Week 1

Question 1

What are the 5 anatomical regions of the brain and what do they contain

Answer 1

Telencephalon - cerebral cortex, subcortical structures and associated white matter

Diencephalon - thalamus, hypothalamus, epithalamus, subthalamus

Mesencephalon - comprised the midbrain

Metencephalon - contains pons and cerebellum

Myelencephalon - medulla

Question 2

Describe the functional divisions of the central nervous system and their function

Answer 2

Anatomical:
CNS: brain and spinal cord
PNS: nerves (12 cranial, 31 spinal), ganglia, nerve endings

Functional divisions (class 1)
Somatic: voluntary control, skeletal muscle
Autonomic: involuntary regulation of physiologic processes
Enteric: independent givers function of GI tract

Functional divisions (class 2)
Sensory: processing input from environment
Motor: both voluntary and involuntary movements through innervation of effected muscles + glands
Integrated: integration of sensory and motor in CNS

Question 3

What is the hind brain

Answer 3

Posterior part of brain including structures such as medulla, pons and cerebellum.

Responsible for essential functions e.g. breathing, heart rate, coordination of motor movements and balance

Question 4

What is in the hind brain

Answer 4

Medulla, pons, cerebellum, locus cornealus, raphe nuclei, reticular formation

Question 5

Outline key components of the midbrain

Answer 5

Aka as mesencephalon
Located between forebrain and hindbrain

Role in motor function, visual and auditory processing and regulation of sleep wake cycle.

Contains:
- tectum: dorsal part of midbrain
- Tegmentum: ventral part of midbrain, involved in motor control, pain perception and autonomic functions
- crus cerebri: bundles of fibres in the midbrain that form part of cerebral peduncles, role in motor function

Question 6

Describe anatomical boundaries delineating the Diencephalon

Answer 6

Contains: thalamus, hypothalamus, epithalamus, subthalamus, third ventricle

Epithalamus contains pineal gland (melatonin) and habenula (regulating neurotransmitter release)

Subthalamus most ventral part of Diencephalon. Lies inbetween thalamus and mesencephalon. Component of basal ganglia involved in motor control and regulation of movement

Surrounded by telencephalon

Question 7

Describe functional organisation of the thalamus

Answer 7

Largest component of Diencephalon.
Paired oval masses of grey matter.
All major sensory pathways relay in thalamus (except olfactory)

Functional divisions:
Reticular nuclei - arousal and pain perception
Sensory nuclei - sensory regulation
Effector nuclei - motor function + launguage
Associative nuclei - high level cognitive functions
Limbic system - mood + motivation

Question 8

Describe function of hypothalamus

Answer 8

DEAL acronym

D = regulates DRIVES such as hunger, thirst and sexual behaviour

E = ENDOCRINE, controls release of hormones from pituitary, growth, metabolism and other functions

A = AUTONOMIC nervous system coordination, heart rate, resp rate and digestion

L = LIMBIC, integrates emotional responses and motivations, links hypothalamus to Limbic system for mood and behaviour regulation

Homeostasis:
- controls ANS, neuroendocrine system and limbic system receiving sensory information from circumventricular organs (highly permeable areas of BBB) and sensory and autonomic circuits (pathways provide visceral and somatosensory input via neuronal signals)

Question 9

Anatomy and function of the pituitary

Answer 9

Hypothalamus pituitary complex is like command centre of endocrine system.

Anterior produces own hormones in response to hormones sent from thalamus.

Posterior pituitary is an extension of neurons of the hypothalamus.

Question 10

Describe anatomical boundaries of the hypothalamus

Answer 10

Anterior - lamina terminalis and optic chiasm
Posterior - imaginary line sloping antero-inferiorly from the posterior commissure to the
mammillary bodies
Superior - hypothalamic sulcus
Inferior - tuber cinereum and mammillary bodies

Question 11

Outline key components of the forebrain

Answer 11

Cerebral cortex - outer layer of brain;higher cognitive functions (thinking, reasoning, voluntary movements)

Limbic system - neural network involved in emotions, motivations and memory.

Basal ganglia - groups of deep nuclei involved in motor control, regulation of voluntary movements

Basal forebrain - base of frontal lobes; includes memory, attention, regulation of wakefulness

Question 12

Limbic system: HOME is where the HOHA

Answer 12

H - homeostasis
O - olfaction
M - memory
E - emotion

H- hypothalamus
O - olfactory bulb
H - hippocampus
A - amygdala

Question 13

Describe 4 functional lobes of cerebral cortex

Answer 13

Frontal - executive functions, decision making, motor control

Parietal - processing sensory information and spatial awareness

Occipital - primarily involved in visual processing

Temporal - associated with auditory processing and memory functions

Question 14

Describe the key functional areas of the lobes.

Answer 14

Broca’s area - frontal lobe; speech production and language processing

Wernickes area - temporal lobe; language comprehension and understanding

Primary motor cortex - frontal lobe; voluntary movements and motor function

Primary somatosensory cortex - parietal lobe; processing sensory information

Primary visual cortex - occipital lobe; initial visual processing

Primary auditory cortex - temporal lobe; processes auditory information and sound perception

Question 15

Describe anatomy of ventricular system of the brain

Answer 15

Interconnected fluid filled cavities which work to circulate CSF.

Lateral ventricles —> intraventricular foramen —> third ventricle (Diencephalon) —> cerebral aqueduct —> fourth ventricle —> lateral or medial aperture
—> central canal of spinal cord , brain or subarachnoid space

Question 16

Describe role of ventricular system

Answer 16

Provides mechanical and immunological support to the brain, helps to maintain stable environment for neural function.

Question 17

Describe the meninges layers of the brain and the spaces/potential spaces between them.

Answer 17

Meninge layers:

Dura mater - outermost, tough fibrous.
Arachnoid mater - middle layer, spider like with projections
Pia mater - inner most, delicate layer lining the brain

Spaces/ potential spaces:

Subarachnoid space: real space, CSF travels through
Subdural space: potential space
Epidural space: potential space

Question 18

Describe utility of different imaging modalities for head, brain and spine

Answer 18

MRI - magnetic fields, detailed images
CT
PET - maps function activity in the brain by detecting radioactive tracers that highlight metabolic processes

Question 19

Outline the utility of contrast agents for CT brain and list indications for the main protocols for common CNS conditions

Answer 19

Enhance visualisation of vascular structure, tumours and inflammation.

Indications for contrast CT: intracranial haemorrhage, vascular abnormalities aneurysms, malformations, assessment of tumours, areas of infection/inflammation, evaluation ischaemic stroke.

Iodine - enhances vascular structures and abnormal it’s and abnormalities in CT brain imaging
Gadolinium - improves detection tumours, MS lesions, inflammation, vascular abnormalities.

Question 20

Describe components of nervous system

Answer 20

Neurons - specialised nerve cells transmitting electrical signals

Oligodendrocytes - CNS glial cells produce myelin to insure and speed up signal transmission

Microglia - immune cells of the brain, responsible for defence against infections maintain brain health

Astrocytes - star-shaped, provide structural support, regulate neurotransmitters, in BBB

Schwann cells - facillitate nerve impulse in PNS by wrapping around axons and forming myelin sheaths

Ependymal cells - line the ventricles of brain and spinal cord, produce CSF

Question 21

Describe the structure of the BBB

Answer 21

Composed of specialised endothelial cells, BBB features tight junctions that restrict passage of most substances ensuring tightly regulated micro environment.

Astrocyte foot processes and pericytes contribute to structural and functional integrity.

Question 22

Transport mechanisms across BBB

Answer 22

Diffusion - passive movement of lipid soluable across the BBB facilitated by the lipid bilateral of endothelial cells

Carrier mediated - transport of molecules through BBB with assistance of carrier proteins that embedded into cell membrane

Receptor-mediated - selective and controlled transport where substances to specific receptors on endothelial cell surface facillitate entry into brain.

ABC transporters - active transport facilitated by ATP-binding cassette (ABC) transporters, pump various molecules out of BBB, limiting entry into brain

Question 23

What is transcytosis and efflux

Answer 23

Transcytosis:
- transport process across BBB involving internalisation of molecules into vesicles on one side of endothelial cell and the release on other sides

Efflux:
- refers to active transport process in which molecules, typically drugs or toxins are pumped out of cells by specialised transport proteins such as ABC transporters.

Question 24

Describe the difficulties the BBB provides for delivery of drugs to the CNS

Answer 24

• tight junctions limit passive diffusion of many drugs particularly larger molecule sizes and poor lipid solubility.
• presence of efflux transporters such as ABC transporters, actively pump out drugs that reach endothelial cells.
• BBB limits permeability to hydrophilic molecules

Question 25

Describe the development of the 5 divisions of the brain.

Answer 25

Egg + sperm = zygote —> blastocyst —> ectoderm, mesoderm, endoderm Focusing on ectoderm: —>neuroectoderm —> neural plate —> Neural groove —> neural tube (becomes CNS) —> neural crest (becomes PNS) —> prosencepalon, mesecencephalon and rhombencepalon Prosencephalon = telencephalon, Diencephalon Mesencephalon = same Rhombocephalon = metecephalo, myelincephalon

Question 26

Outline how the CNS controls voluntary movement, including the hierarchy of motor movement and sensory pathways.

Answer 26

Voluntary movement involves coordinated action of many muscles; needed to be activated right time for voluntary action to occur. Under concious control initiated and directed by individuals will

Question 27

Components of the motor system

Answer 27

- cerebral cortex: responsible for complex cognitive functions and voluntary motor control - basal ganglia: groups of nuclei involved in motor control, coordination, and procedural learning - cerebellum: coordinates movements, balance and posture - brainstem: vital for basic life functions, breathing, heartbeat, pathways for nerve fibres - motor neurons: transmit signals from CNS to muscle enabling voluntary movements

Question 28

Describe control of voluntary muscle, with a focus on the corticospinal tract.

Answer 28

- voluntary muscle movement primarily controlled by corticospinal tract. - originates in the primary motor cortex - signals travel through internal capsule —> cerebral peduncles and pons —> descends in spinal cords lateral columns —> fibres synapse with LMNs in spinal cord in ventral horn (efferent) —> these LMN synapse with skeletal muscles directly causing voluntary movement

Question 29

Describe differences between UPN lesions and LMN lesions

Answer 29

Damage to UMN = spacisity, ridgid muscles tone, babinski reflex positive, fasiculations absent and hyperreflexia Damage to LMNs = muscle weakness, flaccid muscle tone, atrophy, hyporeflexia, babinski negative, fasiculations present

Question 30

Describe transmission of somatosensation, with a focus on the spinothalamic and DCML pathways

Answer 30

- anterior spinothalamic tract carries crude touch and pressure - lateral spinothalamic tract carries pain and temp - DCML transmits proprioceptions, vibration and fine touch Sensory fibres from skin enter spinal cord and synapse with second order neurons in dorsal horn (afferent). Fibres cross to opposite side of cord and ascend to thalamus (ventral posterior nucleus). Sensory fibres ascend ipsilateral lay in the dorsal of spinal cord, synapse with 2nd order neurons in the medulla forming medial leminiscus, these 2nd order neurons deccusate to opposite side and ascend to thalamus. Synapses with 3rd order to somatosensory cortex

Question 32

Describe how the organisation of the sensory and motor systems can change in response to injury, such as amputation, or training.

Answer 32

Following amputation: - sensory and motor systems undergo reorganisation adapting to new neural patterns - cortical remapping, adjacent cortical areas may expand to the former region - can lead to alter end sensory perceptions i.e. phantom limb sensations - motor areas a change, areas take over function of limb allow for prosthesis use Training dependent plasticity - brains ability to reorganises and adapt responding to repeated training - changes in size and activation patterns of brain regions associated with task -

Question 33

Describe arterial blood supply to brain

Answer 33

Receives 20% of cardiac output Divided into anterior and posterior circulation Internal carotid arteries provide 80% to the anterior and vertebral arteries 20% to the posterior.

Question 35

Describe the anterior circulation of blood to the brain

Answer 35

Internal carotid ascends laterally on neck entering skull through carotid canal. Supplies the anterior cerebral artery. Courses anteriorly above the optic nerve and between the cerebral hemispheres to supply medial aspects of frontal and parietal lobes. Middle cerebral artery travels laterally in the Sylvian fissure supplying lateral surfaces of the cerebral hemispheres

Question 36

Describe the posterior circulation and key vessels

Answer 36

Vertebral - ascends through transverse foramina of cervical vertebrae to form basilar artery Basilar - forms union of vertebral arteries. Supplies brainstem and cerebellum Posterior cerebral artery - courses posteriorly along the cerebral peduncle supplying the occipital and inferior temporal lobes Posterior inferior cerebellar - arises from the vertebral artery to supply the posterior inferior aspect of cerebellum Anterior inferior cerebellar artery - arises from basilar artery to supply anterior inferior aspect of cerebellum Superior cerebellar - arises from the basilar artery to supply the superior aspect of the cerebellum

Question 37

Describe segments of MCA (M1 to M4)

Answer 37

M1 = proximal segment of cerebral artery extending from origin to Sylvian fissure M2 = insular segment transversing within the Silvyan and supplying the insular cortex. M3 = opercular segment continuing distally along lateral surface of brain. Supplying operculum and adjacent cortical areas M4 = cortical segment consisting of small branches penetrating the cerebral cortex to -or vide blood to specific functional areas

Question 38

Clinical manifestations of MCA, PCA and ACA

Answer 38

MCA = contralateral hemiparesis; contralateral hemianopia, dysarthria, global aphasia, alexia, a graphic, apraxia, hemineglect (non-dominant), anosognpsia (non-dominant) PCA = contralateral homonymous hemianopia (occipital), cortical blindness, memory deficits, behaviour, hemisensory loss ACA = contralateral lower limb hemiparesis, contralateral lower limb hemianesthesisa, urinary incontinence

Question 39

Describe venous drainage from the brain

Answer 39

Cerebrum, cerebellum and brainstem are drained by veins which empty to dural venous sinuses Dural venous sinuses are valveless venous channels between 2 layers of the dural mater. Straight, superior and inferior Sagittal sinuses are found in the falx cerebri of dura mater converging at the confluence of sinuses From confluence the transverse sinus continues bilaterally and curves into the sigmoid to meet opening of jugular veins. The cavernous sinus drains the opthalamic veins; blood returns to internal jugular vein via superior or inferior petrosal sinuses

Question 40

Explain cerebral venous thrombosis, risk factors and clinical features

Answer 40

Formation of blood clots in the cerebral venous system. CVT symptoms typically develop slowly and can vary based on size and location. Risk factors: hypercoagubility, OCP, obesity, pregnancy, head and neck infections, trauma Clinical features: severe and persistent headache, focal neurological deficits such as hemiparesis and/or visual disturbances, altered mental state such as confusion or coma.

Question 41

Describe the pathogenesis of the common causes of ischemic stroke including clinical features and potential complications

Answer 41

Thrombosis or embolism of cerebral arteries leading to ischaemia and infarction of brain tissue. Clinical features: hemiplegia (damage to motor areas), aphasia (impairment or loss of language ability, speaking, understanding or expressing), ataxia. (Lack of coordination of voluntary muscle movements), dizziness, visual field deficits, headache, dysphasia (difficulty swallowing) Complications of stroke: deep vein thrombosis, cognitive impairment, urinary incontinence, seizures, dysphasia

Question 42

Describe the pathogenesis of atherosclerosis, thrombosis, and embolism in the context of an ischaemic stroke.

Answer 42

Atherosclerosis - progressive narrowing and hardening of arteries due to build up of plaques. Leads to reduced blood flow. Thrombosis - formation of a blood clot (thrombus) within a blood vessels, which can obstruct blood flow and may lead to stroke. Embolism - sudden blockage of vessel by an embolus, detached clot, air bubble or other foreign material travelling through blood stream.

Question 43

Define transient ischameic attack

Answer 43

Characterised as a short period of symptoms similar to that of a stroke. Spontaneously resolves within 24 hrs.

Question 44

Describe haemorrhagic transformation in the context of ischaemic stroke

Answer 44

Conversion of an ischaemic stroke or brain injury into escape of blood into previously ischaemic tissue. Primarily occurs at the site of a repurfusion injury. Haemorrhagic transformation can worsen the outcome; this is a significant risk of repurfusion therapy. Ischaemic —> repurfusion therapy —> return of blood flow to arteries —> blood flows through the leaky arteries —> blood moves into brain parenchyma —> haemorrhagic transformation Ischaemia —> damage to blood vessels —> blood vessels become leaky —> blood flows through leaky arteries —> blood moves into brain parenchyma —> haemorrhagic transformation

Question 45

Describe the pathogenesis of haemorrhage stroke, common causes and clinical features.

Answer 45

Occurs when a blood vessel in the brain ruptures leading to bleeding within or around the brain tissues. This rupture can be caused by weakened vessels walls, aneurysms or arteriovenous malformations. Loss common than ischaemic but severe rapid neurological damage due to direct impact of bleeding on brain structures. Clinical features: thunderclap headache, neck stiffness, vomiting, hypertension, neurological signs such as weakness, numbness, slurred speech, visual disturbances.

Question 46

Describe pathogenesis of hypertension in context of haemorrhagic stroke.

Answer 46

Dysregulation of baroreceptors Rupture of blood vessel in initial haemorrhage leads to increase in intracranial pressure. To maintain perfusion to the brain, baroreflex attempts to compensate by increased BP causing further bleeding in a vicious cycle. Rupture of blood vessel —> increased ICP —> compensation via baroreflex —> secondary hypertension —> further bleeding —> increased ICP = cycle repeats

Question 47

What is a berry aneurysms. Describe common locations of berry aneurysms and potential symptoms associated with their presence

Answer 47

Small rounded outpuching/bulge that appears on a weakened area of a blood vessel in the brain, typically at junctions where arteries branch off (e.g. circle of Willis) Developmental defects in elastic lamina or acquired defects in an artery, often exacerbated by hypertension. Rupture of these aneurysms can result in a subarachnoid haemorrhage or intracranial haemorrhage. SAH most common causing immediate death in 30% following rupture and 85% undiagnosed until rupture. Clinical signs: headaches, nausea, vomiting, neck pain/stiffness

Question 48

Common complications of haemorrhagic stroke

Answer 48

Mass effect - compression of surrounding brain tissue due to the haemorrhage; can damage surrounding structures. Perihaematomal oedema - swelling of brain tissue around the haemorrage Hydrocephalus - build-up of CSF in ventricles Vasospasm - narrowing of blood vessels in brain often occurring after haemorrage, can lead to decreased blood flow and further complications.

Question 49

Specify the investigations used to make a diagnosis of stroke/TIA

Answer 49

As fast as possible - time is brain! CT and MRI gold standard. CT = provides rapid visualisation of haemorrhagic strokes and detects acute changes in brain structure. CT angiography following normal CT. MRI = offers detailed imaging of both acute and chronic stroke lesions, aiding in precise diagnosis and treatment planning Vascular imaging = helps identify underlying vascular abnormalities and assesses blood flow, crucial for determining stroke aetiology and guiding therapeutic interventions

Question 50

Name stroke territories and describe role of CT, MRI and vascular imaging in Assesment of stroke

Answer 50

Stroke territories: - anterior circulation perfumed by internal carotid arteries supplying frontal, parietal and temporal lobes. As well as basal ganglia and internal capsule. - posterior circulation perfumed by vetebral and basilar arteries, provides blood to brainstem, cerebellum, occipital lobes and portions of thalamus and temporal lobes. CT angiogram - visualises arteries; used for aneurysm, stroke and vascular is CT venogram - visualises veins; used for dural venous sinus thrombosis DSA - primarily used for radiologic guided treatment of above conditions

Question 51

Describe acute management of stroke/TIA

Answer 51

Rapid Assesment and diagnosis. Time sensitive interventions: thrombylotic therapy with tissue plasminogen activator (tPA) or mechanical thrombectory aim to restore blood flow. Haemorrhagic strokes may require measures to control bleeding and stabilise vital signs along with intensive care to prevent complications such as cerebral oedema and increased ICP

Question 52

Describe drug classes utilised for secondary prevention of stroke/TIA and mechanism of action

Answer 52

Mechanism of action: Thrombolytics (tPA) - dissolves clots by converting plasminogen to plasminogen which breaks down fibrin. Antipaltelets - inhibits platelet aggregation and activation. Preventing new blood clots Statin - reduces cholesterol synthesis by inhibiting HMG-CoA redcutase, lowering levels of LDL cholesterol reducing stroke risk

Question 53

Describe drug classes utilised for secondary stroke/TIA prevention including contraindications

Answer 53

Thrombolytics - recent intracranial haemorrhage, recent surgery, active bleeding, diathesis Antiplatelets - active bleeding, history of haemorrhageic stroke, liver disease Statin - active liver disease, pregnancy

Question 54

Describe drug classes for secondary prevention of strok/TIA including side effects

Answer 54

Thrombolytics - excessive external bleeding Antiplatelets - gastrointestinal bleeding Statin - muscle pain; weakness; liver enzyme abnormalities

Question 55

Classifications of TBI: differentiation between mild, moderate and severe

Answer 55

Can be classified mild, moderate or severe depending on the Glasgow coma scale: mild TBI = 13-15, unconscious <30 mins, amnesia <24hrs Moderate TBI = 9-12, unconscious 30 min to 24hr, amnesia 1-7 days Severe TBI = 0-8, unconscious >24hr, amnesia >7days

Question 56

Mechanism of TBI

Answer 56

Brain damage in TBI caused by rotational and/or linear acceleration forces, or by blunt trauma with impact deceleration. Direct impact, acceleration-deceleration, blast injury.

Question 57

Focal vs diffuse TBI

Answer 57

Focal TBI = involves specific area of brain characterised by localised damage such as contusions or hematomas, often caused by direct impact or acceleration-deceleration forces. - focal neurological deficits Diffuse TBI = affects more widespread areas of brain. Involves diffuse axonal injury (stretching or tearing of axons) leads to widespread disruption of neural pathways. - diffuse injury: impaired consciousness, cognitive deficits and diffuse neurological impairments

Question 58

Intracranial bleeding: epidural vs Subdural

Answer 58

Epidural haemorrhage - between surface of skull and outer layer of dura mater. Arterial bleeding following skull fracture leading to rapid expansion of haematoma, can cause raised ICP. Subdural haemorrhage - occurs between dura and arachnoid mater, usually due to tearing of bridging veins as a result of shearing forces. Accumulation of blood over a slower period compared to epidural.

Question 59

Describe role of secondary injury following traumatic brain injury.

Answer 59

Primary refers to the immediate damage caused by initial impact or trauma. - e.g. contusions, intracranial bleeds, diffuse axonal injury, diffuse vascular injury Secondary TBI injury t occurs in period following initial trauma. Involves cascade of biochemical and physiological events such as inflammation, ischaemia and excitotoxicity; leads to further damage potentially worsening initial injury. - e.g. neuro inflammation, cerebral oedema, oxidative stress, secondary axonal injury, hypoxia/ischaemia,

Question 60

What is concussion? Outline Pathophysiology of concussion

Answer 60

Form of mild TBI: functional rather than structural impairment. Cascade of secondary injury arising from primary mechanical injury. No abnormality seen on imaging. No routine tests currently exist to diagnose. Mechanism: Mechanical force disrupts cell membranes —> indiscrimative release of neurotransmitters —> Widespread ionic fluxes —> depolarisation of neurons —> membrane pumps restore ionic gradients —> hyperglycolosis to generate ATP —> energy crisis —> cognitive impairment and altered conciousness

Question 61

What is evidence of axonal injury in blood? What does it suggest?

Answer 61

Elevated concentrations of axonal proteins such as tau and neurofilament proteins. Can be seen sometimes in samples from those experiencing symptoms of concussion. Increased levels suggest axon lysis and degeneration indicative of structural damage to axons. Damaged axons in brain do not typically regenerate, hence presence of elevated proteins post concussion suggests potential for permanent brain damage.

Question 62

Describe current difficulties in diagnosis of concussion

Answer 62

- Heterogenous presentation - Subjective nature of symptoms - Challenging to diagnose based on clinical assessment - Conventional imaging may fail to detect subtle structural changes in concussion leading to under diagnosis or misdiagnosis - lack of universally diagnosed bio markers or objective diagnostic tests

Question 63

Explain the like between concussion, particularly repeated concussions, may lead to later development of neurodegenerative diseases

Answer 63

Initial brain injury sets off cascade of biomechanical processes including inflammation and neuronal damage. Can persist or worsen with repeats. Disruptions in cellular function and signally pathways may accelerate accumulation of abnormal proteins such as tau and beta-amyloid, characteristic of diseases like alheizmers and Parkinson’s. Cumulative effects of concussions can lead to chronic inflammation and oxidative stress, exacerbating neuronal damage increasing risk of conditions like chronic traumatic encephalopathy (CTE)

Question 64

Investigations for TBI including the utility of CT brain

Answer 64

CT brain - uses x rays to produce detailed cross-sectional images of the brain GCS - neurological Assesment tool evaluating conciousness based on eye, verbal and motor responses. MRI - assess for soft tissue damage and abnormalities with high resolution imaging. SCAT5 - clinical Assesment tool for evaluating concussion symptoms, cognitive function and balance

Question 65

Indications for CT in TBI investigation

Answer 65

In presence of moderate or severe TBI or mild TBI GCS less than 15 2 or more hours after injury. Focal neurological deficits, skull fractures, clinical suspicion of skull base fractures, extremes of age, dangerous mechanism of injury, retrograde amnesia lasting more than 30 mins, severe headache with more than 2 episodes of vomiting.

Question 66

Describe current acute management of TBI

Answer 66

DR ABCDE - airway, breathing, circulation, disability, exposure Haemodynamic stability - ensure adequate blood pressure and perfusion to brain to bore vent secondary injuries. C-spine precautions - immobilisation of cervical spine Anti-convulsants - medications to prevent or control seizures, can exacerbate brain injury. Sedatives/analgesics - manage pain and agitation while maintaining cerebral perfusion