Phase 2 - Neuro Flashcards

Question

Epidemiology of Ischaemic Stroke

Answer 1

- 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

Answer 2

- 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)

Answer 3

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

Answer 4

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

Answer 5

- 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)

Answer 6

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**, pons Contralateral hemiparesis + pure motor/sensory loss (or mix of both)

Answer 7

- 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

Answer 8

- 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

Answer 9

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 side Secondary 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

Answer 10

- Ischaemia can cause oedem within next 48hrs -> **Hemicraniectomy** (remove part of skull) - but can cause disability

Answer 11

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**

Answer 12

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

Answer 13

20% of strokes

Answer 14

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)

Answer 15

- 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

Answer 16

- 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 ICP 2ndry - fix clotting - lower BP <150 systolic - Statins

Answer 17

- 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

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

- Marfan's/Ehlers Danlos - HTN - POLYCYSTIC KIDNEY DISEASE - TRAUMA - Increased age - FHx

Answer 22

- 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)

Answer 23

- meningitis (no thunder clap headache + has infection) - migrane (no meningism or thunderclap)

Answer 24

- 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

Answer 25

- 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 CSF If vasospasm pr delayed cerebral ischaemia -> refer to neurosurgeon

Answer 26

Rupture of BRIDGING VEIN due to SHEARING

Answer 27

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

Answer 28

- 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 - Papilloedema Focal neurology later e.g. CN3 palsey

Answer 29

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

Answer 30

If <10mm size; midline shift <5mm; no significant neurological dysfunction - consider prophylactic antiepileptics - normalise coag profile but STOP ANTICOAG 10mm 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 cateracts If chronic -> give antiepileptics Give IV MANNITOL to lower ICP

Answer 31

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

Answer 32

- 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

Answer 33

- 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)

Answer 34

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

Answer 35

- ABCDE - URGENT SURGERY - MANNITOL to reduce ICP

Answer 36

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

Answer 37

Oft used for headaches but causes worsening of headache

Answer 38

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)

Answer 39

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

Answer 40

Increasing incidence 55% malig 9th most common - commonest cause in younger ppl (men <45, women <35) Only 3% of all cancers Non 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

Answer 41

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

Answer 42

- 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)

Answer 43

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)

Answer 44

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

Answer 45

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

Answer 46

- 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

Answer 47

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

Answer 48

- 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

Answer 49

- 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)

Answer 50

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

Answer 51

- Hemiparesis - Hemisensory loss - Visual field defect - Dysphasia

Answer 52

- 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 cancer Also: - Age >50 - New onset CHANGE in previously existing headache

Answer 53

- 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 causes Unusual to do lumbar puncture - Raised ICP can cause herniation upon puncturing

Answer 54

- 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)

Answer 55

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

Answer 56

- 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)

Answer 57

- 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)

Answer 58

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

Answer 59

- 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

Answer 60

- 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

Answer 61

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

Answer 62

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

Answer 63

A condition characterised by recurrent epileptic seizures unprovoked by any immediate identified cause Any 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

Answer 64

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

Answer 65

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

Answer 66

- 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

Answer 67

- 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

Answer 68

- Prolonged convulsive seizure lasting 5mins or more or - consecutive recurrent seizures without recovery in-between

Answer 69

- 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

Answer 70

- 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

Answer 71

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

Answer 72

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

Answer 73

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)

Answer 74

- 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

Answer 75

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

Answer 76

- 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

Answer 77

- 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

Answer 78

- 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 suspected Specific: - 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.

Answer 79

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

Answer 80

- 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

Answer 81

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

Answer 82

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

Answer 83

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

Answer 84

- 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

Answer 85

- 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

Answer 86

- 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

Answer 87

- 5% mortality when treated (higher risk if meningococcal) - 20% permanent effects

Answer 88

- Lyme disease (Borrelia burgdorferi) - Leptospira Chronic causes: - TB (higher risk if close contact + immunocomp) - Syphilis (Treponema pallidum) Viral: - Occassionally Poliovirus Fungal: - Chronic - Cryptococcal (typically in poorly controlled HIV) Parasitic

Answer 89

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

Answer 90

- Commonly get spread from extracranial infections ascending e.g. via naso pharynx or ear infection - Less common = haematogenous spread - Direct - via brain surgery Bacteria 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

Answer 91

- 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

Answer 92

- Abnormal clotting - Petechial rash (bleeding) - **Raised ICP**

Answer 93

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

Answer 94

- Subarachnoid haemorrhage - Migraine - Flu + other viral illness - Sinusitis - Brain abscess - Malaria

Answer 95

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

Answer 96

- Clostridium tetani - G +ve anaerobe - Around 8 day incubation period

Answer 97

- 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

Answer 98

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

Answer 99

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

Answer 100

Viral infection - inoclation via animal saliva in broken skin Travels retrogradely along nerves - Incubation period = 2 weeks - many years Higher incidence in tropical countries + russia

Answer 101

- Paresthesia at bite - Furious or paralystic presentation

Answer 102

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

Answer 103

- 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)

Answer 104

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

Answer 105

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

Answer 106

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

Answer 107

Anoxia (low oxygen) Low birth weight

Answer 108

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)

Answer 109

Around 5000 ppl in UK **Median life expectancy = 2-4 yrs** 10% live >10yr 75-80% die within 5 years 1 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)

Answer 110

- **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**

Answer 111

- 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 treat Specific: - 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)

Answer 112

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 > Flexors LMN (ant spinal cord to muscles): - HYPOtonia (flaccid) + muscle wasting - HYPOreflexia - YES FASCICULATIONS - NO babinski - Generally reduced power

Answer 113

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 atrophy Extra motor: - **Emotional lability (rapid, oft exaggerated changes in mood - potentially inappropriate laughing/crying)** - Frontotemporal Dementia (5% - uncommon) - Cognitive problems - Parkinsonism + general fatigue

Answer 114

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

Answer 115

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

Answer 116

- 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

Answer 117

Anterior horn - Post- Polio Motor nerve - Neuropathy or myelopathy e.g. Vit B12 deficiency - spine/brain lesion/compresion Muscle - Myasthenia gravis - Lambert Eaton syndrome

Answer 118

- 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

Answer 119

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

Answer 120

1. Idea of movement (pre-motor cortex/association cortex) 2. Activation of UMNs in motor cortex 3. Impulse via corticospinal tract 4. Modulation by: - cerabellum - fine tuning - Basal ganglia - green signal to move 5. MOVEMENT + somatosensory info obtained by sensory tracts

Answer 121

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

Answer 122

- 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

Answer 123

- **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

Answer 124

- **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, climate Basically a combination of Environment, genetic predisposition + chance

Answer 125

- 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

Answer 126

T + B cell mediated -> immune cascade - Type 1 = macrophages - Type = 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 thing myelin sheath with short intranodes -> less effective - Transmission becomes TEMPERATURE DEPENDANT (Uhtoff's phenomena) - If the axon is damaged it cannot be remyelinated

Answer 127

Active: - **High lymphocyte infiltration -> hypercellular plaque edge + they are present peri-venously (macrophages + t cells)** - 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 mainor blood brain barrier disruption - Plaques are GLIOSED (i.e. Fibrosis) Both have variable oligodendrocyte loss

Answer 128

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 - Intranuclear ophthalmoplegia (from medial longitudinal fasiculus lesion) All can be affected by **Uhtoff's phenomenon - transient worsening of neurological symps in heat**

Answer 129

Combination of nystagmus, intention tremor + scanning/staccato dysarthria - characteristic of cerebellar lesion in MS

Answer 130

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

Answer 131

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

Answer 132

AI - SLE, Sjogrens - Polysrteritis nodosa - Acute disseminated encephalomyelitis Infectious disease - Lyme disease - Syphilis - AIDS Adrenomyeloneuropathy Mitochondrial encephalopathy Cardiac embolic event

Answer 133

- 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: Injectionsite 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

Answer 134

- 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

Answer 135

- 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)

Answer 136

- 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

Answer 137

Amitriptyline (tricyclic antidepressant) or Levodopa

Answer 138

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

Answer 139

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

Answer 140

- Increases with age - Prevalence = 1 in 200 >70s -> 3% of > 65y/o - **Mean survival 10-15 years** 2nd most common neurodegenerative condition after dementia

Answer 141

- INCREASED AGE - FHx - MALES (3:2 male:female) - LESS COMMON IN SMOKERS (60% lower risk)

Answer 142

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)

Answer 143

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 SIGNALS STRIATUM TO STOP FIRING TO Substantia nigra PARS RETICULUM - the signelling to the pars reticulum normally inhibits movement so when the nigrostriatal pathway stops working -> loss of inhibition of [the inhibition of movement] -> 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

Answer 144

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) - Problems doing up buttons, writing smaller (fine motor dysfunction) - Small stepped gait, may drag one foot -> Slower, REDUCED ARM SWING (ASYMETRIC AT FIRST) - Hypomimia (mask-like face) 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** - including orthostatic hypotension - **Constipation (>⅔ of all pts >60 y/o)** - Increased urinary frequency (Usually NOT incontinence tho) - Sleep disorders - **Anosmia occurs early on**

Answer 145

- Incontinence - Dementia - SYMMETRY - Early falls

Answer 146

- Hx - Observations (asymmetrical small-stepped gait with stooped posture, reduced arm swing) - DaTSCAN AKA SPECT (inject gamma radioactive substance) -> shows reduced dopamine supply to striatum

Answer 147

- UMN lesions - Normal pressure hydrocephalus - 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

Answer 148

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) - **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/ **Monoamino-oxidase-B (MAO-B) inhibtors** (weaker) - Reduce breakdown/recycling of dopamine - **Selegiline, Rasagiline**

Answer 149

- 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

Answer 150

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

Answer 151

SLOWLY PROGRESSIVE, AUTOSOMAL DOMINANT neurodegenerative disorder characterised by CHOREA, INCOORDINATION, COGNITIVE DECLINE, PERSONALITY CHANGES + PSYCHIATRIC SYMP Eventually leads to immobility, mutism (can’t speak) + inanition (exhaustion from lack of nutrition)

Answer 152

- 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

Answer 153

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

Answer 154

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

Answer 155

- 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)

Answer 156

- 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

Answer 157

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

Answer 158

- Rigidity = Tone increased over entire radius of joint movement - Spasticity = increased tone then decreased tone

Answer 159

- L3/4 = KNEE - L5 = Big toe - S1 = ANKLE

Answer 160

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)

Answer 161

- Trauma - Tumour - Ischemic/infarct - Infectious disease e.g. TB - Inflam disease e.g. MS

Answer 162

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

Answer 163

- 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

Answer 164

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

Answer 165

- 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

Answer 166

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

Answer 167

- OBESITY - Drugs e.g. Tetracycline

Answer 168

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

Answer 169

- 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

Answer 170

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.

Answer 171

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

Answer 172

- 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%)

Answer 173

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

Answer 174

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

Answer 175

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

Answer 176

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

Answer 177

- 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 mins** Headache needs to start during aura or within 60 mins of aura for it to be classified as migraine with aura

Answer 178

CLINICAL unless other path suspected

Answer 179

- 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

Answer 180

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

Answer 181

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

Answer 182

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

Answer 183

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

Answer 184

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

Answer 185

Diagnosed clinically - 5 similar attacks with relevant Sx Treatment: - Acute = TRIPTANS (sumatriptan) - Preventative = Verapamil (CCB)

Answer 186

- MS (20x more likely) - Increased AGE - FEMALE Triggered by: Eating, Shaving, Talking, Brushing teeth (INNOCUOUS STIMULI TO AFFECTED AREA)

Answer 187

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 face Can have reoccurring paroxysmal attacks from a fraction of a second to 2 minutes NO CLINICALLY identifiable neurological deficit

Answer 188

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

Answer 189

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)

Answer 190

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

Answer 191

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

Answer 192

- Jaw deviates to affected side - loss of Corneal reflex - Trigeminal neuralgia

Answer 193

- Facial droop w/ NO FOREHEAD SPARING - ie Bell's palsey - can get parotid infalmmation

Answer 194

IMPAIRED GAG reflex - impaired swallowing, resp, vocal Think JUGULAR FORAMEN LESION

Answer 195

- Hearing loss - Loss of balance Typically from skull signs e.g. Paget's, compression or middle ear disease

Answer 196

Can't shrug shoulders/turn head against resistance

Answer 197

Tongue deviation to side of lesion

Answer 198

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

Answer 199

X linked recessive mutation of DYSTROPHIN gene - almost exclusively affects boys tho female carriers may also experience some muscle weakness Muscle 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 tests Only supportive treatments exist. - Corticosteroids (PREDNISOLONE) can increase muscular strength - Physio - Braces/splints - assistive devices e.g. wheelchairs, computer tech, lifting devices

Answer 200

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

Answer 201

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

Answer 202

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

Answer 203

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

Answer 204

- 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)

Answer 205

Typically affects PERIPHERIES - GLOVE + STOCKING DISTRIBUTION - Motor mostly caused by GUILLAIN BARRE - Sensory mostly caused by T2DM other causes: Vasculitis, Malig, B12 def, RA Diagnosed by identifying underlying cause (Bloods, serology, ESR/CRP) Treat with Analgesia (e.g. AMITRIPTYLINE) + treat underlying cause

Answer 206

- Changes in brainstem blood flow lead to UNSTABLE TRIGEMINAL + basal thalamus nuclei

Answer 207

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

Answer 208

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

Answer 209

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, Polio Treat with braces, orthotics, physical therapy or surgery to fuse foot + ankle

Answer 210

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

Phase 2 - Neuro Flashcards

(235 cards)