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292 Cards in this Set
- Front
- Back
Diencephalon
|
-btw cerebral cortex and brainstem
-medial to internal capsule -divided in the midline by the 3rd ventricle |
|
dienchephalon subdivisions
|
-epithalamus
-dorsal thalamus (aka thalamus) -ventral thalamus -subthalamus -hypothalamus |
|
Epithalamus parts
|
-habenuclear complex (limbic)
-pineal gland (serotonin) -posterior commissure (links nuclei) |
|
Habenuclear complex
|
-part of epithalamus
-involved in limbic pathway |
|
pineal gland
|
-part of epithalamus
-synthesizes seratonin and converts it to melatonin |
|
posterior commissure
|
-part of epithalamus
-links pretectal and other nuclei of the two sides -just below pineal gland |
|
Dorsal thalamus (thalamus) parts
|
-thalamic nuclei provides a strong link to the cerebral cortex
-external medullary lamina -internal medullary lamina |
|
Ventral thalamus
|
-reticular nucleus of thalamus
-ventral geniculate nucleus (LGNv) |
|
Subthalamus
|
-subthalamic n. (Luys) and zona incerta
-located btw the hypothalamus and the dorsal thalamus -involved with basal ganglia and extrapyramidal activity |
|
Hypothalamus function
|
-controlling center of ANS
-neurobehavioral functions and regulation of hormones released by the hypophysis |
|
parts of the hypothalamus
|
-hypothalamic nuclei
-infundibulum -hypophysis (pituitary gland) -hypohyseal portal system |
|
thalamus blood supply
|
-branches of PCA
-branches of ACA -branches of internal cartoid, ant communicating, and post comm |
|
function of dorsal thalamus
|
-relay of all sensory info to cortex (except smell)
-info about motor activities to cortex -integrates sensory info and projects to assoc cortex -relays emotional and affective info -part of "Papez circuit" --> limbic -alertness, arousal, sleep |
|
Anterior nuclear group of thalamus
|
-afferent input: mamillary body
-projects to: cingulate gyrus -limbic functions |
|
Lateral-ventral tier of thalamus
|
-VA, VL, VPL, VPM, LGN, MGN
-motor, somatic sensation, vision, audition |
|
ventral anterior thalamus
|
-afferent: globus pallidus
-projects to: premotor cortex (area 6) -motor functions |
|
ventral lateral thalamus
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-afferent: dentate nucleus of cerebellum
-projects to: motor and premotor cortex (areas 4 and 6) -motor functions |
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VPL of thalamus
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-afferent: dorsal column- med lemniscus and spinothalamic
-projects to: somatosensory cortex (areas 3, 1, 2) -somatic sensation of contralat body |
|
VPM of thalamus
|
-afferent: sensory nuclei of trigeminal nerve
-projects to: somatosensory cortex (areas 3, 1, 2) -somatic sensation of contralat face |
|
LGN of thalamus
|
-afferent: retinal ganglion cells
-projects to: primary visual cortex (area 17) -vision |
|
MGN of thalamus
|
-afferent: inferior colliculus
-projects to: primary auditory complex (areas 41, 42) -audition |
|
Lateral-dorsal tier of thalamus
|
-lateral dorsal, lateral posterior, pulvinar
-emotional expression and sensory integration |
|
lateral dorsal nucleus of thalamus
|
-afferent: cingulate gyrus
-projects to: cingulate gyrus -emotional expression |
|
lateral posterior nucleus of thalamus
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-afferent: parietal cortex
-projects to: parietal cortex -sensory integration |
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pulvinar nucleus of thalamus
|
-afferent: superior colliculus, POT lobes
-projects to: POT lobes -sensory info integration |
|
medial dorsal nucleus of thalamus
|
-afferent: amygdaloid nuclear coplex, olfactory, hypothalamus
-projects to: prefrontal cortex -limbic functions |
|
diffuse-projection nuclei of thalamus
|
-midline nuclei
-intralaminar nuclei (CM, CL, PF) -reticular nucleus |
|
Midline nuclei of thalamus
|
-afferent: reticular formation and hypothalamus
-projects to: basal forebrain -limbic functions |
|
Intralaminar nuclei of thalamus
|
-CM, CL, PF (surrounded by internal medullary lamina)
-afferent: reticular formation, spinothalamic tract, globus pallidus, cortical areas -projects to: basal ganglia and cortex -role in pain, sleep, wakefulness |
|
reticular nucleus of thalamus
|
-afferent: cortex, thalamus, brainstem RF
-projects to: thalamic nuclei -modulates thalamic activity |
|
thalamic syndrome
|
-usually damage to VPL
-initially, transitory contralat hemianalgesia -then painful sensations with noxious stimuli -later, pain from pressure, touch, vibration -later, dysesthesia -threshold for pain, temp, tactile is raised on ipsilat side (once threshold is reached, pain has strong emotional overtone) |
|
functional characteristics of non-specific syndrome
|
-activated by repepitive, low-freq stimulation
-cortical recruitment response that waxes and wanes -control the level of excitability of neurons over wide areas of cortex |
|
anatomical organization of cortex
|
-derived from telencephalon
-subdivided into archicortex (hippocampus/dentate gyrus), paleocortex (olfactory), neocortex (large) |
|
Frontal lobe
|
-precentral gyrus
-superior and middle frontal gyri -inferior frontal gyrus (orbital, triangular, opercular) -prefrontal cortex -orbital gyri -gyrus rectus |
|
Parietal lobe
|
-postcentral gyrus
-sup parietal lobule -inf parietal lobule (supramarginal and angular gyri) -precuneus -paracentral lobule |
|
Temporal lobe
|
-sup, middle, inf temporal gyri
-fusiform (occitotemporal) gyrus -parahippocampal gyrus -hippocampus |
|
occipital lobe
|
-lateral occipital gyri
-cuneus and lingual gyri |
|
cortex blood supply
|
-ACA, MCA, PCA
-ant and post comm -all from circle of Willis |
|
major venous drainage of cortex
|
-superior sagittal sinus, inf sagittal, striaght sinus, transverse sinus, sigmoid sinus
-drain into internal jugular |
|
Archicortex structure
|
-hippocampus and dentate gyrus
-3 layers |
|
Neocortex structure
|
-6 layers
-I: molecular layer (cells sparse) -II: ext granular layer -III: ext pyramidal layer -IV: int granular layer -V: int pyramidal (large cells) -VI: multiform layer (mix of cell types) |
|
axons in cerebral cortex
|
myelinated axons run in horizontal bands and vertical bundles
|
|
functional units of cortex: columns and modules
|
-each column extends through the 6 layers
-columns of cortical neurons are interconnected within the same hemisphere and btw the two hemispheres -functional columns form modules in various cortical areas (ie visual) |
|
Brodmann's 3, 1, 2
|
-postcentral gyrus
-primary somatosensory |
|
Brodmann's 4
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-precentral gyrus
-primary motor |
|
Brodmann's 17
|
-cuneus and lingual gyrus
-primary visual |
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Brodmann's 41, 42
|
-transverse gyri of Heschl
-primary auditory |
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Brodmann's 44, 45
|
-Broca's area of speech
|
|
general function of cortex
|
-perception of somatic, visual, auditory, olfactory sensation
-planning and executing voluntary movements -emotions and behavior -mental functioning -memory |
|
lesion of primary motor cortex
|
contralateral paralysis
|
|
lesion of primary sensory cortex
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contralat loss of somatic sensation
|
|
lesion of primary visual cortex
|
contralat hemianopia
|
|
lesion of supramarginal gyrus (area 40)
|
astereognosis (can see and feel object but can't recognize meaning)
|
|
lesion of angular gyrus (area 39)
|
-dominant side alexia and agraphia
-nondominant: spatial distorion and contralat neglect (only draw one side of clock) |
|
lesion of Broca's (area 44, 45)
|
-dom: motor aphasia
-nondom: difficulty expressing emotional aspect of language |
|
Auditory loss
|
-need BI-lateral loss of areas 41 and 42 for complete hearing loss
|
|
dominant side Wernicke's
|
sensory aphasia or receptive aphasia
|
|
non-dominant side Wernicke's
|
difficulty understanding emotional language
|
|
hypothalamus is functionally related to which systems:
|
-ANS
-endocrine -limbic |
|
hypothalamus location
|
-makes up walls and floor of third ventricle
-separate from thalamus by hypothalamic sulcus -optic chiasm and lamina terminalis anteriorly -mammillary bodies posteriorly |
|
median eminence
|
-ant part of infundibulum
-where hypothalamic neurons release factors carried by the portal vessels to the anterior pituitary |
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tuber cinereum (gray protberance)
|
-bulge located btw the optic chiasm and mammillary bodies
|
|
hypothal zones
|
-lateral, medial, periventricular
-medial and lateral zones separated by the fornix and mammilothalamic tract |
|
lateral zone of the hypothal
|
-loose neuronal cell groups
-transversed by the fibers of the medial forebrain bundle -lateral preoptic nucleus, lateral hypothalamic area, lateral tuberal nucleus (tuberomammillary) |
|
lateral preoptic nucleus
|
-part of lateral zone of hypothal
-anterior portion -telecephalic developmentally -role in nonREM sleep |
|
lateral hypothalamic area
|
-part of lateral zone of hypothal
-induces eating when stimulated (ablation causes anorexia and starvation) -median forebrain bundle runs through it (lots of functions) |
|
lateral tuberal (tuberomammillary) nucleus
|
-ventrolateral surface of lateral zone of hypothalamus
-large neurons that release histamine as a NT to forebrain -globally projecting -attention and arousal -inhibited during sleep |
|
medial zone of hypothalamus
|
-lots of cells- compact
-preoptic, supraoptic (anterior), tuberal (middle), and mammillary (posterior) regions PSTM |
|
preoptic area
|
-part of medial zone of hypothal
-telencephalic origin -contains medial preoptic nucleus (regulates gonadotropin secretion from adenohypophysis) -INAH1-4 including sexually dimorphic INAH3 reg by testosterone |
|
supraoptic area
|
-medial zone of hypothalamus
-contains suprachiasmatic, anterior hypothalamic, paraventricular and supraoptic nuclei |
|
suprachiasmatic nucleus
|
-immediately dorsal to optic chiasm
-receives direct input from retina -role in circadian rhythms |
|
anterior hypothalamic nucleus
|
-btw suprachiasmatic and paraventricular nuclei
-WARM sensing -stimulatory drive of PNS |
|
bilateral lesion of anterior hypothalamic area results in...
|
-hyperthermia
(loss of warm-sensing neurons) |
|
paraventricular nucleus
|
-heterogeneous with difference output signals
-neurons that release AVP- water conservation -oxytocin- milk let down and release -CRH- stress responsive -other neurons project to interomediolateral cell column to excite symp pregang neurons |
|
supraoptic nucleus
|
-contains neurons that synthesize AVP and oxytocin
-project to neurohypophysis via supraopticohypophyseal tract) where they release into general circulation |
|
tuberal area
|
-part of medial zone of hypothalamus
-contains dorsomedial, ventromedial, and arcuate nuclei |
|
dorsomedial hypothalamic nucleus functions
|
-stim= aggression and savage behavior
-also functions in bp regulation |
|
ventromedial nucleus
|
-stim= urge to eat
-satiety center |
|
bilateral lesion of ventromedial nucleus
|
-hyperphagia
-savage behavior |
|
arcuate nucleus
|
-in tuber cinereum
-controls release of ant pituitary hormones via projections to median eminence and portal vasculature -prominent role in feeding behavior |
|
mammillary area of hypothalamus
|
-consists of posterior nucleus and mammillary nucleus
|
|
posterior hypothalamic nucleus
|
-part of mammillary area of hypothalamus
-COLD sensing neurons |
|
bilateral lesion of posterior nucleus of hypothalamus
|
-complete inability to thermoregulate = poikilothermia
-axons from anterior part (warm sensing) pass through here and are also destoyed |
|
mammillary nucleus
|
-learning and memory, part of limbic system
-input from hippocampus via fornix -project to ant nucleus of thalamus via mammillothalamic tract -damage=memory disturbance |
|
periventricular zone of hypothalamus
|
-contains paraventricular nucleus
-layer of cells lining the wall of the third ventricle at supraoptic and tuberal levels |
|
hypothalamus connections with what portions of the neuraxis?
|
-basal forebrain regions (limbic)
-brainstem regions (ANS) |
|
fornix
|
-tract to deliver axonal projections from hippocampus to mammillary bodies
-divides lateral and medial hypothalamus |
|
mammilothalamic tract
|
-from mammillary bodies to ant nucleus of the thalamus
-key part of Papez circuit |
|
stria terminalis
|
-amygdaloid complex to medial zones of hypothalamus
|
|
medial forebrain bundle
|
-most complex fiber pathway in CNS
-at least 50 distinct parts -extends through entire lateral hypothalamic zone -interconnects reiongs from septal nuclei to brainstem |
|
supraopticohypophyseal tract
|
-from supraoptic and PVN to neurohypophysis
-oxytocin or AVP to post pituitary |
|
tuberoinfundibular tract
|
-arcuate nucleus to hypophyseal portal system at the median eminence of the infundibulum
-release into portal vasculature |
|
hypothalamospinal tract
|
-descending axons that drive spinal cord pregang neurons of SNS and PNS
|
|
hypothalamospinal tract pathway
|
stress-related input (amygdala, prefrontal cortex) --> PVN --> brainstem --> spinal cord --> pregang symp neurons
|
|
3 fundamental capacities of the hypothalamus
|
-access sensory info from entire body
-establishes a biological set point for temp, blood osmolarity, glucose, Na, hormone levels -when a deviation from set point is detected, it responds by adjusting the autonomic, endocrine, and behavioral responses to restore homeostasis |
|
major regulatory functions of the hypothalamus
|
-body temp
-feeding and energy metabolism -emergency response to stress -bp and electrolyte composition -reproduction functions |
|
heat dissipation
|
-anterior hypothal nucleus senses heat
-trigger dissipation via sweating, cutaneous vascular dilation, accel respiration by activation of PNS |
|
disease-associated fever
|
-inflammatory cytokines and pyrogens act on anterior hypothal
-alter set points |
|
cold sensitivity
|
-neurons in posterior hypothalamus
-trigger heat conservation via sympathetic outflow and activation of appropriate endocrine responses to alter metabolic rate |
|
stress responsiveness in the hypothalamus
|
-afferent regulatory control by prefrontal cortex, limbic forebrain, brainstem
-CRH synthesized and released -ant pituitary sim adrenal to release cortisol --> liberates energy sources |
|
arcuate nucleus and feeding
|
-set 1 of neurons: AgRP and NPY --> signal increased feeding and decrease in metabolism
-set 2 of neurons: POMC and CART --> signal decreased feeding and increased metabolism |
|
brainstem satiety center
|
-nucleus solitary tract
-integrates signals from arcuate nucleus about feeding |
|
gherlin
|
-released from stomach just prior to a meal
-acts on AgRP/NPY -increase food intake |
|
PPY
|
-released from GI tract immediately following a meal
-acts on POMC/CART -decreases food intake |
|
leptin
|
-released from fat cells
-decreases food intake |
|
craniopharyngioma
|
-tumor from Rathke's pouch
-pressure on optic chiasm --> bitemporal hemianopsia (tunnel vision) -pressure on hypothal: adiposity, diabetes insipidus, temp reg disturbances, somnolence |
|
hypothal disturbances of memory
|
-posterior hypothal lesions involving mammillary complex
|
|
Klein-Levin syndrome
|
-hypothal lesion in adolescent males
-bulemia, hypersomnolence, hypersexuality -may result in decreased dopaminergic tone |
|
41 yo man with MS. Acute onset of hypothermia; dies of sudden cardiac arrest. Where's the lesion?
|
-bilateral anterior and posterior nuclei of hypothal
|
|
21 yo man with MS. Begins drinking and peeing lots. No hx of diabetes insipidus. Where is the lesion?
|
-over supraoptic nucleus
-can't produce AVP --> can't absorb water |
|
lesion of lateral hypothalamus
|
-causes weight loss
(normall, lateral hypothal makes you grow laterally bc it stimluates appetite) |
|
lesion of medial hypothalamus
|
-causes weight gain
(normally inhibits appetite) |
|
Prader-Willi syndrome
|
-deletion of chrom 15q
-chronic feeling of hunger/ insatiable appetite |
|
ANS controls...
|
-pupillary control
-cardiovascular -GI -genitourinary -point and shoot |
|
ANS spinal cord lesions...
|
-weakness
-sensory loss -GI: constipation, retention -GU: urgency, incontinence -sex: vaginal dryness, pain, ED, anorgasmia |
|
autonomic bowel dysfunction
|
-constipation and retention
-can cause disrupted breathing -impaction |
|
autonomic urinary control
|
-PNS: constricts bladder wall
-SNS: constricts urinary sphincter |
|
normal urinary continence
|
-inhibit parasymp (relax bladder wall)
-stimulate symps (constrict sphincter) |
|
normal urination
|
-stim parasymps (constrict bladder wall)
-inhibit symps (relax sphincter) |
|
Incontinence may arise from...
|
-hyperactive bladder or underactive sphincter
|
|
how do you treat a hyperactive bladder
|
anti-cholinergics to relax bladder wall
|
|
how do you treat an overactive sphincter
|
anti-adrenerics to relax sphincter or intermittent self-catheterization
(if you give anti-cholinergics, worse) |
|
ANS and pupillary control
|
-symp: dilate pupil
-parasymp: constrict pupil |
|
Aniscoria (R eye dilated, L constricted) where could lesion be
|
-R parasymp
or -L symp use ambient light-darkness to differentiate |
|
how do you differentiate btw opp eye symp vs parasymp lesions?
|
-take pt from light to darkness, see if one eye dilates more than the other
-if one fails to dilate properly, lesion is symp ipsilateral |
|
clinical triad of Horner's
|
-small pupil
-ptosis -decreased sweating (sympathetic chain injury) |
|
where could a lesion causing Horner's be?
|
-hypothalamus
-brainstem -thoracic spinal cord -superior cerv gang -carotid plexus |
|
How many neurons are involved in the symp pathway to the eye?
|
-tectospinal spinal tract
-pregang fibers (sup cerv gang) -postgang fibers |
|
internal carotid artery dissection
|
-causes partial Horner's
-blood clot in wall of ICA -arterial wall expands, compressing carotid plexus -small pupil and ptosis, but normal sweating because external carotid plexus is unaffected |
|
why is forehead sweating still intact after an internal carotid artery dissection?
|
the sympathetics to the sweat glands run along the EXTERNAL carotid artery
|
|
what is the main feature of Kluver Bucy syndrome?
|
-increased oral activities
-placidity -hypersexuality |
|
limbic system
|
-site where cortical info and hypothalamic impulses are integrated
-homeostasis (autonomic reg), olfaction, memory, emotion (HOME) |
|
Papez's circuit
|
cingulate --> hippocampus --> fornix --> mammillary bodies --> ant thalamus --> cingulate
|
|
McLean expansion of Papez's circuit
|
-includes association cortex, amygdala, hypothalamus, prefrontal cortex
|
|
what justifies the concept of the limbic system?
|
-common physiologic and neurochemical properties
-intricate anatomic connections -common behavioral associations |
|
common physiologica/neurochemical properties in limbic system
|
-herpes virus has special affinity for these regions
-susceptible to kindling and develop of seizure foci -high density cholinergic innervation and opiate receptors |
|
fornix tract cx
|
hippocampus to mammillary and septal nuclei
|
|
stria terminalis tract cx
|
amygdala to septum and hypothalamus
|
|
ventral amygdalofugal pathway cx
|
amygdala to hypothalamus and brainstem nuclei
|
|
mammillothalamic tract cx
|
mammillary bodies to ant thalamus
|
|
medial forebrain bundle cx
|
hypothalamic nuclei to amygdala and brainstem nuclei
|
|
perforant path cx
|
entorhinal cortex to dentate (hippocampus)
|
|
cingulum tract cx
|
cingulate gyrus to parahippocampal gyrus; hippocampus with midbrain
|
|
outer cortical structures
|
-orbital frontal lobe
-cingulate -entorhinal cortex |
|
cingulate cortex
|
-rostral: emotions and memory
-caudal: visual spatial and memory |
|
orbital frontal lobe
|
-personality
-behavioral control -self awareness |
|
temporal lobe
|
-includes hippocampus, parahippocampus, entorhinal cortex
-memory |
|
inner cortical structures
|
-anterior thalamic nucleus
-mammillary bodies -hypothalamus -septal nucleus |
|
hypothalamus
|
-pleasure center, autonomic, endocrine integration
-neurons project to pituitary, reg ACTH and TSH secretion -maternal behavior, bp, feeding, temp regulation, immune response |
|
amygdala
|
-preservation of SELF behavior
-emotion, social behavior, aggression and defense, sexual behavior, affect regulation |
|
septum function
|
-preservation of SPECIES
-sexual behavior -emotionality |
|
Kluver-Bucy syndrome cause
|
-bilateral large temporal lobe lesions
-include amygdala, hippocampus, uncus -from trauma, herpes, Pick's, Alz's, infarction, focal status epilepticus -increased oral activity, bulemia, hypermetamorphosis, placidity, visual agnosia, hypersexual |
|
Kluver-Bucy syndrome signs
|
-psychic blindness (can't detect meaning of objects based on visual criteria)
-oral -hypermetamorphosis (notice and react to every stimulus) -placidity/ tameness (no rxn to fear or anger) -hypersexual |
|
Geschwind syndrome anatomy
|
-sensory limbic hyperconnection
-strengthening synpatic cx -develops in pts with hx of epilepsy |
|
Geschwind syndrome symptoms
|
-increased philosophic concern
-usually hyposexual -hypergraphia -viscosity (hard to break off conversations) -overly emotionalized world |
|
most pleasurable regions in brain
|
-lateral hypothalamus
-medial forebrain bundle |
|
addictive drugs
|
-mesolimbic dopamine system
-heroin increases neuronal firing rate of dopamine cells -cocaine inhibits reuptake of dopamine |
|
brain pleasure regions
|
-lateral septal region
-portions of amygdala -parts of hippocampus (laterla, medial forebrain bundle, nuc accumbens) -ant cingulate cortex |
|
lesions to ventromedial nuc of hypothalamus
|
-produce pain, rage, or strong aversive rxns and long lasting hyperremotionality
|
|
amygdala lesions
|
-modulation and experience of emotional rxns
-lesions: tameness or reduced emotionability |
|
amygdala in humans
|
-thought to play a major role in the integration of emotions and memory
|
|
septal lesions
|
-changes in sexual behavior
-rage-like attacks and increased irritability |
|
hippocampus lesions
|
-amnestic states
-declarative memory problems |
|
amnestic states can result form lesions in the?
|
hippocampus, dorsal medial nuc of thalamus, mammillary nuclei
|
|
declarative memory
|
-episodic= personal events
-semantic= facts known, not actively remembered |
|
hippocampal formation
|
-hippocampus, dentate gyrus, subiculum
-neocortex has extensive cx with hippocampus and amygdala -efferent=fornix -afferent=perforant path |
|
hippocampus function
|
-formation of episodic memories in humans
-dedicated to spatial mapping in animals |
|
Wernicke Karsakof's syndrome
|
-thiamine deficiency in alcoholics
-confusion, disorientation, oculomotor dysfunction, ataxia -chronic anterorgrade and temporally-graded retrograde amnesia |
|
lesions in Wernicke Karsakoff's
|
mammillary bodies and thalamus
|
|
lesions of cingulate gyrus
|
-emotional blunting
-dec motivation -lowered threshold for fear or startle -decreased pain -OCD |
|
akinetic mutism
|
-associated with bilateral ant cingulate cortex lesion
-can do anything, but absolutely no motivation to do so |
|
Gilles de Tourette syndrome
|
-abnormal ant cingulate
-complex coordinated movement patterns are evoked by electrical stim of AC |
|
bilateral cingulate and orbitofrontal lesions
|
reduced judgement and inability to interpret social cues
|
|
intentional lesions of AC
|
-can relieve obsessive compulsive behaviors
-helpful for some chronic pain patients -associated with sociopathy-- blunted autonomic repsonse to emotional stimuli |
|
disconnecting AC from thalamus
|
-reduced GTS syndromes
|
|
anterior cingulate function
|
-integration of thought, motivation, and emotion with movement
|
|
lesions in AC can cause...
|
-excessive amplification of emotional signals
-amplification of motor behavior -excessive filtering of emotions and motor behavior |
|
orbital frontal lobe syndrome
|
-childlike
-disinhibited, tactless, boastful inattentive, eat gluttonously |
|
frontal/convexity or dorsolateral frontal lobe syndrome
|
-apathetic
-slow -little initiative or spontaneity -vacancy of expression |
|
medial frontal syndrome
|
-akinetic mutism
-inert -speechless -intact sleep wake cycle -loss of drive to move/speak |
|
laterality
|
cerebral hemisphere that is specialized for a group or class of cognitive functions
|
|
dominance
|
-cerebral hemisphere that is specialized for language
-typically L |
|
crossed dominance
|
-condition of R hemisperic dominance for language
|
|
Crowding
|
-condition that occurs after early L hemisphere damage where development of language shift to the R hemisphere
-at expense of development of cognitive capacities typically assoc with R hemisphere (ie visual-spatial skills) |
|
pathological left-handedness
|
-condition of L handedness that has occurred bc of early injury to L hemisphere that causes a shift in natural handedness pattern
|
|
Approx what percent of the entire population is R-handed; and what percent of R handers are L hemisphere dominant for language?
|
90%
95% |
|
Broca's aphasia is characterized by what?
|
-non fluent speech
-poor repetition -relatively spared comprehension |
|
measuring handedness
|
-inventories (range of activities)
-hand used for writing -90% R dextrals, 10% L sinistrals |
|
Intracarotid amobarbital test (IAT) (Wada test)
|
-measures dominance
-catheter: ICA --> barbiture is injected into one hemisphere --> anesthetized --> tests of language -used only when you have brain function abnormalities |
|
fMRI for measuring dominance
|
-based on changes in the ratio of oxyHb to deoxyHb to the brain from moment to moment
-noninvasive -can be performed in healthy individuals |
|
Atypical dominance patterns are more common in what handed people?
|
-left handers
|
|
early brain damage increases what?
|
-incidence of atypical dominance
-particularly in those with left or mixed handedness |
|
Significantly more patients with epilepsy show what dominance pattern?
|
-symmetric and R hemisphere dominance patterns relative to healthy normals
|
|
left-handedness and cerebral dominance patterns
|
-atypical speech representation is more frequent
-negative familial sinistrality have more typical language representation |
|
injury to L hemisphere before age 1
|
-development of language spared
-often generalized cognitive deficit |
|
injury to L hemisphere btw age 1&5
|
-language spared (shifts to non-dominant hemisphere)
-possible visual-spatial deficit (crowding) |
|
injury to L hemisphere after age 5
|
-language no longer spared
-circumscribed language deficits emerge |
|
what injury will cause selective shift of language zones?
|
-selective injury to anterior or posterior speech zones
-causes a shift of the functions associated with that zone only |
|
what injury will cause a complete shift in language function?
|
-injury to the core or central speech zones
-known as crossed-dominance |
|
what hemisphere is usually dominant for language and how is this changed?
|
-left hemisphere dominance for language is the rule
-changed by early brain injury and familial left handedness |
|
lateralization of the hemispheres
|
-relative and complementary
-probably increases with age before puberty, decreases with age thereafter |
|
disorders of speech
|
-involve malfunction of the muslces of speech articulation
-include: mutism, aphonia, aphemia, dysarthria |
|
mutism
|
-absence of speech: organic or elective
-may be psychogenic -extensive bifrontal brain damage of bilateral lesions in supp motor area |
|
aphonia
|
-loss of capacity to produce vocal sound
-due to injury in PNS that enervates muscles of the vocals cords |
|
aphemia
|
-loss of capacity to produce words, can produce sounds
-disconnection syndrom due to a whitematter lesion beneath Broca's that serves as final output pathway for speech production |
|
disorders of language
|
-aphasias
-acquired disturbances of linguistic functions due to injury of the CNS |
|
all aphasias be classified by the integrity of what?
|
-fluency
-comprehension -repetition |
|
how is fluency evaluated
|
-phrase length
-degree of apparent effort in speech production -prosody (preservation of melodic elements of speech) |
|
nonfluent speech
|
-few than 3 words per utterance
-laborious in production -monotonic in delivery |
|
core language zones
|
-Wernicke's area (sup temporal lobe)
-Broca's area (post and inf frontal lobe) -arcuate fasciculus (whitematter connection) |
|
Global aphasias typically occur when?
|
-when the functions of both ant and post aspects of the core language zones are impaired
-no fluency, comprehension or repetition |
|
Transcortical aphasias
|
-repetition of speech is preserved
-loss of fluency (motor) and comprehension (sensory) |
|
when do transcortical motor aphasias occur
|
-lesions to the premotor region
or -SMA lesions |
|
transcortical sensory aphasias occur when?
|
-with lesions of the angular gyrus
or -lesions to poster and inferior temporal lobe |
|
isolation aphasia
|
-lesions of both transcortical motor and sensory aphasias are present
-effectively isolates the core speech zones from the remainder of the hemisphere |
|
Broca's aphasia
|
-nonfluent
-profound impairment in speech articulation -repetition is impaired bc of articulation impairment |
|
Wernicke's aphasia
|
-fluent aphasia
-profound impairment in speech sound recognition and language comprehension -repetition is impaired bc of speech comprehension difficulties |
|
Conduction aphasia
|
-fluent aphasia
-associated with profound impairment in repetition -relatively preserved comprehension -problem with speech sound storage area or arcuate fasciculus |
|
transcortical sensory aphasia
|
-fluent aphasia
-language comprehension deficits at the word level -repetition is preserved |
|
4 levels of consciousness
|
-awake (arousable and maintained without stim)
-sleepy (arousable but falls back asleep) -stupor (arousable but unable to maintain wakefulness) -coma (unarousable with any stim) |
|
diminished level of consciousness indicates what?
|
-a lesion in reticular activating system
-metabolic or structural coma |
|
metabolic coma
|
-affects bilateral cerebral hemisphere
-problem getting nutrients to brain (low glucose, O2, medication overdose) |
|
structural coma
|
-lesion in brainstem or bilateral thalami or bilateral hemispheres
-need both sides |
|
Where is a lesion producing non-fluent aphasia?
|
-inferior frontal lobe in dominant hemisphere (Broca's area)
|
|
Where is a lesion producing fluent aphasia?
|
-superior temporal lobe in dominant hemisphere (Wernicke's Area)
|
|
What is conduction aphasia characterized by?
|
-impaired repetition
-normal fluency and comprehension -lesion in arcuate fasciculus |
|
What is global aphasia characterized by?
|
-impaired fluency, comprehension, and repetition
-pt completely mute, doesn't follow commands, looks blank when spoken to ie complete MCA occlusion |
|
L hemisphere contributes attention...
|
to the R
|
|
R hemisphere contributes attention...
|
bilaterally, but L>R
|
|
R hemisphere lesion causes neglect on which side?
|
severe neglect of the L
|
|
L hemisphere lesion causes attention...
|
-mild neglect of the R
|
|
If you want to look to the L, which frontal eye field sends signal
|
R frontal eye field
|
|
R hemiparesis and eyes look to the L, where is the lesion?
|
left frontal lobe (L frontal eye field and L motor cortex)
|
|
primary sensation
|
-from postcentral gyrus (primary somatosensory cortex)
-pin prick -hot/cold -vibration |
|
cortical sensation
|
-Where or what is it?
-need coordination of senses and multiple brain areas |
|
agraphesthesia
|
can't determine numbers written on palm
|
|
astereognosis
|
can't determine shape of object placed in hand
|
|
Agraphesthesia and astereognosis in an extremity both localize where?
|
to the contralateral parietal lobe
|
|
lesions closer to the optic chiasm are what?
|
usually more incongruous
|
|
posterior occipital lobe mediates vision where?
|
-in the central aspect of the visual fields
|
|
anterior occipital lobe mediates vision where?
|
-in the peripheral aspect of the visual fields
|
|
what artery supplies the tip of the occipital lobe?
|
-mainly the PCA
-can receive collateral flow from the MCW |
|
localization of cognition and emotion in hypothalamus
|
-primitive emotional responses
-fight, flight, feed, mate |
|
localization of cognition and emotion in frontal cortex
|
-highest cognitive function
-control over emotions -judgment, decision making, mortality, compassion, responsibility -reciprocal neg feedback with hypothalamus |
|
localization of cognition and emotion in prefrontal cortex
|
-production and appreciation of art
-beauty as an emotion |
|
localization of cognition and emotion in amygdala
|
-storage of emotional memories
|
|
localization of cognition and emotion in hippocampus
|
-episodic memory
|
|
synaptic plasticity
|
-the ability of synpases to change their strengths in response to experience and a cellular model of learning and memory
-Ca2+ has different responses to increase AMPA threshold or decrease AMPA receptors |
|
glutamatergic receptors in learning and memory
|
-AMPA: basal synaptic transmission
-NMDA receptors: binds Glu and allows Ca2+ to enter and act on AMPA signalers; blocked by Mg2+ (activated when cells are depolar) |
|
studying learning and memory at behavioral level
|
-water maze
-fear conditioning |
|
water maze
|
-hippocampal-dependent task
-spatial memory |
|
cued fear conditioning
|
-amygdala-dep task
-put in a new environment but same stim--> freeze |
|
contextual fear conditioning
|
-hippocampus AND amygdala-dep
-put in conditioned environment and they automatically freeze even without stim |
|
Long-term potentiation (LTP)
|
-enhancing synaptic strength
-induction via learning -maintenance |
|
Long-term depression (LTD)
|
-despressing synaptic strength
|
|
CaMKII
|
-enzyme that phosphorylates targets
-important for LTP -stim by Ca2+ -causes more AMPA receptors so response comes at a lower stimulus |
|
Calcineurin
|
-enzyme that dephosphorylates targets
-important for LTD -stim by Ca2+ -decreases AMPA receptors so more of a stimulus is needed |
|
neurogranin
|
-controls synaptic plasticity balance
-regulates CaMKII availability -increased NG means inc CaMKII |
|
aging and learning/memory
|
-synaptic plasticity imbalance
-changes in levels of CaMKII, calcineurin, NG -LTD begins to dominate over LTP (inc calcineurin, dec NG, dec CaMKII) |
|
TBI
|
external physical force causing impairment
|
|
gen categories of brain injury
|
-congenital (pre-birth or during birth process)
-acquired (after birth process) |
|
types of TBI
|
-blunt/closed
-penetrating/open (skull is fractured) |
|
primary TBIs
|
-skull fx
-contusion -hematoma (subdural or epidural) -intracerebral hemorrhage -diffuse axonal injury -coup-contra-coup |
|
coup-contra coup
|
-contusion at site of impact
-brain slide back -contusion at opposite side |
|
diffuse axonal injury
|
-rotational forces cause stretching and snapping of axons
-unrepairable -ie shaken baby |
|
secondary TBI
|
-evolves over a period of hours/days after inital trauma
-edema -increased intracranial pressure -intracranial infection -epilepsy -hypoxemia |
|
mild TBI
|
-13-15 Glasgow coma scale
-20-60min LOC -<24hr post-traumatic amnesia |
|
moderate TBI
|
-9-12 Glasgow coma scale
-1-24hrs LOC -1-7 days post-traumatic amnesia |
|
severe TBI
|
-3-8 Glasgow coma scale
->24hr LOC ->7 days post-traumatic amnesia |
|
Glasgow coma scale
|
-best eye, motor, verbal response that a clinician can elicit
-can't factor in how much stimulus was required -15=best, 3=worst |
|
high risk groups for TBI
|
-males 15-24 yo
-substance abusers -infants (64% d/t child abuse) -elderly (fall risk) -those with prior brain injury |
|
TBI can result in difficulties with...
|
-executive control functions (memory, money and time management, judgment, concentration, planning, confusion)
-psychosocial and emotional fx -physical abilities |
|
treatment of TBI
|
-acute: stabilize pt
-sub-acute: rehab pt and return to community -chronic: rehab and longterm care |
|
post-TBI evaluation
|
-physical exam and hx and neurological testing
-neurophyschosocial testing to assess intellectual deficits, emotional, behavioral problems -CT/MRI to look for structure changes -PET, fMRI, SPECT to look for fx changes |
|
consequences of CNS injury at cellular injury
|
-neuronal injury
-axonal injury -oligodendrocyte injury/demyelination -astrocyte activation --> scarring -microglia activation |
|
injury to cell body
|
no regeneration of neuron
|
|
regenerating axons in periphery
|
-possible if severed away from cell body
-severed axon retracts and ends seal -distal segment degen's and is phagocytosed by mac's -chromatolysis of Nissl -axon regen follows route of Schwann cells (so axon must be in PNS) |
|
primary mech of SCI
|
-vertebral displacement
-vascular rupture and ischemia (concussive, contusive, shearing, stretching forces) |
|
secondary mech of SCI
|
-membrane-assoc events (lipid hydrolysis)
-vascular events (blood is toxic to neurons) -inflamm (immune recruitment) -biochemical events (NT accumulation, excitotoxicity) |
|
what is necessary for a neuron to regenerate
|
-axon must be in periphery
-cell body can be in PNS or CNS as long as it is intact |
|
clinical definition of SCI
|
-a lesion of the SC that results in paralysis and/or a corresponding loss of sensation
|
|
paraplegia
|
-injury in thoracic/lumbar/sacral regions
-paralysis from waist down |
|
quadriplegia
|
-lesion in cervical region
-paralysis from shoulders down |
|
complete SCI
|
-no motor or sensory in lower sacral or anal area
(ASIA A) |
|
incomplete SCI
|
-some level of motor or sensory below level of injury
(ASIA B-E) |
|
intervention strategies for SCI
|
-limit inital degen/ limit inflamm
-stim axonal growth and regen (best if before scar forms) -block exogenous inhib of regen (myelin, NOGO) |
|
timeline of events in SCI
|
-1st 30 min: vascular compromise, axonal changes
-2hrs: hypoperfusion of cord, microglia and PMNs infiltrate -6hrs: edema, inflamm cells, axolemma rupture -1wk: injury is infiltrated by mac's, Wallerian degen of axons and secondary demyel. occurs |
|
autonomic dysreflexia
|
-post SCI
-abnormal CV episodes -triggered by noxious and non-noxious stimuli |
|
pain syndromes
|
-post SCI
-allodynia -hyperalgesia |
|
Brown-sequard
|
-cord hemisection
-ipsilateral paralysis -contralateral loss of pain/temp |
|
syringomyelia
|
-pain/temp and motor loss increase over time
-occurs as syrinx in middle of cord gets progressively larger |
|
suprapubic catheter
|
-SCI treatment
-improves QOL -limits infections, can limit autonomic dysreflexia episodes |