Neuroscience Test I

Front 1

What does a neuron need in order to survive?

Back 1

To survive, a neuron, just like any other cell:
requires a consistent energy supply of glucose and oxygen (the brain receives 20% of cardiac output)
it needs to be able to make ATP (mitochondria).
It also needs to be able to manufacture and transport proteins throughout the cell—and considering that a neuron can be nearly 3meters long, this is significant.

Front 2

What allows the neuron to adapt in response to increases or decreases in activity in order to support the communication demands in learning, memory, and recovery?

Back 2

The neuron also needs to be able to maintain its physical structure through the regular turnover—including the removal as well as the replacement—of cellular components (i.e., ion channels, receptors, cytoskeletal proteins). This capacity also allows the neuron to adapt in response to increases or decreases in activity in order to support the communication demands in learning, memory, and recovery.

Front 3

Therefore, Signs and Symptoms of nervous system involvement are due to

Back 3

Therefore, Signs and Symptoms of nervous system involvement are due to changes in the neuron’s communication function as well as the innate capacity of the neuron to maintain its structural integrity.

Front 4

Neuronal communication function is determined by:

Back 4

Neuronal communication function is determined by:

Neuron excitability or how easy or difficult it is for
inputs to bring the neuron to threshold.
Neuron capacity to propagate action potentials
down the axon.
Neuron capacity for synaptic communication—
on the presynaptic and postsynaptic sides.
(see slide 11 from Module 1 Topic 2 Part 1)

Front 5

Each of these factors necessary for neuronal communication function can be affected by:

Back 5

Each of these can be affected by:
Failure of the Na+/K+ ATP pump to sustain the concentration gradient across the cell. (see slide 5)
Impaired ion channel function (i.e., trolls don’t work)—flow of ions across the membrane is different interfering with AP propagation and synaptic function. (see slide 6 and 7)
Ionic concentration outside the cell changes. This is especially important with K+. (see slide 7)
Demyelination.

Front 6

Neuronal structural integrity is maintained by:

Back 6

Removal and disposal of old proteins and molecules as part of regular turnover.
Transcribe DNA to synthesize new proteins as part of regular turnover of proteins, in response to injury, in response to changes in activity to either increase or decrease the number of proteins (i.e., receptors)
Transport those proteins within the cell.

Front 7

Problems that result from pathologies that interfere with maintaining structural integrity can include:

Back 7

having too much or too little of a protein
the protein is abnormal
the protein is missing.
These problems will affect the cell’s function—it may alter it, disrupt it, or lead to injury and cell death.

Front 8

What is the effect of changing the potassium gradient outside the cell?

Back 8

Increase in extracellular [K+] (potassium ion concentration) will decrease the concentration gradient for K+ the effect will depolarize the cell due to the drop in [K+] gradient. This means that K+ will not want to leak out of the cell.

Decrease in extracellular [K+] will increase the [K+] gradient which will push more K+ out of the cellthe effect hyperpolarizes the cell.

Front 9

Motor signs and symptoms attributable to "loss of activity"

Back 9

Weakness
Paresis
Paralysis
Hyporeflexia/arreflexia
Flaccid/hypotonia

Front 10

Motor signs and symptoms attributable to "overactivity"

Back 10

Tics
Twitches
“Spasticity”
Hyperreflexia
Hypertonia

Front 11

Somato-sensory signs and symptoms attributable to "loss of activity"

Back 11

Anesthesia
Numbness

Front 12

Somato-sensory signs and symptoms attributable to "overactivity"

Back 12

Paresthesia
Dysesthesia
Tingling
Burning
Radiating pain
Skin crawling
Pins/needles

Front 13

Consciousness signs and symptoms attributable to "loss of activity"

Back 13

Coma
Concussion
Syncope

Front 14

Consciousness signs and symptoms attributable to "overactivity"

Back 14

Hallucinations
Seizures

Front 15

The signs/symptoms reflecting changes in neuron function and physical structure can be:
(extent/duration)

Back 15

The signs/symptoms reflecting changes in neuron function and physical structure can be:

TRANSIENT: the nervous system recovers with no signs/symptoms and no evidence of damage on standard imaging (i.e., CT or MRI).

INJURIOUS: requires a period of repair, regrow, regenerate, and remyelinate. Clinical signs/symptoms may resolve or improve from their original state, but there is evidence of damage or repair on imaging or change in function with evoked potentials (TMS, Nerve conduction, EMG).

KILL THE CELL: leaving the rest of the neurons to remodel and compensate to survive without it. Clinical signs and symptoms plus changes on imaging will persist—but they may improve or get progressively worse. Death can occur from necrosis, apoptosis, or (in the CNS) axonal transection followed by Wallerian Degeneration of the distal axon and death to the proximal axon/cell body.

Front 16

Three categories of onset of signs and symptoms

Back 16

ACUTE: Patient experiences signs/symptoms right away—within minutes up to 24 hours.

SUBACUTE: It takes a few days or weeks for signs/symptoms to be experienced (>24 hours up to 4 weeks)

CHRONIC: It will take months to years to know there are signs/ symptoms (>4 weeks).

Front 17

Options for Evolution of the course of signs and symptoms after onset:

Back 17

Evolution or the course of signs and symptoms after onset:

IMPROVE: after initial peak in signs/symptoms lessen but have not completely resolved.

STABLE/NON-PROGRESSIVE: after reaching max severity, show no major changes over time

PROGRESSIVE: original symptoms increase in severity and/or new symptoms appear over time

RELAPSE/REMIT: periods of signs/ symptoms followed by resolution or improvements. Then they appear again.

Front 18

Topography of signs and symptoms in the body:
(categories for classifying conditions)

Back 18

Topography of signs and symptoms in the body:

FOCAL: Signs and symptoms are confined to a one circumscribed anatomical area or to several contiguous structures in one area of the nervous system—unilateral right, left, or across midline

MULTIFOCAL: more than one area or several non-contiguous areas. If bilateral, assymetrical distribution of signs and symptoms.

DIFFUSE: distributed across wide areas of the nervous system in one level or several, bilateral and symmetrical.

NOTE: topography also assists with localization of the lesion

Front 19

What general temporal profile and topography suggests a mass lesion? (one that is affecting systems based on size/encroachment)

Back 19

Focal and progressive neurological deficits

Front 20

What general temporal profile and topography suggests a vascular condition?

Back 20

acute deficits, which may be focal or diffuse and nonprogressive (ischemia) or progressive (hemorrhage)

Front 21

What general temporal profile and topography suggests inflammatory disorders?

Back 21

subacute, progressive deficits, which may be focal or diffuse

Front 22

What general temporal profile and topography suggests neoplasia?

Back 22

focal, chronic, progressive

Front 23

What general temporal profile and topography suggests degenerative disorders?

Back 23

diffuse, chronic, progressive

Front 24

What general temporal profile and topography suggests metabolic or toxic disorders?

Back 24

diffuse deficits, which may be acute, subacute, or chronic

Front 25

What general temporal profile and topography suggests traumatic lesions?

Back 25

acute (immediate) focal or diffuse deficits that are stable or improve, but they may also manifest as chronic, progressive disorders

Front 26

What general temporal profile and topography suggests a nonmass lesion?

Back 26

diffuse signs and symptoms, whether progressive or not, or nonprogressive signs or symptoms

Front 27

Which types of deficits (reservoir dogs) can be acute?

Back 27

trauma
vascular
toxic/metabolic

Front 28

Which types of deficits (reservoir dogs) can be subacute?

Back 28

inflammation
toxic/metabolic

Front 29

Which types of deficits (reservoir dogs) can be chronic?

Back 29

toxic/metabolic
degenerative
neoplastic

Front 30

Necrosis pathway to cell “explosion” is triggered by what intensity/duration?

Back 30

Necrosis pathway to cell “explosion” is triggered by acute and severe changes in function and/or structure. Energy failure (see next slide) and failure to maintain ionic gradient.

Front 31

1o Necrotic cell death explosion causes mass glutamate release into extracellular space. This triggers...

Back 31

1o Necrotic cell death explosion causes mass glutamate release into extracellular space. This triggers 2o EXCITOTOXICITY setting off necrotic cell death to surrounding cells.

Front 32

Apoptosis pathway to cell death is triggered by...

Back 32

Apoptosis pathway to cell death is triggered by chronic, slow acting sustained or repetitive changes in function and/or structure that trigger intracellular signaling cascade that kills that cell.

Front 33

The pathological processes of Mr. Degenerative diseases (as well as Mr. Neoplastic) start well before clinical signs and symptoms present. How does the nervous system hide this problem for so long?

Back 33

The same mechanisms that permit recovery after injury are the same as those that hide a disease for a period of time: the nervous system is very adaptable.

Synaptic remodeling and unmasking of silent synapses.
Axonal sprouting and collateral innervation of targets by intact neurons
Regions will take on the functions of an injured or destroyed region.
In the PNS axons may regrow.
In both the PNS and CNS there is remyelination.
There is some evidence of neuron regeneration but this is rare.

Front 34

The signs and symptoms of stroke or TIA are the same, but distinct from other things because

Back 34

they happen quickly
Sudden:
numbness or weakness of the face, arm or leg (esp. unilateral)
confusion, trouble speaking or understanding speech
Trouble seeing in one or both eyes
trouble walking, dizziness, loss of balance or coordination
severe headache with no known cause

Front 35

Why is there a need to act fast with strokes?

Back 35

There is a blood-clot dissolving drug that can be administered, and may have an effect on disability if given within the first three hours from the onset of symptoms

Front 36

Most TIA’s neurologic symptoms resolve within...
what's a silent stroke?

Back 36

Most TIA’s neurologic symptoms resolve within <60 minutes. A “silent stroke” is the opposite of a TIA—the individual may not notice neurologic symptoms; however, there is evidence of an infarct/tissue damage on CT scan.

Front 37

What are the "core" and ischemic penumbra?

Back 37

The key pathophysiological concept is the distinction of hypoperfused tissue into operational compartments; tissue that will inevitably die (core) and tissue that may either die or survive (the ischaemic penumbra). Reduction of cerebral blood flow from its normal mean, around 50 mL/100 g per min, to less than 20 mL/100 g per min, results in impaired neural function but preserved tissue integrity; this defines the penumbra. Unless early reperfusion occurs, the penumbra is gradually recruited into the core—ie, the volume of irreversibly damaged tissue grows and the amount of penumbra decreases.

Front 38

Tissue outcome following stroke depends on two factors:

Back 38

Tissue outcome depends on two factors: 1) the severity of flow reduction and 2) its duration. Rescue of the penumbra, either by restoration of blood supply or by interruption of the adverse metabolic or neurochemical cascade, is the basis of acute stroke therapy. Survival of the penumbra is the main determinant of clinical recovery and probably underpins peri-infarct reorganisation. Thus, although mapping the core provides a marker of the inevitable damage, mapping the penumbra shows the potential for recovery.

Front 39

What happens in the brain after a concussion?

Back 39

The sudden stretching of the neuronal and axonal membranes initiates an indiscriminate flux of ions through previously regulated ion channels and transient physical membrane defects. This process is followed by a widespread release of a multitude of neurotransmitters, particularly excitatory amino acids (I.e. gluatmate)], resulting in further changes of neuronal ionic homeostasis. Ionic homeostasis requires extra work from nak pump but it hurts the mitochondria—so it is impaired in its ability to produce glucose. Therefore see an initial spike in glucose utilization followed by a period of depression—this is suggested to be the new marker for neuronal vulenrabiltiy.

Front 40

Why is the brain more susceptible to damage after a concussion?

Back 40

Period of reduced brain energy metabolism—sets up deficits in axons/neurons that were long enough (i.e. length of axon connections between targets) to be injured. Concussion induced pathophysiologic conditions, mainly manifested by energetic metabolic perturbations, make the brain more susceptible to severe and irreversible cellular injury by a second impact of modest entity, creating a disproportion between the trauma severity and the subsequent cerebral damage.

Front 41

Describe the clinical presentation of a concussion

Back 41

This complex pathophysiology represents the modern explanation of the clinical presentation of concussion—a capricious combination of headache, dizziness, insomnia, fatigue, lethargy, uneven gait, nausea/vomiting, blurred vision, attention difficulty, concentration problems, memory problems, orientation problems, self-appraisal problems, expression and speech or language problems, irritability, depression, anxiety, sleep disturbance, problems with emotional control, loss of initiative, blunted affect, somatic preoccupation, hyperactivity, disinhibition, or problems related to employment, marriage, relationships, and home and or school management.”

Front 42

What is second impact syndrome?

Back 42

“A handful of previously published cases have reported on patients (mostly involved in sports-related activities) who, while still having symptoms from a previous head injury, experienced a second injury that unexpectedly and unpredictably led to sustained intracranial hypertension and catastrophic outcomes.”

“Second impact syndrome (SIS), is the occurrence of catastrophic cerebral edema after mTBI/concussion.“

“…within days after a simple blow to the head, [the] intricate biochemical derangement [after concussion] can result in a dangerous state for the brain, generating a situation of metabolic vulnerability to the point that if another equally ‘mild’ injury were to occur, the 2 concussions would show the biochemical equivalence of a severe brain trauma.”

“The reason why SIS is, fortunately, an extremely rare condition is probably because it represents a sort of “perfect storm,” an extremely random and hardly predictable situation generated by the odd combination of the severity of the initial concussion, the time interval between the 2 traumas, and the metabolic state of the brain at the time of the second concussion.”
FROM: The Pathophysiology of Concussion PM R 2011;3:S359-S368

Front 43

What is Chronic Traumatic Encephalopathy (CTE)?

Back 43

What is Chronic Traumatic Encephalopathy (CTE)?
A neurodegenerative disease characterized by a brain that contains deposits consisting of neurofibrillary tangles of tau protein similar to those found in the brains of Alzheimer’s disease (AD) patients. Unlike Alzheimer disease (AD) or many other tauopathies, the tau immunoreactive abnormalities tend to cluster at the depths of sulci, around small blood vessels, and in superficial cortical layers.

Chronic traumatic encephalopathy (CTE), has only been found in individuals with a history of repetitive brain trauma.

Although CTE is associated with a history of repetitive brain trauma, the exact relationship between the acute traumatic injury and CTE is unclear. It has been hypothesized that a neurodegenerative cascade is triggered by repetitive axonal stretching and deformation induced by trauma, particularly in individuals with previous unresolved concussive and/or subconcussive injuries.

Repetitive brain trauma appears to be a necessary variable for the development of CTE but may not be sufficient. All neuropathologically confirmed cases of CTE have had a history of brain trauma exposure but not all individuals with exposure to brain trauma develop CTE. There are many other nongenetic variables to consider when evaluating an individual’s risk of developing CTE (Table 5 next slide ). As stated, all confirmed cases of CTE have had a history of repetitive brain trauma. However, the specific nature of the brain trauma exposure necessary for the development of the disease is not yet known

Front 44

“It is important to note that the clinical presentation of CTE is distinct from the long-term sequelae of a concussion or from PCS. CTE is not the accumulation of symptoms from the earlier injuries.

Rather,

Back 44

“It is important to note that the clinical presentation of CTE is distinct from the long-term sequelae of a concussion or from PCS. CTE is not the accumulation of symptoms from the earlier injuries.

Rather, the symptoms of CTE, like other neurodegenerative diseases, results from the progressive decline in functioning of neurons or of the progressive neuronal death. That is, when there is sufficient disruption of normal neuronal functioning, symptoms specific to the area(s) of that disruption will begin to exhibit…. the symptoms of CTE begin insidiously and are apparently unrelated to earlier impairment. In other cases, PCS symptoms may completely abate months or years before the onset of CTE symptoms. In still other cases, there may be overlap; that is, the PCS symptoms may begin to abate but CTE symptoms gradually worsen at the same time. Typically, CTE symptoms present in midlife, usually years or decades after the end of exposure to repetitive brain trauma (ie, retirement from sports).”

Front 45

Early clinical presentation of Chronic Traumatic Encephalopathy
vs.
Later clinical presentation of CTE

Back 45

memory
executive dysfunction - planning
depression and/or apathy
emotional instability
impulse control problems - "short fuse"
suicidal behavior

vs.

Worsening memory impairment
Worsening executive disfunction
language difficulties
aggressive and irritable behavior
apathy
motor disturbance, including parkinsonism
dementia

Front 46

What are the grey matter structures in the PNS?

Back 46

Gray matter: Ganglia with cell bodies
Dorsal root ganglia (cell bodies for all sensory neurons with a receptor in the periphery—both somatosensory as well as the ANS axons). Proximal to IV foramen.
ANS efferent ganglia—for example, the paravertebral ganglia in the sympathetic chain (see figure on the right). ANS peripheral ganglia have the cell bodies for the second neuron i.e. the “post-ganglionic cell bodies.” Distal to IV foramen. NOTE: there are additional autonomic ganglia--we will discuss them during Module 3.

Front 47

What are the white matter structures in the PNS?

Back 47

White matter: Nerves—axons and myelin from Schwann cells surrounded by connective tissue.
Axons—classified by size/diameter, myelination, speed/conduction velocity, and information carried (motor, sensory, ANS). Synonym for axon: “fiber”
Myelin sheath around the axon—formed by Schwann cells.
Connective tissue coverings and blood supply:
Endoneurium—surrounds the axon and its myelin sheath. Weak.
Perineurium—surrounds a fascicle or bundle of axons and the capillaries. Strong tubule of collagen/elastin. Necessary for axon regrowth after trauma.
Epineurium—surrounds the entire nerve—all the fascicles/bundles and the aterioles/venules that supply the deeper capillaries. (figure on the right shows nerve in the muscle belly leaving a synapse in the muscle on its left, travelling next to blood vessels next to it on its right).

Front 48

What are the anatomical structures of the Peripheral Pathway—between the spinal cord and the Somatic receptors/effectors?

Back 48

What are the anatomical structures of the Peripheral Pathway—between the spinal cord and the Somatic receptors/effectors?

Roots
Spinal Nerve
Rami
(Plexus)
Peripheral Nerve

Front 49

The different axons in the periphery are categorized by:

Back 49

FUNCTION CARRIED—Somatosensory, Somatomotor, Autonomic sensory and motor
DIAMETER/SIZE
MYELINATION
SPEED/AP CONDUCTION VELOCITY.

see chart for specifics
FUNCTION CARRIED because of the associated receptor/effector—column on the right.
SIZE—Diameters range between 1μm – 20μm diameter
SPEED/AP CONDUCTION VELOCITY—ranges between 0.5m/sec(1.12mph) up to 120 m/sec(268mph)
MYELINATION—unmyelinated axons have smaller diameters, have slower conduction velocities and carry autonomic information as well as slow pain and warm temperature. Myelinated axons are larger, have faster conduction velocities and carry motor, proprioceptive, discriminative touch, fast pain, and cold temperature.

Front 50

Somatosensory Modalities:
(what different things can be perceived)

Back 50

Touch—mechanoreceptors for fine, crude
Pain—nociceptors fast, slow and specialized thermo, mechano, and chemoreceptors
Proprioception—mechanoreceptors for motion, position
Temperature—thermoreceptors for cold, warm
Visceral:mechano (i.e. distention), chemo, thermo (for core temp), nociception

Front 51

How are neuron fibers organized in terms of axon conduction velocity?

Back 51

Notice that proprioceptors in the muscle (Ia, Ib), the joint capsule receptor (Aα), and the alpha motor neurons have the same values. These are the fastest axons.
Both II and Aβ have the same values—they are the second fastest.
Next are the gamma motor efferents.
The smallest myelinated axons are the III, Aδ, and B PNS motor efferents.
The remaining fibers—IV and C are the smallest and unmyelinated.

Front 52

Do unmyelinated axons have a relationship with schwan cells?

Back 52

apparently so! still embedded in the cytoplasm... weird

Front 53

Motor pool

Back 53

Motor Pool—distribution of all the lower motorneuron cell bodies in the spinal cord that innervate the soleus.

Most references state that the soleus is innervated by the tibial nerve—and by spinal nerve roots L5, S1, S2.

What this means: motorneurons whose cell bodies are between L5 and S2 send their axons out the ventral roots at L5, S1, and S2. These axons go to the spinal nerves L5, S1, S2, then to the ventral rami. Then they enter the lumbosacral plexus to emerge in the Sciatic nerve, and then branch off into the Tibial nerve to eventually innervate the soleus muscle.

Front 54

Motor Unit:

Back 54

Motor Unit: One motor unit in the soleus—a single motor neuron from the motor pool and the muscle fibers it innervates. Motor neurons can innervate a few muscle fibers up to 1000’s of skeletal muscle fibers (dots in the figure showing motor unit in soleus)

Front 55

Compare somatic motor system to the autonomic motor system:

Back 55

Compare somatic motor system to the autonomic motor system:
ANS uses a two neuron efferent-relay to get to target tissue
Unlike the motor system which uses one alpha motor neuron to transfer info from the CNS to innervate skeletal muscle, ANS efference uses two neurons to innervate their targets

Where the innervation of a muscle can be traced back to relatively precise spinal levels (i.e., Biceps innervated by neurons whose cell bodies are found between C5 and C6 spinal levels), the innervation of the body by the SNS is much more diffuse//imprecise.

Front 56

Differences between sympathetic and parasympathetic systems

Back 56

Pre-ganglionic cell bodies and Target Tissues:
Sympathetic: T1-L2
• Organs of head, neck, trunk, & external genitalia
Adrenal medulla
• Sweat glands in skin
• Piloerector muscles of hair
• ALL vascular smooth muscle—skin, muscle, organs
Sympathetic system is distributed to essentially all tissues in the body (because of vascular smooth muscle)

Parasympathetic: CNIII, VII, IX, X & S2-S4
• Organs of head, neck, trunk, & external genitalia
Parasympathetic system NEVER reaches limbs or body wall—does not influence skeletal muscle or skin

Front 57

QUESTION: How do the SNS post-ganglionic axons get into the spinal nerves of C1-S5 when the pre-ganglionic cell bodies are only located between T1 and L2?

Back 57

Sympathetic
Pre-ganglionic cell bodies T1-L2
Thoracolumbar spinal cord

Pre-ganglionic axons exit from T1 – L2 ventral roots
of the spinal cord and enter the sympathetic chain (paravertebral ganglia).

Prior to synapsing on the post-ganglionic neuron, the pre-ganglionic axon can travel rostrally or caudally to another spinal nerve root level in the sympathetic chain.
Sympathetic
Post-ganglionic cell bodies for Body
(skin, muscles)
Paraverterbral sympathetic chain C1-S5


Post-ganglionic axons exit from
C1-S5 spinal nerves to go to periphery

Front 58

Pre-ganglionic -> post-ganglionic innervation of the SNS

Back 58

Innervation of:
Skin—smooth muscle of blood vessels to vasodilate and vasoconstrict, sweat glands & piloerector muscles

Skeletal Muscle—blood vessels vasoconstrict


T1-T5 preganglionic C1-T2 post-ganglionic to head, neck, UE

T6-T12 preganglionic T1-L3 post-ganglionic to the torso

T12-L2 preganglionic L2-S5 post-ganglionic to the pelvis and LE.

Front 59

Sensory neurons in the peripheral nervous system are pseudo-unipolar meaning

Back 59

meaning...one axon extends from the cell body and bifurcates (see slide 7 for a different image).

The distal branch/ peripheral axon is the sensory afferent fiber connected to the receptor.
The proximal branch / central axon is the branch that enters the spinal cord dorsal root.
The cell body is in the dorsal root ganglion.

Front 60

Neurodiagnosis step 1: Are the signs/symptoms neurologic?

Back 60

Clinical question 1: Which system(s) has(have) signs/symptoms?
There are 5 major functions of the nervous system that produce signs/symptomswe can test with our clinical tests:
Motor
Sensory
Cognition/mental status
Consciousness
Internal Regulation (ANS)

Front 61

Neurodiagnosis step 2: Where is the lesion?

Back 61

Clinical question 2: What is the distribution of the signs/symptoms—where are they in the body and what is their quality?
Anatomical level: Brain, Brainstem/Cerebellum, Spinal Cord, Peripheral
Where in that level—structure/structures?
Topography: focal, multifocal, diffuse
Left, right, midline, bilateral

Front 62

Neurodiagnosis step 3: What is the lesion pathology?

Back 62

Trauma/physical injury
Vascular
Inflammatory
Degenerative
Neoplaßstic
Toxic/Metabolic
Congenital

Clinical question 3:When did the signs/symptoms start? How have they changed since the start?
Onset: Acute, Subacute, Chronic
Evolution/Course: stable, improving, progressive (worsen, addition of other symptoms/signs), relapse/remit)

Front 63

What constitutes the BRAIN/SUPRATENTORIAL LEVEL of the nervous system?

Back 63

BRAIN/SUPRATENTORIAL LEVEL
Cerebral hemispheres: cerebral cortex & subcortical white matter
Basal Ganglia
Thalamus
Hypothalamus
Cranial nerves I and II

Front 64

What constitutes the BRAINSTEM & CB/POSTERIOR FOSSA/INFRATENTORIAL LEVEL of the nervous system?

Back 64

BRAINSTEM & CB/POSTERIOR FOSSA/INFRATENTORIAL LEVEL
Midbrain—CN III, IV nuclei
Pons—CN V, VI, VII, VIII nuclei
Medulla—CN VIII, IX, X, XI, XII nuclei
Cerebellum
Ascending and descending white matter tracts between brain & brainstem, brain & spinal cord, brainstem & spinal cord

Front 65

What constitutes the SPINAL CORD LEVEL of the nervous system?

Back 65

SPINAL CORD LEVEL
Ascending and descending white matter tracts to and from brain & brainstem.
Origin for the spinal nerves peripheral nerves (i.e. nuclei=motor pools)

Front 66

Peripheral Region Lesions:
Systems affected that can produce peripheral symptoms and their qualities:

Back 66

Motor—LMN signs (weakness, hyporeflexia, atrophy**)
Sensory—Light touch, Sharp/Dull, 2pt Discrimination, Temperature, Vibration
ANS—local sweat, vasodilation/constriction in region supplied by the nerve

Front 67

3. Pathology—sign/symptoms by target of process (myelin, axon, NMJ, neuron cell type, effector/receptor)

Diffuse—

Back 67

Diffuse—bilateral, symmetrical Polyneuropathy
Typically caused by inflammation, degeneration, neoplastic, or toxic/metabolic.
May be specific to myelin, fiber/neuron cell type (large or small diameter, long or short axons), NMJ, effector/receptor, and/or myelin.

Front 68

3. Pathology—sign/symptoms by target of process (myelin, axon, NMJ, neuron cell type, effector/receptor)

Focal—

Back 68

confined to single nerve root, plexus, or peripheral nerve, right or left Mononeuropathy
Typically caused by trauma—entrapment/compression or cut/laceration. Maybe by local vascular infarct.
Affects all fibers in nerve. Acute or subacute onset

Front 69

3. Pathology—sign/symptoms by target of process (myelin, axon, NMJ, neuron cell type, effector/receptor)

Multifocal—

Back 69

Multifocal—multiple focal lesions (non-contiguous). If present bilaterally, will be asymmetrical

Front 70

To do its job, a neuron needs

Back 70

1. level of excitability
2. maintain ability to propogate action potentials
3. ability to do synaptic transmission

Front 71

what three things are necessary for cell survival

Back 71

1. adequate and continuous energy supply (glucose, O2
2. turn energy into ATP
3. make/transport proteins

Front 72

What electrical changes can interfere with neural function?

Back 72

1. failure of sodium/potassium pump
2. impaired ion channels
3. altered ion concentration outside the cell
4. demyelination

Front 73

What somatosensory info travels in the doral columns and what is in the spinothalamic tract?

Back 73

dorsal columns - light touch, proprioception, vibration
(synapse on contralateral brainstem, travel on ipsilateral side)

spinothalamic - pain, temp, crude touch
(synapse in spinal cord, cross, and go up)

Front 74

Where are the preganglionic and postganglionic cell bodies of the autonomic nervous system?

Back 74

preganglionic sympathetic cell bodies in lateral horn of spinal cord,
postganglionic sympathetic cell bodies in paravertebral ganglion

Front 75

What fibers are responsible for crude touch?

Back 75

C fibers

Front 76

what fibers are responsible for fine/light touch?

Back 76

ABeta fibers

Front 77

What nerve roots do sympathetic neurons come from?

Back 77

T1-L2, but travel to all levels

Front 78

What sensory neurons and sensations are big/fast?

Back 78

Abeta
mechano
discriminate touch
proprioception

in dorsal columns

Front 79

What sensory aspects are small/slow?

Back 79

c fibers, A delta
pain
temp
crude touch

synapse, cross, ascend in spinothalamic tract