Neurology Flashcards

Question

Thrombectomy eligbility? (NICE)

Answer 1

Up to 24 hours of acute ischaemic stroke if CTA shows proximal occlusion and salvageable brain tissue Take into account: The patient's overall clinical status NIHSS (score >5) Pre-stroke Rankin Scale (score <3, measure of disability)

Answer 2

-Intracranial hemorrhage or history of -Known structural cerebral vascular lesion or neoplasm -Ischemic stroke, neurosurgery or HI within 3 months -Low platelet count -Active bleeding -Uncontrolled HTN

Answer 3

TACS Hemiplegia, Homonymous hemianopia, Higher cortical dysfunction (dysphasia, dyspraxia, neglect) PACS 2/3 above LACS Pure hemi-motor or/and hemi-sensory loss POCS One needs to be present: -CN palsy and a contralateral motor/sensory deficit -Bilateral motor/sensory deficit -Cerebellar dysfunction -Homonymous hemianopia

Answer 4

Stroke SOL Cerebral palsy MS Brown-Sequard syndrome **In addition: Stroke mimic**

Answer 5

Speech: -Comprehension by asking simple instructions (1, 2, 3 stage commands, receptive aphasia) -Repetition (baby hippopotamus) (conduction aphasia and expressive aphasia) -Confrontation naming (anomia) -Spontaneous speech (dysarthria, agrammatism, word retrival, hestitancy) -Reading and writing ## Footnote -In most patients speech is L lateralised, so always offer to check if R hemiparesis/hemisensory loss -Broca's (non-fluent, agrammatism) L MCA infarct affceting PIF cortex -Wernicke's (fluent but meaningless) L MCA affecting PST cortex -Conduction aphasia (impaired repition) inferior parietal -Also anomic (word finding) and global aphasia

Answer 6

-SOL -Seizure +/- Todd's paralysis -Metabolic (hypoNa, hypoglycaemia, Wernicke's) -Hemiplegic migraine -Functional **-CNS infection e.g. abscess** -MS

Answer 7

The NIHSS is a stroke severity scale, a systematic assessment to measure the neurological deficits seen with acute stroke

Answer 8

Expressive dysphasia: “I knew what I wanted to say, but I couldn’t get it out” Receptive dysphasia: “I wasn’t able to understand anyone, they were speaking gibberish” Dysarthria: “My speech was really slurred, it sounded like I was drunk”

Answer 9

(PICA stroke) Vertigo, vomiting Ipsilateral ataxia (fall towards side of lesion) Also: Ipsilateral Horner's, ipsilateral facial loss of pain and temperature Contralateral loss of pain and temperature sensation

Answer 10

-Monocular: ipsilateral retinal or optic nerve lesion -Bitemporal hemianopia: optic chiasm -HH: means lesion is retro-chiasmal, contralateral optic tract or optic radiation -Homonymous superior quadrantanopia: contralateral temporal optic radiation lesion -Homonymous inferior quadrantanopia: contralateral pituirary optic radiation lesion -HH with macular sparing: occipital cortex

Answer 11

Inherited: muscular dystrophy or myotonic dystrophy Endocrine: Cushing's, thyrotoxicosis, hyperparathyroidism, diabetic amyotrophy **Inflammatory: polymyositis or MG (if fatiguable)** Metabolic: osteomalacia Malignancy: paraneoplastic, LEMS

Answer 12

Wheelchair Catheter if spinal plaques INO, RAPD/optic atrophy/reduced VA Sensory and UMN signs DANISH Other features: Fatigue depression cognitive Autonomic (urinary, impotence, bowel problems) Uthoff's (heat-induced condution block of partially demyelinated fibres) Lhermitte's (neck flexion results in electric shock sensation, indicates dorsal column involvement or cervical cord)

Answer 13

Requires dissemination in time and space McDonald criteria allows MS to be diagnosed after a single attack using paraclinical tests

Answer 14

RRMS 85%, can progress to secondary progressive with a median age of 15 years PPMS 15%

Answer 15

Clinical diagnosis plus: -CSF oligoclonal bands -MRI lesions in brain or spinal cord (typical **T2 hyperintense lesions in periventricular white matter**) -Visual evoked potentials delayed velocity but normal amplitude (optic neuritis)

Answer 16

MDT (specialist nurses, PT, OT, orthotics team, social worker, neuropsychologist, SLT) Disease modifying drugs e.g. natalizumab, interferon-beta, glatiramer Vitamin D replacement --- **Symptomatic drugs:** -Methylprednisolone shortens relapses but doesn't alter prognosis -Anti-spasmodics e.g. baclofen or botox injections -Gabapentin, pregabalin, amitriptyline for neuropathic pain -Laxatives and intermittent catheterisation/oxybutynin -SSRIs for depression -Amantadine for fatigue --- **In pregnancy:** Reduced relapse rate during pregnancy but increased in post-partum period Safe for foetus 2% risk of MS in children

Answer 17

Idiopathic demyelinating disorder of the CNS characterised by demyelinating plaques separated in both space and time Characterised as an autoimmune disease but aetiology incompletely understood Thought to be both genetic and environmental factors at play (EBV, smoking, vitamin D deficiency)

Answer 18

Impairment of ipsilateral adduction Normal abduction in contralateral eye with nystagmus Results from medial longitudinal fasciculus

Answer 19

-Demyelination (MS) -Infarction (of midbrain or pons) ## Footnote Less commonly infection (Lyme), inflammation (sarcoid), trauma, SOL

Answer 20

-Myopathic facies -Bilateral ptosis -Frontal balding -Dysarthria -Myotonia 'grip my hand and let go' or 'screw eyes up then open' -Wasting and weakness of distal muscles -Percussion myotonia -Areflexia -Cataracts -PPM scar -Diabetes ## Footnote N.B. Differentials would be myotonia congenita or channelopaties (the familial periodic paralyses)

Answer 21

Clinical features **'Dive-bomber'** potentials on EMG Genetic testing for DM1 (or DM2 if negative) Also ECG (+/- echo), HbA1c and opthalmology assessment ## Footnote N.B. CK may be normal or mildly evelated No indication for muscle biopsy

Answer 22

DM1 is trinucleotide repeat disorder affecting DMPK gene on chromosome 19, demonsrates genetic anticipation, presents younger DM2 is tetranucleotide repeat disorder affecting chromosome 3, presents later Autosomal dominant

Answer 23

-MDT (PT/OT, orthotics, SLT) -No treatment for weakness -Mexiletine may help myotonia (often not needed) -Advise against GA -Genetic counselling Follow-up: -Yearly ECG and low threshold for cardiology referral -Investigate OSA symptoms -Investigate if suspicion of diabetes -Yearly assessment for cataracts

Answer 24

FBC, ESR, CRP, U+Es, LFTs, HbA1C, TFTs, complement EMG (axonal or demyelinating) and nerve conduction MRI cervical spine (to rule out radiculopathy)

Answer 25

Amitriptyline, duloxetine, gabapentin, or pregabalin

Answer 26

Bilateral: autoimmune (MG), genetic (myotonic dystrophy), **congenital, infection (treponemal)**, mitochondrial disorder (CPEO) Investigations: ice or edrophonium test, ACh and MUSK antibodies, CT thorax, treponemal antibodies, muscle biopsy for ragged red fibres (CPEO) --- Unilateral: 3rd nerve palsy (see causes), Horner's (pupil small, see causes) Investigations: HbA1c, ESR, ANA, ENA, ANCA, MRI brain/cord, CT thorax, angiography

Answer 27

Ptosis 'Down and out' eye Pupil enlarged if surgical or compressive, normal if medical or ischaemic

Answer 28

Surgical causes often impinge on superficially located papillary fibres: **-PCOM aneurysm** -SOL -Trauma -Raised ICP (false localising sign) Medical causes (ALL THE Ms): **-Microvascular ischaemia secondary to diabetes or HTN** Also: -Congenital -Other causes of complex opthalmoplegia but this would not cause an isolated CN3 palsy

Answer 29

Bedside: BP and BM Bloods: -HbA1c and lipids -AChR antibodies and anti-MUSK and TFTs -ESR +/- autoimmmune screen to look for vasculitis -Lyme serology Imaging: MRI ## Footnote N.B. In CN3 need urgent MR-A or CT-A to look for PCA which would need urgent neurosurgical input

Answer 30

Treat cause Eye patch or prism glasses DVLA

Answer 31

N.B. Depresses the aDducted eye -Affected eye will look a bit higher and more outwards -Head tilt towards unaffected side -Vertical diplopia when looking down -When eye aDducted it won't depress

Answer 32

N.B. LR aBducts -Convergent squint (eye deviates a little more medially as unopposed action of medial rectus) -Affected eye can't move out -Horizontal diplopia which is worsened when they attempt to look towards the affected side

Answer 33

-MG or thyroid -Stroke (especially brainstem) -Inflammation (MS, sarcoidosis or vasculitis) -Infection (e.g. Lyme) -Opthalmoplegic migraine -Miller Fisher (if ataxia and areflexia) -Mitochondrial disease with CPEO (symmetrical so no diplopia) -Cavernous sinus pathology (3, 4, 6)

Answer 34

DANISH N.B. Cerebellar hemisphere lesions produce **ipsilateral** limb signs Midline lesions cause truncal ataxia In cerebellar nystagmus, fast phase direction changes with changing of gaze (not the case for vestibular lesions, where fast phase is always away from side of lesion)

Answer 35

-Paraneoplastic -Alcohol (Wernicke's subacute or degeneration chronic) -Sclerosis (MS or Miller Fisher syndrome) -Tumour/trauma -Recessive (Friedrich's, ataxia telangiectasia) or dominant (spinocerebellar ataxia) -Iatrogenic (phenytoin toxicity)/infective (VZV or Lyme or cerebellitis) -Endocrine (hypothyroidism) -Stroke (cerebellar or brainstem vascular event) ## Footnote STS = lesions of the ipsilateral cerebellar hemisphere Remaining = lesions of the vermis or global cerebellar degeneration

Answer 36

Bloods: FBC (MCV), B12 and folate, TFTs Consider anti-TTG, anti-GAD and viral serology MRI brain Or CT if acute Consider: LP (MS) or genetic testing (FA) or paraneoplastic screen

Answer 37

-Weakness and wasting of small muscles of hand -Loss of reflexes in upper limbs -Loss of pain and temperature sensation cape-like (preserved of joint position and vibration sense) -Signs may be asymmetrical

Answer 38

Arnold-Chiari malformation Spinal cord SOL Cervical spondylosis Trauma

Answer 39

Combination of LMN and UMN with preserved sensation

Answer 40

Progressive disease of unknown aetiology **Axonal degeneration** of U and LMN Divided into 4 types: -ALS most common (combined upper and lower, spastic weakness in legs) -PLS (just UMN) -Progressive spinal muscular atrophy (only LMN) -Progressive bulbar palsy (LMN brainstem signs)

Answer 41

**Muscle** Inherited: muscular/myotonic dystrophy, spinal muscular atrophy or spinobulbar muscular atrophy (Kennedy's) Inflammatory myositis: polymyositis/dermatomyositis (proximal, anti-Mi2 and ANA, CK) Inclusion body myositis (proximal UL, distal LL needs biopsy) Endocrine: Cushing’s, thyroid disease, acromegaly Metabolic: osteomalacia, ion channelopathies **NMJ** Autoimmune: MG (proximal, fatiguable) **Neuropathy:** Demyelinating: CIDP or MMN Paraneoplastic **AHC** Infection: post-polio MND (some subtypes)

Answer 42

-Clinical diagnosis -VGKC (Isaac's) and GM1 (MMN with CB) antibodies -EMG shows denervation (rules out NMJ or demyelination) -MRI brain spinal cord to exclude lesions which may mimic

Answer 43

-MDT as treatment is largely supportive (PT, OT, orthotics, specialist nurses, dietician, SLT, nutrition, palliative care depending on disease stage) -**Riluzole** slows disease progression by 3 months but doesn't improve function or QoL -**Regularly screen** for speech, swallow, weight, development of FTD and IMPORTANTLY respiratory complications (FVC and early morning gas) -May need **communication aids, PEG and NIPPV** -Baclofen (spasticity), anti-cholinergic (salivation)

Answer 44

'BRT' -Hypomimia and reduced movements -Coarse pill-rolling 2-5Kz tremor -Bradykinesia -Cogwheel rigidity -Gait is shuffling and festinant, reduced arm swinging -Speech hypophonic and monotonous Also do: -Ataxia (MSA) -Vertical eye movements and axial rigidity (PSNP) Say you would do: -L/S BP and bladder scan (MSA) -Cognitive impairment (LBD, PSNP, NPH) -Pulse and carotids (vascular Parkinsonism which is normally LL and bilateral affecting gait) -Ask about medication history (secondary Parkinsonism)

Answer 45

-PD -Parkinson's plus (MSA, PSNP (both symmetrical), corticobasal degeneration (asymmetrical)) -Drug-induced (prochloperazine, **metoclopramide, antipsychotics**) **-Vascular (acute basal ganglia stroke or diffuse SVD)** -Lewy body dementia -Wilson's disease -Post-encephalitis

Answer 46

MSA-P: tremor, rigidity, bradykinesia MSA-C: cerebellar and **autonomic** dysfunction causing collapse, incontinence, dry mouth, swallow problems, urinary retention or incontinence etc.

Answer 47

History (anosmia, constipation, cognition, hallucinations, mood, sleep, drugs, atherosclerotic RF) Formally assess cognition, L/S BP and bladder scan Clinical diagnosis, can be aided by a trial of dopaminergic agent **Bloods:** If <40 years, do copper and caeruloplasmin (Wilson's disease) **Imaging:** MRI brain (vascular changes, atropghy in certain areas may point towards certain differentials, ventricular enalrgement NPH) DaT scan (differentiates PD from drug-induced, will show decreased dopamine uptake)

Answer 48

MDT (SN, PT, OT, SLT) Levo-dopa with peripheral dopa-decarboxylase inhibitor e.g. co-beneldopa (nausea, later wearing off and peak-dose dyskinesias) Dopamine agonists e.g. ropinirole sometimes used in younger patients (slightly less effective and higher risk of impulsivity) Also: MAO-B inhibitors (occasionally), anticholinergics (tremor-predominant) Also: COMT-inhibitors (for Levodopa wearing off) **More advanced therapies which would be started under specialist guidance include:** DBS, apomorphine infusions/rescue injections **In addition, we should:** Manage constipation, mood disorders and sleep disorders

Answer 49

-More frequent dosing -Drugs to reduce dopamine breakdown (COMT inhibitor) -Add MAO-B or dopamine agonist ## Footnote Consider MR dosing N.B. Consider amantadine or DBS in refractory tremor or bothersome dyskinesias

Answer 50

Loss of dopaminergic neurons in the substantia nigra

Answer 51

Resting (Parkinsonism) Action tremor: Postural: BET, dystonic tremor, alcohol Kinetic: ipsilateral cerebellar lesion

Answer 52

-Bilateral cerebellar signs -Combined UMN and LMN signs (leg wasting, reduced power, and **absent reflexes** due to peripheral neuropathy with **upgoing plantars** due to corticospinal tract degeneration) -Posterior column signs (loss of joint vibration and proprioception) Also: -Kyphoscoliosis -Optic atrophy -High-arched palate -SN deafness -Murmur of HOCM -Diabetes

Answer 53

Mixed upper and lower MN signs e.g. absent ankle jerks but upgoing plantars: -SCD -MND -Conus medullaris lesion -Treponemal -Dual pathology e.g. cervical myelopathy and peripheral neuropathy of any cause Other causes of ataxia

Answer 54

-B12 and vitamin E -Brain and spinal cord imaging (to rule out alternative pathology) -NCS and EMG (peripheral nerve involvement) -Genetic testing for hereditary ataxias **-For complications, ECG, echo and HbA1c**

Answer 55

-Autosomal recessive neurodegenerative disorder **-Frataxin gene -Trinucleotide repeat** -Onset during teens -Survival rarely exceeds 20 years from diagnosis -Association between HOCM and dementia

Answer 56

Ptosis Miosis Anhydrosis Central causes: Brain stem causes: MS, Wallenberg's Pre-ganglionic causes: Neck: branchial plexus lesion, Pancoast's tumour Post-ganglionic: Carotid artery dissection, cavernous sinus mass

Answer 57

Dilated pupil with poor response to light and sluggish response to accommodation With absent or diminished **ankle reflexes** Benign condition

Answer 58

Small irregular pupil, which **accommodates** but doesn't react to light Atrophied and depigmented iris Usually a manifestation of quaternary syphilis but can also be caused by DM

Answer 59

**-Ischaemic optic neuropathy (arteritic i.e. GCA or non-arteritic i.e. microvascular ischaemia, long-sighted, usually bilateral) if OLDER** **-Demyelination (MS, NMO) if YOUNGER** -Glaucoma -A SOL e.g. optic glioma -Inflammatory (SLE, sarcoidosis) and infection (Lyme and treponemal) -Hereditary (Leber’s or RP) -Compressive e.g. thyroid eye disease, pituitary tumour -Drugs e.g. ethambutol -Nutritional (B12, folate) ## Footnote Interpret RAPD with caution as whilst it suggests an optic neuropathy, can also be present in retinal disease (reflects the difference in optic nerve signal input between the eyes) So can also be positive in: -Retinal detachment -Central retinal artery occlusion Stages of damage: If normal, this means retro-bulbar optic neuritis If swollen, damaged around optic nerve head Pale optic disc in optic atrophy Always ask for: -Full neurological examination -Slit lamp -Visual fields

Answer 60

-2 or more cutaneous neurofibromas -Cafe-au-lait 6 or more -Axillary freckling -Lisch nodules -Hypertension -Neuropathy with palpable nerves -Optic glioma

Answer 61

-Angiofibromata -Periungal fibromas -Shagreen patch -Ash leaf macules Other associations: -Cystic lung disease -Polycystic kidneys or renal angiomyolipomata or RCC -Retinal phakomas -LD

Answer 62

-Bilateral ptosis -Complicated bilateral extra-ocular palsies -Myasthenic snarl -Nasal speech, poor swallow -Proximal muscle weakness with fatiguability -Sternotomy scars (thymectomy) -FVC N.B. Can either be generalised or ocular MG

Answer 63

Thyrotoxicosis Thymomas DM RA SLE

Answer 64

-Ice/edrophonium test **-FVC is the most important bedside test** -Anti-AChR antibodies in 80% -Anti-MuSK often positive if above negative -Consider VGCC antibodies if ?LEMS **-TFTs** -EMG decrement with repetitive stimulation and 'jitter' is characteristic -Also CT/MRI of the mediastinum (thymoma in 10%)

Answer 65

-MDT (SLT, OT, PT, opthalmology) -Treat as per Sussman protocol with pyridostigmine and steroids +/- steroid sparing agent -Consider admission when initiating steroids for observation of 'steroid dip' **-Thymectomy** -Consider PLEX or IVIg in severe or refractory disease **-Avoid medications e.g. aminoglycosides, quinolones, beta blockers -Counsel on risk factors for crisis including infections, volume depletion, aspiration, and drugs** -Monitor for swallow and respiratory compromise Myasthenic crisis: -ITU for I+V if FVC 15 mL/kg or less -PLEX or IVIg ## Footnote N.B. Pyridostigmine not used in crisis as increases secretions N.B. If oMG and no generalised symptoms within 2 years, can more confidently diagnose oMG N.B. 'Steroid dip' can be observed when starting steroids, especially with large doses (admit for observation if starting higher doses in more severe cases)

Answer 66

-Pelvic then pectoral weakness plus autonomic (dry mouth and sphincter) with ptosis later -Diminished reflexes that become brisker after exercise -70% paraneoplastic (SCC) To investigate: -VGCC antibodies and EMG (increment on repetitive stimulation) -EMG reduced CAMP amplutide with supramaximal stimulus which increases after exercise, jitter -Investigate for underlying neoplasia Treatment: -Treat cause (immunosuppress if no cancer) -Potentiate synaptic transmission with 3,4-diaminopyridine for symptom control

Answer 67

UMN weakness spares the forehead and eye closure LMN involves the forehead and eye closure Bell's phenomenon: eyeball normally rolls up on attempted eye closure (visible if orbicularis oculi weakness)

Answer 68

-Rapid onset 1-2 days -HSV-1 implicated -Induced swelling and compression of the nerve within the facial canal causes demyelination and temporary conduction block -Prednisolone within 72 hours onset plus aciclovir if severe -Remember eye protection (artificial tears, tape eye closed at night) -80% full recovery -More common in pregnancy, and outcome may be worse

Answer 69

**Myopathy** Inclusion body myositis Muscular dystrophy **NMJ** MG **Peripheral nerve** Bilateral Bell's i.e. post HSV Bilateral Ramsey Hunt i.e. post-VZV Lyme GBS **AHC** -MND **Brainstem** -Sarcoidosis -Malignant -Infective -With VI pontine demyelination or CVA -With **V, VI, VIII** and DANISH, suspect CP angle e.g. acoustic neuroma -With VIII suspect auditory canal e.g. cholesteatoma

Answer 70

Presents with headaches: -Postural, valsalva, vomiting -Visual obscurations (blurring, field loss) -Pulsatile tinnitus -Can get diplopia from CN VI false localising sign Investigations: -Formal visual field assessment and fundoscopy -MRI (+/- MRV) -LP with opening pressure (normal CSF) Exclude secondary causes raised ICP: -Venous obstruction -AV malformations -Addison's -Drugs (vitamin A, anabolic steroids) Treatment: -If no visual loss, acetazolamide and weight loss -If visual loss, LP, optic nerve fenestration, VP shunt

Answer 71

CHL: -Cerumen -Otitis externa/media -Cholesteatoma -SOL -Trauma -Otosclorosis SNHL: -Presbycusis or noise-induced -Labrinthitis or Meniere's -Ototoxic drugs -Infection e.g. CMV -SOL affecting cerebellopontine angle e.g. acoustic neuroma -Demyelination

Answer 72

Acute: -Stroke (asymmetrical) **-Hyperglycaemia -Polycythaemia** More chronic: -Sydenham's chorea (post-infective, rare) -SLE -Huntington's (trinucleotide repeat disorder, anticipation)

Answer 73

Hypokinetic (bradykinesia, akinesia) Hyperkinetic (chorea, dystonia, tremor, myoclonus, tics)

Answer 74

MDT (neurologists for symptom management, neuropsychiatrists, neuropsychologists, dieticians as increased BMR, OT and PT) Genetic counselling

Answer 75

**Painless:** -Ischaemic optic neuropathy (GCA (transient) versus non-arteritic ischaemic ON) -Retinal ischaemia (amaurosis fugax) (transient) -Retinal artery or vein occlusion -Retinal detatchment -Vitreous haemorrhage or PVD -Papilloedema (transient) **Painful:** -Optic neuritis (pain on eye movement) (e.g. MS/NMO) -Uveitis -Acute angle closure glaucoma -Corneal ulceration or keratitis -Trauma -Leber's -Migraine (transient) ## Footnote See causes of optic neuropathy below

Answer 76

-Opthalmologist or neurology If GCA: -Inflammatory markers (GCA) -Urgent rheumatology review with USS temporal artery +/- biopsy If amaurosis fugax: -HbA1c and lipids -Urgent TIA clinic with carotid dopplers and Holter If thinking optic neuritis: -B12 and folate -Anti-MOG and aquaporin 4 antibodies -MRI brain and spinal cord +/- orbit -LP -VEP to evaluate optic nerve function -If ?inflammatory autoimmune screen and ACE -If ?infective consider treponemal screen

Answer 77

Stroke SOL N.B. PITS

Answer 78

-Pituitary adenoma (galactorrhoea, acromegaly, Cushing's) Causes bitemporal superior quadrantanopia -Craniopharyngioma Causes bitemporal inferior quadrantanopia ## Footnote C(h)IPS

Answer 79

-Congenital -Trauma -Microvascular ischaemia (associated with DM, HTN) **-Raised ICP causing false localising sign e.g. IIH** N.B. CN6 long route

Answer 80

-Congenital -Traumatic (susceptible as thin nerve and long intracranial course) -Microvascular ischaemia (diabetes or hypertension)

Answer 81

Lesions affecting CP angle: Usually an acoustic neuroma Meningioma Arachnoid cyst

Answer 82

MND GBS Syringobulbia MG Poliomyelitis N.B. Due to diseases affecting nuclei of 9-12 (LMN lesion) Pseudobulbar is due to lesions affecting corticobulbar tracts (UMN lesion)

Answer 83

++wasting and LMN signs ++fasciculations (if no fasciculations, just say 'old polio') Shortened limbs Preserved sensation

Answer 84

Infects CNS and destroys anterior horn cells This causes paralysis, an asymmetrical weakness which affects LLs more than ULs

Answer 85

After a period of prolonged stability following infection, individuals who have been infected and recovered begin to experience new signs and symptoms: muscle atrophy, weakness, pain, fatigue

Answer 86

CN 9-11 SOL Lymphoma, TB, sarcoid

Answer 87

Pyramidal weakness (weakness more distal in upper limbs) Hyper-reflexia Spasticity Sensory loss May be unilateral or bilateral N.B. Would be LMN signs in cervical radiculopathy

Answer 88

Half spinal cord Paralysis and proprioceptive deficits ipsilateral Loss of pain and temperature sensation on the contralateral side ## Footnote As spinothalamic tract ducussates right away in the spinal cord

Answer 89

Pain followed by flaccid, areflexic paralysis (patchy involvement of muscles supplied by C5-C6) Peri-scapular wasting NCS/EMG: sensory motor loss of amplutide with normal velocities, dennervation in muscles after 2 weeks Differentials: adhesive capsulitis, cervical radiculopathy, neoplastic plexopathy, mononeuritis multiplex Treatment: prednisolone and PT

Answer 90

-Duchenne's (x-linked, calf hypertrophy, CM, CK >10,000) -Becker's (x-linked, milder, CK >10,000) -Facioscapulohumeral (AD, face and shoulder, can't whistle or close eyes, winged scapula) **-Limb-girdle (shoulders and pelvis)** -Myotonic -Oculopharyngeal

Answer 91

X-linked Translocation results in absence of dystrophin

Answer 92

Rigidity is not velocity dependent Spasticity is velocity dependent

Answer 93

Spinal cord compression e.g. due to neoplasia or trauma or disc disease Spinal cord ischaemia Demyelination: MS **Nutritional deficiencies (vitamin B12, E, copper)** **Inflammatory: neuromyelitis optica, SLE** **Infection: retroviral, treponemal** Inherited such as HSP or SCAs or Friedrich's (if also cerebellar signs and peripheral neuropathy) MND (PLS variant)

Answer 94

Bloods (B12 and copper) MRI brain and spinal cord Urgency determined by speed of onset of symptoms Condier LP (MS) and genetic studies (HSP)

Answer 95

X linked spinobulbar muscular atrophy LMN X-linked recessive Perioral fasciculations pathognomic Androgen insensitivity Slow progression

Answer 96

Pure UMN signs, hemiparesis or hermisensory, cerebellar signs

Answer 97

Mixed UMN signs and CN palsies and crossed signs

Answer 98

Sensory level, LMN signs at level of lesion, UMN signs below, bowel or bladder dysfunction, isolated dorsal column or spinothalamic tract signs, Brown-Sequard

Answer 99

Purely motor signs, mixed UMN and LMN signs with fasciculations

Answer 100

LMN and sensory signs attributable to one or more roots

Answer 101

LMN and sensory signs affecting more than one root e.g. whole limb

Answer 102

Either: Glove and stocking sensory > LMN signs i.e. length dependent OR: Sensory and LMN signs attributable to one peripheral nerve e.g. radial, ulnar, peroneal

Answer 103

Fatiguable weakness No sensory features

Answer 104

No fatigability No sensory features

Answer 105

-Cerebellar: broad-based, fall towards side of lesion (DANISH) -Extra-pyramidal: shuffling, festinant, slow turning circle and axial rigidity, reduced arm swing, stooped (bradykinesia, bradyphrenia, resting tremor) -Sensory: stamping, Romberg's +ve -Proximal weakness: difficulty rising from chair -Foot drop: high-stepping gait, cannot stand on heels -Hemiplegia: spastic arm flexion and leg extension, circumduction of leg, toe walking -Paraplegia: 'like walking through mud', spastic leg extension -Antalgic: due to pain

Answer 106

L5/S1 lesion Peroneal nerve Peripheral neuropathy Muscular Explanations: Common peroneal nerve palsy: wasting of tibialis anterior, weak ankle dorsiflexion (L4/5), eversion (L5/S1) +/- sensory loss on outside of leg and across foot Causes: fracture or pressure on the neck of fibula L4, L5 root lesion: weakness of ankle dorsiflexion and inversion (eversion can be preserved (L5/S1) +/- weakness of hip abduction, reflexes normal, sensory signs in the L4, L5 dermatomes Causes: prolapsed intervertebral disc Peripheral neuropathy: unilateral or bilateral foot drop, weakness of all muscles in foot (including plantar flexion), normal movements at hip, and knees are flexible, stocking sensory loss Causes: Guillain-Barre syndrome, chronic inflammatory demyelinating polyradiculopathy (CIDP), lead toxicity, porphyria, drugs, congenital (Charcot Marie Tooth) Sciatic nerve lesion: (ask about hip trauma or surgery) or lumbrosacral plexus lesion (obstetric injury)

Answer 107

Chorea (jerky and fleeting) Athetosis (writhing and sinuous) Hemiballismus (ballistic and unilateral)

Answer 108

Pendular Jerk (fast phase towards lesion in central and away in peripheral)

Answer 109

Bacterial meningitis WCC (neutrophils) Raised protein Low CSF to serum glucose ratio Viral meningitis: WCC (leukocytes) Normal or raised protein CSF to serum glucose ratio normal N.B. Bacterial: Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b (Hib) Viral: Enteroviruses Complications of bacterial meningitis: Shock, raised ICP, hydrocephalus Seizures Hearing loss Cognitive

Answer 110

Variable paralysis and sensory loss in the legs, orthopaedic deformities, neurogenic bowel and bladder, hydrocephalus, and Chiari II malformation Prevented with folic acid RF: Poor maternal diet, maternal diabetes, teratogens e.g. MTX or Na valproate