Quiz 5 Flashcards

0
Q

Which neurotransmitter is important for muscle contractions?

A

Acetycholine

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1
Q

What is apraxia?

A

Inability to perform voluntary movements

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2
Q

What part of the brain is critical for procedural memory?

A

Basal Ganglia

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3
Q

Major structures involve in motor movement.

A

Primary motor cortex - this structure is responsible for motor movement execution
Parietal cortex- becomes active before making the movement, meaning it plans the movement before it is executed. ( damaged to this region results in apraxia and contralateral neglect)
Dorsolateral prefrontal cortex- it is involve in strategy making (similar to parietal cortex function)
Secondary motor cortex- this structure helps initiate motor movements ( initiation of motor movements)
Premotor cortex- externally generates motor movements (catching a ball when is thrown at you)
Supplementary motor area- works as a sequencer and planner (voluntary movements)

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4
Q

Basic organization of primary motor cortex and somatosensory motor cortex.

A

Somatotopic organization- things attached close to each other on body are similarly mapped out on brain
Disproportionate Representation: more premotor cortex area dedicated to areas of body used the most (hands, face muscles)
Plasticity: with the constant use of a body part, brain representation of that body part expands
Lateralization: left primary motor cortex controls motor function in right side of body (vice versa)
Precentral Gyrus

Somatosensory Cortex: somatotopic organized in terms of layout 
Postcentral Gyrus
Disproportionate Representation 
Plasticity 
Lateralization
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5
Q

What is the knee-jerk-reflex? ( state other possible terms to refer to this reflex)

A

Tap on the knee–> sensory nerve responds to muscle stretch–> sends signal to spinal cord–> connects to motor neuron from single synapse–> motor neuron stimulates quadriceps to contract and reduce stretch.
This reflex is also known as the monosynaptic stretch reflex

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6
Q

Which are the positive symptoms of PD?

A

Tremor at rest ( usually appear as disease progresses not when onset takes place)
Muscular rigidity
Involuntary motor movements
Oculogyric crisis- eyes tend to shift involuntary to one side and freeze for a few seconds
Dyskenisia- decrease in voluntary movements and increase of involuntary movements, similar to tics or chorea.

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7
Q

Which are the negative symptoms of PD?

A

Disorders of posture(fixation)- odd positions
Disorders of locomotion
Disorder of speech
Akinesia (moderate to later)is the inability to initiate movement, due to problems with selecting and activating motor programs in the brain. It is a common consequence of Parkinson’s disease caused by dopamine loss in the direct pathway of movement.
Masked facial expression- emotionless expresion
Festination- involuntary tendency to take short steps while walking, accelerating steps while walking
Bradykinesia - abnormal slowness in movement.
Hypokinesia - abnormally diminished motor function or activity.

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8
Q

What is festination?

A

Hard time engaging walking, but once it starts it is hard to slow down.

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9
Q

What is the cogwheel rigidity?

A

Occurs when there is also a tremor and is characterized as “stop and go” effect during range of motion maneuver . (Sort of stop motion effect)

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10
Q

In PD, how do tremors change as disease progresses? Do tremors stop during some behaviors?

A

Tremors start in one limb and are mild, however! As PD progresses tremors will worsen. The tremors may transfer to the other side of the body and is not unilateral anymore.
Tremor usually stop as patients try to reach for something or try to execute volitional movement, meaning that once an action is executed (e.g., reaching for an object), the tremors may cease temporarily.

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11
Q

What neurotransmitter is depleted in patients with PD? How can you get a measure of dopamine levels in a living PD patient?

A

Dopamine (DA)
In patients with PD, DA levels are left at 10% ( due to cells dying in the substantia nigra)
Measuring levels of homovanillic acid in urine (urine test). HMA is a DA metabolite. Higher volumes of it mean higher volumes of DA being metabolized.

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12
Q

What is the primary drug use to treat patients with PD? Why is this drug use rather than dopamine?

A

L-Dopa is used to treat patients with PD because it can cross the blood barrier. The problem with dopamine is that it get metabolized before it crosses the blood barrier. L-Dopa is often paired with Cardidopa, which prevents L-Dopa from being metabolized. In addition, some negative effects of this drug is that patients develop some psychotic symptoms similar to those of schizophrenia and that it helps patients just for a while, but then the drug has no effect on treating PD and patient tend to get worse. Its targets are rigidity and bradykinesia, it has no effect on posture or balance.

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13
Q

Review PD with dementia. When do the symptoms of dementia begin in patients with PD with dementia?

A

30% of patients get this (develop this condition)
70 years+ develop this disease, usually after 10-15 years of first onset at age 60 patients are diagnosed with PD
Psychotic symptoms : hallucinations
PD: mild cognitive impairment

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14
Q

Do PD patients who do not show dementia still show some level of cognitive impairment?

A

Show attention and cognitive problems, executive functioning problems
Memory problems: there is a major decrease in procedural memory
Visuospatial line orientation test
Patients show prospective, episodic, short term memory, procedural, source and retrieval memory dysfunction as well.

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15
Q

Review the basic motor symptoms associated with Huntington’ disease (HD). Are motor symptoms typically the first problems observed in HD patients?

A

Early: fideting and minor hyperkinesia (cant keep still)
Increased hyperkinesia as desease progresses, movements become more exaggerated
Substaining muscle contraction: cannot do ( stikck tongue out and hold it there)
Chorea exaggerated patterns, almost like if they were dancing
Dysarthia problems with motor programming speech dysphasia a cognitive speech problem
Show cognitive impairments way before you can see motor dysfunction
Cognitive impairments happen first then motor dysfunction compared to PD, mood swings are often seen in HD patients

16
Q

Review the genetics of HD (e.g. which chromosome is affected, CAG repeats, etc.). Do 100% of HD patients show a family history?

A

Autosomal dominant: if one parent has it, offspring has a 50/50 chance of also getting it
Chromosome 4: normally people have repeats, but more than 39
Trinucleotide repeat CAG
<28= no HD
29-34= no HD, increase risk for offspring
35-38= possible HD, increased risk in offspring
39+= HD
1-3% of HD patients have no family history, this desease is familial

17
Q

Review the basic differences between focal and generalized seizures

A

Focal seizures (60% of the seizures cases are focal) - also called parietal seizures, they receive the term focal because they are focused in one specific part of the brain, they occur in one side only, they do not spread. Are chacterized by the prescence of auras, warning signals for individuals before a seizure occurs, these are sensations like nausea, a particular smell, particular sounds, each aura varies depending onthe individual. No lost of conciousness takes place.

Generalized seizures- abnormal electrical activity, which affects both sides of the brain, they cause complete lost of consciousness, the person may fall or stumble over.

18
Q

What is the difference between a simple focal seizure and a complex focal seizure?

A

Simple focal seizure- person remains concious, remove from reality
Complex focal seizure- change or complete lost of concious, waking up from a dream, repetetive behavior patterns (automatism)few secods, may be a minute.

19
Q

What technique is used to measure seizure activity in the brain?

A

EGG
CT
MRI

20
Q

What is a febrile seizure?

A

Febrile seizures- very common in children, this type of seizure is trigger by a fever higher of 100 (102-103), which eventually causes the brain to response with a seizure.

21
Q

What is status epilepticus?

A

Status epilepticus- this occurs when a seizure last for more than 5 mins, or the person enters into another seizure without recovery ( one seizure follow by another seizure ) this is can be life threatening because it could cause the person have a heart attack or failure to breath.

22
Q

What drugs are used to treat seizures and how do they work? Do the drugs work for all patients? What can be done if the drugs do not work?

A

Antiepileptic drugs affect gabba, making it more efficient, decreasing activity in the brain(Phenobarbital- gaba agonists use for many years older, Dilantin-, Tegretol, Neurotonin - new drug, ) sedatives.
Around 20% of the people do not benefit from drugs, but there are surgical procedures that could be used to treat them. Surgery (alternatives to medication in order to treat seizures)
Removal of seizure focus (like patient HM)
Multiple subpial transection cuts into the cerebral cortex, this happens when the seizures occur in an area that cannot be remove
Corpus callosotomy cutting the corpus collosum
Hemispherectomy- rare procedure consisting in removing one brain hemisphere

23
Q

What do you do if you see someone having a seizure, what should you not do?

A

Roll the person on his or her side to prevent choking on any fluids or vomit.
Cushion the person’s head.
Loosen any tight clothing around the neck.
Keep the person’s airway open. If necessary, grip the person’s jaw gently and tilt his or her head back.
Do NOT restrict the person from moving unless he or she is in danger.
Do NOT put anything into the person’s mouth, not even medicine or liquid. These can cause choking or damage to the person’s jaw, tongue, or teeth. Contrary to widespread belief, people cannot swallow their tongues during a seizure or any other time.
Remove any sharp or solid objects that the person might hit during the seizure.
Note how long the seizure lasts and what symptoms occurred so you can tell a doctor or emergency personnel if necessary.
Stay with the person until the seizure ends.

24
Q

Do seizures cause significant brain damage?

A

Not most of them, but if is a seizure that last more than 5 minutes or one after the other with no recovery period could cause some significant damage

25
Q

Review the differences between absence, clonic, tonic, atonic, and clonic-tonic seizures.

A

Absence seizures- daydreaming, then go back to what they were doing
Petit mal seizures - no shaking, compulsion, minor twitching, they are just staring, then come back to do what they were doing
Tonic seizures- muscle tone increases, arm upper arm back and legs,muscles get very rigid
Clonic seizures - jerking of the muscles, twitching of the body (both sides of the body) seen in head and arms
Atonic seizures - lose muscle tone, this causes them to fall
Tonic-clonic seizures -
Grand mal seizures- increase of muscle tone and muscle jerking, lost of consciousness.