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Flashcards in Neuro Deck (421):

Name the physical features of the frontal lobe

Precentral gyrus (primary motor cortex)
Superior frontal gyrus
Middle frontal gyrus
Inferior frontal gyrus


Name the physical features of the parietal lobe

Postcentral gyrus
Supramarginal gyrus
Angular gyrus


Name the physical features of the temporal lobe

Superior temporal gyrus
Middle temporal gyrus
Inferior temporal gyrus
temporal pole


Name the physical features of the occipital lobe

Occipital pole
Preoccipital notch


Name the main features visible on the medial aspect of the brain

Corpus callosum
Cingulate gyrus
lateral, third ventricles
Pons and medulla


What is the function of the cingulate gyrus?

Gateway to the frontal cortex, higher functioning, and the flight and fight areas of the brain


Describe the precentral gyrus and its associations

It is the primary motor cortex, and it is arranged in a homuncular fashion. This means that the part for the face is located basally, then eyes, hands, torso, legs etc. It is associated with the motor planning area of the frontal cortex, which includes broca's area, eye fields and exter's area.


Describe the rest of the frontal lobe and its overall function

The frontal lobe contains the superior, middle and inferior frontal gyri. Its function is in intelligence, behaviour, personality, mood and cognitive function.


Describe the SMAGLA and the overall function of the parietal lobe

SMAGLA is associated with reading and writing, respectively, and have connections to the eye fields and exter's area. The parietal lobe is associated with spatial awareness, 3d recognition and abstract awareness on the LHS, and music, non verbal communication and nuance on the RHS.


Describe Wernicke's area and the primary auditory cortex

Wernicke's area surrounds the primary auditory cortex on the superior temporal gyrus. The auditory cortex receives input from CNVIII to separate deep vs high sound pitches. Wernicke's area interprets the sound, and has a connection to broca's area called the arcuate fasciculus. It also has a connection to the SMG.


Describe the overall structure of the temporal lobe and its function

The temporal lobe has superior, middle and inferior gyri. It is involved in mood, memory, aggression and intelligence.


Describe the different aphasias that can form and how to tell two apart

Connectional aphasia: Understand what is being said and can verbalize, but the response is not appropriate
Sensory aphasia: Lesion in Wernicke's area. CCannot understand what is being said but can produce words.
Motor aphasia: Can understand what is being said but cannot verbalise
Can tell the difference by asking for a written response to a verbal question


Describe the occipital lobe's structure

It has the primary visual cortex at the occipital pole, which then dives deep. It also has a secondary cortex surrounding it and dipping into the temporal lobe, which is used to interpret the raw info given by the primary


What is the difference ebtween allocortex and neocortex?

Most of the brain's cortex is neocortex, which is made of 6 distinct cell layers
Allocortex has 3 layers of mixed cell type, and only covers a very small portion of the inferior brain. It is associated with fight or flight, the hippocampus and the olfactory centre


What are the 6 layers of the cerebral cortex and what is its general pattern?

I: Molecular
II: External granular
III: External pyramidal
IV: Internal granular
V: Internal pyramidal
VI: Multiform
The upper 3 layers are involved in information from brain to the brain
The lower 3 layers are involved in relaying information between the brain and spinal cord


Describe the molecular layer of the cerebral cortex

Nonspecific cells. Important for development as it's where radial fibres stick into the neocortex and allow its integration into the brain


Describe the external granular layer of the brain

Made of small granular neurons, which receive sensory input from other brain areas (eg. ears)


Describe the external pyramidal layer of the brain

Cells taking info to other cortex areas. They only carry information a short distance and so are small cells (10-40um)


Describe the internal granular layer of the cortex

Granular cells that receive sensory input from the periphery


Describe the internal pyramidal level of the cortex

Betz cells. Large motor neurons of the pyramidal tract (UMNs). 60-120um.


Describe the multiform layer of the cortex

Integrate different sensory inputs of the brain


What can afferent and efferent fibres also be called when in the brain?

- Efferents can also be called corticofugal.
- Afferents can also be called Corticopetal


What are the major forms of arrangement of these six layers, and where are they likely to be found?

It can be homotypical- around equal amounts of each cell type. Found where many types of info are received and sent. Eg. Prefrontal cortex, parietal cortex, temporal cortex
Heterotypical is divided into two categories
Agranular hetero typical is when there are more pyramidal cell types as their primary function is projection to other areas or to the spinal cord. Areas III and V are increased, while II and IV decrease. Eg. Primary motor cortex

Granular heterotypical is where there are more granule cells as the primary function is reception of info. II increases, IV increases massively, and III and V decrease. Eg. Primary somatosensory, visual or auditory cortices.


Describe the circle of willis

Posterior cerebral arteries join the middle cerebral arteries via the posterior communicating arteries. The middle cerebral arteries (arising from internal carotids) join to the anterior cerebral arteries via anterior communicating arteries


Describe the circulation of the posterior brain

2 vertebral arteries join to form the basilar, which then give anterior cerebellar, superior cerebellar, pontine and posterior cerebral arteries


Describe the structure and associated function of the internal capsule

The anterior internal capsule takes info to the frontal lobe from the thalamus (eg. memory)
The curve in the internal capsule is called the genu. It separates the lens and the caudate nucleus
The outer posterior IC takes motor information from the primary motor cortex to the spinal cord
The inner posterior IC takes sensory info from the spinal cord to the primary sensory cortex.
These two areas are arranged in a homuncular fashion, with the genu representing the face, and the rest of the body located more posteriorly


What does each thalamic nucleus do?

The ventroposterior nucleus is responsible for receiving sensory information and sending it out to the primary sensory cortex. The medial part represents the face and the lateral represents the body.
The VAVL nuclei receives info from the basal ganglia and sends it to the motor planning area
The Anterior nuclear group allows memories to be retrieved from and sent to the frontal cortex via papez's circuit.
The medial and lateral groups integrate sensory input from the association cortices, with the lateral being particularly involved in secondary visual information.
The lateral geniculate body receives visual information from the eyes and sends it to the primary visual cortex
The medial geniculate body receives auditory information from the ears and sends it to the primary auditory cortex.
The Intralaminar nuclear group is responsible for consciousness.


What are the overall functions of the thalamus?

Monitors and gatekeeps info for higher cortex
Integrating regionalized brain function
Motor planning and refining


Describe the reticular sheet

A membrane beneath the thalamus which controls UMN sensitivity


Describe papez's circuit

Info is sent in a circle from the anterior thalamic nuclei, to the cingulate gyrus, to the parrahippocampal gyrus, to the hippocampus, to the fornix, to the mamillary body, and back to the anterior thalamic nuclei.
The cingulate gyrus also communicates with the frontal cortex.


Describe the basic shape and ending of the spinal cord

There are two enlargements- the cervical and lumbar.
The cord terminates at the bottom of L1, and forms the cauda equina. The filum terminale of this is attached to the base of the coccyx.
The arachnoid mater terminates at S2 level, and the dura mater ends at S3.


What are rexed's laminae?

10 subdivisions of the gray matter of the spinal cord
1. Posteromarginal nucleus
2. Sustantia gelatinosa
3-4. Nucleus proprius
7. Intermediate zone
8-9. Medial and lateral motor columns


Describe the functions of the different parts of the gray matter of the spinal cord in terms of non discriminative sensation

The posteromarginal nucleus and substantia gelatinosa perform the same function in pain and temperature sensation, although the SG has opioid receptors, so pain referred here can be lessened with analgesics. A further neuron carries the information either to area 8/9, which has LMNs necessary for creating a polysynaptic reflex, or decussates at the anterior white commissure, to be transferred to the brain via the lateral spinothalamic tract.


Describe the functions of the different parts of the gray matter of the spinal cord in terms of discriminative sensation

The nerve fiber enters either directly to the gracile/cuneate fasciculi (25%) or else enter areas 3/4 or the dorsal nucleus of clark. These then conglomerate to form another neuron stretching from the gray matter into the dorsal funiculus, which prevents increasing spinal cord size superiorly.
Alternately, the fiber could go into area 8/9 to provide a myotactic reflex (although this is slow due to unmyelinated fibers)


Describe the functions of areas 5-7 of the gray matter

5-6: Abdominal and internal organs' sympathetic supply
7: Intermediate zone for sympathetic input.


Describe where sensory vs motor neurons are located in the thalamus, cortex and spinal cord

Sensory fibers are located posteriorly, motor are anterior


Describe the function of the gray matter in terms of motor input

UMNs descend via the motor columns, allowing motor info to travel down to the spinal cord. These move into areas 8/9, where they synapse with LMNs and exit via the ventral root


Describe the organization of the midbrain

Most anterior is the crux cerebri, which transmit motor info from the primary motor cortex to the spinal cord, helping to start off the corticospinal pathway. It is arranged in a homuncular fashion, with face medial and body lateral for each of the legs.
Posterior to this is the substantia nigra, which produces dopamine
Deep to this is the tegmentum, which also extends through the brainstem. It is here called the midbrain tegmentum, and receives sensory info from the spinal cord, sending it to the brain.
Most posteriorly are the superior (sight reflex) and inferior (sound reflex) colliculi, made of 4 nerve fibers. Collectively they are called the tectum or corpora quadrigemina


Describe the arrangement of the pons part of the brainstem

Most anterior is the pons, which is overlaid by the basilar artery
It contains the pontine nuclei, which form a conduit from the cortex to the cranial nerve nuclei via the brainstem. This then transmits motor info to the face.
This overlays the pontine tegmentum, then the fourth ventricle, and most posteriorly is the cerebellar peducle, which transmits info to and from the cerebellum


Describe the arrangement of the medulla part of the brainstem

Most anteriorly is the medullary pyraminds, which are where motor info decussates
This overlays the medullary tegmentum, where the gracile and cuneate nuclei are found, and also contains the inferior olives, which coordinate exchange of info between the spinal cord and cerebellum


Describe the corticospinal pathway

It begins in the primary motor cortex before descending through the crus cerebri in the midbrain, into the pons, and then 85% cross over in the medullary pyramids. It then forms the lateral corticospinal tract, which descends into area 8/9 of the gray matter before exiting the ventral root. 15% descends straight down, and crosses over the anterior white commissure. It is thought that these are axial muscle fibers


Describe the corticobulbar tract

It begins in the primary motor cortex before descending through the crus cerebri in the midbrain. Once it enters the pons it synapses with the nucleus of the cranial nerve it supplies, which then runs out of the pons to the face


Describe the dorsal column- medial lemniscus pathway

It enters the spinal cord through the dorsal root ganglion, before entering the gracile/cuneate fasciculi. Then it runs up the dorsal funiculus before synapsing at the gracile/cuneate nuclei. They decussate as internal arcuate fibers, and run up the medial meniscus pathway. They enter the thalamus at the VP nucleus, and then run through the internal capsule to the homuncular part of the primary somatosensory cortex


Describe the lateral spinothalamic tract

Enters the dorsal root ganglion, into regions 1/2 of the gray matter. It then synapses, and decussates at the anterior white commissure. It ascends in the lateral spinothalamic tract, where it then joins the medial lemniscus pathway and enters the VP nucleus of the thalamus. From there it runs in the internal capsule to the homuncular part of the primary somatosensory cortex.


What is the mnemonic used to remember the functions of each of the cranial nerves?

Some Say Marry Money But My Brother Says Big Brains Matter More


What are the 12 cranial nerves?

1: Olfactory
2: Optic
3: Optothalamic
4: Trochlear
5: Trigeminal
6: Abducens
7: Facial
8: Vestibulocochlear
9: Glossopharyngeal
10: Vagus
11: Accessory
12: Hypoglossal


Where do each of the nerves exit the brain?

Cribiform Plate: I
Optic Canal: II
Superior Orbital Fissure: III, IV, V1, VI
Foramen Rotundum: V2
Foramen Ovale: V3
Internal Accoustic Meatus: VII, VIII
Jugular Foramen: IX, X, XI
Hypoglossal Canal: XII


What is the function of the Olfactory nerve and what can happen if it goes wrong?

- Smell
- Fright and flight response
as only input into the limbic
system e.g. smell burning -->
Run fast
- Issue can cause loss of smell sensation


What is the function of the optic nerve and what can happen if it goes wrong?

- Transmits visual information
- There is a chiasma where the medial fibers of each nerve decussate. If there is a lesion before the chiasma, there will be full blindness in one eye
If there is a lesion post chiasma, there will be partial blindness


What is the function of the oculomotor nerve and what can happen if it goes wrong?

Innervates ciliary muscle, sphincter of pupil and all external eye muscles except superior oblique muscle and
lateral rectus muscle
Muscles: Superior rectus, medial rectus, inferior rectus,
inferior oblique
- Damage --> Loss of light reflex,
dilated pupil (Decreased tone
of the constrictor pupillae
muscle), downward, abducted
eye on the affected side due to
the unopposed action of the
superior oblique and lateral
rectus muscle


What is the function of the trochlear nerve and what happens if it goes wrong?

"Innervates superior oblique muscle (pulley) - pulls eye
up and outwards"
Trochlear nerve palsy - downward, inwards gaze


What is the function of the trigeminal nerve and what happens if it goes wrong?

Takes info about sensation back to the brain. It innervates skin as well as internal mucoase.
- V1 = Carries info from Opthalmic division
- V2 = Carries info from maxillary division
- V3 = carries info fromMandibular division.
ALSO HAS MOTOR FUNC. innervates chewing muscles. Innervates some salivary glands
- Trigeminal neuralgia = sudden
attacks of pain which are
triggered by touching the face,
chewing, speaking or brushing


What is the function of the abducens nerve and what happens if it goes wrong?

"Innervates lateral rectus
muscle (involved in lateral
gaze - used in visual tracking
or fixation on an object)"
- Abducens nerve palsy -->
The affected eye turns in
towards the nose and is unable
to abduct properly
(double vision)


What is the function of the facial nerve and what happens if it goes wrong?

- Motor = Muscles of facial
- Parasympathetic =
submandibular, sublingual,
lacrimal glands
- Sensory = anterior 2/3 of
tongue, soft palate
- Facial nerve palsy - facial paralysis
due to a lesion in the facial nerve
(symptoms also include dry mouth
and altered taste. Called bell's palsy and is due to compression of the nerve through the facial canal.


What is the vestibulocochlear nerve and what happens if it goes wrong?

Transmits sound (Cochlear)
and balance (Vestibular)
information from inner ear
to the brain
Damage to nerve - hearing loss,
vertigo, false sense of motion, loss
of equilibrium, nystagmus, motion
sickness, tinnitus


What is the function of the glossopharyngeal nerve and what happens if it goes wrong?

- Sensory = posterior 1/3 of
tongue, tonsil, pharynx,
middle ear
- Motor - stylopharyngeus,
upper pharyngeal muscles,
parotid gland
- Damage to glossopharyngeal nerve
= loss of taste (esp bitter & sour
flavours), trouble swallowing,
absent gag reflex


What is the function of the vagus nerve and what happens if it goes wrong?

- Parasympathetic input to
GI system and Heart
- Motor = heart, lungs,
palate, pharynx, larynx,
trachea, bronchi, GI tract
- Sensory = heart, lungs,
trachea, bronchi, larynx,
pharynx, GI tract, external
- If diabetes has damaged the
vagus nerve, it can cause
gastroparesis: muscles of the
stomach and intestine arent able to
efficiently move food through the
GI system. Symptoms : nausea,
vomiting, heartburn, constipation,
abdominal bloat, stomach spasms
and decreased appetite


What is the function of the accessory nerve and what happens if it goes wrong?

- Stemocleidomastoid (Tilt
& rotate head)
- Trapezium (elevate
Accessory nerve disorder - inability
to shrug shoulders and rotate head


What is the function of the hypoglossal nerve and what happens if it goes wrong?

Tongue muscles & strap
muscles by ansa
cervicalis. Also controls hyoid bone alongside some spinal nerves
Paralysed tongue, or deviated
away from injured side. See
problems swallowing, chewing,


Where are the cranial nerve nuclei? (generally)

I & II: Allocortex/Limbus
The rest sit within the midbrain and hindbrain
There can be multiple nerves associated with one nucleus, or one nucleus associated with one nerve


What are the different categories of sensory vs motor nerves?

Sensory can be:
- General somatic (skin)
- General visceral (organs)
- Special somatic (sight, sound, balance)
- Special visceral (taste/smell)
Motor can be:
- General somatic (skeletal)
- General visceral (smooth)
- Special visceral (pharyngeal arches)


What are the different patterns of sensory loss?

- Localized numbness
- Generalized one sided numbness
- Loss of sensation below a spinal level
- Glove and stocking loss
- Dermatome loss
- Trunk or plexus loss


How do different spinal cord lesions present?

- Can give weakness below a certain sensory level even if no discriminative sensation is lost. This is because a partial lesion can preserve the posterior columns, so pinprick sensation must be tested to determine whether the ventrolateral areas have been compromised
- Can give bilateral signs or paralysis
- Central lesions can also spare the posterior columns and power as they compress the anterior white commissure.
Hemicord lesions cause motor weakness and loss of discriminative sensation on the same side as the lesion, and loss of non discriminatve sensation on the opposite side to the lesion


How do PNS lesions present?

Mononeuropathy can be an AI disease, vasculitis or nerve compression. Sensory loss and weakness in the supplied area
Polyneuropathy presents as motor, sensory or a combination of both. Different issues can affect myelinated or unmyelinated fibers, or even myelin itself.
Eg. Diabetes attacks axons so it starts in the longest (feet) before moving into the hands
Plexus lesions (eg. slipped disc) is a single nerve issue in a dermatome
Guillain Barré syndrome is an example of a demyelinating disease


How do UMN vs LMN symptoms present?

UMN issues show weakness, increased tone and reflexes. Half body or spinal level may be affected
LMN issues show weakness, decreased tone and reflexes. They are due to nerve root or peripheral distal issues


What is the best way to do a sensory exam?

Keep questions unslanted, ie. does this feel the same as this?
Do it at the end of an interview to confirm a hypothesis, rather than to generate one


What are some common sensory exams and how do you do them?

Light touch: Dab a cotton wisp onto the skin, looking for lack of perception, no difference in perception, or different quality of perception (ie felt as pain)
Pinprick: Lightly touch the sharp end to the skin, but not hard enough to puncture. Can also use to differentiate sharp vs. dull
Joint position: Stabilize the joint with hand and then move it while the patient's eyes are closed, asking them to tell you in which direction it's being moved
Vibration: Press a tuning fork to the pulp of middle finger or big toe, and then bony prominences if necessary. See if vibration is felt and how long for (approx. 8 sec is normal)
Graphaesthesia: Can patient recognize a digit traced on their palm?


How do you move when testing sensation?

Move randomly when testing for any numbness
Move from numb area outwards when testing for border of numbness.


What are the three goals of anaesthesia and how are these achieved?

- Hypnosis- normally and IV or volatile agent
- Immobility- normally a muscle relaxant
- Autonomic Areflexia- normally opioids
Modern anaesthesia uses balanced anaesthesia, with different drugs for different purposes


What is the mechanism of uptake and release of volatile agents?

PI > PA > Pa > Pbr (start of anaesthesia)
PI < PA < Pa < Pbr (end of anaesthesia)


How do volatile anaesthetics work?

They likely modulate gaba in the brain and glycine in the spinal cord to reduce synapse transmission


What is the MAC and what factors affect it?

Minimal alveolar concentration producing immobility on standard surgical stimulus in 50% of patients. It is usually expressed as a percentage. The lower the percentage the more potent the drug.
Factors increasing MAC include young age, hyperthermia, hyperthyroid, drugs, and heavy alcohol
Factors decreasing MAC include old age, hypothermia, hypothyroid, drugs, pregnancy and low O2/High CO2


How is volatile anaesthetic dosing monitored?

The FI is compared to the FE, adjusting for minute ventilation, FA and transfer into the blood to estimate blood concentration.


What are the effects of volatile anaesthetics?

Hypnosis, immobility and amnesia
Decreased CMRO2, and increased CBF and ICP- so there are protective and harmful factors for neuro
Peripheral vasolilation, lower BP. Unchanged HR and SV
Resp depression, impaired reflexes to hypoxia and hypercapnia.


What are some of the features of NO?

Odourless, non flammable inhaled anaesthetic
Low potency
Low blood-gas solubility, rapid onset
Nausea and vomiting


What are some of the features of isoflurane?

Potent inhaled anaesthetic, good CVS stability


What are some of the features of sevoflurane?

Non pungent and least resp. depression- good for gaseous induction anaesthesia
Low solubility, rapid onset
Theoretical renal toxicity


What are some of the features of desflurane?

- Pungent inhaled anaesthetic
- Low blood gas solubility, rapid onset and offset


What are some categories of IV anaesthetic and how do they work?

Barbituates (thiopentone)
Phenols (propofol)
Imidazoles (Etomidate)
Benzodiazepines (Midazolam)
All but ketamines act on GABA receptors to enhance GABA, increase Cl- current and cause hyperpolarization
Ketamines act on NDMA receptors in PCP receptrs to antagonize glutamate, suppress excitation and cause analgesia


How do IV agents act in the body?

They are highly lipid soluble and cross the blood-brain barrier
Drug is taken up by well perfused organs, and then decrease blood concentration and they see a concentration drop as the drug leaves the well perfused organs and is metabolized in the liver or is redistributed to tissues.


Describe some of the properties of thiopentone

Very rapid onset and offset, with slow clearance so accumulation will occur
Metabolized in the liver
Causes decreased PVR and BP, as well as rep depression and reflex loss
Mostly used in emergency cesarians and ED


Describe some of the properties of propofol

Moderately rapid onset and offset, with fast clearance allowing for maintenance infusions
Metabolised in liver
Significant decrease in PVR and BP, resp. depression and loss of airway reflexes
It is the standard IV anaesthetics as it reduces CBF and ICP, has less of a hangover and can be used for maintenance


Describe some of the properties of etomidate

It shows CV stability, less resp depression and rapid clearance. However, it shows adrenocortical inhibition, which prevents HPA axis functioning and reduces stress hormones, which are important for recovery


Describe some of the properties of ketabine

Stimulates CVS and preserves resp reflexes and drive
Increased CMRO2, CBF and ICP so not good for neurosurgery
Good for shock but slow and dysphoric emergence


Describe total intravenous anaesthesia, and its pros and cons

Avoids inhalation, and complications of this (malignant hyperthermia, PONV, increased ICP)
However, it's expensive and unable to be effectively monitored.


Describe the structure of local anaesthetics

They have a hydrophobic aromatic group at one end, a hydrophilic amide group at the other end, and are linked together by either amides or esters.


How does the link of local anaesthetics affect their properties?

- Esters are more rapidly metabolized, and so have shorter action, and are more allergenic. Amides have the opposite. Additionally, lengthening the alkyl chain length increases the lipid's solubility, making it more potent.


What are some examples of ester vs amide local anaesthetics?

Esters include cocaine, procaine, benzocaine, tetracaine
Amides are prilocaine, lignocaine, bupivacaine, and ropivacaine


What is the main property of local anaesthetics that determines their speed of action?

Their pKa. The closer their pKa to physiological, the more free base there will be in the body, allowing it to enter the cell and block nerve transmission from the inside


What is the fastest acting local anaesthetic?

Mepivacaine, followed by lignocaine


What does protein binding have to do with duration of action for LAs?

The higher the degree of protein binding, the longer the duration of action.


How are LAs metabolised?

Esters by plasma cholinesterases
Amides by liver metabolism


Describe the properties of lignocaine

Low solubility and potency
Low pKa so fast onset
Low protein binding so short duration
Ideal for short surgical procedures


Describe the properties of bupivacaine

More potent, longer lasting and slower onset compared to lignocaine. May cause cardiac arrest before the neurotoxicity warning sign. Ideal for nerve blocks for analgesia


Describe the general properties of cocaine, prilocaine, and ropivacaine

Cocaine- ester, topical to nose, vasoconstrictor
Prilocaine- amide, safest, used in IV regional anaesthesia with a tourniquet to prevent arrest
Ropivacaine- amide, slow onset, long acting but less CVS toxicity


How do you assess LA toxicity?

Allergic reactions are rare, however, CNS and CVS toxicity can develop, of which CVS is much more life threatening
Thankfully they are dose dependent, and CNS tends to occur earlier than CVS- simply watch for neuro and don't give any more!


How do you administer LAs topically, and why?

They can be topical to the skin in a mixture of LAs in oil. This allows most to be free base and cross the skin. It is used in insertion of IV cannulae in children
Topical to mucus membranes: Cocain has the added advantage of vasoconstriction. Used for instrumentation of the nose/mouth/pharynx as in awake intubation


How do you administer LAs to the soft tissue?

For minor interventions like a mole removal, you use a fast, short duration agent
For post op pain relief you use a slow, long duration agent


What is a peripheral nerve block?

The LA ins infiltrated around a specific nerve or plexus. Sensory fibers are more susceptible, but motor nerves can also be affected. USed for surgery without a GA, or postop pain relief


What is a neuraxial blockade?

LA is injectd into the intrathecal space below L2. It produces a profound distal motor and sensory block, allowing major distal surgery while awake


What is an epidural anaesthetic?

A small catheter is inserted into the epidural space and LA is infused around the spinal nerves nearby. It can be done at any level, and produces a distal sensory and motor blockade. It allows maintenance infusion, and is excellent for postop and labour analgesia


What do NMBAs do?

They paralyse patients undergoing surgery or requiring intubation. They do not sedate, cause amnesia, or have analgesic effects.


Why are NMBAs necessary for intubation?

They paralyze the vocal cords, decreasing damage and postop hoarseness. It also allows control of ventilation intraoperatively, allowing oxygen consumption to be decreased and barotrauma to be prevented. Ventilating also lowers ICP.


What are the 3 areas of the NMJ and their general functions?

Presynaptic- ACh synthesis and storage. Release of ACh and reuptake of Ch
Synaptic cleft: Side of AChE, ACh crosses
Postsynaptic- AChRs anchored in folds


Describe the events at synapse including quantal theory

ACh is stored in vesicles. Ca2+ flows into the cell after an AP, causing the ACh vesicles to fuse with the presynaptic membrane and release ACh into the cleft. The number released is proportional to Ca2+. usually about 200 units with 5000 ACh each. About half are immediately hydrolysed, though more is released than necessary for a single transmission. Approx. 500000 AChRs are bound, allowing Na+ to flow in and causing endplate depolarization.


Describe AChRs

Ligand gated ion channels with 5 subunits each- 2a, b, y, e. Both a units must be bound simultaneously, causing a conformation change, opening the channel and allowing ions to flow in.


Describe AChE

An enzyme present primarily in the synaptic cleft, and to some extent in the extrajunctional area. It is secreted by the muscle and attached to the basal lamina by collagen.


Describe depolarising muscle relaxants

Known as Sux (suxamethonium). It is similar in structure to ACh, and is comprised of 2 ACh molecules bound together. It mimics the effect of ACh by causing depolarization, although it causes fasciculation (a brief flicker of movement) and then relaxation lasting 3-5 mins. It is not hydrolyzed by AChE, but by pseudocholinesterase. Its neuromuscular blocking activity is terminated by diffusion into the plasma. Its time of action depends on the time taken to excrete it.


What are some of the side effects of Sux?

It cannot be reversed pharmacologically
Fasciculations and postoperative myalgia
Cardiac dysrhythmias
Increased ICP, IGP and IOP
Malignant hyperpyrexia
Masseter spasm


What are the positives of Sux?

It provides the quickest, most reliable relaxation for airway control, giving excellent intubating conditions with minimal time for aspiration. It is mainly emergent


Describe how non-depolarising NMBAs work

They are positively charged quaternary N compounds
They compete with ACh and bind to one or both a subunits, preventing ACh binding and opening of the ion channel. As only one molecule of the drug is required to do this, it is biased towards favouring the antagonist
Blockade starts when receptors are more than 70% occupied, and is complete when more than 90% are occupied


What are the two ways of grouping Non depolarising NMBAs?

Chemical structure: Aminosteroies have ammonium on a steroid- Rocuronium, Vecuronium and Pancuronium. Benzylisoquinolones have 2 ammonium joined by methyl. Atracurium, Cisatracurium and Mivacurium
Duration of action: Short acting (Mivacurium)
Intermediate acting: Atracurium, Vecuronium, Rocuronium
Long acting: Pancuronium


Describe atracurium

A NMBA with an intermediate duration and a 3-5 minute onset. It has 2 elimination pathways- Hoffman is nonenzymatic, and dependent on temperature and pH. Its inactive products are excreted. It is also partly removed by renal excretion and ester hydrolysis. It can cause histamine, hypotension and tachycardia. Its advantages are in elderly or kidney dysfunction patients as it is not dependent on renal excretion


Describe mivacurium

3x more potent than atracurium, slow onset of 3-5 mins short duration of action, hydrolysed by pseudocholinesterases. Less histamine. Used mainly in ambulatory surgery


Describe rocuronium

Rapid onset and intermediate duration. Used for rapid sequence induction instead of Sux, but longer duration. Can have anaphylaxis. 90% hepatic elimination


Describe vecuronium

Intermediate duration. Show onset, but no CV side effects. Active metabolites, renally excreted- means it accumulates in renal failure. Used ful in CVS disease patients, with least anyphylaxis and histamine


Describe pancuronium

Long duration of action, high potency and slow onset. Longest duration. Increases BP, HR and CO, so ideal for long cardiac surgery. Minimal histamines. Difficult to reverse


Describe the perfect NMBA

Rapid onset
Titratable effect
Easily reversible
No histamine or anaphylaxis
No haemodynamic effects
Inactive metabolites
No accumulation
Low cost


How can you reverse NMBAs?

You cannot reverse depolarising NMBAs.
Strategies for reversing the others include titrating perfectly for their duration of action, but this is hard as both patients and surgeons can be unpredictable.
Additionally, you could accelerate their reversal, which is safer and more reliable. It can be acheived by increasing the concentration of ACh at the receptor, or decreasing the NMBA.
Increasing ACh is done by using AChE inhibiting drugs, although these act on all receptors throughout the body. This means they have side effects such as bradycardia, bradyarrhythmias, bronchospasm, salivation and increased bowel motility. To counteract these, antimuscarinic agents are given in combination


What is sugammadex?

A perfect antidote for rocuronium and vecuronium, by selectively binding rocuronium and rendering it incapable of binding to the AChR. It favours movement of rocuronium from the NMJ to the plasma, allowing muscle function to return within 2 minutes.


How do you monitor a neuromuscular blockade?

Stimulate the peripheral nerve, assessing the response of the muscle. A stimulator is connected to the ulnar nerve, and 4 stimuli 0.5 seconds apart are given at a frequency of 2hz. The movement of adductor pollicis is assessed, with the TOF count and the TOF ratio. TOF is the number of twitches seen, TOF ratio is the ratio of the 4th to 1st twitch as a percentage.
Intact neurotransmission shows four twitches of identical height.
Recovery from a neuromuscular block causes twitches to come back slowly.


What is TOF fade?

A deficiency of neuromuscular transmission requiring intervention. It is only seen in non-depolarising NMBAs. Different muscle groups respond differently. The diaphragm is less susceptible than peripheral nerves, so adductor pollicis is used as a proxy. It shows


What is double burst stimulation?

The fade of the second twitch is compared to the first. Two to three short bursts of stimuli are administered twice, comparing the twitches. Full recovery is two equal twitches.


What are the five basal ganglia?

The caudate nucleus, putamen (collectively called the striatum), globus pallidus, hypothalamus, and substantia nigra.


What is the function of the basal ganglia?

They smooth out and plan motor movement.


What are the three capsules of the basal ganglia?

The internal capsule, external capsule (separating the claustrum from the putamen) and the extreme capsule (separating the alimentary cortex from the basal ganglia)


What are the claustrum and alimentary cortex?

Claustrum is the centre for visual attention
The alimentary cortex represents the GI system.


Describe the direct and indirect pathways of the basal ganglia

Direct pathway is GLUT from planning area to striatum, GABA to GPi, GABA to VaVL and GLUT to planning
Indirect pathway is GLUT from planning to striatum, GABA to GPe, TABA to subthal, GLUT to GPi, GABA to VaVL and GLUT to planning


What is the nigrostriatal pathway?

Dopamine pathway between the substantia nigra pars reticulata, and then the SN pars compacta to the striatum. It produces dopamine which is then transferred back to the striatum, holding the cells at a tonically active state


How does the pathology of huntingtons disease occur?

The pathway from the striatum to the GPe is inhibited. The fibres from GPe to SUT aren't inhibited, and are free to inhibit the GLUT pathway to GPi. GPi then in turn inhibits the VaVL less, allowing uninhibited firing of the VAVL nucleus to the planning area.


What are the symptoms of and treatment of huntington's disease?

Symptoms include behavioural and cognitive changes, hyperkinesia and involuntary movements. It is due to trinucleotide repeats within the base sequences. Males hand down longer copies of repeats, with women handing down the same length. Therefore, genetic anticipation can happen, where longer and longer chains cause the offspring to get it earlier and more violently than their parents.


What are the symptoms of parkinson's disease, and how does this relate to its

It's due to a failure of the nigrostriatal pathway, which produces dopamine. The lack of dopamine means that the striatum is unable to fire, leading to hypokinesia, emotionally flat moot, tremor at rest (esp. pill rolling) and rigidity.
It can be treated with oral levodopa (although this can cause toxicity), a pallidotomy, or thalamotomy, on one side of the brain, or deep brain stimulation (an adjustable pacemaker implant)


What are the different nuclei within the cerebellum and what do they do?

Fastigial nucleus: Sends info on proprioception to the reticular formation and lateral vestibular nucleus, to be transferred to the lower montorneuron pool.
The interpositus nucleus sends information on automated movement to the red nucleus, which then sends the information via the rubrospinal tract to LMNs
The dentate nucleus sends info on fine movement to the red nucleus and Vent. Lat nucleus, which then sends it ot UMNs and LMNs.


How is the cerebellum divided and what do each of the parts do?

It has lateral part, intermediate part, and vermis. There is also and anterior lobe, posterior lobe, and focculonodular lobe.
The neocerebellum receives input from pontocerebellar and olivocerebellar fibres, for fine motor control, rebound reflex and correction of movement (ie when somebody bumps into you while walking).
The palaeocerebellum is in the intermediate part, and receives proprioception info from the spinocerebellar fibres and olivocerebellar fibres
The archicerebellum is in the flocculonodular lobe and is the first part to develop. It receives vestibular info from the bod


What happens when there are issues with different parts of the cerebellum?

Issue with neocerebellum means issues with fine movement, like an intention tremor
Issue with the palaeocerebellum means there is an issue with postural instability
Issue with archicerebellum means there are problems with general balance, eye movements become quick, cannot focus.


What are the peduncles of the cerebellum and what goes through them?

The inferior peduncle receives info from the olivocerebellar fibres, and vestibulocerebellar fibres from the inf olive and vestibular nucleus
The middle cerebellar peduncle receives fibres from the pontine nuclei
The superior cerebellar peduncle receives info from the cerebellum's nuclei and redirects it to the thalamus, vestibular nucleus, inf. olive, spinal cord etc,


Define drug tolerance and sensitization

Tolerance to a drug is the reduction in response to a drug after repeated administrations. It may be innate or acquired. Sensitization is the opposite process


What is physical drug dependence and withdrawal syndrome?

Physical dependence is the state that develops as a result of tolerance, produced by the resetting of homeostatic mechanisms in response to repeated drug abuse.
Withdrawal syndrome is the evidence of physical dependence- usually characterised by CNS hyperarousal. It is characteristic to the drug category and tends to cause the opposite effects of the drug itself. For example, opioids cause restlessness, cravings, nausea, aches, anxiety, tachycardia when withdrawn.


How is the mesolimbic system involved in addiction?

The stimulis hits the ventral trigeminal area, which gives a pleasurable sensation. It then continues through the nucleus accumbens, where it ends in the prefrontal cortex. Dopamine is the important neurotransmitter in this pathway.


What is substance dependence syndrome?

Continued use of a substance despite problems related to it
Withdrawal symptoms
Dependence is three of these (addiction), one or two indicates abuse.


What are the three sources of substance dependence?

The agent, host or environment.


How does the agent create substance abuse?

Reinforcement is the property that makes the user want to take the drug again- associated with central neurotransmitters and the rapidity of onset of the drug and its method of use.


How does the host create substance abuse?

People show variability in their pharmacokinetic response to drugs, pharmacodynamic response, and their behavioural response to drugs. Some people have polymorphic inheritance for propensity to addiction. Innate tolerance also occurs. Some physiological changes prevent addiction (ie. those with increase alcohol dehydrogenase will never be alcoholics)
Psychiatric disorders can also increase the risk of drug addiction


How does the environment create addiction?

Societal norms and their view of addiction. Additionally, peer pressure, low employment and low educational levels are important.


Describe alcohol as an addictive drug

It's a CNS depressant (but a stimulant at low doses). It impairs recent memory, motor coordination, and causes sedation in high doses.
As tolerance develops, sedation is reduced but the lethal dose is unchanged- more dangerous.
Withdrawal symptoms include craving, tremor, irratability, nausea, tachycardia, etc.
Delerium tremens is caused by long term alcohol abuse and subsequent withdrawal. It shows agitation, confusion, hallucination, sweating etc.


How is alcohol metabolized?

It is metabolized in the liver by alcohol dehydrogynase. The decay is relatively quick for the first few drinks, but changes to zero order once the process becomes saturated, allowing a dangerous buildup.


What can long term use of alcohol cause?

Liver cirrhosis, myopathy, endocrine issues, FAS, mental retardation.


How are opioids as drugs of addiction?

It is used mainly as an analgesic, although its prescription rate has skyrocketed and its affordability plummeted. This has lead people to source cheaper versions from other sources.
There are short acting rapid onsets (morphine, fentanyl) and long acting slow onsets (methadone)


Describe heroin as a drug of addiction

It is the most important opioid of abuse, and is illegal in USA and NZ.
It is associated with abnormal pituitary function, irregular menses, reduced sexual performance, high mortality.


What are the withdrawal symptoms of opioids?

Craving, restlessness, irritability, pain sensitivity, nausea, cramps dysphoria, anxiety
Signs include dilated pupils. sweating, piloerection, tachycardia etc.


Describe cocaine as a drug of addiction

It blocks transporters that recover dopamine from the synapse, leading to increased dopaminergic stimulation. This results in arousal, enhanced performance, increase in HR and BP
Repeated doses lead to stereotyped behaviour, irratibility, violence, and addiction in some users.
Toxicity can result in arrhythmias, psychosis, seizure etc.


Describe meth as a drug of addiction

It releases high levels of dopamine, enhancing mood and body movement. It is neurotoxic, and damages dopamine and serotonin containing cells.
Toxicity includes CNS issues increased wakefulness, increased physical activity, decreased appetite etc.


Describe cannabinoids as a drug of addiction

Burning cannabis leaves contain over 61 cannabinoids, and is the commonest illegal drug in the US. The drug activates cannabinoid receptors in the brain, which results in a high, a reduction in cognitive function, reaction time, learning and memory long term. Anxiety attacks and hallucination may also occur.


Describe propofol as a drug of addiction

- Anaesthetic induction agent with a very narrow therapeutic index


Define epilepsy

A condition in which patients have recurrent, unprovoked epileptic seizures. This comprises an abnormal and excessive electrical discharge from neurones in the cerebral cortex, and is often associated with a loss of consciousness.


What can cause epilepsy?

Can be structural, genetic or metabolic dysfunction


What are the different categories of seizures?

Partial seizures involve neurones in one part of the brain only. A generalized seizure involves all the neurones of the brain


What is the physiology of a seizure?

An imbalance between excitatory and inhibitatory neurotransmitters. It is caused by the synchronous activation of large numbers of hyperexcitable neurones. This can be propogated by normal and abnormal pathways
It can involve GLUT.
NMDA receptors open the channel for Na+, K+ and Ca2_ cations, and is activated by NMDA
Non-NMDA receptors are activated by AMPA and kainic acid, not NMDA. It is permeable to Na+ and K+, but reasonably impermeable to Ca2+. It's rapidly activated and inactivated
It can also involve GABA. Seizures can be caused by blocking of GABA, activation of GLUT receptors, blocking glycine or K+ channels, and unblocking NMDA receptors.


How do you treat epileptic seizures?

Can block Na+ channels (phenytoin). It stabilizes Na+ currents and prevents repetetive firing from sustained depolarization
It also enhanses GABA and reduces GLUT


What are some mutations that can cause epilepsy?

Na+ channel mutation can cause severe myoclonic epilepsy of infancy (causes intellectual impairment) as well as benign epilepsy
Ca2+ channel mutations in the thalamus cause hyperpolarized thalamic neurons, producing cortical depolarization. It is especially common for absence seizures.


What are the different ways of causing an epileptic seizure?

Anatomic rearrangement of local circuits
Frequency dependent changes in synaptic efficacy
Changes in local receptors


How does anatomic rearrangement of local circuits cause epilepsy?

Excitatory axons have collateral branches activating neurones in local regions of the CNS. They can contribute to feedback inhibition or excitation, of which inhibition is typically more powerful., If there is neuronal death, new circuits grow in to replace them, forming new uninhibited circuits


How does a change in local receptors cause epileptic seizures?

NDMA receptors may change, and it can be either perpetuated by seizures or by mutation from birth. This is the principle of kindling, where a repeated exposure to subthreshold stimulation produces spontaneous seizures.


Describe different generalised seizures

A generalized seizure involves both hemispheres of the brain, and may have major or minor motor manifestations.
Types can be- tonic- sustained contraction of muscle
Clonic- regular repeated jerks
Tonic clonic- sustained followed by jerks
Myoclonic- brief jerks of axial and limb muscles
Epileptic- brief contractions of limbs and axial, with an initial myoclonic component.
Absence- go completely blank
Frontal lobe- sudden, abrupt limb posturing


Describe partial seizures

They preserve consciousness, and only involve a certain part of the brain
Can be visual, somatosensory, auditory, psychic, abdominal, olfactory, versive, or focal motor
Complex partial seixures have a loss of consciousness and are unresponsive.


Why do we need sleep?

Most likely to do with synaptic shrinkage. This allows the brain to tidy up and lose unnecessary memories, to permit the formation of new circuits the next day


What are the different sleep stages?

1- on the verge of sleep
2- light sleep
3- deep sleep
4- unwakeable
REM- dreaming


What sort of things are necessary to ask in a sleep history?

Sleep onset, interruptions, quality, extra sleep features (ie snoring, sleep walking)


What are the 3 main groups of sleep symptoms?

Excessive daytime sleepiness


What is insomnia?

Inability to get enough sleep. Can be primary or secondary (due to to substances, neurological condition), circadian, jet lag, or shift work disorder.
It can be due to thinking style- more likely to be insomniac if you are a perfectionist, overthinker or a controlling type.


What is excessive daytime sleepiness?

- Difficulty in maintaining the desired level of wakefulness
- Falling asleep at inappropriate times
- Excessive amount of sleep
- Can be idiomatic, due to substances, circadian rhythm disorder, deprivation or narcolepsy


What is parasomnia?

Limb movements, restless limb


How do you manage sleep disorders? General

First step is getting the diagnosis correct. Then examine possible psychological, behavioural and biological factors


What are countermeasures for sleep deprivation?

Sleeping, or taking short naps.


How do you enhance sleep?

Mindfulness, avoiding stimulating substances, activities and devices
Minimize alcohol
Only go to bed when tired, and get up at the same time
Physical bed
Only use bed for sleep and sex


What are the benefits of sleep?

- Better health
- Better relationships


What are common causes of hearing loss in children?

Otitis media
Infections Trauma


What are common causes of hearing loss in adults?

Age related
Noise exposure
Ototoxic drugs (aminoglycoside antibiotics and cytotoxic drugs)


What are the consequences of hearing loss?

- Increased falls and dizziness
- Reduced cognition
- CNS issues
- Dementia risk increases
- Poor speech and language
- Social isolation
- Decreased literacy, learning, education and employment
- tinnitus
- Depression


How does sound travel from the environment to the inner ear?

These structures are located in the temporal bone
Sound is transmitted through the middle ear to the inner ear, where the vibrations are transduced into neural activity by the sensory cells. In the cochlea, the organ of corti separates the complex sounds into individual frequency components.


What are the components and functions of the outer ear?

The outer ear is made up of the pinna and external auditory meatus, and terminates at the tympanic membrane. It protects the middle ear, is important or sound localization, secretes wax from cerumen glands and cleanses the ear itself.


Describe the middle ear and its components

The middle ear is filled with air, and sits within the temporal bone. It begins at the tympanic membrane, and communicates inf/ant with the nasopharynx via the eustacian tube.
It contains the ossicular chain, made of the malleus, incus and stapes. The stapes articulates with the oval window of the internal ear.
It has a mucosal lining


What is the function of the eustacian tube?

It aerates the middle ear, enabling it to maintain equal air pressure across the tympanic membrane. However, infection can enter the middle ear using this route, causing middle ear disease, and contributing to otitis media with effusion.


What is the function of the ossicular chain?

The bones conduct airborne sound to the oval window. A change in their structure or misattachment causes a conductive hearing loss.


What is the overarching function of the middle ear?

It acts as an impedance transformer, overcoming the mismatch in density between air and inner ear fluid. This allows our auditory system to be much more sensitive.


How does the middle ear transfer sound?

The increased surface area of the tympanic membrane transfers more energy onto the smaller stapes foot plate. The malleus arm is also longer than the incus, allowing generation of greater leverage and force on the stapes.


What is the overall difference between conductive and sensorineural hearing loss?

Conductive is due to outer or middle ear damage, while sensorineural is due to sensory or neural elements of the inner ear


What structures make up the inner ear?

There are three semicircular canals and vestibule of the vestibular system, as well as the spiral cochlea, which contains the organ of corti (sensory organ).


Describe the cochlea

It is a fluid filled tube spiralling around a bony core called the modiolus, which contains the auditory nerve and vascular supply. The fluid is called perilymph, which has a composition similar to ECF (lots of Na+, small K+)


Describe the cochlear duct

It is a cavity lying within the perilymphatic cavity. The floor of this is called the basilar membrane, projecting from the modiolus, that has the organ of corti sitting on it. It divides the perilymph space into the scala vestibuli above and scala tympani below. The space between is the scala media. It contains endolymph, which has a high K+ and low Na+ concentration. This is produced by the stria vascularis on the lateral duct.


Describe the organ of Corti

It is attached to the basilar membrane of the cochlear duct, and is comprised of approx 20k hair cells, named for the stereocilia projecting apically into the endolymph


Describe the classification of hair cells

Inner hair cells comprise 25% of cells and have a single row. These are responsible for the afferent fibres, type I myelenated fibres, which take sensory information to the cortex
Outer hair cells comprise 75% of cells and sit in 3-5 rows. They only take 10% of afferent fibres to the brain, and these are small and unmyelinated. They receive efferent fibres and function as motor cells, enhancing the wave motion of the balisar membrane, to increase the sensitivity and frequency selectivity of the ear. This is energy expensive, but necessary to overcome the friction of the fluids vs corti.
Sound causes them to mechanically oscillate in a frequency specific matter, due to their motor proteins (prestin) in their membranes


What is the function of the round window in the inner ear?

It relieves the pressure created by the stapes pressing in the oval window. This helps a whiplike sound wave form along the basilar membrane


Describe how the sound wave triggers depolarization of hair cells

The basilar membrane varies in mass and stiffness- it's small and stiff at the base, which changes as it goes. As the wave of displacement travels along, it rises in amplitude and slows. For a particular frequency, the wave reaches peak amplitude at the region corresponding to it, and then dissipates. Therefore, the basal cochlea responds to high frequency, and apical to progressiely lower.
The movement of the wave over the stereocilia causes shearing forces to open the transduction channels running from shaft down to tip of the cilia. This causes the rushing in of potassium ions, which triggers an action potential


Describe the transduction channels

They run from the shaft of one stereocilium to the tip of an adjacent one. The anchor on the shaft is made of myosin, with a MET channel on the adjacent tip allowing the ions in. The bridge itself is made of E. Cadherin 23.
These channels are very vulnerable to excessive sound as they maintain tension. They are unlikely to grow back if broken.


Describe the potassium recycling within the cochlea

K+ diffuses out of the hair cells and into the scala tympani. This is very fast due to high difference in concentrations, so there's no need for high energy channels, reducing the need for a great blood supply.
This then flows back into the stria vascularis to be reproduced, via fibroblasts with gap junctions.


How does the cochlea separate frequency?

Place coding: The base of the organ of corti is narrow and stiff. Individual hair cells respond to particular frequencies depending on their location, and this is reflected in the auditory nerve. It has differences in tonotopicity, with each fibre only responding to a certain range of frequencies and intensities. The best frequency is determined by the location of the hair cell it innervates. Basal hair cells have high frequencies, while apical cells have low frequencies.
Volley Principle: Discharge rates are sychronized with frequency of stimulus. These are locked on to a single cycle of stimulus, so they only detect the ones they are synched to. This is known as phase locking, and only occurs in the auditory nerve for frequencies lower than 1-2000hz


How does the cochlea determine intensity?

Intensity is determined by both the number of fibres activated, and their rate of firing. Discharge rates increase with intensity.


Describe how sensorineural deafness occurs within the cochlea

It can be due to congenital abnormalities, infection, drugs, fluid homeostatic disturbances, trauma, noise exposure, age or idiopathy.
It is due to damage to sensory or neural structures of the cochlea. It is the msot common form of deafness, and can cause loss of hearing sensitivity at frequencies damaged, loss of discrimination, poor loudness balance and tolerance, and poor speech recognition. It is due to the loss of fine frequency tuning and intensity detection methods, and these cells do not regenerate.


What is the pathway from cochlea to cortex?

Cochlear nuclei (sensory integration with vest. system)
Sup. Olivary complex (binaural integration, localization and focus on speech)
Inf. colliculus (sens integration, sound localization and visual enhancement of sound)
Medial geniculate body (radiates to heschel's gyrus in temp. lobe)
Auditory cortex


How does hearing loss affect the cochlea's tonotopicity?

It becomes disturbed, with high frequency areas being taken over by low frequency ones


Why is binaural hearing important?

It is used for lound localisation and complex auditory perception. It is done using differences in intensity between the ears (for high frequency) and differences in timing of reception between the ears (for low frequencies). This is because low frequency sounds tend to wrap around the head and so produce little intensity difference.
Most sound responses are greater when heard binaurally. Above the cranial nucleus level, binaural responses dominate


How do cells receiving inputs from both ears localize sound?

Cells in the SOC, IC, MGB and cortex receive inputs from both, and are either excited by both ears (EE) or excited by one and inhibited by the other (EI)
These cells are divided into low freq units sensitive to time differencs (MSO) or to level differences (LSO)


Describe the parts of the cochlear nucleus

The dorsal part projects to the midbrain, while the ventral goes directly to the superior olive


What is tinnitus?

Reduced inhibition of the dorsal cranial nucleus, causing a phantom sound


What are the main types of hearing loss?

Conductive- outer/middle ear damage
Sensorineural- inner ear damage
Mixed- both
Central- issues with nerves or cortex


What do we need to find in a hearing exam?

Onset of loss- rapid vs. gradual, constant vs. fluctuating
Precipitating factors
Assoc. symptoms- tinnitus, vertigo etc.


How do we use tests to determine between conductive and sensorineural hearing loss?

Weber test involves placing a tuning fork on the frontal bone and seeing whether it is heard. This will be referred to the better ear if sensorineural loss, or else not heard at all. In conductive loss, it will be referred to the deafer ear, or still heard.
Rinne test involves striking a tuning fork and holding it on the mastoid process, and then in front of the ear. It will be heard in the bone but not air in conductive hearing loss, and not heard in either for sensorineural


What are some potential causes of conductive deafness?

Osteosclerosis or arthritis
Ossicle issues


Describe microtia

The pinna is not developed but inner ear is normal


Describe glue ear

The eardrum has fluid built up behind it, so sound cannot travel through


Describe mastoiditis

Pus behind the ear builds up, putting pressure on and blocking nerve conduction


What are some potential causes of sensorineural deafness?

Can be congenital - hereditary, delayed hereditary
Can be acquired- noise induced, trauma, infection, ototoxicity.


How do the different hearing losses perceive sounds?

Conductive sounds muffled, maybe tinnitus
Sensorineural has frequency and speech discrimination issues with sound distortion, loudness imbalance, tinnitus and missing frequencies


Describe central auditory disorders

This is issues in auditory processing. It can be amlyaudia (lazy ear), hyperacusis (hypersensitivity) or tinnitus. Mainly caused by peripheral injury or developmental/neurological disorders


Describe some behavioural assessment of hearing

Audiometry- give a pure tone at air and bone conduction, then speech. Normal is hearing below 20Db. Bone conduction bypasses the middle ear and so can confirm conductive hearing oss
Speech audiometry- assess comprehension and detection of speech. It can be affected by background noise etc. and needs to be age appropriate
Tympanometry- assesses ear drum mobility and pressure This is important as a negative eardrum pressure can suck infections into the middle ear via the eustachian tube. It also assesses the integrity of middle ear muscles


What are some physiological assessments of hearing?

- Neural activity of the cochlea and brain centres can be studied in disabled, very young, or people with no behavioural measure
- ABR tests obtain hearing thresholds
Screening for every newborn NZer a few days after birth


What are some treatments for congenital hearing loss?

Hearing aids
Sign language
Implantable hearing aids or teeth conductors- good for conductive loss


Describe cochlear implants

A silicone stent with 22 electrodes. This is inserted into the cochlea of people with no sensory cells. it stimulates the first 2/3 of the cochlea, but needs a good nerve supply
It is ideal for very young children or adults with good language- this is because plasticity for language starts to close at 5 years.


What are some recent developments in hearing technology?

Can have fully implanted cochlear implants
Drugs given via implants to stimulate nerve growth
Bilateral implants
Preservation of residual hearing
Cochlear nucleus implants


How does the brain get imaged on CT?

The bone is visible as bright white, with grey matter grey, white matter dark grey, CSF and fat dar, muscle medium grey and blood showing low-high intensity
It can have vascular contrast, but this doesn't cross the BBB. It is iodinated in CTs. The contrast enters tumours and strokes due to the presence of leaky vessels. However, it can exacerbate poor kidney function
They are fast, available, provide 3D imaging and have an immediate cost. They're great for looking at strokes, and whether it's still bleeding. They can also do tumours, abscesses and trauma


How does the brain get imaged on X ray?

It can be used to check vertebral body and process alignment, as well as the prevertebral soft tissue. Can show spurs on vertebrae, which is a sign of osteoarthritis, as well as examining aneurysms and their repair
It's cheap, easy and fast
However, it uses radiation, and only shows limited TD info. It is overused in head trauma as it can only show skull fracture, which is not always involved in brain trauma


How does the brain get imaged on MRI?

There are two most common types:
T1 shows CSF as hypointense and fat as hyperintense
T2 shows CSF as hyperintense and fat as hypointense
The DWI signal for early strokes appears bright on MRI due to the restriction of water moving out of the cell- this is more useful for stroke imaging than CTs
DTI tractography can trace axon bundles, making it good for signal planning.
Functional MRIs can give locations of tumour and relation to the cortex responsible for a function
It is good as it gives no radiation, is great for the brain, is versatile, can have contrast manipulated, shows immediate early ischaemia, tumours, angiography with gadolinium contrast, and shows a multiplanar view that is good for prenatal imaging
However, it takes a long time and has poor access, is expensive, motion sensitive, needs lots of experience, and has some safety issues. The gadoliunium contrast can also be taken into bones


What are tips for imaging the brain and describing the results?

Describe the patient, side of lesion, why it's important, appearance, location, and other features. Look at history, image and then cues around it.


Is MRI and CT better for imaging stroke, tumour, reconstrction, angiography or spine?

Stroke- both
Tumour- both
Bony reconstruction- CT
Angiography- MRI (slight)
Spine- MRI


How is US used to image the brain?

Paediatric through fontanelles- good for ventrices and haemorrhage


What are the major effects of opioid analgesics? What is its limit?

Analgesia and impaired consciousness
However, the analgesia doesn't apply to neuropathic pain (only nociceptive and inflammatory pain)


How can opioids be administered?

Can be oral, parenternal (intramuscular/venous/intermittent/PCA)


What are opiates vs opioids?

Opiates are derived from opium poppies, derived naturally (eg. morphine, heroin, codeine)
Opioids are synthetic narcotics mimicing its function- eg. pethidine, fentanyl, methadone etc


How do opiates act on opioid receptors?

They can activate Gi proteins to inhibit adenylate cyclase, and decrease the Ca2+ channels permeability and block release of neurotransmitter
They can also increase K+ conductance in the postsynaptic membrane, causing hyperpolarization and decreased response


What are the different opioid receptors and where are they primarily located?

mu receptors are located in the CNS, along with kappa receptors. Delta receptors tend to be more around the pleasure pathways


Describe how receptors are synthesized in peripheral inflammation

In the periphery, receptors are synthesized due to inflammation by the dorsal root ganglion. This is transferred all over the neuron, so opioids can attach to all of these to cause decreased pain. Additionally, inflammatory cells attracted can also produce endogenous opioids.


Describe what activation of Mu-1, Mu-2 and kappa receptors can do

Mu-1 produces analgesia only
Mu-2 produces analgesia, as well as other side effects, euphoria and physical dependence
Kappa produces analgesia and dysphoria


Describe the various agonists and antagonists in opioid analgesics

Agonists activate all subclasses, but with varying affinities
Antagonists cause a lack of activity in all receptor classes
Agonist-antagonists agonize one type and antagonize another
Partial agonists cause activity at one or more but not all receptor types


Describe the adverse effects of opioids

- Respiratory depression, drowsiness, dizziness, constipation, ileus, itching, nausea/vomiting, bradycardia and hypotension


What are semi synthetic vs fully synthetic opioids?

Semisynthetics include bup-re-norphine, oxycodone and di-acetyl morphine
Full synthetics include fentanyl, pethidine, methadone and tramadol


What are some of the body's endogenous opioids?



What happens when there is a withdrawal from opioids?

BP changes, HR and RR may increase, GI has cramps, N&V, diarrhoea
Neuromuscular issues, pilorection, sweating


How do you manage opioid withdrawal?

- Give methadone or bup-re-norphine, with clonidine, or another adjunctive to manage sside effects (ie diarrhoea). This involves one opioid being replaced with another, which is then slowly withdrawn
OR rapid detox treatment is done within 2 hours. Under GA the patient is not subject to withdrawal. Give high doses of naltrexone, followed by maintenance to reduce relapse


Describe morphine and its side effects

Powerful analgesia, sedation, cough suppression.
Causes miosis, alatered mood, N&V, addiction, resp depression, constipation, itching and hypotension (due to histamines), biliary colic and bradycardia.
Can be administered orally, IV, epidural or intramuscularly
Metabolized in the liverto an inactive form as well as some morphine 6-glucuronide, which has at least half the potency
Excreted in urine


Describe pethidine and its side effects

It's s synthetic opiate designed as an anticholinergic. It gives less marked miosis, dry mouth, tachycardia, and can be given in tablet form. It is metabolized and conjugated in the liver, although it gives the product norpethidine, which may accumulate in renal failure to cause seizures and hallucinations.
It interacts with MAOI to cause coma, convulsions etc.


Describe fentanyl and its side effects

Synthetic opioid with a fast onset. Strong agonist of mu receptors, 100x more potent than morphine
Given by IV, IM, transdermally. transmucosal lozenges, nasal spray or sublingual tablets


Describe iontophoresis

A method of transdermal PCA as the drug and an intert agent are placed on the skin, connected by a power supply. When the electric field is on, the drug is ionized and allowd to move through the skin


Describe methadone and its side effects

Fully synthetic, well absorbed from all routes of administration. Rapid analgesia onset. No cognitive impairment, no euphoria, safe in renal and liver failure
Used for chronic or neuropathic pain, opioid withdrawal and detox


Describe tramadol and its side effects

It's a synthetic codeine analog, weak mu opioid receptor agonist
Inhibits serotonin uptake so may cause serotonin syndrome if administered to an SSRI patient
Caution for epilepsy patients


Describe codiene and its side effects

Treats mild to moderate pain
Marketed as single ingredient and combination drugs
Can cause drowsiness and constipation, physical dependence, etc.
Some patients are slow vs rapid metabolizers


What are the opioid antagonists?

Naloxone, naltrexone


Describe nitrous oxide and its side effects

Powerful analgesic normally given 50% with Oxygen. Used in maternity, field and wound dressing
Can cause euphoria, nausea and vomiting, bone marrow depression


What are some co analgesics?

Adjuvent drugs are those whose primary indication is for a purpose other than pain relief, but they demonstrate some analgesic enhancement
Eg. some tricyclic antidepressants, anticonvulsants, anxiolytics, corticosteroids and others


List the symptoms of cerebellar disease

Truncal and gait ataxia
Limb ataxia
Abnormal eye movement
Nausea and vomiting
Normal or reduced tone
Normal power, tendon reflexes, plantar response and sensation


Describe truncal and gait ataxia

Unsteady while sitting, walks unsteadily with broad base
Side to side steps
Cannot walk heel toe


Describe limb ataxia

Clumsiness and difficulty writing. Reboud after displacement of limb
Intention tremor, overshooting of finger nose finger etc
Impaired rapid alternating movements (dysdiadochokinesia)
Issues judging pressure of grip


Describe dysarthria

Loss of articulation producing slurred and staccato speech. This is different from brocas stroke as it's about the physical formation of the words


What are the abnormal eye movements that can come with cerebellar disease

Nystagmus- rhythmic oscillatory movements of one or both eyes when held at extremes of movement
Oscillopsia- environment moves
Broken pursuit of eve motion when tracking a moving target
Square wave jerks- eye flicks up and around when trying to hold straight


Describe some of the causes of cerebellar disease

Multiple sclerosis
Ischaemic stroke

Also congenital or inherited defects, tumours, infections and metabolic disorders


What are the features of an upper motor neuron lesion?

No wating or fasciculation, increased tone with spastic catch, reduced power, increased tendon reflex. Extensor tendon reflex (babinsky reflex), and reduced rapid alternating movements


What are the features of a lower motor neuron lesion?

Increased muscle wasting and possible fasciculations (random jerks). Normal or decreased tone, decreased or absent reflexes, flexor plantar response and normal rapid alternating movements


What are the features of a pyramidal lesion?

No wasting or fasciculations, increased tone, normal power, normal tendon reflexes, flexor plantar response, reduced rapid alternating movement.


What is the pathway for a muscle stretch reflex?

Muscle stretched so golgi tendon organ stretches
1a nerve afferent fires
Sent to dorsal horn of assoc spinal cord level
Monosynaptic connections with alpha motor neurons to the same or synergystic muscle
Also synapses with an inhibitor alpha motor neuron for antagonist muscles


What are the different classes of reflexes?

0 is absent
+ and ++ are normal and brisk normal
+++ are exaggerated
++++ are clonus (give repeated contractions)


What are reflexes?

Involuntary, stereotypical and non fatiguing movements
Response is dependent on strength of stimulus
There is variation between people
Can be increased by activiating assoc muscles
Can be increased when anxious and decreased when sleeping


What would be seen with a spinal cord lesion at C5?

LMN issues at C5 & 6
UMN and sensory issues below


What are some of the symptoms of movement disorders?

Paralysis- can be mono/hemi/para/tetraplegia
Paresis (weakness)
Abnormalities of muscle tone (spasticity, rigidity)
Ataxia- can be decomposition (jerkiness) or dysmetria (over or undershooting)
Involuntary movements- eg. tremor and dyskinesia
These can be focal or diffuse, and acute or chronic


What are some example of focal and diffuse or acute and chronic movement disorders?

Focal acute: trauma or vascular issue
Focal chronic: tumour
Diffuse acute: toxin or infection
Diffuse chronic: Neurodegenerative


Where are (lower) motoneurons, and what are their types?

They can be in the spinal cord (anterior horn) or in the brainstem for CN III-VII and IX-XII
These may be alpha motoneurons- innervate extrafusal muscle for force generation- or gamma motoneurons- innergate intrafusal muscle fibres to control stretch receptor excitability


What pathways are alphamotoneurons involved in?

Descending tracts- pyramidal, rubrospinal (red nucleus), vestibule-spinal (coordination), tecto-spinal (head and eye coordination) and reticulospinal (muscle tone)
Also brainstem or spinal interneurons that synapse with them- like Ia inhibitory interneurons
1a afferents from muscle spindles


What makes up a motor unit?

Dendrites, cell body, axon, axon collateral, NMJ, muscle fibres


What is myotonic muscular dystrophy?

Progressive watsting and weakness of muscles due to CTG repeats causing defective myotonin. It's dominant inherited, and causes myotonia (muscle stiffness) and failure to relax after contraction, even in the heart.
In children this is duchenne's which is progressive wasting and weakness, due to defective dystrophin


What is myasthenia gravis?

AI disease resulting in fewer ACh binding sites due to smaller junctional folds. This results in smaler amplitudes of end plate potentials, reducing transmission and causing weakness without wasting. It can be helped by blocking ACh esterase with tensilon, and treating the side effects (GI) with atropine


What is botulism?

Food poisoning and muscle paralysis caused by clostridium botulinum. It is endocytosed, and proteolyses the membrane proteins involved in ACh release at all peripheral cholinergic synapses, preventing transmission. It causes weakness of striated and smooth muscles. In infants it can cause constipation, lethargy, difficulty feeding, paralysis and respiratory arrest


What is the result of injury to axons?

Distal segment shows wallerian degenration, where the myelin deteriorates, transmission ability is lost and axon survival factor becomes lost. The proximal segment undergoes chromatolysis, where the histological stain colour changes due to migration of lysosomes into the dendrites
In the periphery it can regenerate by 1-2mm per day, and is facilitated by schwann cells. It can re-innervate and give some return to function
In the CNS this regeneration does not occur


What is a stroke?

A group of disorders involving haemorrhage or occlusion of brain blood vessels
It may be ischaemic (vessel blockage) or haemorrhaginc (rupture of vessels). It is mostly focal but can also be global (eg. caused by cardiac arrest)


What are the risk factors of stroke?

Genetic polymorphisms


Describe the anatomy of a stroke

The cells in the region with the greatest blood loss rapidly die by necrotic death. Surrounding this is the penumbra where nerve cells die by slower apoptotic mechanisms. Necrotic death is too rapid for intervention, so apoptotic death is the one targeted by therapy


What causes delayed cell death?

Release of glutamate, causing transporter saturation
Calcium influx
Free radical production
Activation of macrophages (called microglia) which release NO, superoxide, cytokines etc.
Activation of intrinsic mechanisms


What are the two main categories of glut receptor

Ionotripic (ligand gated)
Metabotropic (g protein linked)


Describe ampa receptors

They are ligand gated ion channels with various subunits. Those with GluR2 subunits pass sodium but not calcium, while those with R3 but not R2 pass calcium only. Ischaemic injury downregulates the R2 subunit, causing increased Ca2_ influx


Describe kainate reeptors

Ligand gated ion channels which cause influx of sodium


Describe NMDA receptors

Ligand and voltage gated channels. It needs deoplarization with glutamate and glycine to open the channel. Mg2+ occupies and blocks the channel, so depolarisation causes an efflux of Mg2+
PCP binds inside the channel blocking ion flow.


Describe metabotropic receptors

G protein coupled receptors
Group 1 activate phospholipase C and depolarize neurons. Group II inhibit adenylate cyclase and inhibit neurotransmitter release


Describe the pathway from stroke to cell death

Stroke causes increased glutamate, activating AMPA, NDMA and G gouple receptors
This causes increased influx of Ca2+, causing apoptosis, and increased Na+, Cl- and H2O influx, causing necrosis


How does calcium cause nerve cell death?

It activates calcium sensitive enzymes that carry out the cell suicide program
it is suggested that these are mediated by caspase enzymes that cleaves substrates- esp. caspase 3


How can strokes be treated?

TPA causes thrombolysis but must be given soon after stroke
Glutamate antagonists don't work so far- it's complex
Free radical scavengers
Anti inflammatories


How do glial cells interact with stroke?

Astrocytes link neural activity to blood, flow, allowing survival promotion. Astrocytes can be an important target for drug intervention. By keeping them alive it means that the neurovascular unit is maintained.
Maintaining pericyte integrity promotes new vessel formation


Describe the symptoms of parkinsons disease

It can be tremor at rest (often asymmetrical,
Bradykinsesia or slowness of movement- emotionless face, impaired rapid alternating movement, abnormal gait, freezing, short steps
Postural abnormalities ie stoop


How do you diagnose parkinsons disease?

Needs at least 2/4 of TRAP


Describe the onset of parkinsons disease

It's gradual onset and often asymmentrical. Symmetrical onset indicates and abnormal parkinsons progression (ie medication driven)
Premotor symptoms develop slowly, then it's normally 1-2 years before diagnosis. Treatment starts, a few years in the honeymoon phase. Motor symptoms develop over 10 or so years, with disability lasting after that


What are the non motor symptoms of parkinsons?

Asomnia, constipation, pain, loss of smell, REM sleep behaviour disorder- ie acting out dreams


What are the pathological changes associated with parkinsons disease?

It occurs when the substantia nigra's dopaminergic neurons deteriorate. It can cause synucleinopathy, and predisposes certain regions of the brain. The disease progression is topographically predictable. The longer parkinsons is in the body for, the more space it affects in the brain


Describe levodopa treatment of parkinsons

Levodopa is given with an enzyme inhibitor of peripheral converting enzymes to ensure the maximum amount reaches the brain
It has a short half life, so leads to large fluctuations. This means infusion should be used, with an agonist


What are surgical treatments of parkinsons?

Pallidotomy or thalamotomy. Transplant using fetal tissue
DBS inhibiting overactive neurons without destroying them


What does clonidine have to do with parkinsons?

It blocks dopamine receptors for the treatment of nausea, but can also cause parkinsonian symptoms by blocking CNS dopamine receptors


What is the function of astrocytes?

They are important for brain function, including release and uptake of neurotransmitters, expression of receptors, regulation of synaptic transmission, electrical conduction, neurotrophin production, and possibly generation of new neurons
They are also responsible for immune activation and scar tissue formation
There are multiple types of astrocyte


What are the different categories of astrocyte within the cortex?



Describe protoplasmic astrocytes

Most common, reside in layers 2-6 of neocortex
Processes do not overlap
One domain might cover 10 nerve cells, many synapses and 5 blood vessels. They are important in regulation of blood flow.


Describe fibrous astrocytes

Found in the white and gray matter with intermingling processes. They serve a support role for neurons and help to form scar tissue


What is gliotransmission?

The process of release of transmitters from astrocytes, acting on neurons. It may have a great use in terms of normal brain function- eg. memories may be encoded in astrocytes, astrocytes can induce sleep via caffeine receptors etc


What are microglia?

They survey the microenvironment of the brain, and act in a role similar to macrophages They mediate the immune response, phagocytose debris, sculpt the brain during development and modulate neurotransmission


What are pericytes?

They encase endothelial cells in capillaries and maintain the BBB.


What are some targets in the brain for drugs?

Enzymes, structural proteins, uptake proteins, ion channels, receptors and transducer proteins


How does chemical neurotransmission occur?

Chemical messengers can be released across the synaptic cleft, causing ion channel opening, and or generation of a second messenger. These can be excitatory or inhibitory. Termination is acheived by metabolism and/or reuptake by transporter proteins
The effects of drugs will depend on which neurotransmitters it affects, and the anatomical localization of that particular system


What are the different categories of neurotransmitters?

These can be monoamines (serotonin, noradrenaline, dopamine- from VTA and substantia nigra)
Can be amino acids, like GABA, GLUT, gycine
Can be ACh


What is the difference between neuromodulators and neurotrophic factors?

Neuromodulators have slower pre and post synaptic responses. They are released by nerve cells and astrocytes
Neurotrophic factors are released by non neuronal cells and neurons, and work over long time scales. They act on TKRs to mediate growth morphology and functional properties


What are neurotransmitters (general)?

They can be fast acting, and work via ion channels, or be slow acting via G coupled protein receptors


What is polio?

An acute viral infection that is usually focal. It causes degeneration of motoneurons and muscles. Modified polio viruses can be used to treat brain cancer (glioblastomas)


What are the disease facts assoc with ALS?

Most are sporadic, 10% have familial form Death is usually within 2-5 years unless benign form


What are the symptoms of ALS?

Progressive muscle wasting, weakness and atrophy leading to paralysis
Dysphagia (need percutaneous endoscopic gastronomy) and dysarthria
Respiration impairment
Increased stretch reflexes and spastic tone, with fibreillations and fasciculations
No involvement of extraocular, anal and bladder muscles, or sensory/intellectual capabilities


What causes ALS?

Progressive degeneration of motoneurons a and y in the spinal cord, brainstem motoneurons (but not III, IV or V)
Upper motoneuron degeneration causing spasticity


What are some theories of how ALS occurs?

Autoimmune- antibodies against Ca2+ channels
Neurotrophic- reduced neurotrophic factors that promote motoneuron survival
Oxidative stress hypothesis- mutation of superoxide dismutase, allowing free radicals to build up
Fas induced sensitivity- increased sensitivity to Fas activation, increasing toxic NOS expression
Excitotoxic- increased GLUT due to decreased glut transporter activity. Reduced expression of GluR2 in AMPA, predisposing them to higher calcium fluxes and oxidative damage
TDP-Fus mutation- normally in the nucleus but some for shifts to the cytoplasm, aggregating and affective neuron function


How do you treat ALS?

There is no effective drug available. There is a small benefit to Riluzone (blocks GLUT), baclophen (GABA agonist), and dexpramipexole (improves mitochondrial function with low DA receptor affinity


What factors are integrated to acheive balance?

Visual, vestibular, proprioceptive, and superficial sensory information. Feedback about the head and eyes is independent of each other, as the eyes can be fixed while the head is moving
It also has input into cognition, involves self motion perceptions, self consciousness, spatial navigation learning, memory and object recognition


What kind of movement does the vestibular system provide?

Linear and angular acceleration


What is vertigo and what causes it?

A derangement in vestibular finction- incolves sense of losing balance, disorientation and nausea. Accompanied by ANS symptoms. Ie. motion sickness when there is a mismatch between propriosensation inputs


Describe the structure of the vestibular system?

The vestibular nuclei in the brainstem receive info via CVIII. Fibres project from here to the cerebellum, oculomotor nuclei and spinal cord.
The inner ear contains the sensory organs for vestibular as well as auditory info. The vestibular system consists of three semicircular canals called the horizontal, anterior and posterior canals. They contain perilymph. These semicircles are paired with the one on the opposite side of the head (and with post, to create a line of direction)
Each have an ampulla at one margin of the canal, containing the crista ampullaris and cupula a genatinous structure covering it.
The otolithic organs )macula utriculus and macula sacculus) are located in the bestibule, with the utricle horizontal and the saccule vertical


How is angular acceleration detected by the vestibular system?

When the endolymph within the ampullae moves due to its inertia, it displaces the cupula. If this displacement of the stereocilia is in the direction of kinocilium (one larger hair), the cell will be depolarized, whereas away from the kinocilium hyperpolarizes it. After inertia settles the cell returns to a steady state of firing.


How is linear acceleration detected by the vestibular system?

The maculae sensory cells in the utriculus and sacculus contain calcium carbonate, which gives them mass and enough inertia to detect gravity. This allows it to provide static and up/down movement info for the head.
When the movement of hairs is towards the kinocilium it is excited, and vice versa. When the head is held tilted, it simply reaches a steady state of firing.


What happens if the vestibular system is off?

Can mess with vestibuloccular reflex- can't keep eyes adjusted to head movement. Eye movement can be a proxy for this
Loss of posture and muscle tone maintenance
No function in space- tend to see atryphy here


Why doesn't the vestibular system get activated by sound?

The stapes sits over the saccule, and there is an empty space next to the cochlea- however there is a pressure gradient in the cochlea rather than the vestibular system


What is supplied by the sup and inf vestibular nerves?

Sup: Utricle, and Saccule, int/ant semicircular canals
Inf: Post saccule and post semicircular canal


How are cilia oriented in the vestibular system?

In the semicircular canals are in opposite direction- movement in the head in one direction excites one side and inhibits the other. The comparieson between the two allows determination of direction
In the macula, they hair cells are oriented in different directions so that tilt will depolarise and hypolarise different cells on the same side


What is schizophrenia and what are its symptoms?

A disorder of abnormal thought, perception, behaviour, mood and attention
Positive symptoms are delusions and auditory hallucinations
Negative symptoms are withdrawal and flattened mood


What is the dopamine theory of schizophrenia causes?

Dopamine- overactivity of dopamine systems from the frontal cortex, NA, olfactory and ventral striatum
Amphetamines that increase DA release cause psychosis and exacerbate symtpms. All antipsychotic drugs block DA receptors


What is the GLUT theory of schizophrenia causes?

Decreased glutamate leads to schiz
Due to PCP giving the best model of psychosis, which is an antagonist of the NDMA glut receptor
It is possible that it is a combination of increased DA and decreased GLUT that causes the symptoms


What are the drugs used to treat schizophrenia?

Typicals include chorprozamine- tricyclic dopamine antagonist. However it is an antimuscarinic agent, and produces dry mouth with increased PNS stimulation Haloperidol also antagonises dopamine
Atypicals are Clozapine, although it can cause decreased neutrophils


What are the mechanisms of the schizophrenia drug?

All are dopamine antagonists, with typicals having equal D2 and D4 affinity, with clozapine having a 10x greater D4 affinity
However, typicals show extrapyramidal side effects like dyskinesia and parkinsonian effects
This could be due to the D2 affinity difference, or location of action


What is depression?

An episodic, recurrent illness with periods of spontaneous remission.


What are the two main types of depression?

Unipolar- affects mood, appetite, tiredness, negative self concept. Can be endogenous (unknown origin) or reactive (triggered by environmental event)
Bipolar- manic depression. Mood fluctuates between depression and mainia, where there is heightened mood, iritability, poor decision making , delusion and hallucinations


What is the simple monoamine theory and why is it problematic?

It suggessts that depression is due to a decrease in brain monoamines (eg. serotonin). However, while antidepressants do work by inactivating monoamine reuptake or breakdown, it only works after weeks of chronic use


How do antidepressant drugs work?

First generation: Tricyclics block monoamine reuptake, though they decrease adrenoreceptors and cause antimuscarinic action
Monoamine oxidase inhibitors irreversibly prevent breakdown of monoamines
Second generation: Moclobemide selectively inhibits MAOs
Fluoxetine is an SSRI


How does lithium carbonate help manic depression?

It stabilizes both phases, and may dampen neurotransmission


How does depression affect neurogenesis?

Stress impairs neurogenesis , and this decrease may have something to do with depression development. Treatment of depression helps to generate new brain tissue


What do facial effects have to do with reundancy in stroke?

Upper face is innervated by both sides of the brain, whereas the lower face only receives fibres from the contralateral side. This means a lesion is more likely to appear in the lower face


Describe what the possible consequences of an internal capsule lesion coule be

Ant limb: Lesion can cause head and neck muscle weakness (mainly lower face)
Post limb contains corticospinal fibres so can cause UMN issue contralaterally
Sublenticular nucleus has auditory fibres- opp side deafness
Retrolenticular has visual info from lat geniculate body to visual cortex- can cause contralateral blindness
Also cranial nerve fibres


How do NSAIDS work?

They inhibit COX1 an COX2, though newer agents only inhibit COX2
They are mostly reversibly and incomplete, apart from aspirin, which selectively acetylates a serine residue of the enzyme and irreversibly inactivates it


What do NSAIDS do?

They decrease inflammation and relieve mild pain by reducing PGs. They are also antipyretics and anticoagulants (decrease thromboxane)


What are prostaglandins?

Lipid compoudnds with a wide spectrum of biological actions
- sensitize spinal neurons to pain, induce labour, regulate inflamm responses, platelet response, cell growth etc


What is arachidonic acid?

Synthesized from linoleate- liberated by activation of phospholipase. Goes on to be converted to Prostaglandins, prostacycline and thromboxane by cox1 and cox2.
Converted to leukotrines by leukocytes
These are all eicosanoids


Why should the different COX enzymes be activated or inhibited by NSAIDS?

Cox 1 is always functioning for many bodily functions, so it shouldn't be inhibited as it can affect other organs when given long term
COX2 is involved in making inflammatory PGs, and so should be inhibited
However, selective COX-2 inhibitors are assoc with GI issues, MI and stroke


How are NSAIDS processed by the body?

They are lipophilic, absorbed rapidly and fully. They have low first pass metabolism and a high decree of protein binding, giving a small Vd
Action onset is slow, metabolized into inactive products by the liver
NSAIDS will displace other medications eg. digoxin, so will free them to act more in the body
Enzyme inhibitors and inducers may enhance or decrease their activity


What are the side effects of NSAIDS?

GI issues
Renal issues
Liver toxicity
Pregnancy/lactation problems
Reye's syndrome


How does aspirin work?

It is salicylic acid, bound to acetyl for better tolerance. This then binds to serum albumin, conjugated with glycine and glucuronic acid to be excreted in the urine. It competes with uric acid and so can exacerbate gout
It irreversibly acetylates COX1, inhibiting platelet adhesion. While this does reduce MI and stroke risk, and spares PG12, a vasodilator, high doses can inhibit prostacyclins (also vasodilators) and cause the opposite effect


What can NSAIDS do the GI and bleeding?

It can increase operative blood loss, and increase haematoma risk for epidurals
It also inhibits a protective PG against gastric acid damage. This causes increased acid secretion and acidity, as well as reduced mucus synthesis and thickness
It also causes diarrhoea, N&V etc.


Describe how aspirin relates to asthma

It can induce asthma in a severe and life threatening way
Presents as rhinitis and flushing, then asthma and polyps after a later stage
This is because inhibition of COX causes decreased bronchodilator PGs, as well as lipoxygenases, which cause bronchospasm


What is reye's syndrome?

Acute metabolic encephalopathy, with children more prone after a viral illness


How do NSAIDS affect the kidneys and gestation>

NSAIDS can be assoc with renal failure in susceptible patients, including papillary necrosis, interstitial nephritis, and ATN
NSAIDs can inhibit labour and close patent ductus arteriosus in premmies


Describe apracetamol

An unknown method of analgesia and antipyretic
Weak anti-inflam
Few side effects, but can cause fatal hepatic damage due to N-acetyl benzo quinone once glutatione stores run out- N acetyl cystiene can augement glutatione reserves to bind the toxic metabolite


Where is the CSF found?

In the ventricles and subarachnoid space


Where and how is the CSF produced?

It is formed mainly by the choroid plexus in the lateral ventricles. Some is produced by brain IF by bulk flow
The choroid plexus is found in the ventricles, and forms a network of fenestrated capillaries surrounding a single row of epithelial cells. The ventricular surface of the epithelium has a microvilli brush border.
The first step in production is filtration across the choroidal capillary wall- dependent on hydrostatic capillary pressure
Secondly, the epithelium actively secretes it, including vitamins, glucose and amino acids


What is the route of CSF circulation?

It flows from the lateral to third ventricle through the foramina of monro. It then flows through the cerebral aqueduct to the fourthe ventricle. From the fourth ventricle, it leaves via a midline and two lateral foramina, entering the subarachnoid space. it collects in cisterns surrounding the brainstem, and also circulates in the subarachnoid space of the spinal chord and brain.


How is CSF absorbed?

It is mostly done via the small arachnoid villi and larger arachnoid granulations. These are heriations of the arachnoid membrane into the lumina of the sup saggital sinus.
Some is also absorbed where nerve roots exit the spinal canal, before the dura sleeves them off
It is done by unidirectional bulk flow, relying on hydrostatic pressure. Unless CSF production is well above max absorption, this allows compensation of any increase or decrease in CSF production
Some solutes (lipophilic) are reabsorbed by diffusion into the brain and capillaries


What does the CSF normally consist of?

Few white blood cells, no RBCs, small amount of protein and some glucose depending on blood glucose and rate of its metabolism in the brain


How do you test CSF composition?

With a lumbar puncture
Patient has local anaesthesia and is lying in the left lateral recumbent position. Needle inserted into L3/4 and pressure is measured and sample removed


What are some conditions that can cause variance in the CSF composition?

Meningitis- increased WBC and proteins, maybe decreased glucose
Subarachnoid haemorrhage- increased RBCs, causing xanthochromia- yellow colour due to bilirubin from RBC breakdown
Tumours- tumour cells present


What are the functions of the CSF?

Homeostasis- maintains a constent environment for neurons and glia by facilitating entry of some metabolites, and removing toxic or unnecessary substances
Mechanical protection- it cushions the brain from impact with the skull vault during movement and trauma
Countering increases in ICP (increases reabsorption)
Conducting hormones


What is ICP normally?

Approx. 5-15mmHg


What are the two methods of measuring intracranial pressure?

Lumbar puncture- although this is useless and potentially dangerous in transtentorial herniation due to lagging of spinal CSF pressure behind intracranial
Intracranial pressure monitoring- can be inserted into lateral ventricle or epidural space


What is the Monro-Kellie doctrine?

There are three intracranial components- the brain, CSF and blood.
These components aren't able to be compressed, so an increase in one needs to be followed by a decrease in another to maintain ICP


What are the compensatory mechanisms of the cranium in terms of maintaining ICP?

- Displacement of CSF from the intracrnial cavity into the spinal subarachnoid space
Collapse of cerebral veins, reducing IC blood volume
Increase in CSF absorption
Some distensibility of the lumbosacral dura


What can cause ICP compensatory mechanisms to fail?

Increase in brain volume by a space occupying lesion or oedema
Increase in CSF volume due to obstruction of flow or reduced absorption (rarely, overproduction of CSF)
Increase in blood volume by cerebral venous outflow obstruction, or loss of autoregulation


What is brain oedema?

Increased brain water content. Can be due to
- Vasogenic oedema (increased ECF due to increased endothelial cell permeability)
- Cytotoxic oedema- swelling of cells due to energy depletion and ATP sodium pump failure, allowing hypertonic and hyperosmotic cells- or acute plasma hypoosmolality
- Interstitial oedema- hyperosmolality of periventricular white matter due to transpendymal absorption of CSF


What are the types of cerebral herniation?

- Displacement of one cerebral hemisphere across the midline (midline shift) which can compress the midline structures
- Herniation of medial temporal lobe through the tentorial notch, compressing the upper midbrain, occulomotor nerves and post cerebral artery
- Herniation of the inf cerebellum from the posterior fossa into the spinal canal, which compresses the underlying medulla
Herniation of cingulate gyrus beneath the falx
Upward herniation of the superior cerebellum through the tentorial notch


What is cushings sign?

Arterial hypotension, bradycardia and slow resp rate.
This is due to decreasing blood to the medulla, distorting it and preventing its management of life supporting function


How does arterial blood pressure affect ICP

- Arterial blood pressure- dependent on cerebral blood flow. Cerebral perfusion pressure = MAP - ICP
Normally, Cerebral blood flow is constant due to autoregulation. Vasoactive factors mediate their constriction and dilation. A loss of cerebral autoregulation causes blood flow and blood volume to vary with any change in arterial blood pressure


What besides arterial blood pressure affects ICP?

- Venous pressure- rapid compression of jugular veins cause immediate CSF pressure rise
- Intrathoracic pressure- increased intrathoracic reduces venous return and increases ICP
- Posture- ICP is higher lying down than erect
- PaCo2- hypercapnia causes vasodilation, increasing blood flow and increasing CSF pressure
- PaO2- hypoxia causes arteriole dilation, increasing cerebral blood volume, flow and ICP- although less pronounced than changes due to PaCo2
- Temperature- blood flow increases linearly with increasing core temperature


What is a thunderclap headache and what does it indicate?

It is a sudden headache due to subarachnoid haemorrhage
It is associated with neck stiff ness due to pus and blood inflaming them, as well as loss of consciousness (potential)


What is the function of the blood brain barrier?

Regulation of ionic balance
Facilitation oftransport of essential substances into the brain
Barrier against entry of potentially harmful molecules


What are the features of the blood brain barrier?

Endothelial cells have no fenestrations, but they do have tight junctions. This limits the movement of even smaller molecules between cells, separating the plasma from the ECF of the brain
They also have fewer pinocytotic vesicles, with a thicker basement membrane and more mitochondria (due to high active transport requirement)
Astrocyte foot processes are very closely tied to the walls- allowing regulation of ions and brain volume


What factors affect the transport of a molecule across the BBB?

- Molecule size
- Lipid solubility (more soluble is easier)
- Ionisation at physiological pH
- Protein binding restricts entry
- Presence of specific transport pathways (ie facilitated diffusion, active transport


What are some disorders of the BBB?

- Tight junction disruption, allowing molecules to move between cells
- Proteolysis of basement membranes
- Disruption endothelial glial interactions
- Altered specific transporter function
- Formation of new, leaky blood vessels as in tumours
- Sometimes, can primarily affect the BBB- eg. loss of GLUT1 glucose transporter in the brain
Meningitis also breaks down the barrier, causing presence of WBCs and protein in the CSF


What is the pattern of muscle weakness in hemiparesis pyramidal weakness?

In the upper limbs, the flexors can be weak, but still stronger than the extensors
In the lower limbs, the extensorts may be week, but are still stronger than the flexors


What can cause hemiparesis?

Subdural hematoma- midline shift, compressing motor cortex
Left frontal meningioma- causes changes in cognition and personality, as well as pyramidal weakness
Thrombus in middle cerebral artery leading to stroke
Atrial fibrillation leading to multiple fragments of clots, causing many small strokes
Subarachnoid haemorrhage


What is used to test dysplasia?

Get the patient to name something, say something and do something


What is a new possibility for treatment of stroke?

Solitaire stent retriever- thread a catheter into the blocked artery, surround the embolus with chicken wire esque stuff and pull it back out.


What are the changes in memory associated with normal aging?

Variable loss of memory
Reduced processing and decreased attention
Divided-switching attention
Reduced working memory
Reduced episodic and some reduced semantic memory


What is dementia?

A complex of symptoms, not a diagnosis
A decline from previous level of function in terms of memory, and one or more other cognitive functions such as abstract thinking, judgement, language and praxis, or change in personality
This change must be of sufficient magnitude to interfere with the patient's usual activities of life, such as work, social life or relationships


Where is memory held within the body?

Mainly the brain, in the hippocampal formation. Some motor memory is held within the spinal cord


What is delirium?

Acute deterioration of cognitive function associated with known or presumed organic cause


What is SDAT?

Senile dementia of the alzheimer's type
It involves findings of extensive, progressive neuron loss, and findings of tangles and plaques
This shows shrinkage of gyri, with widened sulci and ventricles, and shrunken amygdala and hippocampus


Describe neurofibrillary tangles

Found within neurons of SDAT brains, especially in the cortex and hippocampus. Their presence correlates well with cognitive impairment
They are made up of paired helical filaments- polymers composed of z-protein
Normally it functions to stabilize microtubules, to maintain cell structure and shape


Describe extracellular plaques

They are a histological finding of small spherical deposits found in extracellular spaces of the cortex and hippocampus. They are formed of insoluble P-amyloid. Some are found in normal patients, but they are a universal finding of the SDAT brain
Diffuse plaques may represent an early stage of the disease, while neuritic plaques have an amyloid core within a cluster of nerve endings.


What is the theory of cholinergic depletion?

It is thought that, as SDAT brains show a reduction in ChAT synthesis of AChE, there is a large reduction in AChE that causes alzheimers
This causes a defecit in presynaptic neurotransmission
This loss is bilaterally symmetrical but variable.
It may be due to loss o cholinergic innervation of the cortex, as cortical nicotinic receptors are significantly reduced
So far, replacement therapy has produced limited results, and does not provide a complete explanation


What is the amyloid theory of Alzheimers?

It is increased amyloid protein in the brain which leads to plaque formation, depletion, damage of the cortex and dementia
It can be removed by immunotherapy, although there have been problems with immune reactions etc


What are treatment bases of alzheimers?

Generally there is no cure- symptoms only
Can use immunotherapy or increase neurotransmitter use. Reversing cholinergic defects has been attempted, and drugs such as donepezil show a 40% benefit


What are the important components of taking a clinical evaluation for vestibular system function?

- Ear exam
- Eye movement
- Head thrust
- Fukudu stepping
- Fistulae
- Dix hallpike movement
- Lab tests


What do we need to know about a vestibular history?

Whether it's a true vertigo or not (are you moving?)
Precipitating and associated factors


What can be told about the vestibular system on examination, and what does this tell us?

If there is any nystagmus- the fast phase is the direction it is moving in.
Remember COWS- cold (inhibitory) moves to the opposite side of the lesion, while warm (excitatory) moves to the same side as the movement.


What can the head thrust test tell us?

it involves the head at 30 degrees downward so the lateral semicircular canal is horizontal. Turn the head quickly to each side to look for a catch up saccade- the lesion in one side of the brain will have eyes staying to that side and then flicking back


What does the fukuda standing test tell us?

Have the person stand with eyes closed and arms straight out. Then march. The person will start turning to the direction the lesion is in.


What is the calorics test?

Patient lies with the LSCC up and cosd water poured into the ear- the nystagmus goes towards the opposite- if warm it will go towards the same ear


What is the dix hallpike test?

This tests the posterior semicircular canal. The patient lies down with their head haning back- turn their head to one side. BPPV will show nystagmus in the side turned to the ground.


Define pain

An unpleasant sensory and emotional experience associated with actual or potential tissue damage


What are the components of pain?

- Affective: mood and emotion
- Autonomic: Increased HR, RR, BP, sweating
- Motor: withdrawal, immobilization, vocalising
- Sensory: Actual feeling of pain


Define pain threshold and give factors that affect where it sits

The point at which a stimulus is perceived as pain
- Factors include personality, stress, anxiety, culture, emotion etc


What is pain tolerance? Give factors that will increase or decrease it

Pain tolerance is the duration or intensity of pain that an individual will tolerate before initiation of overt pain responses
Tolerance can increase due to distraction, alcohol, faith etc
It can decrease due to repeated exposure, fatigue, or sleep deprivation


Define allodynia, paraesthesia, causalgia and nociception

Allodynia: Pain due to stimulus that is not normally painful
Paresthesia: Abnormal sensation of burning, numbness, tingling etc
Causalgia: Sustained burning pain and allodynia after traumatic nerve lesion
Nociception: Sensory process of detecting tissue damage


What are nociceptors?

Free nerve afferents. They can be A delta or C fibres. They are distributed throughout the body, and are stimulated by noxious mechanical, thermal or chemical stimuli


What are the four basic processes of nociception?



What are C vs A delta fibres?

C fibres are small, unmyelinated and slow, whereas A delta are fast, myelinated and medium. These are quick intense pain, whereas C are slow throbbing pain
Both are primary afferent fibres


What is transduction of pain?

Sensory cells convert external painful stimuli into electrical signals, which occurs in primary sensory cells


What is transmission of pain?

Pain is transferred from primary afferents to the dorsal horn, to brain stem, to thalamus, to sensory cortex. It can be done with electrical or neurotransmitter signals


Describe the classes of second order neurons in the dorsal horns

Nociceptive specific fibres are in laminae I and II, activated only by noxious stimuli
Wide dynamic range are in lamina V, activated by noxious and innocuous stimuli


What are neurotransmitters?

Chemical substances that allow nerve impulses to move from one neuron to another across a synapse. They can be excitatory or inhibitory


What structures are involved with pain perception?

The reticular system- autonomic and motor responses
The limbic system: emotional and behavioural responses
Somatosensory cortex- perception and interpretation of sensation


Describe the Gate control method of pain dampening

1. Segmental inhibition: AKA gate control theory- a non painful stimulus can block transmission. Pain fibres open the gate, while A beta fibres carrying light touch closes the gate. The brain itself can also open or close the gate
This is due to inhibitory interneurons in the sminal cord that make enkephalin, which blocks pain transmission


Describe the descending inhibitory nerve system

Descending axons transmit impulses from brain stem to spinal cord to reduce painThe stimulus stimulates periaqueductal gray area, which activates neurons to LC and NRM. This causes release of enkephalin in the spinal cord


Describe the theory of pain amplification

It's also called windup. This is the process of increased AP output by DH cells in response to sustained low frequency input from nociceptive afferents via C fibres to the DH neurones
It causes increased ca2+ in DH cells, leading to them becoming more responsive- leading to hyperalgesia


Describe nociceptive pain

Due to stimuli from somatic and visceral structures after tissue damage. Mediateors such as K+, prostaglandins, bradykinin etc are released and act on nociceptors
They usually are opioid sensitive


Describe neuropathic pain

Due to damaged neuronal structure. usually opioid resistant, but sensitive to co-analgesics, such as tricyclics, electrical pulses etc
It can be peripheral (pains and needles, burning, shooting, stinging) or central (thalamic sensory relay nuclei affected after stroke, spinal cord compression)
Can also be complex regional pain syndrome


Describe CRPS

Caused by ajor injury or minor trauma
Shows as severe debilitating pain with abnormal circulation, temp, sweating, functionolaesa, atrophy and hair/skin changes
Treatment invovles PT, SNS blocks and meds


Describe inflammatory pain

Post traumatic pain including tissue damage and inflammatory mediators
Non neurogenic inflammation is due to inflam substance release from BV and CT due to tissue damage
Neurogenic damage is due to inflammatory cells releasing mediators that act on other areas, causing primary and secondary hyperalgesia


Describe referred pain

Somatic structures have nerves that feed into the same DH inputs as internal structures, so pain feels like it's coming from a dermatome level


Describe the mechanism of chronic pain

Pain and inflammation causes neurotransmitter release onto second order neurons. However, if not treated in time,, they can also cause activation of nearby glial cells, which release their own cytokines to keep the pain going. As a result, pain can be generated in the DH even after the periphery has healed


What are the behavioural and psychological changes assoc with chronic pain

Sleeping disorders
unpleasent sensation


What is the most useful method of assessing pain?

Scale of 1 to 10
Mild is less than four
Moderate if five to six
Severe is more than seven


What are some causes of spinal cord injuries?

Most frequently it is traumatic injuries
Can also be malignant tumours, demyelination, disc protrusion or syringomyelia. The cervical region is the most vulnerable


Describe the consequences of T8 spinal cord left side hemisection

Motor issues: Monoplegia in left leg due to loss of inputs from corticospinal and rubrospinal tract
Hyperreactive reflexes in left leg due to increased motoneuron excitability from imbalance of symp inputs from reticulospinal and vestibulospinal tracts
Sensory issues: Loss of pain and temp on RHS
Loss of discriminative sensation in LHS


Describe spinal schock

Occurs for first 1-3 days after complete spinal cord transection: A temporary period of areflexia due to loss of facilitatory inputs from reticulospinal and vestibulospinal tracts
- Flaccid paralysis in both legs
- All conscious sensation lost
- Areflexia
- Decreased BP due to loss of sympathetic tone
- Absence of thermal sweating (but red skin)
- Atonic bladder and bowels
- Sexual organ dysfunction


Describe te symptoms of spinal cord transection after spinal shock is over

Recovery of muscle tone and hyperreflexia (spastic)
Spontaneous bladder.rectum voiding
Variable or increased BP due to disrupted baroreception
Flexor reflex returns after months
Extensor babinski reflex
Paraesthesia from affected regions


What are the two methods of recovery of CNS systems after transection

Sprouting of presynaptic terminals
Denervation supersensitivity due to increased receptor expression on post synaptic membrane


What are ways of managing resp/motor skills in quad/paraplegic patients?

Quads- may need artificial ventilation or resp pacemaker if lesion is above C3
Para: Can use parasetp (microcomputer muscle control)or rewalk (exoskeleton) to gain mobility


How do you stimulate CNS regeneration?

Antibodies to neutralise growth inhibithing MAG or NOGO-A
Neurotriphin 3
Tissue bridges with fetal spinal cord, peripheral nerve grafts, schwann cells or olfactory glial cells- allows potential recovery of function, but harder than in PNS due to oligodendrocytes being used instead of schwann cells
Neural stem cell use