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70 Cards in this Set
- Front
- Back
- 3rd side (hint)
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What does basal ganglia refer to
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Caudate, putamen, globus pallidus, subthalamic nucleus and substantia nigra
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What is the most important role of the basal ganglia
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Planning, executing and termination of the movement and lesion on any part of the BG will cause involuntary movements
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What are the characteristics of myoclonus
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It basically refers to the hiccups, startle
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What part of basal ganglia is implicated in HD
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Caudate nucleus
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------------------------------------------------- dystonia and Wilsons
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Putamen and Wilson is caused by ↑ in Cu accumulation
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-------------------------------------------- hemiballismus
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SUBTHALAMIC NUCLEUS
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-------------------------------------------- PD
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Substantia nigra
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What tract handles the goal oriented movements
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Corticospinal
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What is the role of the supplementary motor area
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Rehearsal of a movement before it is actually accomplished, ↑ blood flow to the muscles
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What is striatum or neocortex?
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Putamen (controls motor function) and caudate (which is involved in the cognition, behavior and eye controls)
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Lentiform nucleus
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Putamen and GPI
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Corpus striatum
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Caudate putamen, GPI
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What nucleus is involved with the addiction
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Nucleus accumbens
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What nucleus does the limbic system i.e. emotions
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Amygdloid nucleus
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What happens with caudate atrophy
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Huntington’s disease, and the brain shrinks to 1/3rd of it’s original size
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What are the SnS of HD
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Fixed posture, dystonia, ↑ Cu due to Wilson, chews up the caudate, same thing can happen to putamen
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Where would the lesion be seen if the patient was exposed to ↑ levels of CO
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GP
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What is the most common location for metabolic lesions and how do they present
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Metabolic lesions happen in the GPI and they are usually symmetric
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What is pars compacta
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It is called substantia nigra and is the key implicated region in the PD
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Where is subthalamic nucleus and how is it effected
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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
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What is GPI similar to
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SnR, it is believed that these structures were morphologically similar and were separated during development
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What is the direct motor loop pathway
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Motor cortex→ striatum→ Gpi→ thalamus→ motor cortex
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What is the in direct pathway
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Motor cortex→ GPE→ STN→GPI→THA→MOTOR CORTEX. The route taken via GPE makes it indirect
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What are the + points
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STN→ +GPI, THALAMUS→ + MOTOR CORTEX, MOTOR CORTEX→ + ON STRIATUM
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WHAT ARE THE INHBITORY POINTS
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STRIATUM→ - GPE AND GPI, AND STN,GPE→ -STN GPI→ - THALAMUS
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What is the output center of the basal ganglia
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GPI
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What are the excitatory and inhibitory NT for basal ganglia
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+ is glutamate, - is GABA
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What are hypokinetic movements
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Overactive GPI, it ↓ thalamus effect by ↑ it’s inhibitory effect on the thalamus and this causes ↓ stimulation of the cortex by the thalamus
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What are hyperkinetic movements
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These are abnormally ↓ input of GPI, thalamus excitatory effect is ↑ and there are movements because the thalamus continuously + the motor cortex
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Parkinson disease
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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
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What are the clinical symptoms of the PD
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Resting tremor, bradykinesia (slowness of movements), rigidity (↑ muscle tone with passive movements), and postural (poor balance)
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What are the typical symptoms
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Shaking In one hand, slowness, ↓ facial expression, losing balance and micrographia (small handwriting)
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What is the histologic hall mark for PD
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Lewy bodies, these are cytoplasmic, eosinophilic inclusion bodies
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What effect does the DA↓ have on the motor loop
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It → to overactive thalamus because of ↓ effects of direct pathway and ↑ effect of the direct pathway
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What is the rate limiting step in the synthesis of DA
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It is called the tyrosine OH
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What is the drug of choice for PD
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Sinemet, it is a combination of carbidopa and L dopa
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What is the function of the carbidopa
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It ↓ AADC, which has the ability to convert L-dopa into dopamine
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Why do we ↓ AADC
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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
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What is the other component of the sinemet
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L-dopa, converted to DA
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How is DA metabolized
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Via MOA and COMT pathway
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Why do we (X) COMT
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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
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What effect does the caffeine and nicotine have on PD
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Protective
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What is another type of drug that works on the PD patients and usually is the first choice
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Anticholinergic agents
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What id the main drug that can ↓ down the progression of the disease
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None, but it is currently under research
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What happens as the disease progresses
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There are other symptoms that needto addressed like depression, dementia, psychosis (hallucinations), and dementia, and dyskinesia and chorea
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What is the reason for dyskinesia? Who is at risk?
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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
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Is PD genetic
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Yes, there is a genetic propensity to the disease, PARK8 gene test is recommended in the patients that have children
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What is the biomolecular reason to get PD
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Parkin protein is not cleaved properly and in cases of SPORADIC PARKINSON, the proteasome is not working
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What enzyme↓ would be implicated in PD
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Tyrosine OH, it is needed to make DA
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What is the difference between Chorea and dystonia
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Chorea→ random movements
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What is hemiballismus
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It is extreme form of chorea, it is usually ballistic
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What if a child is born with tyrosine OH ↓
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This child will never be normal, w/out medication the child will have tremors and with medication the child will have chorea and dystonia
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Dystonia?
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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
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Lesion in the right putamen→
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Left sided dystonia
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Focal dystonia
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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)
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Generalized dystonia
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Effects the entire body, usually DYT1 gene, these patients are given narcoleptics and surgical lesioning of the GPI bilaterally is helpful.
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HD characteristics
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chorea and dysartheria
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None
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Hemiballismus
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Violent chorea this is due to lesion in the STN
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Huntington’s disease
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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
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What kind of disorder is Huntington
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It is a motor disorder
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What’re some of the features of the HD
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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
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What is the most common age of onset
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39 years, but can range from age 2-70
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What is a genetic phenomenon that can be observed with HD
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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
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is HD maternally or paternally transmitted
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It is paternally transmitted via anticipation
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What is TARDIVE DYKSKINESIA
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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
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What are some of the classic signs of TD
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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
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What are TICS and TOURETTE’S syndrome
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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,
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What is parakinesia
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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
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What is a major source of treatment for all of these movements disorders
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Canabanoids i.e. Marijuana
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What is the difference between Chorea and dystonia
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Chorea→ random movements
Dystonia→ repeating same type of movements |
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