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Take 2: Electric Boogaloo > Phase 2 - Neuro > Flashcards

Phase 2 - Neuro Flashcards

1
Q

Define meningitis

A

Inflammation of the pia and arachnoid mater. Oft caused by organisms infecting the CSF.

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2
Q

Define meningism

A

A set of symptoms indicative of some kind of meningitis, not necessarily of an infective cause (e.g. chemical meningitis/post-surgical)- Stiffness of neck- Severe headacje- Photophobia

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3
Q

Symptoms of infective meningitis

A
  • Pyrexia- Malaise; N+V- May have NON-BLANCHING PURPURIC RASH - characteristically HAEMORRHAGIC in meningococcal (n meningitidis) meningitis - Meningism- Kernig (can’t extend knee when hip is flexed)- Brudzinski sign (knee + hip automatically flex when neck flexed while lying down)
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4
Q

Causes of infective meningitis

A
  • 80% - viruses: - Enteroviruses (Echo virus, Coxsackie virus) - historically Polio - Herpes simplex - Mumps - Lymphocytic chorio meningitis virusBacterial (notifiable):- Neonates: - E coli - Group B (found in genital tract - 25% at child-bearing age) - Listeria monocytogenes - Pinpoint to small, semi transparant colonies with narrow haemolytic zone on Blood Agar - S pneumoniae- infants: - N meningitidis - Strep pneumoniae - H influenzae - a G -ve bacillo-coccus - fastedious, requires Factors V+X- Adults: - Neisseria meningitidis - Strep pneumoniae - both are diplococci but Neisseria is G -ve- Elderly: - Strep pneu - N mening - Listeria monocytogenesListeria affects extremes of age, immunocompromised (including pregnant women + DM)- crowded environment + non-vaccination = RFxViral more common, bacterial more severe
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5
Q

Define encephalitis

A

Inflammation of cerebral cortex

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6
Q

Symps of encephalitis

A
  • Lethargy + fatigue- decreased level of consiousness- Fever- Headache- Encephalopathy, Focal neurology - esp Temporal lobe -> e.g. aphasia- occasionally - fitsCombined with meningism = meningo-encephalitis
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7
Q

Causes of encephalitis

A

Usually viral:- Herpes simplex - 95%- Vaicella zoster- Parvovirus- HIV- Measles- MumpsOccassionally - toxoplasma gondii from cats

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8
Q

Lab investigations for meningitis/encephalitis

A

MRI HEAD for Encephalitis (unilateral inflam) - do first to check ICPCSF obtained via LUMBAR PUNCTURE - ‘gin-clear’, pressure <15cm of H2O (fast - analysed within couple of hours)- analysed for:- cell count- Gram film- Protein- Glucose- Culture on blood/chocolate agar- PCR - enteroviruses, HSV, VZV, s pneum, n mening - CONTRAINDICATED in raised ICP due to risk of tentorial herniation/coningBlood - cultures + PCR for S pneum + N meningNose + throat swabs - blood/chocolate agar + PCR for enterovirusStool PCR for Enterovirus

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9
Q

CSF lab findings consistent with bacterial infection

A
  • Neutrophil predominant leucocyotosis - Raised protein (from dying bacteria, acute phase antibacterial proteins + Ab)- Reduced CSF glucose to serum glucose ratio (Neutrophils + bacteria use up)
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10
Q

Empirical treatment for bacterial meningitis

A

IV cefotaxime/ceftriaxone (3rd gen cephalosporins)- broad spectrum against all common CNS bacteria- good CNS penetration+ IV DEXAMETHASONE (corticosteroid) adjuvent therapy (ie simultaneously)- reduce risk of long term neurological complications- start at same time/immediately prior to starting antibiotics (ie as soon as bacterial diagnosis confirmed)If Immunocomp give AMOXICILLIN - covers ListeriaIf Px presents to GP with non-blanching, purpuric rash -> give IM BENZYLPENICILLIN + immediate hospital referral

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11
Q

Antibiotic therapy for Listeria monocytogenes CSF infection

A

IV AMOXICILLIN - HIGH DOSE + FREQUENCY- 2g every 4-6hrs- start as soon as diagnosed or empirically if suspicion of bacterial meningitis in Immunocomp patient.May add IV GENTAMICIN as adjunctive Abx

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12
Q

When is a lumbar puncture not required in diagnosing bacterial meningitis

A

If the patient presents with the carachterisitc haemorrhagic rash + meningism -> strong clinical suspicion of MENINGOCOCCAL SEPTICAEMIA + meningitis- lumbar puncture is unnecessary + may be harmful if there are any coag abnormalities secondary to meningococcal sepsis- diagnosis can be confirmed by peripheral blood culture or peripheral blood molecular testing (PCR) for N meningitidis

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13
Q

What actions should be taken if a patient is confirmed to have meningococcal meningitis

A
  • Notify Public Health England- Close contacts should be offered antibiotic prohphylaxis - usually single dose of ORAL CIPROFLOXACIN (fluoroquinolone)
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14
Q

CSF lab findings consistent with viral meningitis/encephalitis

A
  • predominantly lymphocytic response- only moderately raised protein- CSF glucose is >50% of the level of the paired serum sample glucose
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15
Q

Treatment for encephalitis

A

IV ACICLOVIR for HSV or VZVIf enterovirus -> self limiting, no antiviral needed just supportive measures where necessary

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16
Q

Define Transient Ischaemic Attack

A

Sudden onset neurological Deficit that lasts for less than 24hrs, caused by focal brain, spinal cord or retinal ISCHAEMIA WITHOUT EVIDENCE OF ACUTE INFARCTION - not a medical emergency so doesn’t require immediate hospitalisation

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17
Q

Epidemiology of TIA

A
  • 90% = ICA (anterior)- 10% vertebral (posterior)
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18
Q

Causes of TIA

A

CAROTID THROMBO-EMBOLI- thrombosis- emboli (fat from atheroma or thrombus, typically from heart) - remember AFib = risk factor for stroke!

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19
Q

RFx for TIA

A

Almost same as IHD/stroke

    • Smoking: Increased Alcohol
    • Diabetes T2
    • HTN
    • AFib
  • Obesity/hypercholesterolaemia
    • VSD
  • Also:- FHx of stroke/TIA
    • Age >55
    • Higher risk in males
      • (-genetics may play a factor)
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20
Q

Presentation of TIA

A

Focal neurology - sudden onset; typically lasts 5-15mins, can last up to 24hrs:

  • ACA -> weak/numb contralateral leg
  • MCA -> contralateral hemiparesis - esp forehead sparing face drooping
    • temporal = receptive dysphasia; frontal = Expressive dysphasia
  • Posterior CA -> Contralateral homonymous hemianopia w/ macular sparing (occipital cortex)
  • Vertebral A -> Cerebellar syndrome (DANISH - sensory + motor) - potential Brainstem infarct (loss of basic vital functions) - Cranial nerve lesions 3-12-
    AMAUROSIS FUGAX -> occlusion/reduced blood flow to RETINA via OPTHALMIC, RETINAL or CILIARY ARTERY
  • BAD PROGNOSIS - oft indicates oncoming STROKE
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21
Q

Dx of TIA

A

Clinical - same as stroke- FAST (face, arms, speech, time)

ABCD2 (no longer advocated by NICE)

  • Age >60 (1 point)
  • BP >140/90 (1)
  • Clinical Sx (unilateral weakness = 2; slurred speech, no weakness = 1)
  • Duration (>1hr = 2; <1hr = 1)
  • T2DM (1)
  • score >6 = urgent referal to nerology, >4 = high risk TIA
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22
Q

Tx of TIA

A
  • Refer to specialist assessment within 24hrs (7 days) of onset
    - Start STATIN (simastatin 40mg)
  • Acutely =
    • Immediate ASPIRIN/Clopidogrel 300mg
    • Treat BP if raised
  • Long term prophylaxis = CLOPIDOGREL 75mg (or MR diapyramidole) + ATRVASTATIN 80mg

Don’t drive till seen by specialist

  • If High risk need to be assessed within 24hrs
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23
Q

Classification of ischaemic stroke

A

TOAST classification (subtypes of ischaemic stroke):

  • Large vessel disease (atherosclerosis) - (mc - 50%)
  • Small vessel disease (occlusion) (25%)
  • Cardioembolic (esp AFib -more common in elderly, female) (20%)
  • Cryptogenic (no RFx + can’t find cause - undetermined aetiology)
  • (+ rarities = 5%)- Rarities (other aetiologies not covered by above)
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24
Q

Define iscahemic stroke

A

Episode of NEUROLOGICAL DYSFUNCTION caused by FOCAL cerebral, spinal or retinal INFARCTION (lasting more than 24 hrs)

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25
Q

Epidemiology of Ischaemic Stroke

A
  • 80-85% of strokes- 25% of ischaemic strokes in young people (<45 y/o) is caused by DISSECTION- Better prognosis/outcomes if treated on a dedicated stroke unit vs conventional ward- 84% return home but few return to work
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26
Q

Causes/RFx of Ischaemic strokes

A
  • Large vessel = atheroma (obesity) -> thromboembolism
  • Small vessel = HTN, DIABETES, SMOKING + AGE -> microatheromas
  • Cardioembolism
    • Mural thrombus, (HF?)
    • AFib, Atrial septal defect
    • Endocarditis
    • Dissection (carotid/vertebral)
      - trauma/cervical manipulation (e.g. getting head pulled back at hairdresser’s)
      - Vigorous physical activity (e.g. weight lifting)
      - Vasculopathy (fibromuscular dysplasia, Marfan’s -> weaker, more likely to tear)
      - Causes stenosis/aneurysm of medium-sized arteries -> reduced perfusion/wall can break
  • Sympathomimetic drug abuse (e.g. dopamine, NAd, Adr etc.)
    - Increased stimulation of sympathetics -> peripheral vasoconstriction + reduced systemic compliance -> increased blood flow/pressure during systole -> more likely to tear
  • Rarities
    • Vasculitis (string of beads - microaneurysms) - consider renal involvement
    • Venous thrombosis (back pressure -> swelling -> blocks blood supply) - oft have thrombophilia (consider in post-partum, infection, dehydration, malig) - shows up as papilloedema
    • Haem conditions like SCD or aPL syndrome -> increased coagulability
    • Hyperviscosity syndrome e.g. Polycythemia vera
  • Idiopathic
  • Other RFx:
    • MALE- Main = increased AGE (>65), HTN, SMOKING
    • Migraine with aura (concurrent sensory disturbance) (esp in younger women) -> causes brain hypoperfusion
    • FHx; genetic factors
    • Previous TIA (increased risk of stroke in around 10 days after)
    • Alcohol
    • DM+lipids + cardiac disease
    • Carotid bruit (indicates stenosis)
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27
Q

Pathophysiology of ischaemic stroke

A

Large vessel:

  • Atherosclerosis - esp at bifurcations/curvature/confluence (carotid bifurcation, aortic arch + basilar artery respectively) - most common
  • Rupture -> thromboembolism further up brain vessel (e.g. MCA - unlikely to have atherosclerosis, much more likely to have embolism)

Small vessel:

  • Small, deep perforator/penetrating arteries blocked by the formation of in situ microatheromas or lipohyalinosis (concentric thickening of small cerebral arteries -> narrowing of lumen -> occlusion)
    • Looks like small holes/cobweb mesh at post-mortem (lacunae)
  • Microatheroma -> weakens vessel

Cardioembolism (blood stasis forming thrombus/pathogenic colonies in heart -> embolism from heart - Oft get big clots)

Dissection - increased strain on vessels - esp CAROTID/VERTEBRAL - or reduced ability of vessels to comply with increased strain -> wall breaks

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28
Q

Presentation of anterior circulation stroke

A

Anterior circulation (stemming from internal carotid):- Dominant hemisphere affected (usually left, even in left-handed people) - Language dysfunction - Expressive or Receptive dysphasia - Dyslexia - Dysgraphia- Non-dominant hemisphere affected: - Anosognosia - Neglect (unaware of paralysed side of body) - Denial of weakness - Visuospatial dysfunction - Dressing/gait apraxia - Either hemisphere -> - Hemiparesis (one side paralysis) - Hemisensory loss - Visual field defect

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29
Q

Presentation of posterior circulation of iscaemic stroke

A
  • Unsteadiness (cerebellar involvement)- Visual disturbance - Homonymous hemianopia w/ MACULAR SPARING (occipital lobe) - Prosopagnosia (can’t regnise faces)- Slurred speech- Headache more common than in anterior stroke- Vomiting (can be mistaken for viral infection - oft leads to late diagnosis)
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30
Q

What specifically does a lacunar stroke affect/present with

A

It is just a small vessel ischaemic stroke affecting the LENTICULOSTRIATE ARTERIES which supplies deep brain structures-> ischaemia/infarct of basal ganglia, internal capsule, thalamus, ponsContralateral hemiparesis + pure motor/sensory loss (or mix of both)

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31
Q

Stroke vs non-stroke

A
  • Stroke usually more abrupt (within secs)- Strokes usually more focal- Strokes usually cause loss of function (non-strokes = =ve symps e.g. flashes of light in visual field - migraine)- Max neurological symptoms at beginning for strokes - for non-strokes can get worse over time
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32
Q

DDx for stroke

A
  • Todd’s paresis - after effect of EPILEPTIC SEIZURE- Space occupying lesions e.g. tumours- Infection (esp in elderly) - can cause decompensation in areas previously affected by stroke- Metabolic disorders - hyper/hyponatraemia, hypoglycaemia, alcohol/drugs (cannabis/cocaine), thyroid dysfunction- MS (oft in younger) - can have episodes years apart, recover fully inbetween- Functional neurological disorder (stressful situations - linked to PTSD)- Migraine
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33
Q

Treatment of ischaemic stroke

A

Hyperacute:- IV Thrombolysis within 4.5 hours of starting stroke - prevents progression -> TISSUE PLASMINOGEN ACTIVATOR or ALTEPLASE (if at risk of bleeding may take aspirin/other anti-platelet) - Drugs can be administered via catheter to brain - If proximal M1 (stem of MCA) occlusion (v. large) - thrombolysis only works in ⅓ of cases - Mechanical thrombectomy - wire fed up femoral artery in groin -> fed up to brain -> grab clot + pull out - Needs to be given within 6 hrs (or within 24hrs if sufficient penumbra on CT perfusion); - works best if they had good function before stroke (e.g. could walk unaided) + had large proximal artery occlusion (internal carotid or proximal M1/M2 segment)- Carotid atherosclerosis -> remove surgically within a week (ENDARTERECTOMY) - Urgent if 50-99% stenosis on symp sideSecondary prevention:- ANTIPLATELETS - Aspirin 300mg for 2 weeks -> lifelong clopidogrel 75mg- Warfarin/DOAC if AFib/mural thrombus- STATINS - reduces risk of future vascular attacks (aim to lower LDL by >40% + keep total cholesterol <3.5)Lower plasma LDL, inhibit cholesterol synthesis (in liver), stabilise atheromas + are anti-inflammatory- LOWER BP - ACEI, THIAZIDEs, CCBs

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34
Q

Complications of ischaemic stroke

A
  • Ischaemia can cause oedem within next 48hrs -> Hemicraniectomy (remove part of skull) - but can cause disability
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35
Q

Define Haemorrhagic stroke

A

2 types:- Primary Intracerebral: RAPIDLY developing clinical signs of NEUROLOGICAL DYSFUNCTION attributable to a FOCAL COLLECTION OF BLOOD within brain PARENCYMA/VENTRICULAR SYSTEM - not caused by trauma - more acute than ischaemic- Subarachnoid: RAPIDLY developing NEUROLOGICAL DYSFUNCTION AND/OR HEADACE due to bleeding into subarachnoid space - not caused by trauma

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36
Q

Define haemorrhagic stroke

A

2 type:- Primary Intracerebral: RAPIDLY developing clinical signs of NEUROLOGICAL DYSFUNCTION attributable to a FOCAL COLLECTION OF BLOOD within brain PARENCYMA/VENTRICULAR SYSTEM - not caused by trauma - more acute than ischaemic- Subarachnoid: RAPIDLY developing NEUROLOGICAL DYSFUNCTION AND/OR HEADACE due to bleeding into subarachnoid space - not caused by trauma

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37
Q

Epidemiology of Haemorrhagic strokes

A

20% of strokes

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38
Q

Causes of haemorrhagic stroke

A

2 types -> Intracerebral + subarachnoid- Intracerebral: -HTN - Amyloidosis - Arteriovenous malformation - Aneurysm rupture- Subarachnoid: - Aneurysm rupture - esp BERRY ANEURYSM (feels like Thunderclap headache/hit on head by cricket bat)

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39
Q

Presentation of haemorrhagic stroke

A
  • Focal neurological symps- RAISED INTERCRANIAL PRESSURE -> papilloedema, more generalised symps - risk of TENTORIAL HERNIATION - CONING: hernitation of medulla/brainstem through foramen magnum- oft Midline shift
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40
Q

Treatment of haemorrhagic stroke

A
  • DO NOT GIVE/STOP ANTICOAGS- Aggressively Reduce BP <150 systolic (e.g. RAMIPRIL) - unless underlying structural cause, GCS <6, early surgery or poor prognosis- Neurosurgery referral - May clamp broken vessel/use coil to give structural support - For arteriovenous malformation -> surgical removal; shrink with radiation; chemically block blood flow to malformed are- IV mannitol for raised ICP2ndry- fix clotting- lower BP <150 systolic- Statins
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41
Q

Dx of stroke

A
  • 1ST LINE (+ gold for bleeds) = NCCT HEAD (fast, cheap) - ischaemia looks normal in first few hours; Haemorrhage = HYPERDENSE BLOOD- Gold = MRI BRAIN with DIFFUSION WEIGHTED IMAGING (for ischaemic) - measures changes in water movement across cell walls to show exact affected area- Bloods (including vasculitis screen) - WCC, Plts, Cholesterol/Lipid screen - PT/aPTT- ECG +/- 72 hour tape (irregular heart rhythms -> can indicate stroke) - esp in cardioembolic- Carotid Doppler US - common area of atherosclerosis -> need to remove or can thrombose (need to image within few days of stroke)- ECHO (for cardioembolic)- CT/MR angiogram of head + neck - e.g. for dissection or carotid occlusion
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42
Q

What is Romberg test

A

Determines if your balance issues are related to the function of your dorsal column by removing the visual and vestibular components that contribute to maintaining balance(need at least 2 of: proprioception, vision, vetibular input - to normally maintain balance)Just stand still w// eyes closed + arms crossed- used to identify cerebellar damage

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43
Q

DANISH acronym

A
  • Dysdiadochokinesia- Ataxia (gait and posture)- Nystagmus- Intention tremor- Slurred, staccato speech- Hypotonia/heel-shin test
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44
Q

Define subarachnoid haemorrhage

A

Bleeding into subarachnoid space typically due to BERRY ANEURYSM RUPTURE (circle of Willis - esp at anterior commisure artery junction) or Trauma

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45
Q

RFx for Subarachnoid haemorrhage

A
  • Marfan’s/Ehlers Danlos- HTN- POLYCYSTIC KIDNEY DISEASE- TRAUMA- Increased age- FHx
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46
Q

Sx of subarach haem

A
  • SUDDEN ONSET OCCIPITAL THUNDERCLAP HEADACHE (berry aneurysm rupture) - 50% have SENTINAL HEADACHE (throbbing ocipital pain) preceding for weeks - 0 -> 10 severity instantly (worst headache ever)- Meningism (but no meningitis)- Kernig’s sign - can’t straighten leg when hip flexed to 90 degrees (stiff hamstring)- Brudzinski’s sign - severe neck stiffnes -> hips + knees flex when neck is flexed/elevated in lying position- reduced Glasgow Coma Score- nerve palsy CN 3 + 6 (fixed dilated pupil + raised ICP signs)
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47
Q

DDx subarach haem

A
  • meningitis (no thunder clap headache + has infection)- migrane (no meningism or thunderclap)
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48
Q

Diagnosis of subarach haemorrhage

A
  • 1st + Gold = NCCT HEAD (diagnostic) - star shaped white area - If +ve -> CT angiogram (to see extent of rupture)- If -ve -> LUMBAR PUNCTURE (but wait around 12 hours as results are most sensitive after 12hrs) - will see XANTHOCHROMIA after 12hr (CSF = yellowish from RBC haemolysis)Can get vasospasm or delayed cerebral ischaemia - usually 3-14 days after haemorrhage - indicated by:- drop of 2 or more GCS - new focal deficit occuring 3-14 days after; not attributable to other causes
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49
Q

Tx of subarach haemorrhage

A
  • 1st line - cardiopulmonary support if GCS <= 8; >8 = support + monitoring- NIMODIPINE (CCB - decreases vasopressin + BP - reduced risk of delayed ischaemia) - stop/reverse anticoag if needed - anticonvulsant where needed- Gold - NEUROSURGERY - endovascular coiling or surgical clipping- if acute hydrocephalus - ventriculostomy or lumbar drainage of CSFIf vasospasm pr delayed cerebral ischaemia -> refer to neurosurgeon
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50
Q

Define subdural haemorrhage

A

Rupture of BRIDGING VEIN due to SHEARING

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51
Q

RFx for subdural haemorrhage

A
  • TRAUMA (e.g. DECELERATION injuries)- Coagulopathy/anticoag use- AGE >65- CHILD ABUSE (SHAKEN BABY SYNDROME)- Cortical atrophy (e.g. dementia, excessive alcohol)
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52
Q

Sx of subdural haem

A
  • GRADUAL ONSET - has a LATENT PERIOD - small bleeding -> accumulation + AUTOLYSIS of blood -> Symps after days/weeks/months - characterised by evidence of trauma, headache, N+V + loss of function- Signs of RAISED ICP - CUSHING’S TRIAD (bradycardia, irregular respirations, widening pulse pressure) - Fluctuating GCS - PapilloedemaFocal neurology later e.g. CN3 palsey
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53
Q

Dx of subdural haem

A

NCCT HEAD -> CRESENT shaped haematoma, NOT CONFINED to suture lines - midline shift- acute = hyperdense- subacute = isodense- chronic (or late) = HYPOdense (darker than brain)Alt MRI/plain skull x-ray

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54
Q

Tx of subdural haem

A

If <10mm size; midline shift <5mm; no significant neurological dysfunction- consider prophylactic antiepileptics- normalise coag profile but STOP ANTICOAG10mm or more; midline shift >5mm; significant/expansile neurological dysfunction- SURGERY - BURR HOLE CRANIOTOMY (make 2 burr holes - irrigate clot with saline + suction) - Trauma craniotomy (frontotemporoparietal craniotomy, durotomy, removal of clot) - Hemicraniotomy (oft done when considerable cerebral swelling/intraparenchymal lesions)Address cause of fall e.g. from arrhythmia or cateractsIf chronic -> give antiepilepticsGive IV MANNITOL to lower ICP

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55
Q

Extradural/epidural haemorrhage

A

TRAUMA esp to MIDDLE MENINGEAL ARTERY due to damage to pterygoid bone (around ear)

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56
Q

RFx for extradural haemorrhage

A
  • Typically 20-30 y/o - HEAD TRAUMA - less likely to occur in older as dura more firmly adhered- v rarely can get extradual contralateral to a subdural bleed - surgery to remove subdural can then allow extradural to rapidly expand if not identified
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57
Q

Presentation of extradural haemorrhage

A
  • Initial event -> Lucid interval - may last hours-days-weeks -> RAPID DETERIORATION due to RAISED ICP - old blood clots become haemolysed + TAKE UP WATER (osmotically active) -> increase ICP by increasing volume- Reduced GCS (coma, confusion)- RAISED ICP (cushing triad, papilloedema)
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58
Q

Dx of extradural haem

A
  • NCCT HEAD -> (LENS shaped) BICONVEX hyperdense bleed - CONFINED TO SUTURE LINES - midline shift- Alt MRI or Plain skull XR
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59
Q

Tx of extradural haem

A
  • ABCDE- URGENT SURGERY- MANNITOL to reduce ICP
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60
Q

Complication of intracranial haemorrhage

A

BRAINSTEM/TONSILLAR HERNIATION/CONING -> Compressed respiration centres -> resp arrest (-> death)- due to untreated raised ICP

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61
Q

Issue with codeine in headaches

A

Oft used for headaches but causes worsening of headache

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62
Q

Types of primary brain tumours

A

Classified based on cell of origin + area- GLIOMAS (most common) - Astrocytoma (astrocytes - maintain homeostasis + neuronal metabolism - 90% - 2nd mc pediatric cancer overall - Oligodendrocytoma/oligodendroglioma (myelinating cells) - Ependymoma (ependymal cells lining ventricles)- Meningioma- In sellar region - e.g. Craniopharyngioma, Pit adenoma- Germinomas (rare, usually pediatric, cancerous, usually in pit/pineal region)- Cranial nerves = SCHWANNOMA (e.g. VIII nerve = acoustic neuroma)- Haematopoetic (primary CNS lymphoma)

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63
Q

Most common cause of brain tumour

A

SECONDARY METS - Non-small cell LUNG cancer (main cause) + small cell lung cancer- BREAST- Malignant Melanoma- Renal cell cancer- Gastric cancer/COLORECTAL- Testicular

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64
Q

Epidemiology of brain tumours

A

Increasing incidence55% malig9th most common - commonest cause in younger ppl (men <45, women <35)Only 3% of all cancersNon germinomatous pineal tumours = 90% male - esp during puberty 10-19 y/o- Grade 2 gliomas - slow growing but undergo anaplastic transformation:AVERAGE SURVIVAL = 10 YEARS (astrocytomas worse - 3-5 yrs) - Even if it goes anaplastic - better prognosis than de novo high grade- Grade 3 gliomas - survival = 3-5 yrs- Grade 4 - survival = 12 months

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65
Q

Median age affected by diff grades of primary brain tumours

A

Grade 2 = 35Grade 3 = 45Grade 4 = 60

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66
Q

Causes/RFx for primary brain tumours

A
  • Majority idiopathic- Ionising radiation (esp if in childhood e.g. for leukaemias - esp meningiomas)- 5% family Hx-Associated genetic syndromes: - neurofibromatosis type 1 (nerve tumour disease) - tuberous sclerosis (mostly benign tumours, diff parts of body), - Hippel-Lindau disease (tumours + cysts - usually benign) - white males - Immunosuppression (CNS lymphoma)
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67
Q

Classification system used for brain tumours

A

WHO classification system - based on histology, molecular markers + genetic factors (brain tumours only spread in CNS so no TNM classification - medulloblastomas can drop down spine but still inside CNS)

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68
Q

Grading of primary brain tumours

A

graded according to how fast they grow + how likely they are to grow back (based on morphology) - also by WHO- Garde 1 = low grade (low proliferation potential), benign (discrete) + associated with long term survival- Grade 2 = low grade (typically benign but can transform into malig) - has ATYPIA + infiltrative but low mitotic activity -> can recur as high-grade- Grade 3 = high grade. ANAPLASTIC (loss of mature/specialised features) + increased mitotic activity. Malignant.- Grade 4 = high grade, v aggressive (reproduce rapidly). Anaplasia, mitotic activity + microvascular proliferation +/- necrosis - has disseminating potential

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69
Q

Complication associated with pineal region masses especially

A

tend to cause OBSTRUCTIVE HYDROCEPHALUS - tend to cluster in midline + compresses aqueduct -> signs + symptom of raised intracranial pressure

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70
Q

Monroe-Kellie Doctrine

A
  • Skull fixed box consisting of Brain parenchyma (80%), Blood supply (10%), CSF (10%) - Brain = 1400ml - Blood = 150ml - CSF = 150ml- If change in make up of intracranial structure -> initially compensation - Increased CSF drainage via ventricular system - Increased venous drainage via dural venous sinuses- non-linear relationship so as volume continues to increase, pressure suddenly rapidly increases: ie decompensation = signs/symps
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71
Q

Presentation of Brain tumour

A

Depends on type, grade + site- typically if progressive over day/s weeks -> consider tumour- but if long Hx of isolated headache -> probably not tumour (only 2% of brain tumour Px)Symps:- Headache - from raised ICP (24% 1st symp) - Associated N+V - Worse when lying down/at night -> worse in morning; can wake Px up (caused by pressure increase when lying down) - Exacerbated by coughing, sneezing, drowsiness (all increase ICP)- New onset/different SEIZURES (>80% - always check for brain tumours in adults presenting with seizures) - more likely in temporal lobe tumours - Focal neurological symptoms- Non-focal symptoms - Blurred vision from papilloedema - Cognitive problems - Personality/behavioural changes (e.g. disinhibtion or loss of motivation - could potentially be specific to frontal lobe) - Cushing’s triad (bradycardia, irregular breathing/respirations, widened pulse pressure - raised BP but reduced HR)Signs:- Papilloedema- Focal neurological deficit- False localising (e.g. Diplopia due to 6th nerve palsey from raised ICP)BRAIN METS associated with a lot of OEDEMA (so raised ICP symps)+ lethargy + weight loss

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72
Q

Examples of the effects of seizures affecting different lobes e.g. in brain tumours

A
  • Temporal lobe = affects emotions -> dread, deja/jamais vu- Frontal lobe = motor, problem solving + personality/mood -> limb jerking, head/eye deviation, absence seizures- Parietal = sensory -> sensory disturbance e.g. spreading tingling- Occipital = vision -> +ve visual disturbance e.g. aura
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73
Q

Examples of focal neurological symps (not seizures)

A
  • Weakness/loss of voluntary control (primary motor)- Loss of skin sensation (primary somatosensory)- Reduced problem solving; change in personality (frontal lobe)- Speech disturbance: - Expressive dysphasia (Broca’s - immediately anterior to primary motor, in frontal) - Receptive dysphasia (Wernicke’s - posterior temporo-parietal border, in temporal)- Hearing/memory problems (Temporal)- visual loss with macular sparing (Primary visual - occipital)- Loss of balance/co-ord (ataxia - Cerebellum)- loss of consiousness, breathing or heart rate (brain stem)
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74
Q

Low grade vs high grade brain tumour symps

A
  • Low grade - oft asymp till seizures or incidentally found- High grade - raised intacranial pressure/rapidly progressing neurological deficit
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75
Q

4 examples of focal neurological deficit

A
  • Hemiparesis- Hemisensory loss- Visual field defect- Dysphasia
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76
Q

When is an urgent referral required for potential brain tumours/RED FLAG SIGNS

A
  • Headache + other signs of raised ICP- Headache with focal neurology (check for visual field defect as well)- New onset focal seizure- Rapidly progressive focal neurology even without headache- Past Hx of cancerAlso:- Age >50- New onset CHANGE in previously existing headache
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77
Q

Dx of brain tumours

A
  • 1st line + diagnostic = MRI Head +/- spine with contrast (gadolinium) (Diffusion weighted imaging) - T1 weighted = black CSF -> tumour = hypointense - T2 weighted = white CSF -> tumour = hyperintense (remember by thinking of Michael jackson) - perfusion MRI to check level of malignancy (more perfused) - can do functional MRI to check if any functional areas affected (if slow growing tumour - brain may have adapted + functional centres may be displaced to different sites than expected) - Can do CT head if acute presentation (rule out haemorrhage, herniation etc) or if MRI unavailable/contraindicated- Brain BIOPSY (determines grade based on histology, molecular markers + genetics)- Othalmological evaluation; visual field testing (if issue suspected)- CT chest/abdo/pelvis - check for secondary causesUnusual to do lumbar puncture - Raised ICP can cause herniation upon puncturing
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78
Q

Prognostic factors of low grade gliomas

A
  • Histology type- AGE- Size of tumour- Rate of growth- Location- Crossing midline- Presenting features- Performance status (score that estimates Px ability to perform activities of daily living independently)
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79
Q

Prognostic factors of high grade gliomas

A
  • IDH status (mutation is favourable)- Performance status- Extent of resection- Older age at time of surgery
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80
Q

3 molecular/genetic variations particularly associated with brain tumours

A
  • MGMT methylation (big prognostic factor!) - if unmethylated - radiochemotherapy = less effective- IDH mutation - IDH wildtype results in progression of diffuse glioma to grade 4 Glioblastoma - IDH mutant more likely to -> grade 2/3 Oligodendroglioma or Astrocytoma - Still risk of grade 4 Astrocytoma- Chromosome 1p19q loss (in oligodendroglial)
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81
Q

DDx of brain tumours

A
  • Stroke (more sudden onset)- Abscesses (typically thinner wall on imaging - surgical emergancy) - Check Temp, WCC, CRP + MRI DWI- Lymphomas - can spontaneoulsy regress with steroids - makes diagnosis difficult if trying to biopsy- MS (may have had similar episode years in the past)
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82
Q

Treatment of Low grade glioma

A
  • SURGERY - EARLY RESECTION (risk of neuro damage)- Radiotherapy + early chemo -> prolongs survival but risk of long-term issues e.g. dementia
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83
Q

Treatment of high grade gliomas

A
  • STEROIDS (DEXAMETHOSONE) - increases WCC but REDUCES OEDEMA- Optimise clotting/coag- MAXIMAL SAFE SURGICAL RESECTION/Debulking (remove radiographically identified area of tumour + surrounding area as long as it is not functionally important) - 5-ALA guided (pink drink that causes tumour to glow pink under ultraviolet light) - Awake craniotomy -> allows CORTICAL MAPPING (checking effects of stimulating areas on Px) -> supramaximal resection - may choose to not debulk if in functionally important area as unable to take out much anyways- Intensive Radiotherapy- Chemo = TEMOZOLOMIDE, PCV
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84
Q

Complications of surgery

A
  • Wound infection- CSF LEAK- Neuro deficit- Seizures- Hydrocephalus (potentially due to blood in ventricles -> poor reabsorption of CSF)- Thrombus related: DVT/PE, MI, CVA (ie stroke/TIA)- recurrence/death
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85
Q

Factors affecting effectiveness of high-grade glioma treatment

A
  • Various routes can be affected- Interpatient variability- Intratumoural heterogeneity- Difficult to cross blood-brain barrier
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86
Q

What is a glioblastoma multiforme

A

AKA grade 4 astrocytoma - fast growing + v aggressive - invasive

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87
Q

Define a diagnosis of epilepsy

A

A condition characterised by recurrent epileptic seizures unprovoked by any immediate identified causeAny of the following:- At least 2 unprovoked seizures occuring more than 24hrs apart- One unprovoked seizure + at least 60% probability of further seizures occuring within 10 years of 2 previous unprovoked seizures- Diagnosis of epilepsy syndrome - a typically idiopathic cause of recurrent seizures

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88
Q

Define seizure

A

The transient occurrence of changes in behaviour, sensation or cognitive processes due to abnormal excessive, hypersynchronous neuronal activity in the brain

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89
Q

Pathophys of epileptic seizures

A

Shifting of balance between GABA and glutamate leading to increased glutamate stimulation + GABA inhibition -> Increased EXCITATION

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90
Q

Classification of epileptic seizures

A
  • Focal - limited to 1 hemisphere - Motor or non-motor - Retained awareness = simple - impaired awareness = complex - Can be focal to bilateral spreading- Generalised (originates in bilaterally distributed networks) - cortical or subcortical but not necessarily both simultaneously - always loss of consiousness
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91
Q

Types of seizures

A
  • Tonic-clonic (Most common) - oft in phases: tonic phase = high frequency (continuous epileptic acitivity) -> rigidity, clonic = lower frequency but oft larger amplitude -> contraction- Absence seizures (common in children, rarer in adults) - can be v quick + hard to spot- Myoclonic = brief, shock-like muscle contractions- Tonic = sudden onset, widespread muscle rigidity- Atonic = spontanous muscle relaxation
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92
Q

Define status epilepticus

A
  • Prolonged convulsive seizure lasting 5mins or moreor- consecutive recurrent seizures without recovery in-between
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93
Q

Epidemiology of Epilepsy

A
  • around 1% affected- Higher incidence in low-income countries- Higher rates in people with learning difficulties- Highest risk of incidence in infants and ppl >50 y/o - BIPHASAL DISTRIBUTION 2/3 treated with just monotherapy but 30% (usually with co-morbidities) don’t respond well to treatment
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94
Q

Causes/RFx of Seizures

A
  • Symptomatic epilepsy (most common in elderly) - Head trauma - oft presents with LoC >30 min + amnesia > 30min - could be iatrogenic - Cerebrovascular disease (infarct, haemorrhage, venous thrombosis) - Brain tumour- Metabolic disorders (hypoglycaemia, hypo/hypernatraemia, hypo/hypercalcaemia - typically not K+)- Infections - v severe response to systemic - typically only in young children - Encephalitis- Drugs - Isoniazid, Tricyclic antidepressants - Alcohol misuse, cocaine- Neurodegenerative disease e.g. Alzheimer’s (rarer)- Sclerosis e.g. Mesial temporal sclerosis (common cause of focal)- Idiopathic epilepsy (oft) - can have genetic component esp in absence, myoclonic + primary generalised tonic clonic seizures
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95
Q

Common triggers of acute attacks of epilepsy

A
  • Stress- Periods (esp few days before menstruation starts)- Lack of sleep- Fever- Too much alcohol- Flashing lights less common
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96
Q

Simple vs complex focal seizures

A
  • Simple = no basal ganglia/thalamus involvement; no loss of consciousness- Complex = BG + thalamus involved -> loss of consciousness
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97
Q

General stages of epileptic seizures

A

Stages:- Prodrome (mood signs, up to days before)- Aura (NOT ALWAYS - typically in temporal) - minutes before- Ictal event i.e. seizure- Post ictal period (only if loss of consciousness) - Headache - Confusion + lowered GCS - Dysphasia - Amnesia - Todd’s Paralysis (if motor affected) - SORE/BLEEDING tongue (ESP in epileptic seizures - due to TONGUE BITING)

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98
Q

Common characteristics of epileptic seizures

A
  • Duration typically 30-120s- +ve ictal symps- Post ictal if loss of consiousnness- stereotypical seizures; an individual will have same type(s) throughout life- Can OFT OCCUR IN SLEEP- Common phenomena: tongue biting, incontinence, deja vu etc
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99
Q

Characteristics of tonic clonic presentation

A
  • no aura- tonic phase = rigidity + high frequency spasms- clonic phase = significant jerking of limbs- UP GAZING OPEN EYES- INCONTINENCE- TONGUE BITING
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100
Q

Characteristic absence seizure presentation

A
  • oft childhood- staring into space (secs to mins)- adults may have deja vu + AUTOMATISMS (LIP SMACKING, rapid blinking, stroking clothing) - may show head deviation- 3Hz SPIKE ON ECG
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101
Q

Presentation of focal seizures

A
  • Temporal: Aura, dysphasia, POST ICTAL PERIOD- Frontal: JACKSONIAN MARCH (spreading of symp from one spot to rest of body) + Todd’s paralysis/palsey- Parietal: Parasthesia- Occipital: Vision changes
102
Q

Dx of seizures

A
  • History- ALWAYS CHECK BLOOD GLUCOSE, FBC, U+E, renal function, LFTs, metabolic panel (check underlying) - Urinalysis- ECG after 1st to check potential cardiac issues- May do CXR to check for pneumonia- Ab testing if autoimmune encephalitis suspectedSpecific:- EEG (Electroencephalogram) - ideally within 72hrs - May show PHASE REVERSAL (indicative) - 3Hz wave in absence seisure - consider using provoking manouvers; doing sleep deprived EEG - if diagnostic difficulties -> ambulatory EEG (up to 48hr)/short-term video EEG - avoid if suspected SYNCOPE = false +ve- MRI/CT head - examine HIPPOCAMPUS, bleeds, tumours etc- Whole genome sequencing if initially <2y/o, clinical features suggest genetic cause, or has other feature e.g. autism, learning disability etc.
103
Q

Tx for epilepsy

A

If first seizure - need to be seen within 2wks- if mild may not need treatment; avoid trigger; stop driving- 1st line = monotherapy (lowest possible dose) - Anti-Epileptic Drugs - SODIUM VALPROATE (contraindicated in females of childbearing age - teratogenic) - CARBAMAZEMPINE - Phenytoin can affect bioavailability of other drugs + doesn’t work for absence siezures - May also use Lamotrigine - Ethosuximide only works for absence seizures - Rufinamide is good for generalised- 2nd line = monotherapy (highest possible dose)- 3rd = Alt mono or combination therapy- If refractory to medical -> surgical: - curative only if focal -> resection or hemispherectomy - palliative in generalised -> Tractotomy (sever corpus - typically in kids) or Electrostimulation (e.g. vagal nerve stimulation - stimulates for 30s every 5min)- if v. refractory -> consider reducing monotherapy

104
Q

complications of epilepsy

A
  • Status epileptics - TREAT with BENZODIAZEPINES: - IV LORAZEPAM 4mg; give AGAIN if not initially work - if still not working IV FOSPHENYTOIN- Sudden unexpected death - esp after tonic clonic
105
Q

Define syncope

A

Paroxysmal event in which changes in behaviour, sensation and cognitive processes are caused by an insufficient blood or oxygen supply to the brain

106
Q

Characteristics/presentation of syncope

A
  • Duration 5-30s- Recover WITHIN 30s- Situational- Typically from sitting/standing- Rarely from sleep- PRESYNCOPAL SYMPS- Cardiogenic syncope - less warning, history of heart disease
107
Q

Define Non-epileptic/functional/dissociative seizures

A

Paroxysmal event in which changes in behaviour, sensation and cognitive function are caused by mental processes associated with psychosocial distress- linked to PTSD

108
Q

Carachteristics/presentation of non-epileptic seizures

A
  • Situational- Duration 1-20 MINUTES- Dramatic motor phenomena or prolonged atonia - oft semi purposeful movements - agonist-antagonist action -> TREMOR - Hip thrusting v characteristic- Oft EYES CLOSED- May have ictal crying/speaking- Surprisingly rapid/slow post ictal recovery- Oft History of psych illness or other somatoform disorders
109
Q

Mode of action of main anti-epileptics

A
  • Sodium valproate inhibits GABA degradation + stimulates GABA synthesis -> inhibitory action on neuron- Carbemazepine + lamotrigine - Inhibit NA+ INFLUX via Voltage-gated Na+ channels (prevents increase in excitability + formation of action potential)- Retigabine - Increases Voltage-gated K+ channel activity -> K+ efflux reduces neuronal excitability- Pregabalin + gabapentin - Inhibit Ca2+ voltage gated channel -> inhibits Ca2+ influx which normally drives neurotransmitter release- Levitiracetam - inhibits SV2A which is required for release of neurotransmitters for vesicles
110
Q

Primary prevention of pneumococcal infection

A
  • PCV (pneumococcal conjugate vaccine) vaccine in children <2 - at 12 weeks + 1 year- PPV (pneumococcal polysaccharide vaccine) in >65 y/o + anyone >2 y/o with long-term health conditions (e.g. serious heart/kidney condition)May not be recommended in pregnancy/breastfeeding
111
Q

Epidemiology of bacterial meningitis

A
  • 5% mortality when treated (higher risk if meningococcal)- 20% permanent effects
112
Q

Uncommon causes of infective meningitis

A
  • Lyme disease (Borrelia burgdorferi)- LeptospiraChronic causes:- TB (higher risk if close contact + immunocomp)- Syphilis (Treponema pallidum)Viral:- Occassionally PoliovirusFungal:- Chronic - Cryptococcal (typically in poorly controlled HIV)Parasitic
113
Q

RFx for acute + chronic Meningitis

A

Acute:- Students- Travel- ImmunocompChronic:- small children- Immunocomp

114
Q

Pathophys of meningitis

A
  • Commonly get spread from extracranial infections ascending e.g. via naso pharynx or ear infection- Less common = haematogenous spread- Direct - via brain surgeryBacteria multiply in CSF + use up glucose -> infiltration by WBC which also use up glucose- both of above produce protein waste products-> leaking of CSF -> brain oedema
115
Q

Dx of meningitis

A
  • Assess GCS (lowest 3 - coma, highest 15 - normal)- 1st line = Blood cultures (Px oft bacteraemic) - give empirical medsa at this point- LUMBAR PUNCTURE (gold) - Do CT HEAD first if: - Aged >60 - Immunocomp - Hx of CNS disease - Seizures <1 week - GCS<14 - Focal neurological signs - Papilloedema - Atypical Hx- Test for HIV
116
Q

When is lumbar puncture contraindicated

A
  • Abnormal clotting- Petechial rash (bleeding)- Raised ICP
117
Q

How can Cryptococci be identified

A

can be seen on microscopy with India ink stain - has clear halo around cryptococcoi

118
Q

DDx for meningitis

A
  • Subarachnoid haemorrhage- Migraine- Flu + other viral illness- Sinusitis- Brain abscess- Malaria
119
Q

Complications of meningitis

A
  • DIC (in meningococcal septicaemia)- WATERHOUSE FRIEDRICHSEN syndrome (adrenal insufficiency caused by intradrenal haemorrhage due to meningococcal DIC)
120
Q

Tetanus pathogen

A
  • Clostridium tetani - G +ve anaerobe- Around 8 day incubation period
121
Q

Pathophys of Tetanus

A
  • C tetani spores are found in soil - oft innoculation through skin from gardening tools- They produce toxins: - Teanolysin (tissue distruction) - Tetanospasmin (simultaneous muscle contraction) - Travels retrogradely along axons + intereferes with neurotransmitter release - leads to increased neuron firing + unopposed muscle contraction + spasm
122
Q

Presentation of tetanus

A

Risus sardonicus - facial contraction (rictus grin)Opisthotonos - whole body contraction -> awkward bent shape due to strength of back muscles

123
Q

How long does a tetanus vaccination stay effective

A

10 years

124
Q

Treatment for symptomatic tetanus

A
  • Supportive: muscle relaxants + paracetamol/cooling- Ig - mop up toxin- METRONIADZOLE to clear residual bacteria
125
Q

Rabies pathophys + epidemiology

A

Viral infection - inoclation via animal saliva in broken skinTravels retrogradely along nerves- Incubation period = 2 weeks - many yearsHigher incidence in tropical countries + russia

126
Q

Presentation of rabies

A
  • Paresthesia at bite- Furious or paralystic presentation
127
Q

Tx of rabies

A
  • Fatal once CNS symps present - manage with sedatives (palliation)- Prophylaxis: - pre-exposure vaccine - Post exposure vaccine + Ig infused around wound
128
Q

Most Characteristic presentation of brain lesions in different parts of the brain

A
  • Cerebral = widespread contralateral- spinal cord lesions - oft bilateral + from a certain level- cerebellar lesion - loss of co-ord + IPSILATERAL- peripheral nerves = glove + stocking distribution- Brainstem - esp cranial nerve palsies (has a lot of weird presentations including irregular breathing/apnea, dysfunction of basic physiological functions etc)
129
Q

What structures pass through the cavernous sinus and what important area of the brain does it pass next to

A

Structures:- Along the lateral sides from top to bottom: - Occulomotor (CN3) - Trochlear (CN4) - Trigeminal 1st branch (CN5) - Trigeminal 2nd branch (CN5)- Most medial important structure: - Internal carotid artery- Around the internal carotid: - Autonomic plexus- Between the carotid + plexus and the more lateral nerves, right at the bottom of the sinus - Abducens (CN6)They pass on either side of the sella turcica + pit gland

130
Q

Medical vs Surgical 3rd nerve palsey

A

The parasympathetic fibres which control pupillary constriction are on the outside of CN3- Surgical 3rd nerve = caused by COMPRESSION + ALWAYS HAS FIXED DILATED PUPILS because compression is coming externally so parasymp fibres will be first to get affected - emergency! Could be tumour or aneurysm- Medical 3rd nerve = usually from MICROVASCULAR cause e.g. Diabetes - normally presents with double vision (occulomotor controlled eye muscle not working so eye turned down + out) but doesn’t necessarily have pupillary involvement as microvascular complications affect from inside out - less urgent

131
Q

Define cerebral palsey

A

Non-progressive brain damage before or during neo-natal period (time of onset v important - specifically a congenital condition)- occurs due to some physical/functional dysfunction - not genetic- can present with wide range of physical/mental impairment

132
Q

RFx for cerebral palsey

A

Anoxia (low oxygen)Low birth weight

133
Q

Define MND + name its subtypes

A

Progressive neurodegenerative disorder affecting UMN or LMN or both- Most common = Amyotrophic lateral sclerosis (affects both UMN + LMN)- Primary lateral sclerosis (mostly UMN)- Primary muscular atrophy (mostly LMN)

134
Q

Epidemiology of MND

A

Around 5000 ppl in UKMedian life expectancy = 2-4 yrs10% live >10yr75-80% die within 5 years1 in 10 familial?- INCREASED INCIDENCE WITH AGE- Life expectancy for ALS = 18M - 3 1/2 yrs - worse outcomes associated with increased CO2 retention- Slightly higher in males than females- (Spinal muscular atrophy - CHILDREN)

135
Q

Causes/RFx of ALS

A
  • AGE - peak incidence 6075 y/o- Genetic predisposition/FHx - 15-20% associated with SOD1 gene mutations- Environmental risk (as shown by the fact it affects old age - step-wise progression - exact mechanism unclear) - e.g. smoking, agricultural chemicals, lead exposure, v high levels of physical activity
136
Q

Pathophys of MND/ALS

A
  • Commonly caused by GGGGCC repeat expansion in C9orf72 gene - can be transcribed to form toxic substance- ALS charachterised by TDP-43 protein aggregation inside neurons -> NEURON DEATH- Affects Corticospinal (motor) tract (cortex, brain stem, ventral cord) - typically neuron death starts 12-18 months before symps start -> difficult to treatSpecific:- Diaphragm too weak in MND so can’t get enough O2 during REM sleep -> Build-up of CO2 -> brings out of REM sleep - poor sleep, doesn’t feel well rested - MORNING HEADACHES from CO2 build-up- ONEUF’S NUCLEUS + OCCULOMOTOR NUCLEI ar NOT AFFECTED -> NO BLADDER/INCONTINENCE or EYE symps (unlike in MS)- Affects motor neurons so no sensory dysfunction (unlike in MS or Polyneuropathies)
137
Q

UMN lesion vs LMN lesion

A

UMN (motor cortex to anterior spinal cord):- Hypertonia (rigidity, spasticity)- HYPERreflexia- NO fasciculations- Babinski sign/upgoing plantars- Power variation: - In arms: Flexors > Extensors - Legs: Extensors > FlexorsLMN (ant spinal cord to muscles):- HYPOtonia (flaccid) + muscle wasting- HYPOreflexia- YES FASCICULATIONS- NO babinski- Generally reduced power

138
Q

Presentation of ALS

A

3 key presentations:- LIMB onset (75%) - Upper extremity weakness - Spastic unsteady gait; foot drop - Propensity for falls - Painful muscle spasms + Hyper-reflexia- BULBAR onset (worse prognosis) - Oropharyngeal weakness -> Choking problems - Dysarthria/Dysphasia (will sound diff depending on if UMN or LMN) - Sialorrhoea + drooling - Jaw spasms/bruxism (teeth grinding- RESPIRATORY onset (typically more delayed diagnosis due to wide DDx + simmilarity to sleep apnea) - Dyspnoea - Sleep disturbance - Fatigue - Morning headaches (from accumulation of CO2 overnight- General: - Reduced appetite/increased metabolism + weight loss - Progressive stooping + muscle atrophyExtra motor:- Emotional lability (rapid, oft exaggerated changes in mood - potentially inappropriate laughing/crying)- Frontotemporal Dementia (5% - uncommon) - Cognitive problems- Parkinsonism+ general fatigue

139
Q

What causes fasiculations

A

normal posture is maintained by continuous firing; loss of some LMN -> nearby LMN take over -> larger motor units -> becomes big enough to see flickers of muscle movement beneath skin- hence why it only appears in LMN lesions

140
Q

What is split hand sign

A

Disproportionate increased wasting of thenar muscles copmared to hypothenar- in MND

141
Q

Dx of ALS

A
  • Whole brain + spine imaging to discount lesions/compression- Clinical diagnosis - based on RFx + presentation - Electromyography shows FIBRILLATION POTENTIALS due to deinnervation of LMN - Consider genetic testing - offer counselling first if for a family member- Mainly tests to rule out DDx
142
Q

DDx of MND

A

Anterior horn- Post- PolioMotor nerve- Neuropathy or myelopathy e.g. Vit B12 deficiency- spine/brain lesion/compresionMuscle- Myasthenia gravis- Lambert Eaton syndrome

143
Q

Tx of MND

A
  • MDT management - including speech therapy, voice banking, wheel chair etc- RILUZOLE 50mg orally BD (antiglutamatergic) - 3 months life gain - Need to monitor LFTs - can cause mild hepatitis- NON-INVASIVE VENTILATION (esp bipac - helps with inhalation + exhalation) - monitor resp function with FVC or SVC or SNIP (<40cm H2O = nocturnal hypoxia - 6 m mortality predictor)- Oft MND Px have v high metabolic rate so give PEG stomach tube for additional nutrition
144
Q

Complications of MND

A

Resp failure, Aspiration pneumonia, Swallowing failure- eventually resp failure is what kills people usually

145
Q

Organisation of movement (give the main stages of the process)

A
  1. Idea of movement (pre-motor cortex/association cortex)2. Activation of UMNs in motor cortex3. Impulse via corticospinal tract4. Modulation by: - cerabellum - fine tuning - Basal ganglia - green signal to move5. MOVEMENT + somatosensory info obtained by sensory tracts
146
Q

Define Multiple Sclerosis

A

An inflammatory, Type 4 hypersensitivity reaction against the myelin sheath and oligodendrocytes which causes demyelination + damage of CNS neuronsHas a pre-clinical and clinical phase

147
Q

Diagnostic criteria for MS

A
  • MCDONALD CRITERIA: 2 or more CNS lesions disseminated in time + space- can be evidenced by an MRI scan w/ gadolinium contrast+ exclusion of differential conditions
148
Q

Epidemiology of MS

A
  • Commonest onset in 20-35/40 y/o - affects younger to middle aged people- Commonest cause of chronic neurological disability in young adults- Reduced risk -> Fish consumption; living closer to equator- The age at which immigration to an area with higher incidence occurs is important - the younger age at migration = greater increase in risk- 20-30% monozygotic concordance- 4% ish risk for other close relatives
149
Q

Causes/RFx of MS

A
  • FEMALES - most commonly caucasian- 20-40 y/o- Autoimmune disease; or just having HLA antigens (the more present = higher risk)- FHx- EBV (similar epitomes present in CNS)- Nutritional deficiencies e.g. Vit D- Environment: Latitude, Diet, Sanitation, Socioeconomic status, climateBasically a combination of Environment, genetic predisposition + chance
150
Q

Types of MS

A
  • Relapsing remitting: Sx, complete/incomplete recovery, Sx…- Primary progressive: gradual deterioration without recovery- Secondary: Relapsing remiting -> more linear progressive deterioration (75% of RR cases)- Progressive relapsing
151
Q

Pathophys of MS

A

T + B cell mediated -> immune cascade

  • Type 1 = macrophages
  • Type 2 = antibodies
  • Mainly Autoreactive TH1 cells are activated which cause direct damage to myelin, axons + oligodendrocytes via inflammation, as well as activating B cells, macrophages, complement.
  • Initially if only myelin sheath damaged - the axon can be remyelinated
    • leads to uniformly thin myelin sheath with short intranodes -> less effective
    • Transmission becomes TEMPERATURE DEPENDANT (Uhtoff’s phenomena - Sx worse when hot)
  • If the axon is damaged it cannot be remyelinated
152
Q

Active vs inactive lesions in MS

A

Active:

  • High lymphocyte infiltration -> hypercellular plaque edge (esp MACROPHAGES + activated microglia associated with active lesions) + B and T CELLS are present peri-venously
  • Demyelination + breakdown products present
  • EXTENSIVE BLOOD BRAIN BARRIER DISRUPTION
  • Older active plaques may have central gliosis

Inactive:

  • HYPOCELLULAR PLAQUE
  • Demyelination present but NO BREAKDOWN PRODUCTS present (atrophy but no active inflammation)
  • Moderate to minor blood brain barrier disruption
  • Plaques are GLIOSED (i.e. Fibrosis)

Both have variable oligodendrocyte loss

153
Q

Typical Presentation of MS

A

Only UMN signs/symps

  • Spinal cord:
    • Weakness (1st symp in 48%)
    • Paresthesia
    • Spasticity + other pyramidal signs
    • Lhermitte’s sign (electric shock-like sensation radiating doewn spin +/- into limbs on flexion of neck - can be painful)
    • Bladder/bowel + sexual dysfunction (less common)
  • Optic nerve -> Optic neuritis (painful loss/impairment of vision, esp affecting colour - typically unilateral)
  • Brainstem (less commonly affected)
    • Double vision, Nystagmus + vertigo
  • Cerebellar white matter
    • Charcot’s neuro triad: Dysarthria, Nystagmus, Intention tremor
    • ATAXIA
    • Fatigue (which can cause apparent exacerbation of other symps)
    • Neuropathic Pain
    • Cognitive issues; Depression; Neurobehavioural symps e.g. pathological laughing/crying
  • Internuclear ophthalmoplegia (from medial longitudinal fasiculus lesion - normally connects ipsilateral occulomotor and contralateral abducens)

All can be affected by Uhtoff’s phenomenon - transient worsening of neurological symps in heat

154
Q

What is charcot’s neurological triad

A

Combination of:

  • nystagmus,
  • intention tremor
  • scanning/staccato dysarthria

characteristic of cerebellar lesion in MS

155
Q

Features suggesting a diagnosis of MS needs to be re-evaluated

A

No objective neuro deficits
No objective evidence for dissemination of lesions
Strongly positive family Hx (for something?)
Progressive disease from outset in young patients
Localised disease or they have no eye involvement
No CSF abnormalities
Pain as predominant symptom

156
Q

Diagnosis of MS

A

McDonald’s Criteria
- Clinical Hx
- Neuro exam

  • Diagnostic = MRI BRAIN + CORD w/ GADOLINIUM CONTRAST
    • Shows dissemination in space + time as the gadolinium shows how long the lesions have been there
  • Evoked Potentials - shows slowed conduction (unspecific)
    • VEP (visual evoked potentials) specifically can pinpoint lesions associated with optic nerve lesions
  • LUMBAR PUNCTURE + CSF ELECTROPHORESIS - may show Oligoclonal IgG banding (non-specific)
    • compare with peripheral blood - should be localised to CNS
157
Q

DDx for MS

A

AI- SLE, Sjogrens- Polysrteritis nodosa- Acute disseminated encephalomyelitisInfectious disease- Lyme disease- Syphilis- AIDSAdrenomyeloneuropathyMitochondrial encephalopathyCardiac embolic event

158
Q

Tx of MS

A
  • For acute episodes/relapses -> IV METHYLPREDNISOLONE (or oral prednisolone) - not diseaase modifying; or plasma exchange
  • Prophylaxis -> BETA-INTERFERON (subcut every other day) - disease modifying
    • slight adverse effects include: Injection site reaction, flu-like symps, mild intermittent lymphonpneia, mild-moderate rises in liver enzymes
    • typically reduce after taking for a few months

most intensive = autologous stem cell transplant

Treating early + aggressively could improve prognosis+ Treat symps

159
Q

Treatment for spasticity

A

BENZODIAZEPINES

  • Oral baclofen or DIAZEPAM
  • If focal/disabling -> peripheral nerve block with phenols, alcohol, BoTox etc
  • Severe -> INTRATHECAL baclofen or Functional neurosurgery

remove triggers (UTIs, bed sores) + give physio

160
Q

Treatment for tremor

A
  • ORAL BETA BLOCKERS, Low dose BARBURITES, Gabapentin, Carbemazepine, even Isoniazid
  • Orthotic devises e.g. weighted wrist bands; computer-controlled mechanical damping devices
  • THALAMIC SURGERY (stereotactic thalamotomy; Thalamic electrostimulation)
161
Q

Treatment for sexual dysfunction

A
  • Counselling- Treat spasticity + incontinence- Yohimbe? Sildenafil (viagra - aslo cause pulm smooth muscle relaxation) - can interact with anti-anginals/hypertensives to cause hypotension- Penile prostheses- For females: Gels, topical local anaesthetics
162
Q

Treatment for pathological laughing/crying

A

Amitriptyline (tricyclic antidepressant) or Levodopa

163
Q

Which supportive services + organisations are oft involved in MS care

A
  • MS societies- Medical/nursing + MS clinics- Clinical psychology/counselling- Disability advisory- Physio/occupational therapy; speech- Social services- Mobility, continence, vocational, housing services
164
Q

Define Parkinson’s Disease

A

Chronic, progressive neurodegenerative disorder characterised by BRADYKINESIA with at least one of REST TREMOR or RIGIDITY

165
Q

Epidemiology of Parkinson’s

A
  • Increases with age- Prevalence = 1 in 200 >70s -> 3% of > 65y/o- Mean survival 10-15 years2nd most common neurodegenerative condition after dementia
166
Q

RFx and protective factors for Parkinson’s

A

RFx:

  • INCREASED AGE
  • FHx
  • MALES (3:2 male:female)
  • previous head injury

Protective:

  • LESS COMMON IN SMOKERS (60% lower risk)
  • physical activity
  • caffeine intake
167
Q

Causes of Parkinson’s

A

Inherited- Monogenic mendelian inheritence (but parkinson gene - v rare)- Susceptibility factors i.e. presence of risk factors (x3 ish increased risk)Environmental- Pesticides, herbicides (toxin induced)

168
Q

Pathophys of Parkinson’s

A

Basically a combination of OXIDATIVE STRESS + MITOCHONDRIAL DYSFUNCTION -> cell death in SUBSTANTIA NIGRA PAS COMPACTUM - site of dopaminergic neurons which radiate out to supply dopamine to striatum in basal ganglia

  • NIGROSTRIATAL PATHWAY excites the direct pathway and inhibits the indirect pathway
  • dopamine stimulates D1 receptors in striatum which causes GABA release and inhibition of Substantia nigra PARS RETICULUM and Globus pallidus INTERNA which sends GABA signals to the thalamus
  • sending GABA to the thalamus results in DISINHIBITION of the thalamus and SIMULATION OF MOVEMENT
  • when the nigrostriatal pathway stops working the INHIBITORY INDIRECT KEEPS FIRING -> DISINHIBITION of SUBTHALAMIC NUCLEUS leading to EXCITATION of GPi/SNr and INHIBITION OF THALAMUS -> DIFFICULTY INITIATING MOVEMENT
  • Intracytoplasmic inclusion bodies - LEWY BODIES canb e found in affected ragions
  • Can also get cell loss + dysfunction in other parts of the brain + potentially outside nervous system
169
Q

Presentation of Parkinson’s

A

Characteristic:
- RESTING TREMOR (initially unilateral) + some postural tremor - PILL-ROLLING tremor
- RIGIDITY - pain/stiffness; problems turning in bed
- cogwheel rigidity (jerky limb movement) - lead pipe rigidity (maintained stiffness)
- BRADYKINESIA (better upon initiation of movement, gradually deteriorates)
- POSTURAL INSTABILITY

Other motor:

  • fine motor dysfunction
    • micrographia
    • difficulty doing up buttons
  • Small stepped gait, may drag one foot -> Slower, REDUCED ARM SWING (ASYMETRIC AT FIRST)
  • Hypomimia (mask-like facies + Decreased blinking)
  • Hypokinetic dysarthria
  • Dysphagia (bradykinesia of pharyngeal muscles)

Slow progression - always starts asymmetrically

Non-motor:

  • Depression and anxiety - 20-40% (v common + diff to treat)
  • Potentially also phobias, hallucinations etc
  • Dementia (20%) - esp in old/severely affected
  • Autonomic problems
    • orthostatic hypotension
    • Constipation (>⅔ of all pts >60 y/o)
    • Increased urinary frequency (Usually NOT incontinence tho)
    • Sleep disorders
    • Anosmia occurs early on
170
Q

Which symps are not typically present in INITIAL parkinson’s

A
  • Incontinence- Dementia- SYMMETRY- Early falls
171
Q

Dx of Parkinson’s

A

Clinical

  • Hx- Observations (asymmetrical small-stepped gait with stooped posture, reduced arm swing)

To distinguish from essential tremor and drug induced/vascular/psychogenic Parkinsonism:

  • DaTSCAN AKA SPECT (inject gamma radioactive substance) -> shows reduced dopamine supply to striatum

May use a structural MRI if in doubt (eg atypical features)

172
Q

DDx for Parkinson’s

A
  • UMN lesions
  • Normal pressure hydrocephalus (Dementia, gait disturbance / falls, INCONTINENCE)
  • LEWY BODY DEMENTIA
    • remember that in Parkinson’s dementia, the Parkinsonism comes BEFORE the dementia; in Lewy body dementia with parkinsonism, the Dementia comes before the Parkinsonism
  • MULTIPLE SYSTEM ATROPHY
    • prominent AUTONOMIC dysfunction
      - e.g significant postural hypotension, constipation
    • EARLY postural instability
    • poor response to levodopa
  • Progressive Supranuclear Palsy
    • early instability + falls
    • vertical GAZE Palsy
    • axial rigidity
  • Corticobasilar Degeneration (apraxia, aphasia, alien hand syndrome)
  • Wilson’s disease (associated liver disease)
  • Dementia Pugilistica (secondary to repeated head trauma)
  • Drug induced Parkinsonism (esp calcium channel blockers, antipsychotics)
173
Q

Treatment of Parkinson’s

A

No cure or disease modifying treatment- Treatments aim to reduce loss/increase availability of dopamine (oft given in combination)

  • Levodopa/L-DOPA = strongest
    • need to be taken up by remaining neurons + converted to dopamine in brain so given in combination with a dopa decarboxylase inhibitor which prevents it from being broken down in systemic circulation
      • e.g. levodopa + cardiodopa = co-careldopa; or co-beneldopa
    • oft started early + has better effect but increased risk of SE (including motor SE like Off-dyskinesia)
    • Diff types:
      • Dispersible release - kick start in morning
      • Standard release - during day
      • Slow release - overnight (if needed)
  • Non- ergot Dopamine agonists - act directly at post-synaptic (boosts dopamine action - works short-mid term)
    • Oft 1st line if <60 y/o
    • Significant “soft” side effects - e.g. tiredness, hyper impulsivity disorders e.g. gambling, hypersexuality
    • Ropinirole, Pramipexole; Rotigotine (available in patches)
  • COMT inhibitors - used in conjunction with levodopa to extend effectiveness (reduces off time)
    • Entacapone, opicapone
      - ( remember it like L-capone - Entacapone is given with levodopa to make it last Longer)
  • Monoamino-oxidase-B (MAO-B) inhibtors (weaker) - Reduce breakdown/recycling of dopamine - Selegiline, Rasagiline
174
Q

Late stage complications in Parkinson’s

A
  • Meds start wearing off more quickly- On-Dyskinesias - Hyperkinetic, choreiform movement when drugs work- Off-Dyskineasia - Fixed, painful dystonic posturing (sustained muscle contraction), typically of feet, when drugs don’t work- Freezing - ie unpredictable loss of mobility- Dementia
175
Q

Which drugs should you not give in Parkinson’s

A

Anticholinergics- SE = Cognition, confusion, systemic - makes symps worse

176
Q

Define Huntington’s

A

SLOWLY PROGRESSIVE, AUTOSOMAL DOMINANT neurodegenerative disorder characterised by CHOREA, INCOORDINATION, COGNITIVE DECLINE, PERSONALITY CHANGES + PSYCHIATRIC SYMPS

Eventually leads to immobility, mutism (can’t speak) + inanition (exhaustion from lack of nutrition)

177
Q

Epidemiology of Huntington’s

A
  • Typically presents in mid-life: 35-55 (60+ = severe)
  • Full penetrance (everyone with the mutation will develop the symptoms)
  • Shows anticipation - can accumulate more triplet repeats with each generation which can cause it to present earlier/more severely
  • Male = Female
178
Q

Pathophys of Huntington’s

A

Repeat expansion of CAG trinucleotide in Huntingtin gene at N-terminal end on chromosome 4

Autosomal DOMINANT

179
Q

Presentation of Huntington’s

A

Cardinal features:

  • Chorea (pt oft unaware of fidgeting or tries to make movements look normal) - first/most common
    • Random + unpredictable
  • Dementia
  • Psychiatric problems
    • Personality change, depression, psychosis, disinhibition/unusually anxious behaviour
  • impaired work performance
  • Others:
    • Abnormal eye movements:
      • Slowed saccadic eye movements (saccedes = rapidly switching gaze from 1 point to other)
      • Broken pursuit
    • Ataxia
    • some parkinsonism (rigidity, slow finger movements) later on in disease progression
180
Q

Dx of Huntington’s

A
  • CLINICAL DIAGNOSIS (+ve FHx + characteristic presentation)
  • CAG repeat testing -> confirms (if necessary)
    • Less than 28 = normal
    • > = 40 - +ve result -> almost definitely will develop Huntington’s during lifetime
  • Consider MRI/CT brain - May show CAUDATE/STRIATAL ATROPHY (oft not definitively present early + unspecific)
181
Q

Tx of Huntington’s

A
  • No cure
  • 1ST LINE = Extensive COUNSELLING
  • Consider non-pharm e.g. physio, speech/language therapy, nutritional support
  • Treat symps:
    • Dopamine agonist or TETRABENAZINE (a VMAT2) for CHOREA
      - also works for Parkinsonism
    • SSRI for Depression (consider electroconvulsive therapy if refractory)
    • Neuroleptics (HALOPERIDOL) for psychosis
    • Risperidone for aggression
    • Mood stabilising anticonvulsants for behavioural problems
    • SSRIs/Benzodiazepines for prominent anxiety/insomnia
182
Q

Essential tremor

A

v common (DDx for parkinson’s) - 5% > 65 y/o- but no associated Structural pathologyPresents with POSTURAL/ACTION TREMOR (as opposed to rest tremor/pill rolling in Parkinson’s)- No increased tone- No impaired fine finger movementsTreat with B BLOCKERS (contraindicate in asthma); Primidone (anti-epileptic - initally low dose)- consider Gabapentin, clonazepam if needed

183
Q

Rigidity vs Spasticity

A
  • Rigidity = Tone increased over entire radius of joint movement- Spasticity = increased tone then decreased tone
184
Q

Which Nerve roots are associated with which deep tendon reflexes

A
  • L3/4 = KNEE- L5 = Big toe- S1 = ANKLE
185
Q

Presentation + associated pathophys of Brown Sequard syndrome

A

Below level of lesion:- Ipsilateral motor weakness - Corticospinal (decussates in medullary pyramids)- Ipsilateral loss of fine touch, 2 point discrimination + proprioception - DCML dysfunction (decussates in medulla)- CONTRALATERAL loss of PAIN + TEMP - Spinothalamic (decussates 1-2 spinal levels above where it enters) - can have ipsilateral loss of pain/temp at level of lesion (spinothalamic may not have crossed over yet)Partial loss of innervation to bladder + anus -> urinary urgency + poor anal tone (may present as constipation)

186
Q

Causes of Brown Sequard syndrome

A
  • Trauma- Tumour- Ischemic/infarct- Infectious disease e.g. TB- Inflam disease e.g. MS
187
Q

Define lateral medullary syndrome

A

Lesion in lateral part of medulla oblongata - typically caused by a vascular event, esp a Vertebral artery stroke (or posterior inferior cerebellar artery)

188
Q

Presentation of Lateral medullary syndrome

A
  • Ipsilateral: - Horner’s syndrome; - Limb ataxia - Loss of facial sensation of pain + temp and reduced corneal reflex - Dysrthria + Dysphagia- Contralateral loss of PAIN + TEMP below lesion- Vertigo, dizziness- Nystagmus- N+V, hiccups
189
Q

Presentation of Horner’s syndrome

A

TRIAD of:- Facial hypo-/anhidrosis (reduced sweating)- Miosis (abnormally constricted pupils)- Partial ptosisCaused by DISRUPTED SYMPATHETIC SUPPLY

190
Q

Presentation of raised ICP

A
  • Postural, worse on lying down - Worse on waking- Worse on coughing, sneezing, straining (valsalva)- Nausea/vomiting- Papilloedema (tho may be absent if acute) - blurred border on funcoscopy- +/- focal signs
191
Q

Define Idiopathic Intracranial HTN + give classic presentation

A

Headache caused by raised ICPSx:- Visual disturbance - check acuity + feilds- Papilloedema + other raised ICP Sx

192
Q

RFx for Idiopathic Intracranial HTN

A
  • OBESITY- Drugs e.g. Tetracycline
193
Q

Investigations for Idiopathic Intracranial HTN

A
  • CT +/- contrast = NORMAL - Exclude 2ndry cause and cerebral venous sinus thrombosis- CSF - HIGH OPENING PRESSURE but normal constituents
194
Q

Management of Idiopathic intracranial HTN

A
  • Modify RFx (obesity, drugs like tetracycline)- Monitor visual fields (Goldman fields)- Pharm: - Acetazolamind - Topiramate - Diuretics- Conside repeated LPs, CSF shunt and optic nerve fenestration if v severe
195
Q

What is a medication overuse headache

A

Headache present for >= 15 days/month linked to the regular use of one or more symptomatic treatment drugs for >3 months. If a headache was previously present, it has worsened during drug use.

196
Q

Which medications are linked to medication overuse headaches

A

Used for 10 or more days/months for >3 months:- Ergotamine-Triptans- Opiods- Combination analgesiaAny of the above used for 15 or more days/months for >3 months without overuse of any specific drug + Simple analgesics

197
Q

What is a Migraine + epidemology

A
  • Episodes of recurrent headache characterised by usually unilateral, throbbing/pulsing pain distribution and N+V or photo/phonophobia. May or may not have premonitory visual disturbance (aura)- Most common cause of Recurrent headache- commonly undiagnosed (48%)
198
Q

RFx for migraine

A
  • FEMALES- Working age (esp <40)- Oestrogen (oral contraception)- FHx- Education, income + socioeconomic status to some degree
199
Q

Common triggers for Migraines

A

Think CHOCOLATE- Chocolate(/coffee?)- Hangovers- Orgasms- Cheese- Oral contraceptives- Lie ins- Alcohol- Tumult (increased NOISE)- Exercise

200
Q

Progression of Migraine (stages)

A
  • PRODROME (days before) - mood signs- AURA (can start up to 60 mins before attack) - commonly zig zag lines- THROBBING HEADACHE lasting 4-72 hrs
201
Q

Sx of Migraine

A

2 of the following:- UNILATERAL PAIN- PULSING/THROBBING- MODERATE-SEVERE- Aggravation by routine physical activityAt least 1 of:- N+V- Photophobia/phonophobia+ not attributed to another disorder -> NORMAL NEURO EXAM

202
Q

Sx of aura in migraine with aura

A
  • NO motor weakness- FULLY REVERSIBLE VISUAL symps (positive or negative) - OR: fully reversible dysphasia+ 2 of following:- HOMONYMOUS visual symos and/or UNILATERAL SENSORY symps- at least 1 symp develops over 5 or more mins OR diff symps occur in succession over 5 or more mins- each symp lasts between 5-60 minsHeadache needs to start during aura or within 60 mins of aura for it to be classified as migraine with aura
203
Q

Dx of migraine

A

CLINICAL unless other path suspected

204
Q

Tx of Migraine

A
  • Life style mod + manage triggers (e.g. avoid tea + coffee, esp at night)
  • Acute:
    • Paracetamol/NSAIDs + TRIPTAN (contraindicated if CVD)
      • consider just paracetamol, nsaids or ASPIRIN 900mg if prefer monotherapy
    • consider Anti-emetics (can also help with reduced gastric motility)
  • Preventative:
    • PROPANOLOL or Topiramate (contraindicated in preg)
    • 2nd line = AMITRIPTYLINE (tricyclic antidepress) + consider acupuncture
  • If not responding to at least 3 prior pharm treatments + are not experiencing medication overuse -> BOTULINUM TOXIN type A
    • Psych/behavioural therapy
    • Surgical treatments
205
Q

Define Tension headache + epidemiology

A

Bilateral generalised headache which can radiate to neck. Most common primary headache. Commonly triggered by STRESS.

206
Q

Sx of tension headache

A

Need 10 or more attacks to diagnose- Lasts 30 mins - 7 days- At least 2 of following: - Bilateral (may spread to trapezius) - PRESSURE/TIGHTENING (not pulsating - like tight band around head) - mild-moderate intensity - NOT aggravated by routine activity- NO N+V- Either photo or phonophobia

207
Q

Management of Tension headache

A

Diagnosed CLINICALLY from Hx Treat with SIMPLE ANALGESIA - Aspirin/paracetamol

208
Q

Define cluster headaches

A

Unilateral periorbital pain w/ autonomic features. LASTS 15-180 MINS. Can be episodic or chronic.- Episodic = ≥ 2 cluster periods lasting 7 days to 1 year separated by pain free periods lasting ≥1 month- Chronic attacks occur for more than 1 year without remission or with remission lasting <1 month

209
Q

Sx of cluster headaches

A

Need at least 5 attacks to be diagnosed- Very/Severe UNILATERAL ORBITAL, SUPRAORBITAL and/or TEMPORAL pain lasting 15-180 MINS if untreated - oft CRESCENDO character- Accompanying IPSILATERAL CRANIAL AUTONOMIC FEATURES and/or sense of restlessness/agitation - face flushing - red conjunctiva + lacrimation - ptosis - miosis - rhinorrhoea (runny nose)- Frequency: 1 every other day - 8 per day- Not attributed to another disorder

210
Q

Management of cluster headaches

A

Diagnosed clinically - 5 similar attacks with relevant Sx

Treatment:

  • Acute = TRIPTANS (sumatriptan)
  • Preventative = Verapamil (CCB)
211
Q

RFx for Trigeminal neuralgia

A
  • MS (20x more likely)- Increased AGE- FEMALETriggered by: Eating, Shaving, Talking, Brushing teeth (INNOCUOUS STIMULI TO AFFECTED AREA)
212
Q

Sx of trigeminal neuralgia

A

Need at least 3 attacks to diagnose- SEVERE, Electric SHOCK-like pain (stabbing, shooting, sharp) which only affects areas supplied by trigeminal (spares angle of jaw; neck)- oft Precipitated by innocuous stimuli to the affected side of the faceCan have reoccurring paroxysmal attacks from a fraction of a second to 2 minutesNO CLINICALLY identifiable neurological deficit

213
Q

Tx for trigeminal neuralgia

A

CARBEMAZEPINE (anticonvulsant) - 2nd line includes lamotrigine, gabapentin, pregabalin, baclofen+ consider surgery if nothing else works(simple analgesia doesn’t work)

214
Q

CN3 lesion Sx

A

Occulomotor- Ptosis- Down + out eye- Fixed dilated pupil IF parasympathetic fibres along outside of nerve affected (more common in surgical 3rd nerve palsey i.e. raised ICP; or if Edinger-Westphal nucleus affected - contains parasympathetic preganglion)

215
Q

CN4 lesion Sx

A

Diplopia on LOOKING DOWN - typically due to TRAUMA (quite unusual)

216
Q

CN6 palsey Sx

A

Adducted eye. Can’t abduct. - oft sign of raised ICP

217
Q

CN5 palsey Sx

A
  • Jaw deviates to affected side- loss of Corneal reflex- Trigeminal neuralgia
218
Q

CN7 plasey Sx

A
  • Facial droop w/ NO FOREHEAD SPARING - ie Bell’s palsey - can get parotid infalmmation
219
Q

CN9 + 10 palsey Sx

A

IMPAIRED GAG reflex - impaired swallowing, resp, vocalThink JUGULAR FORAMEN LESION

220
Q

CN8 lesion Sx

A
  • Hearing loss- Loss of balanceTypically from skull signs e.g. Paget’s, compression or middle ear disease
221
Q

CN11 lesion Sx

A

Can’t shrug shoulders/turn head against resistance

222
Q

CN12 lesion Sx

A

Tongue deviation to side of lesion

223
Q

Common causes of cranial nerve pathology

A

3-12 originate from brainstem so oft from brainstem injury (trauma, tumour, MS, posterior stroke)3-6 (excludin the mandibular nerve - trigeminal v3) also pass through cavernous sinus so consider raised ICP

224
Q

Duchenne Muscular dystrophe

A

X linked recessive mutation of DYSTROPHIN gene- almost exclusively affects boys tho female carriers may also experience some muscle weaknessMuscle is replaced by ADIPOSE tissue.Commonly present with GOWER’S SIGN (have to climb up themselves to get up - esp in young children) and SKELETAL DEFORMITIES (scoliosis, hyperlordosis)Diagnosis happens via PERINATAL TESTS + DNA genetic testsOnly supportive treatments exist. - Corticosteroids (PREDNISOLONE) can increase muscular strength- Physio- Braces/splints- assistive devices e.g. wheelchairs, computer tech, lifting devices

225
Q

Pathophys of Charcot-Marie-Tooth syndrome

A

Inherited sensory + motor PNS POLYNEUROPATHYCaused by an AUTOSOMAL DOMINANT MUTATION on Chromosome 17 - PUP22 GENE

226
Q

Presentation of Charcot Marie Tooth

A

Commonly present between 5-15 tho sometimes don’t present till middle age- Foot drop (common peroneal palsey)- STORK LEGS (v thin calves + distal limbs in general)- HAMMER TOES (Curled up)- HIGH ARCHED FEET (pes cavus)- decreased deep tendon reflexes

227
Q

Management of Chracot Marie Tooth (Dx + Tx)

A

Dx:- Nerve conduction studies- Nerve biopsy- Genetic testingTx = supportive:- orthotics + physio

228
Q

What is Creutzfeld-Jakob disease

A

Idiopathic misfolded proteins deposited in cerebrum + esp in cerebellum -> severe cerebellar dysfunctionA PRION disease - varient version was transmitted from cows with Bovine spongiform encephalitis and has been linked to transmission via blood products.

229
Q

Mechanisms that cause peripheral neuropathy

A
  • Demyelination (Guillain Barre, B12 def)- Axonal damage (T2DM, infection, endocrine)- Nerve compression (RA)- Vasa nervorum infarction (nutrient vessels)- Wallerian degeneration (nerve cut; distal part dies - surgery, trauma)
230
Q

Polyneuropathy

A

Typically affects PERIPHERIES - GLOVE + STOCKING DISTRIBUTION- Motor mostly caused by GUILLAIN BARRE- Sensory mostly caused by T2DMother causes: Vasculitis, Malig, B12 def, RADiagnosed by identifying underlying cause (Bloods, serology, ESR/CRP)Treat with Analgesia (e.g. AMITRIPTYLINE) + treat underlying cause

231
Q

Pathophys of Migraine

A
  • Changes in brainstem blood flow lead to UNSTABLE TRIGEMINAL + basal thalamus nuclei
232
Q

Claw hand

A

ULNER NERVE PALSEY (C8 + T1 roots)- 4th + 5th fingers claw upTx = Splint + simple analgesia

233
Q

Wrist drop

A

RADIAL NERVE PALSY (C5-T1) - mostly innervates arm extensorsTx = Splint + simple analgesia

234
Q

Foot drop (+ causes + Tx)

A

Peroneal nerve palsey (branch of sciatic so stems from L4-S3)- back of knee to front of shin -> DORSIFLEXORS-> associated pain/numbness- Injuries- Joint replacement-Childbirth- Diabetes- Neuro conditions: stroke, MS, cerebral palsey, Charcot-Marie-Tooth- Muscle disorders: ALS, muscular dystrophy, PolioTreat with braces, orthotics, physical therapy or surgery to fuse foot + ankle

235
Q

When is thrombolysis contraindicated

A
  • stroke in past 3 months- severe stroke-active malignancy- diabetes (relative contraindication - severe hypo/hyperglycaemia just increases risk of haemorrhage)
236
Q

Define myesthenia gravis

A

Chronic autoimmune disorder of POST-SYNAPTIC membrane at NEUROMUSCULAR JUNCTION.

Characterised by fatigability

237
Q

Myesthenia gravis epid

A

BIMODAL PRESENTATION (when looking at both sexes)

  • FEMALES tend to be affected YOUNGER (25 - 40 y/o)
    - Linked to AUTOIMMUNE
  • MALES tend to be OLDER (~60 y/o)
    • Linked to THYMOMA
238
Q

RFx for Myesthenia Gravis

A
  • FHx / PHx of AI conditions
  • Genetic markers (HLA gene + single nucleotide polymorphisms)
  • Immune checkpoint inhibitors (cancer Tx)
239
Q

Myesthenia Gravis pathophys

A

3 main types:

  • 85% = Nicotinic Acetylecholine Receptor (AChR) Antibodies (IgG class 1 + 3)
    • Bind to postsynaptic ACh receptor + COMPETITIVELY INHIBIT ACh binding
      - they can also cross-link AChR causing INTERNALISATION of those receptors so fewer are available on the post-synaptic surface membrane
    • More AChR Ab bind with more EXCERTION so there are fewer and fewer receptors available
    • This leads to progressively less effective stimulation of the muscle with increased activity (presenting as fatigability)
    • The Ab clear with rest
    • When the Ab bind, they also activate the COMPLEMENT SYSTEM (as they are IgG class 1+3) at nmj -> POSTSYNAPTIC CELL DAMAGE
  • Ab against Muscle-specific kinase (MuSK - more common in black women) + Low-density lipoprotein receptor-related protein 4 (LRP4)
    • normally induces the creation + aggregation of AChR at the nmj so fewer of these proteins = fewer AChR
  • 10% = THYMOMA
240
Q

Px of myesthenia gravis

A

Muscle fatigability: STARTING FROM HEAD + NECK; spreading to rest of body

  • Eyes: Ptosis + Diplopia (tends to be earliest)
  • Face: Myesthenic snarl
  • Jaw weakness
  • Bulbar weakness (cn 9-12):
    - Dysphagia
    - Dysarthria (NASAL)
  • Neck weakness
  • PROXIMAL LIMB weakness with NO EVIDENT WASTING + NORMAL REFLEXES + SENSATIONS
  • Resp weakness: SOB

Worse in evening

241
Q

Examinations for Myesthenia Gravis

A

To test fatigability:

  • Repeated blinking -> exacerbates ptosis
  • Prolonged upward gazing -> exacerbates Diplopia
  • Repeated abduction of one arm 20 times -> Unilateral weakness when comparing both sides
  • Cogan’s lid twitch: prolonged downward gazing -> breif overshoot of lid retraction triggered by suddenly returning eyes to primary position

Test for FORCED VITAL CAPACITY

Check for thymectomy scar

242
Q

Investigations for Myesthenia gravis

A
  • Serology:
    • AchR Ab (if this is +ve don’t necessarily have to check other Ab)
    • Anti-MuSK Ab
    • LRP4 Ab
  • Electrophysical nerve stimulation (IF SERONEGATIVE)
    - EMG (electromyography) -> DECREMENTAL response on repetitive stimulation
    - SFEMG (single fibre) -> increased jitter or complete block with repeated stimulation
  • CT CHEST (to check thymus)
  • Serial pulm function (PEF?) IF SOB / suspected crisis/pre-crisis

Diagnostic if in doubt:

  • Edrophonium test
243
Q

Edrophonium test

A
  • Pts given EDROPHONIUM CHOLRIDE (or neostigmine) - a RAPID + SHORT acting ACETYLCHOLINEESTERASE INHIBITOR
  • Temporary increase in muscle power
244
Q

Myesthenic Sx DDx

A
  • Myesthenia gravis
    • worsens with exercise
  • Lambert Easton myesthenic syndrome (paraneoplastic syndrome from small cell lung cancer)
    - IMPROVES with brief exercise
  • Botulism
  • Penicillamine-induced Myesthenia Gravis
  • Primary MYOPATHIES (proximal muscle weakness but generally not as much fatigability)
245
Q

Myesthenia gravis Tx

A
  1. Acetylecholine esterase inhib: PYRIDOSTIGMINE, neostigmine
  2. Immunosuppression: CORTICOSTEROID, AZATHIOPRINE, Ciclosporin, Methotrexate
  3. Anti-B cell receptor Ab - RITUXIMAB

Oft THYMECTOMY works

If severe consider:

  • IVIg
  • Plasma exchange
246
Q

Myesthenic crisis

A

Acute exacerbation of MG with SEVERE RESP WEAKNESS (oft triggered by other illness e.g. LRTI)

  • FVC 15ml/kg or LESS and or Negative Inspiratory Force 20 cm H2O or less (normal >= 70 cm H2O)

Tx:

  • Non-invasive / mechanical BiPAP
  • IVIg or Plasma exchange
  • Supportive (VTE, ulcer prophylaxis, nutrition + hydration etc)
    (may require tracheostomy + PEG)
247
Q

Lambert Eaton myesthenic syndrome

A
  • Ab attack PRE-synaptic CALCIUM CHANNALS
  • Px:
    • Proximal limb weakness
    • DIMINISHED muscle stretch REFLEXES
    • IMPROVES with brief EXERCISE
    • Autonomic Sx: Dry mouth, constipation, impotence
  • Eyes only OCCASIONALLY involved at Px
  • Ix:
    - Voltage gated Ca channel Ab +ve (almost always AChR -ve)
    - Low cAMP that increase with rapid stimulation
  • Tx:
    - PREDNISOLONE + IVIg
248
Q
A
249
Q

Main DDx for cluster headaches

A

Other headaches and ACUTE CLOSED ANGLE GLAUCOMA (Tho this normally has blurry vision + halos around lights)

250
Q

What criteria is used in the diagnosis of Parkinson’s

A

UK Parkinson’s disease society brain bank clinical diagnostic scan

  • presence of BRADYKINESIA + at least one of following
    • muscular rigidity
    • resting tremor (4-6Hz)
    • postural instability (not caused by visual, vestibular, cerebellar or proprioceptive dysfunction)
  • need to rule out differentials (e.g. consider multiple system atrophy if early autonomic dysfunction)
  • at least 3 or more of the following supporting positive criteria also need to be present:
    • unilatéral onset
    • resting tremor
    • PROGRESSIVE disease
    • persistent asymmetry affecting same side
    • good response to levodopa (70-100%)
    • response to levodopa for more than 5 years
    • severe levodopa-induced chorea
    • disease course lasting >10 years

Take 2: Electric Boogaloo (20 decks)

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