Neurology

Question 1

What do the internal carotids supply?

Answer 1

Anterior 2/3rds of cerebral hemispheres and basal ganglia

Question 2

What supplies the circle of willis?

Answer 2

internal carotids and basilar

Question 3

What happens with a anterior cerebral artery occlusion?

Answer 3

frontal and medial cerebrum, weak contralateral legs (sometimes arms), facial sparing

Question 4

What happens with a middle cerebral artery occlusion?

Answer 4

lateral part of each hemisphere, occlusion = contralateral hemiparesis, hemisensory loss, contralateral homonymous hemianopia, dysphasia, visuo-spatial disturbance

Question 5

What happens with a posterior cerebral artery occlusion?

Answer 5

occipital lobe, contralateral homonymous hemianopia

Question 6

What happens with a vertebrobasilar artery occlusion?

Answer 6

cerebellum, occipital brainstem; occlusion = hemianopia, cortical blindness, diplopia, vertigo, ataxia, dysarthria, dysphasia, hemi/quadriplegia

Question 7

what to ask for a headache (red flags)?

Answer 7

SOCRATES, red flags = >60yrs, thunderclap, infective, hx malignancy

Question 8

what to ask for weakness (red flags)?

Answer 8

SOCRATES, red flags = loss of sphincter control [spine problem like cancer, trauma, cauda equina syndrome], sudden onset [stroke], progressive, resp/swallowing problems

Question 9

what to ask for visual disturbance (red flags)?

Answer 9

blur, monocular/binocular, diplopia, photophobia, speed of onset, pain in eye

Question 10

what to ask for speech disturbance (red flags)?

Answer 10

confusion, dysarthria, dysphonia [laryngeal problems, resp muscle weakness], comprehension/receptive/wernickes, production/expressive/brocas, repetition [conductive dysphasia, arcuate fasciculus]

Question 11

what to ask for dysphagia (red flags)?

Answer 11

neuro [bulbar and pseudobulbar palsy], mechanical (achalasia/stricture), solids/liquids, pain, nasal regurg, coughing, speed of onset), sensation (pain, odd distrubtion, +ve/-ve [numbness, paraesthesia], speed of onset

Question 12

what to ask for blackouts (red flags)?

Answer 12

hx from pt/bystander, loss of consciousness, posture, provocation and prodrome, frequency, duration, tongue biting, incontinence, cyanosis, confusion after, shaking, chest pain, palpitations, fhx, driving

Question 13

Indicators of raised ICP?

Answer 13

worsens when strain like coughing/sneezing, also have papilloedema, diplopia, difficulty concentrating

Question 14

Symptoms from nox use?

Answer 14

B12 deficiency = paraesthesia, blindness, confusion, wernickes

Question 15

What is hemiballismus?

Answer 15

one arm goes out and moves

Question 16

5 tests to determine cognition?

Answer 16

AMT10 test, AVPU, MMSE, MOCA, ACE-R

Question 17

What does the MOCA test?

Answer 17

for the younger population like PD; short term memory, visuospatial, attention, conc, working memory, language and time and place orientation

Question 18

What is intranuclear ophthalmoplegia?

Answer 18

when nystagmus means eyes can’t communicate with each to move to look together at something

Question 19

Bell’s palsy

Answer 19

can’t close the eye; affected side cannot move/show expression

Question 20

Describing CT head?

Answer 20

patient demographics, type of scan (non-contrast CT), what plane the scan is in, describe what see (e.g. high attenuation lesion, left hemisphere, midline if centred or not), describe lesion; attenuation means area of colour different to what it should be (high = white, iso = middle tone and low = dark); extra/intra axial (inside or outside the brain when on an axial plane)

Question 21

Causes for ischaemic stroke?

Answer 21

hypoperfusion, thrombus, embolus, cerebral venous sinus thrombosis

Question 22

treatment options for ischaemic stroke (pharma)?

Answer 22

aspirin as prevention (300mg 2wks then long-term anticoag [clopidogrel or dipyridamole]); thrombolysis/thrombectomy (alteplase; check Cis, best within 90mins)

Question 23

Types of ischaemic stroke?

Answer 23

total anterior circ infarct, partial anterior, lacunar (basal ganglia, internal capsule, thalamus [consciousness impaired], pons; ataxic hemiparesis, pure motor/sensory/both, dysphasia), posterior

Question 24

S+Ss of stroke?

Answer 24

facial weakness, arm drift, abnormal speech, eyes deviate to the side of the lesion; if spinothalamic/corticospinal/dorsal column affected then hemiplegia, facial weakness, numbness, reduced sensation, reduced muscle tone, spasticity, hyperreflexia, weakness in tongue and sternocleidomastoid, carotid bruit; brainstem affects CNs (locked in syndrome)

Question 25

cerebral cortex stroke?

Answer 25

aphasia, dysarthria, apraxia, visual field deficit, memory loss

Question 26

cerebellar stroke?

Answer 26

ataxia, co-ordination, vertigo

Question 27

ischaemic stroke risks?

Answer 27

stimulants, sickle cell, air pollution, MI, arrhythmias, cerebral venous sinus thrombosis (increase venous pressure exceeding arterial pressure), >45yrs, men

Question 28

treatment for venous sinus stroke?

Answer 28

LMW heparin and then warfarin

Question 29

TIA S+Ss?

Answer 29

cerebral ischaemia symptoms lasting <24hours; can get amaurosis fugax and less severe symptoms of stroke

Question 30

TIA management?

Answer 30

ABCD2; stop driving for month

Question 31

Management for stroke (not treatment)?

Answer 31

protect airway; bg 4-11mmol/L, bp only if thrombolysis; nbm until screen swallow, CT/MRI in 1hour if unusual/thrombolysis/haemorrhagic, otherwise 24hours

Question 32

Causes of haemorrhagic stroke?

Answer 32

SAH/cerebral haemorrhage; from cerebral amyloid angiopathy, cerebral AV malformation, intracranial aneurysm

Question 33

Management and treatment of haemorrhagic stroke?

Answer 33

bloods, CT head, stop anticoag/antiplatelet etc, ICPDs (the compressive squeezing leg stockings), reverse with vit K and beriplex (beriplex is faster acting for warfarin), aggressive bp control (140-160mmHg)

Question 34

What is neuroplasticity?

Answer 34

part of brain dies their function is taken over by other part of the brain

Question 35

Stroke investigations?

Answer 35

hypertension, 24 our ECG for AF, vasculitis, prothrombotic states, hypo/hyperglycaemic, thrombocytopenia, hyperviscous, genetics, carotid artery stenosis with carotid doppler/MRI

Question 36

Stroke complications?

Answer 36

high ICP, low GCS when HTN, aspiration pneumonia (ng feed), pressure sores, depression, cognitive impairment

Question 37

What does CHADSVASC stand for (when to treat with AF)?

Answer 37

Congestive heart failure, Hypertension, Age ≥ 75 (2), Age 65-74, Diabetes mellitus, Stroke/TIA/thrombo-embolism (2), Vascular disease, Sex Female

Question 38

What does HASBLED stand for (warfarin or DOAC)?

Answer 38

Hypertension, Abnormal liver function, Abnormal renal function, Stroke, Bleeding, Labile INRs, Elderly (Age >65), Drugs, Alcohol use ≥ 8u / week

Question 39

Hx for muscle weakness?

Answer 39

onset, proximal/distal, progressive, predisposing events, SOCRATES, symmetrical or not, local or diffuse, pain/motor/sensory, sphincter control, deformity, swelling, stiff, loss of movement/function; MRC grading

Question 40

S+Ss UMN?

Answer 40

bulk normal, tone high, strength low, no fasciculations, high reflexes; corticospinal/pyramidal tracts (contralateral); groups of muscles; spasticity in stronger muscles (leg extensors and arm flexors); Babinski reflexes and clonus positive

Question 41

S+Ss LMN?

Answer 41

reduced bulk, normal/decreased tone, low strength, may have fasciculations, low or no reflexes; anywhere distal to anterior horn (nerve roots, plexuses, peripheral)

Question 42

What do the peripheral small nerves transmit?

Answer 42

pain and temp along spinothalamic tracts

Question 43

What do the peripheral large nerves transmit?

Answer 43

proprioception and vibration

Question 44

Common weakness causes?

Answer 44

steroid myopathy, statin myopathy, metabolic and endocrine, myotonic dystrophy, UMN/LMN, hypocalcaemia, hypokalaemia, anaemia, post viral, malignancy, infection, low CO, Guillain-Barre

Question 45

Why would CK be raised?

Answer 45

inflammatory/proximal myopathy and anterior horn cell disease

Question 46

S+Ss in weakness?

Answer 46

stairs, chairs, hair; wasting; facial weakness; neck weakness; contractures; scoliosis (Duchenne); eye movements rare

Question 47

S+Ss in peripheral neuropathy?

Answer 47

chronic and slow progressing, sensory/motor/both, trophic changes (dryness, thin skin, deformity of nails, hair loss, ulcers), large fibre is more numbness and small fibre is more painful and burning sensation, ataxia, numbness, muscle wasting, paraesthesia

Question 48

Causes of peripheral neuropathy?

Answer 48

Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, hereditary sensorimotor neuropathies (charcot-marie-tooth), diphtheria, porphyria are all motor; B12 and folate lack, diabetes, alcohol/drugs, metabolic abnormalities, leprosy, amyloidosis are sensory

Question 49

What is mononeuritis multiplex?

Answer 49

painful, asymmetrical, motor; subacute; inflammatory mediated

Question 50

What can cause mononeuritis multiplex?

Answer 50

vasculitides like churg strauss, connective tissue like sarcoid; ischaemic infarction of vasa nervosum from vasculitis

Question 51

Median nerve (C6-T1) control?

Answer 51

controls LOAF (lumbricals, opponens, policis, abductor pollicis brevis, flexor policis brevis)

Question 52

Ulnar nerve (C7-T1) control?

Answer 52

can’t cross fingers, weakness of medial flexors, medial 2 lumbricals (claw hand)

Question 53

Radial nerve (C5-T1) control?

Answer 53

opens fist, BEAST (brachioradialis, extensors, abductor pollicis longus, supinator, triceps)

Question 54

Brachial plexus S+Ss damage?

Answer 54

pain/paraesthesia along arm

Question 55

Phrenic nerve (C3-5) S+Ss damage?

Answer 55

orthopnoea

Question 56

Lateral cutaneous nerve of the thigh S+Ss damage?

Answer 56

anterolateral burning thigh pain

Question 57

Sciatic S+Ss damage?

Answer 57

affect hamstring and all muscles and senses below knee

Question 58

Common peroneal damage S+Ss?

Answer 58

foot drop, weak ankle dorsiflexion, sensory loss over foot dorsum

Question 59

Tibial nerve damage S+Ss?

Answer 59

can’t stand on tiptoes, invert foot, flex toes, sensory loss on sole

Question 60

Investigations for neuropathies?

Answer 60

Neuro screen, vasculitic screen, EMG/NCS, CSF, nerve biopsy

Question 61

Treatment and management for neuropathies?

Answer 61

gabapentin/pregabalin/amitriptyline; remove underlying cause; prednisolone if inflammatory or vasculitis

Question 62

Guillain Barre pathophysiology?

Answer 62

• AI against myelin (T cells and macrophages or IgG if axonal); post infection

Question 63

Common GBS post infections?

Answer 63

resp/GI –campylobacter jejuni, flu, EBV, cytomegalovirus, varicella zoster, herpes simplex, zika

Question 64

GBS S+Ss?

Answer 64

numbness distally, ascending weakness (1/2 day – 2wks to be max), paraesthesia, bifacial weakness, cranial neuropathies, areflexia, flaccid tetra/paraparesis

Question 65

GBS investigations and results?

Answer 65

raised CSF protein, few cells; EMG slow nerve conduction; use IVIgs or plasmapheresis, DVT prophylaxis, BP, ECG, monitor swallow

Question 66

GBS differentials?

Answer 66

spinal shock syndrome, botulism, myasthenia, lyme disease, toxins

Question 67

GBS complications?

Answer 67

severe weakness, aspiration, resp failure, autonomic instability (monitor all of these – bp fluctuation and arrhythmia), hyporeflexia, ataxia, ophthalmoplegia, resp failure (breathing muscles failure)

Question 68

Treatment for GBS?

Answer 68

ABCD, ABG, ECG, early anaesthesia, infection, supportive management of resp function, IVIg; improvement 2 days-6 months; LP (elevated protein); MRI, bloods; plasmapheresis

Question 69

What is autonomic instability?

Answer 69

tachycardia, bradycardia, hyper/hypotension

Question 70

Pathophysiology of myasthenia gravis?

Answer 70

• AI against nicotinic Ach receptors (abs = MuSK, LRP4)

Question 71

MG S+Ss?

Answer 71

thymus dysfunction common (hyperplasia/thymoma); repetitive use of muscle = weakness shows; fatigueable weakness (proximal limbs, neck and face [head droop and ptosis], extraocular [complex diplopia], bulbar, speech); other AI diseases; no wasting/fasciculations; sensation, reflexes normal; dysphonia rare; reflexes normal

Question 72

What population is mg common in?

Answer 72

3rd decade for women and 6th/7th for men

Question 73

MG investigations?

Answer 73

tensilon test, achr abs (if -ve then NCS/EMG), EMG, CT thorax (thymoma), thyroid; if lift the ptosed eye then the other should ptose; anti-achr/anti-musk abs

Question 74

MG treatment and management?

Answer 74

achesterase inhibitors (pyridostigmine – stop ach breakdown at NMJ), immunosuppressants (steroids, azathioprine/methotrexate/mycophenolate), thymectomy, stop antispasmodics/muscle relaxants, assess severity, bone protection (PPI), IVIg (for crisis), treat infections early and aggressively with abx; for severe generalised used rituximab

Question 75

What can trigger myasthenic crisis?

Answer 75

infection, over/underdosing, abx/antiarrhythmics/beta blockers, disease progression, emotions, hypokalaemia, pregnant

Question 76

How to manage myasthenic crisis?

Answer 76

review and think about breathing and monitor

Question 77

Pathophysiology of MND?

Answer 77

• Degeneration of MN in motor cortex and anterior horns of spine

Question 78

MND investigations?

Answer 78

LP, NCS/EMG/MRI

Question 79

What is UMN only MND?

Answer 79

primary lateral sclerosis

Question 80

What is LMN only MND?

Answer 80

primary muscular atrophy

Question 81

What is both L and UMN MND?

Answer 81

amyotrophic lateral sclerosis

Question 82

What is bulbar only MND?

Answer 82

progressive bulbar palsy

Question 83

MND S+Ss?

Answer 83

asymmetrical weakness; bulbar/limb onset; no sensory/visual/BB; 2-5yrs survive; UMN is pyramidal signs (spastic, increased tone, hyperreflexive, weakness), LMN (flaccid dysarthria, loss of tone, loss of reflexes, weakness); >40yrs, stumbling spastic gait, foot drop, proximal myopathy, weak grip, should abduction and sometimes aspiration pneumonia

Question 84

What is MND diagnosis from?

Answer 84

clinical supported by electrophysiology; sensory should be normal in NCS, motor can be normal (as compensatory innervation can make up for the loss) or abnormal; Awaji-Shima criteria for ALS (give EMG findings [fasciculations, fibrillations] for active denervation with re-innervation as much weighting as clinical findings; need at least two muscles that this is true for)

Question 85

MND differentials?

Answer 85

radiculopathy, CIDP, myopathy, MG

Question 86

What is MND treatment and management?

Answer 86

MDT, riluzole (inhibits glutamate release and NMDA receptor antagonist); antimuscarinic for stop drooling; blend food for dysphagia; exercise; palliative; find way of communicating effectively

Question 87

What can cause a coma?

Answer 87

drugs, anoxia, mass lesions, injury, infections, infarcts, metabolic, epilepsy, SAH, sometimes psych, hypothermia, venous sinus occlusions, tumour; hx, previous events, suicide attempts, travel

Question 88

What does GCS assess?

Answer 88

eye, motor and verbal in consciousness

Question 89

What exams are needed in assessing coma?

Answer 89

trauma, skull, fever, hypothermia, breath odour, needle marks, liver disease, convulsion, alert bracelet, skin colour, GCS (may not be able to maintain airway), eye reactions, focal deficits, meningism, bp, pulse, emergency bracelet, resp/carido/neuro/abdo

Question 90

What investigations are needed in assessing coma?

Answer 90

bloods, imaging, LP, EEG

Question 91

What S+Ss for cocaine use?

Answer 91

seizures, tic-like movements, crack is anxiety, confusion, paranoia, visual hallucinations, psychosis, stroke

Question 92

What is status epilepticus?

Answer 92

persistent seizure activity for 30 mins+ either continuous or intermittent without recovery

Question 93

Causes of status epilepticus in adults?

Answer 93

usually anticonvulsant/alcohol withdrawal (pabrinex or thiamine), cerebrovascular disease, metabolic disorders (lactic acidosis, high K+, sugar, CO2, low Na), renal, autonomic (hyperpyrexia, failure of cerebral autoreg, vomiting, incontinence), CVA

Question 94

Assessment of status epilepticus?

Answer 94

rule out infection with LP, CT, EEG when less obvious to diagnose, O2, cardiac and resp assess, blood glucose

Question 95

Emergency treatment of status epilepticus?

Answer 95

IV benzodiazepine (midazolam/diazepam rectal if can’t swallow – give IV phenobarbital after trying IV lorazepam) fit more than 5 mins, if no work then give antiepileptic drug IV (phenytoin, levetiracetam, sodium valproate, phenobarbital), if this doesn’t work then general anaesthesia and intubation

Question 96

Sudden onset headache causes?

Answer 96

SAH, cerebral venous thrombosis, dissection carotid/vertebral, bacterial meningitis, encephalitis, cerebral abscess, acute haemorrhage

Question 97

SAH S+Ss?

Answer 97

thunderclap, dizzy, vomiting profusely, ptosis, eye movements painful, pupillary reflexes normal, stiff neck, photophobia, spontaneous onset, low GCS, 3rd CN palsy

Question 98

SAH treatment?

Answer 98

surgical clipping or endovascular coiling

Question 99

Sudden onset headache investigations?

Answer 99

CT (better closer to event), MRI, LP (xanthochromia 12hours to 2wks after – yellow CSF)

Question 100

Two types of acute neuropathies?

Answer 100

acute demyelinating or motor axonal

Question 101

Acute neuropathy S+Ss?

Answer 101

peripheral paraesthesia then pain, then starting to fall even if early 30s from weakness

Question 102

Acute neuropathy investigations?

Answer 102

NCS

Question 103

Investigations for transient LOC?

Answer 103

12 lead ECG, CT head, EEG, home recording, bloods

Question 104

Pathophysiology of epilepsy?

Answer 104

clinical manifestation of abnormal and excessive discharge of cerebral neurones, resistance of excitatory neurones firing in refractory period is decreased; upregulation of excitatory circuits and down-regulation of inhibitory, brain structure may have changed, failure of GABA neurotransmission, if epileptic then tendency to unprovoked seizures

Question 105

Epilepsy PMH?

Answer 105

childhood development, head injury, neurosurgery, stroke, malignancy, AI, neurodegenerative, LD, drugs, metabolic disorders

Question 106

Epilepsy S+Ss?

Answer 106

simple/complex partial seizures (simple = aura) or generalised tonic clonic (may have aura, stiffen, jerk, grunting, cyanosis, eyes open, 1-2mins, 20mins post-ictal confusion/headache or 1-2 hours, lateral tongue biting, urinary incontinence, injury), myoclonic jerks, absences (SEE PHASE 2A NOTES, brief and appear to drift off), without warning, loss of awareness, awake/asleep, childhood/teenage onset, aura, focal motor activity, automatisms, epigastric sensations, nausea, abnormal taste/smell, SUDEP (most common cause of death)

Question 107

Common epilepsy triggers?

Answer 107

early morning, sleep deprivation, alcohol, photosensitivity; tramadol

Question 108

DVLA notification for epilepsy?

Answer 108

car 6 months and 12 months after, HGV 5 years then 10 years

Question 109

Epilepsy tests?

Answer 109

EEG, MRI, ECG, 3-12 month review

Question 110

Treatment and management of epilepsy?

Answer 110

= AEDs, levetiracetam (most commonly used), lamotrigine, valproate (not used for women of childbearing age - teratogenic), lots of SEs common, adjunctives = clozabam, topiramate, focal use carbamezapine/levetricetam/lamotrigine

Question 111

What is complex epilepsy and how is it treated?

Answer 111

not controlled for 2 years, unsuccessful with 2 AEDs, bad SEs from AEDs, psych comorbidity, unilateral structural lesion; vagal nerve stimulation, surgery for refractive focal epilepsy (anterior/medial temporal lobe resection), SUDEP in uncontrolled

Question 112

Whats is syncope from transient global hypoperfusion?

Answer 112

from lack of blood/oxygen flow to the brain so loss of oxygen

Question 113

What is reflex syncope and causes?

Answer 113

neural – vasovagal from emotion/pain/standing, situational [cough, effort, micturition] from sneeze, carotid sinus hypersensitivity from head turning

Question 114

What is cardiogenic syncope and causes?

Answer 114

Wolff-Parkinson-white, bruguda syndrome, arrhythmogenic right ventricular dysplasia; fewer prodrome symptoms than the other causes of syncope; Stokes Adams attacks

Question 115

What is orthostatic hypotension and its causes?

Answer 115

drugs, autonomic failure, hypovolaemia, PD, diabetes, MSA

Question 116

What is neurogenic syncope and its causes?

Answer 116

inappropriate activation of PNS [vagal nerve] and decrease of SNS

Question 117

Give the different types of syncope?

Answer 117

anxiety, factitious (Munchausens), hypoglycaemia; when vessels don’t constrict to bring blood flow to brain when stand up), structural cardiac disease, cerebrovascular, substance abuse, psychogenic (panic attacks), reflex, cardiogenic, neurogenic and orthostatic

Question 118

PMH of syncope?

Answer 118

previous faints, poor oral intake, PMH

Question 119

Syncope S+Ss?

Answer 119

prodrome = hot, dizzy, visual crowding, ear ringing, pale; S+Ss = pallor during, brief, jerks if upright, fainting prodrome, loss of consciousness ask, <20 secs to some minutes, nausea, sweating, blurred vision, chest pain, dyspnoea, palps, recovery v quick

Question 120

Syncope investigations?

Answer 120

don’t need CT, triggers, change in med, postural tone loss, sudden death, 24 hour tape, tilt table, autonomic function tests; ECG, ECHO

Question 121

What is a psychogenic non-epileptic seizure (NEAD)?

Answer 121

– appears like epileptic but no ictal cerebral discharges; from psych distress (childhood sexual abuse or just stress); may have epilepsy as well

Question 122

Differentials of a NEAD?

Answer 122

hypoglycaemia/acute hydrocephalus, never really think about TIA

Question 123

Difference in hx of NEAD to epilepsy?

Answer 123

no urinary incontinence/tongue biting/tonic clonic movements/unexplained anxiety/deja vue

Question 124

PMH of NEAD?

Answer 124

birth, febrile seizures, CNS infections/head injuries, psych problems; DH = antidepressants and tramadol; SH = psych, alcohol, drugs, driving, psychosocial

Question 125

NEAD S+Ss?

Answer 125

subjective symptoms, eyes usually closed, partially responsive, wax and waning symptoms, emotional, long, tired and washed out post-ictal, random but gradual onset, awake or asleep, over 2 mins, violent thrashing, side to side head, asynchronous movements, may have aura and partner may be aware

Question 126

NEAD treatment and management?

Answer 126

neuropsychotherapy and don’t give anti-epileptics

Question 127

Causes of unilateral vision loss?

Answer 127

vascular (amaurosis fugax, central retinal vein occlusion, anterior ischaemic optic neuropathy), optic neuritis, retinal detachment, vitreous haemorrhage, acute angle closure glaucoma

Question 128

What is central retinal vein occlusion and some S+Ss?

Answer 128

cotton wool spots, multiple retinal haemorrhages, pale optic disc, cherry red spot in macula, ocular equivalent of a stroke

Question 129

What is an anterior ischaemic optic neuropathy?

Answer 129

posterior ciliary artery occluded, supplies optic nerve head, papillodema] - GCA

Question 130

What happens with a retina detachment?

Answer 130

flashes/floaters with decrease in vision, retina peeled away, curtain covering vision, surgical repair

Question 131

S+Ss of vitreous haemorrhage?

Answer 131

flashes/floaters with low vision with diabetic retinopathy, red tinge from blood, blurred vision, visual loss

Question 132

S+Ss acute angle closure glaucoma?

Answer 132

painful red eye with N+V, treat with bright room

Question 133

Treatment acute angle closure glaucoma?

Answer 133

pilocarpine [constricts pupil] or timolol drops [beta blocker], surgery/laser treatment

Question 134

Loss of vision investigations?

Answer 134

hx and exam, visual evoked potential/MRI, fluorescein angiography, tonometry (for glaucoma in eye pressure), US

Question 135

What is a clinically isolated symptom?

Answer 135

first episode of symptoms from inflammatory demyelination

Question 136

Normal ophthalmoscopy?

Answer 136

macula, optic nerve and photo orientation mark

Question 137

Abnormal ophthalmoscopy?

Answer 137

if inflamed optic nerve head (papillitis) but behind nerve is normal; swollen optic disc = anterior ischaemic optic neuropathy; central retinal artery occlusion = cherry red spot at macula; central retinal vein occlusion = dilation of branch veins, cotton wool patches and multiple retinal haemorrhages

Question 138

MS pathophysiology?

Answer 138

lesions in CNS (white matter in optic nerve, brainstem, basal ganglia and spinal cord – at least 2+ and 30 days or more between attacks), inflammation and destruction of myelin; loss of oligodendrocytes means myelin loss and progresses to axonal loss; remyelination at first but less successful as progresses; more astrocytes as neurone loss; inflammation from T cells

Question 139

MS associations?

Answer 139

EBV and herpes simplex, smoking, stress and diet

Question 140

MS S+Ss?

Answer 140

blindness/hemianopia, optic neuritis (reduced/loss of vision in eye), diplopia, horizontal nystagmus, lateral rectal weakness, facial weakness (pain bursts, cough, hiccough, paraesthesia, complex gaze palsies), sometimes deafness, acute demyelination in brainstem means positional vertigo, ataxia, vomiting, visual auditory attention loss, amnesia, depression, damage in posterior column of cervical cord (tightness, burning, pulling, twisting, tearing), loss of thermal/pain sensation, loss of leg sensation (triad associated with cauda equina), impotence in men, loss of thermoregulation, UMN signs (spastic and brisk reflexes), optic atrophy, cerebellar signs, internuclear ophthalmoplegia, dysarthria, incontinence, L’Hermitte’s, worse with heat

Question 141

MS tests?

Answer 141

MRI gives high T2 signal lesions in white matter (mainly periventricular)

Question 142

MS diagnosis?

Answer 142

presence of multiple CNS lesions, symptoms longer than 24 hours and disseminated in time and space (>1 month apart); relapses from viral infections, stress; McDonald criteria; 4 types = relapsing/remitting, secondary progressive (after RR), primary progressive and progressive remitting

Question 143

MS treatment?

Answer 143

amantadine for fatigue, exercise, baclofen/gabapentin for spasticity, amitriptyline for emotions, for relapses give oral methylprednisolone for 5 days; interferon beta 1a/1b (disease modifying)

Question 144

Optic neuritis causes?

Answer 144

= acute demyelinating, ischaemic optic neuropathy, corticosteroid responsive (AI), post infection, post vaccination, infections, vitamin B12 low, drugs (amiodarone, ethambutol), viral infection in kids

Question 145

Optic neuritis S+Ss?

Answer 145

triad of visual impairment (worsened by hot shower), pain around eye (worsened by movement), impairment of colour vision, others = light flashes, Uhthoff’s phenomenon (body gets overheated in demyelinating – hot weather, hot tubs etc), Pulfrich’s phenomenon (still target moves in ellipsis laterally), fatigue, decreased pupillary light reaction, arcuate defects, scotoma, RAPD, dyschromatopsia (loss of colour vision)

Question 146

Optic neuritis treatment?

Answer 146

refer to ophthalmologist/neurologist, methylprednisolone in acute, MRI, neuro assessment, normally resolves on its own or sometimes with steroids, 6wk recovery, risk increased for developing MS

Question 147

Neuromuscular emergencies?

Answer 147

* Swallowing – if structural then liquids ok until disease progresses but neural is if both solids and liquids from onset * MND – speech precedes swallowing problems (RED FLAG) * MANAGEMENT – abcd, ABGs, early anaesthetic help, infection?, treat underlying cause * Type 2 resp failure – from respiratory muscle failure (MG – myasthenic crisis)

Question 148

Proximal myopathy S+Ss and causes?

Answer 148

affects hair, stairs and chairs, not reflexes, specific muscles, not paraesthesia/bladder weakness; kids = Duchenne muscular dystrophy, adults from corticosteroids use

Question 149

Neuromuscular syndromes S+Ss and causes?

Answer 149

fatigable, repeatable; writing, walking, brushing teeth; MG, Lambert-Eaton (defective ach release at presynaptic nerve so proximal muscle weakness [voltage gated calcium channels], extraocular/bulbar not usually involved, can have bilateral partial ptosis

Question 150

Neuromuscular syndromes treatments?

Answer 150

corticosteroids and immunosuppressants [pyridostigmine and IVIg])

Question 151

Peripheral neuropathy types and S+Ss?

Answer 151

large fibre = signs seen before symptoms; small fibre = pain and burning in feet at night; trophic changes (shiny skin, loss of hair, dryness and nail changes)

Question 152

Radiculopathy causes, areas and S+Ss?

Answer 152

usually C6-7 (bicep/tricep wasting) and L5-S1 (L5 dorsiflexion and S1 plantar flexion); sciatic from spinal degeneration and nagging pain (more shooting and sharp) with numbness and weakness; pancoasts tumour = ulnar radiculopathy in smokers; cauda equina syndrome (incontinence, saddle paraesthesia); spinal claudication (pain down one or both legs only with walking – easy to treat)

Question 153

Vertebral pain syndrome S+Ss?

Answer 153

aching, nagging pain isolated to before joint, arthritic; relieved by rubbing and heat; paraesthesia, weakness and numbness, reduced ROM

Question 154

Myelopathy S+Ss?

Answer 154

spinal cord; signs before symptoms; UMN (Babinski, clonus, loss of fine motor movements, Hoffman’s, hyperreflexia, cross adductors and deltoid/pectoral reflex)

Question 155

Cavernous sinus syndrome S+Ss?

Answer 155

CN 3, 4, 5, 6 palsies

Question 156

Spinal claudication causes?

Answer 156

canal stenosis or cauda equina syndrome

Question 157

What syndromes cause nerve thickening?

Answer 157

Charcot-Marie-Tooth or leprosy

Question 158

What does an EMG do?

Answer 158

record electrical activity of skeletal muscle; diagnosis for neuromuscular/motor control diseases; assesses fasciculations and voluntary movements

Question 159

What can EMG be used for assessing?

Answer 159

neurogenic disorders (see gaps between interference indicating axonal loss and see tiny little discharges/fibrillations between this, also see this in myopathy; fibrillations are always pathological); myopathy (full and early motor activation, low amplitude); myotonia (wax and wane in spontaneous firing, in muscle fibre membrane channelopathies); use single fibre for looking for NMJ disorders

Question 160

What does NCS do?

Answer 160

evaluates function and ability of electrical conduction of sensory/motor nerves

Question 161

What types of NCS are there?

Answer 161

motor and sensory (peripheral nerve stimulation), F-wave study (supramaximal stimulation of a motor nerve and record action potentials sent to its muscle) and H-reflex study (stimulation of nerve and record reflex electricity in muscle in limb)

Question 162

When is a brain biopsy needed?

Answer 162

for tumour, infection and inflammation diagnosis; stereotactic brain needle biopsy (small hole into skull and needle guided by CT/MRI), scar can cause seizures

Question 163

When is a muscle biopsy needed?

Answer 163

for distinguishing myopathy from neuropathy in weakness and low muscle tone

Question 164

When is a nerve biopsy needed?

Answer 164

indicate damage to myelin sheath, damage to small nerves, axonal destruction and neuropathies

Question 165

What is a GCA score for?

Answer 165

• Level of consciousness in those with trauma brain injury

Question 166

What is abnormal, moderate and severe from a GCA score?

Answer 166

3-14 abnormal (moderate = 9-12 and 8 or below is severe)

Question 167

When is an angiography used?

Answer 167

aneurysms, stenosis, atherosclerosis, vasculitis, AV malformation, thrombosis and vasospasm

Question 168

What are angiography SEs?

Answer 168

TIA, loss of consciousness and hemiplegia

Question 169

When is an LP used?

Answer 169

= meningitis, SAH, hydrocephalus, benign intracranial hypertension, medulloblastoma, inject meds (spinal anaesthesia, chemo)

Question 170

LP complications?

Answer 170

headache, nausea responding to analgesia and fluids, paraesthesia

Question 171

What may increased CSF pressure in LP mean?

Answer 171

congestive HF, cerebral oedema, SAH, meningeal inflammation, hydrocephalus

Question 172

What may decreased CSF pressure in LP mean?

Answer 172

subarachnoid blockage, severe dehydration, hyperosmolality; pleocytosis (WBC presence – leukaemia, mets, recurrent epileptic seizures)

Question 173

What may granulocytes in LP mean?

Answer 173

Bacterial meningitis

Question 174

What may RBCs in LP mean?

Answer 174

intracranial haemorrhage

Question 175

What may low glucose in LP mean?

Answer 175

lymphoma, leukaemia, fungal TB

Question 176

What may high lactate in LP mean?

Answer 176

CNS cancer, MS, traumatic brain injury, brain abscess, hydrocephalus, resp alkalosis

Question 177

What may high protein in LP mean?

Answer 177

spinal block

Question 178

What may oligoclonal bands in LP mean?

Answer 178

MS

Question 179

When is a spine/brain MRI used?

Answer 179

• For tumours, abscesses, congenital abnormalities, aneurysms, venous malformation, haemorrhage, subdural haematoma, MS, encephalomyelitis, herniated discs, spinal cord compression

Question 180

When is an MRI contraindicated?

Answer 180

pacemakers, cochlear implants, implanted drug infusion pumps, metal implants

Question 181

What is a T1 and T2 MRI?

Answer 181

T1 = CSF dark and for anatomy, T2 = CSF light and white matter dark so useful for pathology

Question 182

What is a FLAIR MRI?

Answer 182

white matter plaques for seeing demyelination

Question 183

When is a CT head most useful for?

Answer 183

Trauma and spiral for kids who can't keep still

Question 184

Other uses for CT head?

Answer 184

intracranial haematomas, brain contusions, oedema, foreign bodies, brain injury, haemorrhage, stroke, tumours, hydrocephalus, disease, skull malformation

Question 185

What is an EEG?

Answer 185

Non-invasive testing electrical activity in the brain (voltage fluctuations)

Question 186

What is an EEG for?

Answer 186

epilepsy (sometimes during seizure – localise it and distinguish from others), sleep disorders, coma, encephalopathies, brain death, depth of anaesthesia, cerebral perfusion in endarterectomy, SAH brain damage

Question 187

What is rhythmic activity in EEG?

Answer 187

divided by frequency; abnormal activity = epileptiform/non-epileptiform, focal (can identify area of cortical irritation during seizure)/diffuse (more for generalised epilepsy)

Question 188

What are transients in an EEG?

Answer 188

spikes and are abnormal and can be epileptiform (that identify epilepsy)

Question 189

Pathophysiology of Huntington's?

Answer 189

• Progressive, neurodegenerative from CAG repeat on 4q, AD inheritance; more glutamines so huntingtin accumulates in neurones of dorsal striatum and caudate nucleus

Question 190

HD S+Ss?

Answer 190

(30-50yrs onset) = chorea (involuntary movements – peaks and declines, worsened by stress/anxiety/depression), impairment of voluntary, akathisia (feeling restless), rigidity and spasticity later unless childhood onset (can get myoclonus), bradykinesia, dysphagia later (can be cause of death – aspiration, weight loss), dysarthria, falls common, incontinent, sleep disturbance, lose driving ability; cognitive = disruption in planning, organisation, lack of initiative, perseveration, impulsivity, irritable, temper, low spatial perception, low self-awareness, difficulty learning new, lack of time awareness; psych = depression, mania, anxiety, apathy, delirium, sexual disorders, OCD

Question 191

HD treatment and management?

Answer 191

supressing chorea (neuroleptics like haloperidol, fluthenazine; benzodiazepines; dopamine depleting agents like tetrabenazine and reserpine but they do have SEs and see psych crib sheet, can worsen dysarthria), relieving stiffness (benzodiazepines but can cause bradykinesia), reliving spasticity (tizanidine = alpha2 agonist), antiparkinsonian meds for rigidity and bradykinesia; other management = PEG feeds for dysphagia, calorie content assessed, hydration and maybe puree food

Question 192

Parkinson's pathophysiology?

Answer 192

low dopamine in pars compacta of substantia nigra; circuits to basal ganglia affected = motor, oculo-motor, limbic, orbitofrontal; can be from alpha-synuclein bound to ubiquitin in damaged cells (Lewy body – in olfactory bulb, medulla oblongata, pontine at first)

Question 193

Risk factors for PD?

Answer 193

genes like PARK 1, 4, 5; heavy metals; pesticides; FH; 2nd most common neurodegenerative disease; 7-14 years expectancy

Question 194

PD S+Ss?

Answer 194

primary parkinsonism; motor with autonomic dysfunction/neuropsych/sleep disturbance; 4 main symptoms = tremor (at rest not in sleep/voluntary movement pill rolling), rigidity (cog wheel/lead pipe neck and shoulders first), bradykinesia (start with fine motor), postural instability; others = fast shuffling and forward flexed gait, asymmetrical arm swing; cognitive in early disease (memory affected like recalling, dementia); mood difficulty (depression, anxiety, apathy); low facial expressions; quiet speech; hallucinations/delusions; sleep problems, orthostatic hypotension, constipation, vision abnormal, impaired smell and pain sense; other symptoms = progressive supranuclear palsy, multiple system atrophy, cortico-basal degeneration, lewy body dementia

Question 195

PD diagnosis?

Answer 195

on hx and examination and rule out PSP and multiple system atrophy; CT/MRI

Question 196

PD treatment and management?

Answer 196

no cure; levodopa dopamine analogue standard used 30mins before meals but later in disease gives motor complications like chorea (also in diagnostic stages to see if improves with it); carbidopa and benserazide are peripheral dopa decarboxylase inhibitors; tolcapone inhibits COMT breaking down dopamine; bromocriptine and pramipexole are dopamine agonists (similar to levodopa); selegiline and rasagiline are MAO-B inhibitors that block dopamine metabolism in basal ganglia; amantadine for motor symptoms; exercise programmes; dysphagia so use thickeners; MDT

Question 197

Causes and red flags of an acute headache?

Answer 197

hx of cancer; above 50yrs (GCA, mets, temporal arteritis); thunderclap/worst ever/vomit at onset (SAH [LP after 12 hours if CT head negative and still suspect but not valid after 12 days, can look for aneurysm after this time using CT angiography], can also get cerebral vasoconstrictive syndrome [from drugs like sumatriptan or over the counter]); meningism (LP, kernigs, Brudzinski, fever, tachycardia, non-blanching rash, CRP); raised ICP signs (worse in morning, papilloedema can eventually get tunnel vision [can look like optic neuritis from MS which is more diffuse headache with pain on movement and visual changes early (scotoma); also look like diabetic papillitis], worse on straining/leaning forward, vomiting; pressure from LP pressure over 30 is abnormal, 14 is normal); idiopathic intracranial hypertension and normal pressure hypertension can cause blindness (losing weight can help, surgery); medication (GTN, nitrates, omeprazole); sleep apnoea (worse in morning); hypertension; sinusitis (can be worse in morning); psychogenic (worse in morning too)

Question 198

Differentiating between migraine and TIA?

Answer 198

migraine more +ve symptoms; more tingling than numbness in migraine; aura in migraine but usually hemianopia in TIA; more weakness with TIA; sudden onset with TIA and migraine more gradual

Question 199

Temporal arteritis S+Ss and risks?

Answer 199

scalp tenderness; risk of amaurosis fugax (TIA of posterior ciliary artery) and posterior circulation stroke

Question 200

What is a chronic headache?

Answer 200

more than 3 months

Question 201

Causes of chronic headache?

Answer 201

migraine and chronic daily syndrome headaches (medication overuse – rebound headaches from stopping it)

Question 202

Migraine prevention and acute treatment?

Answer 202

prevention = propranolol 1st line, 2nd line tricyclics, topiramate 3rd line, 4th line candesartan or valproate if no contraindication; for acute = NSAID with triptan

Question 203

What does DANISH stand for for cerebellar syndrome?

Answer 203

dysdiadochokinesia, dysmetria, ataxia, nystagmus, intention tremor, slurred speech, hypotonia

Question 204

What side is affected in cerebellar syndrome?

Answer 204

Ipsilateral

Question 205

Give an overview of peripheral neuroanatomy?

Answer 205

anterior horn, nerve, muscle; ventral roots are motor and dorsal is sensory

Question 206

Give the controls of nerves C5, 6, 7, 8, T1 and 2?

Answer 206

Over deltoid, index finger, middle finger, little finger, inner arm, apex of axilla

Question 207

Give the controls of nerves L2, 3, 4, 5, S1 and 2?

Answer 207

Anterior medial thigh, over the knee, medial aspect of tibia, dorsum of foot to big toe, lateral heel, popliteal fossa

Question 208

winging scapular causes?

Answer 208

Long thoracic nerve = serratus anterior; Accessory = trapezius (uncommon); Dorsal scapular = rhomboids (rare)

Question 209

What is progressive supranuclear palsy and what areas of the brain are affected?

Answer 209

• Gradual deterioration in specific volumes of the brain; neurofibrillary tangles seen; basal ganglia, brainstem, cerebral cortex, spinal cord, dentate nucleus affected; can have Pick’s disease

Question 210

Progressive supranuclear palsy S+Ss?

Answer 210

loss of balance, bumping into objects, fast walking, personality change, bradykinesia, visual symptoms; later = dementia, dysarthria, dysphagia, difficulty moving eyes, neck stiffening, incontinence, constipation

Question 211

Progressive supranuclear palsy treatment?

Answer 211

no cure; amantadine, levodopa for neck dystonia, rivastigmine for cognition

Question 212

Progressive supranuclear palsy complications?

Answer 212

pneumonia (cause of death), Richardson syndrome (postural instability, supranuclear vertical gaze palsy, frontal dysfunction), PSP (asymmetrical tremor, initial levodopa response), infection

Question 213

What is multiple system atrophy and what areas of the brain are affected?

Answer 213

• Neurodegenerative affecting substantia nigra, striatum, ANS; onset 50-60s; gliosis and astrocyte proliferation and Papp-Lantos bodies

Question 214

What is multiple system atrophy S+Ss?

Answer 214

autonomic dysfunction, parkinsonism, ataxia; sometimes ED or postural hypotension; later sleep disorders, constipation, vocal cord paralysis, difficulty regulating body temp, sometimes cognitive impairment; no cure

Question 215

Meningitis S+Ss?

Answer 215

severe headache, nuchal rigidity, sudden high fever, altered mental state, photophobia, phonophobia, Kernig’s, brudzinski’s sign, petechial rash, bulging fontanelles <6 months

Question 216

Meninigitis complications?

Answer 216

sepsis, DIC, gangrene, focal seizure, CN abnormal

Question 217

Meningitis causes?

Answer 217

viral (herpes simplex, VSV, HIV, mumps), bacterial, fungal, protozoa, sarcoidosis, SLE, malignant

Question 218

Meninigitis risks?

Answer 218

HIV and immunosuppressants

Question 219

Meningitis tests?

Answer 219

FBC/CRP/blood cultures, LP, hyponatraemia common in bacterial

Question 220

Meningitis treatments?

Answer 220

prophylaxis for close contacts (rifampicin, ciprofloxacin, ceftriaxone); IV fluids, mechanical ventilation, third generation cephalosporins (ceftriaxone), meningococcal then use benzylpenicillin, if h.influenzae then use corticosteroids, viral supportive and acyclovir, fungal with amphotericin B

Question 221

What is encephalitis?

Answer 221

• Sudden onset inflammation of brain

Question 222

Encephalitis S+Ss?

Answer 222

acute fever, headache, confusion, seizures, irritable, poor appetite

Question 223

Encephalitis causes?

Answer 223

viral = rabies, herpes simplex, polio, measles; bacterial = meningitis

Question 224

Encephalitis tests?

Answer 224

MRI T2 hypersensitivity in median temporal, EEG, LP, bloods, urinalysis

Question 225

Encephalitis treatment?

Answer 225

steroids reduce swelling, sedatives, antivirals/biotics

Question 226

Brain tumour S+Ss?

Answer 226

high ICP, headaches, frontal lobes (poor reasoning, personality change, inappropriate social, poor planning, decreased speech), temporal (memory loss, hearing loss, difficulty in language comprehension), parietal (poor interpretation of languages, decreased pain sense, poor spatial/visual awareness), occipital (poor/loss vision), cerebellar (poor balance, muscle movement, posture), brainstem (bp, swallowing, heartbeat)

Question 227

Primary brain tumours?

Answer 227

• Meningiomas benign; primary = glial cells (malignant); pituitary adenomas and nerve sheath

Question 228

Brain tumour tests?

Answer 228

CT/MRI BBB disruption; EEG

Question 229

Mets to become brain tumour?

Answer 229

lung, breast, malignant melanoma, kidney, colon

Question 230

Brain tumour prognosis?

Answer 230

medullablastoma (good), glioblastoma multiforme (bad), oligodendrogliomas (incurable – slow progressing)

Question 231

History for spinal cord injury?

Answer 231

• Traumatic or not; mechanical, toxic and ischaemic; level is lowest level of full sensation and function; complete is everything below level function lost; sensory exam = 0 for absent, 1 for impaired and 2 for normal

Question 232

What is a romberg test for?

Answer 232

balance/proprioception; cerebellum, vestibulum

Question 233

What does a pronator drift show?

Answer 233

pyramidal lesion, power

Question 234

Cord compression causes?

Answer 234

canal stenosis, herniated discs, tumours (mets, astrocytoma, neurofibroma, meningioma)

Question 235

Cord compression S+Ss?

Answer 235

bilateral leg weakness, bladder/anal sphincter giving hesitancy and frequency, look for motor, reflex and sensory level

Question 236

Cord compression tests?

Answer 236

spinal MRI, biopsy, bloods, CXR

Question 237

Cord compression treatments?

Answer 237

urgent dexamethasone with specific therapy for malignancy and drainage and abx for abscesses

Question 238

Cord vascular problems causes?

Answer 238

epidural haemorrhage, spinal cord ischaemia (aortic dissection, aortic aneurysm repair, inferior venecal thrombosis)

Question 239

Altered sensation from spinal cord causes?

Answer 239

peripheral neuropathy, CNS disorders (stroke/MS), nereve root lesions, spinal cord compression, hyperventilation, circ disturbance (Raynaud’s/PVD/embolic)

Question 240

Inflammatory spinal cord injury causes?

Answer 240

acute transverse myelitis, neuromyelitis optica (spinal cord and optic nerve, brainstem, aquaporin-4 ab, longitudinal lesion in MRI)

Question 241

Infection spinal cord injury causes?

Answer 241

abscess (bacteria/tuberculosis), herpes simplex, chronic meningitis, meningo vascular syphilis, cytomegalovirus, schistosomiasis

Question 242

What is central cord syndrome and its S+Ss?

Answer 242

damage of cervical, weakness of arms, legs spared, spared sacral sensation; loss of pain, light touch and pressure below injury; usually from neck hyperextension in elderly with spinal stenosis

Question 243

What is cervical spondylosis?

Answer 243

degeneration of annulus fibrosis ad osteophyte formation narrowing spinal cord and traps cord

Question 244

Cervical spondylosis S+Ss?

Answer 244

neck stiffness, crepitus, brachialgia (arm pain), forearm/wrist pain, L/Hermitte’s, LMN signs if radiculopathy, UMN if cord compression

Question 245

Cervical spondylosis management?

Answer 245

urgent MRI, specialist referral, if not urgent then analgesia and gentle activity; may need laminectomy/laminoplasty

Question 246

What is anterior cord syndrome and its S+Ss?

Answer 246

anterior cord damage or reduction in supply to anterior cord; below level = motor, pain and temp sensation lost

Question 247

What is Brown Sequard sydrome?

Answer 247

hemisection of spinal cord (loss of motor, proprioception, vibration ipsilateral, pain and temp loss contralateral)

Question 248

What is posterior cord syndrome?

Answer 248

posterior spinal artery infarct; loss of proprioception, vibration

Question 249

What is cauda equina syndrome and its S+Ss?

Answer 249

saddle paraesthesia, bowel disturbance, urinary incontinence, paraesthesia, spasticity, sexual dysfunction, leg weakness areflexic and flaccid, back pain and may radiate down legs; from conus medullaris syndrome, ruptured intervertebral disc, tumour, fecal impaction

Question 250

Pathophysiology of neurosarcoidosis?

Answer 250

chronic, non-inflammatory; non-caseating granulomas in different parts of body, 10% of those with sarcoidosis

Question 251

S+Ss of neurosarcoidosis?

Answer 251

cranial nerve abnormality (usually CN7), decrease in visual perception, seizures, meningitis, depression, psychosis, peripheral neuropathy, Sometimes dyspnoea, arthralgia, jaundice, HF

Question 252

Neurosarcoidosis treatment?

Answer 252

prednisolone, immunosuppressants (methotrexate and cyclophosphamide)

Question 253

What is muscular dystrophy?

Answer 253

Progressive weakness and muscle wasting

Question 254

5 types of muscular dystrophy?

Answer 254

Duchenne, Becker’s, FSH, limb girdle, myotonic

Question 255

Features of duchenne?

Answer 255

most progressive; FH, features, lab findings (mostly CK), myopathic EMG, muscle biopsy

Question 256

Features of Becker?

Answer 256

More benign than duchenne

Question 257

Features of facioscapulohumeral?

Answer 257

slow progressing of facial, scapular, humeral and peroneal; life expectancy normal and takes 10 yrs to show symptoms

Question 258

Features of limb girdle?

Answer 258

hip and shoulder; 20-30years onset; cardiac and resp symptoms

Question 259

Features of myotonic?

Answer 259

AD inheritance; facial and distal muscle weakness/wasting, myotonia (tonic muscle spasm), frontal balding, cataracts, pulmonary hypoventilation, mild mental retardation; can use mexiletine

Question 260

Common causes of movement disorders?

Answer 260

PD (rest or re-emergent), benign essential tremor (postural), drug induced (alcohol, neuroleptics, beta agonists), thyrotoxicosis, intention usually from cerebellar

Question 261

Less common movement disorder causes?

Answer 261

Huntington’s, chorea, liver failure, tics/jerks/spasms, cerebellar disorder, wilson’s

Question 262

Wilson's S+Ss?

Answer 262

asymmetrical and variable tremor, difficulty speaking, excess salivation, ataxia, clumsy hands, personality changes, high copper, kayser-fleischer rings, caeruloplasmin used to treat

Question 263

Essential tremor causes?

Answer 263

action, postural; onset after 65 with cognitive impairment

Question 264

Essential tremor management and treatment?

Answer 264

avoid caffeine/stress; use beta blocker (propranolol)

Question 265

What is hemiballismus?

Answer 265

proximal hemichorea contralateral to lesion in subthalamic nucleus; recovers spontaneously over months

Question 266

What is athetosis?

Answer 266

slow, repetitive, purposeless movements; mainly from cerebral palsy but if pseudoathetosis from severe proprioceptive loss

Question 267

What is myoclonus?

Answer 267

sudden involuntary focal or general jerks from cord, brainstem or cerebral cortex; can have asterixis in wrists from liver/kidney problems; can also have benign essential myoclonus

Question 268

What is a tardive syndrome?

Answer 268

twisting and choreiform movements of proximal/trunk muscles from dopamine antagonists

Question 269

How is a tardive syndrome treated?

Answer 269

Treat with tetrabenazine and withdraw drugs in question

Question 270

What is dystonia?

Answer 270

prolonged muscle contractions causing abnormal posture

Question 271

Types of dystonia?

Answer 271

Idiopathic general, focal and acute

Question 272

How to treat general dystonia?

Answer 272

anticholinergics and muscle relaxants

Question 273

How to treat focal dystonia?

Answer 273

inject with botox

Question 274

How to treat acute dystonia?

Answer 274

neuroleptics and some anti-emetics like metoclopramide and cyclizine if from drugs

Question 275

Some complications from acute dystonia?

Answer 275

torticollis [head pulled back], trismus [oropharyngeal spasm] and oculogyric spasm [eyes drawn up]

Question 276

Common causes of abnormal gait?

Answer 276

stroke, childhood hip disorders, PD, cerebral palsy, MS, spinal cord compression, joint disorders

Question 277

Uncommon causes of abnormal gait?

Answer 277

cerebellar problems, peripheral neuropathies, myopathies, GBS, polio, MND

Question 278

What is spastic gait?

Answer 278

stiff, circumduction of legs

Question 279

What causes spastic gait?

Answer 279

UMN lesions

Question 280

What is extrapyramidal gait?

Answer 280

flexed posture, shuffling feet, postural instability

Question 281

What causes extrapyramidal gait?

Answer 281

PD

Question 282

What causes steppage gait?

Answer 282

foot drop from MS, GBS, peroneal nerve injured, prolapsed intervertebral disc

Question 283

What causes difficulty turning?

Answer 283

Cerebral/basal ganglia

Question 284

What is myopathic gait?

Answer 284

waddling, can’t stand from sitting, cannot climb stairs; hip girdle weakness

Question 285

What is psychogenic gait?

Answer 285

doesn’t follow any other gait disorder pattern

Question 286

What is ataxic gait and causes?

Answer 286

looks like a novice on an ice rink (widened base and unsteady); multi-infarct states and normal pressure hydrocephalus

Question 287

What causes frontal gait disorder and what is it?

Answer 287

cerebral tumours, subdural haemorrhage, hydrocephalus, multiple lacunar infarcts; slow, shuffling, wide, hesitation, poor posture

Question 288

What is paraparesis?

Answer 288

bilateral leg weakness and hyperreflexia

Question 289

What is scissor gait?

Answer 289

spastic cerebral palsy

Question 290

What is trendelenburg gait?

Answer 290

hip abductor weakness/pain and L5 radiculopathy

Question 291

Common causes of vertigo?

Answer 291

benign positional vertigo, Meniere’s, vestibular neuronitis, brainstem stroke, postural hypotension

Question 292

Uncommon causes of vertigo?

Answer 292

arrhythmia and MS; o Ototoxicity = aminoglycosides, loop diuretics, cisplatin o Acoustic neuroma = schwannoma from vestibular nerve, unilateral hearing loss and vertigo later, slow growing o Trauma = petrous temporal bone, cerebellopontine angle affected then can interfere with auditory nerve o Herpes zoster = if erupts over external auditory meatus

Question 293

Questions to ask pt for vertigo?

Answer 293

vertigo, disequilibrium, presyncope, lightheaded

Question 294

What is a benign paroxysmal positional vertigo (BPPV)?

Answer 294

detached otoliths in utricles and saccules when head stopped moving so vertigo

Question 295

What are causes of BPPV?

Answer 295

idiopathic, head injury, spontaneous degeneration of labyrinth, post viral, post-stapes surgery, chronic middle ear disease

Question 296

What RFs are there for BPPV?

Answer 296

older (50yrs), women, Meniere’s, anxiety, migraine

Question 297

BPPV S+Ss?

Answer 297

worse on head movement (side to side), sudden onset attacks 20-30secs, nausea, worse in morning, hearing unaffected

Question 298

Examinations for BPPV?

Answer 298

= ear drum, CNs, Dix-Hallpike test (should see nystagmus)

Question 299

BPPV red flags?

Answer 299

unilateral hearing loss, new onset headache, focal neuro signs, atypical nystagmus, cerebellar signs

Question 300

BPPV treatment and management?

Answer 300

reassure that resolves and 50% recur, Epley’s manoeuvre

Question 301

What is menieres?

Answer 301

disorder of inner ear from change in volume in labyrinth

Question 302

RFs for menieres?

Answer 302

allergy, AI, genetics, Na/K disturbance, vascular, viral infection, 40-60yrs

Question 303

Menieres S+Ss?

Answer 303

vertigo, tinnitus, fluctuating hearing loss, aural pressure sense, attacks 2-3 hours and in clusters, start off unilateral, some unexplained falls, earlier = vertigo attacks more common and loner remission but then middle stage = vertigo with pre-giddiness and sensorineural hearing loss and tinnitus worse, late = vertigo less, hearing loss worse

Question 304

Menieres tests?

Answer 304

CNs, ears, cervical spine, Hallpike manoeuvre, exclude: other ENT, intracranial, systemic illness, audiometry, MRI brain

Question 305

What menieres treatment is there?

Answer 305

vertigo attacks with prochlorperazine, lifestyle changes, trial of betahistine, vestibular rehab, hearing support, local steroid injections

Question 306

Causes of vestibular neuritis/labyrinthitis?

Answer 306

usually from reactivation of latent herpes simplex, peak onset 40-50yrs; others = AI, microvascular ischaemic insults, URTI prior, viral, systemic disease

Question 307

Labyrinthitis S+Ss?

Answer 307

when inflammation of membranous labyrinth and damage to vestibular and auditory organs, sudden and incapacitating vertigo, exacerbated by movement, hearing loss, N+V

Question 308

Labyrinthitis complications?

Answer 308

cochlea trauma from vertebrobasilar ischaemia, meningitis, Meniere’s and aminoglycosides

Question 309

Labyrinthitis differentials?

Answer 309

stroke, TIA, tumour

Question 310

Labyrinthitis examinations?

Answer 310

CNs, ear, gait, mastoid tenderness, Weber’s, head-impulse, nystagmus

Question 311

What causes conductive hearing loss?

Answer 311

wax, otosclerosis, otitis media, glue ear

Question 312

What causes chronic sensorineural hearing loss?

Answer 312

environment noise, inherited, presbycusis (loss of acuity for high freq before 30)

Question 313

What causes sudden sensorineural hearing loss?

Answer 313

ENT immediately; noise, gentamicin, mumps, acoustic neuroma, MS, vasculitis, stoke

Question 314

What tests for sudden sensorineural hearing loss?

Answer 314

ESR, FBC, LFT, Panca, viral titres, TB, evoked response audiometry, CXR, MRI, lymph, nasopharyngeal culture

Question 315

What can tinnitus cause?

Answer 315

Depression and insomnia

Question 316

What causes tinnitus?

Answer 316

inner ear damage, hearing loss, wax, excess noise, injury, otitis media, post-stapedectomy, menieres, aspirin, loop diuretics, aminoglycosides

Question 317

How to treat tinnitus?

Answer 317

exclude serious; psych support; tinnitus coping training; drugs don’t tend to help but can try hypnotics at night or misoprostol; masking with white noise/hearing aid; cochlear nerve section = drastic

Question 318

What are the common causes of headaches?

Answer 318

non-organic pain syndromes, sinusitis (dull, constant ache over frontal and maxillary sinuses with post-nasal drip, worse bent over), migraine, meningitis, SAH, raised ICP, cranial arteritis, encephalitis (uncommon), venous sinus thrombosis (subacute with papillodema), tropical illness, intracranial hypotension

Question 319

Examinations for headache?

Answer 319

fundoscopy, bp, temporal artery palpation, neuro exam, cognition

Question 320

What can intracranial venous thromboses cause?

Answer 320

seizures, less common then arterial, death from trans tentorial herniation or oedema

Question 321

Dural venous sinus S+Ss?

Answer 321

mainly sagittal or transverse; mainly headaches, vomiting, papilloedema, seizures, unusually cerebellar signs (sigmoid)

Question 322

Cortical vein S+Ss?

Answer 322

stroke-like focal symptoms over days; seizures, sudden headaches

Question 323

Types of tension headache?

Answer 323

episodic (<15 day per month) or chronic (usually meds)

Question 324

Tension headache S+Ss?

Answer 324

pressure/tightness mild-moderate, N+V, gradual in onset and variable duration, responsive to OTC

Question 325

Tension headache examination?

Answer 325

head, neck, fundoscopy, bp

Question 326

Tension headache treatment?

Answer 326

ibuprofen first, amitriptyline for chronic

Question 327

Migraine types?

Answer 327

either with aura and headache, without aura and headache or without headache and aura; first as child then improves as older, FH

Question 328

Migraine S+Ss?

Answer 328

tired, irritable, depressed, difficulty conc, CHOCOLATE aggravating factors, headache last 4-72 hours, unilateral, pulsating, severe, N+V, photo/phonophobia, aura in 1 eye then spread, unilateral paraesthesia, allodynia, can have dysphasia/dysarthria, ataxia, hemiparesis, ophthalmoplegia

Question 329

Migraine red flags?

Answer 329

papilloedema, new seizure, abnormal neuro, new onset cluster

Question 330

Migraine diagnosis?

Answer 330

without aura cannot until 5 attacks, menstrual migraine after falling oestrogen, pulsing, worsens with exercise, unilateral

Question 331

Migraine treatment and management?

Answer 331

address triggers, simple analgesic (aspirin/ibuprofen), prochlorperazine (N+V), diclofenac suppository if V, triptans (5HT1 receptor agonists), prophylaxis if 2+ per month and include beta blocker and amitriptyline, if not this then sodium valproate; acupuncture if treatments don’t work and sometimes cold/hot pack during attack; stop oral contraception as can worsen, should get ease of headache during pregnancy

Question 332

Cluster headache risks/triggers?

Answer 332

head injury, smoking, alcohol, sleep disruption, heat, exercise, solvents; episodic = 2wks to 3months, chronic = 1 yr without remission

Question 333

Cluster headache S+Ss?

Answer 333

bouts of 12 wks and at night, pain without aura rapidly over 10 mins, intense, penetrating, behind or around eye, forehead and temple, 45-90mins, restless, ipsilateral lacrimation, rhinorrhoea, nasal congestion

Question 334

Cluster headache red flags?

Answer 334

change in headache pattern, new headache over 50, systemic illness, personality change, ICP high

Question 335

Cluster headache treatment?

Answer 335

stop smoking, limit alcohol, good sleep, if acute then SC sumatriptan, O2; prophylaxis = verapamil (ECG monitor fortnightly) and if not then lithium

Question 336

SAH causes?

Answer 336

usually from berry aneurysms in circle of Willis or arteriovenous malformations, mean age 50

Question 337

RFs for SAH?

Answer 337

Ehlers-Danlos, Afro-Caribbean, marfans, neurofibromatosis, FH

Question 338

SAH S+Ss?

Answer 338

thunderclap headache for few secs, vomiting, seizures, meningism 6 hours after, some with confusion, if after head injury then decreased consciousness and hemiparesis; prodrome of 3wks = headache, diplopia, dizziness, orbital pain

Question 339

SAH examinations?

Answer 339

consciousness, ophthalmoscopy, neck stiffness, neuro, bp increase, if had seizure then AV malformation, CT in 24hours and angiography following, LP if CT negative but still suspect (xanthochromia), ECG, kernigs sign

Question 340

SAH treatment and management?

Answer 340

reduce bleeding and complications, endovascular obliteration by coiling/clipping, intubation/ventilation/NG feed may be need, nitroprusside for hypertension, GCS check, keep hydrated to stop hyponatraemia

Question 341

SAH complications?

Answer 341

cerebral ischaemia from vasospasm treated with nimodipine, hydrocephalus by ventricular drainage/LP, cognitive impairment

Question 342

Other headaches?

Answer 342

primary stabbing (trigeminal neuralgia), primary cough, primary exertional (brough on by exercise 5mins-48hours), primary sexual (orgasm), primary thunderclap

Question 343

Common causes of delirium?

Answer 343

hypoxia (COPD, pneumonia, pulmonary oedema, resp depression risk drugs, heart problems, anaemia, cyanide), metabolic disorders, drug abuse, iatrogenic, CNS (subdural, infections, postictal), infection, environment, delirium tremens (uncommon in alcohol withdrawal)

Question 344

Head injury investigations?

Answer 344

GCS; haemodynamics; neuro; other injuries; CT head and cervical if <13 GCS, abnormal X-ray, cervical injury

Question 345

Head injury treatment?

Answer 345

immobilise cervical spine (GCS<15, neck pain, focal neuro, paraesthesia), ABC, A+E (for: high energy injury, lose consciousness, amnesia, persistent headache, focal neuro signs, vomiting, seizures, visible trauma, suspected skull fx, >65, bleeding hx, anticoagulation, drug/alcohol, non-accidental injury)

Question 346

Head injury neurosurgery?

Answer 346

decreasing GCS, progressive focal neuro, persistent coma, unexplained confusion >4hours, CSF leak

Question 347

Head injury A+E management?

Answer 347

high dose mannitol, prophylactic AEDs, early nutritional support

Question 348

Head injury complications?

Answer 348

raised ICP, amnesia, CSF leak, meningitis, intracranial haemorrhage, skull fx, diffuse axonal injury, seizures, concussions, cognitive impairment

Question 349

What is an extradural haematoma?

Answer 349

blood between dura and bone

Question 350

Causes of extradural haematoma?

Answer 350

fx of temporal/parietal bone damaging middle meningeal artery/vein; also in spinal column after LP/epidural

Question 351

Extradural haematoma S+Ss?

Answer 351

headache, seizures, CSF otorrhoea/rhinorrhoea, decrease in GCS, facial nerve injury, limb weakness, visual field defects; Spinal – numbness, paraesthesia, altered reflexes, urinary incontinence

Question 352

Extradural haematoma investigations?

Answer 352

XR skull/spine; CT (crescent shaped blood clot)

Question 353

Extradural haematoma treatment?

Answer 353

maintain airway, trauma assess; ICP raised = osmotic diuretics; burr holes

Question 354

Extradural haematoma complications?

Answer 354

neuro deficits, post traumatic seizures 1-3months

Question 355

Subdural haematoma types and pathophysiology?

Answer 355

acute, subacute (3-7 days post), chronic (2-3wks after); tearing of bridging veins of venous sinuses/bleeding from damaged cortical artery

Question 356

Subdural haematoma causes?

Answer 356

Blunt head trauma

Question 357

Risks for getting a subdural haematoma?

Answer 357

elderly, kids, alcoholics

Question 358

Subdural haematoma S+Ss?

Answer 358

shortly after moderate-severe injury, LOC, progressive if chronic, hx anorexia and N+V, neuro deficits (focal limb weakness, speech tricky, personality change)

Question 359

Subdural haematoma investigations?

Answer 359

GCS, vital signs, neuro, external trauma, FBC, U+Es, LFTs, coagulation screen, CT head (lens shaped clot)

Question 360

Subdural haematoma treatment and management?

Answer 360

severe = cervical spine immobilise, ABC, intubate, ventilate, mannitol if high ICP, treat coagulopathy, emergency craniotomy, clot evacuate

Question 361

Subdural haematoma complications?

Answer 361

cerebral oedema, raised ICP, recurrent haematoma, seizures, permanent neuro deficit

Question 362

Disordered cognition common causes?

Answer 362

acute confusional state (delirium – surgery, systemic infection, head injury, drugs, withdrawal, metabolic, hypoxia, stroke, nutritional [b12]), dementia

Question 363

Disordered cognition S+Ss?

Answer 363

cognition impaired, perception, consciousness, memory, disorientated, sleep disorder, hallucinations, hyper/hypoactive

Question 364

Disordered cognition uncommon?

Answer 364

AIDS, myxoedema, vasculitis, neoplastic, Huntington’s, hydrocephalus, vit deficiency, CJD

Question 365

Dementia definition?

Answer 365

neurodegenerative with decline in many cognitive areas; diagnosis = hx, cognition testing, examine, rfs, med review

Question 366

Dementia types?

Answer 366

AD, vascular (don’t use ach inhibitors/memantine), lewy body (cognitive, hallucinations, later parkinsonism, don’t use antipsychotics), fronto-temporal (behaviour change, disinhibited, emotional unconcern)

Question 367

Dementia treatment?

Answer 367

memory clinic, no cognition affecting drugs, massage/music/aromatherapy, SSRI if depressed

Question 368

Alzheimer's S+Ss?

Answer 368

>40yrs, global cognitive impairment, visuo-spatial loss, memory, verbal, executive planning, anosognosia (don’t understand things like plots of films), later is agnosia, behaviour change, irritable, psychosis

Question 369

Alzheimer's RFs?

Answer 369

environmental, genetic, other psych problems, beta amyloid peptide build-up plaques, loss of ache, downs

Question 370

Alzheimer's management and treatment?

Answer 370

ache inhibitors (donepezil, rivastigmine, galantamine but can exacerbate heart block and peptic ulcers), antigultamatergic (memantine), antipsychotics only for non-cognitive, specialist memory service and bp control

Question 371

Causes of raised ICP?

Answer 371

mass lesions, neoplasms, abscess, focal oedema from infection/trauma, CSF circ disturbance, venous sinus obstruction, diffuse brain oedema, idiopathic intracranial hypertension

Question 372

S+Ss raised ICP?

Answer 372

headache (red flags – nocturnal, early morning, coughing and moving head exacerbates), papilloedema, vomiting, lethargy, irritable, slow decision making, abnormal behaviour, pupillary changes, unilateral ptosis, hemiparesis, hypertension, slow irregular pulse

Question 373

Raised ICP investigations?

Answer 373

CT/MRI head, glucose, renal function, electrolytes, osmolarity, monitor ICP in severe head injury, abnormal CT and GCS3-8

Question 374

Raised ICP management and treatment?

Answer 374

maintain arterial O2 tension, normal vascular volume; treat = avoid pyrexia, manage seizures, CSF drain, head off bed, analgesic (morphine), sedate (IV propofol), neuromuscular blockade, mannitol, hyperventilate; depressive craniectomy is last line

Question 375

What is hydrocephalus?

Answer 375

increase in CSF in ventricles; causes usually impaired absorption and increased secretion

Question 376

Pathophysiology of hydrocephalus?

Answer 376

ventricular dilation; CSF permeates in periventricular white matter = damage; types = non-communicating/obstructive where CSF obstructed in ventricles, communicating = communication with ventricles and SA space from problem out of ventricles (thickening of leptomeninges, increase in CSF viscosity), ex vacuo = secondary to brain atrophy (Alzheimer’s), congenital = from no antenatal care, maternal hypertension, pre-eclampsia, foetal alcohol use; acquired = supratentorial masses, intraventricular haematoma, tumours

Question 377

Hydrocephalus S+Ss?

Answer 377

infants = rapid head circ increase, increased limb tone; adults acute = headache, vomiting, papilloedema, impaired up gaze; gradual onset = cognitive deterioration, neck pain, N+V, double vision, incontinence

Question 378

Hydrocephalus investigations?

Answer 378

CT (dilated lateral and 3rd plus abnormal 4th = posterior fossa mass, dilated lateral and 3rd + 4th normal = aqueduct stenosis)

Question 379

Hydrocephalus treatment?

Answer 379

LP if communicating, no treatment if asymptomatic and stopped, shunt and external ventricular drain

Question 380

What is normal pressure hydrocephalus?

Answer 380

ventricular dilation in absence of CSF change

Question 381

S+Ss normal pressure hydrocephalus?

Answer 381

gait abnormal, urinary incontinence, dementia, pyramidal tract signs, brisk reflexes

Question 382

Causes normal pressure hydrocephalus?

Answer 382

SAH, meningitis, idiopathic, head injury, CNS tumour

Question 383

NPH investigations?

Answer 383

MRI/CT show ventricles, large volume LP shows normal CSF pressure, papilloedema none

Question 384

NPH treatment?

Answer 384

acetazolamide (carbonic anhydrase inhibitor), repeated LP, ventriculoperitoneal shunt

Question 385

Causes of dysphagia?

Answer 385

Alzheimer’s, brain tumours, ALS, GBS, HD, PD, CNS infections, stroke, trauma, polio, cerebral palsy, MS, muscular dystrophy; resp failure = ALS, MG, muscular dystrophy

Question 386

Bulbar palsy S+Ss?

Answer 386

tremulous lips, weak/wasted/fasciculations tongue, drooling, absent palatal moving, dysphonia, articulation, neuro deficits in limbs (flaccid, weak, fasciculations)

Question 387

Bulbar palsy causes?

Answer 387

diphtheria, polio, MND, syringobulbia, CVA, brainstem tumours, GBS

Question 388

Pseudobulbar palsy definition?

Answer 388

disease of corticobulbar tracts, bilateral

Question 389

Pseudobulbar palsy S+Ss?

Answer 389

paralysed tongue, absent palatal movements, dribbling, paralysed facial muscles, hyperreflexia of jaw, nasal regurg, emotionally labile, increased tone, reflexes and weak

Question 390

Pseudobulbar palsy causes?

Answer 390

CVA, MND, MS, injury, high brainstem tumours, neurosyphilis

Question 391

What is dysarthria and dysphasia?

Answer 391

• Speech disorder from muscle control (dysarthria), impairment of language (dysphasia)

Question 392

Two types of dysphasia?

Answer 392

receptive dysphasia = difficulty comprehension, excessive dysphasia = difficulty in understanding

Question 393

Causes of dysarthria?

Answer 393

UMN of cerebral hemisphere or LMN lesions of brainstem

Question 394

Dysarthria S+Ss associated with causes?

Answer 394

slurred and weak voice is pseudobulbar palsy; slurred staccato from cerebellar lesions in MS; dysrhythmia, dysphonia, monotonous in PD; indistinct articulation, hypernasal, bilateral weakness in MND

Question 395

Causes of dysphasia?

Answer 395

lesion of dominant hemisphere from CVA, dementia, injury

Question 396

Dysphasia S+Ss associated with causes?

Answer 396

fluent but doesn’t make sense; excessive S+Ss = not fluent but understand how to construct; conduction = lesions of arcuate fasciculus, posterior parietal and temporal; deep = lesions of temporal lobe and word repetition problems

Question 397

What is optic neuritis?

Answer 397

inflammation of optic nerve

Question 398

Optic neuritis S+Ss?

Answer 398

triad = eye pain, reduced vision, reduced colour vision, others = light flashes, Uhthoff’s phenomenon, Pulfrich’s phenomenon, fatigue, low pupillary light reflex, papillitis; develops over hours/days and worse in heat

Question 399

Optic neuritis investigations?

Answer 399

MRI, CXR for atypical (sarcoidosis), LP

Question 400

Optic neuritis causes?

Answer 400

demyelinating ON

Question 401

Optic neuritis management?

Answer 401

from demyelination and compensatory neuronal recruitment; use methylprednisolone or interferon beta

Question 402

What is papilloedema?

Answer 402

optic disc swelling from high ICP

Question 403

Papilloedema causes?

Answer 403

non-arteritic anterior ischaemic optic neuropathy, optic neuritis, intracranial patho (tumour, haemorrhage, trauma, infection, abscess, resp failue) o If unilateral – ADON, retinal vein occlusion, diabetic papillopathy o Bilateral – papilloedema, toxic optic neuropathy, malignant HT

Question 404

Papilloedema S+Ss?

Answer 404

hours/wks, enlargement of blind spot, blurred vision and vision obscurations

Question 405

Bell's palsy S+Ss?

Answer 405

abrupt (usually after sleep) with complete unilateral facial weakness and ipsilateral ear ache; ageusia (low taste); can’t wrinkle forehead; sound hypersensitivity; others = unilateral mouth drooping, drooling, food trapped in gum + cheek, can’t close eye (red), ectropion, speech tricky, conjunctivitis

Question 406

Differentials of Bell's (if rash, bilateral, UMN signs, other CNs, limbs affected)?

Answer 406

infective (Lyme’s, meningitis), brainstem lesions, tumours, systemic disease (GBS, sarcoidosis)

Question 407

Bell's management?

Answer 407

Most completely recover; within 72hours prednisolone; protect eyes with glasses and artificial tears

Question 408

What inheritance is type 1 and 2 neurofibromatosis?

Answer 408

AD

Question 409

NF1 S+Ss?

Answer 409

café-au-lait spots, freckling in skin folds, dermal neurofibromas (can become papillomas), nodular fibromas, lisch nodules, mild LD, nerve root compressions, some get malignancy, GI bleeds and obstructions, cystic lesions, scoliosis

Question 410

NF2 S+Ss?

Answer 410

more likely to get a bilateral vestibular schwannoma/malignancy; can get sensorineural hearing loss, tinnitus and vertigo

Question 411

NF1 management?

Answer 411

MDT

Question 412

NF2 management?

Answer 412

Brain MRI and treat malignancy

Question 413

What is the syrinx?

Answer 413

tubular cavity close to or in cervical cord canal

Question 414

What causes syringomyelia?

Answer 414

basilar invagination, masses, blocked CSF circ

Question 415

Syringomyelia S+Ss?

Answer 415

absent pain and temp sensation; wasting/weakness of hand (claw); others = horner’s, UMN leg, body asymmetry; can get syringobulbia

Question 416

Syringomyelia management and treatment?

Answer 416

MRI imaging; decompress at foramen magnum

Question 417

S+Ss delirium?

Answer 417

cognitive (lower conc, slow response, confusion, disorientated in time), perception (hallucinations), physical (lower mobility and movement, restless, agitated, change in appetite, sleep disturbance; all with fluctuations), social (lack of cooperation, withdrawal, change in mood, delusional); hypo/hyperactive

Question 418

Delirium management?

Answer 418

holistic; treat cause; avoid sedation if possible (antipsychotics first – haloperidol or olanzapine)

Question 419

What is narcolepsy and patho?

Answer 419

• Narcolepsy – chronic neuro condition producing disruption to normal sleeping pattern; excessive sleepiness; starts around adolescence o Thought to involve hypocretin (orexin) o Triggers – head trauma, infection and change in sleep habits o Usually have normal amount of sleep but is fragmented and a lot during the day; don’t have as much REM

Question 420

Narcolepsy S+Ss?

Answer 420

o Presentation – triad of excessive daytime sleepiness (EDS), hypnagogic hallucinations and sleep paralysis  EDS – persistent sleepiness, nap during ADLs, excessive fatigue, automatism (episodes where seem awake but lack full awareness and behave inappropriately); autonomic (pupils abnormal, fainting spells, ED, night sweats, gastric problems, low body temp, systemic hypotension, dry mouth, heart palps, headache, extremities dysthermia); sleep paralysis = pts aware but can’t open/move eyes, sense of inability to breathe

Question 421

Cataplexy definition?

Answer 421

sudden loss of muscle tone, preserved consciousness and power in response to strong emotion; only from narcolepsy (5%); last few seconds/minutes

Question 422

Cataplexy S+Ss?

Answer 422

can be slight facial drooping to no muscles working aside from diaphragm; slurred speech, blurred vision, diplopia; hearing, awareness and consciousness intact; few times per day or less than 1 per year; usually bilateral weakness

Question 423

Narcolepsy investigations?

Answer 423

Epworth sleepiness scale; sleep studies (nocturnal polysomnography); EEG; brain MRI to exclude lesions

Question 424

Narcolepsy diagnosis?

Answer 424

excessive daytime sleepiness daily for 3months or more; cataplexy (may be there or not); not due to another condition; nocturnal polysomnography then MSLT

Question 425

Narcolepsy differentials?

Answer 425

OSA, drug/toxins, seizures, syncope, TIA, sleep paralysis, psychosis

Question 426

Narcolepsy management and medications?

Answer 426

good sleep hygiene, strategic daytime naps, reg exercise, family and friends educations, no known cure for cataplexy; stimulants for EDS, modanafil for EDS and may help with cataplexy, antidepressants (tricyclics) can improve sleep paralysis or hypnagogic hallucinations, benzos sometimes used o EDS – first-line = modanafil, 2nd = methylphenidate, 3rd = modanafil with sodium oxybate

Question 427

Narcolepsy complications?

Answer 427

poor conc, memory, falls/injuries in cataplexy, status cataplecitcus (if meds stopped abruptly), obesity, metabolic syndrome, impulsive

Question 428

Shingles definition and S+Ss?

Answer 428

* Symptoms in dermatome; pain and rash (mild to severe; dull or stabbing); not usually widespread; usually chest, abdo and eye * Rash 2-3 days after pain; red blotches and fluid filled blisters; can get scarring; lasts 2-4wks; sometimes fever; contagious through blisters until dry; only get shingles as a reactivation of own chickenpox (immunosuppressed/stress)

Question 429

Shingles management and medications?

Answer 429

* Management – loose clothing; ice; emollients when itchy (calamine); dressing for blisters * Pharma – NSAIDs, paracetamol, sometimes opiates if painful; if neuropathic pain then tricyclics or gabapentin; antivirals = acyclovir, famciclovir, valaciclovir (for over 50s, shingles in eye/ear, immunocompromised, moderate/severe pain, moderate/severe rash); steroids to reduce inflammation

Question 430

Dopamine effect and receptors?

Answer 430

D1-5 receptors and mood and reward-seeking behaviour

Question 431

Dopamine agonists and conditions for?

Answer 431

pramipexole/ropinirole/levodopa/apomorphine (parkinson’s), cabergoline (hyperprolactinaemia, acromegaly), chlorpromazine (schizophrenia), metoclopramide (nausea)

Question 432

Serotonin effects and receptors?

Answer 432

5HT1-7 receptors and many effects

Question 433

Serotonin agonists and conditions for?

Answer 433

lithium (mood stabiliser), sumatriptan (migraine), buspirone (anxiety), fluoxetine/sertraline (depression), ondansetron (nausea), mirtazapine (depression), olanzapine/clozapine (psychosis)

Question 434

Types of amino acids and their effects?

Answer 434

glutamate and aspartate = excitatory on NMDA and non-NDMA in epilepsy and CNS ischaemia; GABA inhibitory

Question 435

GABA agonists and their conditions for?

Answer 435

gabapentin/valproate (epilepsy and neuro pain), benzos (sedation), baclofen (spasticity), alcohol

Question 436

Glutamate antagonist and what for?

Answer 436

memantine for dementia

Question 437

Ach receptors?

Answer 437

muscarinic and nicotinic receptors

Question 438

Peripheral agonists of ach?

Answer 438

glaucoma (pilocarpine), myasthenia gravis (anticholinesterases)

Question 439

Peripheral antagonists of ach?

Answer 439

asthma (ipratropium), incontinence, dry secretions pre-op, dilate pupils, increase HR (atropine)

Question 440

Ach inhibitors for dementia?

Answer 440

donepezil, galantamine, rivastigmine

Question 441

Ach treatment for drug-induced parkinsonism?

Answer 441

procyclidine, trihexyphenidol

Question 442

Types of histamine and purine treatments and what for?

Answer 442

cyclizine (antihistamine and nausea), purinergic receptor blocker (chronic pain)

Question 443

Types of neuropeptides and what for?

Answer 443

exogenous opioids (wide range of analgesic and mood related effects); aprepitant (low chemo nausea)

Question 444

Types of receptors for noradrenaline and adrenaline and their effects?

Answer 444

alpha and beta 1-2; alpha receptors = arteriolar vasoconstriction and pupillary dilation (peripheral); beta 1 = high pulse and myocardial contractility; beta 2 = bronchodilation, uterine relaxation, arteriolar vasodilation

Question 445

What is clonidine for?

Answer 445

refractory hypertension

Question 446

What are tricyclics and venlafexine for?

Answer 446

SNRIs and 5HT for depression

Question 447

What is a TIA?

Answer 447

• No infarction; brief episode of neurological dysfunction from temporary focal cerebral ischaemia (loss of O2 to specific part of brain matter)

Question 448

Pathophysiology of TIA?

Answer 448

small vessel occlusion (usually by atherothromboembolism from carotid but also cardioembolism giving microemboli and hyperviscosity of blood); usual risk factors for what would cause these (like for an MI)

Question 449

S+Ss TIA?

Answer 449

sudden loss of function but then resolved after some minutes; most affect anterior circulation of brain (weak contralateral leg and sometimes arm; weakness on one side of body [hemiparesis]; dysphasia; amaurosis fugax [loss of vision in one eye] – think of what would happen in a stroke: FAST where face refers to eyes); posterior circ (diplopia, vertigo, vomiting, choking and dysarthria [not quite incoherent speech but difficult to understand], ataxia, hemianopia – think that posterior is more to do with how you would feel at top of high building – VERTIGO AND FEELING ILL AND STRUGGLING TO WALK PROPERLY)

Question 450

Diagnosis of TIA?

Answer 450

based on description usually; bloods (look for anything that could lead to blood thickening); carotid artery doppler ultrasound for stenosis; all the scans (CT, ECG)

Question 451

TIA treatment?

Answer 451

score risk of stroke after TIA (ABCD2 – SEE PAGE 38 – if score above 6 see specialist immediately); antiplatelets, anticoagulant for any other complications like AF etc, statins, control CV risk

Question 452

Stroke definition?

Answer 452

Rapid onset (last more than 24 hours) neurological deficit by infarction

Question 453

What is ABCD2?

Answer 453

A — Age: 60 years of age or more (1 point) B — BP (at presentation) 140/90 mm Hg or greater (1 point) C — Clinical features Unilateral weakness, 2 points Speech disturbance without weakness, 1 point. D — Duration (60 minutes or longer, 2 points, 10–59 minutes, 1 point) D — presence of diabetes: 1 point

Question 454

Carotid ischaemic stroke S+Ss?

Answer 454

weakness of face, arm, legs; amaurosis fugax (painless loss of vision); impaired language

Question 455

Posterior circ stroke S+Ss?

Answer 455

dysarthria, dysphagia, diplopia, dizziness, ataxia, diplegia

Question 456

Anterior circ stroke S+Ss?

Answer 456

supplies frontal lobe bits so motor function affected and superior bits of parietal so a bit of integrating sensory information to give an output (leg weakness and sensory disturbance, apraxia, incontinence, drowsiness as consciousness from frontal lobe lost, decrease in spontaneous speech; MAINLY ONE SIDED)

Question 457

Middle cerebral artery stroke S+Ss?

Answer 457

bits of frontal lobe again (mainly motor for head, neck and arms MAINLY FOR BOTH SIDES and this also incorporates speech areas – broca’s and wernicke’s) and a bit of parietal to do with visual for sight (hemianopia)

Question 458

Posterior cerebral artery stroke S+Ss?

Answer 458

to do with supplying the occipital lobe (SEE END OF PAGE 43 FOR SPECIFICS OF BLINDNESS)

Question 459

Vertebrobasilar artery stroke S+Ss?

Answer 459

supplies loads including cerebellum and pons linking cerebrum to cerebellum so can be v dangerous; motor, speech, visual and consciousness (basically all of the mentioned effects can be felt here)

Question 460

Lacunar stroke S+Ss?

Answer 460

small strokes subcortically; deep penetrating arteries occluded; no cortical features; due to small vessel disease; pure motor hemiparesis, ataxic hemiparesis, clumsy hand and dystharthria, pure hemisensory, mixed sensorimotor

Question 461

What does spinothalamic tract do?

Answer 461

lateral = pain and touch and medial = crude touch and on same side but cross before thalamus

Question 462

What does spinocerebellar tract do?

Answer 462

proprioception (that’s input for cerebellum) and dorsal ipsilateral cerebellum and ventral contra and ipsilateral cerebellum

Question 463

What does the spinoreticular tract do?

Answer 463

deep/chronic pain

Question 464

What does the corticospinal tract do?

Answer 464

Control of voluntary muscles and pass to Cerebral peduncles (above this is pyramids [ventrolateral sulcus on lateral border of pyramid on either side continuous with spinal cord] to mark the corticospinal tract and can also see the decussation later in the midbrain like pyramids of Giza)

Question 465

What does the tectospinal tract do?

Answer 465

head Turning for visual stimuli

Question 466

What does the rubrospinal tract do?

Answer 466

spinal Reflexes

Question 467

What does the vestibulospinal tract do?

Answer 467

like wearing a VEST for some at the gym who has big muscles for muscle tone and posture

Question 468

What do the mammillary bodies do?

Answer 468

Make new Memories

Question 469

What does the cerebellum do and what inhibits it?

Answer 469

excites motor control and Basal ganglia Blocks/inhibits it (thalamus)

Question 470

What is a generalised tonic-clonic/grand mal seizure?

Answer 470

(think like how you would imagine a jerky seizure and stiff limbs like normal epilepsy) - no aura usually; lose consciousness; tonic phase = rigid limbs; clonic phase = some generalised muscle jerking for a couple of mins

Question 471

What is a typical absence/petit mal seizure?

Answer 471

child; looks like child has zoned out for a couple of seconds and may not realise even had a seizure; can lead to tonic-clonic in later life

Question 472

What is a myoclonic seizure?

Answer 472

sudden isolated jerk of part of the body and can throw them to the ground with an uncontrolled limb

Question 473

What is a tonic seizure?

Answer 473

increase in muscle tone and stiffening (REMEMBER TONIC = STIFFENING)

Question 474

What is an atonic seizure?

Answer 474

loss of muscle tone

Question 475

What is a simple partial seizure?

Answer 475

no post-ictal symptoms and no impairment of awareness and memory and usually frontal lobe (THINK SIMPLE MEANS NO COMPLICATIONS AFTER)

Question 476

What is a complex partial seizure?

Answer 476

affects awareness and memory (so usually temporal lobe therefore as affects speech understanding, memory and emotion as connected to the hippocampus etc); post-ictal confusion common

Question 477

What is a partial seizure with secondary generalisation?

Answer 477

can start as partial but spread to general and cause convulsions

Question 478

What hormone is raised after an epileptic rather than a non-epileptic attack?

Answer 478

Raised prolactin

Question 479

Triad of normal pressure hydrocephalus S+S?

Answer 479

incontinence, confusion, dementia