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What are the Basal Ganglia?
are a series of deep nuclei deep in the cerebrum. They all grey matter and they act in coordinating movement (helps to control movement). We don't know a lot about them, in fact what we do know is what happens when they damage. They are found lateral to the internal capsule which is lateral to the thalamus.
Strokes often effect the basal ganglions because the very small vessel that supply them often get clogged with fat and other particles. Hence common place for strokes
The basial ganglion is an old part of the brain connected to old pathways – so it deals with very basic movements.
Name the basak ganglia?
- Basal ganglia according to most text consider..
- Caudate Nucleus - Corpus striatum – this is the largest and most important in fucntion
Putamen - Corpus striatum
Corpus striatum – the caudate and putamen together are called the corpus striatum.
- Globus Pallidus -
Some text also call these basial ganglia
- Sub thalamic nucleus – found in the diencephalon
- red nucleus
- substantia nigria – in the mid brain
What is the corpus striatum?
Corpus striatum – the caudate and putamen together are called the corpus striatum.
What is the lenticular nucleus?
the putman and globus pallidus together are called lenticular nucleus
What is the direct and inderect pathway?
direct pathway – cortex → striatum → globus pallidus(internal segment) /substantia nigra (pars reticular) → supplementary motor area = this pathway is a facilitatory pathway which excites the supplementary motor cortex.
indirect pathway - it is an inhibitory pathway – so it inhibits the cortex
What is the pathology caused by the most common form ofdamage to the basal ganglia?
Most common damage to this area is degeneration of the substantia nigra which creates dopamine and this loss of dopamine leads to Parkinson’s disease . This creates a mix of positive (example: resting tremor) and negative symptoms (example:bradykinisia = slow movement ).
Name the signs of Parkinson’s disease?
- Parkinson’s disease . This creates a mix of positive (example: resting tremor) and negative symptoms
- (example:bradykinisia = slow movement ).
- 4 cardinal symptoms of parkinson's disease
- resting tremor
- muscle rigidity – cog wheel rigidity
- bradykinisiea – slow movement or hard to get moving
- postural instability - this occurs later in the disease
Other possible symptoms linked to to basal ganglion problems – because they are highly linked to the extra pyramidal pathways. The basal ganglion coordinate movement in the extra pryamidal pathways , which are rubrospinal, retecrospinal, vestibulo and tectospinal.
shuffling gait – this is when they have a hurried shuffling gait and they can't seem to stop themselves
- festination – or hurried gait were the pt starts shuffling
- on and they can't stop themselves
- pedestal turning
- retropolsion gate – is when the pt tries to turn and they start walking backward
- mask like face - no expression and a blank stare
- micrograffti – all movements get smaller
Chorea - in Latin means choreography or dance like movements - a pt with this has jerky movements of the arms and facial twitches – so jerky involuntary purposeless movements of the body and especial the arms and legs.
Huntington's chorea causes damage to what areas of the CNS and what causes it?
Huntington's chorea is common form of chorea which is an inherited genetic defect or trait and it is a form of chorea were you find defects in the cerebrum and in the Corpus striatum.
What is the cerebral cortex and the cortex?
Cerebral cortex – 80% of the brain – large dome that covers most of the rest of the brain – it is highly convoluted and folded, to increase surface area (cerebellem is also folded for the same reason). This is the part of the brain that creates advanced movements.
Cortex - means bark of tree in Latin – so it the outer layer – in the brain the outside is grey matter and this is were most of the interesting stuff happens. The inside of the brain has white matter that carries things around.
6 layers of cells, top to bottom, make up the fold of the cortex.
Define Gyrus, sulcus and fissure?
- Gyrus – means circle in greek it is a up swelling
- sulcus – crack
- fissure – big crack, example: longitudinal fissure which separates the left and right hemispheres.
What is the corpus callosum?
The corpus callosum contains most of the commissar fiber and hence connects the right and left hemispheres. Though posterior and anterior callosum do help with this but most of the fiber go across the corpus callosum.
Name the three types of fibers found within the cerebrum?
Within the cerebrum there are 3 tracts or fibers
- Projection fibers/tracts – are white fibers which brings
- thing into or out of the cortex – 3rd order neuron are also called projection neurons and start on the thalamus and go some were in the cortex.
- Intra-hemisphere connection are know as association
- fibers/tracts – they are basicly interneurons within a hemisphere.
Commissure fibers/tracts – these connect inter hemisphere so they connect left to right hemisphere
Why would a pt have their corpus callosum severed?
pt who have epileptic seizures can have there corpus callosum to prevent one hemisphere form effecting the other. This is called split brain. Experiments use these because you can give the right hemisphere a piece of information without any cross over to the left to sere what each hemisphere does by itself
Name the lobes of the cerebrum?
5 lobes of the cerebrum
- frontal - separated from the parietal by the central sulcus
- (also called the fissure of Rolando after luigi Rolondo a anatomist)
- parietal – is separated from the occipital by the parietal
- occipital sulcus
temporal - separated from the frontal lobe by the lateral sulcus or fissure of Sylvius.
- insula – or island of Reil – is small lobe deep within
- the temporal lobes and it not usually as convoluted as the other lobes
What is the Calcarine fissure and why is it important?
Calcarine fissure– is on the back of the occipital lobe – and this is important because below it is the lingual gyrus and above it it is the Cuneate gyrus. This is were the visual cortex is. The lens of the eye inverts the image so the image being processed by the brain is upside down in the back of the visual cortex.
The calcarine fissure is where the primary visual cortex is concentrated. The central visual field is located in posterior portion of the calcarine sulcus and the peripheral visual field in the anterior portion.
What is the Lingual gyrus ?
Lingual gyrus - The lingual gyrus of the occipital lobe lies between the calcarine sulcus and the posterior part of the collateral sulcus; behind, it reaches the occipital pole; in front, it is continued on to the tentorial surface of the temporal lobe, and joins the parahippocampal gyrus. The lingual gyrus is so-named because it resembles the tongue in shape. This region is believed to play an important role in dreaming and vision, especially in recognizing words, regardless of size, font, etc.
Name the 3 prominent gryi of the temporal lobe?
On the Temporal lobe there are 3 prominent gryi – these are the three big fold that make up the temporal lobe
- superior temporal gryus
- middle temporal gryus
- inferior temporal gryus
What is the Angular gryus and why is it important?
Angular gryus - is a fold that wraps around the end of the lateral sulcus – strokes can happen here
What is a lobotomy and who invented?
A protugese surgeon named António Egas Moniz developed frontal lobotomy (sticks an ice pick up the noise into the frontal lobe and go side to side and separate the frontal lobe form the rest of the brain) – to treat psychotics – it made them totally docile and very passive and they lost all social graces, if they need to pee they would just pee right in the corner – 1949 here got the noble prize for this technique – one pt tried to kill him for what was done to him.
Why do some lower animals have frontal lobes?
Many higher animals such as dolphins and whales have very large frontal lobes. In lower animals this is smaller but if they do have one it is usually designed for smell, sense that a very important sense in animals.
What are the 3 major function of the cerebral cortex that other parts of the brain don't due?
- reception and interpretation of sensory information –
- conscious perception – so projection neurons form the thalamus go to sensory cortex and each of the special senses get sent to all the places on the cerebral cortex and then they get interpreted by the cerebral cortex as to what they are. All conscious perception are a function of the cerebral cortex. Many senses such as proprioception are sent to the cerebellum but they not consciously perceived there.
Organized complex motor behavior – so it organizes very complex movements like learning to dance or pole vault – without this we can only do simply movements.
Memory – storage of learned experiences. We lay down memory distributed throughout the cortex.
- Conscious perception of senses – areas in the cortex are
- specified for certain senses
Were is the Somatosensory cortex or primary somesthetic area and what does it do? and what # on broadman's map does it occupy?
Somatosensory cortex or primary somesthetic area– 1,2,3 on broadman's map – it is on the post central gryus which is on the parietal lobe behind the central sulcus. This is the are of the cerebral cortex which receives all body sensation so every sensation except the special senses , pain , temperature touch, proprioectption, force form the trunk body and face and other parts all go to this cortex through the thalamus. It is somatotopically organized. More sections of the cortex are devoted to the face and hands so they are much more sensitive because of this. Which is why you can discriminate things better there. Example the the 2 point test – were you poke a patient with two pencils on different parts of there body and you will find that on the back they need to be far a part to tell that there are two pencils but on your hand or phase you could tell very easily even when its only two mm apart. So there is unequal representation of the body here. The anterior cerebral artery covers the top of this gryus and the Middle cerebral artery cover the upper parts of this gryus.
What is Broadman map?
Broadman was a french neurologist who labeled the area of the brain, creating a numbered map of the brain.
What are poles?
Poles: The tips of the brain front and back are called poles – there is a frontal pole and occipital pole
Were is the primary visual area on broadman map and in general?
On the occipital pole – area 17 on BM is the primary visual area or visual cortex – this is were the optic nerve ends up so retinal information goes through the optic nerve optic tract and optic chaism and ends on the back of the head.
Were is the auditory reception area on broadmans map? and auditory association areas number?
Auditory reception area – area 41 and 42 on BM – this is were sound get projected to.
Auditory association area –area 22 also called Wernicke's area.
Were does the sense of smell get processed?
Olfaction – get projected to the inside of the temporal lobe – you cant see it because it inside
Were is tatse located in general and on broadman map?
Taste – is at the very bottom at the somatosensory area 43 on BM on the bottom of the lateral sulcus. Primary Gustatory area.
Are there difference between sensory center bilaterally?
All of these areas and association areas are bilateral so they exists on the both sides of the brain but there are differences between the hemisphere. So there can be processing differences or deficits between the hemispheres.
What is Brocas area and were is it located and why?
Language centers is unilateral – Brocas area is usually on the left hemisphere. So if you lose as a child you can transfer this to the other side of the brain. Though this is unlikely in adults , but common in children. 70% of people have this on the left a few have it on the right side. Some people can have a bilateral language center but this is linked to stuttering.
Broca's Area – left hemisphere on the frontal lobe – language and speech area so if damaged by a lesion you can write but you can't speak.
what is a CLEM test and why do we use it?
CLEM test - Can use conjugate lateral eye movement – tells us which hemisphere a pt is using by the way there eyes are moving so you will look to the opposite side from the part of the brain that they using when answering a question. That is lateralization of the hemispheres. So have the pt stare at a card and them ask them question , math, spacial and see were there eyes go. Women tend to be less lateralized then males. Can use this technique to determine which hemisphere a pt likes to use and then can structure you lesson to them either through demonstration or verbal instructions or other such methods. So you want to structure your education towards which hemisphere they like to use. SO teacher should use the best of both worlds.
What is the primary motor cortex and what number is it on broadman's map?
Primary motor area – Area 4 on BM – is on the precentral gryus - lasts stop on the way before being sent down the motor cortex. So stimulating this causes a movement like bending the elbow not an action like throwing a javelin. We stimulated this during surgery to get this map. As with the sensory cortex we have an unequal distribution on the body map within the motor cortex which is why we have far more control of hands, face leg and other parts then and hence why we can make finer movements with those parts. If you lost the middle cerebral artery then we would lose the hand and UE and if lost anterior cerebral artery we would lose lower extremities. There is also a specila area for eye movements. There is also an association center for motor areas.
What is the premotor cortex?
Infront of the cortex is a premotor cortex – which is an association area for the primary motor cortex and it is were the responses are organized.
List some Cerebral Global symptoms from strokes to the cerebral cortex?
- Apraxia – without practice – this is the inability to
- perform a learned (skilled) purposeful action. Damage to the frontal lobe will cause this. So you can control you arms and the muscles are fine, but you can't combine these movements together to do a skill like walking or feeding myself.
- Agraphia – ability to write is gone – usually caused by a
- stroke in the angular gyrus – kind of a type of apraxia
Aphasia – problems with language or the symbols associated with it – aphasia is often associated with a stroke in the angular gryus
sensory or receptor aphasia – can't understand language – can't see , it read it , hear it
visual aphasia – without words – can't understand words on a piece of paper so you can't read , even though before the stroke or problem you could.
auditory aphasia – can read perfectly but can't understand spoken words usually caused by damage to Wernikies area.
- motor or verbal aphasia - can't write it or speak it
- expressive aphasia – can read and understand spoken words but can't speak due to damage to Broca's area.
Alexia – without word or words blindness
Agnosia – means without knowledge in Greek – so this is something they don't know or without knowledge. So the visual cortex is fine but you look at something and you don't know what it is. You can have visual or tactile agnosia, so don't know what your seeing or touching. Also caused by strokes to the right angular gyrus. Pt with due this do odd things like brush hair with apple when they have visual agnosia. Often caused by strokes to the right angular gryus which goes aroudn the corner of the lateral gryus.
SN: Famous book written by oliver sacks called “the man who mistook his wife for a hat”
- Neglect – many types or terms used for this hemispatial,
- hemiagnosia, unilater neglect - A severe from of agnosia is called
neglect – were the pt totally ignores one side of the body and world. This is usually associated with damage to the right angular gryus (right hemisphere). In most pt this is Caused by right hemisphere damage so it is a left sided agnosia, though can happen in the left hemisphere but it is very rare for some reason. Pt with the right side neglect will due odd things like shaving the right side of the face but not the left side, they will even eat only food of the right side of there plate but not the left. They don't believe there is a left side of the world. In extreme cases they have tried to cut there arm off because they don't believe it there limb they though it was an alien being because they don't believe that the left side of the world exists. So to them there is no left side of the world. Need to know were to stand and how to interact and were to put things like, were to put the TV in there rooms and how to place mirrors all of these things trying to force them to realize there is a left side. This can be broken down into input and output neglect.
- Output – don't output motor commands to the left side -
- wont shave or move left side in extreme cases have tried to cut of left arm because they refuse to believe they have a left side to there body. So you don't interact with the left hand side of the world
- Input –don't acknowledge sensory information from the
- left side of the world - is sensory neglect you don't hear, feel or see the left hand side of the world
- Dysarthria – problems with articulation of word due to a
- mechanical problem , not the same as aphasia – example if your tongue was paralyzed.
Name and describe the catagories of receptors?
Categories of receptors
- Mechanoreceptors - Most important to us is the mechno
- receptors. They respond to mechanical deformation of the receptor form stretch, pressure,vibration or just pushing on the skin fires these receptors. It is the mechanical deformation of the receptor that causes them to fire.
- Proprioceptors are a subset of mechano receptors which
- provide you with knowledge of were you are in space and how your moving. So they tell us the displacement of the muscles in space.
Thermoreceptors – pick up hot and cold- these are important to us when using modalities
- Chemoreceptors – sense damaged skin, nerve and tissue
- damage by the chemicals they release when damaged.
Expalin proprioception and kinestethis?
proprioception and kinestethis – proprioception is were you are so its static information and kinesthesia (a sub category of propricoception) is how your moving such as the speed a joint is moving at, such as how fast the knee is bending. Often it is considered a subset of proprioception.
What are nocieptors and polymodal nociceptors?
Nociceptors – are a subset of our mechano and thermo receptors that sense pain. Usually can sense pain in terms of temperature or pressure.
Polymodal Nociceptors - are pain receptors that can sense more then one mode of pain, so they can respond to pain from temperature , pressure and what ever. They give rise to c fiber (type 4 – the last type, unmyelinated slow conducting slow fibers). So the pain coming out of these receptors is the slow dull aching type of pain.
C fiber is type 4 nerve fibers – unmyelinated slow conducting small fibers.
What receptors are responsible for sharp dull and why do we use such tests?
Thermo and mechano receptors that give raise to – type III fibers (a delta) also unmyleinated - are responsible for sharp prickly pain sensations.
Sharp dull test are used to test if pain sensation is working – so this is when you stick a person with a pin and they just feel dull pain or pressure. Novicane creates the same sort of effect, because it means can't detect sharp pick pressure.
What is analgesic?
analgesic (also known as a painkiller) is any member of the group of drugs used to relieve pain (achieve analgesia). The word analgesic derives from Greek an- ("without") and algos ("pain").
What are B fibers?
B fibers – Nerve fibers in these group, are myelinated with a small diameter. they are the preganglionic fibers of the autonomic nervous system. Preganglionic fibers have a low conduction velocity.
Explain what Free Nerve Endings are and what they do?
Free Nerve Endings (I, IV) - these are the most undeveloped receptors with no real structures they are really just nerve endings in the skin - these don't have a receptor it is just a free nerve end. There is disagreement over what sensation these transmits. Most consider that they give rise to a delta and C and a beta (type II fiber) fibers – which give rise to many sensation such as touch (C fiber and a delta's) , heat and cold (free nerve endings going into a C fiber) , pain (a delta, C fibers) , pressure.
Root hair plexus – is a slightly modified free nerve ending which wraps around hair roots in the skin and sense the pressure or movement of the hair they are a rapidly adapting receptor
Expalin and define Merkel’s discs?
Merkel’s discs (type II fibers) – slightly modified epidermal cell – slow adapting receptor that responds to pressure. So pushing on the skin provokes these to give you the sense of pressure. a beta (II)
Explain Meissner’s corpuscle?
Meissner’s corpuscle (type II fibers) – these are the one found in your hair less skin, they are superficial in the skin – These are very important in discriminating touch , so they are what tells you if somethin a fly or water or hand that touching you. Or if there two things touching the skin or one thing. So used in two point touch test. slowly adapting receptors A beta (II)
Explain Pacinian Corpuscle ?
- Pacinian Corpuscle (type II fibers) – very common throughout the body – are found deeper down in the skin, they are lamilated which means they have layers.
- These CT layers are filled with fluid and the receptors in the center of these fluid filled layers which dampens the stimuli to it. These onions deep within the skin are very response to vibration. They are rapidly adapting receptors. The layers of this onion and
- the water between act as a dampener so they don't sense things after the first push, so they sense tapping but not a constant pressure. Example: push on a water filled balloon and you feel but you wont feel it if you hold it after the initial push, but you would feel taping this is how these receptors work.
very rapidly adapting receptor A beta (II fibers)
Explain End bulbs of Krause?
- End bulbs of Krause (type III fiber) – usually cold receptors or temperature receptors
- Cold receptor a beta (III) – not important in therapy
Expalin Ruffini’s Corpuscle?
Ruffini’s Corpuscle (type II fibers) –slowly adapting receptor, thought to be skin stretch and maybe temperature , some debate about this. Slow adapting receptor a beta (II)
Name all the Cutaneous & Subcutanteous receptors?
- Free Nerve Endings (I, IV) -
- Merkel’s discs (type II fibers)
- Meissner’s corpuscle (type II fibers)
- Pacinian Corpuscle (type II fibers) –
- End bulbs of Krause (type III fiber) - Cold receptor a beta (III)
- Ruffini’s Corpuscle (II)
- muscle spindles
- golgi tendon organs
Explain the GTO?
- golgi tendon organs – or GTO – is found in the interface between the muscle fibers and the tendon at both ends of the tendon, so its in series with muscle fibers.
- They are named after Camillo Golgi, noble prize in 1906 for physiology. Collagen fibers of the tendon coming out of the muscles into the tendon are all wrinkled like spaghetti strands and there are little axons woven between the splits in the strands and so when you increase the force the collagen which is lose floppy strands of spaghetti straighten so they were crinkled but start straightening and the gaps get smaller and this squeezes the axon terminal that have threaded themselves between them, this signals force so the
- more you stretch the collagen (muscle and tendon) the more force is sent into the axon. So it force sensation. that the receptor transmit.
- Ib affernt fiber (unipolar neurons) – goes out of this receptor and into the dorsal Grey horn and into the spinal cord. Cell body is in the dorsal root ganglion. It Cans sense .1 of a gram of force. So this signal then
- travels to the brain up the proprioception pathways which are the dorsal columns the fasciculis cuntanus (UE) and gracilis (LE) and goes up to the nucleus cutaneous or fracilis and then crosses over through a secondary neuron to the thalamus and then to the somato
- sensory cortex through a 3rd order neuron. IF this was
- the arm this would be on the side of the somato sensory cortex and as such would be supplied by the middle cerebral artery. SO sense the GTO senses force it is responsible for the deactivation of the muscle in response to high force, so when there a lot of force the
- GTO sends a signal through the I b neuron which goes in hits an interneuron in the spine and then comes back out and turns the muscle off. So at high forces the GTO will turn the muscle off (autogenic inhibition) to protect it. So if the bones are about to break or the muscle rip from heavy lifting the GTP turns of the muscle.
Technique which uses this in therapy is contract relax or hold relax PNF patterns – which is when you the pt contract there limb against you once you stretched the limb and then have them relax and you can go further back in the stretch because the GTO turns of the muscles so they can be stretched more. So there important in many stretching techniques.
GTO – an important receptor found in the juncture between the muscle and the tendon – it job is to sense force both consciously and unconsciously. This information is sent up the facciuclis cuntaneus and gracilis , it is also sent up spinocerebellar tracts to the cerebellum. GTO also inhibits the muscle it comes form which is called autogenic inhibition or inverse miotatic reflex.
What does the GTO do?
- Monitors tension developed in muscle
Prevents muscle damage during excessive force generation
Stimulation results in reflex relaxation of muscle Inhibitory neurons send IPSPs to muscle fibers – this is called the inverse myotatic reflex or autogen inhibition
Ability to voluntarily oppose GTO inhibition may be related to gains in strength. This ability to oppose this is what may be responsible for the early force gain we find when we start exercising. So we get stronger before we hypertrophy the muscle because there is neurological changes in the CNS which modulate the GTO inhibitions to let us produce more force.
What artery would have to die to mess with sensation from the arm?
Somatosensory cortex has arm on the side not in the crack so it supplied the middle cerebral artery.
Explain rapidly/slowly adapting receptors?
rapidly adapting receptors – are quick to respond to a signal but it turns itself off quickly. So even if there still pressure or stimuli it wont register it after a short time. So ti signals if touched or trigger quickly but then turns of and doesn’t continue to fire if the stimuli remains. Example: bend a hair on your arm and you can feel it but if you hold it you can't feel it any more, because it rapidly adapting.
Slow adapting receptors – are slower to activate, but continue to send a signal for as long as they triggered.
Explain how the GTO effect early force gains from exercise?
The ability to oppose the GTO inhibition helps in force production and early strength gains seen when a person exercises. Because it takes 6-8 weeks for physiological changes in the muscle to happen but you can lift more weight within the first few week, this is because you train the nervous system to recruit the right muscle in the right order and because you learn to stop the GTO form inhibiting the muscle. So you modulate the GTO inhibition to get more force gains.
List the feature of receptors other then the GTO/MS?
- Free Nerve Endings – bare dendrites –
- least modified
- Pain mainly Ad and C
- Cold and heat Ad and C
- Touch Ad and C
- Root hair plexus Ab (II) rapidly adapting
- Merkel’s discs
- Modified epidermal cells of stratum
- basale Ab (II)
- Slowly adapting receptor
- Steady skin indentation – pressure
- Meissner’s corpuscle
- Located in dermal papillae -- egg shaped
- Dendrite enclosed by connective tissue
- [mechanical filter]
- Numerous in finger tips and other
- hairless skin
- Tongue, lips, eyelids
- Slowly adapting receptor Ab (II)
- Touch receptor – lighter touch than
- Merkels disc
- Discriminative touch
- Pacinian Corpuscle
- Deeper than meissner’s corpuscle in skin – also around joints and tendons
- Lamellated like onion
- Very widespread
- Very rapidly adapting receptor Ab (II)
- d/t fluid filled spaces in lamella = damper
- Fine pressure
- End bulbs of Krause
- Cold receptor Ad [III]
- Ruffini’s Corpuscle
- Slowly adapting receptor Ab (II)
- Skin stretch
- Some say heat?
Explain the MS?
Muscle Spindles – fusiform or muscle shaped capsules within the body of the muscle itself. They lay along side or parallel to the muscle. Within these capsule there are specialized muscle fibers called intrafusal fibers. Within the spindle you will find two bag fiber (they are also called nuclei bag fibersbecause they have more then one nuclei and they are found in the bulge or bag in the center of the cell). One of those fibers is the dynamic bag fiber and the other is the other is the static bag fibers. Near them you will find several nuclei chain fibers (called this because nuceli arrange themselves in a chain down through the fiber). At the end of all these fibers we find the specialized skeletal muscle fibers. The equatorial region (or middle of the fibers) has no muscle fibers it just ligamentous non contractile tissues. The center of these fibers have receptors in them. The ends have the contractile elements.
the receptors is the non contractile equatorial regions - Two types of fibers arise form the MS type type Ia and type II fibers. The type Ia fiber has branches that go to every type of interfusial fiber so it has receptor terminals on all of them the nuclei bag and chain fibers, this is called the annulo spiral ending or primary endings which give rise to the type 1a afferent. The type II fiber innervates all the fibers except the dynamic bag. This is called secondary endings or flow spray endings (because it looks like a bunch or spray of flowers). All the endings of these neurons are on the equatorial regions. However the ends of these fibers have a contractile elemenent due to the muscle fibers at the ends of the interfusial fibers and so it has to have a motor neuron going to it. Which is the gamma motor neurons.
What type of lower motor neuron goes to interfusial or extrafusial fiber?
Contractile portion of MS – the intrafusal muscle fibers at the end of the fibers has a gamma motor neuron going to it. There is a dynamic gamma motor neuron which goes to the dynamic bag fiber and the static gamma motor neurons which goes to the static bag and the chain fibers.
Alpha motor muscle goes to normal muscles or extrafusal fibers.
Explain how slow versus fast stretching effects the firing of fibers in the MS?
- Example: stretching a muscle effects on Type 1a and type II fibers – if we stretch on the hamstring with a ramp stretch – so you stretch and then hold and then push a little further and then hold hold at the new angle and then repeat. So during this stretch the MS
- sends signals down each fibers to tell muscle length.
- With a slow stretch
- Type Ia – would fire a roughly steady stream of signals telling the body that you are at a certain amount of stretch.
- Type II – would fire more as we are stretching and less before and when holding the stretch.
- With a fast stretch
- Type Ia would fire even more during the stretch
Type II – fires at the same rate
Explain what Type Ia and II fibers from mucle spindles do?
Type Ia afferent also called dynamic or phasic afferent because it tells us the rate of stretch – once the stretch stop it goes back to resting level. So tells us the rate of stretch.
- Type II – is the static afferent so it only care that we are
- being stretched or the amount of stretch not how fast we are being stretched – so constantly tells the brain the amount of stretch.
Explain what fires the MS?
passive stretch - every time you passively stretch a muscle it activates the MS – example: patella reflex – these neurons (Type Ia and type II) form a reflex arc – so when you tap the patella tendons you activate the MS and Ia and Type II fibers carry a signal out of the MS and go into the dorsal root of the spine and then synapse with the alpha motor neurons in the ventral grey horn which signals a contraction of the quads and you get the reflex. This is an example of the myottatic reflex.
example:stretch reflex - Antgonis/agonist – knee jerk reflex – so we whack the quads tendon with a hammer which tugs on the quads minutely which stretches the quads – the MS in the quads detect this slight stretch and trigger the quads to fire. So this is a passive stretch of the muscle. This can't be inhibited but can be enhanced by the jendrassik manuever. Which is when you grit you teeth or clenching you fist increases the level of the reflex. This increases the stimulation to the cord by sending back ground stimulation into the cord which gets the ventral grey horns throughout the cord becomes hyper facciliated or ready to fire so it takes less stimulation to trigger them.
relaxation the extarfusal fibers you will stretch the MS - similar to passive stretch activation -
example: if you held a dumbell curl held out at full length, then as you get tired the weight will sink ten degrees, the MS in the biceps detect this and send a signal to the cord which causes the biceps to fire and bring the elbow back up to resting length. When the MS detect the stretch they send into the cord a signal saying that I have been stretched ten degrees give me ten degrees of activation of the biceps. However there is a delay in that system , due to having to synapse into the cord. SO by the time the biceps get the response , the arm is now 20 degrees lower then it was at start.
This is why we have a type Ia afferent because it tell us how the speed at which we are being stretched so it allow us to predict (lets us predict the future) were your going to be so it tell you how much more force to use to counteract the drop. SO it predictive as well as velocity dependent. IT not a perfect system though which is why if we try and hold the weight perfectly still you see a ten Hertz tremor (10 cycles per second) due to this lag constantly be corrected for.
contraction of the intrafusal fibers -when the muscle is contracted the intrafusal fibers also contract to perserve tension which means while the muscle is shorter they stay contracted which keeps firing the MS.
contract the intrafusal fibers and you can't help but stretch the inside of the MS to cause it to fire (basis of mertons servomechanism theory – not accurate but we do set are muscles some time using gamma gain)
What is reciprocal inhibition?
reciprocal inhibition – so to reduce tone in a muscle you activate the opposite muscle- is when you turn off the antogonist muscle when you turn on the agnonist - this is useful in PT and in stretching in general– in pt with stroke when you want to reduce tone in a muscle you turn on the msucle antogonistic to it, which decrease its tone and relaxes it.
Example of reciprocal inhibition: can't swing the knee extension if hamstrings are on so – what happens is that the Ia and Type II send signal to the ventral horn side branches of them in the spine go to the antogonist muscle so if you turn on the quads these side branches turn off the hamstring.
This is also the the thing that makes your head snap up when you fall asleep and tip forward.
Define the jendrassik manuever. ?
jendrassik manuever. Which is when you grit you teeth or clenching you fist increases the level of the reflex. This increases the stimulation to the cord by sending back ground stimulation into the cord which gets the ventral grey horns throughout the cord becomes hyper facciliated or ready to fire so it takes less stimulation to trigger them.
Under the traditional approach explain the causes of spasticity?
Traditional approach - If we lose the higher control of the reflex the muscle take on a life on there own (go haywire)– and we get spasticity
Some people say the MS get facilitated
Other says it the alpha motor neurons pulls in the cord that get facilitated which causes the signal to go round and round because the muscle gets stuck in a loop – so this is spasticity which is not hypertonicity – it is a specific type of hypetonicity – for it is a non linear increase of muscle tone due to velocity of muscle stretch. So the faster you stretch a muscle the more it resits this is due to the I a afferent fiber. So a pt with spastic muscle doesn't like to be stretched quickly. So bounce approach wont work with them. So the stretch reflex has a life of there own.
Why due we have gamma motor neurons and muscle fiber in the MS?
When you stretch a muscle such as the biceps (4 cm) the MS spindles fires and the arm goes up. However if you contract the muscle the MS gets all floppy due to the loss of tension. So when you stretch it again but not back to normal length it wont fire because the MS is to floppy to detect stretch. So with only a passive component it could not detect stretch below it resting length. Which is why we have intrafusal fibers , for when the muscle contracts the gamma motor neurons also fire the intrafusal fibers contract which keeps the MS at the same length as the extrafusal fibers so that at any muscle length they can detect stretch.
Were are the most MS found?
You find more MS in muscle which are very finely controlled muscles such as the hands and the eyes. Because the eyes must be controlled carefully. Also found in large # in postural muscles like the soleus.
What is alpha gamma activation or linkage?
IS part of the current theory of muscle control in which you activate the gamma and alpha motor neuron at the same time.
Explain Merton's follow up servomechanism?
The original concept of muscle control – was called Merton's follow up servomechanism – people originally though that when you stimulate the brain with an outside electrical current they find that the signal goes down the gamma motor neuron first and sets the MS to a set length which would feedback into the cord and this would fire the alpha motor neuron. So they thought that setting the MS controlled the muscle by contracting intrafusal fibers first to cause the extrafisual fibers to contract.
So gamma motor neurons go to the intrafisual fibers within the MS , which causes it to contract the ends (which is the interfusial fibers) which stretches the middle or receptor part of the MS which causes the receptor to fire and send signals down the type Ia and Type II fibers which feedback into the spinal cord were they synapse with alpha motor neurons going to a muscles like the biceps which causes it to contract to get rid of the stretch on the MS, because if the biceps is shorter then it not on stretch. However the MS interfisual muscle fibers can't move muscle on its own even if you contracted all of them at once.
However there was a delay in this system which disproved this. Because when the brain sends a signal the alpha and gamma fire at the same time. So you shrink the MS and muscle at same rate and length.
What is Autogenic inhibition.?
THis is when the GTO causes the reverse mitotic reflex. Which is when these Force receptor turns muscle off at high forces which is called Autogenic inhibition.
Explain what fiber arise from the MS and what they do?
Muscle spindle – has interfusial fibers within it and it has different types of sensory fiber come out of it.
Ia monitors rate of stretch. So we have a type Ia afferent because it tell us the speed at which we are being stretched so it allow us to predict (lets us predict the future) were your going to be so it tell you how much more force to use to counteract the drop. SO it predictive as well as velocity dependent. IT not a perfect system though which is why if we try and hold the weight perfectly still you see a ten Hertz tremor (10 cycles per second) due to this lag constantly be corrected for.
Type II gives you the amount of static stretch. Thought to be the primary receptors in determining joint angle. We have joint receptors but these are more important because we know the angle of the elbow based on the stretch of the muscles around the joint.
the receptors is the non contractile equatorial regions of the MS- Two types of fibers arise form the MS - type Ia and type II fibers.
The type Ia fiber has branches that go to every type of interfusial fiber so it has receptor terminals on all of them the nuclei bag and chain fibers, this is called the annulo spiral ending or primary endings which give rise to the type 1a afferent.
The type II fiber innervates all the fibers except the dynamic bag. This is called secondary endings or flow spray endings (because it looks like a bunch or spray of flowers).
Type II (static) afferent comes off all but the dynamic bag.
All the endings of these neurons are on the equatorial regions. However the ends of these fibers have a contractile elemenent due to the muscle fibers at the ends of the interfusial fibers and so it has to have a motor neuron going to it. Which is the gamma motor neurons.
Why is bounce stretcht generally less efective then a held stretch?
Stretching – you get more stretch out a static stretch then a bounce stretch because the bouncing is more inhibited because the IA and type II both fire but if you go down and hold the Ia turns of leaving only the Type II to oppose you, so when your not going through a velocity stretch any more the I a turns off and you get less resistance to a stretch if you hold the stretch.
What is gamma gain?
Gamma gain – if I want my elbow to be held at 90 degrees I set my inter and extra fusial muscle at a certain length or gain and if my biceps gets stretched after this and I will detect this– – the MS must shrink at the same rate as the muscle it in or it useless. So gamma system keep contracting the interfusial fibers to allow the MS to be continually sensitive to stretch in any part of its ROM this is the myototic reflex. MS job is to to turn on the muscle it comes out and hence cause that muscle to contract , hence knee jerk reflex (inverse mitotic reflex) is caused by the MS.
Example: reflex – You tap the persons patella tendon with a hammer and this causes stretch of the MS which cause a signal to go up the Ia afferents to the cord where they synapse with the alpha motor neurons going to the quads and cause the quads to contract. But you can't contract the quads unless you turn of the hamstring so there is an inhibitory inter neuron going to the alpha motor neurons going to the hamstrings and turning them off.
What is a Renshaw cell and what does it do?
Renshaw cell –are inhibitory cell within the inter neuron - it job is to turn of the alpha motor neuron that it came from originally– this is called recurrent inhibition – so though it is an inhibitory neuron, but it also inhibits the inhibitory neuron for the agonists. So a nerve won't fire for ever because it turns it of. Also turns off other alpha motor neurons near the one it came from . It is thought to focus activity down certain highly facilitated pathways by turning off the noise within a segmental level. Turns of the alpha motor pool , so only the strongest signal can blast through. - primary point: Inhibitory neurons within the segmental level and they are responsible for recurrent inhibition which is turning off the alpha motor neuron that initially turned the renshaw cell on. So inhibit agonist and excite the antigonist. Lot of debate about these cell in the literature.
- So as the alpha motor neurons as it fires down to the muscle it sends a collateral to the renshaw cell which turns of the alpha motor neuron it came from and it inhibits the inhibitory neurons for the
What is spasticity and why doe sit happen?
Spasticity – loss of inhibition from a supraspinal levels it is the stretch reflex that is hyper facilitated. A non linear increase in resistance to motion based on velocity of stretch. So the faster you stretch some ones spastic muscle the more it resits you. So spasticity is a term reserved for the resistance caused by the stretch reflex.
Why it happens - many places within the reflex arc can causes spasticity.
Loss of descending control at the segmental level due to a lesion lets the reflex go crazy.
Some say the alpha motor pools on the segmental level are hyper facilitated.
- Some people argue ti the MS themselves that are hyper
- facilitated – hence why a small stretch causes them to fire Some argue that the gamma motor neurons are hyper facilitated in the ventral grey horn and hence are close to threshold then a slight stretch may cause them to fire to the interfusial making them fire which will feedback and turn on the extra fusail fibers,
May be deliberate attempt in spastic dysplegia child to give themselves some tone because they were born with inadequate tone in gastrocs
Name treatments for spasticity?
- Botox - destroys the motor end plates with botox
- Baclofen – to much there floppy and worthless to little does nothing , put a pump into subarchnoiud space all day long. Can be taken orally but have to put such high doses to get across BBB that it makes the child very drowsy and floppy.
Dorsal rhizotomy – if there is to muscles contraction they can go in and cut some of the rootlets toi try and reduce the drive to the alpha motor neurons some doctor will do this and some wont- can also be sued to reduce spasticity.
e stim to spastic muscle or strengthen it (Boobath which is the traditional approach says never do this because of the stretch reflex). But a spastic muscle is a weak muscle so strengthening it regains more function and often reduces spasticity.
List and explain the cord mediated reflexed we care about?
Cord mediated reflexes
flex withdra reflex - is when you put you limb on a painful stimulus (example stand on a thumb tact) and these pain signals go into the spinal cord and synapses with the alpha motor neuron for the flexors and cause you to pull the limb away – this is a segmental reflex so doesn't require the brain to do this. This is why you feel the pain a second after you pull away.
- crossed extensor reflex – (example: if put foot on thumb tact the flexor withdraw reflex pulls your foot up off the thumb tact however then you would fall over because you only have one leg on the ground so to counter this you have the crossed extensor reflex - this reflex saves you) – the opposite limb extends in reaction to the
- flex or withdraw reflex. So Contra-lateral limb extends as the ipsilateral limb flexes.
- Extensor thrust reflex – this is why if you push on a
- babies feet he pushes against you , because he thinks it the floor, so gentle pressure on the foot pads creates push. In a stroke pt this can be a problem because if they don' have adequate inhibitory control of this then when they put there foot down and they go bolt up right and stand rigid which prevents them from starting gait. So
- this hyper reflex (or to powerful reflex) is a problem , but we can use BW supported systems to overcome this, by lowering them down to the ground gentle and not putting full weight onto the ground, because not provoking the primitive thrust reflex .
Explain some fo the tonic reflex we care about?
Tonic reflex –more complex reflex that control the tone of certain groups of muscles– so they control one part of the body in relation to another.
- ATNR asymmetric tonic neck reflex – this is the classic
- reflex you see in babies were if you turn the head to the left and the arm will extend when the other arm flexes so the baby will take on the fencing position. It is thought o cordinate basic reaching with looking. Should disappear within 6-8 months but in CP pt can have an obligatory reflex which can cause issues. Reemerges in some pt with brain damage. This is also why when the head is
- towards the wrist extension is stronger but if you look away flexion is stronger. Used to think this was due to the neck receptors but it actually the perception of the head in space that causes this not the receptors. People used to think was due to neck receptors but they found that if you turn your head to the side and hold it there you will feel like you head is drifting towards mid
- line even though it is not. So it some kind of perception of the head in space and not the stretch reflex in the neck that causes this.
Symmetric tonic reflexes is when both he limbs do the same thing – Example: if you flex the neck of a baby the arms flex and the leg extends and this is though to be left over from when we were quadrupeds and wanted to get down to drink. Tilt the neck back and the arms extend. Which is why children have trouble diving because when they put there arms out the head goes back.
- Tonic Labyrinthine reflex – based on the position of the
- head in space so were it is tilted Example: TLR if put a baby on its back and the head back all limbs extend but put head horizontal with the face down the whole body will flex causing the baby to curl up into a ball on the bed. Can also cause issue for brain damaged pts.
What is fictive locamotion and what did it prove?
Fictive locamotion - Some sensory feed back may come from the ventral roots.(never think of this in the boards) – so grillner paralyzed cut the brain stem , cut the dorsal roots and then he paralyzed the muscle with quria. Then he put electrodes on the ventral roots and shocked the cord, not phasicly just back ground stimulation and out of the ventral horn comes the flex extend commands so the cat was still electrically trying to walk. There are CPG or neural oscilators or spinal pattern generators , which create walking without any input or brain , these neural circuits is thought to be in the cord. So we are trying to put electrodes in the spine and get a person walking without the brain. Are these circuits learned or developed with experience, to test this they used kittens and cut the midbrain at birth before it can walk and do this experiment and the kitten will walks so these CPG are built in or prewired circuits there at birth.
What did Pearsons work find?
CPG – pearson did a lot of work on cockroaches gait – and found the CPG for there gait and thinks it is the same pattern for animals and even humans. So each leg still has the same swing and stance phase. Or flex extend in most creatures.
To go faster all animals reduce stance phase while swing phase remains the same throughout different speeds of gait.
How do the CPG for wlaking and standing work?
Command neuron in the brain toniclly activate the extensors (so they are always on (always background signals to them) to make us stand up , this is postural tone) when we want to run we send a signal to the CPG which periodically turns on the flexor muscles using this burst generator which also turns off the extensors (decreases there back ground tone). So you actually control the flexor with the burst generator and if you damage the flexor burst generator natural stance is extension because nothing is inhibiting it.
How is the brain involved in walking?
We don't need a brain to walk in most situations. Example: a normal cat you wouldn't have any activity coming down the corticospinal tract when walking on a treadmill but if you put blocks on the treadmill then his corticospinal tract would go nuts because it has to dodge the blocks and so it has to adjust the normal gait patterns.
CPG is why a chicken can walk without a head but to change the gait pattern you need a brain to modify the CPG.
Exlpain how pain and temp sensation get to the brain?
pain and temperature – different receptors receive signals and send this down the neuron into the dorsal root were it synapses in the dorsal grey horn. Then this second order neuron cross through the dorsal white commisser to the other side of the cord and then it goes up the lateral spinalthalmic tract. The lateral spinothalmic tract goes all the way up the cord and Ends in the thalamus at a nuclei called the ventral posterior lateral nuclei or VPL this is were the second order neuron ends. This is were the third order neuron picks it up and takes it to the somato sensory center.
What are rex's laminae?
- Within the grey matter of the cord there are layers or
- laminia which are labeled with Roman numerals 1-10, back to front. Called rex's laminae.
What are the two types of fibers tht carry pain/temp sensation and in what areas of the cord do they synapse?
2 basic fibers coming in a delta (type 3 fibers) and c fibers (type 4 fibers)
a delta fiber synapses in laminae I and V in the layers of
the grey matter – they then it directly synapses with secondary order neurons starting in laminae I and in laminae 5 which go across the white comminsere and then go up the lateral spinothalmic tract to the VCL.
C fibers (type 4) – synapse in laminae II (also called the
substantia gelatinosa) with an interneuron which then connects to a second order neuron in laminae I. Cross the middle line and go up the lateral spinothalmic tracts.
What do A beta do?
A beta fibers –are fibers that carry signals from other sense such as (mechanoreceptors) are pressure , proproception, other sensory and they come in and synapse on the dendrites. These can close the gate to pain hence why we shake our hand.
What spinal tract carries pain and how is it orginized?
So when pain enters the cord and it enters the lateral spinothalmic tract – which is itself somatotopgraphicly organized so the LE are more lateral or peripheral and the UE are in the inside or deeper in the tract.
What is Lissauer tract and what do sit do?
Lissauer tract - is the very tip of the dorsal grey horn or the dorsal lateral fasciulis of Lissauer.
- The posterolateral tract (fasciculus of Lissauer, Lissauer's tract, tract of Lissauer, dorsolateral fasciculus, dorsolateral tract, zone of Lissauer) is a small strand situated in relation to the tip of the posterior column close to the entrance of the posterior nerve roots. It contains centrally projecting axons carrying discriminative pain and temperature information (location, intensity and quality), which enter the spinal column ascend or descend one or two spinal segments in this tract before penetrating the grey matter of the dorsal horn where they synapse on second-order neurons. The axons of these second-order neurons cross the midline
- and ascend in the anterolateral quadrant of the contralateral half of the spinal cord, where they join the spinothalamic tract. The second-order neurons ultimately synapse on neurons in the ventral posterior lateral nucleus (VPL) of the thalamus.
IF there was a lesion at T5 were would you lose pain and temp sensation?
lesion at T5 – lose pain and temp contra laterally one or two segments below this lesion (ex brown sequard) because of the collateral's so you would not lose T5 or T6 but you would lose T7 because of Lissauers tract.
What is tractomy and why is done?
tractomy – is when we deliberately cut a spinal tract such as the lateral spinothalmic tract which is done to cut the pain pathway in cases of severe untreatable pain which can't be managed by meds. This works in part due to the somato topergraticly organized.
What nerve handles paain and temp sensations for the face?
Trigeminal nerve – carries most of the sensation from the face including pain and temp. Can see pain and temperature dissociation in this nerve.
What is redicular pain?
IT is one type of neuralgia. In which pain radiates down the nerve from the site of the lesion – so it nerve root irritation, type pain.so burning shooting types of pain.
Neuralgia – nerve pain
Define reffered pain and list some common refferd pain patterns?
Refered pain – is when an organ refers pain to a nerve which it shares components – is were part of the skin hurts ex: arm burning but there is nothing wrong with the arm or the nerves going to that arm, so if T1 and T2 dermotomes are hurting in the left arm (sometimes can be in the right but is rarer) but nothing else is wrong then that may be a heart attack. So this happens because T1 and T2 nerve roots also run to the hearts and though msot organs don't have pain receptores the covering around them due and when they get inflamed they mombard the cord with pain so when the covering around organs (heart in this case) become irritated they trigger nerves which share nerve roots with the arm and because there is overlap with nerves from the arm the brain becomes confused and you feel pain in a diff place.
Lungs – refer pain to the back of the neck and the top of the shoulder ( because the phrenic nerve has nerve roots of C3,4,5 so the dermotomes of C3,4,5 is were it sends pain).
Back and shoulder pain – can be from gall bladder or kidneys. - this is very tough because have to determine if it muscle or organ pain. So when a person comes in with pain of the back or chest you need to see if you can make this problem worse or better because if can't then it probably not a muscle , ligament, or nerve it is probably organ.
Explain analgestic versus anesthesia?
analgestic – blocks pain only example: is lidocain which is a synthetic form of cocain which numbs you to pain. So they would have lost there sharp feeling because that pain receptors, so you can feel pressure but not pain.
anesthesia – is lack of sensation so an anesthetic block all sensation.
Name and explain one of the firts pain med used?
Morphine – was one of the first general anesthetic drugs. It is derived from opium or popies. It is very powerful but it is very addictive. Named for morpheous greek god of forms and dreams. When on morphine you can see shapes and form floating aorund your head because it is an hallucinogen.
- Alcohol – was used for pain relief for many years.
- Ether – first westernized manufactured anesthetic in the
What is belladona , why is it called this and hwo does it work?
Deadly Night shade - In the middle ages they used a plant in Europe were you picked the berries and crushed the berries and it was powerful anesthetic. Renaissance ladies would squirt this drug in there eye to create big black pupils which was considered more attractive - (belladona = means beautiful ladies) = deadly night shade is one of the most deadly/toxic plants in the western hemisphere– 2 berries can kill a kid and 5-10 can kill an adult , one leaf can kill an adult. The berries taste sweet. So used as anesthetic in the middle ages in very controlled doses and the Romans often used to kill each other. Death berries or devils cherries. This works to dilate the eye because the eye is controlled by two muscle a sphincter muscle and another that looks more like strands and is part of the ANS . SN goes to the Radial muscle (pulls the pupil wider), and the PS goes to the sphincter muscle and makes the pupil smaller. SN: cognitive effort makes the pupils dilate. - So when belladona is thrown in the eye it is a parasympathetic antognist which destroys the PN supply to the eye causing the SN to overcome the PN and hence the radial muscle dilates the eye. So it an anti colergent drug because it block colerigent fibers - atropine is a synthetic drug made from this commonly used by doctors to dilate the eye. This is done to look in the back of the eye for optic neurosis or chocked disc were the optic disc pushes into the back of the eye, because in some cased the optic disc pushes forward due to cerebal herniation. It is also injected in the heart to speed up the heart when the ehart is stopped due to heart attacks or other pathologies. Soldiers used to carry atrophin pens because it was a antidote for nerve gases that stop the heart and cause heart attacks.
How do beta blockers work?
To decrease the heart you give them a sympathetic antagonist which block the SN, this is used in pt who have high blood pressure (hypertension) (example of general sympathetic antagonist: beta blockers which slows the heart rate down due lower blood pressure) – you most watch out of pt with this because there heart rate responses will be blunted so in a stress test they would run to death before the heart rate went up past 90 due to the beta blocker inhibiting this signal.
What are Barbiturate and what thes troy behind there name?
Barbiturate -a class of very powerful narcotics (very addictive) and hypnotics and sedatives used for general anestetics. Now used for anticovulsent example Phenobarbital was used for grand mall seziers. It was first created by Adolf Von Bire who founded the bear asprin company. The drug was finished by emilo fisher who carried on his work and produced barbitates.
Adolf Von Bire which is now bear apsrin company – first to work on this and his student carried on his work and made barbiturates (urate means urine), He condensed melonic acid with urine. The story goes that on his way to work he would pick up Barbra’s pee (girl who worked in coffee shop) because needed a lot of urine to create this drug and he would take that to his lab and work with her pee.
Explain the Ventral or anterior spinocerebellar tract?
- Ventral or anterior spinocerebellar tract – carries proprioception from a few lower thoracic and mostly lumbar and sacral regions (leg info) – it is also a redundant system – information enters the cord and it synapses in the lateral/ventral grey horn area and then two neurons take over, one goes left and the other right. So two projection neurons arise form this, so it a bilateral tract so info form the legs goes up both anterior spinocerebllar tracts all the way to the cerebellum. Goes through the superior cerebellar perduncle. Most of that signal crosses over to go in the same hemisphere as the limb so R leg to R hemisphere, so even the information that comes up contralterally will cross over in the brain
- stem to it original side before going into the cerberum. SO this is why cerebellar lesion tend to be ipsilateral, so they would lose tone on right side and fall to the right side. Cross before the cerebellar.
Name the spinal tracts that carry information to the cerebellum and why they important?
- There is a Dorsal spinocerebellar tract , anterior spinocerebellar tract, and cuneocerebellar tract- All these tract take proprioception information into the cerebellar for unconscious proprioception, which
- help coordinate movement and muscle tone and other rapid responses to posture. So these tract can work without a cerebrum. SO these tract adjusts muscle tone before we are consciously aware of what we are doing, example: how heavy is this milk (cerebellum tell us to add more force to carry it). So damage to the cerebellum cause loss of proprioception tot he cerebellum and hence causes ataxia and otherlow level coordination issues.
Explain the pathway for simple curde touch and pressure?
- Pressure and simple or crude touch – first order neuron in the skin send info in through the dorsal root ganglion and it synapses in the dorsal grey horn and the second order neuron cross over the cord and then ascends in the ventral or anterior spinothalmic tract. (lateral spinothalmic tract is pain is temp) and then it ascends all the way up the tract (contralaterally) to VPL (ventral posterolateral nucleus of the thalamus) then third order
- neuron takes over and takes it to somatic sensory cortex. When that 1st order neuron comes into the cord it gives of a collateral which ascends ipsilateral which goes all the way up the cord and every segment above were it came in it gives of a side branch which synpases with another second order neuron that cross the midline and then goes up contralateraly but stops in the cord and does not go to the brain stem. So it is a very redundant system. So with a spinal cord lesion you very rarely lose this sensation , you would have to damage the entire cord to take out this pathway. Testing this pathway – push on pt skin very specifiably using Semmes Weinstein or Von Frey hairs – which are a little metal
- handle with monofillament coming out of it and you will have a whole set of these and you will push them on the skin starting small and working up and you will list the number of the one they could first feel and there is certain number (.75) which they must have for
- protective responses so in diabetics this can mean problems with injury and lesion will occur. Used on feet of diabetics. ??
Explain the pathwya for concious proprioception?
- conscious proprioception (this system is called the dorsal lemeniscal system)- all the GTO and muscle spindles go up this way - so first order neuron comes in to the cord and immediately ascends ipsilaterally up the dorsal collumns in the FC or FG and they ascend all the way up the cord and end in the medual just rostral and above the decisation of the pryamids of the medulla were the motor fibers cross. These propriceptive fibers End on nucleus C or G and then ascend contralterally in the medial lemniscus which is the pathway of fibers that takes this information up to the thalamus and the VPL
- and the thrid order neuron take sit from the thalamus to the cortex where it goes to the somatosensory cortex and then the info is interpreted by the association cortex. This is the pathway for conscious perception, vibration (comes from parcinian corpusels),
- proprioception and fine discriminator touch so how far two object are
- apart on the skin.
- there is a side branch off of that first order neuron that
- goes to the ventral grey horn and synapses which is what creates reflexes such as the knee jerk reflexes. There is another collateral that goes to the lateral base of the grey horn (in laminae 7) which is called clacks nucleus or nucleus dorsalis (start of the posterior spinocerebellar tract) – you find this column of nuclei all the way down the cord between T1 and L2 (end of cord) – this synapse
- is with second order neurons which (blue tract on slide) come out and go up the dorsal spinocerebelar tract (or posterior spinocerebellar tract) , which goes all the way up the cord and goes into the cerebellum through the inferior perduncle into the cerebellum. It is an ipsilateral tract so if it comes in the left it goes into the left nucleis dorsalis and ascends up the left posterior spinocerebellar tract and goes into the left hemisphere of the cerebelelum through the left inferior perduncle. If neurons come in below L2 just ascend up the cladua equina and enter the lower levels of the spinal cord and ascend into the nucleuis dorsalis's lower levels. Infromation from the arms (T1 and above) comes into
- the cord and don't synapse and take an upward bend and go to the ACN (accessory cunate nucleus or lateral cunate nucleus) which sits lateral to the cunate nucleus which is the end of the FC. So this proprioception from the arms comes up to the ACN and goes into the
- cerebellum through the cuneo-cerebellar tract, which goes from the lateral cunate nucelus in the medulla to the cerebellar cortex via the inferior cerebellar perduncle.