Tourette's Syndrome Essay Flashcards
Tourette’s syndrome (TS)
Involves a number of clinical features including verbal and motor tics
Tics
the most obvious and distinguishing symptom
brief actions (motor)
vocalisations (verbal)
Range in complexity
simple recurrent acts like blinking and coughing, involving one muscle group
complex multiple co-occuring tics or elaborate action sequences, involving multiple motor groups
Most common misconception about TS
People with the condition use inappropriate language and blurt out curse words
Often seen on TV and in movies
This is often not the case
Known as coprolalia
1 in 10 people
Complex tic
Hard to suppress/control
Embarrassing/ashamed
Tics
Involuntary
Unwilled
Unchosen
Involuntary urge
Voluntarily releasing tic to relieve urge
Prevalence, stress, comorbidity
1 in 100 (1%) population
Most find it gets better by late teens/early adulthood
Not understood why
Worse with stress - same as OCD
Comorbid with ADHD and OCD
First line of treatment for TS
Habit reversal therapy
Two step process - awareness and competitive response training
Tic occurs, person acknowledges it, tells therapist, therapist gives counter response e.g sit on hand
Psychological intervention first line because physiological mechanism not fully understood
Pharmacological treatments second line include
antiepileptics and neuroleptics (control gaba and glutamate balance)
Dopamine blockers
haloperidol
risperidone
control tics
SE: weight gain, IRM
Experimental techniques
transcranial magnetic stimulation
deep brain stimulation
invasive
not as common
Mechanism not fully understood but thought to
primarily include BG
in typical motor control
signals encoding motor plans from cortex enter cortico-striatal-thalamo-cortical circuit via putamen
in TS dysregulation within basal ganglia
likely compromises inhibitory striatal outflow facilitating direct over indirect pathway activity
as consequence, thalamic output to motor cortex
predisposes production of actions not signalled through corticostriatal pathway or weakly signalled
postmortem data
revealed key insights into striatal dysfunction in TS with 50% reduction in GABAergic interneurons
similar to HD chorea
reduction in GABA interneurons - unwanted movements
findings in TS brains consistent with
altered neural migration during development
Animal models
injection of GABA antagonist bucucilline into putamen leads to brief recurrent actions that closely resemble human tics
potential mechanisms involving dysregulated synaptic communication and architecture include
neurologins
neurexins
GABAergic
glutamatergic AMPA receptor signalling suggested
as well as mitochondrial function disturbances
proposed to alter energy balance within BG
