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MBBCh 2- PHSL2004A > 11. CNS (Motor) (2) > Flashcards

11. CNS (Motor) (2) Flashcards

1
Q

What are the cerebellum and associated systems?

A
  • The cerebellum and associated systems are central to producing coordinated movement
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2
Q
  • Weakness caused by UMN or LMN problems will produce _____ movement —-> Weakness of muscle is the cause
A

uncoordinated

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3
Q
  • Damage to cerebellum or associated systems =
A

= muscle strength entirely intact, but ataxic/uncoordinated movement will be noted

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4
Q
  • The cerebellum also controls movement through the __________ system.
A

extrapyramidal

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5
Q

What does the extrapyramidal system consist of? (2)

A
  • The extrapyramidal system consists of several nuclei in the brainstem where UMNs are found —-> Red nucleus, reticular nucleus and vestibular nuclei
  • It also includes the tracts in the spinal chord conveying the axons of the UMNs in these nuclei Rubrospinal, reticulospinal, and vestibulospinal tracts
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6
Q

What is the function of the UMNs in the extrapyramidal nuclei? (3)

A
  • These UMNs target the same LMNs as the corticospinal tracts, but do not produce purposeful muscle contraction
  • Their role is to induce contraction of any muscle group when it is required for posture.
  • Without appropriate posture, coordinated movements would not be possible
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7
Q

Pyramidal vs Extrapyramidal systems:

A
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8
Q

What does the cerebellum produce? (2)

A
  • The cerebellum produces coordinated movements by comparing motor plans with actual movements and fine tuning the motor outputs
  • The cerebellum must therefore receive information about the plan for movement and the actual movement itself.
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9
Q

How does the cerebellum signal movement that has occurred in the best way possible? (2)

A
  • The best way to signal the movement that has occurred is through position receptors
  • info about the motor plan comes from the primary, pre- and supplementary motor cortices
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10
Q

What are the cerebellar afferents? (4)

A
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10
Q

What are the cerebellar afferents? (4)

A
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11
Q

What are the cerebellar efferents? (4)

A
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12
Q
  • With regards to cerebellar outputs, both pyramidal and extrapyramidal systems are modified
  • Therefore 3 functions influence the Friday of movement =
  • If any of these functions are disturbed =
A

= somatic proprioception, vestibular function and the cerebellum
= ataxia

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13
Q

What is the mechanism of coordinated movement?

A
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14
Q

Distinguishing different causes of ataxia:
* Asking patients to stand with their legs together with their eyes closed —>

A
  • Asking patients to stand with their legs together with their eyes closed —-> An ataxic patient will be unstable and tend to overbalance
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15
Q

Distinguishing different causes of ataxia:
* If patient opens eyes and balance is improved when they look at their feet to detect position —->

A
  • If patient opens eyes and balance is improved when they look at their feet to detect position A somatic proprioceptor problem (+’ve Romberg test)
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16
Q

True or false
* Neither cerebellar or vestibular problems can be fixed by looking at the position of the feet

A

True

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17
Q

How is ataxia caused?
* Vestibular problems —> (2)

A
  • Vestibular problems Ataxia is caused by inability to detect position but it is the position of the head that is detected and one cannot see the position of the head
  • Vestibular problems are caused either by damage to vestibular apparatus,vestibulocochlear nerve or nucleus of the nerve
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17
Q

How is ataxia caused?
* Vestibular problems —> (2)

A
  • Vestibular problems Ataxia is caused by inability to detect position but it is the position of the head that is detected and one cannot see the position of the head
  • Vestibular problems are caused either by damage to vestibular apparatus,vestibulocochlear nerve or nucleus of the nerve
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18
Q
  • Vestibular problems are caused either by damage to the vestibular apparatus, vestibulocochlear nerve or nucleus of the nerve
  • This kind of damage is usually associated with _____ and abnormal tests of hearing —–>
A

vertigo
Rinne’ and Webber’s

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19
Q

Summation of distinguishing the different causes of ataxia:

A
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20
Q

How does the cerebellum integrate information?

A
  • Afferent information to the cerebellum activates two areas Cells in the deep cerebellar nuclei (DCN) and cortical cells
21
Q

How is the ability of the cerebellum to fine-tune movement determined? (2)

A
  • The ability of cerebellum to fine-tune movement is determined by too much activation of the DCN being compensated for by inhibitory GABA effects produced by cortical cells
  • Since DCN cells are the outputs from the cerebellum, damage will reduce motor outputs
22
Q
  • Damage to cortical cells will increase motor outputs from the cerebellum —>
A

Influences muscle tone

23
Q

Vestibulo-ocular reflex & cerebellar control:
What is the purpose of VOR and how is it mediated?

A
  • VOR maintains our ability to look forward while turning the head to listen for the sound of danger behind us
  • VOR is mediated by activation of the semicircular canal when turning the head which through the vestibular nucleus controls III, IV and VI CN nuclei
24
Q

Abnormal cerebellar function
V A N I S H D D T

A
25
Q

How are dysdiadochokinesis and dysmetria detected?

A
26
Q

How must effective movement be performed? (2)

A
  • Effective movement has to be spontaneous and performed without thought (automatic)
  • Every movement we make, we first learn and then store as motor memories (the motor plan) Found in pre motor and supplementary motor cortices
27
Q

What does the thalamus activate and how does this link to the motor cortex? (2)

A
  • The thalamus is used to activate these memories
  • The signal to activate these memories comes from the motor cortex but to retrieve the plan for movement, motor memories first activate a circuit (the basal ganglia circuit)
28
Q

How is automatic movement produced?

A
29
Q

How do normal basal ganglia function?

A
30
Q

How do the basal ganglia function in recalling motor memories to enable movement?

A
  • To access motor memories, the inhibitory effects of the basal ganglia on the thalamus (via GABA) need to be removed
  • These inhibitory effects are in place to stop the recall of motor memories at inappropriate times
  • To prevent basal ganglia inhibition of thalamic cells, dopamine in the striatum has two effects mediated through direct and indirect pathways
  • The effects of dopamine via either pathway are to decrease the GABA effects on thalamic cells and hence to recall motor memories
31
Q

How does Parkinson’s disease work? (4)

A
  • As in Parkinson’s disease, loss of dopamine results in an inability to retrieve motor memories automatically & general decrease in movement (bradykinesia)
  • This is expressed in a decreased facial expression, an inability to stop walking or stop moving forward when the need to stop occurs
  • When walking: Patients do not swing their arms
  • When sitting: Patients will hardly move which will eventually lead to catatonia (no movement at all)
31
Q

How does Parkinson’s disease work? (4)

A
  • As in Parkinson’s disease, loss of dopamine results in an inability to retrieve motor memories automatically & general decrease in movement (bradykinesia)
  • This is expressed in a decreased facial expression, an inability to stop walking or stop moving forward when the need to stop occurs
  • When walking: Patients do not swing their arms
  • When sitting: Patients will hardly move which will eventually lead to catatonia (no movement at all)
32
Q

What is ballismus? (2)

A
  • When certain components of basal ganglia are lost, it can prevent the inhibitory effects of GABA on the thalamus
  • This causes the retrieval of motor memories at inappropriate times which result in bizarre movements (ballismus)
33
Q

What are Association cortices? (2)

A
  • information from primary cortices are further processed in association cortices to serve more advanced functions
  • Association cortices can either process a single primary function (unimodal association cortices) or several primary functions simultaneously (heteromodal/poly modal/multimodal association cortices)
34
Q

What is the function of the unimodal association cortices?

A
  • The unimodal association cortices for motor function are the supplementary and pre motor cortices which carry a motor plan
35
Q
  • Somatosensory cortex integrated several somatosensory sensations to detect size and shape of objects using touch.

What happens if damage occurs to these areas? (2)

A
  • Damage results in the inability to identify shapes drawn on the hand or objects placed in the hand may not be detected with the eyes shut
  • These are knows as agraphasthaesia and astereognosis
36
Q
  • The visual association cortex processes two distinct streams of neural information derived from the primary visual cortex: (2)
A

Dorsal and ventral streams

37
Q

What is the function of the dorsal stream?

A
  • The dorsal stream takes primary visual information and processes it for the detection of distance (depth), size, and motion.
  • Patients with disturbances of this area may see perfectly well, but cannot judge difference in the size of objects (simultanagnosia) or distances between objects
38
Q

What is the function of the ventral stream?

A
  • The ventral stream takes primary visual information and processes it to allow for the detection of shape and colour
39
Q

What are Heteromodal association cortices? (2)

A
  • Further integration of somatosensory and visual information provides a sense of spatial awareness
  • Damage to this area result in patients ignoring certain areas of their bodies (neglect syndrome)
39
Q

What are Heteromodal association cortices? (2)

A
  • Further integration of somatosensory and visual information provides a sense of spatial awareness
  • Damage to this area result in patients ignoring certain areas of their bodies (neglect syndrome)
40
Q

What is Wenicke’s aphasia?

A
  • Further integration of visual and auditory information provides an understanding of language and damage to this area results in patients unable to understand language even though they will think they do and will speak fluently without making much sense
  • This is called sensory/receptive aphasia or a Wenicke’s aphasia
40
Q

What is Wenicke’s aphasia?

A
  • Further integration of visual and auditory information provides an understanding of language and damage to this area results in patients unable to understand language even though they will think they do and will speak fluently without making much sense
  • This is called sensory/receptive aphasia or a Wenicke’s aphasia
41
Q
  • Visual information is further processed more anterior,y in the _______ lobe
  • This allows for the recognition of a particular item
  • Damage to this area results in patients having intact ____ and an ability to recognise a face as a human face but not from a particular person
A

temporal
vision

42
Q

What is Broca’s area?

A
  • Further processing of language occurs in a heteromodal association cortex in the frontal lobe = Broca’s area
  • This area translates language into a motor component of speech
43
Q

What happens if there is damage to Broca’s area? (2)

A
  • Damage cause a motor or expressive aphasia = Broca’s aphasia
  • They can understand language but he ability to express language is affected and speech is non-fluent
44
Q
  • In most people these regions are found in the left hemispheres only but in some left-handed people these regions are found in the right side of the brain only
  • In most people damage to the___ _____ is responsible for aphasias
A

left isotherm

45
Q
  • The _______ and _______ prefrontal cortices are responsible for executive and cognitive function
  • These areas are where the short-term memory is held before being processed for long term memory
A

ventrolateral
dorsolateral

46
Q

What is Broadman’s area? (2)

A
  • Brodman’s areas are responsible for generating a sense of pleasure or reward, emotional well-being, happiness and a sense of worthiness
  • Damage to these areas = emotional disturbances that occur in depressive illnesses and schizophrenia
47
Q

How is long-term memory?

A
  • To acquire long-term memory, info derived from primary sensory and association cortices must first be processes by the hippocampus formation in the medial part of the temporal lobe before being transferred to association cortices all over the brain for long-term storage
48
Q

What happens if there is damage to the temporal lobe?

A
  • Damage to the temporal lobe One may remember everything that occurred prior to the damage but no new memories may be developed = anterograde amnesia
49
Q

How does one get retrograde amnesia?

A
  • Damage to the frontal, parietal or temporal lobe association cortices like in Alzheimer’s Old memories are lost but new memories may be gained = retrograde amnesia

MBBCh 2- PHSL2004A (19 decks)

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