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
