Block 5: Cortical Functions, Cerebrum Flashcards
What does series processing refer to and how is it different than parallel processing?
- 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
Define divergence and convergence.
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
Besides series and parallel processing, how else can sensory pathways be modulated?
Descending pathway information
How does a hyperpolarization in a photoreceptor cell become depolarization in a ganglion cell?
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!
What are the three visual cortex areas and what do they encode for?
- Ocular dominance columns: depth perception
- Orientation columns: edge –> motion
- “Blob” cells: color perception
What is strabismus and what does it result in infants under the age of 6 months old and young children?
- 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.
Define cortical achroma.
Cortical achroma = cannot see color and cannot identify things (ventral stream lesion)
Define ideomotor apraxia.
Ideomotor apraxia = cannot execute movements that are dependent on sight (dorsal stream lesion); loss of gestures (waving goodbye) and using tools
Define orofacial apraxia.
Inability to make specific facial movements
Define ideational apraxia.
Inability to perform sequential actions (socks before shoes; associated with frontal cortex too)
Define prosopangnosia.
Prosopagnosia = inability to recognize faces (caused by a bilateral lesion of inferior temporal cortex)
Define visual agnosia.
Visual agnosia = inability to recognize an object by sight (caused by damage to unimodal visual cortex)
Define astereognosia.
Astereognosia = inability to recognize an object by touch alone (caused by damage to unimodal somatosensory cortex)
Define associative visual agnosia.
Associative visual agnosia = can identify objects, but not name them (damage to posterior parietal cortex)
Define finger agnosia.
Finger agnosia = inability to identify their fingers (damage to angular gyrus of dominant parietal cortex)
What agnosias signify Gerstmann syndrome and where is the lesion located?
finger agnosia, acalculia, agraphia, and right-left confusion
- Lesion in lateral parietal lobe
What is the primary language pathway?
- Input from primary auditory and visual cortices
- Gerschwind’s territory (recognition, labelling items)
- Wernicke’s area (language comprehension)
- Arcuate fasiculus
- Broca’s area (language generation)
- Primary motor cortex (stimulate voluntary muscles that control speech - CN IX, X, XII)
What are the stages of speech production?
- Airstream from lungs (diaphragm - phrenic nerve)
- Vibration of vocal cords
- Filtering vocal tract - formation of vowels
- Produce speech sounds (consonants)
Define receptive aphasia and where in the language pathway there is a deficit.
Receptive aphasia = patient is unable to comprehend written and spoken language
Deficit in Wernicke’s area
Define conductive aphasia and where in the language pathway there is a deficit.
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
Define expressive aphasia and where in the language pathway there is a deficit.
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
Define global aphasia and where in the language pathway there is a deficit.
Global aphasia = patients have problems generating and comprehending speech; does not have a distinct pattern, impacts entire pathway
What speech deficits would be expected in a patient that has a lesion in Gerschwind’s area?
Inability to come up with words; on the tip of their tongue
What is spatial neglect and what cerebral hemisphere does it affect and its specific location?
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
Define tactile agnosia.
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
Define auditory agnosia.
Auditory agnosia = patient with unimpaired hearing fails to recognize or appreciate a meaning with a perceived sound
- Lesion in superior temporal lobe
Define anosognosia.
Anosognosia = loss of disease awareness
- Lesion in parietal lobule (right)
What are the regeneration inhibitor proteins found in the CNS? How are these molecules treated pharmacologically?
NogoA, MAG - released upon neuronal damage
- Tx: targeted antibodies; inhibit signalling pathway by increased [cAMP]
What causes glial scars to form and what are they made out of? How are glial scars degraded?
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
What myelin-derived inhibitors do CNS neurons express which limits their ability to regenerate?
NogoR, p75NTR
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?
- CSPG form perineuronal nets which induces maturation of GABA neurons
- tx: chondroitinase and PT
What are the clinical and histological characteristics of oligodendrogliomas?
Clinical: seizures, mean survival = 5-10 years; 10% of adult gliomas, can be found in children
Histology:
- Cytoplasmic halos
- Calcified structures
What are the clinical and histological characteristics of ependymomas?
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
What are the clinical, histological, and genetic characteristics of medulloblastomas?
Clinical: children, usually located in cerebellum
Histology: Homer-Wright rosettes, mitoses
Genetics: isochromosome 17 - i(17)(q10) - long arm duplicated
What are the clinical and histological characteristics of meningiomas?
Clinical: benign arachnoid cell tumor; slow-growing
Histology: syncytial pattern (swirling), psammoma bodies (calcium deposits)
