HMB200H1 Study Guide - Final Guide: Globus Pallidus, Anterior Grey Column, Visual Cortex

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1. Describe the spinal cord and spinal nerves. How does spinal cord injury result in

tetraplegia or paraplegia?

There are 31 spinal cord segments, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral

and one cossygeal. Lesion from C4 and C6 results in tetraplegia, T6 and L1

result in paraplegia

2. Differentiate upper and lower motor neurons.

Upper motor neurons commends fro voluntary motor action at motor

cortex of the frontal lobe

Lower motor neurons exist in the spinal cord, which regulated muscle

activity

3. Describe the role of the prefrontal cortex, premotor cortex and primary cortex

(M1) in movement.

Prefrontal cortex: planning

Premotor cortex: sequence organization and mirror neurons.

Primary motor cortex: movement production

4. Describe the process of mental rehearsing/visualizing a motor action.

Frequent imagining of movement sequences may induce plasticity in the

motor cortex because the neuronal activity is almost identical in the

premotor cortex in visualizing and executing action.

5. Describe how the motor cortex might represent ‘movement repertoire.’

The regions of the motor homunculus represents categories of movement

6. Explain post-stroke cortical plasticity. Explain how rehabilitation interacts with

this plasticity.

In stroke, the affect area begins to shrink in cortical size. But due to

plasticity of the motor cortex, undergoing constriaint-induce movement

therapy can reshape the region.

7. Explain the lateral and anteromedial pathway systems that descend the spinal

cord.

Lateral pathway system consists of lateral corticospinal tract, anterior

corticospinal tract, rubrospinal tract.

Anteromedial pathway system: vestibulospinal tract, reticulospinal tract,

tectospinal tract

8. Differentiate the lateral and anterior corticospinal tract.

Lateral corticospinal tract: carries info for movement of limbs and digits.

Cross over at medulla.

Anterior corticospinal tract: carries info for movement of body's midline

(trunk) cross over at lower motor neurons

9. Describe the representation of motor neurons for different muscles that is

present in the spinal cord.

There is topographic mapping of muscles in the spinal cord. Ex, the lateral

portion of the ventral horn is for finger and arm movement while the

medial is for trunk movement.

10.Discuss the role of the basal ganglia in movement. Give the indirect and direct

pathways. Describe the role of dopamine and dopamine receptors in these

pathways.

Basal ganglia is a network of structures that's included in coordinating

movements

Indirect: Cortex -> Striatum -> Globus Pallidus external -> Subthalamic

nucleus -> Globus Pallidus internus -> Thalamus

○

Direct: cortex -> Striatum -> globus pallidus internus -> thalamus

○

Dopamine plats a role at the level of striatum via the substantia nigra. D1

receptors excites striatum / D2 receptors inhibit striatum

11.Where in these pathways might the effects of deep brain stimulation (DBS) be

important?

The indirect pathway might be important for DBS. Electrodes are planted in

subthalamic nucleus (STN) or globus pallidus internus (GPi)

12.Describe the role of the cerebellum in movement. Describe the importance of

the inferior olive and spinocerebellar tracts (which relay information to the

cerebellum).

Cerebellum plays an important role in posture, balance and coordination

Inferior olive and spinocerebellar tract relate this important info

about errors to the cerebellum

Inferior olive sends copy of instruction

Spinothalamic tracts send feedback from actual movement

○

13.Describe the posterior column-ML system and the anterior spinothalamic

system.

Posterior column-medial lemniscus system involves with fine touch and

pressure. Cross over at medulla

Anterior spinothalamic system involves pain and temperature. Cross over at

spinal cord

14.Be familiar with the effects of unilateral lesions.

Unilateral lesion leads to ipsilateral loss of fine touch and pressure

sensation

Contralateral loss of pain and temperature

sensation

15.Be familiar with spinal cord reflexes.

Knee jerk reflexes involves stretch of quadriceps muscle which send signals

to the spinal cord and synapses with motor neuron sending info back to

quadriceps to contract

16.Differentiate the subregions of the somatosensory cortex.

Primary somatosensory cortex (S1): Brodmann 1, 2, 3a, 3b. Received info

from body

Secondary somatosensory cortex (S2): Brodmann 5, 7. receive info from S1

17.Describe nociceptive processing in the brain. Describe how individual differences

in pain sensitivity might be related to differences in brain activity. Describe how

chronic pain might be reflected in gray matter changes.

Pain is represented in the insula, PFC and anterior cingulate. Anterior

spinothalamic pathways.

Individual differences in pain are correlated with differences in the activity

of prefrontal cortex, anterior cingulate and somatosensory cortex.

In chronic pain, there are decrease gray matter density in somatosensory

cortex and motor cortex, as well as increase in middle occipital gyrus

18.Describe the gate control of pain in the spinal cord.

Gate control of pain involves fine touch/ pressure path synapsing onto an

inhibitory interneurons of the pain pathway, therefore touch activates an

inhibitor of pain

19.Describe the regulation of pain by the periaqueductal gray. How might this

system be sensitive to opioid drugs?

Periaqueductal gray and rostroventral medulla modulates pain. PAG

neurons are normally inhibited by GABA neuron. When PAG is active, RVM

can modulate pain in the spine via inhibitory synapse. Opioids such as

morphine act on the u-opioid receptors of the inhibitory PAG interneurons.

Turning them off can relieve pain.

20.How many senses do we have?

We have 5 sense because we could have more depending on the definition.

Vision, smell, taste, hearing, touch / equilibrioreception,

thermoreception, nociception

○

21.Describe the visual pathway. Give all important stops (i.e. synapses) in the

pathway.

Light enter and hits pigments of the photoreceptors (rods or cones) which

synapse onto bipolar cells (either light on or off) and ultimately into

ganglion cells (parvocellular and magnocellular). These ganglions form the

optic tract leading to the Lateral geniculate nucleus and ultimately primary

visual cortex (V1)

22.Differentiate rods and cones in terms of expression and function.

Rods: function well in night time, don't respond to colors.

Cones: function well in day time, respond to colors, responsible for high

acuity vision.

23.What are feature detection neurons?

Feature detection neurons are specialized to respond to different stimulus

features, such as orientation, color, direction and size.

24.What pathways are used in vision-guided action and vision-guided recognition?

Dorsal stream: vision-guided action

Ventral stream: vision guided recognition

25.What is the fusiform gyrus and what might it do?

Fusiform gyrus is an area located at the temporal lobe and it recognize faces

Study notes 8

Thursday, April 5, 2018

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Document Summary

12:31 am: describe the spinal cord and spinal nerves. There are 31 spinal cord segments, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and one cossygeal. Lesion from c4 and c6 results in tetraplegia, t6 and l1 result in paraplegia: differentiate upper and lower motor neurons. Upper motor neurons commends fro voluntary motor action at motor cortex of the frontal lobe. Lower motor neurons exist in the spinal cord, which regulated muscle activity: describe the role of the prefrontal cortex, premotor cortex and primary cortex (m1) in movement. Primary motor cortex: movement production: describe the process of mental rehearsing/visualizing a motor action. Frequent imagining of movement sequences may induce plasticity in the motor cortex because the neuronal activity is almost identical in the premotor cortex in visualizing and executing action: describe how the motor cortex might represent movement repertoire. ". The regions of the motor homunculus represents categories of movement: explain post-stroke cortical plasticity.

Related Questions

To investigate Neilâs symptoms further, doctors referred him to a neurologist, Dr. Bonasera, that specialized in motor disorders. Dr. Bonasera noted that Neil exhibited diminished right dorsalis pedis and posterior tibial pulses. His cognitive tests were normal. Tests of the cranial nerves were normal, with the exception of occasional slurred speech. His motor tests revealed generally slowed movements. Neil was experiencing pain and stiffness in the shoulder joints, which could explain his restricted range motion. Dr. Bonasera tested the motor strength of his finger extensors (4+/5), hip flexors (4/5), and various muscle groups in his arms and legs (5/5). There were tests for dysmetria (i.e., lack of coordination) and dexterity, which were normal yet slowed. Neil did have difficulty lifting his legs for some of the examinations, and he walked with a shuffling gate, often keeping both feet close together for a narrow base of support. He took very small steps and often stooped over while walking. When placing one foot in front of the other in a tandem walking stance, he would fall to either side and was unable to regain his balance. Sensory examination was normal, deep tendon reflexes were normal, and the Babinski sign was absent bilaterally. There were no Parkinsons-like symptoms, increased motor tone, or muscle fasciculations observed in testing.

Just one day later, another neurologist noted brisk reflexes and bilateral Babinski signs. Doctors performed magnetic resonance imaging (MRI) of the brain to reveal an infarct in the right caudate nucleus and an infarct in the right cerebellum. Doctors prescribed intense physical therapy. Neil saw some improvements for articulation, but he continued to struggle with the speed of speech and began to experience weakness of the tongue on his left side. CT angiograms revealed an aneurysm of the infrarenal aorta extending into the right common iliac artery. A spinal MRI revealed degenerative disease of the cervical spine (C4-C5) with a mild central canal stenosis. No such degeneration was present in the thoracic or lumbar spine. However, Neil did have mild impingement of the right L3-L5 nerve roots. A lumbar puncture revealed normal CSF pressures, cell counts, and composition. Neil continued physical therapy and experienced significant improvements in speech, walking, and balance. He also commented that his muscle soreness and fatigue had improved.

Neil continued his physical therapy while recovering at home. However, his symptoms worsened over the following weeks. Neil grew progressively weaker, occasionally falling. He required assistance for walking, and he was experiencing some numbness in both hands. He was admitted to a hospital, where he underwent a neurological examination. Cognitive and cranial nerve tests were normal. There were no fasciculations of the neck or tongue muscles. He was able to rotate and extend the neck with normal strength, however neck flexion seemed to be compromised. Neil exhibited widespread fasciculations in his arms and legs, and the muscles of these limbs had mildly atrophied. Motor tests were conducted for the arms and legs (4/5), and wrist extensors and intrinsic muscles of the hand (3+/ 5). Neil exhibited hyperactive deep-tendon reflexes and positive Babinski signs bilaterally. Sensory examinations were unchanged.

Based on the compounding symptoms and rapid progression of the disease, doctors suspected that Neil was suffering from amyotrophic lateral sclerosis (ALS), a disease that results in the destruction of upper and lower motor neurons. To confirm this diagnosis, neurologists conducted a series of tests., including nerve conduction tests and needle EMG. Nerve conduction tests of the motor and sensory nerves revealed normal conduction velocities with low amplitude compound motor action potentials, and normal sensory nerve potentials. There were abundant fasciculations and characteristics that suggested remodeling of motor units following denervation. Furthermore, EMG suggested net motor unit loss. There was no evidence of demyelination. Based on these results, doctors confirmed the diagnosis of ALS. For the following weeks, Neil experienced physical therapy aimed to help him preserve his strength and energy. He soon began to experience difficulty swallowing, and his cough progressed. Soon thereafter he developed pneumonia, was placed on a feeding tube, and ultimately died just 15 weeks after his initial hospitalization.

5. Electromyography involves recording electrical activity from muscle fibers. Justify Neil's low amplitude compound motor action potentials given his diagnosis of ALS. Be sure to describe how a muscle fiber initiates and propagates action potentials, and state how that process differs in the case of ALS.

6. Motor unit remodeling includes a reduction in the number of motor units, atrophy of muscle fibers, and an increased number of fibers per motor unit. Describe how motor unit remodeling may be indicative of ALS. Be sure to describe the typical structure and function of a motor unit, a typical distribution of motor unit (and fiber types) within a muscle, and how motor unit remodeling could contribute to Neil's weakness.

7. Based on the etiology of the disease, justify the finding of hyperactive deep-tendon reflexes and positive Babinski signs bilaterally in a patient suffering from ALS. Be sure to describe a typical reflex, and describe how descending inhibition may modulate a reflex response.

8. Justify why Neil's motor tests progressively worsened, whereas sensory, and cognitive tests remained unchanged. Be sure to describe the central and peripheral nervous system structures required for perception versus movement, and identify where deficits may be found in a patient with ALS.

HMB200H1 Study Guide - Final Guide: Globus Pallidus, Anterior Grey Column, Visual Cortex

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