100% satisfaction guarantee Immediately available after payment Both online and in PDF No strings attached
logo-home
Neurology - Summary $7.79   Add to cart

Summary

Neurology - Summary

 6 views  0 purchase
  • Course
  • Institution

Neurology - Summary Table of all neurological conditions organised by history findings, examination findings, investigation findings and management according to Australian guidelines.

Last document update: 10 months ago

Preview 2 out of 9  pages

  • December 26, 2023
  • December 26, 2023
  • 9
  • 2022/2023
  • Summary
avatar-seller
Stroke and Vascular Disease
Info History/RF Examination Investigation Management
Migraine Ax – unclear; genetic predisposition potential triggers – 1 Prodrome (hrs-days) – food cravings, mood changes, photophobia, To exclude other Dx Lifestyle – avoid known triggers;
Primary alcohol, nicotine, poor sleeping habits, emotional stress, phonophobia, osmophobia headache diary to identify triggers;
headache weather changes, hormonal changes in women 2 Aura - positive phenomena i.e visual sparkles, flashing lights; negative Bedside – regular sleep cycle, regular meals,
characterised by (menstruation, hormone intake – OCP) phenomena i.e vision loss; sensory changes – paresthesia; speech stress Mx
recurrent Pathophys – language Sx; hemiplegic migraine i.e aura involving motor weakness Mild-moderate
episodes of Neurogenic inflammation – inflammation (vasodilation, 3 Main event Bloods – Nonopioid analgesia (aspirin or
unilateral, fluid and protein extravasation, etc) caused by the Throbbing, drilling, ice pick to the head, burning FBE, UEC, CRP, ESR (↑ in temporal ibuprofen or other NSAID +
localised pain action of neuro-peptides on blood vessels Unilateral usually, but can shift sides during attack arteritis) paracetamol)
that can be Cortical spreading depression – slow wave of electrical Fronto-temporal pain distribution If nauseated – metoclopramide
accompanied by activity → ? auras + activating the nerves that sense Vomiting Triptan (serotonin agonists) – can
N/V and pain in the meninges + change the function of blood 4-72hrs duration, worse in PM w/ gradual onset be given subcut if more severe
Imaging –
sensitivity to vessels 4 Postdrome/hangover – decreased mood, concentration difficulty, Refractory pts
MRI brain w/ contrast – concerning
light and sound Trigeminovascular system – group of nerve cells that fatigue and so on Ergots/ergotamine
headaches – identifies space-
sense pain in the face and covering of the brain – causes (vasoconstrictor) via serotonin
occupying lesions or ischaemia
Chronic, neurogenic inflammation via the release of a substance; RF – Female; OCP use; FHx; Overuse of analgesia; altitude; stress; lack of receptor agonist, but also action on
CT head – looking for intracranial
genetically normal pulsations of the vessels are sensed by CNV as sleep dopamine and NA
haemorrhage, raised ICP
driven, episodic, painful stimuli Paraenteral Mg (for migraine +
neurological Common migraine – no aura, paroxysmal headache +/- aura)
vomiting; classic migraine – aura, paroxysmal Clinical Dx Other anti-emetic (chlorpromazine
disorder
headache, N+V Other – – an anti-psychotic)
N/V, photophobia, fever, neck pain/stiffness, loss of weight or appetite, LP if thinking meningitis Stronger NSAID (Ketorolac)
Epi – early-mid-life; more common in females trauma, aura – flashing lights/loss of vision, speech, movement or CSF culture Prophylaxis – antiepileptics, TCA,
sensation, seizure propranolol, CCB (verapamil)
NO objective sensory or motor neurological signs
Stroke Pathophys – PC – face change, heavy arm etc, Bedside – BSL (elevated in AIS); ECG + ACUTE
Sudden onset of Ischaemic (~85%) – sudden onset neurological Sx Vitals, BSL, GCS (important to Telemetry – AF, STEMI/NSTEMI, prev Ischaemic – DRSABCD
neurological Arterial thrombosis (formation in artery i.e local); large <30min – TIA; >30min – stroke track progression of stroke) ischaemic events Ensure haemodynamic stability
deficits of a vessel – stenosis or occlusion of ICA, vertebral or Pain Rapid neurological assessment (HTN is expected; treat if >200)
vascular basis w/ intracranial a leading to insufficient blood flow beyond Headache (NIHSS score /42 – favours MCA Bloods – FBE, UEC (?electrolytes, Stroke admission
infarction of CNS lesion; small vessel/lacunar – chronic HTN and DM Neck pain strokes) contrast for CT) Thrombolysis – IV alteplase tPA if
tissue cause vessel wall thickening and decreased luminal Weakness in arms or legs Troponin (intramural thrombus → <4.5hr from Sx onset
diameter Sensory changes on limbs or face stroke) Endovascular clot retrieval if <6hr
TIA – same thing Cardioembolic (blockage of cerebral arterial flow from a Visual changes – all vision or part Coag studies – pro-thrombotic from Sx onset
but w/o cardiac source) – AF usually, left ventricular aneurysm, of vision BAC/drug screen – cerebellar Neurosurg referral
infarction rheumatic valve disease, prosthetic heart valves, recent Speech – expressive or receptive presentation Haemorrhagic – DRSABCD

, MI, IE, paradoxical embolus (patent foramen ovale) aphasia, dysarthria HbA1c Surg Mx – IV cannula, NBM
AIS – w/ Systemic Hypoperfusion (global cerebral ischaemia) – Ax – AF, hyperlipidaemia, previous Lipid profile Tranexamic acid (considered if
infarction inadequate blood flow to the brain secondary to cardiac TIAs Coags – thrombocytopaenia NOAC or bleeding)
arrest, arrythmia, MI, severe respiratory failure; affects RF – age, male, post-menopausal BP control via BB
watershed areas b/w major cerebral arterial territories women, atherosclerotic RF (HTN, Imaging – Reverse anti-coag
Haemorrhagic (~15%) – DM, smoking, hyperlipidaemia, Non-contrast CT head – rule out ICH, Neurosurg referral for Mx; surgical
Intracerebral haemorrhage – hypertensive – rupture of obesity), embolic RF (AF, SAH evacuation
small microaneurysms causing intraparenchymal COCP/HRT, IVDU), FHx or PMHx CT angiography – will tell us how Ongoing – statin, aspirin, BB,
haemorrhage usually at the putamen, thalamus, much tissue is dead (umbra) + how clopidogrel, SNAPW, treat
cerebellum and pons; trauma, amyloid angiopathy, SAH – sudden onset, thunderclap much can be saved (penumbra) underlying Ax (AF, carotid
vascular malformations, vasculitis, drug use headache; worst headache ever CT perfusion endarterectomy/revascularisation),
SAH – cerebral aneurysms (saccular/berry), AVM, MRI – DWI, FLAIR DM control, HTN control
trauma (blunt, penetrating) TTE Long term antithrombotic therapy
Non-AF – antiplatelets – aspirin,
DDx – peripheral vertigo, migraine, delirium, seizures, clopidogrel
Complete – carotid a doppler studies AF – anti-coagulation – warfarin,
electrolyte disturbances for stenosis, lupus anti-coag + anti DOACs
cardiolipin, ESR/CRP, blood cultures, Dedicated stroke unit
fasting serum lipids, echocardiogram
(IE or thrombus)
ACA MCA ICA (gives off ACA/MCA) PCA (supplies occipital lobe) ICH
Contralateral weakness - LL>>face, UL Contralateral weakness - Face, Very similar to ACA/MCA Contralateral homonymous Headahce
Contralateral sensory loss - LL>>face, UL UL>>LL syndrome heminaopia Increased ICP signs - N/V, Cushing's
Personality change Contralateral sensory loss - Face, Also gives off opthalmic a - Alexia w/o agraphia triad - bradycardia, irregular
Abulia, disinhibition, executive dysfunction UL>LL temporary monoocular vision loss Contralateral hemibody pain respirations, widened pulse
Akinetic mutism - no movement or speech Ipsilateral gaze deviation (towards Midbrain syndromes pressure
Speech unclear or dysarthric side of lesion) Watershed areas - hypoxic Ax Diplopia and ataxia
Contralateral homonymous MCA/ACA zone - Proximal UL/LL Lacunar Infarcts SAH
heminaopia (lesion at visual weakness, sensory loss Pure motor stroke Worst headache ever - thunderclap
radiations) MCA/PCA zone - visual Pure sensory stroke Meningeal signs
If L dominant: dysfunction Mixed sensorimotor Increase ICP signs - N/V, Cushing's
Broca's Aphasia - expressive Ataxic hemiparesis - weakness + loss triad
Wernicke's Aphasia - receptive of coordination
If R non-dominant: Dysarthria
Apraxia - inability to perform
learned movements on command
Sensory/visual neglect

Intracranial Epidural haemorrhage: bleeding between the dura EDH – Bedside – BSL EDH
Haemorrhage mater and the calvarium; middle meningeal a (red High impact history Conservative if small
Bleeding within lemon) Initial LOC → lucid interval → coma Bloods – Evacuation of the clot
the skull Epi – 20-30yr males, good prognosis CN III palsy – down + out FBE, UEC, LFT, CRP, coags, VBG, SDH
Ax – head trauma – MVA, falls + assaults, 70-95% have High ICP – headaches, vomiting, confusion, seizures, aphasia blood cultures – if febrile Conservative Mx - generally benign
Encompasses pterion fracture SDH – if conservative is appropriate
epidural, PPx – high impact → skull fracture + tears of middle Older pt falls ~days ago Evacuation of the clot
meningeal a Anticoagulants Imaging – -Burrhole or craniotomy
subdural, CTB –
subarachnoid Subdural haemorrhage: bleeding between the dura and Progressive neurological decline -If surg – 50-90% mortality
the arachnoid layer (subdural space); damage to High ICP Sx as above EDH – Red lemon, midline shift, SAH
and intracerebral ventricular compression
haemorrhage. bridging veins (blue banana) SAH – DRS ABCD
Epi – common in infant/toddlers Sudden, onset, severe ‘thunderclap’ headache, +/- sentinel headache SDH – Blue banana Address ICP – bed elevation,
Ax – non-accidental injury in infants/toddlers (physical may occur 1-2 weeks before, high ICP + mass effects – LOC, N/V, SAH – starfish of death hypoventilation, BP control
Cx – tonsillar abuse); falls in elderly (atrophy of vessels -> friable) confusion + seizures ICH – hyperdense lesion where the Analgesia – Panadol
herniation, PPx – trauma + friable blood vessels in elderly → Meningism – photophobia, neck stiffness, headache; Kernig’s haemorrhage occurred Nimodipine PO for 21d – CCB to

The benefits of buying summaries with Stuvia:

Guaranteed quality through customer reviews

Guaranteed quality through customer reviews

Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.

Quick and easy check-out

Quick and easy check-out

You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.

Focus on what matters

Focus on what matters

Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!

Frequently asked questions

What do I get when I buy this document?

You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.

Satisfaction guarantee: how does it work?

Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.

Who am I buying these notes from?

Stuvia is a marketplace, so you are not buying this document from us, but from seller nikitagoyal. Stuvia facilitates payment to the seller.

Will I be stuck with a subscription?

No, you only buy these notes for $7.79. You're not tied to anything after your purchase.

Can Stuvia be trusted?

4.6 stars on Google & Trustpilot (+1000 reviews)

75323 documents were sold in the last 30 days

Founded in 2010, the go-to place to buy study notes for 14 years now

Start selling
$7.79
  • (0)
  Add to cart