Lec 22 Flashcards
Name treatments for PD and details
Drug replacement for dop - Use Levadopa (precursor to dop).
Surgical removal of basal ganglia nuclei
deep brain stimulation
Replace deteriorated cells with new ones that produce dop
Details of Levadopa (mech + problems)
Use Levadopa (precursor to dop).
- oral drug
- lasts 4 hours, must take routinely
- manages tremor, rigidity,
Problems
- drug wears off so must schedule it
- over medication leads to dyskinesias (unregulated movements)
- after long term use, unwanted movements can start happening
- postural instability and falls are not managed by this drug.
can you give a person straight dopamine
no - will not uptake it
details of surgery for PD
cause intentional lesion to globus pallidus or thalamus.
This reduces inhibition on movement.
problem - may get other damage, not reversible
describe deep brain stimulation for PD patients
implant electrode into part of brain while patient awake to get the perfect spot. Ask them to move and see what works.
implant to globus pallidus or smtg
electrode attached to power pack that send signals.
Shuts off certain neurons.
Can turn it on and off and is reversible.
very affective
describe cell transplant for PD
New area of search
transplant stem cells that would produce dop
What is Huntington’s
description (1), details (5)
degeneration of striatal cells (caudate + putamen)
- leads to large lateral ventricle
- mostly cells for indirect path affected (therefore excessive facilitation
- see deficits in cognitive and motor function.
- onset at 30-50 years
- progressive - leads to death
- there is a genetic component on parent have = 50% chance child will get, both parents have =100%
- no known cure
describe huntingtons chorea
describe dystonia
frequent, non-rhythmic involuntary movements
dystonia - abnormal sustained positions of limbs/trunk/face
describe (5) affects of Huntington’s
Chorea - jerky movements
Dystonia - sustained positions
Abnormal eye movement
Dementia
Depression and anxiety
treatments for Huntington’s
anti-dopaminergic meds
- because mostly affects indirect path (does inhibition of movement) you get more movement. Therefore, by giving anti-dop meds, mostly trying to get direct path to stop reducing inhibition (sub nig give pos signal to direct path and neg signal to indirect path)
Lesions - thalamotomy (would reduce positive signal)
Deep brain stimulation - target certain areas like with PD treatment
athetosis
slow involuntary writhing movements with intermittent dystonia (sustained positions)
hemiballismus + mechanism
how treat?
purposeless ballistic movements (often circular)
mech - subthalamic nuc lesion decrease indirect path output -> dec inhibition = increased movement
treat with neuroleptics (drugs) but can cause parkinson-like symptoms
What is usual age range for tourette syndrome
males or females get?
is there genetic component?
what area does it affect?
co-morbidities
- early childhood onset, reduces by adulthood
- males 4:1
- yes
- affect striatal cells for dop in basal ganglia (overactive = more random movements)
- co = ADHD AND OCD
symptoms of tourettes
tics
vocalia - vocal tics
echolalia - repeat what heard
what makes up the basal ganglia
striatum
- cuadate nuc
- putamen
Glob pall
- internal seg
- ext seg
subthal nuc
substantia nigra
- pars compacta
- pars reticulata
treatment for tourettes
is there cure
- psychotherapy to deal with stresses as result
- dopamine blockers - long term use can lead to symptoms
- deep brain stim in thal to reduce tics
- music can reduce tics
no cure
