NEURO Flashcards

Question

# ```NEURO Intro to Sensory Systems and Somatosensation by Dr Murphy``` Why are receptive fields not the same across the body? ## Footnote *LOB: Describe how pressure on a fingertip is converted to a receptor potential and explain, with examples, the factors that influence sensitivity, selectivity, spatial and temporal resolution of the signal

Answer 1

Small field require more innervation If that was all over the body thered be so much information But also it requires more space in the cortex. The brain has prioritised what is important.

Answer 2

Sensory systems use this to amass a response for threshold Needs a noticeable change in firing rate for small changes in pressure But can saturate if response is proportional to pressure. So receptors adapt at difference rates to overcome saturation. By damping down response to constant stimuli, then moments when stimulus strength changes is highlighted. = vigorous response to small changes. **Damping constant stimuli responses enhances the detection of stimulus strength changes, fostering a vigorous response to minor alterations.** ***Extra:*** Rate coding was originally shown by Edgar Adrian and Yngve Zotterman in 1928. In this simple experiment different weights were hung from a muscle.**As the weight of the stimulus increased, the number of spikes recorded from sensory nerves innervating the muscle also increased**

Answer 3

In pressure sensation How closely the measured activity corresponds to the timing of the actual neuronal activity. Rapidly adapting receptors= high temporal resolution Slowly adapting receptors= low temporal resolution Rapidly adapting receptors, such as those found in Meissner's corpuscles, exhibit high temporal resolution. These receptors quickly respond to changes in pressure but rapidly adapt to sustained pressure stimuli. Conversely, slowly adapting receptors, like those in Merkel cells, demonstrate low temporal resolution. They maintain firing rates over prolonged periods in response to sustained pressure, providing continuous information but with slower response kinetics.

Answer 4

A sensory nerve ending with mechanically gated channels surrounded by connx tissue lamellae and gel. Firm pressure Large RF Rapid adaptation Deep in skin.

Answer 5

Changes depending on slowly changing sustained pressure or rapidly chnaging pressure. Non myelinated nerve ending is able to sustain many mechanical gated channel changes. ?Role of aplification such as vibration?

Answer 6

Mehcnoreceptors respond to deformaiton of the membrane, and stretch detectors and tension monitors provide input.

Answer 7

Stretch detectors (Ia and II) in muscle spindles The Golgi tendon organ is a proprioceptor that monitors and signals muscle contraction against a force (muscle tension),

Answer 8

Contain many intrafusal fibres- nuclear chain and bag Type II and Type IIa stretch sensitive ensory afferents Stretchy passive centre type II respond in proportion to the amount of change in length type Ia respond in proportion to the rate of change in length

Answer 9

Contractile poles interact with γ motor neurones

Answer 10

When muscles are stretched due to changes in body position, **intrafusal** muscle spindles detect this stretch and signal the CNS to adjust muscle tone accordingly. This feedback loop helps in maintaining proper muscle length and tension to support posture against the force of gravity.

Answer 11

1. Biceps stretch as weight is added to cup (top up the tipple) 2. Centres of intrafusal muscles are stretched (Ia and II) 3. Afferent to spinal cord (type II as amount of stretch has increased) 4. Motor neurones are excited 5. Muscle contracts a little more strongly.

Answer 12

1. Brain reduces excitation of α and γ motor neurones of bicep 2. Bicep lengthens, intrafusal muscle fibre pole stretch but centres dont change. RELAX 3. Antangonist muscle activated 4. Tricep shortens

Answer 13

Gamma control refers to the result on gamma motor neurones. **Regulating sensitivity!** Gamma motor neurons are a type of motor neuron that innervate the intrafusal muscle fibers within muscle spindles. These neurons regulate the sensitivity of the muscle spindle by adjusting the tension in the intrafusal fibers. **When gamma motor neurons are activated, they cause contraction of the intrafusal muscle fibers within the muscle spindle. This adjustment in tension maintains the optimal sensitivity of the muscle spindle** Think of when an elastic band is already stretched, it wont stretch more. The sensitivity is reduced.

Answer 14

Stepping on uneven ground causes the ankle to roll rapid unintended stretch of the calf muscle activates type Ia stretch afferents very rapid reflex causes a sharp contraction of that same muscle, preventing a fall / damage to the ankle This is the reflex that is tested clinically by tapping tendons

Answer 15

* Brain initiates and controls voluntary movements. * Signals from the brain travel through the spinal cord to the muscles. * Spinal cord facilitates movement execution and coordination. * Contains networks of neurons, including motor neurons and interneurons. * Inhibition mechanisms within the spinal cord regulate muscle activity. * Helps fine-tune and coordinate muscle movement. * **Pre-synaptic inhibition**: * Regulates **sensitivity** of stretch reflex (Ia reflex). * Adjusts muscle tone during voluntary movements. * GABAergic (metabotropic) slow in onset and long-lasting, * **Post-synaptic inhibition:** * Affects excitability of motor neurons and interneurons. * Refines motor output for smooth and coordinated movement. * glycinergic (ionotropic) fast and transient non-specific | are part of the spinal circuitry controlling movement, incl gait cycle

Answer 16

Primary Afferent Dorsal Columns Synapse in dorsal column nuclei Ascends in medial lemeniscus Synapse with specific thalamic nucleus (vent post) Ascends via internal capsule Primary SS area.

Answer 17

Inhibitory interneurones synapse between primary and secondary afferents Dampens down responses to homogenous stimuli So it can be **highlighted where stimulus strength changes** Like turning down the radio so you can see the door number when driving **Sharpens spatial responses**

Answer 18

Neural adaptation or sensory adaptation is a gradual decrease over time in the responsiveness of the sensory system to a constant stimulus.

Answer 19

**Adaption and lateral inhibition damp down responses to homogenous (same) temporal and spatial stimulation** Respond strongly to small changes over a very large stimulus range Increases **DYNAMIC RANGE** Dynamic range is the ratio between the largest and smallest values that a certain quantity can assume. **Lateral inhibition enhances the perception of edges and contrasts in sensory stimuli. By suppressing the activity of neighboring neurons, lateral inhibition sharpens the spatial resolution of sensory systems and improves the ability to detect fine details.** **Adaptation is the process by which sensory receptors decrease their response to a continuous or repetitive stimulus over time. Helps focus on new or changing stimuli.** | Think photography and exposure points.

Answer 20

determines the type of stimulus you would use in a clinical setting and the interpretation of the results

Answer 21

determines the dimensions of test stimuli

Answer 22

determines the temporal characteristics of test stimuli temporal resolution refers to the ability to distinguish two points in time For example, fMRI has high spatial resolution but low temporal resolution, while EEG has high temporal resolution but low spatial resolution.

Answer 23

4 areas area 3a – proprioceptors area 3b – skin area 1 – skin area 2 – both

Answer 24

columns 1) fine detail 2) texture 3) damage 4) vibration 5) skin stretch

Answer 25

Phantom limb Epileptic Activity (phatom sensations) Synaesthesia (auditory activates colour processing)

Answer 26

“an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

Answer 27

* Warning system * Sensory experience * Trigger for emotional and behavioural response such as fight/flight * Doesnt always correlate with receptor activation (stress, anxiety) * Can be caused by dysfunctional neural pathways

Answer 28

The dorsal horn Laminae I II V

Answer 29

**Aδ** Axon thin and myelinated NT is glutamate *sharp immediate pain **C** Axon thinner and unmyelinated many NT incl glutamate and substance P *delayed aching pain

Answer 30

Primary pain Aδ Found in intrafusal muscle fibres instant reflex to pull away

Answer 31

Specific fibres in the muscle can be categorised as intrafusal or extrafusal. Intrafusal are specialised fibres that act as sensory organs Extrafusal are muscle fibres for force which contract.

Answer 32

C fibres are also activated Inflammation builds Too slow for immediate reflex but good for "irritation" to check and address

Answer 33

* Primary afferent * Ascends in Dorsal column * Synapse in Medulla in dorsal column nuclei * Ascends in medial lemniscus * Synapse in specific thalamic nucleus * Ascends in internal capsule to primary SS area of cortex.

Answer 34

* Nocicpetor primary afferent * Synapse in dorsal horn (spinal cord) * Ascends in spinothalamic tract * Synapse in specific thalamic nucleus * Ascends in internal capsule to primary SS area of cortex

Answer 35

1. stimulate SS cortex= local sensation 2. stimulate SS thalamus = local sensation "sharp hot electric" 3. lesions in primary SS cortex reduces sensation

Answer 36

The nociceptors synapse and highjack the medial pain pathways.

Answer 37

As the medial pain pathway passes through the brainstem, multiple targets have autonomic and modulatory control Whilst passing through the thalamic nuclei to the cortex, passing to the hypothalamus amygdlaa and frontal cortex relates pain to higher order brain function.

Answer 38

“normal” pain due to tissue damage, which stimulates nociceptor nerve endings

Answer 39

hyperalgesia (increased pain from painful stimuli) allodynia (non-painful stimuli become painful)

Answer 40

Inflammatory soup results in both hypersensitisation and depolarisation This hypersensitisation goes on to amplify depolarisation This in turn releases inflammatory mediators and cycles

Answer 41

Via "turning off/ blocking" desending modultion Specifically: * orbitofrontal cortex * anterior cingulate cortex * periaqueductal grey (stem) * Raphe magnus (nuclei stem) * locus coeruleus (nuclei stem) These supress nociceptor pathways at first synapse.

Answer 42

Activate regions of the brain required for descending modulation via opioids Activate the pathways directly at the synapse at the inhibitory interneurones at the spinal cord (opioids) Placebo and coping strategies incl CBT to mimic the survival instinct to activate the descending modulation. Acupuncture and TENS may be placebos or may activate local circuits

Answer 43

More perception of pain Different levels of pain tolerance.

Answer 44

Anxiety can up regulate the negative effects of the descending modulation which via Serotonin and a different receptor Up regulates pain at the Aδ and C fibres.

Answer 45

In high stress situations the limbic centres prioritise survival. For survival and "coping" pain may need to be dialled down (think massive trauma and not feeling pain) This stress activates the descending modulation at the anterior cingulate and insular contex (limbic structures) This then synapses at the inhibitory interneurones to reduce pain.

Answer 46

pain that results from nociceptor responses to pathological conditions

Answer 47

* Persistently high glucose (poorly controlled diabetes) * Direct injury to nociceptors (spontaneous pain) * Microinflammation and sensitisation (hyperaglesia and allodynia) * Alterations in central pathway **Neurogenic pain** ## Footnote allodynia= pain due to a stimulus that does not normally provoke pain.

Answer 48

pain caused by abnormal cns processing such as * unbalanced descending control systems * dysfunction of inhibitory systems in spinal cord * excess long-term potentiaiton after injury (nerve trauma) or persistent activation (diabetic neuropathy) * central sensitisation

Answer 49

* **Peripheral Nerve Injury**: * Damaged nerves cause abnormal pain signaling, leading to increased sensitivity. * **Central Sensitization**: * Prolonged pain input results in heightened spinal cord and brain sensitivity, amplifying pain perception. * **Ectopic Discharges:** * Abnormal nerve firing generates spontaneous pain sensations. * **Peripheral Neurotransmitter Alterations:** * Imbalance in neurotransmitter release disrupts pain regulation. * **Neuroinflammation:** * Immune responses release pro-inflammatory molecules, contributing to pain. * **Maladaptive Plasticity:** * Abnormal synaptic changes perpetuate chronic pain states. * **Peripheral Sensitization:** * Increased sensitivity of sensory neurons at the injury site exacerbates pain perception

Answer 50

* reduces pain by improving mood and coping ability (think decending modulation * chemically increases transmission in descending anti-nocicpetive pathway

Answer 51

Tissue damage triggers inflammation. Inflammation releases mediators that sensitize pain receptors. Pain serves as a protective mechanism. Sensitization of pain receptors amplifies pain perception. * Prostaglandins * Cytokines * Bradykinin * Histamine * Nerve Growth Factor (NGF) * Substance P

Answer 52

act as anxiolytics Boost GABAergic inhibition Boost spinal cord inhibition

Answer 53

Block high firing AP during seizures Reduce activity at synapses with long-term potentiation

Answer 54

Neurogenic pain mechanisms characterised by * chronic release of peptides from C fibres * inflammation * abnormal glial activity Seen often in chronic peripheral spinal cord injury (highly immunogenic causes)

Answer 55

* LAs produce a loss of pain sensation without affecting consciousness * Act locally * Prevent perception of pain by CNS - block generation/conduction of action potentials (APs) by inhibiting voltage-gated Na+ channels

Answer 56

*Take procaine and lidocaine as examples* * Aromatic benzyl group * Basic Group * C=O (ester or amide) * Local anaesthetics are weak bases (pKa of 7-9) * Act as proton acceptors at physiological pH (7.2) * Act as proton donors in alkaline conditions (pH>pKa)

Answer 57

* Local anaesthetics are weak bases (pKa of 7-9) * Act as proton acceptors at physiological pH (7.2) WHY? Water everywhere! *When considering the pH and pKa of cell internal and external and thinking about channels opening to depolarise.*

Answer 58

Ester bonds susceptible to hydrolysis Procaine has shorter t1/2 than lignocaine

Answer 59

Ester bonds susceptible to hydrolysis Procaine has shorter t1/2 than lignocaine

Answer 60

* Block Na+ channels * Block generation and conduction of action potentials (APs) * No APs, no information sent to CNS, no perception of pain

Answer 61

Termed use-dependent drugs, **only work when high activity** Less side effects, low activity neurones not affected Principle of other drugs; anti-epileptic, class I cardiac anti-arrhythmic Prevents the downstream channels from reclosing

Answer 62

Alkaline pH makes more drug into non-ionised form (LA), which can cross the ‘fatty’ myelin sheath and axonal membrane Inside the cell (pH 7.2), more drug becomes ionised into the LAH+ form, which blocks the Na+ channel "ion-trapping"

Answer 63

LA + H3O <=> LAH+ +H2O Inside cell favours LAH+ Outside cell favours LA

Answer 64

LAs block small diameter axons before large ones LAs usually block un-myelinated before myelinated fibres Nociceptive impulses are conducted in Aδ fibres (small diameter myelinated axons) and C fibres (unmyelinated axons)

Answer 65

If enter brain: * stimulation * tremor * agitation * convulsions * CNS depression * respiratory depression *

Answer 66

Blocked Na+ channels, reduced Ca2+ influx, Reduced contraction force Reduces cardiac output Reduces vasulcar tone as increased vasodilation Reduced blood pressure

Answer 67

* **Surface anaesthesia**: applied to mucosal surface e.g., bronchial (bronchoscopy), nose, cornea – LAs do not cross skin very well * **Local nerve block:** LA injected close to sensory nerve, e.g., dentistry * **Spinal anaesthesia**: LA injected into subarachnoid space between 2nd and 5th lumbar vertebrae enters straight into CSF, e.g., surgery when inappropriate to use general anaesthetic, frail/elderly patient * **Epidural**: LA injected into epidural space – outside meninges, where it diffuses to and blocks nerve roots. e.g., childbirth

Answer 68

**Vasoconstriction keeps the LA localised to the area of injection** * Adrenaline causes vasoconstriction * reduces possibility of systemic toxicity * Prevents bleeding * Also prolongs the LA action RISK: Local hypoxia - particular extremities: fingers, toes, nose Absorption of adrenaline = arrhythmia

Answer 69

Grey matter make up 40% of brain tissue and have ***no energy reserves*** and are intolerant to hypoxia Without O2 - neuronal damage occurs in several minutes The brain has a very high O2 consumption, so constantly requires a high blood flow (x10 higher than body average)

Answer 70

High number of capillaries Highly permeable **diffusion area is very high** Auto-regulation (myogenic response) is well-developed Local metabolic vasodilatation is well-developed

Answer 71

The myogenic mechanism is how arteries and arterioles react to an increase or decrease of blood pressure to keep the blood flow constant

Answer 72

Keep cerebral flow around **60ml/min/100g** via influencing Mean pressure (mmHg) arterial Less than **60ml/min/100g** and **60mmHg** Mentaal confusion and syncope can occur. ## Footnote Remember HR 60, Brain 60

Answer 73

* The brain autogregulates flow around 60ml/min/100g * and requires * PaCO2 of 40 * PaO2 of 100 ## Footnote Thik logically about these graphs, when flow is low...

Answer 74

Cerebral arteries ‘outside’ the brain receive dense innervation from sympathetic nerves Cerebral arterioles ‘within’ the brain have little sympathetic innervation Perivascular nerves (C-fibres, nociceptors)

Answer 75

Perivascular nerves **(C-fibres, nociceptors**) release **Serotonin** and Calcitonin gene-related peptide mediate the pain of vascular headaches in strokes and the later phase of migraine through **vasodilation**

Answer 76

Pain from headaches can be reduced by understanding pain mediation and cause of headache Inflammation causes vasodilation so administering serotonin sumatriptan (5-HT1B agonist) Constricts of blood vessels Calcitonin gene-related peptide (CGRP) inhibitors for migraine, Constriction of blood vessels Reduces CGRP-mediated vasodilation

Answer 77

in walls of carotid arteries changes in blood pressure (BP) BP = Cardiac output (CO) x Total Peripheral Resistance (TPR) CO = blood flow (both have units of volume/time) So BP gives information about blood flow.

Answer 78

Effect of increasing in BP on baroreflex

Answer 79

* a baroreflex to high bp * stimulation of carotid sinus nerve results in activation of * Switch off Sympathetic, Switch on parasympathetic * Vessel relaxation -> reduced TPR – reduced BP * SA node reduced HR and Mycoardial contractility reduced- reduced cardiac output **Reduces Blood pressure**

Answer 80

* a baroreflex to low bp * stimulation of carotid sinus nerve results in activation of * Switch on Sympathetic, Switch off parasympathetic * Vessel contraction -> increased TPR – increased BP * SA node increased HR and Mycoardial contractility increased- increased cardiac output * NOTE: * Venoconstriction Increased venous return * Increased Starling’s law Greater preload * greater SV and BP * Also prevents postural hypotension **Increases Blood pressure**

Answer 81

Nerve that receives from carotid baroreceptor to the brain

Answer 82

Adrenaline secretion, Vasopressin (ADH) secretion, Stimulation of RAAS – Ang II production

Answer 83

* Located in CAROTID and AORTIC BODIES * Stimulated by * low O2 (hypoxia) * High CO2 (hypercapnia) * H+

Answer 84

Asphyxia (low O2/high CO2) Shock (systemic hypotension) Haemorrhage (when BP below range of baroreflex) **Drives cardiac regulation and regulates ventilation**

Answer 85

Severe hypotension or shock can result in inadequate tissue perfusion, leading to anaerobic metabolism and the production of lactic acid, which can contribute to metabolic acidosis and potentially elevate blood CO2 levels.

Answer 86

80 mmHg to 180 mmHg for mean arterial pressure (MAP)

Answer 87

* Nociceptive sympathetic afferents found in ventricles of heart * stimulated by acidic conditions (lactate during ischaemia) * C fibres * C Fibres converge on same neurones in spinal cord as somatic afferents, e.g., from skin areas Referred pain * Spinothalamic tract * Leads to a pressor response * Increase sympathetic NS * Vasoconstriction (think pale in MI), sweaty, tachycardia

Answer 88

* Brain stem nuclei are important: * Baroreceptors stimulate Nucleus tractus solitarius NTS * which stimulates Caudal ventral lateral medulla CVLM * which inhibits Rostral ventral lateral medulla RVLM * RVLM is switched off * switch off sympathetic nerves, so parasympathetic are the only ones working * DEPRESSOR reflex ## Footnote NOTE RVLM does not switch ON parasympathetic but rather switches off sympathetic so only parasympathetic is present.

Answer 89

* Brain stem nuclei are important: * Baroreceptors ***cant***stimulate Nucleus tractus solitarius NTS * NTS ***cant*** stimulate Caudal ventral lateral medulla CVLM * the inhibitory pathway between CVLM and RVLM is switched off * so the RVLM continues to stimulate sympathetic activity * sympathetic activity turned on * PRESSOR reflex

Answer 90

* stimulate inhibitory pathway NTS neurone * NTS switches off CVLM inhibition of RVLM * RVLM is switched on * Sympathetic activity increased * Pressor response *

Answer 91

* Stimulation of the NTS stimulates hypothalamus and limbic system (high brain order) as well as Nucleus ambiguus * stimulates N. Ambiguus, * Switch on vagus, * Reduce HR * Reduce BP

Answer 92

High brain orders can stimulate the Inspiratory Centre Inhibitory input from Inspiratory Centre, Inhibit N. Ambiguus, Switch off vagal nerve, Sinus tachycardia

Answer 93

Limbic system (‘emotional centre’) directly stimulates nucleus amiguus ** TURNS ON vagus nerve and PARASYMPATHETIC** heart rate drops blood pressure drops **cerebral flow drops** **loss of conciousness**

Answer 94

**due to a severe quick loss of cerebral flow** limbic system (‘emotional centre’) directly stimulates nucleus amiguus switches ON vagus nerve heart rate drops blood pressure drops cerebral flow lost faint

Answer 95

When lying down, central venous pressure is same across body Distribution of blood is equal When standing up, blood pools in legs due to gravity (about 1L) **less return of blood to the heart** (low CVP) Less return of blood, less stretch heart, less output, low stroke volume (starlings law) Affects cerebral blood flow, as pressure is reduced.

Answer 96

Warmth - causes further venodilatation and ‘pooling’ Bed rest – supine position for length of time changes baroreceptor threshold) Drug side effects – e.g., CCB - vasodilators

Answer 97

Lesion occupies space causing ICP. When ICP raises above MAP, get constriction of cerebral vessels. 1) Sympathetic response increases blood pressure to try and restore flow 2) Baroreceptor then detect high blood pressure and trigger a parasympathetic response via the vagus nerve. This induces bradycardia, or slowed heart rate | Cushing's Triad.

Answer 98

Blood vessels – contribute to all aspects of hypertensive organ damage. Blood vessels themselves undergo atheroma and aneurysm formation in large vessels, elastic reduplication in small vessels. Heart: left ventricular hypertrophy, left heart failure (LHF). Increased load causes concentric left ventricular hypertrophy

Answer 99

Kidney: nephrosclerosis, renal failure Thickened renal arterioles Glomerulosclerosis Granular cortical atrophy due to nephrosclerosis – loss of a glomerulus causes atrophy of the nephron.

Answer 100

Brain: microaneurysms and stroke, ischaemic cortical atrophy/ dementia.

Answer 101

* Eye: retinal capillary damage, haemorrhages, exudates. * Early hypertensive retinopathy * ‘Nicking, of retinal veins by overlying arterioles, normally they run alongside. * Moderate hypertensive retinopathy * Straightened, wider capillaries * Flame shaped haemorrhages * ‘Cotton wool’ spots * (later)‘Hard’ exudates around macula * Late chronic or ‘malignant’ acute hypertensive retinopathy * Papilloedema * Haemorrhage

Answer 102

**Pathophysiology**: Tear in the aortic intima allows blood to flow between layers, creating a false lumen. Often caused by hypertension, atherosclerosis, and mechanical stress. **Appearances**: Sudden, severe chest or back pain. Symptoms may include shortness of breath, neurological deficits. Physical exam findings: blood pressure differences between arms, murmurs, signs of organ ischemia. Diagnosis confirmed with imaging (CTA, MRA).

Answer 103

Changes in the luminal diameter of the arterioles are the most important component in regulating systemic arterial blood pressure. The resistance of flow is equivalent to the fourth power of the diameter. Therefore, a 50% decrease in the lumen results in a 16-fold increase in the pressure. (http://emedicine.medscape.com/article/1201779-overview) **Smaller vessels for HT, larger for atheroma**

Answer 104

True aneurysms are when the entire wall of the vessel bulges. Sometimes part of the wall is cut or torn, usually by trauma, and the inner layers bulge through the tear – some people would term this a false aneurysm because not all layers are affected.

Answer 105

Aneurysms occur at points of weakness * usually due to atheroma * sometimes due to inflammatory damage (e.g. syphilis) * occasionally due to connective tissue abnormalities (e.g. Marfan’s) * sometimes follow trauma, e.g. partial medial tear, often due to a traffic accident *

Answer 106

False aneurysms occur if the artery wall is punctured (e.g. during an arteriogram or angioplasty) and blood tracks out into adjacent tissue, but is contained locally by scar tissue. This expands as further blood is pumped out of the vessel wall.

Answer 107

typically occur at the bifurcations of the arteries in the Circle of Willis. Their rupture usually causes subarachnoid haemorrhage

Answer 108

This is usually secondary to atheroma and may: -Rupture, causing intraperitoneal haemorrhage and death -Throw off thromboemboli, causing ischaemia and gangrene

Answer 109

This can be due to -Aortic dissection (‘dissecting aneurysm’) -Syphilitic aneurysm Both develop due to weakening of the media and may rupture, causing haemopericardium and cardiac tamponade

Answer 110

typically occur in cerebral arteries in patients with hypertension. Their rupture causes intracerebral haemorrhage

Answer 111

Most aneurysms are secondary to atheroma and are fusiform (spindle shaped) Saccular aneurysms often occur after focal damage to a vessel, eg infection (eg bacteria may lodge in an atheromatous plaque) ‘Berry’ aneurysms are saccular and are due to focal vessel wall weakness at the point of bifurcation

Answer 112

Rupture Thrombosis Thromboembolism

Answer 113

* Aortic dissection (‘Dissecting aneurysm’): * Typical of elderly person with medial degeneration or Marfan’s syndrome - a congenitally weak media * tear in the intima, typically aortic root, allows blood to enter the aortic wall and form a parallel track. * Cerebral microaneurysm – typical of hypertension

Answer 114

* Definition: sudden onset of neurological deficit, due to cardiovascular cause. * Strokes are commonest in elderly men. * Modifiable factors strongly associated with stroke are hypertension, atrial fibrillation, smoking, diabetes mellitus and high cholesterol. * Effects are dictated by site and extent of damage and availability of speedy interventional treatment.

Answer 115

**Ischaemic: (80%)** Thrombo-embolic: sources include thrombus over atheroma at carotid bifurcation; mural thrombus from heart **Haemorrhagic (20%)** most commonly due to rupture of cerebral microaneurysm secondary to hypertension

Answer 116

The core of an infarct will undergo irretrievable and irreversible necrosis The adjacent territory is only relatively ischaemic, as there may be a degree of compensation from nearby blood supplies If arterial perfusion can be restored within 3 hours, much of the ‘penumbra’ territory may be salvaged. Some benefit to treatment up to 6 hours later. | "almost shadow"

Answer 117

Cerebral lesions due to strokes are soft due to liquefaction necrosis of the brain tissue. When this is cleared by macrophages, cystic spaces remain in the brain. | like a scar

Answer 118

Typically seen in diabetes and/or hypertension, usually with extensive small vessel atheroma. Affect deep penetrating arterioles – typically to basal ganglia, brainstem, thalamus and deep white matter, small lesions 2-15mm. Tiny cystic infarcts may be devastating, eg if internal capsule is involved, a 2mm infarct may cause a dense hemiplegia, if white matter can be clinically silent but contribute to vascular dementia.

Answer 119

Transient ischaemic attack’ – neurological deficit lasting < 12-24 hours Likelihood of full blown stroke within 5 yrs = 30% 4-20% incidence within 90 days (half within 48 hours) Risk is a factor of: Age, Blood Pressure, Clinical Symptoms, Duration > 1 hour, Diabetes Indication for immediate investigation and intervention

Answer 120

Definition: A thrombotic stroke occurs when a blood clot (thrombus) forms within an artery that supplies blood to the brain. Cause: Usually associated with atherosclerosis, a condition where fatty deposits (plaques) build up on artery walls. Outcome: The clot can block blood flow to a part of the brain, leading to tissue damage and neurological deficits

Answer 121

Definition: An embolic stroke happens when an embolus (a blood clot or other debris) forms elsewhere in the body and travels through the bloodstream to the brain, where it blocks a blood vessel. Cause: Common sources of emboli include the heart (due to conditions like atrial fibrillation) or other large arteries. Outcome: Similar to thrombotic strokes, embolic strokes can cause sudden and severe neurological symptoms.

Answer 122

Smoking cessation: tax++ on cigarettes. Aspirin for those at risk (risk reduction for stroke 25%) Decrease salt intake (↓BP 5mmHg should ↓strokes by 40%) Treat atrial fibrillation: warfarin (70% protection vs aspirin, but greater risk of haemorrhagic complications). New direct oral anticoagulants developed. Fast recognition of TIA.

Answer 123

**True Aneurysm:** Involves all three layers of the arterial wall (intima, media, and adventitia) and is bounded by arterial tissue. ie) Fusiform Aneurysm, Saccular Aneurysm **False Aneurysm (Pseudoaneurysm):** Involves a defect in the arterial wall with extravasation of blood that is contained by surrounding tissues or structures rather than arterial layers. ie) Traumatic Pseudoaneurysm (stab) or Iatrogenic Pseudoaneurysm (complication of atrial access in angiography,)

Answer 124

Definition: Intracerebral hemorrhage occurs when there is bleeding within the brain tissue itself, often from a ruptured blood vessel. Cause: Hypertension (high blood pressure) is a common cause, but other factors like trauma, blood vessel abnormalities, or blood disorders can contribute. Outcome: The bleeding results in pressure on surrounding brain tissue, leading to neurological damage. Symptoms can be sudden and severe.

Answer 125

Definition: Subarachnoid hemorrhage is bleeding into the space between the brain and the thin tissues that cover it (subarachnoid space). Cause: Commonly caused by the rupture of an aneurysm (a bulging, weakened area in the wall of an artery). Outcome: Blood in the subarachnoid space can lead to increased pressure and irritation of the brain, causing symptoms such as a sudden severe headache ("thunderclap headache"), nausea, vomiting, and neurological deficits.

Answer 126

Subarachnoid haemorrhage often follows ruptured Berry aneurysm; blood is confined beneath pia/arachnoid and follows the brain contours. Subdural haematoma formation is the result of trauma. Blood clot lies between the arachnoid and dural meninges

Answer 127

**regions of the brain that lie between the territories supplied by two major arteries. ** These areas are more susceptible to ischemia because they are at the border or "watershed" between the blood supply from two different arterial sources. **Hypoperfused areas** Example: Infarct at border between middle and anterior cerebral artery supply in patient with profound hypotension due to MI

Answer 128

Antiplatelet therapy Aspirin Clopidogrel Dipyridamole Thrombolysis (best within 3 hours, may have functional benefit up to 6 hours later) Evacuation of clot

Answer 129

Smoking cessation: tax++ on cigarettes. Aspirin for those at risk (risk reduction for stroke 25%) Decrease salt intake (↓BP 5mmHg should ↓strokes by 40%) Treat atrial fibrillation: warfarin (70% protection vs aspirin, but greater risk of haemorrhagic complications). New direct oral anticoagulants developed. Fast recognition of TIA.

Answer 130

creating the right number of nerve cells

Answer 131

1. Neurogenesis – creating the right number of nerve cells 2. Migration & differentiation – getting the right cells to the right place. 3. Axon guidance – growing an axon to the right target area. 4. Synaptogenesis – making connections with potentially useful partners. 5. Activity-dependent refinement – testing and perfecting the neural circuit.

Answer 132

Neuroblasts and neuroepithelial cells migrate to form the cerebral cortex. Cells born earlier settling in deeper layers and later-born cells populating surface layers.

Answer 133

Elements of the early neural tube. Neuroepithelial cells, or neuroectodermal cells, form the wall of the closed neural tube in early embryonic development. neuroblast or primitive nerve cell is a postmitotic cell that does not divide further and which will develop into a neuron after a migration phase

Answer 134

Molecules released by the developing brain guides the migrating cells Instruct gene expression and behavioural pattern.

Answer 135

Transformation of neurblasts into specific cell types. Remember the different brain neurocytes- glial astrocyte etc.

Answer 136

Neuroblasts migrate by elongating and reorganizing. Morphogenic signaling molecules released by the developing brain guide these cells. Extension of Axons and Dendrites to form connections. Guidance signals direct cells to specific target regions- precise and targetted connections.

Answer 137

Morphogenic signaling molecules guide neuroblasts during migration, influencing gene expression and behavior. Such as directing axons to where they are required.

Answer 138

Axonal growth requires traction, achieved by binding to the extracellular matrix. Specific proteins within the matrix guide axons along designated tracks and prevent penetration into forbidden areas. "including actin filament bundles and the mechanisms controlling their remodeling."

Answer 139

Formation of synapses. Originally nerve cells make trial synapses, and these need to be fine controlled and selected for efficiency as the trial synapses are too dense and suboptimal

Answer 140

Identifying and strengthening active synapses while eliminating less useful ones. LTP is typically induced by **the repeated and coordinated firing** of the pre-synaptic neuron (sending signals) and the post-synaptic neuron (receiving signals).

Answer 141

Long-term potentiation (LTP) is a process involving persistent strengthening of synapses that leads to a long-lasting increase in signal transmission between neurons. **changes in the efficiency of neurotransmitter release, alterations in receptor sensitivity, and modifications in the structure of synapses.**

Answer 142

Plasticity, the brain's ability to change, must be controlled as development progresses. Different brain regions have critical periods during which plasticity is possible, closing afterward. Structure- Neurones Functional- alterations in neurotransmitter release or receptor sensitivity. Synaptic- changes in the strength of synapses,

Answer 143

Different brain regions have critical periods during which plasticity is possible, and many of these periods close, making plasticity impossible thereafter." "The example of a child's brain adapting to a congenital eye problem emphasizes the importance of early intervention before critical periods close."

Answer 144

Ocular dominance columns contribute to the perception of depth and the integration of visual information from both eyes. They play a role in binocular vision and stereopsis, which is the ability to perceive depth and three-dimensional structures. Each column is specialized to process visual input from one eye. This organization ensures that the brain receives and processes information from both eyes but maintains the specificity of each eye's input. Ocular dominance columns develop during early postnatal life through a process called visual experience-dependent plasticity, with exposure to visual stimuli

Answer 145

"Consider a girl with a mutation in one copy of the doublecortin gene." "Depending on gene expression, some cells migrate normally, forming a seemingly normal cortex, while others do not, resulting in a double cortex." epilepsy

Answer 146

NDMA leading to increased glutamate release, receptor numbers, and dendrite and bouton size.

Answer 147

Developmental Traumatic Traumatic brain injury Traumatic spinal cord injury Ischaemic (e.g. stroke) Hypoxic (e.g. cardiac arrest) Inflammatory (e.g. multiple sclerosis) Neurodegenerative conditions (e.g. Alzheimer’s, Parkinson’s) Infection (e.g. meningitis, encephalitis) Tumours

Answer 148

**USUALLY ALL** Neurons Glial cells Astrocytes Microglia Oligodendrocytes (myelin) Blood - brain barrier CSF

Answer 149

a group of permanent disorders of the development of movement and posture that are attributed to non progressive disturbances that occurred in the developing foetal or infant brain. **disturbances of sensation perception, cognition, communication, behaviour, epilepsy, and by secondary musculoskeletal problems.”**

Answer 150

a group of permanent disorders of the development of movement and posture that are attributed to non progressive disturbances that occurred in the developing foetal or infant brain. **disturbances of sensation perception, cognition, communication, behaviour, epilepsy, and by secondary musculoskeletal problems.” **

Answer 151

Reduction of whole brain oxygenation Preferentially affects the most metabolically active parts of the brain Grey matter Cerebral cortex Basal ganglia

Answer 152

Multiple sclerosis: inflammation → demyelination → neuronal dysfunction Demyelination disease The cerebrospinal fluid is tested for oligoclonal bands of IgG on electrophoresis, which are inflammation markers found in 75–85% of people with MS High signal in the spine on T2 MRI

Answer 153

Presented with headache , nausea and vomiting , reduced level of consciousness, myoclonic jerks and pyrexia. Right occipital lobe brain abscess, ventriculitis and hydrocephalus

Answer 154

Fate of neuron following axotomy and target loss Loss of trophic factors and support Fate of neurons which lose their normal input, i.e. denervation Loss of normal input → change in synaptic balance

Answer 155

Severed axons in the **PNS can regrow**, if their nerve sheath remains intact the layer of myelin and connective tissue that surrounds and insulates nerve fibers

Answer 156

Regrowth of severed axons Occurs effectively in **mammals’ peripheral nervous system only** Myelin is of critical importance: provides a guide tube for the sprouting end of a severed neuron to grow through extending axon guided to its destination as it during development

Answer 157

Glial scar formation (gliosis) is a reactive cellular process involving proliferation of astrocytes and microglia after injury to the CNS shown to have both beneficial and detrimental effects. Regenerates a tissue barrier after blood-brain barrier compromise and promotes revascularisation of injured brain. BUT: , neuro-developmental inhibitors are secreted by astrocytes that prevent axon regrowth and regeneration.

Answer 158

hippocampus (dentate gyrus) near the lateral ventricles (subventricular zone), supplying the olfactory bulb Both important for memory, so perhaps memory does “grow”.

Answer 159

Having one brain area take over the functions damaged in another area

Answer 160

Compensation Presynaptic neurons sprout more terminals Can even get reorganisation Neurorehabilitation capitalises on the way the brain normally learns to relearn lost function. This approach of using learning, alone and in combination with other therapies, promotes adaptive neural plasticity

Answer 161

Hemispherectomy in young children Outcome can be surprising good Language reorganisation and relative intellectual preservation In blind people portions of visual cortex may be used for reading Braille and other non-visual functions

Answer 162

Change in balance of excitation and inhibition - ‘unmasking’ Strengthening or weakening of existing synapses - longterm potentiation or depression Change in neuronal membrane excitability Anatomical changes - sprouting of new axons/synapses

Answer 163

1. Some specific techniques might be effective transmission in corticospinal pathways reorganisation of brain maps/activity performance of movement 2. Therapy might need to be task specific 3. Intensity might be important 4. Timing might be important

Answer 164

Cell replacement: neurons, oligodendrocytes Very limited evidence that this occurs “Bystander” effects: Intrinsically neuroprotective Anti-inflammatory Anti-apoptotic Delivery of trophic factors Overcome natural inhibitors

Answer 165

a noninvasive procedure that uses magnetic fields to stimulate nerve cells in the brain to improve symptoms of depression. The treatment coil is applied to the head above the left prefrontal cortex. This part of the brain is involved with mood regulation, and therefore, is the location where the magnetic fields are focused. These magnetic fields do not directly affect the whole brain; they reach only about two to three centimeters into the brain directly beneath the treatment coil

Answer 166

Cerebellum receives **input** from the cerebral cortex, particularly the **motor** and **premotor** areas . Motor planning and initiation signals originate in the cortex and are transmitted to the cerebellum for refinement of movement patterns.

Answer 167

tightly connected to the brainstem, especially the pontine nuclei. The **pontine nuclei relay** information from the cerebral cortex to the cerebellum **via the middle cerebellar peduncle.**

Answer 168

influencing motor coordination and balance Input from middle peduncle

Answer 169

medial limb position and touch

Answer 170

posture, limb movement and eye movement

Answer 171

equilibrium, balance and posture

Answer 172

Inferior Peduncle The cerebellum receives information from the vestibular system, which plays a crucial role in maintaining balance and spatial orientation. This input is essential for the cerebellum's involvement in postural adjustments and coordination.

Answer 173

Efferent fibers from the cerebellum project to the spinal cord through the superior, middle, and inferior cerebellar peduncles. These connections modulate and fine-tune motor commands, contributing to the smooth execution of movements.

Answer 174

The cerebellum projects to the thalamus, forming a closed loop with the cerebral cortex. This loop is crucial for motor learning and the coordination of voluntary movements.

Answer 175

Molecular Layer Purkinje Cell Layer Granular Layer

Answer 176

Contains **stellate** and **basket** cells, as well as the **parallel** **fibers** (axon terminals of granule cells) and **Purkinje** **cell** **dendrites**. This layer is involved in **the integration of signals.**

Answer 177

Composed of Purkinje cells, which are large, **inhibitory** neurons with extensive dendritic trees. Purkinje cells **receive inputs from parallel fibers** and provide the main **output of the cerebellar cortex.**

Answer 178

Contains granule cells, the most numerous neurons in the cerebellum. Granule cells send parallel fibers through the molecular layer, providing **excitatory** input to Purkinje cells.

Answer 179

The cerebellum receives information about intended movements from the cerebral cortex and actual movements from sensory systems. It compares these signals, detects errors, and sends corrective signals to the motor centers to refine motor output. ## Footnote *LOB: Outline the basics of the physiological function of the cerebellum and its effects on descending motor systems

Answer 180

Motor Learning: fine tuning Coordination and timing of muscle contractions: smooth execution Coordination and Timing: precise timing and coordination of muscle contractions, Balance and Posture: integration of vestibular input Influence on Descending Motor Pathways ## Footnote *LOB: Outline the basics of the physiological function of the cerebellum and its effects on descending motor systems

Answer 181

Above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves

Answer 182

Pyramidal weakness (extensors of ULs and flexors of lower limbs) Slow or uncoordinated active movement Fatigability Spasticity Clonus Positive Babinski Extensor or flexor spasms Mass reflex Dysynergic patterns of co-contraction during movement Associated reactions and other dysynergic stereotypical spastic dystonias

Answer 183

“ a motor disorder characterized by a velocity dependent increase in the tonic stretch reflex (muscle tone) with exaggerated tendon jerks, resulting from hyper excitability of the stretch reflex, as one component of the upper motor neurone syndrome” (Lance 1980) | MUST KNOW LANCE 1980

Answer 184

“Spasticity is a disordered sensori-motor control, resulting from an upper motor neurone lesion, presenting as intermittent or sustained involuntary activation of muscles” (Pandyan 2005) Implies that spasticity can now be used to describe the entire range of signs and symptoms that are collectively described as the positive features of the UMN syndrome Narrows it sufficiently to exclude the negative features.

Answer 185

Restricts normal movement Excessive/inappropriate movement Pain Interferes with function: active or passive Tissue damage Soft tissue/joint changes

Answer 186

Remove noxious stimuli Physical therapy Oral medication Focal intervention Inteathecal intervention Orthopaedic surgery Neurosurgery

Answer 187

Baclofen Tizanidine Dantrolene Diazepam Clonazepam Gabapentin Oromucosal CBD/THC

Answer 188

Botulinum Toxin Local anaesthetic Phenol

Answer 189

Baclofen Phenol Into spine- subarachnoid space. WHY? ITBaclofen : higher CSF concentrations (up50 times) with lower baclofen dose (up100 times)

Answer 190

BTX-A cleaves off the protein that is attached to the cell membrane (SNAP25) and therefore prevents the vesicle from binding with it thus preventing the release of acetylcholine into the synapse.

Answer 191

A neurolytic chemical that causes coagulation of nervous tissue and denaturing of proteins, which leads to cell damage, axonal degenration and indiscriminate destruction of motor and sensory nerves when injected intrathecally. When injected with glycerol, with careful position of the patient you can target just motor nerve roots Degree of damage and duration of effect may vary with some patients needing repeat injections.

Answer 192

a condition in which pupils respond differently to light stimuli shone in one eye at a time due to unilateral or asymmetrical disease of the retina or optic nerve

Answer 193

Painful eye movement Colour vision impaired Optic discs looks pale at presentation Most common cause is demyelination (inflammatory) Monocular vision loss. | Optic neuritis occurs when swelling damages the optic nerve

Answer 194

Inflammation of the disc

Answer 195

* MRI brain and orbits with contrast (+/- cord if any other history) * Overall risk of developing Multiple Sclerosis is 50% * 25% if no lesions on MRI * 72% if 1+ lesions present on MRI * Treatment is with 5 days high dose corticosteroids

Answer 196

Same swelling at the disc No high pressure symptoms

Answer 197

Vascular: ischaemic, haemmorhagic "hit back of head" common phrase for subarachnoid haemmorhage MUST EXCLUDE

Answer 198

Occulomotor Trochlear Abducens Cranial nerve 6: LO6- no elevation. (they lead to eye movement- if misaligned they cause double vision) Midbrain or Pons error Length of cranial nerves Neuromuscular junction (myesthenia gravis) Muscle disease

Answer 199

drooping eyelid on right hand side

Answer 200

Nausea Sore Neck

Answer 201

Cranial nerve III (oculomotor nerve) supplies: - Levator palpebrae superioris (motor fibres) - Superior rectus, medial rectus, inferior rectus and inferior oblique (motor fibres) - Constrictor pupillae (parasympathetic fibres) **Cranial nerve III (oculomotor nerve) palsy results in:** - Inability to lift the eyelid - Unopposed action of lateral rectus and superior oblique muscles - Unopposed action of sympathetic pupillary fibres

Answer 202

With pain must ?bleeding

Answer 203

difficulty moving the right eye in any direction | Can not relate it to one specific CN

Answer 204

Opthalmic veins drain into the cavernous sinus.

Answer 205

Opthalmic veins drain into the cavernous sinus.

Answer 206

The forehead is supplied by both sides of the brain so stroke occuring in the brain can be overcome by the additional supply

Answer 207

Bell's palsy is an** unexplained episode of facial muscle weakness or paralysis **that usually resolves on its own and causes no complications. Affects full length of the nerve, therefore, dry eyes, change in taste sensation, hyperacusis * Not normally painful, but may be preceded by strange sensation in face * Idiopathic Management – 50-60mg prednisolone for 5-10days Complications – Corneal ulceration, dry eyes, ectropion, crocodile tears, synkinesis. Tape the eye to protect the cornea from abrasions. Prognosis – 25% recover completely, 70% recover almost completely The branches of the facial nerve can get mixed up: salivatory tears and motor can mix up. Feels "strange sensation"

Answer 208

**Severe ear pain** * Vesicular rash in EAM or pinna * Taste dysfunction * Hyperacusis **Investigations**: * Viral PCR (VZV) * Swabs of vesicular rash * HIV test **Management**: * Aciclovir * Analgesia

Answer 209

Also known as: * Vestibular schwannoma- shwann of 8th affected pressing on 7th and cerebellar later Benign tumour 7% of patients with acoustic neuroma also have Neurofibromatosis Type 2. NF-2 is associated with bilateral acoustic neuromas NF-2 has autosomal dominant inheritance.

Answer 210

Typical features of MND in general: * No sensory involvement * Wasting and fasciculations * Brisk reflexes with upgoing plantars * “Anterior horn cell disease” * Progressive signs and symptoms – degenerative * Treatment with Riluzole Amyotrophic lateral sclerosis (ALS) o Mixed UMN and LMN signs Progressive bulbar palsy (PBP) o UMN and LMN bulbar dysfunction o If dysfunction spreads to affect other areas, then referred to as bulbar-onset ALS Primary lateral sclerosis (PLS) o Predominantly UMN signs o Longer survival than ALS Progressive muscular atrophy (PMA) o Predominantly LMN signs o Longer survival than ALS

Answer 211

9-12 Speech Swallowing error lower motor neuron lesion either at nuclear or fascicular level in the medulla or from bilateral lesions of the lower cranial nerves outside the brain-stem.

Answer 212

2. Voltage gated calcium channels open 3. ↑[Ca2+]i initiates vesicle fusion with the presynaptic membrane

Answer 213

How neurotransmitters enter the vesicles | Have an appreciation nothing more at this stage

Answer 214

Ligand-gated ion channels FAST synaptic transmission

Answer 215

GPCRs - G-protein coupled receptors (mostly) SLOW signal modulation

Answer 216

Synthesis: Derived from dietary amino acids. Release: Exocytosis from vesicles in presynaptic terminals. Receptor Binding: Acts on ionotropic receptors. Receptors abundant in cortex, basal ganglia, sensory pathways Termination: Reuptake and enzymatic degradation. **Function: Excitatory (glutamate) or inhibitory (GABA).**

Answer 217

* Glu from either glucose (Krebs cycle) or glutamine. * Glutamine is synthesised in astrocytes (glial cells). * EAAT = excitatory amino acid transporter. * GLnT = glutamine transporter, * VGlut = vesicular glutamate transporter. Instead of being recaptured directly by neurons, most of the glutamate released during synaptic activity is diverted to astrocytes via high-affinity excitatory amino acid transporters (EAATs), converted to glutamine, and then shuttled back by the concerted work of multiple glutamine transporters

Answer 218

Ionotropic and metabotropic

Answer 219

Glutamate excitotoxicity: epilepsy Stroke Depression

Answer 220

NMDA, AMPA & Kainate (ionotropic) Metabotropic (G-protein coupled/ modulatory)

Answer 221

Glutamate receptor (pre- and post synaptic) Role in synaptic plasticity (hippocampus) Role in memory, stroke

Answer 222

γ-aminobutyric acid inhibitory amino acid neurotransmitter Mostly via inhibitory interneurons Highest density in nigrostriatal (dopaminergic) system Synthesised from Glutamate

Answer 223

**BOTH** GABAA receptors presynaptically have slow inhibitory effects therefore GABA fast & slow transmission GABAB receptors inhibit voltage-gated calcium channels and opens K+ channels therefore reducing post synaptic excitability

Answer 224

## Footnote Picrotoxin is a non-competitive antagonist and only used in research.

Answer 225

**GABA A** Structure: The GABA A receptor is a pentameric ligand-gated ion channel, meaning it consists of five subunits arranged around a central pore. Mechanism: It is a ligand-gated ion channel, responding to the binding of the neurotransmitter gamma-aminobutyric acid (GABA). **GABA B** Structure: The GABA B receptor is a dimer, meaning it consists of two subunits. Mechanism: It is G-protein coupled, meaning it activates intracellular signaling pathways through G-proteins.

Answer 226

**Baclofen** activation results in the inhibition of the release of various neurotransmitters, including glutamate, opioids, and even GABA itself. Antispastic Effect Baclofen may have implications for drug addiction. **Gamma-Hydroxybutyrate (GHB): **is a partial agonist of GABA B receptors. Mechanism: GHB shares some similarities with GABA and can partially activate GABA B receptors.

Answer 227

anxiety disorders, epilepsy, schizophrenia and insomnia

Answer 228

Synthesis: Derived from tyrosine. Release: Exocytosis from noradrenergic nerve terminals. Receptor Binding: Acts on adrenergic receptors. GPCR Termination: Reuptake and enzymatic degradation. Function: Involved in the "fight or flight" response.

Answer 229

Tyrosine Tyrosine hydroxlyase

Answer 230

Synthesis: Derived from tyrosine. Release: Exocytosis from dopaminergic nerve terminals. Receptor Binding: Acts on dopaminergic receptors. Termination: Reuptake and enzymatic degradation. Function: Involved in reward, motivation, and motor control

Answer 231

The α2 adrenergic receptor is found both on the post synaptic and presynaptic terminal. It is important in regulation Too much NA? It can bind to the presynaptic which then inhibits NA release. Excess NA? Reuptaken via NA transporter then broken down by MAO monoamineoxidase

Answer 232

Low NA? Need to increase levels in synaptic media **Cocaine** blocks NA re-uptake so more NA circulate in synapse **Block MAO** so no breakdown **Amphetamine** enters vesicles displacing NA into cytoplasm, increase NA leakage out of neuron

Answer 233

Synthesis: Derived from tyrosine. L-DOPA and Dopa decarboxylase Release: Exocytosis from dopaminergic nerve terminals. Receptor Binding: Acts on dopaminergic receptors. Termination: Reuptake and enzymatic degradation. Function: Involved in reward, motivation, and motor control

Answer 234

**Substantia nigra projects to the striatum**: for control / initiation of voluntary movement **mesocorticolimbic from dopamine neurone to hippocampus and amygdala**: rewards and emotion

Answer 235

Heroin, Cocaine etc upregulate the mesocorticolimbic pathway Addition results

Answer 236

Nicotinic (ionotropic / fast) Muscarinic (G-protein coupled / slow) M1 excitatory ( M1 receptors in dementia) M2 presynaptic inhibition (inhibit Ach release) M3 excitatory glandular/smooth muscle effects (side effects) M4 and M5 function not well known

Answer 237

Synthesis: Produced in the cell body and processed in the Golgi apparatus. Release: Often co-released with other neurotransmitters. Receptor Binding: Acts on specific peptide receptors. Termination: Diffusion and enzymatic degradation. Function: Modulate pain perception, mood, and other complex behaviors. ## Footnote Examples include substance P, enkephalins, and oxytocin.

Answer 238

Arousal Epilepsy (mutations of nAChR genes) Learning and memory (KO mice) Motor control (M receptors inhibit DA), pain, addiction Involved in schizophrenia, ADHD, depression, anxiety, Alzheimers

Answer 239

basal forebrain complex / septohippocampal pathway and nucleus basalis cognitive function / Alzheimer’s disease and motor control septum to hypothalamus

Answer 240

The D2 dopamine receptor is found both on the post synaptic and presynaptic terminal. It is important in regulation Broken down by MAO B

Answer 241

D1 and D2 receptors in striatum, limbic system, thalamus & hypothalamus D3 receptors in limbic system NOT striatum D4 receptors in cortex & limbic system Targetting specific receptors can aleviate specific symptoms. Target D3 for mood and addiction Target D1 for parkinsons

Answer 242

Substantia nigra to basal ganglia (Parkinson’s disease)

Answer 243

Midbrain to limbic cortex

Answer 244

Synthesis: Derived from tryptophan and tryptophan hydroxylase. Release: Exocytosis from serotonergic nerve terminals. Receptor Binding: Acts on serotonin receptors. Termination: Reuptake and enzymatic degradation. Function: Regulates mood, appetite, and sleep.

Answer 245

5HT receptors are found pre-synaptic. Too much serotonin binds here and promotes reuptake and less release. serotonin is also broken down by MAO

Answer 246

**5-HT receptors (14 subtypes)all G-protein coupled except 5-HT3** 5-HT1 **inhibitory**, limbic system – mood, migraine 5-HT2 (5-HT2A), excitatory, limbic system & cortex 5-HT3 **excitatory**, medulla – vomiting 5-HT4 presynaptic facilitation (ACh) – cognitive enhancement 5-HT6 and 5-HT7 – novel targets, cognition, sleep

Answer 247

usually take the neurotransmitter back up into the pre-synaptic terminal

Answer 248

Autoreceptors:inhibit cell firing and transmitter release at the terminal regions

Answer 249

Synthesis: Synthesized from choline and acetyl coenzyme A. Release: Exocytosis from cholinergic nerve terminals. Receptor Binding: Acts on cholinergic receptors (nicotinic and muscarinic). Termination: Broken down by acetylcholinesterase. Function: Involved in muscle contraction, memory, and attention.

Answer 250

Synthesis: Produced in the cell body and processed in the Golgi apparatus. Release: Often co-released with other neurotransmitters. Receptor Binding: Acts on specific peptide receptors. Termination: Diffusion and enzymatic degradation. Function: Modulate pain perception, mood, and other complex behaviors.

Answer 251

Noradrenergic Serotonergic Dopaminergic Cholinergic

Answer 252

**Noradrenergic** Locus Coeruleus **Serotonergic** Raphe Nuclei **Dopaminergic** Substantia Nigra and Ventral tegmental Area **Cholinergic** Basal Forebrain and Brain Stem Complexes

Answer 253

Small set of neurons at core Arise from brain stem One neuron influences many others Synapses release transmitter molecules into extracellular fluid

Answer 254

Remember Raphe means Seam so S for serotonin.

Answer 255

Literally diffuses and activates different areas More of a widespread affect Have a "modulatory" action

Answer 256

Dopamine Serotonin Noradrenaline

Answer 257

Histamine H1 (arousal) and H3 (presynaptic / constitutively active) Functions: sleep / wake, vomiting Purines Adenosine (A1, A2A/2B) and ATP (P2X) Functions: sleep, pain, neuroprotection, addiction, seizures, ischaemia, anticonvulsant Neuropeptides Opioid peptides , ,  Functions: pain

Answer 258

Neuropeptide Synthesis: Transcription Translation Post-translational Modification Packaging and Transport Release Challenges in Neuropeptide Synthesis: Complexity of Processing Post-translational Modifications Cell-Specific Synthesis Low Abundance Vesicle Packaging Regulation and Function

Answer 259

Lipid mediators -Products of conversion of eicosanoids to endocanabinoids -act on CB1 (inhibit GABA, glutamate release) - involved in vomiting (CB1 agonist block it, MS, pain, anxiety, weight loss/rimonabant CB1 antogonist)

Answer 260

Control the pituitary

Answer 261

**Primary** No underlying structural abnormality Theoretically a genetic condition Not a medical emergency in most cases **Secondary** A structural cause Medical emergencies in most cases ?Back of head ?Subarachnoid worst case

Answer 262

**Primary** No underlying structural abnormality Theoretically a genetic condition Either polygenetic like **migraines** Change in the chemical activity in the pain centres of the brain Involved nerves and blood vessel changes in some cases, as well as external factors like muscles of face and skull

Answer 263

There is some structural or biochemical abnormality MRI scan not always the answer Can be due to changes in pressure within brain (high or low) Systemic diseases e.g. giant cell arteritis in >55 years of age Vascular e.g. bleeds, subarachnoids Lesions: tumour, although often the headache is due to pressure

Answer 264

Profuse vomiting Fever Low conscious levels Confusion or speech abnormalities Neurological symptoms e.g. weakness, speech disturbance Pressure dependent features (worse on lying down, coughing, straining)

Answer 265

Previously GP advice to CT for reassurance but reassurance only lasts approx 3 years so not good cost: benefit SYMPTOMS: * Focal neurological symptoms or abnormal neurological exam * New onset headache in anyone known to have a malignancy or HIV positive * Headache with low GCS or new seizure * Thunderclap headache (think SAH) * Headache which starts after standing and goes on lying down (low pressure) * Significant head injury * Headache with aura lasting >2 hours * New onset headache with aura * New onset cluster headaches *

Answer 266

The commonest cause of headaches 19th most disabling condition in the world Headache starts of one sided or frontal or back of head Builds up over half an hour Throbbing and pressing in nature Recurring disabling attacks lasting 4-72 hours Association with nausea and/or photophobia and phonophobia (at least one of these) With or without aura (usually visual patterns or spots of blurred vision)

Answer 267

**Primary** * *Migraines (with or without aura)* * *Cluster headaches* * *Stabbing/ice pick headaches* * Thunderclap headaches * Coital headaches * Cough headaches **Secondary** * Analgesia overuse headache * Subarachnoid haemorrhage * Meningitis * Tumour * Raised intracranial pressure * Low intracranial pressure | Red flags in italics

Answer 268

Pre-empt treatment: manage triggers (sleep, hydration, food) Acute treatment: pain management asap Prevent chronic migraines: decrease number of migraine days/severity Sleep routine (sleep and wake similar times in day) Food-eat regularly and try not to skip meals Hydration Manage stress levels/meditation Exercise regularly (not necessarily vigorously!) Best evidence: Triptans (sumatriptan 50mg oral, 6mg s/c; zolmitriptan 2.5mg oral etc) Aspirin 900mg stat dose or ibuprofen 600-800mg stat dose Naproxen 500mg Prochlorperazine IV Opiates e.g. codeine 30-60mg stat dose (not for regular use) Sodium valproate intravenous in refractory cases (hardly used) Corticosteroid e.g. prednisolone 60mg as last resort | Red flags in italics

Answer 269

Second most common primary headache syndrome (suicidal headache) Severe unilateral headache usually around the eye with autonomic features Eye watering/red/swelling Facial sweating/redness/swelling Nasal dripping Smaller pupil of affected eye Lasts 15-30 minutes; 1-8 times a day Usually at night after a couple of hours of sleeping Always on the same side during that cluster Patient is restless, unable to sit or sleep, agitated, feels like banging his head

Answer 270

Headache cause both **anxiety** and chronic headache causes **depression** Often patients are not taken seriously and are not managed well by those who first see them By the time they see a specialist, they are at the final hope stage as they feel not listened to Many people are told to have **CBT** and mental health treatment** rather than headache treatment** Both need to happen together to make an impact outcome

Answer 271

Nausea Vomiting Loss of Apetite Postural Hypotension Insomnia, Vivid Dreams, inverted sleep-wake cycle Confusion hallucination, delusions

Answer 272

Dopamine precursor- LDopa Dopamine Agonist COMT inhibitor MAOb inhibitor Anticholinergic

Answer 273

* Levodopa (L-dopa)/does not cure disease/prolongs the quality of life * Immediate precursor of dopamine, first line treatment if motor symptoms impact on quality of life * Undergoes significant peripheral metabolism * Combined with peripheral decarboxylase inhibitor (carbidopa, benserazide) decr dose needed, decr side effects * Decarboxylation * Dopa decarboxylase not rate limiting, perhaps conversion in remaining DAergic neurons * Conversion in NAergic or serotonergic neurons (Dopa decarboxylase nonspecific) * -First line of treatment if quality of life is impaired

Answer 274

Stimulate the reward system too D2 receptors Hypersexuality Gambling Addiction ***Impulse Control disorder*** 3.5 - 13.6% of Dopamine agonist treated PD patients

Answer 275

Psychotic like effects ?Schizophrenia symptoms Hallucinations, behavioural changes DA release (amphetamine) produces ‘schizophrenia’ (Carlsson 2000) **D2** agonists produce stereotyped behaviour (not D1)

Answer 276

CTZ- chemoreceptor trigger zone vomitting center, medulla outside BBB packed with D2 LDopa will stimulate CTZ

Answer 277

Incr akinesia (inability to initiate movement)/natural progression Dyskinesias (involuntary writhing movements) Psychiatric symptoms, dementia, visual hallucination, confusion

Answer 278

Movements depend on amount of LDopa, loss of a lot of neurones in later stages Uptake into brain depends on many factors, so drug usage is varying, Rapid oscillations in mobility (‘on-off’ effect), fluctuating plasma levels (LDopa acts even without DA neurons) Duration of dose action decr’d (‘end of dose’ deterioration)-narrow therapeutic window ## Footnote Therapeutic window narrows over time.

Answer 279

Usually used ad hoc to L-Dopa further into PD progression L-dopa sparing effects, may delay development of ‘on-off’ effects Only 50% of patients respond to DA agonists alone Side effects: nausea, vomiting, psychiatric symptoms Ergot derivatives – fibrotic changes leading to valvular heart disease Newer DA agonists (ropinirole, pramipexole), longer duration of action – lower tendency for dyskinesia Side effects include confusion, delusions, sleep disturbances, predispose to compulsive behaviours (excessive gambling, over eating, sexual excess/reward) Pramipexole – antioxidant effects & protective effect on mitochondria

Answer 280

Not as effective as L Dopa Inc DA release, Dec amine uptake, direct DA agonist, anti-muscarinic Less effective than levodopa Effectiveness reduces over time ***Side effects less severe***

Answer 281

Selegiline – selective MAOB inhibitor (no peripheral effect vs non selective (cheese effect MAOa inhibitors) Decr DA metabolism, used as adjunct to levodopa Protect against MPTP toxicity – no evidence of neuroprotective role in patients Low risk of hallucinations, fewer adverse effects Entacapone – COMT inhibitor Slows elimination of levodopa More adverse effects Low risk of hallucinations

Answer 282

***Doesnt delay neurodegeneration but helps with quality of life for a longer duration*** **MAOB inhibitor**, selegiline (no non selective MAO effects) Decreases metabolism of L-dopa in brain and potentiates effect Protect against MPTP toxicity – no evidence of neuroprotective role in patients **Catechol-O-methyl transferase (COMT) inhibitor**, entacapone Slows elimination of L-dopa, incre t½ & augments action Dopamine agonists (bromocriptine) (after 5 year LDOPA)

Answer 283

Not used a lot, useful in early stages in young people to decr tremor, rigidity Not to be used on old people (memory problems, confusion) Corrects overactivity of central cholinergic neurons from reduced inhibitory DA activity Reduces sialorrhoea Associated with troublesome side effects (dry mouth, impaired vision, urinary retention)

Answer 284

**Basal Ganglia** Muscle rigidity, stiffness Tremor at rest Hypokinesia, bradykinesia motor activity difficult to initiate & stop

Answer 285

Parkinson’s disease (progressive neurodegenerative) **hypokinesia** Loss of DAergic neurons in nigrostriatal tract Huntington’s disease **Hyperkinesia** (jerky involuntary movement, dementia) Loss of GABAergic neurons in striatum

Answer 286

Loss of DAergic inhibition of GABAergic cells **Increased** activity of GABAergic neurons in globus pallidus **Decreased** activation of cortical areas (difficulty initiating movements)

Answer 287

Complex disturbances of other transmitter systems ACh, NA, 5-HT and GABA Cholinergic interneurons in striatum strongly inhibited by DA Hyperactivity of cholinregic neurons linked to PD symptoms (tremor, bradykinesia) DA/Ach imbalance

Answer 288

"Consider deep brain stimulation for people with advanced Parkinson's disease whose symptoms are not adequately controlled by best medical therapy. " Surgical approaches Implantation of electrodes – deep brain stimulation Implantation of foetal nigral tissue into striatum Synaptic connections formed but limited clinical benefit so far Side effects - severe dyskinesias

Answer 289

**EARLY** Dopamine Agonists – mild effect Ropinorole Pramipexole Rotigotine Cabergoline MAOB-Inhibitors – mild effect Selegiline Rasagiline Levo-dopa – moderate to good effect Co-careldopa Co-beneldopa (usually the first line of treatment if quality of life impaired) No treatment **ADVANCED** Addition (prolongs quality of life) Dopamine agonists (adverse effects, hallucination) MAOB-inhibitors (less adverse effects) COMT inhibitors (adverse effects) Apomorphine (non selective dopamine agonist) injection or sub cutaneous infusion Levodopa gel infusion (jejunal) Deep brain stimulation (DBS) – STN/GPi

Answer 290

***Not all patients have the triad*** **BRADYKINESIA** (or akinesia or hypokinesia) (needs decrement- loss of speed and amplitude of movement) +/- Rigidity +/- Tremor +/- Postural & gait disturbance

Answer 291

Cardinal motor signs (triad) Axial Motor Non-Motor Neuropsychiatric and Emotional

Answer 292

Hypomimia (facial expression)(mask) Hypophonia (soft voice) Short steps, shuffling gait Micrographia

Answer 293

Act out your dreams Kicking, flailing Early feature

Answer 294

The first essential criterion is **parkinsonism**: **Bradykinesia** in combination with at least 1 of rest **tremor** or **rigidity** Then supporting criteria, red flag and exclusion criteria.

Answer 295

* **suggesting atypical or Ddx** * symetrical onset * Early cognitive impariment or behavioural change **(DLB)** * Easly autonomic distrbance **(MSA)** * Easly falls and postural instability **(PSP)** * Bulbar signs - dysarthria, dysphagia * Cerebellar signs * Presence of toher movemnt disorders * Sudden onset or rapid stepwise profression * Lack of response to levodopa

Answer 296

neurofibrillary tangles within neurones (not all neurones) extra-cellular senile plaques- insoluble protein neruonal depletion in cerenral cortex and hippocampus ATROPHY | silver stains

Answer 297

**Plaques** β amyloid peptides. Insoluble, aggregates **Tangles** Tau protein Small structural protein in all neurones, keeps axons in shape, crinkles | single cell transcriptomics will tell us more.

Answer 298

Amyloid (Pet), Tau (CSF), Neuronal Atrophy (scan) But removing Amyloid or Tau doesnt cure Alzheimers.

Answer 299

Amyloid Precursor Protein (APP) on C/s 21 Presenilin-1 and 2 When cleaved incorrectly will release Amyloid beta peptides. Rare, inherited 30-70yo symptomatic. Down's syndrome has additional C/s21= ?similar symptoms

Answer 300

Over 65 y 40% >80yo ApoE (C/s 19) lipid transport APOE E2 E3 E4 E4 increases risk 8 fold BUT E4 not a deterministic gene.

Answer 301

Cognitive decline Severe, progressive but healthy adults Memory Loss Brain atrophy (mainly cortical grey matter and hippocampus) **Phrases**: Alzheimers Type pathology AND/OR Alzheimers Type Syndrome

Answer 302

Sometimes A β peptides can dimerise and form oligemers They cannot be dissolved Form β sheet (like prions) Form plaques Plaques contain metals (natural) If APP is cleaved by β secretase rather than α then Aβ more likely to form Pre-senilins are co-factors for γ-secretase (cleaves to Aβ)

Answer 303

PIB Scans Molecule that can bind to Aβ

Answer 304

Hyper-phosphorylated tau protein (normally phosphorylated but not to this extent) Tau dilaments are inside neurone axons in cerebral cortex This causes it to fold and crinkle It cannot do its role.

Answer 305

Aβ can accumulate around microvessels when cleaved- the waste products are transported to be removed. From the plaques to the blood vessel wall Can accumulate. Amyloid clearing drugs can cause this Haemmorhagic side effects

Answer 306

**abnormal aggregation or hyperphosphorylation of tau protein**

Answer 307

Often in people with Parkinson’s Disease, overlaps with PDD Neuropathology. **Lewy bodies (arrows) Contain α-synuclein**, encoded by SNCA Often co-morbid with AD: A-beta, CAA Not all neurones Mainly substantia nigra- parkinsons

Answer 308

Heterogenous clinical syndrome characterized by frontotemporal lobar degeneration. Abnormal protein deposits: MAPT (tau), TDP43, C0orf72 (mRNA), FUS Subtypes: ***FTLD-tau,*** FTLD-TDP, FTLD-FET **Tau forms Pick bodies** Did not find excessive amyloid Can affect up to whole cerebral cortex by the same mechanisms.

Answer 309

Not very common as a single primary disease But vascular pathology often VERY present in AD Concentric fibrous thickening Not atheroma Not cerebral amyloid angiopathy

Answer 310

G1i) A decline in memory (both verbal and non verbal). Most evident in the learning of new information. G1ii) Decline in other cognitive abilities. ‘planning and organizing and in general processing of information. - Decline objectively verified by informant and quantified cognitive assessments - Can be quantified as mild, moderate or severe G2) Awareness of environment is preserved (i.e. not delirium) G3) Decline in emotional control or a change in social behaviour (lability, irritability, motivation, apathy) G4) Symptoms present for > 6 months | Cannot diagnose in an acute confusion state.

Answer 311

* Depression (‘depressive pseudodementia’) * Intracranial space-occupying lesions (e.g. tumour; subdural haematoma) * Temporal lobe seizures (‘transient epileptic amnesia’) * Normal ageing (‘benign senescent forgetfulness’)

Answer 312

* Depression (‘depressive pseudodementia’) * Intracranial space-occupying lesions (e.g. tumour; subdural haematoma) * Temporal lobe seizures (‘transient epileptic amnesia’) * Normal ageing (‘benign senescent forgetfulness’)

Answer 313

* Alzheimer’s disease (AD).* (50-60%) * Vascular dementia. * (10-15%). * Dementia with Lewy bodies. * (15-20%). * Frontotemporal * (4-6%) – but 20% <65

Answer 314

HISTORY * Some awareness of failing memory * Concentration and general knowledge ok Family * 2-3 years decline, repetitive * Preserved language and practical skills, some problems managing accounts Physical: not to note ACE-III * Some impairment on attention * Impaired memory (normal registration but very poor delayed recall) * Mild impairment on naming * Language and visuospatial reasonably intact

Answer 315

* Depression & Anxiety * Psychosis and Hallucinations (Secondary) * "Absolutely certain they left the purse on the table and therefore an intruder has come in" * Agitation, wandering, aggression, anxiety, shouting out, day-night reversal (What is driving these symptoms?) * Personality change * Disimhibition and apathy

Answer 316

* Increasing Age * Vascular risk factors (HT, AF, smoking) * Family history * ApoE4 * Hypothyroidism * Head Trauma * Lower education (lesser cognitive reserve ie) constant exams)

Answer 317

Cholinesterase Inhibitors -Donepezil tablet --*Common side effects include nausea, trouble sleeping, aggression, diarrhea, feeling tired, and muscle cramps.* -Rivastimine patch/tablet NMDA receptor Antagonist -memantine Other Symptom Management

Answer 318

IgG1 monoclonal Ab that binds with high affinity to Aβ soluble protofibrils NOT A CURE Both groups had worsening symptoms The drug DOES reduce plaques but not in a large cohort 6 strokes in the lexanemab-treated group Infrastructure to prescribe is not accessible

Answer 319

PDD diagnosed if parkinsonian symptoms have existed for at least 12 months prior to dementia. DLB if both motor and cognitive symptoms develop within 12 months, or cognitive prior to motor. Which one comes first? **TRIAD** Visual Hallucinations- LBD and Delirium Parkinsonism Fluctuating cognitive performance.

Answer 320

Cholinesterase Inhibitors Rivastigmine – patch or BD tablets NMDA receptor antagonist Memantine Avoid antipsychotics Quetiapine Clozapine Need to be careful between options. If remove dopamine not good but need to treat visual hallucinations

Answer 321

* 2 Language Subtypes * -semantic * -progressive non-fluent aphasia, * Behavioural variants, * Alteration in personality and social conduct * Disinhibition or apathy, related to serotonin levels? * Perseveration. Utilisation behaviour. * Poor function on verbal fluency, trail making tests, cog estimates, proverbs * Frontal Lobe Battery *

Answer 322

The cause of the disorder is **thiamine (vitamin B1) deficiency.** This can occur due to Wernicke **encephalopathy**, eating disorders, malnutrition, and alcohol abuse. WE is characterized by the presence of a triad of symptoms: **Ocular disturbances (ophthalmoplegia) Changes in mental state (confusion) Unsteady stance and gait (ataxia**) A study on Wernicke-Korsakoff syndrome showed that with consistent thiamine treatment there were noticeable improvements in mental status after only 2–3 weeks of therap

Answer 323

Psychiatrist assessment, diagnosis, overall management strategy, medical management, complex decisions. CPN monitor mental state and risks. Support/educate patient and carers. O.T. assess home environment, living skills (i.e safety in kitchen), provide aids/adaptations. Psychologist psychometry, analysis of challenging behaviour. Social work assess for MOW, day care, home carers, permanent care (i.e nursing home). In-patient care.

Answer 324

ABC charts: Before the defined behaviour (antecedent) During the defined behaviour (behaviour) After the behaviour had taken place (consequence)

Answer 325

Examples: Donepezil, Rivastigmine, Galantamine Mechanism of Action: In Alzheimer's disease, there is a **deficiency of acetylcholine**, a neurotransmitter involved in memory and learning. Cholinesterase inhibitors block the activity of **acetylcholinesterase**, an enzyme that breaks down acetylcholine. By inhibiting acetylcholinesterase, these drugs **increase the levels of acetylcholine** in the brain, which may temporarily improve cognitive function and slow down the progression of symptoms.

Answer 326

Example: Memantine Mechanism of Action: Glutamate is an excitatory neurotransmitter that plays a role in learning and memory. In Alzheimer's disease, **excessive stimulation of N-methyl-D-aspartate (NMDA) receptors by glutamate can lead to neuronal damage.** Memantine is an NMDA receptor antagonist that **modulates glutamate** activity by blocking excessive activation, helping to protect neurons from **excitotoxicity**.

Answer 327

Example: Aducanumab Mechanism of Action: Aducanumab is a monoclonal antibody designed to **target and clear beta-amyloid plaques**, which are characteristic pathological features in Alzheimer's disease. By binding to beta-amyloid, aducanumab aims to facilitate the removal of these plaques from the brain, potentially slowing down the progression of the disease. Not very successful

Answer 328

dependence refers to physical reliance on a substance Dependence is characterized by the symptoms of tolerance and withdrawal. emergence of physical and emotional withdrawal symptoms Not always addiction

Answer 329

If you develop a tolerance to a substance, it becomes less effective for you

Answer 330

* A chronic relapsing disorder characterised by: * Compulsion to seek and take the drug * Loss of control in limiting intake * Emergence of a negative emotional state (dysphoria, anxiety, irritability) ## Footnote DSM-V: A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by two (or more) of the following occurring with a 12 month period

Answer 331

* Acute reinforcement (social) * Escalating/ compulsive use * Dependence Resolving addiction (Relapse occurs here) * Withdrawal * Protracted Withdrawal * Recovery In Heroin use: Biggest hurdle: Maintenance of drug-free state as 70% relapse

Answer 332

Occurs in circuits for * reward prediction and pleasure * Cognitive control * learning and memory * motivation drive

Answer 333

* Hippocampus (memory) * Amygdala (Emotion) * Extended Amygdala (stress/ negative reinforcement) * Mesolimbic (reward) (Dopiminergic pathways)

Answer 334

* Opioids - Agonist at mu (and delta and kappa) opioid receptors * Cocaine - Dopamine transporter blocker - indirect DA agonist * Amphetamine - Dopamine releaser - indirect DA agonist * Alcohol - Facilitates GABAA + inhibits NMDA receptor function * Nicotine - Agonist at nACh receptors * Cannabinoids - Agonist at CB1 receptors * Phencyclidine - NMDA receptor antagonist * Hallucinogens - 5-HT2A agonists

Answer 335

methylphenidate & MDMA Release cytosolic monoamines (DA) Amphetamine-like drugs are taken up into nerve terminals by neuronal uptake transporters and cause release of monoamines from nerve terminals. Release DA and NA but behavioural effects likely to be linked to DA.

Answer 336

* Pharmacological effects: * incr alertness and locomotor stimulation ( inc aggression) * Euphoria / excitement * Stereotyped behaviour * Anorexia * decr physical and mental fatigue (improves monotonous tasks) * Peripheral sympathomimetic actions ( incr blood pressure & decr gastric motility) * Confidence improves/lack of tiredness

Answer 337

Blocks catecholamine reuptake (incr DA, stimulant effect) *Pharmacokinetics*: HCl salt, inhaled and i.v. administration Nasal inhalation less intense, leads to necrosis of nasal mucosa Freebase form (‘crack’), smoked, as intense as i.v route

Answer 338

Pharmacological effects: Euphoria Locomotor stimulation Fewer stereotyped behaviours than amphetamine Heightened pleasure Lower tendency for delusions, hallucinations and paranoia

Answer 339

Opioids produce intense euphoria via acting on MOP (μ opiod receptor) Diamorphine (heroin) high abuse potential Tolerance Seen within 12 – 24 hours

Answer 340

* **Neuroplasticity:**Structural and functional changes in reward and self-control brain regions. * **Dysregulation of Reward** Pathways: Blunted response to natural rewards and enhanced craving for drugs. * **Learning and Memory Hijacking**: Drug cues become strongly associated with drug reward, driving craving and relapse. * **Stress Response Dysregulation**: Increased stress sensitivity and dysregulated stress hormone release. * **Impaired Inhibitory Contro**l: Dysfunction in decision-making areas leads to compulsive drug-seeking behavior. * **Development of Tolerance and Withdrawal**: Increased drug tolerance and withdrawal symptoms drive continued drug use. * **Altered Motivation and Hedonic Set Point:** Decreased responsiveness to natural rewards and increased drive for drug consumption

Answer 341

Opioids inhibit HPA axis in humans Cocaine activates HPA axis

Answer 342

Inhibition of MOP in ventral tegmental area Results in mesolimbic inhibition pathway being dampened Nucleus accubens is less activated Nucleus accumbens reward centre is activated "taking drug is rewarded" Locomotion, drug seeking, dis inhibition

Answer 343

Mechanism of action: Potentiates GABA-mediated inhibition Inhibits presynaptic Ca2+ entry through voltage-gated Ca2+ channels Inhibits transmitter release Disinhibits mesolimbic DAergic neurons (incr reward) Induces the release of endogenous opioid peptides Reward effect  by naltrexone (endogenous opioid involvement)

Answer 344

Pharmacological effects Slurred speech, motor in-coordination, incrd self confidence, euphoria Impaired cognitive and motor performance Higher levels linked to labile mood: euphoria and melancholy, aggression and submission

Answer 345

Pharmacological effects nACh receptors, α4β2 subtype Receptors, ligand-gated cation channels (pre- and post-synaptic) Enhance transmitter release and neuronal excitability icluding opioid peptides Cortex & hippocampus (cognitive function) and ventral tegmental area (DA release and reward) ιncr alertness, decre irritability (dependent on dose and situation)

Answer 346

Opioids inhibit HPA axis in humans Cocaine activates HPA axis

Answer 347

via desensitisation Think opiods working on receptors With repeated opioid exposure, the receptors become less responsive due to internalization of the receptors or other mechanisms that make them less available for binding the initial effects of the opioid diminish. To compensate, the brain may adapt by reducing the number of receptors available or by altering downstream signaling pathways reduced responsiveness need for higher doses to achieve the same effects. neuroplasticity, plays a role in opioid tolerance

Answer 348

* **Psychostimulants**: deep sleep, lethargy, depression, anxiety & hunger * **MDMA** (ecstacy):Depression, anxiety, irritability, incr aggression * **Heroin**: Sweating, gooseflesh (cold turkey), irritability, aggression * **Nicotine**: Irritability, hunger, weight gain, impaired cognitive and motor performance, craving (persisting many years) * **Alcohol**: Tremor, nausea, sweating, fever, hallucinations, Seizures, confusion, agitation, aggression

Answer 349

* Reward activation in nucleus accumbens, reinforces the use of opioids. * Prolonged exposure to opioids induces neuroadaptations to counteract the enhanced neurotransmitter release. * As the brain adapts to the regular presence of opioids, a state of dependence develops. * chronic presence of opioids alters the normal release of neurotransmitters. * **Withdrawal and NEGATIVE REINFORCEMENT * **

Answer 350

**Outer Segment:** Contains stacked membranous disks containing visual pigments. Visual pigments consist of opsins (proteins) bound to chromophores (retinal). **Inner Segment:** Houses the cell's organelles, including mitochondria for energy production. Connected to the outer segment by a cilium. **Cell Body:** Contains the nucleus and other cellular machinery. Integrates signals from the outer segment. **Synaptic Terminal:** End of the photoreceptor where neurotransmitters are released. Communicates with bipolar cells in the retina.

Answer 351

* Light passes all structure * Hits the Rods * UV converts Rhodopsin to Opsin and Retinol * Which activates G protein to create phosphodiesterase to breakdown cGMP * Breakdown of cGMP results in channels being closed. * Sodium Channels close, reducing sodium influx. * Rod becomes hyperpolarised less glutamate is released. * Glutamate cannot exit the Rod to effect the Bipolar cells. Glutamate has an inhibitory effect on Bipolar cells So the ON bipolar cell generates a potential And the OFF bipolar cell does not.

Answer 352

* Location: The RPE is situated in the posterior part of the eye, covering the outer surface of the neural retina. * Structure: It consists of a single layer of pigmented cells that are tightly packed together. * Pigmentation: RPE cells contain melanin, which gives them a dark color. This pigment absorbs excess light and helps protect the retina from phototoxicity.

Answer 353

* **Phagocytosis**: * RPE cells actively phagocytose and digest the membranous discs shed from the outer segments of photoreceptor cells. * This process is crucial for maintaining the health and function of photoreceptors. * **Visual Cycle**: * RPE is involved in the regeneration of visual pigments. * It converts all-trans-retinal back to 11-cis-retinal, allowing the recycling of the chromophore necessary for phototransduction. * **Nutrient Transport:** * RPE provides nutrients, including glucose and ions, to the photoreceptors. * It helps maintain the ionic balance essential for the proper functioning of photoreceptor cells. * **Barrier Function:** * RPE forms a barrier between the choroid (vascular layer) and the photoreceptors. * This barrier is critical for regulating the transport of substances between the blood supply and the retina. * **Maintenance of Blood-Retinal Barrier:** * RPE cells contribute to the blood-retinal barrier, preventing the entry of potentially harmful substances from the blood into the retina. * **Protection from Phototoxicity:** * RPE absorbs excess light and protects the retina from phototoxicity by converting it into heat. * Secretion of Growth Factors: * RPE secretes various growth factors that support the survival and maintenance of retinal cells.

Answer 354

**Age-Related Macular Degeneration (AMD):** AMD is a common condition where the RPE deteriorates over time. This can lead to a loss of central vision due to the degeneration of photoreceptors in the macula. **Retinitis Pigmentosa:** Inherited retinal disorder where mutations affect the function of photoreceptor cells and the RPE. RPE dysfunction can contribute to the degeneration of photoreceptors. **Diabetic Retinopathy:** Diabetes can lead to damage of the blood vessels in the retina and compromise RPE function. This can result in vision impairment and, in severe cases, blindness. **Choroidal Neovascularization:** Abnormal blood vessel growth from the choroid into the retina can disrupt the normal functioning of RPE cells. This is often associated with conditions like wet AMD. **Toxic Insults:** Exposure to certain toxins or drugs can damage RPE cells. This damage can interfere with the support RPE provides to photoreceptors. **Inflammatory Conditions:** Inflammatory diseases affecting the eye, such as uveitis, can lead to RPE dysfunction. Inflammation can compromise the barrier function of RPE. **Inherited Disorders:** Certain genetic disorders can result in abnormalities in RPE function. These may manifest as a part of broader conditions affecting the retina.

Answer 355

A visual receptive field refers to the specific region of the visual field to which a neuron, such as a retinal ganglion cell (RGC) or a neuron in higher visual processing areas, responds. In other words, it is the area in the visual space that, when stimulated, influences the activity of that particular neuron. **The term receptive field refers to the region of visual space where changes in luminance influence the activity of a single neuron.**

Answer 356

* **Location**: RGCs are found in the innermost layer of the retina, closest to the vitreous humor. * **Axons Form the Optic Nerve**: The axons of RGCs converge at the optic disc to form the optic nerve. The optic nerve carries visual information from the retina to the brain. * **Output Neurons**: RGCs are the primary output neurons of the retina. They integrate signals from photoreceptor cells (rods and cones) and bipolar cells and generate action potentials to transmit visual information. * **Receptive Fields**: RGCs have receptive fields, specific regions in the visual field to which they respond. The receptive fields have a center-surround organization, where light stimulation in the center can have different effects than stimulation in the surround. * **Visual Processing**: RGCs play a crucial role in the initial processing of visual information. They contribute to the formation of the retinotopic map, where neighboring cells in the retina project to neighboring locations in the visual cortex. * **Types of RGCs:** * **On-Center/Off-Surround: These RGCs are excited by light in the center of their receptive field and inhibited by light in the surround.** * **Off-Center/On-Surround: These RGCs are inhibited by light in the center and excited by light in the surround.** * * **Projection to the Brain:** The axons of RGCs project to several brain structures, with the majority converging at the lateral geniculate nucleus (LGN) in the thalamus. From there, visual information is further processed and sent to the visual cortex for higher-level interpretation. * **Role in Visual Perception**: RGCs are essential for the perception of visual stimuli, including the detection of edges, contrast, and motion. * **Selective Response**: Different types of RGCs have selective responses to various features of visual stimuli, such as color, intensity, and direction of motion.

Answer 357

* **Center-Surround Organization:** * RGCs exhibit a center-surround organization in their receptive fields. * The receptive field is divided into two regions – the central excitatory region and the surrounding inhibitory region. * * **Excitatory Center:** * Light falling on the central region of the receptive field (center) elicits an excitatory response. * Different RGCs may have receptive fields that respond best to light of a specific intensity, orientation, or location within their center region. * * **Inhibitory Surround:** * Light falling on the surrounding region (surround) elicits an inhibitory response. * The inhibitory surround is crucial for edge detection and contrast enhancement. * * **On-Center/Off-Surround and Off-Center/On-Surround Cells:** * RGCs can be classified into different types based on their response to light in the center and surround. * On-Center/Off-Surround cells are excited by light in the center and inhibited by light in the surround. Off-Center/On-Surround cells show the opposite response.

Answer 358

he inhibitory surround enhances the contrast sensitivity of RGCs. It helps in detecting edges and boundaries in the visual scene, as the response is stronger when there is a transition from light to dark or vice versa.

Answer 359

RGCs exhibit adaptation to prolonged exposure to uniform light levels. Continuous stimulation of the center or surround may lead to a reduction in the response, allowing the cells to adapt to different lighting conditions.

Answer 360

RGCs exhibit adaptation to prolonged exposure to uniform light levels. Continuous stimulation of the center or surround may lead to a reduction in the response, allowing the cells to adapt to different lighting conditions. *think about dimmable lights* Dimming the lights corresponds to reduced stimulation: When RGCs are exposed to lower levels of light, they adapt by becoming more sensitive to the dim environment. Restoring normal light represents adaptation: RGCs adapt to the new visual conditions, allowing them to respond optimally to the restored normal light level. Brightening the lights corresponds to increased stimulation: If there is a sudden increase in light intensity, RGCs initially respond strongly, but adaptation sets in, making them less sensitive to the heightened brightness

Answer 361

Parvocellular (P) Ganglion Cells: *colour to brain cortex* Magnocellular (M) Ganglion Cells: *motion and brightness to cortex* Koniocellular (K) Ganglion Cells: *colour vision ?bluelight* Direction-Selective Ganglion Cells: *respond to direction promote motion info* Orientation-Selective Ganglion Cells: *perception of object shapes and boundaries.* Brisk-Sustained *Brisk-Sustained cells respond continuously to a sustained stimulus changes in environmnet * and Brisk-Transient Ganglion Cells: *respond only to the onset or offset of a stimulus. * Changes in environment

Answer 362

**Parvocellular (P) Ganglion Cells:** Color information High spatial resolution: (small receptive fields), allowing for detailed analysis of the visual scene. **Magnocellular (M) Ganglion Cells:**I Motion information: sensitive to changes in luminance Low spatial resolution (larger receptive fields), providing a broader view **Koniocellular (K) Ganglion Cells:** Color information They have smaller cell bodies and are often considered an intermediate type between P and M cells. **Direction-Selective Ganglion Cells:** respond more strongly to motion in a specific direction. **Orientation-Selective Ganglion Cells:** sensitive to the orientation of lines or edges in the visual scene **Brisk-Sustained and Brisk-Transient Ganglion Cells:** **Sustained** : maintain their response over time, providing sustained information about stimuli. **Transient** : respond strongly to the onset or offset of a stimulus.

Answer 363

**Spatial Integration**: Neurons in higher visual areas integrate signals from multiple retinal ganglion cells, enhancing the overall perception of visual features. **Temporal Integration**: Higher-level cells can integrate information over time, allowing for the perception of dynamic visual scenes and changes in the environment. **Complex Feature Detection**: Neurons at higher levels can detect more complex features, such as shapes, objects, and textures, by combining the responses of multiple retinal ganglion cells. **Top-Down Processing:** Feedback from higher visual areas to lower levels modulates the processing of visual information, influencing the perception of specific features or patterns.

Answer 364

often referred to as the** dorsal and ventral pathway**s, respectively, are two major streams of information processing in the visual system,** originating from the primary visual cortex (V1) and extending to higher visual areas.**

Answer 365

* Also referred to as the "where" or "how" pathway. * Extends from the primary visual cortex (V1) to the parietal cortex. * Specialized for processing spatial location, motion perception, and the control of self-movement. * Involved in spatial awareness, directing attention, and guiding motor actions based on visual information ** Primary Visual Cortex (V1): Middle Temporal Area (MT or V5): Posterior Parietal Cortex:**

Answer 366

Also known as the "what" pathway. Extends from the primary visual cortex (V1) to the infero-temporal cortex. Specialized for object recognition, color perception, and the integration of visual details. Involved in identifying and recognizing objects, discriminating between visual features, and forming a holistic perception of scenes. **Primary Visual Cortex (V1): Inferior Temporal Cortex: Fusiform Face Area (FFA): Parahippocampal Place Area (PPA):**

Answer 367

Infero-Temporal (Ventral) Cortical Pathway: **Location**: The infero-temporal pathway extends from the primary visual cortex (V1) to the infero-temporal cortex. **Object Recognition:** Ventral Stream Function: Specialized for processing the identity and features of objects. Role in Object Recognition: Critical for identifying and recognizing objects, including their shape, color, and texture. **Color and Detail Perception:** Ventral Stream Function: Processes detailed visual information, including color and fine details. Role in Visual Discrimination: Contributes to discriminating between objects based on visual features. Perception of Faces: Ventral Stream Function: Particularly important for the perception of faces. Role in Face Recognition: Involved in recognizing and distinguishing faces. **Integration of Visual Information:** Ventral Stream Function: Integrates visual information across different features to form a holistic perception of objects. Role in Scene Perception: Contributes to the perception of complex scenes and the integration of visual elements into a coherent whole.

Answer 368

**Location**: The parietal pathway extends from the primary visual cortex (V1) to the parietal cortex. **Spatial Location Processing:** Dorsal Stream Function: This pathway is involved in processing the spatial location of visual stimuli. Role in Object Localization: It helps in determining where objects are located in the visual field. **Motion Perception:** Dorsal Stream Function: Specialized for processing motion and detecting the speed and direction of moving objects. Role in Perception of Movement: Involved in tracking moving objects and perceiving the motion of the observer or the environment. **Spatial Attention:** Dorsal Stream Function: Involved in directing spatial attention to specific locations in the visual field. Role in Spatial Perception: Contributes to spatial awareness and the ability to focus attention on relevant visual stimuli. **Control of Self-Movement:** Dorsal Stream Function: Plays a role in the control of self-movement and guiding motor actions based on visual information. Role in Motor Planning: Contributes to planning and executing motor actions based on the spatial information extracted from the visual scene.

Answer 369

**UP** FEF -> Sup. Colliculus -> riMLF -> Post Commissure -> Inf Oblique and S Rectus **DOWN** FEF -> Sup. Colliculus -> riMLF -> Tegmental Midbrain -> Inf Oblique Nucleus, Superior Rectus Nucleus **Right**: Left Cerebral cortex -> Right Pons -> Right CN6N and via interneurones Left CN3 N **Right Peripheral** Visual Cortex -> Left Occipital Parietal Field -> FEF -> Sup. Colliculus -> LPPRF -> R CN6 N and via interneurones L CN3N

Answer 370

Pursuit eye movements involve **tracking a moving object** to maintain **foveal vision** on the target. The **primary visual cortex (V1) processes the motion** information and sends signals to the middle temporal area (MT) and medial superior temporal area (MST). From these areas, **signals are sent to the frontal eye fields (FEF) and supplementary eye fields (SEF)**, which are involved in the planning and initiation of pursuit movements. The **cerebellum, particularly the flocculus and vermis**, is crucial for **processing and integrating visual** motion signals. The **vestibular system** contributes to **gaze stabilization** during pursuit by providing **information about head movement.** The **oculomotor system generates motor commands that drive the smooth pursuit eye movements**, minimizing retinal slip to keep the target on the fovea. Visual Cortex -> Higher Order -> FEF -> SEF -> DLPN -> Flocc -> CN3 N CN6N If error then saccade takes over and jerky movement

Answer 371

**Vergence eye movements involve the simultaneous movement of both eyes in opposite directions to maintain binocular fusion.** The **visual cortex,** particularly the disparity-selective cells, **processes binocular disparit**y information. The **midbrain and brainstem areas,** such as the midbrain reticular formation and interstitial nucleus of Cajal, are involved in the **generation of vergence commands.** Neural Control: **Disparity signals** from the visual cortex are processed in the **midbrain**, leading to the generation of vergence commands. Vergence eye movements are executed by the contraction or relaxation of the extraocular muscles to bring the eyes to the correct convergence or divergence angle. The oculomotor nerve (cranial nerve III) controls the medial rectus muscles for convergence and lateral rectus muscles for divergence.

Answer 372

**Saccadic** * rapid * voluntary gaze shift * superior colliculus (initiated) * Brainstem and cranial nerve nuclei (controlled) **Pursuit** * tracking a moving target * coordinated by visual processing area, cerebellum, vestibular system **Vergence** * disconjugate * maintain binocular vision * controlled by visual cortex, midbrain, CN3 * Each type of eye movement is orchestrated by specific neural pathways to achieve accurate and coordinated visual behaviors.

Answer 373

While the dorsal and ventral pathways are described separately, there is evidence of interactions and feedback between them, allowing for a more integrated and cohesive perception of the visual environment. **Both pathways receive feedback connections from higher-order visual areas and other brain regions.** Interaction between the pathways contributes to the **integration of object recognition** with action planning.] But understood as two pathways,

Answer 374

* **Pigment Epithelium:** * Location: Outermost layer, adjacent to the choroid. * Function: Absorbs excess light and provides nourishment to the photoreceptor cells. * **Photoreceptor Layer**: * Rod Cells: More sensitive to low light conditions, allowing for peripheral vision. * Cone Cells: Responsible for color vision and detailed visual acuity in brighter light. * Location: Rods and cones are the first layer of cells in contact with incoming light. * **Outer Nuclear Layer:** * Contains cell bodies of photoreceptor cells. * Outer Plexiform Layer: * Location: Synaptic connections between photoreceptors and bipolar cells. * **Inner Nuclear Laye**r: * Contains cell bodies of bipolar, horizontal, and amacrine cells. * **Inner Plexiform Layer:** * Location: Synaptic connections between bipolar cells, ganglion cells, and amacrine cells. * **Ganglion Cell Layer:** * Ganglion Cells: Transmit visual information from the retina to the brain via their axons, forming the optic nerve. * Amacrine Cells: Modulate signals between bipolar and ganglion cells. * Horizontal Cells: Facilitate communication between photoreceptors and bipolar cells. * **Nerve Fiber Layer:** * Location: Consists of ganglion cell axons forming the optic nerve. * Inner Limiting Membrane: * Location: Innermost layer, in contact with the vitreous humor.

Answer 375

* **Photoreceptors to Bipolar Cell**s: Photoreceptors synapse with bipolar cells in the outer plexiform layer. * **Bipolar Cells to Ganglion Cell**s: Bipolar cells synapse with ganglion cells in the inner plexiform layer. * **Horizontal and Amacrine Cells**: These cells facilitate lateral communication between photoreceptors and bipolar cells or between bipolar cells and ganglion cells.

Answer 376

* Cornea and Lens: * Incoming light first passes through the cornea and lens, which focus and direct the light onto the retina. * * Photoreceptor Layer: * Light reaches the outermost layer of the retina, where photoreceptor cells (rods and cones) are located. * Photoreceptors contain light-sensitive pigments that undergo chemical changes in response to light. * * Phototransduction in Photoreceptors: * When light strikes the photoreceptor cells, it triggers a cascade of chemical reactions. * In rod cells, the pigment rhodopsin undergoes changes, while in cone cells, different pigments respond to specific wavelengths, including those corresponding to different colors. * * Signal Generation in Photoreceptors: * The chemical changes in the photoreceptor cells result in the generation of electrical signals. * * Outer Plexiform Layer: * Photoreceptors synapse with bipolar cells in the outer plexiform layer. * Bipolar cells play a role in transmitting the signals from photoreceptors to the next layer. * * Bipolar Cell Layer: * Bipolar cells process and transmit the signals received from photoreceptors. * * Inner Plexiform Layer: * Bipolar cells synapse with ganglion cells in the inner plexiform layer. * Interactions with horizontal and amacrine cells also occur, modulating and refining the signals. * * Ganglion Cell Layer: * Ganglion cells receive the processed signals and generate action potentials. * * Nerve Fiber Layer: * Ganglion cell axons, now in the form of action potentials, travel through the nerve fiber layer. * * Optic Nerve: * Ganglion cell axons converge to form the optic nerve, carrying the neural signals away from the eye. * * Transmission to the Brain: * The optic nerve transmits the signals to the visual processing areas of the brain, particularly the thalamus and visual cortex, where further processing and interpretation of the visual information occur. * **

Answer 377

The fovea is a small, central pit within the macula, which is a specialized area in the retina. It is densely packed with cone cells, which are photoreceptor cells responsible for color vision and detailed visual acuity. The fovea has the highest concentration of cone cells in the entire retina.

Answer 378

Visual acuity refers to the sharpness or clarity of vision, particularly the ability to see fine details. It is a measure of how well the eye can distinguish between two points that are close together. Measured via Snellens Conditions such as nearsightedness (myopia), farsightedness (hyperopia), astigmatism, and other eye disorders can affect visual acuity.

Answer 379

**cornea** optical bending **acqueous humor** maintains eye shape and nourishes cornea and lens **lens** Fine-tines as the curvature can be adjusted to allow for accomodation **ciliary muscle** autonomic control via parasympathetic- accommodation by bending lens **zonule/ suspensory ligaments** tension in the suspensory ligaments, controlled by the ciliary muscles, alter the shape of the lens during accommodation. **pupils** size is controlled by iris

Answer 380

* Parasympathetic Nervous System (PNS) Control: The main controller of the ciliary muscles is the parasympathetic division of the autonomic nervous system. * **CN3** **Nerve**: The parasympathetic signals originate from the oculomotor nerve (cranial nerve III), specifically the ciliary ganglion. * **Release** of **Acetylcholine**: Parasympathetic stimulation causes the release of acetylcholine at the nerve endings within the ciliary muscle. * **Muscle** **Contraction**: Acetylcholine binds to receptors on the ciliary muscle, leading to its contraction. * **Lens** **Accommodation**: Contraction of the ciliary muscle reduces tension on the suspensory ligaments (zonules), allowing the lens to become more rounded and increasing its refractive power for close-up vision. *

Answer 381

* Parasympathetic and Sympathetic Control: Both divisions of the autonomic nervous system influence the iris muscles, but their effects are opposing. * Parasympathetic Control (Constriction): * Preganglionic parasympathetic fibers from the oculomotor nerve synapse in the ciliary ganglion. * Postganglionic fibers release acetylcholine, causing contraction of the circular (constrictor) muscles of the iris. * This results in miosis, or constriction of the pupil, which limits the amount of light entering the eye. * Sympathetic Control (Dilation): * Sympathetic fibers originate from the superior cervical ganglion. * Norepinephrine is released and acts on the radial (dilator) muscles of the iris. * This causes mydriasis, or dilation of the pupil, allowing more light to enter the eye.

Answer 382

* Light-sensitive photoreceptor cells (rods and cones) in the retina convert light into neural signals. * Ganglion cells in the retina transmit these signals via their axons, forming the optic nerve. * **Optic Nerve:** * The optic nerve carries visual information from each eye to the optic chiasm. * At the optic chiasm, fibers from the nasal (medial) halves of the retinas cross over, while fibers from the temporal (lateral) halves remain uncrossed. * **Optic** **Chiasm**: * Fibers from the nasal half of each retina cross over to the opposite side. * Fibers from the temporal half of each retina remain on the same side. * This arrangement allows for the integration of visual information from both hemifields of the visual field. * **Optic** **Tracts**: * After the optic chiasm, the crossed and uncrossed fibers form the optic tracts. * The optic tracts carry visual information towards the lateral geniculate nucleus (LGN) in the thalamus. * **Lateral** **Geniculate** **Nucleus** (LGN): * The LGN is a thalamic nucleus that receives visual input from the optic tracts. * From the LGN, visual information is relayed to the primary visual cortex in the occipital lobe. * **Optic** **Radiations**: * Fibers from the LGN form optic radiations, which project to the primary visual cortex (striate cortex or V1) in the occipital lobe. * **Primary** **Visual** **Cortex** (V1): * The primary visual cortex is located in the calcarine sulcus in the occipital lobe. * It is responsible for the initial processing of visual information, including the detection of basic visual features such as orientation, contrast, and motion.

Answer 383

unilateral optic nerve lesions result in monocular blindness in the affected eye. Bilateral optic nerve lesions lead to complete blindness.

Answer 384

bitemporal hemianopia. This visual deficit involves the loss of vision in the temporal halves of both visual fields.

Answer 385

Unilateral optic tract lesions result in homonymous hemianopia on the contralateral side. Bilateral optic tract lesions can cause bilateral homonymous hemianopia.

Answer 386

Lesions in the LGN can lead to visual deficits affecting specific regions of the visual field, depending on the location and extent of the damage.

Answer 387

primary visual cortex can lead to a variety of visual deficits, including cortical blindness or scotomas (localized visual field defects).

Answer 388

High cone density Direct light (no scattering via other layers) Concentration of cells to transmit to optic nerve Central fixation Fewer Rod (few low acuity cells) Limited spatial summation (1:1)

Answer 389

The vestibular apparatus is a system within the inner ear responsible for detecting and processing information related to balance and spatial orientation. It consists of structures such as: **Semicircular Canals:** Three canals oriented in different planes (horizontal, anterior/posterior, and lateral). Detect rotational movements of the head. **Utricle and Saccule:** Located in the vestibule of the inner ear. Utricle is sensitive to horizontal movements. Saccule is more sensitive to vertical movements. Contain specialized areas called maculae, which house hair cells. **Maculae Hair Cells:** Found in the utricle and saccule. Detect linear accelerations and changes in head position. Maculae consist of hair cells, supporting cells, and a gelatinous layer topped with otoliths. Otolith movement bends hair cell stereocilia, generating electrical signals. **Cristae Hair Cells:** Found in the ampullae at the base of the semicircular canals. Detect rotational movements. Cristae consist of hair cells, supporting cells, and a gelatinous structure called the cupula. Head rotation causes fluid movement, bending the cupula, and stimulating hair cells.

Answer 390

* Rotation of the head leads to fluid movement within the semicircular canals. * The movement of the cupula in the ampullae of the canals stimulates hair cells. * Hair cell stereocilia bend, initiating the generation of electrical signals. * The vestibular nerve transmits these signals to the brain, providing information about the direction and speed of head rotation.

Answer 391

* Linear acceleration or changes in head position cause movement of the otoliths within the utricle and saccule. * This movement bends the stereocilia of hair cells in the maculae. * Bending of stereocilia generates electrical signals, which are transmitted via the vestibular nerve. * The brain interprets these signals to perceive linear accelerations and changes in head position. *

Answer 392

* **coordination of eye movements against head movements** * ensuring stable vision during head motion * involve the vestibular system, brainstem nuclei, and the cerebellum. * Short- and long-term modulation of VOR responses are influenced by the cerebellum.

Answer 393

**Vestibular Hair Cells:** Angular and linear head movements are detected by hair cells in the semicircular canals and otolith organs (utricle and saccule) of the vestibular apparatus. **Vestibular Nerve (Vestibulocochlear Nerve - Cranial Nerve VIII)**: Sensory signals from vestibular hair cells are transmitted to the brainstem via the vestibular nerve. **Vestibular Nuclei:** Vestibular nuclei are located in the brainstem and receive input from the vestibular nerve. These nuclei process vestibular signals and send commands to the ocular motor nuclei. **Ocular Motor Nuclei:** Vestibular signals reach the ocular motor nuclei, such as the abducens nucleus and the oculomotor nucleus. These nuclei control the extraocular muscles responsible for eye movements. **Eye Movements:** The coordinated activation of extraocular muscles ensures that the eyes move in the opposite direction of head movements, maintaining a stable visual field.

Answer 394

**Short-Term Modulation by Cerebellum:** **Flocculonodular Lobe of the Cerebellum:** receives input from the vestibular nuclei and projects to the vestibular nuclei and the brainstem ocular motor nuclei. **Purkinje Cells:** inhibit the vestibular nuclei. During rapid head movements, signals from the vestibular system are transmitted to the cerebellum. **Adaptation**: The cerebellum can modulate the strength of the VOR in response to repetitive stimuli. This short-term adaptation **allows for rapid adjustments to changes in head movement patterns.**

Answer 395

**Cerebellar Learning:** The cerebellum is involved in long-term adaptation and learning of VOR responses. Over time, the cerebellum **adjusts the strength of the VOR based on sensory experiences and feedback.** **Plasticity**: Long-term changes in VOR strength occur through s**ynaptic plasticity** in the cerebellum. The cerebellum** refines the VOR based on visual and proprioceptive feedback.**

Answer 396

During rapid head movements, signals from the vestibular system reach the cerebellum. The cerebellum, **through inhibitory signals from Purkinje** cells, modulates the strength of the VOR by a**djusting the firing rate** of the vestibular nuclei. This rapid adaptation allows for adjustments in eye movements to compensate for changes in head movement patterns. The cerebellum aids in compensating for head accelerations, **ensuring that the eyes move appropriately** to stabilize the visual field.

Answer 397

Dysfunction in cerebellar modulation of the VOR can lead to disorders such as gaze instability, dizziness, and difficulties maintaining visual focus during head movements. Nystagmus Ataxia Vertigo Ocular Dysmetria Impaired Smooth Pursuit Movements: Can be caused by cerebellar lesions, MS, Friedreich's ataxia, spinocerebellar ataxias, Toxic-Metabolic Causes, Degenerative Disorders:

Answer 398

Vertigo, a sensation of spinning or dizziness, often results from disturbances in the vestibular system. The semicircular canals and otolith organs detect head movements and linear accelerations, contributing to spatial orientation. **Peripheral Causes:** * **Vestibular Neuritis:** Inflammation of the vestibular nerve can result in sudden-onset vertigo. * **Benign Paroxysmal Positional Vertigo (BPPV):** Dislodged otoliths in the semicircular canals can cause brief episodes of vertigo triggered by specific head movements. * **Meniere's Disease:** Inner ear disorder characterized by recurrent vertigo, hearing loss, and tinnitus. Experiencing unnatural movements, especially without corresponding visual cues, can induce vertigo, nystagmus, and motion sickness due to the sensory conflict between the vestibular and visual systems.

Answer 399

Nystagmus refers to involuntary, rhythmic eye movements. Abnormalities in the vestibular system can cause pathological nystagmus, disrupting the coordination of eye movements with head motion. **Peripheral and Central Causes:** * **Peripheral Nystagmus:** Conditions affecting the vestibular nerve or inner ear, such as vestibular neuritis or BPPV. * **Central Nystagmus:** Dysfunction in central vestibular pathways, often related to neurological disorders like multiple sclerosis or brainstem lesions. Experiencing unnatural movements, especially without corresponding visual cues, can induce vertigo, nystagmus, and motion sickness due to the sensory conflict between the vestibular and visual systems.

Answer 400

Motion sickness results from a sensory conflict between visual and vestibular inputs. The brain receives mixed signals about motion, leading to nausea and other symptoms. **Sensory Conflict:** Motion sickness arises due to a conflict between visual and vestibular signals during motion. In situations like reading in a moving vehicle, the eyes perceive stillness while the vestibular system senses motion, leading to nausea and discomfort.

Answer 401

Motion sickness may have evolved as a protective mechanism to prompt individuals to avoid ingesting potentially harmful substances. The mismatch between visual and vestibular signals could signal exposure to toxins or spoiled food. Motion sickness arises when there is a discrepancy or conflict between the signals received by the visual system and the vestibular system. For example, when a person is reading in a moving vehicle, the eyes perceive a stationary book (visual input), while the vestibular system senses the motion of the vehicle. The sensory conflict triggers an autonomic nervous system response, leading to symptoms such as nausea and vomiting. The body perceives the conflicting signals as a potential ingestion of toxins or poison, prompting a protective response to expel the perceived harmful substance. The vestibular nuclei in the brainstem process signals related to motion and acceleration. The autonomic nervous system, including the emetic center in the brainstem, is activated in response to the sensory conflict.

Answer 402

The vestibular system, as part of the body's sensory apparatus, helps detect and respond to potentially harmful substances. Vestibular reflexes, including the VOR, contribute to maintaining stable vision and preventing disorientation. Clinical Connection: While the vestibular system itself is not an anti-poison system, it contributes to overall sensory integration. Certain toxins affecting the vestibular system can result in symptoms such as nausea, dizziness, and impaired coordination.

Answer 403

M1 Muscarinic Acetylcholine Receptor (mAChR) Antagonists: These drugs block the M1 subtype of muscarinic acetylcholine receptors. Example: Scopolamine. Clinical Application: Used in the treatment of vestibular-related nausea and vomiting. Scopolamine, in particular, is known for its anticholinergic effects, which can **reduce vestibular input** and help alleviate symptoms. H1 Histamine Receptor Antagonists: These drugs block H1 receptors, which are histamine receptors. Examples: Meclizine, dimenhydrinate. Clinical Application: Used to treat motion sickness and vestibular-related symptoms by **reducing the effects of histamin**e, especially in the vestibular system. Dopamine Antagonists: Examples: Promethazine, prochlorperazine, droperidol, metoclopramide. Mechanism of Action: **Block dopamine receptors, primarily in the chemoreceptor trigger zone (CTZ)** and central nervous system, reducing the vomiting reflex.

Answer 404

* 1. Outer Ear: * Pinna (Auricle): * The outer ear collects sound waves from the environment. * Its unique shape helps in capturing sound waves from different directions. * Ear Canal (Auditory Canal): * The ear canal funnels sound waves toward the eardrum. * The length and shape of the ear canal influence its resonance properties. * 2. Middle Ear: * Eardrum (Tympanic Membrane): * The eardrum vibrates when sound waves hit it. * The eardrum's stiffness and surface area influence its response to different frequencies. * Ossicles (Malleus, Incus, Stapes): * Vibrations from the eardrum are transmitted to the three tiny bones (ossicles) in the middle ear. * These bones act as a lever system to amplify the mechanical vibrations. * 3. Inner Ear: * Cochlea: * The cochlea is the primary organ for hearing and is shaped like a snail shell. * It is filled with fluid and contains the basilar membrane, which runs the length of the cochlea. * Hair Cells: * Hair cells are the sensory receptors responsible for converting mechanical vibrations into electrical signals. * Two types of hair cells: inner hair cells (IHCs) and outer hair cells (OHCs). * Hair cells are arranged along the basilar membrane, forming the Organ of Corti.

Answer 405

High-frequency sounds are detected near the base of the cochlea, closer to the stapes. Low-frequency sounds are detected toward the apex (tip) of the cochlea. This theory suggests that different frequencies stimulate different regions of the basilar membrane.

Answer 406

The cochlea is tonotopically organized, meaning that specific frequencies are spatially represented

Answer 407

**Sound Wave Transmission:** Sound waves travel through the ear canal and cause the eardrum to vibrate. The ossicles amplify these vibrations, transmitting them to the oval window. **Fluid Movement in the Cochlea:** Vibrations of the oval window create pressure waves in the fluid of the cochlea. These pressure waves travel along the basilar membrane. **Hair Cell Activation:** Hair cells are deflected as the basilar membrane moves. Stereocilia (tiny hair-like structures on hair cells) bend, opening ion channels and generating electrical signals. **Auditory Nerve Activation:** Activated hair cells transmit signals to the auditory nerve fibers. The auditory nerve carries these signals to the brain for processing.

Answer 408

**Mechanical Displacement:** Sound waves cause the basilar membrane in the cochlea to vibrate. This vibration displaces the hair bundles on the apical surface of hair cells, specifically the stereocilia. **Stereocilia Deflection:** When the hair bundles are deflected, it leads to the opening of ion channels located on the stereocilia. The direction and extent of deflection depend on the amplitude (intensity) of the sound wave. **Influx of Ions:** The opening of ion channels allows the influx of ions, particularly potassium, into the hair cell. This influx generates a receptor potential in the hair cell. **Release of Neurotransmitters:** The receptor potential triggers the release of neurotransmitters (e.g., glutamate) from the base of the hair cell. **Activation of Auditory Nerve Fibers:** Neurotransmitters activate auditory nerve fibers synapsing with the hair cell. **The frequency of action potentials in the auditory nerve is proportional to the loudness (intensity) of the sound.**

Answer 409

**Place Coding:** Different frequencies of sound waves cause maximal displacement of the basilar membrane at specific locations along the cochlea. High-frequency sounds maximize displacement near the base, while low-frequency sounds maximize displacement toward the apex. **Hair Cell Activation:** Hair cells at different locations along the cochlea respond preferentially to specific frequencies based on the place principle. **Tonal Map:** The cochlea is tonotopically organized, creating a tonal map where specific frequencies are spatially represented. Higher frequencies are represented at the base, and lower frequencies are represented toward the apex. **Frequency Discrimination**: The brain interprets the pattern of activated hair cells to distinguish between different frequencies, allowing for accurate frequency discrimination.

Answer 410

**Phase Locking:** Hair cells exhibit phase locking, meaning they can follow the frequency of a sound wave with high temporal precision. The timing of action potentials in auditory nerve fibers is synchronized with the phase of the sound wave. **Temporal Coding:** The timing of action potentials provides information about the temporal structure of sounds, such as the duration and timing of auditory events. **Auditory Nerve Firing Pattern:** Rapid changes in sound wave cycles can lead to corresponding rapid changes in the firing pattern of auditory nerve fibers.

Answer 411

Comapre the moment a sound reaches the two ears

Answer 412

The loundness of sounds between the two ears. | L for lateral l for loud

Answer 413

* **Iner Hair Cells (IHCs):** * **Main Transducers:** IHCs are the primary transducers of sound waves into electrical signals. * **Auditory Signal Transmission**: They play a central role in transmitting auditory signals to the brain through the auditory nerve. * **Responsible for Hearing Sensation**: The majority of the information about sound is transmitted through the IHCs. * * **Outer Hair Cells (OHCs):** * **Amplification:** OHCs amplify the mechanical vibrations of sound waves within the cochlea. * **Frequency Selectivity**: They enhance the sensitivity and frequency selectivity of the auditory system. * **Modulation**: OHCs can be modulated by the brain to adjust their sensitivity, contributing to the fine-tuning of the cochlea's response to different frequencies.

Answer 414

**Primary Auditory Cortex (A1):** Initial cortical processing of auditory information. Tonotopic organization based on frequency. Perception of basic auditory features. **Secondary Auditory Cortex (A2):** Further processing of complex auditory information. Higher-level analysis of auditory stimuli. Integration with other sensory modalities.

Answer 415

**Broca's Area:** Location: Typically in the left frontal lobe, specifically in the posterior part of the frontal gyrus. Function: Essential for language production and grammatical processing. Involved in the planning and coordination of speech movements. **Wernicke's Area:** Location: Typically in the left temporal lobe, often in the posterior part of the superior temporal gyrus. Function: Critical for language comprehension. Involved in understanding and processing the meaning of spoken and written words. **Primary Auditory Cortex (A1) and Surrounding Areas:** Location: In the superior temporal gyrus. Function: Initial processing of auditory information, including speech sounds. Contributes to the analysis of sound frequency and basic auditory features.

Answer 416

Involved in orienting movements of the head and eyes towards sound sources. Coordinates with visual inputs for spatial localization.

Answer 417

**Damage to Hair Cells:** Hair cells in the cochlea are susceptible to damage from exposure to loud noises, ototoxic medications, and aging. Example: Prolonged exposure to high-intensity noise (e.g., from industrial machinery, concerts, or firearms) can lead to hair cell damage and sensorineural hearing loss. **Degeneration of Auditory Nerve Fibers:** Damage to auditory nerve fibers can occur due to genetic factors, infections, tumors, or vascular issues. Example: Acoustic neuroma, a benign tumor of the vestibulocochlear nerve, can compress the auditory nerve fibers and lead to sensorineural hearing loss. **Vascular Insufficiency:** Inadequate blood supply to the cochlea can result in ischemic damage to hair cells and auditory nerve fibers. Example: Atherosclerosis, which leads to narrowing or blockage of blood vessels supplying the inner ear, can cause sensorineural hearing loss. **Ototoxic Medications:** Certain medications, such as some antibiotics (e.g., gentamicin), chemotherapy drugs, and nonsteroidal anti-inflammatory drugs (NSAIDs), can damage hair cells and auditory nerve fibers. Example: Aminoglycoside antibiotics like gentamicin are known to cause sensorineural hearing loss when used at high doses or for prolonged periods. **Genetic Factors:** Inherited genetic mutations can affect the structure and function of components of the auditory system, leading to sensorineural hearing loss. Example: Connexin 26 gene mutations are associated with congenital sensorineural deafness, where affected individuals are born with hearing loss due to abnormalities in cochlear function. **Age-related Changes:** Degenerative changes in the inner ear structures, including loss of hair cells and auditory nerve fibers, are common with aging (presbycusis). Example: Presbycusis often manifests as a gradual, progressive sensorineural hearing loss, particularly affecting high-frequency sounds. **Autoimmune Disorders:** Autoimmune conditions, such as autoimmune inner ear disease (AIED), can result in inflammation and damage to inner ear structures, including hair cells and auditory nerve fibers. Example: AIED can lead to sudden sensorineural hearing loss or progressive bilateral hearing loss. **Traumatic Injury:** Head trauma or sudden changes in air pressure (barotrauma) can cause damage to the cochlea or auditory nerve, resulting in sensorineural hearing loss. Example: Temporal bone fractures, commonly associated with head trauma, can disrupt the delicate structures of the inner ear and lead to sensorineural deafness

Answer 418

Age-related loss of hearing from the base of the cochlea

Answer 419

Fusion of the stapes to the bone

Answer 420

Death of hair cells in the spiral organ (organ of Corti)

Answer 421

Potassium enters through mechanically-gated channels at the tips of the stereocilia

Answer 422

Definition: Conductive hearing loss occurs when there is a problem with the transmission of sound waves from the external ear to the inner ear. Causes: Blockage or damage to the ear canal (e.g., earwax impaction). Otitis media (infection or inflammation of the middle ear). Problems with the ear ossicles (small bones in the middle ear). Perforation of the tympanic membrane (eardrum). Characteristics: Typically involves a reduction in the ability to hear faint sounds. Conductive hearing loss can often be addressed or improved through medical or surgical interventions.

Answer 423

High frequency

Answer 424

Rupture of the membranes in the cochlea due to Barotrauma

Answer 425

Loss of protective secretions within the external meatus

Answer 426

Definition: Sensorineural hearing loss occurs when there is damage to the inner ear (cochlea) or the auditory nerve pathways. Causes: Aging (presbycusis). Noise-induced damage. Viral infections affecting the inner ear. Certain medications. Genetics. Characteristics: Difficulty hearing faint sounds, as well as understanding speech, especially in noisy environments. Sensorineural hearing loss is often permanent, and treatment options may include hearing aids or cochlear implants.

Answer 427

**Ascending** **Spinothalamic** 1) Anterior = crude touch and pressure 2) Lateral= pain **Ascending** **Dorsal** 1) Gracile = Lower than T6 2) Cuneate = Above T6 Both for proprioception and vibration

Answer 428

1) sensory nerve synapses in the dorsal/anterir horn of grey at the substantia gelatinosa 2) Decussates across to the Spinothalamic tract (white matter) (opposite side) and travels to the thalamus 3) Synapses in the thalamus and travels to the somatosensory cortex via the internal capsule | NT: Glutamate.

Answer 429

1) sensory nerve enters the dorsal column (same side) and ascends to the medulla oblongata 2) Synapses in the dorsal nuclei and decussates (at the/forming medial lemniscus) and arises in the dorsal column (opposite side) to the Thalamus 3) The thalamus synapses to the somatosensory cortex via the internal capsule. | NT: Glutamate

Answer 430

Not 1,2,3 but UMN in brain LMN in cord to tissue. * Motor cortex at pyrimidal cells via corona radiata, * via internal capsule and midrbain (ant.crus cerebri) and pons (basillar pons) * Travels through medulla via pyramidal tracts decussating at the base of medulla. (90% decussate here, 10% at cord) * Moves via the corticospinal tract * UMN LMN synapse at the border **The pathway finishes at the function (LMN to effector)** | NT: Glutamate until effector Ach

Answer 431

1) light passes all structures to hit the retina at the back 2) Phototransduction of the Rods: Photo excitation via UV breaks rhodopsin into opsin (active) and retinal 3) Active opsin activates transducin (g protein) to produce phosphodiesterase 4) Phosphodiesterase breaks down cGMP 5) Photocurrent: 5) This shuts sodium hannels and the rod becomes hyper polarised. 6) Proportional to the depolarisation, less glutamate is released. 7) Glutamate has an inhibitory effect on "ON bipolar cells", the lack of glutamate means the metabotropic cells can cascade and produce an Act Pot 8) Glutamate has an excitatory effect on ionotropic "OFF Bipolar cells" so the sodium channels are closed and no Act Pot are generated.

Answer 432

**Rods function mainly in dim light and provide monochromatic vision. Cones function in well-lit conditions and are responsible for the perception of colour through the use of a range of opsins

Answer 433

3 Rods to 1 Bipolar 1 Cone to 1 Bipolar **Metabotopic (ON cells)** High cGMP High Glutamate Inhibited ON Cells ON Cells have no Act Pot **Ionotropic (OFF cells)** High cGMP High Glutamate AMPA receptor controls Na Channel Glut activates AMPA Na open, Na rushes in Cell is depolarised. Act Pot occur.

Answer 434

Semicircular canals Ampulla Utricle Saccule

Answer 435

Ampulla of the Semicircular canal- Rotational Utricle- linear acceleration Saccule- linear acceleration

Answer 436

The ampulla contain cupula made of a gelatinous layer containing Type 1, 2 hair cells, stereocillia and support cells. There are no otoliths.

Answer 437

The utricle is responsible for x axis acceleration The saccule is responsible for y axis accerleration They do not contain cupula Otolith crystals sit on top of a gelatinous layer (thinner than cupula) These otoliths interact with the T1 and T2 hair cells Ototlith movement activates hair cells. Forward motion pushes the otoliths backwards. Think about how youre pushed to your seat in a rollercoaster at fast acceleration. But tilt works on gravity! like holding a rainstick!

Answer 438

The hearing system can encode all of these. Pitch is **frequency**. Volume is loundness or intensity or **amplitude** Timbre is **attribute**

Answer 439

NO! The yellow is basilar a main structural element that separates the cochlear duct from the tympanic duct and determines the mechanical wave propagation properties of the cochlear partition The red is organ of corti- highly varied strip of epithelial cells allows for transduction of auditory signals into nerve impulses' action potential.

Answer 440

Cochlea encodes frequency with base high pitch and apex low pitch. Pressure runs along the basilar membrane and wave moves the hair cells. The cochlear nerve spans the cochlear. Cochlear fibres run through the basiclar membrane of the organ of corti The basilar membrane is narrower and stiffer at the base (near the oval window), responding better to high-frequency sounds. Towards the apex, it widens and becomes more flexible, responding better to low-frequency sounds. Inside the cochlear are mutliple membranes and hair cells. Inner hair cells encode sound and are NOT connected to the tectorial membrane Outer hair cells encode amplification and are connected to the tectorial membrane The tectorial membrane is acellular and amplifies faint noises. It also stores Ca2+ for depolarisation. Reisners membrane contains nutrients and is implicated in meniers disease.

Answer 441

Endolymph and Perilymph: Endolymph is the fluid within the scala media of the cochlea, and perilymph is the fluid in the scala vestibuli and scala tympani. The differences in ion composition between these fluids play a role in the generation of the electrical signals in the hair cells. Note that only the surface of the organ of Corti is bathed in endolymph (notably the stereocilia of the hair cells), whilst the main body of hair cells and support cells are bathed in perilymph.

Answer 442

The perilymph in the vestibular duct and the endolymph in the cochlear duct act mechanically as a single duct, being kept apart only by the very thin Reissner's membrane The high potassium content of the endolymph means that potassium, not sodium, is carried as the de-polarizing electric current in the hair cells. This is known as the mechano-electric transduction (MET) current.

Answer 443

Medial Geniculate Nucleus is **AUDITORY** Lateral Geniculate Nucleus is **VISUAL**

Answer 444

Superior Olivary body is **AUDITORY** Lateral olivary body is pre cerebellar

Answer 445

**Purpose**: Saccade: Rapid, voluntary movements that redirect the line of sight from one point to another. Saccades are used to shift the eyes quickly to a new target. Pursuit: Smooth, continuous eye movements used to track a moving object, keeping the eyes fixated on it as it moves. **Nature**: Saccade: Jerky and rapid eye movements. Pursuit: Smooth and continuous eye movements. Speed: Saccade: Fast movements that occur in a fraction of a second. Pursuit: Slower movements that are maintained over a longer duration. **Voluntariness**: Saccade: Voluntary, under conscious control. Pursuit: Also voluntary, but often involves more automatic, reflex-like mechanisms, especially in response to moving objects. **Neural** Pathways: Saccade: Involves the superior colliculus, frontal eye fields (FEF), and parietal eye fields (PEF), with signals sent to the brainstem and oculomotor neurons. Pursuit: Involves cortical areas such as FEF and PEF, the superior colliculus, brainstem structures, and the cerebellum to coordinate smooth tracking. **Target** Characteristics: Saccade: Typically directed towards stationary or briefly appearing targets. Pursuit: Used to track moving targets, maintaining gaze on the target as it moves across the visual field. Eye Movement Patterns: Saccade: Involves a series of discrete, ballistic eye movements. Pursuit: Involves a sustained, smooth tracking of a moving object. **Accuracy**: Saccade: Aims for accurate redirection of gaze to a specific target. Pursuit: Aims for accurate and continuous tracking of a moving target.

Answer 446

* Ataxia: Lack of voluntary muscle coordination, unsteady gait. * Dysmetria: Inaccurate judgment of movement range or force. * Intention tremor: Tremor during purposeful movements, worsens with approach. * Hypotonia: Decreased muscle tone, floppy appearance, postural instability. * Dysarthria: Slurred speech due to muscle coordination impairment. * Nystagmus: Involuntary eye oscillations, various types, gaze-related. * Vertigo: Sensation of spinning, dizziness, vestibulocerebellar dysfunction. * Cognitive impairments: Executive function, attention, spatial cognition difficulties sometimes. * Incoordination of eye movements: Eye movement coordination issues, smooth pursuit affected.

Answer 447

The direct and indirect basal ganglia loop Both receive dopamine but the indirect MSENIT utilises D2 receptors for an inhibitory affect. **M**SI**T** **M**SE**N**I**T** Where bold is exitatory

Answer 448

Locked in syndrome

Answer 449

Lateral Medullary: Ipsilateral Wallenberg Medial Medullary: Contralateral Dejenre

Answer 450

Medial Frontal and Parietal Lobes Contralateral weakness, urinary inctoninence, behavioural changes

Answer 451

Lateral Frontal and Parietal Lobes Contralateral jemiparesis/plegia to face arm leg Aphasia Neglect, Homonymous hemianopia. B&W Aphasia

Answer 452

Occipital lobe, thalamus, Hypothalamus, MB, Cerbellum