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Neurology Flashcards

1
Q

Findings suggesting not mononeuritis multiplex

A

Would do full exam but…

in generalised inflammatory neuro condition would expect some degree of arreflexia

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2
Q

Management of neuropathic pain

A

Amitryptiline
Pregabalin/gabapentin
Duloxetine
Topical therapies eg capsasum

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3
Q

Further investigation of neuropathy

A

NCS
NMG - shows any regeneration
MRI neck if worried about radiculopathy

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4
Q

Causes of (sensory) peripheral neuropathy

(Chronic conditions/Nutrition/Toxins/Autoimmune)

A

Chronic; Diabetes, Hyperthyroidism, malignancy

Nutrition: B12, B1, B6

Toxins; Uraema, ETOH, Chemo, ABx

Auto immune: CIDP, sarcoid, ANCA +ve vasculitis, RA

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5
Q

What bedside tests could you do to narrow down possible causes of peripheral neuropathy?

A

Opthalmoscopy ?diabetic retinopathy
Urine dip ?glucose
BM

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6
Q

Blood tests to Ix peripheral neuropathy

A

FBC ?macro anaemia
U+Es ?uraemia
LFTs ?alcohol
TFTs
B12
Auto immune screen, ESR
immunoglobulins, electrophoresis
HbA1c

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7
Q

Further Examination if ?stroke

A

AF - heart, pulse
Right Carotids ?bruit
Heart murmur
BP

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8
Q

Further Ix for stroke

A

MRI
ECG/24 hr/ 5 day tape
Echo ?Structural issue
BP
Carotid doppler

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9
Q

What does macular sparing (in homonymous hemianopia) suggest?

A

Posterior cerebral artery stroke (as occipital lobe gets blood from MCA)

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10
Q

Significance of corneal reflex

A

Lost in trigeminal nerve palsy but remaisn if hemispheric issue

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11
Q

Limb signs you would expect if ?Stroke

A

increased tone
weakness
sensory loss
hyperreflexia

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12
Q

Secondary prevention of stroke

A

ACEi/BP control
statin
antiplatelet

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13
Q

What does high stepping gait/foot drop suggest?

A

Sensory ataxia

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14
Q

What questions are important when taking history in Charcot Marie Tooth?

A

FHx
Auto dom
would expect family member to be affect

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15
Q

What tests do you do to investigate for Charcot Marie Tooth?

A

Neurophysiology - demyleinating vs axonal
Genetic testing

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16
Q

Why is the distinction between demyelinating and axonal neuropathies helpful or
important in the investigation of Charcot-Marie-Tooth?

A

Multiple types of CMT
Type I - demyelinating
may mutations can cause CMT phenotype

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17
Q

What treatments are available for CMT?

A

No disease modifying treatments
Need to diagnose and test family members
MDT
Physio
Orthotics eg to help drive, correct foot drop
OT

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18
Q

Examination findings for CMT

A

Orthotics
Foot drop/high stepping gait
Distal muscle wasting
High arched feet/pes cavus

inverted champagne bottle (preserved thigh muscle)

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19
Q

Cause of sudden onset myelopathy (spastic paraparesis)

A

Spinal infarct

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20
Q

What other features would suggest MS?

A

Cranial nerve - optic neuropathy RAPD with pale optic disc, intranuclear opthalmoplegia
hx of relapse/remittign

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21
Q

Ix ?MS

A

MRI brain and spine
LP - oligoclonal bands

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22
Q

Initial tx of MS

A

High dose IV steroids eg methylprednisolone (needs neg urine ip and infection ruled out first). Counsel for steroids

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23
Q

What to counsel for steroids?

A

Insomnia
Personality change/mania
GI upset/ulcer
AVN of hip
High BMs

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24
Q

Differentials of cerebellar syndrome

A

Stroke
MS
ETOH
Genetic/paraneoplastic

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25
Q

What imaging do you use to Ix cerebellar syndrome

A

MRI
much better than CT at visualising posterior fossa

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26
Q

Management of cerebellar syndrome?

A

MDT
PT to maintain strength and function
OT for adaptions at home

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27
Q

Lifestyle advice for cerebellar syndrome

A

Occupation - risk, adaptions
PMHx and meds - anything worsening sx eg dizziness
ETOH will exacerbate cerebellar sx

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28
Q

Cerebellar ataxia vs Sensory ataxia

A

CA - nystagmus, dysarthria, wide gait
SA - impaired sensation, proprioception and vibration

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29
Q

Rhombergs positive - Sensory or Cerebellar ataxia?

A

Sensory

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30
Q

UMN signs

A

weakness without atrophy
hyperreflexia
increased tone
spasticity
rigidity
tremor
chorea

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31
Q

Differentials for MND

A

Spinal muscular atrophy (X linked)
Kennedys disease
Multifocal motor neuropathy with conduction block

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32
Q

Ix for ?MND

A

EMG
MRI

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33
Q

Features of MND

A

Upper and lower motor neurone, axonalwasting and fasiculation, weaknessusually spastic but cna be flaccid
Asymmetrical

speech disturbance
Rapid and aggressive
Cognitive/behaviour disturbance - frontotemporal dementia ax
NO SENSORY LOSS or cerebellar

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34
Q

Features of Multifocal motor neuropathy with conduction block

A

Distal weakness
Clumsiness

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35
Q

Management of MND/ALS

A

Specilist neuro team and neuro nurses
Riluzole (expnesive and only short increase in survival)
MDT/PT/OT
SALT/dietician - weight, swallowing ?PEG
Resp - early morning ABG, FVC (may need NIV, cough assist)
Comms aids
Cognitive testing

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36
Q

Compressive causes of Brown Sequard

A

Tumour (Primary/secondary)

Disc Herniation

Spinal stenosis

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37
Q

Auto immune Causes of Brown Sequard

A

MS

SLE

Sarcoid

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38
Q

Infective causes of Brown Sequard

A

HIV

Varicella

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39
Q

Nutritional causes of Brown Sequard

A

B12 deficiency

Copper deficiency

Hereditary spastic paraparesis

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40
Q

Time frames of causes of myelopathy

A

Minutes - vascular

Days - Traums/disc herniation

Days- weeks - Demylenation/lupus

Month - Nutrition

Years - genetic

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41
Q

What is Brown Sequard

A

Weakness/paralysis one side,

Loss of sensation other

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42
Q

Nutritional deficincies causing peripheral neuropathy

A

B1

B6

B12

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43
Q

Drug causes of peripheral neuropathy

A

ETOH

TB meds (ethambutol, isoniazid)

ABx - Nitro, Dapsone, Metro

Cardio - Hydralazine, Amiodarone, Propanalol

Phenytoin, Clochinine, Chloroquinine

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44
Q

Immune causes of peripheral neuropathy

A

RA

GPA

CIDP

GBS

HIV

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45
Q

Follow up ix for Diabetic neuropathy

A

Fundoscopy

HbA1c

L/S bp

Urinalysis

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46
Q

Differentials of Motor Neurone Disease

A

Spinal Muscular Atrophy

Kennedys (peri oral fasiculation)

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47
Q

Managament of Motor Neurone Disease

A

Riluloze

MDT

esp SALT ?PEG

Resp ?NIV

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48
Q

Weakness + wasting + fasiculations +UMN

NO SENSORY disturbance

A

Most likely Motor Neurone Disease

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49
Q

What is Kennedys syndrome

A

X linked spino bulbar muscular atrophy

Only LMN

Peri oral fasiculations are pathognomonic

X linked recessive w androgen insentivity

Progresses v slowly (unlike ALS)

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50
Q

Cerebellar syndrome + hyperreflexia + up going plantars

A

Spinocerebellar syndrome

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51
Q

What specifically would you like to know in Hx for cerebellar syndrome to ax cause?

A

Fhx - Fredreichs or ataxia telangectasia

Drugs - phenytoin

Stroke risk factors

Relapsing remitting sx ?MS

Endo probs

Red flags malginancy ?paraneoplastic

ETOH

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52
Q

Muscle wasting + scars + deformity + older patient + weakness + NO sensory issues +LMN signs

A

Post polio syndrome

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53
Q

How would you manage GBS?

A

Monitor FVC, if FVC <1.5 ?vent support, ABG

IV immunoglobulin/plasma exchange

If unwell ICU

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54
Q

How would you manage CIDP?

A

Neuropathic pain management

DMARD

Steroids/IV immunogloubin/DMARDS

MDT

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55
Q

Presentation fo Hereditary Spastic Parapesis

A

Increased tone

Non sustained clonus

Brisk reflexes

Promixal weakness

Spastic gait

Decreased vibration and proprioception, sensation

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56
Q

Differentials of Spastic Parapesis

A

Acute w back pain - Compressive eg disc hernia

Sudden - vasular eg spinal stroke (althought spascity comes later)

Days - inflammatory - MS, transverse myelitis, VZV

Chronic - B12

HIV, TLV1, tumours, lateral sclerosis

57
Q

How would you investigate spastic parapesis

A

MRI spine

Genetic testing

Reversible causes eg B12, infection

58
Q

Differentials of flaccid paralysis

A

1) MND, poliomyelitis
2) Cauda equina
3) trauma/tumour abcess
4) Motor neuropathies

: inflam - GBS, CIPD

Infectious - HIV, lyme disease

Toxins - lead, arsenic

Metabollic - diabetes

Drugs - gold, ciclosporin

Congenital - CMT

5) NMJ - MG, Lambert Eaton
6) Myopathies

59
Q

Casues of spastic paraparesis

A

1) Demyelination - MIS
2) Cord compression
3) Trauma
4) Anterior horn cell disease
5) Cerebral palsy

60
Q

Cuases of spastic paraparesis with sensory level

A

1) Cord compression
2) Cord infarct
3) Transverse myelitis

61
Q

Spastic paraparesis and dorsal column loss (joint position sense and vibration):

A

Demyelination (Multiple sclerosis)

Friedreich’s ataxia

Subacute combined degeneration of the cord

Syphilis

Parasagittal meningioma

Cervical myelopathy

62
Q

Spastic paraparesis and spinothalamic loss (pain and temperature):

A

Syringomyelia

Anterior spinal artery infarction

63
Q

Spastic paraparesis and cerebellar signs:

A

Demyelination (Multiple sclerosis)

Friedreich’s ataxia

Spinocerebellar ataxia

Arnold Chiari Malformation

Syringomyelia

64
Q

Spastic paraparesis and small hand muscle wasting

A

Cervical myelopathy (C5-T1)

Anterior horn cell disease (motor neuron disease)

Syringomyelia

65
Q

Spastic paraparesis and UMN signs in upper limbs:

A

Cervical myelopathy (above C5)

Bilateral strokes

66
Q

What other questions would you ask of PD?

A

Hallucinations

Cognitive dysfunction

67
Q

Differentials of Parkinsonism

A

Lewy Body - sx preceding by cog impairment or hallucinations

MSA - postural hypotension, urinary incontinence, cerebellar signs

PSNP - can’t look up

Vascular Parkinsonism - lower limbs, B/L sx

68
Q

Non motor sx of Parkinsons

A

Anosmia

Cognitive impairment

Mood disorder

Pain

Constipation

69
Q

Treatment options for Parkinsons

A
  • anti cholinergics
  • COMT inhibitors
  • MOAB
  • Dopaminergics
    • levodopa
    • dopamine agonists
70
Q

Side effects of dopaminergic tx for Parkinsons

A

Impulsivitiy

Disinhibition

71
Q

Side effects of dopaminergic treatments for Parkisnsons

A

Levodopa - on/off

Dose related dyskinesia

72
Q

Dx if Parkinsons sx + cerebellar signs

A

MSA

73
Q
A
74
Q

Features suggestive of migraine

A

Unilateral

throbbing

Light aversion

phonophobia

nausea

Aura

Triggers

75
Q

Red flags of headache

A

Thunderclap headache

Reaches maximal pain within 1-2 mins

Confusion

Pyexia

Neck stiffness photophobia

Early morning/ postural cariation

Neurology

1st headache >55

76
Q

Causes of chorea

(tic like sudden movements)

A

Stroke - acute onset, asymmetric

Hyperglycaemia, polycythaemia

SLE

Huntingtons

Syndehams chorea (Group A strep)

Meds - levodopa, neuroleptics

77
Q

Tell me about Huntingtons

A

trinucleotide repeat

Genetic anticipitation - affected earlier/ more severe each generation

No disease modifying treatments

Autosomal dominant

AIDs

78
Q

How can you differentiate between NMJ disordersn (eg myasthenia) and myopathy

A

ACH antibodies, anti MUSK

EMG - MG decreases with repetitive stimulation

79
Q

How do you manage myasthenic crisis?

A

Steroids

FVC monitoring ?ventilation

d/w ICU

80
Q

Management of myasthenia

A

CT chest ? thymoma ?resection

Pyridostigmine

Steroids/steroid sparing agents

IV immunoglobulin

?thymectomy

81
Q

Management of Freidrichs ataxis

A

Echos, ECGS (inc exercise induced) - risk of arrhytmias and cardiomyopathy. May need ICD

MDT

Genetic counselling

Auto recessive, problem with frataxin gene

Check B12 and vit E as deficiency can mimic

82
Q
A
83
Q

Anterior cerebral artery stroke

A

Contralateral hemiparesis and sensory loss, lower extremity > upper

84
Q

Middle cerebral artery stroke

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

85
Q

Posterior cerebral artery stroke

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia

86
Q

Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain) stroke

A

Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

87
Q

Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)

A

Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

88
Q

Anterior inferior cerebellar artery (lateral pontine syndrome)

A

Symptoms are similar to Wallenberg’s (see above), but:
Ipsilateral: facial paralysis and deafness

89
Q

Basilar artery

A

‘Locked-in’ syndrome

90
Q

TACS

A

All three:

  1. Unilateral weakness and/or sensory deficit of the face, arm and leg
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction (dysphasia, visuospatial disorder)
91
Q

PACS

A

Two of:

  1. Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction (dysphasia, visuospatial disorder)
92
Q

POCS

(brainstem/cerebellum)

A

One of POCS:

  • Cranial nerve palsy and a contralateral motor/sensory deficit
  • Bilateral motor/sensory deficit
  • Conjugate eye movement disorder (e.g. horizontal gaze palsy)
  • Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
  • Isolated homonymous hemianopia
93
Q

LACS

A

One of the following:

Pure sensory stroke

Pure motor stroke

Sensori-motor stroke

Ataxic hemiparesi

94
Q

Lateral medullary (WALLENBURG) syndrome

Occlusion of posterior inferior cerellar artery

A

Ipsilateral: cerebellar, horners, loss of trigeminal pain/sensation

Contra: loss of pain and sensation

95
Q

Lower limb dermatomes

A
96
Q

Upper limb dermatomes

A
97
Q

Shoulder abduction myotome

A

C5

98
Q

Shoulder adduction myotome

A

C6/7

99
Q

Elbow flexion myotome

A

C5/6

100
Q

Elbow extension myotome

A

C7

101
Q

Wrist extension myotome

A

C6

102
Q

Finger extension mytome

A

C7

103
Q

Finger and thumb abduction myotome

A

T1 (ulnar and median respectively)

104
Q

Presentation of syringomyelia

A

Weakness/wasting small muscles hand

Loss of reflexes upper limbs

Loss of pain and temp (spinothalamic) in upper limbs and chest, preserved joint and vibration

Charcot joints

Upgoing plantars, kyphoscoliosis

Can have cerebellar, cranial nerve or horners

105
Q

What is syringomyelia

A

Fluid filled expanding caivty in C spine

Expands ventrally, so affects

  1. spinothalamic pain and temp, then
  2. anterior horn cells - LMN
  3. Corticospinal - UMN signs below syrinx

usually spares dorsal column proprioception

ax with Arnold Chiari/spina bifida

106
Q

Hereditary Sensory Motor Neuropathy - Charcot

Features

A
107
Q

Causes of predominatnly sensory peripheral neuropathy

A

DM

ETOH

Drugs - isoniazid, vincristine

Vit deficiency - B12, B1

108
Q

Causes of predominantly motor peripheral neuropathy

A

GBS, botulism (acute)

Lead toxicity

Porphyria

HSMN

109
Q

Causes of mononeuritis multiplex

A

DM

SLE/RA

PAN/Churg Strauss

HIV

Malignancy

110
Q

Presentation of Friedreichs Ataxia

A

Young, wheelchair, visual/hearing impairment

Pes cavus, kyphoscoliosis

B/L cerebellar ataxia

Leg wasting, absent reflexes, up going plantars

Posterior column - vibration and joint positiion

High arched palate

HCOM

DM

111
Q

Inheritance of Fredreichs

A

Auto recessive

Onsent in teenage years

20 year surival from diagnosis

HCOM, dementia

112
Q

Facial Nerve Palsy + VI palsy

A

MS + stroke

(Pons affected)

113
Q

Facial nerve palsy + V, VI ,VII palsy and cerebellar signs

A

Tumour eg acoustic neuroma

Cerebellar pontine angle

114
Q

Facial nerve palsy + VIII palsy

A

cholestaetoma/abcess

(auditory/facial canal)

115
Q

Facial nerve palsy + scars/parotid mass

A

Tumour/trauma

116
Q

Features of Bells Palsy

A

Rapid onset 1-2 days

HSV-1

Swelling and compresion of nerve within facial canal causes demyelination and conduction block

More common and worse outcome in pregnancy

All of the face so LMN

(UMN spares forehead)

117
Q

Management of facial nerve palsy

A

Steroids if within 72 hour of onset

Aciclovir if severe

Eye protection

70-80% fully recover

118
Q

Causes of facial nerve palsy

A

Herpes Zoster - Ramsay Hunt

Mononeuropathy - Lyme disease, DM, sarcoid

Tumour/trauma

MS/stroke

B/L: GBS, Sarcoidm Lyme, MG, B/L Bells

119
Q
A
120
Q

Features of MG

A

B/L ptosis, snarl trying to smile

Nasal speech

Proximal muscle weakness with fatiguability

Sternotomy scars from thymectomy

121
Q

Lambert Eaton

A

Diminshed reflexes - become brisker after exercise

Lower limb girdle weakness

Ax with malignancy eg SCLC

Antibodies block pre synaptic calcium channel

Anti voltage gated calcium antibodies

122
Q

Causes of B/L extra ocular palsies

(Opthalmoplegia)

A
  • MG
  • Graves
  • Mitochondiral cytopathies eg Kearns Sayre syndrome
  • Miller Fisher GBS
  • Cavernous sinus pathology
123
Q

Causes of B/L ptosis

A

Congenital

Senile

MG

MD

Kearns Sayre

B/L Horners

124
Q

Features of Tuberous Sclerosis

A

Skin • Ash leaf, Shagreen

Respiratory •  Cystic lung disease

Abdominal •  Renal enlargement - polycystic ,renal angiomyolipomata •  Transplanted kidney •  Dialysis fistulae

Eyes • Retinal phakomas (dense white patches) in 50%

CNS •  Mental retardation may occur •  Seizures

Auto dom

Railroad track on XR Skull

125
Q

Skin changes Tuberous Sclerosis

A

Angiofibromas

Periungual fibroma

Shagreen Patches

Ash Leaf Marks

126
Q
A

Ash Leaf

Neurofibromatosis

127
Q

Shagreen patch

A

Varying spider neavi usually on lower back

Tuberous Sclerosis

128
Q

Features of neurofibromatosis

A

Cutaneous neurofibromas

6 or more cafe au lait

Axillary freckling

Lisch nodules - harmatomas iris

HTN (RAS, phaeochromocytoma)

Lung fibrosis

Neuropathy with palable enlarged nerves

Visual impairment

Auto dom

129
Q
A

Cafe au lait spots

>6 neurofibromatosis

130
Q
A

Lisch nodules

Neurofibromatosis

131
Q
A

Cutaneous neurofibromas

Neurofibromatosis

132
Q

Features of Horners syndrome

(PEAS)

A

Ptosis

Enopthalmos

Anhydrosis

Small pupil (myosis)

+- flushed skin ipsiaterally to Horners pupul due to loss of sympathetic vasomotor tone

Look for scare in nek

133
Q

Causes of Horners syndrome

A

Tumour in neck/chest

Pancoast tumour

Carotid dissection

Stroke

Syringomyelia

134
Q
A

3rd nerve palsy

Partial ptosis

eye is down and out due to unopposed lateral rectus and superior oblique

135
Q

Causes of a pale disc

PALE DISCS

A

PRESSURE* : tumour, glaucoma and Paget’s

ATAXIA: Friedreich’s ataxia

LEBER’S

DIETARY: ↓B12, DEGENERATIVE: retinitis pigmentosa

ISCHAEMIA: central retinal artery occlusion

SYPHILIS and other infections, e.g. CMV and toxoplasmosis

CYANIDE and other toxins, e.g. alcohol, lead and tobacco

SCLEROSIS* : MS

136
Q
A

ARMD

Drusens spots

wet if new vessel formation

Risk factors •  Age, white, FHx, smoking

•  Wet - higher incidence CAD/Stroke

Tx •  Ophthalmology referral

•  Wet - intravitreal anti‐VEGF ( can increase CBV CB risk)

Prognosis • most blind in affected eye within 2 years

137
Q
A

Retinitis pigmentosa

Blind, loss of peripheral vision, begins with reduced nigth vision

“bone spicule” pigmentation, optic atrophy, ax cataracts

ax with ataxia - Fredreichs, Kearns-Sayre, deafness - Kearns Sayre

Cogenital/acquired (post retinits), vit A can slow progression

138
Q

Causes of proximal myopathy

A

polymyositis/dermatomyositis. SLE, vasculitis, RA, systemic sclerosis. Cancer (paraneoplastic: carcinomatous neuromyopathy) Drugs (statins, steroids) Infections (bacterial infections, HIV, CMV, EBV, Hepatitis) Endocrine (thyroid, addisons, osteomalacia, cushings, acromegaly, diabetic amyotrophy) Toxins (alcohol)

139
Q

Anti epileptics in pregnancy

A
  • If seizure-free before conception , likely to remain so
  • Most have normal pregnancies
  • Some low risk, but inadequate seizure control is higher risk - aim for lower appropriate dose
  • Valproate is contraindicated in preg ( birth defects and developmental disorders, cardiac+NTD ) so only if really necessary
  • Lamotrogine effectiveness may be reduced by oestrogen contraception

Lamotrigine or Keppra are best

  • Risks of Status to m+b - more common in preg due to preg + sometimes changing meds , but also reg repeated seizures carries risk (esp tonic-clonic)
  • Remember folate replacement

PACES (7 decks)

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