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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
-afferent: dentate nucleus of cerebellum
-projects to: motor and premotor cortex (areas 4 and 6)
-motor functions
VPL of thalamus
-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
-afferent: parietal cortex
-projects to: parietal cortex
-sensory integration
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
-precentral gyrus
-primary motor
Brodmann's 17
-cuneus and lingual gyrus
-primary visual
Brodmann's 41, 42
-transverse gyri of Heschl
-primary auditory
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
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
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