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296 Cards in this Set
- Front
- Back
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what are the 4 major components of the diencephalon?
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epithalamus
thalamus hypthalamus subthalamus |
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what does the epithalamus contain?
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pineal body
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waht is the thalamus bounded by?
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ant and post commissures
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waht does the subthalamus contain?
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subthalamic nucleus of the basal ganglia
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what are the 3 majore categories of thalamic nuclei?
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relay nuclei in the thalamus
intralaminar nuclei in the thalamus reticular nucleus in the thalamus |
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waht do the relay nuclei in the thalamus receive?
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inputs from numerous pathways and project to cerebral cortex
receive MASSIVE reciprical connections back from the cortex: corticothalamic fibers |
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all sensory modalities sends imputs to the thalamus with the exception of
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olfaction
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relay nuclei for pain, temp from body via waht tract? what part of cortex?
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tract: ALS from body
relay: VPL S1 cortex |
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relay nuclei for fine touch via what tract? what part of cortex?
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DC-ML
relay: VPL S1 cortex |
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relay nuclei for pain, temp from body via waht tract? what part of cortex?
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CN V
relay: VMPM S1 cortex |
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what relay nuclei for fine touch from head? via waht tract? portion of cotex?
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CN V
VPM S1 cortex |
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what relay nuclei for visual sensory? via aht tract? what area of cortex?
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optic tract
LGN V1 cortex |
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what relay nuclei for auditory sensory? via waht tract? what area of cortex?
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brachium of inf coliculus
MGN A1 cortex |
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what relay nuclei for taste? via waht tract? what portion of cortex?
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central tegmental tract
VPM T1 |
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what relay nuclei for balance? via waht tract? what portion of cortex?
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MLF
VPL 3a, insular |
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motor is relayed to what nuclei?
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Va and VL
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all output to thalamus is coming from what layer of cortex?
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6
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output from cortex to CP, CS, CB, CR (all except thalamus) is coming from what layer?
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layer 5
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input from thalamus to cortex is into what layer?
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layer 4
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what are cortex layers 2/3 for?
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send info ispi , axons throughout cortex
into corpus collosum |
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thalamocortical tracts via waht layer?
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4
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corticothalamic tracts via waht layer?
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6
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mediodorsal (MD) of thalamus receives imput from?
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amygdala, olfactory cortex, basal ganglia(nucleus accumbuns)
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ant nucleus of thalamus receives imputs from where?
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mammillothalamic tract, fornix
*impt nucleus for memory |
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waht thalamic nuclei is impot in memory?
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ant neucleus
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where does the fornix come from? where does it go?
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from temporal lobe, dives into hippocampus, ends in mammillary bodies *can go directly to thalamus inot ant nucleus
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lesion to hippocampus?
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short term memory loss
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where is the VPL located?
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postcentral gyrus
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damage to VPL?
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contra loss of body sensory
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damage to VPM?
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contral loss of sensation to face
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R thalamus projects to right or left postcentral gyrus?
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R post central gyrus
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fornix delivers what modality to where? what area of cortex recieves this info?
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memory to ant nucleus in thalamus from hippocampus
cingulate cortex : Posterior |
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stria terminalis delivers what modality to where? what area of cortex recieves this info?
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emotions to medialdorsal nucleus from amygdala and olfactor cortex
prefrontal cortex and cingulat cortex: ANTERIOR |
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medial dorsal nucleus is the relay for waht?
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emotions
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intralaminar nuclei in the thalamus are the relay for what?
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ascending reticular activating system (ARAS) for arousal
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fxn of intralaminar nuclei?
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activates entire cortex when BRAINSTEM reticular formation is activated
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waht is the reticular nucleus in the thalamus?
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thin sheet of neurons jsut lateral to the rest of the thalamus and medial to the internal capsule
*only nuclei of the thalamus that does not project to the cortex |
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what is the only thalamic nuclei that does not project to the cortex?
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reticular nuclei
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output from the reticular nuclei in thalamus? via?
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to the THALAMUS!!
pure inhibitory GABA-ergic neurons-regulates thalamic activity |
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output of hippocampus?
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fornix to mamilary bodies (hypothal) to thalamus
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waht is the ant commisure?
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fibers connecting temporal lobes
ant boundary to hypothal |
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does loss of one type of memory impair the other type?
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no
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what arethe 2 types of memory?
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declarative memory: facts,events that canbe recalled and declared ex: autobiographical events and facts
procedural memory: no available to conscious awareness ex: motor skills, habits..driving, riding a bike |
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what do declarative memories require?
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intact limbic structures: medialtempral lobe(hippocampus), medial diencephalon
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who do produral memories require?
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intact basal ganglia and cerebellum b/c motor skills
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how do lesions to the basal ganglia or cerebellum affect memory?
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affect procedural memory and produce observable movmt disorders
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time frame of immediate memory? short term? long term?
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immediat: seconds duration
short term: seconds to minutes long term: very long |
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what is immeidate memory? capacity?
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total of ALL sensory info immediately after it has been processed by the sensory systems
capacity is very large must be converted into a more stable form or it wil be rapidly lost with newer icoming sensations |
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why do we need to take notes in class?
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b/c the sensory info coming in is immediate memory and lasts only for seconds
it needs to be converted into a more stable form or it will be rapidly lost with newer incoming info |
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what does short term memory require? capaicity?
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requires constant atttention to remain in short term memory
capacity is very limited: 7+/-2 pieces of info (phone number) must be CONSOLIDATED into long term memory or memories in short term will be lost as soon as attention shifts |
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capacity of long term memory? how are they formed?
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long term memories are very RESISTANT to forgetting
capacity is vast long term memories are formed through a process called CONSOLIDATION |
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when are memories vulnerable?
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in the process of being consolidated they are vulnerable to a variety of insults: head trauma, seizures, electroconvulsive shock
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is forgetting normal? when is it not?
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forgetting is normal
amnesia is the pathological loss of memories |
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what is retrograde amnesia?
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loss of accumulated long term memories due to damage to areas of brain where long term memories have been stored
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what is anterograde amnesia?
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inabilty to form new memories (hippocampus) and is a result of damage to areas of the brain involved with consolidation of memories
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what is the location of immedite and long term memory?
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high level sensory/ association cortices
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what type of amnesia is it when you can't recog or remember familar faces?
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face agnosia or prosopagnosia: specific retrograde amnesia du to lesion in inf temporal cortex
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waht type of amnesia is it when you have trouble forming memories of new faces?
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specific type of anterograde amnesia due to lesions in inf temporal cortex
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magnocellular pathway processes?
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motion: watching salsa dancers
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waht is the top down manner of memory?
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smell, voice, motion to bring back memories and guide the bottom up recognition process
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what is the bottom up recognition process?
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ex: visual info sent to V1 then V2 then V3 and you recognize the face
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where are auditory aspects of memory stored?
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in high order auditory cortical areas
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how does consolidation occur?
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by strenghening synaptic connections b/n neurons in multiple neocortical areas
*plasticity ex: memory of individual person becomes respresented in declarative memory by the strenthening of synapses connecting neurons in ares of visual cortical areas (color of hair), auditory areas (sound of their voice) language areas of the cortex (name of person) and even olfatory areas of the cortex (body odor) |
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waht does consolidation of memory require?
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set of interconnected limbic structures: cingulate gyrus, hippocampus, mamillary bodies
but the structurs are not participants in long term storage of memories, only in the consolidation of declaritive memories |
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how can the hippocampus talk to the ant thalamus?
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directly via fornix
or indirectly after fornix reaches mammillary bodie then have mamillothalamic tract |
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waht components are needed for short term memory + consolidation/
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hippocampus
mammilary bodies ant thalamus cingulate gyrus |
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bilateral damage to medial temporal lobe damaging hippocampus, entorhinal cortex and parahippocampal gyrus produces?
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dense global anterograde amnesia
* this can also occur with damage only to hippocampus but is less severe |
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what is the #1 site for epileptic seizures?
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temporal lobe
need at least 1 temporal lobe to allow consolidation to occur |
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what are the 4 major arease w/n the hippocampal formation
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from enterorhinal cortex:
dentate gyrus CA3 CA1 subiculum output via mamilary bodies, hypthal |
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what area of the hippocampus is very sensitive to anoxia and ischemic insult?
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CA1: contains pyramidal cells
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bilateral lesion ot medial diencephalon resuls in?
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bilateral damage to mammillary bodies and ant thalamus
also produces a dense global anterograde amnesia *this is the majore output from hippocampal formation |
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damage to ant nucleus of thalamus or fibers in mammillo-thalamic tract can also produce?
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global anterograde amnesia
like bilateral medial temporal lobe lesion and bilateral medial diencephalon lesion |
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the consoldation of memory is ____ (time)
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gradual and cumulative
takes place over hours and days |
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strenthening or potentiation of synapses involved in memory requires what?
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activity dependent process
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process of strengenthening memory synaes s called waht?
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long term potentiation (LTP)
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waht synaptic connections are strenthened in hippocampal formaton/
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excitatory pyramidal neuron to pyramidal neuron
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describe how synaptic connections are stregthened b/n pyramidal cells in hippocampal formation
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CA3 dendrite rleases Glu onto postsynaptic CA1 membrane
both ionotropic (direct) Glu R's: non NMDA and NMDA R the non NMDA will depol (Na enters) get EPSP and now NMDA R opens and allow Ca to enter cell Ca stimulates Ca dependent enzymes that increase the sensitivty of postsyanptic neuron to Glu via PKC phosph of nonNMDA R's and rlease of retrograde factors that act on presynaptic mem |
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how do we retrieve memories?
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a stimulus feature associated with the original memory reactivates one of the cortical areas where one of the aspects of the memory is stored
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characteristics of memory retrieval
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memory recall is variable: attempts to recall memory may not succeed in reactivating all areas of where the memory is stored
sometimes incorrect: activate inappr area *recognition is easier than recall: external stimulus which prompts recognition provides a partial clue for ractivation of some cortical areas where teh memory is stored |
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how is recognition different than recall?
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recognition is easier: external stimulus provies a clue for reactivation of some cortical areas where memory is stored
recall is self generated stimulus for the reactivaton of the cortical areas where teh memory is stored |
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if you lesion the primary visual field on R, lose what visual field?
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L
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waht is Brodman 17?
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V1: knowing/cognition
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where are mirror neurons located and what are they for?
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prefrontal cortex
planning, goal setting |
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what are the "silent" areas-substrate of highest brain fxn, cognition, knowing?
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association cortex
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what are the 3 main association areas?
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prefrontal: location of delay-specific neurons and mirror neurons
parietal: location of attention specific neurons temporal: location of recognition specfic neurons |
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importance of prefrontal association cortex?
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planning behavior, setting goals, recognizing behaviors
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importance of parietal association cortex?
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attending to complex stimuli
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importane of temporal association cortex?
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recognizing and identifying objects
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what regions are responsible for the info processing that goes on b/n sensory input and motor output?
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association cortecies
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what cotex is essential for PLANNING approprate behavioral responses?
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frontal
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what cortex is responsible for ATTENdING to complex stimuli in the external and internal environment?
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parietal
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what cortex is responsible for IDENTIFY simule?
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temporal
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insteand of thinking of one hemi being dominant, what do whe think?
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complementary specialization of the hemispheres
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which hemi is responsible for sequential and analytical processes?
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Categorical hemi: left hemi (dominant)
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what hemi is responsible for visuospatial relations?
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Representational hemi: R hemi (non dominant)
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what is the handness of 90% of pop? which of their hemis is categorical?
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Right
categorical hemi is 96% of R handed individuals is Left Hemi |
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what percent of r handed ppl have a right hemi for categorial analysis?
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4%
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what perdent of pop is left handed? how many of them have their left hemi as categorical?
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10% pop Left handed
70% have L hemi as categorical 15% right |
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which hemi specializes in declarative memory?
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Left
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what does the Left hemi specialize in?
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intellectual
rational verbal analytical thinking declarative memory *categorical hemi |
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Lesions in Left Hemi cause what?
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language disorders whereas extensive lesions in the representational hemi do not
*can still sing with ppl that have lesion on L |
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are pts with left hemi lesions aware of their disability?
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yes, and often depressed
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what does the Right Hemi specialize in?
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percieving and in emotional, nonverbal, and intuitive thinking and in procedural memory
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which hemi is for procedural memory?
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Right hemi
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sustained attention to a polymodal task is a fxn of what hemi?
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Right: Representational
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which hemi is involved with recognition of objects by their form and the recognition of musical themes?
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R: Representational
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lesions of Representational hemi produce waht?
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agnosias: inabilty to recognize objets by a particaular sensory modality even though sensory modality is in check: can't identify pen but can see it, can feel it
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agnosias are lesions where?
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in temporal and parietal lobes of representational hemi
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a lesion in the inf parietal lobe is the primary region responsbile for?
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attention
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are pts with lesion of representational hemi aware of their disability?
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no unlike in categorcial hemi and ar unconcerned even euphoric and unable to recognize emotions in other individuals
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what is the word for someone that is unaware of their disablity?
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anosognosia as seen in lesions of representational hemi
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which associaiton cortex is responsible for cognitive behavior and motor planing; maintenance of an person's personality?
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prefrontal cortex
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carrying out motor tasks involving memory or in relation to sensory inputs is whose job?
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prefrontal cortex
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lesoins in which cortex are interpreted as a change in the patient's character?
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prefrontal cortex
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waht woul a frontal lesion cause?
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pts become boastful of physical prowess and little restraint in conversation, unale to plan for future
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where is Broca's area located?
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inf frontal gyrus
part of prefrontal cortex Brodman 44, 45 |
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what is Broca's aphasia? cna be caused by?
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difficulty in expressing thoughts either in written (agraphia) or in spoken language (non fluent, expresive or motor aphasia)
sup MCA damage |
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where is wenicke's area located?
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brodman 22
left post temporal lobe |
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in terms of association cortex, where is the limbic system located?
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prefrontal cortex
emotional behavior and memory |
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lesions of the categorical (L) parietal and temporal lobe produce?
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aphasia: disorder of language
Wernicke's Conduction aphasia anomic aphasia global aphasia |
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what is Wernicke's aphasia?
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difficulty in comprehending speech and in reading
"verbal diarrhea" |
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higher sensory fxns and language are a fxn of what 2 association cortices?
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parietal-temporal association cortex
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lesions of categorical (usually L) parietal-tempral lobe produce?
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aphasia: disorder of language
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diff b/n Broca's and Wernicke's?
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brocas: comprehension but non fluent speech (broken speech)
wernicke: no comprehension, but fluent speech |
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what is a conduction aphasia?
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fluent aphasia like Wernickes
lesion in auditory cortex: no trouble speaking or hearing but has trouble putting words together or conjuring up words |
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what is anomic aphasia?
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damage to angular gyrus: Categorical Hemi
unable to NAME objects |
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what is global aphasia?
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loss of all language skills (comprehension, speaking, writing and reading)
lesion on Left Categorical |
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agnosia can occur with damage to what hemi?
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left or right
parietal-temporal |
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waht is Agnosia?
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"not Knowing": inability to recognize a complex sensory stimuli such as an object even though the sensory pathways and perception of the object are intact
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what is astereognosis?
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form of agnosia: left or Righ hemi
inablity to recognize the form of objects by touch alone, with no major somatic sensory deficits |
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what is prosopagnosia
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form of agnosia: left or right hemi
uni or bi temporal lobe damage inablity to IDENTIFY old faces or remember new faces-no vision pathway deficits |
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face-blindnes is called?
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prosopagnosia
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what is Gerstmann's syndrome? 4 things assoicated with the syndrome?
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parietal lobe lesion: R or L
1. confusion b/n R and L 2. difficulty in saying which finger was touched 3. dysgraphia: writing diablity 4. dyscalculia: inabilty to do math calculations |
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waht is apraxia/
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inabilty to perform an acton in response to a verbal command "unlock the door" in the absence of any defect in comprehension, incoordination ,ro motor weakness
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waht is aprosody?
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loss of emotional exprssion
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damage to parietal lobe=
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attention deficits
ex: Contralateral Neglect due to lesion of R, representational Pareital lobe parietal = attending |
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massive lesion in Right parietal lobe?
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assive lesion in the right parieto-occipital region this … resulted in an inattention to or neglect of the left half of external space.
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hallmark of contralateral neglect?
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The hallmark of contralateral neglect is an inability to perceive and attend to objects, or even one's own body, in a part of space, despite the fact that visual acuity, somatic sensation, and motor ability remain intact. Affected individuals fail to report, respond to, or even orient to stimuli presented to the side of the body (or visual space) opposite the lesion
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waht is the primary lobe for attention?
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inferior parietal lobe, is the primary cortical region (but not the only region) governing attention
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which side is contralateral neglect mostly problematic?
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contralateral neglect syndrome is specifically associated with damage to the right parietal cortex. The unequal distribution of this particular cognitive function between the hemispheres is thought to arise because the right parietal cortex mediates attention to both left and right halves of the body and extrapersonal space, whereas the left hemisphere mediates attention only to the right.
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why is a lesion of LEFT parietal lobe not as bad as a RIGHT parietal lobe lesion?
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left parietal lesions tend to be compensated by the intact right hemisphere. In contrast, when the right parietal cortex is damaged, there is little or no compensatory capacity in the left hemisphere to mediate attention to the left side of the body or extrapersonal space.
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what ares of the brain will be stimulatated when asked to attend to the RIGHT visual field? LEFT visual field?
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A subject has been asked to attend to objects in the left visual field; only the right parietal cortex is active. (B) When attention is shifted from the left visual field to the right, the right parietal cortex remains active, but activity is apparent in the left parietal cortex as well. This arrangement implies that damage to the left parietal lobe does not generate right-sided hemineglect because the right parietal lobe also serves this function.
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how do agnosias of Left temporal lobe compare with those of Right temporal lobe?
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lesions of the right temporal lobe lead to agnosia for faces and objects, whereas lesions of the corresponding regions of the left temporal lobe tend to result in difficulties with language-related material
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waht is the #2 neuro disease?
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epilepsy
#1=stroke |
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waht does the EEG measure?
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electrical activity of the neurons in the cortex
measures the activity of the cortical neurons changes in response to behavioral states and pathologies such as coma and epilepsy |
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activit of the EEG is due to?
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cortical neurons post synaptic potentials
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which EEG wave has the greatest freq? lowest?
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beta: >13Hz (14-40)
delta: <4Hz |
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frequencies of EEG waves?
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beta: >13
alpha: 8-13 theta: 4-8 delta: <4 |
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waht does an EEG voltage represent?
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EEG voltage signal represents a difference between the voltages at two electrodes
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do the EEG scalp electrodes pick up AP's?
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calp electrodes are not sensitive enough to pick out individual action potentials
Instead, the EEG picks up the activity of large groups of neurons, which produces a greater voltage than the firing of an individual neuron |
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what does low amp, high freq imply?
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Faster frequencies and lower amplitudes indicate that the subject is more aroused and alert, whereas low-frequency, high-amplitude waves are associated with the deepest levels of sleep.
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waht are the principal source of EEG potential?how are they oriented?
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pyramidal cells
they are orientaed perpendicular to the surface of the brain they line up dipoles and field potentials summage AP's are NOT the source of the EEG, too fast to summate |
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how are EEG waves crated?
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extracellular current flow associated with the summated synaptic potentials in activated pyramidal cells
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what happens when cortical neurons fire synchronosly?
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their bipotentials summate, producing large amp/high voltage brain waves at low freq(slow rate)
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waht happens when coritcal neurons fire Asynchronously?
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their bipotentials summate, producing small amp (low voltage) brain waves at a fast rate(high freq)
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when do we see Beta waves?
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active, awake, thinking
Eyes open REM sleep state |
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when do we see alpha waves?
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relaxed, relative mental inactivity
eyes closed highest amp over the ocipital, posterior region of head |
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why do we see the highest amp alpha waves over the occipital, posterior region of head?
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b/c eyes are closed and all extracll feild potentials are the same
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when do we see theta waves?
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awake youth <30yrs
drowsiness NON REM sleep |
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when do we see delta waves?
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NON REM sleep/Stage 4
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what are the axis for EEG?
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voltage (y) against time
voltage of EEG dtermines its amplitude |
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what happens to the voltage of EEG by the time it reaches scalp?
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decreased bc attentuated by meninges, CSF, dura, bone , scalp
on surface: 10-100microV amplitude |
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how are the 21 electrodes arranged on the head?
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odd on left
even on right |
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summation of synchonously firing neurons will generate what?
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the slowest freq and highest amp EEG waves
ex: delta brain waves voltage: >74micor V (beta are <75) |
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highest amp of all brain wave ptterns?
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delta waves >74microV
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lowest amp of all brain wave patterns?
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beta waves <75microV
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when and where are alpha brain waves prnoucned?
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over the occipital cortex in awake, relaxed humans with EYES CLOSED
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EEG pattern changes rapidly with what?
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eys going from open to closed and vice versa
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what does it mean when waves are abnormal on 1 or 2 channels?
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lesion is local , focal
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what happens when you alert the pt that had their eyes closed? how will the bran waves change?
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they open their eyes, blocking the alpha rythm, producing less synchronized activity and more low voltage and high freq activity (beta waves)
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how will hyperventilation change wave patterns?
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increase alveolar ventilationg will drop partial pressure of CO2 in lung alveoli, blood and brain
(nl Va is 4L/min, nl PaCO2 is 40mmHg) will see slowing of waves in nl subject generalized-synchonous sizure discharge or absence seizure in abnl pt |
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affect of hyperventialation on brain waves of nl pt?
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slowing of waves
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affect of hyperventialtion in abnl pt?
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generalized -synchronous seizure discharge or absence seizure
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what is the physiologic response to intermittient photic stimulation (flashing light 1-30cps)?
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photic driving of the occipital EEG
will cause rythmic EEG activity with same freq as flasing light |
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whta is teh photoconvulsive response to intermittent photic stimulation?
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occurs at 15cps in pts with epilepsy
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waht are some ways to enhance existing EEG abnormalaties?
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hyperventialtion: absence seizure
intermittent photic stimulation: will photconvulse at 15cps in pts with epilepsy audtiroy stimulation sleep deprivation |
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auditory stimulation and sleep deprivation are mimicers of what?
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abnormal EEG
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what is the lobe most likely to have abnromal EEG actvity?
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temporal lobe
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what is partial or focal epilepsy?
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form of seizure that begins in a restricted brain region and REMAINS LOCAL or spreads to adjacent cortex
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state of pt in partial/focal epilspy?
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pt remains conscious
EEG spikes only on a few channels |
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ex of pertial/focal epilepsy
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jacksonian motor seizure
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what is a generalized or NON focal epilepsy?
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form of seizure that involves large parts of the brain right at the start of the seizure
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state of pt in gerneralized/non focal epilepsy?
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pt is unconscous
EEG siezure activity on all EEG channels at teh same time |
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ex of generalized non focal epilspsy?
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Absence seizures (petit mal): spke and wave
Grand mal seizure: alternative pds of tonic and clonci bod mvmts |
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waht is an Absence sizure?
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3Hz spike and wave
pt doesn't fall***, but they are unconscious |
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what is a grand mal sizure?
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pt falls, and they are unconscous
alternating tonic (pds increased muscle tone) and clonic (jrky mvmts) |
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what must you be careful of with postop hyponatremic pts?
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after surgery pts are hyponatremic b/c increased ADH
must bring Na levels back up SLOWLY, bc overly rapid elevation of plasma Na may cause neurologic symptoms in the pt bc hypotnoic bain cells intially cuase brain to swell then if you Tx too fast, brain cell will shrink too fast |
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is the sleep/wake cycle dependent on the visual system or zeitgebers (time cues)?
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no, it is a endogenous generator but w/o the normal zeitgebers to entrain the sleep/wake cycle to 24hrs, the human sleep/wake will increase to 26hrs
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what would happen ot the sleep/wake cycle w/o the zeitgebers
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the sleep/wake cycle will increase to 26hrs
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what is neural system regulating circadian rhtym?
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suprachiastmatic nucleus in ant hypothal
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what are the circumventricular organs?
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they lack BBB
pinal gland area postrema subfornical organ |
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job of subfornical organ?
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sense hyper or hypo natremia and send axons to cause para and supraoptic nuclei to fire
**osmo R |
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how do retinal luminance receptors regulate circadium rhtyms?
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retinal luminance is monitered by MELANOPSIN (not rhodopsin) to the suprachiasmatic nucleus then to super cervial ganglion and finally to pineal gland where melanin is released in the DARK into the blood
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when is melanin released?
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melanopsin r's sense retinal LUMINENCE (not contrast) and send info to Suprachiasmatic nucleus which then goes to super cevical ganglion then to the pineal gland
the pineal gland secretes melatonin form the pineal gland into the blood |
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what tract goes from the mamillary bodies to the ant thalamus?
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mamillothalamic tract
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when are the 2 major sleep "gates" during 24hr?
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one during evening
one during mid afternoon |
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what are the 3 states of consciousness of the brain?
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1. wake
2. rapid eye mvmt sleep (REM) 3. NON-REM sleep (NREM) |
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what do we use to identify the states of consciusness?
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EEG, EMG, EOG
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state of EEG, EMG, EOG during wake?
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EEG: low voltage, high freq beta waves
EMG: high EOG: eye moving up down and left to right, fast eye mvmts |
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how is NON REM identified on the basis of EEG, EMG, and EOG?
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EEG: high voltage, low freq
EMG: low EOG: none |
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how is REM identified on the basis of EEG, EMG and EOG?
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EEG: low voltage, high freq (beta)
EMG: none (paralyzed except diaphragm) EOG: eyes moving up/down , left/right (CN 3,4,6 NOT paralyzed) |
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awake state is associated with what type of wave/
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beta
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what 3 factors was REM identified based on?
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1. low or absent muscle tone
2. bursts of rapid eyeball mvmt 3. brain waves similar to beta waves |
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what is the REM state also refrred to as?
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Paradoxical sleep or desynchronized sleep
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is REM separte from orthodox sleep?
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yes, the rest of sleep is called NON REM sleep
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80% of ppt woken up in REM report waht?
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vivid, active dreams
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waht type of drams to ppl woken up from REM have?
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vivid, active
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how do we know that the brain is AUTOstimulated in REM?
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b/c of the presence of beta waves, a highly active brain wave pattern
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state of mm in REM?
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atonic (except extraocular mm, diaphraghm) so the body is paralyzed while the brain is being activated
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state of alpha motor neurons in REM?
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inhibited; afferent sensory input inhibited
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is afferent sensory input during REM inhibited or active?
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inhibited
inhibt alpha motor neurons going out, and sensory going in |
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what is Phasic REM
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encompasses ABRUPT changes in respiration, blood pressure, heart rate as well as whole body twitches and jerks in assoicateion with bursts of rapid eye mvmts (saccadic)
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when do we see whole body twitches and jerks?
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in phasic REM in assoication with burst of rapid eye mvmts (saccadic0
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how many REM sleep periods are there per night?
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4 or 5
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what percent of total sleep time each night is spent in REM?
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20% with each REM pd lasting 20 min
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how long do each REM period last?
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20min
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which REM of the night is the shortest?
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first REM of the night
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how do lenght of REM change during the night?
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first one is shortest
each successive REM sleep pd becomes longer than the previous one |
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what is the ultradian rhythm?
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less than 24hr rythym of 90-100 min during which REM and NREM alternate with each other
ex: NR-70min then R-20min next cycle NR-60min and R-30min (each successive REM is longer) |
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when is REM sleep more prominent?
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in the latter portion of the night
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if each REM gets successivley longer, what happens ot Stage IV sleep?
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decreases and might only see stage 2 NREM in latter portions of night
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NREM makes up what percent of sleep?
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80%
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NREM is also called?
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Slow wave sleep=delta waves
synchronized sleep |
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what are the 4 stages of NREM?
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1: brief transition phase, drowsy state b/n wake and sleep, low voltage with mixed EEG freq
2: signs of spindles and K complexes in EEG 3: 20%-50% of EEG has DELTA waves 4: >50% has DELTA waves |
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what is stage 1 NREM?
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BRIEF transition phase
drowsy state b/n wake and sleep low voltage mixed EEG frq |
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in what NREM stage do we see spindles nd K complexes?
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stage 2
spindles = NREM longer (can also see spindles in 3) |
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what is stage 3? stage 4?
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20-50% of EEG has DELTA waves : 3
>50% has DELTA waves: 4 |
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voltage and freq in stage 4?
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increase voltage
low freq |
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as we progress through the sleep stages what happens?
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incrase amplitude
decrease freq |
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high freq spike clusters are seen when?
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spindles
stage 2 NREM |
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how long does it roughly take to get from stage 1-4?
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1 hr
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why is stage 4 sleep called deep sleep?
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most difficult stage to awaken someone from
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early portion of sleep is composed of what stages of NREM?
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stages 3/4 the delta stages
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what happens to stage 3/4 as the night progresses?
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less stage 3 and 4
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how does waking someone in NREM diffrent from waking someone in REM?
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woken in REM: vivid dreams (flying)
woken in NREM: report mental acivity but NO vivid dream reports (ex: bland dreams like balancing checkbooK) |
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what type of mvmts do we see in NON REM?
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slow rolling eye mvmts in ANY STAGE
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what is thes state of skeletal mm in NREM?
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NOT paralyzed, but muscle tone is less than in the awake state
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which stages of sleep are dificult to awak from?
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stage 3 and 4
adults: not alert chilcren: very confused |
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waht are some things seen in children in NON REM sleep that dissappear at puberty?
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sleepwalking (somnambulism)
bed wetting (enuresis) night terrors (pavor nocturnus) |
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what is pavor nocturnus?
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night terrors that disseapear at puberty
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waht is somnabuliusm?
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sleepwalking that disseapears at puberty
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what is enuresis?
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bed wetting that disseapears at puberty
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what happesn to sleeping time per day with age?
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decreases espcially NREM sleep
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what happens to REM sleep with age?
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much greater as a baby then with age decreases and stays at ~20%
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amt of REM in newborn?
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50% REM
nl 20% |
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how many hrs do infants sleep? how much of that is in REM?
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16h/day
50% (8hr) REM |
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how many hrs do adults sleep? how much of that is in REM?
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8hr/day
20% REM |
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waht happesn to stage 4 with age?
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decresae
absent in old age |
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what does sleep require?
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active process that requires brainstem and hypothalamus to be intact
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what are the brainstem and hypothalamus needed for?
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sleep!
b/c sleep is active process |
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waht is the ascending reticular activating system critical for?
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maintenance of consciousness
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where is teh ascending reticular activating system located?
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uppper brainstem-diencephalic jxn
midbrain and pons area electrically stimulating a group of cholinergic neurons that lies near the junction of the pons and midbrain causes a state of wakefulness and arousal (the name “reticular activating system” was therefore given to this region of the brainstem |
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lesions in ARAS produce waht?
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coma
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waht is the ARAS composed of?
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interconnected systems regulated by the pontomescencephalic reticular formation system
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waht makes 5HT?
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raphe nucleues
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waht makes NE?
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locus ceruleus
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waht makes Ach?
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nucleus basalis of Meynert
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activity of what type of neurons is impt in REM sleep?
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activity of cholinergic neurons in the reticular activating system is a primary cause of wakefulness and REM sleep, and that their relative inactivity is important for producing non-REM sleep.
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which neurons are active during the awake state?
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monoaminergic and cholinergic systems are active during the waking state and suppress REM sleep.
increase in Ach, NE, 5HT |
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how does the activity of cholineric neurons and NE and 5HT change with NREM?
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decreased activity of the monoaminergic and cholinergic systems leads to the onset of non-REM sleep
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how do levels of Ach, 5HT and NE change with REM?
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In REM sleep, the monoaminergic and serotonin neurotransmitter levels markedly decrease, while the cholinergic levels increase to approximately the levels found in the awake state.
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fxn of sleep?
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unknown: impt for maintenance of CNS and PNS fxn
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what happens in sleep deprivation?
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prolonged wakefullness is associated with progressive malfxn of the mind and nervous system: difficulty concentrating, irritable, decreased motor skill performance (can't drive car)
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after total sleep deprivation, what does recovery sleep show?
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rebound in NONREM stage 3 and 4 that occurs 1st
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if you are deprived of all sleep (NON and REM) waht happens when you finally do get to sleep?
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NON REM stage 3 and 4 occur first
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which type of sleep is critical for life?
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REM
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what happens in recovery sleep after being REM sleep deprived?
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REM sleep rebound wich makes up the previous REM sleep loss
can go straight from wake to REM state and REM lasts long time |
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what happens to the REM latency in recovery sleep from REM deprivation?
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decrease in REM sleep latency (time to first REM period), increase in the REM sleep pd duration
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narcolepsy is a disorder of what type of sleep
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REM disorder
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waht is narcolepsy?
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REM sleep disorder
pts have trouble staying awake during the DAY sleep attacks of 5-30min duration (attacks b/c sleep is ACTIVE) |
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latency of REM in narcoleptics?
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very short-sleep onset REM (go from wake to REM with no muscle tone)
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what do narcoleptic dogs lack?
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hypocretins-orexins (HO), peptides in hypothalamus, which project to reticular acitivating system
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waht type of pts lack hypocretins-orexcins, peptides in hypthalamus, that project to reticuar formation?
|
narcoleptics
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if narcoleptics have sleep attacks during the day, waht hapens to them at night?
|
disrupted night sleep
fragmented but sleep no longer than normal go from W-NR-R-W-NR-W |
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what pts are subject to cataplexy? what iss this?
|
narcoleptics
TRANSIENT muscular paralysis immediatly following sudden emotion (anger, laughter, sex) pt is conscious but CAN'T move |
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in cataplexy, is the pt conscious?
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yes, but cannot move: transient msucle pralysis seen in narcoleptics
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what can cataplexy develop into ?
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REM sleep with sleep onset hallucinations
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what is sleep paralysis and who do we see this in/
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transeint muscular paralysis while drifiting into or out of sleep
seen in narcoleptics pt is conceous but cannot move |
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what is similar b/n sleep paralysis and cataplexy?
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pt is consceous but cannot move
both transient muscle paralysis cataplexy: following sudeen emotion paralysis: while drifting into or out of sleep |
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what pts are subject to cataplexy, sleep paralysis, and hallucinations?
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narcoleptics
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when do narcoleptics have hallucinations?
|
start of sleep: hypnAGOGIC
end of sleep: hypnOPOMPIC hypnagogic can occcur with cataplexy |
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waht is DIMS?
|
insomina: Disorder of initiating and maninting sleep
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differentiate difficulty falling asleep b/n normal, narcoleptic and insomniac?
|
normal: 15-20min
narcoleptic: 2-3 min insomniac: 1-3 hours |
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if you have insominia, what happens to your NON REM latency?
|
increasing greatly
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what is sleep apnea?
|
lack of breathing mvmts during sleep
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what can sleep apnea lead to?
|
daytime sleepiness b/c difficulty in maintaing a normal sleep pattern
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waht are the 3 types of sleep apnea?
|
obstructive
central mixed |
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what is obstructive apnea?
|
airway obstructed (soft tissue occlude airway) in spite of huge swngs in intrapleaural (esophageal) pressure
pressure becoms very negative |
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waht is central apnea?
|
airway is OK
NO swing in esophageal pressure seen resp ctners in medulla stop firing |
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what is mixed apnea
|
central sleep apnea develops into an obstructive apnea
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how do you improve sleep apnea?
|
weight redxn or surgery will improve sleep pattern
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waht is CPAP?
|
continous positive airway pressure seen with sleep apnea: put in splint to keep airway open
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what is REM sleep behavior disorder (RSBD)?
|
excessive mvts during REM sleep: pt has pathological absence of muscle atonia during REM sleep: muscle tone stays high, get up and act out dreams but this is not sonombolism
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who is REM sleep behavior disorder seen in ?
|
elderly males
muscle tone stays high and they get up and act out dreams |
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how does REM sleep compare physiologically to NREM and wake?
|
intermediate but with a very large standard deviation: HR can exceed awake state thefore impt to give drug to decrease REM in MI patient
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when during sleep are physioogic patterns wthe lowest?
|
NREM which is 80% of total sleep
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