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70 Cards in this Set

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What does basal ganglia refer to
Caudate, putamen, globus pallidus, subthalamic nucleus and substantia nigra
What is the most important role of the basal ganglia
Planning, executing and termination of the movement and lesion on any part of the BG will cause involuntary movements
What are the characteristics of myoclonus
It basically refers to the hiccups, startle
What part of basal ganglia is implicated in HD
Caudate nucleus
------------------------------------------------- dystonia and Wilsons
Putamen and Wilson is caused by ↑ in Cu accumulation
-------------------------------------------- hemiballismus
-------------------------------------------- PD
Substantia nigra
What tract handles the goal oriented movements
What is the role of the supplementary motor area
Rehearsal of a movement before it is actually accomplished, ↑ blood flow to the muscles
What is striatum or neocortex?
Putamen (controls motor function) and caudate (which is involved in the cognition, behavior and eye controls)
Lentiform nucleus
Putamen and GPI
Corpus striatum
Caudate putamen, GPI
What nucleus is involved with the addiction
Nucleus accumbens
What nucleus does the limbic system i.e. emotions
Amygdloid nucleus
What happens with caudate atrophy
Huntington’s disease, and the brain shrinks to 1/3rd of it’s original size
What are the SnS of HD
Fixed posture, dystonia, ↑ Cu due to Wilson, chews up the caudate, same thing can happen to putamen
Where would the lesion be seen if the patient was exposed to ↑ levels of CO
What is the most common location for metabolic lesions and how do they present
Metabolic lesions happen in the GPI and they are usually symmetric
What is pars compacta
It is called substantia nigra and is the key implicated region in the PD
Where is subthalamic nucleus and how is it effected
It is below the thalamus and is mainly affected by microbes, mainly AIDS virus and histplasmosis. This causes the formation of abscess and this usually presents on the contralateral side, i.e. abscess on the left and problems in the right
What is GPI similar to
SnR, it is believed that these structures were morphologically similar and were separated during development
What is the direct motor loop pathway
Motor cortex→ striatum→ Gpi→ thalamus→ motor cortex
What is the in direct pathway
Motor cortex→ GPE→ STN→GPI→THA→MOTOR CORTEX. The route taken via GPE makes it indirect
What are the + points
What is the output center of the basal ganglia
What are the excitatory and inhibitory NT for basal ganglia
+ is glutamate, - is GABA
What are hypokinetic movements
Overactive GPI, it ↓ thalamus effect by ↑ it’s inhibitory effect on the thalamus and this causes ↓ stimulation of the cortex by the thalamus
What are hyperkinetic movements
These are abnormally ↓ input of GPI, thalamus excitatory effect is ↑ and there are movements because the thalamus continuously + the motor cortex
Parkinson disease
Problem with the SN, loss of dopamine producing cells, and the loss of neurons in the zona compacta, and the remaining neurons contain lewy bodies, MAIN CAUSE IS ↓ DOPAMINE
What are the clinical symptoms of the PD
Resting tremor, bradykinesia (slowness of movements), rigidity (↑ muscle tone with passive movements), and postural (poor balance)
What are the typical symptoms
Shaking In one hand, slowness, ↓ facial expression, losing balance and micrographia (small handwriting)
What is the histologic hall mark for PD
Lewy bodies, these are cytoplasmic, eosinophilic inclusion bodies
What effect does the DA↓ have on the motor loop
It → to overactive thalamus because of ↓ effects of direct pathway and ↑ effect of the direct pathway
What is the rate limiting step in the synthesis of DA
It is called the tyrosine OH
What is the drug of choice for PD
Sinemet, it is a combination of carbidopa and L dopa
What is the function of the carbidopa
It ↓ AADC, which has the ability to convert L-dopa into dopamine
Why do we ↓ AADC
Because it is found in ↑ concentration in the blood, will convert the administered L-dopa into DA and no DA will go to the brain
What is the other component of the sinemet
L-dopa, converted to DA
How is DA metabolized
Via MOA and COMT pathway
Why do we (X) COMT
It has the ability to convert the DA to a dead end substance that can’t be used by the brain, so we treat the PD patients with COMTAN
What effect does the caffeine and nicotine have on PD
What is another type of drug that works on the PD patients and usually is the first choice
Anticholinergic agents
What id the main drug that can ↓ down the progression of the disease
None, but it is currently under research
What happens as the disease progresses
There are other symptoms that needto addressed like depression, dementia, psychosis (hallucinations), and dementia, and dyskinesia and chorea
What is the reason for dyskinesia? Who is at risk?
This is usually seen in the patients that take sinemet, there is a 70% chance of forming chorea if you are on sinemet, it the patient is ↓ 40 yo, 100% will develop chorea with in 3 years
Is PD genetic
Yes, there is a genetic propensity to the disease, PARK8 gene test is recommended in the patients that have children
What is the biomolecular reason to get PD
Parkin protein is not cleaved properly and in cases of SPORADIC PARKINSON, the proteasome is not working
What enzyme↓ would be implicated in PD
Tyrosine OH, it is needed to make DA
What is the difference between Chorea and dystonia
Chorea→ random movements
What is hemiballismus
It is extreme form of chorea, it is usually ballistic
What if a child is born with tyrosine OH ↓
This child will never be normal, w/out medication the child will have tremors and with medication the child will have chorea and dystonia
Is repeated stereotypical movements, involuntary, writhing, jerking, twisting and this is due to lesion in the putamen, this is usually ↓ Gpi output, so the thalamus ↑active
Lesion in the right putamen→
Left sided dystonia
Focal dystonia
Mainly seen in adults and involves one part of the body, usually idiopathic, examples includes cervical dystonia, blepharospasm (↑ blinking), oromandibular dystonia, spasmodic ( they have a hoarse voice, put finger on the side of the mouth and the voice gets better)
Generalized dystonia
Effects the entire body, usually DYT1 gene, these patients are given narcoleptics and surgical lesioning of the GPI bilaterally is helpful.
HD characteristics
chorea and dysartheria
Violent chorea this is due to lesion in the STN
Huntington’s disease
Classic basal ganglia disorder that causes the involuntary movements i.e. chorea, AD genetic, can cause sever emotional problems like apathy, depression, irritability, withdrawal, anxiety also it can cause cognitive problems like↓ memory, verbal fluency, coordination, calculating and planning. There’s is 10-15% suicide rate
What kind of disorder is Huntington
It is a motor disorder
What’re some of the features of the HD
Chorea, dysartheria (slurred speech),abnormal eye movements, difficulty shifting gaze quickly, inability to maintain muscle contraction, ‘milk maid grip’, dysphagia, poor coordination and poor balance
What is the most common age of onset
39 years, but can range from age 2-70
What is a genetic phenomenon that can be observed with HD
Anticipation in the CAG repeats, an effected parent can have multiple repeats and those would be expanded form generation to generation. The diseased allele is located on the chromosome 4, and the number of repeats has to ↑ than the normal 17-30, these repeats will coded for a misfolded Huntington’s protein
is HD maternally or paternally transmitted
It is paternally transmitted via anticipation
Persistent involuntary abnormal movements caused by the drugs like DA inhibitors, this is usually an iatrogenic disorder and can be a permanent condition main drug that’s implicated is Halidol
What are some of the classic signs of TD
Abnormal movements of the mouth and the tongue, possibly due to striatal DA receptor super sensitivity, this can be prevented by showing care to use drugs that inhibit DA activity especially if they are not antipsychotics mainly compazine
What are TICS and TOURETTE’S syndrome
Tics are intermittent movements or sounds, mainly motor and vocal (anytime the patients move air through their vocal cords they will have an echo), these can be caused by ↑# or sensitivity to DA. Halidol can ↓ TICS but it can cause TD,
What is parakinesia
Taking random movements and turning them into purposeful movements, like if you are in the habit of touching your face, you will pretend to fix your glasses
What is a major source of treatment for all of these movements disorders
Canabanoids i.e. Marijuana
What is the difference between Chorea and dystonia
Chorea→ random movements
Dystonia→ repeating same type of movements