Flashcards in Physiology Deck (142):
Describe the physiology of an neurone from beginning to end and the function of each division
1. Dendrite- Stimulated by environmental changes/ activity of other cells
2. Cell Body- nucleus (loose chromatin + prominent nucleolus); mitochondria (lots), rER, GA, Cytoplasma (perikaryon)
3. Axons- conduct AP, regenerative
4. Synaptic Terminals- send signal out to another neurone/ organ/ muscle/ gland
What characteristics does a neurone have to ensure are not lost?
Long Living + amitotic (divide without mitosis)
Axons can grow back if damaged
What part of the neurone, if damaged cannot grow back?
Neuronal cell body- irreversible damage
What are the 3 types of neurone? How do they differ and where are they found?
1. UNIPOLAR- Cochlear Nucleus- NO dendrite, 1 synapse
2. MULTIPOLAR- Brain- 1 neurone, multiple synaptic terminals
3. BIPOLAR- Olfactory Mucosa (retina- rods + cones)- 1 dendrite, 1 synapse
4. PSEUDOUNIPOLAR- DRG- 1 dendrite, 1 synapse but DONT have to go through cell body
What is the action of Schwann Cells and Oligiodendrocytes?
Schwann Cells (PNS) + Oligiodendrocytes (CNS) form myelin sheaths around axons by secreting a membrane that wraps around axon to help carry nerve impulses.
Salatory connection- AP can jump via nodes of ranvier
What is the difference between myelinated and non-myelinated axons in PNS?
Non- myelinate axons in PNS still wrapped in Schwann Cells but myelin sheath not fully formed
Where are myelinated axons found?
White Matter + Tracts (bundles of axons carrying specific information throughout white matter)
Where are unmyelinated axons found?
Grey Matter + Nuclei
What are the subtypes of glial cells in the PNS? Where are they found + what is their function?
1. Satellite Cells (PNS)- Surround neuronal cell bodies
2. Schwann Cells (PNS)- Myelination
What are the subtypes of glial cells in the CNS? Where are they found + what is their function?
1. Oligiodendrocytes (CNS)- Myelination
2. Astrocytes (CNS)- most common, surround synapses + capillaries (BBB) + help in K buffering
3. Microglia (CNS)- Phagocytosis, scar tissue formation
4. Ependymal- Line Ventricles
What is the BBB made from? What is its function?
Maintains a stable brain environment and stops harmful AA + ions from entering.
Tight Junction via endothelium
Thick basal lamina
Astrocytic foot process'
NOT in hypothalmus + posterior pituitary
Where is the BB absent?
Hypothalamus + Posterior Pituitary
What must the composition of a drug be to pass the BBB?
Lipophilic + Vectorial to pass
What kind of reflexes are there?
Involuntary stereotypical pattern of response brought on via a sensory stimulus
1. Sensory Reflex- Mediated at level of spinal chord
2. Monosynaptic- stretch reflex
3. Polysnaptic- flexor reflex
What is the stretch reflex?
Controls muscle tone + posture
1. Tendon streched
2. Intrafusal muscle fibres stretched
3. Sensory neurone activated
4. Monosynaptic Reflex Arc/ Polysynaptic Reflex Arc to inhibitory interneurone
What is the Flexor (+ crossed extensor) Reflex?
1. Pain Stimulus
2. Sensory Neurone Activated
3. Polysynaptic Reflex Arc
= Flexion and Withdrawl from noxious stimulus + Crossed Extensor Responds to contralateral weight bearing limb (weight bearing limb)
What does the autonomic NS innervate? What are its 2 classifications and key features?
Involuntary control of smooth muscle, cardiac muscle + glands (visceral organs)
2 neuronal pathway
1. Sympathetic - Thoracolumbar outflow with preganglia near spinal chord + postganglionic fibres targeting every cell in the body.
2. Parasympathetic- Cranialsacral outflow with preganglia near target organ + post ganglia at exocrine glands + heart.
What is a nerve conduction study?
Examine nerve function of peripheral nerves + muscles
Conduction Velocity (speed on an impulse along a nerve) measured via-
Distance between impulses/ Time taken between impulses
What are sensory studies? What can they show?
Stimulate sensory nerves- measure sensory + motor function
Show conduction block (slow/ stopping of impulses due to loss of salutary conduction.
NOTE: Below loss whatever gets through will be conducted as normal
What is Electrophysiolohgy? What does it look for?
Identify section where conduction block/ demyelination has occurred eg./ ulnar neuropathy
What is Electromyography (EMG)? What can it be used to diagnose?
Fine needle in muscle measure difference between outer sheath and inner core- allows you to isolate AP from individual muscle fibres within one motor unit/ can record 2 muscle fibres within 1 motor unit (should be same/ little/ no delay between stimualtion)
In NMJ disease this relationship is lost= Jitters eg./ Myaesthsia Gravis (autoimmune)
What is Electroencephalogram? What can it be used to diagnose?
Electrical activity (of cortical neurones) WITHIN the brain
eg./ Epilepy, Encephalopathy, Sleep + altered consciousness
Electrodes on scalp
Ambulatory- day + night
Video telemetry + film
What are the 3 types of sensory receptors?
1. Mechanoreceptors- Pressure/ load
2. Chemoreceptors- pH
3. Thermoreceptors- Temperature
4. Nociceptors- Noxious/ Damaging stimuli via free nerve endings
5. Proprioceptors- Sense of body in space via muscle spindles
What are the 4 types of complex sensory structures? What are they tuned into?
Meissners- Light touch
Pacinian- Deep Pressure
What is the process of signal transduction?
Sensory receptors stuck in skin , whole cell sending info- transduce adequate stimulus to a depolarisation (generator potential- size encodes intensity of stimuli)- V gated Na channels open- AP produced (frequency of AP corresponds to intensity of stimuli)- Receptive field encodes location of stimulus- axons bring to CNS
What are receptive fields?
Neurones within small fields that provide modality (type of receptor activaion), intensity + location
Acuity (resolution) is different due to 2 point discrimination (if big receptive field won't be able to differentiate between 2 point as same neurone activated)
What type of primary afferent fibres do you get and how are they different from each other?
Aβ- Large, myelinated, fast (30-70ms)=touch, pressure + vibration
Aγ- Small.=, myelinated, slow (5-30ms)= cold, fast pain, pressure
C- Unmyelinated, slowest (0.5- 2ms)= warmth + pain
How do mechanoreceptive (A⍺ + Aβ) fibres transmit sensory information?
Up through IPSILATERAL dorsal column- synapse in cuneate + gracile nuclei-
2nd order fibres cross over at midline (decussate) in brainstem- project to reticular formation, thalamus + cortex
How do thermorecepetors + nociceptors (Aγ + C) fibres transmit sensory information?
Immediate synapse into dorsal horn- 2nd order cross at midline- up through anterolateral tract- to reticular formation, thalamus + cortex
What does adaptation have to do with processing sensory information?
Generator potential produced at sensory terminals
1. Rapid Adapting (||||||)- Fades, cells bodies loose threshold fast and stop firing eg./ loose ability to feel heat.
2. Slow Adapting (| | |)- Keep firing in response to strained stimuli eg./ muscle spindles are always aware where muscle is
What does convergence have to do with processing sensory information?
Several Neurones synapsing into one
Reduced acuity (as merge receptive fields)
Underline 'referred pain'
1. Specific- convergence is of the same modalities./ Reffered pain of a heart attack going to L arm
2. Non-Specific- Convergence between 2 different modalities. Don't know field/ stimulus just alert brain to region in distress
What does lateral inhibition have to do with processing sensory information?
Activation of 1 sensory input causes lateral inhibition of the others- better definition of boundaries (easier for brain to pick up important info)
What type of pain is there and what is it caused by?
1. Sharp Stabbing- Aγ (localised)
2. Diffuse Throbbing- C (harder to localise)
3. Acute- Chronic (long term changes in synaptic changes in thalamus + cortex)
4. Visceral Pain- Reffered Pain (poorly localised)
5. Phantom Limb Pain- Nueroma comes over damaged axons- fires AP- change in thalamus
How does nociceptive sensory information enter the spinal chord?
Asses Acute Pain
1. Afferent nociceptive fibres enter via dorsal root (cell bodies lie in DRG just outside spinal chord)
2. Nociceptive fibres synapse in superficial layers of the dorsal horn
3. 2nd order fibres cross close to region of entry and ascend via contralateral spinothalamic tract
What is the gate control theory of pain summarised?
The gate control theory of pain asserts that non-painful input closes the "gates" to painful input, which prevents pain sensation from traveling to the central nervous system. Therefore, stimulation by non-noxious input is able to suppress pain.
How does the gate control theory of pain work?
1. When no input comes in, the inhibitory neuron prevents the projection neuron from sending signals to the brain (gate is closed).
2. Normal somatosensory input happens when there is more large-fiber stimulation (or only large-fiber stimulation). Both the inhibitory neuron and the projection neuron are stimulated, but the inhibitory neuron prevents the projection neuron from sending signals to the brain (gate is closed).
3. Nociception (pain reception) happens when there is more small-fiber stimulation or only small-fiber stimulation. This inactivates the inhibitory neuron, and the projection neuron sends signals to the brain informing it of pain (gate is open).
4. Descending pathways from the brain close the gate by inhibiting the projector neurons and diminishing pain perception.
How can pain sensation be lost using the gate control theory?
If you rub or shake your hand after you bang your finger, you stimulate normal somatosensory input to the projector neurons. This closes the gate and reduces the perception of pain.
What is the analgesic pathway of NSAIDS?
Inhibit cycle-oxygenase (within archandonic acid) which produces prostaglandins- decreasing bradykinin release (less noxious stimuli to stimulate small fibres (γ/C) so inhibitory neurone is not activated- no signals up to brain
What is the analgesic pathways of opiates?
Eg./ Morphine (released epidurally)
Inhibit AP firing at nerve terminals
What is the analgesic pathway of local anaesthetics?
Block Na AP so all axonal transmission
What is trans-cutaneous electrical nerve stimulation (TENS)?
Electrical stimulation activates large diameter innocuous mechanorecpetors (in same body segment of painful stimulus)- endogenous opiod peptides (from interneurones in dorsal horn) activate Mu receptors stopping progression from 1st to 2nd order neurones
Where is area 4? What is its function?
Frontal Lobe Area 4= precentral gyrus- primary motor cortex
Involved in somatic representation of the contralateral half of the body via the Motor Homunculus
What is the motor homunculus?
Neurones in the PNS are related to moving a muscle group. Amount of motor cortex taken up doesn't vary on size but dexterity eg./ Hands and face take up large areas but trunk, toes, feet and genitals take up very small areas
What is area 44, 45? What is its function?
Frontal Lobe Inferior frontal gyrus- Brocas area of motor speech
= formulates speech via muscle movement
What is the job of the prefrontal cortex?
Higher cognitive functions- Intellect, judgement + prediction/planning
What is the function of the parietal lobe?
What is area 3,2, + 1's function?
Post central gyrus- primary sensory area (general sensations from contralateral side of the body) Sensory homunculus
What is the sensory homunculus?
Neurones/ Area proportional to degree of sensation in area eg./ Abdomen, pharynx and face take up large area but trunk and extremities take up fairly small sections
What is the job of the superior parietal lobe?
Interprets general sensory + consciousness/ awareness of contralateral half eg./ something in pocket
What is the job of the inferior parietal lobe?
Interface between somatosensory cortex + visual + auditory areas
In dominant areas= language function
Where is Wernicks area? What is its function?
Back part of temporal lobe, comprehension and understanding of speech
Most people have on Left lobe (remember dominant is contralateral to what 'handed' you are) even most left handed people have Wernicks in LHS.
What are areas 41 + 42?
Primary Audiotory cortex (Hechts convolutions) + Wernicks Area (in dominant hemisphere)
What kind fo fibres are in the inferior surface of the temporal lobe? What is their function?
Fibres from olfactory tract- concooius appreciation of smell
What is the function of the occipital lobe? What are the 2 important areas in it?
Area 17- Primary visual cortex
Area 18 + 19- Visual Association cortex (interprets visual images)
Where is the limbic lobe? What is its function?
Cingluate Gryrus (above the corpus callous)
Memory (info repeats around)
What areas of the brain interpret language?
Area 44, 45- Parietal Lobe Brocas Area (motor speech)
Wernicks Area- Temporal Lobe (dominant) auditory association
Describe the production and flow of CSF
1. CSF produced by the choroid plexus (lateral ventricle, 3rd roof + 4th roof/caudal) by active production (ATP) Na pumped into subarachnoid space and water follows (from BV)
2. Lateral Ventricle- Foramen of Munro- 3rd ventricle- Cerebral Aqueduct- 4th ventricle- Foramen of Magendie + Luschka- Around brain and spinal chord- Subarachnoid Space (most here)- Arachnoid Granulations (villi open when ICP is 3-5cm greater than dural venous sinus pressure= passive)- Venous Blood System
What is cognition? How is it achieved?
Cognition- integration of sensory information to make sense
Cerebellum integrates (multiple parallel processing unit)
Gives us the ability to learn and remember events due to nueronal plasticity ( neurones adapt their connections in response to learning)
What is the function of the subdivisions of the limbic system? What is its main function overall?
Instinctive behaviours- thirst, sex + hunger. Balances reward + punishment (drive for all concious behaviour) if an experience is neither rewarding or punishing you will forget as nothing to learn from
1. Hypothalamus- Emotion + ANS response
2. Hippocampus- Learning + memory (start)
3. Cingulate Gyrus- Emotion
4. Amygdala- Emotion + memory
What is the job of the hippocampus?
Learn + Formation new memories
What are the 4 different types of memory?
1. Immediate/ sensory- Few seconds, visual (<1s), auditory (<4s)
2. Short Term- seconds/hrs boring memory
3. Intermediate long-term- Hours/ Feels
4. Long Term- lifelong
A- Declaritive/ Explicit- Episodic (events), semantic (words, rules, language needs hippocampus)
B- Procedural/ Reflective? Implicit- Aquired slowly through repetition + motor memory (cerebellum independent of hippocampus)
How is short term/ long term memory produced?
Each synapse is in a reverberating circuit (excitatory)
If insignificant- reverb fades- no consolidation
Visual (<1s), Auditory (<4s)
If significant- reverb (harder when tired)- consolidation- long term memory
How is intermediate long-term memory produced?
Chemical changes at presynaptic neurones
Inc Ca entry to presynaptic terminals= Inc neurotransmitter release, strengthening the synapse
How is memory recalled?
Frontal Cortex + Limbic System enter significant memories into the papez circuit (cingulate gyrus- hippocampus- mammillary bodies- anterior thalamus) and back
This reverb between frontal cortex + papez means components laid down in different areas eg./ visual, auditory etc
What is contained in the circuit of Papez?
Cingulate gyrus- Hippocampus- Mamillary Bodies- anterior thalamus
Why do smells provoke long term memories?
Olfactory stimuli are relayed from olfactory tract through amygdala + hippocampus to prefrontal cortex (travels through limbic system)
What kind of sleep enforces long term memory consolidation/ reinforce weak circuits?
What kind of matter is found in the spinal chord?
White Matter- Nerve tracts from neurones
Grey Matter- Neurones (10layers- reed lamina)
-Low Threshold Mechano. Aβ (3+4)
-Nociceptive Specific Aγ+C (1+2)
-Wide Dynamic Range- noxious/non Aβ (5)
What is the pathway of pain?
1. STIMULI(tissue damage) picked up by Aγ (myelinated, fast) + C (unmyelinated, dull)
2. Nociceptors go into DRG (cell bodies) and in through dorsal horn
3. Synapse + decussation (Rexed Lamina 2,5) and goes up via-
A- Lateral Spinothalamic Tract- terminates at ventroposterior thalamic nuclei (fast + slow pain + temp to somatosensory cortex= spatial, temporal + initial pain)
B- Anterior-Ventral Spinothalamic Tract- medial thalamus- cingulate cortex + hippocampus (limbic, emotional component) + prefrontal cortex + insula + basal ganglia- descend from brain to dorsal horn-
How is peripheral sensitisation involved in pain modulation?
Spontaneous Pain- Spontaneous activity in nerve fibres
Change in nociceptors due to inflammatory mediators any stimuli eg./ thermo/mechano is a trigger
Innocuous (weak)- Allodynia- Decreased threshold for a response (range at which stimuli becomes noxious changes).
Hyperalgesia- Exaggerated response to normal/ supranormal stimuli
Spontaneous- Spontaneous pain in nerve fibres (dying nerve injury)
How is central sensitisation involved in pain modulation?
Response of 2nd order neurones to normal input (noxious + non)
1. Wind-up- winding up response to the input in activated synapses- homosynaptic activity- progressive Inc over course of stimuli mediated by neurotransmitter P + CGRP
2. Classical- Opening up of new synapses (heterosynaptic activity- glutamate)-NMDA. Outlast initial stimuli as keeps going but at low levels
3. Long Term Potential- Activated synapses by very intense potential (glutamate- NMDA + AMPA)
What is the difference between acute and chronic pain?
Acute < 1month, Physiological (obvious tissue damage), resolves on healing, protective, noxious stimuli, usually nociceptive.
Chronic >3-6mnths Pathological (pain beyond expected healing), no purpose, not always noxious stimuli (nociceptive/ neuropathic/ mixed)
What is nociceptive pain?
Nociceptors respond to noxious stimuli- typically localised at site.
Throbbing, aching/ stiff
Resolve when tissue heals/ chronic eg./ osteoarthritis.
Responds to analgesics
What is neuropathic pain?
Caused by primary lesion/ dysfunction in somatosensory NS eg./ neuroma
Painful lesion (pain may not be at site but in territory) almost always chronic
Responds poorly to analgesics
How do you treat 'pain'?
1. Transduction- NSAIDS, ICE, rest, LA blocks (peripheral nerve blocks)
2. Transmission- nerve blocks, opioids (act of spinal dorsal horn), anticonvulsants, surgery
3. Perception- education, cognitive behaviour therapy, graded motor imaging
4. Descending modulation- placebos, opioids, antidepressants, surgery- spinal chord stimulation
How is the motor system a hierarchy?
TOP TEIR: Cerebral Cortex (Motor cortex- plan, initiate + direct voluntary movement via visual, olfactory, auditory, emotional, intellect) + Basal Ganglia (gates proper initiation of movement) + Cerebellum (sensory motor coordination of ongoing movement)
MIDDLE TEIR: Corticospinal Tracts + Brainstem Nuclei (control spinal reflexes to coordinate posture and balance)
+ Sensory Neurones (integrate sensory input in)
LOWER TEIR: Descending control pathways- Motor Neurones Pools (⍺motor-neurones) on skeletal muscle)- Proximal Muscles mapped by medial motor neurones eg./ shoulder, Distal Muscles mapped by lateral motor neurones eg./ fingers
What kind of fibres are found in the dorsal horn?
How does the stretch reflex occur?
1. Stretch muscle causes intramural fibres in muscle spindles stimulates annular spiral ending (of muscle spindle afferents)
3. AP release- DRG- monosynaptic reflex- excitatory stimulation of ⍺motor neurones in ventral horn- back to muscles extrafusal fiibres- contraction
4. + motor neurones of antagonistic muscles are inhibited by interneuronal connections within the spinal chord
What are the important spinal chord levels of reflexes? Why is it important to know these?
Able to localise a problem by what reflexes are present/ absent
How does the flexor/ withdraws reflex work?
Mediated by nociceptors (pain receptors in skin, muscle + joints via Aγ fibres)
Polysnaptic (1 branch affects lots of muscles so difficult to localise) + Protective
Inc sensory Ops from pain receptors- excitatory interneurones- Inc activity in flexor muscles + antagonist extensors inhibited (via inhibitory interneurones)
Slower reflex than stretch as nociceptive fibres have a smaller diameter so conduct slower
What is the golgi tendon reflex?
Activated when damage is likely/ excessive load= Inc tension in tendon- inhibits neurone + muscle relaxes
Can be overridden by-
1. Strong descending inhibition hyperpolarising ⍺motor neurones
2. Descending inhibition of γmotor neurones (muscle spindles)
What is Babinskis sign?
Damage to CS tract- big toes up ( can also get in epileptic seizures + <1y/o as motor system not fully developed
What are the 3 ascending spinal tracts? What do they carry?
1. Lateral Spinothalamic- Pain + Temperature (
2. Anterior Spinothalamic- Light touch + Pressure
3. Fasiculus Gracilis + Cuneatus- Discrimitive touch, vibration sense + proprioception
Describe the pathways of ascending spinal tracts (anterior spinothalamic + fasiculus Gracilis + cuneatus )
1. Proprioceptors pick up touch, pressure etc
2. 1st order neurone picks up- Dorsal root- up column to medulla
3. Reaches gracile + cuneate nuclei- synapses- DECAUSSATION
4. 2nd order neurone travels up lemniscus in pons (contralateral) to VPL in Thalamus
5. 3rd order neurone to post central gyrus (parietal lobe)
NOTE: lesions above decussation control contalateral sensory loss whereas lesions below decasussation (below gracile + cuneate nuclei) control ipsilateral sensory loss)
Describe the pathway of ascending spinal tracts (lateral spinothalamic) why is it different?
1. Proprioceptors pick up extreme pain + temperature
2. 1st order neurone picks up and brings in through dorsal root of spinal chord
CROSSES AT LEVEL OF ENTRY (via 2nd order neurone)
3. Travels up to VPL in Thalamus- 3rd order neurone- post central gyrus (parietal lobe)
Crosses at level of entry as need to deal with immediately so more urgent pathway
NOTE: lesion will always cause contralateral sensory loss (if in spinal chord)
What are the 4 descending motor tracts? What do they carry?
1. Coricospinal- ⍺motor neurones- skilled motor to extremities
2. Reticulospinal- ⍺+ γ motor neurones- control of voluntary motor function- pontine + medullary subgroups, balance + body position
3. Rubospinal- ⍺+ γ motor neurones-facilitate flexors, inhibit extensors (balance control)
Describe the pathways of descending spinal tracts (motor)
1. Primary Motor Cortex (Cerebral Cortex- Area 4 + premotor + supplementary motor cortex in area 6 2xmaps)- down through corticobulbar tract- through cerebral peduncle
2. Collect to form a pyramid in upper medulla
DECAUSSATE (20% don't)- white matter of spinal chord- grey matter
3. Synapse to LMN at level it needs out- 2nd order neurone
4. Out via ventral horn to skeletal muscle
How is the cerebellum involved in coordination?
- ipsilateral proprioceptive tracts
- vestibular nuclei (balance + posture)
And calculates best way to coordinate muscles to ensure smooth muscle coordination
Sends info to cerebellar peduncles- cerebral cortex
What is the main difference between ascending and descending spinal tracts?
Ascending- 3 order neurones and carry sensory information to the post central gyrus (sensory homunculus) it decussates at gracile and cuneate nuclei (AS,FGC) or right away at the dorsal root of the spinal chord (pain- LS)
Descending- 2 order neurones and carry motor information from the precentral gyrus (motor homunculus) out via the ventral horn to skeletal muscles it decussates at the pyramid in the upper medulla
What are the differences between the corticospinal + rubospinal tracts? What would the difference in lesions be here?
Corticospinal is longer + more important than rubospinal
Both Synapse at ventral horn + at interneurones- muscle
Corticospinal starts in Motor cortex (4 +6) and descends through the internal capsule- thalamus- medulla- cross at pyramids. Rubospinal tract starts in red nucleus (midbrain) and crosses at the medulla (earlier)
1. A lesion affecting both tracts= loss of fine movements of arms + hands, can't move shoulders, elbows, wrists + fingers.
2. A lesion higher up (affecting CST only) will result in same deficits but after a few months functions reappear as RuST taken over
Describe the pathways and function of the vestibulospinal + tectospinal ventromedial pathways
Vestibulospinal- Descending, acts on ⍺+ γ motor neurones- stabilises head + neck. From vestibular nucleus- crosses at medulla- splits and sends info to both sides
Tectospinal- Descending, ensures eyes remain stable as body moves. From superior colliculus and crosses at medulla
What do areas 5+7 have?
Carry mental image of the body in space (proprioceptors, somatosensory + visual)
What is the function of area 6?
Where fine movement is made, imagined + seen ( if seen before- empathy, lost in autism)
How is the direction of a neurone determined?
Each neurone has a preferred direction when stimulated
Activity in increased before movement (firing less in other directions)- responses of all neurones combined- population vector- direction of movement
How do you correct postural instability?
Via feedback- Change in body position- brain vestibular nuclei- spinal chord motor neurones- correction
How does a feedforward mechanism effect movement?
BEFORE movement begins
Cortex- brainstem reticular formation nuclei- anticipatory adjustments
eg./ Contract biceps to pull handle but FIRST contract gastrocneimum leg muscle to ensure stability
What is the motor loop?
Feedforward/ predictive mechanism for higher level gait control
Information from the cortex (prefrontal, motor + sensory) is shared- excitatory (glutamergic) input to -
1. putamen- globus pallidus internal-GP external (before limb movements)
2. caudate + S.Nigra (before eye movements)- GP external- At rest GP neurones are actively inhibiting VL but excitation of putamen inhibits inhibitory GABAergic
- releases VLO (from ventral lateral nucleus of thalamus)- excitatory- boost SMA activity= feedforward mechanism
What parts of the brain aid sleep and consciousness?
Sleep- Hypothalamus + Suprachiasmatic Nuceli (electrical stimulation supports sleep via melatonin from pineal gland)
Conciousness- Hypothalamus + Suprachiasmatic Nuceli (orexin) + Reticular Foramen (via serotonergic neurones)
Describe the sleep cycle
inhibitory peptide signals dominate- excitatory neurones in ascending Reticular Activating System (reticular foramen- seratonergic) are relaxed- inhibitory cells fatigue- stimulate excitatory pathways in CNS + PNS- +ve feedback from PNS + CNS sustains wakefulness- active cells fatigue + excitatory signals fade- inhbitory peptide signals dominate etc
How does an Electro Encephalogram (EEG) look like in different levels of consciousness?
Electrodes placed on scalp (record neurones)
1. Relaxed, Awake- high frequency, high amplitude synchronised ⍺ waves (large net voltage but slow rising (Anasthesia- epilepsy)
2. Alert, Awake- High frequency, Low Amplitude, Asynchronised βwaves. (+ve/ -ve) net voltage change small
3. Theta Waves- Low Frequency, varying amplitude in sleep in kids/ emotional stress in adults.
4. Delta Waves- Low Frequency, Low Amplitude, in deep sleep (night terrors)
What are the stages of a sleep cycle?
1. Slow wave non-REM sleep, light, easily roused
2. Eye-movements stop, sleep spindles (rapid bursts), frequency slows
3. Difficult to rouse (spinal activity declines), very slow, Amp Inc again
4. Difficult to rouse, exclusively delta waves
What stages of sleep are difficult to rouse? Sleep talking also occurs here
Stages 3 + 4
What is REM sleep?
Look awake of EEG (as HR + RR inc)- dream here
Eye muscles show rapid activity but inhibitory projections from pons to spinal chord make all other muscles rigid
Depended on cholinergic pathways within Reticular Foramen and their projections to Thalamus, Hypothalamus + Cortex
NOTE: Anticholergics prolong REM sleep
Remember dreams here (nightmares)
Decreases with age, none in elderly
What is the physiological importance of sleep?
Neuronal Plasticity, Learning + Memory (synapses in brain adapt to receiving info)
Clear waste from CNS
Conserve Body Energy (C02 cerebral consumption inc during REM sleep)
How does sleep follow a circadian rhythm?
Suprachiasmatic Nucleus (hypothalamus, above optic chiasm) neurones have a 24hr cycle (optic nerve placement means they are sensitive to light and dark queues)
Damage would loose melatonin + orexin so loose circadian rhythm
What pathway do nerves take from external (PNS) to internal (CNS)
Sensory Input ( Visceral- organs, General- touch temp + pain, Special- taste smell hearing + balance)- Afferent Ap- DRG- Dorsal Horn- CNS- Ventral Horn- efferent- somatic motor (striated muscle)/ preganglionic- postganglionic efferent- Visceral/ Autonomic (smooth muscle in glands)
How many pairs of cranial nerves are there?
What is the Order of the 12 cranial nerves?
Describe the pathway and function of CN1 and clinical tests of its function
Foramina in cribriform plate (ethmoid bone)- SENSORY- SMELL
Clinical Test: Unilateral/ Bilateral smelling loss
Describe the pathway and function of CN2 and clinical tests of its function
Optic Canal- Optic Chiasm (cross)- Optic Tracts- SENSORY- VISION
Clinical Test: visual acuity (Snellings chart, visual fields, pupillary reaction, fundoscopy, colour vision (Ischara Plate)
Describe the pathway and function of CN3 and clinical tests of its function
Midbrain- Superior Orbital Fissure- SOMATIC MOTOR to Superior, Medial rectus, Inferior Rectus + Inferior Oblique Muscles + VISCERAL MOTOR to contract ciliary muscle (accomidation)
Clinical Test: Light Reaction (contract in light, dilate in dark), Movement (Up, Down + In)
Describe the pathway and function of CN4 and clinical tests of its function
Midbrain- Superior Orbital Fissure- SOMATIC MOTOR to Superior Oblique
Clinical Test: Ptosis (dropping of eyelid)
Movements (down + rotate)
Describe the pathway and function of CN5 V1 and clinical tests of its function
Pons- Trigeminal Ganglia
V1 Opthalamic- Superior Orbital Fissure-GENERAL SENSORY- Cornea, forehead, scalp , eyelids, sinuses, nose + mucosa of the nasal passages.
Clinical Test: Sensation in this division eg./ on the forehead + Corneal Reflex
Describe the pathway and function of CN5 V2 and clinical tests of its function
Pons- Trigeminal Ganglia
V2- Maxillary- Foramen Rotundum- GENERAL SENSORY- maxilla, maxillary teeth, TMJ, mucosa of nose, maxillary sinuses + palate
Clinical Test: Sensation in this area eg./ side of mouth
Describe the pathway and function of CN5 V3and clinical tests of its function
Pons- Trigeminal Ganglia
V3- Mandibular- Foramen Ovale- GENERAL SENSORY- mandible, mandibular teeth, TMJ, Anterior 2/3 of tongue + SOMATIC MOTOR- muscles of mastication, digastric, tensor vili platinum, tympanic
Clinical Test- Sensation in the area eg./ Jaw
Jaw Jerk Reflex
Describe the pathway and function of CN6 and clinical tests of its function
Pons + Medulla- Superior Orbital Fissure- SOMATIC MOTOR (lateral rectus)
Clinical Test: Eyemovements, abducts
Describe the pathway and function of CN7 and clinical tests of its function
Pons + Medulla- Internal Acoustic Meatus- Stylomastoid Foramen- SOMATIC MOTOR (facial expression, stapedius, digastric); VISCERAL MOTOR (submandibular, sublingual, lacrimal, nose + palate glands); SPECIAL SENSORY (taste anterior 2/3 of tongue + soft palate) GENERAL SENSORY (external acoustic meatus)
Clinical Test: Screw up face (muscles of facial expression)
Describe the pathway and function of CN8 and clinical tests of its function
Pons + Medulla- Internal Acoustic Meatus- spilts into cochlear and vestibular branches- SPECIAL SENSORY (cochlea, semicircular duct, utricle, saccle)
Clinical Test: hearing Rinnes + Webers
Describe the pathway and function of CN9 and clinical tests of its function
Medulla- jugular foramen- SPECIAL SENSORY (taste to posterior 1/3 of tongue); VISCERAL SENSORY (carotid bodies, carotid sinus); GENERAL SENSORY (cutaneous sensation via middle ear + posterior oral cavity); VISCERAL MOTOR (to parotid gland); SOMATIC MOTOR (stylopharyngeus- swallow)
Clinical Test: with vagal
Describe the pathway and function of CN10 and clinical tests of its function
Medulla- Jugular Foramen- SPECIAL SENSORY (tase in epiglottis + palate)- GENERAL SENSORY- (auricle + external acoustic meatus sensation); VISCERAL SENSORY (pharynx, larynx, trachea, bronchi, oesophagus, stomach, intestine); VISCERAL MOTOR (bronchi, gut + heart); SOMATIC MOTOR (pharynx, larynx, palate + oesophagus)
Clinical Test: palate movement, gag reflex, speech, cough
Describe the pathway and function of CN11
Medulla + Spinal Chord- Jugular foramen- SOMATIC MOTOR (soft palate, pharynx, larynx, SCM + trapezius)
Describe the pathway and function of CN12
Medulla- Hypoglossal Canal- SOMATIC MOTOR (muscles of tongue)
Describe how the Glasgow Coma Scale verbal score is calculated
3- Innaproppriate Words
2- Incomprehensible Sounds
Describe how the Glasgow Coma Scale motor scale is calculated
6- Obeys commands
5- Moves to localise pain
4- Flexion withdraw from pain
3- Abnormal Flexion
2- Abnormal Extension
Describe how the Glasgow Coma Scale eyes is calculated
3- To sounds
2- To pressure
What are the important GCS markers?
Describe inter cranial space
Cranium is filled with blood, CSF, brain + others
Skull is a fixed space (after 1 1/2 years when fontanelles fuse).
Compensate for an increase eg./ via tumour, clot by shunting to other places- spinal dura (CSF out via foramen magnum), blood to periphery, pupil herniation, temporal lobe herniates- pressure on tentorium
When these compensatory mechanisms fail= Inc ICP
What is the function of the frontal lobe? How can you test this?
Voluntary control of movement- precentral gyrus
High Order- restraint, initiative, order
Primitive Reflexes (child)
Saccadic Eye Movements
Stroop Test (colour vs Words), coherence, spell backwards
What is the difference between Broca + Wernicks influence?
Both involved in speech
Brocas is motor speech in the frontal lobe
Wernicks is language development in the dominant (left) temporal lobe
Need Brocas, Wernicks + white matter between in order to repeat
What is the function of the parietal lobe? How can you test these?
Somatosensory area (body maps)
Multimodality Assimulation (info from other areas)
Astereoagnosia (identify object by touch)
Dysgraphasthesia (draw on hand)
2 point discrimination
eg./ gerstmans syndrome
What is the function of the temporal lobe?
Process Auditory Input
Emotion (amygdala-limbic system)
Encode long term memory
What is the function of the occipital lobe?
What are the clinical features of cerebellar disease?
D- Dysdiadochokinesia (rapid alt movements)
A- Ataxia (gait/uncordination)
I- Inatension Tremor
S- Slurred Speech
P- past Pointing nose
What is the difference between radiculopathy and myelopathy of the spine?
Radiculopathy- single dermatome/ myotome (group of muscles), LMN, unilateral weakness, lose reflex.
Myelopathy- Cervical/ Thoracic chord, UMN, bilateral= colonus, up-going planters, Inc tone, Hoffmans Sign, brisk reflexes, proprioception impaired.
What is Hoffmans sign? What is its clinical significance?
Flick middle finger nail and thumb curls in
Shows cervical/ thoracic UMN spinal damage
Describe the spread of cardiac output to brain tissue
Brain receives 15% cardiac output= 55-60mL/100g of brain tissue per minute
- Grey Matter= 75mL/100g/min (higher metabolism)
- White Matter= 45mL/ 100g/min
Where are cell bodies kept?
Nerve Cell bodies- DRG
Neuronal Cell bodies- Grey Matter
What affects cerebral blood flow?
Cerebral Perfusion Pressure (blood pressure gradient across the brain CPP= MAP-ICP)
Conc. Arterial CO2 + Arterial PO2
What is the numerical value of ischemia + cell death?
Ischemia= 20mL/100g/min (can be rectified)
Cell Death= 10mL/100g/min (permanent)
What is cerebral autoregulation?
Ability to maintain constant BF over a wide range of CPP (blood pressure gradient across brain) 50-150mmHg
Dec CPP= Cerebral arterioles dilate
Inc CPP= Cerebral arterioles constrict
What is the BBB composed of?
Astrocytic Foot Process'
Tight Junction capillary endothelium
Capillary lumen (lipid, amino acid + sugar soluble)
-Compliance- change in volume observed for for a given change in pressure (dV/ dP)
- Elasticity- change in pressure observed for a given change in volume (dP/dV)