Psychology Unit 3
Section A– Disorder
Autism Spectrum Disorder
Characteristic
ASD is a lifelong, developmental disorder of communication and how the individual
understands the world around them.
DSM-5 & ICD-11 are two classification systems, both of which include 2 broad categories of
symptoms when diagnosing ASD – 1. Communication issues, 2. Repetitive behaviours.
Social-emotional reciprocity is an example of a communication issue. This is where the
individual with ASD may not use verbal communication to share interests or emotions with
others. They are less likely to respond to other people’s attempts to begin a conversation, for
example, not engaging in small talk with the cashier at the supermarket. Alternatively, they
may respond inappropriately such as talking about something irrelevant to the conversation,
for example in detail about their favourite subject.
Non-verbal communication is a further communication issue. This is any communication
which does not involve spoken words. An individual with ASD may avoid eye contact when
being spoken to. This can be one of the first behaviours parents notice in their children.
Additionally, gestures may be misunderstood, for example not making sense of a parent
putting their hand up to say ‘stop’ when a child is doing something they shouldn’t. Or not
understanding facial expressions, such as when someone is angry with them.
In addition, an individual with ASD may lack theory of mind where they are unable to see
other people’s perspectives which can lead to a lack of empathy. For example, a person with
ASD who is feeling happy may assume others also feel this way. For example, not asking a
friend who has fallen over if they are ok. As a result, the individual may have problems
developing and maintaining relationships with their peers.
Repetitive behaviours include echolalia, where an individual repeats words or phrases they
have heard. For example, a child with ASD may repeat phrases from cartoon characters on
the TV. Stimming is also a common characteristic of those with ASD where they engage in
self-stimulatory repetitive behaviours. For example, flapping arms or flicking fingers when
anxious as a way to self-soothe. Rather than engaging with role-play, the child may
repeatedly line up toys in size order.
Those with ASD tend to stick to routines and may find a change distressing. For example, a
late-night phone call which disrupts the normal bath-story-bed routine may cause the child to
overreact and have a meltdown as a result of this unexpected change. As a result, the
individual may experience anxiety in situations when neurotypicals would not.
,Finally, those with ASD have an unusual reaction to sensory input. The senses tend to be
heightened, such as an intense dislike for having one’s hair brushed, as well as a
heightened sense to sound. For example, a busy shopping centre may cause a sensory
meltdown as the child struggles to cope with the overdose of sensory stimulation such as
bright lights / loud music/rustling of shopping bags/crowds of people talking.
, 1. Biological
Amygdala Dysfunction
(AO1)
One biological explanation is the amygdala dysfunction theory. The amygdala has
been implicated in ASD as it is crucial for social and emotional responses. Although
in adulthood there is no difference in the volume of the amygdala between those with
and without ASD, a key difference lies in childhood with a 6-9% increase in volume
in those with ASD (Nordahl 2012). This early growth may lead to abnormalities in the
connections between neurons in the amygdala which may damage its functioning.
Baron-Cohen stated that as the amygdala has many neural connections with the
the frontal lobe, that damage to the amygdala could lead to the social and emotional
deficits found in those with ASD, such as difficulty processing social information. This
could link to one of the behaviours seen in those with ASD where they struggle to
understand non-verbal communication such as gestures, as well as social rules such
as not standing too close to another person. Through using fMRI scans the ‘eyes
task’ suggested that the left amygdala (involved when we infer other people’s
emotions from their facial expressions - especially their eyes) are impaired in those
with ASD.
Genetic Predisposition
(AO1)
One biological explanation for ASD is that there is a genetic predisposition. Among the
general population (who do not have any relatives with ASD) there is a 0.11% chance of an
individual developing ASD (Szatmari). If a sibling already has a diagnosis, the risk of
developing ASD increases to 2.2%. Bailey et al analysed data from the British Twin Study
and found a concordance rate for MZ twins of 60% and 0% for DZ twins. When the study
included social or cognitive impairments, they found an increase in concordance rates - 92%
for MZ and 10% for DZ. As MZ twins share 100% DNA compared to DZ twins sharing 50%,
it, therefore, suggests there is a genetic component due to the greater concordance rate for
MZ twins.
Genetic mutations, which can occur during reproduction, help further explain the
genetic component of ASD. In a study of 3730 children with autism spectrum
disorder or developmental delay, researchers found 15 CHD8 mutations (Bernier).
Furthermore, ASD can be non-syndromic (ASD is the only disorder diagnosed) or syndromic
(occurring with some other condition which may have a genetic cause). One condition which
is known to co-occur in syndromic ASD is Fragile X syndrome (FXS). Around 60% of those
with Fragile X syndrome also meet the diagnostic criteria for ASD which may suggest that an
FMR1 mutation may also be a genetic factor in the development of ASD.
Finally, de novo mutations may account for simplex ASD (where there is no family history of
ASD). De novo copy number variations account for about 10 to 25% of cases of ASD. De
novo gene mutations may explain more severe cases of ASD while genetic inheritance
(inheritance of faulty genes from parents) may explain less severe cases of ASD. Due to the
various genes which may be involved, this helps to explain why autism is a spectrum
disorder where the severity between siblings can vary. For example, siblings where one child
is high functioning, whereas the other child is non-verbal.
, (AO3)
1. + Supporting evidence –
Colvert et al (2015) assessed 6,423 twin pairs for autistic traits using questionnaires,
observations and interviews. Concordance rates of MZ twins ranged from 77% to
99% whereas DZ twins' concordance ranged from 22% to 65%.
(+) externally valid research showed MZ twins had much higher concordance than
DZ twins due to sharing 100% DNA.
(-)Joseph suggested that MZ twins are more likely to be brought up in similar
conditions and be treated similarly, (eg. be in the same class at school, and have
similar friends and experiences). Hence, the high concordance rates of MZ twins may
be due to shared nurture rather than shared biology.
2. - Inconsistent findings –
Hallmayer found that the heritability of ASD is 55% whereas Bai's study showed 80%
heritability.
(+)Both suggest a clear biological component which supports the explanation.
(-) Yet, findings are inconsistent meaning that research into the role of genes is not
reliable, questioning the external validity and external reliability of the supporting
evidence and the explanation.
3. + Deterministic explanation –
The explanation sees ASD as a result of genetic mutations eg.CHD8 (biological
determinism). This may help change the public perception or tackle stigma as the
individual has no free will eg. when having a public outburst due to sensory
sensitivities. Additionally, it is more ethical than alternative explanations eg. not
seeing ASD as the cause of poor parenting, unlike the refrigerator mother
explanation.
4. - Too reductionist –
Focus on nature (genes) not nurture. Landrigan suggested that there may be
possible environmental triggers for ASD such as prenatal influences - toxic chemicals
and viruses that the mother is exposed to while carrying her baby - may have a role
to play in damage to the brain of the developing child. Therefore, genes alone may
be only a partial explanation of ASD. Diathesis-stress model for a more holistic
explanation.
Both
(AO3)
1. +Genetics supporting evidence - Colvert - 77-99% concordance for MZ twins
compared to 22- 65% for DZ twins. This externally valid research using 6,423
participants supports the genetic explanation as MZ twins share 100% of DNA. Yet,
shared nurture, not nature? (Joseph- MZ twins are treated similarly). MZ
concordance is not 100%.
2. -Amygdala dysfunction contradictory evidence - Nordahl vs Herbert - inconsistent
findings for amygdala dysfunction - early childhood growth of the amygdala
contradicts Herbert et al who found a smaller amygdala compared to controls.
Section A– Disorder
Autism Spectrum Disorder
Characteristic
ASD is a lifelong, developmental disorder of communication and how the individual
understands the world around them.
DSM-5 & ICD-11 are two classification systems, both of which include 2 broad categories of
symptoms when diagnosing ASD – 1. Communication issues, 2. Repetitive behaviours.
Social-emotional reciprocity is an example of a communication issue. This is where the
individual with ASD may not use verbal communication to share interests or emotions with
others. They are less likely to respond to other people’s attempts to begin a conversation, for
example, not engaging in small talk with the cashier at the supermarket. Alternatively, they
may respond inappropriately such as talking about something irrelevant to the conversation,
for example in detail about their favourite subject.
Non-verbal communication is a further communication issue. This is any communication
which does not involve spoken words. An individual with ASD may avoid eye contact when
being spoken to. This can be one of the first behaviours parents notice in their children.
Additionally, gestures may be misunderstood, for example not making sense of a parent
putting their hand up to say ‘stop’ when a child is doing something they shouldn’t. Or not
understanding facial expressions, such as when someone is angry with them.
In addition, an individual with ASD may lack theory of mind where they are unable to see
other people’s perspectives which can lead to a lack of empathy. For example, a person with
ASD who is feeling happy may assume others also feel this way. For example, not asking a
friend who has fallen over if they are ok. As a result, the individual may have problems
developing and maintaining relationships with their peers.
Repetitive behaviours include echolalia, where an individual repeats words or phrases they
have heard. For example, a child with ASD may repeat phrases from cartoon characters on
the TV. Stimming is also a common characteristic of those with ASD where they engage in
self-stimulatory repetitive behaviours. For example, flapping arms or flicking fingers when
anxious as a way to self-soothe. Rather than engaging with role-play, the child may
repeatedly line up toys in size order.
Those with ASD tend to stick to routines and may find a change distressing. For example, a
late-night phone call which disrupts the normal bath-story-bed routine may cause the child to
overreact and have a meltdown as a result of this unexpected change. As a result, the
individual may experience anxiety in situations when neurotypicals would not.
,Finally, those with ASD have an unusual reaction to sensory input. The senses tend to be
heightened, such as an intense dislike for having one’s hair brushed, as well as a
heightened sense to sound. For example, a busy shopping centre may cause a sensory
meltdown as the child struggles to cope with the overdose of sensory stimulation such as
bright lights / loud music/rustling of shopping bags/crowds of people talking.
, 1. Biological
Amygdala Dysfunction
(AO1)
One biological explanation is the amygdala dysfunction theory. The amygdala has
been implicated in ASD as it is crucial for social and emotional responses. Although
in adulthood there is no difference in the volume of the amygdala between those with
and without ASD, a key difference lies in childhood with a 6-9% increase in volume
in those with ASD (Nordahl 2012). This early growth may lead to abnormalities in the
connections between neurons in the amygdala which may damage its functioning.
Baron-Cohen stated that as the amygdala has many neural connections with the
the frontal lobe, that damage to the amygdala could lead to the social and emotional
deficits found in those with ASD, such as difficulty processing social information. This
could link to one of the behaviours seen in those with ASD where they struggle to
understand non-verbal communication such as gestures, as well as social rules such
as not standing too close to another person. Through using fMRI scans the ‘eyes
task’ suggested that the left amygdala (involved when we infer other people’s
emotions from their facial expressions - especially their eyes) are impaired in those
with ASD.
Genetic Predisposition
(AO1)
One biological explanation for ASD is that there is a genetic predisposition. Among the
general population (who do not have any relatives with ASD) there is a 0.11% chance of an
individual developing ASD (Szatmari). If a sibling already has a diagnosis, the risk of
developing ASD increases to 2.2%. Bailey et al analysed data from the British Twin Study
and found a concordance rate for MZ twins of 60% and 0% for DZ twins. When the study
included social or cognitive impairments, they found an increase in concordance rates - 92%
for MZ and 10% for DZ. As MZ twins share 100% DNA compared to DZ twins sharing 50%,
it, therefore, suggests there is a genetic component due to the greater concordance rate for
MZ twins.
Genetic mutations, which can occur during reproduction, help further explain the
genetic component of ASD. In a study of 3730 children with autism spectrum
disorder or developmental delay, researchers found 15 CHD8 mutations (Bernier).
Furthermore, ASD can be non-syndromic (ASD is the only disorder diagnosed) or syndromic
(occurring with some other condition which may have a genetic cause). One condition which
is known to co-occur in syndromic ASD is Fragile X syndrome (FXS). Around 60% of those
with Fragile X syndrome also meet the diagnostic criteria for ASD which may suggest that an
FMR1 mutation may also be a genetic factor in the development of ASD.
Finally, de novo mutations may account for simplex ASD (where there is no family history of
ASD). De novo copy number variations account for about 10 to 25% of cases of ASD. De
novo gene mutations may explain more severe cases of ASD while genetic inheritance
(inheritance of faulty genes from parents) may explain less severe cases of ASD. Due to the
various genes which may be involved, this helps to explain why autism is a spectrum
disorder where the severity between siblings can vary. For example, siblings where one child
is high functioning, whereas the other child is non-verbal.
, (AO3)
1. + Supporting evidence –
Colvert et al (2015) assessed 6,423 twin pairs for autistic traits using questionnaires,
observations and interviews. Concordance rates of MZ twins ranged from 77% to
99% whereas DZ twins' concordance ranged from 22% to 65%.
(+) externally valid research showed MZ twins had much higher concordance than
DZ twins due to sharing 100% DNA.
(-)Joseph suggested that MZ twins are more likely to be brought up in similar
conditions and be treated similarly, (eg. be in the same class at school, and have
similar friends and experiences). Hence, the high concordance rates of MZ twins may
be due to shared nurture rather than shared biology.
2. - Inconsistent findings –
Hallmayer found that the heritability of ASD is 55% whereas Bai's study showed 80%
heritability.
(+)Both suggest a clear biological component which supports the explanation.
(-) Yet, findings are inconsistent meaning that research into the role of genes is not
reliable, questioning the external validity and external reliability of the supporting
evidence and the explanation.
3. + Deterministic explanation –
The explanation sees ASD as a result of genetic mutations eg.CHD8 (biological
determinism). This may help change the public perception or tackle stigma as the
individual has no free will eg. when having a public outburst due to sensory
sensitivities. Additionally, it is more ethical than alternative explanations eg. not
seeing ASD as the cause of poor parenting, unlike the refrigerator mother
explanation.
4. - Too reductionist –
Focus on nature (genes) not nurture. Landrigan suggested that there may be
possible environmental triggers for ASD such as prenatal influences - toxic chemicals
and viruses that the mother is exposed to while carrying her baby - may have a role
to play in damage to the brain of the developing child. Therefore, genes alone may
be only a partial explanation of ASD. Diathesis-stress model for a more holistic
explanation.
Both
(AO3)
1. +Genetics supporting evidence - Colvert - 77-99% concordance for MZ twins
compared to 22- 65% for DZ twins. This externally valid research using 6,423
participants supports the genetic explanation as MZ twins share 100% of DNA. Yet,
shared nurture, not nature? (Joseph- MZ twins are treated similarly). MZ
concordance is not 100%.
2. -Amygdala dysfunction contradictory evidence - Nordahl vs Herbert - inconsistent
findings for amygdala dysfunction - early childhood growth of the amygdala
contradicts Herbert et al who found a smaller amygdala compared to controls.
