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Neurology Flashcards

1
Q

Describe the tract of the olfactory nerve.

A
  • olfactory cells of nasal mucosa
  • olfactory bulbs
  • pyriform cortex via cribriform plate
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2
Q

Describe the tract of the optic nerve.

A
  • retinal ganglion cells
  • optic chiasm
  • optic tract
  • lateral geniculate body
  • optic radiation
  • primary visual cortex in occipital cortex
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3
Q

What should you examine when testing the optic nerve?

A
  • optic discs with ophthalmoscope
  • pupillary responses
  • visual acuity (using Snellen chart)
  • visual fields and blind spot
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4
Q

Discuss the papillary light reflex.

A
  • retinal ganglion cells
  • optic nerve
  • pretectal area
  • synapse with Edinger-Westphal nucleus
  • parasympathetic signals via oculomotor nerve which synapse with ciliary ganglion
  • post-synaptic nerves innervate iris sphincter muscle
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5
Q

An optic tract lesion of which area would cause bitemporal hemianopia?

A

optic chiasm

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6
Q

A lesion of the optic tract would lead to which visual field defect?

A

contralateral homonymous hemianopia

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7
Q

Which visual tract defect arises from a right sided Meyer’s loop lesion?

A

left homonymous superior quadrantanopia

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8
Q

Right homonymous inferior quadrantanopia is caused by a lesion where?

A

left optic radiations before they are joined by fibres from Meyer’s loop

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9
Q

List the structures that the oculomotor nerve innervates.

A

Motor: inferior oblique, superior, medial and inferior recti muscles AND levator palpebrae superioris
Para: ciliary muscle, pupillary constrictor muscles

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10
Q

Which nerve supplies the superior oblique muscle and what movement does it cause?

A
  • trochlear nerve

- depresses adducted eye and intorts abducted eye

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11
Q

What is internuclear ophthalmoplegia?

A

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

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12
Q

What causes internuclear ophthalmoplegia? Which disease is it commonly seen in?

A

results from lesion of medial longitudinal fasiculus

MS

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13
Q

What results from ipsilateral disruption of cervical sympathetic chain?

A

Horner’s syndrome

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14
Q

List the features seen in Horner’s syndrome.

A
  • miosis
  • ptosis
  • anhidrosis
  • apparent enophthalmos
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15
Q

Name some causes of cervical sympathetic chain disruption.

A

congenital, brainstem stroke, cluster headache, apical lung tumour, MS, carotid artery dissection

  • cervical rib
  • syringomyelia
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16
Q

Describe the function of the trigeminal nerve.

A
  • sensory: face (ophthalmic, mandibular, maxillary) and anterior 2/3 tongue
  • motor: masseter, temporalis, medial and lateral pterygoids
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17
Q

Which sensory component of the trigeminal nerve does herpes zoster ophthalmicus affect? How is it treated?

A

V1

oral aciclovir

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18
Q

Describe the function of the facial nerve.

A

motor: muscles of facial expression
sensory: taste (anterior 2/3 tongue)
para: salivary and lacrimal glands

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19
Q

What clinical differences are seen between upper and lower facial motor neurone lesion?

A

upper: weakness of inferior facial muscles
lower: weakness of superior and inferior facial muscles

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20
Q

Describe the corneal reflex. (3 points)

A
  • lightly touch cornea with cotton wool
  • afferent = V
  • efferent = VII
  • test of pontine function
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21
Q

What is the function of CNVIII? What structures does it innervate?

A

vestibulocochlear nerve

balance: nerve endings within semi-circular canals to cerebellum and spinal cord
hearing: cochlear to auditory cortex in temporal lobes

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22
Q

Discuss the function of the glossopharyngeal nerve and the structures it innervates.

A
  • sensory: taste (posterior 1/3 tongue), proprioception for swallowing (pharyngeal wall), blood pressure receptors (carotid sinuses)
  • motor: swallow and gag reflexes (pharyngeal muscles), lacrimation (lacrimal glands)
  • para: salivation (parotid glands)
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23
Q

What is seen in glossopharyngeal palsy?

A

deviation of uvula away from the side of lesion

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24
Q

Discuss the function of the vagus nerve and the structures it innervates.

A
  • sensory: chemoreceptors (blood oxygen conc, carotid bodies), pain receptors (resp and GI tract), sensation (external ear, larynx, pharynx)
  • motor: HR and stroke volume (pacemaker and ventricles), peristalsis (GI tract smooth muscles), air flow (bronchial smooth muscles), speech and swallowing (larynx and pharynx)
  • para: smooth muscles and glands of same areas as motor, as well as thoracic and abdo areas
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25
Q

What is the function of the spinal accessory nerve?

A

head rotation and shoulder shrugging - sternocleidomastoid and trapezius muscles

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26
Q

Which nerve is responsible for the motor component of the tongue?

A

hypoglossal

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27
Q

What would be seen in a left-sided hypoglossal palsy?

A

tongue deviation to left

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28
Q

Discuss the nucleus location of each of the cranial nerves.

A

forebrain: I, II
midbrain: III, IV
pons: V, VI, VII, VIII
medulla: IX, X, XI, XII

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29
Q

Which cranial nerves exit the skull via the superior orbital fissure?

A

III, IV, V1, VI

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30
Q

Discuss where the three components of the trigeminal nerve exit the skull.

A

V1: superior orbital fissure
V2: foramen rotundum
V3: foramen ovale

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31
Q

CN VII and VIII exit the skull through what?

A

internal acoustic meatus

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32
Q

The jugular foramen allows the passage of which cranial nerves and vessels?

A

IX, X and XI
internal jugular vein
sigmoid and internal petrosal sinus

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33
Q

CN XII exits the skull via which canal?

A

hypoglossal canal

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34
Q

Discuss radial nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.

A
  • entrapment at spiral groove ‘saturday night palsy’
  • wrist and finger drop, usually painless
  • sensory: lateral aspect of back of hand
    motor: wrist and finger extension, elbow flexion in mid-pronation (brachioradialis)
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35
Q

Discuss ulnar nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.

A
  • entrapment at medial epicondyle (ulnar groove)
  • history of trauma to elbow, weak grip, usually painless
  • sensory: medial aspect of hand
    motor: wrist flexion, index and pinkie abduction, thumb adduction
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36
Q

Discuss median nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.

A
  • entrapment within carpal tunnel at wrist
  • history of intermittent nocturnal pain, numbness and tingling (often relieved by shaking hand), positive Tinel’s sign/Phalen’s test, weak grip
  • sensory - lateral palm of hand
  • motor: LOAF
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37
Q

Discuss femoral nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.

A
  • haemorrhage/trauma
  • weakness of quadriceps and hip flexion, numbness in medial skin
  • sensory - lateral leg
  • motor - knee extension, hip flexion and adduction
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38
Q

Discuss common peroneal nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.

A
  • entrapment of fibular head
  • trauma, surgery or external compression, acute onset foot drop, usually painless
  • sensory: lateral leg
  • motor: ankle dorsiflexion, great toe extension
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39
Q

What is mononeuritis multiplex? List some common causes.

A

simultaneous or sequential development of nerve palsy of 2 or more nerves

causes: diabetes, vasculitic, RA, lupus, Sjogren’s syndrome, hep C, HIV, sarcoidosis, lymphoma

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40
Q

Distinguish between a primary and secondary headache including examples of each.

A 
primary = headache and its ass. features is the disorder (no underlying cause) e.g. migraine, tension, cluster
secondary = secondary to underlying causes e.g. subarachnoid haemorrhage, space-occupying lesion, meningitis, temporal arteritis
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41
Q

List some ‘red flag’ features which suggest secondary headache.

A

Systemic symptoms (fever, weight loss)
Neurological signs or symptoms
Older age of onset
Onset is acute ( <5 mins)
Previous headache history is different or absent
Triggered headache (valsalva, exertion or posture)

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42
Q

Which signs suggest a secondary headache on examination?

A

systemic: reduced conscious level, BP, pyrexia, meningism, skin rash, temporal artery tenderness
cranial nerve: pupillary responses, visual fields, eye movements, fundoscopy

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43
Q

Name 4 upper motor neurone signs to look for in headache clinical exam.

A
  • pronator drift
  • increased tone
  • brisk reflexes
  • extensor plantar response
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44
Q

Name 4 cerebellar signs that may be seen in headache examination.

A
  • nystagmus
  • past-pointing
  • dysdiadochokinesis
  • broad-based ataxic gait
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45
Q

Give a description of the pathophysiology of migraine.

A
  • primary dysfunction in brainstem sensory nuclei (V, VII - X)
  • pain results from pain sensitive cranial blood vessels and their innervating trigeminal fibres
  • aura: cortical spreading depression
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46
Q

List the stages of migraine and give a description of each.

A
  • prodrome - up to 48 hrs before headache, mood disturbance, restlessness, hyperosmia, photophobia, diarrhoea
  • aura - recurrent reversible focal neurological symptoms, develops over 5-20 mins and lasts <60mins, visual aura (scotoma, flashing lights, fortification spectrum), sensory aura often starts in hand and migrates up arm
  • headache - throbbing or pulsatile, moderate-severe, gradual onset, 4-72 hours, unilateral in 60%, can radiate, aggravated by routine physical activity
  • associated symptoms - N&V, photophobia, phonophobia, osmophobia, mood disturbance, diarrhoea
  • postdrome
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47
Q

Give examples of visual aura seen in headache.

A

zigzag fortification spectrum, visual field loss, negative scotoma, positive scotoma

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48
Q

What are two complications of migraine?

A
  1. Medication overuse headache: headache 15+ days per month associated with frequent use of acute relief meds
  2. Chronic migraine: headache on 15+ days per month
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49
Q

Discuss the management of migraine.

A
  • lifestyle: avoid triggers, reduce caffeine/alcohol, encourage regular meals and sleep patterns
  • acute management: simple analgesia, triptans, antiemetic
  • prophylaxis: beta-blockers, tricyclic antidepressants, anti-epilepsy
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50
Q

Define a thunderclap headache.

A

abrupt-onset of severe headache which reaches maximal intensity <5mins (and lasts >1hr)
should be considered as subarachnoid haemorrhage until proven otherwise

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51
Q

What are the causes of thunderclap headache?

A
  • subarachnoid haemorrhage
  • intracerebral haemorrhage
  • arterial dissection
  • cerebral venous sinus thrombosis
  • bacterial meningitis
  • primary headaches
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52
Q

How do you investigate a thunderclap headache?

A
  • bloods
  • 12 lead ECG
  • urgent CT brain
  • lumbar puncture (xanthochromia - subarachnoid haemorrhage)
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53
Q

What is a normal intracranial pressure?

A

7-15 mmHg

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54
Q

What are some causes of increased ICP?

A
  • mass effect: tumour, infarction with oedema, haematoma, abscess
  • increased venous pressure
  • obstruction to CSF flow/absorption: hydrocephalus, meningitis
  • idiopathic
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55
Q

What are some key history findings in a raised pressure headache?

A
  • worse on lying flat, improved on sitting
  • worse in morning
  • persistent N&V
  • worse on valsalva
  • worse with physical exertion
  • transient visual obscurations with change in posture
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56
Q

List some examination findings in raised pressure headaches.

A
  • optic disc swelling - papilloedema
  • impaired visual acuity
  • restricted visual fields
  • CN III palsy
  • CN VI palsy
  • focal neurological signs
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57
Q

What are the two major causes of low pressure headache?

A
  • post-lumbar puncture - most resolve spontaneously

- spontaneous intracranial hypotension - spontaneous dural tear, following valsalva

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58
Q

Does lying down relieve a high or low pressure headache?

A

low

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59
Q

Discuss the clinical presentation of neuropathy including motor, sensory and autonomic.

A

motor: weakness/muscle atrophy
sensory: large - sensory ataxia/loss of vibration sense/numbness/tingling, small - impaired pin prick/temperature/painful burning/numbness/tingling
autonomic: postural hypotension, erectile dysfunction, GI disturbance, abnormal sweating

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60
Q

Define length-dependent axonal neuropathy.

A
  • diffuse involvement of peripheral nerves
  • age > 50 yrs
  • starts in toes/feet
  • symmetrical and slowly progressive
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61
Q

What are some causes of length-dependent axonal neuropathy?

A
  • diabetes
  • alcohol
  • nutrition deficiency (B12 and folate)
  • others: immune e.g. RA, lupus, renal failure, hypothyroidism, drugs, infections, myeloma
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62
Q

What is Guillain-Barre syndrome?

A
  • acute inflammatory autoimmune demyelinating neuropathy
  • progressive ascending weakness over days
  • flaccid, quadraparesis with areflexia +/- respiratory/bulbar/autonomic involvement
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63
Q

Describe the aetiology of GB.

A

post-infectious autoimmune e.g. camplyobacter, CMV, EBV

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64
Q

How is GB treated?

A

IV Ig or apheresis

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65
Q

Define myasthenia gravis.

A

autoimmune disorder: antibodies to ACh receptor at post-synaptic NMJ - fatiguable weakness of ocular, bulbar, neck, resp and/or limb muscles

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66
Q

What is myasthenia gravis associated with?

A

other autoimmune disorders

? thymic hyperplasia and thymoma

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67
Q

What investigations should be carried out if myasthenia gravis is suspected?

A
  • antibodies to AChR present

- abnormal single fibre EMG and repetitive nerve stimulation

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68
Q

Discuss the management of myasthenia gravis.

A
  • pyridostigmine (anti-ACh esterase)

- immunosuppressive therapies (steroids and IV Ig)

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69
Q

Give a detailed definition of stroke.

A

central nervous system infarction (which includes brain, spinal cord and retinal cells attributable to ischaemia), based on objective evidence of focal ischaemic injury in a defined vascular distribution or clinical evidence of the former with other aetiologies excluded.

70
Q

What are the signs and symptoms of stroke?

A
  • acute onset
  • right weakness: leg/face and arm/hemiparesis (sensory and motor cortex)
  • dysphasia (Broca’s and Wernicke’s area)
  • visual disturbance: right homonymous heminopia (optic tract runs in MCA region)
  • acute light-headedness
71
Q

List four classes of stroke according to Oxfordshire Community Stroke Project.

A
  1. Total anterior circulation syndrome: proximal MCA or ICA occlusion - hemiparesis, hemianopia, higher cortical dysfunction
  2. Partial anterior circulation syndrome: branch MCA occlusion - isolated higher cortical dysfunction or 2 of: hemiparesis, hemianopia, higher cortical dysfunction
  3. Posterior circulation syndrome: perforating arteries, PCA, cerebellar occlusion - isolated hemianopia or brainstem syndrome
  4. Lacunar syndrome: perforating artery/small vessel disease - pure motor or pure sensory or sensorimotor stroke or ataxic hemiparesis or clumsy hand-dysarthritis
72
Q

Define intracerebral haemorrhage.

A

a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma

73
Q

Define stroke caused by intracerebral haemorrhage.

A

rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma

74
Q

List common causes of an intracranial bleed.

A 
trauma
small vessel disease
amyloid angiopathy
blood vessel abnormalities
blood clotting deficiencies
tumours
drugs: cocaine, amphetamine
75
Q

Describe the differences in treatment approach in ischaemic stroke vs haemorrhagic stroke.

A

ischaemic: IV thrombolysis, thromboectomy aspirin, stroke unit, hemicranectomy
haemorrhagic: BP control, stroke unit, neurosurgical evaluation

76
Q

3% of strokes are caused by aneurysmal SAH. How do aneurysms form and rupture?

A
  • increased haemodynamic stress
  • activation of endothelial cells
  • recruitment of inflammatory cells
  • outward vascular remodelling
  • adapted and stabilised aneurysm
  • sustained inflammation and remodelling leads to rupture
77
Q

List predisposing factors that may lead to aneurysmal SAH.

A
  • smoking
  • female sex
  • hypertension
  • positive family history
  • ADPCK, coarctation of aorta
78
Q

What are the clinical history and examination findings in ASAH?

A

history: sudden onset headache, LOC, seizures, visual, speech and limb disturbances, sentinel headache
exam: photophobia, meningism, subhyaloid, haemorrhages, vitreous haemorrhages, speech and limb distrubances, pulmonary oedema

79
Q

What is the use of CT in the investigation of ASAH?

A
  • confirms diagnosis
  • clues to aetiology
  • identifies complications: infarction, haematoma, hydrocephalus
  • prognostic: Fisher grade
80
Q

Besides CT, what other investigations are useful in ASAH?

A
  • LP: xanthochromia
  • MRA
  • DSA: stroke, diabetes
  • hyponatraemia
  • ECG changes
  • elevated troponin levels
  • ECHO
81
Q

Describe the resuscitation process following ASAH.

A
  • bed rest
  • fluids - saline
  • anti-embolic stockings
  • nimodipine
  • analgesia
  • doppler studies
82
Q

How can cerebral artery aneurysms be managed?

A
  • surgical clipping
  • endovascular coils, stents and glue
  • conservative
83
Q

What are the complications associated with aneurysms and how would you manage them?

A
  • rehaemorrhage - immediate repair
  • delayed ischaemia - fluid management, nimodipine, inotropes, angioplasty
  • hydrocephalus - LP, shunt
  • hyponatraemia - hypertonic saline, fludrocortisone
  • ECG changes
  • LRTI, PE, UTI
  • seizures
  • DVT
84
Q

What is consciousness and what factors affect it?

A

it reflects level of arousal and presence of cognitive behaviour
factors: trauma, elevated ICP, fever, seizure, sepsis, medications etc.

85
Q

Describe the scoring used in the Glasgow Coma Scale in adults.

A 
EYE OPENING
4 spontaneous
3 to verbal command
2 to pain
1 none
VERBAL
5 oriented
4 confused
3 inappropriate
2 incomprehensible sounds
1 none
MOTOR
6 obeys command
5 localised pain
4 normal flexion
3 abnormal flexion
2 extension
1 none
86
Q

How is GCS modified for young children?

A

verbal scale is not appropriate in non-verbal children
5 appropriate words, smiles, fixes/follows
4 consolable crying
3 persistently irritable
2 restless, agitated
1 none

87
Q

How is GCS used to classify head injury?

A

14-15: minor
9-13: moderate
<8: severe

88
Q

Discuss the WFNS grading system of SAH.

A 
I: GCS 15 and -ve focal signs
II: GCS 13-14 and -ve focal signs
III: GCS 13-14 and +ve focal signs
IV: GCS 7-12 and +/-ve focal signs
V: GCS 3-6 and +/-ve focal signs
89
Q

What is multiple sclerosis?

A
  • idiopathic inflammatory demyelinating disease of CNS
  • acute episodes of inflammation are associated with focal neurological deficits e.g. weak leg, visual loss and urinary incontinence
  • deficits usually develop gradually, last for more than 24hrs and may gradually improve over days to week
  • later in untreated disease patients becomes more disabled
90
Q

List subtypes of MS.

A
  • primary progressive MS
  • secondary progressive MS
  • benign MS
  • relapsing remitting MS
  • progressive relapsing MS
91
Q

Name some syndromes that can develop into MS.

A
  • optic neuritis
  • clinically isolated syndromes
  • transverse myelitis
  • radiologically isolated syndromes
92
Q

Discuss optic neuritis in relation to MS.

A
  • painful visual loss that comes on over a few days caused by inflammation of optic nerve
  • 30% develop MS by 5yrs
  • 50% develop MS by 15yrs
  • risk of MS depends on MRI scan and oligoclonal bands
93
Q

Discuss transverse myelitis in relation to MS.

A
  • inflammation of the spinal cord
  • weakness
  • sensory loss
  • incontinence
94
Q

What are clinically isolated syndromes relating to MS?

A
  • single episode of neurological disability due to focal CNS inflammation
  • may be first attack of MS
  • can happen after infection and not be related to MS
95
Q

What is the criteria for MS diagnosis?

A

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

96
Q

What causes MS?

A

genetic factors, sunlight/vit D exposure, viral trigger (EBV), smoking

97
Q

When would you suspect MS?

A
  • neurological symptoms that develop over a few days
  • a history of transient neurological symptoms that have lasted for more than 24hrs and spontaneously resolved
  • ‘hidden relapses’ e.g. optic neuritis, bell’s palsy, labyrinthitis, sensory symptoms, bladder symptoms
98
Q

List common symptoms of MS.

A
  • optic neuritis
  • nystagmus
  • dysarthria
  • dysphagia
  • muscle weakness and spasm
  • paraesthesia
  • bowel and urinary incontinence
  • diarrhoea or constipation
  • urinary frequency or retention
99
Q

How would you investigate suspected MS?

A
  1. MRI brain and cervical spine with gadolinium contrast:
    - demyelination in 2 regions can indicated dissemination in space
    - enhancing and non-enhancing areas of demyelination can indicate dissemination in time
  2. LP - oligoclonal bands, cell counts, glucose, protein
  3. Bloods - exclude other conditions
  4. Visual evoked potentials - subclinical optic neuritis
  5. CXR - exclude sarcoidosis
100
Q

What are oligoclonal bands and what is their relevance in MS?

A
  • Ig bands seen in blood and spinal fluid after protein electrophoresis
  • presence of bands in CSF but not blood suggests Ig production in CNS
  • supports diagnosis of MS but can be seen in other conditions
101
Q

Define relapse in relation to MS.

A

a relapse usually involves a new neurological deficit that lasts for more than 24hrs in the absence of pyrexia or infection

102
Q

Define pseudo-relapse in relation to MS.

A

a pseudo-relapse is the reemergence of previous neurological symptoms or signs related to an old area of demyelination in the contect of pyrexia or infection

103
Q

How is relapse in MS managed?

A
  • 1g of IV methylprednisilone for 3 days or 500mg of oral methylprednisiline for 5 days
    AND
  • PPI for gastroprotection
  • ideally prescribe at 9am to avoid sleep disruption
104
Q

Discuss the medications available for MS.

A

dimethyl fumurate, alemtuzamab, natalizumab

105
Q

What is the definition of dementia?

A
  • progressive cognitive decline
  • interfere with the ability to function at work or at usual activities
  • represent a decline from previous levels of functioning and performing
  • is not explained by delirium or major psychiatric disorder
106
Q

Describe the cognitive history of a patient with dementia.

A

MEMORY - impaired ability to acquire and remember new information e.g. repetition, forgetfulness, getting lost
EXECUTIVE FUNCTION - impaired reasoning and handling of complex tasks, poor judgement e.g. poor decision making, poor risk assessment, poor financial management
VISUOSPATIAL - impaired visuospatial abilities e.g inability to recognise faces, can’t dress or cook for self
LANGUAGE - impaired language functions e.g. difficulty thinking of words, speech hesitations

107
Q

What is the purpose of the Addenbrokes cognitive assessment? And what does it examine?

A
  • 100 questions to assess severity and pattern of impairment in dementia
  • examines memory, attention/concentration, language, visuospatial, executive function
108
Q

Which type of disorder is likely in deficit in ACEr of:

  1. Episodic memory
  2. Semantic memory
  3. Attention/conc
  4. Naming/fluency
  5. Visuospatial
A
  1. Alzheimer’s
  2. Semantic dementia - frontotemporal dementia
  3. Delirium
  4. Progressive non-fluent aphasia
  5. PD plus syndrome or variants AD
109
Q

How are seizure and epilepsy related?

A

seizure - episode of neuronal hyperactivity

epilepsy - at least two unprovoked episodes of seizure

110
Q

What are the features of focal (partial) epilepsy?

A
  • history trauma/birth injury
  • focal aura/sequelae (including gustatory/sensory/motor features) e.g. left arm increased tone = right sided motor area lesion
  • post-attack confusion/drowsiness
  • automatisms - plucking movements or fiddling, precedes seizures
  • nocturnal events
  • long lasting deja vu
111
Q

What are the features of genetic generalised epilepsy?

A
  • photosensitivity
  • age of onset = 8-26
  • alcohol or sleep deprivation
  • myoclonus
  • lack of aura
  • seizures within 2hrs of awakening
  • family history of IGE
  • EEG abnormal
112
Q

What are the DDx for epilepsy?

A
  • syncope
  • non-epileptic attack disorder
  • migraine
  • narcolepsy
  • transient global amnesia
  • panic attacks
113
Q

Define status epilepticus.

A

> 2 seizure without full recovery of neurological function between seizures
OR
continuous seizure activity >30 mins
MEDICAL EMERGENCY with recognised mortality

114
Q

Name the three drugs normally used in the treatment of focal epilepsy.

A

lamotrigine
carbamazepine
levetiracetam

115
Q

Name the three drugs normally used in the treatment of generalised epilepsy.

A

valproate
levetiracetam
lamotrigine

116
Q

What should you do if you see someone in a seizure?

A
  • keep them out of harm’s way
  • put them in recovery position
  • if movements stop and no impairment of ABCs, does not need hospitalisation once recovers awareness
117
Q

Discuss the pathology of Parkinson’s disease.

A
  • loss of dopaminergic neurones within substantia nigra
  • surviving neurones contain Lewy bodies
  • PD manifests clinically after loss of approx. 50% of dopaminergic neurones
118
Q

What are some of the suggested mechanisms for LB formation?

A
  • oxidative stress
  • mitochondrial failure
  • excitotoxicity
  • protein aggregation
  • interference with DNA transcription
  • nitric oxide
  • inflammation
  • apoptosis
  • trophin deficiency
  • infection
119
Q

Describe the pathological progression of PD.

A

Six stages:
1-2: medulla/pona and olfactory nucleus = presymptomatic or premotor e.g. loss of smell
3-4: midbrain - substantia nigra = parkinsonism
5-6: neocortex involvement = development of PD dementia

120
Q

What are the main clinical parkinsonism features?

A
  • bradykinesia - slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions
  • resting tremor - asymmetric
  • rigidity
  • postural instability
121
Q

List some of the non-motor symptoms of PD.

A
  • neuropsychiatric: dementia, depression, anxiety
  • autonomic: constipation, nocturia, erectile dysfunction, sweating, postural hypotension
  • sleep: REM sleep behaviour disorder, restless legs syndrome
  • other: reduced olfactory function, fatigue, pain and sensory symptoms
122
Q

What investigations would you undertake in suspected PD?

A
  • bloods: TFTs, copper/caeruloplasmin
  • structural imaging: CT/MRI brain normal in PD, abnormal in vascular parkinsonism
  • functional imaging: imaging of presynaptic dopaminergic function using DAT SPECT is abnormal in degenerative parkinsonism
123
Q

Discuss the treatment of PD.

A
  • L-dopa
  • dopamine agonists
  • MAO-B inhibitors
  • COMT inhibitors
  • advanced stage = deep brain stimulation of subthalamic nucleus
124
Q

Discuss the use of L-dopa in PD.

A
  • taken up by dopaminergic neurones and decarboxylate to dopamine within presynaptic terminals
  • prescribed alongside carbidopa which reduced side effects
125
Q

What are the adverse effects and long term motor complications of L-dopa?

A
  • peripheral: N&V, postural hypotension
  • central: confusion, hallucinations
  • fluctuations in motor response after 5 yrs
  • dyskinesia
126
Q

Ropinirole and pramipexole are examples of which type of PD drug? And how do they work?

A

dopamine agonists - act directly on post-synaptic striatal dopamine receptors (D2)

127
Q

What are the side effects of dopamine agonists?

A

dopaminergic side effects and somnolence, impulse control disorders and nightmares

128
Q

Which type of drug works by preventing dopamine breakdown by binding irreversibly to monoamine oxidase?

A

MAO-B inhibitors e.g. selegiline, rasagiline

129
Q

Name two COMT inhibitors and describe their mechanism of action.

A

entacapone, tolcapone - inhibit catechol-o-methyltransferase results in longer L-dopa half life

130
Q

Discuss the degenerative and secondary causes of parkinsonism.

A
  • degenerative: dementia with Lewy bodies, progressive supranuclear palsy, multiple system atrophy
  • secondary: drug-induced (dopamine antagonists), CVD, toxins, infection
131
Q

Define Parkinson’s disease.

A

common slowly progressive asymmetrical neurodegenerative disorder predominantly affecting elderly

132
Q

What investigations are needed in epilepsy?

A

brain imaging - CT or MRI
EEG - brain waves, take 1hr, lying at rest with photic stimulation
systemic provocations

133
Q

What is the mechanism of carbamazepine?

A

Voltage gated Na+ channel blocker on pre-synaptic membrane. Blocks the Na+ influx; reduces neuronal excitability and decreases the action potential.

134
Q

With which anti-epileptic should you avoid alcohol and grapefruit juice?

A

carbamazepine

135
Q

Describe the mechanism of action of sodium valporate.

A

Weak sodium ion channel blocker. Inhibitor of GABA degrading enzymes, increased GABA stops action potential.

136
Q

Which anti-epileptics can increase risk of Stevens-Johnson syndrome?

A

sodium valporate
phenytoin
lamotrigine

137
Q

How does lamotrigine work?

A

Varied mechanism of action. Inhibits voltage-gated Na+ channels and/or Ca2+ channels. Acts on pre-synaptic neuronal membrane, reduces action potential and excitatory signals.

138
Q

Discuss the mechanism of action of Levetiracetam.

A

SV2A is a synaptic vesicle protein required for neurotransmitter release. Drug blocks this and reduced neurotransmitter release. Induces an anti-epileptic effect

139
Q

What is the most common gene mutation that causes PD?

A

PARK8 (LRRK2) - 70% chance of developing PD

140
Q

Look over clinical neuroanatomy lecture.

A

DON’T SKIP THIS!!

141
Q

Which infectious syndromes do bacterial microbes give rise to in the CNS? Name the three most common pathogens.

A
  • meningitis, meningo-encephalitis, abscess

- meningococcus, pneumococcus, listeria

142
Q

Which pathogens most commonly cause encephalitis as well as meningitis?

A 
enterovirus
HSV
VZV
HIV
mumps
143
Q

Cryptococcosis is an example of a fungal microbe. Which syndromes do these commonly lead to in the CNS?

A

meningo-encephalitis

mass lesion

144
Q

Which type of microbe is toxoplasmosis?

145
Q

What is meningitis? Differentiate between acute and sub-acute.

A
  • inflammation of meninges
  • acute: bacterial or viral
  • sub-acute: bacterial (listeria, TB)
146
Q

What are the signs and symptoms of meningitis?

A
  • headache
  • neck stiffness
  • reduced GCS
  • fever
  • confusion (cerebritis/encephalitis)
  • rash: purpuric and/or petechial but macular early on (meningococcal)
147
Q

What are the risk factors for developing pneumococcal BM?

A

70% underlying disorder

  • middle ear disease
  • head injury
  • neurosurgery
  • alcohol
  • immunosuppression (HIV)
148
Q

Immunosuppression and pregnancy are risk factors to developing which type of BM?

149
Q

What are some distinguishing factors of pneumococcal meningitis?

A
  • focal signs
  • seizures
  • VIII palsy
  • other pneumococcal infection signs e.g. endocarditis, CAP, ENT
150
Q

List factors which are associated with poor prognosis in bacterial meningitis.

A
  • pneumococcus
  • reduced GCS
  • CNS signs
  • older age > 60yrs
  • CN palsy (pneumococcal)
  • bleeding (meningococcal)
151
Q

What investigations would you undertake for suspected meningitis?

A
  • history and exam (throat, cranial nerves)
  • blood cultures and PCR
  • throat culture, viral gargle
  • FBC, UEs, LFTs, CRP
  • lumbar puncture - cell count, gram stain, culture, PCR, protein, glucose, viral PCR
152
Q

LP should routinely be performed before CT. When should CT be arrived out first?

A
  • GCS < 12
  • CNS signs
  • papilloedema
  • immunocompromised
  • seizure
153
Q

When is a lumbar puncture contraindicated?

A
  • brain shift
  • rapid GCS reduction
  • resp/cardiac compromise
  • severe sepsis
  • rapidly evolving rash
  • coagulopathy
154
Q

Which antibiotic is first line therapy in possible bacterial meningitis?

A

IV ceftriaxone 2g 12hrly

155
Q

Discuss the definitive antibiotic therapy for meningococcal, pneumococcal and listeria BM

A
  • meningococcal: IV ceft or benpen 5 days
  • pneumococcal: IV ceft or benpen 10-14 days
  • listeria: IV amox (stop ceft) 21 days - increase if complications
156
Q

Should corticosteroids be used in BM?

A

YES for proven BM

10mg QID dexamethasone 4 days

157
Q

Discuss mechanisms put in place to prevent meningoccal infection. (5 points)

A
  • primary: childhood immunisations - HIB, pneumo, mening
  • secondary: chemoprophylaxis
  • travel to high prevalence areas: ACWY
  • asplenia, complement deficiency: men boosters, HIB and pneumo
  • cochlear implants: pneumo booster
158
Q

How is viral meningitis diagnosed and managed?

A
  • only after exclusion of BM

- consider aciclovir only if immunocompromised or confused (encephalitis)

159
Q

How would you investigate viral encephalitis?

A
  • history: confusion, fever, seizures
  • lymphocytic CSF (normal glucose), PCR
  • EEG
  • MRI
160
Q

Discuss the effects of intra-cerebral TB.

A
  • sub-acute (weeks)
  • may be unmasked during TB Rx
  • CN lesions III, IV, VI, IX
161
Q

How would you treat intra-cerebral TB?

A
  • steroids

- Rx for one year (RIF, INH, Pyraz, Etham)

162
Q

How does HIV brain disease develop and in what ways does it manifest?

A
  • unrecognised/untreated infection and marked immunodeficiency or lifestyle
  • encephalitis
  • dementia
  • neuro-syphilis
  • opportunistic
163
Q

What is PMLE?

A

progressive focal multifocal leucoencephalopathy - progressive motor dysfunction

164
Q

In which patients does PMLE develop?

A

immunocompromised, HIV, anti-TNF, transplant, JCV

165
Q

Which pathogen commonly gives rise to intra-cerebral toxoplasmosis?

A

toxoplasma gondii

166
Q

How does intra-cerebral toxoplasmosis manifest?

A

headache, seizures, focal CNS signs

167
Q

How would investigate suspected intra-cerebral toxoplasmosis?

A

IgG and IgM - blood

PCR - CSF

168
Q

Which drugs are used in the treatment of toxoplasmosis?

A

sulphadiazine + pyramethamine

169
Q

How is CSF investigated in cryptococcal meningitis?

A

india ink
cryptococcal antigen
culture

170
Q

Amphotericin B and flucytosine are used in the treatment of which pathogen causing meningitis?

A

cryptococcal

Phase 3 (10 decks)

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