Functionality and Pathology of Swear Words

Question 1

Does strategic swearing only have negative effects?

Answer 1

No, it can have positive meaning as well: context needed to ground the meaning of the intended use, e.g., embarrassment, emphasis, solidarity

Question 2

How much of the spoken content does swearing make?

Answer 2

≈ 0.5%

Question 3

How is swearing/cursing traditionally understood?

Answer 3

as inflicting harm or horror on someone by invoking the aid of a supernatural power, also foul or taboo language (sex, excrement, related body parts)

Question 4

What are taboo gestures necessary for?

Answer 4

taboo gestures, e.g. sexual obscenities of dominance involving ostentatious phallic, are necessary for the purpose of shocking an opponent and self-protection

Question 5

What messages do swear words convey?

Answer 5

1. image of toughness and strength, ignoring formality
2. evolutionary indicator of potential threat
3. avoidance of sensitive topics in sake of social norms

Question 6

What is automatic swearing? What can it be needed for?

Answer 6

Expressing negative emotions may result in both tension reduction and aggressive drive reduction

It is useful for pain relief (cf. swearing in the native language vs. the second language)

Question 7

What is rage circuit?

Answer 7

Pain activates “rage circuit”:
a part of the amygdala -> the hypothalamus -> the gray matter of the midbrain
It communicates that the situation at hand is deeply affecting

Question 8

Are taboo words just like other words?

Answer 8

No, taboo words comprise a unique class of words neurologically distinct from normal language use

evidence from selective preservation of swearing in aphasic patients

Question 9

Where does strategic swearing engage?

Answer 9

strategic/purposeful swearing engages the left hemisphere

Question 10

What are the regions involved in automatic swearing?

Answer 10

• right hemisphere, which is involved in emotion-related functions
• limbic system
• basal ganglia

Question 11

What is coprolalia? Copropraxia?

Answer 11

Coprolalia is a pathological use of swear words, copropraxia — of obscene gestures

Question 12

Can coprolalia and copropraxia be a symptom in various conditions?

Answer 12

Yes, of course
e.g.
* stroke
* epilepsy
* neurodegenerative disorders
* Gilles-de-la-Tourette syndrome

Question 13

What are the main symptoms of Gilles de la Tourette-Syndrom

Answer 13

simple and complex motor and phonic tics (distinction is disputed):
* simple motor, e.g blinking, head jerking
* complex motor, e.g. touching, jumping or distorted posture
* simple phonic, e.g. sniffing, throat clearing, coughing
* complex phonic, e.g. linguistically meaningful verbalizations and utterances

Also not so often symptoms (<10% of all patients):
* coprolalia/copropraxia,
* echolalia/echopraxia,
* palialia/palipraxia

Question 14

How many tics have to be present for GTS diagnosis?

Answer 14

several motor tics and one or more phonic tic for more than one year

Question 15

What are premonitory urges?

Answer 15

Feelings of tightness, tension or itching accompanied by mounting sense of discomfort or distress and relieved by tic performance.
They can be suppressed with mounting discomfort but rebound after suppression.

Question 16

Describe epidemiology and etiological features of GTS

timecourse, prevalence in population, heritability, risk factors

Answer 16

• nursery school onset (4-6 y.o), highest severity at 10-12 y.o, then decline, however possible to develop it later, after a seizure, for example
• prevalence around 1%, 3-4 times more common in boys
• 0.77 estimated heritabilty
• no gene associated with it
• pre and perinatal factors (maternal stress, gestational smoking, infections) => activating microglia and altering synaptic connections
• maternal autoimmune disease associated with 29% increase of GTS in boy

Question 17

Is there pure GTS or is it usually accompanied by other conditions?

Answer 17

> 90% of patients don’t have ‘pure GTS’

• comorbid conditions
  
  • OCD, OCB (disorder vs. behaviour)
  • ADHD (Attention deficit hyperactivity disorder)
  • migraine in 25-26% of GTS
• coexistent conditions (no identified genetic or etiological overlap)
  
  • depression <- social deprivation
  • anxiety
  • substance abuse
  • learning disorder
  • suicidality

Question 18

What is the hypothesised pathomechanism of GST?

Answer 18

• dysfunction of cortico-basal ganglia-thalamic-cortical circuitry => selecting contextually appropriate behavioural patterns and suppressing inappropriate ones is failed
• among several transmitter systems, there is most solid evidence for dopamine:

VTA innervates the frontal cortex and ventral striatum -> influences transmitter release in both glutamatergic cortical and GABAergic (direct and indirect pathway) striatal neurons

glutamate, GABA, acetylcholine, noradrenaline, histamine, cannabinoids

Question 19

What are the treatment options for GTS?

Answer 19

• behavioural therapy
• medication: anti-psychotic drugs (dopamine antagonists, haloperidol) and anti-adrenergic drugs
• deep brain stimulation (basal ganglia — last resort for desperate cases)

NB!
* waxing-and-waning nature of GTS with a tendency to improve on the long run discourages
* partial or full remission in later adolescence (90% of the adults still have tics, but they are not distressful anymore?)