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Phase 2A > Neurology > Flashcards

Neurology Flashcards

1
Q

Differentiate between CNS & PNS?

A

CNS = brain & spinal cord, collection of cell bodies = nuclei

PNS = outside the CNS
collection of cell bodies = ganglia

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2
Q

What connects the CNS & PNS?

A
  • 12 cranial nerves - brain & head and neck
  • 31 spinal nerves - spinal cord and periphery
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3
Q

the Autonomic nervous system:

  • what is it
  • where is it
  • what are its divisions
A
  • system beyond conscious control, e.g. viscera, smooth muscle, glands, heart
  • part in CNS part in PNS
  • sympathetic and parasympathetic divisions
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4
Q

What is the sympathetic nervous system

A
  • essentially fight or flight system
  • ganglia close to spinal cord
  • supply visceral organs and structures of the superficial body organs
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5
Q

Effect of the sympathetic nervous system

A
  • **increases** heart rate & force of constriction in heart
  • **vasoconstriction**
  • **bronchoDILATION**
  • sphincter contract
  • decreased gastric secretion & motility
  • male ejaculation
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6
Q

Major structure of the sympathetic nervous system?

A

Sympathetic trunk - two chains of ganglia lying close to spinal cord (one on each side)

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7
Q

Neurotransmitter of sympathetic nervous system and receptor?

A

Preganglionic: Acetyl-choline ACh to nicotinic receptors
Effector cell: Noradrenaline to adrenergic receptors

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8
Q

What is the parasympathetic nervous system

A
  • essentially the rest and digest system
  • some ganglia in brain, some near the organs
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9
Q

Major structure of the sympathetic nervous system?

A

Cranial nerves 10, 9, 7, 3

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10
Q

Neurotransmitter of sympathetic nervous system and receptor?

A

Preganglionic: Acetyl-choline ACh to nicotinic receptors
Effector cell: Acetyl-choline ACh to muscarinic receptors

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11
Q

Effect of the sympathetic nervous system

A
  • **decrease** heart rate and force of contraction
  • **vasodilation**
  • **bronchoCONSTRICTION**
  • increased gastric motility and secretion
  • spincter relaxation
  • male erection
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12
Q

How many pairs of spinal nerves do we have

A

31 - 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal

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13
Q

Where is the motor cortex located

A

Precentral gyrus, **frontal lobe**!!

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14
Q

Where is the somatosensory cortex located

A

Postcentral gyrus, **parietal lobe**!!

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15
Q

Where is the visual cortex located

A

**Occipital lobe**

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16
Q

Where is the auditory cortex located?

A

Lateral fissure, **temporal lobe**

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17
Q

What is the frontal lobe responsible for?

A

higher intellect, personality, mood, social conduct and language (in dominant hemisphere only)

remember by teens - they’ve not developed frontal lobe properly yet lol also pituitary tumour in optic chiasm can cause mood changes

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18
Q

What is the parietal lobe responsible for?

A

language on dom
sensory perception and integration on nondom

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19
Q

What is the temporal lobe responsible for?

A

memory and language primary auditory cortex is here!!

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20
Q

What is the occipital lobe responsible for?

A

vision - primary visual cortex is here!

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21
Q

If a patient has
- recognition deficits (agnosias) - e.g. cannot recognise basic sounds or faces

Where has the cerebrovascular accident occurred?

A

Temporal lobe

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22
Q

If a patient has

  • personality and behavorial changes
  • inability to solve problems

Where has the cerebrovascular accident occurred?

A

Frontal lobe

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23
Q

If a patient has
- visual field defects

and this is a cerebrovascular accident - where has this occurred?

A

Occipital lobe

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24
Q

If a patient has
- attention deficits, e.g. contralateral hemispatial neglect syndrome (does not pay attention to a side of body)

Where has the cerebrovascular accident occurred and what is the relation to the side of the body neglected?

A

Parietal lobe

Lesion would be on the opposite of the neglected body side

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25
Q

What is the cerebellum responsible for?

A

Generally, movement

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26
Q

Which neoplasm causes bitemporal hemianopia?

A

pituitary adenoma

ah the good old days

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27
Q

What is a dermatome

A

area of skin supplied by a single spinal nerve

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28
Q

What is a myotome

A

muscles supplied by a single spinal nerve

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29
Q

Name cranial nerves in order!!

(mnemonic & names)

A

Oh Oh Oh They Traveled And Found Voldemort Guarding Very Ancient Horcruxes.

Olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, vestibulocochlear, glossopharyngeal, vagus, accessory, hypoglossal

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30
Q

Nerves for sensory, motor or both?

(mnemonic)

A

Some say money matters but my brother says big brains matter most

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31
Q

Parasympathetic nerves?

(mnemonic & which)

A

1973

10 - vagus
9 - glossopharyngeal
7 - facial
3 - oculomotor

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32
Q

Nerves of the eye?

(mnemonic & what they stand for)

A

SO4 LR6 3

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33
Q

How would you interpret the results of CN I tests

A

If **anosmia**: causes are

  • meningioma
  • trauma - skull or cribriform plate
  • Parkinson’s
  • mucus block / covid / genetics
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34
Q

How would you test CN II

A

visual acuity

  • distance - Snellen chart & pinhole
  • colour vision - ishihara plates

fields

  • neglect / inattention
  • field - formal is **Amsler chart**
  • blind spot

optic disc
- fundoscopy

Pupil

  • pupillary light reflex (direct - ipslateral, consensual - contralateral, swing check relative afferent pupillary defect)
  • accomodation reflex - distant to near
  • size, shape
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35
Q

Visual field defects - key in investigation?

A

Test one eye while covering the other! Patient often do not realise

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36
Q

**bitemporal hemianopia**

  • what is it?
  • pathology?
A
  • loss of temporal visual field in both eyes
  • optic chiasm tumour
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37
Q

**Homonymous field defects**

  • types
  • pathology?
A
  • hemianopias or quadrantanopias
  • same side of visual field in each eye
  • pathology is behind optic chiasm in visual pathways: stroke, tumour, abscess
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38
Q

**Scotoma**

  • what is it?
  • pathology?
A
  • absent or reduced vision surrounded by areas of possible vision
  • wide range, including demyelinating (MS, DM)
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39
Q

**Monocular vision loss**

  • what is it?
  • pathology?
A
  • total loss of vision in one eye secondary to optic nerve pathology or ocular disease
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40
Q

How would you interpret results of a fundoscope exam?

A

if papilloedema, causes are

  • usually **ischaemia** - intracranial bleed possible
  • **hypertension** - systemic, intracranial (benign & malignant → suspect a brain tumour!)
  • **headache**
  • **brain tumour** causing compression
  • prolonged CNS infection
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41
Q

Nerves of the eye again!!

(mnemonic & what they stand for)

A

SO4 LR6 3

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42
Q

Strabismus

  • what is it?
  • pathology?
  • how would you assess it?
A
  • condition where eyes do not properly align with each other when looking at an object
  • pathology affecting III, IV & Vi (and/or) can all cause strabismus
  • test by corneal reflex test / Hirschberg test and or cover test
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43
Q

How would you test CN VII?

A

By facial expressions:

  • raising eyebrows
  • closing eyes
  • blowing out cheeks
  • smiling
  • pursing lips
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44
Q

How to differentiate between a Facial Palsy and a stroke?

A

stroke is forehead sparing whereas the nerve palsy is not!!

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45
Q

Differentiate between Bell’s palsy and facial palsy?

A

Facial palsy is termed Bell’s palsy when it is idiopathic

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46
Q

Define stroke?

A

neurological deficit lasting longer than 24 hours due to vascular compromise

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47
Q

What are ischaemic strokes? Subclassify?

A

Reduction in cerebral blood flow due to arterial occlusion or stenosis

= anterior / middle / posterior cerebral artery / lacunar
(thrombotic / embolic)

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48
Q

How can you distinguish haemorrhagic and ischaemic strokes?

A

No reliable way

tho intracerebral more often associated with severe headaches or coma → ICP ++

patients on anticoag: assumed to have haemorrhage unless proven otherwise

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49
Q

Associated risk factors for ischaemic strokes?

A

AF - higher risk of thrombus / embolus

atherosclerosis

shock

vasculitis

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50
Q

What are haemorrhagic strokes? Classify?

A

Ruptured blood vessels leading to reduced blood flow

Intracerebral / subarachnoid / intraventricular

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51
Q

Risk factors for strokes?

A

Hypertension, age, AF

Smoking, diabetes, hypercholesterolaemia, polycythaemia

medications - HRT, combined oral contraceptive pill

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52
Q

FAST tool to identify stroke in community?

A

Face, Arm, Speech, Time

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53
Q

Tool used to identify strokes in ER?

A

ROSIER

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54
Q

Differentiate stroke from bell’s palsy?

A

Stroke = forehead sparing = Upper motor neuron lesion

Bell’s palsy = everything on face = Lower motor neuron lesion

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55
Q

Investigations for Stroke?

A

Head CT
→ rule out haemorrhagic before thrombolysis & LP
→ aspirin 300mg stat post CT

LP - MUST if CT normal
not before 12h - xanthochromia

Pulse, BP, ECG
look for AF / if high BP then must maintain!! 20% will compromise cerebral perfusion

Bloods
thrombocytopenia & polycythaemia - rule out hypoglycaemia

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56
Q

3 layers of meninges of the brain?

A

IN → out

Pia mater, arachnoid mater, dura mater

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57
Q

Risk factors for an extradural haemorrhage?

A

Young patient with traumatic head injury + ongoing headache

periods of improval then rapid decline (haematoma getting larger to compress intracranial contents)

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58
Q

How might an extradural haemorrhage appear on CT?

A

Lentil / lemon, biconvex

Limited by cranial sutures!

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59
Q

How might a subdural haemorrhage appear on CT?

A

Crescent

Not restricted by suture lines!

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60
Q

Risk of subdural haemorrhage?

A

elderly, alcoholic patients

→ atrophy in brian = more likely to rupture

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61
Q

How might an subarachnoid haemorrhage appear on CT?

A

Star / around the brain

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62
Q

Causes of subarachnoid haemorrhage?

A

Usually ruptured cerebral aneurysm
= berry aneurysm = 80%

arterio-venous malformations

others: enceph, vasculitis, tumour, idiopathic

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63
Q

Risk for subarachnoid haemorrhage?

A

Hypertension, smoking, excessive alcohol consumption, cocaine

sickle cell anaemia

fam hx, also black female 45-70

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64
Q

Symptoms of a subarachnoid haemorrhage?

A

Sudden and severe thunderclap headache hitting on the back of the head

→ Most severe at beginning, short period

N+V, collapse, seizure
can present with meningism

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65
Q

How should you treat haemorrhagic strokes (4)?

A

Do not give antiplatelets!!

Reverse anticoagulants

Control hypertension

Nimodeipine

Decompression of raised ICP
Mannitol (diuretic) / Burr holes

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66
Q

What is nimodepine?

A

a CCB

Prevent & tx of ischaemic neurological defects following aneurysmal subarachnoid haemorrhage

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67
Q

How might you reverse warfarin?

A

Human Prothrombin Complex (Beriplex) & Vitamin K

if unavailable - fresh frozen plasma

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68
Q

Direct Oral anticoagulants (DOAC) reversal:

Agents for Dabigatran, rivaroxaban, apixaban?

A

Dabigatran = Idarucizumab

Rivaroxaban & Apixaban = Andexanet alfa
(R&A = direct factor Xa inhibitor)

(D = direct oral anticoag)

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69
Q

Surgical interventions for intracranial bleeds?

A

Coiling - place platinum coils into aneurysm and seal it off from artery

Clipping

→ not indicated unless ruptured

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70
Q

Complications of intracranial haemorrhages?

A

Vasospasm - can result in brain ischaema

Hydrocephalus - buildup of fluid in ventricles
(LP or shunt)

Seizures

(prevent with nimodipine)

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71
Q

Features of anterior cerebral artery stroke?

A

Limb dysfunctions
gait apraxia, truncal ataxia, incontinence

**Sensory loss, mostly in lower limbs**
amarosis fugax (transient vision loss)
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72
Q

Features of middle cerebral artery stroke?

A

Upper limbs > lower limbs

Facial / speech features
facial droop, aphasia
homonymous hemianopia
hemineglect in non dominant hemisphere

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73
Q

Features of posterior cerebral artery stroke?

A

Heavy visual features

visual agnosia - cannot interpret info but can see
colour naming / discriminating problems

double vision, visual field defects

contralateral homonymous hemianopia w/ macular sparing
(loss sight same side both eyes)

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74
Q

Features of a lacunar stroke?

A

lacks true cortical signs: aphasia, visuospatial neglect, gaze deviation, visual field defects

Involves limbs more than head
pure sensory impairment / motor stroke, ataxic hemiparesis (weak in leg), clumsy hand etc

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75
Q

Treatment principles, ischaemic stroke?

A

Thrombolysis = up to 4.5 hours since onset of symptoms

Thrombecttomy = 6-24 hours since onset

Clopidogrel 24 hours after both

if both unsuitable: aspirin daily 2weeks then lifelong clopidogrel

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76
Q

What is thrombolysis?

A

give within 4.5 hours of onset
ischaemic stroke
→ once excluded primary ICH with CT!

Alteplase = tissue plasminogen activator, breaksdown clots & reverse stroke

Monitor for complications e.g. IC / systemic haemorrhage = repeat CT

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77
Q

What is thrombectomy?

A

= mechanical removal of clot

give 6-24 hours since onset of symptoms
→ must confirm occlusion on imagine

→ clopidogrel 24 hours after

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78
Q

How might you prevent stroke?

A

Platelet tx
Clopidogrel 75mg daily ± aspirin
(alt dipyridamole)

Cholesterol treatment
atorvastatin 80mg
(alt simvastatin)

Tx modifiable risk factos
AF = warfarin / DOAC
BP - ACEi

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79
Q

Mechanism of statins?

A

Inhibit HMG-CoA, thereby decreasing production of LDL levels

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80
Q

Define transient ischaemic attack?

A

neurological deficit lasting less than (or up to) 24 hours

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81
Q

Management for TIA’s?

A

If on anticoag → immediate admission

aspirin 300 mg stat
daily until specialist review

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82
Q

What is epilepsy?

A

a recurrent tendency to have spontaneous, intermittent, abnormal electrical activity in parts of the brain, manifesting in seizures

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83
Q

What is a seizure?

A

transient episodes of abnormal electrical activity in the brain as caused by excessive, hypersynchronous neural discharge

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84
Q

Diagnostic criteria, epilepsy?

A

= at least 2 or more unprovoked seizures occurring > 24hrs apart to DIAGNOSE EPILEPSY

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85
Q

What is syncope? Risk factors?

A

= loss of consciousness due to hypoperfusion to brain

Risk - prolonged upright position, sweating, nausea, issues w/ heart / BP etc

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86
Q

Differentiate non-epileptic seizures to epileptic seizures?

A

Non epileptic = situational, situational, with pre-ictal anxiety

Epileptic = result from sleep, can have incontinence & sleep

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87
Q

General advice for patients with epilepsy?

A

→ CANNOT DRIVE = inform DVLA
until free of day time seizures for minimum a year

→ try not to swim alone, avoid dangerous sports, leave door open when taking bath

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88
Q

Causes of epilepsy?

A

⅔rd idiopathic, often familial

Post CNS infection → cortical scarring ‘sclerosis’

Space occupying lesion, stroke, alzheimer’s / dementia, alcohol withdrawal

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89
Q

Risk factors for epilepsy?

A

Fam hx

Premature born babies

Abnormal blood vessel in brain
arterio-venous malformations

Use of drugs - cocaine

Alzheimer’s / dementia

stroke / brain tumour / infection

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90
Q

DIfferentials for epilepsy?

A

Syncope = most common

  • *Dissociative (non-epileptic) seizures**
  • situational, durational, dissociative
  • eyes closed, can cry / speak, same f but larger amp
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91
Q

Investigations & Diagnosis for epilepsy?

A

> 2 seizures 24 hours apart

→ diagnosis of exclusion

EEG (checks for which type)

MRI brain (structural problems / tumours)

CT head - space occup lesion

exclusions - ECG for heart

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92
Q

4 stages of epileptic attacks?

A

Prodrome = change of mood or behaviour

aura = deja vu, strange feeling in gut, flashing light

ictus = the seizure, 30-120s

Post-ictally = after seizure

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93
Q

Examples of post-ictally behaviour?

A

Amnesia

Headache, confusion, myalgia and sore tongue (might be bitten)

Temporary weakness after focal seizure in motor cortex = todd’s palsy

dysphagia following temporal lobe seizure

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94
Q

What are generalised seizures?

A

Bilateral, symmetrical & synchronous motor manifestations

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95
Q

What are focal seizures?

A

Features referable to one part of a hemisphere

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96
Q

Floaters in vision field / visual flashes

Which lobe can the seizure be located to?

A

Occipital lobe
= visual

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97
Q

Pins and needles, pricking, ants are crawling over skin

Which lobe can the seizure be located to?

A

Parietal lob

= sensory seizures

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98
Q

Hallucinations, lip smacking / grabbing, plucking, sense of deja vu

Which lobe can the seizure be located to? Feature post-ictally?

A

Temporal lobe

Post ictally = dysphagia

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99
Q

Head / leg movements, posturing, start from one point then → whole body

Which lobe can the seizure be located to? Post-ictally features?

A

Frontal lobe
= motor

  • *Post ictally = weakness**
    assoc. Todd’s palsy = paralysis of limbs involved for hours
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100
Q

What is status epilepticus? How would you manage it?

A

→ seizures lasting > 5 minutes or > 3 seizures in one hour
= medical emergency

IV lorazepam 4mg, repeat aft 10 minutes if seizure continues

If still = IV phenobarbital or IV phenytoin

Other options
buccal midazolam, rectal diazepam

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101
Q

What are Tonic-clonic seizures?

A 
tonic = muscle tensing
clonic = muscle jerking
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102
Q

What are absent seizures?

A

→ typically in children

blank, stares into space and abruptly returns to normal

often don’t realise, 10-20s,
> 90% grow out of it

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103
Q

Feature of absent seizure on EEG?

A

3Hz spike and wave activity!

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104
Q

What are atonic seizures?

A

Drop attacks = sudden loss of muscle tone and cessation of movement = fall

typically > 3 minutes, begin in childhood

differential is lennox-gastaut syndrome

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105
Q

What are myoclonic seizures?

A

→ usually in children, as a part of juvenile myoclonic epilepsy

sudden brief muscle contractions, like a sudden ‘jump‘

= a violently disobedient limb or be suddenly thrown to the ground

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106
Q

If a child presents with myoclonic seizure, test you should do?

A

Genetic testing

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107
Q

Treatment principles for epilepsy?

A

For generalised seizures

→ 1st = sodium valproate
→ 2nd = lamotrigine or carbamazepine

Reverse for focal seizures

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108
Q

Sodium valproate

Class / mechanism / SE / CI?

A

antiepileptics

increase GABA activity → relax the brain

SE = teratogenic, liver damage & hepatitis, hair loss, tremor

CI = girls & women of reproductive age!

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109
Q

Carbamazepine

Class / Mechanism / SE?

A

antiepileptic

Inhibit neuronal sodium channels

SE - agranulocytosis (carbimazole also)/ aplastic anaemia / CYP450

(also for trigeminal neuralgia)

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110
Q

Lamotrigine

class / SE

A

antiepileptic

also for bipolar disorder

SE Stevens-Johnson syndrome / DREE = life threatening rashes!!
+ leukopenia

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111
Q

Surgical options to treat seizures?

A

Surgical resection = if single defined cause or area

Vagal nerve stimulation / disconnection

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112
Q

What are infantile spams?

A

West syndrome, rare

start around 6m infancy, clusters of full body spasms

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113
Q

Treatment for infantile spams?

A

1st line prednisolone & vigabatrin

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114
Q

What is Parkinson’s?

A

Degeneration of the pars compacta in substantia nigra of brain leading to decrease in dopamine

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115
Q

Causes & risk factors of Parkinson’s

A

No known cause
Genetic mutations - PINK1, Parkin etc

Risk
Pesticide exposure, MPTP in illegal opioids
male, age, fam history
! non smoker = higher !

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116
Q

Presentation of Parkinson’s?

A

TRAP
+ sleep disturbances / anosmia

T = tremor = resting!
pill rolling tremor

R = rigidity
cogwheel rigidity, esp in arms

A = akinesia / dyskinesia
reduced arm swing, shuffling gait, soft voice, reduced blinking, drooling

P = postural instability
& forward tilting

→ NO WEAKNESS

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117
Q

Differentials for Parkinson?

A

Benign essential tremor

Dementia with lewy bodies

Progressive suprenuclear palsy

if on Levodopa
high response = lewy body dementia
(hallucinations, agitation, confusion)
low response = Multi-system atrophy

(symmetrical, worse on mvt, no other parkinson features, better with alcohol)

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118
Q

Investigations for Parkinson’s?

A

CT / MRI

PET with fluorodopa
localises dopamine deficiency in basal ganglia

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119
Q

What might you find on an autopsy of a Parkinson patient?

A

Lewy body depositions = eosinophilic protein aggregations in substantia nigra, cytoplasm rich in eosin

disappearance / fading of the substantia nigra

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120
Q

Most effective tx for Parkinson’s?

A

Levodopa = 1st line

if motor symptoms not affecting patient’s QoL then others or levodopa

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121
Q

Levodopa

class / mechanism / SE

A

synthetic dopamine (precursor)
→ boost patient’s dopamine level
→ give with COMT

SE less effective over time, if dose too high = dyskinesia (N+V, arrhyth, chorea, dystonia)

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122
Q

COMT inhibitors

Examples / Mechanism?

A

entacapone, tolcapone

Inhibition of breakdown of dopamine by Catechol-O-Methyl Transferase enzymes

used in conjunction w/ levodopa

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123
Q

Dopamine Receptor Agonists

Examples / mechanism / SE

A

bromocriptine / cabergoline

= stimulate dopamine receptors

SE impulse control disorders, hallucinations, excessive daytime somnolence

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124
Q

MAO-B inhibitors

Examples? Mechanism?

A

Selegiline, rasagiline

Inhibits breakdown of dopamine by Monoamine oxidase-B enzymes

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125
Q

Surgical tx options for Parkinson’s?

A

Deep brain stimulation

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126
Q

Define dementia?

A

Clinical syndrome characterised by significant deterioration in cognitive skills → impairment of normal function

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127
Q

Reversible causes of dementia & tx (5)?
aka differentials of dementia?

A

alcohol
hypothyroidism (THR)
vitamin B12 deficiency
Syphilis (penicillin)
Normal pressure hydrocephalus
(ventriculoperitoneal shunt)

128
Q

What is an Normal pressure hydrocephalus?

A

= abnormal venous drainage of cerebrospinal bluid → backup of fluid & hydrocephalus

symptoms = dementia, urinary incontinence, magnetic gait

MRI - no cortical atrophy, ventriculomegaly of all ventricles, patent cerebral aqueduct

Tx ventriculoperitoneal shunt

129
Q

Irreversible causes of dementia? (Types of dementia)?

A

Alzheimer’s disease

Vascular dementia

Lewy body dementia

Frontotemporal dementia

130
Q

Briefly outline pathophysio of Alzheimer’s?

A

neurofibrillary tangles & beta amyloid plaques affect function of neurons → interrupt key neuron process → cell death

131
Q

What can be found on a brain biopsy in someone with Alzheimer’s?

A

Neurofibrillary tangles (tau protein aggregations) & beta amyloid plaques

Widespread cerebral atrophy esp. cortex & hippocampus

132
Q

Key presentation of Alzheimer’s?

A

Memory loss

Loss of personality, intellect & language

133
Q

Investigations for Alzheimer’s?

A

= Exclude

CT / MRI → hippocampus & cortex atrophy

definitive is actually brain biopsy but obv impossible until death

134
Q

Treatment option for Alzheimer’s?

A

Symptomatic
Cholinesterase inhibitors
(+ACh levels)

NMDA receptor antagonists

Depression = SSRI

135
Q

Key presentation vascular dementia?

A

Step wise steady & gradual deterioration related to region (and a history) of stroke / TIAs

136
Q

Symptoms of vascular dementia?

A

Urinary incontinence, cranial nerve palsy, focal neurological deficits

137
Q

Treatment for vascular dementia?

A

None to reverse

→ Prevent another stroke
= BP, lifestyle, smoke, antiplatelet = aspirin

(nimodepine is ischaemic)

138
Q

Key presentation frontotemporal dementia?

A

< 65 years

Personality change, lack of social inhibition

139
Q

What might you find on an imaging scan of frontotemporal demential patient?

A

Atrophy of frontal & temporal lobes

sparing other lobes!

140
Q

Treatment for frontotemporal dementia?

A

No tx available to delay progression

SSRI = behavoural symptoms
(setraline, citalopram)

Atypical antipsychotics = psychosis

141
Q

Symptoms of Parkinson’s disease & lewy body dementia?

A
  • *= Parkinsonism**
  • *= TRAP**

Tremor (resting)

Rigidity (esp in arms)

Akinesia / bradykinesia

Postural instability

142
Q

Differentiate Parkinson’s disease dementia x Lewy body dementia?

A

→ sequence of events

Parkinson’s = Parkinsonism THEN dementia

Lewy body = dementia THEN Parkinson

143
Q

If on Levodopa, how might you differentiate Lewy body dementia x Parkinson’s disease dementia?

A

Responds well = Parkinson’s d.d.

If 3 tions: hallucination, agitation & confusion → Lewy body dementia as patients are dopamine sensitive

144
Q

Other features of lewy body dementia?

A

Recurrent visual hallucinations

Flunctuating attention / alertness / cognition

Sleep disturbances

145
Q

Tx for Lewy body dementia?

A

Cholinesterase inhibitors = improve symptoms, but don’t slow progression

Levodopa = helps with motor impairment but risk of developing delirium

→ CI antipsychotics (worsen!)

146
Q

What is Huntington’s disease?

A

Autosomal dominant

genetic condition, progressive deterioration in the nervous system

147
Q

Genetic stuff for Huntington’s?

A

Trinucleoside repeat disorder = CAG

Genetic mutation on HTT gene on chromosome 4

148
Q

What is anticipation?

A

= in Huntington’s

each successive generation have more repeats in gene
= earlier age of onset
= increased severity of disease

149
Q

Presentation - Hungtington’s?

A

30-50 years, but can be earlier or later

Chorea
= involuntary, purposeless movements
= parakinesia = try to incorporate into purposeful mvt

Dementia
= cognitive decline

Behavior changes
= cognitive, psychiatric, mood problems,

dysarthria / dysphagia / dystonia + parkinson’s

150
Q

How might you diagnose Hungtington’s chorea?

A

blood PCR for CAG repeats

MRI = atrophy of caudate & putamen, enlargement of the lateral ventricles

151
Q

Tx for Hungtington’s?

A

No tx for slow or stop

Symptomatic relief / MDT in QoL

speech & language / genetic counselling / advanced directives

chorea = antipsychotics, benzodiazepine

152
Q

Prognosis for Huntington’s?

A

Progressive condition

LE 15-20 years after onset

death often due to respiratory, e.g. pneumonia, but also common is suicide 😞

153
Q

Before any headache investigation - one thing to rule out?

A

Idiopathic cranial hypertension

154
Q

Signs of raised intracranial pressure?

A

headache, vomitting, reduced levels of consciousness, papilloedema

Cushing’s triad
widening pulse pressure, bradycardia, irregular breathing

155
Q

Presentation & risk - idiopathic intracranial hypertension

A

headache, blurred vision, enlarged blind spot, papilloedema, ± 6th nerve palsy

risk → obesity, female, pregnancy, drugs (COCP, steroids, tetracyclines, lithium)

156
Q

Signs of papilloedema?

A

Optic nerve swelling & blurring of the disc margins

cotton wool spots, silver wiring,
hard exudates, retinal haemorrhage

→ seen on a fundoscope

157
Q

Tx Idiopathic intracranial hypertension?

A

1st line = Weight loss

Diuretics = acetazolamide

Topiramate (anticonvulsant) = also cause weight loss

Surgery
optic nerve sheath decompression and fenestration

158
Q

Thunderclap headache?

A

Subarachnoid haemorrhage!

159
Q

Thunderclap headache?

A

Subarachnoid haemorrhage!

160
Q

Presentation of tension headaches?

A

Aches across the forehead in a band pattern

Pressing & tightening
come and go

no N&V

161
Q

Tx Tension headaches?

A
  • *Basic analgesia**
  • *= aspirin / paracet / ibuprofen**

Consider amitriptyline

Relaxation techniques & hot towels to local area

162
Q

Tension headache associations

A

stress / depression / alcohol / skipping meals / dehydration

163
Q

Triggers of migraines?

A

= chocolate

Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie in’s
Alcohol
Tumult - loud noise
Exercise

164
Q

Risk factors for migraines?

A

females, positive family history

165
Q

Presentation of migraine?

A

moderate to severe intensity

  • *pounding or throbbing in nature**
  • *nausea & vomiting**

± aura
± photophobia, phonophobia

166
Q

What is aura & examples?

A

prodrome / postdrome to migraine

visual = flashing light, zigzag lines, lose part of vision, black holes in visual field

sensory = parasthesia

speech or language = problems saying / understanding words

167
Q

Diagnostic criteria for migraines

A

5 attacks

168
Q

Acute management for migraines?

A

oral triptan ± paracetamol
or other analgestics = aspirin / paracetamol

169
Q

Preventive management for migraines?

A

Topiramate / propanolol

→ amitriptyline

→ 10 sessions of acupuncture over 5-8 weeks

  • *Riboflavin** (vit B12)
  • *Botulinum Toxin type A** = last line

(CI teratogenic / asthma)

170
Q

Presentation of cluster headaches?

A

→ headache + unilateral,
ipslateral eye concentrated

red, swollen, watering eye

miosis = constrict,
ptosis = eyelid droop

nasal discharge, facial sweating

→ 5 to diagnose
→ episodic, can wake pt

171
Q

Triggers of cluster headaches?

A

Alcohol, strong smells, exercise

172
Q

Acute treatment for cluster headaches?

A

100% 15L O2
15-20 minutes via non-rebreathable mask
CI if COPD

Triptan = SC sumatriptan 6mg
→ serotonin receptor agonist = reduce vascular inflammation

173
Q

Preventive measures for cluster headaches?

A

1st line CCB = verapamil

Avoid alcohol during cluster period

Corticosteroids may help during cluster period (prednisolone short course 2-3 weeks to break cluster)

174
Q

Presentation - trigeminal neuralgia?

A

Intense facial pain, similar to electric shock / shooting pain lasting seconds to minutes

related to eating

175
Q

Branches of the trigeminal nerve?

A

Ophthalmic (v1)

Maxillary (V2)

Mandibular (V3)

→ any combination can be affected)

176
Q

Tx trigeminal neuralgia?

A

1st = oral carbamazepine

2nd oral phenytoin, gabapentin & lamotrigine

Surgical - microvascular decompression / gamma knife surgery

(anticonvulsants)

177
Q

Associations & triggers - trigeminal neuralgia?

A

5-10% multiple sclerosis

triggers: cold weather, spicy food, caffeine, citrus fruits, brushing teeth, cough / sneeze

178
Q

Medication overuse headache - diagnostic criteria? triggers?

A

Headache present ≥ 15 days / month

Triggers = opioids, triptanss, combination analgesic (paracetamol + codeine / opiates)

179
Q

Present sinusitis?

A

Headache associated with inflammation of sinuses

→ if tender over the sinus = DIAGNOSTIC

facial pain behind nose, forehead and eyes

180
Q

Treatment sinusitis?

A

Resolve in 2-3 weeks, mostly viral

tx

  • *nasal irrigation with saline**
  • *prolonged = steroids nasal spray**
181
Q

Cervical spondylosis - present & diagnose?

A

Degenerative changes in cervical spine = diag by exclusions

Neck pain worsened by mvt

182
Q

Hormonal headache - present & tx?

A

related to low oestrogen, nonspecific tension like headache

→ 2 days before & first 3 days of menstruation, menopause, pregnancy

= 2 out of 3 menstrual cycles for diagnosis → headache diary

183
Q

What is Horner’s syndrome?

A
  • *ptosis, miosis, anhydrosis**
  • *→ all on the same side**

flushing on one side of the face and that side doesn’t sweat. The eye on the same side has a smaller (constricted) pupil with a drooping or weak eyelid.

184
Q

Define meningitis?

A

inflammation of meninges

185
Q

What is meningism?

A

Neck stiffness / photophobia /
Kernig’s sign

= pain & resistance on passive knee extensions with hips fully extended

186
Q

Presentation - meningitis?

A

triad
Fever, headache, neck stiffness / leg pains

N + V, photophobia, rash (non blanching)

187
Q

Causes of meningitis?

A

Bacterial / viral / fungal / parasitic

188
Q

How might you treat primary meningitis?

A

IV / IM Benzylpenicillin

or IM ceftriaxone

189
Q

Secondary tx for meningitis?

A

GCS assessment

Blood cultures + broad spectrum antibiotics

Steroids
= IV dexamethasone to reduce tissue inflammation, damage & reduce morbid

usually - CT before LP

DIAGNOSTIC = Lumbar puncture
CI: coagulation disorders, rash, raised intracranial pressure

190
Q

Initial antibiotics for meningitis? Any to add?

A

Ceftriaxone or cefotaxime

if allergy = (erythro?)

if immunocompromised + amoxicillin
(risk of listeria)

if travel hx + vancomycin
(risk of penicillin resistance)

191
Q

If there is a rash - most likely causative organism? special response?

A

Rash = most likely
neisseria meningitidis

→ inform PHE
→ identify close contacts: prophylactic antibiotics = ciprofloxacin / rifampicin

192
Q

Causative bacteria for meningitis? (6+2)

A

GRAM NEG
Neisseria meningitidis
E coli
Haemophilius influenza B

GRAM POS
Listeria spp.
Strep pneumoniae
Group B strep.

Chronic
Mycobacterium Tuberculosis
Syphilis

193
Q

Meningitis in - neonates, pregnant ladies, immunosuppressed patients, elderly

A

Listeria spp.

194
Q

Causes of meningitis in adults (2)?

A

Neisseria meningitidis
Strep pneumoniae

195
Q

Viral causes of meningitis?

A 
Herpes Simplex (HSV)
Varicella Zoster (VZV)
Enterovirus
196
Q

Fungal causes of meningitis?

A

Cryptococcal spp.

197
Q

Cause of meningitis when LP / CSF is

‘fibrin web’ appearance
high WBC = lymphocytes
high protein
low glucose

A

Fungal / TB
→ PCR for M. TB

198
Q

Cause of meningitis when LP / CSF is

cloudy
high WBC = neutrophil / granulocytes
high protein
low glucose

A

Bacterial

199
Q

Cause of meningitis when LP / CSF is

clear
high WBC = lymphocytes
high protein
normal glucose

A

Viral

PCR for HSV, VZV & enterovirus

200
Q

How might you test for TB?

A

Phenol auramine / Ziehl-Neelson stain

201
Q

Differentiate between TB / bacterial causes of meningitis as appeared on CSF?

A

Bacterial = neutrophils / other granulocytes

TB / fungal = neutrophils = lymphocytes

202
Q

Differentiate between TB / fungal and viral caused meningitis as appeared on CSF?

A

viral = glucose normal

TB / fungal = high glucose

203
Q

Signs of sepsis?

A

= prolonged refill time

cold hands and feet
decreasing BP
evolving rash

204
Q

Sepsis 6 tx?

A

Give
oxygen
fluid resuscitation
IV antibiotics

Take
Blood cultures
Urine putput
Lactate

205
Q

What is encephalitis?

A

Inflammation of the cerebral cortex
= severe abnormalities in function of brain

206
Q

Causes of encephalitis?

(name essential at least)

A

usually Viral
→ Herpes Simplex virus
→ Varicella zoster virus

MMR, EBV, HIV if immunocompromised, CMV, Coxsackie

  • *Tropical**
  • *mozzie bite**: Japanese encephalitis / West Nile
  • *animals**: tick borne / rabies
207
Q

Present - encephalitis?

A

acute flu-like illness, hours to days
fevers, seizures

altered GCS - confusion, agitation, drowsiness, coma

  • *± meningism**, mostly absent
  • *check travel tx / animal bite**
208
Q

Investigations / initial management encephalitis?

A

IV Acyclovir

Contrast enhanced CT
must preceed LP

Lumbar Puncture
high lymphocytes
high protein
normal glucose

viral PCR
(throat swab & MSU)

blood culture, toxoplasma IgM titre, malaria film, gram film → negative

209
Q

Treatment for encephalitis?

A

if HSV or VZV = acyclovir
PCR at the end of cycle

others mostly supportive
→ lots of neuro rehab

210
Q

Cause of tetanus?

A

Clostridium tetani
gram pos rod, anaerobic spore
in soil & house dust

inoculation through skin

211
Q

TETANUS CARDS

A
212
Q

RABIES CARDS

A
213
Q

CJD CARDS

A
214
Q

What is Guillan Barre syndrome?

A

Acute, inflammatory polyneuropathy

→ ascending neuropathy resulting in weakness & reduced reflexes

215
Q

Risk factors for Guillan Barre syndrome?

A

peak 15- 35, 50-75

males > females

after pregnancy (delivery)

216
Q

Causes of Guillan Barre?

A

History of preceeding illness
Diarrhea or a respiratory illness
→ Campylobacter jejuni = most common
→ causes gastroenteritis

Viral causes
Cytomegalovirus (CMV), Epstein Barr, Zika, HIV

Post vaccinations

217
Q

Pathophysio - Guillan Barre?

A

Immune mediated damage to peripheral nerves
= molecular mimicry
= antibodies generated in response to pathogen incorrectly cross react with body’s own cells

218
Q

Presentation - Guillan Barre?

A

Prodrome = usually gastroenteritis & flu like illness

Ascending neuropathy = symmetrical
feet → facial / respiratory
→ reduced reflexes
→ weakness
→ peripheral neuropathy
→ loss of sensation

219
Q

What is Miller Fisher syndrome?

A

Variant of Guillan Barre

= ataxia, areflexia, ophthalmoplegia
with anti-GQ1B antibodies
(component of nerves)

220
Q

Differentials for Guillan Barre?

A

Lyme disease

sarcoidosis

Thiamine deficiency

Neoplasms

221
Q

Investigations for Guillan Barre?

A

DIAGNOSTiC = Nerve conduction studies
= reduced signal through nerve, prolonged distal motor latency ± conduction block

Lumbar puncture at L4
high protein, normal cell count, normal glucose

Spirometry = monitor FVC
decrease FVC = admit to ITU for maintenance of airways

Bloods → check for IgA deficiency, if yes cannot tx IV IG = severe allergic reaction

222
Q

Treatment of Guillan Barre?

A

Plasmaphoresis

IV Immunoglobulin
CI: IgA deficient patients → anaphylaxis!

(plasma exchange)

223
Q

Complications of Guillan Barre?

A

Respiratory failure, infection, cardio dysfunction & pulm embolism

→ monitor BP, FVC, low limb stockings & LMWH prophylaxis for venous thrombosis

224
Q

Tx neuropathic pain?

A

gabapentin / carbamazepine

(anticonvulsants)

225
Q

Criteria for assessment for tx pathways, Guillan Barre?

A

Hughes Disability score

226
Q

What is myasthenia gravis?

A

Neuromuscular autoimmune disorder, due to antibody mediated blockage of neuromuscular transmission

227
Q

Risk & aetiology, myasthenia gravis?

A

20-30’s females
60-70’s males

228
Q

Pathophysio of myasthenia gravis?

A

Acetylcholine receptor antibodies (ACH`r-Ab / anti ACh) binds to ACh receptors at neuromuscular junction

= prevents binding of ACh & subsequent depolarisation needed for muscle contraction

229
Q

AChR-Ab

produced by? ways it affects NMJ?

A

produced by B lymphocytes

prevents binding by ACh

cross link ACh-R = internalisation & destruction

Complement mediated damage of post synaptic membrane

230
Q

What type of hypersensitivity reaction is myasthenia gravis?

A

antibody mediated = type II

231
Q

Other antibodies in Myasthenia Gravis?

A

AChR-Ab = 80-90%

anti MuSK protein
anti LRP protein

232
Q

Associations - Myasthenia Gravis?

A

Thymus abnormalities
85% hyperplasia, 15% thymoma

autoimmune associations
Grave’s SLE, rheum art

Transient MG - caused by D-Penicillamine treatment for Wilson’s disease

233
Q

Clinical presentation - Myasthenia Gravis

A

hallmark = fatiguability of muscles
increasing weakness with use
→ common at the end of the day or following exercise

Signs by region
Limbs = arms > legs
can’t hang up laundry / comb in one go

Myasthenic sneer = facial muscles
expressionless, poor smile
dropped head at the end of day

bulbar = count to 50 = voice smaller
ophthalmic

234
Q

Investigations for myasthenia gravis?

A

Ice pack test
ptosis improve after application of ice
(neuromuscular transmission better at lower muscle temp)

Cogan’s lid twitch
patient to follow pen down … and suddenly up = lid will overshoot and twitch

Bloods for AChR-Ab, MuSK & LRP4
if negative = Electromyography (90% sensitivity)

Thymus assessment (CT chest)
+ thyroid function test (highly assoc)

235
Q

Pharmacological treatment (with class) for myasthemia gravis?

A

1st = pyridostigmine

2nd = Prednisolone
corticosteroids

3rd = immunosuppressants
azathioprine = inhibit purine synthesis
risk of marrow failure

236
Q

Class of pyridostigmine? Mechanism? SE?

A

Acetylcholinesterase Inhibitors

prevent hydrolysis or acetylcholine and increase effect at NMJ

SE cholinergic = secretions, diarrhoea, GI upset, bronchospasm, sweating, urinary incontinence

→ avoid during acute myasthenic crisis

237
Q

Other management options, myasthenia gravis?

A

FVC manage, speech and language team

IV Immunoglobulin
if severe respiratory or bulbar symptoms
alt plasmaphoresis

Thymectomy for thymomas

High dose steroids if ventilated
initially worsen then better

238
Q

What is a myasthenic crisis?

A

Worsening weakness that requires respiratory support, e.g. intubation / ventilation

239
Q

Presentation - myasthenic crisis?

A

Severe limb weakness, diplopia

Hypoxia
quiet breathing, reduced chest expansion, tachy, HP

sats & ABG can be normal

240
Q

Tx myasthenic crisis?

A

Urgent admission to hospital

intubation / non invasive ventilation

FVC / single breath count = BEST investigate !!!
all to be assessed by speech & language team & regularly FVC assess

241
Q

What is Lambert Eaton syndrome?

A

Antibodies against voltage gated calcium channels on presynaptic junction

ACh release reduced = muscle weakness

242
Q

Causes of Lambert Eaton syndrome?

A

Autoimmune related
both MNJ & autonomic ganglia
90% seropositive

50-60% have underlying malignancy
small cell lung CA, lymphoproliferative

STRONG relate w/ T1DM, Thyroid diseases

243
Q

Presentation Lambert Eaton syndrome?

A

hallmark = strength increases with repeated effort / exercise!

Proximal muscle weakness
→ in the morning

dry eyes, dry mouth, sexual dysfunction, sphincter issues, postural hypotension

244
Q

Management - Lambert Eaton syndrome?

A

ACh inhibitor = pyridostigmine
(goes both ways_

3, 4 diaminopyridine = blocks K channel in nerve terminal & potentiates action

treat cancer / use steoids may also help

245
Q

What is Isaac’s syndrome?

A

Peripheral nerve hyperexcitability due to antibodies against voltage gated potassium channels

cramps, fasciculations, hyperhydrosis, myokymia, exercise intolerance

246
Q

What is Multiple Sclerosis?

A

Chronic progressive condition that involves demyelination of the myelinated neurones in the CNS

247
Q

Causes & risk of Multiple Sclerosis?

A

Autoimmune = T cell mediated

20-40’s, women!!!

Others
genetics / Epstein Barr virus / low sun or vit D / smoking & obesity

248
Q

What are myelins? Produced by which cells?

A

Myelin = sheath of the axons of neurones in CNS
→ produced by oligodendrocytes = affected in MS

249
Q

Pathophysio of multiple sclerosis?

A

Inflammation around myelin & infiltration of immune cells = damage to myelin

Plaques of demyelination occur around veins (perivenular) & have a predilection for distinct CNS sites:

optic nerves, ventricles of brain, corpus callosum, brainstem & cerebellar connections etc

250
Q

Type of reaction for Multiple Sclerosis?

A

Type 4 = cell mediated hypersensitivity

(T cells / B cells / macrophages)

251
Q

Symptoms of Multiple Sclerosis?

A

Charcot’s neurologic triad +3

Dysarthria = plaques in brainstem
speech / eat / swallow / talk = throat

Intention tremor = plaques in motor pathways
limb weakness & spasms, tremors, ataxia

Nystagmus = plaques in eye nerves
optic neuritis, diplopia
loss of vision / pain

Paraesthesia = plaques in sensory pathways

Lhermitte’s sign
electric shock runs down back & radiate to limbs when bending neck

Plaques in ANS
Incontinence / sexual dysfunc / bowel symptoms

252
Q

Mneumonic for Multiple Sclerosis symptoms?

A

LOVDIP

Lhermitte’s sign, limb weakness

Optic neuritis

Vertigo

Diplopia

Incontinence

Paraesthesia

253
Q

Immediate treatment with optic neuritis?

A

seen urgently by ophathalmologist

Steroid treatment, 2-6 weeks recovery

254
Q

What are the four disease patterns of multiple sclerosis? Briefly describe each one? Which is the most common?

A

Replasing / remitting MS (80%)
no increase in disability between bouts months apart

Secondary progressive MS
over time from RRMS disability progression becomes constant

Primary Progressive MS
steady disability progression

Progressive relapsing MS
steady disability + bouts superimposed

255
Q

Differentials for MS?

A

SLE

Parkinson’s

Motor neurone disease

256
Q

Diagnostic criteria & investigations?

A

Criteria = 2 or more attacks disseminated in time & space (affecting diff parts of CNS)

DIAGNOSTIC = MRI
90%+ white matter plaques

Lumbar puncture = CSF shows IgG bands (antibodies)

Electrophysiology = visual evoked potential studies → delayed conduction = demyelination

257
Q

How might you differentiate between active & chronic lesions of MS?

A

use Gadolinium contrast in MRI

Lesions that are enhancing = break in BBB & uptake gd = active

Not enhancing = old

258
Q

Current pharmacological treatment for MS?

A

→ disease modifying = induce remission with no evidence of disease activity

Monoclonal antibodies = IV alemtuzumab, natalizumab

dimethyl fumarate

259
Q

How might you treat an acute MS attack?

A

steroids = oral methylprednisolone 500mg daily for 5 days / IV 1g / day if severe

if frequent relapses = anti-inflammatory cytokines
SC interferon 1A / 1B reduce relapse and lesion accumulation

→ 2nd line = plasmaphoresis / stem cell transplant

260
Q

How might you symptomatically treat MS?

A

exercise to maintain activity & strength

neuropathic pain = amitriptyline / gabapentin

depression = SSRI

Urgen incontinence = anticholinergic medications = oxybutynin

spasticity = gabapentin / botox

261
Q

What is Charcot Marie Tooth syndrome?

A

dysfunction in myelin or axons causes weakness and impaired sensory perception due to improper signalling

262
Q

Nature of Charcot Marie Tooth syndrome? aetiology?

A

inherited = auto dom!

affects peripheral motor & sensory pathways

before 10 or later than 40

263
Q

Pathology of CMT?

A

Loss of myelin on peripheral neurones OR loss of peripheral neurones

progressive loss of
→ motor in feet & legs
→ sensory in hands & feet

264
Q

Present - CMT?

A

High foot arches = pes cavus

Distal muscle wasting = inverted champagne bottle legs

Weakness, sharp pain & numbness in hands and legs

= trip a lot, clumsy, feet slap the ground when walking, can’t run

265
Q

Management for CMT?

A

no tx, for cause or prevent progression

physio, occup, podiatrist

ortho surgeon to correct disabling joint deformities

266
Q

Differentiate Charcot Marie Tooth & MS?

A

MS = disease of brain & spinal cord
→ CNS
mvt, sensory, thinking

CMT = disease of peripheral nerves
→ PNS
weakness & sensory perception
signal can’t get to brain

267
Q

Causes of peripheral neuropathy?

A

A alcohol

B B12 deficiency

C cancer & chronic kidney disease

D diabetes
& drugs - isoniazid, amiodarone, cisplatin

E every vasculitis

268
Q

What are Duchenne & Becker’s muscular dystrophies

A

Genetic disorder characterised by progressive muscle degeneration and weakness

both → x-linked recessive

269
Q

What are dystrophins?

A

proteins which keeps muscle cell intact

lack of dystrophins = become fragile & easily damaged

270
Q

Pathophysio of Duchenne’s & Becker’s?

A

Duchenne = no functional dystorphins made

Becker = dystrophin protein only partially functional

271
Q

Characteristic presentation of Duchenne & Becker’s muscular dystrophies?

A

hallmark = muscle weakness

Gower’s manoeuvre = walks hands to legs before getting up

Enlargement of calves

Difficulty jumping, running & walking, clumsy, waddling gait, lumbar lordosis (spine curve inwards)

272
Q

Compare and contrast Duchenne & Becker muscular dystrophy in terms of presentation?

A

Duchenne = early childhood, usually 2-3, boys
→ proximal body muscle to distal

Becker = teens to early adulthood, men 5-60
→ begins hips and pelvic, thighs & shoulders

273
Q

Complications of Duchenne & Becker muscular dystrophies?

A

Cardiomyopathy & respiratory symptoms (weakened organs)

Adrenal insufficiency (from steroids)

Growth retardation
late puberty, lack of testosterones,

274
Q

Investigations for the MD’s?

A

Screen = Creatinine kinase
= enzyme released by muscle when damaged
= usually 10-100x value (>200)

Diagnostic = genetic testing

then test for liver function

275
Q

How might you treat the muscular dystrophies?

A

Corticosteroids = slow progress
prednisolone

ataluren = if genetic defect
→ allows ribosome to read through premature stop codons that causes incomplete dystrophin synthesis

Supportive = bone health & hormones (from steroids), supply with vitamins

276
Q

What are motor neurone diseases?

A

= umbrella of rare degenerative neurological illness affecting the motor neurones

→ rare progressive ultrimately fatal

277
Q

Risk & pathology of motor neurone diseases?

A

Genetic component
→ surviving motor neurones contain abnormal protein TDP-43

Fam hx

links: smoking, heavy metal exposure, certain pesticides

278
Q

How are MND classified? Examples?

A

Upper motor neurones, lower motor neurones, mixed neurones (ALS, progressive bulbar)

279
Q

Differentiate UMN lesion from LMN lesion?

A

UMN = spasticity (+tone), hypereflexia, plantars,

LMN = wasting, fasciculation, absent nerve conduction
weakness corresponding to lower cord nerves

Diff = in UMN forehead will be spared = stroke

280
Q

Example of an upper motor neurone disease?

A

Primary lateral sclerosis
= loss of Betz cells in motor cortex, mainly UMN signs, marked leg weakness & pseudobulbar palsy

281
Q

Example of a lower motor neurone disease?

A

Progressive muscular atrophy
= weakness & wasting of distal muscle, fasciculations & absent reflexes

282
Q

Example of a mixed motor neurone disease?

A

Amylotrophic lateral sclerosis ALS
= classic & most common
= distal & proximal muscle weakness & wasting, spasticity, hyperreflexia

283
Q

Typical presentation of ALS?

A

Triad of
Limbs

Bulbar

Respiratory

284
Q

The motor neurone disease on its own & second most common?

A

Progressive bulbar palsy
= only bulbar muscles = talking & swallowing
→ involves cranial nerve nuclei

285
Q

Typical presentation for MNND?

A

Limb onset = 75%
→ distal asymmetric weakness of the arms / hands
= grip / shoulder abduction issues

  • *→ lower limb symptoms**
  • *= stumbling gait, foot drop,** tripping, loss of power, wasting
286
Q

Typical progressive presentation of MND?

A

Bulbar onset (25%)
→ dysarthria, wasting & fasciculations of tongue, dysphagia, slurred speech

Respiratory (5%)
dyspnoea, orthopnoea, poor sleep, reduced appetite, weight loss

287
Q

Distinguish MND from Myasthenia Gravis & Multiple sclerosis?

A

MND never affects eyes movements - MG

MND will not have sphincter disturbances - MS

288
Q

How might you investigate motor neurone disease?

A

Upper = imaging, from the lesion upward

Lower = nerve conduction studies NCS / Electromyography (EMG)

ALS = + creatinine kinase

289
Q

Diagnostic criteria of ALS?

A

El Escorial diagnostic criteria

Definite = LMN + UMN in 3 regions

Probable = LMN + UMN in 2 regions
or (LMN +) UMN in 1 region
+ EMG acute denervation in ≥ 2 limb

  • *Possible** = LMN + UMN in 1 region
  • *Suspected** = LMN, or UMN, only
290
Q

Complications / links of MND?

A

Frontotemporal dementia

Death causes = respiratory failure or pneumonia

291
Q

Only medication to slow progression of ALS / MND?

A

Riluzole
prolongs life for 3-4 months

292
Q

Tx for MND muscle cramps?

A

1st = quinine
SE prolongs QT interval

2nd = baclofen

→ consider exercise programs

293
Q

Tx for MND salivation problems?

A

1st = antimuscarinics
propantheline, SC glycopyrroate (less cognitive effects = preferred for cognitive impairment)

botox type A if doesn’t work

294
Q

Tx for respiratory symptoms in MND?

A

treat reversible causes of worsening respiratory impairment before considering meds

opioids / benzodiazepines

non-invasive ventilation at home for those with respiratory impairment

295
Q

Supportive measures for ALS?

A

Bulbar - blend food, gastrostomy

non invasive ventilation

296
Q

What is corticobulbar palsy / pseudobulbar palsy?

A

UMN lesion of bulbar muscles due to bilateral lesions above the mid pons

297
Q

Presentation of corticobulbar / pseudobulbar palsy?

A

Slow tongue movements & speech

jaw jerk

pharyngeal & palatal reflexes

Pseudobulbar effect
→ weeping unprovoked by sorrow
→ mood incongruent giggling
= emotional incontinence without mood change

298
Q

Tx corticobulbar palsy?

A

dextromethorphan + quinidine

299
Q

Which spinal tract is the descending upper motor neurone?

A

Corticospinal

decussate at the medulla

300
Q

Which spinal tract is responsible for proprioception, vibration & 2 point discrimination?

A

Dorsal column
= ascending sensory tract

decussate at medulla

301
Q

Which spinal tract is responsible for pain and temperature?

A

Spinothalamic tract
= ascending sensory tract

decussate IMMEDIATELT at spinal cord

302
Q

What are common causes of spinal cord compression?

A

acute = vertebral body neoplasm
most common

Disc herniation

Disc prolapse
(bulge within the disc itself)

303
Q

Presentation - spinal cord compression?

A

Sensory loss below the level of lesion (sensory level)

304
Q

What is sciatica?

A

S1 nerve root compression

Sensory loss in back of leg to lateral aspect of little toe (sciatic nerve distribution)

305
Q

How will L5 nerve root compression present?

A

Sensory loss / pain in lateral leg & medial side of big toe

306
Q

Investigations for spinal cord damage?

A

do not delay!!

MRI = gold standard

biopsy / surgical exploration for identifying masses

307
Q

Treatment for spinal cord compression?

A

if malignancy = IV dexamethasone

Epidural abscess = surgically decompress and antibiotics given

Neurosurg refer stat
→ decompression
laminectomy / microdisectomy

(reduce inflammation & oedema)

308
Q

How many vertebrae and pairs of spinal cord are there in the spinal coloumn?

A

33 vertebrae, 31 spinal cords

7 (8) cervical, 12 thoracic, 5 Lumbar, 5 sacral, 4 (1) coccygeal

309
Q

How many intervertebrae discs are there?

A

23

310
Q

Where does the spinal cord end?

A

L2, conus medullaris

311
Q

What is the cauda equina?

A

5 lumbar 5 sacral 1 coccygeal

nerve roots distal to the level of termination at L1/L2

LMN!!!

312
Q

Muscular presentation of someone affected by cauda equina?

A

Flaccid & areflexic

313
Q

Causes of cauda equina?

A

Spondylolisthesis = top vertebra slips forward (sink into body), nerve root comes above the vertebra below

Herniation of lumbar disc
L4/5 or L5/S1

Tumours / mets

spinal stenosis / ankylosing spondylitis

trauma / post op haematoma

314
Q

Present cauda equina?

A

Variable leg weakness
→ flaccid & areflexic (LMN signs)

Bilateral sciatica

Saddle anaesthesia

Bladder / bowel dysfunction, erectile dysfunction

315
Q

Investigations of cauda equina?

A

MRI to localise lesion

knee flexion - tests L5-S1,
ankle plantar flexion tests S1-S2
straight leg raising = L5 S1
femoral stretch = L4

316
Q

Treatment for cauda equina syndrome?

A

= EMERGENCY
refer to neuro immediately

decompression of the nerve stat to avoid irreversible paralysis

→ microdisectomy, epidural steroid for pain, surgical spine fixation if slipped disk, spinal fusion = reduce pain from motion → nerve root

Phase 2A (12 decks)

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