neuro 01

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neuro 01
2012-02-12 16:19:31

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  1. What is Ataxia?
    uncordinated movements
  2. What is Hypotonia?
    – less muscle tone then normal
  3. What is Athetosis?
    Athetosis is a symptom characterized by involuntary convoluted, writhing movements of the fingers, arms, legs, and neck. – writhing movements
  4. What is Dysmetria ?
    Dysmetria – also called past point – this is the inability to hit a target with a limb , hence it alternate name for a person trying to point at something will point slightly to the side of the target.
  5. What is Dysdiadochokinesia ?
    Dysdiadochokinesia - dysdiadochokinesis, dysdiadokokinesia, dysdiadokokinesis, or DDK (from Greek dys "bad", diadocho "receive", kinesia "movement") is the medical term for an inability to perform rapid, alternating movements.
  6. What are sign and symptoms?
    Symptoms – are the subjective reports of the pt about things there experiencing.

    Signs – are observable and provocable response. These are what we use special test for.
  7. What is somnolence?
    Somnolence – Hard time sleeping
  8. What is the Glasgow coma scale score?
    Glasgow coma scale score – is a core used by ER doctors to classify a person based on their responses, a pt is placed in the range 3-15; patients with scores of 3-8 are usually said to be in a coma. The total score is the sum of the scores in three categories verbal, motor and eye opening responses which includes their response to pain stimuli. A pt's score is correlated with their function and chances/rate of recovery. It is highly predictive of function recovery so a bad score at the beginning of treatment means they unlikely to recover as well or at all.
  9. What is Afebrile?
    Afebrile – no fever
  10. What is Euvolemic?
    Euvolemic – normal blood volume
  11. What is Fundoscopy?
    Fundoscopy – is a test, were a doctor shines a light into a pt's eyes and looks in a pt eye to check for abnormalities and signs of things like optic nervritis, or a pushed in optic disk due to cerebral herniation.
  12. What is Pronator drift?
    Pronator drift – when a pt's arm gradually pronates involuntarily, it is a sign of brain damage.
  13. What is Romberg sign?
    Romberg sign/test – is when you have a pt stand still with there legs together , this is done to test the pt's balance, so can they stand up without swaying. There are several version of this test in some you may also have the pt close there eyes while standing with legs together.
  14. What is hyper-reflexic?
    hyperreflexic – exaggerated reflexes
  15. What is a epidural hematoma?
    Epidural hematoma – upon the dura – so it is a bleed between the dura matter and the cranium. On a CT scan this shows up as a white area that pushing in on the brain.
  16. Explain a subduralhematoma?
    Subdural hematoma – beneath the dura mater. - So it is a bleed – on a CT scan it shows up as a dark area such as an absence of the ventricles.

    • subdural hematoma - also known as a subdural haemorrhage
    • (SDH), is a type of haematoma, a form of traumatic brain injury. Blood gathers within the outermost meningeal layer, between the dura mater, which adheres to the skull, and the arachnoid mater, which envelops the brain. Usually resulting from tears in bridging veins which cross the subdural space, subdural hemorrhages may cause an increase in intracranial pressure (ICP), which can cause compression of and damage to delicate brain tissue. Subdural hematomas are often life-threatening when acute. Chronic subdural hematomas, however, have better prognosis if properly managed. In contrast, epidural hematomas are usually caused by tears in arteries, resulting in a build-up of blood between the dura mater and skull.
  17. What is Aterial Brutis?
    Aterial Brutis – the sound of turbulence from the blood flow in the neck caused by atherosclerosis which can be heard while using a stethoscope to listen to the neck.
  18. What is Ptosis?
    Ptosis – drooping eye lid on one side of the face
  19. What is miosis?
    Miosis – pupil is very small (pin point) and fixed, and hence unreactive to light.
  20. What is Babinski sign?
    Babinski sign – is when you scratch the bottom of the foot, if the pt is normal their feet will curl, but if they instead dorsiflex , or extend all the toes except the big toe, then they have this sign.
  21. What is Aphasia? and what is motor aphasia?
    Aphasia – is a pathology were a pt has problems with language, however there are many types of aphasia and they can effect a pt ability to speak, write, read or hear language. However no matter which type they have, all cause issues with communication.

    Motor aphasia – is a problem producing spoken language – 99% of pt with this pathology have a focal lesion in the middle cerebral artery.
  22. What is Brocas area?
    Brocas area – this is the language center of the brain also called the speech center – the speech center is one of the few parts of the brain that not bilateral, or in other words there is only one speech center. If a person does have two speech centers (bilateral) then they often have a stutter, perhaps due to this redundancy. This area is located on the left side of the brain, above the left lateral fissure on the frontal lobe. This area is supplied by the middle cerebral artery.
  23. Name the 3 cerebral arteries?
    Cerebral arteries

    Anteroir cerebral atery – supplies most of the medial and superior surfaces of the brain and the frontal pole. (frontal pole: the anterior extremity of the frontal lobe of the cerebrum.)

    Middle cerebral artery – Supplies the lateral surface of the brain and the temporal pole.

    posterior cerebral artery – supplies the inferior surfaces of the brain and the temporal pole.
  24. What is cerebral arterial circle?
    Cerebral arterial circle – is a roughly pentagon shaped circle of vessels on the ventral surface of the brain. It is an important anastomosis at the base of the brain between the four arteries; two vertebral and two internal carotid arteries that supply the brain. The arterial circle is formed sequentially in an anterior to posterior direction by the

    • Anterior communicating artery
    • Anterior cerebral arteries
    • internal carotid arteries (2)
    • posterior communicating arteries
    • posterior cerebral arteries
  25. Name and explain the types of lesion and give an example?
    Focal lesion – is a lesion or injury in one specific area, such as in one single artery.

    Multifocal lesion – means injury or lesion in many sites, example: MS

    • The fact that MS is a multifocal lesion is the key to diagnosing it for it is only the fact that a patient
    • will have a number of weird unrelated symptoms such as Tingling in the hand weakness in the legs and blurred vision which indicate that it is caused by multiple unrelated lesions and hence is MS.

    Diffuse lesion – doesn't have one or multiple focus of the lesion instead there is lots and lots of systemic issues , example: diabetes
  26. what is the central?
    Central sulcus – a crack between the two loves frontal and parietal.
  27. Were does prociception come from and how does it travel to the brain?
    Prociception = ipsilateral = come from GTO , muscle spindles – these fibers cross over in the bottom of the brain stem – so they become contralteral in the brain stem but remain ipsilateral in the spine.
  28. How does pain and sensation travel up the cord?
    Sensation/Pain = travel contralateral through the spine – cross at segemental level so contralateral in the cord
  29. Name the cells in the PNS and CNS which sheath nerves and explain the difference between them?
    Schwan cells (neurolemmocyte) – produce the myelin sheaths in the peripheral nervous system – only wraps one neuron. – create the myelin sheaths in the PNS - produces the myelin sheathing or membrane around the peripheral axons in the PNS. They form by wrapping the Schwan cell around the axon over and over again until it forms a double membrane around the axon, in the process most of its cytoplasm is squeezed out of the cell. During this process the schwan cell myelinates down the whole but it leaves gaps called nodes of ranvier – these gaps allow for saltatory conduction – which literally means jumping conduction in latin – this is when the electrical imbalances jumps form one gap to the next speeding up conduction. In essences these nodes act as booster stations.

    oligiodendrocytes – (literally means few branch cells – they wrap around several neurons) myelinates several neurons of the central nervous system.
  30. What are Neuroglial cells?
    Neuroglial cells – means nerve glue – this is the supportive cells in the nervous system that are not neurons.
  31. Name the characteristic of a neuron?
    Special characteristics neurons -

    • Specialized for conduction –
    • though other cells can become excited or even conduct only neurons are designed to conduct down along there lengths.
    • Very sensitive to O2 deprivation – hence they will die very quickly without O2 – this is why with stroke pt we need to get them to an ER at once to prevent loss of brain cells. (there is only 10 sec of O2 in the brain at any time)

    Neurons don't have any Mitotic appuratus – hence no mitotis – so once you kill a nerve cells it wont regrow . If we could regrow nerves we would be able to cure parkinson, stroke and other diseases that cause neuron damage.

    However there is one place in the nervous system were neuron can and do regrow all of the time this is the olfactory nerves which are continuously dieing and regrowing.
  32. Explain what inhibitory neurons do and how they cna effect each other?
    inhibitory neuron – turns off neuron signal – can decrease or out right stop the signal depending on other neurons near by. So if activated a inhibitory neuron will decrease a signal being sent through it, however if this inhibitory neuron is attached to another inhibitory neuron then the second neuron can inhibit the inhibition effect of the first inhibitory neurons there by resulting in an uninterrupted signal from the presynaptic neuron before the inhibitory (and post synaptic) neuron.

    They also fight normal neurons to try and cancel a signal and prevent the axon hillock form firing for this reason they tend to be closer to the axon hillock them most neurons to increase the chances that they will be able to inhibit a neurons signal.
  33. Define decremental conduction ?
    In an axon conduction is all or nothing but within a denrite conduction you get decremental conduction.

    decremental conduction – literally means decay or to die of – this is when the strength of a signal decays as it travels away from the source (neuron) , which means that sometimes the signal will not reach the axon hillock or if it does it will be a lot weaker then the original signal.
  34. Explain what the axon hillock?
    Axon hillock – is the part of the neuron located on the soma were the axon starts – it is the integration center of the neuron – it absorbs all the different signal sent from various denrites integrates them and decides if the sum of these signals is strong enough to fire an action potential.

    Hence the father a neuronal attachment (axon) is from the axon hillock the more likely it's signal is to die off and not trigger an action potential and the closer a it is to the axon hillock the more likely it is to fire the action potential.

    Inhibitory neurons – fight normal neurons to try and cancel a signal and prevent the axon hillock form firing for this reason they tend to be closer to the axon hillock them most neurons to increase the chances that they will be able to inhibit a neurons signal.
  35. Name and define the types of summation?
    Types of summation

    temporal summation – is when a neuron fires lots of times very rapidly, these weak signals will then add up to a stronger signal in the denrite and therefore are more likely to trigger the axon hillock.

    Spacial summation – this when 2 or more signals from axon terminal that are close together in space both fire a signal and these signals add up to a stronger signal with a greater chance of firing the action potential at the axon hillock.
  36. What is the Soma?
    Cell body – also called the soma or perikaryon – is the trophic segment – this is the part of the cell which nourishes the rest of the cell. It contains all the normal cell organells and components with the exception of the mitotic aparratus.
  37. What are nissle bodies and what do they do?
    Nissle bodies – discrete granular bodies of variable size that occur in the cell body and dendrites but not the axon of neurons, are composed of RNA and polyribosomes, called also Nissl granules. These are found in others of the body but are very prominent in neurons. Within neurons they produce micortubles that have two functions.

    • They create the internal skeleton for the nerves
    • they form neurofibrils which are made of long pipes that make up the center of the axon – these tubes are responsible for transporting varies things such as nutrients and neurotransmitters and other things up and down the axon to and from the soma. This is how neurotransmitters which are create din the cell body get the to the axon terminals for release.
  38. What is the Axon?
    Axon – is the long wire like structure on a neuron which ends in axon terminals at the synaptic junction. There length ranges from smaller then 1mm to longer then a meter. This is the conductive element of a neuron.
  39. What is the axolemma and why is it important?
    axolemma - is the outer layer of axon - is the cell membrane surrounding an axon. It is responsible for maintaining the membrane potential of the neuron, and it contains ion channels through which ions can flow. When this occurs, the voltage inside the axon changes, and depolarization or hyperpolarization of the membrane can occur. Adequate depolarization can lead to an action potential, which travels down the axon in a self-propagating manner as more ion channels open due to stimulation by the influx of positive ions. If the axolemma is damaged, it becomes unable to perform its vital role of maintaining the concentration gradient of ions inside and outside of the cell. When ions move down their concentration gradient into the cell, they can cause a number of different cellular processes that may lead to cell damage or cell death.
  40. Explain the method of transports used inside of an axon?
    Methods of transportation within the axon

    Axonal transport – this is a very fast very direct transport system that runs to and from the soma to the axon terminals – which means it does 2 way transport of Various things. Example: neurotransmitters are sent down to the axon terminals and stuff like waste products and samples of nerve growth factor are sent up to the cell body. Unfortunately this system is also used by bad things like the rabies to infect the cell body.

    Axoplasmic flow – this is a slow and one way transport system – this system involves the movement of things through the streams of protoplasm, from proximal to distal. The advantage of this system is that it move very big stuff which can't be moved by axonal transport. Travels only about a mm a day.
  41. What is the axon terminals?
    Axon terminal – is one side of the synapse and this is were synaptic bulps are located which release neurotransmitters into the synaptic cleft.

    Neural transmission is very fast but it does go to the synapse and the synaptic gap does cause a slight delay.
  42. Explain Acetylcholine? and what breaks it down?
    Acetylcholine – this is an exicitory neurotransmitter found in the nerve cells of motor neurons of the somatic motor system. Specifically, acetylcholine is released by cholinergic fiber/neurons. Most post synaptic neurons have receptors capable of reching Ach.

    cholinesterase is a family of enzymes that catalyze the hydrolysis of the neurotransmitter acetylcholine into choline and acetic acid, a reaction necessary to allow a cholinergic neuron to return to its resting state after activation. Or in other words it breaks down acetylcholine so it doesn't hang around and over stimulate a synapse.
  43. Explain Myasthenia gravis, and what drug is it treated with?
    Myasthenia gravis – (names means grave muscle weakness) is a pathology were antibodies sit on some of the acetylcholine receptors there by blocking them , so that acetylcholine can't act as effectively on the far side of the synaptic junction. This is why we give such a pt neostigmine which will cause the acetylcholine to hang around longer which gives it more of a chance of triggering the few unblocked receptors. The primary symptoms of this disease is muscle weakness. This disease tends to attack cranial nerves first, in particular it effects the fascial nerve first. Most common symptoms in pt developing this disease is tired and weak fascial muscles , this effect is worse at the end of the day. It can also effect swallowing and this can cause choking. This becomes lethal if it effects the vagus. For exterme causes the pt may carry neostigmine.

    Neostigmine (Prostigmin, Vagostigmin) is a parasympathomimetic that acts as a reversible acetylcholinesterase inhibitor. Or in other words it is a drug which inhibits the effects cholinesterase there by keep acetylcholine around longer. This is used to treat diseases such as Myasthenia gravis.
  44. Name the Neurotransmitters we care about?
    • Acetylcholine
    • Dopamine
    • epinephrine and nor epinephrine
    • Serotonin
    • Glutamate
    • Substance P
    • GABA – gamma aminobutyric
  45. Explain Parkinson's disease and treatment?
    Parkinson's disease (also known as Parkinson disease, Parkinson's, idiopathic parkinsonism, primary parkinsonism, PD, or paralysis agitans) is a degenerative disorder of the central nervous system. The motor symptoms of Parkinson's disease result from the death of dopamine-generating cells in the substantia nigra, a region of the midbrain; the cause of this cell death is unknown. Early in the course of the disease, the most obvious symptoms are movement-related; these include shaking, rigidity, slowness of movement and difficulty with walking and gait. Later, cognitive and behavioural problems may arise, with dementia commonly occurring in the advanced stages of the disease. Other symptoms include sensory, sleep and emotional problems. PD is more common in the elderly, with most cases occurring after the age of 50.

    Symptoms include: rolling tremors and gait disturbances – they will shuffle and then freeze and be unable to move during which they will shake. Another symptom is micrograffi.

    Modern treatments are effective at managing the early motor symptoms of the disease, mainly through the use of levodopa and dopamine agonists ( is treated with L Dopa which is a precursor to dopamine which is small enough to pass through the mengines into the CNS were it help create higher levels of dopamine). As the disease progresses and dopaminergic neurons continue to be lost, a point eventually arrives at which these drugs become ineffective at treating the symptoms and at the same time produce a complication called dyskinesia, marked by involuntary writhing movements. Diet and some forms of rehabilitation have shown some effectiveness at alleviating symptoms. Surgery and deep brain stimulation have been used to reduce motor symptoms as a last resort in severe cases where drugs are ineffective.
  46. What is Micrografti ?
    Micrografti – or very small handwritting
  47. What is epinephrine and nor epinephrine?
    • epinephrine and nor epinephrine – Epinephrine (also known as adrenaline) is a hormone and a neurotransmitter. It increases heart rate, constricts blood vessels, dilates air passages and participates in the
    • fight-or-flight response of the sympathetic nervous system. In chemical terms, adrenaline is one of a group of monoamines called the catecholamines. It is produced in some neurons of the central nervous system, and in the chromaffin cells of the adrenal medulla from the amino acids phenylalanine and tyrosine.

    Norepinephrine(INN) (abbreviated norepi or NE) is the US name for noradrenaline(BAN) (abbreviated NA, NAd, or norad), a catecholamine with multiple roles including as a hormone and a neurotransmitter. Areas of the body that produce or are affected by norepinephrine are described as noradrenergic. The terms noradrenaline (from the Latin) and norepinephrine (derived from Greek) are interchangeable, with noradrenaline being the common name in most parts of the world. However, to avoid confusion and achieve consistency, medical authorities have promoted norepinephrine as the favoured nomenclature, and this is the term used throughout this article. One of the most important functions of norepinephrine is its role as the neurotransmitter released from the sympathetic neurons affecting the heart. An increase in norepinephrine from the sympathetic nervous system increases the rate of contractions. As a stress hormone, norepinephrine affects parts of the brain, such as the amygdala, where attention and responses are controlled. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle. It increases the brain's oxygen supply. Norepinephrine can also suppress neuroinflammation when released diffusely in the brain from the locus coeruleus. When norepinephrine acts as a drug, it increases blood pressure by increasing vascular tone (tension of muscles) through α-adrenergic receptor activation; this causes a compensatory reflex that results in a drop in heart rate, "reflex bradycardia". Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase.[8] It is released from the adrenal medulla into the blood as a hormone, and is also a neurotransmitter in the central nervous system and sympathetic nervous system, where it is released from noradrenergic neurons in the locus coeruleus. The actions of norepinephrine are carried out via the binding to adrenergic receptors.
  48. What does serotin do? What drug inhibits its uptake?
    Serotonin – important in weight loss – this is a neurotransmitter used in the reticular formation – which is a network of neurons in the brain stem that keep us awake, damage to this system will lead to comma or sleep.

    Prosac – inhibits the reuptake of serotonin. So happy pill.
  49. What is GABA? name a GABA agnoist?
    GABA – gamma aminobutyric - is the chief and the most inhibitory neurotransmitter in the mammalian central nervous system. It plays a role in regulating neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone.

    Baclofen – is a drug used in PEDs for children with spastic dsyplesia or cerebral palsy. Is a powerful GABA agnost which means it mimics GABAs – however dosage must be carefully calibrate because to much makes the pt sleep but the right amount can reduce spasticity. This delivered to the pt through a implanted pump.
  50. What is Botulizing toxin used for?
    Botulizing toxin – or botox – is a toxin natural created by some of the bacteria that cause food poisoning. This drug is used to reduce the spasticity in a muscle by killing the motor end plates at synaptic junction. Example: kids with hyper contraction of the gastrocs have this done, it is very painful.
  51. What is Glutamate?
    Glutamate – common neurotransmitters found throughout the nervous system, in fact almost every neuron has a receptor for this neurotransmitter. This is an excititory neurotransmitter which causes calcium to enter the next cell. However to much of this will cause excessive calcium release which will cause the next cell to burn up, because calcium is what drives internal metabolism so to much of it entering the cell will cause it to run itself to death. So to much glutamate will run a cell to death. Inhibitor drugs for this neurotransmitter are used to help treat strokes. This can be a neurotoxin because concentration can cause excitotxity – or in other words to much glutamate makes for to much calcium release , which floods into a cell causing it overwork itself to death.
  52. What is the most commonly used drug to effect the synapses?
    Most common drug used to effect the synapses is caffine , it is an excitory drug which lowers post synaptic membrane potential.
  53. Why is Curare dangerous?
    Curare – blocks Ach neurotransmitter receptors sites on the muscle.
  54. What is substance P?
    Substance P enhances sensitivity to pain – is found/released by noriceptos in response to stimuli such as injury. They are a poly peptide, neurotransmitter involved in pain, which can be found in dorsal roots of pain fibers. It is also a mitogen. So it act to enhance pain and in regeneration of a damaged area.
  55. What is a mitogen?
    Mitogen – is a substance which stimulates the area around it to grow and bud off, so it causes mitossi in near by cells.
  56. Name the second messenger systems?
    • Types of second messenger systems
    • DAG– diacylglycerol
    • IP3= inositol triphosphate
    • Arachindonic acid
    • nicotinic
    • Muscarinic
    • Catecholamines
  57. Name the types of receptors on post synaptic membranes and explaine the difference between the two?
    Receptors on postsynaptic membrane

    Type I receptor – are fast acting because they are directly linked to ion channels – so they quickly (within millisecs) open ion channels when triggered.

    Some neurotransmitter can activate two types of receptor (Type I and Type II) ?? An example is Ach which can trigger nicotinic receptors which are fast type one receptors (which acts at motor end plates in muscularjunction) and muscarinic which is a slow type II receptor which acts on cardiac muscle and sweat glands.

    Type II receptor – is a slow receptor – when triggered it will take seconds to minutes to trigger a response , but these receptors continue to trigger a response for a long period time. These receptors also have to use a second messenger system. So the receptor triggers other things which trigger the second messenger receptor which is linked to ion channels.
  58. Explain myelin sheath healing?
    myelin sheaths in the PNS create a neurolemma or outer-layer of myelin around the neurons, however this doesn't happen in the CNS. This matter because when a neuron is damaged in the PNS the myelin dies and then the part of the axon was severed will die and the rest of the axon will wither back to the soma, but the myelin sheath (neurolema) is left behind as a sort of pipe. The damaged neuron will then send/grow out multiple new axon tendrils which will search for this tube. If one of them finds it they will then grow down it and the other tendrils with die off. Then a new schwann cells will replace the old dead neurolemma and the nerve will have fully regenerated. However. If the gap is to big this may not happen because the axons may not be able to find the tube, if this happens then the nerve will fail to regenerate. This process is very slow 1mm a day. In rare cases a axon tendril can grow into the wrong tube and then other effects are possible.
  59. What is the most common demyelinating disease of the CNS? explain its sign and symptoms? Give a factor that makes devoloping it less common? How is/was it diagnoised?
    Most common demylinating disease is MS – which is a problem with attacks on the myelin in the CNS but not in the PNS. This is when the mylein sheath in CNS are destroyed leaving behind plaques (scars) which disrupt nervous functions.

    There is more then one type of MS – some cause slower degeneration and other forms have a faster progression and the pt may grow worse quickly.

    • Detection
    • MRI – can see plaques

    Before the were MRI's doctors used to look for a weird collection of signs and symptoms – because the plaques would form randomly in the CNS causing random unrelated symptoms.

    Symptoms of MS – MS symptoms come and go as the diseases moves in and out of remission (or relapse) slowly growing worse.

    Ataxia – poor coordination (or poor motor control)

    Eye issues – common in the early stages – such as blurred vission , due to optic nerve issues , or diplopia = double vision

    Tingling in extremities (toes in fingers) , common early symptoms


    Intention tremor – tremor in limbs when the person is intending to move

    Fatigue – this can be very bad, during a flare up even putting on a heavy sweat shirt can can make a pt's arm to heavy to lift, another example would be sheets a pt in a flare up might not even be able to turn over with a sheet on them.

    • Dysarthia – (you will find this and not aphasia in MS pt's) this is when there is a mechanical issue with producing speech. Pt's with this tend to speak in a very robotic manner. Example: broken jaw, or
    • nerve issues with tongue.

    (uncommon symptom) inappropriate laughter

    Bowel and bladder issues – problems with voiding can lead to infections which can and often does kill the pt.

    • Clinical Note: some patient find that it is sitting (hanging over a toilet) on a toilet which makes it hard to pee, so some pt may find they can only pee if they
    • squat over a bucket.

    • Lhermitte's sign, - sometimes called the Barber Chair phenomenon, is an electrical sensation that runs down the back and into the limbs. In many patients, it is elicited by bending the head forward. It can also be evoked when a practitioner pounds on the posterior
    • cervical spine while the neck is flexed; this is caused by
    • involvement of the posterior columns. Lhermitte's
    • sign is named for Jacques Jean Lhermitte, a French neurologist and neuropsychiatrist. Thus it is incorrect to spell the term as "L'hermitte's sign". The sign suggests a lesion of the dorsal columns of the cervical cord or of the caudal medulla. Although often considered a classic finding in multiple sclerosis, it can be caused by a number of conditions, including transverse myelitis, Behçet's disease, trauma, radiation myelopathy, vitamin
    • B12 deficiency (subacute combined degeneration), and compression of the spinal cord in the neck from any cause such as cervical spondylosis, disc herniation, tumor, and Arnold-Chiari malformation.
    • This also happens in spinal menigitis.

    There is no know cause or way to prevent MS. Also there is no animal model of MS which makes it hard to study. MS may be an autoimmune disease.

    MS has 25% rate of concordance. Were as a disease like schisphenia has a 60% concordance rate.

    Chances of developing MS if you live in a cold climate 50/100,000, the chance of contracting MS decreases if you grew up or at least spent up till your teen years in a warmer climate, this may have something to do with the thalamus but we don't really understand why this is yet. So the warmer the climate you were raised in the less chance of developing MS you have. Example: a pt who grew up in Denver has 10x greater chance of developing MS then a pt who grew up in new Orleans and 50x the chance of someone who grew up in new Mexico. Korea – has almost no cases of MS. When a pt develops MS heat is bad for them and may make there conditions worse, so cold is better for them.
  60. Explain treatments for MS?
    Treatments for MS

    MS pt's are often put on corticosteriods such as prednizone to decrease inflammation and suppress their immune system. This is done because some believe it is an autoimmune disease.

    Betaseron is a multiple sclerosis (MS) medication that is available by prescription. It comes as an injection and is injected just under the skin every other day. Clinical studies show that people who took the drug experienced fewer MS relapses and had fewer lesions after two years of taking it. While most people tolerate the medication well, potential side effects include weakness, headaches, and flu-like symptoms. It increases/enhances the immune system. Why this works for some pt and immunosupressent work for other is unknown.

    PT treat MS by trying to decrease its signs in symptoms this is done in many ways , including energy concentration, moderate exercise (to much is bad and so is to little so it takes some skill to set this up) or even just by reducing the movements they have to make in ADLS.

    Most cases of MS occur between ages 20-40 – there has never been a case in people of less then 10 or over 60 years old. It is most common in white women (3/1 to male female ratio) of northern European descent between the ages of 20-40.
  61. Most common Demylinating disease of the PNS?
    • Guillain-Barre syndrome - is an acute polyneuropathy, a disorder affecting the peripheral nervous system. Ascending paralysis, weakness beginning in the feet and hands and migrating towards the trunk, is the most typical symptom, and some subtypes cause change in sensation or pain as well as dysfunction of the autonomic nervous system. It can cause life-threatening complications, in particular if the breathing muscles are affected or if there is autonomic nervous system involvement. The disease is usually triggered by an infection. The diagnosis is usually made by nerve conduction studies and with studies of the cerebrospinal fluid. With prompt treatment by intravenous immunoglobulins or plasmapheresis, together with supportive care, the majority will recover completely.
    • or to put it another way

    is a serious disorder that occurs when the body's defense (immune) system mistakenly attacks part of the nervous system. This leads to nerve inflammation that causes muscle weakness.
  62. What are the 3 structural names of neurons?
    Types of neurons by structure – you can tell which structural type of neuron a neuron is by how many projections it has from the soma.

    Bipolar – are the neurons of the specialized senses and are usually linked to cranial nerves

    Unipolar – 90% of sensory neurons are unipolar – they are often found in ganglion and specifically in the dorsal root ganglion.

    • Multipolar – almost all the other neurons in the CNS are
    • multipolar
  63. Define efferent/afferent?
    • Motor neurons = efferent – or outgoing nerves
    • Sensory neurons = afferent – in going neurons
  64. Define Dorsal Rhizotomy ?
    Dorsal Rhizotomy – is when surgeons cut some of the dorsal roots – this is done in cerebral palsy pts to reduce spascticity.
  65. Define the types of neurogilia cells?
    Neuroglial cells – nerve glue

    Oligiodendrocytes – cell provide myelin covering

    Microglial cells – there primary job is phagocytosis – eat junk in the CNS

    • Astrocytes – look like stars – there a different types
    • but there primary job is to support the interface between capillary and neurons and hence form the blood brain barrier.

    • Ependymal cells – produce the CSF – they are found in
    • groups or clumps of cells called choroid plexus which are glud to locations within the different centricles.

    • Satilite cells – found in the PNS support (this structural
    • support holds unipolar neurons steady) neurons in the dorsal root ganglion
  66. Define orthograda and retrograde?
    Orthograde or antigrade transport – is transport away from a cell body, both axoplasmic flow and axional transport are examples of this.

    Retrograde transport – transportation to the cell body from down the axon. This is a fast form of transport and in neurons only axonal transport counts as this form of transport.
  67. What effect does stimulating a nerve more have on newuroal transmission?
    Stimulating a nerve more won't increase the speed or amplitude of the action potential for once it fires it fires but it will increase the frequency or number of times it fires. So this would frequency modulation like with FM radio.
  68. What is GABA?
    GABA most well know and cited NT – gama amino butenic acid – can be an excititory in some places in the nervous system but is usually inhibitory
  69. List and define the refectory periods in neural transmission?
    Absolute refractory period – the time when no matter how hard you stimulate the axon there is no chance that it will fire – this last for 1/2 a millisecond after the first depolrization after this you have the relative refractory period

    Relative refractory period – this is the stage when a neuron can be fired but it requires greater levels of stimulus then normal to fire it. So a weak stimulis can't trigger it but a stronger stimulis can cause it to firer more often so the strength of stimulus is coded as frequency modulation or FM.

    These two effects create the change in signals
  70. What is Saltitory conduction?
    Saltitory conduction – the myelin sheath prevents any depolarization beneath it by blocking the ion channels , which causes the signal to die off at the sheath , which causes the signal to passively spread down the axon within the cell underneath the myelin – so this current flows down the axon passively and a passive signal is much faster and uses less energy then an active signal because you don't need to depolerize or repolerize the axon. Also it saves energy because none is required. However the signal dies of due to resistance in the axon. Within a mm or so the signal is gone, but right before it dies off there is a node of ranivia which refires the signal by depolarizing the axon in that area and this keep happening until it gets to the end of the axon. This is why this is faster and more energy efficient then unmyelinated axons. However it does take energy to have the axon sheathed with myelin.
  71. Explain speed of conduction?
    Speed of conduction = the square root of the membrane resistance / by the axon resistance

    The wider the axon the less resistance there is in the axon which means the bigger the axon is the faster it goes and this is even more true with myelinated axons.
  72. What is a Generator potential?
    Generator potential – need this to create an action potential – this is the cummulation of signals at the axon hillock. They are coded amplitude modulation (AM) so the stronger amplitude the greater the signal. you need a generator potential to get an axon potential because they generate the action potential -
  73. define decremental conduction?
    decremental conduction - transmission of an electric impulse in which the amplitude of the impulse decreases with distance.
  74. List the fiber types of neurons and there diameters?
    A fiber – don't need to know the speed but know the thickenes -

    • a alpha motor neurons – Diameter 12-20 um- the biggest fibers we have – there large size allows for the quick activation of muscles – conduction at 120 m a sec or 270 mile/hour. – more prone to injury from pressure palsy and ischemia due to there size. Hence with a brachio plexus injury these are the fiber hurt first.
    • A beta – 5-12 um
    • a gamma – 3-6 um
    • a delta - 2-5 um
    • B fibers - <3 um
    • C fibers – .3-1.3 um - unmyelinated – slow pain - .5-2 mm a sec -

    Small fibers like c fibers are easier to stimulate then big fibers with e-stim. Smaller diameter fibers are also more effect by drugs and anesthetics and ice. This is also true of ice hence why an ice cuff works to deafferent people for experiments because it shuts down the small sensory fibers first (used to deafferent someone for experiments).
  75. List the other classifiaction system for neuron Fibers?
    Fiber types (sensory only) – other classification system

    • type Ia – fibers form a muscle spindle (afferent) –
    • larger correspond to a alpha so are large and fast – gives you the rate or velocity of stretching of muscles

    • Type Ib – a alpha – goes to golgi tendon organ – this
    • detects force through the muscular tendonis junction

    • Type II – a beta – smaller then type I – also goes from
    • the muscle spindles – tells you how much your muscles have been stretched or the amount of stretch or static length. So it tells you something like I have been stretched to five inches.

    Type III – a delta – pain, Temperature

    Type IV – c fibers – deep aching pains
  76. Were does the spin start and end and what are the two imporant structures wihtin it?
    Spinal cord – start of the cord is in the foreamen magnum in the occipital bone – below that is the cord above that is the lowest part of the brainstem the medulla oblongata. The cord ends at about L2, at the conus medularis which is cone shaped swelling, the cord grows faster then the spine so it stops at L2 but the nerve roots keep going becoming the claudia equina.
  77. How many pairs of spinal nerves, cranial nerves and bones in the spine do we have?
    • Pairs of spinal nerves - 8-12-5-5-1
    • Bones in the spine – 33 (vertebrae) 7-12-5-5-4
    • Cranial nerves: 12
  78. explain a spinal tap?
    Spinal tap – is when CSF is removed form the spine from between the pia matter and the archnoid space. It is taken from below L2 usually Between L3-4 or L4-5 because there is no spine there so there is no risk of spinal damage.
  79. List the layer of the mengies and the space between them?
    Meninges – 3 layers of protective layers around the brain and cord

    • Epidural space – is a cushing layer between the bones of
    • the spine and skull and the dura mater - just a fatty space

    dura mater – tough mother – outlayer of meninges – goes all around the cord – it is very tough CT. Looks like plastic and is hard to remove from brain and bone in dissection because sticks to both.

    • Subdural space - potential space – no real gap unless
    • there is some kind of pathology involved

    • arachnoid mater – spider web – because it looks like a
    • spiders web as it send projection inward to connect with the pia mater.

    • Subarachnoid space – held open by the spider web like
    • projections and this is were we find the CSF.

    • pia mater – gentle mother – is a thin membranous sheath
    • which folds around every fold and crack of the brain and spinal cord

    All three layers go around the whole of the CNS.
  80. What are the Denticulate ligaments?
    These three sheaths are stabilized in the spinal cord by the denticulate ligaments and hold the cord so it doesn’t bang around in the back bone.
  81. Define and explain what the venous sinus and the arachnoid villi are?
    Dural or venous sinus - At the top of the brain the dura mater separates out , and this happens in other specific area of the brain. The outer layer stick right to the bone and inner layer is pulled in.

    So it splits into two layers endosteil (in the bone) or periosteal layer (around the bone) – this layer stick with the bone meningeal layer – this layer hangs inward

    Creating a venous sinus in the crack and fissures in the brain the most important and biggest of these sinus being the superior longitudinal sinus. It is the start of venous outflow from the brain. Or place were blood from the brain gets out.

    So blood comes in through vertebral arteries and the internal carotid arteries is turned into CSF and gets out through these venous sinus.

    Venous sinus – also important in CSF circulation because this is were we put the CSF back into the blood through the Arachnoid villi.

    Arachnoid villi – are protrusions from the subarachnoid space into the superior sagital sinus were we pump CSF back into the blood inside of venous sinus
  82. what are the properties and origins of CSF? What do doctors test it for?
    CSF – look like thinner egg whites because it has no blood in it. If there is blood in it they test for cerebral hemorrhage. If you do a spinal tap and there is blood in it then you have a spinal hemorrhage and this is very dangerous. There is a high concentration of proteins, sugar, sodium in CSF. If a pt has very low sugar in their CSF then this is bad – worst case scenario this could mean there is a infection sense bacteria like to live on sugar Example: streptococcus or bacterial meningitis.

    • Epedimial cells (a type of neuroglilial ) make CSF in the
    • ventricles in groups called a coriod plexus. They are responsible for filtering the blood and putting it into the sub arachnoid space.

    Epedymal cells are cilliated ot help keep CSF moving.

    Brain doesn't have a lymphatic system so the CSF act sort of like a lymphatic system for the brain getting rid of stuff.

    Coroid plexus – filter part of blood out and put it into the sub-arachnoid space.
  83. Explain ventricles and the flow of CSF in them? What are the two biggest potential bottle necks?
    There are 4 ventricles in the brain– two biggest are the lateral ventricles which communicate with a third ventricle which is in mid-line , which communicates with the fourth ventricle through the cerebral aqueduct.

    • So CSF is pushed down the lateral ventricles in to
    • the 3rd and then into the 4th, and around the
    • brain.

    The cerebral aqueduct can become a bottle neck because it can get to narrow or get blocked.

    • As CSF tries to go from the 4 ventricle into the cord , through the median aperture this small tube can also
    • become a bottle neck.

    if the shape of the ventricles changes then something is wrong example: brain tumor.
  84. How CSF is in the body at any moment and how much is made every day? what is the effect of a blockage of CSF in the brain in children?
    At any given time 200mL of CSF in the system (5-6 fluid ounces) – but you make 500mL a day but it being constantly created and dumped out of the brain – so there is a continual build up of pressure around the ventricles. So if it doesn't get absorbed as fast as it's made or you get a blockage in one of the bottle necks (such as the cerebral aqueduct) you can get hydrocephalis or water on the brain. This is a build up of CSF in the brain. In children because there skull hasn’t fused yet there head will just expand to accommodate it as the pressure form the ventricles just cause the fontal to give so the head expands, usually they place a shunt in to one of the ventricles to siphon some of this out and into the stomach, because it can lead to issues.
  85. What should we worry about if a child has spinobifida and the parent say he in a bad mood,having a bad day, sick, dizzy, confused or balance is off?
    Shunts are common in kids with spinobifida , because they often have hydrocephalis with the spinabifida so many have shunts.

    This can mean that the shunt is blocked, this is quite common and the first symptom is that the child behavior and motor control is off and this will get worse. It very important that these be dealt with at once.
  86. What are the symptoms of bacterial meningitis and how do you make sure it is bacterial meningitis ?
    bacterial meningitis – a very bad an infection inside of the pia mater and arachnoid layer – very dangerous and lethal – symptoms are high fever headaches and neck pain – the difference between it and the flue is that you will see neck guarding, hence limits sign – were they wont flex the neck.

    Limits sign – is when a pt stiffens up around the neck , so thier is neck guarding to avoid pain from stretching the meninges.