Block 5: Cortical Functions, Cerebrum

Question 1

What does series processing refer to and how is it different than parallel processing?

Answer 1

• Series processing occurs when a stimulus activates a first order neuron which then activates a second order neuron which activates a third order neuron –> labelled line theory
• Parallel processing involves signal divergence where inputs from one receptor go to two or more second order neurons

Question 2

Define divergence and convergence.

Answer 2

Divergence: signal input from one receptor cell goes to two or more second order neurons

Convergence: inputs from two cells synapse on one postsynaptic cell

Question 3

Besides series and parallel processing, how else can sensory pathways be modulated?

Answer 3

Descending pathway information

Question 4

How does a hyperpolarization in a photoreceptor cell become depolarization in a ganglion cell?

Answer 4

It all depends on the bipolar cell actions. Some bipolar cells do not change their response from a PR (off response). Other bipolar cells actually flip the signal to become an on response; this is typically done through amacrine cells providing an inhibition of a inhibition –> excitation!

Question 5

What are the three visual cortex areas and what do they encode for?

Answer 5

• Ocular dominance columns: depth perception
• Orientation columns: edge –> motion
• “Blob” cells: color perception

Question 6

What is strabismus and what does it result in infants under the age of 6 months old and young children?

Answer 6

• Strabismis = muscle imbalance that results in misalignment of visual axes within the two eyes

Under 6 months old, infants with strabismus develop diplopia (double vision).

In younger children, suppression of the weaker eye visual field occurs and results in amblyopia.

Question 7

Define cortical achroma.

Answer 7

Cortical achroma = cannot see color and cannot identify things (ventral stream lesion)

Question 8

Define ideomotor apraxia.

Answer 8

Ideomotor apraxia = cannot execute movements that are dependent on sight (dorsal stream lesion); loss of gestures (waving goodbye) and using tools

Question 9

Define orofacial apraxia.

Answer 9

Inability to make specific facial movements

Question 10

Define ideational apraxia.

Answer 10

Inability to perform sequential actions (socks before shoes; associated with frontal cortex too)

Question 11

Define prosopangnosia.

Answer 11

Prosopagnosia = inability to recognize faces (caused by a bilateral lesion of inferior temporal cortex)

Question 12

Define visual agnosia.

Answer 12

Visual agnosia = inability to recognize an object by sight (caused by damage to unimodal visual cortex)

Question 13

Define astereognosia.

Answer 13

Astereognosia = inability to recognize an object by touch alone (caused by damage to unimodal somatosensory cortex)

Question 14

Define associative visual agnosia.

Answer 14

Associative visual agnosia = can identify objects, but not name them (damage to posterior parietal cortex)

Question 15

Define finger agnosia.

Answer 15

Finger agnosia = inability to identify their fingers (damage to angular gyrus of dominant parietal cortex)

Question 16

What agnosias signify Gerstmann syndrome and where is the lesion located?

Answer 16

finger agnosia, acalculia, agraphia, and right-left confusion
- Lesion in lateral parietal lobe

Question 17

What is the primary language pathway?

Answer 17

1. Input from primary auditory and visual cortices
2. Gerschwind’s territory (recognition, labelling items)
3. Wernicke’s area (language comprehension)
4. Arcuate fasiculus
5. Broca’s area (language generation)
6. Primary motor cortex (stimulate voluntary muscles that control speech - CN IX, X, XII)

Question 18

What are the stages of speech production?

Answer 18

1. Airstream from lungs (diaphragm - phrenic nerve)
2. Vibration of vocal cords
3. Filtering vocal tract - formation of vowels
4. Produce speech sounds (consonants)

Question 19

Define receptive aphasia and where in the language pathway there is a deficit.

Answer 19

Receptive aphasia = patient is unable to comprehend written and spoken language

Deficit in Wernicke’s area

Question 20

Define conductive aphasia and where in the language pathway there is a deficit.

Answer 20

Conductive aphasia = good comprehension and able to produce speech with lots of pauses and gaps; commonly detected as a problem in comprehension though

Deficit in arcuate fasiculus

Question 21

Define expressive aphasia and where in the language pathway there is a deficit.

Answer 21

Expressive aphasia = patient has a difficult time generating speech, no problems with comprehension; have impaired verbal and oral expression and an inability to organize speech

Deficit in Broca’s area

Question 22

Define global aphasia and where in the language pathway there is a deficit.

Answer 22

Global aphasia = patients have problems generating and comprehending speech; does not have a distinct pattern, impacts entire pathway

Question 23

What speech deficits would be expected in a patient that has a lesion in Gerschwind’s area?

Answer 23

Inability to come up with words; on the tip of their tongue

Question 24

What is spatial neglect and what cerebral hemisphere does it affect and its specific location?

Answer 24

Spatial neglect = failure to acknowledge half of the world

Occurs in the non-dominant cerebral hemisphere; posterior parietal cortex

Occurs in ~50% of right-hemisphere strokes

Results as a lack of attention paid to half of the visual field: right hemi –> left visual field; left hemi –> both right and left visual fields

Question 25

Define tactile agnosia.

Answer 25

Tactile agnosia = inability to correlate surface texture, shape, size, and weight of an object and compare it to a previous experience.

• Lesion is parietal association cortex

Question 26

Define auditory agnosia.

Answer 26

Auditory agnosia = patient with unimpaired hearing fails to recognize or appreciate a meaning with a perceived sound

• Lesion in superior temporal lobe

Question 27

Define anosognosia.

Answer 27

Anosognosia = loss of disease awareness

• Lesion in parietal lobule (right)

Question 28

What are the regeneration inhibitor proteins found in the CNS? How are these molecules treated pharmacologically?

Answer 28

NogoA, MAG - released upon neuronal damage

• Tx: targeted antibodies; inhibit signalling pathway by increased [cAMP]

Question 29

What causes glial scars to form and what are they made out of? How are glial scars degraded?

Answer 29

CNS neuronal injury causes local excess production of astrocytes which act as a physical barrier around axons. The glial scar is made of CSPG (chondroitin sulfate proteoglycan) core and unbranched polysaccharides surrounding it.

• Use chondroitinase to degrade CSPG

Question 30

What myelin-derived inhibitors do CNS neurons express which limits their ability to regenerate?

Answer 30

NogoR, p75NTR

Question 31

What factors contribute to the closure of the “critical period” in brain plasticity? What can be done pharamacologically to enhance this time period of plasticity?

Answer 31

• CSPG form perineuronal nets which induces maturation of GABA neurons
• tx: chondroitinase and PT

Question 32

What are the clinical and histological characteristics of oligodendrogliomas?

Answer 32

Clinical: seizures, mean survival = 5-10 years; 10% of adult gliomas, can be found in children

Histology:

• Cytoplasmic halos
• Calcified structures

Question 33

What are the clinical and histological characteristics of ependymomas?

Answer 33

Clinical: found in children, located near fourth ventricle; adult variant in spinal cord; slow growing - poor prognosis (mean =4 years)

Histology: pseudorosettes - vasculature in middle

Question 34

What are the clinical, histological, and genetic characteristics of medulloblastomas?

Answer 34

Clinical: children, usually located in cerebellum

Histology: Homer-Wright rosettes, mitoses

Genetics: isochromosome 17 - i(17)(q10) - long arm duplicated

Question 35

What are the clinical and histological characteristics of meningiomas?

Answer 35

Clinical: benign arachnoid cell tumor; slow-growing

Histology: syncytial pattern (swirling), psammoma bodies (calcium deposits)