S34 cerebral cortex Flashcards
SMA syndrome
three stages:
global akinesia that was worse contrallaterally, with arrest of speech immediately posteratively
- sudden recovery few days later with persistent reduction in contralateral motor activity, emotional facial palsy, and reduction in spontaneous speech
- subtle disturbance involving alternating hand movements
primary sensory cortex
somatic sensation
hearing
vision
vestibular
gustatory
olfactory
secondary somatosensory area
immediately posterior to the primary sensory cortex
larger receptive fields compared to the primary sensory Cortex
responde to touch, pressure, pain, and limb position from BOTH SIDES OF THE BODY
Somatotopic Organization
Lesions of the secondary somatosensory area
impairment of tactile discrimination, deficits in 2-point discrimination, precise localization, position sense, stereognosis
primary and secondary auditory areas
receive auditory information from the geniculate nucleus
binaural (but more contralateral)
pure word deafness
bilateral lesions (or unilateral left-side lesions)
disconnects auditory association (respond only to auditory stimuli, retention of auditory info) from wernicke’s area
cannot understand or repeat spoken words, but they respond appropriately to sounds and understand written language
Lateral geniculate nucleus
receives information in a retinotopic pattern representing the contralateral visual field
Neurons of LGN form the
geniculocalcarine tract (optic radiations)
projecting to Primary visual cortex of the occipital lobes
the cuneus
receives impulses from the Upper quadrant of ipsilateral side of both retinas
corresponds to Lower quadrant of contralateral visual field
Lingual gyrus
receives impulses from the lower quadrant of ipsilateral side of both RETINAS
Corresponds to UPPER QUADRANT of CONTRALATERAL Visual Field
Cortical blindness
pupillary light reflexes remain intact, but no useful vision
results from complete bilateral destruction of striate cortex
Anton’s syndrome:
- patients with cortical blindness who claim that they can see
visual association areas
respond to complex aspects of visual stimuli such as form, motion, color, speed and direction
Visual association area lesion
can result in discrete deficits in naming of visual stimuli affecting some categories but not others.
primary taste area
brodmann’s area 43- receives input from ventoposteromedial (VPM) nucleus
two major heteromodal association
temporoparietal areas
prefrontal areas
temporoparietal association area
receives input from auditory, somatosensory, visual, and olfactory area
input and output to paralimbic cortex
affected by motivation and reward
heavily connected with the following thalamic nuclei: medial part of the pulvinar nucleus and lateral posterior nucleus
Infarction of internal capsule most frequently results from occlusion of the
lenticulostraite branches of the middle cerebral artery
Infarction of internal capsule most frequently results in
contralateral conditions:
tactile hypesthesia
anesthesia
hemiparesis (with the babinski sign)
lower facial weakness
homonymous hemianopia
thalamic syndrome (dejerine and roussy) usually caused by
occlusion of a posterior thalamoperforating artery
thalamic syndrome classic signs
contralateral hemiparesis
contralateral hemianesthesia
elevated pain threshold
spontaneous, agonizing, burning pain (hyperpathia)
athetotic posturing of the hand (thalamic hand)
left-sided lesions in the temporoparietal association area
disorders of language
disturbed spatial integration
wernicke’s aphasia
damage of the angular gyrus
Alexia (inability to read) Anomia (inability to name objects) Agraphia (inability to write) Finger Agnosia Constructional apraxia Right-Left confusion
alexia
inability to read
anomia
inability to name objects
agraphia
inability to write
gerstmann’s syndrome
Alexia
anomia
agraphia
finger angosia
temporoparietal association area right-sided lesion
disturbances in integration of personal and extra personal space- SENSORY NEGLECT
result in dressing apraxia, constructional apraxia, neglect of left-sided space and lack of insight about these deficits
bilateral lesions in the temporoparietal areas
visual, spatial, and language defects
Bilateral lesions of posterior parietal lobe
balint’s syndrome:
inability to gaze towards the peripheral field
difficulty in reaching out and touching objects accurately
inattention to objects in peripheral visual field
temporoparietal association area other distrubances
mood disturbances;
anger or apathy
related to interruption of connects with the limbic system
prefrontal association area
respond to multiple sensory inputs
respond to the behavioral importance of the inputs
emotional processing
planning
decision making
prefrontal association area unilateral lesions
neglect of contralateral side of extra personal space
prefrontal association area bilateral lesions
complete loss of civility and normal behavior or judgment.
disregard for social graces, concern for others, and cleanliness
paralimbic areas
Primarily mesocortical areas that essentially form a ring of tissue along the medial edge of the cerebral hemisphere, extending laterally to the insula
Receive information from the heteromodal association areas
Involved in learning & memory, drive & affect, social behavior.
visual agnosia
failure to recognize objects visually in the absence of a defect in visual acuity or intellectual impairment
in purest form, same objects can be identified by touch or hearing
prosopagnosia (agnosia for familiar faces)
caused by: bilateral lesions of the temporal aspect of visual unimodal association areas (inferior temporal gyrus)
tactile agnosia
inability to recognize objects by touch when tactile and proprioceptive sensibility remain intact
caused by lesions of supra marginal gyrus
auditory agnosia
failure of patient with intact hearing to recognize specific sounds including speech, music, or familiar noises.
caused by bilateral lesions of the posterior part of the superior temporal convolution
apraxias
loss of ability to carry out correctly certain movements
- in absence of any weakness or other primary deficits
usually results from a disconnection between the planning area and the execution area
dsyarthria
disturbance in execution of speech
- occurs without a disorder of language
aphonia
inability to produce sound
aphasia
disorder of language caused by defect in production or comprehension of vocabulary or syntax
broca’s aphasia
confluent or motor aphasia
produces slow, broken language
poor sounds and grammar
understands spoken and written word
extremely frustrating
often accompanied by right-sided hemiplegia
wernicke’s aphasia
fluent or sensory aphasia
produces spoken language more rapidly than normal but somewhat nonsensical
poor comprehension of spoken and written word
circumlocutions, paraphasia
no associated weakness
conduction aphasia
damage to pathway between wernicke’s area and brook’s area
- poor repetition
- fluent aphasia
- intact comprehension
