Tourette's Syndrome Essay Flashcards

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1
Q

Tourette’s syndrome (TS)

A

Involves a number of clinical features including verbal and motor tics

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2
Q

Tics

A

the most obvious and distinguishing symptom

brief actions (motor)
vocalisations (verbal)

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3
Q

Range in complexity

A

simple recurrent acts like blinking and coughing, involving one muscle group

complex multiple co-occuring tics or elaborate action sequences, involving multiple motor groups

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4
Q

Most common misconception about TS

A

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

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5
Q

Tics

A

Involuntary
Unwilled
Unchosen
Involuntary urge
Voluntarily releasing tic to relieve urge

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6
Q

Prevalence, stress, comorbidity

A

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

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7
Q

First line of treatment for TS

A

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

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8
Q

Pharmacological treatments second line include

A

antiepileptics and neuroleptics (control gaba and glutamate balance)

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9
Q

Dopamine blockers

A

haloperidol
risperidone
control tics
SE: weight gain, IRM

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10
Q

Experimental techniques

A

transcranial magnetic stimulation
deep brain stimulation
invasive
not as common

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11
Q

Mechanism not fully understood but thought to

A

primarily include BG

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12
Q

in typical motor control

A

signals encoding motor plans from cortex enter cortico-striatal-thalamo-cortical circuit via putamen

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13
Q

in TS dysregulation within basal ganglia

A

likely compromises inhibitory striatal outflow facilitating direct over indirect pathway activity

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14
Q

as consequence, thalamic output to motor cortex

A

predisposes production of actions not signalled through corticostriatal pathway or weakly signalled

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15
Q

postmortem data

A

revealed key insights into striatal dysfunction in TS with 50% reduction in GABAergic interneurons

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16
Q

similar to HD chorea

A

reduction in GABA interneurons - unwanted movements

17
Q

findings in TS brains consistent with

A

altered neural migration during development

18
Q

Animal models

A

injection of GABA antagonist bucucilline into putamen leads to brief recurrent actions that closely resemble human tics

19
Q

potential mechanisms involving dysregulated synaptic communication and architecture include

A

neurologins
neurexins
GABAergic
glutamatergic AMPA receptor signalling suggested

20
Q

as well as mitochondrial function disturbances

A

proposed to alter energy balance within BG