Test 5 Flashcards

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1
Q

What is apraxia?

A

Inability to execute motor movement when asked to

Someone says “brush your hair” but you cant show them how but you know how to

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2
Q

Which neurotransmitter is important for muscle contractions?

A

Acetylcholine

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3
Q

What part of the brain is critical for procedural memory?

A
Basal ganglia
(knowing how to do things, motor skills)
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4
Q

Review the 11 major structures involved in motor movements (e.g. premotor cortex, primary motor cortex, etc.).

A
  1. prefrontal cortex- planning, goal-oriented
  2. parietal cortex- spatial awareness of where you are in the world
  3. primary motor cortex (precentral gyrus)- plans and executes motor movement
  4. secondary motor cortex- initiating motor movement
    4a. pre motor cortex- initiation of external motor movement (ducking when you see a ball coming)
    4b. supplementary motor cortex- initiate self-generated motor movement (pick up a glass)
  5. frontal eye fields- moving the eyes
  6. cerebellum- balance and coordination
  7. basal ganglia- motor movement, how to do something
  8. cuadate nucleus- where to respond in space (reach and miss)
  9. putamen- strength of motor response (pick up eggs vs hammer)
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5
Q

what 2 cortex combined represent the highest level of the motor control hierarchy?

A

parietal and prefrontal cortex

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6
Q

Review the basic organization of primary motor cortex

A

Primary Motor Cortex= Sends the signals to execute the motor movement.
Precentral Gyrus= Controls voluntary motor movement
Somatotopic Organization= Map of your body and how/which neurons are used. Your body is laid out like a map.
Disproportionate Representations= Not proportional to the actual size of the body part. Some areas take up more/less space.More important body parts that require more fine motor control have more brain area dedicated to them.
Plasticity =Representation of brain areas can change over time with experience.
Lateralization= Brain controls opposite side of the body.Right Primary Motor controls left side of body, and vice versa.

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7
Q

Review the basic organization of somatosensory cortex

A

Somatosensory Cortex (post central gyrus)= Ability to register touch/pain on the body.
Postcentral Gyrus= Controls sensory function from the body.
The sensory system communicates with the motor system - they are close to one another in the brain in order to work together.
Somatotopic Organization= Same mapping and same disproportion as the other system.
Disproportional Representations =Not proportional to the actual size of the body part. Some areas take up more/less space
Plasticity= If you get a lot of sensory information on your hand, you are going to develop larger representation in the hand.
Lateralization= Touch on the right side of the body, activates the left somatosensory cortex.

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8
Q

what is astereoagnosia?

A

cant recognize an object by touching it

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9
Q

what is ataxia?

A

reach and miss

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10
Q

what is akinesia?

A

absence of ability to make voluntary movement

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11
Q

what is hyperkinesia?

A

increase in size of motor movement (exaggerated step)

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12
Q

what is hypokinesia?

A

deduction in motor movement (shuffle feet)

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13
Q

what is bradykinesia?

A

slow motor movement

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14
Q

what is the knee- jerk reflex?

A
  1. Tap on the patellar tendon stretches the quad
  2. Sensory nerve responds to the muscle stretch
  3. By sending a signal to the spinal cord, where it connects to a motor neuron through a signal synapse
  4. Motor neuron stimulates the quad muscle to contract and reduce the stretch
  5. Quad contracts, extending the lower leg
    * spinal cord mediated
    * only involves one synapse
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15
Q

Primary symptoms of PD

A

Tremor at rest (typically begins in one limb)
Muscle rigidity (stiff)-Cogwheel rigidity
Bradykinesia: slowness in motor movement
Posture disturbances (tend to bend over)
Impaired balance (often fall)- no righting reflex

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16
Q

Seondary symptoms of PD

A

Disorders of posture (stooped)
Involuntary motor movements
Oculogyriccrisis: eyes shift and become frozen
Dyskinesia: abnormality/impairment in voluntary motor movement, parts of body move back
Micrographia: write really small
Disorders of locomotion (freezing and festination)
disorders of speech
Masked facial expression (extrapyramidalsymptoms: overlap with lewy-body dementia)

17
Q

What is festination

A

problem with gait, characterized small and fast steps (makes it more likely to fall)

18
Q

What is cogwheel rigidity?

A

part of muscle rigidity, one of the primary symptoms of PD. When you try to move one limb but are vey rigid

19
Q

How do tremors change as the disease progresses? Do the tremors stop during some behaviors?

A

Tremors get worse as the disease progresses, however they stop briefly while sleeping or during deliberate movements (touching your finger tip to another persons)

20
Q

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

A

Dopamine is reduced by 80-90% in the brain of a PD patient

Urine test- dopamine comes out as homovanillic acid in urine and is a way to monitor decreased levels of dopamine

21
Q

What is the primary drug treatment for patients with PD? Why is this drug used rather than dopamine?

A
Stalevo is the most commonly prescribed treatment (combo or Ldopa, Carbidopa, and Entcapone) 
Dopamine is not used because it cannot pass the blood brain barrier to get to the brain
Levadopa (L-dopa) combined with Carbidopa (Sinemet)- helps more L-dopa get in the brain
combination of L-dopa and Carbidopa are pretty effective 
COMT inhibitors (Entcapone): blocks enzyme that breaks down dopamine to get more in pathway
Dopamine Agonists: increase synthesis of dopamine
Requip and Mirapex: fewer side effects, less wave off, can cause drowsiness and hallucinations
22
Q

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

A

Large variety don’t show dementia
Dementia with lewy bodies
Memory problems
Executive function is impaired
Psychotic symptoms: dellusions, hallucinations
Attention problems
Age of onset with PD is between 50 and 60 where primary symptoms develop
10% before age 40
patients live 10-20 years after diagnosis
About a 10- 15 year gap after PD diagnosis to dementia diagnosis
40% of patients show RSBD before the onset of PD

23
Q

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

A

Over 50% will perform in the cognitively normal range on tests
PD patients who do not show dementia can show some level of cognitive impairment in the domains listed.Sometend to be more impaired in certain domains than others, there is no profile for people with PD because it varies so much
Attention/Concentration
Executive Function: planning,problem solving, abstract thinking, rule acquisition set shifting, perseverations. initiating/inhibiting actions, fluency
Memory: prospective memory (remembering to remember), episodic memory, STM, procedural memory, source memory, recall vs. retrieval
Visuospatial: line orientation

24
Q

Review the basic motor symptoms associated with Huntington’ disease (HD).

A

chorea:body is moving excessively; can’t control their movements
hyperkinesia: exaggerated movements
problems sustaining muscle contraction
Dysarthia: problems with motor component of speech
Dysphasia: cognitive speech problem

25
Q

Review the basic cognitive symptoms associated with Huntington’ disease (HD).

A
Early symptoms
forgetful
focusing and maintaining attention
As it progresses:
Concentration/attention
 Learning
Memory/retriecal (episodic memory, STM, procedural, and source memory)
Executive function
Visuospatial Processing
Slow processing speed
Language is relativelypreserved
Apraxia
26
Q

Review the basic emotional symptoms associated with Huntington’ disease (HD).

A
Personality
Anxiety/Depression
Mania
Mood swings
OCD behaviors
Schizophrenic like symptoms
Hallucinations and delusions
27
Q

Are motor symptoms typically the first problems observed in HD patients?

A

Cognitive/Emotional problems are typically the first problems observed in HD patients.Motor symptoms are usually used to make diagnosis

28
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

Chromosome 4 mutation
If you have enough CAG’s repeats you will get Huntington’s disease
<28 CAG’s in a row = no HD
29-34 CAG’s in a row = no HD for you, BUT increased risk for offspring
35-39 CAG’s in a row = possible HD, increased risk in offspring
39+ CAG’s in a row = you WILL have HD
the more repeats you have the earlier you are going to get it
100% of HD patients DO show a family history

29
Q

Review the basic differences between focal and generalized seizures.

A

Focal seizures- affect one part of the brain
Subtypes- simple focal and complex focal
Generalized seizures- affect both sides of the brain
Subtypes- absence, tonic, clonic, atonic, and tonic-clonic

30
Q

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

A
Simple focal seizure
don’t lose consciousness 
may experience odd smells, tastes, sensations
complex focal seizures
change in consciousness 
feels like a dream 
may have strange/repetitive behavior 
experience aura/ warning signs
31
Q

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

A

EEG- best way
Subdural EEG- measures brain activity with electrodes directly on the brain
MRI or CT- rule out others
PET or fMRI- evidence of underactivity in brain sections

32
Q

What is a febrile seizure?

A

seizure is induced by a high fever (above 102)

33
Q

What is status epilepticus?

A

seizures that last more than 5 min or multiple seizures without consciousness for 5 minutes, can be life threatening

34
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- GABA agonists (makes GABA work better)
No, 20% of people do not respond
If drugs don’t work, surgeries such as, removal of seizure focus (most common), multiple subpial transection (cuts in white matter around it), corpus callosotomy (cut corpus callosum), or hemispherectomy (remove 1 hemisphere).

35
Q

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

A

DO
o1. Roll the person on his or her side to prevent choking on any fluids or vomit.
o2. Cushion the person’s head.
o3. Loosen any tight clothing around the neck.
o4. Keep the person’s airway open. If necessary, grip the person’s jaw gently and tilt his or her head back.
o5. Remove any sharp or solid objects that the person might hit during the seizure.
o6. Note how long the seizure lasts and what symptoms occurred so you can tell a doctor or emergency personnel if necessary.
o7. Stay with the person until the seizure ends.
DO NOT
oDo NOT restrict the person from moving unless he or she is in danger.
oDo 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.

36
Q

Do seizures cause significant brain damage?

A

Majority of the time we see very few individuals having significant brain damage due to seizures, for most the brain looks perfectly fine on an mri.

37
Q

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

A
All affect consciousness 
Absence- zone out, then resume 
Clonic- repeated jerking movement 
Tonic- rigid and stiff (usually arms, back, and trunk) 
Atonic- lose muscle tone, limp 
Clonic/tonic- stiff muscle and jerky