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Neurology Flashcards

1
Q

Types of stroke

A

1) Ischaemic
- Embolic / atheroscelrotic
2) Haemorrhagic
- Intracerebral / sub-arachnoid / extradural / subdural
3) Venous

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2
Q

Cause of lacunar infract?

A

Local atheromatous disease 2o HTN / smoking

Infarction up to 1.5cm

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3
Q

Common RFs stroke

A

1) Smoking
2) HTN
3) DM
4) AF
5) TIAs
6) Carotid artery stenosis
7) FHx

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4
Q

Types of lacunar infarct?

A
  • Pure motor
  • Sensorimotor
  • Pure sensory
  • Ataxia-hemiparesis - hemiparesis with ataxia disproportionate to weakness
  • Dysarthria
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5
Q

Ix of large vessel ischaemic stroke

A

1) Carotid and vertebral arteries - occlusion / dissection
2) Cardiac structure and rhythm
3) Prothrombotic tendency

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6
Q

Anterior cerebral artery occlusion signs

A

1) Contralateral LL weakness and sensory impairement (sometimes mild in UL)
2) Loss of voluntary micturition -> incontinence

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7
Q

Middle cerebral artery occlusion signs

A

1) Contralateral weakness and sensory impairment of face and arm, more than leg
2) Homonymous quadrant/hemi-anopia
3) Expressive +/- receptive dysphasia

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8
Q

ACA supply

A

Parasaggital cortex

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9
Q

MCA supply

A

Lateral surface of frontal, temporal and parietal lobes

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10
Q

Posterior circulation stroke vessels

A

All supplied by vertebral arteries

Includes basilar arteries and it s perforators

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11
Q

PICA

A

Posterior inferior cerebellar artery

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12
Q

PICA syndrome.. aka..

A

Lateral medullary synbdrome
Wallenberg’s syndrome

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13
Q

PICA syndrome signs

A

1) Impairment of pain/pinprick - ipsilateral in face, contralateral trunk and extremities
2) Dysphagia / hoarsnessess / impaired gag
3) Ipsilateral horners

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14
Q

AICA

A

Anterior inferior cerebellar artery

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15
Q

AICA syndrome

A

1) Ipsilateral face sensory impairment
2) Contralateral trunk and extermities pain and pinprick impairment
3) Ipsilateral paralysis of face and muscle of mastication
4) Ipsilateral hemi-ataxia

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16
Q

PCA occlusion

A

1) Contralateral homonymous hemianopia
2) Contralateral loss of pain / temp sensation
3) Memory deficits
4) Cortical blindness and visual defecits
5) Third nerve palsy and contralateral hemiplegia (Weber’s syndrome)

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17
Q

Top of basilar syndrome

A

1) Loss of vertical eye movements
2) Pupillary abnormalities
3) Coma
4) Locked-in syndrome

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18
Q

Blood supply spinal cord

A

2/3 is supplied by anterior spinal artery

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19
Q

Commonest area of spinal cord infarction

A

Upper thoracic cord (as is a watershed area)

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20
Q

Signs of spinal cord infarction

A

1) Acute flaccid paralysis (later spasticity)
2) Loss of sphincter control
3) Anasthesia to pain/temp (spinothalamic), but preservation of joint position vibration (dorsal columns)

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21
Q

Causes of ischaemic stroke (4)

A

1) CARDIAC
- AF/ valvular disease / endocariditis / prosthetic valve

2) ARTERIAL TREE PATH
- Carotid / aortic atherosclerosis / dissection / vasculitis

3) HAEMATOLOGICAL
- Sickle / Polycythaemia / Thrombocytopenia / antiphospholipid

4) Non-atherosclerotic vasculpopathy
- Drug misuse / Mitochondrial disease / CADASIL

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22
Q

% stroke due to haemorrhage

A

10%

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23
Q

Deep intracerbal haemorrhage

A

Usually related to HTN especially close to basal ganglia

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24
Q

5 most common causes of intracerebral haemorrhage:

A

1) HTN
2) Anticoagulation
3) Trauma
4) Tumour
5) Aneurysm

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25
Q

Most common cause of subarachnoid haemorrhage

A

Intracranial aneurysm (85%)

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26
Q

Complications of subarachnoid haemorrhage

A

1) Vasospasm - give nimodipine
2) Hydrocephalus
3) Rebleeding
4) Seizures
5) Pulmonary oedema
/ arrhythmia

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27
Q

Cushings triad

A

Bradycardia, wide pulse pressure, high BP

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28
Q

Signs of venous infarction

A

1) Signs of raised ICP - headache / papilloedema / VI CN palsy
2) Seizures
3) Focal signs
4) Altered consciousness

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29
Q

Causes of venous infarction

A

1) Raised oestrogen
2) Dehydration
3) Sepsis
4) Thrombophilia

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30
Q

DDx stroke

A

SOL
Viral encephalitis
Neuroinflammatory E.g. MS
Migrane
Metabolic E.g. hypoglycaewmia
Epilepsy E.g. Todd’s paresis

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31
Q

Immediate Ix stroke

A

Obs
Glucose
12 lead ECG
CT head +/- head and neck angiography

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32
Q

Mx post stroke

A

SLT assessment
CXR ?aspiration
Thrombophilia screen
24hr ECG & TTE
MRI brain

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33
Q

Thrombolysis window

A

3-4.5 hours dependent on local guidelines

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34
Q

Contraindications to thrombolysis

A

Prev. intracranial haemorrhage
Stroke / head injury in last 3/12
Active bleeding
Prev. GI bleed / varices / liver disease
Surgery or trauma last 14 days
Pericarditis / pancreatitis
Recent lumbar puncture
Uncontrolled HTN

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35
Q

Bleeding risk with thrombolysis

A

6% if treated within 3 hours

Risk rises with time

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36
Q

Acute complications of stroke

A

1) Raised ICP
2) Haemorrhagic transformation
3) Aspiration -> pneumonia

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37
Q

Evidence for thrombolysis

A

NINDS trial - increased patients with minimal disability from 38% -> 50%, NNT 8, NNT improved outcome 3

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38
Q

Secondary prevention ischaemic stroke

A

1) Aspirin 300mg for 2 weeks then Clopi 75mg OD
2) ACEi
3) Statin

?anticoag
?carotid endarterectomy if >70%

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39
Q

Whats is NIHSS

A

Assess severity of stroke
Max score 42
Score 5-20 = thrombolysis

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40
Q

Ix subarachnoid haemorrhage

A

CT head
If CT head normal, LP ?xanthochromia

Digital subtraction angiography gold-standard

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41
Q

Tx Subarachnoid haemorrhage

A

1) Supportive Care - avoid hyperthermia / hyperglycaemia
2) Stop antiplatelet/anticoag
3) Commence nimodipine
4) Neurosurgical review

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42
Q

What is MS?

A

CNS inflammation disseminated in time and space

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43
Q

MS Epidemiology

A

Typically 20 -40
Females 2x more likely

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44
Q

MS Aetiology

A

Both genetic (HLA II alleles & IL-7 receptor alpha) and enviromental factors (viruses / Vit D deficiency)

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45
Q

What is optic neuritis?

A

Pain on movement of eye, commonly associated with changes in vision (acuity / colour / RAPD)

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46
Q

Cause of diplopia in MS?

A

CN VI palsy
Internuclear opthalmoplegia

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47
Q

Presentation of spinal cord lesion in MS?

A

Sensory disturbance
Paraparesis
+/- urinary/bowel dysfunction

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48
Q

Late features of MS

A

Weakness and spasticity
Cerebellar signs
Cognitive impairment

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49
Q

Uhtpoff’s phenomenon

A

Worsening of neurological symptoms with rise in body temp (e.g. after shower)

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50
Q

MS - CNS or PNS

A

CNS! does not cause isolated peripheral neuropathy

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51
Q

MS clinical course

A

85% relapse-remitting

After 20 years most develop secondary progressive MS

Others are primary progressive

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52
Q

How is MS diagnosed?

A

CLINICALLY - need to exclude mimics

Blood tests inc. ESR, ANA, ANCA, dsDNA, ENA, anti-phospholipid, B12 and treponema serology

MRI - periventricular white matter lesions, typically in corpus callosum

Visual evoked potentials if involving optic pathway

CSF usually normal, may have mildly raised WCC

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53
Q

Revised McDonald Criteria in MS

A

Diagnosis can be made in clinically isolated syndrome if new T2 lesion is demonstrated within 30 days of clinical onset

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54
Q

Mx acute relapse MS

A

Steroids - quicker symtpom resolution, no prognostic

Rule out infection

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55
Q

Symptomatic Mx in MS

A

Physiotherapy
Anti-spastics - baclofen / botox
Laxatives
Intermittent self-catheterisation

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56
Q

Disease-modifying therapy in MS

A

According to Association of British Neurologists:

1) Beta-interferon / glatiramer acetate - must be ambulant with evidence of active disease

2) mABs - Natiluzimab in those with severe active disease (alemtuzumab is also used

3) Oral - fingolimod in RRMS

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57
Q

MS Mimics

A

1) Vasculitides / Auto-immune conditions - E.g. SLE, Sjogrens, Behcets, Sarcoid

2) Vascular - recurrent TIAs/stroke, CADASIL, Fabry’s

3) Mitochondrial - MELAS

4) Infection - Lyme / HIV / syphilis

5) Metabolic - B12 deficiency

6) Leucodystrophies

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58
Q

What is neuromyelitis optica?

A

Demyelination of spinal cord and optic nerve - mediated by antibody against aquaporin-4

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59
Q

Rating scale for disability in MS?

A

Expanded disability status scale

0-10

0=normal
5= ambulatory for 200m
10= death due to MS

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60
Q

Why would beta-interferon / glatiramer acetate be stopped?

A

Adverse reactions - injection site, flu like symptoms, AI hepatitis

Neutralising antiboides to beta-interferon, continue with glatiramer acetate

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61
Q

Cause of Parkinsonism?

A

1) Parkinson’s disease
2) Drug induced (neuroleptics / anti-emetics / valproate)
3) Parkinsons Plus Syndrome - Progressive supranuclear palsy / MSA / corticobasal degeneration
4) Lewy body dementia
5) Vascular parkinsonism
6) Rarer - toxins / Wilsons

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62
Q

Signs that point away from PD?

A

Symmetry of symptoms
Tardive dyskinesia
Early falls, especially backwards
Supranuclear gaze palsy
Early autonomic disturbances
Early dementia & visual hallucinations

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63
Q

PD definition

A

Movement disorder characterised by bradykinesia, tremor and rigidity

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64
Q

What is chorea?

A

Unpredictable jerky movements affecting different body parts in a random fashion

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65
Q

Causes of chorea?

A

Sydenham’s chorea - rheumatic fever
Drug-induced
Pregnanct
Polycythaemia ruba vera
Cerebral infarction

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66
Q

What is hemi-ballismus?

A

Ballistic movements of arm

Vascular lesion in subthalamic nucleus

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67
Q

What is athetosis?

A

Writhing movements of the limbs, usually more distally

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68
Q

What is dystonia?

A

Sustained involuntary contractions _> abnormal posture

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69
Q

What is tremor?

A

Involuntary rhythmic movements

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70
Q

Parkinsonian tremor

A

Low frequency rhythmic tremor
Present at rest
Worse on distraction
Alleviated by movement

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71
Q

Essential tremor

A

Postural or on action
Family history
Better with alcohol / beta blockers

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72
Q

Cerebellar tremor

A

Absent at rest
Exacerbated by goal-directed movement

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73
Q

Abnormal gait in peripheral neuopathy?

A

Yes, sensory ataxic gait - can expect midline ataxia and Rombergs +ve

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74
Q

Cause of peripheral neuropathy?

A

Metabolic
- Diabetes
- Hypothyroidism
- Uraemia
- Vit B1/6/12 deficiency

Toxic
- Alcohol excess
- Chemotherapy
- Antibiotics

Immune-mediated
- CIDP (chronic inflammatory demyelinating polyneuropathy
- Sarcoidosis
- ANCE +ve vasculitis
- RA

Paraneoplastic
- Either solid organ - lung - or those associated with paraproteinaemia

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75
Q

Further Ix peripheral neuropathy

A

Bedside tests for evidence of DM
- CBG
- Urinalysis - proteinuria
- Fundoscopy - retinopathy

Blood
- FBC ?macrocytic anaemia
- Urea and electrolytes, renal function
- LFTs ?transaminitis
- TFTs
- B12
- ESR ?inflammatory conditions
- HbA1c

Neurophysiology
- Nerve conduction ?demyelinating vs. axonal
- Length dependence - non-length depenendent likely inflammatory

76
Q

Charcot-Marie Tooth Findings

A

Tone - Flaccid
Power - reduced distally
Areflexia
Reduced sensation

LL>UL

77
Q

C-M-T genetics

A

Autosomal dominant, therefore need to check FHx

78
Q

C-M-T Ix

A

Neurophysiology
- Demyelinating vs. axonal
- Helps delineate subgroups

Genetic testing (blood) to confirm diagnosis and phenotype

Involve Neuro (neuromuscular disorder)

79
Q

Demyelinating vs. axonal in C-M-T

A

C-M-T Type 1 = demyelinating

80
Q

C-M-T

A

No disease modifying treatments

Involve MDT
- Physiotherapy
- Orthotics - bilateral AFOs
- Occupational therapy

Diagnosis helpful as genetic conditions
Explains to patient

81
Q

L homonymous hemianopia, reduced sensation L face & reduced hearing L ear

A

R hemispheric lesion
Could be R MCA infarct

82
Q

Extra exam findings when expecting a stroke?

A

Irregularly irregular pulse ?AF
Carotid bruits ?stenosis
Murmur ?valvular heart disease

Check BP

83
Q

Posterior cerebral artery stroke - what visual signs do you get?

A

Macula sparing

84
Q

Chronic Stroke Ix & Mx

A

MRI Brain
Prolonged ECG - check rhythm
Carotid doppler - severe stenosis ?endarterectomy
BP monitoring
TTE ?structural cardiac cause

85
Q

What is macula sparing?

A

Preserved central vision - happens with PCA stroke

86
Q

Lower limb spastic paraparesis causes

A

Acute
- Vascular - spinal cord infarct
Chronic
- Disc prolapse
- Inflammatory - MS
- Neoplasia

87
Q

What is INO?

A

Lesion in medial longitudinal fasiculus - resulting in failure of eye to adduct and nystagmus in other eye

Common in MS

88
Q

Causes of cerebellar ataxia

A

Acute
- Stroke - ischaemic or haemorrhagic
Relapsing/remitting
- MS affecting cerebellum
Chronic
- EtOH - check social hx
Genetic
Paraneoplastic

89
Q

Cerebellar signs

A

Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

90
Q

Ix Cerebellar Ataxia

A

MRI

Superior vs. CT to image posterior fossa

91
Q

Management of ataxia

A

Should try and address the underlying aetiology

Involve MDT - retain function & independence
- Physio - mobility
- OT - Equipment/adaptions at home

Lifestyle advice - assess occupation to reduce risk, medication side effects, EtOH Hx (can exacrbate therefore reduce/stop)

92
Q

Ataxia DDx

A

Sensory vs. cerebellar

Sensory in UL
- Pseudoathetosis - writhing of fingers outstretched with eye close
- Struggle to finger nose with eyes close
Sensory in LL
- Looks where placing feet
- Swaying with Romberg’s when eyes closed

Cerebellar signs - nystagmus, slurred speech

93
Q

What do you do if reflexes cannot be elicited?

A

Jendrassik maneuver

POTENTIATES the reflex

94
Q

Causes of sensory ataxia

A

Central
- Spinal cord pathology (dorsal column damage)
Peripheral
- Neuropathy - usually damaged to large myelinated fibres

Can be central and peripheral - Eg. B12 deficiency

95
Q

Speech impairment MND

A

Bulbar dysarthria

96
Q

DDX MND (with Lower signs)

A

Spinal muscular atrophy
Kennedy’s disease
Multifocal neuropathy with conduction block (which is treatable!)

97
Q

MND Ix

A

Neurophysiology
- EMG - look for fibrillation / fasiculations
- Nerve conduction studies - conduction block / dymelination

Imaging - MRI

98
Q

MND key features in Hx

A
  • Asymmetrical
  • Rapid progression
  • Behavioural / cognitive impairment (secondary to frontotemporal dementia)
  • Family Hx (familial Hx vs. Kennedy’s disease)
99
Q

Mx MND

A

Refer to Neurology & MND CNS

Drugs - Riluzole (can improve prognosis by months)

MDT
- Physio improve mobility
- OT - adaptations / equipment at home/work
- SLT - assess swallow
- Dieticians - nutrition (?Needs PEG)
- Review Resp function - FVC monitoring (may progress to needing NIV at night)

100
Q

MND other name

A

Amyotrophic Lateral Sclerosis

101
Q

Signs in MND

A

Both upper and lower, absence of sensory signs

102
Q

Medical term for increased sensation

A

Hyperaesthesia

103
Q

History of onset in myelopathy

A

ACUTE (mins)
- Vascular
Acute (days)
- Trauma / disc herniation
Sub-acute (days-weeks)
- Autoimmune (demyelination / SLE)
Chronic (weeks-months)
- Nutritional (B12 / Cu) / malignancy
Chronic (Months/years)
- Genetic

Screen for other neuro features / relapse-remitting cause
Screen for malignancy fetures - FLAWS
FHx

104
Q

Unilateral increased tone with weakness

A

Unilateral spastic paresis

105
Q

Unilateral pyramidal findings (increased tone, brisk reflexes and weakness) with contralateral spinothalamic dysfunction

A

Partial brown-sequard syndrome

106
Q

What is a myelopathy?

A

Spinal cord dysfunction

107
Q

How do you localise level of myelopathy?

A

Need to do full upper + lower limb and CN neurological examination.

Would not expect any findings on examination of CNs

108
Q

Signs of optic neuropathy

A

Pale disc & relative afferent pupillary defect - lesion in optic nerve

109
Q

Ix of myelopathy

A

MRI of spinal cord

Urgency dependent on timing of onset and severity of symptoms

110
Q

Treatment of spinal cord compression secondary to malignancy

A

High dose steroids
Radiotherapy vs. surgery

111
Q

Perioral fasciulations

A

Pathognomic of Kennedy’s disease, always mention MND

112
Q

Cerebellar ataxia signs - DDx

A

Acute
- Stroke - infarct vs. haemorrhage (usually unilateral signs
- Cerebellitis (infection e.g. varicella or autoimmune)
- Demyelination

Chronic
- EtOH
- Nutritional deficieinces
- Previous surgery or trauma

113
Q

Cerebellar Ataxia - Ix

A

Acute - CT head to r/o acute stroke
Chronic - MRI much superior

114
Q

Key questions in Hx for patient with cerebellar ataxia

A

1) Onset and progression of symtpoms
2) Screen for other neurological signs or symptoms ?relapsing-remitting
3) RFs - Alcohol / Drugs / nutrition
4) Systemic features, inc. malignancy
5) FHx

115
Q

What is staccato speech?

A

Broken / choppy speech

116
Q

Oscillopsia

A

Where objects appear to be jumping in vision

117
Q

Peripheral neuropathy and cerebellar signs - cause

A

More likely to be toxic cause e.g. EtOH

118
Q

Dysfunction of motor function - where is lesion?

A

Could be:
- Anterior horn cells
- Motor neurones

119
Q

Investigations for suspected MND

A

1) Full Hx - symptom onset and progression
2) Complete full neurological exams
3) Nerve conduction studies, looking for evidence of denervation

120
Q

Kennedy’s disease vs. ALS/MND

A

ALS is rapidly progressive

Kennedy’s
- X-lined - look for family Hx
- Much more slower onset

121
Q

Kennedy’s disease vs. ALS/MND on clinical exam

A

Perioral fasiculations only in Kennedy’s disease

122
Q

Management of Kennedy’s disease

A

Via MDT

Regular Neurology follow up, focussed on symptomatic management

OT/Physio to maintain function & independence & optimise home and work setting

SLT & dietician - assess swallow and optimise diet to reduce risk of aspiration

Neuropsychologist - to come to terms with condition

Can perform early morning blood gas to identify patients with respiratory muscle weakness -> refer for ventilatory support

123
Q

Kennedy’s disease other name

A

X-linked spinobulbar atrophy
Only lower motor neurones are affected
Slow progression
Associated with androgren insensitivity

124
Q

How is Kennedy’s disease confirmed?

A

Genetic testing

125
Q

Use of nerve conduction studies in Kennedy’s disease?

A
  • Confirm denervation
  • Assess extent of involvement
  • Assess for any unexpected sensory involvement
126
Q

What is arachnodactly? What conditions is it associated with?

A

Long , thin, curved fingers
Associated with Marfan’s

127
Q

Marfan’s syndrome inheritance

A

Autosomal dominant
Affects fibrillin 1 gene

128
Q

Cardiac complications of Marfans

A

Aortic root / aorta diltatation
Aortic regurgitation
Mitral valve prolpase

129
Q

Indications of aortic root replacement in patient’s with Marfans?

A

Aortic root > 50mm
or >45mm in individuals with FHx Aortic dissection
Aortic root expansion >3mm/year

130
Q

Causes of breathlessness in Marfans?

A

Valvular incompetence
Ischaemic heart disease
Arrhtythmia
R/o IE

131
Q

Progressive weakness in a patient with previous Polio

A

Post polio syndrome

symptoms include progressive muscle weakness, pain in the muscles and joints, and tiredness

132
Q

Management of post polio syndrome

A

MDT approach

Regular neurology review - consider neuropathic analgesia

Physiotherapy and occupational therapy to maintain mobility/function and optimise home and work settings

Neuropsychology to help patient come to terms with diagnosis

133
Q
A
134
Q

5 UL screening tests

A
  1. Pronator drift
  2. Quick release of fists
  3. Push ?scapula winging
  4. Finger to nose ? Coarse ataxia
  5. Scars on head or neck
135
Q

Difference between spasticity and rigidity 

A

 spasticity is velocity dependent

136
Q

Where is spasticity maximal?

A

At extreme extension

137
Q

Complications of L Dopa therapy

A

Dyskinesia
Impulse control disorders

138
Q

Ddx proximal myopathy

A

Statin related
Thyroid disorders
Polymyositis
Dermatomyositis
Paraneoplastic
Statin related

139
Q

Myelopathy causes

A

Very acute - vascular
Acute - compressive eg disc herniation
Days - inflammatory - MS (transverse myelitis) or infective (most likely VZV)
Weeks - Vit b12 -> Subacute combined degeneration of the cord / TB / HTLV1
Months - tumours or neuro degeneration (primary lateral sclerosis)

Positive family history. Consider hereditary spastic paraparesis.

140
Q

Ix Myelopathy

A

MRI spine - timing dependent on the timing of onset of symptoms

141
Q

Non limb symptom associated with a myelopathy

A

Consider bladder dysfunction

142
Q

Bloods tests in myelopathy

A

Check for reversible causes
Cu and B12

143
Q

How to confirm diagnosis of hereditary spastic paraparesis

A

Genetic testing with NGS

144
Q

Clinical examination of Parkinsonism - DDx

A

Idiopathic Parkinson’s Disease
Parkinsons Plus - PSP / MSA
Vascular Parkinsonism - clasically present with gait abnormality
LB dementia

145
Q

Non-motor symptoms of Parkinson’s Disease

A

Anosmia
Sleep - REM / turning over in bed / broken sleep
Constipation
Cognitive
Mood
Pain
Autonomic dysfunction

146
Q

Medical management of PD

A

Dopaminergic - Levodopa / Dopamine agonists
MAOi
COMTi
Anti-cholinergics

Can be delivered by tablet, patches, disperisble medications
Dopaminergic medications can also be delivered via a pump, typically in late disease

147
Q

Side-effects of dopaminergic medications

A

Impulse Control disorders
On-Off phenomenon

148
Q

Management of PD

A

MDT

Neuro - medical therapy
Physio - improve function and mobility
OT - Improve home and work environment
SLT - review swallow and speech
PD CNS - continuity and support
Role of support groups

149
Q

Signs of parkinonism and cerebellar signs

A

MSA

150
Q

Sign of PSP

A

Vertical supranuclear gaze palsy

151
Q

Hemiparesis

A

Most likely differrential is stroke

152
Q

How to assess speech

A

Assess understanding of commands
- close your eyes
- 2 step - touch L ear with R hand

Repeat phrases
- baby hippopotamuses
- 42 west register street

Test naming
- Can you tell me what you had for breakfast
- What is this object

153
Q

Management of stroke outside thrombolysis window

A

A->E manner

once stable
- Take Hx
- Check for mimics - blood glucose (hypoglycaemia) & urine dip (infection)
- ECG
- Bloods - FBC, Renal, Liver, TFTs, HbA1c, cholesterol
- CT head - exclude haemorrhage
- Bedside swallow assessment
- Antiplatelet as soon as haemorrhage ruled out

Management on stroke unit

153
Q

Neuro signs associated with raised ICP

A

Papilloedema
CN VI palsy
Normal visual fields

154
Q

Features of migraneous headache

A

Unilateral
Throbbing
Photophobia & phonophobia
Triggers - foods, stress, sleep deprivation
Usually have similar episodes previously

154
Q

Red flags in headache Hx

A

Very acute onset - maximal intensity in seconds to mins - thunderclap -> subarachnoid haemorrhage

Present with other unwell symptoms ?meningitis

Insidious onset ?SOL
- Worse in early morning
- Associated with visual change or focal neuro defecit

Age >55

155
Q

Tx Migraine

A

Analgesia
- 1st: Paracetamol + NSAID
- Avoidance of opioid
- Consider triptan therapy in acute phase - oral / nasal / SC

Lifestyle
- Healthy diet / sleep / exercise
- Avoid triggers

Prophylaxis
- Propranolol / Topiramate

156
Q

Inflammatory neuropathies

A

Acute
- GBS
Chronic
- CIDP

Looks for any extra-neural manifestations - E.g. arthopathy

157
Q

Neuropathy with waxing-waning course

A

?Inflammatory
?associated with AI disease

158
Q

Patient presenting with chorea - DDx

A

Acute presentation - hypoglycaemia, polycthaemia & Vascular cause

Autoimmune - SLE-related

Genetic - Huntington’s disease (particularly with family Hx)

Post-rheumatic fever - rare in UK

159
Q

Management of Huntington’s disease

A

No Disease-modifying therapy

MDT approach
- OT/PT
- Neuropsychiatry - treat mood disturbance
- Neuropsychology
- Dietician (involuntary movements increase basal metabolic rate)

160
Q

Extra tests to perform in patients with involuntary movements

A
  • Check for bradykinesia
  • Check eye movements
161
Q

Patients presenting with weakness, but normal examination - where can lesion be?

A

NMJ - ?Myasthenia gravis
Myopathy

162
Q

Characteristics of NMH pathology

A

Should demonstrate a fatiguability on repeated stimulation

163
Q

Differentiating between NMJ and myopathy

A

Neurophysiological tests
ACh receptor Ab +ve in MG

164
Q

Clinical examination findings & Hx in myasthenia gravis

A

Fatigue ptosis - should resolve with ice pack placed over eye
Complex opthalmoplegia

Symptoms getting worse by end of day
Worse after exercise
Diplopia, dysphonia, dysphagia

165
Q

Triad miller-fisher

A

Ataxia, areflexia, opthalmoplegia

166
Q

Treatment of myasthenic crisis

A

A -> E approach
Monitor FVC
Escalate to senior and ICU ?ventilatory support

Confirm diagnosis with ACh Abs & Neurophysiological studies (single fibre EMG)

CT Chest ?thymoma

167
Q

Medical therapy for myasthenia gravis

A

Pyridostigmine (cholinesterase inhibitor)
Steroids can be used in acute crisis
May want to consider steroid-sparing agents in longer term

168
Q

What is Lambert-Eaton syndrome

A

Proximal muscle weakness that improves with repeated use

Associated with pre-synaptic Ca channels
Associated with reduced ACh release

169
Q

Therapies sometimes required in myasthenic crisis

A

I&V
IVIG
Plasma exchange

170
Q

Combination of UMN and LMN signs in young ataxic patient

A

In keeping with both a cerebellar and sensory ataxia

In young patient, could be genetic, eg friedrichs ataxia

171
Q

Other Ix in Friedrichs ataxia

A

Want to do blood tests to rule out reversible causes - E.g. B12

Imaging - mri brain and spine - to rule out compressive pathology

Neurophysiology studies

Diagnosis will be made with genetic testing

172
Q

Common mortality complication in Friedrichs

A

Cardiomyopathy and arrhythmia

Need serial ECG and echo monitoring

Those with arrhythmia may need cardio referral and iCD

173
Q

Management of MDT

A

MDT
- neuro
- OT/PT
- orthotics
- genetic conselling

174
Q

Genetics of Friedrichs

A

Autosomal recessive
Trinucleotide repeat disorder
Disorder of Fratqxin gene

175
Q

Complains of diplopia with normal eye movements. What to check?

A

Fatiguability of upward gaze
Myasthenia gravis

176
Q

EMG findings myasthenja gravis

A

Degradation of action potentials with repeated movements

177
Q

Antibodies Myasthenia Gravis

A

Anti-Achetylchokine receptor abs
Anti-MuSK

178
Q

What is required when someone presents with ocular MG?

A

Follow up for 2 years as generalisation likely to happen within that time period

179
Q

Management of generalised MG

A
  1. Pyridostigmine
  2. Ct chest to rule out thymoma
  3. Steroids +/- steroid sparing agents
  4. If resistant, consider IVIG
180
Q

Young patient. Leg weakness. Distal atrophy with calf hyper trophy.

A

Think of muscular dystrophy

181
Q

Types of muscular dystrophy

A

Duchenne
Beckers
Ocular pharyngeal
Myotonic
Facioscapulohumeral
Limb girdle

182
Q

Typical Ix findings in a muscular distrophy

A

Raised creatine kinase
EMG demonstrating myopathic changes
MRI to rule out inflammatory causes
Genetic testing to confirm variant

183
Q

Management of muscular dystrophy

A

MDT management

SLT to assess swallow
Cardiac screening
OT/PT

PACES (6 decks)

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