Sensory and Motor Circuits Flashcards

1
Q

There are four somatosensory circuits, what are they?

A

Lemniscal, Anterolateral (spinothalamic), spino-cerebellar, Trigeminal

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2
Q

Large motor neurons are especially vulnerable to insult from ischemia, toxicity, bacteria, etc, so that early symptoms of peripheral nerve disease often first show up how?

A

Epicritic rather than protopathic losses.

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3
Q

What is the gracile fasciculus?

A

Dorsal root axons from the lower trunk and limbs that enter at lower thoracic and lumbosacral levels.

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4
Q

What is the cuneate fasciculus?

A

Upper trunk and limb axons that enter the spinal cord at upper thoracic and cervical levels ascend as the cuneate fasciculus.

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5
Q

The gracile fasciculus and cuneate fasciculus if cut would cause what?

A

Epicritic losses ipsilaterally.

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6
Q

Where do the gracile fasciculus and cuneate fasciculus synapse? Where do they go from there?

A

In the medulla. The information is picked up by second-order neurons whose cell bodies lie in the gracile and cuneate nuclei. Axons of these cells exit the nuclei cross to the other side in the medulla at which time they are renamed the medial lemniscus.

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7
Q

What would damage to the right medial lemniscus produce?

A

Epicritic symptoms on the patient’s left side of the body.

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8
Q

Where does the medial lemniscus synapse? What happens to the information from there?

A

In the ventral posterolateral nucleus of the thalamus (VPL). Information is then picked up by the third-order neurons, which carry it to the post central gyrus (S1, or Brodmann’s area 3,2,1) via the internal capsule.

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9
Q

What do epicritic symptoms include the loss of?

A

Stereognosis: Cannot recognize tactile shapes placed in the hand (astereognosis)
Two-point tactility: cannot separate the location of 2 simultaneous touches near each other on the skin Position sense:cannot state the position of the limb without visual cues
Vibration: Insensitivity to high frequency stimulation
Simple touch: Largely intact, just less sensitivity.

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10
Q

The size of the dorsal root axon diameter in the Anterolateral system is _________, while in the Lemniscus system they are __________?

A

Small-diameter.

Large-diamter.

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11
Q

What happens if you damage the anterolateral tract on one side? Why?

A

It will cause protopathic symptoms on the opposite side of the body. This is because most of the AL tract neurons first cross the midline before ascending to the brain.

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12
Q

Anterolateral tract axons synapse diffusely and at the level in the brainstem, but where do most terminate? What is the fate of the rest of the axons?

A

In the reticular formation. A few make it to the thalamus where they terminate in the ventral posterolateral nucleus of the thalamus as well as sever other nuclei including the dorsomedial and intralaminar nuclei. Signals then pass via the internal capsule to primary somatosensory cortex (post central gyrus, SI, 3,1,2 of Brodmann)

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13
Q

What does reduced “protopathic” mean?

A

Pain: reduced or no sense of pain from a pinprick or from chronic internal pain.
Temperature: reduced or lost sense of warming and cooling of the skin.
Simple touch: Largely intact, but reduced sensitivity

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14
Q

In the spino-cerebellar system where do signals from muscle spindles and joint receptors enter the CNS?

A

Via the dorsal roots and after one or more synapses, spino-cerebellar tracts carry this information to the same side of the cerebellum.

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15
Q

In the spino-cerebella system axons from the leg and lower trunk ascend as part of the gracile fasciculus, where do the axons terminate?

A

They terminate in the dorsal nucleus of Clarke or Clarke’s nucleus in the thoracic cord. Second order neurons from Clarke’s n. ascend to the cerebellum along the lateral rim of the white matter as the dorsal spinocerebellar tract.

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16
Q

In the spino-cerebella system a second component from the arm and upper torso ascends with the cuneate fasciculus to the medulla, where do they synapse?

A

They synapse in the accessory (or lateral) cuneate nucleus. Second-order neurons carry the signals to the cerebellum as the cuneo-cerebellar tract.

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17
Q

Why are the clinical effects of pathology of the spino-cerebellar system rarely seen?

A

They are rarely damaged in isolation.

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18
Q

In the Trigeminal system where do axons of the trigeminal nerve conveying epicritic sensation synapse? Where do second-order neurons travel?

A

In the principal or chief sensory nucleus of CN 5 and in the pontine part of the spinal nucleus of CN5. Second-order neurons leave these nuclei, cross the midline, and join the medial lemniscus en route to the thalamus (ventral posteromedial nucleus). Subsequent neurons forward the signals to the post central gyrus.

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19
Q

What is the pathology of the pontine portion of the trigeminal system?

A

There will be epicritic losses of the head and neck. The symptoms are on the same side if the pathology lies before the crossing (in the trigeminal nerve or nuclei). Pathology after the crossing (medial lemniscus, thalamus, cortex) will cause losses on the opposite side of the patient’s face.

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20
Q

Where do axons from the second portion of the trigeminal nerve travel? What information do they contain?

A

They convey protopathic information and descend toward the spinal cord as the spinal tract of CN5, synapsing along the way in the adjacent caudal portion of the spinal nucleus of CN5. Second-order neurons leave the caudal part of the spinal nucleus, cross the midline, and project largely to the reticular formation.

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21
Q

Describe the pathology of the caudal portion of the spinal trigeminal tract (in medulla) and nucleus of CN5:

A

Cause protopathic losses on the same side of the head. Pathology after the crossing (ie. from the reticular formation), particularly at a pontine or midbrain level, will affect the opposite side of the head.

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22
Q

A third sensory component of the trigeminal nerve carries proprioreceptive input from the face. What path do the axons take?

A

Axons in the trigeminal nerve are continuous with the neurons of the mesencephalic nucleus of CN5, these axons, called the mesencephalic tract of CN5 continue through the mesencephalic nucleus of CN5 to synapse with neurons of the motor nucleus of CN5 for jaw reflexes, and via the reticular formation before projecting to the cerebellum.

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23
Q

The trigeminal nerve also has a motor component, where do the axons come from and where do they go?

A

Axons arise from cells in the motor nucleus of CN5 in the pons and innervate the muscles of mastication on the same side. Pathology of the trigeminal nerve will both reduce facial sensation and weaken the jaw of the patient. The jaw may jut to the side of injury when opened.

24
Q

What are the two descending networks that carry motor commands to the brainstem and spinal cord?

A

Pyramidal system: direct cortical input

Brainstem-spinal system: indirect cortical control (sometimes called extra-pyramidal)

25
Q

Where do axons in the pyramidal system arise?

A

From cells in all lobes of neocortex, but especially the frontal and parietal lobes.

26
Q

Where does the cortico-bulbar tract descend? What does it control?

A

It descends through the brainstem and controls neurons of all the cranial nerve nuclei.

27
Q

Describe the unilateral pathology of the cortico-bulbar tract:

A

There will be weakened movement of the head and neck on opposite side of the body, because most of the CB fibers arising on the left will cross to control cranial nerve nuclei on the right side of the brain just rostral to the level of the cranial nerve nucleus being affected. However, for most of the CN n. there is also an ipsilateral component. For this reason only the CN 12 and CN 7 areas are affected by a unilateral CB lesion.

28
Q

Describe the route of the cortico-pontine tract:

A

IIt descends to terminate on the pontine nuclei in the basis of the pons. Axons from these nuclei forward the signals to the cerebellum on the opposite side. Isolated damage to this tract does not occur clinically.

29
Q

Where does the cortico-spinal tract descend? What does it control?

A

Through the brainstem and spinal cord. It controls motor neurons of the trunk and limbs

30
Q

In the brainstem how do CS axons descend, describe:

A

On the same side as their cortical origin. Then most cross the midline in the caudal medulla (pyramidal decussation) continuing on the opposite side of the spinal cord (lateral corticospinal tract) to reach their targets. Only a small number of axons continue ipsilaterally (ventral/ anterior corticospinal tract).

31
Q

Describe pathology in the brainstem:

A

Pathology in the brainstem therefore impairs movement mainly on the opposite side of the body. Pathology in the spinal cord (below the decussation) will affect movement on the same side of the body.

32
Q

Usually pathology damages the pyramidal and brainstem-spinal tract together causing what?

A

Marked weakness or outright paralysis of the affected muscles. The limbs become hyperreflexic over time.

33
Q

Where do the brainstem-spinal pathways originate? What do they control?

A

In the brainstem from nuclei. Collectively they control the muscles of the neck, trunk, and limbs.

34
Q

How do the brainstem-spinal pathway lesions compare to the pyramidal tracts?

A

In general they are mimic them in that pathology in the brainstem will affect movement on the opposite side of the body; pathology in the spinal cord will affect the movement of the same side of the body. Isolated damage is rare.

35
Q

What controls bot the Pyramidal and Brainstem-spinal pathways?

A

The motor cortex

36
Q

What is the general rule if the pathology is in the peripheral nerves:
Why?

A

It will lie on the same side as the symptoms. This is because peripheral nerves (dorsal roots, ventral roots, and all cranial nerves except trochlear) do not cross.

37
Q

What is the general rule if the pathology is in the spinal cord:
Why?

A

It will be in the same side as all of the symptoms, except the pain and temperature loss. This is because the lemniscal and the motor tracts remain uncrossed through the spinal cord, but the anterolateral tracts cross at or near the level of entry.

38
Q

What is the general rule if the pathology is in brainstem:

Why?

A

It will lie on the same side as the most rostral symptom, but be on the side opposite the caudal symptoms. The most rostral symptom will tend to be caused by damage to the cranial nerve nucleus, or its axons that project ipsilaterally, so the symptom will be on the same side as the damage. Caudal symptoms are due to damage to the descending motor axons that cross below the level of damage to innervate the CN n., thereby causing contralateral symptoms

39
Q

What is the general rule if the pathology is in the forebrain:
Why?

A

It will lie opposite the symptoms. This is because the pathways in the forebrain are not primary axons and are all crossed (except olfactory)

40
Q

What is the general rule if the pathology is in the cerebellum:
Why?

A

Pathology will be on the same side as the symptoms. (just memorize this for now)

41
Q

What are the two factors that maintain muscle tone? (the same circuit is also responsible for the deep tendon reflexes)

A

1 - The sensory fibers from muscle spindles which, synapse on motor neurons in the cord, constantly excite the motor neurons with a baseline barrage of APs.
2- The corticospinal and the indirect motor pathways; descending motor tracts maintain a baseline level of excitability in the lower motor neurons.

42
Q

How can one distinguish between dorsal (sensory) and ventral (motor) peripheral nerve damage?

A

Muscles will show very early signs with fasciculations (slight quiverings) and after a time atrophy will be apparent. Sensory nerve pathology does not cause this muscle death.

43
Q

What does weakness accompanied by increased tone indicate?

A

The pathology is not in the peripheral nerves, but somewhere along the course of the descending CNS motor tracts.

44
Q

If there is a motor neuron lesion and paralysis of the face how do you distinguish between an UMN or LMN pathology?

A

UMN is due to pathology of the forebrain, or the corticobulbar tract and will only the lower quadrant of the face will be paralyzed and on the opposite side. If LMN damage than from forehead to chin is affected.

45
Q

At the optic chasm describe what happens to the two optic nerves:

A

Axons from the nasal half of each retina (temporal visual field) cross, while those from the temporal retina (nasal visual field) do not cross. These retinal axons then enter the optic tract, which wraps around the thalamus and the crus cerebra.

46
Q

Damage to which pathway would have the most severe effect on vision?

A

The Geniculo-calcarine pathway.

47
Q

Where do axons carrying information about the upper half of the visual field travel and terminate?

A

They pass deep to the cortex of the temporal lobe and terminate in the cortex of the inferior bank of the calcimine sulcus (lingual gyrus). Thus, pathology of the temporal lobe, or of the inferior bank of the visual cortex could eliminate some of your upper visual field.

48
Q

Where do axons carrying information about the lower half of the visual field travel and terminate?

A

They pass deep to the parietal lobe and terminate in the cortex forming the superior bank of the calcimine sulcus (cuneus gyrus). Consequently damage to the parietal lobe or superior bank of visual cortex can result in scotomas in the lower visual field.

49
Q

In respect to visual pathways what affect does the hypothalamus have?

A

It governs long-term reactions to light (circadian rhythm). One of the projections from the region of the hypothalamus receiving optic input is to the pineal body, a region that is related to these seasonal changes in light.

50
Q

In respect to visual pathways what affect does pretectum have?

A

It functions like a light meter. It receives bilateral input from the two eyes and it contains cells that calculate the total light energy entering the eye. These cells cross the midline to the other pretectal nucleus or project to the Edinger-Westphal nucleus of the same side, the parasympathetic component of oculomotor complex.

51
Q

In respect to visual pathways what affect does the superior colliculus have?

A

It is certainly involved in moving the eyes, head, and axial muscles. Some evidence suggests this optic input to the colliculus permits a very rapid orientation of our eyes and body to a visual event.

52
Q

What does bi-temporal hemianopia suggest?

A

A pituitary tumor pushing on the optic chiasm

53
Q

Describe the path of CN8:

A

It carries auditory information from the cochlea to the brain. It terminates in two nuclei, the dorsal and ventral cochlear nuclei, which lie on the surface of the inferior cerebellar peduncle. The second order neurons project to several nuclei on both sides of the brain (bilateral mixing). All of the information eventually ascends the brainstem in the lateral lemniscus. Most terminates on the inferior colliculus, which in turn projects to the medial geniculate nucleus, and ultimately to Heschl’s gyrus by traveling through the posterior limb of the internal capsule

54
Q

What would a unilateral brainstem lesion at the second order axon and beyond of the CN8 cause?

A

It will NOT cause hearing deficits, because much of the information from both ears will escape injury.

55
Q

If a patient has lost hearing in one ear what must be true of her pathology? If the patient has hearing loss in both ears?

A

Her pathology must be in the ear, in CN8, or in the cochlear nuclei. It is not deeper in the brain than that. For both ears the pathology must be bilateral.

56
Q

What is Heschl’s gyrus called?

A

Primary auditory cortex, A1, Brodmann 41,42. It is the primary sensory cortex for audition. It is important for distinguishing sound patterns.

57
Q

What would damage to Heschl’s gyrus cause? What would damage to Heschl’s gyrus in both hemispheres cause? What else could cause the same thing?

A

Little deficit. In the left hemisphere Wernicke’s area is a secondary auditory area that mediates the perception of language. Damage to Heschl’s gyri in both hemispheres or damage to the left auditory cortex and the corpus callosum results in an inability to understand spoken language (word deafness).