Neurology and Neuroscience Flashcards
Describe the cerebral cortex
Covers brain surface, contains grey matter, folded with gyri and sulci, organised into lobes
Microscopicly it’s organised into layers and columns. Layers being: molecular layer, external granular, external pyramidal. Internal granular, internal pyramidal then multiform. Then columns: being small pyramidal neurone at the top, then granule/stellate neutron then large pyramidal
Also classified on cytoarchitecture into 52 regions that relate to function
Describe the lobes of the brain
FRONTAL LPBE: motor function, language, cognitive function (executive function like planning), attention ], memory
PARIETAL LOBE; sensation (touch, pain), sensory aspects of language, spatial orientation and self, perception
OCCIPITAL LOBE: visual info
TEMPORAL LOBE: auditory info processing, emotions, memories
LIMBIC LOBE: learning, memory, emotion, motivation, reward
INSULAR CORTEX: visceral sensations, autonomic control, interception, auditory processing, visual-vestibular integration
Describe the internal structure of the brain
Grey matter has neuronal cell bodies and glial cells, White matter had myelinated neurones are arranged in tracts
Describe white matter tracts in detail
White matter tracts connect cortical areas.
Association fibres: connect areas within the same hemisphere. Examples: Superior Longitudianal Fasciculus which connects frontal and occipital lobes, Inferior Longitudinal Fasciculus which connects the parietal and occipital lobes (both longitudinal Fasciculus connect to occipital, the superior is longer m]and starts and frontal whereas inferior is shorter and starts at temporal lobe), arcuate Fasciculus which connects frontal and temporal lobes, uncinate fasciculus which connects anterior frontal and temporal lobes (arcuate arcs around the limbic lobe, uncinate makes a upside down u shape at bottom of brain.
Commissural fibres: connect homologous structure in the left and right hemispheres. Examples include:Corpus callosum (top one) and anterior commissure
Projection fibres: connect cortex with lower brain structures like the thalamus brain stem and spinal cord. Examples:afferent is towards cortex, efferent is away from cortex, fibres that are deeper to cortex radiate as corona radiata and the corona radiate converges into internal fibres
Describe primary and secondary cortices
Primary cortices : function is predicatable, organised topographically, symmetry in left and right
Secondary/association cortices: function less predictable, not organised topographically, left and right symmetry weak or absent
Describe the primary and association cortices of each lobe in the brain
Frontal Lobe
- Primary Cortices: Primary Motor Cortex which controls fine, discrete, precise movements and provides descending signals to create movement
- Association Cortices: 1) Supplementary Area: involved in planning complex movements (internally cued- memory based tasks like reciting piano) 2) Premotor Area: involved in planning movements, active prior to voluntary movements (externally cued- visually guided task like sight reading). Supplementary is superior/medial to premotor)
Parietal Lobe:
-Primary Cortices: Primary Somatosensory which processed somatic sensations such as fine touch, vibration, proprioception, pain, temperature, two point discrimination which arise from receptors in the body
- Association Cortices: Somatosensory association which interprets the significance of sensory information such as recognising objects put into your hand, awareness of self and personal space.
Somatosensory association is behind primary somatosensory and only at the top part
Occipital Lobe:
-Primary Cortices: Primary Visual which processes visual stimuli
- Association Cortices: Visual Association which gives meaning and interpretation of visual input.
primary visual is in centre ish at very back and visual association surrounding
Temporal Lobe
- Primary Cortices: Primary Auditory which processes auditory stimuli
- Association Cortices: Auditory Association which gives meaning and interpretation of auditory input
Primary auditory is in centre and auditory association surrounds
Describe the other association areas
Prefrontal Cortex: attention, adjusting social behaviour, planning, personality expression, decision making
Broca’s Area: (just behind prefrontal cortex) production of language
Wernicke’s area: (below somatosensory association and Infront of visual association) understanding of language
Describe what happens when there is a lesion to the primary Cortices and the association cortices
Frontal Lobe Lesion: change in personality and inappropriate behaviour
Parietal Lobe Lesion: contralateral neglect so if lesion is in right hemisphere then lack of awareness of self and extra personal space on left side. E.g only draw half a daisy or identify objects on half the side of a plate
Temporal Lobe Lesion: leads to agnosia (can’t recognise), if resection anterior medial part of temporal lobe then anterograde amnesia (can’t form memories)
Primary Visual Cortex: blindness in corresponding visual field
Visual Association: problems in interpreting visual information e.g prosopatnosia which is face blindness
Brocka’s: expressive aphasia: poor speech production but can comprehend
Wernicke’s: receptive aphasia: poor comprehension but speech production is fine.
(Brockas and Wernicke’s communicate through arcuate fasciculus)
How is cortical function assessed
IMAGING: PET which measures blood flow to different brain regions and fMRI which measures amount of blood oxygen in a brain region
ENCEPHALOGRAPHY: EEG measures electrical signals produced by the brain, MEG measures magnetic signals made by the brain. You produce event related potentials from stimuli and measure the signals as a response such as visual evoked potentials and somatosensory evoked potentials. The potentials create waves which show the sequential activation of neural pathways e.g for, shoulder to brain stem, thalamus, and to the somatosensory cortex.
BRAIN STIMULATION: TMG (transcranial magnetic stimulation) uses electromagnetic induction to stimulate neutrons, can assess the functional integrity of circuits (aka if stimulate a motor area for hand will hand move). Can also investigate neural interactions controlling movement after injury and work out what brain areas are responsible for what functions. tDCS (transcranial direct current stimulation) uses low direct current over scalp to increase or decrease firing rates
STRUCTURE IMAGING; DTI (diffusion tensor imaging) based on diffusion of water molecules, them when use tractography with it can reconstruct neural tracts in 3D to asses integrity
What is MS and what are the main symptoms
MS is an autoimmune disorder which results in loss of myelin from neutrons in the CNS
Main Symptoms: blurred vision, fatigue, difficulty walking, numbness/tingling, muscle stiffness
Describe the different waves in peripheral nerve stimulation
Peripheral nerve stimulation can be used, it depolarises a nerve and can induce muscle contraction by activating sensory or motor axons. Assesses neuromuscular transmission
. Activation of motor axons can cause AP to travel across the nerve and cause muscle contraction (twitch), electromyography will record this fast response as the M (motor) wave. M shaped large wave
The same stimulus can cause activation of sensory neurons, the action potential can travel to the spinal cord and activate lower motor neurons in the spinal cord, the AP will spread along the motor neuron to the muscle causing contraction aka a twitch. This later response is the H- reflex. Similar to shape of M wave but no M shape. slower because has to go through the whole process, whereas motor neurons are the last step before contraction. H reflex looks like ventricular tachycardia ice peak
A large electrical stimulus can cause activation of the motor or axons to conduct antidromically. AP travel across motor neuron to spinal cord (opposite way to normal should be spinal cord to motor neurone) and this can activate lower motor neurones in the spinal cord which the AP will travel across to the muscle and cause a twitch. This causes the F-wave ( a tiny little wave)
In peripheral nerve stimulation what are the terms that describe which way the stimulation travels
Orthodromic- travels in the normal direction of nerve fibre. E.g sensory neurone to spinal cord to lower motor neurone to muscle
Antidromic- travels in opposite way to normal nerve fibres. E.g motor neurone to spinal cord back to motor neurone
Describe brain stimulation
Transcranial magnetic stimulation (TMS) used to cause cortical motor stimulation, activated]s the upper motor neurones, AP travel from upper to lower motor neurones and causes muscle contraction, will cause a motor evoked potential
Describe the difference between central and peripheral motor conduction time
The total motor conduction time is the time from brain to muscle (MEP latency)
Peripheral motor conduction time is to and from spinal cord to muscle is the (M latency + F latency -1)/2
Central motor conduction time is total motor conduction time (TMCT) minus peripheral motor conduction time (PMCT)
How would MS affect central and peripheral motor conduction time
Brain stimulation (cmct) longer than usual MEP latency, so total conduction time delayed
Peripheral nerve stimulation, normal F wave latency so no issue with lower motor neurones and the conduction time is normal.
Describe the blood supply to the brain and the arteries within the brain
common carotid artery (internal carotid artery supplies brain from this) and vertebral artery.
inside the brain (circle of willis): the vertebral arteries on each side merge on the brain stem to become the basilar artery. the basilar artery then branches into two posterior cerebral arteries. from the posterior cerebral arteries on both sides there is a posterior communicating artery that links posterior cerebral to middle cerebral. the internal carotid artery is what branches to make these two middle cerebral arteries. from middle cerebral artery there is the anterior cerebral artery then at the top the anterior communicating artery
describe the venous drainage of the brain
cerebral veins drain into venous sinuses in the dura mater. These sinuses include: superior sagittal sinus, inferior sagital sinus (falx cerebri is inbetween these two), the combination of the inferior sagittal sinus and the great cerebral vein creates the straight sinus which drains to the confluence of sinuses at the back of the head, confluence of sinuses then drain into the transverse sinus then the sigmoid sinus then the internal jugular veins
Describe the four types of haemorrhage what they are caused by and some symptoms
Extradural- due to trauma, takes immediate effect as it is an arterial bleed which is high pressure
Subdural- due to trauma but only see clinical effects in days as it is a venous system thats disrupted which is lower pressure. Symptoms: persistant headache as pressure builds, this puts pressure on brainstem so lose consciousness, mute and drowsy
Subarachnoid- ruptured aneurysms
Intracerebral- spontaneous hypertensive
intracerebellar-would have rapid onset, no injury, drowsy, speech slurred, wobbly eye, unsteady
Define a stroke and the types of strokes
a cerebrovascular accident
transient ischaemic attack- rapidly developing focal disturbance of brain function of vascular origin that resolves in 24 hours. blood flow to brain temporarily blocked
Infarction- degenerative changes which occur in tissue following artery blockage
Cerebral ischaemia- lack of blood supply to tissue resulting in permanent damage
what is a thromboembolic stroke
formation of a blood clot which blocks a small blood vessel
What are the risk factors for stroke
Age
Hypertension
Cardiac disease
Smoking
Diabetes Mellitus
Obesity- Atherosclerosis
From knowledge of the vasculature of the brain, describe cerebral artery perfusion. From this how would you find out which artery has been occluded
When looking at a whole brain: the anterior cerebral artery supplies the very outer rip of the top of the brain, the middle cerebral artery the majority of the sides and the posterior cerebral artery mainly the occipital lobe
From half of a brain: the anterior cerebral artery supplies the majorityfrom the top to the bottom of the limbic lobe. the middle cerebral artery supplies a tiny bit at the anterior inferior position and the posterior cerebral artery still the occipital lobe and the base of the brain
Would know which artery has been occluded as in a cadavers brain whatever the artery supplies will look wetter and more dead
Describe what would happen if the anterior, middle and inferior cerebral arteries were blocked
Anterior cerebral artery: paralysis of contralateral structures, leg more likely than arm or face. Abulia which is disturbance of intellect, executive function and judgement, loss of appropriate social behaviour. As through frontal lobe has been affected. May get urinary issues too
Middle cerebral artery: classic stroke. contralateral hemiplegia usually in the arm (muscle weakness), contraslateral hemisensory deficits, hemianopia, aphasia if a left sided lesion (langauge deficit). arm, upper limb, face, lip, mouth, wernickes speech area
Posterior cerebral artery symptoms: visual deficits homonymous hemianopia (field loss deficit in the same halves of the visual field of each eye), visual agnosia (cant identify object)
Describe the organisation of the brain in terms of function and order
Hierarchal organisation: higher order of hierarchy are involved in more complex tasks like planning movement, lower order areas involved in execution of movement. The motor cortex receives info from other cortical areas and sends commands to the thalamus and brainstem. However, there are feedback loops as the basal ganglia and cerebellum receive info from the motor cortex and help to plan the movement by fine tuning it- the cerebellum gets information from proprioceptors and knows the position of limbs. The motor cortex and cerebellum then both pass the command to brainstem which both contracts facial, head and neck muscles and then passes to the spinal cord and contracts muscles of body
Functional segregation: motor systems arranged into different areas that control different movements
Describe the descending tracts
PYRAMIDAL tracts- e.g. corticospinal and corticobulbar. pass through pyramids of medulla, go from motor cortex to spinal cord or cranial nerve nuclei, used for voluntary movements go body and face
EXTRAPYRAMIDAL tracts- e.g. vestibulospinal, tectospinal, reticulospinal, reburospinal. These do not pass through pyramids and go from brainstem nuclei to spinal cord. Are responsible for automatic movements for balance, posture and locomotion
Describe the pathway of the corticospinal tract
This descending tract carries motor related information to the spinal cord. Upper motor neurones in the precentral gyrus aka primary motor cortex begin the movement plan, the fibres come together to create a bundle, this travels through the coronal radiata into the internal capsule and the cerebral peduncle of the midbrain. This stretches to the medulla where 80% of fibres decussate, they then extend and synapse onto alpha or gamma motor neurones in the spinal cord. The fibres that decussate make the lateral corticospinal tract which acts on the limb muscles. The fibres that do not decussate and continue on the ipsilateral side create the anterior corticospinal tract which innervates trunk muscles.
Describe the cortiobulbar tract
Corticobulbar tract carries upper motor neuron input to motor nuclei of trigeminal (for jaw muscle movement), facial (facial muscle movement), trochlear, abducens and oculomotor (eye movemnts), and hypoglossal (tongue) nerves.
For voluntary movement of the face (and neck)
What are the extrapyramidal tracts and what do they do
Vestibulospinal: stabilises head during body movements, coordinated head movements with eye movements and mediates postural adjustments.
Reticulospinal: from medulla and pons, control postural stability and changes in muscle tone associated with voluntary movement
Tectospinal: superior colliculus of midbrain. controls orientation of the head and neck during eye movements
Rebruspinal: red nucleus of midbrain, innervates lower motor neurones of flexors of upper limb
Describe what symptoms different lesions of the motor tract would cause
UPPER MOTOR NEURONE LESION
Negative sign- loss of voluntary mototr function, paresis (graded weakness of movement), paralysis/plegia (loss of voluntary muscle activity)
Positive sign- increased abnormal motor function as lost inhiitory descending input, spasticity (increased muscle tone), hyper-reflexia (exaggerated reflexes), clonus (abnormal muscle oscillation), babinskis sign (stimulate underside of foot and patient will extend foot).
LESION OF INFERIOR PARIETAL LOBE (primary somatosensory), THE FRONTAL LOBE (premotor cortex, supplementary area)
causes apraxia- disorder or skilled movement. Stroke and dementia are the most common- in a MRI will see an infarct to one of these areas in the brain)
LOWER MOTOR NEURONE LESION
weakness, hypotonia, hyporeflexia, muscle atrophy, fasciculations (twitch due to damaged motor neurones making spontaneous AP). fibrillatioons (spontaneous twitching of individual muscle fibres)
What is motor neurone disease and the symptoms
Progressive neurodegenerative disorder of the motor system.
Upper motor neurone sign- spasticity (inc tone), brisk limb and jaw reflexes, babinskis sign, loss of dexterity, dysarthria (difficulty speaking), dysphagia (difficulty swallowing).
Lower motor neurone signs- weakness, muscle wasting, tongue fasciculations and wasting, nasal speech, dysphagia
Describe the basal ganglia and the circuitry of how it works
Basal ganglia refers to a group of subcortical nuclei in the brain responsible for motor control, located in the cerebrum. Activity doesn’t cause movement independently but activate different areas of the brain
Can see the basal ganglia via coronal sections from anterior to posterior of the brain. In more anterior sections will see the putamen connected to the caudate nucleus (the combination of putamen with thalamus is called the striatum) with the nucleus accumbens. Further back the amygdala appears at the very posterior part.
Posterially, the caudate nucleus is with the thalamus. Underneath these two are the putamen and external globus pallidus.
Circuitry: How information flows through basal ganglia back to the cortex for proper movement. Begins in the cortex then travels to the striatum (putamen and thalamus) then 1-INDIRECTLY to globus pallidus external , to subthalamic nucleus and globus pallidus (internal). or DIRECTLY can just go from striatum to internal globus pallidus. From here it goes to the thalamus to supplementary motor area, the substantia nigra and the striatum,
Describe disorders that are caused due to a problem in the basal ganglia circuitry
PARKINSONS DISEASE
Degeneration of dopaminergic neurones in the substantia nigra which project to the striatum. This causes movements to not be as strong or forceful and to increase activity of unwanted movement.
Symptoms: bradykinesia (slowness of small movements), hypomimic face (expressionless), akinesia (difficulty to initiate movement), rigidity (muscle tone increase), tremor at rest - pill rolling
HUNTINGTONS DISEASE
Genetic neurodegenarative disease, chromosome 4, autosomal dominant, CAG repeat.
Degeneration of GABAergic neurones in the striatum (in caudate first then putamen). Less inhibition so more unwanted movements. Chore(ograph)ic - choreic movements rapid jerky involuntary (like dance) hands and face affected first then legs and rest of body. Speech impairment, difficulty swallowing, unsteady gait, later will get cognitive decline and dementia. On scan will see larger ventricles and the bottom right of the right ventricle and vice versa will be very thin.
BALLISM
Usually from stroke affecting the subthalamic nucleus. Experience sudden, uncontrolled flinging of extremities, symptoms occur contralaterally.
Describe cerebellum anatomy, what different areas do and what would happen if there was damage to those areas
In posterior cranial fossa, separated from cerebrum by the tentorium cerebeli. Cerebellum coordinates and predicts movement
VESTBULOCEREBELLUM: horizontal aross the centre of the cerebellum. Responsible for regulation of gait (walking), posture and equilibrium, coordinates head with eye movements
If damages: gait ataxia (uncoordinated movement), tendency to fall
SPINOCEREBELLUM: middle verticle area or cerebellum (medial half). Responsible for coordination of speech, adjustment of muscle tone, coorination of limb movements
If damaged: (degeneration and atrophy of this area associated with chronic alcoholisim) affects mainly legs, abnormal wide gait and stance
CEREBROCEREBELLUM: lateral half of each side. Responsible for coordination of skilled movements, cognitive function, attention, processing of language and emotional control.
If damaged:affects mainly arms skilled coordinated movements, tremor and speech
What are the main signs of cerebellar dysfunction
ATAXIA- less movement coordination and accuracy, posture and gait disturbed so stagger and wide based stances look drunk
DYSMETRIA- inappropriate force and distance for movements
INTENTION TREMOR- increasing oscillation of a limb during purposeful movement
DYSDIADOCHOKINESIA- cant perform rapidly alternating movements
SCANNING SPEECH- staccato
What are the types of motor neurone found in the brainstem and spinal cord, what do they do
Alpha motor neurones, innervate extrafusal muscle fibres of skeletal muscle to cause contraction. They are clustered in motor neurone pools which contain all the alpha motor neurones needed to innervate a single muscle
Describe a motor unit and the types of motor unit
A motor unit is a single motor neurone together with all the muscle fibres that it innervates. If one motor unit is stimulated all muscle fibres within contract
Type 1 - Slow, S, smallest cell body diameter, small dendritic trees, thinnest acons, slowest conduction velocity. high myoglobin content, red colour, high aerobic capacity, low anaerobic capacity
Type IIA - Fast Fatigue Resistant FR, larger diameter cell bodies, larger dendritic trees, thicker axons, faster conduction velocity. High myoglobin content, pink colour, moderate aerobic capacity, high anaerobic capacity
Type IIB- Fast Fatiguable FF, larger diameter cell bodies, larger dendritic trees, thicker axons, faster conduction velocity. Low myoglobin, white colour, low aerobic capacity, High anaerobic capacity
as inc across types cell body, dendritic trees, axon thickness and conduction velocity increases. However as go down numbers myoglobin decreases, colour becomes paler, aerobic capacity decreases
Describe how the brain regulates the force a muscle produces
RECRUITMENT- smaller units recrited first- type 1->IIA->IIB, more force needed then more recruited this allows fine control. The motor unit recruited last is the first to be derecruited
RATE CODING- slow units fire at lower frequencies, as firing rate increases the force produced increases. As more units are recruited the motor units that were already recruited increase their firing rates
What is the term used when motor units fire at a frequency too fast to allow the muscle to relax between AP’s
Summation
What are neurotrophic factors
A type of growth factor that prevent neuronal death. The motor unit and fibre characteristics are dependent on the nerve innervating them e.g if switched slow to a fast twitch muscle then fibre characteristic would change
When might motor units change properties
IIB to IIA most common after training muscles
Type I to II if reconditioning such as no gravity or due to spinal cord injury
Ageing loses type I and II, mostly II so slower contraction times in aged muscles
What is a reflex
Automatic response to a stimulus that doesnt reach the level of consciousness, also known as a monosynaptic reflex
How can reflexes be influences/ controlled to a degree
Jendrassik manoevre - decerebration such as clench teeth, make fist, etc makes the reflex becomes larger
This is because the CNS exerts inhibitory and excitatory regulation on the stretch reflex. Inhibitory control normally dominated, decerebration however reveals excitatory control. likewise, brain damage can cause rigidity and spasticity as it influences this reflex.
How does the supraspinal control of reflexes work
Muscle is stretched activating sensory neurones which go to the spinal cord into the dorsal root ganglia and synapse onto lower motor neurones. Lower motor neurones can be alpha or gamma.
Alpha motor neurones associated with the shortening muscle are firing causes contraction
At the same time the NT’s synapse onto an interneurones to inhibit the alpha motor neurone of the antagonist muscle so it stretches
Propriospinal neurones (a type of interneurone) are activated which regulates gamma motor neurones activates gamma motor neurones of contracting muscle and inhibits the relaxed muscle. gamma motor neurones control muscle spindle fibres so want the muscle spindle fibre to contract with muscle to stay taught and signal to the body about subsequent motor activity.
terminals of afferent fibres activated by these lower motor neurones to control the muscle
Describe issues associated with motor neurones lesions and signs associated with them
Hyper-reflexia - overactive reflexes, lose descending inhibition associated with upper motor lesions
Clonus hyper-reflexia is involuntary and rhythmic muscle contractions
Babinski sign - stimulate sole of foot, if big toe curls upwards then its abnormal and a positive babinski sign. Toes curl upward in infant tho which is normal
Hypo-reflexia - below normal or absent reflexes associated with lower motor neurones
Describe signs that theres a problem with upper motor neurones and signs for lower motor neurones
UppErMN (lose inhibition mechanism)- hypErtonic, clonus (hyper-reflexia and rhythmic muscle contractions), power weakness, brisk reflexes, no wasting or fasciculations
stiff, cramps, , spasticity, tongue move slowly, gag reflex brisk, jaw jerk increase, deep tendon reflex brisk
LOwerMN- flaccid/hypOtonia, power weakness of distal, reflex reduces, wasting, fasciculations
tongue wasting, fasciculations,
probelms with both- slurred speech, difficulty swallowing, tripped, difficulty holding things and reaching up, weakness in limbs, weight loss, breathless
In motor neurone disease what PATHWAYS are affected
pyramidal tracts (corticospinal and corticobulbar). for motor movements
In motor neurone diseas why are abdominal reflexes (superficial reflex) absent but deep tendon relxed brisk
hallmark of a corticospinal tract lesion
what is a fasciculation
involuntary and abnormal firing of a single motor neurone
Explain denervation and reinnervation
When a motor neurone dies all of the fibres that were supplied by it die, they loose their nerve supply and are denervaterd. Reinnervation occurs when the axons of the remaining motor unit grow and reach out to the denerved muscle fibres. The resulting motor unit is less stable and prone to ectopic generation of electrical stimuli in the distal axon that causes contraction of muscle fibres aka fasciculations
Describe the two main types of headaches and examples of them
Primary Headaches:
1) Migraine
2)Tension-type headaches
3)Trigeminal autonomic cephalagias (cluster headaches)
Secondary Headaches
where the headache is caused by another condition or disorder
Describe primary Headaches in more detail
If a primary headache is long lasting- over 4 hours- then it is likely a migraine or a tension type headache
If a primary headache is short lasting then likely a trigeminal autonomic cephalalgia
What four key findings suggest a secondary headache
AGE- new onset or different headaches in a person over 50
ONSET- sudden, abrupt onset of severe (thunderclap)
SYSTEMIC SYMPTOMS- fever, neck stiffness, rash, weight loss
NEUROLOGICAL SIGNS- confusion, impaired consciousness, focal neurology, swollen optic discs
Describe types of migraine
Can be episodic where they are recurrent or chronic
Characteristics: unilateral, pulsating, moderate to severe pain, physical activity aggravates it, can last hours to days.
Usually one or both of : Nausea/vomiting and photophobia/phonophobia
May have auras which are array of symptoms that reflect focal cortical or brainstem dysfunction, less than 30 mins and before a headache . See the expanding C shape and visual disturbance increases with time.
Describe the phases of a migraine
Premonitory: yawning, polyuria, mood change, irritable, light sensitive, neck pain, concentration difficulty
Aura: Visual, sensory numbness, weakness, speech arrest
Headache: Head and body pain, nausea, photophobia
Resolution: rest and sleep
Recovery: mood disturbed, food intolerance, feeling hungover
Describe migraine management
Lifestyle factors: avoiding triggers, creating a routine diet, sleep, exercise and mindfullness routine.
If this doesnt work then pharmacological therpy which can be:
- Acute/abortive: fast acting such as paracetamol, NSAIDS, Prokinetics, Triptans
- Strategy which are preventative in the long term such as nasal sumatriptan (serotonin a HT1 antoagonist), , B-blockers, serotonin antagonists
Describe tension type headaches
Feels like tight muscles around head and neck
Lasts 30 mins can be longer
Bilateral
Mild or moderate
No added features (no nausea or vomiting photophobia or phonophobia
What is the treatment for tension type headaches
Reassurance
Individual attacks- give aspirin or paracetomol
Describe cluster headaches
Severe unilateral pain
15-180 mins
Ipsilaterally one of the following: conjunctival redness and/or lacrimation, nasal congestion and/or rhinorrhoea, eyelid oedema
May also experience: forehead and facial sweating, miosis and/or ptosis, a sense of restlessness or agitation, not associated with brain lesion on MRI
What is the treatment of cluster headaches
Acutely: Triptan (nasal or subctaneously give), High flow oxygen (oxygen inhibits neuronal activation in trigeminocervical complex and the symptoms are all trigeminal autonomic symptoms)
Prevention: Verapamil (calcium channel inhibitor for prophylaxis), block the greater occipital nerve.
Avoid: paracetomol, NSAIDS, oral tiptans, ergots or opioid as no effect
Compare the differences between all three types of primary headaches
MIGRAINE- unilateral can be bilateral, pulasating, mod-severe, physical activity aggravates, nausea/vomiting or photophobia/phonophobia, 1/2 per month
TENSION TYPE HEADACHE- bilateral, pressing, tightening, pulsating, mild-mod, featurless
CLUSTER HEADACHE- Unilateral (never bilateral), very severe, restlessness, ipsilateral to pain may be: conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, eyelid oedema, 1-3 per day and daily for 2-3 months, short headaches every few hours
Describe the hearing organ and vestibular organ
Hearing organ: capture high frewuency motion (sound)
Vestibular organ: capture low frequency motion (movements)
What 2 things is sound made of
Frequency/pitch: (Hz) is the cycles per second and gives the perceived tone
Amplitude/loudness (dB) is sound pressure, the amplitude/height of sound wave
Describe the outer ear, its functions and how it produces sound
The outer ear functions are:
to capture sounds and focus it on the tympanic membrane
to amplify sounds of upper range of speech frequencies by resonance in canal
protect the ear from external threats
The external ear is comprised of the auricle (pinna) which is made of elastic cartilage, concha and the tympanic membrane
The tympanic membrane converts vibrations and air into mechanical movement and will move at the same Hz as the sound
Describe the middle ear, its functions and how sound travels through
Mechanical amplification of sound.
Borders: tympanic membrane and oval window
When the tympanic membrane is hit, it vibrates malleus bone which vibrates incus which vibrates stapes. Stapes is anchored onto the oval window so when is hit the mechanical stimuli will vibrate the fluid in the cochlea.
Within the middle ear are the tensor tympani and stapedius muscles. Stapedius muscle connects to stapes and a motor branch of the facial nerves can cause it to contract to dampen
Describe the inner ear, its functions and how sound travels through
Hearing part of the ear
TRANSDUCES vibration into nervous impulses.
comprised of oval window and cochlea
Mechanical movement in middle ear through the stapes tapping on the oval window causes movement in fluid which moves the basilar membrane, will reach its peak at what ever part responds to that sound frequency
Describe the cochlea in detail, its structure etc
Cochlea has 3 fluid filled compartments: scala vestibuli and scala tympani, they both contain perilymph high in sodium) and are bony structures. Inside these compartments is scala media which is membranous with a vestibular membrane side and a basilar membrane side. It contains endolymph which is high in potassium. Scala media also contains the hearing organ/ Organ of Corti as it lies in the basilar membrane. Basilar membrane is arranged tonotopically : Higher frequency sound moves the first part (narrow and tight), lower frequency moves the apex which is wider
The stapes bone will tap on the oval window, and cause fluid movement in the scala vestibuli, this will move the scala media which has the tectorial membrane and basilar membrane which will move the organ of corti back and forth. This causes sterocilia hair deflection towards the kinocilium which will open K+ ion channels and depolarise the cell. Depolarisation allows Ca2+ channels to open and causes the excitatory glutamate neurotransmitter release which propagates a auditory signal to the afferent vestibulocochlear nerve. Hyperpolarisation where the stereocilia move away from the kinocilium causes hyperpolarisation which closes K+ channels
Describe the hearing organ in detail
Has two types of hair cells: Inner hair cells and Outer hair cells.
The tectorial membrane is above these hair cells which allows hair deflection to depolarise the cell.
Movement in basilar membrane is translated into electrical impulses in the organ of corti, when basilar membrane vibrates moves the hair cells and their sterocillia which opens ion channels and causes NT rlease to propagae auditory signal to vestibulocochlear nerve
Whats the difference between the hair cells
Inner- Afferent info to auditory nerve, TRANSDUCE sound into nerve impulse, 1 layer of inner
Outer: EFFERENT of auditory nerve, modulate sensitivity of response (brain says if too much) 3 layers of outer
After the neurotransmitter has been released to the afferent vestibulocochlear nerve what pathway is taken next
signals stimulate spiral ganglions in the cochlea and send a signal via the cochlear nerve to the ipsilateral cochlear nuclei in the pons . Auditory information crosses at the superior olive (contralaterally). Then the signal goes ipsilaterally to the inferior colliculus and then the medial geniculate body (thalamus) then finally reaches the auditory cortex
What are the types of hearing loss and their causes
ANATOMICAL
-conductive hearing loss: problem in outer (wax or foreign body) or middle ear (otitis- will see bubble or otosclerosis)
-sensorineural hearing loss: sensory cochlea (noise, prebycusis-age, ototoxicity- chemo or AB’s) or auditory nerve hearing loss (acoustic neuroma- a unilateral tumour)
-central hearing loss: brain and the brainstem
TIMING
-sudden hearing loss: min to day
-progressive hearing loss: months to years
What tests can be used to assess hearing
whisper in one ear whilst rubbing fingers in other
tuning fork- weber (fork on top of head, should hear equally in both ears, if more on one side then its defective) or rinne test (next to ear, if bone conduction better is defective) test presence of gross hearing loss
audiometry: audiogram plots hearing thresholds to define hearing loss, should stay between 0-20dB
osteoacoustic emissions: cochleas outer hair cells produces low intensity osteoacoustic sounds as they expand and contract. can be used to assess newborn hearing
On audiometry testing how would conductive and sensorineural hearing loss patterns differ
Conductive: bone conduction is high as nerves are working, air conduction falls below 20dB
Sensorineural: bone and air conduction fall at higher frequencies
How is hearing loss treated
Underlying cause: remove ear wax, treat infection
Hearing aids
Cohlear implants
Brainstem implants
Movement and gravity changes are sense by mechanical sensors (canals and otoliths), CNS integrates this info and cause ocular reflex and postural control
What does the vestibular system provide information about
To detect and infrom about head movement and position
spatial orientation/balance
keep images fixed during head movements
Describe the vestibular systems anatomy in detail
Vestibule is continuous with cochlea, the saccule (otolith organ) joins to the cochlea, this joins to the utricle (otolith organ), the otolith organs cells are located on the maculae, cells are horizontal in utricle and vertical in saccule.
The maculae is basically hair cells, a gelatinous matrix and otoconia on top (carbon crystals). Maculae detect linear acceleration. The utricle connects to the three semicircular canals (anterior, lateral and posterior) which detect angular acceleration. These canals are filled with endolymph when the head rotates the fluid moves through the canal that corresponds to the plane of movement. Endolymph (high in K+) flows into the ampulla (at each end of canal) which has the crista which contains has hair cells and is surrounded by the cupula which is what moves against hair cells.
What movement do each of the otolith organs sense
Utricle is horizontal movement like head tilts. Utricle lies horizontally so tilts move otoconia into gel and moves the hair cells
Saccule is acceleration or deceleration in vertical plane (ball sacks hang vertical). Saccule stands vertically so gravity and elevator pulls upa nd down
How do hair cells generate potential
Hair cells have a resting potential and a basal discharge (if in constant acceleration will be basal)
If towards the kinocilium then depolarises the cell and increases/excites/stimulates in nerve discharge
If away from kinocilium then hyperpolarisation and reduces/inihibts the nerve
How do hair cells generate potential
Hair cells have a resting potential and a basal discharge
If towards the kinocilium then depolarises the cell and increases/excites/stimulates in nerve discharge
If away from kinocilium then hyperpolarisation and reduces/inihibts the nerve
How is information passed higher up
info travels thru vestibulocochlear nerve to vestibulospinal tract to vestibula ganglion to vestibular nuclei in the pons where primary afferents end
What are the two vestibular reflexes
Vestibulo-ocular reflex- eyes can stay fixed in retina when moving. Vestibular ad oculomotor nuclei connection: eye movement opposite to head movement but same velocity and amplitude
Vestibuo-spinal reflex- if slip feel sudden acceleration and will stop the fall.
What disorders may arise from the vestibular system and what would the presentation be
- TIming and Laterality
acute + unilateral = imbalance, dizziness, vertigo and nausea
slow + uni/bilateral = imbalance and nausea / NO VERTIGO - Balance disorders
peripheral vestibular organs such as vestibular organ or CN 8 = vestibular neuritis(acute) , benign paroxysmal positional vertigo (intermittent) or menieres disease/migraine (recurrent), schwannoma vestibular (progressive)
central vestibular disorders such as CNS = stroke (acute) , multiple sclerosis (progressive) or tumours
What are the red flags of vestibular disorders and what three things should be checked
Headache
gait problems
Hyper-acute onset
hearing loss
more than 4 days of symptoms
Check: eyes, legs and ears
If a patient presents with intemittent dizziness and vertigo what test needs to be used and what is the likely diagnosis
Dix Hallpike Test
Benign Paroxysmal Positional Vertigo: periphera disorder where otoliths from utricle detach from maculae and float in the semicircular canals causing a larger endolymph flow wehn the head moves whcich will cause a larger reaction when the head moves qicky = vertigo. common to attac when lying down or getting up
If a patient is acutely dizzy what test should be used and what are the two likely diagnoses
HINTS exam
Head Impulse Test:move head see if eyes move with, if do then vestibulocochlear nerve
Nystagmus: retina moving back and forth quickly : unidriectional= peripheral origin, changes direction or vertical = central/ stroke
Test Skew: a vertical misalignment of eyes = stroke
Looks for vestibular neuritis or stroke as those are two acute causes
Name the parts of the eye:
Lateral and medial canthus
Pupil, iris, sclera
Caruncle (the pink)
Limbus: border between cornea and sclera
Describe the lacrimal systems innervation and what happens
Tears can be basal, emotional or a reflex
Afferent signals come from stimulation of the cornea, and travel to cranial nerve 5 the trigeminal- specifically V1 the ophthalmic branch
Efferent signals are parasympathetic and act on the lacrimal gland
Neurotransmitter used is acetylcholine
Causes the lacrimal gland to secrete a tear which drains through the two puncta on the medial lid margin, they flow through the superior and inferior canaliculi, gather in the tear sac and exit trough the tear duct into the nasal cavity
What is the tear film, it’s role, explain it
Maintains smooth cornea to air surface, makes sure the cornea has an oxygen supply as cornea has no blood vessels, removes debris by blinking and is a bacteriacide.
SMOOTH, O2 SUPPLY, FOREIGN OBJECTS, CLEAN
Has three layers
- Superficial lipid layer: reduces tear film evaporation. (Made by meibomian glands along lid margin)
- Aqueous layer: tear film - is the thickest layer, a lubricant.
- Mucinous layer: keeps closely attached to eye and maintains surface wetting
Which layer of the tear film is in close contact with the eye
Mucinous layer
Which layer of the tear film protects the tear film from evaporation
Lipid layer
What glands produce lipids for the tear film
Meibomian Glands
What is the thin transparent tissue that covers the outer surface of the eye?
Conjunctiva - begins at outer edge of cornea, covers the visible part of the eye and lines inside of the eyelids. Nourished by tiny blood vessels.
Describe the layers that cover the back of the eye
Sclera- tough, opaque, protects the eye (outer layer), high water content, connects with cornea
choroid pigmented and vascular nourishes the eye goes all the way around
Retina- neurosensory tissue inside eye, very thin, responsible for capturing the light that enters the eye and sends to brain through optic nerve
What is the cornea, name it’s layers from most superficial to innermost ?
Transparent, dome shaped window covering front of the eye. Low water content.
Powerful reflecting surface, 2/3 of eyes focusing power.
Epithelium -> Bowman’s membrane-> Stroma (contributes to transparency) -> Descemets membrane-> endothelium ( pumps fluid out of cornea and prevents oedema, glucose passes over from between the iris and cornea and nourishes the eye as has no blood vessels.)
Anterior epithelim
Bowmans membrane
Central stroma
Descemets membrane
Endothelium
If the cornea is hydrated what happens
Becomes white.
The cornea has a low water content so by hydrating it it becomes white like the sclera which has high wster content
What is the lens and its functions
Behind the iris, is an acellular capsule has inner elongated cell fibres.
Is transparent, has refractive power, 1/3 of the eyes focusing power
What nerve transmits info from the eye to the brain
Optic nerve which connects the the back of the eye near the macula, visible portion is the optic disk
What is the optic nerve blind spot
Where the optic nerve meets the retina there are no light sensitive cells, is the optic disk
What is the macula
Centre of retina , highly sensitive for detailed central vision and tasks like reading that require central vision
What is the central of the macula called and what is its function
Fovea, high concentration of cones to see detail, low concentration of rods
Describe central and peripheral vision
Central: CONES detail day vision, colour vision, reading, facial recognition. Has fovea which is high concentration of cone receptors. Loss of foveal vision = poor visual acuity
Peripheral vision: RODS shape, movement, night vision, navigation. Loss of visual field= unable to navigate in environment
Describe the structure of the retina
3 layers:
Outer layer= photoreceptors for light detection : 1st order neuron
Middle layer= bipolar cells 2nd order neurones, signal processing to improve contrast sensitivity, and regulate sensitivity
Inner layer: retinal ganglion cells 3rd order neurones, transmit signal from eye to brain
What are the two types of photoreceptors
Rods- SCOTOPIC: longer outer segment, more sensitive to light than cones but slow response, night vision, peripheral. FAR AWAY FROM FOVEA IS MORE ROD CELLS
Cones-PHOTOTOPIC: less sensitive but faster, daylight vision and colour vision. FOVEA HAS MORE CONE
cones= central= focus = detail = colour = day vision/photopic
rods= peripheral = sensitive to light= slow = night vision/scotopic
What are the different type of cone cells and what are they sensitive to
S cones : blue (wavelengths of 400-430)
M cones: green (WL of 530-560)
L cones: red (WL of 560-600)
Why arent rod cells sensitive to colour
used for night vision and spatial recognition not sensitive to colours
What are the most common colour vision deficiencies
Deuteranomaly: cant see red
Protanomaly: red looks greenish, green is still green
Protanopia: red becomes green and green is yellow
Deuteranopia: green and red look orange and rest of spectrum is blue .
Tritanopia- pink and blues only
Tritanomaly-
What is the name for full colour blindness
Achromatopsia
What is the test used for colour blindness
Ishihara test
What effect does refraction have on light
velocity changes
the lights path changes
How is the index of refraction calculated
Index of refraction is the speed of light in a vacuum divided by the speed in a medium. (will always be bigger than one and unitless as the speed in a medium is always smaller than air)
Describe what happens when light meets a medium
The incident ray hits the medium, some is reflected back, some is refracted through the boundary.
Angle of incidence always is equal to angle of reflection
the angle of refraction changes . all measured from the actual light ray to the normal line of the graph
What are the two types of lenses
Convex: Converging lens, takes the light rays and brings then to a point
Concave: Diverging lens, takes light rays and spreads them out
What is the term for an eye that has an adequate correlation between axial length and refractive power and parallel light rays fall directly on the retina
Emmetropia
What is ametropia
mismatch between axial length and refractive power. Parallel light rays dont fall on the retina
can be myopia, hyperopia, astigmatism or presbyopia
What happens in myopia, what are the main causes and the symptoms
Short sighted
parallel rays converge at focal point anterior to retina (should converge on)
In the myopic eye, the eyeball becomes elongated, causing the focal length of a lens to decrease, resulting in difficulty seeing objects afar, cornea is also move curved, think thinner, so goes thru easily
Causes
Excessive long globe causes axial myopia (long eyeball)
Excessive refractive power causes refractive myopia (medium slows too fast)
Symptoms
blurred distance vision, squints to try to improve acuity, headache
How is myopia treated
Concave lens (neg lens)- spreads out as reaches a focal point too quickly
Contact lens
Remove lens to reduce eyes refractive power
What is hyperopia, the causes and the symptoms
Farsightedness
parallel rays converge at a focal point posterior to retina
shortened hyperopic eye shape has an increased focal length of a lens, resulting in blurry near vision.
Causes:
excessive short globe is axial hyperopia
insufficient refractive power is refractive hyperopia (medium doesnt slow the rays enough)
Symptoms:
visual acuity early on: cant read fine print, or near vision suddenly and intermittently blurs, tiredness or weak printing makes worse
eyepain, headache, burning sensation in eyes
amblyopia (lazy eye)
How is hyperopia treated
Converging (positive) lens (helps it to converge early)
cataract extraction with a converging lens
contact lens
intraocular lens
what is astigmatism
parallel rays focus in two lines due to the cornea being misshaped (not domed)
is hereditary
refractive media is not spherical so they refract differently along one meridan rather than the meridian perpendicular to it. Meridians need to be perpendicular e.g at 90 and 180 to connect at one point, if it was 90 and 170 it wouldnt line up Causes 2 focal points so the object is represented as two sharply defined lines
What are the symptoms of atigmatism
headache, eyepain
blurred and distorted vision
head tilting and turning
What is the treatment of astigmatism
if regular: cylinder lenses with spherical lenses (convex or concave) focuses light into a line not a point
irrregular: rigid cylinder lenses and surgery
What are the components of the near response
Pupillary Miosis : Sphincter Pupillae contracts, to increase depth of field
Convergence: Medial recti from both eyes align both eyes towards the object
Accomodation: Circular cilliary muscle contracts and changes the shape if the lens to increase refractive power for near vision, it thickens the lense
What is presbyopia
loss of accomodation (focus on near objects). Happens after 40 yrs old, distant vision is in tact. use reading glasses to increase refractive power
What is the treatment of presbyopia
convex lenses as rays converge behind retina so need convex to converge further forward.
reading glasses
bifocal glasses
trifocal glasses
progressive power glasses
How is presbyopia corrected
Spectacle lenses : monofocal or multifocal
Contact lenses: used for cosmetic, athletes or specific jobs
What are the types of optical correction and their advantages and disadvantages
Contact lenses
- need daily cleaning , expensive, risk to infectious keratitis, giant papillary conjunctivitis, corneal vascularisation, chronic conjunctivitis
Intraocular lense
replace cataract crystalline lense
best for aphakia, avoid magnification and distortion that spectacle lense causes
are monofocal so will always need reading glasses
Intraocular lense insertion is surgical so can be done through :
keratorefractive surgery/laser
Intraocular surgery
What manoeuvres are used for Benign Paroxysmal Positional Vertigo
Epley manoeuvre
Semont manoeuvre
Describe the layers at the front of the eye
Cornea which joins to sclera
Uvea which contains iris, ciliary body and choroid- choroid pigmented and vascular nourishes the eye goes all the way around, the ciliary body is nearer the front then the iris which is just behnd the cornea and controls light levels by using tiny muscles which dilate and contract the central pupil.
Lens and suspensory ligament behind
What two structures are powerful refractive surfaces and allow the eye to focus
Cornea (2/3 focusing power)
Lens (1/3 of focusing power)
What lens is surgically inserted for the correction of myopia and astigmatism
ICL- Staar intra-collamer lens
Describe the visual pathway including neurone order
Rod and cone photoreceptors are first order neurones, the ligh passes to retinal bipolar cells which are second order and then to the retinal ganglion cells which are third order and include
the optic nerve to optic chiasm (where half the fibres cross) to the optic tract, the ganglion nerve fibres then synapse at lateral geniculate nucleus then onto optic radiation which is the 4th order neurone in the thalamus then to primary visual cortex
Describe how lesions anterior, at and posterior to the optic chiasma would affect vision
Anterior to optic chiasma such as optic nerve will only affect one eye: monocular blindness
At the optic chiasma: damages the nasal retina visual info in both eyes which is responsible for temporal vision, bitemporal hemianopia.
Posterior to will affect both nasal and temporal vision as fibres decussate at the optic chiasma. if right sided lesion get left homonymous hemianopia in both eyes and visa versa. Both sides on opposite visual field/ same side of vision
If only affect the temporal side of the fibres (aka non crossing fibres) will result in nasal hemianopia of the other eye
Lesions in optic radiation= quadranopia because the lateral geniculate splits into two further fibres
Lesions to the visual cortex= macular sparing
Describe the origin of crossed and uncrossed fibres and what visual field they are responsible for
Crossed fibres from nasal retina responsible for temporal field vision
Uncrossed fibres from temporal retina responsible for nasal field
What are the causes of bitemporal hemianopia
Pituitary gland tumour as the pituitary is under the optic chiasm
If a patient has a stroke what visual issue will they have
Homonymous hemianopia
Damage to the primary visual cortex causes what
Contralateral homonymous hemianopia with macular sparing.
also due to stroke.
The macula recieves dual blood supply so supplied with blood
What is the function of the pupil
Regulates light input
Describe what the pupil does in light and dark
In light: reduces spherical abberations, glare and bleaching of photo-pigments, increases depth of field, pupil constricts (parasympathetic CN8)
In dark: increases light sensitivity, lets more light in , pupil dilated (sympathetic nerve)
Describe the pupillary reflex
AFFERENT: Photosensitive retinal ganglion cells receive visual information, the info travels on the optic nerve synapses on the pretectal nucleus (exit before the lateral geniculate nucleus) and then synapse on the Edinger-Westphal Nuclei
EFFERENT: Edinger-Westphal Nuceli is parasympathetic and used in the efferent pathway to travel with the oculomotor nerve efferent and synapses at the ciliary ganglion the pupillary sphincter to constrict both pupils
There is a direct and consensual reflex. The eye that light shines into directly reflexes, but the other one does to; the consensual reflex
Explain the defects that can be seen in the pupillary reflex
Right/Left Afferent Defect: optic nerve defective. If right optic nerve is damaged when light is shone in the right eye there will be no pupil constriction, if shone in left then normal reaction
Right/Left Efferent Defect: damage to the oculomotor nerve, damage to right of CN3 means right eye will never contract but left will contract whether left or right is stimulated.
Unilateral Afferent Defect: different response depending on which eye is stimulated
Unilateral Efferent Defect: same unequal response doesnt depend on eye stimulated
What test is used to diagnose RAPD
RAPD: relative Afferent Pupillary Defect
Swinging torch test: when light swings to undamaged side then pupils constrict which is normal. When light swings to damaged eye both pupils dilate
What are the terms to describe eye movement
Duction: movement in one eye
Version: both eyes move in same direction
Vergence: both eyes in opposite direction outwards
Convergence: both eyes move in when viewing a near object
supraduction, supraversion
infraduction, infraversion
dextroversion: right
levoversion: left
What are the two speeds of eye movement called
Saccade: 900 degrees: a short fast burst focus on stationary objects
-reflexive saccade, scanning saccade, predictive saccade, memory guided saccade
Smooth pursuit: 60 degrees: slow movement : focus on moving targets
Name the extraocular muscles and their function
Four lateral muscles:
Superior rectus: moves eye up
Inferior rectus: moves eye down
Lateral rectus : eye moves laterally/abducts
Medial rectus : eye moves medially/adducts
Superior Oblique :moves eye down and out/depressed and abducted (string pulling towards top of nose) is under superior rectus, on temporal side
Inferior oblique : moves eye up and out / elevated and abducted (string pulling to side of jaw) is over inferior rectus, on nasal side
Describe the innervation of extraocular muscles
Oculomotor CN3 Superior Branch
superior rectus and levator palpebrae superiosis to raise eyelid
Oculomotor CN3 Inferior Branch
inferior rectus, medial rectus, inferior oblique, parasympathetic nerve constricts pupil.
Trochlear CN4
superior oblique
Abducens CN6
lateral rectus (abducens abducts the eye so lateral rectuh)
How are the intraocular muscles tested
Medial rectus tested by adducting eye
lateral rectus tested by abducting the eye
Superior rectus tested by abducting and elevating
Inferior rectus by abducting and depressing
Superior Oblique by elevating and adducting
Inferior Oblique by depressing and adducting
For the oblique muscles adducting puts in line with their function of abducting
for sup and inf rectus muscles abducting puts in line with their function of going up and down
Describe what would happen in third and sixth nerve palsy
Third nerve palsy: eye down and out with a droopy eyelid
Fourth nerve palsy: one iris higher than the other
Sixth nerve palsy: Affected eye cannot abduct (double vision worse when looking to affected eye side
What reflex test is used to test visual acuity in pre verbal children
Optokinetic Nystagmus reflex
looks for smooth pursuit following a moving pattern and a fast reset saccade looking at the beginning of the pattern again
What are the causes of 3rd nerve palsy and their treatments
Medical lesion: microvascular disease due to hypertension, diabetes mellitus (affects vasculature to the nerve so the central part, the parasympathetic fibres run on outer side so pupils are spared). Control of condition is the treatment
Surgical lesion: posterior communicating artery aneurysm, would also affect the pupil. Neurological opinion needed
What is pilocarpine and how does it work
Muscarinic receptor agonist which acts on M3 receptors in the iris sphincter muscles, results in contraction of the muscle (miosis) and pupil constriction even if parasympathetic system is damaged
If the pupillary light reflex is slow to react and causes rapid constriction of of the slow pupil when pilocarpine is added where is the damage
To the parasympathetic ciliary ganglion
What is the term used to described light-near dissociation
Adie’s pupil : caused by reinnervation that happens when the ciliary ganglion is damaged. This causes upregulation of postsynaptic receptors but the reinnervation is aberrant so fibres targeting the ciliary body target the pupil instead so pationt gets meiosis with near accommodation
What signs are telling of Alzheimers dementia
Head turning to verify their answer with family, vague answers, unsure of routes.
Initial episodic memory deficits secondary to medial temporal lobe dysfunction
Epsiodic memory which is memory of particular episodes in life is impaired, this memory is dependent on medial temporal lobes including the hippocampus and entorhinal cortex
on MRI see large ventricle and widened sulci, also see black hippocampus
What are the biomarkers of Alzheimers and what is the primary event
Amyloid spreading is the primary event, then Tau spreads causin injury and dysfunction which alters brain structure and leads to gmild cognitive impairment and dementia
How can Alzheimers be tested
Lumbar puncture, look if there is Beta Amyloid and Tau in CSF
If a patient is not having memory issues, states they have visual hallucinations, REM sleep disorder (talking, shouting, lashing out during sleep) what type of dementia is it and how will it present on a scan
Dementia with Lewy bodies
aggregation of alpha synuclein monomer to alpha synuclein oligomer to fibril to lewy body
On a scan: hippocampus is preserved
On dopamine transporter scan will see less areas lit up,will not be bright because alpha synuclein in Lewy bodys causes neurodegeneration of dopaminergic neurons. If it were alzheimers caudate and putamen would be bright yellow/white lit up
How will fronto-temporal dementia present and what MRI changes
problems with memory, speech mixed up, cant name objects angry/frustrated rude, personality changes
MRI : volume loss in temporal lobes and frontal operculum (in saggital section is behind the eye). see large black spaces either side of the central ventricle
What two cognitive tests are used to assess dementia
MoCA: montreal Cognitive Assessment :good sensitivity as a screening tool, easy to use but takes a long time
ACE test: Addenbrooks cognitive ecamination: quick and easy, but may depend on the users education level
Define meningitis
Inflammation of meninges - viral or bacterial
will see lots of t cells in sub arachnoid
Define encephalitis
Inflammation of brain tissue due to infection or autoimmune
What is cerebral vasculitis
inflammation of blood vessel walls
What is the name of the vessels that plunge into the brain substance and form a network capillaries
Pial vessels
What makes blood brain barrier
Capillaries At the blood brain barrier have endothelial cells that have tight junctions which reduces solute and fluid leak across.
Astrocytes help form these tight junctions.
What happens if there endothelial layer of the blood brain barrier is disrupted
Causes collagenous disruption and fibrogen leakage, erythrocytes or fibrogen get into the brain parynchyma as the astrocytes end-feet change, they retract and open so immune cells can then invade
What does encephalitis present with
Flu like with pyrexia and headache
develops into: confusion/disorientation, seizures, fits, personality/behaviour changes, difficulty speaking, weakness, loss of consciousness
fever, seizure, behaviour change, confusion, disorientation
What are the causes of encephalitis
Viral Infection: Herpes, measles, Chickenpox, Rubella
Insect bites (mosquito, tick), bacterial and fungal infection, trauma or autoimmune (attack Ca2+/H+ channel)
What are the treatments of encephalitis
Antivirals (acyclovir), steroids, antibiotics, analgesics, anti convulsants, ventilation, corticosterodis for inflammation, immune suppresant
What medical condition causes demyelination of the CNS
Multiple Sclerosis
What is MS, how does it present
Inflammation as CD3 T-cells and CD20 B-cells infiltrate, Demyelination, Axonal Loss, Neurodegeneration
Come in with initial problem then later a different- relapsing-remitting pattern which is liked to inflammatory activity, eventually becomes progressive, neurodegeneration activity so dont recover just gets worse.
What is meningitis and its causes
inflammation of meninges
Bacterial causes: meningococcal, pneumococccal, Hemophilus influenzae B (Hib) or streptococcal
can be viral or fungal
take a lumbar puncture then do I.V AB
What is an infection of the spinal cord called
Myelitis
(brain and spinal cord = encephalomylitis)
What is the difference between encephalitis and meningitis causes
encephalitis is viral mostly snf meningitis is bacterial coccus
How does meningitis present
sudden fever, severe headache, nausea/vomiting, double vision, drowsiness, sensitivity to bright light, stiff neck and rash
What are the key differences between encephalitis and meningitis presentations
Envephalitis patients always have findings like weakness, visual disturbance, aphasia, cerebellar findings and behaviour changes as well as seizures. Gradual symptoms
Meningitis dont have focal neurological findings until later in presentation and are more likely to have photophobia, vomiting and neck stiffness. Sudden symptoms
Diagnostic tests for encephalitis and meningitis
Neurological examination, CT, MRI, lumbar puncture, blood, urine analysis
Encephalitis: HIV, normal gluocse, raised protein and lymphocytes. on CT see sulci and gyri lit up
Meningitis: high WBC, low sugar/glucose,
How is meningitis treated
I.V antibiotics, analgesics, corticosteroids to reduce inflammation, immune suppressors
similar to encephalitis
What are some of the long term effects of meningitis
Learning disabitlities, memory loss, poor concentration, clumsy, headaches, deafness, loss of balance, epilepsy, speech and visual problems
