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How common is Dyskinetic CP?

(2017. Monbaliu + Dan)

It is the second most common type


What is dyskinetic CP usually cased by?

(2017. Monbaliu + Dan)

Non-progressive lesions to the basal ganglia or thalamus


In dyskinetic CP (DCP) what two major movement disorders are presented together most of the time?

(2017. Monbaliu + Dan)

Dystonia and choreathetosis


Is the pathology for both movement disorders in dsykinetic CP known? And what is the current hypothesis (3 parts)?

(2017. Monbaliu + Dan)

-It is largely unknown

-Emerging hypothesis are
1. an imbalance between indirect and direct basal ganglia pathways
2. disturbed sensory processing
3. impaired plasticity in the basal ganglia


What can exacerbate dystonia? And what can relieve it?

(2017. Monbaliu + Dan)

- emotion, cognitive tasks, stress, pain and intention to move

-it is always released by sleep


Are dystonia and choreathetosis usually generalised? And where is the higher severity?

(2017. Monbaliu + Dan)

-usually both generalised over all body regions

-higher severity in the upper limbs than lower limbs- and both movement disorders increase with activity


What are some key clinical presentations of dyskinetic CP? (5 parts)

(2017. Monbaliu + Dan)

1. Motor impairments—-often more severe than other types of CP
2. Non-motor co-morbidities—more than half intellectual impairment, anarthria (non-verbal), and epilepsy
3. Visual and hearing ——-impairments common
4. Underweights——More than half
5. Verbal communication ———is always always affected


What does dystonia refer to? And how could dystonia be described?

(2017. Monbaliu + Dan)

-Refers to abnormal postures, involuntary twisting and repetitive movements- due to sustained muscle contractions

-Most accurately described as a neuronal network disorder


What pathways exist in the basal ganglia? And how do they operate and might operate in people with dyskinetic CP?

(2017. Monbaliu + Dan)

-A direct, excitable pathway: controls voluntary movement
-An indirect inhibitory pathway: inhibits unwanted movement

For dyskinetic CP there is an imbalance between the direct and indirect pathways, an over activity in the direct pathway and under activity of the indirect. Causing excessive moment and loss of inhibition


What might lead to abnormal sensorimotor integration? And cause what?

(2017. Monbaliu + Dan)

Abnormal plasticity during motor learning

And cause consolidation of abnormal motor engram

Therefore, therapeutic mama gets have little effort on dystonia because bad motor memories are difficult to erase


What do studies in deep brain stimulation (DBS) find?

(2017. Monbaliu + Dan)

-Reduction of dystonia rather than effects on function, quality of life, or choreathetosis


What is hypothesised about the pathophysiology of inherited Dystonia vs secondary Dystonia of dyskinetic CP?

(2017. Monbaliu + Dan)

-hypothesised that difference pathophysiology and therefore different responses in treatment and differences in motor cortex plasticity + cerebellum function in the modulation of dystonia features


What might explain the modest and delayed effects of DBS in people with dyskinetic CP?

(2017. Monbaliu + Dan)

Abnormal plasticity

Altered neuronal cortex- basal ganglia network


What evidence is there for rehabilitation strategies for dyskinetic cerebral palsy?

(2017. Monbaliu + Dan)

Very little evidence and current practice based on clinical expertise


Given the potential of brain plasticity what two areas of research are warranted for dyskinetic CP management?

(2017. Monbaliu + Dan)

-Cognitive learning

-Motor learning


What evidence is there for pharmacological treatment of dyskinetic CP?

(2017. Monbaliu + Dan)

Very little evidence

-Those without MRI abnormalities (although can take years to show) possibilities of dopamine-responsive mimic to be considered

-Some studies showing intrathecal baclofen to decrease dystonia


What depleting agenda can influence hyperkinetic component of dyskinesia?

(2017. Monbaliu + Dan)

Dopamine-depleting agents

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