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Phase 2a Flashcards > Neurology > Flashcards

Neurology Flashcards

1
Q

Branches of aortic trunk? R CCA and L CCA bifurcate at what level? Ascend in what structure? Once in cranial cavity run in what?

A 
Brachiocephalic trunk--> R common carotid and right subclavian arteries
L common carotid 
L subclavian 
Approx C3-C4
Carotid sheath
Cavernous sinus
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2
Q

Cervical internal carotid has no what? Anterior and medial to what? Posterior and lateral to what? Ascends behind and then medial to what?

A 
Narrowings/ dilatations/ branches
Internal jugular vein 
ECA at origin 
ECA
(Rare carotid-basilar anastomoses)
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3
Q

Petrous ICA penetrates what bone and runs horizontally in what? Small branch where and small potential connection with what?

A

Temporal bone- anteromedially in carotid canal
Middle/ inner ear- caroticotympanic artery
ECA- vidian artery

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4
Q

Turns superiorly at what? Enters what thing? Pierces dura at level of what? Small branches supply what 3 things Potential small connections with ECA via what?

A 
Forman lacerum 
Cavernous sinus 
Level of anterior clinoid process 
Dura, cranial nerves 3-6 and posterior pituitary
ILT
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5
Q

Ophthalmic artery is usually what and passes into what? Superior hypophyseal arteries/ trunk supply what? Posterior communicating artery runs backwards above what to connect with the PCA? Anterior choroidal artery supplies what things?

A

Intradural- into the optic canal
Pituitary gland, stalk, hypothalamus and optic chiasm
CN3 to connect with PCA
Choroid plexus, optic tract, cerebral peduncle, internal capsule and medial temporal lobe- for vision and motor control

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6
Q

What the middle cerebral artery? M1 runs laterally to what? M2 runs in what? M3 emerge onto the what? M4 are what?

A 
Larger of the 2 terminal ICA branches
Laterally to limen insulae 
In the insular cistern 
The brain surface 
Vessels on the brain surface
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7
Q

What does M1 supply?

A

Lentiform nucleus (putmen and globus pallidus)
Caudate nucleus
Internal capsule

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8
Q

What is the anterior cerebral artery? A1 runs medially to connect with contralateral ACA via what? A2 runs in interhemispheric fissue to what? A3 are cortical branches from what arteries?

A

Smaller of 2 terminal ICA branches
Via anterior communicating artery
Genu of corpus callosum and 2 cortical branches
Callosomarginal and pericallosal arteries

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9
Q

Vertebral arteries arise from what? Enters foramina transversarium at what level? Turn laterally at what? Loop posteriorly on what? Through foramen magnum anterolateral to what?

A 
Subclavian arteries- left may directly from arch 
C6
C2
C1
Medulla
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10
Q

Extracranial VA branches supply what?

A

Neck muscles, spinal meninges(cervical spine,) spinal cord- cervical cord, anastomoses with other neck vessels- ECA branches

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11
Q

Intracranial VA branches?

A

Anterior spinal artery, small meduallary perforators, posterior inferior cerebellar artery (PICA) supplies medullar and inferior cerebellum

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12
Q

The VAs unite to form what? Runs anterior to what? Multiple perforating arteries to what? Bilateral anterior inferior cerebellar arteries supply what? Also what arteries?

A 
Basilar artery 
Pons 
Brainstem 
Cerebellum, 7&8 CNs
Bilateral superior cerebellar arteries (SCAs)
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13
Q

The 2 PCAs arise from what? Partially encircle what to supply what things? Also, the medial and lateral posterior choroidal arteries supply what things?

A

Terminal bifurcation of the basilar artery
Midbrain—> thalamus, geniculate bodies, cerebral peduncles and tectum
Tectum, thalamus and choroid of the 3rd and lateral ventricles

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14
Q

What cortical territories does the posterior cerebral artery supply?

A

Inferior temporal lobe- anastomoses with the MCA vessels
Posterior third of the interhemispheric surface- anastomoses with the ACA
Visual cortex and occipital lobe

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15
Q

Classification of headaches?

A

Primary- tension, cluster, migraine, secondary- meningitis, encephalitis, GCA, medication overuse, venous thrombosis, tumour, SAH
Other- trigeminal neuralgia

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16
Q

Red flags for headaches?

A

Fever, photophobia/ neck stiffness, new neurological symptoms, dizziness, visual disturbance, sudden onset occipital headache, worse on coughing/ straining, postural, worse on standing/ lying/ bending over, severe enough to wake the patient, vomiting, history of trauma, pregnancy (pre-eclampsia)

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17
Q

History for headaches?

A

Time, pain- severity, quality, site and speed, associated, triggers +/-, response- during attack/ function/ medication useful, between attacks- normal persisting symptoms, any change in attacks

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18
Q

Examination for headaches? Fundoscopy to look for what?

A

Fever, altered consciousness, neck stiffness, Kernigs sign, focal neurological signs- fundoscopy, always check BP also
Papilloedema- indicates raised intracranial pressure- may be due to brain tumour, benign intracranial hypertension or intracranial bleed

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19
Q

Symptoms of a migraine?

A

Visual/ other aura lasting 15-30 mins followed by unilateral, throbbing headache/ isolate aura with no headache
Episodic severe headaches without aura- often premenstrual, usually unilateral, with nausea, vomiting +/- photophobia/ phonophobia, may be allodynia

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20
Q

Criteria of migraine with no aura?

A

> 5 headaches lasting 4-72h + nausea/ vomiting (or photo/ phonophobia) + any2 of: unilateral, pulsating, impairs/ worsened by routine activity
1 of: nausea and/or vomiting, photophobia and phonophobia

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21
Q

2 criteria of migraine with aura?

A

> 1 reversible aura symptom: visual- zigzags, spots, unilateral sensory- tingling, numbness, speech- aphasia, motor weakness- ‘hemiplegic migraine’
2 of: >1 aura symptom spreads gradually over >5m and/ or >2 aura symptoms occurring in succession, each aura symptom lasts 5-60m, >1 aura symptoms is unilateral, aura accompanied/ followed within 60m with headache

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22
Q

Triggers for migraines (CHOCOLATE)?

A

Chocolate, hangovers, orgasms, cheese, oral contraceptive pill, lie-ins, alcohol, tumult, exercise

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23
Q

DD for migraine? Tx?

A

Cluster/ tension headache, cervical spondylosis, increased BP, intracranial pathology, sinusitis/ otitis media, caries, TIAs may mimic migraine aura

NSAIDs- ketoprofen and dispersible aspirin= similar efficacy to oral 5HT agonists- triptan and ergot alkaloids
Non-pharm= warm/ cold packs to the head, rebreathing into paper bag may help abort attacks
Avoid triggers, stop pill
X3 prophylaxis= propanolol/ topiramate, acupuncture, amitriptyline

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24
Q

Features of cluster headache? Presentation?

A

May be due to superficial temporal artery smooth muscle hyperreactivity to 5HT- there are hypothalamic grey matter abnormalities too, autosomal dominant gene= role too, onset at any age; commoner in smokers

Rapid onset severe unilateral, orbital, supraorbital/ temporal pain
15-180 mins long, middle of night/ morning hours after REM sleep usually
Other symps: ipsilateral eye lacrimation and redness, rhinorrea, miosis and/ or ptosis

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25
Q

Tx of cluster headaches?

A 
Acute= subcut sumatriptan, 100% O2 through non-rebreathable mask for 15 mins
Prevention= veramipil, lithium carbonate, prednisolone
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26
Q

Classification and cause of tension headaches?

A

Episodic TH- <15d per month, chronic TH- >15d per month, can med induced, also ass with depression
Neurovascular irritation refers to scalp muscles and soft tissues

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27
Q

Presentation and tx of tension headaches?

A

Generalised mild-mod pain pressing/ tightening pain bilaterally
30 mins- 7 days

Simple- ibuprofen, aspirin
Chronic- TCA e.g. amitriptyline

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28
Q

4 criteria of trigeminal neuralgia?

A

> 3 attacks of unilateral facial pain, pain in >1 division of trigeminal nerve with no radiation, pain must 3 of: paroxysmal attacks lasting from 1-180 seconds, severe intensity, electric shock-like/ shooting/ stabbing/ sharp, precipitated by innocuous stimuli to affected side of face, no neurological deficit

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29
Q

Tx of trigeminal neuralgia?

A

1st line= carbamezapine 100mg

2nd and 3rd line= lamotrigine, phenytoin or gabapentin, surgery= rhizotomy, stereotactic radiosurgery etc

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30
Q

Presentation of GCA headache?

A

Tender, thickeneded, pulseless temporal arteries, jaw claudication- pain on chewing, scalp tenderness–> pain on combing hair, visual disturbance–> amaurosis fugax (can be irreversible,) systemic features–> malaise, fever, lethargy, weight loss, polymyalgia rheumatic features

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31
Q

Invest and tx of GCA?

A

Bloods= -ANCA, ESR>50, raised CRP and ALP, lowered Hb
Temporal artery biopsy- necrotising arteritis with inflammation

High dose prednisolone (40mg)+ low dose aspirin (75mg)
PPI and bisphosphonate also

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32
Q

Symptoms of CNS infection? Non-blanching rash? 20% bac meningitis sufferers have what?

A

Headache, neck stiffness, photophobia, altered consciousness
Meningococcal septicaemia
Skin scars, amputation, hearing loss, seizures, brain damage

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33
Q

Bacterial causes of meningitis- acute and chronic? Fungal chronic? Acute viral?

A

N.meningitidis, s.pneumoniae, listeria spp, group B strep, h. influenzae B, e.coli
Mycobacterium (TB,) syphilis

Crytococcal

Herpes simplex, varicella zoster, enterovirus

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34
Q

Advice to GP for meningitis tx? >1hr what ABs alternatively? In hospital? For N.mengitidis?

A

IM benzylpenicillin 1200mg if signs of meningococcal disease
Cefotaxime, ceftriaxone
ABC, assess GCS, blood cultures within an hour, broad spec ABs, steroids- IV dexamethasone
Identify close contacts, Ciprofloxacin

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35
Q

What is encephalitis? Causes? Non-infective? Clinical pres?

A

Inflammation of brain parenchyma
Herpes, entero, poliovirus, coxsackie, measles, mumps, varicella
Other: Japanse, tickborne, rabies, West Nile, dengue
AI and paraneoplastic

Flu-like, fever, headaches, confusion, nausea, vomiting, altered GCS, cognitive impairment, seizures, +/- meningism

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36
Q

Invest and tx for encephalitis?

A

MRI head within 24-48 hours, lumbar puncture- lymphocytic CSF, viral PCR

Mostly supportive, IV acicyclovir is suspected HSV/ VZV within 30 mins, phenytoin for seizures

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37
Q

Initial infection with herpes zoster is what? Reactivation? Varicella lies dormant in what? RFs for reactivation? Present? Give what?

A

Chickenpox
Shingles
DRG
Old age, poor immune system, chickenpox <18 months age
Dermatomal distribution of rash and pain
Oral acyclovir

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38
Q

Ascending sensory system has what things? Lat spinothalamic tract crosses where? Descending motor system?

A

Posterior columns, lat spinothalamic tract, thalamus

Internal capsule, pyramidal decussation, corticospinal tract

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39
Q

Reticular activating system is peri-aqueductal gray matter/ floor of fourth ventricle leading to what?

A

Alertness, sleep/wake, REM/ non REM sleep, respiratory centre, cardiovascular drive

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40
Q

MRI images- colour of T2 and T1? Disorders affecting brainstem?

A

White and black
Tumour- meningioma, schwannoma, astrocytoma, metastasis, hemangioblastoma, epidermoid
Inflammatory- MS, metabolic- central pontine myelonecrosis, trauma, sponta haemorrhage- AVM, aneurysm, infarction- vertebral artery dissection, infection- cerebellar abscess from ear

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41
Q

Criteria for brainstem death? Location for common benign tumours?

A

Pupils, corneal reflex, caloric vestibular reflex, cough reflex, gag reflex, respirations, response to pain
Cerebellopontine angle

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42
Q

What is MS? Typically presents in who? Common sites? Types?

A

Chronic AI disorder of CNS- plaques of demyelination
Optic nerves, brainstem, cervical spinal cord
Relapse and remitting, primary progressive, secondary progressive

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43
Q

Typical MS symptoms?

A

Optic neuritis, spasticity and other pyramidal signs, sensory S&S, Lhermitte’s sign, nystagmus, double vision, vertigo, bladder and sexual dysfunction

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44
Q

Ix of MS? Management?

A

MRI brain and spine, evoked potentials, LP= oligoclonal IgG bands in CSF

Acute: steroids= methylprednisolone, chronic: 1st line= beta interferon, glatiramer acetate, 2nd line= natalizumab

Symptoms- tremor= BB, spasticity= baclofen, PT, OT, MDT

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45
Q

What is epilepsy? Prodrome then what x3?

A

Recurrent tendency to have spontaneous, intermittent and abnormal electrical activity in a part of the brain, manifesting as seizures.
Prodrome–> aura–> ictal symptoms- dependent on part of brain affected–> post-ictal symptoms- headache, confusion, amnesia etc

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46
Q

What are partial (focal) seizures? Symptoms of temporal, frontal, occipital and parietal?

A

Limited to one hemisphere
Temporal= smell/taste abnormalities, auditory phenomena, automatisms- lip smacking, walking without purpose, memory phenomena- deja-vu
Frontal: motor phenomena, may –> to Jacksonian march(spreading clonic movement)
Occipital–> visual phenomena
Parietal–> sensory disturbances- tingling, numbness etc.

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47
Q

What are generalised seizures? Absence? Myoclonic? Tonic? Tonic-clonic? Atonic?

A

Simultaneous LoC<10s, abrupt onset and termination
Myclonic= sudden, brief jerking of limb/ face/ trunk
Tonic= increased tone
Tonic-clonic: 1) Tonic phase- LoC and increased tone of limbs 2) Clonic phase (rhythmical jerking of limbs)
Atonic= no LoC, sudden loss of muscle tone e.g. drop of hand or fall

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48
Q

Seizure treated with carbamazepine, lamotrigine? Sodium valproate? Valproate? Valproate, ethosuximide? Valproate/ levetiracetam? Carbamazepine is CI in what seizures?

A 
Partial(focal)
Tonic-clonic
Tonic, atonic
Absence
Myoclonic

Tonic, atonic, absence and myoclonic

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49
Q

What is status epilepticus? Tx in community, hospital? If seizures continue?

A

Seizure>5m- emergency
Open and maintain airway, give O2 and gain IV access
Community–> buccal midazolam or rectal diazepam
Hospital–> IV lorazepam/ diazepam
Phenytoin

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50
Q

What is SUDEP? More common in what?

A

Sudden unexpected death in epilepsy- in uncontrolled epilepsy and may be related–> nocturnal seizure-ass apnoea or asystole

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51
Q

What is non-epileptic attack disorder?

A

Uncontrollable symptoms, no learning disabilities, and CNS exam, CT, MRI, and EEG= normal, may coexist with true epilepsy
Changes in behaviour, sensation and cognitive function caused by mental processes ass with psychosocial distress
Situational, last 1-20 mins
Dramatic motor phenomenoa or postical atonia
Eyes closed and crying/ speaking
Rapid/ slow postictal recovery
History of psych illness/ other form
Vagal nerve stimulation

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52
Q

What is syncope?

A

Paroxysmal event- changes in behaviour, sensation and cognitive processes are caused by insufficient blood sugar/ O2 supply to brain
Often situational
Parasyncopeal symptoms- light headed
5-30 seconds, recovery within 30 seconds
Cardiogenic- less warning, history of heart disease
Common for BP and HR to drop
Fainting can involved jerking

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53
Q

Missile and non-missile head injuries? Lesion distribution? Time course damage following injury? Focal and diffuse damage after non-missile trauma?

A

Dura mater remains intact
Diffuse, focal
Primary- immediate biophysical forces of trauma, secondary- sometime after, physiological responses, effects of hypoxia, infection

Focal= scalp, contusions, lacerations, skull= fracture, meninges= haemorrhage, infection, brain= contusions, lacerations, haemorrhage, infection
Diffuse axonal injury, vascular injury, hypoxia- ischaemia, swelling

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54
Q

Blunt head trauma? Focal damage? Angled/ pointed objects–> what fractures? Flat surfaces?

A

Focal damage- scalp lacerations
Skull fracture, implies considerable force, increased risk of haematoma, infection and aerocele
Localised - often open/ depressed
Linear fractures- can extend–> skull base (contrecoup fractures)

55
Q

People affected by subdural haematomas? Why? Cause of bleeding? Levels of consciousness?

A

Elderly and alcoholics
Brain atrophy, vein stretching, increased likelihood to fall
Rupture of bridging veins running from cortex–> venous sinuses
Fluctuating levels, ICP gradually rises over some weeks

56
Q

Cause of bleeding from extradural haematoma? Level of consciousness? x4 features of ICP?

A

Fracture of temporal bone–> tear of middle meningeal artery
Brief period- then lucid interval of improvement, then condition rapidly deteriorates as ICP increases

Headache, vomiting, confusion, seizures

57
Q

Investigation of subdural and extradural haematomas? Why is LP contraindicated? What shaped is extradural? Subdural?

A

CT head
Coning
Egg-shaped
Sickle-shaped

58
Q

Management of SDH and EDH?

A

ABCDE= first, then osmotic diuresis with mannitol to treat raised ICP, surgery: SDH- emergency evacuation via Burr hole craniotomy, EDH= clot evacuation

59
Q

Aetiology of subarachnoid haemorrhage? RFs?

A

Usually result of bleeding from berry aneurysm at branching points of Circle of Willis- origin of anterior comm artery, joining of pos comm artery with ICA
Congenital AV malformations
Idiopathic
Smoking, alcohol, HTN, bleeding disorders, Marfan + ED syndromes, autosomal dominant PKD

60
Q

Pres of SAH?

A

Sentinel headache in 3 weeks prior to SAH due to small warning bleeds
Symps= sudden onset severe occipital thunderclap headache, others= nausea, vomiting, neck stiffness, seizures, drowsiness

Signs= meningism, fundoscopy- intraocular haemorrhages, signs of increased ICP, focal neurology e.g. pupil changes and other signs of 3rd nerve palsy if pos comm artery aneurysm

61
Q

Invest and tx of SAH?

A

CT head= white star-shape due to blood in basal cisterns
Lumbar puncture- wait 12 hours= xanthochromia(yellowing)= breakdown of RBCs–> increased bilirubin

Nimodipine- decreases cerebral artery vasospasm so prevents cerebral ischaemia
Surgery- coiling(endovascular obliteration) preferred to clipping

62
Q

2 key surface antigens on influenza A? Types in humans?

A

Haemagglutinin(15 subtypes)- virus binding and entry–> cells i.e. grappling hook for getting in
Neuraminidase(9 subtypes)- Bolt Cutters for getting out
H1-H4, N1-N2 and maybe H5

63
Q

Genetics of influenza? Why are there seasonal epidemics?

A

8x single-stranded RNA segments, gene re-assortment can happen in infections as genome= segmented
Genes swapping during co-infection with human and avian flu virus
No proof reading mechanism= prone to mutation
Antigenic drift

64
Q

Influenza B features? C? Transmission? Infection and comps?

A

Prone to mutation, sporadic outbreaks less severe, often children
Minor disease, mildly symptomatic/ asymptomatic
Aerosols, coughs and sneezes, hand to hand, other contact
Upper and/or lower symptoms+ fever, headache, myalgia, weakness
Bacterial pneumonia, mortality higher with underlying health conditions- chronic cardiac and pulm diseases, old age, chronic metabolic disease, chronic renal disease, immunosuppressed

65
Q

Tx options for influenza? Peaks when? Incubation? Infections from symptoms= days after?

A

Supportive- oxygenation, hydration/ nutrition, homeostasis maintain, prevent/ treat secondary infections
Antivirals to reduce transmission, severity and duration
1-4 days, 4-5 days after
December-March

66
Q

Avian flu features? Most seasonal flu=? Controlling?

A

Ruffled feathers and depression, mutation–> highly pathogenic= 100% mortality
SE Asia- close proximity poultry and people, 50-80%= in small rural households
Secondary bacterial pneumonia, H5N1= primary viral pneumonia
Cull affected birds, quarantine, biosecurity, vaccination, antivirals, PPE, reduced risk co-infection

67
Q

Swine flu features? Managing early stages flu?

A

Reassortment swine, avian and human flu, different from human flu
Sensitive to Oseltamivir and Zanamivir, seasonal not effective
40+ some immunity

Containment phase- case identify- swabs, case Tx, contact tracing, increased prophylaxis, tx phase= treat cases only, National Flu Pandemic Service

68
Q

Infection control measures? Managing cases?

A

Hand hygiene, cough etiquette, universal precautions and PPE, surgical masks, non aerosol generating procedures, patient segregation, reduced social contact, flu surgeries
Call centres, non-medical= algorithm, patient/ relative= antivirals, home delivery, hospital admission criteria

69
Q

Anti-viral drugs how many courses to cover what % attack rate? Most effective when? Issues?

A

30 million for 50% attack rate
Mostly Tamiflu and some Relenza, within 24-48 hours
Reduced hosp admission by 50% and disease duration by 24 hours
Resitance, side effects, who given, distribution

70
Q

Limited role of face masks?

A

Only if worn correctly, changed freq, removed properly, disposed safely, used + good universal hygiene procedure, run out, how many per day?

71
Q

Staff issues with flu? Impact on schools and other services? Pop-wide interventions?

A

Anxiety to work, adequate protection, access to antivirals, risk to family, staff segregation, redeployment, staff recycling, organisations sharing staff
NHS staffing if schools close?, distribution and transport, prisons, education, business

Travel and mass gatherings, restrictions, school closures, voluntary home isolation, screening people into UK ports

72
Q

MERD coronavirus? SARS?

A

Bats–>camels, lots of outbreaks due to Hajj

Caused by SARS-COV virus

73
Q

What are adverse events a product of? What are sharp-enders more likely to be? What model of causation? What is culture?

A

Many causal factors
The inheritors rather than the instigators, remedial efforts directed at removing error traps and strengthening defences
‘Swiss-cheese’ model

Shared values and beliefs that interact with an organisation’s structure and control systems–> behavioural norms

74
Q

What is healthcare harm? Occupational and transport safety figures focus on what more? What is human error?

A

Broadly defined- includes smaller/ less serious events and larger events and fatalities
On mortality and larger incidents of harm
Failure of a planned action/ sequence of mental/ physical actions to be completed as intended/ use of wrong plan achieve an outcome

75
Q

What are never events? Latent failure? Active failure? Organisational system failure? Technical failure?

A

Serious, largely preventable patient safety incidents if correct measures implemented e.g. wrong site/ implant, retained object, wrong rate of admin etc

Removes practitioner- organisational policies, procedures, resource allocation= less apparent
Direct contact with the patient
Indirect involving management, culture, knowledge

Indirect failure of facilities/ external factors

76
Q

3 factors contributing to adverse events? Confirmation bias? Anchoring? Diagnosis momentum? Flow?

A

Clinical complexity, poor communication- good= SBAR, complex systems
Evidence to confirm rather than discomfirming evidence e.g. tests
Lock onto salient features in initial presentation and failing to adjust in light of later information

Once labels are attached, gathers momentum until becomes definite and all other possibilities excluded

Error–> report–> learn from it–> share it–> inform patient and apologise (duty of candour)

77
Q

Distinguishing motor neurone disease from MS and polyneuropathies? From myasthenia gravis?

A

No sensory loss/ sphincter disturbance

Eye movements not affected

78
Q

Features of UMN disease?

A

Hyper-reflexia, hyper-tonia, spasticity, Babinski +ve, DISUSE ATROPHY

Hypo-reflexia, hypo-tonia, denervation atrophy, Babinski -ve

79
Q

Features of MN disease?

A

Dysfunction of MOTOR neurones, no sensory disturbances, destruction in anterior horn cells of brain and spinal cord
4 types= most patients= mixed picture, ALS= most common, SOD-1 gene

80
Q

Meaning of paresis? Paralysis? Ataxia? Apraxia?

A

Impaired ability to move body part
Can move body part- no will
Will movements= clumsy, ill-directioned/ uncontrolled
Disorder of consciously organised patterns of movement/ impaired ability to recall acquired motor skills

81
Q

What can affect UMN and LMN? Investigating UMN disease? Median age and how many years fatal?

A

Fasciculations- varied picture

EMG, raised creatinine kinase due to muscle destruction
60 years, 2-4 years

82
Q

Tx for MN disease?

A

Anti-glutamatergic drugs: Riluzole- Na+ channel blocker inhibiting glutamate, CI= renal/ liver, prolongs life 3 months, SE= vomiting, pulse increase, somnolence, headache, vertigo, LFT increases

Symptoms= tracheostomy, ventilator, NG tube
PT/OT/ MDT
Drooling= amitryptyline, propantheline
Joint pain and distress= NSAIDs, then opioids

Death= due to resp failure due to pneumonia

83
Q

3 cardinal symptoms of brain tumour? Features of increased ICP? Cardinal physical sign?

A

Raised ICP–> headache, reduced conscious level, nausea, vomiting
Progressive neurological deficity, epilepsy- more focal seizures

Worse in morning, increased by coughing, sometimes relieved by vomiting
Papilloedema

84
Q

Causes of secondary tumours? Tx options?

A

Non small cell lung tumour, small cell lung, breast, melanoma, renal cell, GI, unknown primary
Chemo/radiotherapy, surgery, best supportive care
Surgery for: absent/ controlled primary disease, age<75, good performance status

85
Q

Most primary where origin? Most freq, that occur in adults? Most common in 4th-5th decade?

A

Glial cell
Astrocytoma
Oligodendroglioma

86
Q

Gliomas graded what? Grade I? II? III? IV?

A

Pilocytic-‘Paediatric’
Benign- premalignant
Anaplastic astrocytoma- cancer (malignant)
Glioblastoma multiforme(GBM)- most common phenotype, given time= all gliomas–> GBM, prognosis=<1 year

87
Q

2 pathways–> malignant gliomas?

A

1) Common= initial genetic error of glucose glycolysis, mutation of IDH-1–> excess of 2-hydroxyglutarate, gen instability in glial cells and inappropriate mitosis
2) Less common= no IDH mutation, catastrophic gen mutation, poor prognosis- even low grade

88
Q

How classify brain tumours? Aim to determine what?

A

Histologically A and E, immunohistochemistry and mol/ cytogenetics
Tumour type, grade, prognostic factors, additional markers

89
Q

Tx of brain tumours?

A

Temozolomide- smaller pro-drug crosses BBB, methyl–> guanine preventing DNA replication- can be reversed by MGMT from tumours–> resistant
Chemo and radiotherapy
Dexamethasone- most powerful oral/IV, improves brain performance in all tumours, reduced inflam and oedema, no later than 2pm

90
Q

Most common cancers metastasising to brain?

A

Lung, breast, colorectal, prostate

91
Q

Commonest cause of dementia? Early degeneration of what brain section? Frontal lobes? Temporal lobes?

A

Alzheimers disease- medial temporal lobe–> temporal neocortex, frontal and parietal ass areas
Motor movements, motor speech-Brocas area, personality, planning
Hearing, language comprehension, semantic knowledge, memory, emotional behaviour

Selective amnesia and language impairments–>complex attention–> visuospatial, sustained attention–> global deficits

92
Q

Differentials of dementia?

A

Vascular/ mixed dementia- sub-cortical frontal pattern- attention and motor difficulties, visuospatial difficulties
With Lewy bodies- fluctuating cognition, pronounced disturbances in attention, working memory and early visuoperceptual deficitis
Depressive pseudodementia

93
Q

Psych changes in dementia?

A

Subtle behavioural changes- inattentiveness, mild cog dulling, social and emotional withdrawal and agitation
Apathy, disengagement
Psychotic= delusions, hallucinations, anxiety

94
Q

Pre-clinical AD?

A

Memory impairment= first marker, poor perf on episodic memory tests, general cog function= preserved, daily living= intact, score above 24/30 on MMSE, high risk–> AD

95
Q

Examination for AD?

A

History- cog function via 6 CIT- year, month, address, with 5 parts, count 20-1, months in year in reverse, repeat address
Blood tests- B12, folate, iron, neuropsychology
MRI- atrophy, function assessed- energy and blood supply= PET and SPECT, functional MRI- networks

96
Q

Management of dementia?

A

Prevention= healthy behaviours, support= socially and cognitively, carers courses
Meds for mood and anxiety- acetylcholinesterase inhibitors- memantine (anti-glutamate,) control vasc factors

97
Q

What are somatisation disorders? Conversion disorder? Pain disorder? Dissociative disorders?

A

When physical symptoms caused by mental/ emotional factors
No medical explanation for brain/ neurological symptoms
Persistent pain cannot be attributed to physical disorder

Cause physical and psychological problems, short lived/ longer
Of movement/ sensation
Dissociative dementia- info about themselves, past, skill, not knowing how got there

Dissociative identity disorder- uncertain about identity, may feel presence of others

98
Q

Who’s hierarchy of needs? ABC of self-care?

A

Maslow’s
Awareness
Balance
Connection

99
Q

What is myasthenia gravis characterised by? Associated with what in 10%

A

Weakness and fatigability of ocular, bulbar and proximal limb muscles- ptosis, talking and chewing problems, swallowing
IgG ABs–> AChR at post-synaptic membrane at NMJ
Thymic tumour

100
Q

What drugs can aggravate myasthenia gravis? Investigations?

A

BBs, lithium, some ABs
Bedside- count to 50/ keep arm outstretched
Bloods- anti-AChR ABs in blood, anti-MuSK ABs
Tensilon test(rarely performed)
CT/MRI for thymoma

101
Q

Tx for myasthenia gravis?

A

Anticholinesterases- pyridostigmine, immunosupressants- prednisolone, azathioprine
Plasmapheresis- IVIG in myasthenic crisis
Thymectomy

102
Q

What is expert medical generalism?

A

HC–> all patients on list with any HC need

Focus on whole person

103
Q

Only output of cerebellum? Symptoms of cerebellar ataxia? Examination?

A

Purkinje cells
Slurring speech- staccato, swallowing difficulties, oscillopsia, clumsiness, tremor, loss precision, unsteadiness in dark, stumbles and falls

Gait, limb ataxia, eye movements, speehc, sensory ataxia, other signs

104
Q

Signs of cerebellar dysfunction? (DASHING)

A

Nystagmus, dysarthria, action tremor, dysdiaochokinaesia- impaired ability rapid movements, truncal ataxia, limb and gait ataxia

105
Q

Clinical severity ataxia?

A

Mild= mobilising independently/ walking aid, moderate= 2 walking aids/ frame, severe= wheelchair dependent, SARA= rating and assessment of ataxia

106
Q

Majority of children brain tumours where? Adults? Most meningiomas what grade?

A

Posterior fossa
Supraentorial
Grade I

107
Q

Normal ICP in adults? Types of herniation syndromes?

A

<15mmHg
Uncal herniation
Tonsil herniation
Subfalcian (cingulate) herniation

108
Q

Formation of dopamine? Where is it produced? 3 cardinal triad of Parkinson’s?

A

L-tyrosine–>L-DOPA–>dopamine
Substantia nigra- apoptosis here–> PD

Tremor- worse at rest, 4-6 cycles/ sec= slower than cerebellar tremor
Rigidity/tone–> ‘cogwheel rigidity’, felt during rapid pronation/ supination
Brady/ hypokinesia- slow to initiate movement, low amplitude excursions in repetitive actions, reduced arm swing, festinance- shuffling, freezing at obstacles, expressionless face

109
Q

Causes of Parkinson’s?

A

Reduction in dopamine secreting cells of substantia nigra- lightens, reduce dopamine to striatum, reduced neuronal transmission from basal ganglia to cortex

110
Q

Diagnosing Parkinson’s?

A

Tremor and/or hypertonia with bradykinesia; exclude frontotemporal dementia and cerebellar disease
Signs worse on one side
MRI rule out structural pathology

111
Q

Differentials for Parkinson’s?

A

Benign essential tremor
Parkinson-plus syndromes- VIVD- vertical gaze palsy, impotence/ incontinence, visual hallucinations, interfering activity by limb, diabetic/ htn patient
Drugs- antipsychotics, metoclopramide, prochlorperazine
Rarer= trauma, Wilson’s disease, HIV

112
Q

Drugs to increase dopamine supply? Decrease dopamine breakdown? Help tremor?

A

Co-careldopa- L-DOPA (levodopa)+ carbidopa
Dopamine receptor agonists–> ropinirole/ rotigotine

MAO-B inhibitor–> rasagilline/ selegiline
COMT inhibitor–> entacapone/ tolcapone

Anticholinergic- amantadine

113
Q

Non-pharm for Parkinson’s?

A

Deep brain stimulation, surgical ablation of overactive basal ganglia

114
Q

Cardinal features of Huntingdon’s disease?

A

Chorea- fidgety (not aware of abnormal movements), dementia, psychiatric issues-pers change, depression, psychosis+ FH

115
Q

What triplet of Huntington gene is repeated? Atrophy of which part of the brain–> depletion of GABA? Early features?

A

CAG>39 repeats needed
Striatum
Depression, self-neglect, irritability, behavioural issues etc.
Advanced= chorea and rigidity, dementia

116
Q

Differentials for HD?

A

Sydenham’s chorea, benign hereditary chorea, drug induced, other dyskinesias, other causes of dementia

117
Q

HD examination?

A

Abnormal eye movements, chorea, ataxia- heel–>toe walking issues, ‘touch of Parkinsonism’- rigidity, slowness fine finger movements

118
Q

Conventional HD tx?

A

Chorea- neuroleptic- sulpiride, depression= SSRIs- seroxate, psychosis= neuroleptic- Haloperidol, aggression= Risperidone

119
Q

What is Guillain Barre-syndrome? Triggered by what infections?

A

Acute neuropathy, inflammatory and demyelinating

Campylobacter jejuni, EBV, CMV

120
Q

Presentation of Guillain Barre?

A

Progressive onset limb weakness after viral illness, loss of reflexes, often sensory and motor disturbances

Severe–> resp depression, vital capacity should be monitored if suspected

121
Q

Investigations of Guillain Barre? Tx?

A

Mainly clinical, nerve conduction studies, LP= high protein in CSF

IVIG, ventilation if resp muscles involved

122
Q

What is the cauda equina? Causes of compression? Presents? Diagnosis and tx?

A

Bundle of spinal nerves from level L1/2
Back pain, saddle anaesthesia, loss of bowel/bladder control
MRI
Surgical decompression

123
Q

Nerves affected by mononeuropathies? Causes of polyneuropathies? (DAVID)

A

Median, radial, sciatic, common peroneal

Diabetes, alcohol, vit def- B12, infective- GB, drugs (isoniazid)

124
Q

Causes of carpal tunnel syndrome? Tests? Tx?

A

Pregnancy, obesity, hypothyroidism, RA
Tinnel’s and Phalen’s
Pain relief, splint, steroid injection, surgery

125
Q

Aetiology of TIA and stroke?

A

Thrombosis in situ, embolism from heart(valve disease, mural thrombus- AF)/ carotid, CNS bleed- ass with HTN, aneurysm rupture, head injury, young patient= vasculitis, thrombophilia, SAH

126
Q

Modifiable and non-modifiable RFs for stroke?

A

HTN, smoking, hyperlipidaemia, obesity

DM, male, vasculitis, hypotension

127
Q

3 features of total anterior circulation syndrome (TACS)- large cortical stroke in ACA/MCA territories?
PACS- partial in ACA/MCA territories?

A

Contralateral weakness and/or sensory deficit of face, arm and leg, homonymous hemianopia, higher dysfunction- dysphasia, visuospatial disorder

Contralateral weakness, homonymous hemianopia, higher dysfunction

128
Q

Posterior circulation syndrome (POCS) one of what features? What is Lacunar syndrome? One of what features?

A

Cerebellar/ brainstem syndrome- quadriplegia, locked in syndrome LoC, isolated homonymous hemianopia, cranial nerve palsy AND contralateral/ sensory deficit

Subcortical stroke due to small vessel disease: pure motor stroke, ataxic hemiparesis- ipsilateral weakness+clumsiness(mostly legs,) pure sensory- contralateral numbness, tingling, pain or burning
Mixed sensorimotor stroke
Clumsy hand dysarthria

129
Q

Investigation for stroke? 1st and 2nd line for ischaemic? Tx for haemorrhagic?

A

Distinguish between hemorrhagic and ischaemic stroke –> CT brain
Thrombolysis, then aspirin 300mg for 2 weeks, then clopidogrel 75mg OD

Control BP: B-blocker, Beriplex if warfarin-related bleed, clot evacuation
Rehab= physio, OT, SALT
Anti-hypertensives, statins

130
Q

What is a TIA?

A

Sudden onset global neurological deficit lasting <24h, with complete clinical recovery -usually 5-15m

131
Q

Features of carotid/ anterior blockage? Vertebrobasilar/ posterior?

A

Hemiparesis- unilateral weakness and/or hemisensory loss
Amaurosis fugax–> descending loss of vision in one eye(ipsilateral retinal/ ophthalmic artery embolism,) Broca’s dysphasia

Hemisensory symptoms
Diplopia, vertigo, vomiting, dysarthria–> slurred speech, ataxia
Hemianopia(ophthalmic cortex) or bilateral visual loss

132
Q

ABCD2 score for TIA?

A

Age>/=60= 1 point
BP>/= 140/90= 1 point
Clinical features: unilateral weakness= 2 points, speech disturbance without weakness= 1 point
Duration of symptoms: >60 mins= 2 points, 10-59 mins= 1 point
Diabetes= 1 point

133
Q

What tx following TIA, if ABCD2>4, >1 TIA/ week/ AF/ on anticoagulant?

A

Antiplatelet- aspirin 300mg or clopidogrel 300mg unless on anticoagulant therapy
Statin- simvastatin 40mg
If on AC therapy= admit for imaging to rule out haemorrhagic stroke

134
Q

Secondary prevention following TIA?

A

Lifestyle, control RFs, clopidogrel and statin prescribed

For patients with 50-90% carotid stenosis= carotid endarterectomy

Phase 2a Flashcards (14 decks)

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