to amplified responses

EEG

very good spatial resolution: direct recording of what you do, what happens in the first msec after the S, reflects the first stages  of elaboration of a S

good to understand WHEN some modulations happen

fMRI

if you want to know WHERE these modulations happen

sensory modulation disorder

-        All sensory modulation disorders (with pain associated, with increased sensitivity to other S…) are all given by an imbalance between excitatory inputs and inhibitory inputs on the cortical level

-        There is a cortical hyperexcitation and that would be accompanied by sensory modulation alteration

what causes sensory hypersensitivity in patients?

-        An increase in unpleasantness is always reported

-        Sometimes accompanied by increase in intensity

-        The question remains whether there’s an increase gain, a modified interpretation of deficient inhibition

-        Research is limited to some chronic pain conditions

temporal order judgement task (TOJ)

you receive (on 2 body parts), in very rapid succession, 2 stimuli → indicate which arm was stimulated first or second

attentional bias to a bodypart

then the S on the other arm have to be presented a certain msec before, in order to be perceived as simultaneous  → different temporal interval

point of subjective simultaneity

you’re going to perceive the S faster when your focused on that body part

when both S are perceived at the same time, but they are never at the same there → there’s always going to be a slight interval between the 2

corollarly effect

the increase in non-nociceptive responses is corollary

what is this reflecting?

2 hypothesis:

1. arousal model

2. attention model

arousal model

you respond to all S more when you’re in a condition of nociceptive hypersensitivity  (you have a change in physiological parameters that make you respond in that way to all the S)

• do we have an increase in arousal after HFS

attention model

you would have mechanical hypersensitivity, but then also perceptual bias on the arm that wasn’t measured (because the test wasn’t the best one …) → the attentional shift is the other explanation

• how much of the N140 increase is related to attention?

attentional model: study

Tried to replicate the results of the tactile increase (from the study of Vandenbroeke)  by also adding another element → a block of attention (asked pp to pay attention to the stimulated arm or to the control arm)

• perceived tactile intensity: changed

• An increase in the N1 of the vibrotactile S applied onto the sensitized arm

• Increase in N140 is also present when controlling for attention

• Attention alone doesn’t explain the increased amplitude

arousal model: study

Measured skin conductance levels (SCL) and heart rate variability (HRV) → during the intense pain that was given and then mapped it at different time points after the stimulation

• SCL: They didn’t find any evidence that there was a change after HFS → no evidence for a change in arousal

• the same for HRV

they didn’t really find an increase in autonomic nervous system activity after HFS

HFS

increases NA activity, and SCL if HFS is intense → the increase disappears fast