18.5 - Tourette's Flashcards
How does Tourettes differ from schizophrenia, bipolar MDD and anxiety disorders?
the specificity of its symptoms
explain the case of RG
developed tics at 15
what are tics
involuntary, repetitive, stereotyped movements or vocalizations
what is a symptom Tourettes shares with schizophrenia
echolalia
how effective was RG’s medication
99% symptom elimination
What is of the utmost importance for the wellbeing of those with Tourettes
the understanding of their peers, family and friends, as well as their support - really all the difference in outcomes
when does Tourettes onset
- what are symptoms usually like at onset? Do they remain this way?
typically early in life (childhood, adolescence)
- some motor tics life eye blinking, head movements
- no, they gradually become more complex and severe
describe some common complex motor tics
hitting and touching objects, squatting hoppin twirling lewd gestures
what are common verbal tics
- inarticulate sounds like barking
- Coprolalia (swearing)
- echolalia
- palilalia - repetition of ones own words
Do Tourette’s symptoms ever stop worsening? explain
Yes, they tend to peak after a few years, then gradually subside
what is the prevalence of Tourettes
0.3-1% of the pop
are there gender differences in prevalence?
- describe
yes, males 4x more frequent in childhood
- less profound as they mature
Is there a genetic component to Tourettes?
yes - 50% conc. in monozygotic, 10% in dy
what two disorders do some Tourettes patients display symptoms of
ADHD, OCD, or both
can Tourettes patients control their tics?
- yes and no
- they are involuntary, but they can be temporarily suppressed with concentration and effort
how have we misunderstood the nature of tic suppression
believed it would result in a rebound, where they become more frequent and extreme
- this is not the case
why is the neural basis of Tourettes more amenable to study than the other disorders in this chpt
bc its fuckin obviously Tourettes - well defined with clearly observable symptoms
what are the impediments to the study of Tourettes
- lack of a strong link to a particular gene
- greatest - symptoms subside with age, means ppl rarely are under care for the disorder when they die, tf no postmortem studies
what does the lack of availability of post mortem brain studies mean for our studies on the neural pathology underlying Tourettes
- why is this a problem
study is based entirely on brain imaging studies
- hard to conduct bc of the requirement of the patients to stay motionless
where has most of the research on cerebral pathology in this disorder led us?
- describe the findings about this area
to focus on the striatum (caudate plus putamen)
- smaller striata volumes
- fMRI activity in PFC and caudate nuclei during tic suppression
what do the activations of PFC and caudate nuclei during tic suppression tell us (in theory0
that decision to suppress tics emerges from PFC, which initiates suppression by acting on the caudate nuclei
what other area of the brain has been implicated in Tourettes? describe (ie - types of synapses, role this seems to play)
the cortical-striatal-thalamic-cortical brain circuits,
- dopaminergic and GABAergic signalling therein
- brain circuits are implicated in motor learning including habit formation
are brain differences in Tourettes localized to the striatum and the cortical-striatal-thalamic-cortical structures?
Nope, they seem to be widespread
- example - thinning in the sensorimotor cortex grey matter
- particularly prominent in areas controlling the face, mouth and larynx
where does treatment for Tourettes typically begin
not with tics
- patients, family members, friends and teachers are education about the syndrome
- then treatment focusses on the ancillary emotional problems like anxiety and depressin
when to we start to treat tics
only once we have educated the support group and treated ancillary emotional problems
how do we treat tics
usually with antipsychotics
- reduce tics by around 70%
- very often refuse to take them bc of the adverse effects
what is the success of antipsychotics in treating tics amenable to
the belief that the disorder is related to an abnormality in the cortical-striatal-thalamic-cortical circuit, bc this signal relies heavily on dopamine
