Neuro 2 Flashcards

Question

What are the sensory receptors of the otolich organs?

Answer 1

Sensory apparatus of utricle + saccule = maculae Macula in utricle orientated in horizontal plane >Saccule - vertical plane Maculae also have set of cilia, protruding into otolith membrane >Embedded within this membrane are CaCO3 crystals - otoliths

Answer 2

Tilt of head Otoliths greater density than endolymp, moves otoliths first + the otolith membrane in which they are embedded >Distorts jelly + moves cillia Backward - direction of kinocilium - depolarisation Forwards away, hyperpolarisation, decreased APs

Answer 3

Projections from vestibular nuclei on one side project ipsilaterally, bilaterally and contralaterally to desc motor pathways (+extraocular nuclei - from muscles) Vestibular nuclei receive input from proprioceptors signalling limb + body position, also from neck and eye muscles Vestibular nuclei then project via thalamus to cerebral cortex kinaesthesia (the perception of movement + body position)

Answer 4

Tonic labryinthe reflexes Dynamic righting reflexes Vestibulo-occular reflexes

Answer 5

Keep axis of head in a constant relationship with the rest of the body. Use information from maculae and neck proprioceptors.

Answer 6

Afferents from semi-circular canals project and connect (within the vestibular nuclei) to afferent fibres travelling to the extraocular nuclei >have strong input to influencing eye movement. visual system sends powerful descending projections which control posture. >demonstrated by increased difficulty experienced with balance with closed eyes

Answer 7

People with destruction of vestibular apparatus can still maintain good balance if movement is relatively slow and eyes are open. But lost immediately on closing eyes.

Answer 8

Static | Dynamic

Answer 9

Tilted head, eyes intort/extort to compensate, so that over a certain range, the image stays the right way up.

Answer 10

series of saccadic eye movements that rotate eye against direction of rotation of head and body so original direction of gaze is preserved despite head rotating. The extent of eye movement is restricted; when eyeball comes to the end of its range of movement, rapidly flicks back to the zero position i.e. straight ahead. If rotation continues the slow phase starts again, then flicks back. By convention, direction of nystagmus is the direction of the rapid flick back R rotation = R nystagmus

Answer 11

Post rotatory | Caloric stimulation

Answer 12

Subjects rotated in Barany chair. If rotate to left - during acceleration get left nystagmus. At end of rotation, for ~20 seconds, during deceleration get a right nystagmus. Due to endolymph catching up - now pushing cupula in opposite direction.

Answer 13

When outer ear washed with cold or warm fluid, temperature difference from core gets through thin bone and sets up convection currents which affect the endolymph. Warm fluid causes nystagmus towards affected side, cold away from affected >(COWS – Cold Opposite, Warm Same). Stimulation without movement can cause nausea + vomiting

Answer 14

Powerful maintained stimulation of the vestibular system - can give rise to kinetosis Motion sickness is most likely to occur if visual and vestibular system inputs to the cerebellum are in conflict e.g. if the vestibular system indicates rotation but the visual system does not. cerebellum generates a “sickness signal” to hypothalamus to bring about ANS changes >BP decrease, dizziness, sweating + pallor

Answer 15

Unknown exactly Something below level of mid pons actively sending inhibitory impulses to cortex Suggested that reticular formation at brain stem (associated with state of conciousness) >Sends projections to thalamus + higher cortical areas >Drugs blocking serotonin inhibit sleep, unknown how Some sort of compound, probably peptide, in CSF contributes towards sleep

Answer 16

Suprachiasmatic nuclei (SCN) in thalamus role in induction of sleep Electrical stimulation of SCN can promote sleep Damage to SCN disrupts sleep/wake cycle

Answer 17

Hypothalamus releases orexin (hypocretin) - excitory neurotransmitter needed for wakefulness Orexin active in waking state Stop firing during sleep Defective causes narcolepsy

Answer 18

Look at behaviour, speech patterns, content, writing, calculating skills Brain activity - EEG (Electroencephalogram)

Answer 19

Alpha Beta Theta Delta

Answer 20

Alpha - relaxed awake | High frequency, high amplitude

Answer 21

alert awake | Higher frequency, lower amplitude

Answer 22

Deep sleep; Awake: common in children , emotional stress + frustration in adults low frequency, vary in amplitude

Answer 23

deep sleep | Low frequency, high amplitude

Answer 24

Asyncrhnous waves due to multiple processes | NOT due to low activity

Answer 25

5 stages: 1-4, 4-3-2-5, back and forwards 1 slow wave, non REM sleep. Slow eye movements, light sleep easily roused. >High amplitude low frequency theta waves 2 Eye movements stop, frequency gets slower >Rapid waves called sleep spindles (occur in burts) - cluster of 12-14hz 3 High amplitude, very slow (2hz) delta waves interspersed with short episodes of faster waves, spindle activity slows 4 Exclusively delta waves >3+4 = deep sleep 5 (REM sleep - dreams occur. Fast waves - like when being awake

Answer 26

Sleep in first few hours Most restful Associated with decreased vascular tone (and BP), respiratory + basal metabolic rates (decrease in BP) Dreams occur but rarely remembered

Answer 27

5-30 mins every 90 min, often more frequent later Dreams mostly occur in REM Eye muscles show burst of rapid activity - profound inhibition of all other skeletal muscles due to inhibitory projections from pons to spinal cord. >Prevents acting out REM sleep dependent on cholinergic pathways within reticular formation + their projections to thalamus, hypothalamus + cortex. Anticholinesterases increase amount of time in REM sleep >HR/RR irregular, brain metabolism increases >EEG mimics beta waves Very difficult to arouse person from them

Answer 28

Impairment results in: Loss of cognitive function Loss of physical performance Sluggishness Irritability

Answer 29

``` Neuronal plasticity Learning + memory Cognition Clearance of waste products from CNS Conservation of whole body energy Immune function ```

Answer 30

``` Insommnia Sleep terrors Nightmares Somnambulism (sleep walking) Narcolepsy ```

Answer 31

Chronic inability to obtrain necessary quality/amount of sleep for daytime behavious a) Chronic, primary - no identifiable cause b) Temporary, secondary insommnia - response to pain, bereavment or other crisis

Answer 32

Strong visual component seen in REM. Waking will result in nightmare stopping Terror - occur in deep delta sleep, common in ages 3-8 >Occur early in night >Children thrash + scream - may sit/stand up with eyes open but not awake >Often fail to recognise parents >Child doesn't remember episode next morning

Answer 33

Occurs only in non-REM often 4, more common in children/young adults Walk with eyes open, can see + avoid objects, carry out complex tasks No memory of episode

Answer 34

Enter directly into REM with little warning Very dangerous Linked to dysfunctional orexin release

Answer 35

Biological body clock ~ 24hrs Entrained, with light having effect Nerve fibres pass through SCN - potential cause, but not only factor as blind people still have same body clock If SCN destroyed, body clock rhythm lost

Answer 36

Thought processing Integration of all sensory information to make sense of situation Requires ability to remember Requires motivation

Answer 37

Limbic system

Answer 38

Most primitive part of cortex Four areas - hypothalamus, hippocampus (associated with memory), cingulate gyrus, amygdala Collectively responsible for instinctive behaviour, and emotive - driven by reward, punishment`

Answer 39

Electrical stimulation of certain areas in limbic system in conscious patients -> intense feelings of wellbeing, euphoria + sexual arosual (reward areas) Other areas terror anger, pain - punishment areas Central spects to learning - form affective components of sensory experiences

Answer 40

Experiences neither rewarding or punishment barely remembered - habitation Rewarding/punishing remembered

Answer 41

Central to learning + formation of memories People with bilateral hippocampal damage - both immediate (sensory) memory but unable to form long term memories Reflexive memory intact

Answer 42

Immediate/sensory Short-term Intermediate Long-term

Answer 43

ability to hold experiences in the mind for a few seconds. Based on different sensory modalities. Visual memories decay fastest (<1s), auditory ones slowest (<4s).

Answer 44

seconds - hours. "Working Memory" short term tasks such as dialling a number, mental arithmetic, reading a sentence. Associated with reverberating circuits.

Answer 45

hours to weeks e.g. what you did last weekend. | Associated with chemical adaptation at the presynaptic terminal.

Answer 46

hours to lifetime. e.g. where you grew up and your childhood friends. Associated with structural changes in synaptic connections.

Answer 47

Short-term memory is an electrical phenomenon. It depends on maintained excitation from reverberating circuits i.e. they need to be constantly refreshed. Reverberating circuit keeps memory alive. If deemed significant, consolidation of memory If insignificant, reverberation fades If refreshing effect disrupted, presents as amnesia

Answer 48

Anterograde | Retrograde

Answer 49

Inability to recall events following injury >Either short lived or permenant Destruction of hippocampus results in permanent inability to form new memories

Answer 50

Can't remember events leading up to event (short term, long term normally unaffected) >Often presents with anterograde If thalamus damaged, hippocampus spared, only retrograde amnesia seen

Answer 51

Chemical changes in presynaptic neuron Increasing Ca2+ entry to presynaptic terminals, Increases neurotransmitter release ("strengthens" synapse"

Answer 52

Structural changes at synapses >Increase in NT release sites on presynaptic membrane. >Increase in number of NT vesicles stored and released. >Increase in number of presynaptic terminals At same time greater change in graded membrane potential in post-synaptic cell (EPSP) is often observed. This “strengthens the synapse”, is called Long Term Potentiation forms basis of much learning and memory.

Answer 53

Declarative | Procedural/ Reflexive/Implicit Memory:

Answer 54

Abstract memory for events (episodic memory) words, rules and language (semantic memory). Is based mainly in the hippocampus.

Answer 55

Acquired slowly through repetition. Includes motor memory for acquired motor skills (tennis), and rules based learning such as, in the UK, always driving on the left. Thinking about these skills (“memories”) often impairs performance! Is based mainly in the cerebellum. Is independent of hippocampus

Answer 56

Similar process in cerebellum during motor learning Selective strengthening of synaptic connections through repetition (minutes --> hours) >During which, simply exists as electrical activity General anaesthesia or electrical convulsion, prevent memories of experiences immediately before event being consolidated (memories will be lost) Requires attention New memories coded, then stored in sensory association areas of cortex Stored alongside similar memories

Answer 57

Frontal cortex gates a papez circuit Reverberating activity then continues between the Papez circuit, frontal cortex, sensory and association areas until the consolidation process is complete. Different components of the memory are laid down in different parts of the cortex, eg visual component in the visual cortex, auditory in auditory cortex, etc. As such, recall can be evoked by multiple associations. Many memories have strong emotional components to them, ie pleasant or unpleasant.

Answer 58

``` Mechanoreceptor Chemoreceptor Thermoreceptor Nocioreceptors Proprioreceptors ```

Answer 59

They transduce their adequate stimulis into depolarisation (receptor (generator) potential Size of receptor potential encodes intensity of stimulus receptor potential then evokes firing of action potentials for long distance transmission >frequency of action potentials encodes intensity of stimulus receptive field encodes location of stimulus gives information on the modality, intensity & location of the stimulus

Answer 60

Density of innervation + size of receptive fields

Answer 61

Aα & Aβ eg muscle spindles, golgi tendon organs etc

Answer 62

project straight up through ipsilateral dorsal columns synapse in cuneate & gracile nuclei the 2nd order fibres cross over midline (decussate) in the brain stem & project to reticular formation, thalamus and cortex

Answer 63

synapse in the dorsal horn the 2nd order fibres cross over the midline in the spinal cord project up through the contralateral spinothalamic (anterolateral) tract to reticular formation, thalamus and cortex

Answer 64

causes loss of touch, vibration, proprioception below lesion on ipsilateral side

Answer 65

causes loss of nociceptive & temperature sensation below lesion on contralateral side

Answer 66

How the receptors respond to the stimuli In rapidly adapting receptors, they stimulate lots to start with, and then stop firing until the stimulus is removed (with a few as it gets removed) In slowly adapting receptors, action potentials are fired for the duration of the stimulus

Answer 67

Where multiple neurones feed into a single neurone >saves on neurones >but reduces acuity >may underlie referred pain >May also result in multiple stimuli triggering a single neurone - nonspecific pathways Will know there is stimulus, but not sure which it is

Answer 68

activation of one sensory input causes synaptic inhibition of its neighbours gives better definition of boundaries cleans up sensory information

Answer 69

Activated by low pH, heat (via ASIC, TRPV1 etc) local chemical mediators (eg bradykinin, histamine, prostaglandins)

Answer 70

NSAIDs TENS - trans cutaneous electric nerve stimulation Opiates

Answer 71

reduce sensitivity of nociceptors block transmitter release in dorsal horn (hence epidural administration) activate descending inhibitory pathways

Answer 72

prostaglandins sensitise nociceptors to bradykinin NSAIDs are analgesic (and antipiretic & anti-inflammatory) because they inhibit cyclo-oxygenase which converts arachidonic acid to prostaglandins so NSAIDs work well against pain associated with inflammation

Neuro 2 Flashcards

(96 cards)