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Phase 3A > Neurology > Flashcards

Neurology Flashcards

1
Q

Functional division of the pyramidal tracts?

What are pyramidal tracts responsible for?

A

Corticospinal tracts-lateral and anterior
Corticobulbar tracts

Responsible for voluntary control of musculature of body and face

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2
Q

Structure of corticospinal tracts/what path do they follow?

A

Originate at cerebral cortex and pass through medulla oblongata

  • Lateral corticospinal tract (90%) decussate at medulla and terminate in the ventral horn (at all segmental levels)
  • Anterior tract remains ipsilateral and decussates/terminates in cervical/upper thoracic segmental levels
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3
Q

What do the extrapyramidal tracts do?
What tracts are there?
Where do they originate, and which decussate?

A

Involuntary and autonomic control of all musculature eg muscle tone, balance, posture, locomotion
All originate at the brainstem
Vestibulospinal and reticulospinal don’t decussate
Rubrospinal and tectospinal decussate

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4
Q

How many pairs of spinal nerves are there?

A

31

8C, 12T, 5L, 5S, 1C

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5
Q

What would examination of an UMN lesion show?

A

Normal muscle bulk, increased tone, decreased strength, no fasciculations, hyperreflexia (brisk)

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6
Q

What would examination of a LMN lesion show?

A

Decreased bulk/wasting, normal or decreased tone, decreased strength, may have fasciculations, decreased or absent reflexes

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7
Q

Name peripheral neuropathies (polyneuropathy) that are predominantly motor loss

A

Guillain barre syndrome (GBS), chronic inflammatory demyelinating neuropathy (CIDP ie chronic version of GBS), hereditary sensiromotor neuropathies (HSMN eg Charcot-Marie-Tooth disease), diphtheria, porphyria

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8
Q

Name peripheral neuropathies (polyneuropathy) that are predominantly sensory loss

A

Deficiency states eg B12/folate, diabetes, alcohol/toxins/drugs, leprosy, amyloidosis, metabolic abnormalities eg uraemia

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9
Q

Defining features of polyneuropathy?

A

Usually chronic and slowly progressive, starts in legs and longer nerves, can be sensory/motor/both

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10
Q

What is mononeuritis multiplex?

A

Painful, asymmetrical, sensory and motor neuropathy, subacute presentation.
Inflammatory/immune mediated.
Common causes=vasculitides eg Churg Strauss and connective tissue disorders eg sarcoid

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11
Q

Name 2 common mononeuropathies

A

Carpal tunnel syndrome-median nerve compression in flexor retinaculum
Common peroneal nerve in the leg
Ulnar nerve at the elbow
Radial nerve in the axilla

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12
Q

What investigations are involved in a neuropathy screen?

A

FBC, ESR, U+E, glucose, TFT, CRP, serum electrophoresis, B12 and folate, anti gliadin, (TPHA and HIV)

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13
Q

What investigations are involved in a vasculitic screen?

A

FBC, ESR, U+E, Cr, CRP, ANA, ANCA, anti dsDNA, RhF, complement, cryoglobulins

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14
Q

Principles of treatment of inflammatory neuropathy?

And vasculitic neuropathy?

A

Inflammatory eg CIDP: prednisolone with steroid sparing agent such as azathioprine
Vasculitic eg with Wegners: prednisolone with immunosuppressant such as cyclophosphamide

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15
Q

How does GBS arise?

What is it?

A

Autoimmune response leading to demyelination
Post infectious- respiratory or GI (campylobacter)
Subacute (<6 weeks), ascending paralysis/numbness/areflexia

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16
Q

What will you see on LP with GBS?

A

Raised CSF protein

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17
Q

How to manage GBS?

A 
Treat with IV Ig or plasmapheresis
Supportive
Monitor FVC
Consider ITU review
Recovery may take weeks to years
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18
Q

What is Myasthenia Gravis?

A

Autoimmune disorder with antibodies against nicotinic ACh receptors
Commonly due to thymus dysfunction- hyperplasia and thymomas
Results in generalised and fatiguable weakness

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19
Q

Different potential presentations of MG?

A

Proximal limbs, neck and face (head drop and ptosis), extraocular (complex diplopia), bulbar (speech and swallow issues especially in elderly), ocular (seen in 10-25%)

NB/ at risk of other AI diseases

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20
Q

How to investigate for MG?

A

Tensilon test used in the past
Look for AChR antibodies
EMG-looking at NMJ
CT thorax (breathing)

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21
Q

How to treat MG?

A

Acetycholinesterase inhibitors eg pyridostigmine
Immunosuppressants- steroids started slowly, azathioprine/methotrexate/mycophenolate
Thymectomy if indicated

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22
Q

What is a myasthenic crisis?

A

Severe weakness including respiratory muscles-high risk of death
Caused by infection/natural disease cycle/under or overdose of medication
Urgent reviews by anaesthetists and neurologists needed

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23
Q 
What is MND? 
UMN or LMN?
How to diagnose?
What is spared?
Survival?
A

Degeneration of motor neurons in motor cortex and anterior horns of spinal cord. Asymmetric weakness. Bulbar or limb onset.
UMN and LMN signs
LP/EMG/MRI to rule out, mainly a clinical diagnosis
No sensory, visual or bladder/bowel involvement
Usually 2-5 years survival

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24
Q

Name 2 common muscle disorders

A

Steroid myopathy, statin myopathy, metabolic and endocrine myopathies, myotonic dystrophy

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25
Q

Name 2 uncommon muscle disorders

A

Duchenne and Becker + most muscular dystrophies eg FSHD (facioscapulohumeral muscular dystrophy)
Inflammatory muscle disease eg polymyositis
Mitochondrial disorders

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26
Q

What is the WHO definition of a stroke?

A

Clinical syndrome consisting of rapidly developing clinical signs of focal disturbance of cerebral function, lasting more than 24 hours or leading to death with no apparent cause other than a vascular origin

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27
Q

What are the common symptoms of a carotid territory stroke?

A

Weakness of face, leg, arm, amaurosis fugax, impaired language

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28
Q

What are the common symptoms of a posterior circulation stroke?

A

Dysarthria, dysphasia, diplopia, dizziness, ataxia, diplegia

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29
Q

Proportion division of types of stroke?

A

Ischaemic- around 85%

Haemorrhagic- around 15%

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30
Q

What is the Oxford stroke (Bamford) classification of stroke?

A

Total anterior circulation stroke
Partial anterior circulation stroke
Lacunar syndrome
Posterior circulation syndrome

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31
Q

How to differentiate TACS from PACS (Bamford)?

A

TACS has all 3 of; unilateral weakness, homonymous hemianopia and higher cerebral dysfunction
PACS has just 2 out of 3

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32
Q

How to identify Lacunar syndrome (Bamford)?

A

One of following: pure sensory stroke, pure motor stroke, sensori-motor stroke, ataxic hemiparesis

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33
Q

How to indentify posterior circulation syndrome (Bamford)?

A

One of the following:
CN palsy and a contralat motor/sensory deficit
Bilat motor/sensory deficit
Conjugate eye movement disorder eg gaze palsy
Cerebellar dysfunction eg ataxia/nystagmus/vertigo
Isolated homonymous hemianopia or cortical blindness

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34
Q

Potential signs of an anterior circulation infarction

Which arteries is this?

A

Arteries=middle and anterior cerebral arteries
Contralateral weakness, contralateral sensory loss/inattention, dysarthria, dysphasia (receptive/expressive), homonymous hemianopia/visual inattention, higher cortical dysfunction

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35
Q

What is the underlying pathology of a lacunar stroke?

A

Occlusion of deep penetrating arteries. Affects small volume of subcortical white matter.
Small vessel disease-arterial wall disorganisation, microatheroma, lipohyalinosis

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36
Q

General flow diagram of how to manage a stroke

A

think FAST/recognition
ABCDE, bloods. Brief history and exam, BP, NIHSS
Urgent CT head +/- CTA
Thrombolysis +/- mechanical thrombectomy or aspirin
Investigate cause, screen and prevent complications, secondary prevention, rehab

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37
Q

When can you give thrombolysis? What with?

A

IV administration of tissue plasminogen activator eg alteplase
Within 4.5 hours of symptom onset (or time they were last seen well)

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38
Q

Name 4 CIs to thrombolysis

A

Suspect SAH, active bleeding, symptoms only minor or rapidly improving, low platelets, recent heparin treatment, recent warfarin treatment and INR elevation, recent post MI pericarditis, recent LP, BP over 185/110 consistently, BG <3 or >20, pregnancy, active pancreatitis

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39
Q

What is involved in post-thrombolysis care?

A

Aggressive BP monitoring, vigilance for complications, 24 hour CT head (haemorrhagic transformation)

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40
Q

What is mechanical thrombectomy? Time window?

A

Recanalisation of the culprit vessel
6 hour time window for anterior circulation stroke
Can be used alongside IV thrombolysis, but a limited resource

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41
Q

What investigations are used after the initial management of stroke?

A 
Bloods-FBC, ESR, U+Es, lipids, LFTs, CRP, clotting screen, glucose and HbA1c
ECG +/- 72 hour tape
Carotid doppler USS
Echo
MRI

For a young patient/atypical stroke consider HIV and vasculitic screen, thrombophilia screen, homocysteine. Cardiac investigations, vasc imaging eg CTA

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42
Q

Management after stroke investigations?

A

MDT approach
Lifestyle: smoking/drugs/alcohol cessation, diet modifications, exercise, driving advice
Medical: VTE assessment, hydration, NG feeding+/- PEG, spasticity (physio, botox), monitor for infection
Secondary prevention
Surgical: eg carotid endarterectomy

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43
Q

What is involved in secondary prevention after an ischaemic stroke?

A

Antiplatelets: 300mg aspirin po/pr for 2 weeks and clopidogrel lifelong
Anticoagulation: if in AF may need to wait for 2 weeks- HASBLED and CHADSVASC scores
Hypertension: target <130/80
Cholesterol: statin, aim for 40% reduction in non-HDL cholesterol

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44
Q

How to manage a haemorrhagic stroke? (drugs and corresponding)

A

Reversal of any anticoagulation
Warfarin= beriplex and vitamin K
Heparin= protamine
LMWH= potentially reversible with protamine
Apixaban/rivaroxaban/edoxabana=possibly reversible with beriplex
Dabigatran=idarucizumab

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45
Q

Red flags in a headache history

A

New headache over 60 years, thunderclap, infective symptoms, history of malignancy

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46
Q

Red flags in a history of weakness

A

Loss of sphincter control, sudden onset, progressive, respiratory or swallowing problems

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47
Q

Red flags in a history of visual disturbance

A

Any other associated symptom eg headache and visual loss in an older person

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48
Q

Important aspects in a history of speech disturbance

A

Comprehension (receptive/Wernicke’s dysphasia)
Production (expressive/Broca’s dysphasia)
Repetition (conductive dysphasia, arcuate fasciculus- connecting brocas and wernickes)
Articulation/dysarthria (cerebellar, bulbar, pseudo-bulbar donald duck speech)
Phonation/dysphonia (eg resp muscle weakness)

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49
Q

What are some mechanical and neurological causes of dysphagia?

A

Mechanical= stricture and achalasia

Neurological= bulbar and pseudo-bulbar palsy, brainstem pathology, MG, MND

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50
Q

Describe the AMT

What are some other cognitive state assessment methods

A

AMT/abbreviated mental test score:
Tell pt to recall address, age, time, year, recognise two people, DOB, dates of 2nd world war, name of present monarch, name of hospital, count 20 to 1

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51
Q

What do you see in CN3 palsy?

A

eye looking down and out with ptosis (ipsilateral)

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52
Q

What is internuclear ophthalmoplegia?

A

Disorder of conjugate lateral gaze. Lesion in medial longitudinal fasciculus.
Ipsilateral to eye that fails to adduct across

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53
Q

Difference between UMN and LMN lesions of facial nerve

A

UMN lesions spare the forehead

LMN lesions=Bells palsy doesn’t spare the forehead

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54
Q

Rinne’s test- describe the finding

A

In conductive hearing loss, bone conduction is louder than air conduction
(In sensorineural deafness, air conduction is louder than bone conduction)
Normal=air conduction louder than bone conduction

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55
Q

Weber’s test- describe the finding

A

In conductive hearing loss, sound is heard louder on side of affected ear
(In sensorineural deafness, sound heard louder of intact ear)
Normal=equally loud

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56
Q

Difference between spasticity and rigidity?

A

Spasticity=amplitude and velocity dependent- “clasp knife”,affected pyramidal tracts

Rigidity=independent of amplitude and velocity, lead pipe, cogwheel (rigidity an tremor together), affected basal ganglia

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57
Q

How to recognise cerebellar lesion/coordination?

A

DANISH

Dysdiadokinesis, ataxia, nystagmus, intention tremor, speech, hypotonia

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58
Q

What are considered neurological emergencies?

A 
Coma
Sudden or subacute new headache
Weakness
Visual loss
Status epilepticus
Other eg acute loss of bladder function, hemiballismu, severe chorea, severe dysphagia
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59
Q

What subtypes of weakness are there, when considering neurological emergencies?

A

Generalised +/- respiratory failure
Acute/subacute para/quadriplegia
Acute hemi/monoplegia (stroke)

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60
Q

Describe GCS

A

Glasgow coma score
Eye opening: 1=none, 2=to pain, 3=to voices, 4=spontaneously
Motor response: 1=none, 2=extension to pain, 3=flexion to pain, 4=withdraw from pain, 5=localises to pain, 6=obeys commands
Verbal response: 1=none, 2=groans, 3=inappropriate words, 4=confused speech, 5=orientated

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61
Q

Name 5 common causes of coma

A

Drugs/toxins (opiates), anoxia, mass lesions (bleeds), infections (HSE, bacterial meningitis), infarcts, metabolic (hypoglycaemia, DKA, hepatic encephalopathy, uraemia), SAH, epilepsy

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62
Q

Name 2 uncommon causes of coma

A

Mass lesions (tumours), hypothermia, psychiatric, venous sinus occlusions

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63
Q

What is status epilepticus?

A

Official definition: Persistent seizure activity for 30 mins or more-continuous or intermittent attacks without recovery of consciousness
Practical definition: convulsive seizure activity with loss of consciousness for over 10 mins

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64
Q

What warrants status epilepticus in different seizure types?

A

Generalised tonic-clonic= 5 mins
Focal=10 mins
Absence=10-15 mins

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65
Q

What are potential consequences of status epilpeticus?

A 
Increased CNS metabolic consumption
Mortality
Rhabdomyolysis
Renal failure
Metabolic acidosis
Hyperthermia
Heart and other organ effects
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66
Q

How to manage status epilepticus?

A

1st line= benzodiazepine eg IV lorazepam/diazepam/clonazepam or rectal diazepam

2nd line=antiepileptic drug IV eg phenytoin (will need cardiac monitoring) or sodium valproate

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67
Q

What is sudden onset headache with third cranial nerve palsy or painful third nerve palsy until proven otherwise?

A

Subarachnoid haemorrhage

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68
Q

Potential causes of sudden severe headaches?

A

SAH, cerebral venous sinus thrombosis, dissection-carotid/vertebral, infection-bacterial meningitis/encephalitis/cerebral abscess, acute haemorrhage/acute infarcts, pituitary apoplexy

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69
Q

What are SAHs usually caused by?

A

Rupture of saccular aneurysm

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70
Q

Signs and symptoms of SAH?

A

Acute severe localised headache (“hit by a hammer”)
Meningism (nausea, vomiting, stiff neck, photophobia)
Double vision
Ptsosis
Sometimes-sezures, low GCS, sudden death

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71
Q

Investigations after suspected SAH?

A

CT ASAP-sensitivity decreases with time
CTA or MRA
LP 12 hours after event
CSF xanthochromia if presenting late

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72
Q

How does GBS present?

A

Can be demyelinating or axonal, acute/subacute, immune mediated, multifocal polyradiculoneuritis

Numbness starts distally, progressive ascending weakness, bifacial weakness and other cranial neuropathies, flaccid tetra or paraperesis, areflexia

Potential different presentations: paraparetic, pharyngeal-cervical-brachial weakness, bifacial weakness with paraesthesia, Miller-Fisher syndrome (less severe form of GBS)

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73
Q

What are potential dangers of GBS?

A

Severe weakness, aspiration, resp failure, autonomic instability (severe sudden hypotension and cardiac arrhythmias)

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74
Q

Main management principles of GBS?

A

Monitor FVC and ECG
Always admit. Let ITU know early if VC less than 1L
DVT prophylaxis, BP, monitor swallow

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75
Q

How to treat GBS?

A

IV Ig or plasma exchange

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76
Q

When is a spinal cord emergency suspected?

What must be ruled out and how?

A 
Acute/subacute onset
bladder-bowel weakness
saddle anaesthesia
leg weakness
constant sensory deficit
significant pain

Rule out cord compression via MRI

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77
Q

What will a lesion of the R dorsal column at L1 result in?

Common causes?

A

Absences of light touch, proprioception and vibration in the right leg
Common causes= MS, penetrating injuries, tumour compression

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78
Q

What will a lesion of the R fasciculus cuneatus at C3 result in?
Common causes?

A

No light touch, vibration or proprioception in R arm and R trunk
Common causes= MS, penetrating injuries, tumour compression

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79
Q

What will a lesion of the R lateral corticospinal tract at L1 result in?
Common causes?

A

UMN signs in the R leg (weakness, hyperreflexia, hypertonia)

Common causes= penetrating injuries, lateral compression from tumours, MS

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80
Q

What will a lesion of the R lateral spinothalamic tract at L1 result in?
Common causes?

A

Absence of pain and temperature sensation in the left leg

Common causes= penetrating injuries, MS, compression from tumours

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81
Q

What will a lesion of the anterior gray and white commissures at C5-C6 result in?
Common causes?

A

Central cord syndrome!
Absence of pain and temperature sensation in c5 and c6 dermatomes in both upper extremities
Common causes= post traumatic contusion, syringomyelia, intrinsic spinal cord tumours

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82
Q

What will a complete transection of the R half of the spinal cord at L1 result in?
Common causes?

A

Brown-Sequard syndrome!
Absence of light touch, proprioception, vibration in R leg. UMN signs in R leg. Absence of pain and temperature sensation in L leg
Common causes=penetrating injuries, tumour compression, MS

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83
Q

What will complete transection of the spinal cord at L1 result in?
Common causes?

A

Both legs will have absence of light touch, vibration and proprioception. UMN signs in both legs/paraplegia. No pain or temp in either leg.
Common causes=trauma, tumours, transverse myelitis, MS

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84
Q

What will complete transection of the dorsal columns in the cervical region result in?
Common causes?

A

No light touch, vibration or proprioception from neck down

Common causes= trauma, posterior tumour compression, MS, vitamin B12 deficiency

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85
Q

What will complete transection of the lateral spinothalamic tracts with DC sparing in the cervical region result in?
Common causes?

A

Anterior cord syndrome!
UMN signs bilaterally below the lesion (damage to lateral corticospinal), LMN signs bilaterally at the level of the lesion (damage to LMN in ventral horns), no pain nor temp bilaterally below the lesion level
Common causes=anterior spinal artery occlusion, MS, occlusion of artery of Adamkiewicz during AAA repair

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86
Q

Presentation of cauda equina?

Common causes?

A 
SPIN= saddle anaesthesia, pain/paralysis, incontinence bladder/bowel, numbness
Causes= compressive (discs and tumours), non compressive- inflammatory/infiltrative/granulomatous, vascular (spinal dural fistula)
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87
Q

What are the different types of focal seizures?

A

Simple partial seizures (aura), complex partial seizures (loss of consciousness), secondary generalised tonic clonic seizures

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88
Q

What are the different types of generalised seizures?

A

Generalised tonic clonic seizures, myoclonic jerks, absences (a/w 3 second spike and wave on EEG)

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89
Q

Causes of syncope?

A

Reflex-vasovagal, situational, carotid sinus hypersensitivity
Cardiogenic- conditions that predispose to transiet tachyarrythmias, bradyarrhythmias, cardiac ischaemia, structural heart disease
Orthostatic hypotension- drugs, autonomic failure

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90
Q

What types of heart block have a high risk of progression to asystole?

A

Complete/3rd degree heart block
Mobitz type II 2nd degree heart block
Incomplete trifascicular block-RBBB, LAD, 1st degree heart block

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91
Q

TLOC during exercise is what type of TLOC until proven otherwise?

A

Cardiogenic

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92
Q

What are PNES?

A

Psychogenic non-epileptic seizure
Episodes of movement, sensation or experience that resemble epileptic seizures but without ictal cerebral discharges
Physical manifestation of psychological distress
A/w comorbid psychopathology and with childhood sexual abuse

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93
Q

Common features of a generalised tonic clonic seizure?

A

No trigger, may have aura, stiffening/jerking of limbs/vocalization or grunting/cyanosis/eyes open, 1-2 mins, post-ictal confusion for about 20 mins, lateral tongue bite, urinary incontinence, injury
NB/tramadol use lowers seizure threshold, and ask about alcohol/recreational drug use

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94
Q

Characteristics of syncope?

A

Triggers, typical fainting prodrome, pallor, may have jerks if in upright position, brief. No post-ictal period, rapid recovery. Look for hypotensive medications

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95
Q

Characteristics of PNES?

A

May be situational, eyes often closed, often wax and wane, may be emotional. Often very prolonged. Post ictal is variable but almost always tired/washed out
Look for antidepressants or psychotic medications. SH very important

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96
Q

Investigations for TLOC?

A

12 lead ECG for all TLOC
Neuroimaging- CT not indicated in syncope but in epilepsy (MRI is better)
EEG in very frequent seizures
Recordings of the event

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97
Q

Myotome, dermatome and reflex associated with c5/c6 root?

A

Elbow flexion, thumb, biceps reflex

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98
Q

Myotome, dermatome and reflex associated with c7 root?

A

Elbow extension, middle finger, triceps reflex

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99
Q

Myotome and dermatome a/w c8/t1 root?

A

Hand myotome and medial hand/forearm dermatome

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100
Q

Myotome, dermatome and reflex a/w L5 root?

A

Dorsiflexion
Dermatome=big toe, dorsum of foot
No reflexes

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101
Q

Myotome, dermatome and reflex a/w S1 root?

A

Plantarflexion
Little toe, sole and heel
Ankle jerk

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102
Q

Describe the normal volumes of the ventricular system?

A

CSF produced at 500ml/24 hour
Total CSF volume=120ml
Capacity of ventricular system=20ml
Normal pressure 5-15cm H2O

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103
Q

Symptoms and signs of hydrocephalus?

A

Symptoms: headache, vomiting, visual disturbance, gait unsteadiness
Signs: drowsiness, papilloedema, limitationof upward gaze, reduced visual acuity

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104
Q

Shapes of extradural haematoma and subdural haematoma on CT?

A 
Extradural= lemon shaped
Subdural= quarter moon
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105
Q

What are the characteristics of a migraine?

A

Moderate to severe
Unilateral and throbbing lasting 4-72 hours
Migraine with or without aura or silent migraine (aura and no headache)
Aura can last 5 minutes to an hour
May have prodromal stage (mood, energy levels, appetite, behaviour changes)
Often nausea, vomiting, photo/phonophobia

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106
Q

What could be in the aura phase of a migraine?

A

Visual problems-blind spots, flashing lights, zig-zag patterns
Numbness or tingling
Feeling dizzy or off balance
Dysphasia

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107
Q

Common triggers for migraines?

A

Menorrhoea, stress, tiredness, certain foods or drinks, exercise

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108
Q

How to treat a migraine?

A

Paracetamol/aspirin/ibuprofen can help reduce symptoms but beware medication overuse headache
Triptans (cause blood vessels around brain to constrict)
Anti-emetics
Transcranial magnetic stimulatoin

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109
Q

How to prevent migraines?

A 
Topiramate (antiepileptic)
Propranolol
Amitriptyline
Botulinum toxin type A for chronic migraine (headaches on over 15 days a month, 8 of which must be migraine)
Acupuncture
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110
Q

What are the characteristics of a tension headache?

A

Bilateral ache
May feel neck muscles tighten and feeling of pressure behind eyes
Usually 30 mins-few hours but can last several days

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111
Q

Common causes of tension headaches?

A

Stress and anxiety, squinting, poor posture, tiredness, dehydration, missing meals, lack of exercise, bright sunlight, noise, certain smells

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112
Q

How to manage tension type headaches?

A

Simple analgesia
Relaxation techniques
Trigger avoidance

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113
Q

What are the characteristics of a cluster headache?

A

Excruciating, unilateral, often around the eye
More common in men, tend to start in 30s or 40s
Sharp, burning or piercing sensation
Associated symptoms: red or watering eye, ptosis and swelling of 1 eyelid, miosis in 1 eye, sweaty face, blocked or runny nostril
Lasts 15 mins to 3 hours, typically occur between 1-8 times a day
Often at same time of day

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114
Q

How to manage cluster headaches?

A

Specialist treatment: sumatriptan injections or nasal spray, o2 therapy, zolmitriptan nasal spray

Newer= transcutaneous vagus nerve stimulation.

Chronic=stimulation device implantation.

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115
Q

How to prevent cluster headaches?

A

Avoid triggers eg don’t drink alcohol during a cluster bout, avoid strong smelling chemicals, avoid exercise
Verapamil as soon as headache begins and continue until bout is stopped
If verapamil doesn’t work, consider corticosteroids, lithium and local anaesthetic injections into back of head

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116
Q

What are the characteristics of temporal arteritis?

A

Frequent, severe headaches
Pain and tenderness over temples
Jaw pain while eating or talking
Vision problems eg diplopia or loss of vision in 1 or both eyes
Highly associated with developing polymyalgia rheumatica

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117
Q

How to diagnose temporal arteritis?

A

Ultrasound scan of temples
Examination of temples- tender temporal arteries
Biopsy of temporal arteries (giant cell infiltration)

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118
Q

How to treat temporal arteritis?

A

Prednisolone
Initial high dose for a few weeks, then lower steroid dose for longer term

Potential others: low dose aspirin, PPIs, bisphosphonate therapy, immunosuppressants

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119
Q

Causes of cerebellar disorder?

A

Vascular (Stroke or TIA)
Space-occupying (hydrocephalus or posterior fossa tumours/abscesses)
Nutritional (Wernicke’s encephalopathy, vit E deficiency, gluten sensitivity)
Infections (meningo-encephalitis, HIV, toxoplasmosis, Creutzfeldt-jakob disease)
Toxins (alcohol, mercury, CO poisoning)
Drugs and drug OD
Trauma
MS
Genetic
Metabolic and endocrine (eg inherited metabolic disorders)
Congenital (eg cerebral palsy)
Idiopathic

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120
Q

Describe presentation of cerebellar disorder?

A

ATAXIA (different depending where in cerebellum) eg truncal, limb (lesions of cerebellar hemisphere cause ipsilateral signs), Riddoch’s sign, acute-onset, subacute, episodic, chronic progressive

DYSARTHRIA -spluttering stoccato speech

Larger writing

TREMOR- unilat, bilat or truncal

Nausea and vomiting

Cerebellar cognitive affective syndrome

DYSDIADOCHOKINESIS

NYSTAGMUS

May have mild hypotonia and hyporeflexia

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121
Q

Features of simple partial seizures?

A

Auras/Focal seizures without impaired consciousness
Most commonly from temporal lobes, sometimes frontal lobes, rarely other lobes
Focal motor signs, autonomic signs (flushing, sweating, vomiting), sensory signs (flashing lights, unpleasant odours, tastes, vertigo, pain, paraesthesia), psychic symptoms (deja vu, depersonalisation, fear)

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122
Q

Features of complex partial seizures?

A

Focal seizure with impaired consciousness
Automatic behaviours eg plucking at clothes, fiddling, lip smacking, chewing, grimacing
Post-ictal confusion and amnesia

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123
Q

Features of tonic-clonic seizure?

A

/Grand mal
Tonic stage= lose consciousness, body goes stiff and may fall to floor
Clonic stage= limbs jerk about, may have incontinence, may have lateral tongue bite
Post ictal drowsiness, confusion, headache, myalgia, incontinence

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124
Q

Features of an absence seizure?

A

/Petit mal
Lose awareness of surroundings, mainly affect children
stare blankly, look like daydreaming, flutter eyes, may make slight jerking movements of body and limbs.
Last up to 15 seconds and amnesia afterwards

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125
Q

Features of a myoclonic seizure?

A

Some or all of body suddenly twitches and jerks
Often happen soon after waking up
Last a few mins and might lose consciousness

126
Q

Features of an atonic seizure?

A

All muscles relax so may fall to the ground, sudden loss of tone
Quick recovery

127
Q

Features of a tonic seizure?

A

All muscles become rigid, maybe causing a fall

Quick recovery

128
Q

Which anti-epileptic to prescribe for focal seizures?

A

Lamotrigine, Carbamazapine are first line

129
Q

Which AED for tonic clonic seizures?

A

Sodium valproate or lamotrigine if not suitable

130
Q

Which AED for absence seizures?

A

Ethosuximide or sodium valproate

Lamotrigine if above are unsuitable

131
Q

Which AED for myoclonic seizures?

A

Sodium valproate

Topiramate if unsuitable

132
Q

Features of narcolepsy?

A

Lack of hypocretin/orexin in brain (regulates wakefulness)

Excessive daytime sleepiness, sleep attacks, cataplexy, sleep paralysis, excessive dreaming and waking in the night

133
Q

How to manage narcolepsy?

A

No cure
Frequent, brief, evenly spaced naps throughout the day
Strict bedtime routine
Stimulant medication eg modafinil, dexamphetamine, methylphenidate
Consider antidepressants

134
Q

How to diagnose narcolepsy?

A

Rule out sleep apnoea, epilepsy, depression, hypothyroid and a previous head injury
See if secondary narcolepsy-head injury, brain tumour, MS, encephalitis
Sleep analysis- Epworth sleepiness scale, polysomnography, measure hypocretin levels

135
Q

What is cataplexy?

A

Sudden temporary muscle weakness or loss of muscular control.
Commonly experienced by those with narcolepsy
Typical symptoms= jaw dropping, head slumping, leg collapsing, slurred speech, double vision
Usually triggered by strong emotions

136
Q

How to manage cataplexy?

A

Sodium oxybate

Antidepressants eg fluoxetine, venlafaxine, imipramine

137
Q

What is shingles/what causes it?

A

Viral infection by varicella-zoster virus

After chickenpox virus lies inactive in nerve tissue near nervous system, when it reactivates=shingles

138
Q

Describe the presentation of shingles?

A

First signs=tingling or pain in an area of skin, headache or feeling unwell
Unilateral itchy rash after a few days- red blotches, then itchy blisters, then scabbed over, painful skin after the rash has gone
Can take up to 4 weeks for rash to heal

139
Q

Potential complications of shingles?

A

Postherpetic neuralgia
Vision loss (ophthlmic shingles)
Neurological problems eg encephalitis, facial paralysis, hearing/balance problems
Skin infections of blisters

140
Q

Management of shingles?

A

Avoid pregnant women who haven’t had chickenpox, people with weakened immune system, babies less than 1 month
Shingles vaccination for people in their 70s
Paracetamol, keep rash clean, wear loose-fitting clothing, cool compress

141
Q

What is the pathaphysiology of Wernicke-Korsakoff syndrome?

A

Drinking alcohol prevents body from getting enough thiamine/vit B1- this is vital for neurones to work
2 stages
stage 1=intense inflammation=wernicke’s encephalopathy
stage 2=if encephalopathy not treated quickly, may developl korsakoff’s syndrome=similar to dementia

142
Q

What are the symptoms of wernicke’s encephalopathy?

A

Disorientation, confusion and mild memory loss (most common sxs)
Difficulty controlling eye movements-nystagmus and conjugate gaze palsies
Poor balance, wide based gait
Undernourished

Triad= acute confusion, ataxia, ophthalmoplegia

143
Q

How to manage suspected wernicke’s encephalopathy?

A

May need MRI to confirm
Immediately stop drinking alcohol
High dose IV thiamine hydrochloride

144
Q

Causes of wernicke’s encephalopathy?

A

90% cases=alcohol abuse
Also could be:
Starvation, postbariatric surgery, GI malignancy, chronic dialysis

145
Q

What are the symptoms of Korsakoff’s syndrome/Wernicke-Korsakoff syndrome?

A

Confabulation and memory loss (global amnesia)

146
Q

What is the pathaphysiology of Huntington’s disease?

A

CAG triplet expansion repeat in the huntingtin gene
Number of repeats determines phenotype eg over 39=100% penetrance
Autosomal dominant, shows anticipation

147
Q

Presentation of Huntington’s disease?

A

Neuropsychiatric=progressive personality change, behavioural abnormalities, depression, cognitive impairment, psychosis
Motor= chorea, parkinsonism, dystonia, slowing of saccades
Weight loss

148
Q

What is the treatment of Huntington’s disease?

A

No disease-modifying treatment
Supportive
Atypical antipsychotics-dual action on chorea and psychosis
Symptom support-chorea, depression, psychosis

Death usually within 15-20 years of diagnosis

149
Q

How can you manage chorea?

A

Atypical antipsychotics, tetrabenazine, amantadine

150
Q

What is the pathaphysiology of Parkinson’s disease?

A

neurodegenerative a/w Lewy bodies
loss of dopaminergic neurons in the substantia nigra pars compacta
imbalance of dopamine and ACh in striatum

151
Q

What are the symptoms of parkinson’s disease?

A

Bradykinesia/hypokinesia, resting tremor, rigidity, postural instability
Loss of sense of smell, constipation, urinary frequency/urgency, REM sleep disorder, visual hallucinations, sialorrhoea, depression/memory impairment

152
Q

What could you see on examination of a person with Parkinson’s disease?

A 
Hypomimia, quiet speech
Cranial nerves are normal
Lead-pipe rigidity 
Cog-wheeling
Resting tremor 4Hz (3-5)
Brady/hypokinesia
Stooped posture
Shuffling gait, unilateral reduced arm swing, freezing of gait 
Postural instability
Micrographia
153
Q

What are the treatments for parkinson’s disease?

A

Speech therapy and physio. Deep brain stimulation

Levodopa, dopamine agonists, MAO B inhibitors, anticholinergic agents, amantadine, COMT inhibitors

154
Q

Pros and cons of levodopa?

A

pros= most effective drug for bradykinesia/akinesia, some improvement in tremor/rigidity. Can be combined with peripheral decarboxylase inhibitor to prevent postural hypotension eg levodopa+carbidopa=sinemet, levodopa+benserazide=madopar

Cons=rarely improves postural instability, nausea at first, GI absorption varies with different meals, motor fluctuations (get worse with longer duration)-dyskinesia/wearing-off/dystonic posturing

155
Q

Examples of dopamine agonists?

A

Pramipexole, ropinirole, bromocriptine, cabergoline, rotigotine, apomorphine

156
Q

Issues with dopamine agonists?

A

nausea, somnolence, a/w mood disorders and impulse control disorders, withdrawal syndrome. Can sometimes cause confusion and hallucinations.

157
Q

What leads to vascular dementia?

A

Any ischaemia/hypoperfusion of brain tissue eg TIA and stroke

158
Q

How to diagnose vascular dementia?

A

Clinical assessment and history

CT or MRI

159
Q

What are the symptoms of Alzheimer’s disease?

A

Early stages=memory lapses
Middle stages=increasing confusion and disorientation, obsessive/repetitive/impulsive behaviour, delusions, aphasia, disturbed sleep, mood changes, hallucinations
Later stages=hallucinations and delusions can get worse, dysphagia, weight loss, incontinence, gradual loss of speech, significant memory problems (short and long term)

160
Q

What is the pathaphysiology of Alzheimer’s disease?

A

Amyloid deposits forming plaques in neural tissue
Tau deposits-neurofibrillary tangles
Decreased ACh
Atrophy of brain

161
Q

How to treat Alzheimer’s disease?

A

No cure
Acetylcholinesterase inhibitors eg donepezil, galantamine and rivastigmine for early-mid stage disease
Memantine (blocks glutamate receptor) for mod-severe
BPSDs-coping strategies, risperidone/haloperidol if absolutely necessary
Social support

162
Q

What are BPSDs?

A

Behavioural and psychological symptoms of dementia:

eg increased agitation, anxiety, wandering, aggression, delusions and hallucinations

163
Q

What is the pathaphysiology of normal pressure hydrocephalus?

A

Primary NPH=idiopathic (most)
Secondary NPH= previous IVH/SAH/scarring from meningitis

Abnormal build up of CSF leading to ventricular enlargement with a normal LP opening pressure

164
Q

What are the signs and symptoms of NPH?

A

Magnetic gait-bilateral
Cognitive disturbance-psychomotor behaviour deficits and bradyphrenia (dementia like symptoms)
Urinary urgency progressing to incontinence

165
Q

How to diagnose NPH?

A

Firm diagnosis can’t be made-categories as either probably, possible or unlikely NPH
MRI head: lat and third ventricles out of proportion to sulcal enlargement
CSF flow studies

166
Q

How to treat NPH?

A

Neurosurgery for consideration of VP shunt

167
Q

What are the 3 types of hydrocephalus?

A

Congenital, acquired, normal pressure

Also communicating and non-communicating

168
Q

What can cause congenital hydrocephalus?

What are the potential complications?

A

Spina bifida, maternal infection eg mumps or rubella

Long-term complications:
learning disabilities, speech and memory problems, short attention span, vision problems eg squint or vision loss, epilepsy, coordination issue

169
Q

What can cause acquired hydrocephalus?

A

Brain or spinal cord tumours, infections of CNS eg bacterial meningitis, injury or stroke

170
Q

Signs and symptoms of acquired hydrocephalus?

A

Headaches (may be worse in the morning). Neck pain, nausea, vomiting, sleepiness, confusion, blurred vision or diplopia, gait disorders, incontinence

171
Q

Signs and symptoms of hydrocephalus in infants?

A

Rapid increase in head size, unusually large head, bulge on fontanel, vomiting, feeding issues, sleepiness, irritability, eyes fixed downwards (“sun setting”), seizures

172
Q

How to treat hydrocephalus?

A

Shunt or endoscopic third ventriculostomy (ETV)

Rehab therapies ad educational interventions

173
Q

What is the commonest form of brain tumour?

A

Brain metastases, commonly from lung/melanoma/breast

174
Q

Potential presentations of brain tumours?

A

Raised ICP-vomiting, diplopia
Headache-dull, constant or throbbing, progressive, may be worse at night and waking the patient
Seizures
Focal deficits-weakness, sensory loss, aphasia

175
Q

What are the different types of primary brain tumour?

A

Meningioma (1/3 of primary)

Gliomas (around 1/3 of primary); astrocytoma, oligodendroglioma, ependymoma, schwannoma, craniopharyngioma

176
Q

Describe a meningioma

A

Attached to dura (10% arise from spinal cord)
Slow growing, often asymptomatic and incidental findingss
More common in older female patients

177
Q

Describe a glioma

A

Fast growing generally and normally younger patients

178
Q

Describe the brain tumour grading/classification (WHO)

A

Grade I= lowest grade tumours eg pilocytic astrocytoma
Grade II= lower grade malignancies eg fibrillary astrocytoma
Grade III= higher grade malignancies eg anaplastic astrocytoma
Grade IV= highest-grade malignancies eg glioblastoma multiforme

179
Q

Describe the pathaphysiology of multiple sclerosis

A

Autoimmune inflammatory disorder of CNS characterised by widespread demyelination throughout CNS as well as diffuse neuronal loss (degeneration of oligodendrocytes)

180
Q

Describe the epidemiology of MS

A

RFs: onset generally in 20s, female (2:1), smoking, EBV exposure, low vitamin D, childhood obesity, genetics-HLA-DRB1

181
Q

What are the different forms of MS?

A

Relapse-onset (95%)

Progressive-onset (5%)

182
Q

What are the most characteristic syndromes seen at initial presentation and relapse in MS?

A

Optic neuritis, transverse myelitis, sensory disturbance, UMN weakness, cerebellar syndrome, brainstem syndromes eg internuclear ophthalmoplegia

183
Q

What is Lhermitte’s sign?

A

Paroxysmal shock-like sensations down back and limbs on neck flexion in MS

184
Q

What is Uhtoff’s phenomenon?

A

Paroxysmal worsening of symptoms on heat exposure in MS

185
Q

What is the MacDonal 2010 criteria?

A

For a diagnosis of MS: dissemination in space (relapse and radiological) and dissemination in time (clinical and radiological)

186
Q

What can be seen on LP in MS?

A

Oligoclonal bands

187
Q

How would you treat a relapse of MS?

A

Steroids

188
Q

What disease modifying therapies are available for MS?

A

(No proven benefit in progressive MS)

Interferon beta, glatirameracetate, daclizumab, natalizumab, alemtuzumab, fingolimod

189
Q

What management options have proven benefit in progressive MS?

A

Ocrelizumab

Haematopoietic stem cell transplantation

190
Q

What symptomatic treatment can you use in MS?

A 
Nociceptive pain-NSAIDs, TENS, physio
Neuropathic pain-gabapentin, amitryptilline, TENS
Trigeminal neuralgia-Carbamazapine
Bladder dysfunction-self catheterisation
Spasticity-baclofen
191
Q

What are the different types of MND?

A

Amyotrophic lateral sclerosis, Progressive muscular atrophy, primary lateral sclerosis, progressive bulbar palsy, flail arm syndrome

192
Q

How does ALS manifest?

A

Begins with distal, asymmetric limb weakness which progresses proximally

Limb muscles: UMN and LMN signs
Bulbar muscles; dysarthria, dysphagia, pseduobulbar effect (sudden inappropriate laughing or crying, uncontrollable)
Axial muscles: head drop, postural instability
Respiratory muscles: initially dyspnoea on exertion and nocturnal hypoventilation, later=neuromuscular resp failure
Cognitive=a/w frontotemporal dementia

193
Q

How to diagnose MND?

A

Exclusion of differentials-bloods, LP, EMG, NCS (reduction in number of motor axons), MRI brain and spinal cord

194
Q

What treatment options are there for MND?

A

Supportive care eg baclofen for spasticity, SLT, alternative feeding routes, NIV, tracheostomy, muscarinic antagonists eg hyoscine hydrobromide for sialorrhoea

Riluzole= disease-modifying drug, extends survival by a few months and extends tracheostomy-free survival

195
Q

What are the symptoms of cerebral palsy and when do you notice them?

A

Start to notice symptoms during first 2-3 years of life
Problems with movement, coordination and developmemt eg developmental milestone delays, hypotonia, weakness, clumsy movements, spasms, tremors, walking on tiptoes

Potential other symptoms: feeding/drooling/swallow issues, constipation, speaking issues, epilepsy, GORD, scoliosis, dislocating hips, urinary incontinence, hearing loss, learning disability, squint/reduced vision

196
Q

What are the 4 main types of cerebral palsy?

A

Spastic cerebral palsy-rigidity
Dyskinetic cerebral palsy -switch between rigidity and floppiness
Ataxic cerebral palsy- balance and coordination issues
Mixed cerebral palsy

197
Q

Causes of cerebral palsy?

A

Prenatal issues: periventricular leukomalacia, maternal infection eg rubella and toxoplasmosis, stroke, injury to unborn baby’s head

Problems during or after birth: asphyxiation during difficult birth, meningitis, serious head injury, choking or nearly drowning, very hypoglycaemic, stroke

Risks: premature birth, low birthweight, part of multiple birth, mother taking cocaine/smoking/drinking

198
Q

How to diagnose cerebral palsy?

A

MRI or cranial ultrasound
EEG if seizures
General lab tests
Identify where issues are eg vision, hearing, speech, intellect, development and movement

199
Q

What is neurofibromatosis type 1?

A

Autosomal dominant genetic condition causing (usually benign) tumours to grow along nerves

200
Q

What are the symptoms of neurofibromatosis type 1?

A

Often mild and no serious health problems

Skin: cafe au lait spots, freckles in unusual places eg armpits, tumours on or under skin=neurofibromas

Some children develop learning and behavioural problems-ADHD and ASD

Tumour on optic pathway (optic pathway glioma)-rarely symptomatic but may interfere with vision

Some develop hypertension due to renal artery stenosis

Physical development: scoliosis, bigger head, small size and lower weight

Migraines, rarely brain tumours

201
Q

What is the treatment for NF1?

A

Regular monitoring. May include physio, psychological support and pain management

202
Q

What are the main symptoms of neurofibromatosis type 2?

A

Tumours leading to hearing loss, tinnitus and balance problems
Cataracts
Skin tumours
Peripheral neuropathy
Brain: headaches, vomiting, seizures, visual disturbances
Spinal cord: back pain, muscle weakness, unpleasant sensations

203
Q

What is mosaic NF2?

A

Milder form of NF2 where symptoms are milder and often restricted to certain area or side of body

204
Q

What monitoring is required in NF2?

A

Annual MRI scans
Annual eye tests for cataracts
Annual hearing tests

205
Q

What are the causes of meningitis?

A

Bacterial: Streptococcus pneumoniae, Neisseira meningitidis, Listeria monocytogenes (elderly and immunocompromised), Haemophilus influenzae (children), Gram negatives (elderly and immunosuppressed), TB (immunosuppressed), staphylcocci (neurosurgery patients)

Fungal: cryptococcus neoformans
Viral: HSV2, enterovirus

206
Q

What is the presentation of bacterial meningitis?

A

Fever, headache, meningism (photophobia and neck stiffness), confusion/decreased GCS, sepsis developing over a few days

207
Q

What could be seen on examination of someone with bacterial meningitis?

A

Septic, rash (non-blanching, petechial/purpuric)
Decreased GCS
Cranial neuropathis, papilloedema
Meningism: photophobia, neck stiffness (passive and active), Brudzinski sign and Kernig’s sign

208
Q

What is Brudzinksi’s sign?

A

Neck flexion leading to hip flexion

209
Q

What is Kernig’s sign?

A

Hip flexion prevents knee extension

210
Q

How to investigate for bacterial menigitis?

A

Bloods-culture, FBC, U+E, coagulation: neutrophilia and increased CRP
LP: increased WCC (neutrophilia), increased protein, decreased glucose

CT head-prior to LP if decreased GCS/raised ICP/focal neurological deficit/seizures

211
Q

What antibiotics for bacterial meningitis?

A

In GP: IM or IV benzylpenicillin asap

Secondary care: initially empiric then narrow once cultured. Ceftriaxone. Add ampicillin for elderly/immunocompromised.

212
Q

Overall management of bacterial menigitis?

A 
IV antibiotics
Dexamethasone in pneumococcal disease
Iv fluids
Treat close contacts with oral ciprofloxacin
Notify PHE
213
Q

What is the pathaphysiology of encephalitis?

A

Inflammation of the brain. Usually caused by virus (most commonly=herpes simplex virus). Potential other viruses=mumps, measles, flu, varicella zoster virus.

214
Q

What are the symptoms of encephalitis?

A

Fever, headache, muscle aches, tired, nausea and vomiting

Meningism, coma, seizures

215
Q

How to diagnose encephalitis?

A

CT or MRI to rule out other causes and rule out signs of raised ICP

LP, bloods.

May have EEG

216
Q

How to manage encephalitis?

A

Antiviral-aciclovir without hesitation
Antibiotics if suspecting meningitis
Supportive: fluids, antipyretic, oxygen etc

217
Q

What is horner’s syndrome?

A

Disruption of sympathetic nerves supplying the eye

Triad of partial ptosis, miosis (leading to anisocoria/difference in size of pupils) and anhidrosis

218
Q

What is the presentation of horner’s syndrome?

A

Ptosis, anhidrosis, facial flushing if preganglionic lesion, orbital pain/headache is postganglionic lesion

219
Q

Name some potential causes of Horner’s syndrome

A

Central (first order) nerve lesions: stroke, MS, pituitary tumour, basal meningitis, neck trauma, syringomyelia

Preganglionic (second order) nerve lesions: apical lung tumour eg Pancoast, lymphadenopathy, lower brachial plexus trauma, aortic aneurysms, trauma to chest, neuroblastoma

Postganglionic (third order) nerve lesions: cluster headaches or migraine, herpes zoster, internal carotid dissection, temporal arteritis

220
Q

How can you test for Horner’s?

A

Cocaine eye drops- dilation of pupil normally, but no response in Horner’s syndrome
Apraclonidine-little effect on normal pupil but causes dilation of Horner’s pupil

221
Q

How can you classify strabismus?

A 
Congenital or acquired
Right, left or alternating
Permanent or intermittent
Manifest or latent
Concomitant (non-paralytic-size of deviation does not vary with direction of gaze) or incomitant (paralytic-direction of gaze does affect size)
Primary secondary or consecutive
Infantile
Situational
222
Q

How to examine for strabismus?

A

Hirschberg’s test (pen torch should be central bilaterally, if lies on inner margin of the pupil=exotropia, if on outer margin=esotropia)
Cover/uncover test
Alternate cover test

223
Q

What normally causes paralytic squint?

A

Damage to extraocular muscles of their nerves- CN III, IV, VI
Isolated nerve palsy or multiple nerves
Myopathies- tend to be bilateral

224
Q

Describe presentation of third nerve cranial palsy?

Common causes?

A

External ophthalmoplegia with partial or complete mobility problems (various degress of squint), may be internal ophthalmoplegia (partial or incomplete impairment of pupillary reactions)
Ptosis

CC: aneurysm, tumour, trauma, pituitary apoplexy, herpes zoster, leukaemia. Ischaemic microvascular disease=pupil sparing

225
Q

Describe presentation of fourth nerve palsy?

Common causes?

A

Binocular vertical diplopia, difficulty reading, sense that things are tilted

CC: trauma, vasculopathy, demyelinating disease

226
Q

Describe presentation of sixth cranial nerve palsy?

Common causes?

A

Horizontal diplopia which is worse for distance than near vision and most pronounces on lateral gaze on affected side

CC: vasculopathy and trauma, idiopathic

227
Q

What might be the cause of multiple nerve palsies causing strabismus?

A

Arteriovenous fistula, cavernous sinus tumours, pituitary apoplexy, herpes zoster, cavernous sinus thrombosis

228
Q

Differences between UMN and LMN lesions of facial nerve?

A

UMN= only affect lower face due to contralateral innervation

LMN=ipsilateral weakness of entire face

229
Q

What is the potential presentation of Bell’s Palsy?

A

Sudden weakness of one side of the face. Not forehead sparing. May have drooping of the mouth, drooling, inability to close eye, excessive tearing in one eye. May have impaired or altered sense of taste and sensitivity to loud noise

230
Q

How to manage Bell’s Palsy?

A

Try to see within 72 hours of onset. Steroids (prednisolone) and antiviral medication (aciclovir)

231
Q

What are the clinical features of facial nerve lesions?

A

Weakness of muscles of facial expression, hyperacusis, impaired corneal reflex (afferent CN V efferent CN VII), dry eyes, dry mouth, loss of taste in anterior 2/3 of tongue

232
Q

What are the symptoms of trigeminal neuralgia?

A

Episodes of brief, sharp, stabbing pain in trigeminal (usually V2 or V3) nerve distribution triggered by light touch, cold air or facial movements
Episodes last for seconds and followed by refractory period during which further attacks do not occur

233
Q

Causes of trigeminal neurlagia?

A

Classical=idiopathic
Peripheral causes= herpes zoster, trauma, cavernous sinus lesions
CNS causes=demyelination, infarction

234
Q

How to manage trigeminal neuralgia?

A

Treat underlying causes eg if due to grinding teeth, wear a mouth guard
First line=carbamazapine (not nice), nicer=amitriptyline

235
Q

What is bovine papular stomatitis?

A

A virus that affects cattle, can be transmitted to humans

236
Q

What is bulbar palsy?

A

Result of diseases affecting lower cranial nerves VII-XII. Speech deficit due to paralysis or weakness of muscles of articulation

237
Q

Causes of bulbar palsy?

A

Broad classification= muscle disorders, diseases of motor nuclei in medulla and lower pons, intramedullary nerves of spinal cord diseases, diseases of peripheral nerves supplying the muscles

Examples: diphtheria, poliomyelitis, MND, syringobulbia, brainstem tumours, GBS

238
Q

Presentation of bulbar palsy?

A

Tremulous lips, weak and wasted tongue with fasciculations, drooling, absent palatal movements, dsyphonia (rasping tone due to vocal cord paralysis, nasal tone if bilat palatal paralysis), articulation-difficulty pronouncing r sounds and progressively can’t do consonants

239
Q

What is pseudobulbar palsy?

A

Results from disease of corticobulbar tracts.

240
Q

Presentation of pseudobulbar palsy?

A

Paralysed tongue, palatal movements absent, persistent dribbling, facial muscles may also be paralysed, exaggerated reflexes, nasal regurg, dysphonia, dysphagic, emotional lability may be present

241
Q

Causes of pseudobulbar palsy?

A

Cerebrovascular events, demyelinating disorders, MND, high brainstem tumours, head injury, neurosyphilis

242
Q

What is sciatica?

A 
Sciatic nerve (L4-S3) irritated or compressed 
Pain radiating along path of sciatic nerve, branching from lower back down through hips, buttocks and down leg. 
Commonly due to herniated disk or bone spur or spinal stenosis
243
Q

Symptoms of sciatica?

A

Pain radiating from lumbar spine to buttock and down back of leg, to a level below the knee, sometimes felt in foot and great toe.
Some may experience numbness, tingling or muscle weakness. Prolonged sitting can aggravate. Normally unilateral.

244
Q

How to manage sciatica?

A

Exercises and stretches. Physiotherapy.

Consider analgesia- NSAIDs or may need specific treatment for neuropathic pain eg gabapentin or amitriptyline

245
Q

Define radiculopathy?

A

Condition due to compressed nerve in the spine

246
Q

What is sciatica?

A 
Sciatic nerve (L4-S3) irritated or compressed 
Pain radiating along path of sciatic nerve, branching from lower back down through hips, buttocks and down leg. 
Commonly due to herniated disk or bone spur or spinal stenosis
247
Q

Symptoms of sciatica?

A

Pain radiating from lumbar spine to buttock and down back of leg, to a level below the knee, sometimes felt in foot and great toe.
Some may experience numbness, tingling or muscle weakness. Prolonged sitting can aggravate. Normally unilateral.

248
Q

How to manage sciatica?

A

Exercises and stretches. Physiotherapy.

Consider analgesia- NSAIDs or may need specific treatment for neuropathic pain eg gabapentin or amitriptyline

249
Q

Define radiculopathy?

A

Condition due to compressed nerve in the spine

250
Q

What causes spinal stenosis?

A

Natural ageing process normally-degenerative changes leading to partial constriction

251
Q

What do patients with spinal stenosis normally complain of?

A

Back and leg pain on walking, numbness or weakness, both legs or just one.
Classically can walk 50-500m and then have to stop as pain and numbness gets worse.
Improvement on sitting down or leaning forward
Normally no pain in the leg at rest

252
Q

How to manage spinal stenosis?

A

First: simple analgesia, improve mobility/strength/fitness, weight loss if applicable, walking as best as possible, static bike cycling, may need neuropathic analgesia

Second: may need spinal injections, nerve blocks, consider surgery

253
Q

What is anterior cord syndrome?

A

Incomplete cord syndrome predominantly affecting anterior 2/3 of spinal cord

Motor paralysis below level of lesion and loss of pain and temperature at and below level of lesion. Fine touch/vibration/proprioception spared

Normally due to ischaemia of that portion due to anterior spinal artery reduced blood flow- commonly aortic surgery

254
Q

What is brain herniation?

A

Life-threatening condition with shift of brain tissue into adjacent space due to mass effect

Different patterns: subfalcine, transalar, transtentorial (uncal and central, ascending), tonsillar, extracranial, paradoxical

255
Q

What could cause brain herniation?

A 
Any intracranial mass:
intracranial haemorrhage (extradural, subdural, intracerebral), cerebral swelling (infarction, periabscess oedema), tumours, cerebral abscess
256
Q

If signs of raised ICP, should you do a LP?

A

NO- can lead to herniation!! Acute pressure gradient resulting in downwards displacement of cerebrum and brainstem

257
Q

Difference between coma and stupor?

A

Coma= unrepsonsive, unrousable state

Stupor= unresponsive, rousable state

258
Q

Potential causes of coma

A

Post-ictal
Anoxic
Metabolic-hypoglycaemia, hyponatraemia, acidaemia, uraemia, liver failure, myxoedema, Wernicke encephalopathy
Toxic-opiates, benzos, tricyclics, alcohol, neuroleptics
Coma with focal signs: vascular event
Coma with signs of meningism: SAH, meningitis, encephalitis

259
Q

How to initially assess coma?

A 
Resuscitation: Airway and C spine
Breathing
Circulation
Diabetes ( 50ml 50% dextrose, consider thiamine if suspicious of Wernicke's)
Drugs (consider naloxone)
Epilepsy (if ongoing, lorazepam)
Fever (meningitis, encephalitis?)
GCS
Herniation (evidence of coning-pupil, check tone and reflexes in all 4 limbs)
Investigate
260
Q

What will opiate misuse pupils look like?

A

Pinpoint, equal ,unreactive

261
Q

What will a pontine lesion pupils look like?

A

Pinpoint, equal

262
Q

What will metabolic encephalopathy pupils look like?

A

Small and reactive, equal

263
Q

Symptoms of a brain abscess?

A 
May develop quickly or slowly 
Headache (severe, localised, can't be relieved by pain killers)
Changes in mental state eg confusio
Nerve function- weakness, slurred speceh or paralysis
Fever
Seizures
Nausea and vomiting
Stiff neck
Visual changes

NEUROLOGICAL EMERGENCY

264
Q

What causes of brain abscess?

A

Infection in the skull- half the cases; persistent otitis media, sinusitis or mastoiditis

Infection through bloodstream (1 in 4 cases), immunocompromised especially. Cyanotic heat disease, pulmonary AV fistula, dental abscess, lung infections, endocarditis, peritonitis, cystitis

Infection after a head injury- (1 in 10 cases)- skull fracture due to penetrating injury, gunshot/shrapnel wound

rarely a complication of neurosurgery

265
Q

How to treat a brain abscess?

A

IV antibiotics or antifungal if several absecesses, small (<2cm), deep, menigitis coexisting, hydrocephalus

Surgery and then antibiotics after : simple aspiration (burr hole using CT scan) or craniotomy

266
Q

Describe steroid myopathy?

Management?

A

Arms, legs and pelvis symmetrically affected most
Increasing intolerance to exercise as muscles weaken with use and pain increases

Mx: reduce or stop steroids. Increase muscle strength. If not possible to stop, switch fluorinated steroids eg dexamethasone to nonflourinated eg prenisone

267
Q

What are the inflammatory myopathies?

A

Chronic (long-standing) muscle inflammation, muscle weakness and sometimes muscle pain

Polymyositis, dermatomyositis, inclusion body myositis, necrotising autoimmune myopathy

268
Q

Describe polymyositis

A

Affects skeletal muscle, bilaterally. Onset normally between 30 and 60.

Variable presentation. Untreated may lead to issues with swallow, speaking, rising from seated, climbing stairs, lifting objects

269
Q

Describe dermatomyositis

A

Skin rash (patchy, purple or red) preceding or accompanying progressive muscle weakness

Rash usually on eyelids or on muscles used to extend joints

270
Q

Describe inclusion body myositis

A

Most common form of inflammatory myopathy in people over 50, more common in men

Slow progressive muscle weakness and wasting of proximal and distal muscles (typically thighs and forearms), bilat usually. Multi-protein aggregates

Falling and tripping usually first noticeable symptoms. Weakness in wrists and fingers. Difficulty swallowing in half of cases.

271
Q

Describe necrotising autoimmune myopathy

A

Weakness in upper and lower body. Similar to polymyositis and dermatomyositis.

Occurs alone or after viral infections, a/w cancer, in connective tissue disorders or in statins

272
Q

How to diagnose inflammatory myopathies?

A

Bloods-muscle enzymes and autoantibodies, physical exam, biopsy

273
Q

How to manage chronic inflammatory myopathies?

A

Cannot be cured but symptomatic management- medication, physical therapy, exercise, heat therapy, orthotics and assistive devices, rest

High dose steroids. May consider immunosuppressants

274
Q

Name 2 metabolic myopathies

A

Myopathies due to something lacking-rare

Carnitine deficiency, lactate dehydrogenase deficiency, phosphoglycerate kinase deficiency,

275
Q

Describe myotonic dystrophy

A

Genetic condition causing progressive muscle weakness and wasting

Typically affects skeletal muscle and commonly electrical conduction system of heart, resp, swallow, bowel etc

276
Q

Describe statin induced myopathy

A

Spectrum: myalgia, myositis, rhabdomyolysis, asx increase in concentration of creatine kinase

Commonly: fatigue, flu-like symptoms, nocturnal cramping

277
Q

Describe muscular dystrophy

A

Inherited diseases with a lack of dystrophin- causes problems with walking, swallowing and muscle coordination

278
Q

Name some of the better known muscular dystrophies

A

Duchenne, Becker, congenital, myotonic, limb-girdle, facioscapulohumeral (FSHD), emery-dreifuss, distal muscular

279
Q

What are the symptoms of poliomyelitis?

A

Flu-like illness 3 to 21 days after infection

Polio virus can attack nerves in spine and base of brain, causing paralysis usually in legs

280
Q

Potential long term problems of polio

A

Muscle weakness, atrophy, contractures, deformities

281
Q

Describe the cervical dermatomes

A

c2= temple and forehead
c3=neck, posterior cheek
c4= shoulder, clavicle, upper scapula
c5=deltoid, anterior aspect of arm and base of thumb
c6=anterior arm, radial side of and to thumb and index finger
c7=lateral arm and forearm to index, long and ring fingers
c8=medial arm and forearm to fingers (long, ring, little)

282
Q

Describe the thoracic dermatomes

A

t1=medial side of forearm to base of little finger
t2=medial side of upper arm to medial elbow
t3-t6=upper thorax
t5-t7=costal margin
t8-t12=abdomen and lumbar region

283
Q

Describe the lumbar dermatoms

A

l1=back, trochanter and groin
l2=back, front of thigh to knee
l3=back, upper buttock, anterior thigh and knee, medial lower leg
l4=medial buttock, lateral thigh, medial leg, dorsum of foot, big toe
l5=buttock, posterior and lateral thigh , lateral leg, dorsum of foot, medial half of sole, first/second/third toes

284
Q

describe the sacral dermatomes

A

s1=buttock, thigh and posterior leg
s2=buttock, thigh and posterior leg
s3=groin, medial thigh to knee
s4=perineum, genitals, lower sacrum

285
Q

myotome c5 action?

A

shoulder abduction

286
Q

what myotome for elbow flexion and wrist extension?

A

c6

287
Q

c7 myotome action?

A

elbow extension

288
Q

What myotome for finger flexion?

A

c8

289
Q

what does t1 do?

A

finger abduction

290
Q

myotome for hip flexion?

A

l2

291
Q

myotome for knee extension?

A

l3

292
Q

myotome l4 action?

A

ankle dorsiflexion

293
Q

myotome l5 action?

A

great toe extension

294
Q

what does s1 do?

A

ankle plantarflexion

295
Q

What are potential causes of myopathies?

A

steroids, inflammatory, metabolic, myotonic, statin, muscular dystrophy, polio

296
Q

Describe primary lateral sclerosis

A

Loss of cells in the motor cortex. UMN signs only

297
Q

Describe progressive muscular atrophy

A

LMN only, distal before proximal muscles affected. Has the best prognosis for MND

298
Q

Describe progressive bulbar palsy

A

CN ix-xii affected= palsy on tongue, muscles of chewing and facial muscles affected due to loss of function of brainstem nuclei. Carries worst prognosis

299
Q

What are these repeats for?

GAA, CTG, CGG, CAG

A

GAA=Friedrich’s ataxia
CTG=myotonic dystrophy
CGG=fragile X syndrome
CAG=Hungtington’s

300
Q

What are the features of Parkinson’s plus syndromes?

A

Bilateral, symmetrical symptoms, eye signs=progressive supranuclear palsy (impaired vertical gaze, nasal donald-duck voice secondary to pseduobulbar palsy, increaseing frequency of falls)

301
Q

What is transient global amnesia? How to manage?

A

Transient loss of memory function, repeatedly ask the same question, no recall of events after the attack
Unknown aetiology
Mx= reassurance

302
Q

Describe an essential tremor

A

Most common cause of titubation
Relieved by alcohol and sleep. Worse on movement and during stress
Can be fh (autosomal dominant)

303
Q

Management of essential tremor

A

Propranolol first line

Primidone can be used

304
Q

Potential causes of chorea

A

HD, SLE, pregnancy, thyrotoxicosis, wilson’s disease, ataxic telangiectasia, anti-phospholipid, oral contraceptive pill, l-dopa, antipsychotics

305
Q

How to differentiate between essential tremor and pd?

A

DAT scan

306
Q

What are the autonomic symptoms that can be experienced in PD?

A

orthostatic hypotension, constipation, N/V, urinary symptoms, seborrhoea, heat intolerance, sexual dysfunction, hypersalivation, sweating

307
Q

Features indicative of idiopathic intracranial htn

A

BMI (obese), symptoms of raised ICP

308
Q

What drug in brain herniation

A

Mannitol

309
Q

Low GCS, slow breathing, pin point pupils?

Management?

A

Opiate OD

Naloxone (short half life)

310
Q

Low GCS, slow breathing, normal pupils?

Management?

A

Benzo OD

Flumazenil (huge caution in epilepsy)

311
Q

Pupils big and arrhythmia?

A

Tricyclic OD

No specific treatment

Phase 3A (8 decks)

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