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Phase 3 > Neurology > Flashcards

Neurology Flashcards

1
Q

List risk factors for stroke

A

Hypertension

Diabetes

Atrial fibrillation

Smoking

Hyperlipidaemia

Sleep apnoea

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2
Q

Describe the different types of stroke

A

Ischaemic – blockage of blood vessels (85%)

Haemorrhagic – burst blood vessels (15%)

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3
Q

Describe the clinical presentation of large vessel stroke

A
  • Cortical signs
    > Right brain: right gaze preference, neglect
    > Left brain: left gaze preference, aphasia
  • MCA
    > Arm > leg weakness

> LMCA: aphasia

> RMCA
> Neglect
> Topographical difficulty
> Apraxia
> Constructional impairment
> Anosognosia (lack of insight - doesnt uderstand or perceive illness)

  • ACA
    > Leg > arm weakness, grasp
    > Muteness, perseveration (stay on same thought), abulia (lack of willpower)
    > Personality change
  • PCA
    > Contralateral hemianopia
    > Memory loss/confusion
    > Ataxia
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4
Q

Describe the clinical presentation of a small vessel stroke

A

Lenticulostriate perforating arteries supplying deep white matter

No cortical signs

Cause sensory or motor loss, or both

Equally distributed - lacunar syndromes

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5
Q

Describe the clinical presentation of a posterior circulation stroke

A

Crossed signs

Cranial nerve findings

Headache

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6
Q

Describe brainstem stroke syndromes

A

Combination of cranial nerve abnormalities and crossed motor/sensory findings e.g.

> Double vision - diplopia

> Facial numbness or weakness (CN V)

> Slurred speech

> Difficulty swallowing

> Ataxia

> Vertigo

> Nausea and vomiting

> Hoarseness

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7
Q

Describe the causes of haemorrhagic strokes

A
  • Uncontrolled hypertension

> Spontaneous rupture of a small artery deep in the brain
Typically in the basal ganglia

  • Aneurysm
  • Arteriovenous malformation (AVM)
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8
Q

Describe the acute treatment of ischaemic stroke

A

tPa – tissue plasminogen activator (alteplase)
> Must be used within 4.5 hours of onset
>Reduces disability risk by 30% but an ICH risk

Mechanical clot retrieval - thrombectomy

Aspirin
Double statin dose

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9
Q

What are the contraindications for the use of tPa

A

Haemorrhage

SBP > 185 or DBP > 110

Recent surgery, trauma or stroke

Coagulopathy

Seizure at onset of symptoms

NIHSS > 21

Age > 80

Glucose < 2.2

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10
Q

Describe the pathophysiology of MS

A

Idiopathic inflammatory demyelinating disease of the CNS

Acute episodes of inflammation are associated with focal neurological deficits

Demyelination results in loss of neurological function

> Weak leg
Visual loss
Urinary incontinence

Deficits usually develop gradually, last more than 24h and may gradually improve over days to weeks

MS is diagnosed when there is evidence of 2 or more episodes of demyelination disseminated in space and time

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11
Q

Describe the subtypes of MS

A
  • Relapsing remitting Multiple Sclerosis (RRMS)
    > Unpredictable attacks which may or may not leave permanent deficits followed by periods of remission
  • Primary progressive multiple sclerosis (PPMS)
    > At least 1 year of disease progression
    > Steady increase in disability without attacks
  • Secondary progressive multiple sclerosis (SPMS)
    > Initial relapsing-remitting multiple sclerosis
    > Suddenly begins to decline without periods of remission
  • Benign multiple sclerosis (BMS)
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12
Q

Describe the causes of MS

A

Genetics

Sunlight / vitamin D exposure

Viral trigger – EBV

Multifactorial – smoking

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13
Q

Which syndromes may develop into MS?

A
  • Optic neuritis
    > Painful visual loss that comes on after a few days
    > Can resolve after a few weeks
    > 30% will develop MS within 5 years, 15% within 15 year
  • Clinically isolated syndromes
    > Single episode of neurological disability due to focal inflammation of brain or spinal cord
    > Can be a first attack of MS or be due to infection
    > Can include optic neuritis and transverse myelitis
  • Transverse myelitis
    > Inflammation of the spinal cord
    > Leg weakness, sensory loss, incontinence, sexual dysfunction
    > Causes: MS, viral infections
  • Radiologically isolated syndromes
    > Incidental findings that look like MS; may or may not develop MS
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14
Q

Describe the investigations used in MS

A
  • MRI brain + cervical spine with gadolinium contrast

> Dawson’s finger: radiographic feature of demyelination, reflects perivenular inflammation

> Evidence of demyelination in 2 regions e.g. periventricular and spinal cord - dissemination in space

> If enhancing and non-enhancing areas of demyelination – dissemination in time

  • Lumbar puncture
    > Oligoclonal bands in CSF
  • Bloods (exclude other conditions)
    > B12/folate
    > Serum ACE (sarcoidosis)
    > HIV, Lyme and syphilis serology
    > ESR/CRP
    > ANA/ANCA/RF
    > Aquaporin-4 antibodies: if transverse myelitis / optic neuritis
    > Calcium (sarcoidosis)
  • Visual evoked potentials
    > Measure conduction of nerve signals in optic nerve to identify subclinical optic neuritis
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15
Q

What is the definition of a relapse and a pseudorelapse in MS?

A

Relapse
> New neurological deficit lasting >24h in the absence of pyrexia or infection

Pseudo-relapse
> Reemergence of previous neurological symptoms or signs related to an old area of demyelination in the context of heat or infection

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16
Q

What is the steroid regime for an MS relapse?

A

1g of IV methylprednisolone for 3 days OR

500mg of oral methylprednisolone for 5 days and

PPI for gastroprotection

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17
Q

Describe treatments for MS

A

RRMS
> Alemtuzumab
> Natalizumab
> Anti-CD20: ocrelizumab, ofatumumab, rituximab
> Fingolimod
> Dimethyl fumarate
> Cladribine
> Stem cell transplants

Progressive MS
> PPMS - ocrelizumab
> SPMS - siponimod

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18
Q

Describe a relative afferent pupillary defect (RAPD) and its causes

A

Aka Marcus Gunn Pupil

Pupil remains dilated in one eye despite exposure to bright light – swinging light test

Shows unilateral optic nerve or retinal dysfunction

Causes

  • Disease of retina

> Retinal detachment

> > Floaters
Flashes of light
Shadow in vision field

> Retinal ischaemia

  • Optic nerve disease

> Optic neuritis

> > Pain with eye movement
Loss of vision

> Inflammation from multiple sclerosis

  • Severe glaucoma

> Headaches
Nausea/vomiting
Eye redness
Blurred vision

  • Trauma
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19
Q

List the different types of primary and secondary headaches

A

Primary
- Migraine
- Tension headaches
- Trigeminal autonomic cephalgias

Secondary
- Thunderclap headaches
- High pressure headaches
- Low pressure headaches
- Neuralgias

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20
Q

Describe tension type headaches

A

At least 10 episodes of headache occuring on <1 day/month on average

Lasting from 30 minutes to 7 days

Characteristics
> Bilateral location
> Pressing or tightening (non-pulsating) quality
> Mild or moderate intensity
> Not aggravated by routine physical activity

> No nausea or vomiting

> No more than one of photophobia or phonophobia

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21
Q

Describe the pathophysiology of migraine

A

Interaction between primary afferent nociceptive neurons / trigeminovascular system / brainstem / thalamus / hypothalamus / cortex

Calcitonin gene related peptide (CGRP)

Not a primary vascular problem

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22
Q

Describe the diagnostic criteria for migraine

A

At least 5 attacks

Headache attacks lasting 4-72h when untreated

Characteristics
- Unilateral location
- Pulsating quality
- Moderate or severe pain intensity
- Aggravated by routine physical activity

At least one of the following
- Nausea and/or vomiting
- Photophobia and phonophobia

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23
Q

Describe the phases of migraine

A

Prodrome: hours-days

  • Yawning
  • Polyuria
  • Depression
  • Irritability
  • Food cravings
  • Poor concentration
  • Sensitivity to light and sound
  • Poor sleep

Aura: 5-60m
- Visual
- Sensory
- Language
- Motor

Headache: 4-72h
- Throbbing headache
- Nausea
- Vomiting
- Photophonophobia
- Worse with activity

Postdrome: 24-48h
- Depression
- Euphoria
- Poor concentration
- Fatigue

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24
Q

Describe the acute treatment of migraine

A

Avoid opiates

Simple analgesics – aspirin 900mg or ibuprofen 400-600mg

Triptans
> Sumatriptan 50-100mg
> All oral triptans are gastrically absorbed – may not work if patient is vomiting
> Only work once headache starts

Early or persistent vomiting
> Add antiemetic – metoclopramide 10mg or prochlorperazine 10mg
> Consider nasal zolmitriptan or subcutaneous sumatriptan

No response
> Try other triptans OR triptan + NSAID

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25
Q

Describe migraine prophylaxis

A

Lifestyle advice, triggers

Prophylaxis if >4-5 disabling headaches per month

Use headache diaries

For each medication, determine efficacy at 3 months
> If ineffective, wean medication and try another one
> If effective, continue 6-12 months

Agents
> Propranolol
> Topiramate
> Amitriptyline
> Candesartan
> Flunarazine

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26
Q

Describe the treatment of refractory or chronic migraine

A

Onabotulinumtoxin A

> Chronic migraine
>15 headache days per month
MOH previously addressed
Failed on at least 3 prophylactics

CGRP inhibitors – monoclonal antibodies
> Erenumab

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27
Q

Describe cluster headaches

A

At least 5 attacks

Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes when untreated

Signs ipsilateral to the headache
> Conjunctival injection or lacrimation
> Nasal congestion or rhinorrhoea
> Eyelid oedema
> Forehead and facial sweating
> Forehead and facial flushing
> Sensation of fullness in the ear
> Miosis or ptosis

Sense of restlessness or agitation

Occurring with a frequency between one every other day and 8 per day

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28
Q

Describe trigeminal neuralgia including its treatment

A

One-sided intense, stabbing paroxysmal facial pain

Triggered by wind, chewing, touch

Other symptoms
- Facial muscle spasms
- Autonomic symptoms
> Lacrimation
> Diffuse conjunctival injection
> Rhinorrhoea

Investigations

> MRI
> Trigeminal nerve distorted and compressed by superior cerebellar artery

Treatment
> Carbamazepine
> Surgical microvascular decompression

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29
Q

Describe raised pressure headaches

A

Characteristics

> Worse on lying flat

> Improve on sitting up

> Worse in the morning

> Persistent nausea/vomiting

> Worse on valsalva e.g. coughing, laughing, straining

> Worse with physical exertion

> Transient visual obscurations with change in posture

Examination findings

> Optic disc swelling – papilloedema

> Impaired visual acuity / colour vision

> Restricted visual fields / enlarged blind spot

> IIIrd nerve palsy

> VIth nerve palsy – false localising sign

> Focal neurological signs

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30
Q

Describe thunderclap headache including causes

A

First and worst headache – subarachnoid haemorrhage

Severe sudden onset headache

Typically maximum onset within 1 minute, typical duration >1h

Medical emergency, same day specialist assessment

Non-contrast CT scan (NCCT) within 12h onset
> If CT normal, lumbar puncture
> For blood products – oxybilirubin

If CT/LP normal consider other investigations
> MRI
> MR/CT venogram
> MR/CT angiogram

Causes

  • Subarachnoid haemorrhage
  • Intracerebral haemorrhage
  • Aortic dissection – vertebral or carotid
  • Cerebral venous sinus thrombosis
  • Ischaemic stroke
  • Bacterial meningitis
  • Spontaneous intracranial hypotension
  • Pituitary apoplexy
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31
Q

Describe the course, tract and pathology associated with the olfactory nerve

A

Smell

Course
> Travels through the ethmoid bone and lays upon the cribriform plate
> Arises from the cerebrum

Tract
> Olfactory cells of nasal mucosa
> Olfactory bulbs
> Pyriform cortex – temporal lobe, near hippocampus

Pathology
> Hyposmia
> Normal ageing
> Viral URTI
> Chronic rhinitis or sinusitis
> Head trauma
> Neurodegenerative disorders – Parkinson’s, Alzheimer’s

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32
Q

Describe the function and tract associated with the optic nerve

A

Vision

Enter: optic canal
Arises from the cerebrum

Tract
> Retinal ganglion cells
> Optic chiasm
> Thalamus
> Primary visual cortex – occipital lobe

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33
Q

Describe the examination of the optic nerve

A

Optic discs with ophthalmoscope
> Papilloedema: raised ICP
> Optic atrophy: previous optic neuritis

Pupillary reflexes
> Direct and consensual light reflexes
> Swinging light test for RAPD
> Accommodation reflex

Visual acuity - Snellen chart

Visual fields and blind spot: confrontation

Colour vision: Ishihara colour plates

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34
Q

Describe the physiology of the pupillary light reflex

A

Light is shone into the the left eye and the travels via the optic tract and synapses at the pretectal nucleus

Interneurones then synapse with both Edinger-Westphal nuclei

Post-ganglionic fibres run with ciliary nerves and terminate on sphincter pupillae

Pupillary constriction in both eyes (direct and indirect) when a light is shone in one

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35
Q

Describe different types of visual field defects

A

Optic - ipsilateral monocular visual loss

Optic chiasm - bitemporal hemianopia

Optic tract - contralateral homonymous (affecting both visual fields) hemianopia

Parietal upper optic radiation - contralateral homonymous inferior quadrantanopia

Temporal lower optic radiation - contralateral homonymous superior quadrantanopia

Occipital visual cortex - contralateral homonymous hemianopia (macular sparing)

Most common tumours impacting anterior visual pathways
> Pituitary adenoma
> Meningioma
> Craniopharyngioma

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36
Q

Describe eye muscles and movements associated with them, as well as their assessment

A

Assessment – smooth pursuit – draw H shape in the air

Oculomotor nerve

> Superior rectus
> Elevation of eyeball
> Also adduction and medial rotation

> Inferior rectus
> Depression of eyeball
> Abduction and lateral rotation

> Medial rectus
> Adducts the eyeball

> Lateral rectus
> Abducts the eyeball

> Inferior oblique
> Elevation of the eyeball
> Abduction and lateral rotation

Trochlear nerve

> Superior oblique
> Depression of eyeball
> Abduction and medial rotation

> Abducens nerve
> Lateral rectus

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37
Q

Describe the function and tract of the oculomotor nerve

A

Eye movements
> Inferior oblique
> Superior, medial and inferior rectus

Levator palpebrae superioris – keeps upper eyelid open

Lens accommodation: ciliary muscles

Pupil constriction - parasympathetic
> Ciliary muscles and sphincter pupillae

Arises from the midbrain-pontine junction

Nucleus

> Motor
> Located in the midbrain at the level of the superior colliculus

> Parasympathetic
> Dorsal midbrain – Edinger Westphal nucleus

Exit: superior orbital fissure
> Exits brainstem from the interpeduncular fossa of the midbrain
> Passes through cavernous sinus
> Enters orbit through superior orbital fissure

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38
Q

Describe complete 3rd nerve palsy

A

Ptosis

Pupillary dilatation

Eye in a “down and out” position

Due to unopposed actions of lateral rectus and superior oblique

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39
Q

Describe the function and location of the trochlear nerve

A

Eye movements - superior oblique

Arises from the midbrain
> Level of inferior colliculus

Exit: superior orbital fissure

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40
Q

Describe the function of the trigeminal nerve and its location

A

Arises from pons

3 branches

  • V1 - ophthalmic nerve

> Branches
> Supraorbital nerve
> Nasociliary nerve
> Ciliary branches supply the cornea

> Exit: superior orbital fissure

> Enter: supraorbital foramen

  • V2 - maxillary nerve

> Exit: foramen rotundum
Enter: infraorbital foramen

  • V3 - mandibular nerve

> Exit: foramen ovale
> V3 meningeal branch exits through foramen spinosum

> Enter: mental foramen

> Muscles of mastication:
> Temporalis
> Masseter
> Pterygoids

> Motor to muscles of mastication and general sensory to face

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41
Q

Describe the function and location of the abducens nerve

A

Eye movement (abduction - lateral rectus)

Arises from the pontine-medulla junction

Exit: superior orbital fissure

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42
Q

Describe the function and location of the facial nerve

A

Muscles of facial expression
> Frontalis
> Orbicularis occuli
> Orbicularis oris

Supplies secretory glands
> Sublingual & submandibular glands
> Lacrimal glands

Supplies taste of anterior 2/3 of the tongue

Corneal reflex
> Lightly touch cornea with cotton wool
> Afferent – CN V
> Efferent – CN VII
> Normal response is blinking
> May be lost in pontine lesions

Arises from the pontine-medulla junction

Enter: internal acoustic meatus

Exit: stylomastoid foramen

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43
Q

Describe the location and function of the vestibulocochlear nerve

A

Arises from the pontine-medulla junction

2 nerves

> Vestibular nerve - balance
> Nerve endings within semicircular canals
> Reach cerebellum and spinal cord

> Cochlear nerve - hearing
Reaches auditory cortex in the temporal lobes

Enter: internal acoustic meatus

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44
Q

Describe the testing of the vestibulocochlear nerve

A

Rinne’s test

> Tuning fork is held at the mastoid process and then at the external auditory meatus

> Patient is asked which is louder

BC > AC – conductive deafness

AC > BC – normal or sensorineural deafness

Weber’s test

> Tuning fork is held at the vertex
Patient is asked which ear they hear the vibration loudest in

Normal – same in both ears

Conductive hearing loss – deaf ear

Sensorineural hearing loss – good ear

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45
Q

Describe the function and location of the glossopharyngeal nerve

A

Sensory
> Taste – posterior 1/3 of tongue
> Proprioception for swallowing – pharyngeal wall
> Blood pressure receptors – carotid sinuses

Motor
> Swallow and gag reflex – pharyngeal muscles
> Lacrimation – lacrimal glands

Parasympathetic
> Saliva production – parotid glands

Originates from the medulla, posterior to the olive

Exit: jugular foramen

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46
Q

How is the glossopharyngeal nerve tested?

A

Motor

Ask patient to open mouth and say “ahh”

Watch for elevation of the soft palate

Unilateral weakness of CN IX – deviation of uvula away from the lesion – glossopharyngeal palsy

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47
Q

Describe the function and location of the vagus nerve

A

Sensory

> Chemoreceptors
> Blood oxygen concentration
> Carotid bodies

> Pain receptors (dura)
> Respiratory and digestive tracts

> Sensation
> External ear, larynx and pharynx

Motor

> Heart rate and stroke volume
> Pacemaker and ventricular muscles

> Peristalsis
> Smooth muscles of the digestive tract

> Air flow
> Smooth muscles in bronchial tubes

> Speech and swallowing
> Muscles of larynx and pharynx – recurrent laryngeal nerve

Parasympathetic

> Smooth muscles and glands of the same area innervated by the motor component, as well as thoracic and abdominal areas

Exit: jugular foramen

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48
Q

Describe the function and location of the spinal accessory nerve

A

Exit: jugular foramen

Neck muscles
- Sternocleidomastoid
- Trapezius

Head rotation and shoulder shrugging

Originates from medulla, posterior to the olive

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49
Q

Describe the location and function of the hypoglossal nerve

A

Motor – speech and swallowing

> Muscles of the tongue

Originates from medulla, anterior to the olive

Exit: hypoglossal canal

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50
Q

Describe a hypoglossal nerve palsy

A

Observe the tongue at rest and ask patient to stick out their tongue & move it from side to side

Unilateral/bilateral wasting or fasciculations (at rest)

Unilateral XIIth weakness causes the tongue to deviate towards the side of the lesion

Slow and spastic tongue movements suggest pseudobulbar palsy

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51
Q

Describe internuclear ophthalmoplegia

A

Disorder of conjugate gaze

Failure of adduction of affected eye with nystagmus on lateral gaze in contralateral eye

Can be unilateral or bilateral

Results from lesion of medial longitudinal fasciculus – connects IIIrd and VIth nerve nuclei

Commonly seen in multiple sclerosis (MS)

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52
Q

Describe Horner’s syndrome and its causes

A

Ipsilateral disruption of cervical / thoracic sympathetic chain

Causes
> Congenital
> Brainstem stroke
> Cluster headache
> Apical lung tumour
> Multiple sclerosis
> Carotid artery dissection
> Cervical rib
> Syringomyelia

Consists of
> Miosis
> Ptosis
> Apparent enophthalmos
> Anhydrosis

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53
Q

Describe herpes zoster ophthalmicus

A

Pain may precede vesicles

Shingles affects ophthalmic division of trigeminal nerve
> V2/V3 rarely affected

Elderly and immunocompromised at risk

Treated with oral aciclovir

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54
Q

Describe the radiological appearance of different types of brain haemorrhages

A

Extradural

  • Lenticular or “lens” shape - between dura and bone

Subdural

  • Scalloped appearance; can have layers depending on freshness of bleed

Subarachnoid

  • Blood between sulci
55
Q

Describe Denis’ 3 columns of spinal injury

A

To determine spinal stability: if 1 or more affected, unstable

Anterior
> Anterior longitudinal ligament
> Anterior annulus
> Anterior 2/3 vertebral body

Middle column
> Posterior 1/3 vertebral body
> Posterior annulus
> Posterior longitudinal ligament

Posterior column
> Posterior elements: pedicles, facets, laminae, spinous process
> Posterior ligaments

56
Q

Describe the functions of the different lobes of the brain

A

Frontal lobe

> Emotions
Mood
Insight
Cognitive and creative function
Primary motor area separated from parietal lobe by central sulcus

Parietal lobe

> Sensation
Coordination of signals from other cortices
Primary sensory area separated from frontal lobe by central sulcus

Occipital lobe

> Vision

Temporal lobe

> Memory
Gustatory function
Smell
Hearing

57
Q

List the components of the basal ganglia

A

Basal ganglia
> Caudate nucleus
> Striatum
> Globus pallidus externa and interna
> Substantia nigra pars compacta and pars reticulata
> Subthalamic nucleus

58
Q

Describe the anatomy of the ventricular system

A

Lateral two ventricles
> Each one has a
» Frontal horn
» Temporal horn
» Occipital horn

> Come close together in the midline but are separated by the septum pellucidum

> Connect with third ventricle via interventricular foramina of Munro

3rd ventricle
> Narrow space lying in the diencephalon between thalamus and hypothalamus
> Connects to 4th ventricle via aqueduct of Sylvius (midbrain)

4th ventricle
> Lies in the posterior fossa between brainstem and cerebellum
> Communicates with subarachnoid space via lateral foramina of Luschka and median aperture of Magendie

Most CSF produced by choroid plexus in lateral ventricle, some in 4th ventricles

59
Q

Lis the functions of the CSF

A

Cushions brain against impact/movement and own weight

Provides stable chemical environment for brain

Nutrient & waste exchange between nervous tissue and blood

60
Q

Describe the flow of CSF through the ventricular system

A

Fills lateral ventricles then flows centrally (third ventricle) via the intraventricular foramen of Munro

Then, CSF flows through aqueduct of midbrain and opens up into fourth ventricle

4th ventricle is anterior to the cerebellum and posterior to the pons

Resorbed into venous system via arachnoid granulations

Presence of blood in CSF indicates subarachnoid haemorrhage

61
Q

Describe the areas if the brain responsible for speech and comprehension

A

Wernicke’s area – hearing and understanding speech
> Receptive dysphasia

Broca’s area – speech production
> Expressive dysphasia

Connected via the arcuate fasciculus

62
Q

Describe the anatomy of the spinal cord

A
  • Cervical enlargement
  • Lumbosacral enlargement
  • Cone-shaped ending of spinal cord - conus medullaris
  • End of spinal cord L1/L2 - filum terminale
  • Cauda equina - free nerves
63
Q

List the different sensory and motor tract

A

Light touch, vibration, proprioception – dorsal column medial lemniscal pathway

Pain, temperature – spinothalamic tract

Corticospinal tract - motor tracts
> Fasciculus gracilis - lower limb
> Fasciculus cuneatus - upper limb

64
Q

Describe patterns of sensory loss

A

Generalised peripheral neuropathy – glove and stocking distribution

Specific sensory roots – dermatomal distribution

Single dorsal column lesion – unilateral distribution below level of injury

Transverse thoracic spinal cord lesion – bilateral distribution below level of injury

Unilateral cord lesion (Brown Sequard): ipsilateral loss of light touch and vibration, contralateral loss of pain sensation

Central cord lesion: arm and chest distribution

Mid-brainstem lesion: ipsilateral loss of sensation in face, contralateral loss of sensation in body

Hemisphere (thalamic) lesion: ipsilateral loss of sensation in face and body

65
Q

Describe the knee jerk reflex

A

Striking the patellar tendon causes stretching of the quadriceps muscle

Afferent signal sent through sensory neurons up through dorsal root ganglion

Enters dorsal horn, synapse onto motor neuron
Efferent signal causes contraction of quadriceps

Afferent signal also works through interneuron to have an inhibitory effect on motor neuron going to hamstring

Relaxation of hamstrings

Sensory neuron involved in reflex arc also synapses with an inhibitory interneuron

This neuron synapses ipsilaterally with a motor neuron controlling antagonistic muscles

Antagonistic muscles are relaxed, resulting in contraction of other muscle group - reciprocal innervation

66
Q

Describe the reinforcement of reflexes

A

Jendrassik manoeuvre - teeth clenching or pulling interlinked fingers in opposite directions

Combination of distraction and cortical inhibition from anterior horn cells

67
Q

List the root levels for each reflex

A

Jaw jerk - cranial nerve V

Biceps - C5/6

Tricep C6/7

Supinator C5/6

Knee L3/4

Ankle S1

68
Q

Describe the differences between upper and lower motor neuron problems

A

Upper motor neuron
> Increased / “brisk”
> Localises to brain or spinal cord

> Associated with
> Increased tone
> Extensor plantar response

Lower motor neuron
> Decreased or absent
> Localises to peripheral nerve

> Associated with
> Normal or decreased tone
> “Mute” or flexor plantar response

69
Q

Describe subarachnoid haemorrhage and its causes and predisposing factors

A

Blood vessels reside in the subarachnoid space

Aneurysms rupture into the subarachnoid space, producing a subarachnoid haemorrhage – acute cerebrovascular event

Other causes
> Arteriovenous malformation (AVM)
> Tumour

Predisposing factors
> Smoking
> Female sex
> Hypertension
> Positive family history
> ADPCK
> Ehlers-Danlos
> Coarctation of the aorta

70
Q

Describe the diagnosis of subarachnoid haemorrhage

A

History

> Acute headache
Loss of consciousness
Seizures
Visual, speech and limb disturbance
Sentinel headache

Clinical examination

> Photophobia
Meningism
Subhyaloid haemorrhages
Vitreous haemorrhages – Terson’s syndrome
Speech and limb disturbance
Cardiovascular problems e.g. pulmonary oedema

71
Q

Describe the grading system used to grade the severity of subarachnoid haemorrhage

A

Grade I – GCS 15

Grade II – GCS 13-14 without deficit

Grade III – GCS 13-14 with deficit

Grade IV – GCS 7-12

Grade V – GCS 3-6

72
Q

Describe the investigations used for subarachnoid haemorrhage

A

CT
> Prognostic: Fisher grade
> Based on the amount of bleeding on CT

LP
> Xanthochromia – yellowing of CSF due to bilirubin (takes 8-12h)

Further investigations
> CTA – eGFR
> MRA – eGFR and gadolinium
> DSA (digital subtraction angiography) – stroke, diabetics

Other
> U&Es – hyponatraemia
> ECG changes
> Elevated troponin
> Echocardiography – Takotsubo cardiomyopathy

73
Q

Describe the management of subarachnoid haemorrhage

A

Resuscitation
> Bed rest
> Fluids: 2.5-3.0L normal saline
> Anti-embolic stockings

Nimodipine: calcium channel antagonist
> Prevents delayed ischaemic neurological deficit

Analgesia

Doppler studies

Management
> Endovascular – coils & other devices
> Surgical clipping – early v late
> Conservative

74
Q

List the complications of subarachnoid haemorrhage

A

Rehaemorrhage

Delayed ischaemia

Hydrocephalus

Hyponatraemia
> Cerebral salt wasting syndrome (CSW)
> SIADH

Cardiovascular problems
> Stunned myocardium
> Elevation of troponin
> Arrhythmia
> Wall motion abnormalities
> Sudden death
> LVF - Takotsubo cardiomyopathy

Seizures

DVT/PE

LRTI, UTI

75
Q

Describe cerebral salt wasting syndrome (CSW)

A

Patients excrete large quantities of sodium and consequently fluid

Intravascular volume depleted

Important to establish volume status

Give hypertonic saline + fludrocortisone

76
Q

Describe Takotsubo cardiomyopathy

A

Apical wall hypokinesis – apex of myocardium fails to contract

Associated with development of left ventricular dysfunction and pulmonary oedema

Usually self-resolving

77
Q

Describe the motor features seen in Parkinson’s disease

A

Unilateral pill-rolling tremor
> 4-6 Hz rest tremor
> Becomes bilateral as disease progresses

Postural instability

Rigidity – increased tone, “cogwheel rigidity”

Bradykinesia
> Slowness in initiation of voluntary movement
> Progressive reduction in speed and amplitude of repetitive action

78
Q

List non-motor symptoms of Parkinson’s disease

A

Dementia

Depression, anxiety

Urinary urgency / nocturia, constipation

Erectile dysfunction

Excessive salivation

Low BP / postural hypotension

Speech difficulties

Hallucinations and delusions

Seborrheoic dermatitis / sweating

REM sleep behaviour disorder

Restless leg syndrome

Reduced olfactory function

Fatigue / daytime somnolence

Pain and sensory symptoms

79
Q

Describe causes of parkinsonism

A

Drug-induced
> Dopamine antagonists

Progressive supranuclear palsy (PSP)
> Also cognitive impairment, axial stiffness and difficulty with vertical gaze

Multi systems atrophy (MSA)
> Cerebellar dysfunction & autonomic dysfunction
> Prominent bowel, bladder and BP difficulties

Corticobasal disease (CBD)
> One-sided symptoms and dystonia in affected area

Lewy body dementia
> Visual hallucinations, fluctuations in cognition

Vascular parkinsonism
> Microvascular changes within basal ganglia give rise to lower body parkinsonism
> Leads to gait difficulties, UMN signs
> Does not affect speech, swallowing, upper limbs

80
Q

List the different drug types used in Parkinson’s disease

A
  • L-dopa
  • Dopamine agonists
  • MAO-B inhibitors
  • COMT inhibitors
  • Amantadine
  • Anticholinergics
  • Botulinum toxin
81
Q

Describe the use of L-dopa in the management of Parkinson’s disease including adverse effects

A

L-dopa + carbidopa – Sinemet

L-dopa + benserazide - Madopar

Dosing: 200-1000mg/day across 3-5 doses

Adverse effects

  • Peripheral
    > Nausea, vomiting
    > Postural hypotension
  • Central
    > Confusion
    > Hallucinations
82
Q

Describe the use of dopamine agonists in the management of Parkinson’s disease including side effects

A

Bind to post-synaptic dopamine receptor

Make patient more sensitive to endogenous dopamine

Ropinirole, pramipexoxle, rotigotine, apomorphine

Longer half-life than L-dopa but less effective

Can be prescribed as monotherapy in early disease or adjunct later

Side-effects
> Fewer motor complications than L-dopa
> Dopaminergic side effects
> Daytime somnolence
> Impulse control disorders – pathological gambling, hypersexuality

83
Q

Give examples of MAO-B inhibitors

A

Selegiline, rasagiline

Can be prescribed as monotherapy in early disease or adjunct later

84
Q

Give examples of COMT inhibitors

A

Entacapone, opicapone

Results in longer L-dopa half-life / duration of action

Slow breakdown of Levodopa peripherally

Co-prescribed with L-dopa

Side-effects
> Dopaminergic side-effects
> Diarrhoea

85
Q

Describe the use of amantadine, anticholinergics and botulinum toxin in the management of Parkinson’s disease

A

Amantadine
> Anti-dyskinetic effects
> Side-effects: confusion and livedo reticularis

Anticholinergics
> Trihexyphenidyl, orphenadrine, procyclidine
> Prescribed for anti-tremor effect

> Side-effects
> Confusion
> Urinary retention
> Blurred vision
> Dry mouth

Botulinum toxin
> Roles in sialorrhoea, blepharospasm / eyelid-opening apraxia, other focal dystonia

86
Q

Describe problems seen in advanced Parkinson’s disease

A

Motor
> On/off fluctuations
> L-dopa-induced dyskinesia

Axial
> Gait difficulties – including gait freezing
> Change in posture
> Poor balance / falls
> Speech / swallowing difficulties

Cognitive
> Dementia
> Hallucinations / psychosis

87
Q

Describe alternative treatments for advanced Parkinson’s disease

A

Apomorphine pen injection or subcutaneous pump

Intrajejunal duodopa infusion

Deep brain stimulation (DBS) surgery
> Allows electrical stimulation of subthalamic nucleus
> Targeted, adjustable, non-destructive and reversible way of modulating pathological brain circuits
> 3 implantable components
» Brain leads – electrodes at distal end
» Neurostimulator – implantable pulse generator (IPG)
» Extension wires

88
Q

Describe Parkinson’s disease emergencies

A

Motor
> Severe OFF periods / severe dyskinesia

> Parkinson-hyperpyrexia syndrome
> High temperature
> Muscle stiffness
> High CK
> Can cause renal failure
> Triggered by sudden reduction in Parkinson’s medications – rare complication

Non-motor

> Acute psychosis
Impulsivity
Dopamine dysregulation (excessive L-dopa)
Dysautonomia
> Postural hypotension
> Dysphagia
> Intestinal pseudo-obstruction

Falls

Device-related - DBS ; apomorphine pump

89
Q

Outline causes of loss of consciousness

A

Faints – lack of blood to the brain

Fits – electrical discharge

Other
> Metabolic cause
> Psychiatric / psychological
> Trauma

90
Q

Describe a seizure including the different phases

A

A seizure is a sustained and synchronised electrical discharge in the brain causing symptoms or signs

Phases

> PDS – large and prolonged depolarisation with generation of action potential spikes
> At onset of PDS, AMPA channel opens
> Na+ enters cell triggering depolarisation

> NMDA channel then opens
> Allows Na+ and Ca+ entry

> > Following depolarisation, there is opening of the potassium channels and activation of GABA channels with Cl- entering the cell

> > Both influx of Cl- and efflux of K+ lead to hyperpolarisation of the cell

> Tonic phase – very frequent discharges, muscles are stiff

> Clonic phase – discharges come in clusters and reduce in frequency

91
Q

Describe the excitatory and inhibitory firing of neurons

A

Excitation
> EAA
> Action on NMDA / AMPA / Kainate
> Na+ / Ca2+ influx

Inhibition
> GABA/glycine
> Action on GABA-R
> Cl- influx

92
Q

Describe the different types of seizure

A

Tonic seizure
> Short-lived, <1 minute
> Abrupt
> Generalised muscle stiffening with rapid recovery

Generalised tonic-clonic seizure
> Bilaterally convulsive
> Generalised stiffening
> Subsequent rhythmic jerking of the limbs
> Urinary incontinence
> Tongue biting

Absence seizure
> Behavioural arrest
> Formerly called petit mal seizures
> Brief loss of awareness / responsiveness / blank stare
> Sudden onset / termination - usually no post-ictal state
> Most common in children, 50-100 / day

Atonic seizure
> Sudden onset of loss of muscle tone

Myoclonic seizure
> Brief, ‘shock-like’ involuntary single or multiple jerks

Partial seizures (aka focal seizures)
> With loss of awareness
> With motor phenomena
> With sensory phenomena
> With psychological phenomena
> With cognitive phenomena

93
Q

Describe the causes and classification of epilepsy

A

Causes
> Unknown
> Vascular
> Hippocampal sclerosis
> Infection
> Trauma
> Other
> MCD
> Tumour
> Degenerative

Classification

> Focal epilepsy – localised onset

> Genetic generalised – generalised onset

> Uncertain

94
Q

Describe the management of status epilepticus

A

If seizure is not self-limiting and carries on

> Initial therapy
> Benzodiazepine
> IV lorazepam
> IV/rectal diazepam
> Buccal midazolam

Treat potential cause
> IV glucose if hypoglycaemia
> IV thiamine if alcohol abuse

If seizure continues for further 5 minutes
> Repeat benzodiazepine dosing
> Administer usual AEDs where necessary

If seizure continues
> IV phenytoin or valproate

If seizure continues
> ITU admission
> Sedation with general anaesthetic

95
Q

Describe the long-term treatment of epilepsy

A

Sodium channel blockers
> Reducing pre-synaptic excitability and the ability of action potentials to spread
> Carbamazepine, oxcarbazepine, phenytoin, lamotrigine

SV2A antagonists
> SV2A required for release of neurotransmitter from vesicles
> Inhibited by levetiracetam

N-type calcium channel blocker
> Calcium influx drives neurotransmitter release
> Channel inhibited by pregabalin and gabapentin
> The response of the GABAA receptor to GABA is enhanced by benzodiazepines, barbiturates, felbamate, topiramate

GABA levels are increased by other AEDs
> Tiagabine inhibits the GABA transporter
> Vigabatrin inhibits GABA transaminase (GABAT)
> Felbamate has action on Glu receptors, but its primary mode of action is via inhibition of voltage-gated Na+ channels and some action on GABA transmission
> Topiramate also targets Glu receptors as part of a mixed mode of action, but its primary target is thought to be inhibition of voltage-gated Na+ (and Ca2+)

96
Q

Describe the structural organisation of a peripheral nerve

A

Fasciculi
- Each fascicle is a bundle of axons from individual cells
- Surrounded by perineurium

Epineurium
- Surrounds peripheral nerve
- Tough connective tissue

97
Q

Describe the different types of nerve fibres

A

Large fibres (myelinated)
> Motor nerves
> Proprioception, light touch and vibration

Thinly myelinated fibres
> Light, touch and temperature

Small fibres (unmyelinated)
> Light touch, pain and temperature

98
Q

Describe length-dependent axonal neuropathy

A

Diffuse involvement of peripheral nerves
> Age > 50 years
> Length dependent - starts in toes / feet
> Symmetrical, slowly progressive
> No significant sensory ataxia
> Any weakness is distal and mild

Causes
> Diabetes
> Alcohol
> Nutritional - folate / B12 / thiamine / B6 deficiency
> Immune-mediated: RA, lupus, vasculitis, polyarteritis nodosa
> Metabolic / endocrine
> Renal failure
> Hypothyroidism
> Drugs: isoniazid, cisplatin, amiodarone, gold
> Infectious: HIV, Hep B & C
> Inherited: Charcot-Marie-Tooth, Hereditary neuropathy with liability to pressure palsy (HNPP)
> Neoplastic : myeloma
> Paraneoplastic
> Critical illness

99
Q

Describe Guillain-Barre syndrome

A

Acute inflammatory demyelinating neuropathy

Post-infectious autoimmune aetiology
> Campylobacter
> CMV
> EBV

Progressive ascending weakness over days

Flaccid quadriparesis with areflexia

Can have respiratory / bulbar / autonomic involvement

Treatment - IV immunoglobulin or apheresis

CIDP – chronic form
> Steroid and IVIG responsive

100
Q

Describe nerve conduction studies

A

Axonal v demyelinating motor studies

Axonal – CMAP is half of the size of a normal curve

Demyelinating
> Normal size but delayed conduction
> OR conduction block with temporal dispersion
» Area under the curve is the same but slower and takes longer to peak

101
Q

Describe mononeuritis multiplex

A

Sequential or simultaneous development of neuropathy in 2 or more nerves

Describes a cluster of conditions

Most commonly affects

> Common peroneal
> Weak ankle dorsiflexion
> Sensory disturbance lateral aspect of calf and foot

> Radial
> Wrist / finger drop
> Sensory disturbance – dorsum of hand

> Axillary
> Weakness of shoulder abduction
> Badge of sensory disturbance – inferior deltoid

> Median
> LOAF weakness
> Sensory disturbance

> Femoral
> Weak hip flexion and knee extension
> Sensory disturbance lateral calf and dorsum of foot

Common causes

> Diabetes
Vasculitic – Churg Strauss, polyarteritis nodosa
Rheumatological – RA, lupus, Sjogren’s
Infective – Hep C, HIV
Sarcoidosis
Lymphoma

Investigations
> History and examination
> Nerve conduction studies and EMG
> MRI of plexus with contrast
> LP

Management
> Treat underlying cause
> Symptoms may be irreversible

102
Q

List muscular dystrophies

A
  • Duchenne and Becker Muscular Dystrophy
  • Emery-Dreifus type
  • Limb girdle type
  • Fascioscapulohumeral type
  • Oculopharyngeal type
103
Q

Describe myasthenia gravis

A

Pathogenesis
> Autoimmune disorder
> Antibodies to acetylcholine receptor at post-synaptic NMJ
> Association with other autoimmune disorders
> May be associated with thymic hyperplasia or thymoma

Affects young women in 20s and older men in 70s

Signs and symptoms
> Fatiguable weakness of ocular, bulbar, neck, respiratory and/or limb muscles

Investigations
> Antibodies to AChR present in 85%
> Single fibre EMG and repetitive nerve stimulation abnormal

Management
> Pyridostigmine - Anti-acetylcholinesterase
> Immunosuppressive therapies: steroids, IV immunoglobulin

104
Q

Give examples of cognitive functions which may be affected in dementia

A

Memory
> Repetitive questions or conversations
> Misplacing personal belongings
> Forgetting events or appointments
> Getting lost on a familiar route

Executive function
> Poor understanding of safety risks
> Inability to manage finances
> Poor decision-making ability
> Inability to plan complex or sequential activities

Visuospatial
> Inability to recognise faces or common objects
> Inability to find objects in direct view despite good acuity
> Inability to operate simple implements or orient clothing to body

Language
> Difficulty thinking of common words while speaking
> Hesitation
> Speech, spelling and writing errors

105
Q

Give examples of bedside cognitive assessments

A

Folstein MMSE (30)

Addenbrookes Cognitive Examination (100)
> 4 domains
» Executive function
» Memory
» Language
» Visuospatial

106
Q

Describe the areas of the brain responsible for executive function

A

Behaviour
> Orbitofrontal
> Obeying and recognising social cues
> Appropriate behaviour

Attention / working memory
> Dorsolateral prefrontal cortex

Motivation / goal-driven
> Anterior cingulate

107
Q

Describe the areas of the brain responsible for visual processing and how to test this

A

Ventral stream
> Object recognition – visual agnosia
> Facial recognition – prosopagnosia

Dorsal stream
> Position of object in space – dyspraxia

Testing ACE-r
> Pentagons
> Cubes
> 3D letters
> Dots counting

108
Q

Describe attention and how it is tested

A

Component of consciousness which allows filtering of information to allow one to focus on a particular stimuli

Essential for all aspects of cognition

Pathological process – delirium (or anxiety/depression)

Testing

> ACEr
> Orientation e.g. what is the day/month/year, spell WORLD backwards
> Serial 7s

> Trail making (trails B) - learning and understanding rules

> Proverbs

> Verbal fluency

> Estimates

> Planning

109
Q

Describe pathological processes associated with episodic memory and how it is tested

A

Pathological process

> Early Alzheimer’s disease
> Hippocampal atrophy
> Ventricular enlargement

> Limbic encephalitis

Testing ACEr
> Anterograde memory - address learning
> Retrograde memory – historical famous figures

110
Q

Describe pathological processes associated with semantic memory and how it is tested

A

Semantic dementia (variant frontotemporal dementia) - anterior temporal atrophy
> Loss of knowledge about the world including words

Testing ACEr
> Marked reduction category verbal fluency e.g. give a list of animals in one minute
> Impairment of irregular words (dyslexia) e.g. pint

111
Q

Describe the different forms of language, the pathological processes which can arise and how it is tested

A

3 forms
> Speech – aphasia
> Reading – alexia
> Writing – agraphia

Pathological processes

> Semantic variant – semantic dementia
> Poor confrontation naming e.g. naming common objects
> Impaired single word comprehension
> Poor object/person recognition, surface dyslexia

> Logopenic variant – Alzheimer’s dementia
> Impaired single word retrieval - “thinking of right word”
> Impaired repetition, speech sound errors (phenomic)
> Spared object/person recognition, single word recognition

> Non-fluent variant – progressive non-fluent aphasia (variant FTD)
> Effortful, halting, motor impairment of speech
> Phenomic errors
> Spared object/person recognition, single word recognition

Testing using ACEr
> Naming
> Repetition
> 3 stage command – comprehension
> Reading

112
Q

Describe the pathophysiology of Alzheimer’s disease

A

Starts in temporal lobe – impairment of episodic memory

Hippocampal atrophy and ventricular enlargement

Spreads to parietal and frontal lobes – visuospatial dysfunction

Global atrophy including language centres – language disorder

113
Q

Describe Bell’s palsy and its treatment

A

Unilateral facial weakness evolves over 48h often preceded by ear pain/distorted sounds
> Decreased tear production – ocular dryness
> Hyperacusis
> Ageusia

Causes
> Unknown
> Viral-associated ischaemia, demyelination
» Herpes zoster, herpes simplex
» EBV
» Lyme disease

Treatment
> Steroids – oral prednisolone
> Artificial tears, eye patching
» Long-term: tarsorrhaphy
> Physical therapy
> May resolve spontaneously within weeks-months

114
Q

List the main agents which cause CNS infection

A

Bacterial: meningococcus, pneumococcus, Listeria

Viral: HSV, VZV, enterovirus (D-68), HIV, mumps

Fungal: cryptococcosis

Parasitic: toxoplasmosis

115
Q

Describe the causative agents of meningitis

A

Bacterial or viral

> Streptococcus pneumoniae – gram positive diplococci

> > 70% underlying disorder
> Middle ear disease
> Head injury – CSF leak
> Neurosurgery
> Alcohol
> Immunosuppression (HIV)

> > Neurology
> Focal signs
> Seizures
> VIII palsy
> CAP
> ENT
> Endocarditis

> Neisseria meningitidis – gram negative diplococci

Subacute

> Bacterial – Listeria, TB

> > Listeria monocytogenes – gram positive rods
> Immunosuppression
> Pregnancy

116
Q

Describe the signs and symptoms of meningitis

A

Inflammation of meninges +/- cerebrum (meningo-encephalitis) - inflammatory CSF

Symptoms and signs
> Headache
> Neck stiffness/rigidity
> Reduced GCS
> Fever
> Confusion indicative of cerebritis / encephalitis
> Rash – purpuric +/- petaechial but macular early on (meningococcal)

117
Q

Describe LP findings in meningitis

A

Bacterial
> Low glucose
> High protein
> Neutrophils present
> Lymphocytes in Listeria infection

TB
> Low glucose
> High protein
> Lymphocytes present

Viral
> Normal glucose
> High protein
> Lymphocytes present (also neutrophils early on – esp mumps meningitis)

Fungal
> Low glucose
> High protein
> Lymphocytes present

118
Q

Describe treatment of suspected bacterial meningitis

A

Possible bacterial meningitis
> IV ceftriaxone 2g 12 hourly OR benzyl penicillin
> OR if true penicillin allergy: IV chloramphenicol

> If age > 60, immunosuppressed, alcohol excess, liver disease or Listeria meningitis suspected - add IV amoxicillin to ceftriaxone OR if true penicillin allergy> add IV co-trimoxazole

Bacterial meningitis strongly suspected
> Add IV dexamethasone 10mg 6 hourly (4 days)

Duration of antibiotics
> Meningococcal – 5 days
> Listeria – 21 days (IV amoxicillin – stop ceftriaxone)
> Pneumococcal – 10-14 days
> Haemophilus – 10 days

If high likelihood of pneumococcal meningitis add steroids

119
Q

Describe chemoprophylaxis for meningococcal meningitis

A

Given to contacts

Ciprofloxacin

Rifampicin

120
Q

Describe viral encephalitis and its treatment

A

Confusion, fever +/- seizures

HSV encephalitis
> High mortality rate with neuro sequelae e.g. hearing loss, memory loss
> Lymphocytic CSF
> Normal glucose
> PCR is positive

EEG – temporal lobe changes

Treatment - IV aciclovir 2-3 weeks (HSV, VZV)

121
Q

Describe intracerebral TB

A

Subacute – weeks

May be unmasked during TB treatment

CN lesions usually CN III, IV, VI, IX

Sample widely – early morning urines (EMUs), bronchoalveolar lavage (BAL)

CSF may be normal

Treatment for one year
> Rifampicin
> Pyrazinamide
> Isoniazid
> Ethambutol
> Steroids

122
Q

Describe HIV brain disease

A

Consequence of unrecognised/untreated infection and marked immunodeficiency

> Encephalitis: responds to antiretroviral therapy

> Dementia: does not respond to antiretroviral therapy

> Neurosyphilis – secondary or tertiary
> Responds to penicillin

> Opportunistic
> TB
> Cryptococcus
> Toxoplasmosis
> JC virus – progressive multifocal leuco-encephalopathy

123
Q

Describe intracerebral toxoplasmosis

A

Toxoplasma gondii

Signs and symptoms
> Headache
> Seizures
> Focal CNS signs

> Immunocompromised (HIV)

> Multiple enhancing lesions – basal ganglia

Investigations
> IgG and IgM – blood
> PCR – CSF

Treatment
> Sulphadiazine
> Pyramethamine
> Restore immune function

124
Q

Describe cryptococcal meningitis

A

Immunodeficiency usual – HIV

Space occupying lesion (SOL) or meningo-encephalitis (subacute)

Papilloedema usually present
> Will progress to optic atrophy and blindness if untreated

Can cause pulmonary nodules and skin lesions

CSF
> India ink – classic large capsule
> Cryptococcal antigen (also blood)
> Culture

Treatment
> Amphotericin B
> Flucytosine
> Fluconazole, possible steroids
> If raised ICP – shunt
> Paradoxical worsening with ARVs in HIV

125
Q

Describe the treatment used for acute alcohol intoxication and name complications of chronic alcohol abuse

A

Chlordiazepoxide PRN and IV Pabrinex (vitamin B1)

Complications: Wernicke’s encephalopathy progressing to Korsakoff’s syndrome

126
Q

Describe the Oxfordshire Community Stroke Project (OCSP) classification

A

4 subtypes of ischaemic stroke

1) Lacunar syndrome (LACS)
> pure motor stroke OR pure sensory stroke OR sensorimotor stroke OR ataxic hemiparesis OR clumsy hand-dysarthria

2) Total anterior circulation syndrome (TACS)
> hemiparesis AND higher cortical dysfunction (dysphasia or visuospatial neglect) AND homonymous hemianopia

3) Partial anterior circulation syndrome (PACS)
> Isolated higher cortical dysfunction OR any 2 of hemiparesis, higher cortical dysfunction, hemianopia

4) Posterior circulation infarct (POCS)
> Isolated hemianopia, brainstem or cerebellar syndromes

127
Q

Describe the CHADS-VASc score and at what score do you anticoagulate and with what?

A

C – Congestive Heart Failure/ LV Dysfunction
H – Hypertension
A(2) – Age ≥ 75
D – Diabetes Mellitus
S(2) – Stroke/TIA/Thromboembolism
V – Vascular Disease (e.g. PAD, MI)
A – Age (65-74)
Sc – Sex Category (1 point for F)

If CHA2DS-VASc Score ≥ 2:
offer anticoagulation- (Edoxaban/Apixaban).
If patient has a mechanical valve replacement: Warfarin

128
Q

Discuss management of migraine - acute and prophylactic

A

Acute (1st line)
- Simple analgesics (Paracetamol, Ibuprofen or Aspirin) UPTO 2 twice a week
- Triptans (e.g. Sumatriptan)
- Avoid if patient has CVD
- Give with anti-emetics if vomiting
- Consider anti-emetics if patient is vomiting (Metoclopramide or Prochlorperazine)

If not working - try other Triptans and NSAIDs (2nd line)

Prophylactic
- Lifestyle: diet and hydration, avoid triggers, relaxation activities, headache diaries
- Medication. Consider if:
>4 disabling headaches per month
Not resolved by acute medication, or risk of Medication overuse headache
Offer EITHER of:
- Propranolol
- Amitriptyline
- Topiramate
- Candesartan
- Flunarazine

If ineffective after 3m, wean and try another
If all failed: refer to neurology specialist

avoid opiates

129
Q

Summarise peripheral neuropathies - GBS, length dependent, myasthenia gravis

A

Guillain-Barre Syndrome (medical emergency)
- Ascending weakness (length-dependent) and sensory loss
- Typically after GI infection/ EBV
- Treated with IVIg

  1. Length dependent axonal neuropathies
    - Tend to have a glove-and-stocking distribution, symmetrical
    - Multiple causes (B12/B9, Isoniazid, Diabetes, alcohol, Charcot-Marie Tooth)
  2. Neuromuscular Junction Disorders
    - Myasthenia Gravis (esp younger women, older men)
    - Fatiguable weakness: ptosis, quietening speech, respiratory difficulties
    - Ix: Antibodies to post-synaptic ACh receptors at the NMJ, possible mediastinal mass on CT
    - Treated with Pyridostigmine (anti-AChE)
130
Q

Define Pellagra

A

Pellagra - A deficiency of niacin (vitamin B3). Characterized by the presence of glossitis and “the three Ds”: diarrhea, dermatitis, dementia, and possibly death (the four Ds).

131
Q

Discuss Bamford Stroke Classification

A
132
Q

Describe symtpoms of stroke by location

A

ACA
- Contralateral leg > arm weakness, sensory loss, urinary incontinence
- Personality changes

MCA
-Arm > leg weakness, sensory loss
- Hemineglect/ aphasia

PCA
- Contralateral hemianopia with macular sparing
- Alexia, prosopagnosia etc

Lacunar strokes
- Pure sensory/motor/mixed (no cortical signs such as neglect, aphasia)

Cerebellar strokes
- Consider if vertigo (vomiting), tremors, slurred speech, ataxia, nystagmus etc

133
Q

Describe Cushing’s triad

A

Cushing’s triad refers to signs which indicate increased intracranial pressure (ICP).

These include bradycardia, widened pulse pressure and irregular respirations.

Phase 3 (14 decks)

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