Neurology and Neuroscience

Question 1

Describe the cerebral cortex

Answer 1

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

Question 2

Describe the lobes of the brain

Answer 2

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

Question 3

Describe the internal structure of the brain

Answer 3

Grey matter has neuronal cell bodies and glial cells, White matter had myelinated neurones are arranged in tracts

Question 4

Describe white matter tracts in detail

Answer 4

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

Question 5

Describe primary and secondary cortices

Answer 5

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

Question 6

Describe the primary and association cortices of each lobe in the brain

Answer 6

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

Question 7

Describe the other association areas

Answer 7

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

Question 8

Describe what happens when there is a lesion to the primary Cortices and the association cortices

Answer 8

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)

Question 9

How is cortical function assessed

Answer 9

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

Question 10

What is MS and what are the main symptoms

Answer 10

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

Question 11

Describe the different waves in peripheral nerve stimulation

Answer 11

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)

Question 12

In peripheral nerve stimulation what are the terms that describe which way the stimulation travels

Answer 12

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

Question 13

Describe brain stimulation

Answer 13

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

Question 14

Describe the difference between central and peripheral motor conduction time

Answer 14

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)

Question 15

How would MS affect central and peripheral motor conduction time

Answer 15

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.

Question 16

Describe the blood supply to the brain and the arteries within the brain

Answer 16

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

Question 17

describe the venous drainage of the brain

Answer 17

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

Question 18

Describe the four types of haemorrhage what they are caused by and some symptoms

Answer 18

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

Question 19

Define a stroke and the types of strokes

Answer 19

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

Question 20

what is a thromboembolic stroke

Answer 20

formation of a blood clot which blocks a small blood vessel

Question 21

What are the risk factors for stroke

Answer 21

Age
Hypertension
Cardiac disease
Smoking
Diabetes Mellitus
Obesity- Atherosclerosis

Question 22

From knowledge of the vasculature of the brain, describe cerebral artery perfusion. From this how would you find out which artery has been occluded

Answer 22

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

Question 23

Describe what would happen if the anterior, middle and inferior cerebral arteries were blocked

Answer 23

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)

Question 24

Describe the organisation of the brain in terms of function and order

Answer 24

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

Question 25

Describe the descending tracts

Answer 25

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

Question 26

Describe the pathway of the corticospinal tract

Answer 26

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.

Question 27

Describe the cortiobulbar tract

Answer 27

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)

Question 28

What are the extrapyramidal tracts and what do they do

Answer 28

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

Question 29

Describe what symptoms different lesions of the motor tract would cause

Answer 29

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)

Question 30

What is motor neurone disease and the symptoms

Answer 30

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

Question 31

Describe the basal ganglia and the circuitry of how it works

Answer 31

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,

Question 32

Describe disorders that are caused due to a problem in the basal ganglia circuitry

Answer 32

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.

Question 33

Describe cerebellum anatomy, what different areas do and what would happen if there was damage to those areas

Answer 33

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

Question 34

What are the main signs of cerebellar dysfunction

Answer 34

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

Question 35

What are the types of motor neurone found in the brainstem and spinal cord, what do they do

Answer 35

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

Question 36

Describe a motor unit and the types of motor unit

Answer 36

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

Question 37

Describe how the brain regulates the force a muscle produces

Answer 37

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

Question 38

What is the term used when motor units fire at a frequency too fast to allow the muscle to relax between AP's

Answer 38

Summation

Question 39

What are neurotrophic factors

Answer 39

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

Question 40

When might motor units change properties

Answer 40

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

Question 41

What is a reflex

Answer 41

Automatic response to a stimulus that doesnt reach the level of consciousness, also known as a monosynaptic reflex

Question 42

How can reflexes be influences/ controlled to a degree

Answer 42

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.

Question 43

How does the supraspinal control of reflexes work

Answer 43

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

Question 44

Describe issues associated with motor neurones lesions and signs associated with them

Answer 44

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

Question 45

Describe signs that theres a problem with upper motor neurones and signs for lower motor neurones

Answer 45

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

Question 46

In motor neurone disease what PATHWAYS are affected

Answer 46

pyramidal tracts (corticospinal and corticobulbar). for motor movements

Question 47

In motor neurone diseas why are abdominal reflexes (superficial reflex) absent but deep tendon relxed brisk

Answer 47

hallmark of a corticospinal tract lesion

Question 48

what is a fasciculation

Answer 48

involuntary and abnormal firing of a single motor neurone

Question 49

Explain denervation and reinnervation

Answer 49

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

Question 50

Describe the two main types of headaches and examples of them

Answer 50

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

Question 51

Describe primary Headaches in more detail

Answer 51

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

Question 52

What four key findings suggest a secondary headache

Answer 52

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

Question 53

Describe types of migraine

Answer 53

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.

Question 54

Describe the phases of a migraine

Answer 54

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

Question 55

Describe migraine management

Answer 55

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

Question 56

Describe tension type headaches

Answer 56

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

Question 57

What is the treatment for tension type headaches

Answer 57

Reassurance Individual attacks- give aspirin or paracetomol

Question 58

Describe cluster headaches

Answer 58

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

Question 59

What is the treatment of cluster headaches

Answer 59

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

Question 60

Compare the differences between all three types of primary headaches

Answer 60

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

Question 61

Describe the hearing organ and vestibular organ

Answer 61

Hearing organ: capture high frewuency motion (sound) Vestibular organ: capture low frequency motion (movements)

Question 62

What 2 things is sound made of

Answer 62

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

Question 63

Describe the outer ear, its functions and how it produces sound

Answer 63

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

Question 64

Describe the middle ear, its functions and how sound travels through

Answer 64

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

Question 65

Describe the inner ear, its functions and how sound travels through

Answer 65

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

Question 66

Describe the cochlea in detail, its structure etc

Answer 66

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

Question 67

Describe the hearing organ in detail

Answer 67

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

Question 68

Whats the difference between the hair cells

Answer 68

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

Question 69

After the neurotransmitter has been released to the afferent vestibulocochlear nerve what pathway is taken next

Answer 69

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

Question 70

What are the types of hearing loss and their causes

Answer 70

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

Question 71

What tests can be used to assess hearing

Answer 71

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

Question 72

On audiometry testing how would conductive and sensorineural hearing loss patterns differ

Answer 72

Conductive: bone conduction is high as nerves are working, air conduction falls below 20dB Sensorineural: bone and air conduction fall at higher frequencies

Question 73

How is hearing loss treated

Answer 73

Underlying cause: remove ear wax, treat infection Hearing aids Cohlear implants Brainstem implants

Answer 74

Movement and gravity changes are sense by mechanical sensors (canals and otoliths), CNS integrates this info and cause ocular reflex and postural control

Question 75

What does the vestibular system provide information about

Answer 75

To detect and infrom about head movement and position spatial orientation/balance keep images fixed during head movements

Question 76

Describe the vestibular systems anatomy in detail

Answer 76

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.

Question 77

What movement do each of the otolith organs sense

Answer 77

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

Question 78

How do hair cells generate potential

Answer 78

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

Question 79

How do hair cells generate potential

Answer 79

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

Question 80

How is information passed higher up

Answer 80

info travels thru vestibulocochlear nerve to vestibulospinal tract to vestibula ganglion to vestibular nuclei in the pons where primary afferents end

Question 81

What are the two vestibular reflexes

Answer 81

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.

Question 82

What disorders may arise from the vestibular system and what would the presentation be

Answer 82

- 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

Question 83

What are the red flags of vestibular disorders and what three things should be checked

Answer 83

Headache gait problems Hyper-acute onset hearing loss more than 4 days of symptoms Check: eyes, legs and ears

Question 84

If a patient presents with intemittent dizziness and vertigo what test needs to be used and what is the likely diagnosis

Answer 84

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

Question 85

If a patient is acutely dizzy what test should be used and what are the two likely diagnoses

Answer 85

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

Question 86

Name the parts of the eye:

Answer 86

Lateral and medial canthus Pupil, iris, sclera Caruncle (the pink) Limbus: border between cornea and sclera

Question 87

Describe the lacrimal systems innervation and what happens

Answer 87

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

Question 88

What is the tear film, it’s role, explain it

Answer 88

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

Question 89

Which layer of the tear film is in close contact with the eye

Answer 89

Mucinous layer

Question 90

Which layer of the tear film protects the tear film from evaporation

Answer 90

Lipid layer

Question 91

What glands produce lipids for the tear film

Answer 91

Meibomian Glands

Question 92

What is the thin transparent tissue that covers the outer surface of the eye?

Answer 92

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.

Question 93

Describe the layers that cover the back of the eye

Answer 93

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

Question 94

What is the cornea, name it’s layers from most superficial to innermost ?

Answer 94

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

Question 95

If the cornea is hydrated what happens

Answer 95

Becomes white. The cornea has a low water content so by hydrating it it becomes white like the sclera which has high wster content

Question 96

What is the lens and its functions

Answer 96

Behind the iris, is an acellular capsule has inner elongated cell fibres. Is transparent, has refractive power, 1/3 of the eyes focusing power

Question 97

What nerve transmits info from the eye to the brain

Answer 97

Optic nerve which connects the the back of the eye near the macula, visible portion is the optic disk

Question 98

What is the optic nerve blind spot

Answer 98

Where the optic nerve meets the retina there are no light sensitive cells, is the optic disk

Question 99

What is the macula

Answer 99

Centre of retina , highly sensitive for detailed central vision and tasks like reading that require central vision

Question 100

What is the central of the macula called and what is its function

Answer 100

Fovea, high concentration of cones to see detail, low concentration of rods

Question 101

Describe central and peripheral vision

Answer 101

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

Question 102

Describe the structure of the retina

Answer 102

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

Question 103

What are the two types of photoreceptors

Answer 103

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

Question 104

What are the different type of cone cells and what are they sensitive to

Answer 104

S cones : blue (wavelengths of 400-430) M cones: green (WL of 530-560) L cones: red (WL of 560-600)

Question 105

Why arent rod cells sensitive to colour

Answer 105

used for night vision and spatial recognition not sensitive to colours

Question 106

What are the most common colour vision deficiencies

Answer 106

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-

Question 107

What is the name for full colour blindness

Answer 107

Achromatopsia

Question 108

What is the test used for colour blindness

Answer 108

Ishihara test

Question 109

What effect does refraction have on light

Answer 109

velocity changes the lights path changes

Question 110

How is the index of refraction calculated

Answer 110

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)

Question 111

Describe what happens when light meets a medium

Answer 111

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

Question 112

What are the two types of lenses

Answer 112

Convex: Converging lens, takes the light rays and brings then to a point Concave: Diverging lens, takes light rays and spreads them out

Question 113

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

Answer 113

Emmetropia

Question 114

What is ametropia

Answer 114

mismatch between axial length and refractive power. Parallel light rays dont fall on the retina can be myopia, hyperopia, astigmatism or presbyopia

Question 115

What happens in myopia, what are the main causes and the symptoms

Answer 115

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

Question 116

How is myopia treated

Answer 116

Concave lens (neg lens)- spreads out as reaches a focal point too quickly Contact lens Remove lens to reduce eyes refractive power

Question 117

What is hyperopia, the causes and the symptoms

Answer 117

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)

Question 118

How is hyperopia treated

Answer 118

Converging (positive) lens (helps it to converge early) cataract extraction with a converging lens contact lens intraocular lens

Question 119

what is astigmatism

Answer 119

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

Question 120

What are the symptoms of atigmatism

Answer 120

headache, eyepain blurred and distorted vision head tilting and turning

Question 121

What is the treatment of astigmatism

Answer 121

if regular: cylinder lenses with spherical lenses (convex or concave) focuses light into a line not a point irrregular: rigid cylinder lenses and surgery

Question 122

What are the components of the near response

Answer 122

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

Question 123

What is presbyopia

Answer 123

loss of accomodation (focus on near objects). Happens after 40 yrs old, distant vision is in tact. use reading glasses to increase refractive power

Question 124

What is the treatment of presbyopia

Answer 124

convex lenses as rays converge behind retina so need convex to converge further forward. reading glasses bifocal glasses trifocal glasses progressive power glasses

Question 125

How is presbyopia corrected

Answer 125

Spectacle lenses : monofocal or multifocal Contact lenses: used for cosmetic, athletes or specific jobs

Question 126

What are the types of optical correction and their advantages and disadvantages

Answer 126

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

Question 127

What manoeuvres are used for Benign Paroxysmal Positional Vertigo

Answer 127

Epley manoeuvre Semont manoeuvre

Question 128

Describe the layers at the front of the eye

Answer 128

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

Question 129

What two structures are powerful refractive surfaces and allow the eye to focus

Answer 129

Cornea (2/3 focusing power) Lens (1/3 of focusing power)

Question 130

What lens is surgically inserted for the correction of myopia and astigmatism

Answer 130

ICL- Staar intra-collamer lens

Question 131

Describe the visual pathway including neurone order

Answer 131

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

Question 132

Describe how lesions anterior, at and posterior to the optic chiasma would affect vision

Answer 132

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

Question 133

Describe the origin of crossed and uncrossed fibres and what visual field they are responsible for

Answer 133

Crossed fibres from nasal retina responsible for temporal field vision Uncrossed fibres from temporal retina responsible for nasal field

Question 134

What are the causes of bitemporal hemianopia

Answer 134

Pituitary gland tumour as the pituitary is under the optic chiasm

Question 135

If a patient has a stroke what visual issue will they have

Answer 135

Homonymous hemianopia

Question 136

Damage to the primary visual cortex causes what

Answer 136

Contralateral homonymous hemianopia with macular sparing. also due to stroke. The macula recieves dual blood supply so supplied with blood

Question 137

What is the function of the pupil

Answer 137

Regulates light input

Question 138

Describe what the pupil does in light and dark

Answer 138

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)

Question 139

Describe the pupillary reflex

Answer 139

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

Question 140

Explain the defects that can be seen in the pupillary reflex

Answer 140

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

Question 141

What test is used to diagnose RAPD

Answer 141

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

Question 142

What are the terms to describe eye movement

Answer 142

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

Question 143

What are the two speeds of eye movement called

Answer 143

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

Question 144

Name the extraocular muscles and their function

Answer 144

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

Question 145

Describe the innervation of extraocular muscles

Answer 145

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)

Question 146

How are the intraocular muscles tested

Answer 146

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

Question 147

Describe what would happen in third and sixth nerve palsy

Answer 147

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

Question 148

What reflex test is used to test visual acuity in pre verbal children

Answer 148

Optokinetic Nystagmus reflex looks for smooth pursuit following a moving pattern and a fast reset saccade looking at the beginning of the pattern again

Question 149

What are the causes of 3rd nerve palsy and their treatments

Answer 149

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

Question 150

What is pilocarpine and how does it work

Answer 150

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

Question 151

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

Answer 151

To the parasympathetic ciliary ganglion

Question 152

What is the term used to described light-near dissociation

Answer 152

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

Question 153

What signs are telling of Alzheimers dementia

Answer 153

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

Question 154

What are the biomarkers of Alzheimers and what is the primary event

Answer 154

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

Question 155

How can Alzheimers be tested

Answer 155

Lumbar puncture, look if there is Beta Amyloid and Tau in CSF

Question 156

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

Answer 156

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

Question 157

How will fronto-temporal dementia present and what MRI changes

Answer 157

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

Question 158

What two cognitive tests are used to assess dementia

Answer 158

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

Question 159

Define meningitis

Answer 159

Inflammation of meninges - viral or bacterial will see lots of t cells in sub arachnoid

Question 160

Define encephalitis

Answer 160

Inflammation of brain tissue due to infection or autoimmune

Question 161

What is cerebral vasculitis

Answer 161

inflammation of blood vessel walls

Question 162

What is the name of the vessels that plunge into the brain substance and form a network capillaries

Answer 162

Pial vessels

Question 163

What makes blood brain barrier

Answer 163

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.

Question 164

What happens if there endothelial layer of the blood brain barrier is disrupted

Answer 164

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

Question 165

What does encephalitis present with

Answer 165

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

Question 166

What are the causes of encephalitis

Answer 166

Viral Infection: Herpes, measles, Chickenpox, Rubella Insect bites (mosquito, tick), bacterial and fungal infection, trauma or autoimmune (attack Ca2+/H+ channel)

Question 167

What are the treatments of encephalitis

Answer 167

Antivirals (acyclovir), steroids, antibiotics, analgesics, anti convulsants, ventilation, corticosterodis for inflammation, immune suppresant

Question 168

What medical condition causes demyelination of the CNS

Answer 168

Multiple Sclerosis

Question 169

What is MS, how does it present

Answer 169

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.

Question 170

What is meningitis and its causes

Answer 170

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

Question 171

What is an infection of the spinal cord called

Answer 171

Myelitis (brain and spinal cord = encephalomylitis)

Question 172

What is the difference between encephalitis and meningitis causes

Answer 172

encephalitis is viral mostly snf meningitis is bacterial coccus

Question 173

How does meningitis present

Answer 173

sudden fever, severe headache, nausea/vomiting, double vision, drowsiness, sensitivity to bright light, stiff neck and rash

Question 174

What are the key differences between encephalitis and meningitis presentations

Answer 174

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

Question 175

Diagnostic tests for encephalitis and meningitis

Answer 175

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,

Question 176

How is meningitis treated

Answer 176

I.V antibiotics, analgesics, corticosteroids to reduce inflammation, immune suppressors similar to encephalitis

Question 177

What are some of the long term effects of meningitis

Answer 177

Learning disabitlities, memory loss, poor concentration, clumsy, headaches, deafness, loss of balance, epilepsy, speech and visual problems