3. CNS/PNS Flashcards

1
Q

Name 4 Parasympathetic ganglia kip

A

Parasympathetic ganglia:

  1. Ciliary ganglion innervating the sphincter pupillae and the ciliary muscle
  2. Pterygopalatine ganglion innervating the lacrimal gland and glands of the nasal cavity
  3. Submandibular ganglion innervating the submandibular and sublingual glands
  4. Otic ganglion innervating the parotid gland
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2
Q

Are the parasympathetic fibres myelinated? whats is the neurotransmiter

A
  1. Receive myelinated preganglionic nerve fibres
  2. actelycholine (Ach) as the neurotransmitter.
  3. post-ganglionic fibre is shorter, unmyelinated and also has Ach as the principal transmitter.
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3
Q

Lateral spinothalmaic tract
Contain fibres project to where

Where do they synsapse pass deccusate and pass to where

Where do posterior colums deccusate

how many neurones reuqired to convey sens info to cortex

What is carreid by the ST tract

where is the remained carried by

Where do they pass to

A

The lateral spinothalamic tract contains fibres that project to non-specific thalamic nuclei.

Axons carrying sensory information synapse in the dorsal horn of the spinal cord, decussate and then pass as second-order neurones to the thalamus and reticular formation.

The posterior columns decussate at the brainstem.

Three neurons are rquired to convey sensory information from the periphery to conscious level at the cerebral cortex.

Pain and temperature are associated with the lateral spinothalamic tract whilst the remainder of the touch fibres (not carried by the dorsal columns) are associated with the anterior (ventral) tract. They contain nerve fibres from receptors on the contralateral side of the body.

Fibres from the lateral spinothalamic tracts pass to the thalamus and reticular formation, and they have no direct path to the cerebellum.

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4
Q

Epidural space

Starts where ends where - what shape

Dural sac ends where adults & kids

Pressure - why
Where is it greatest

What does it contain x 5

A

The epidural space extends downwards from the foramen magnum to the sacral hiatus and is triangular in cross-section.

The dural sac ends at S2 in an adult and S3/4 in an infant.

The pressure in the epidural space is subatmospheric (negative), due to transmission of the subatmospheric intrathoracic pressure through the intervertebral foramina.

It is greatest in the upper and middle thoracic regions and lowest in the lumbar and sacral regions, as distance from the thorax increases.

The epidural space contains:

Fat
Epidural veins (Batson's plexus)
Small arteries
Lymphatics, and
Spinal nerve roots.
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5
Q

Enzymes & NT

GABA syhtn by what

COMT Does what

MAOi does what

What metab ach

A

Glutamic acid decarboxylase does synthesise gamma-aminobutyric acid (GABA).

However, catechol-o-methyl transferase and monoamine oxidase metabolise norepinephrine to vanylmethylmandelic acid (VMA).

Monoamine oxidase metabolises serotonin to 5-hydroxyindole acetic acid (5-HIAA).

Cholinesterase metabolises acetylcholine.

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6
Q

CSF
pH - vs plsama

Conc higher or lowe than plasma

Na
Cl
K
Na
Ca
Protein
Bic

Opening pressure

glucose conc vs plamsa

A

CSF has a pH of 7.31, therefore lower than plasma.

It has a lower concentration of potassium, calcium, and protein than plasma. It has a higher concentration of sodium, chloride, bicarbonate and magnesium.

The CSF typically has no cells present but white cells should be less than 4/ml.

The pressure of CSF is typically less than 20 cm of water.

It has approximately two-thirds the glucose concentration of plasma with a concentration of approximately 3.3-4 mmol/L.

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7
Q

Cerebral ischaemia -

Levels of blood flow

normal

EEG Changes

A

Cerebral ischaemia can either be global or focal, either complete or incomplete. At blood flow levels of 30-40 ml/100 g/min EEG changes begin to appear. The EEG changes that suggest poor prognosis are low voltage, poorly reactive rhythms, periodic lateralised epileptiform discharges and fluctuations in underlying rhythms.

Glucose will still be metabolised albeit anaerobically. The waste products of anaerobic metabolism will not be removed efficiently due to reduced blood supply. This results in worse acidosis compared to complete cessation of blood supply.

Studies to prove whether incomplete ischaemia causes more damage than complete ischaemia have been inconclusive. At 30-40 ml/100 g/min causes EEG changes as described above. When the blood flow decreases to 20 ml/100 g/min lactate levels increase. Between 20 ml/100 g/min - 10 ml/100 g/min free radicals are released and evoked potentials begin to disappear.

At flow rates lesser than 10 ml/100 g/min irreversible damage occurs due to water accumulation.

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8
Q

How much does brain weigh % wise body weight
how much CO occurs

How is CBF controlled mainly

over what MAPs

Beyond limits proportional to what

Autoreg mainly controlled by what

A

The brain weighs only 3% of the body weight, but it receives 15% of the cardiac output.

Autoregulation of cerebral blood flow (CBF) occurs between mean arterial pressures (MAP) of 60 - 130 mmHg, over which the CBF is maintained at a constant level.

Beyond these limits the CBF is directly proportional to the mean arterial pressure (not systolic blood pressure).

The mechanism of CBF autoregulation is controlled predominantly by the PaCO2 level, whereas the autonomic nervous system has a minimal role.

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9
Q

How are the following transmiited

Vibration
pain
temperature
proprioception
joint positon
A

Pain is transmitted in the spinothalamic tracts.

Temperature is also transmitted in the spinothalamic tracts.

The impulses responsible for the vibrating sensation are carried in the dorsal column.

Proprioceptive information is transmitted up the spinal cord in the dorsal columns.

Joint position, or proprioception is transmitted up the fasciculus gracillis and cuneatus tracts in the dorsal columns.

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10
Q

genetic code is how many triplets of nucleotides

each codon codes what
is there any exception

Pyrimidine bases are

Purine bases are

what pairs with what

A

The genetic code consists of 64 triplets of nucleotides. These triplets are called codons.With three exceptions, each codon encodes for one of the 20 amino acids used in the synthesis of proteins. Most amino acids are encoded by more than one codon.

Pyrimidine bases are thymidine (T) and cytosine (C).

A and G are purine bases

G always pairs with C and T with A.

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11
Q

What are the opioid receptors

where are they present

A

here are four opioid receptors:

Mu - mu opioid receptor (also known as μ-opioid peptide or MOP) is present in the brain, spinal cord and the periaqueductal grey, produces analgesia, meiosis, euphoria, respiratory depression, bradycardia, constipation
Kappa - the kappa opioid receptor (κ-opioid receptor or KOP) produces analgesia, sedation, miosis
Delta - the delta opioid receptor (δ-opioid receptor or DOP) produces analgesia, respiratory depression
Nociceptin opioid receptor (NOP).
Opioid receptors are inhibitory G protein coupled receptors.

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12
Q

Chemoreceptors

where are they located in brain

what do they respond to

carotid respond to what

Is there another response to hypotension by baroreceptors

A

Medullary chemoreceptors respond directly to changes in CSF pH and therefore hydrogen ion concentration rather than CO2. However CSF pH does not change rapidly in response to CO2, which readily crosses the blood brain barrier (BBB).

The carotid chemoreceptors are primarily stimulated by changes in partial pressure of oxygen in the blood and not hydrogen ions

The buffering capacity of the CSF is less than that of plasma. Hydrogen ions do not directly cross the BBB but do stimulate respiration by an effect on the peripheral chemoreceptors.

As part of the baroreceptor reflex there is respiratory stimulation in response to hypotension

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13
Q

Normal ICP is

A
Intracranial pressure (ICP) is important as it affects cerebral perfusion pressure and cerebral blood flow. 
Normal ICP is between 5 and 13 mmHg.
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14
Q

Constituents within the skull include the

A

Brain (80%/1400 ml)
Blood (10%/150 ml) and
Cerebrospinal fluid (CSF 10%/150 ml).

The skull is a rigid box so if one of the three components increases in volume, then there must be compensation by a decrease in the volume of one or more of the remaining components otherwise the ICP will increase (Monro-Kellie hypothesis).

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15
Q

Primary and secondary injury

A

Primary brain injury occurs at the time of the head injury and is unavoidable except through preventative measures to reduce the incidence of head injury. Secondary brain injury is caused by a reduction in oxygen delivery due to hypoxaemia (low arterial PaO2) or anaemia, a reduction in cerebral blood flow due to hypotension or reduced cardiac output, and factors which cause a raised ICP and reduced CPP. Secondary brain injury is preventable through appropriate management.

T

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16
Q

Techniques that can be employed to reduce ICP are

A

Techniques that can be employed to reduce ICP are aimed at reducing the volume of one or more of the contents of the skull.

Reduce brain tissue volume
Reduce blood volume
Reduce CSF volume.

Techniques to reduce brain tissue volume include:

Tumour resection or abcess removal
Steroids (especially dexamethasone) to reduce cerebral oedema
Mannitol/furosemide or hypertonic saline to reduce intracellular volume
Decompressive craniectomy to increase intracranial volume.

Techniques to reduce blood volume include:

Evacuation of haematomas
Barbiturate coma to reduce cerebral metabolic rate and oxygen consumption and therefore cerebral blood volume

Arterial: avoiding hypoxaemia, hypercarbia, hyperthermia, vasodilatory drugs, hypotension
Venous: patient positioning with 30° head up, avoiding neck compression with ties/excessive rotation, avoiding PEEP/airway obstruction/CVP lines in neck.
Techniques to reduce CSF volume include:

Insertion of external ventricular drain or ventriculoperitoneal shunt to reduce CSF volume (although more a long term measure).

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17
Q

Acromegaly - what is it
what does it secrete

How are they classified

A

In more than 95% of people with acromegaly a benign tumour of the pituitary gland called an adenoma produces excess growth hormone (GH).

Pituitary tumours are labeled either micro- or macro-adenomas, depending on their size. Most GH-secreting tumours are macro-adenomas, meaning they are larger than 1 cm.

The other causes of acromegaly are rare.

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18
Q

CSF produced by what
how much a day
what rate is that

Total volume
where distributed

change icp affect?

A

CSF is produced by the choroid plexus at a rate of 0.3 mL/min. 500 mL are produced per day.

The total volume in an adult is between 125 and 150 mL, with two thirds surrounding the brain and one third surrounding the spinal cord.

Production is unaffected by changes in intracranial pressure (ICP), but absorption by the arachnoid villi is increased when the ICP is elevated.

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19
Q

Adenosine receptors - surface what cells

How many subtype

are a1 a2 present centrally or periph

A1 & A2 with regarads pain

A

Adenosine receptors are expressed on the surface of most cells, and four subtypes are known to exist (A1, A2A, A2B and A3)

The A1 and A2 receptors are present both peripherally and centrally, with agonists at the A1 receptors being antinociceptive and agonists at the A2 receptors being algogenic (that is, activation results in pain).

The role of adenosine and other A1 receptor agonists is currently under investigation for use in acute and chronic pain state

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20
Q

WHat is outside the blood brain barier

Lipid or water solbubiltiy cross

Is it as effective in paeds

is it altered by inflamm

A

he blood brain barrier (BBB) consists of the ultrafiltration barrier in the choroid plexus and the barrier around cerebral capillaries.

The hypothalamus, third and fourth ventricles and the chemoreceptor trigger zone (CTZ) are located outside the BBB (not inside).

Water oxygen and carbon dioxide cross the BBB freely, but glucose is controlled. The ability of chemicals to cross the barrier is proportional to their lipid solubility (not water solubility), and inversely proportional to their molecular size and charge.

The BBB is less effective in neonates than in adults, which explains why there is increased passage of opioids and bile salts (kernicterus) into the neonatal brain.

Meningitis alters the effectiveness and permeability of the barrier, and this effect helps the passage of antibiotics which would otherwise not be able to cross the BBB.

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21
Q

Injury to anterior cord

Hemisection

A

Injury to the anterior spinal cord results in paralysis (motor loss) below the level of the lesion, with proprioception, touch and vibration senses being preserved.

Hemisection of the cord (Brown-Sequard syndrome) results in ipsilateral paralysis and loss of proprioception, touch and vibration sense,

with loss of pain and temperature sensation on the contralateral side.

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22
Q

SNS

arises from where

preganglionic
legnth
myelination

Where doe they synapse
What is the NT here

Post ganglionic
are what length
Myelination
NT

A

The sympathetic nervous system arises from the lateral horns of grey matter of spinal cord at levels T1-L5 (thoracolumbar outflow). They usually have short myelinated preganglionic neurones synapsing in ganglia lateral to the vertebral column. The neurotransmitter at this point is acetyl chloline (Ach).

The longer unmyelinated postganglionic neurones then synapse with effector organ where the neurotransmitter is adrenaline or noradrenaline.

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23
Q

Parasympathetic

orign where
What nerves
where else

Preganglionic neurons
myelin/not
length

NT - what

Post ganglionig
myelinated
length
NT

A

The parasympathetic nervous system has a craniosacral outflow.
The origin of the cranial outflow is in the midbrain and medulla (cranial nerves III, VII, IX and X) and the sacral outflow S2, S3 and S4.

They usually have long myelinated preganglionic neurones synapsing in ganglia close to the target organ. The neurotransmitter at this point is Ach. The shorter unmyelinated postganglionic neurones then synapse with effector organ where the neurotransmitter is again Ach.

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24
Q

Regulation CBF

most improtant
where can this be autoregulated

what level does change w/ pao2

temperatre affect

A

One of the most important factors that regulate cerebral vascular tone is PaCO2. Carbon dioxide induces cerebral vasodilatation and therefore increases CBF. There is a linear increase between a PaCO2 between 20 mmHg (2.7 kPa) and 80 mmHg (10.7 kPa).

There are likely to be areas where auto regulation may have failed locally but not globally. Similarly local vs. systemic acidosis will have similar effects. The CBF does not significantly change until the PaO2 falls below 50 mmHg (6.5 kPa) below which the CBF progressively increases.

Hyperthermia causes an increase in the cerebral metabolic rate for oxygen (CMRO2) and therefore CBF. (CMRO2 and CBF are linked). Hyperthermia secondary to hypothalamic injury can be a late feature of cerebral injury and is therefore not the most likely cause of an increased CBF in this scenario.

25
Q

What does the eeg do

How many wavebands

Describe them
where are they maximal respeictively

what are there frequencies

What is a/w genreal anaestheisa

A

The electroencephalogram (EEG) records electrical activity of the brain from the surface of the scalp by plotting voltage against time.

There are four classical wavebands: alpha, beta, theta and delta.

Alpha rhythm consists of cyclic activity at 8-12 Hz and has maximal amplitude over the occipital and parietal regions. The alpha waves are reduced by visual and mental activity and are augmented by closing the eyes.

Beta waves are fast waves (>14 Hz) are predominantly seen in the frontal region. They are present in awake patients with open eyes.

Theta waves have a frequency of 4-7 Hz and are normally present in children but diminish with increasing age. In adults they may indicate intracerebral pathology. Delta waves are slow waves (1-3 Hz) and tend to be large in amplitude. Delta waves are rarely seen in the healthy waking adult EEG but are prominent and normal during sleep, especially of infants, children, and young adults.

In cerebral ischaemia there is a slowing of high frequency waves with an increase in theta and delta activity.

The EEG changes associated with deepening general anaesthesia is a slowing of electrical activity followed by brief periods of inactivity (burst suppression), finally leading to electrical silence. The appearance of burst suppression on an EEG confirms that the patient is anaesthetised (not emerging from anaesthesia). The lightening of anaesthesia is associated with high-voltage fast waves.

26
Q

Connector of PS are located where

What do they form nuclei of in BS

What nerve roots do they run

what cranial fibres are there
What about the lower ones - where do they relay

A

The connector cells of the parasympathetic part of the autonomic nervous system (preganglionic efferent fibres) are located in the brain and sacral segments of the spinal cord.

Those in the brain form part of the nuclei of origin of cranial nerves III, VII, IX and X and the axons emerge from the brain contained in the corresponding cranial nerves.

The sacral connector cells are found in the grey matter of the second, third and fourth sacral segments of the cord.

The myelinated axons leave the cord in the anterior nerve roots of the corresponding spinal nerves and finally from the pelvic splanchnic nerves.

The cranial preganglionic (efferent) fibres relay in the ciliary, pterygopalatine, submandibular and otic ganglia, whereas those in the pelvic splanchnic nerves relay in ganglia in the pelvic plexuses.

Classically the postganglionic fibres are nonmyelinated and are relatively short in length compared with those of the sympathetic system.

The facial nerve (VII) emerges from the skull through the stylomastoid foramen.

The parasympathetic secretomotor fibres supply the submandibular and sublingual salivary glands, the lacrimal gland and the glands of the nose and palate.

The glossopharyngeal nerve (IX) leaves the skull by passing through the jugular foramen (not stylomastoid foramen) and supplies the parotid salivary gland with parasympathetic secretomotor fibres (not facial nerve).

The vagus nerve (X) also leaves the skull through the jugular foramen.

Each vagus nerve then descends through the neck alongside the carotid arteries and internal jugular veins (within the carotid sheath), traverses the chest before finally piercing the diaphragm with the oesophagus (not aorta) to terminate within the abdomen.

27
Q

What does hyperoxia do to CBF

Why

What does hypoxia

what is normal cbf

A

Hyperoxia is associated with decreased cerebral blood flow. All the other options are associated with an increase in CBF.

Hyperoxia decreases regional CBF by relatively poorly understood mechanisms. The leading hypothesis is that superoxide dismutase enzyme in arteriolar walls is overwhelmed by high concentrations of oxygen to cause a reduction in nitric oxide (a potent vasodilator) production and hence vasoconstriction. The effect is small in comparison to that produced by hypoxia.

Below a PaO2 of around 7-8kPa CBF rises sharply. Above this value a gentle slope downwards is seen, with a reduction in CBF of around 10% with an FiO2 of 1.0.

Normal global CBF is 54 mls/100g of brain tissue per minute.

General anaesthesia is associated with a rise in CBF secondary to vasodilation.

There is a linear relationship between PaCO2 and CBF from around 3.5-10.0 kPa. At 10kPa CBF is around 120 ml/100g. Hence hypercarbia is incorrect.

Hyperoxia is correct, and indeed hypoxia is associated with increased CBF.

Lower plasma viscosity is associated with enhanced blood flow and hence hyperviscosity is an incorrect option

Ketamine increases cerebral metabolic rate and hence blood flow.

28
Q
CSF concentrations
glucose
na
k
mg
hoc3
A

The concentration of glucose in CSF is 64 mg/dL whilst in plasma it is 100 mg/dL.
The concentration of sodium in CSF is 140 mmol/L.
The concentration of potassium in CSF is 2.9 mmol/L, whilst in plasma it is 3.5 mmol/L.
Magnesium has a concentration of 2.2 meq/kg H2O in CSF, whilst in plasma it is 1.6 meq/kg H2O.
The concentration of HCO3- in CSF is 25.1 meq/L, whilst in plasma it is 24.8 meq/L.

29
Q

Nernst eqn calculate what

Normal RMP

What is equation

A

The Nernst equation is used to calculate the membrane potential at which the ions are in equilibrium across the cell membrane.

The normal resting membrane potential is -70 mV (not + 70 mV).

The equation is:
E = (RT / FZ) ln ([X]o / [X]i)

Where:
E is the equilibrium potential
R is the universal gas constant
T is the absolute temperature
F is the Faraday constant
Z is the valency of the ion
[X]o is the extracellular concentration of ion X
[X]i is the intracellular concentration of ion X.
30
Q

Coronary vasculature
how affected by adrenergic system

Stellate ganglia do what to post ganglionic fivres

stim right heart does what
left heart does what

alpha 2 functions med how

Symp nerve to adrenal are pre or post ganglion

A

The coronary vasculature is dilated (beta2), and constricted (alpha1), by the adrenergic system. In the presence of an intact endothelium parasympathetic stimulation leads to a dilatation via the actions of nitric oxide.

The paired stellate ganglia send postganglionic fibres to the heart. Stimulation via the right leads to increased heart rate while via the left leads to increased contractility.

Alpha-2 mediated negative feedback functions by reducing intra-cellular levels of cAMP. Sympathetic nerves reaching the adrenals are pre-ganglionic.

31
Q

main ascending path carrying nociceptive are

Which carries pain and temp
where do they cross
where do they terminate

Spinoreticular tract terminate where

A

The two main ascending pathways carrying nociceptive signals are the spinothalamic tract and the spinoreticular tract.

The spinothalamic tract carries pain and temperature sensation. The second order neurones from the dorsal horn cross to the contralateral spinothalamic tract termination in the thalamus.

At the spinoreticular tract second order neurones terminate in the reticular formation before projecting to the thalamus and hypothalamus.

Posterior (dorsal) columns carry light touch and proprioceptive sentation.

The substantia gelatinosa is in the dorsal horn of the spinal cord.
It receives the primary afferent neurones (Aδ and C) subserving the sensations of pain and temperature.

32
Q

Featurs of autnomic neuropathy

How might one feature be tested at bedside

What are the affects of spinal anaesthesia

A

Features of an autonomic neuropathy include:

Postural hypotension
Cardiac conduction defects
Bladder dysfunction
Gastrointestinal disturbances including delayed gastric emptying.
Postural (also known as orthostatic) hypotension is an abnormal decrease in blood pressure-of at least 20 mm Hg systolic and 10 mm Hg diastolic-within three minutes of standing upright.

A useful bedside test which indicates autonomic dysfunction is a reduction in blood pressure of greater than 20-30 mmHg on standing

There is decreased cardiovascular stability associated with spinal or extradural anaesthesia and patients are at risk of severe hypotension.

A reduced response to hypoglycaemia is also seen.

The pupils constrict or dilate slowly (not rapidly) in response to changes in light intensity.

33
Q

CSF produced where

Where does it enter the blood stream

where does it leave ventricular system

How does hydrocephalus ococur

what is communicating hydrocep

compard to non communicating

A

CSF is produced by the choroid plexuses within the lateral, third, and fourth ventricles of the brain.

Aggregates of arachnoid villi (arachnoid granulations) serve as sites where the CSF diffuses into the bloodstream.

CSF leaves the ventricular system of the brain and enters the subarachnoid space between the arachnoid and pia mater, where it cushions and nourishes the brain.

In certain areas the arachnoid projects into the venous sinuses to form arachnoid villi.

Hydrocephalus occurs when there is obstruction to the outflow of CSF, which can occur if there is blockage of the arachnoid granulations. Communicating hydrocephalus is an abnormal collection of CSF in the absence of any flow obstruction in the ventricles.

Whereas a non-communicating hydrocephalus is an abnormal collection of CSF, with flow obstructed within the ventricular system.

34
Q

Sleep

REM Sleep and age

A

Decreases w/ age

Neonates 50% REM
2 YO 25%
Adult 15-20%

REM - charct eyer movement and characeteists eeg
mix freq low volt saw tooth wave

TONIC ren - reduced muscle activity
phasic - muscle movement and twitch

Atonia of REM =- hyerpol = a motor - prevent act dream

Increasase ADH During sleep

35
Q

Path CSF

A

Ependymal cell chroid - late vent

Choroid plexus

Foramen monro

Aqeuduct sylvius

foramen magendia

Arach vili

36
Q

Brainstem testing CN

A

Pupil response - II (optic)-> III (oculomotor)

Corneal V- VII

Oculovestib VIII-> III IV VI

Gag IX - > X

Cough X-> X

all examined excent I and XII

Pupil constrict

Corneal - Afferent ophthalmic trigem nerve - efferent - CNVII - facial

Oculovestib
Normal
caloric response eye movement toward ipsi ear
horizont nstagmus towards constlater

absence direct and consensual

Gag - posterior pharyngeal wall - observe soft palate contract -Aff gloosopharyngeal - eff vagus

Cough - suction to carina
aff and eff vagus

37
Q

Fibres

A

Aa = motor, proprio 80-120m/s 20um

Ab TOuch pressure 30-70 5-12

Ay motor => spindles 15-30 3-6um

Ad Sharp px temp 12-30 2-5

B Pre ganglionic autonomic 3-15 <3

C post ganglion + dull pain .5-2.5 .4-1.3

38
Q

dorsal root nerve section c3-l2

sequlae
wahts called

A

Hypotonia
loss reflex
loss sensation
(not paralysis / sympathetic sweat gland)

Sensory root
2/3 pass dorsal grey horn s/c
other 2/3 pass gracile + cuneate
sens = pathway reflex arx
monitor tone - spindle

preganglion output to ans - ventral nerve

39
Q

tracts

ascending path

A

Posterior div:
fasisculus gracilis
cuneates

ascend to dorsal column -> nuclei

decussate in medulla

fas grac
-touch, vibr, prop - lower body

fas cun
upper

40
Q

spinothalamic

A

enter cord and decussate to ascend on contralat side

lat spino pain + temp

ant spino - touch + pressure

41
Q

descending path

A

lat corticospinal decuss in medulla
descend scord

motor innervation

ant corticospinal - doesnt deccusate until distal ant horn cell (prox muscles)

42
Q

What is the CN PS innervation

A

III VII IX X

43
Q

Sympathetitc ps to pelvic organs

A

lumbar roots / inferior mesteric ganglion

PS - sacral roots ii IV

44
Q

Which fibres are long

A

Postganglion sympathetic fibres are longer = than PS

as symp cell body not near end organ

45
Q

where are the cell body of sympathetitic system found

A

lateral horn of spinal cord

46
Q

Pathological a waves

A

lundberg a - acute rise icp 5-10 min

drop in cerebral compliance - impending herniaton

always path - require intervention

47
Q

ICP measured how

A

evd
subdural bolt
subdural catheter
intraparenchymal transducer

48
Q

path b wave

A

oscillations icp .5-2 waves. min

unstable ICP

49
Q

lundbeg c

A

interaction pulmonary and cardiac cycle

4-8 wave min
have been seen healthy

50
Q

ICP mon

constit of skull %

How cope rising icp

how much does flow increase paco2 increase

what can abolish response

what pao2 level can rise flow

A

A+B + C waves = affected [ressure change

85% brain
10% csf
5% blood

rising icp = change distrib csf -
increase spinal space + increase reabsoprtion

flow increase linearly for .13kpa increase in pAco2 2-4%

severe hypotension can abolish art response to paco2

rises pao2 <6.7

51
Q

Pain transmission

how is fast transmitted

Slow

A

lamina => thalamus via monosynaptic path

Responsible reflex response to pain -
dull sow - c fibres lam II + III
synapse second order neron - tmit -> polysnaptic system mult reg midbrain pons medulla

52
Q

Visceral nciceptor

A

< dense - somatic nociceptors
poorly loaclaise diffuse midline pain

exhib spatial summation
- if large area stim pain threshold lowered

53
Q

What is the NT at autonoic ganglia

A

Ach @ all autonomic ganglia

all preganglionic relase ach

post ganglionic ach - PS
Nroad NS
except sweat - ach

54
Q

Auditor potential

A

one last disapper -under anaesthesia - measure

forehaed ref elctrode - other mastoid

55
Q

bis

A

relatinship freq component - phased coupling other aspec eeg

compressed spec array - requires eeg amplitude recorded

56
Q

Standing affect intracranial P

cerebral v sinuses

A

normay = 7-15mmg supine
ICP -10 standing = becomes subatmospheric

held open by extravascular tissue -> even when intravascular pressure falls
high risk embolus - sitting positon cranial surgery

57
Q

Mean csf density

A

1.0003g/l

> men

> non preg v preg

lower premenopasal women

58
Q

Pyramidal system

comes where
where it go
where it get name

how many fibres and what % decussate
what do they form

A

Comes fibres from area IV motor cortex -> contrlater motor fibres

Form Pyramids in medulla - (get name)
80-90% decussate 1 million fibres
form lateral cortiocspinal tract

will degen after decortication
concern fine movent