Neuroscience Flashcards
Describe the early development of the CNS.
- proliferation of the ectoderm in the dorsal midline of the embryonic disc - this forms the NEURAL PLATE
- as the plate thickens further it starts to fold up on the sides
- eventually, the two neural folds fuse dorsally to form a tube (lined by NEUROEPITHELIUM, in which the space in the middle is called the NEURAL CANAL
- at the tip of the neural fold you get little bunches of cells called NEURAL CRESTS, these crests separate form the tube and lie unfused alongside them
- at the other end of the process the neural tube lies in the midline, dorsally to the embryo, on the other side there are two strips of neural crest tissue
State what the neural tube and neural crest go on to become.
- Neural Tube = CNS cells
- Neural Crest = PNS cells
State the 3 cell types the arise from neuroepithelium
- neuroblasts 2. glioblasts 3. ependymal cells
Describe neuroblasts.
- precursors for all neurones that have their cell bodies within the CNS
Describe glioblasts
- become neuroglia -> astrocytes, oligodendrocytes etc
Describe ependymal cells.
- lining of ventricles and central canal - remain close to the inner membrane of the neural tube and they spread out and form a lining around the developing ventricular system
State the differentiation of neural crest cells.
- sensory neurones of dorsal root ganglia and cranial ganglia
- post-ganglionic autonomic neurones
- schwann cells
- non-neuronal derivatives
Explain the layout of neuroepithelium.
- almost all cells are attached to BOTH the inner and outer membranes - it’s just that the nuclei are in different positions
- the cross-section shows fat cells going through mitosis at the bottom
Describe the differentiation of neuroepithelium.
- cells withdraw from the outer membrane towards the inner membrane and go through mitosis
- one of the daughter cells will stay attached to the inner cell membrane, it gets bigger and goes into the cell cycle again
- the other daughter cell migrates away from the inner membrane and then develops into neuroblasts
- they develop processes (one will become the axon) and these axons are directed away from the inner membrane again, as the above occurs over and over you end up with THREE layers
- there is one layer by the inner membrane where you get mitosis occurring, another layer where you mainly have cell bodies and another that has mainly axons -> this is the beginning of the difference between grey and white matter
What controls the process of differntiation and migration?
- signalling molecules (sonic hedgehog), secreted by surrounding tissues, interact with receptors on neuroblasts
- control migration & axonal growth by attraction and repulsion
- depends on concentration gradient and timing
Describe the developing spinal cord.
o 2 significant features:
- > neural canal is even smaller compared to the thickness of the wall
- > grey matter has split into TWO different types: -> alar plate - dorsal and basal plate - ventral
o interneurons in the alar plates are becoming specialised to receive sensory information -> information comes from the developing dorsal root ganglia that developed from the neural crest
in the basal plate there are some interneurons and the development of motor neurones -> means the basal plate has a motor function -> the axons leave the spinal cord to go towards muscles
Describe the anatomy of a mature spinal cord compared to a developing spinal cord.
- the neural canal becomes the central canal carrying CSF
- alar plates develop into the dorsal horns
- basal plates develop into ventral horns
- the whole spinal cord is surrounded by a thick layer of white matter
Describe the organisation of the nuclei in the brainstem.
- the cranial nerve nuclei within the brainstem that have a motor function tend to lie more medially (because that’s where the basal plates have ended up after the split)
o Motor = Medial
o Sensory = Lateral
o Autonomic = in between
Explain the development of the brainstem.
- the 4th ventricle develops -> makes a mess of the tubular organisation
- the roof plate starts proliferating rapidly causing the dorsal part of the brainstem expands laterally
- as the roof plate expands it pushes the alar plates aside so they are no longer dorsal to the roof plate, this is the developing brainstem
Describe the appearance of the brain at 4 weeks in an embryo.
o only the most anterior bit of the neural tube develops into the brain
- differentiation of the wall of the anterior neural tube occurs to form THREE primary vesicles:
- > prosencephalon = future forebrain
- > mesencephalon = future midbrain
- > rhombencephalon = future hindbrain
o the rest becomes the spinal cord
Describe the appearance of the brain in an embryo at 5 weeks
- enormous expansion of the top part of the developing forebrain -> telencephalon will become the cerebral hemispheres
- less expansion in the lower part of the developing forebrain because that part becomes the diencephalon
- the developing midbrain doesn’t expand very much
- the developing hindbrain divides in two becoming the pons and the medulla
Describe the structure of the brain in a n embryo of 8 weeks of age.
- as development continues you get more and more growth of the wall of the neural tube
- the space within it has become smaller relative to the wall and this space becomes the ventricular system
- late on, you have the first development of the cerebellum -> out-pouching from the back of the pons
Explain the folding of the developing brain.
o there are THREE flexures: cephalic, pontine and cervical
o as you go through development these flexures become exaggerated -> by 8 weeks, the telencephalon has got so big that it’s starting to move back and cover the diencephalon
Explain the development of the cortex
o the brain has a core of white matter with grey matter around the outside -> opposite to the spinal cord
o the grey matter consists of nuclei that have migrated from the inner membrane of the neural tube
- migration takes place by the neuroblasts attaching themselves to radial glial cells -> have their cell bodies anchored in the inner membrane and have a single long process that goes to the outer membrane
- neuroblasts attach themselves to radial glial cells and climb up towards the outer membrane
- a wave of proliferation near the inner membrane occurs followed by a wave of migration towards the other surface -> one layer of the cortex is formed
- another wave of proliferation and another wave of migration forming the 2nd layer of cortex -> continues until you have SIX LAYERS of cells within the cerebral cortex
Back
What are the general causes for the occurence of developmental disorders.
- genetic mutation and environmental factors such as the mother’s lifestyle, diet and teratogens
What is the cause of schizophrenia
- malfunction of neural development early on in develomet
Name a cause of spina bifida
- folic acid deficiency in vivo
What is cranioarchischisis.
- completely open brain and spinal cord
- incompatible with life -> misscarriage, still born or die shortly after birth
What is anenceephaly.
- open brain and lack of skull vault
- as a consequency patients never have a fully developed brain, usually isnt compatible with life (are still born)
What is encephalocele.
- herniation of the meninges (and brain) -> large bump outside of the skull, usually at the back of the head
What is iniencephaly
occipital skull and spine defects with extreme retroflextion of the head
What is spina bifida occulta
- closed asympatomatic NTD in which some vertebrate are not completely closed
What is closed spinal dysraphism
- deficiency of at least two vertebrate arches
- can become covered by lipoma
What is meningocele
- production of the meninges filled with CSF due to a defect in the skull or spine
What is myelomeningocele
- open spinal cord, which can lead to meningeal cysts
Explain the significance of neural stem cells.
- there are still some germinal cells in the subependymal areas and hippocampus of the adult brain, but in very small numbers with none around mid-60s
- after strokes it is sometimes possible for recovery via these stem cells
- research is being done to see if they can be targetted in other neurodegenerative diseases - Huntington’s being one
Define the brainstem.
- the part of the CNS, exclusive of the cerebellum that lies between the cerebrum and the spinal cord
What are the three major divisions of the brainstem from top to bottom?
- midbrain
- pons
- medulla oblongata
State the role of the pineal gland.
- releases melatonin and is important in regulating circadian rhythm -> does so by light via training from vision
What is the role of the superior colliculus.
- important in the coordination of eye and head movements at the same time (think about watching tennis)
What is the role of the inferior colliculus.
- auditory reflexes, if there is a loud bang you tend to look in the direction of the bang immediately
Which cranial nerve emerges from the back of the brainstem?
- trochlear nerve (CN IV) -> out of the back of the pons
State the role of the trochlear nerve
- suppling one of the extrinsic muscles of the eye (superior oblique muscle in particular)
Which sensory pathways are the dorsal corsal columns involved in.
- fine touch
- proprioception (space perception)
What is very clear from the anteroinferior view of the brainstem?
- the pons
Name the 4 functional subtypes of the cranial nerves.
- General Somatic Afferent (GSA)
- General Visceral Afferent (GVA)
- General Somatic Efferent (GSE)
- General Visceral Efferent (GVE)
Describe the function of the special somatic afferent nerve.
- vision, hearing and equilibrium (only the cranial nerves)
State the function of special visceral afferent nerves.
- smell (CN I) and taste
Name the functions of the special visceral efferent nerves.
- muscles involved in chewing, facial expression, swallowing, vocal sounds and turning the head
What is the general rule about the positioning of motor and sensory nerves?
- motor tend to be medial while sensory tend to be lateral
Describe the arrangement of the general somatic efferent nerve.
o GSE are the most medial of all the pathways
- oculomotor = most rostal -> top of the midbrain
- trochlear = immediately below but still in the midbrain
- abducens = in the pons -> nerve move down before emerging from the ponto-medullary junction
- hypoglossal = in the medulla
Describe the anatomy of the special visceral efferent nerves
o SVE lateral to the GSE (2nd)
- trigerminal = in the pons
- facial = in the pons
- ambiguus = in the medulla (involved in swallowing)
- accessory = in the cervical spinal cord
Describe the anatomy of the general visceral efferent nerves.
o GVE are lateral to the SVE (3rd)
- edinger westphal = in the midbrain (parasympathetic imput into the eye)
- salivatory = three pairs of nuclei at the ponto-medullary border
- vagus = in the pons
What is the anatomy of the special somatic afferent nerve.
o most lateral (6th)
- vestibulocochlear = nucleus mainly resides in the pons but also partly in the medulla
What is the arrangement of the general somatic afferent nerves?
o lateral to the GVA (5th)
- there are THREE trigerminal nuclei, one spans across from the midbrain to the pons, another is completely in the pons while the last starts in the pons and goes all the way down the cervical spinal cord
Describe the arrangement of the general visceral afferent nerve.
o most medial of the sensory nuclei but still lateral to all motor (4th)
- solitarius = 90% in the medulla with a fraction in the pons
Describe the appearance of the midbrain.
- has a typical MICKEY MOUSE appearance
- you can see the cerebral aqueduct then you’re in the midbrain
- cerebral peduncle will vary in appearance
- the inferior colliculus which is low down in the midbrain
- MOST OBVIOUS SIGN IS THE SUBSTANTIA NIGRA -> are dopaminergic neurones which normally produce neuromelanin, a pigment that gives its BLACK colour -> as you get old it gets blacker and blacker
NOTE: In Parkinson’s disease you lose these dopaminergic neurones so a pale substantia nigra could be a sign of Parkinson’s disease
What is the anatomy of the pons?
o the pons is in the region of the 4th Ventricle - just underneath the cerebellum
o MOST PBVIOUS FEATURE ARE THE TRANSVERSE FIBRES
o cerebral peduncles hold onto the cerebrum onto the back of the brainstem
- the main peduncle is the middle cerebellar peduncle
Describe the anatomy of the open/upper medulla.
- the medulla changes a lot as you go down the brainstem
- at the top you still have the 4th ventricle but the rest of the shape is very different to the pons
- MAIN FEATURE = PYRAMIDS start to be seen
- a bit of a bulge in the side of the medulla called the inferior olivary nucleus - this is connected to the cerebellum and is involved in fine tuning motor movements
- inferior olivary nucleus can be seen
Wha is the anatomy of the lower medulla?
o at the junction with the spinal cord the cross-section is very round
o dorsal columns can be seen here (touch and proprioception)
- the smaller of the columns is the gracilis - sensory information from the lower limb
- more laterally you have the cuneatus - sensory information from the upper limb
o central canal can be seen in the cross-section of the lower medulla
o crossing over of the fibres at the pyramidal decussation in the lower medulla
State the signs and symptoms of Lateral Medullary Syndrome.
- vertigo
- ipsilateral Cerebellar Ataxia - problem with gait on the same side of the body as the lesion (broad-based gate with a tendency to shuffle)
- ipsilateral loss of pain/thermal sense (face)
- Horner’s Syndrome - loss of sympathetic innervation to the head and neck -> ptosis, lack of sweating around the eye, hoarseness of voice and difficulty swallowing
- contralateral loss of pain/thermal sense in the trunk and limbs
What is the cause of lateral medullary syndrome?
- caused by thrombosis of the vertebral artery or the posterior inferior cerebellar artery
Using this image match the areas to the consequences of lateral medullary syndrome.
- PICA supplies the shaded section of the medulla
- disturbing the vestibular nucleus = vertigo
- disturbing the inferior cerebellar peduncle = the balance problem
- sympathetic tract = Horner’s Syndrome
- spinothalamic tract = pain and sensory information coming from the body
- damage is catastrophic because everything is packed close together in the medulla
What are the demands of the brain?
- 2% of his body weight (around 1.3 kg)
- 10-20% of CO
- 20% of body oxygen consumption
- 66% of liver glucose
- brain is very vunerable if blood supply becomes impaired
What are the two blood supplies to the brain?
- internal carotid arteries (front)
- vertebral arteries (back)
Name the structure that the ICA and VA give rise to.
- circle of Willis
- cerebral arteries come off the circle
Where do the external carotid arteries supply?
- the face
What arteries supply the cerebral hemispheres?
- internal carotid
Describe the pathway of the vertebral arteries which branch of the subclavian arteries.
- travel through the tranverse foramina in the cervical vertebrate and the foramen magnum and onto the brain
Name the major vessels in the venous drainage of the brain.
- cerebral veins
- venous sinuses
- dura mater
- internal jugular veins
Describe the system of the dural venous sinuses
- running along the top is the superior sagittal sinus, inbetween the two folds of dura, at this point the CSF drains back into the venous system
- along the bottom of the dural fold is the inferior sagittal sinus
- these sinuses run backwards to form a big space filled with blood called the CONFLUENCE OF THE SINUSES -> a bleed at the confluence of sinuses can be terrible
What is the medical term for a stroke?
- cerebrovascular accident (CVA)
Define Stroke.
- rapidly developing focal disturbance of brain function of presumed vascular origin lasting more than 24 hours
What percentage of strokes are due to infarction?
- 85%, the other 15% is due to haemorrhage
Define Transient Ischaemic Attack (TIA).
- rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours
Why are TIA clinically so important?
- a massive risk factor for a stroke -> may have been a small bit of atherosclerotic debris that blocks more distally and resolves itself
State 2 causes of occlusions.
- thrombosis -> formation of a blood clot
- embolism -> plugging of small vessel by material carried from larger vessel
How many people die of strokes each year in the UK?
- 100,000, making it the 3rd most common cause of death
What perecentage of survivors have some kind of damage?
- 70% show an obvious neurological defect
- 50% are permenently disabled
Name 5 key risk factors to having a stroke.
- age
- hypertension
- cardiac disease
- smoking
- diabetes mellitus
Describe the path of the middle cerebral artery.
- extends laterally and emerges through the lateral fissure between the frontal and temporal lobes
State the area which is supplied by the middle cerebral artery.
- it supplies the front 2/3 of the lateral part of the hemisphere
Which section of the brain is supplied by the posterior cerebral artery?
- posterior cerebral artery supplies the medial and lateral parts of the posterior part of the hemisphere
What artery supplies the medial part of each hemisphere?
- the anterior cerebral artery
State the symptoms specific to a stroke caused by disturbance to the anterior cerebral artery.
- paralysis of the contralateral LEG more so than the arm or face -> due to motor homunculus part of the motor cortex that controls the leg is more medial than the part controlling the arm
- disturbance of intellect, executive function and judgement (abulia - absence of willpower)
- loss of appropriate social behaviour
State the symptoms specific to a stroke caused by disturbance to the middle cerebral artery.
- CLASSIC STROKE
- contralateral hemiplegia - more the contralateral ARM than leg -> the lesion is more lateral -> closer to the motor cortex controlling the arms than legs
- contralateral hemisensory deficits
- hemianopia (loss of half the visual field)
- aphasia (if a left sided lesion) - can’t speak -> the language centres are more on the left side of the brain
What are the areas of the brain involved in speech?
- Broca’s Area
Name the symptoms specific to a stroke caused by disturbance to the posterior cerebral artery.
o this leads to visual defects -> supplies the occipital lobe where the primary visual cortex is
- omonymous hemianopia
- visual agnosia (loss ability to recognise things)
Back
What are lacunes?
- a lacune is a small cavity, that appear in deep structures as a result of small vessel occlusion, the exact deficit is dependent on anatomical location
- often caused by strokes
Name a cause of lacunar infarcts.
- hypertension
Name the 4 types of haemorrhagic strokes.
- extradural
- subdural
- subarachnoid
- intracerebral
State the cause and consequence of extradural haemorrhagic strokes.
- trauma
- immediate effects - high pressure arterial bleed -> massive increase in intracranial pressure -> herniation -> will be terminal if surgical intervention to relieve pressure is not carried out
- it treated quickly it has good prognosis
State the cause and consequence of a subdural haemorrhagic stroke.
- trauma
- delayed effects due to lower pressure venous bleed -> blood accumulates in the subdural space -> still an emergency -> good outcome if treated
- not uncommon for them to have been initial unconscious and then to have recovered
State the cause of subarahnoid haemorrhagic stroke.
- usually a ruptured aneurysm
State the cause of intracerebral haemorrhagic stroke.
- spontaneous hypertensive rupture of small vessels
What is the difference between dura in the skull and in the vertebral column?
- vertebral column has a SINGLE LAYER of dura with fat between the bone and the dura
- the skull has TWO LAYERS of dura that are mostly stuck together
What are the two layers of dura in the skull?
- periosteal
- meningeal
Describe an extradural haematoma.
- high pressure arterial supply to the brain leads to the splitting of some of the arteries that are running in the meninges themselves (between the dura and the skull), causing compression of the skull underneath
- the periosteal dura is stuck to the skull so it is only a potential space that is there, which can be filled by blood in an extradural haemorrhage
- usually always due to a blow to the side of the head
Describe a subdural haematoma.
- are slower to cause issues than an extradural haematoma
- is caused by the rupture of VEINS in the skull - so is at much lower pressure
- because of the slow onset of symptoms, patients may initially think that they are ok and then experience symptoms a few hours later
What is the fold of dura that extends between the medial surfaces of the two hemispheres called?
- falx cerebri
What does the peeling apart of the two layers of dura at the top of the falx cerebri form and what is found in this space?
- superior sagittal sinus
- within the gap arachnoid granules are found
How is the CSF filtered?
- it leaks through holes in the arachnoid membrane and enters the superior sagittao sinus
Which vertebrate is the most to likely herniate?
- L5 disk -> change in angle between lumbar vertebra and sacral -> has the most pressure going through it
In terms of meningeal layers, what are the differences between the brain and the spinal cord?
- no epidural space in the brain unless a pathological issue is present but there is in the spinal cord
- two layers/folds of dura around to the brain but only one around the spinal cord
- if there isn’t a space then there is some sort of pathology present -> haemorrhage being one
From the outside travelling inwards, name the meningeal layers and the space linked to them around the spinal cord.
- epidural space
- dura mater
- arachnoid mater
- subarachnoid space
- pia mater
State some clincial relevances of the epidural space.
- can be used to insert anaesthetic or painkillers -> sometimes done in childbirth
- epidural nerve block for pain relief or to carry out surgery
State the clincial relevance of the subarachnoid space.
- sampling of CSF
- insertion of anaesthtics or painkillers-> if there is a good idea of how long a surgery will take it is used instead of a general anaesthetic -> especially in the elderly or those with co-morbidites
- spinal nerve block for pain relief or to make surgery possible
Define dermatomes.
- an area of skin that is supplied by a pair of neurones
Define myotome
muscles that are supplied by a pair of neurones
Which spinal nerve supplies the dermatome that the umbilicus lies in?
- T10
At what point does a nerve become a mixed spinal nerve?
- once the sensory and motor nerve have joined laterally from the roots
Describe the cross section the spinal cord, including some key landmarks.
What is the general rule about sensory neurone crossing in the spinal cord.
- sensory neurones usually cross over when it synapses -> if the neurone synapses when entering spinal cord it will immediatelycross etc
When do discriminative touch and proprioception sensory fibres cross over?
- sensory fibres enter the dorsal horn and travel in the dorsal columns without synapsing in the posterior horn so don’t cross until the medulla
When do pain and temperatue sensory fibres cross over?
- sensory fibres enter the dorsal horn, then may travel up or down 1-2 segments in the Lissauer tract, and synapse in the nucleus proprius before crossing the midline in the anterior commissure and travelling in the spinothalamic tract
At what point do motor neurones cross over?
- all motor neurones cross over deep in the medulla, therefore they always emerge on the ‘correct’ side
Name the major tracts the spinal cord in a clockwise direction form back to front while also stating their function.
o corticospinal tracts = voluntary movement pathway
- lateral = limbs
- anterior = trunk (proximal muscles)
o spinothalamic tract = pain and temperature from contralateral side of body
o dorsal columns = sensory info for fine (discriminative) touch
- fasciculus gracillis – lower limbs
- fasciculus cuneatus – upper limbs
What is the path of the lateral corticospinal tract?
- a neurone travels from the fine motor cortex to the medulla where is synapses and therefore crosses over before a spinal nerve which synapses onto a lower motor neurone before becoming a periphary nerve with other spinal nerves and travelling to an effector/muscle
Name some factors that affect the severity of spinal lesions.
- loss of neural tissue - small if due to trauma but extensive if due to metastases or degenerative disease
- vertical level
- transverse plane
What is the link between the height of a lesion and the level of disability?
- the higher the lesion, the greater the disability
- REMEMBER C3,4,5 keep the diaphragm alive -> segmets which the phrenic nerve emerges from
Why is the brains glucose supply so surplus?
· the brain can’t synthesise or utilise any other source of energy, estimated that the brain use 50-60% of the bodies glucose
· ketones can be metabolised, for a short period of time, if there is a shortage of glucose but glucose is the main nutrient
Describe the stages of lateral corticospinal tract injury including recovery
· Stage 1 - spinal shock: loss of reflex activity below the lesion, lasting for days or weeks = flaccid paralysis
· Stage 2 - return of reflexes (happens over weeks/months): hyperreflexia and/or spasticity = rigid paralysis
What percentage decrease in blood flow to the brain is required before its function becomes significantly impaired?
- 50%
State the consequence of a 4 second interruption of cerebral blood flow.
- unconsciousness
- after a few minutes irreversible damage starts to occur
Describe the symptoms of hypoglycaemia caused by the loss of brain function.
- individual appears disoriented
- slurred speech
- impaired motor function
o similar to be being drunk
What is the blood glucose conc. that if values fall below becomes catastrophic?
- below 2 mM (normally between 4-6mM) it can result in unconsciousness, coma and DEATH
How is cerebral blood flow maintained?
- via autoregulation by stretch-sensitive cerebral vascular smooth muscle which can contact and relax to maintain cerebral blood flow when arterial blood flow is between 60-160mmHg
What happens if the arterial blood flow rises above 160mmHg?
- increased flow can lead to swelling of brain tissue which is not accommodated by the “closed” cranium, therefore intracranial pressure increases -> becomes dangerous
What two factors contribute to local regulation of cerebral blood flow?
- neural
- chemical
Describe the pattern of vascularisation in the CNS tissues.
- arteries enter the CNS tissue from branches of the surface pial vessels, branches penetrate into the brain parenchyma branching to form capillaries which drain into venules and veins which drain into surface pial veins
- no neurone is ever more than 100µm from a capillary
What 4 neural factors alter local cerebral blood flow?
- sympathetic nerve stimulation -> vasoconstriction - only happens when the arterial blood pressure is HIGH
- parasympathetic (facial nerve) stimulation -> facial nerve fibres are innervated by parasympathetic fibres -> causes a slight vasodilation
- central cortical neurones -> neuronal neurotransmitter (catecholamines) release -> vasoconstriction)
- dopaminergic neurones -> produce vasoconstriction -> important in regulating local blood flow to areas of the brain that are more active
Define pericytes.
- cells that wrap around capillaries which have diverse activities e.g. immune function, transport properties, contractile
- effectively a type of brain macrophage
Explain how dopaminergic neurones control local cerebral blood flow.
- when dopaminergic neurones are active, they can cause the contraction of pericytes to decrease the blood flow to a particular area thus diverting blood to other, more active areas of the brain
- dopamine may also cause contraction of pericytes via aminergic and serotoninergic receptors
- IMPORTANT FOR DIVERTING BLOOD TO ACTIVE AREAS OF THE BRAIN
What chemical factors can alter local cerebral blood flow?
- CO2 (indirect) -> vasodilator
- pH -> vasodilator
- nitric oxide -> vasodilator
- K+ -> vasodilator
- adenosine -> vasodilator
- anoxia -> vasodilator
- other (e.g. kinins, prostaglandins, histamine, endothelins)
Explain how CO2 can cause cerebral artery flow to increase.
- H+ ion cannot cros the BBB to influcence smooth muscle cells
- CO2 from the blood or from local metabolic activity gets converted to H+ by carbonic anhydrase in surrounding neural tissue and in the smooth muscle cells -> elevated H+ means decreased pH -> relaxation of the contractile smooth muscle cells and increased blood flow
Where is the CSF formed?
- choroid plexus -> are present in the lateral ventricle, 4th ventricle etc
Name an adaptation that makes the choroid plexus good for CSF formation.
- the capillaries are leaky but, are surrounded by ependymal cells with tight junctions -> can freely lsecrete molecules into the ventricle to make CSF
Describe the flow route of CSF.
lateral ventricles -> 3rd ventricle (via interventricular foramina) -> cerebral aqueduct -> 4th ventricle -> subarachnoid space (via medial and lateral apertures) -> lateral ventricles
State the volume of CSF as well as the amount produced formed everyday.
- volume of CSF = 80 - 150 mL
- volume of CSF formed per day = 450 mL/day
What is the function of the CSF?
- protection (chemical and physical)
- nutrition of neurones
- transport of molecules
What are the functions of the Blood-Brain-Barrier?
- protects the brain tissue from toxins and circulating transmitters like catecholamines
- it also protects the brain from wide variations in ion concentrations
Compare plasma to CSF.
o very similar composition
- amino acids are much lower in CSF, Ca2+ and Na+ are also lower
- CSF has very little protein where plasma has a lot
What is the clinical relevance of there being very little protein in CSF?
- if there is protein in the CSF it is a marker for brain infection, injury or other damage
What is Brown-Sequard Syndrom?
- a rare neurological condition characterized by a lesion in the spinal cord which results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side
What changes occur in a vessel of the CNS parenchyma as it travels away from the pial?
- the junctions become tighter and therefore the vessel become less and less permeable
What classes of molecules can relatively easily cross the BBB?
- lipophilic molecules (alcohol and anaesthetics)
- hydrophobic
How do hydrophilic substances cross throught the BBB and into the brain and CSF?
o only certain hydrophilic substances are allowed through the BBB by means of specific transport mechanisms including:
- water via aquaporin channels
- glucose via GLUT1 proteins
- amino acids via 3 different transporters
- electrolytes via specific transporter systems
What are the general roles of circumventricular organs (CVOs)?
- sampling plasma for toxins -> will induce vomiting
- sensing electrolytes
- regulating water intake
Name some circumventricular organs (CVOs)
- median eminence region of the hypothalamus
- subfornical organ (SFO)
- organum vasculosum of the lamina terminalis (OVLT)
What is special about circumventricular organs?
- even though they are in the brain they lie outside of the BBB and actually have fenestrated capillaries
- molecules can readily pass from the blood to the CSF/ ECF -> vital for their relative functions
- ventricular ependymal lining close to these areas can be much tighter than in other areas, limiting the exchange between them and the CSF
Name some pathological states that cause the breakdown of the BBB.
- inflammation
- infection
- trauma
- stroke
How does the BBB affect the treatment for Parkinson’s Disease?
o a key therapy in Parkinson’s disease is pharmacologically raising the levels of dopamine in the brain, however dopamine cannot cross the BBB
o L-DOPA can cross the BBB via an amino acid transporter, and is converted to dopamine in the brain by DOPA decarboxylase -> is a pharmacology way of increasing dopamine in the brain
- however lots of L-DOPA gets converted before it reaches the brain -> L-DOPA is co-administration with a DOPA decarboxylase inhibitor (carbidopa) -> carbidopa cannot cross the BBB, so does not affect conversion of L-DOPA in the brain
What is the problem of using L-DOPA as a treatment for Parkinson’s Disease?
- lots of L-DOPA is converted to dopamine outside of the brain by DOPA decarboxylase, reducing the conc. of L-DOPA which can cross the brain
- can’t raise does or adverse effects of dopamine appear
How are the problems with L-DOPA overcome for Parkinson’s treatment?
- co-administrating a DOPA carboxylase inhibitor (carbidopa)
- carbidopa cannot cross the BBB so enzymes instead the BBB aren’t inhibited
What is a modality?
- a type of stimulus -> hot, cold, touch, etc
- each modality has a specialised receptors which transmit information through specfic anatomical pathways to the brain
What is registered by mechanoreceptors?
- touch, pressure, vibration
- proprioception -> joint position, muscle length, muscle tension
What receptors sense temperature?
- thermoreceptors
What is the receptor for pain?
- noiceptors
What sensory information is carried by A-alpha fibres?
- proprioception of skeletal muscles
What sensory information is carried by A-beta fibres?
- mechanoreception of skin
What sensory information is carried by A-gamma fibres?
- pain
- temperature
What sensory information is carried by C fibres?
- temperature
- pain
- itch
Define Sensory Receptor.
- transducers that convert energy from the environment into neuronal action potentials
Define Absolute Threshold.
- the level of stimulus that produces a positive response of detection 50% of the time
Describe thermoreceptors, including their activation.
- free nerve endings with high thermal sensitivity
- changes in temperature activates a family of transient receptor potential ion channels
What do Meissner’s corpuscles detect?
- fine discriminative touch
What do Merkel cells detect?
- light touch and superficial pressure
What do Pacinian corpuscles detect?
- deep pressure, vibrations and tickling
What do Ruffini endings detect?
- continuous pressure or touch and strech
How sensitive are mechanoreceptors?
- very -> have a very low threshold
What are tonic receptors?
o detect continuous stimulus strength -> transmit impulses to the brain as long the stimulus is present -> keeps the brain constantly informed of the status of the body
o slowly adapting
- eg. merkel cells-> slowly adapt allowing for superficial pressure and fine touch to be perceived
What are phasic receptors?
o detect a change in stimulus strength -> transmit an impulse at the start and the end of the stimulus
o slowly adapting
- e.g. pacinian receptor -> sudden pressure excites receptor causing a signal, transmits a signal again when pressure is released
Define Receptive Field.
- a region on the skin which causes activation of a single sensory neuron when activated
What is the significance of the receptive fields, when talking about sensitivity?
- finger tips, lips, tongue have high density of innervation with very small receptive fields = more sensitive
- the back has less densely packed innervation with larger receptive fields = less sensitive
What is two point discrimination and how does it tie in with receptive fields?
o minimum distance at which two points are perceived as seperate
- is related to the size of receptive fields -> points can be closer on the hand than the back
What is tranduction?
- sensory receptors generate a receptor potential, a change in their membrane potential, in response to approriate stimulation
Where does the cuneate nucleus recieve input from?
- C1-T6 -> via the cuneate tract
What imputs into the gracile nuclues?
- T7-S4 -> via the gracile tract
In terms of sensory input, what is area 3b involved in?
- tactile discrimination
In terms of sensory input, what is area 1 involved in?
- analysis of texture
In terms of sensory input, what is area 2 involved in?
- stereognosis -> ability to percieve the 3D shape of an object by touch
- has input from muscles and joints and reciprocal connections with the motor cortex -> may inform the motor cortex of sensory consequences of moving
What inputs into the primary somatosensory cortex?
- input from a single type of receptor, and from a specfic location
What inputs into the secondary somatosensory cortex?
- input from the thalamus and primary somatosensory cortex
- many neurons in the SII have bilateral receptive fields -> stimuli in corresponding regions on both sides of the body will evoke a response
How is the secondary somatosensory cortex able to form a whole body perceptual experience?
- inputs from the contralateral body surface arise directly due to decussation (crossing over) of the medial lemniscus
- inputs from the ipsilateral body surface enter secondary somatosensory cortex from the contralateral side via the corpus callosum
- by integrating information from both sides the SII is the first stage in froming whole body perceptual experiences
What are the roles of the secondary somatosensory cortex?
- enable tactile discrimination learned using one hand to be easily performed with the other -> due to its input into the limbic cortex
- important in controlling movement in the light of somatosensory input via its connections with the motor cortex
Explain how we are not aware of the sensations caused by wearing clothes.
- the somatosensory cortex has reciprocal connections with all of the subcortical structures which relay sensory input to it
- the descending pathway is made by the corticospinal (pyramidal) tract either directly or via its connections witht he brainstem reticular nuclei -> these back projections have a somatotopic mapping precisely in register with the ascending dorsal column-medial lemniscal system -> this is the vehicle which somatosensory input is filtered as an attention mechanism
What is the difference between nocieptive and pathological pain?
- nociceptive (acute) has a protective role
- pathological (clinical) is associated with disease and nervous system dysfunction
What is the name given to the area of skin innervated by a dorsal root?
- dermatome
What is conveyed by the anterolateral pathways?
- temperature
- pain
- crude touch sensation
Name 4 characteristics of nociceptors.
- polymodal -> different types of nociceptor respond to different types of stimuli
- free nerve endings -> in terms of structure they are much simpler than mechanoreceptors, usually just free axonal endings of sensory neurones
- high threshold - higher activation threshold than touch receptors
- slow Adapting -> good because if there is a potentially harmful stimulus then you want to be constantly reminded of it so you do something about it
What two sensroy fibres carry nociceptive information?
- A-delta
- C neurone
Describe A-delta fibres.
- large
- fast adapting
- produces pain fast -> alerts you to the potential of some harmful scenario
- fast conducting -> still no where near as fast as touch neurones
Describe C neurones.
- smaller than A-delta neurones
- produces a dull, aching pain -> the role of C neurone mediated nociception is to remind you of the injury so that you guard this part of the body
- slow conducting -> unmyelinated -> ties in with its role/provides a constant reminder
Where does input pass through as it goes from the peripheral to central nervous system?
o the dorsal root
- dorsal root ganglion (body)
- trigeminal ganglia (face)
Where is the dorsal horn situated and how is it organised?
- part of the spinal cord
- organised into rexed laminae (I-VII)
Where exactly does innocuous mechanical stimuli input into the dorsal horn?
- A-beta fibres terminate in lamina III-VI -> deep in the dorsal root
Where exactly does pain and temperature stimuli input into the dorsal horn?
- A-delta and C-fibers terminate in lamina I-II -> supericial
What is the main excitatory neurotransmitter in the dorsal horn?
- glutamate
How do interneurons connect?
- between different laminae and between adjacent peripheral inputs
What is lateral inhibition used for?
- to detect the difference between adjacent inputs
How can rubbing an injured area provide pain relief?
- rubbing the skin stimulates the A-beta fibres -> inhibits stimulated pain fibres by interneuron inhibition
What travels in the dorsal column system?
o innocuous mechanical stimuli
- fine discriminative touch
- vibration
How do A-beta fibres enter the dorsal column pathways?
- through the dorsal horn
Where are the gracile and cuneate nuclei postioned?
- in the medulla
Where do 2nd order neurones of the dorsal column cross the in the medulla?
- caudal medulla -> forms the contralateral medial lemniscus tract -> travels and terminates in the ventral posterior lateral nucleus of the thalamus
Where do 3rd order neurones of the dorsal column project to?
- somatosensory cortex -> size of somatotopic areas in proportional to density of sensory receptors in that body region - somatosensory humunculus
Where do 1st and 2nd order neurons of the spinothalamic tract terminate?
- 1st = dorsal horn
- 2nd = decussate immediately in the spinal cord and form the spinothalamic tract and terminate in the ventral posterior lateral nucleus of the thalamus
What is the spinoreticular tract?
- the pathway which links pain to the limbic cortex and tehrefore emotion
What is the main cause of an anterior spinal cord lesion?
- blocked anterior spinal artery causes ischaemic damage to the anterior part of the spinal cord
What are the symptoms of an anterior spinal cord lesion?
- bilateral loss of pain and temperature below the lesion -> spinothalamic tract is damaged
- retained light touch and vibration sensation -> dorsal column is fine
What is Electrical Perceptual Thresholds (EPT)?
- a technique in which an electronic pulse is passed to the skin
- used to determine the type and location of a spinal cord injury
Define pain.
- an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
State the types of pain.
- nociceptive -> tissue damage, typical ACUTE (e.g. cut skin)
- muscle -> lactic acidosis, ischaemia (e.g. strecthing, fibromyalgia)
- somatic -> well localised (e.g. inflammation, infection)
- visceral -> deep, poorly localised pain (e.g. stomach, colon, IBS)
- referred -> from an internal organ/structure (angina, appendicitis)
- neuropathic -> dysfunctional nervous system
How long does pain last for before it would be counted as chronic?
- 6 months
Define neuropathic pain.
- pain cuased by a lesion or disease of the somatosensory nervous system
What does neurpathic pain feel like?
- sharp, burning, electric shock like
How does neuropathic pain respond to opiates?
- poorly
- anti-depressants are commonly used instead -> particularly TCAs
What is sciatica?
- pain caused in the sciatic nerve due to spinal nerves becoming compressed in the intervertebral foramen
Name 5 examples of neurpoathic pain.
- sciatica
- diabetic neuropathy
- post-herpetic neuralgia
- post-surgical pain
- HIV-induced neuropathy
- chemotherapy indcued neuropathy
- complex regional pain syndrome
Define Allodynia.
- pain due to to a stimulus that does not normal provoke pain
Define Hyperalgesia.
- increased pain from a stimulus that normally provokes pain
Define Sensitisation.
- increased responsiveness of nociceptive neurons to their normal input
- a research driven phrase
Define Hypoalgesia.
- a diminised pain in response to a normally painful stimulus
Define Paraesthesia.
- abnormal sensation, whetehr spontaneous or evoked
How is neuropathic pain diagnosed/assessed?
- questionnaires
- simply examination techniques -> cold/freezing pain, brus, pin prick
What is mechanism behind a repeated painful stimulus becoming more painful when it is repeated?
- intiated by NMDA receptor activation
- Ca2+ mediated synpatic plasticaity in dorsal horn neurons
- increased synaptic strength
- reduced inhibtory influences on dorsal neurons
- persistant activation of NMDA receptors can result in the development of chronic pain
What is the role of monoamines?
- inhibit spinal cord excitability
What is the descending control of nociception with the PAG-RVM axis and locus cereleus?
- PAG-RVM = serotonin
- locus cereleus = noradrenaline
How might endogenous opiods affect peoples pain thresholds?
- endogenous opiods are contained within the PAG and RVM
o they enhance the inhibition from the PAG-NVM axis -> reduces the pain transmission in the dorsal horn by inhibitng glutamate release -> activates spinothalamic neurons and therefore inhibition of pain
- this mechanism works when placebos are given
Name some pain relief drugs that work in the descending control systems?
- opiods
- anti-depressants -> TCA, SNRI, SSRI
What is the mechanism of Serotonin and Norepinephrine Re-uptake Inhibitors (SNRIs) mechanism in descending noradrenaline inhibition?
- binds to the pre-synaptic (sometime post) terminal in the dorsal horn and therefore increases the amount of noradrenaline in the cleft
- noradrenaline binds to alpha 2 receptors -> inhibitory signalling in that neurone
What are the 3 neuropathic pain ‘clusters’?
- sensory loss
- thermal hyperalgesia
- mechanical hyperalgesia
What is Functional Segregation?
- motor systems organised in a number of different areas that controls different aspects of movement
What is meant by Hierarchical Organisation?
- high order areas are involved in more complex tasks -> programme and decide on movements, coordinate muscle activity
- lower level of the hierarchy performs lower level tasks -> execution of movement
Describe the Motor System Hierarchy.
o Level 1 = spinal cord -> mainly involved in reflex movements
o Level 2 = Brainstem -> is the centre of integration of different inputs coming from the vestibular system, the vision system and the auditory system
o Level 3 = Motor Cortex (consists of the: primary motor cortex, premotor cortex and supplementary motor area) -> is where the movements are programmed and where the voluntary movements are initiated
- Level 4 = Association Cortex (contains the parietal and frontal cortex) -> not strictly part of the motor pathway, but it influences the planning and execution of movements
What is the role of the basal ganglia and cerebellum in movement?
- basal ganglia and cerebellum fine tune the corse instruction from the primary motor cortex before it reaches the spinal cord
What is the anatomical pathway which from wanting to move to movement?
Where is the primary motor cortex located?
- precentral gyrus, anterior to the central sulcus
What is the function of the primary motor cortex?
- controlled fine, discrete, precise voluntary movement
- provides descending signals to execute movement
What are the 3 parts of the motor cortex?
- Primary Motor Cortex or M1 - Broadmann’s Area 4
- Premotor Cortex - Broadmann’s Area 6
- Supplementary Motor Area - Broadmann’s Area 6
Where is the motor cortex located?
o all are anterior to the central sulcus
How is the primary motor cortex arranged?
- somatotopic organisation
What is the name of the descending motor pathway?
- lateral corticospinal pathway
- anterior corticospinal pathway
Where does motor pathways decussate, identifying which pathway is each?
- base of the medulla -> POSTERIOR CORTICOSPINAL TRACT
- 5-10% travel ipsilaterally until the spinal cord level -> supply the trunk and the proximal parts of the limbs -> ANTERIOR CORTICOSPINAL TRACT
What are cerebral peduncles?
- structures at the front of the midbrain which arise from the front of the pons and contain the large ascending (sensory) and descending (motor) nerve tracts that run to and from the cerebrum from the pons
What are the 2 parts of the descending/pyramidal system?
- corticobulbar tract -> starts in the cortex, then exits and innervates the muscles in the face
- corticospinal tract -> starts in the cortex and innervates the muscles of the arms and legs
What is the corticobulbar pathway?
- the descending linb which innervates the muscles of the face
Where is the premotor cortex located?
- fronatl lobe anterior to the primary motor cortex
What is the function of the premotor cortex?
- planning of movements
- regulation of externally cued movements
Where is the supplementary motor area located?
- fronatl lobe anterior and superior to the primary motor cortex
What is the function of the supplemetary motor area?
- planning complex movements
- programming sequencing of movements
- regulates internally driven movements (e.g. speech)
- SMA becomes active when thinking about a movement before executing that movement
What is meant by associated cortex?
o brain areas not strictly motor areas as their activity does not correlate with motor output/act
- posterior parietal cortex -> ensures movements are targeted accurately to objects in external space
- prefrontal cortex -> involved in selection of appropriate movements for a particular course of action -> think emotions as control of personality
What are the lower motor neurons?
- spinal cord
- brainstem
What are the upper motor neurons?
- corticospinal
- corticobulbar
What is clincally called pyramidal?
- lateral corticospinal tract
What is clincally known as the extrapyramidal?
- basal ganglia
- cerebellum
Define Paresis.
- graded weakness of movement
What occurs with a upper motor neuron lesion?
o initially you get loss of function (‘negative signs’) -> paresis (graded weakness of movement) or paralysis/plegia
o after a few weeks of having this lesion you will get increased abnormal motor function (‘positive signs’) -> due to the loss of inhibitory descending inputs
- spasticity = increased muscle tone
- hyperreflexia = exaggerated reflexes
- clonus = abnormal oscillatory muscle contraction
Define Spasticity.
- increased muscle tone
Define Hyperreflexia.
- exaggerated reflexes
Define Clonus.
- abnormal oscillatory muscle contraction
Name the tell tale/important sign of upper motor neuron lesions.
- Babinski’s Sign (aka extensor plantar response)
- stroking the plantar side of the foot in a normal person causes the toes will flex, but after upper motor neurone lesions the toes will fan and the big toe will go up
Do upper motor neuron lesions cause muscle atrophy?
o NO muscle atrophy
- will have muscle disuse but this will only lead to partial atrophy -> it’s the lower motor neurones, exiting from the spinal cord that bring nutrients to the muscle
What is Apraxia?
o a disorder in skilled movement NOT caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea)
- patients are NOT paretic (partial motor paralysis) but have lost information about how to perform skilled movements -> not because they’ve lost motor command to the muscle but is instead because they have lost the information on how to perform the skilled movements
What causes Apraxia?
o lesions of the inferior parietal lobe and the frontal lobe (premotor cortex and supplementary motor area)
- any disease of these areas can cause Apraxia, but Stroke and Dementia are the most common causes
Define Chorea.
- a movement disorder that causes involuntary, unpredictable body movements
What are the signs of a lower motor neuron lesion?
- weakness
- hypotonia (reduced muscle tone)
- hyporeflexia (reduced reflexes)
- muscle atrophy - the metabolic trophic support to the muscle is lost
- fasciculations - damaged motor units produce spontaneous action potentials, resulting in a visible twitch
- fibrillations - twitch of individual muscle fibres - these aren’t visible to the naked eye but can be recorded if the patients have needle electromyography
What is Motor Neuron Disease?
- progressive neurodegenerative disorder of the motor system - it is a spectrum of disorders
- MND can affect only upper motor neurones, only lower motor neurones or both -> when MND affects both upper AND lower motor neurones it is called Amyotrophic Lateral Sclerosis (ALS) (MND and ALS are used interchangeably in the UK)
What is the most common cause of death in MND suffers?
- respiratory failure when they can no longer control their respiratory muscles
What are the upper motor neuron signs of MND?
- increased muscle tone (spasticity of limbs and tongue)
- brisk limbs and jaw reflexes
- Babinski’s sign
- loss of dexterity
- dysarthria
- dysphagia
What are the lower motor neuron signs of MND?
- weakness
- muscle wasting
- tongue fasciculations and wasting
- nasal speech
- dysphagia
What makes up the basal ganglia?
- caudate nucleus
- lentiform nucleus (putamen + external globus pallidus)
- subthalamic nucleus
- substantia nigra
- ventral pallidum
- claustrum
- nucleus accumbens
- nucleus basalis of Meynert
What are the functions of the basal ganglia?
- elaborating associated movements (e.g. swinging arms when walking)
- moderating and coordinating movement (suppressing unwanted movements)
- performing movements in order
What is the consequence of of damage to the subthalamic nucleus?
- random, uncontrabble movement -> commonly swinging of the arm
- random movements in Parkinson’s can sometimes be successfully treated by surgically inserting an electrode into the subthalamic nucleus
What is a vertebral feature of Parkinson’s?
- camptocormia -> forwardly arched spine
What is the neuropathology of Parkinson’s?
- neurodegeneration of the dopaminergic neurons that originate in the substantia nigra and project to the striatum
What are the main motor sign of Parkinson’s?
- bradykinesia -> slowness of small movements (doing up buttons, handling a knife)
- hypomimic face -> expressionless, mask-like
- akinesia -> difficulty in the initiation of movements because cannot initiate movements internally
- rigidity -> muscle tone increase, causing resistance to externally imposed joint movements
- tremor at rest -> 4-7 Hz, starts in one hand (“pill-rolling tremor”); with time spreads to other parts of the body
What is the genetic mechanism of Hungtington’s?
- CAG repeats in the Huntington gene on chromosome 4
- autosomal dominant
What is Huntington’s and what are the pathological changes that occur?
- genetic neurodegenerative disorder
- degeneration of GABAergic neurons in the striatum, cuadate and then the putamen -> loss of cuadate nucleus leads to massively enlarged ventricles
What are the motor signs of Huntington’s Disease?
- chorea -> starts with hands and face before progressing legs and rest of the body
- speech impairment
- difficulty swallowing
- unsteady gait
- later stages, cognitive decline and dementia
What are the 3 layers of the cerebellum from the outside in?
- molecular
- Purkinje
- granular
What is the name of the nucleus which reaches and inputs information to the cerebellum?
- central nucleus
What are the 3 divisions of the cerebellum?
- vestibulocerebellum
- spinocerebellum
- cerebrocerebellum
Where is the vestibulocerebellum?
- deep, inner section of the cerebellum
Where is the spinocerebellum?
- medial section of the cerebellum
Where is the cerebrocerebellum?
- lateral area of the cerebellum
What is the role of the cerebrocerebellum?
- co-ordination of skilled movements
- cognitive function -> attention, processing of language
- emotional control
What is the role of the spinocerebellum?
- co-ordination of speech
- adjustment of muscle tone
- co-ordination of limb movements
What is the role of the vestibulocerebellum?
- regulation of gait, posture and equilibrium
- co-ordination of head movements with eye movements
What is the major cause of damage to the vestibulocerebellum and its symptoms?
- tumour
- gait ataxia, tendency to fall (even when sitting with eyes open) -> similar to the symptoms of vestibular disease
What is the major cause of damage to the spinocerebellum and what symptoms does it cause?
Back
- chronic alcoholism
- mainly affects the legs -> causes abnormal gait and stance
What are does damage to the cerebrocerebellum cause?
- mainly affects the arms, skilled co-ordinated movements and speech
What are the main signs of cerebellar dysfunction?
- ataxia -> general impairments in movement co-ordination and accuracy -> disturbances of posture or gait: wide-based, staggering (“drunken”) gait
- dysmetria -> inappropriate force and distance for target-directed movements
- intention tremor -> increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
- dysdiadochokinesia -> inability to perform rapidly alternating movements, (rapidly pronating and supinating hands and forearms)
- scanning speech -> staccato, due to impaired coordination of speech muscles
Describe what triggers transmission across synapses.
o membrane potential of the post synaptic neurone can be altered in two directions by inputs
- can be made be made less negative -> brought closer to the threshold for firing -> excitatory post-synaptic potential (EPSP) or made more negative (hyperpolarised) -> inhibitory post-synaptic potential (IPSP)
o GRADED effects -> post-synaptic neurone fire dependent on the summation of the various inputs
Describe the neuromuscular junction.
- a specialised synapse between the motor neurone and the motor end plate on the muscle fibre cell membrane
What neurotransmitter is used in neuromuscular junctions?
- acetylcholine
What are miniature end plate potentials?
- when recording membrane potential across the muscle fibre, you can see that at any one point there are small changes in membrane potential
- are NOT action potentials but rather just small changes in membrane potential that happens as vesicles are constantly dumping their contents into the synaptic cleft
What are the 4 names for alpha motor neurones?
- alpha motor neurone
- ventral horn cells
- anterior horn cells
- lower motor neurones
Define intrafusal.
- skeletal muscle fibres that serve as specialised sensory organs (proprioceptors) that detect the amount and rate of change in length of a muscle
Define extrafusal.
- standard skeletal muscle fibres that are innervated by alpha motor neurones and generate tension by contracting, thereby allowing for skeletal muscle movement
What do alpha motor neurones innervate?
- extrafusal muscle fibres of the skeletal muscle -> cause skeletal muscle contraction
What are spindles?
- coiled, spring like sensory receptors in the muscle
- when stretched they feedback to the CNS and allows an excitatory reflex to be generated -> what you want when your patella ligament gets hit by a tendon hammer
Define Motor Neurone Pool.
- collection of lower motor neurones that innervate a single muscle
What is the arrangement of alpha motor neurones in the spinal cord?
- extensors = more anterior part of the ventral horn
- flexors = more posterior part of the ventral horn
- proximal = more central
- distal = more lateral
Define Motor Unit.
- a single motor neurone together with all the muscle fibres that it innervates, it is the smallest functional unit with which to produce force
How many muscle fibres are innervated by a single aplha motor neurone?
- it depends on the complexity/control of the movement that is required -> each alpha motor neurone can innervate several muscle fibres -> each muscle fibre is only innervated by ONE ALPHA NEURONE
o muscles in the eye have a low innervation ratio (number of fibres innervated by a single motor neurone) because this needs to be finely controlled
o quadriceps do not need a low innervation ratio because you want power from this muscle rather than delicate control
Under what circumstances can an axon sprout and innervate muscle fibres which are already being innervated?
- pathological ones e.g. when a nerve has been cut
Name the types of motor units>
- slow -> smallest cell body diameter, dendritic trees, thinnest axons -> slowest conduction velocity
- fast, fatigue resistant -> larger cell body diameter, dendritic trees, thicker axons -> faster conduction velocity
- fast, fatigable -> largest cell body diameter, dendritic trees, thickest axons -> fastest conduction velocity
What are the functions of slow and fast motor units?
- slow = not much force but work for a long time -> postural muscles e.g. soleus -> standing all day
- fast = lots of force but tire much faster -> bicep
How are different muscle fibre types distributed through muscle?
- evenly -> produce even force and longetivity across the muscle
How is the muscle force regulated?
o 2 mechanisms by which the brain regulates the force that a single muscle can produce
- recruitment -> recruiting more motor units -> smaller units, generally slow twitch, are recruited first
- rate coding -> changing the frequency with which you send action potentials down the nerves
What are Neurotrophic factors?
- factors that are produced within the nerve and transported throughout the nerve to maintain the nerves integrity and function -> type of growth factor, prevent neuronal death, promote the growth of neurons after injury
- CNS neurones don’t regenerate after injury unlike peripheral nerve - the explanation is that in the CNS you have millions of axons as opposed to a few thousand so the consequences of rewiring incorrectly is not worth it
Is it possible to switch from slow to fast muscle types?
- NO WAY of changing fast to slow or vice versa
- slow to fast is only possible in cases of severe deconditioning or spinal cord injury
- microgravity during spaceflight results in a shift from slow to fast muscle fibre types
- ageing is associated with a loss of slow and fast muscle fibres but with preferential loss of fast fibres -> leaves a large proportion of slow fibres in aged muscle -> is called sarcopenia
What are the corticospinal/pyramidal and extrapyramidal tracts?
- corticospinal/pyramidal tract = voluntary movement pathway
- extrapyramidal tracts = automatic movements in response to stimuli
Define reflex.
- automatic and often inborn response to a stimulus that involves a nerve impulse passing inward from a receptor to a nerve centre and then outward to an effector (as a muscle or gland) without reaching the level of consciousness
What are the components of the reflex arc?
sensory receptor -> sensory neuron -> integrating system within the CNS -> motor neuron -> effector
What is the Hoffman Reflex?
- a way in which the stimulus can be identical every time the reflex is tested -> ensures that the stimulus has the same duration and amplitude so you know that any change in reflex size is NOT due to the input unlike with a tendon hammer
- an electrical stimulus is delievered to a nerve -> the impulse is carried along the sensory fibre to the spinal cord and via a reflex arc back to the muscle
What will be seen in Hoffman Reflexes?
- direct motor response/twitch -> going from the motor neurone that has been stimulated, directly to the muscle causing contraction -> is the M wave (motor wave)
- short time later you will see another response (in the EMG)/twicth -> caused by the action potential in the sensory neurone going back to the spinal cord and exciting the motor neurone -> is the H wave
What is meant by flexion withdrawal and crossed extensor?
- lots of polysynaptic reflexes go up and down the spinal cord to innervate groups of muscle on the same side
- are also reflexes that cross the spinal cord to the other side such that the other limbs do something to keep us upright -> contract one leg if the other is picked up from stepping on something sharp
What is the Jendrassik Manoeuvre?
- there is some descending control of reflexes from the brain from supraspinal centres
- when testing the knee-jerk reflex on someone and you ask them to clench their teeth, the reflex you get when you tap their patellar tendon will be 2 or 3 times greater
What are the cuases of hyper-reflexia and hypo-reflexia?
- hyper-reflexia = upper motor neurone lesions (e.g. strokes) -> leads to clonus and Babinski’s sign
- hypo-reflexia = lower motor neurone lesions
What are the main causes of hearing loss?
- loud traumatic sounds: military, industrial, clubs
- 200 genetic conditions cause hearing problems
- infections – meningitis or congenital (rubella or syphilis)
- drugs -> used for severe heart infections and chemotherapy
- ageing
o hearing loss affects about 10% of the population in the UK
What is sound?
- changes in air pressure
What determines pitch and volume?
- pitch = frequency
- volume = intensity
Describe the decibel scale.
- used to measure th eintensity of sound
- logarithmic scal using base 10
What is the Vestibular system?
- the organ/system which gives spacial orientation
What are the 3 main inputs into the vestibular system?
- visual
- rotation/gravity
- pressure
What are the outputs of the vestibular system?
- ocular reflexes
- postural control
- nausea -> due to imbalance or mismatch of information
What is the role of the outer ear?
- localises sound and channels it into the ear canal
How are the sound waves turned into a noise we can hear and understand?
- sound reaches the tympanic membrane (ear drum) and causes it to vibrate
- after the eardrum are 3 little bones (ossicles): the stapes, the incus and the malleus -> these transmit the vibrations of the tympanic membrane onto the cochlea - the organ of hearing
- after the cochlea, signals are transferred via the vestibulocochlear nerve (CN VIII) into the central pathways
Describe the cochlea.
- organ of hearing
- a snail-shaped organ filled with liquid
- hair cells are the sensory receptors in the cochlea
What is the exact role of the ossicles (little bones in the ear)?
- match the impedance and reduce the loss in energy as the vibration goes from the air to the cochlea
- malleus and incus can have their positions adjusted by the tympanic and stapedius muscles to control the tension of the tympanic membrane -> reduce noise going to cochlea to reduce damage
What is Conductive Hearing Loss?
- hearing loss due to the ear being uncapable of transmitting the vibration of sound waves onto the cochlea
Name some causes of conductive hearing loss.
- cerumen (ear wax)
- infections (otitis)
- tumours
- fluid accumulation in the middle ear can occur due to cold -> far more common in children
- perforated tympanic membrane
- otosclerosis – abnormal bone growth can obstruct ear canal
- barotrauma -> temporary form -> driving down a hill fast or in take off
Describe the contents of the cochlea.
- two liquid-filled chambers
- the Organ of Corti -> includes the basilar and tectorial membrane, hair cells and supporting cells
Describe the function of the basilar membrane.
o an elastic structure with different mechanical properties at either end -> it vibrates at different positions along its length in response to different frequencies -> the base is narrow and tough while the apex is broad and floppy -> higher the frequency the further along the membrane the sound will travel
- breaks complex sounds down by distributing the energy of each component
frequency along its length -> hair cells (receptors) are present along the whole length of the basilar membrane in order to detect all frequencies
What is the function of hair cells in the inner ear?
- receptors of the inner ear -> motion of the basilar membrane deflects the hair bundles of the hair cells
What is the mechanism of hair cells in the inner ear?
- bending of the sterocilia towards the tallest sterocilum due to themotion of the basilar membrane changes the internal voltage of the cell -> ultimately produces an electric signal that travels towards the brain -> is called Mechano-transduction
- sterocilia are connected by filamentous linkages called tip links -> work as small springs stretched by the sterocilia’s sliding
Is the hair bundle process active or passive explain why it is?
o active -> need for an active amplification is due to the large portion of energy that is lost in the viscous damping effects of the cochlear liquids
- sensitivity and the sharp frequency selectivity of the cochlea cannot be explained solely by passive mechanical properties – basilar membrane (BM) impedance
What are the 4 aspects of the active process of hair bundles in the inner ear?
- amplification
- frequency tuning
- compressive non-linearity
- spontaneous otoacoustic emission
What is the role of outer hair cells of the ear?
o electromobility
- when efferent fibres are activated, frequency selectivity and sensitivity is enhanced -> this could be due to OHCs -> their cell bodies shorten and elongate when their internal voltage is changed -> electromobility
What causes electromobility?
- a change in outer hair cells internal voltage -> happens at a rate of 80 kHz
- is due to reorientation of the protein prestin
- the spontaneous back and forth movement might be the cause of
otoacoustic emissions
What is the spiral ganglion?
- hair cells (mostly IHCs) form synapses with sensory neurones in the cochlear ganglion (spiral ganglion)
- neurotransmitters are constantly released at rest but the rate changes in response to a change of the presynaptic voltage, due to MT ion channel gating
- each ganglion cell nd corressponding axon responds best to stimulation at a particular frequency
Why is each inner hair cell attached to multpile spiral ganglion cells?
- enable phase-locking -> a collection of fibres can produce a phase-locked response when a single nerve fibre could not -> if one/some fail you still hear the sound
What is Sensorineural Hearing Loss?
- problem rooted in the sensory apparatus of the inner ear or the vestibulocochlear
nerve (retrocochlear hearing loss) - the most widespread type of hearing loss
Name some cuases of sensorineural hearing loss.
- loud noises – headphones at high volume (temporary or permanent
hearing loss) -> clubs are about 100 dB and concerts about 120 dB - Ménière’s disease -> excess fluid in the cochlea
- genetic mutations affect the Organ of Corti
- aminoglycoside antibiotics are toxic for hair cells -> Streptomyocin
- congenital diseases -> rubella, toxoplasmosis
- ageing (presbycusis)
What is the treatment for sensorineural hearing loss?
- Cochlear Implants -> most hearing loss is due to loss of hair cells -> the implant bypasses the dead cells and directly stimulates the nerve fibres
- do not work if the cochlear nerve is damaged
Where does the cochlear nerve convey its information to?
- the cochlear nucleus of the brainstem -> low frequency neurones are ventrally placed whie high frequency nerones are more dorsal
What is the role of the dorsal cochlear nucleus?
- locates sounds in the vertical plane
- sounds of high frequencies produce intensity differences between the two ears -> high frequency sounds produce constructive and destructive interference
- the ears detect and affect differently sounds coming from different directions due to their asymmetrical shape -> called spectral cues
What are the roles of the different cochlear nucleus neurones?
o T-Stellate Cells -> encode sound frequency and intensity of narrowband stimuli -> their tonotopic array represents sounds’ spectra
o Bushy cells -> produce more sharply but less temporally precise versions of the cochlear nerve fibres -> provide the resolution required to encode the relative time of arrival of inputs to the two ears
What is the role of the superior olivary complex?
- compare bilateral activity of the cochlear nuclei to determine the location of a sound
How does the superior olivary complex function?
o medial superior olive computes the interaural time difference -> sounds are detected at the nearest ear before they reach the other one -> bushy cells carry information about the timing of inputs at every cycle so a map of interaural delay can be formed due to delay lines -> used to locate sound in the horizontal plane
o lateral superior olive detects differences in intensity between the two ears -> neurones are excited by sound arising from the ear in the same side (ipsilaterally) while they are inhibited by opposite sounds (contralaterally)
o SOC neurones feedback to the hair cells -> feedback is used to balance the response from the two ears, but also to reduce the sensitivity of the cochlea
What is the role of the inferior colliculus?
What is the relevance of the superior colliculs?
- auditory and visual maps merge -> neurones are tuned to respond to stimuli with
specific sound directions -> the auditory map here created is fundamental for reflexes in orienting the hear and eyes to acoustic stimuli
What can be detected by the balance system?
- only acceleration
- two types of acceleration -> angular acceleration (turning) and linear acceleration (forward/backwards)
What governs angular and linear acceleration?
- angular acceleration = 3 semi-circular canals -> detect head motion
- linear acceleration = 2 otolith organs (utricle and saccule) -> detect linear acceleration
What is the normal function of the vestibular system?
- subserve perception of movement in space and tilt with respect to gravity
- provide reflex balance reactions to sudden instability of gait or posture ‘vestibulo-spinal reflexes
- stabilise the eyes on earth fixed targets, preserving visual acuity during head movements -> ‘vestibular-ocular reflexes’
- assist control of blood pressure and heart rate during rapid up-down tilts
- assist synchronisation of respiration with body reorientations
- provokes motion sickness when stimulated in unusual motion environments
- provide a reference of absolute motion in space, which helps interpret the relativistic signals of the other senses in creating a perception of spatial orientation
Name some disorders of the vestibular system.
- false perception of movement in space -> ‘vertigo’ (Vestibulo-cortical)
- instability of gait and posture -> ‘vestibular ataxia’ (Vestibulo-spinal )
- inability to stabilise the eyes -> ‘vestibular nystagmus’ in unilateral lesions; ‘oscillopsia’ during head movement in bilateral vestibular lesions (Vestibulo-ocular)
- slight impairment of orthostatic control in the acute phase of vestibular loss
- severe nausea and vomiting in the acute phase of unilateral vestibular loss
- loss of co-ordination on directional reorientation; motion intolerance, oversensitivity to visual motion in the environment
Describe the vestibular labyrinth.
o bony labyrinth -> bounded by petrous temporal bone filled with perilymph
o membranous labyrinth -> filled with endolymph contain the receptor cells
- located within the utricle, saccule and semicircular canals
Describe hair cells within the vestibular system.
o Type 1
- more in number
- direct afferent and indirect efferent
- chalice-like nerve endings form ribbon synapses
o Type 2
- less in number
- direct acting
- simple nerve terminals
What is the anatomy of the eye?
What is the major functions of the tear film?
- protect the eye from drying out
- aid the optical properties of the eye
What are the three types of tears?
- basal tears
- reflex tears due to irritation
- emotional/crying tears
What is the route that tears take?
- tears produced by the lacrimal gland -> drains through the two puncta, opening on medial lid margin -> flows through the superior and the inferior canaliculi -> gather in the Tear Sac and then the Tear Duct -> exit the Tear Duct through the tear duct into the nose cavity
- is a valve where the canaliculi meet the Tear Sac which prevents reflux of tears back onto the surface of the eye
What functions does the tear film play?
- maintain smooth cornea-air surface
- oxygen supply to the cornea
- removal of debris
- bactericide
What are the 3 layers of tear film?
- outer most = superficial oily layer -> reduces tear film evaporation -> produced by Meibomian Glands along lid margins
- middle layer = aqueous tear film -> produced by the tear glands
- inner most = mucinous layer on the Corneal Surface to maintain surface wetting -> produced by Goblet cells
Which layer of the tear film protects the tear film from rapid evaporation?
A) Lipid Layer
B) Water Layer
C) Mucinous Layer
D) All Three Layers
- A
Label the diagram.
What is the conjunctiva?
- the thin, transparent tissue that covers the outer surface of the eye -> begins at the outer edge of the cornea, covers the visible part of the eye, and lines the inside of the eyelids
- is nourished by tiny blood vessels that are nearly invisible to the naked eye -> bleeding in the conjunctiva spreads around -> results in blood shot eyes
What are the 3 layers of the coat of the eye?
- sclera -> hard, opaque connective tissue
- choroid -> pigmented and highly vascular -> the eye is always functioning so requires a lot of energy
- retina -> neurosensory tissue
Describe the sclera.
- high water content
- tough, opaque tissue that serves as the eye’s protective outer coat -> helps maintain the shape
- continuous with the cornea
Describe the cornea.
- transparent, dome-shaped window (convex curvature) covering the front of the eye
- a powerful refracting surface -> provides 2/3 of the eyes focusing power
- acts as both a physical barrier and an infection barrier
- relies on tear film and aqueous fluid, for nutrients and oxygen supply
- low water content -> dehydrated by the inner layer of the cornea - corneal endothelium
What are the 5 layers of the cornea?
- Epithelium -> regenrates very quickly
- Bowman’s Membrane
- Stroma -> thickest layer of the cornea -> contributes towards transparency -> corneal nerve endings provides sensation and nutrients for healthy tissue as no blood vessels are in normal cornea
- Descemet’s Membrane
- Endothelium -> pumps fluid out of corneal and prevents corneal oedema -> no regeneration power and the density decreases with age -> endothelial cell dysfunction may result in corneal oedemaand corneal cloudiness
What are the 3 parts of the uvea?
- the Iris
- the ciliary body
- the choroid
Describe the choroid.
- posterior part of the uvea is the choroid
- lies between the retina and sclera
- is composed of layers of blood vessels that nourish the back of the eye
Describe the iris.
- coloured part of the eye is called the iris
- controls light levels inside the eye similar to the aperture on a camera
- round opening in the centre of the iris is called the pupil
- embedded with tiny muscles that dilate (widen) and constrict (narrow) the pupil size
Describe the structure of the lens.
- outer acellular capsule
- regular inner elongated cell fibres -> transparency
- may loose transparency with age -> cataract
What are the functions of the lens?
- responsible for one third of the refractive power of the eye -> higher refractive index than aqueous fluid and vitreous
- accommodation -> elasticity: muscles constrict -> lens becomes smaller + thicker -> short sight
What is the lens suspended by?
- a fibrous ring known a lens zonules
What issue occurs with the lens zonules with age?
- a problem with short-sightedness -> the lens loses its elastic properties due to ageing of the lenz zonules muscles -> when the muscle constricts, the lens remains wide and thin -> short-sightedness
What is the retina?
- retina is a very thin layer of tissue that lines the inner part of the eye -> responsible for capturing the light rays that enter the eye -> light impulses are then sent to the brain for processing, via the optic nerve
What two features are prominent on the retina, when examined, when someone is looking straight ahead?
- optic nerve head/optic disc
- macula
Describe the macula.
- is located roughly in the centre of the retina, temporal (lateral) to the optic nerve
- a small, highly sensitive part of the retina responsible for detailed central vision
- the fovea is the very centre of the macula -> allows us to appreciate detail and perform tasks that require central vision such reading
What is glaucoma?
- optic neuropathy with characteristic structural damage to the optic nerve, associated with progressive retinal ganglion cell death, loss of nerve fibres and visual field loss
What are the risk factors to glaucoma?
- age
- family history
- accidents
- intraocular pressure (only modifiable risk factor à target)
Where is aqueous fluid secreted from?
- the ciliary body into the anterior chamber
What is the first line treatment for glaucoma?
- prostaglandns analogues -> increased aqueous humour flow and therefore reabsorption
What is the normal intraocular pressure?
- 12 -24 mmHg
What are the 2 types of glaucoma?
- primary open angle glaucoma
- close angle glaucoma
What is the corresponding anatomical landmark for the physiological blind spot?
a. macula
b. fovea
c. optic disc
d. ora serrata
- b. fovea
Describe central/macular vision.
- detail day and colour vision -> fovea has the highest concentration of cone photoreceptors
- used for reading, facial recognition and activities which require focus
What test assesses central vision and what will its loss cause?
- assessed by Visual Acuity Assessment -> loss of foveal vision results in poor visual acuity
Describe peripheral vision.
- for detecting shape and movement in the environment and night vision
- navigation vision -> patients with loss of peripheral vision have problems navigating the world -> extensive loss of visual field leads to the patient needing white stick even with perfect visual acuity
Describe the retinal structure.
- Outer Layer -> photoreceptors (1st Order Neuron) -> detection of light
- Middle Layer -> bipolar cells (2nd Order Neurons) -> local signal processing to improve contrast sensitivity, regulate sensitivity
- Inner Layer -> retinal ganglion cells (3rd Order Neurons) -> transmission of signal from the eye to the brain
What is the function of the retinal pigment epithelium?
- found in the outer thin layer
- transports nutrients from the choroid to the photoreceptor cells and removes metabolic waste form the retina
Describe Rod receptors.
- longer outer segment with photo-sensitive pigment
- 100 times more sensitive to light and movement than cones
- slow response to light
- responsible for night vision (Scotopic Vision)
- allow you to find your position in space and detect movement and judge distance
- 120 million rods
Describe Cone photoreceptors.
- less sensitive to light than rods
- faster response than rods
- responsible for day light fine vision and colour vision (Photopic Vision)
- 6 million cones
Where can one find the highest concentration of Rod Photoreceptors in the retina? a) Optic Disc
b) Fovea
c) 10-20 degrees away from Fovea
d) 20-40 degrees away from Fovea
- d
Describe the frequency spectrum of vision.
- rod vision has only one single peak light sensitivity,at 498 nano-meters wavelength
- S-Cones: with photo-pigment sensitive to short wavelength -> blue
- M-Cones: with photo-pigment sensitive to medium wavelength -> green
- L-Cones: with photo-pigment sensitive to long wavelength -> red
What is the most common collur vision deficiency?
- deuteranomaly -> redued sensitivity to red light
How is colour blindness tested?
- ishihara test -> used for red-green colour perception deficiencies -> colour dotted circles with numbers in
Describe light-dark adaptation of the eyes.
o dark adaptation - from light -> dark)
- retina increases its light sensitivity in dark -> switches from photopic to scoptic vision
- biphasic process
- cone adaptation = 7 minutes
- rod adaptation = 30 minutes -> due to regeneration of rhodopsin
o light adaptation (suppression of light sensitivity going into light)
- occurs over 5 minutes
- bleaching of photo-pigments mediates the process
- neuro-adaptation: Inhibition of Rod/Cone function
- pupil Adaptation (minor) constriction of pupil with light
Which is the commonest form of colourvision deficiency in humans?
a) absence of all cone photoreceptors
b) absence of M-cone (green) photoreceptors
c) abnormal L-cone (red) photoreceptors
d) red-green confusion
- red-green confusion
Define ametropia.
- refers to vision disorders characterized by the eyes inability to correctly focus the images of objects on the retina -> forms include myopia (nearsightedness), hyperopia (farsightedness), and astigmatism
What is refraction?
- based on the idea that light is passing through one medium into another -> as light goes from one medium to another, the velocity changes
- ratio of two speeds can be compared:
In order for light to reach the reina from air, what must light photons pass through?
- tear film -> cornea -> aqueous humour -> lens -> vitreous humour -> retina
What are the application of lenses?
- refraction
What are the two basic types of lenses?
o convex lenses
- light passes through the converging (convex) lens and rays converge towards a focal point
- focal point is at a distance from the central plane of the lens – this distance is proportional to the thickness of the lens -> used by short-sighted people in glasses
o concave lenses
- light disperses around because it is refracted in a divergent way -> focal point is a virtual point -> virtual focal point is in front of the lens
Define emmetropia.
- an eye with a refractive power of 0 -> no visiual defects
Define ametropia.
- presense of a refractive error -> mismatch between axial length and refractive power -> parallel light rays don’t fall on the retina (no accommodation)
What are the 4 types of ametropia?
- nearsightedness (myopia)
- farsightedness (hyperopia)
- astigmatism
- presbyopia
What is myopia?
- short-sightedness -> parallel rays converge at a focal point anterior to the retina
What are the causes of myopia?
- excessive long globe -> axial myopia -> more common
- excessive refractive power -> refractive myopia
What are the symptoms of myopia?
- blurred distance vision
- squint in an attempt to improve uncorrected visual acuity when gazing into the distance
- headache
What are the treatments for myopia?
- concave glasses -> also achieved with contact lenses -> both move focal point slightly backwards
- surgical removal of the lens to reduce refractive power
What is hyperopia?
- long-sightedness -> parellel rays converge at a focal point posterior to the retina
What are the causes of hyperopia?
- excessive short globe (axial hyperopia) -> more common
- insufficient refractive power (refractive hyperopia)
State some symptoms of hyperopia.
- visual acuity at near tends to blur relatively early -> usually more noticable if they are tired
- asthenopic symptoms -> eyepain, headache in frontal region, burning sensation in the eyes, blepharoconjunctivitis
- amblyopia (lazy eye) -> uncorrected hyperopia in one eye leads the brain favouring the other eye -> 5D
What is the treatment for hyperopia?
- convex lenses in glasses of contact lens
- surgical intervention
What is astigmatism?
- caused by a refractive media that is not spherical -> more elliptical -> the cornea is not evenly shaped in terms of the radius
- light refracts differently along one meridian than along meridian perpendicular to it -> results in 2 focal points (punctiform object is represent as 2 sharply defined lines)
What are the symptoms of astigmatism?
- asthenopic symptoms (headache , eyepain)
- blurred vision
- distortion of vision
- head tilting and turning
What is the treatment for astigmatism?
- regular astigmatism -> cylinder lenses with or without spherical lenses (convex or concave)
- irregular astigmatism -> rigid CL or surgery
Describe presbyopia.
- naturally occurring loss of accommodation (focus for near objects) -> onset from age 40 years due to natural loss of lens elasticity
- distant vision intact
- corrected by reading glasses (convex lenses) to increase refractive power of the eye
Which statement is false for Myopia?
a) may be associated with large globe
b) light ray converges behind the retina
c) may be associated with increased corneal curvature
d) unable to see objects clearly at distance without glasses or other optical correction
- b -> converges infront of the retina
In accommodation, which one of the following events does not take place?
a) relaxation of Circular Ciliary Muscle
b) relaxation of Zonules
c) thickening of Lens
d) increase of Lens Refractive Power
- a
What is the pathway down which signals are transmitted in the visual pathway?
- eye -> optic nerve -> optic chiasm -> optic tract -> lateral geniculate nucleus -> optic radiation -> primary visual cortex or striate cortes
WHat perecentage of ganglionic fibres cross at the optic chiasm?
- 53% ganglion fibres cross at optic chiasm
- crossed fibres -> originate from nasal retina -> responsible for temporal visual field
- uncrossed fibres -> originate from temporal retina -> responsible for nasal visual field
What are the results of lesions at the optic chaism and posterior to the optic chiasm?
- Temporal Field Deficit in Both Eyes -> Bitemporal Hemianopia
- Right sided lesion -> Left Homonymous Hemianopia in Both Eyes
- Left sided lesion -> Right Homonymous Hemianopia in Both Eyes
What is the typical cause of bitemporal hemianopia?
- enlargement of the pituitary gland
Describe the primary visual cortex.
- located along the Calcarine Sulcus within the Occipital Lobe (aka the Striate Cortex)
- specializes in processing visual information of static and moving objects
- organised as columns of information from the left and right which are interspersed -> helps judge depth
- a disproportionately large area representing the macular central vision within the PVC
- area above the Calcarine Fissure represents the inferior visual field and below the Calcarine Fissure represents the superior visual field
Describe how a stroke can lead to macular sparing homonymous hemianopia.
- leads to Contralateral Homonymous Hemianopia with Macula Sparing -> area representing the Macula receives dual blood supply from Posterior Cerebral Arteries from both sides
What is the extrastriate cortex?
- area around PVC within the Occipital Lobe
- converts basic visual information, orientation and position into complex information
What causes pupil dilation and constriction?
- constriction = iris muscle contracts to constrict the pupillary aperture
- dilation = radial muscle contracts
Describe the pathway of the pupilary reflex.
o Afferent pathway (Red & Green)
- Rod and Cone Photoreceptors synapsing on Bipolar Cells synapsing on Retinal Ganglion Cells
- Pupil-specific ganglion cells exits at posterior third of optic tract before entering the LGN -> synapses at the Brain Stem (Pretectal Nucleus) -> afferent (incoming) pathway from each eye synapses on Edinger-Westphal Nuclei on both sides in the brainstem
o Efferent pathway (Blue)
- Edinger-Westphal Nucleus -> Oculomotor Nerve Efferent -> synapses at Ciliary ganglion
· Short Posterior Ciliary Nerve à Pupillary Sphincter
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What pupillary response would occur in someone with a right afferent defect?
- no pupil constriction in either eye when right eye is stimulated
What pupillary response would occur in someone with a right efferent defect?
- no right pupil constriction when either eye is stumlated with light
What pupillary response would occur in someone with a unilateral afferent defect?
- different response depending on which eye is stimulated
What pupillary response would occur in someone with a unilateral efferent defect?
- same unequal response between left and right eye irrespective which eye is stimulated
Define duction, in terms of the eye.
- eye movement in one eye, without making any reference to the movement of the fellow eye
Define version, in terms of eye movement.
o movement of both eyes in the same direction
- gazing to the right = dextroversion
- gazing to the left: levoversion
Define vergence, in terms of eye movements.
- movement of both eyes in opposite directions simultaneously
Define convergence, in terms of movements of th eye.
- simultaneous adduction (inward) movement in both eyes when viewing a near object
What is saccade and state the 5 different saccades?
o short fast burst -> up to 900deg/sec
- reflexive saccade to external stimuli
- scanning saccade
- predictive saccade to track objects
- memory-guided saccade
What is smooth pursuit?
- slow sustained movement -> up to 60 degrees per second
- driven by motion of a moving target across the retina
What are the 6 extraocular muscles?
- superior rectus
- inferior rectus
- lateral rectus
- medial rectus
- superior oblique
- inferior oblique
Where is the superior rectus attached and what is its function?
- attached at 12 o’clock
- moves the eye up
Where is the inferior rectus attached and what is its function?
- attached at 6 o’clock
- moves the eye down
Where is the lateral rectus attached and what is its function?
- attached to the temporal side of the eye
- moves the eye towards the temple
Where is the medial rectus attached and what is its function?
- attached on the nasal side of the eye
- moves the eye towards the nose
Where is the superior oblique muscle attached and what is its function?
- attached high on the temporal side of the eye -> passes under the superior rectus
- moves the eye in a diagonal pattern -> down and in
Where is the inferior oblique muscle attached and what is its function?
- attached low on the nasal side of the eye -> passes over the inferior rectus
- moves the eye in a diagonal pattern -> up and out
What eye muscles are innervated by the superior branch of the third cranial nerve?
o Superior Rectus – elevates eye
o Lid Levator – raises eyelid
What eye muscles are innervated by the inferior branch of the third cranial nerve?
o Inferior Rectus -> depresses eye
o Medial Rectus -> adducts eye
o Inferior Oblique -> elevates eye
o Parasympathetic Nerve -> constricts pupil
What eye muscle is innervated by the fourth cranial nerve?
- superior oblique -> depresses the eye
What eye muscle is innervated by the sixth cranial nerve?
- lateral rectus -> abducts the eye
Define supra- and intra version.
- supraversion = elevation of both eyes -> namely simultaneous right and left eye supraduction
- infraversion = depression of both eyes -> namely simultaneous right and left eye infraduction
What occurs in third nerve palsy?
- only muscles not innervated by CN III in the affected eye are working -> lateral rectus muscle and superior oblique muscle
- affected eye down and out with a droopy eyelid (ptosis)
What occurs in sixth nerve palsy?
- sixth nerve palsy presents with deficit in abduction in the affected eye -> made apparent when the patient is asked to abduct the affected eye
- affected eye deviates inwards (unable to abduct)
- double vision worsen on gazing to the side of affected eye
What is mystagmus?
- oscillatory eye movement -> can be physiological or pathological
When is the optokinetic nystagmus reflex clinically useful?
- in testing visual acuity in pre-verbal children by observing the presence of nystagmus movement in response to moving grating patterns of various spatial frequencies
What does oscillopsia indicate?
- nystagmus
What is nystagmus?
- a condition involving involuntay eye movements
What is the most common cause of vertigo?
- benign paroxysmal positional vertigo (BPPV)
What are the red flags for vertigo?
- headache
- gait problems
- hyperacute onset
- hearing loss
- prolonged symptoms -> for more than 4 days
A 65 year old artist with hypertension has a 4 year history of recurrent attacks of violent spinning dizziness with sweating, a sensation of impending doom and nausea. He feels unwell for about an hour afterwards. The attacks occur on looking up. On direct questioning the attacks also occur in bed. What one test would you perform to do to confirm the diagnosis?
1. MRI brain scan
- MRI of the internal acoustic meati
- Hallpike manouevre
- Cardiac monitoring
- Bithermal caloric irrigation
- Hallpike manouevre
A previously well 44 year old businesswoman has a 1 year history of episodic rocking-type dizziness lasting 30-60 minutes. During these episodes she notices that she prefers to lie down in a quiet dark room until the dizziness abates. She has mild asthma, suffered from severe headaches in her 20’s but now only gets the occasional headache (x 1/month). The examination is normal although there was a 10mm postural drop in systolic blood pressure. What is the likely diagnosis?
1. Vertebro-basilar insufficiency
- Postural hypotension
- Benign paroxysmal positional vertigo
- Vestibular migraine
- Cardiac dysrrhythmia
- Vestibular migraine
A previously well 34 year old lawyer developed severe and sudden onset spinning dizziness one evening whilst working out in the gym with weights. The dizziness was associated with nausea, vomiting and headache even though he had no previous headache history. He staggered home and went to bed. The next day he was still the same and vomited whenever he got up to move around. He went to his GP practice and was seen by the nurse who prescribed stemetil for an ear problem. Along with migraine, what is the most likely differential diagnosis?
- BPPV
- Cerebellar stroke
- Meniere’s Disease
- Meningitis
- Vestibular neuritis
- Cerebellar stroke - very fast onset
Briefly summarise grey and white matter in the brain.
- grey matter- > on the surface of the brain -> contains nerve cell bodies
- white matter -> the circuitry -> axons and connections
What is diffusion tensor imaging?
- a MR modality that looks for alignment of water molecules, and coincident activity -> it is a good way of looking at functional connectivity
What are the 3 types of white matter fibres?
- association fibres
- commissural fibres
- projection fibres
Describe association fibres.
What are commissural fibres?
- connections between the two hemisphere to integrate information from different areas -> main one being the corpus callosum
Describe projection fibres.
- long pathways that connect the cortex with the lower brain structures (e.g. thalamus), brainstem and spinal cord
Describe the cortical layers of the grey matter.
o the neocortex (most of the cortex) has a 6-layer structure -> the archicortex has 3 cortical layers
- layer I contains mainly neuropil
- layer II contains generally smaller pyramidal neurons with primarily corticocortical connections
- layer IV is typically rich in stellate neurons with locally ramifying axons; in the primary sensory cortices -> these neurons receive input from the thalamus, the major sensory relay from the periphery
- layer V, and to a lesser degree layer VI, contain pyramidal neurons whose axons typically leave the cortex (output)
Describe columnar distribution in the cortex.
- we have cortical columns
- the neocortex is arranged in layers (lamina structure) and columns there are more dense vertical connections -> these columns are the basis for topographical organization
- neurons with similar properties are connected in the same column
Define primary and association cortices.
- primary cortices: function is predictable, organised topographically, left-right symmetry
- association cortices: function less predictable, not organised topographically, left-right symmetry weak/absent
What functions occur in the occipital lobe?
o primary visual cortex in the occipital lobe
- visual association cortex analyses different attributes of visual image in different places -> form and colour is analysed along the ventral pathway, spatial relationships and movement along dorsal pathway
What processes occur in the parietal lobe?
o primary somatosensory cortex in the post-central gyrus in the parietal lobe
- posterior parietal association cortex creates spatial map of body in surroundings, from multi-modality information
What are the functions of the temporal lobe?
o auditory cortex in the superior temporal gyrus in the temporal lobe
- language, object recognition, memory, emotion
What processes occur in the frontal lobe?
- primary motor cortex (PMC) part of the pre-central gyrus in the frontal lobe
- judgement, foresight, personality, appreciation of self in relation to world -> personalities
What kind of stroke is most likely to cause language deficits?
- left sided
- Broca’s and Wernicke’s areas are both lateralised to the left hemisphere
What is the consequence of a lesion in the fusiform gyrus?
- prosopagnosia -> face blindness
What are the consequences to having a lesion in the occipital cortex?
- lesions affect specific aspects of vision perception
What are the consequences of an injury to the parietal lobe?
- injury may cause disorientation, inability to read map or understand spatial relationships, apraxia, hemispatial neglect
What does injury to the temporal lobe lead to?
- injury leads to agnosia, receptive aphasia
What happens as a result of injury to the frontal lobe?
- injury leads to deficits in planning and inappropriate behaviour
What happens in someone who has no corpus callosum?
- left hemisphere is language dominant while right is is for spatial processing
- in an experiment, a word is flashed briefly to the right field and the patient is asked what they saw -> they will be able to, because the left hemisphere is dominant for verbal processing
- if you flash the word briefly to the left field, the patient doesn’t see anything -> however, they will be able to draw what the word says
o due to dominant activities of the hemispheres on either side, a split callosum is problematic
Why might a patient have their corpus callosum surgically cut?
- severely epileptic -> prevent a global seizure that initiates in one hemisphere
What is the use of functional MRI?
- get information in vivo about connectivity -> particularly in CNS conditions
- usually about monitoring blood flow and glucose metabolism -> glucose use is probably related to functional activity of the brain -> where there is more glucose and more blood flow, there is probably higher activity
Where are the primary olfactory neurones and olfactory bulbs located?
- neurones = mucosa at the top of the nose
- bulbs = inferior surface of the frontal lobes
What is loss of olfaction due to?
- trauma to the ethmoid bone which damage the olfactory neurones
- early sign of Parkinson’s and Alzhemeir’s
- old age
Describe, to the best of current knowledge, how a certain smell is detected?
- the cribriform plate is a very fine layer with small holes making up part of the ethmoid bone -> projecting through the holes are the olfactory receptor cells with a bipolar morphology
- olfactory neurones project into the olfactory bulb, and form glomerular like structures in their interaction with second order olfactory neurones -> cells in the olfactory bulb (second order) are called mitral cells
- second order neurones then project back to the olfactory processing centres -> olfactory tract lies on the inferior surface of the frontal lobe -> mitral cells project back to the olfactory tract, and they split into medial and lateral olfactory stria
- neurones project to two cortical olfactory processing areas -> piriform cortex of the temporal lobe and the orbitofrontal cortex
- connections of olfactory neurones to the brainstem evoke and promote autonomic responses -> e.g. if you smell something you want to eat, you will start salivating
Name 2 clinical defects of smell.
- anosmia = complete loss of smell
- prodromal aura = in temporal lobe epilepsy, the electrical activity before a seizure may provoke a prodromal aura -> in some people this may be a smell -> they smell something and know they will have a seizure
What processes is the limbic system responsible for?
o processes aimed at survival of the individual
- maintenance of homeostasis (hypothalamic function) via activation of visceral effector mechanisms -> modulation of pituitary hormone release and initiation of feeding and drinking
- agonistic behaviour (fight or flight)
- sexual and reproductive behaviour
- memory -> vital in terms of emotional response to stimuli in the environment
What areas are in the limbic system?
- frontal lobe
- thalamus
- hippocampus
- amygdala
- hypothalamus
- olfactory bulb
- cingulate cortex
Describe the Papez circuit.
- main output pathway of the hippocampus is the fornix, which comes out of the inferior horn of the lateral ventricle (the hippocampus sits in the ventricle floor) -> fibres go up, forward and down into the mammillary bodies of the hypothalamus -> a connection to the anterior nucleus of the thalamus via the mamillo-thalamic tract -> projections from the thalamus to the cingulate cortex (just above the corpus callosum) -> to complete the circuit, there are fibres running from the cingulate cortex to the hippocampus (via the cingulum bundle
What is the role of the neocortex?
- information is received from the outside, and integrated at the hippocampus
- provokes a response, which stimulates the hypothalamus to change normal homeostatic activity
- reactions you have are influenced by memories and previous experiences
Where is long term memories stored?
- within the parietal cortex
What are the afferent and efferent inputs into the hippocampus?
- afferent = perforant pathway
- efferent = fimbria/fornix
What are the functions of the hippocampus?
- short-term memory
- learning
Name 2 diseases which have clinical links to the hippocampus.
- Alzheimer’s -> localised atrophy to the hippocampus
- epilepsy
Where is the hippocampus?
- sits in the floor of the ventricle
- the fimbria and fornix can be seen projecting into the mammillary bodies at the base of the diencephalon
- the amygdala is a nucleus buried in the white matter, in the anterior part of the temporal lobe
Describe the cortical atrophy is Alzheimer’s.
- temporal lobe atrophy (shrinkage)
- gyri get thinner and the sulci become wider -> there is less brain substance
- in later stages of Alzheimer’s, the frontal lobe also starts to undergo atrophy
- primary motor cortex, primary sensory cortex and occipital lobe are largely unaffected
Describe plaques and tangles in Alzheimer’s.
- pathology at a cellular level is tangles -> abnormal cytoskeletal proteins
- cytoskeleton breaks down and neuronal cell function breaks down -> differential susceptibility of the cells (some neurones will not be affected)
- senile plaques are observed -> protein is laid down in the hippocampus -> disturbing normal memory function.
Describe the anatomical progression of Alzheimer’s.
- early = hippocampus and entorhinal cortex -> short-term memory problems
- moderate = parietal lobe -> dressing apraxia
- late = fronatl lobe -> loss of executive skills and personality
Where is the amygdola located?
- a nucleus buried in the white matter of the anterior part of the temporal lobe
How is the amygdola connected?
o is highly interconnected with everything else;
- afferent = olfactory cortex, septum, temporal neocortex, hippocampus, brainstem
- efferent = stria terminalis
What is the function of the amygdola?
- fear and anxiety
- fight or flight
What is Kluver-Bucy syndrome?
- a reversion to the basis survival instincts, and exploration of the environment -> YOU BECOME COMPLETELY FEARLESS
- results from localised bilateral lesions in the anterior temporal lobe -> often due to trauma but still incredibly rare
What are the symptoms of Kluver-Bucy syndrome?
- hyperorality
- loss of fear
- visual agnosia
- hypersexuality
o very rare for more than two symptoms to be shown in the same patient
What structures are associated with aggression?
- anterior parts of the hypothalamus
- brainstem
- amygdola
- NT- system -> has a role in serotonin in the raphe nuclei
What is the septum?
· - the membrane between the two lateral ventricles anteriorly, at its base is the septal nuclei
What in the inputs and outputs of the septal nuclei?
- afferent = amygdala, olfactory tract, hippocampus, brainstem
- efferent = stria medularis thalami, hippocampus, hypothalamus
What is the function of the septal nuclei?
- reward
- reinforcement
What is the drug dependency pathway?
- mesolimbic pathway
- dopaminergic neurones are in the midbrain -> fibres project via the median forebrain bundle to the cortex, nucleus accumbens (obssession, compulsion and reward) )and amygdola (reward)
What is the nucleus accumbens involved in?
- obsessive compulsion
- reward
What must be considered when prescribing a Parkinson’s patient dopamine agonsits?
- family must watch for compulsie reward-based behaviour -> may become compulsive gamblers
- stimulation of the mesolimbic pathway causes this effect
What system acts as the control/gateway of consciousness?
- reticular activating system -> starts in the brainstem and influences the activity of the cerebral cortex -> can be direct or indirectly though the intralaminar nuclei in the thalamus
- high activity in this system leads to higher level of arousal
What nuclei and bodies are linked in with the RAS system and therefore aid the ability to fall asleep?
- lateral hypothalamus -> promotes wakefulness via the orexin system
- ventrolateral preoptic nucleus -> promotes sleep from within the naterior hypothalamus
- suprachiasmatic nucleus -> synchronises sleep with falling light -> provides the body with circadian rhythm
What are the effects of sleep depreivation?
o psychiatric -> sleepiness, irritability, stress, mood fluctuations, depression, impulsivity, hallucinations
o neurological -> impaired attention, memory, executive function, risk of errors and accidents
- neurodegeneration -> sleep problems can be a warning sign for neurodegenerative disease
o somatic -> CAN LEAD TO DEATH
- glucose intolerance
- reduced leptin/increased appetite à obesity
- impaired immunity
- increased risk of cardiovascular disease and cancer
How is sleep altered/regulated after sleep loss?
- reduced latency to sleep onset
- increase of slow wave sleep (NREM)
- increase of REM sleep (after selective REM sleep deprivation)
What is the function of sleep?
- restoration and recovery -> but active individuals do not sleep more
- energy conservation -> 10% drop in BMR -> but lying still is just as effective
- predator avoidance by staying still -> doesn’t explain why sleep is so complex
o specific brain functions -> MEMORY CONSOLIDATION
Describe dreams.
- can occur in REM and NREM sleep -> most frequent in REM sleep -> more easily recalled in REM sleep
- contents of dreams are more emotional than ‘real life’
Describe the brain activity during a time of dreams.
- brain activity in the limbic system is higher than in frontal lobe during dreams -> suggests emotion/memory
What are the potential function of sleep?
o no-one really knows but there are some theories
- afety valve for antisocial emotions
- disposal of unwanted memories
- memory consolidation
Name some causes of chronic insomnia.
- physiological -> sleep apnoea (obstructive and central), chronic pain
- brain dysfunction -> depression, fatal familial insomnia, night working
What treatments are available for insomnia?
- treat the cause if possible
- improved sleep hygiene
- sleep cognitive behavioural therapy
- hypnotics (sleeping tablets) -> enhance GABAergic circuits -> inhibitory mechanisms on brain activity
What is narcolepsy?
- falling alseep repeatedly during the day and disturbed sleep during the night
What condition is often linked with narcolepsy?
- ccataplexy -> sudden, brief loss of voluntary muscle tone, often triggered by strong emotions e.g. laughter
What is Lewy-Body disease?
- a type of dementia
- in lewy-body dementia, patients can act out their dreams, often in a very violent way
- sufferes partners will recall being punched in the middle of the night, as the patient is acting out the dream
- Lewy-body disease can often pre-date the onset of other kinds of obvious dementia symptoms by years
What is vigilance?
- wakefulness -> the level of consciousness in terms of how much your RAS is working
Define awareness.
- level and content of consciousness
Describe a graph showing awareness against vigilance.
What is the default-mode network?
- a pathway which is more active at rest/inbetween tasks
What is the pertubational complexity index?
- a method of quantifying brain complexity using transcranial magnetic stimulation and EEG
- a transcranial magnetic stimulator sends a pulse to the brain -> causes reverberation of activity -> this reverberation (activity around the brain) can be measured using EEG
- in patients who have disorders of consciousness (or are asleep/anaesthetised), their response is NOT AS DIVERSE -> measurea/tracks conscious levela
Define a coma.
Define vegetative state.
Define minimally active state.
What is the difference between homonymous hemianopia and visual neglect?
o homonymous hemianopia = loss of half of the visual field, common after stroke
o visual neglect = a higher order problem -> lose conscious awareness of one side.
- if the neglect is on the left side, the patient won’t attend at all to anything on the right side -> if much high order problem -> the patient has completely lost awareness of that side
Describe the glasgow coma scale.
- a clinical means of assessing something about conscious level
- ranges between 3 and 15 -> the lower the score, the higher the severity
- eyes =4, voice = 5 and motor = 6
What are the paramater/scoring systems for the glasgow coma scale?
What are the 4 main categories of causes of coma?
- metabolic
- diffuse intracranial
- hemisphere lesion
- brainstem
What are the metabolic causes of a coma?
- drug overdose
- hypoglycaemia
- diabetes
- ‘the failures’ -> renal, liver etc.
- hypercalcaemia
What are the cause of coma that are classified as diffuse intracanial?
- head injury (trauma)
- meningitis
- SAH
- encephalitis
- epilepsy
- hypoxic brain injury
What are the hemisphere lesional causes of coma?
- cerebral infarct
- cerebral haemorrhage -> subdural or extradural
- abscess
- tumour
What are the brainstem causes of coma?
- brainstem infarct
- tumour
- abscess
- cerebellar haemorrhage
- cerebella infarct
What is shown on this scan?
- extradural haemorrhage
What is shown on this scan?
- subdural haemorrhage
What is shown on this scan?
- diffuse axonal injury
What is shown on this scan?
- posterior fossa lesions -> compresses the brain stem
What is shown on this scan?
- bilateral medial thalamic infarcts
How far can neural crest derived cell migrate?
- capable of migrating over quite large distances
Where do you find the pineal gland?
- in the brainstem on the midline -> unusual as it is not bilateral like the rest of the braintem
What cranial nerves emerge from the midbrain?
- optic nerve
- oculomotor
Which cranial nerve emerges out of the lateral part of the pons?
- trigeminal (V)
What 3 cranial nerves emerge at the ponto-medullary junction?
- most medially = abducens (VI)
- facial (VII)
- most laterally = vestibulocochlear (VIII)
What is Bell’s palsy?
- dysfunction of the facial nerve causes a loss of facial muscle tone -> can lead to drooping of one side of the mouth and therefore drowl
- nearly almost resolves itself
What 4 cranial nerves emerge from the medulla?
- glossopharyngeal (IX) - lateral
- vagus (X) - lateral
- accessory (XI) - lateral
- hypoglossal nerve (XII) - seperate from the others
What is the pyramidal decussation?
- the point of the medulla at which 90-95% of fibres cross over
What is the function of the oculomotor (III) nerve?
- movement of the eye
What is the function of the trigeminal (V) nerve?
- touch and sensation throughout the head and neck through its 3 divisions -> opthalmic, maxillary and mandibular
- is a small root next to the main larger one because the trigeminal also has motor function in mastication
What is the function of the abducens (VI) nerve?
- supplies the lateral rectus -> cause abduction from the midline
What is the function of the facial (VII) nerve?
- innervates facial muscles -> involved in movement of the face
What is the function of the vestibulocochlear (VIII) nerve?
- innervates the inner ear -> involved in balance and hearing
What is the function of the glossopharyngeal (IX) nerve?
- sensory and motor innervation of the tongue and pharynx
What is the function of the vagus (X) nerve?
- main parasympathetic nerve -> projects down into the viscera
What is the function of the accessory (XI) nerve?
- supplies the sternocleidomastoid and trapezius -> turning of the head and shrugging of shoulders
What is the function of the hypoglossal (XII) nerve?
- supplies the musculature of the tongue
Touch sensation from the skin on the forehead is of what functional classification?
a. general viseral afferent
b. general visceral efferent
c. general somatic afferent
d. general somatic efferent
e. special somatic efferent
a. general somatic afferent
What is the role of the general somatic afferent nerves?
- sensation from skin and mucous membranes
What is the role of the general somatic efferent nerves?
- muscles for eye and tongue movements
What is the role of the general visceral efferent nerves?
- preganglionic parasympathetic -> mainly the vagus
What is the role of the general visceral afferent nerves?
- sensation from the GI tract, heart, lungs and other deep organs
What does a pale substantia nigra suggest?
- Parkinson’s disease -> the neurones have been loss so there is no black from the build up of neuromelanin
Which of these cranial nerve nuclei recieves sensory information concerning taste?
a. Edinger-Westphal
b. facial
c. nucleus ambiguus
d. nucleus solitarius
e. pontine trigeminal nucleus
d. nucleus solitarius
Which of the following arteries of the circle of Willis is unpaired?
a. anterior cerebral
b. anterior communicating
c. middle cerebral
d. posterior cerebral
e. posterior communicating
- anterior communicating artery
What are the areas of the brain involved in understanding language?
- Wernicke’s Area
Describe a subarachnoid haemorrhage.
- blood ciculates (often after an aneurysm has ruptured) in the subarachnoid space where CSF usually is
- is an emergency -> quite often it is fatal
Which of these vascular problems is most likely to require rapid neurosurgical intervention?
a. extradural haemorrhage
b. lacunar infarct
c. parenchymal infarct
d. sudural haemorrhage
e. transient ischaemic attack
a. extradural haemorrhage
How many spinal nerve pairing are there?
o 31 pairs of spinal nerves
- 8 cervical
- 12 thoracic
- 5 lumbar
- 5 sacral
- 1 coccygeal
Where do the spinal nerves leave the vertebral column?
- through the intervertebral foramina
What are the two enlargements of the spinal cord?
- cervical enlargement -> has extra motor neurones that go to the muscles of the upper limb
- lumbarsacral enlargement -> has extra motor neurones that go to the muscles of the lower limb
Lesion(s) in what area would cause a loss of the ability to breath?
- C3-C5 -> C3,4,5 keep the diaphragm alive
What area is used to sample the CSF?
- lumbar cistern
Describe the main sensory pathways.
o neuron has cell body in dorsal root ganglion -> neuron either in spinal cord or in medulla, dependent on type of pathway (second order neurons cross from one side to the other)
o third neuron is from thalamus to the cortex
o crossing over: touch = medulla (dorsal column) and pain = spinal cord (spinothalamic tract)
Describe the patella tendon test.
o reflex test
- hitting patella tendon causes muscle to stretch
- stretch signal sent to spinal cord – via muscle spindals
- causes motor neurone to contract muscle
What spinal segmenst have sympathetic outflow from them?
- T1 to L2
What is syncope?
- fainting
What happens if the arterial blood flow falls below 60mmHg?
- comprimised brain function and then possible irreversible brain damage and death
Explain how sympathetic nerve stimulation can alter cerebral blood flow.
- by producing vasoconstriction in the main cerebral arteries -> probably only active when the arterial blood pressure is high
Explain how parasympathetic nerve stimulation can alter cerebral blood flow.
- don’t normally associate the parasympathetic NS with vasculature, however facial nerve fibres are innervated by parasympathetic fibres can cause slight vasodilation
Explain how central cortical neurones can alter cerebral blood flow.
- neurones within the brain itself release a variety of vasoconstrictor neurotransmitters, such as catecholamines -> vasoconstriction
Describe the structure of the blood-brain barrier.
- endothelial cells that line the capillaries in the brain have very tight junctions (non-fenestrated) -> a lot of molecules can’t pass readily through the BBB
- capillaries are also surrounded by pericytes (far more heavily than in periphoral capillaries) that have end-feet that run along the capillary wall -> pericytes contraction makes it more likely for molecules to escape the capillary
- overall it’s mainly the tight junctions between endothelial cells forming the BBB but also pericytes
What is the relationship between anti-histamines and the blood-brain barrier?
- old-fashioned H1 blockers are hydrophobic and could cross the BBB -> since histamine is important in wakefulness and alertness, these antihistamines made people drowsy -> lots of over-the-counter sleeping tablets are old-fashioned anti-hisatmines
- second-generation anti-histamines are polar, therefore don’t readily cross the BBB -> no drowsiness
Label this diagram.
