Download Cell Bio 11- Higher Cortical Function Everything has to go to the

Cell Bio 11- Higher Cortical Function
Everything has to go to the thalamus then cortex (except CN1)
Frontal Lobe
Makes up 1/3 of cerebral cortex
Primary motor, premotor, frontal eye field, supplementary motor, prefrontal, and Broca’s area
Everything supplied by middle cerebral artery (except small amount at hemispheres: ACA legs)
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No motor control over genitals
Primary Motor Cortex: Brodmann Area 4
Somatotopic organization
Size of areas is proportional to the degree of skill involved with movement
Lesions of motor cortex result in paralysis/paresis of contralateral body area
Only place with Lateral cortical spinal tracts (all other cortexes have to feed back to 4)
Premotor Cortex: Area 6
Contains programming for movements
Electrical stimulation produces slower movements of larger groups of muscles compared to area 4
Lesion produces apraxia - inability to perform voluntary movement in the absence of paralysis
Cell Bio 11- Higher Cortical Function
Frontal Eye Field: Inferior Part of Area 8
 Stimulation produces conjugate eye movement to contralateral side
 Lesion produces transient deviation of eyes to ipsilateral side and paralysis of contralateral gaze
 Tries to give you gaze to contralateral side when normal, eyes deviate towards lesion when there is a lesion
Supplementary Motor Area: Parts of Areas 6 and 8
 Medial surface
 Programming for complex movements involving several parts of the body
Prefrontal Cortex: Areas 9, 10, 11, 12, 32, 46, and 47
 Nearly 1/4 of all cortex
 Orbitofrontal area functions in visceral and emotional activities
 Dorsolateral area functions in intellectual activities such as planning, judgement, problem solving and
conceptualizing
 Makes you intellectually capable and socially acceptable
Broca’s Area: Areas 44 & 45 (**Board question!)
 Part of the inferior frontal gyrus
 Functions in speech (control muscles to be able to make up speech)
 Lesion know what you want to say logically but cannot make words
Frontal Lobe-Prefrontal Cortex
 Lesions cause loss of initiative, careless dress, loss of sense of acceptable social behavior
 Prefrontal leucotomy or prefrontal lobotomy were once common surgical procedures to treat patients with
severe behavioral disorders
o Lobotomy: surgical severence of nerve fibers connecting the frontal lobes to the thalamus for relief of
some mental disorders
 Used now for temporal lobe seizures
o Area of brain damaged in “Phineas Gage”
 Under left eye, exits skull. He was a different person (used to be nice, now quarrelsome, bad
tempered, lazy and irresponsible
Parietal Lobe
Makes up 1/5 of total cortex
Primary and secondary somatosensory, gustatory, association
Primary Somatosensory Area: 3,1,2
 Somatotopically organized
 Areas of cortex proportional to sensory discrimination of the area not to the amount of surface area
Secondary Somatosensory Area: Posterior part of area 43
 Somatotopy poorly defined
Primary Gustatory Cortex: Area 43 Anterior part of parietal operculum
 Lesion results in contralateral (mostly) ageusia (the absence or impairment of the sense of taste)
Cell Bio 11- Higher Cortical Function
Parietal Association Cortex : Areas 5,7,39,40
 7: input from visual and motor cortex
 39&40: input from all association areas
o function in hand performance
o neglect syndrome
o astereognosis : loss of the ability to recognize the shapes of the objects by handling them
Parietal Neglect Syndrome
 Failure to recognize side of body contralateral to injury
 May not bathe contralateral side of body or shave contralateral side of face
 Deny own limbs
 Objects in contralateral visual field ignored
 Right hemisphere lesion: problems are very severe (not 50/50 from hemispheres because right side keeps
control of how we view bilaterally)
 Left hemisphere only gives a few (maybe 30%) so the lesion is going to have less effects
Temporal Lobe
1/4 of total cortex
Primary auditory, Auditory association, Visual association, Limbic
Primary Auditory Cortex: Areas 41 &42
 Tonotopic organization
o High frequency sounds posteromedial, and low frequency sounds anterolateral
 Lesion causes difficulty in recognizing distance and direction of sound, especially when the sound comes from
the contralateral side
Auditory Association Cortex: Area 22
 Wernicke’s area (posterior part of 22)
 Language understanding and formulation
 Damage can result in aphasia (slow speech, impaired articulation)
Limbic Temporal Cortex: Visceral function, emotions, behavior, memory
 Stimulation can elicit past events
 Bilateral lesion of 20,21 causes prosopagnosia (a form of visual agnosia) inability to recognize faces. Often
damaged in Alzheimer’s disease
Occipital Lobe
Area 17: striate cortex, primary visual cortex
 Macular vision in posterior part
 Lesion causes homonymous hemianopsia: blindness in one half of the visual field of one or both eyes
Anopsia: don’t see
Hemi: one side lost
Homonymous: same side
 Patient will constantly look over to their blind side, aware of all they may miss otherwise
Occipital Lobe: Areas 18 & 19
 Receive visual info from area-17 bilaterally
 Complex processing for color, movement, direction, visual interpretation
 Lesion can cause visual agnosia (loss of the ability to recognize familiar objects or stimuli)
Cell Bio 11- Higher Cortical Function
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Hemispheric Lateralization of Function
Hemisphere with language function is termed “dominant”
10% of population is left-handed
95% of right-handers have language in left hemisphere
75% of left-handers have language in left hemisphere
Handedness and language dominance develop before speech begins
Right sided= speech problems
Dominant hemisphere also excels in analytical thinking and calculation
Nondominant hemisphere excels in sensory discrimination, emotional/nonverbal thinking, artistic skill, music,
spatial perception and perhaps face recognition
Language Areas of the Brain
Broca’s area (44, 45) , 43 & 45 is the motor speech center
Motor programs for speech production
Projects to motor cortex areas controlling vocal cords, tongue and lips
Lesion causes expressive aphasia with poor articulation, short sentences, slow speech
>> articulation of the sounds that constitute speech >>> primary motor area
o the motor program that activates particular sequences of sounds to produce words is formulated
o Broca’s area >> corresponds to Broadmann’s 44-45
Wernicke’s area >>initial steps of language processing that enable particular sequences of sounds to be
identified/comprehended as meaningful words
o Wernicke’s area >> corresponds to Broadmann’s area 22
Broca’s Aphasia
 (Mostly) Infarct in the left middle cerebral artery (MCA) superior division
 Decreased frequency of spontaneous speech
 Phrase length fewer than 5 words
 More nouns than prepositions
 Lacking prosody (melodious intonation for the meaning of sentence)
 Repetition is impaired
 Comprehension is (relatively) intact
 Right hemiparesis (affecting face & arm, more than leg)
 frustration & depression
Cell Bio 11- Higher Cortical Function
Wernicke’s Aphasia
 Infarct in the left middle cerebral artery (MCA) inferior division territory
 impaired comprehension
 has normal fluency, prosody, and grammatical structure
 “empty”, meaningless, nonsensical paraphasic errors
 Impaired repetition
 contralateral visual field cut (especially right upper quadrant)
 apraxia
 unaware of their deficit (contrast to Broca’s aphasia)
Both areas are MCA territory.
Broca: MCA superior
Wernickes: MCA inferior
Arcuate fasciculus connects the two areas
Lesion: issues with speech
Cannot repeat something back to you because you cannot process together
Cell Bio 11- Higher Cortical Function
Wernicke Disease
 Due to Vitamin B1 (thiamine) deficiency
 Is uncommon in individuals who have a varied diet, but individuals with a history of chronic alcoholism may not
have a well-balanced diet.
 Capillary proliferation, hemorrhage, necrosis, and hemosiderin deposition are often found in the mamillary
bodies and the periaqueductal gray matter, resulting in paralysis of the extraocular muscles.
 If memory problems with confabulation are observed, the diagnosis is Wernicke-Korsakoff syndrome.
Korsakoff’s psychosis
 Is characterized by retrograde memory loss, the inability to form new memories, and a tendency for
confabulation (exaggerating) to compensate for these losses.
 It is caused by thiamine deficiency and commonly accompanies chronic alcoholism. Thiamine is a coenzyme for
transketolase, which participates in the pentose monophosphate pathway of glucose metabolism.
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Chronic alcoholism damages Dorsomedial nucleus of thalamus, which is believed to play a role in memory
formation
A thiamine deficiency is indicated by a change in erythrocyte transketolase activity.
o If enzyme activity increases by more than 15% when thiamine diphosphate is added to the culture
medium, then the thiamine deficieny is considered significant enough to indicate Korsakoff’s psychosis.
Alexia and Agraphia
 impairments in reading and writing
 caused by deficits in central language processing/ not by simple sensory or motor deficits
Visual Information
 Dorsal Pathways: project to parieto-occipital association cortex >> answer the question where?
 Ventral Pathways: project to occipito-temporal association cortex >> what? (analyze form, color, faces, letters)