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1

Causes of aortic stenosis

Senile calcification (60+)

Congenital: biscupid valve (40-60 years), Williams syndrome

Rheumatic fever

2

What is the commonest cause of aortic stenosis

Senile calcification

3

Features of Williams syndrome

Neurodevelopmental disorder characterised by "elfin" facies + low nasal bridge, cheerful demeanor and ease with strangers

Developmental delay

Language deficiencies

Profound visuo-spatial impairment

CV problems e.g. supravalvular aortic stenosis

Transient hypercalcaemia

4

Symptom triad in AS

Angina

Dyspnoea

Syncope (especially with exercise)

5

Symptoms of AS

Triad: angina, dyspnoea, syncope

LVF: PND, orthopnea, frothy sputum

Arrhythmias

Systemic emobli if endocarditis

Sudden death

6

Triad: angina, dyspnoea, syncope

LVF: PND, orthopnea, frothy sputum

Arrhythmias

Systemic emobli if endocarditis

Sudden death

Aortic stenosis

7

Def: supravalvular aortic stenosis

Congenital obstructive narrowing of the aorta above the aortic valve

8

Signs of AS

Slow rising pulse with narrow pulse pressure

Aortic thrill

Forceful, non-displaced apex (pressure overload)

Abnormal heart sounds:

Quiet A2

Early systolic ejection click if pliable (young valve)

S4: forceful atrial contraction vs hypertrophied valve.

Murmur:

ESM, right 2nd ICS sitting forward in end-expiration

Radiating to carotids

9

Abnormal heart sounds:

Quiet A2

Early systolic ejection click if pliable (young valve)

S4: forceful atrial contraction vs hypertrophied valve.

Aortic stenosis

10

Murmur:

ESM, right 2nd ICS sitting forward in end-expiration

Radiating to carotids

Aortic stenosis

11

What are the clinical indicators of severe AS?

Quiet/absent A2

S4

Narrow pulse pressure

Decompensation: LVF

12

DDx of AS

CAD

MR

Aortic sclerosis

HOCM

13

What differentiates clinically between AS and aortic scleorsis

Valve thickening rather than valve narrowing: no pressure gradient

Turbulence leads to mumrmur

ESM without radiation and a normal pulse

 

Doesn't have the narrow PP, slow rising pulse, forceful apex or ECG evicednece of LVF seen in Aortic Stenossi

14

Ix in AS

FVC

U+E

Lipids

Glucose

15

What differentiates between HOCM and AS clinically

HOCM is an ESM murmur which increases intensity with the valsalva (reduces in AS)

 

16

ECG findings in AS

LVH

LV strain: tall R, ST depression, T inversion in V4-6

LBBB or complete AV block due to septal calcification (may need pacing)

17

CXR findings in AS

Calcified AV (esp on lateral films)
LVH

Evidence of failure

Post-stenotic aortic dilatation

18

Aortic stenosis

Arrow= post stenotic dilatation

19

What is diagnostic in AS?

Echo+ doppler

20

Echo findings in AS

Thickened, calcified immobile valve cusps

Can be used to categorise severity

21

What Ix to perform in AS

Bloods

ECG

CXR

Echo+Doppler

Cardiac catheteristaion and angiography

Exercise stress test contraindicated if symptomatic)

22

Aortic stenosis

23

Echocardiography: severe AS

>4,/s jet velocity

>40mmHg pressure gradient

Valve area <1cm^2

24

Use of cardiac catheterisation and angiography in AS

Can assess valve gradient and LV function

Assess coronaries in all patients planned for surgery

25

Use of exercise stress test in AS

Contraindicated if symptomatic

May be useful to assess exercise capacity in asymptomatic patients

26

Medical Mx of AS

Optimise RFs: statins, anti-hypertensives, DM

Monitor with regular F/U (echo)

Angina: beta blockers

Heart failure: ACEI and diuretics

Avoid nitrates

27

Surgical mx of AS

Mechanical/biproshetic

Balloon valvuloplasty

TAVI

28

Implications of surgical replacement of valve in AS

Poor prognosis if symptomatic

Angina/syncope: 2-3y

LVF: 1-2y

29

Indications for valve replacement in AS

Severe symptomatic AS

Severe asymptomatic AS with reduced EF (<60%)

Severe AS undergoing CABG or other valve operation

30

Mechanical vs bioprosthetic valves

Mechanical last longer but need anticoagulation (used in younger patients)

Bioprosthetic: don't require anticoagulation but fail sooner

31

Use of balloon valvuloplasty in AS

Limited use in adults as complication rate is high (>10%) and restenosis occurs in 6-12mo

32

Features of TAVI

Folded valve deployed in aortic root

Increased perioperative stroke risk cf. replacement

Reduction in major bleeding

Similar survival at 1y

Little long term data

33

Cx of TAVI

Major bleeding from entry sites

Stroke

VT

MI

Aortic dissection

Cardiac tamponade

Postoperative AR and paravalvular leak

34

CXR findings in pulmonary oedema

ABCDE

Alveolar shadowing

Kerley B lines

Cardiomegaly (cardiothoracic ratio >50%)

Diversion of the upper lobe

Effusions

Fluid in the fissures

35

Def: obstructive sleep apnoea

Intermitten closure/collapse of the pharyngeal airway-> apnoeic epsiodes duriing sleep

36

RFs for sleep apnoea

Obesity

Male

Smoker

EtOH

Idiopathic pulmonary fibrosis

Structural airway pathology e.,g. micrognathia

NM disease e.g. NMD

37

Ix in OSA

SpO2

Polysomnography is diagnostic

38

Rx of sleep apnoea

Weight loss

Avoid smoking and EtOH

CPAP during sleep

Surgery to relieve pharyngeal obstruction: tonsillectomy, uvulopalatpharyngoplasty

39

Clinical features of obstructive sleep apnoea

Nocturnal

Snoring

Choking, gasping, apnoeic episodes

 

Daytime:

Morning headache

Somnolence

Reduced memory and attention

Irritability, depression

40

Cx of obstructive sleep apnoea

Pulmonary HTN

T2 respiratory failure
Cor pulmonale

41

Assessment scores for sleep Apnoea

Epworth score ( fallling asleep in various situations)

STOP BANG

42

Autonomic complications of DM

Postural hypotension: Rx: fludorcortisone

Gastroparesis: early satiety, GORD, bloating

Diarrhoea: Rx: codeine phosphate

Urinary retention

Erectile dysfunction

43

RFs for aspiration pneumonia

Stroke

Bulbar palsy

Reduced GCS

GORD

Achalasia

44

Mx of aspiration pneumonia

Anaerobes

Co-amoxiclav PO TDS for 7D

45

What is risk feeding

Feeding in individual with unsafe swallow at risk of aspiration

e.g. not able to tolearte NG tube

46

Def: splinted diaphragm

Inhibition of diaphragmatic movement, seen in a variety of disease

47

Draw Einthoven's triangle

48

Draw cardiac electrogram

49

Draw ECG lead arrangement

50

Draw cardiac conduction pathways

51

View: Leads II, III, aVf

Inferior

52

View: I, aVL, V5 + V6

Lateral

53

View: V2-V4

Anteroseptal

54

View: V2-V6

Anterolateral

55

View: V1, V2, V3 (reciprocal)

Posterior

56

Vessel: II, III, aVF

RCA

57

Vessel: I, aVL, V5 + V6

L circumflex

58

Vessel: V2-V4

LAD

59

Vessel: V2-V6

Left main stem

60

Rate on ECG

300/ no of large squares

 

If irregular, use rhythmn strip x 6

61

Componenets of reporting ECG

Demographics

Rate, rhythmn

Axis

P waves

QRS

PR interval

QTc

ST segments

T waves

Extras

 

62

https://www.youtube.com/watch?v=7lcm1HI4fbk

63

Def: MEN

Autosomal dominant functioning hormone tumours in multiple organs

64

MEN1

3 Ps

Parathyroid: adenoma/hyperplasia

Pituitary: adenoma, prolactin or GH

Pancreatic tumours: gastrinoma or insulinoma

 

65

MEN2A

2Ps 1 M

Thyroid medulary carcinoma

Parathyroid

Phaeochromocytoma

Hyperthyroidism

66

MEN2B

1P 2Ms

Phaeochromocytoma

Medullary thyroid carcinoma

Marfanoid habitus/,icosal neuroma

67

Def: DM

 

Multisystem disorder due to an absolute or relative lack of endogenous insulin leading to metabolic and vascular complications

68

Pathophysiology of T1DM

Auotimmune destruction of beta cells leading to an absolute insulin deficiency

69

Presentation of T1DM

Polyuria, polydipsia, weight loss, DKA, starting before puberty

70

Polyuria, polydipsia, weight loss, DKA, starting before puberty

T1DM

71

What HLAs associated with T1DM

HLA-D3 and D4

72

Anti-islet

Anti-GAD abs

T1DM

73

Pathophysiology of T2DM

Insulin resistance and beta cell dysfunction leading to relative insulin deficiency

74

Presentation of T2DM

Polyuria, polydipsia, complications

75

Concordance of T2DM

80% in MZs

76

Associations of T2DM

Obesity

Reduced exercise

Calorie and EtOH excess

77

Diagnostic criteria for DM, symptomatic

Symptoms i.e. polyuria, polydipsia, weight loss, lethargy

+

Raised plasma venous glucose detected once:

fasting >7mM

Random >11.1mM

78

Diagnostic criteria for DM, asymptomatic

Raised venous glucose detected on 2 separate occasions

or 2h OGTT >11.1

79

When is OGTT required?

When borderline fasting or random glucose measurements

80

Normal fasting glucose

<6.1

81

Normal OGTT

<7.8

82

Impaired fasting glucose

6.1-6.9

83

Impaired glucose tolerance

75g OGTT 7.8-11

84

Fasting glucose in DM

>7

85

75g OGTT in Diabetes

>11.1

86

Secondary causes of DM, drugs

Steroids

Anti-HIV

Atypical neuroleptics

Thiazides

87

Secondary causes of DM. pancreatic

CF

Chronic pancreatitis

Hereditary haemochromatosis

Pancreatic Ca

88

Secondary causes of DM, endocrine

Phaeo,

Cushings

Acromegaly

T4

89

Secondary causes of DM, other

GSDs

90

Def: Metabolic syndrome

Central obesity (raiesd waist circumference) and >1 of:

Raised TGs

Reduced HDL

HTN

Hyperglycaemia: DM, IGT, IFG

91

MDT mx of DM

GP

Endocrinologist

Sx

DSN

Dieticians

Chiropodists

Fellow patients

92

What are the 4Cs of DM monitoring

Control, glycaemiic

Complication

Competency

Coping

93

Monitoring DM: Control

Record of complications: DKA, HONK, hypos

Capillary blood glucose: 

Fasting 4.5-6.5

2h post-prandial 4.5-9

 

HbA1c reflects exposure over last 6-8w

Aim 45-50 (7.5-8%)

 

BP, lipids

94

Monitoring Dm, Cxs

Macro: pulses, BP, cardiac auscultation


Micro: fundoscopy, ACR + U+Es, sensory testing plus foot inspection

95

Monitoring DM: Competency

With insulin injections

Checking injection sites

BM monitoring

96

Monitoring DM: coping

Psychoscoial e.g. ED, depression

Occupation

Domestic

97

Lifestlye modificaiton in DM: DELAYS

Diet

Exercise

Lipids

ABP

Asprin

Yearly/6 monthly check up: 4Cs

Smoking cessation

98

Lifestyle modificaiton, DM, diet

Same as that considered healthy for everyone

Reduced total calorie intake

Reduced refined carbs

Increased complex carbs

Increased soluble fibre

Reduced fat (sat)

Reduced Na

Avoid binge drinking

99

Lifestyle modification DM, lipis

Rx of hyperlipidaemia

Priamry prevention with statins if >40y regardless of lipids

100

Lifestyle modification DM, ABP

Reduce Na intake and EtOH

Keep BP <130/80

ACEI best, if afrocarribean descent ACEI + CCB or thiazide

 

101

Issue with beta blockers in DM?

Mask hypos

102

Issue with thiazides in DM

Raise glucose

103

Antiplatelet therapy in DM

Not recommended as primary prevention unles CVD

104

How can the VOR be used to determine whether a comatose patient's brainstem is intact?

In comatose patients, once it has been determined that the cervical spine is intact, a test of the vestibulo-ocular reflex can be performed by turning the head to one side. If the brainstem is intact, the eyes will move conjugately away from the direction of turning (as if still looking at the examiner rather than fixed straight ahead). Negative "doll's eyes" would stay fixed midorbit, and having negative "doll's eyes" is therefore a sign that a comatose patient's brainstem is functionally not intact.

105

Brown's syndrome

Brown's syndrome is a rare form of strabismus characterized by limited elevation of the affected eye. The disorder may be congenital (existing at or before birth), or acquired. Brown syndrome is caused by a malfunction of the Superior oblique muscle, causing the eye to have difficulty moving up, particularly during adduction (when eye turns towards the nose)

106

Draw the movements performed by the eye muscles

107

Characteristic of internuclear opathlmogpleiga

Paresis of eye adduciton in horizontal gaze but not in convergence

Due to lesions on the medial longitudinal fasciculus

 

Internuclear ophthalmoplegia results from a lesion in the MLF. In young people, the disorder is commonly caused by multiple sclerosis and may be bilateral. In the elderly, internuclear ophthalmoplegia is typically caused by stroke and is unilateral. Rarely, the cause is Arnold-Chiari malformation, neurosyphilis, Lyme disease, tumor, head trauma, nutritional disorders (eg, Wernicke encephalopathy, pernicious anemia), or drug intoxication (eg, with tricyclic antidepressants or opioids).

If a lesion in the MLF blocks signals from the horizontal gaze center to the 3rd cranial nerve, the eye on the affected side cannot adduct (or adducts weakly) past the midline. The affected eye adducts normally in convergence because convergence does not require signals from the horizontal gaze center. This finding distinguishes internuclear ophthalmoplegia from 3rd cranial nerve palsy, which impairs adduction in convergence (this palsy also differs because it causes limited vertical eye movement, ptosis, and pupillary abnormalities).

During horizontal gaze to the side opposite the affected eye, images are horizontally displaced, causing diplopia; end nystagmus often occurs in the abducting eye. Sometimes vertical bilateral nystagmus occurs during attempted upward gaze.

108

++ Urea

+Cr

+ Albumin

+ HCt

?Dehydration

109

+Urea

+Cr

+H

+K

+Urate

+PO4

Reduced Ca

?Low GFR

110

Low Na

Low K

Raised HCO3

Raised Urea

Thiazide and loop diuretics

111

Normal Urea and Creatinine

Reduced urate

Reduced PO4

Reduced HCO3

?Tubular dysfunction

112

Raised bilirubin

Raised ALP

Reduced albumin

Raised PT (Raised APTT if end stage)

 

 

Hepatocellular disease

113

Raised bilirubin

Raised ALP

Reduced albumin

Raised PT (Raised APTT if end stage)

 

AST:ALT >2, raised GGT

Alcoholic hepatocellular disease

114

Raised bilirubin

Raised ALP

Reduced albumin

Raised PT (Raised APTT if end stage)

 

AST:ALT <2

?Viral hepatocellular disease

115

Raised ALP

Raised GGT

Raised bilirubin

Raised AST

Cholestasis

116

Raised GGT

Raised MCV

Evidence of hepatocellular disease

?XS EtOH intake

117

Raised K

Reduced Na

?Addison's

118

May show

Reduced K

Raised Na

Raised HCO3

?Cushing's

119

Reduced K

Raised Na

Raised HCO3

?Conn's

120

Raised Na

Raised serum osmolality

Reduced urine osmolality

DI

121

Reduced Na

Reduced serum osmolality

Raised urine osmolality

Raised urine Na

?SIADH

122

Presentation of hyponatraemia <135

N/v, anorexia, malaise

123

Presentation of hyponatraemia: <130

Headache, confusion, irritability

124

Presentation of hyponatraemia: <125

Seizures

Non-cardiogenic pulmonary oedema

125

Presentation of hyponatraemia <115

Coma and death

126

Causes of hypovolaemic hyponatraemia

U Na >20mM

= renal loss

 

Diuretics

Addison's

Osmolar diuresis e.g. glucose

Renal failure (diuretic phase)

 

127

Causes of hypovolaemic hyponatreamia

U<20mM

=extra-renal loss

Diarrhoea

Vomiting

Fistula

SBO

Burns

128

Causes of hypervolaemic hyponatraemia

Cardiac failure

Nephrotic syndrome

Cirrhosis

Renal failure

129

Causes of euvolaemic hyponatraemia

U osmolality >500

SIADH

130

Causes of euvolaemic hyponatreamia

U osmolality <500

Water overload

Severe hypothyroidism

GC insufficiency

131

Mx of hyponatraemia

Correct the underlying cause

Replace Na and water at the same rate at which they were lost

NB: too fast-> central pontine myelinolysis

132

Rate of correction in chronic hyponatraemia?

10mM/d

133

Rate of correction in acute hyponatraemia?

1mM/hr

134

Mx of asymptomatic chronic hyponatraemia

Fluid restrict

135

Mx of symptomatic/acute hyponatraemia/dehydration

Cautious rehydration with 0.9% saline

136

Mx of hypervolaemic hyponatraemia

Consider frusemide

137

Mx of hyponatraemia if seizures/coma

Consider hypertonic saline

138

Def: SIADH

Concentrated urine: Na >20mM, osmolality >500

Hyponatraemia or palsma osmolality <275

Absence of hypovolaemia, oedema or diuretics

139

Causes of SIADH

Resp

CNS

Endo

Drugs

Resp: SCLC, pneumonia, TB

CNS; meningoencephalitis, head injury, SAH

Endo: hypothyroidism

Drugs: cyclophosphamdie, SSRIs, CBZ

140

Which drugs can cause SIADH

Cyclophosphamide, SSRIs, CBZ

141

Rx in SIADH?

Rx cause and fluid restrict

Consider vasopressin R antagonists: demclocycline, vaptans

142

Blood supply of the spinal cord

3 longitudinal vessels:

2 posterior spinal arteries- dorsal 1/3

1 anterior spinal artery: ventral 2/3

Reinforced by segmentel feeder arteries

Longitudinal veins drain intot he extradural vertebral plexus

143

Gross anatomy of the spinal cord

Foramen magnum to L1/L2

Terminates as conus medullaris

Spinal nerves continue inferiorly as cauda equina

Denticulate ligament and filum terminale are pial extensions that supend the cord in subarachnoid space

144

The spinal dura mater is continueous with what?

The neuronal epineurium

145

In what spinal mater is the CSF found?

The subarachnoid space

146

What level does the spinal cord finish at?

L1/L2

147

Describe the formation of spinal nerves

Mixed nerves that originate from the SC forming the peripheral nervous system

Each spinal nerve begins as an anterior (motor) and posterior (sensory) nerve root.

These arise from the spinal cord and unite at the intervertebral foramina forming a single spinal nerve

These nerves leave the vertebral canal and divide into two:

Anterior rami: nerve fibres to the body, both motor and sensory

Posterior rami: nerve fibres to the synovial joints of the vertebral column, deep muscles of the back and the overlying skin.

148

Muscle weakness, paralysis with loss of reflexes

Most commonly caused by vertebral fractures or dislocation, vasculitic disease, arethomatous disease or external compression

Spinal cord infarction

149

Where are 95% of spinal cord ischaemic events?

To the anterior aspect of the spinal cord, with the psoterior columns preserved

150

151

Modality of the dorsal columns?

Fine touch, vibration, proprioception

152

Cell body of the dorsal column?

DRG

153

Decussation of the dorsal column

In medulla, forming the medial leminicus

154

Mode of the lateral corticospinal tract

Motor (body)

155

Cell body of the spinothalamic tract

DRG

156

Decussation of the lateral spinothalamic tract

In cord, at entry level

157

Mode of the lateral corticospinal tract

Motor

158

Cell body of the lateral corticospinal tract

1o motor cotrex

159

Decussation of the lateral corticospinal tract

Pyramidal decussation in the ventral medulla

160

How can the somatosensory tracts be classified?

Conscious: dorsal column-medial leminiscal pathway and the anterolateral system

Unconscious: spinocerebellar

161

Organisation of the dorsal column-medial lemniscal pathway

3 groups

1o neurones: carry sensory information from receptors to the medulla. Signals from the upper limb travel in the fasciculus cuneatus (lateral part of the dorsal column) synapsing in the cuneate nucleus

Signals from the lower limb travel in the fasciculus gracilis (medial part) and synapse in the gracile nucleus)

 

2o:

Begin in either of the nuclei, synapse with 3o neurones in the thalamus. Decussate in the medulla oblongata and travel in the contralateral medial lemniscus to reach the thalamus.

 

3o:

Take sensory signals from the thalamus to the primary sensory cortex of the brain.

162

What is this pathway

DCML

163

Organisation of the anterolateral system

Two tracts:

Anterior spinothalamic: crude touch and pressure

Lateral spinothalamic: pain and temperature

 

1o:

Arise from sensory Rs in the periphery, enter the SC, ascend 1-2 levels and terminate at the tip of the dorsal horn (substantia gelatinosa)

2o:

Carry info from the susbtantita gelatinosa to the thalamus. Arise from synapse with 1o neurone, decussate and here the fibres split into the anterior and lateral tracts. Syanpse in the thalamus

3o

Take sensory signals from the thalamus to the primary sensory cortex of the brain, ascend from the ventral posterolateral nucleus of the thalamus, through the internal capsule, terminating at the sensory cortex

 

 

164

What info is carried by the anterior spinothalamic tract?

Crude touch and pressure

165

What info is carried by the lateral spinothalamic tract

Pain and temperature

166

167

What neural pathway is this?

Spinothalamic

168

What are the individual pathways in the spinocerebellar tracts?

Posterior spinocerebellar tract: proprioceptive info from lower limbs to the ipsilateral cerebellum

Cuneocerebellar tract: carries proprioceptive information from the upper limbs to the ipsilateral cerebellum

Anterior spinocerebellar tract: carries proprioceptive information from lower limbs, decussating twice and terminating in the ipsilateral cerebelllum

Rostral spinocerebellar tract: carries proprioceptive information from the upper limbs to the ipsilateral cerebellum

169

Pattern of sensory loss if DCML lesion in the spinal cord?

Ipsilateral dorsal modalities

170

Pattern of loss in injury to the anterolateral system

Contralteral pain and temperature sensation

171

Brown Sequard Syndrome pattern of loss

DCML: ipsilateral loss of tactile sensation and proprioception

Anterolateral system: contralateral loss of ppain and temperature sensation

Will also involve the descending motor tracts causing ipsilateral hemiparesis

172

Function of thalamic VPL nuceli

Somatosensory body

173

Function of thalamic VPM nuclei

Somatosensoty head

174

Function of thalamic LGN nuclei

Visual

175

Function of thalamic MGN nuclei

Auditory

176

How can the descending tracts be classified?

Pyramidal tracts: originate in the cerebral cotex, carry motor fibres to the spinal cord and brainstem: voluntary control

Extrapyramidal tracts: originate in the brainstem, carry motor fibres to the SC- responsbile for involuntary and automatic control of all musculature.

 

No synapses within the descending pathways.

177

How can the pyramidal tracts be classified?

Corticospinal: musculature of the body

Corticobulbar: musculature of the head and neck

178

Path of the corticospinal tracts

Begin in the cerebral cortex (primary motor cortex, premotor cortex, supplementary motor area)

Neurones converge and desced through the internal capsule

After the internal capsule the neurones pass through the crus cerebri of the midbrain, the pons and into the medulla.

In the most inferior part of the medulla the tract divides in two.

Fibres within the lateral corticospinal tract decussate and terminate in the ventral horn

Anterior spinal tract remains ipsilateral, they then decussate and terminate in the ventral horn of the cervical and upper thoracic segmental levels.

179

What is this pathway

Pyramidal: corticospinal pathway

180

Path of the corticobulbar tracts

Arise from the lateral aspect of the 1o motor cortex, receiving the same inputs as the corticopsinal tracts.

The fibres converge and pass through the internal capsule to the brainstem.

The neurones terminate on the motor nuclei of the cranial nerves. Here, they synapse with LMNs, which carry the motor signals to the face and neck.

NB many of these corticobulbar fibres innervate the motor neurones bilaterally. E.g. the fibres from the left 1o motor cortex act as UMNs

Upper motor neurones for the facial nerve have a contralateral innervation, this only affects muscles in the lower quadrant of the face, below the eyes

UMNs for hypoglossal only provide contralateral innervation

181

UMN innervation of the facial nerve

Upper motor neurones for the facial nerve have a contralateral innervation, this only affects muscles in the lower quadrant of the face, below the eyes

182

UMN innervation of the hypoglossal

Only provides contralateral innervation

183

What are the extrapyramidal tracts?

Vestibulospinal

Reticulospinal

Rubrospinal

Tectospinal

184

Which extrapyramidal tracts decussate?

Rubrospinal and tectospinal, therefore provide contralateral innervation

185

Function of the vestibulospinal

Two pathways: medial and lateral

Arise from vestibular nuclei which receive input from the organs of balance, they convey this info to the SC where it remains ipsilateral.

Fibres in this patheway control balance and posture via lower motor neurones

186

Functions of the reticulospinal tracts

Medial: arises from the pons, facilitates voluntary movements and increases muscle tone

Lateral: arises from the meudlla, inhibits voluntary movements and reduces muscle tone

187

Function of the rubrospinal tracts

Originates from red nucleus.

May play a role in fine control of hand movements

188

Function of the tectopsinal tracts

Begins at the superior colliculus of the midbrain. (receives input from optic nerves)

Neurones decussate

Tectospinal tract coordinates movements of the head in relation to visual stimuli)

189

Supranuclear lesions=

UMN

190

UMN lesion to the hypoglossal

A lesion to the upper motorn neurone will result in spastic paralysis of the contralateral side of genioglossus.

Tongue points to the contralateral side i.e. away from lesion

191

Function of cerebellum and BG

Output to cortex via thalamus

Regulation of posture, locomotion, coordination and movement

192

What is the internal capsule

White matter carrying axonal fibres from motor cortex to pyramids of medullla

Infarction can lead to contralateral hemiparesis

193

Function of the frontal lobe

Cognition and memory

Executive function

Motor cortex

Dominant hemisphere: motor speech (Broca's area)

194

Function of the parietal lobe

Sensory cortex

Body orientation

195

Function of the temporal lobe

Memory

Dominant hemisphere: receptive language (Wernicke's area)

196

Function of the occipital lobe

Visual cortex

197

Draw the homunculus

198

How can you differntiate between primary motor and primary somatosensory cortices

Primary somatosensory is posterior to the central sulcus

199

Draw the blood supply of the brain

200

Brainstem rule of 4

4 structures in the midline beginning with M

4 structures to the side beginning with S

4 cranial nerves in the medulla, 4 in the pons and 4 above the pons

4 motor nuclei that are in the midline are those that divide equally into twleve except for 1 and 2: 3, 4, 6, 12

(5,7,9,11 are in the lateral brainstem)

201

Brainstem rule of 4:

4 medial structures

1: motor pathway (corticospinal tract)

2: medial lemniscus: CL loss of viration and proprioception int he arm and leg

3: MLF: ipsilateral internuclear opthalmoplegia

4: motor nucleus and nerve (3, 4, 6, 12)

202

Brainstem, rule of 4

Lateral structures

Spinocerebellar pathway: ipsilateral ataxia of the arm and leg

Spinothalamic pathway: contralateral alteration of pain and temperature sensation affecting arm and leg

Sensory nucleus of Trigeminal: ipsilateral alteration of pain and T sensation in the trigeminal nerve distribution

Sympathetic pathway: ipsilateral horner's: partial ptosis and a miosis

203

Brainstem rule of 4:

4 CNs in the medulla

9: loss of pharyngeal sensation

10; ipsilateral palatal weakness

11: spinal accessory: ipsilateral wekkness of the trapezius and sternocleidomastoid

12: hypoglossal: ipsilateral weakness of the tongue.

204

Brainstem rule of 4

4 cranial nerves in the pons

5: ipsilateral atleration of pain, T and light tocuh fo the face, sparing the angle of the jaw

6: ipsilateral weakness of eye abduction

7: ipsilateral facial wekaness

8: ipsilateral deafness.

 

205

Brainstem rule of 4

The 4 cranial nerves above the pons

Olfactory

Optic (not in midbrain)

 

Oculomotor:down and out, dilated pupil ipsilaterally

Trochlear: inability to look down when the eye is adducted.

 

206

Blood supply of the brainstem

Medial arteries i.e. basilar, vertebral, anterior spinal artery

Lateral arteries: posterior cerebral and superior cerebellar, anterior inferior cerebellar

207

Medial brainstem syndromes:

Due to para-median branch occlusion

208

Lateral brainstem syndromes

Due to occlusion of the circumferential branches also seen in unilateral vertebral occlusion.

209

If there are signs of both a lateral and medial brainstem syndrome?

?Basilar artery problem

210

Process of NMJ transmission

Presnyaptic volatge gated Ca channels open

ACh released from presynaptic terminal

ACh diffuses across cleft

ACh binds to nicotinic receptors on the post-synaptic terminal

Na influx, leads to depolarisation and SR Ca release, leading to muscle contraction

ACh degraded by acetylcholinesterase and choline is taken up into the presynaptic terminal

211

Targets for NMJ blockade

Block presynaptic chonline uptake: hemicholinium

Block ACh vesicle fusion: botulinum, LEMS

Block nAChR-

Non-depolarising: atracurium, vecuronium

Depolarsing: suxamethonium

212

What are the dopamine pathways in the brain?

Mesocorticolimbic: SCZ

Nigrostriatal: Parkinsonism

Tuberoinfundibular: Hyperprolactinaemia

213

Features of the sympathetic nervous system

Cell bodies from T1-L2

GVE preganglionic fibres synapse at either the paravertebral ganglia, the prevertebral ganglia or chromaffin cells of the adrenal medulla

Preganglionic fibres are myelinated and release ACh at nACHRs

Postganglionic fibres are unmyelinated and release NA at adrenergic receptors except at sweat glands where they release ACh for muscarinic Rs

214

What are the components of the parasympathetic nervous system?

Cranial: CN3, 7, 9, 10

Ciliary, pterygopalatine, submandibular, otic ganglions

Vagus supplies thoracic and abdominal viscera

Sacral: pelvic splanchnic nerves (S2-4) innervate the pelvic viscera

Preganglionic fibres release ACh at nAChRs, post-ganglionic fibres relase ACh at mAChRs

215

Funciton of ciliary ganglion

Ciliary muscle and sphincter pupillae

216

Function of pterygopalatine ganglia

Mucous membranes of the nose, palate and lacrimal gland

217

Function of the submandibular ganglion

Submandibular and sublingual glands

218

Functions of the otic ganglion

Parotid gland

219

Midbrain CN nuclei

3, 4 (5)

220

Pons CN nuclei

5,6,7,8

221

Medullla CN nuclei

5,8,10,11,12

222

VOR

Axons from vestibular neuornes project via MLF to abducens and oculomotor nuclei

Head turns L eyes trun R

Absent Doll's eye sign= brainstem death

223

Features of caloric test of vestibulocoular pathway

Warm-> increased firing of vestibular neurones-> eye turns to the contralateral side with nystagmus to ipsilateral side

Remember fast direction of nystagmus:COWS

Cold: opposite

Warm: Same

Absence of eye movements= brainstem damage on side being tested

224

Which nucleus is involved in the pupillary light reflex?

Direct: Optic nerve-> Edinger Westphal nucleus-> ipsilateral pretectal nucleus, Oculomotor nerve synpases in ciliary ganglion leading to constriction of sphincter pupillae

Consensular: Optic nerve-> Edinger Westphail-> contralateral pretectal nucleus-> oculomotor nerve-> ciliary ganglion-> sphincter pupillae

225

226

227

228

229

230

Pattern of cortical motor deficit?

Hypereflexia proximally in arm or leg

Unexpected patterns e.g. all movements in hand/foot

231

Hypereflexia proximally in arm or leg

Unexpected patterns e.g. all movements in hand/foot

?Cortical lesion

232

Pattern of lesion to internal capsule and corticospinal tracts?

Contralateral hemiparesis with pyramidal distribution

Lesion with epilepsy, reduced cognition or homonymous hemianopia= in cerebral hemisphere

Lesion with contralateral CN palsy= brainstem lesion on the side of the palsy (e.g. Miilar-Gubler syndrome)

233

Contralateral hemiparesis with pyramidal distribution

?Internal capsule/corticospinal lesion

234

Contralateral hemiparesis with pyramidal distribution

With epilepsy, reduced cognition or homonymous hemianopia

=In cerebral hemisphere

235

Contralateral hemiparesis with pyramidal distribution

With contralateral CN palsy=

Brainstem lesion on the side of the lesion

236

Milard-Gubler Syndrome

Lesion of the pons aka ventral pontine syndrome

Symptoms result from the functional loss of anatomical structures of the pons including CNVI and VII and fibres of the corticospinal tract

Paralysis of CNVI leads to diplopia, esotropia (internal strabismus) and loss of eye abduction

Disruption of CNVII leads to flaccid paralysis of the muscles of facial expression and loss of the corneal reflex

Disruption of the corticospinal tract leads to contralateral hemiplegia of the extermities

237

Lesion of the pons aka ventral pontine syndrome

Symptoms result from the funcitonal loss of anatomical structures of the pons including CNVI and VII and fibres of the corticospinal tract

Paralysis of CNVI leads to diplopia, esotropia (internal strabismus) and loss of eye abduction

Disruption of CNVII leads to flaccid paralysis of the muscles of facial expression and loss of the corneal reflex

Disruption of the corticospinal tract leads to contralateral hemiplegia of the extermities

Millar-Gubler syndrome

238

Patern of cord lesion with motor deficit

 Quadriparesis/paraparesis

Motor and reflex level: LMN signs at level of the lesion and UMN signs below

239

 Quadriparesis/paraparesis

Motor and reflex level: LMN signs at level of the lesion and UMN signs below

?cord lesion

240

Pattern of deficit in peripheral motor neuropathy

Usually distal weakenss

In GBS the weakness is proximal (root involvement)

Single nerve= mononeuropathy- trauma or entrapment

Several nerves= mononeuritis multiplex: vasculitis or DM

241

Causes of mononeuritis multiplex

Vasculitis or DM

242

Features of UMN lesions

Motor cells in pre-central gyrus to anterior horn cells in the cord

Pyramidal weakness: extensors in UL, flexors in LL

No wasting

Spasticity: increased tone +/- clonus

Hyperreflexia

Up-going plantars

243

Pyramidal weakness: extensors in UL, flexors in LL

No wasting

Spasticity: increased tone +/- clonus

Hyperreflexia

Up-going plantars

UMN lesion

244

Pattern of deficit in LMN lesions

Anterior horn cells to peripheral nerves

Wasting

fasciculation

Flaccidity: hypotonia

Hyporeflexia

Downgoing plantars

245

Anterior horn cells to peripheral nerves

Wasting

fasciculation

Flaccidity: hypotonia

Hyporeflexia

Downgoing plantars

LMN lesion

246

Pattern of deficit in primary muscle lesions

Symmetrical loss

Reflexes lost later than in neuropathies

No sensory loss

Fatiguability in myasthenia

247

Symmetrical loss

Reflexes lost later than in neuropathies

No sensory loss

Fatiguability in myasthenia

Primary muscle lesions

248

Patterns of sensory deficits

Pain and temp travel in small fibres in peripheral nerves and in anterolateral spinothalamic tracts

Touch, joint position and vibration travel in large fibres peripherally and in dorsal columns centrally

249

Distal sensory loss

Suggestive of a neuropathy

250

Sensory level tells us

Hallmark of cord lesion

251

Spinal nerves:

Neck flexor

C1-C6

252

Spinal nerves:

Neck extensors

C1-T1

253

Spinal nerves:

Supply diaphragm

C3, 4, 5

254

Spinal nerves:

C5, C6

Move shoulder, raise arm, flex elbow

255

Spinal nerves:

C6

Externally rotate (supinate the arm)

256

Spinal nerves:

C6-7

Extend elbow and wrist (triceps and wrist extensors)

Pronate wrist

257

Spinal nerves:

C7, T1

Flex wrist, supply small muscles of the hand

258

Spinal nerves:

T1-T6

Intercostals and trunk above the waist

259

Spinal nerves:

T7-L1

Abdominal muscles

260

Spinal nerves:

L1-L4

Flex thigh

261

Spinal nerves:

L2, L3, L4

Adduct thigh, extend leg at the knee (quadriceps femoris)

262

Spinal nerves:

L4, L5, LS1

Abduct thigh

Flex leg at the knee

Dorsiflex foot

Extend toes

263

Spinal nerves:

L5, S1, S2

Extend leg at the hip

Plantar flex foot

Flex toes

264

Ipsilateral loss of proprioception/vibration and UMN weakness with contralateral loss of pain

Brown-Sequard syndrome

265

Selective loss of pain and temp with conservation of proprioception and vibration (dissociated sensory loss)

Occurs in cervical cord lesions e.g. syringomyelia

266

Cerebellar syndrome

DDANISH

Dysdiadochokinesia

Dysmetria: past-pointing

Ataxia: limb/truncal

Nystagmus: horizontal= ipsilateral hemisphere

Intention tremor

Speech: slurred, staccato, scanning dysarthria

267

Scanning dysarthria

Scanning speech, also known as explosive speech, is a type of ataxic dysarthria in which spoken words are broken up into separate syllables, often separated by a noticeable pause, and spoken with varying force.

268

Causes of cerebellar syndrome

PASTRIES

Paraneoplastic: e.g. from bronchial carcinoma

Alcohol: thiamine and B12 deficiency

Sclerosis

Tumour e.g. CPA lesion

Rare: MSA, Friedrich's, Ataxia Telangiectasia

Iatrogenic: phenytoin

Endo: hypothyroidsim

Stroke: vertebrobasilar

269

What does the ACA supply

Frontal and medial part of cerebrum

270

Contralateral motor/sensory loss in the legs>arms

Face spared

Abulia (pathological laziness)

ACA insult

271

What does the MCA supply

Lateral/external part of hemisphere

272

Contralateral motor/sensory loss in face and arms/legs

Contralateral homonymous hemianopia due to involvement of optic radiation

Dominant hemisphere (L): aphasia

Non-dominant hemisphere: neglect, apraxia

MCA insult

273

What does the PCA supply?

Occipital lobe

 

274

Contralateral homonymous heminaopia with macula sparing

PCA insult

275

What is supplied by the vertebrobasilar circulation?

Cerebellum, brainstem and occipital lobes

Any insult to this circulation can present with a combination of symptoms

276

Combination of symptoms from:

visual- hemianopia, cortical blindness

DANISH

CN lesions

Hemi/quadriplegia

Uni/bilateral sensory sympyoms

?Vertebrobasilar insult

277

Lateral Medullary syndrome as a consequence?

Occlusion of one vertebral A or PICA

278

Features of Lateral Medullary Syndrome (Wallenberg's syndrome0

DANVAH

Dysphagia

Ataxia (ipsilateral)

Nystagmus (ipsilateral)

Vertigo

Anaesthesia: ipsilateral facial numbness and absent corneal reflex, contralateral pain loss

Horner's syndrome

279

Millard-Gubler Syndrome (crossed hemiplegia)

 

Pontine lesion (e.g. infarct)

6th and 7th CN palsy with contralateral hemiplegia

280

Causes of locked in syndrome

Ventral pons infarction: basilar artery

Central pontine myelinolysis

281

Causes of CPA syndrome

Acoustic neuroma, meningioma, cerebellar astrocytoma, metastasis

282

Features of CPA syndrome

Ipsilateral CN5, 6, 7, 8 palsies and cerebellar signs

Absent corneal reflex

LMN facial palsy

LR palsy

Sensorineural deafness, vertigo, tinnitus

DANISH

283

Ipsilateral CN5, 6, 7, 8 palsies and cerebellar signs

Absent corneal reflex

LMN facial palsy

LR palsy

Sensorineural deafness, vertigo, tinnitus

DANISH

CPA Syndrome

284

What is subclavian steal syndrome

Subclavian artery stenosis proximal to the origin of the vertebral artery may lead to blood being stolen from this vertebral artery by retrograde flow

285

Syncope/presyncope or focal neurology on using the arm

Subclavian Steal Syndrome

286

Def: Subclavian Steal Syndrome

Syncope/presyncope or focal neurology on using the arm

BP difference >20mmHg between arms

287

Def: Beck's Syndrome

aka Anterior Spinal Artery Syndrome

Infarction of spinal cord in distibution of anterior spinal artery (i.e. ventral 2/3rds of cord)

288

Causes of Anterior Spinal Artery (Beck's syndrome)

Aortic aneurysm dissection or repair

289

Para/quadriparesis

Impaired pain and temperature sensation

Preserved touch and proprioception

Anterior Spinal Artery Syndrome

290

Structure of muscle weakness differential

Cerebrum/brainstem

Cord

Anterior horn

Roots/plexus

Motor nerves

NMJ

Muscle

291

Cerebral/brainstem causes of muscle weakness

Vascular: infarct, haemorrhage

Inflammation: MS

SOL

Infection: encephalitis, abscess

292

Cord causes of muscle weakness

Vascular: anterior spinal artery infarction

Inflammation: MS

Injury

293

Anterior horn causes of muscle weakness

MND, polio

294

Roots/plexal cause of muscle weakness

Spondylosis

Cauda equina syndrome

Carcinoma

295

Motor nerve causes of muscle weakness

Motorneuropathy e.g. compression

Polyneuropathy e.g. GBS, CMT

296

NMJ causes of muscle weakness

MG

LEMS (Lambert-Eaton)

Botulism

297

With what is myasthenia gravis assocaited?

Thymoma

298

Muscular causes of muscle weakness

Toxins: steroids

Poly/Dermato-myositis

Inherited: DMD, BMD, FSH

299

How can gait disturbance be classified?

Motor

Basal ganglia

UMN bilateral/unilateral

LMN unilateral/bilateral

Mixed UMN and LMN

 

Sensory

Vestibular

Cerebellar

Proprioceptive loss

Visual loss

 

Other

300

Basal ganglia causes of gait disturbance

Festinating/shuffling

PD

Parkinsonism: MSA, PSP, LBD, CBD

301

UMN bilateral cause of gait disturbance

Spastic, scissoring

 

Cord: compression, trauma, hereditary spastic paraparesis, syringomelia, transverse myelitis

 

Bihemispheric: CP, MS

302

Description of spastic gait

Scissoring- bilateral

Cricumducting- unilateral

303

LMN bilateral causes of gait disturbance

Bilateral foot drop

 

Polyneuropathy: CMT, GBS

Cauda equina

304

High stepping gait aka

Foot drop

Unilateral or bilateral

305

LMN uniltaeral causes of gait distrubance

Foot drop-> high stepping gait

 

Anterior horn: Polio

Radicular: L5 root lesion

Sciatic/common peroneal nerve: trauma. DM

306

Causes of mixed UMN and LMN gait disturbance

MND

Ataxia: Friedrich's

SACD

Taboparesis

307

How can hand wasting differential be structured?

Cord

Roots

Plexus

Neuropathy

Muscle

308

Cord causes of hand wasting

Anterior horn: MND, polio

Syringomyelia

 

309

Root causes of hand wasting

Spondylosis, neurofibroma

310

Plexal causes of hand wasting

Compression: cervical rib, tumour: Pancoast's, breast

Avulsion: Klumpke's palsy

311

Neuropathic causes of hand wasting

Generalised: CMT

Mononeuritis multiplex: DM

Compressive mononeuropathy: 

Median- thenar wasting

Ulnar- hypothenar and interossei wasting

312

Muscular causes of hand wasting

Disuse: RA

Compartment syndrome: Volkman's ischaemic contracture

Distal myopathy: myotonic dystrophy

Cachexia

313

Volkman's iscahemic contractiure

Permanent flexion contracture of the hand at the wrist

 

 

314

Causes of Volkmann's ischaemic contracture

Neglected compartment syndrome

Crush syndrome

#: esp those associated with vascular injury

Bleeding disorders

 

Iscahemic leading to contracture of long flexors and extensors in the forearm

 

315

Vestibular causes of gait disturbance

Romberg's +ve:

Meniere's 

Viral labyrinthitis

Brainstem lesion

316

Cerebellar causes of gait disturbance

Ataxis

EtOH

Infarct

317

Proprioceptive causes of gait disturbance

Romberg's +ve

Dorsal columns: B12 deficiency

Peripheral neuropathy: DM, EtOH, uraemia

 

318

Other causes of gait disturbance

Myopathy, MG/LEMS

Medical: postural hypotension, Stokes-Adams, arthritis

319

Causes of blackouts

CRASH

Cardiac

Arterial

Systemic

Head

320

Cardiac causes of blackouts

 

Stokes-Adams Attacks

 

Brady: heart block, sick sinus, long-QT

Tachy: SVT, VT

Structural: weak heat: LVF, tamponade.

Block: AS, HOCM, PE

321

What are the reflexes leading to blackout

Vagal overactvitiy

Sympathetic underactivity= Postural hypotension

322

Features of vagal overactivity

Vasovagal syncope

Situational: cough, effort, micturition

Carotid sinus syncope

 

323

Causes of postural hypotension

STANDUP

Salt deficiency: hypovolaemia, Addison's

Toxins:

Cardiac- ACEI, diuretics, Nitratates, alpha blockers

Neuro: TCAs, benzos, antipsychotics, L-DOPA

Autonomic Neuropathy: DM, Parkinson's GBS

Dialysis

Unwell: chronic bed rest

Pooling, venous: varicose veins, prolonged standing

324

Arterial causes of blackouts

Vertebrobasilar insufficiency: migraine, TIA (doesn't really cause blackouts), CVA, subclavian steal

Shock

HTN: phaeo

325

Systemic causes of blackouts

Metabolic: reduced glucose

Respiratory: hypoxia, hypercapnia

Blood: anaemia, hyperviscosity

326

Head causes of blackout

Epilepsy

Drop attacks

327

Examination following black out

Postural hypotension: difference of >20/10 after standing for 3 mins vs lying down

CV

Neurological

328

Ix following blackout

ECG +/- 24hr ECG

U+E, FBC, Glucose

Tilt table

EEG, sleep EEG

Echo

CT

MRI brain

329

Triggers in cardiogenic syncope

Exertion, drug, unkown

330

Symptoms before in cardiogenic syncope

Palpitations, chest pain, dyspnoea

331

Symptoms during cardiogenic syncope

Pale, slow/absent pulse, clonic jerks may occur

332

Symptoms after cardiogenic syncope

Rapid recovery

333

ix in cardiogenic syncope

ECG

24hr ECG

Echo

334

Trigger for vasovagal syncop

Prolonged standing, heat, fatigue, stress

 

335

Symptoms before vasovagal syncope

Gradual onset: secs-> mins

Nausea, pallor, sweating, tunnel vision, tinnitus

Cannot occur lying down

336

Symptoms during vasovagal syncope

Pale, grey, clammy, bradycardic

Clonic jerks and incontinence can occur but no tongue biting

337

Symptoms after vasovagal syncope

Rapid recovery

338

Ix in vasovagal syncope

Tilt-table testing

339

Trigger to postural hypotensive blackout

Standing uo

Before during and after as for vasovagal

340

Ix in postural hypotension

Tilt-table testing

341

Trigger in arterial causes of blackout

Arm elevation, migraine

342

Before during and after in arterial blackouts

As for vasovagal +/- brainstem symptoms e.g. diplopia, nausea, dysarthria

343

Ix in arterial blackouts

MRA, duplex vertebrobasilar circulation

344

Symptoms of hypoglycaemia

Tremor, hunger, sweating, light-headedness-> LOC

345

Triggers in epilepsy

Flashing lights, fatigue, fasting

346

Symptoms before epileptic epsidoe

Aura in complex partial seizures- feeling strange epigastric rising

Deja/jamais vu

Smells

Lights

Automatisms

 

347

Symptoms during epileptic episode

Tongue biting

Incontinence

Stiffness-> jerking, eyes open

Cyanosis

Reduced SpO2

348

Symptoms after epileptic episode

Headache

Confusion

Sleeps

Todd's palsy

349

Todd's palsy

Post-ictal paresis/palsy

Usually confined to one side

Usually abates after 48hrs

350

Symptoms of drop-attack

Sudden weakness of legs causes older woman to fall to the ground

351

Features of drop attacks

No LOC

Sudden weakness

No post-ictal phase

352

Def: vertigo

The illusion of movement, usually rotatory of patient or surroundings

Worse on movement

353

Def: dizziness

With impaired consciousness= blackout

Without impaired consciousness

Vertigo: vestibular

Imbalance: vestibular, cerebellar, extrapyramidal

354

Causes of vertigo

IMBALANCE

Infection/injury

Meniere's

BPV

Aminoglycosides/frusemide

Lymph

Arterial

Nerve

Central lesions

Epilepsy

 

355

Infective causes of vertigo

Labyrinthitis: post-viral severe vertiog, N+V

Ramsay Hunt

Trauma: to petrous temporal bone

356

Symptoms of Menniere's

Recurrent vertigo (~20 mins) +/- N+V

Fluctuating SNHL

Tinnitus

Aural fullness

357

Lymph, peri, fistula causing imbalance

Connection between inner and middle ears

Traumatic or congenital

Presents with vertigo, SNHL

On examination Tullio's phenomenon may be seen

358

Connection between inner and middle ears

Traumatic or congenital

Presents with vertigo, SNHL

On examination Tullio's phenomenon may be seen

Lymph, Peri fistula

Connection between inner and middle ear

359

Tullio phenomenon

Tullio phenomenon, sound-induced vertigo, dizziness, nausea or eye movement (nystagmus) was first described in 1929 by the Italian biologist Prof. Pietro Tullio. (1881–1941)[1][2] During his experiments on pigeons, Tullio discovered that by drilling tiny holes in the semicircular canals of his subjects, he could subsequently cause them balance problems when exposed to sound.

The cause is usually a fistula in the middle or inner ear, allowing abnormal sound-synchronized pressure changes in the balance organs.[3] Such an opening may be caused by a barotrauma (e.g. incurred when diving or flying), or may be a side effect of fenestration surgery, syphilis or Lyme disease. Patients with this disorder may also experience vertigo, imbalance and eye movement set off by changes in pressure, e.g. when nose-blowing, swallowing or when lifting heavy objects.

360

Arterial causes of vertigo

Migraine

TIA/Stroke

361

Nerve causes of imbalance

Acoustic neuroma/vestibular schwannoma

362

Central lesions causing vertigo

Demyelination, tumour, infarct (e.g. LMS)

363

Epileptic causes of vertigo

Complex partial seizures

364

Conductive causes of hearing loss

WIDENING

Wax or foreign body

Infection: otitis media, OME

Drum perf

Extra: ossicle discontinuity- otosclerosis, trauma

Neoplasia: carcinoma

INury: barotrauma

Granulomatous: Wegener's, Sarcoid

365

Sensorineural causes of hearing loss

DDIVINITY

Developmental

Degenerative

Infection

Vascular

Inflammation

Neoplasia

Injury

Toxins

lYmph

366

Developmental causes of sensorineural hearing loss

Genetic: Alport's, Waardenburgs

Congenital: TORCH

Perinatal: anoxia

367

Degenerative causes of sensorineural hearing loss?

Presbyacusis

368

Infective causes of sensorineural hearing loss

VZV, measles, mumps, IFV

Meningitis

369

Vascular causes of sensorineural hearing loss

Ischaemia of internal auditory artery-> sudden hearing loss and vertigo

Stroke

370

Inflammatory causes of hearing loss

Vasculitis

Sarcoidosis

371

Neoplastic cause of sensorineural hearing loss

CPA tumours: acoustic neuroma

 

372

What is the commonest cause of unilateral SNHL

Acoustic neuroma

373

Toxins causing sensorineural hearing loss

Gentamicin

Frusemide

Aspirin

374

lYmph causes of sensorineural hearing loss

Endolymphatic hydrops= Menier'es

Perilymphatic fistula= ruptured round window

 

375

Def: tremor

Regular, rhythmic oscillation

376

Types of tremor

RAPID

Resting

Action/postural

Intention

Dystonic

377

Features of resting tremor

4-6Hz, pill-rolling

Abolished on voluntary movement

Increased with distraction (e.g. counting backwards)

Caused by Parkinsonism

 

Rx with Da agonists, antimuscarinic e.g. procyclidine

378

4-6Hz, pill-rolling

Abolished on voluntary movement

Increased with distraction (e.g. counting backwards)

Caused by Parkinsonism

 

Rx with Da agonists, antimuscarinic e.g. procyclidine

Resting tremor

379

Features of action/postural tremor

6-12Hz

Absent at rest

Worse with outstretched hands or movement

Equally bad at all stages of movement

380

6-12Hz

Absent at rest

Worse with outstretched hands or movement

Equally bad at all stages of movement

Action/postural tremor

381

Causes of postural tremor

BEATS

Benign essential tremor

Endocrine: thyrotoxicosis, reduced glucose, phaeochromocytoma

Alcohol withdrawal (or caffeine, opioids)

Toxins: beta agonists, theophylline, VPA, phenytoin

Sympathetic: physiological tremor may be enhanced e.g. anxiety

382

Features of intention tremor

>6Hz, irregular, large amplitude

Worse at end of movement e.g. past pointing

383

>6Hz, irregular, large amplitude

Worse at end of movement e.g. past pointing

Intention tremor

384

Cause of intention tremor

Cerebellar damage

385

Features of dystonic tremor

Variable

Causes are mostly idiopathic/ as for dystonia

386

Features of benign essential tremor

Autosomal dominant

Occur with action and worse with anxiety, emotion, caffeine

Arms, neck, voice

Doesn't occur during sleep

Better with EtOH

387

Autosomal dominant

Occur with action and worse with anxiety, emotion, caffeine

Arms, neck, voice

Doesn't occur during sleep

Better with EtOH

Benign essential tremor

388

Def: myoclonus

Sudden, involuntary jerk

389

Causes of myoclonus

Metabolic: asterixis (L, R, raised CO2)

Neurodegenerative diseases (lysosomal storage disorders)

CJD

Myoclonic epilepsies e.g. infantile spasms

390

Metabolic causes of asterixis

Hepatic flap (ammonia)

Renal flap (azotemia- urea)

Electrolyte: hypoglycaemia, hypokalaemia and hypomagnesaemia

Drugs: barbiturate, EtOH, phenytoin, primidone

391

Benign Essential Myoclonus

Autosomal dominant

Childhood onset, frequent generalised myoclonus without progression

May respond to valproate

392

Def: dystonia

Prolonged muscle contracture-  unusual joint posture or repetitive movmenets

393

Idiopathic generalised dystonia

Often autosomal dominant

Childhood onset: starts in one leg and spreads on that side of the body over 5-10 years

394

Idiopathic focal dystonia

Commonest form of dystonia

Confined to one part of the body

Worsened by stress

395

What are the types of idiopathic focal dystonia?

Spasmodic torticollis

Blepharospasm

Oromandibular

Writer's/Musician's cramp

396

Types of acute dystonia

Torticollis, trismus and or occulogyric crisis

397

Trismus

Reduced opening of the jaw caused by spasm

398

Drugs causing acute dystonia

Neurlopetics

Metoclopramide (NB pregnant women)

L-Dopa

399

Rx in acute dystonia

Procyclidine (antimuscarinic)

400

Def: chorea

Non-rhythmic, purposeless, jerky, flitting movements

e.g. facial grimacing, flexing/extending the fingers

401

Causes of chorea

Huntington's

Sydenham's

Wilson's

L-Dopa

402

Def: athetosis

Slow, sinuous, writhing movements

403

Causes of athetosis

Cerebal palsy

Kernicterus

404

Hemiballismus

Large amplitude, flinging hemichorea

Contralateral to a vascular lesion in the subthalamic nucleus: often in elderly diabetics

Recovers spontaneously over moths

405

Which region of the brain is involved in hemiballismus

Subthalamic nucleus

406

What causes tardive syndromes

Delayed onset following chronic exposure to dopamine antagonsts e.g. antipsychotics, antiemetics, L-Dopa

407

How can tardive syndromes be classified?

Dyskinesia: orobuccolingual, truncal or choreform movements

Dystonia: sustained, stereotyped muscle spasms of twitching or turning

Akathisia: unpleasant sense of inner restlessness +/- repetitive movements e.g. pacing

408

Rx in tardive syndromes

Change e.g. to atypical or slowly withdraw drug

Dyskinesia: tetrabenazine

Akathisia: beta blocker

409

Def: dementia

Chronically impaired condition that affects multiple domains without impairment of consciousness

Acquired and progressive

410

PC in AD

Progressive, global, cognitive decline

411

RFs for AD

ApoE4

Presenilin 1/2 muts

DS

412

Ix in AD

MRI- medial temporal lobe atrophy

413

Rx in AD

Cholinestarse inhibitors e.g. donepezil, rivastigmine if MMSE is 10-20

414

Ix in Vascular dementia

MRI- extensive infarcts or small vessel disease

415

Sudden onset, stepwise deterioration, patchy deficits in cognition

Vascular RFs

?Vascular dementia

416

Pathophysiology of LBD

Lewy Bodies in occipito-parietal cortex

417

Rx in vascular dementia

Manage predisposing factors

418

Fluctuating cogntiive dysfunction, visual hallucinations, parkinsonism

LBD

419

Rx in LBD

Cholinesterase inhibitors

420

Disinhibition, personality change, early memory preservation, progressive aphasia

Frontotemporal dementia

421

This is the most severe form of aphasia, and is applied to patients who can produce few recognizable words and understand little or no spoken language. may often be seen immediately after the patient has suffered a stroke and it may rapidly improve if the damage has not been too extensive. However, with greater brain damage, severe and lasting disability may result.

Global aphasia

422

In this form of aphasia, speech output is severely reduced and is limited mainly to short utterances of less than four words. Vocabulary access is limited and the formation of sounds is often laborious and clumsy. The person may understand speech relatively well and be able to read, but be limited in writingoften referred to as a 'non fluent aphasia' because of the halting and effortful quality of speech.

Broca's aphasia

Expressive aphasia

423

This term is applied to patients who have sparse and effortful speech, resembling severe Broca's aphasia. However, unlike persons with Broca's aphasia, they remain limited in their comprehension of speech and do not read or write beyond an elementary level.

Mixed non-fluent aphasia

424

In this form of aphasia the ability to grasp the meaning of spoken words is chiefly impaired, while the ease of producing connected speech is not much affected. THowever, speech is far from normal. Sentences do not hang together and irrelevant words intrude-sometimes to the point of jargon, in severe cases. Reading and writing are often severely impaired.

Receptive aphasia (Wernicke's)

425

This term is applied to persons who are left with a persistent inability to supply the words for the very things they want to talk about-particularly the significant nouns and verbs. As a result their speech, while fluent in grammatical form and output is full of vague circumlocutions and expressions of frustration. They understand speech well, and in most cases, read adequately. Difficulty finding words is as evident in writing as in speech.

Anomic aphasia

426

. Unlike other forms of aphasia that result from stroke or brain injury, PPA is caused by neurodegenerative diseases, such as Alzheimer's Disease or Frontotemporal Lobar Degeneration. PPA results from deterioration of brain tissue important for speech and language. Although the first symptoms are problems with speech and language, other problems associated with the underlying disease, such as memory loss, often occur later.

Primary progressive aphasia

427

Ameliorable causes of dementia

Infection:

Viral: HIV, HSV, PML

Helminth: cysticerosis, toxo

 

Vascular:

Chronic SDH

 

Inflammation

SLE, carcoid

 

Neoplasia

 

Nutritional:

Thiamine deficiency

B12 and folate deficiency

Pellagra (B3/niacin deficiency)

 

Hypothyroid

 

Hypoadrenalism

 

Hypercalcaemia

 

Normal pressure hydrocephalus

 

(Depression)

428

Def: delerium

Globally impaired cognition and impaired consciousness

429

Disorientation to person, time and place

Reversal of sleep-wake cycle (hyperactive at night)

Labile mood

Illusions, delusions and hallucinations

Cognitive impairment: memory, language, concentration

Delirium

430

Causes of ACS

DELIRIUMS

Drugs: opiods, sedatives, L-DOPA

Eyes, ears and other sensory deficits

Low O2 states: MI, stroke, PE

infection

Retention

Ictal

Under-hydration/nutrition

Metabolic: DM, post-op, sodium ,uraemia

SDH or other intracranial pathology

431

Ix in ACS

Bloods: FBC, U+Es, LFTs, glucose, ABG

urine dip

Septic screen

ECG, LP

432

Mx of delirium

ID and Rx underlying cause

Surround with familiar people

Nurse in moderately, lit quiet room

Help to orientate to time and space

Find glasses, hearing aids

Avoid sedatives if possible but if disruptive@

Haldol 0.5-2mg PO/IM

Chlorpromazine 50-100mg PO/IM (avoid in elderly)

433

Causes of acute headache

VICIOUS

Vascular

Infection/inflammation

Compression

ICP

Opthalmic

Unknown

Systemic

434

Vascular causes of acute headache

Haemorrhage: SAH, intracranial, intracerebral

Infarction: esp. posterior circulation

Venous: sinus/cortical thrombosis

435

Infective/inflammatory causes of acute headache

Meningitis

Encephalitis

Abscesss

436

Compressive causes of acute headache

Obstructive hydrocephalus: tumour

Pituitary enlargement: apoplexy

437

bleeding into or impaired blood supply of the pituitary gland at the base of the brain. This usually occurs in the presence of a tumor of the pituitary, although in 80% of cases this has not been diagnosed previously. The most common initial symptom is a sudden headache, often associated with a rapidly worsening visual field defect or double vision caused by compression of nerves surrounding the gland. This is followed in many cases by acute symptoms caused by lack of secretion of essential hormones, predominantly adrenal insufficiency

Pituitary apoplexy

438

Reduced ICP causes of acute headache

Spontaneous intracranial hypotension: acute dural CSF leak

Worse on standing initially

439

Ophthalmic cause of acute headache

Acute glaucoma

440

Unknown causes of acute headache

Cough, exertion, coitus

441

Systemic causes of acute headache

HTN: Phaeo, pre-eclampsia

Infection: sinusitis, tonsillitis, atypical pneumonia

Toxins: CO

442

Causes of chronic headache

MCD TINGS

Migraine

Cluster headaches

Drugs:

Analgesics, caffeine, vasodilators: Ca2+ antatgonists, nitrates

 

ICP:

raised: tumour, aneurysm, AVM, benign intracranial HTN

reduced: spontaneous intracranial hypotension

 

Neuralgia


GCA

 

Systemic:

HTN

Organ failure: uraemia

443

Ix in headache

Blooods

Urine

Micro: cultures, serology (enterovirus), HSV, HIV, syphillis, crypto, CSF

 

Radiology:

Non-contrast CT

SAH: blood in sulci, cisterns, white: 90% sensitivity in first 24h

 

MRI: MRA: anerusym

MRV: sinus thrombosis

 

Special: CSF

 

444

What is the normal opening pressure of CSF?

5-20cm H2O

445

Raised opening pressure CSF

SAH, meningitis

446

Reduced CSF opening pressure

Spontaneous intracranial hypotension

447

Cause of CSF xanthochromia

Yellow appearnce of CSF due to bilirubin, detected by spectrophotometry

Blood in CSF e.g. in SAH

448

CSF:

Turbid apperance

Polymorphonuclear cells

100-1000 cells

Reduced glucose (<1/2 plasma)

Raised protein (>1.5)

Bacterial meningitis

449

CSF:

Fibrin web appearance

Lympho/monoculear

10-1000 cells

Reduced glucose (<1/2 plasma)

Raised protein (1-5)

TB meningitis

450

Clear CSF

Lympho/monoculear

50-1000 cells

>1/2 plasma glucose

Mild raised protein (<1)

Viral meningitis

451

Sudden onset, worst ever occipital headache

Meningisim, focal signs, reduced conciousness

?SAH

452

SAH

Dense material in the basal cisterns and fissures is due to acute bleeding into the subarachnoid space

Blood in the subarachnoid space can fill or partly fill the sulci, fissures, basal cisterns and ventricles

Blood in the ventricles may be the only sign of subarachnoid haemorrhage

When a CT scan is acquired the patient lies supine and any blood in the lateral ventricles will collect posteriorly

Calcification of the choroid plexus is a normal finding which should not be mistaken for intraventricular blood

453

Headache, vomiting, seizures, vision, papilloedema

Saggital venous sinus thrombosis

454

Headache +/- mastoid pain, focal CNS signs, seizures, papilloedema

Transverse venous sinus thrombosis

455

?Venous sinus thrombosis

MRV

456

Thunderclap headache

Stroke-like focal symptoms over days

Focal seizures common

Cortical vein thrombosis

457

Def: CVST

Cerebral venous sinus thrombosis (CVST) is the presence of acute thrombosis (a blood clot) in the dural venous sinuses, which drain blood from the brain. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body, and seizures. The diagnosis is usually by computed tomography (CT/CAT scan) or magnetic resonance imaging (MRI) employing radiocontrast to demonstrate obstruction of the venous sinuses by thrombus.[1]

Treatment is with anticoagulants (medication that suppresses blood clotting), and rarely thrombolysis (enzymatic destruction of the blood clot). Given that there is usually an underlying cause for the disease, tests may be performed to look for these. The disease may be complicated by raised intracranial pressure, which may warrant surgical intervention such as the placement of a shunt.

458

Fever, photophobia, neck stiffness, Kernig's +ve

Purpuric rash

Reduced consciousness

Meningitis

459

Fever, odd behaviour, fits, focal neurology, reduced consciousness

Encephalitis

460

Constant unilateral eye pain radiating to forehead

Reduced acuity, haloes, N+V

Red eye, cloudy cornea

Dilated, non-responsive pupil

Acute glaucoma

461

Bilateral/vertex-bitermopral non-pulsatile band-like headache

Tension headache

462

Unilateral throbbing

N+V, phono/photophobia

Prodrome->aura-> headache

Migraine

463

Rapid onset, very severe pain around/behind one eye

Red, watery eye, nasal congestion

Miosis, ptosis

Attacks lasting 15mins-3hrs 1-2x/day mostly nocturnal

Episodes last 4-12w, can be chronic or episodic

Cluster headaches

464

Rx in cluster headache

?Neuroimaging- GP/neurologist discussion

 

Acute:

Subcutaenous or nasal triptan: e.g. subcut sumatriptan 6mg (most rapid and effective)

Arrange provsiion of home and ambulatory oxygen therapy: 100% O2 at 12l per minute via a non-rebreathe mask and a reservoir bag

 

(Do not offer paracetamol, aspirin, NSAIDs, or oral triptans for acute treatment)

 

Prophylactic: verapamil

465

Acute Rx in cluster headache

Subcut/nasal triptan

100% O2

466

Cluster headache prophlyaxis

Verpamail

467

Paroxysmal hemicranias

Cluster-like headache lasting 5-45 mins 5-30 times/day

468

SUNCT

Short-lasting unilateral neuralgia with conjunctival injection and tearing, attacks last 15-60s, recure 5-30x/hr

469

Hemicrania continua

Continuous cluster-like headache

470

Rx of hemicranias

All repsond well to indomethacin

471

Paroxysms of unilateral intense stabbing pain in trigeminal distribution

Triggered by washing area, shaving, eating talking

Male >50y

 

Trigeminal neuralgia

472

What is significant in trigeminal neuralgia

2o in 14%:

Compression of CNV

MS

Zoster

Chiari malformation

473

Ix in trigeminal neuralgia

Ix: exclude 2o cause with MRI

474

Rx in trigeminal neuralgia

Carbamazepine (100mg BD and titrate slowly)

Specialist involvement if doesn't work (Lamotrigine and gabapentin are alternatives)

 

 

Surgical: microvascular decompression

475

Episodic headache becoming daily chronic headache

Using OTC analgesia >6d/m

Analgesia overuse

476

Headache worse in morning, stooping, visual problems, obese woman

Raised ICP headache

477

Headache worse when sitting or standing

Reduced ICP headache

478

Preauricular pain on chewing

Associated with crepitus

Earache, headache

TMJ dysfunction

479

GCA

rule of 60

>60y

ESR >60

pred 60mg

480

Unilateral temple/scalp pain and tenderness

thcikened, pulseless temporal artery

Jaw claudication, amaurosis fugax, sudden blindness

Associated with PMR in 50%

GCA

481

Ix in GCA

ESR +++

Raised plt

Raised ALP

Reduced Hb

Temporal artery biopsy

482

Rx in GCA

High dose prednisolone (60mg/d PO) for 5-7d

Opthalmology involvement

Guided by symptoms and ESR

Give PPI and bisphosphonate

Start 75mg OD aspirin

 

Steroid dose is gradually tapered over 1-2y with most patients reaching complete remission

483

Epidemiology of migraine

8% prevalence

F>M

484

RFs Migraine

Obesity

PFO

485

Pathophysiology of migraine

Vascular: cerebrovascular constriction-> aura, dilatation -> headache

Brain: spreading cortical depression

Inflammation: activation of CNV nerve terminals in the meninges and cerebral vessels

486

Migraine triggers

CHOCOLATE

Cheese

OCP

Caffeine

alcohOL

Anxiety

Travel

Exercise

487

Symptoms of migraine

Headache

Prodrome (50%)
Aura (20%)

488

How can migraine be classified

With aura (classical migraine)

Without aura (common migraine)

489

Features of migraine headache

Aura lasting 15-30 mins then unilateral, throbbing headache

Phono/photophobia

Nausea/vomiting

Allodynia

Often premenstrual

490

Features of migraine prodrome

50%

Precede migraine by hours-days

Yawnings

Food cravings

Changes in sleep, appetite or mood

491

Features of migraine aura

20%

Precedes migraine by minutes and may persist

Vsiual: distortion, lines, dots, zig-zags, scotoma, hemianopia

 

Sensory: paraesthesia (fingers-> face)

 

Motor: dysarthria, ataxia, ophthalmoplegia, hemiparesis (hemiplegic migraine)

 

Speech: dysphasia, paraphasia

492

Diagnostic criteria for migraine

Typical aura and headache or

>5 headaches lasting 4-72h with either n/v or photo/phonophobia and >2 of:

unilateral

pulsating

interferes with normal life

worsened by routine activity

493

DDx migraine

Cluster/tension headache

Cervical spondylosis

HTN

Intracranial pathology

Epilepsy

494

Acute management of migraine

1st line- combination therapy

Oral triptan e.g. (sumatriptan 50/100mg) and an NSAID e.g. ibuprofen

or an oral triptan and paracetamol

If monotherapy preferred consider oral triptan, NSAID or aspirin (900mg every 4-6h) or paracetamol

Consider adding an anti-emetic e.g. metoclopramide, domperidone, prochlorperazine even in the absence of N+V

495

Preventative treatment of migraine

1st line

Topiramate or propranolol

2nd line

Amitryptilline

3

Acupuncture

 

Riboflavin may be effective in reducing migraine frequency and intensity

496

NB re Topiramate in pregnancy

Assoicated with fetal malformations and can impair hormonal contraception

497

Epidemiology of SAH

9/100,000

35-65yrs

498

Causes of SAH

Rupture of saccular aneurysms (80%)

AVMs (15%)

499

RFs for SAH

Smoking

HTN

EtOH

Bleeding diathesis

Mycotic aneurysms (bacterial infection of arterial wall- SBE)

FHx (close relatives have 3-5x risk

500

What are the sites of Berry Aneurysms

Junction of posterior communicating with IC

Junction of anterior communicating with ACA

Bifurcation of MCA

501

What conditions are associated with SAH?

Adult PKD

Coarctation of the aorta

Ehlers Danlos

502

Sudden severe occipital headache

Collapse

Meningism: neck stiffnes, N/V, photophobia

Seizures

Drowsiness-> coma

?SAH

503

Sentinal headche

6% of SAH patients experience sentinal headache from small warning bleed

504

Signs of SAH

Kernig's

Retinal or subhyaloid haemorrahge

Focal neurology: at presentation suggests aneurysm location, later deficits suggest complications

505

Kernig's sign

Kernig's sign. Kernig's sign (after Waldemar Kernig (1840–1917), a Russian neurologist) is positive when the thigh is flexed at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance). This may indicate subarachnoid hemorrhage or meningitis.

506

Brudzinski's sign

Jozef Brudzinski (1874–1917), a Polish pediatrician, is credited with several signs in meningitis. The most commonly used sign (Brudzinski's neck sign) is the appearance of involuntary lifting of the legs when lifting a patient's head off the examining couch, with the patient lying supine.

507

DDx for SAH

In 1o care, 25% of those with thunderclap headache have SAH

50-60% have no cause found

Rest: meningitis, intracerebral bleeds, cortical vein thrombosis

508

Ix of SAH

CT

LP

509

CT sensitivity in SAH

Detects >90% of SAH within first 48h

510

LP in SAH

If CT -ve and no CIs, >12h after start of headache

Xanthochromia due to break down of bilirubin

511

Mx of SAH

Frequent neuro obs: pupils, GCS, BP

Maintain cerebral perfusion pressure, keep SBP >160

Nimodipine for 3w (reduces cerebral vasopsasm)

Endovascular coiling (preferable to surgical clipping

512

Complications of SAH

Rebleeding (20%): commonest cause of mortality

Cerebral ischaemia: due to vasospasm: commonest cause of morbidity

Hydrocephalus: due to blockage of arachnoid granulations, may require ventricular or lumbar drain

Hyponatraemia: dont Mx with fluid restriction

513

Mx of saccular aneruysm

Young patients with aneurysms >7mm in diameter may benefit from Sx

514

Def: stroke

Rapid onset, focal neurological deficit due to a vascular lesion lasting >24h

515

Pathogenesis of stroke

Infarction due to ischaemia (80%)

or intracerebral haemorrhage (20%)

516

Parthophysiology of ischaemic stroke

Atheroma: large e.g. MCA

Small vessel perforators (lacunar)

517

Pathophysiology of embolic stroke

Cardiac (30% of strokes): AF, endocarditis, MI

Atherothromboembolism e.g. from carotids

518

Aetiology of haemorrhagic stroke

Raised BP

Trauma

Aneurysm rupture

Anticoagulation

Thrombolysis

519

Rarer causes of stroke

Watershed stroke: sudden reduction in BP e.g. sepsis

Carotid artery dissection

Vasculitis: PAN, HIV

Cerebral vasospasm 2o to SAH

Venous sinus thrombosis

Anti-phospholipid syndrome, thromobphilia

520

RFs for stroke

HTN

Smoking

DM

Raised lipids

FHx

Cardiac: AF, valvular disase

Peripheral vascular disease

Previous Hx

Ethnicity: raised in blacks and asians

Raised PCT/Hct

OCP

521

Cardiac causes of stroke

AF: 4.5%/y

External cardioversion: 1-3%

Prosthetic valves

Acute MI esp. large anterior

Paradoxical systemic emboli

Cardiac sx

Valve vegetations

522

Ix in determining cause of stroke

ID risk factors for further strokes:

HTN

Cardiac emobli

Carotid artery stenosis

Bleeding/thrombotic tendency

Hyperviscosity

Metabolic

Vasculitis

 

523

Identifying aetiology of stroke:

HTN

Retinopathy

Nephropathy

Big heart on CXR

524

Identifying aetiology of stroke:

Cardiac emboli

ECG +/- 24hr tape for AF

Echo: mural thrombus, hypokinesis, valve lesions, ASD, VSD

525

Identifying aetiology of stroke:

Cartoid artery stenosis

Doppler US +/- angio

Endarterectomy beneficial if >70% symptomatic stenosis

526

When is endarterectomy beneficial in context of carotid artery stenosis?

If >70% symptomatic stenosis

527

Identifying aetiology of stroke:

Bleeding/thrombotic tendency

Thrombophilia screen

Thrombocytopenia

528

Identifying aetiology of stroke:

Hyperviscosity

PCV

SCD

Myeloma

529

Identifying aetiology of stroke:

Metabolic

Glucose

Lipids

Hyperhomocystinaemia

530

Identifying aetiology of stroke:

Vasculitis

Raised ESR

ANA

531

What is used to classify Stroke?

Oxford/Bamford classification

Based on clinical localisation of inffarct

S= syndrome: prior to imaging

I= infarct after imaging when atheroembolic infarct confirmed

532

TACS=

Total anterior circulation stroke

533

What arterial territory involved in TACS?

Large infarct in carotid/ MCA, ACA territory

534

Clinical features of TACS

All 3 of:

1. Hemiparesis (contralateral) and/or sensory deficit (>2 of face, arm and leg)

2. Homonymous hemianopia (contralateral)

3. Higher cortical dysfunction

- Dominant (L usually): dysphasia

- Non-dominant: hemispatial neglect

535

All 3 of:

1. Hemiparesis (contralateral) and/or sensory deficit (>2 of face, arm and leg)

2. Homonymous hemianopia (contralateral)

3. Higher cortical dysfunction

- Dominant (L usually): dysphasia

- Non-dominant: hemispatial neglect

TACS

536

PACS=

Partial anterior circulation syndrome

537

Territory affected by PACS?

Carotid/MCA and ACA territory

538

Clinical features of PACS

2/3 of TACS criteria, usually:

1. Hemiparesis (contralateral) and or sensory deficit

2. Higher cortical dysfunction

Dominant: dysphasia

Non-dominant: neglect, constructional apraxia

 

Deficit is less dense and/or incomplete

539

2/3 of TACS criteria, usually:

1. Hemiparesis (contralateral) and or sensory deficit

2. Higher cortical dysfunction

Dominant: dysphasia

Non-dominant: neglect, constructional apraxia

 

Deficit is less dense and/or incomplete

PACS

540

POCS=

 

Arterial territory affected?

Posterior circulation stroke

 

Infarct in vertebrobasilar territory

541

Clinical features of POCS?

Cerebellar syndrome

Brainstem syndrome

Contralateral homonoymous hemianopia

542

LACS
 

Arterial territory affected?

Lacunar stroke

 

Small infarcts around basal ganglia, internal capsule, thalamus and pons

543

What is there an absence of in LACS?

Higher cortical dysfunction

Homonymous hemianopia

Drowsiness

Brainstem signs

544

What are the 5 LACS syndromes?

Pure motor: posterior limb of internal capsule- commonest

Pure sensory: posterior thalamus (VPL)

Mixed sensorimotor: internal capsule

Dysarthria/clumsy hand

Ataxic hemiparesis: anterior limb of internal capsule, weakness and dysmetria

545

Ischaemic pointers in stroke

Carotid bruit

AF

Past TIA

IHD

546

Haemorrhagic pointers in stroke

Meningism

Severe headache

Coma

547

Brainstem infarcts, clinical features

Complex signs depending on relationship of infarct to CN nuclei, long tracts and brainstem connections

548

Brainstem infarct, region affected

Hemi/quadraparesis

Corticospinal tracts

549

Brainstem infarct, region affected

Conjugate gaze palsy

Oculomotor system

550

Brainstem infarct, region affected

Horner's syndrome

Sympathetic fibres

551

Brainstem infarct, region affected

Facial weakness (LMN)

CN7 nucleus

552

Brainstem infarct, region affected

Nystagmus, vertigo

CN8 nucleus

553

Brainstem infarct, region affected

Dysphagia, dysarthria

CN9 and 10

554

Brainstem infarct, region affected

Dysarthria, ataxia

Cerebellar connections

555

Brainstem infarct, region affected

Reduced GCS

Reticular activating system

556

Which artery affected in LMS/ Wallenberg's syndrome

PICA or vertebral artery

557

Features of LMS/ Wallenberg's syndrome

DANVAH

Dysphagia

Ataxia

Nystagmus

Vertigo

Anaesthesia: ipsilateral facial numbness and absent corneal reflex, contralateral pain loss

Horner's syndrome

558

Features of Millard-Gubler syndrome

Pontine infarct

6th and 7th CN nuclei + corticospinal tracts:

Diplopia

LMN facial palsy and loss of corneal reflex

Contralateral hemiplegia

559

DDx for stroke

Head injury +/- haemorrhage

Glucose derangement

SOL

Hemiplegic migraine

Todd's palsy

Infections: encephalitis, abscesses, Toxo, HIV, HTLV

Drugs e.g. opiate overdose

560

Acute management of stoke

Resuscitate

Monitor

Imaging

Medical

Surgical

Stroke Unit

Secondary prevention

Rehabilitation

561

Resuscitation in stroke

ABC

Ensure patent airway: consider NGT

NBM until swallowing assessed by SALT

Don't overhydrate: risk of cerebral oedema

562

Monitoring in acute mx of stroke

Glucose: 4-11mM: sliding scale if DM

BP <185/110 for thrombolysis NB Rx of HTN can reduce cerebral perfusion

Neuro obs

563

Imaging in acute stroke

Urgent CT/MRI

CT used to exclude 1o haemorrhage

Diffusion-weighted MRI is most sensitive for acute infarct

564

Medical management of stroke

Consider thrombolysis if 18-80 years and <4.5hrs since onset of symptoms

Alteplase

CT 24h post thrombolysis to look for haemorrhage

Aspirin 300mg PO/PR once haemorrhagic stroke excluded +/- PPI, clopidogrel if aspirin sensitive

565

Cerebral perfusion pressure

(CPP) = MAP – ICP or CVP (whichever is highest)

566

Surgical Mx of stroke

Neurosurgical opinion if ICH

May coil bleeding aneurysms

Decompressive hemicraniectomy for some forms of MCA infarction

567

Features of stroke unit

Specialist nursing and physio

Early mobilisation

DVT prophylaxis

568

1o prevention of stroke

Control RFs: HTN, lipids, DM, smoking, cardiac disease

Conisder life long anticoagulation in AF (use CHADS2)

Cartoid endarterectomy if symptomatic 70% stenosis

Exercise

569

Secondary prevention of stroke

Risk factor control as for primary prevention, start a statin after 48h

Aspirin/clopidogrel 300mg for 2w after stroke then either

clopidogrel 75mg OD (preferred option)

Aspirin 75mg OD + dipyridamole MR 200mg BD

Warfarin instead of aspirin/clopidogrel if cardioembolic stroke or chronic AF, start from 2w post-stroke. Don't use aspirin and warfarin together

Carotid endarterectomy if good recovery and ipsilateral stenosis

570

Features of post-stroke rehab

MENDS

MDT: physio, SALT, dietician, OT, specialist nurses, neurologist, family

Eating: screen swallowing: NG/PEG if unable to take. Screen for malnutrition (MUST tool)

Neurorehab: physio and speech therapy

DVT prophylaxis

Sores: must be avoided at all costs

571

MUST tool

‘MUST’ is a five-step screening tool to identify

adults,

who are malnourished, at risk of malnutrition

(undernutrition), or obese. It also includes management guidelines which can be used to develop

a care plan.

572

OT purpose

Impairment: paralysed arm

Disability: inability to write

Handicap: can't work as accountant

 

OT aims to minimise diability and abolish handicap

573

Px stroke

10% recurrence

574

Px PACS

20% mortality

1/3 survivors independent

2/3 of survivors dependents

575

Px TACS

60% mortality

5% independance

576

Def: TIA

Sudden onset focal neurology lasting <24h due to temprorary occlusion of part of the cerebral circulation

~15% of strokes are preceded by TIAs

577

Symptoms usually brief

Global evenets e.g. syncope/dizziness are not typical

Signs mimic those of CVA in the same arterial territory

TIA

578

Signs of causes of TIA

Carotid bruits

Raised BP

Heart murmur

AF

579

Causes of TIA

Atherothromboembolism from carotids is the main cause

Cardioembolism: Post-MI, AF, valve disease

Hyperviscosity: polycytheamia, SCD, myeloma

580

DDx for TIA

Vascular: CVA, migraine, GCA

Epilepsy

Hyperventilation

Hypoglycaemia

581

Ix in TIA

Aim: to find cause and define vascular risk

Bloods: FBC, U&E, ESR, glucose, lipids

CXR

ECG

Echo

Carotid doppler +/- angiography

Consider diffusion weighted MRI

582

Mx of TIA time to intervention

Intervention within 72h-> 2% strokes @90d

Intervention within 3w: 10% strokes @90d

583

Mx of TIA

ACAS

Antiplatelet therpay/anticoagulate

Cardiac risk factor control

Assess risk of subsequent stroke

Speciliast referral to TIA clinic

584

Antiplatelet/anticoaglant therapy in TIA

Aspirin/clopidogrel 300mg/d for 2w then 75mg/d, add dipridamole MR to aspirin

Clopidogrel preferred for LT

 

Warfarin if cardiac emboli: AF, MI, MS- after 2wks

 

 

585

How is risk of stroke subsequent to TIA assessed?

ABCD2 score

586

Px of TIA

Combined risk of stroke and MI is 9%/year

3x increased in mortality in comparison to TIA free populations

587

Components of ABCD2 score

Age >60

BP >140/90

Clinical features: unilateral weakness (2 points), speech disturbance without weakness (1)

Duration:

>1h (2 points)

10-59 mins (1 point)

DM

 

Maximum of 7 points

588

Score cut offs for ABCD2

Score >4-> TIA clinical within 24hours

Score <4: TIA clinic within 1w

589

ABCD2 prognosis

Score >6: 8% risk of stroke within 2d, 35% risk within 1w

Score >4

 

All patients with suspected TIA should be seen by specialist within 1w

590

Def: SDH

Bleeding from bridging veins between cortex and sinuses

Haematoma between dura and arachnoid

Often due to minor trauma that occured a long time previously- especially deceleration injuries

591

Bleeding from bridging veins between cortex and sinuses

Haematoma between dura and arachnoid

Often due to minor trauma that occured a long time previously- especially deceleration injuries

SDH

592

RFs for SDH

Elderly: brain atrophy

Falls: epileptics, alcoholics

Anticoagulation

593

Headache

Fluctuating GCS, sleepiness

Gradual physical or mental slowing

Unsteadiness

?SDH

594

Signs in SDH

Raised ICP can lead to tentorial herniation

Localising signs occur late

595

CT/MRI findings in SDH

Crescenteric heamatoma over one hemisphere

Clot goes from white-> grey with time

Mid-line shift

596

Crescenteric heamatoma over one hemisphere

Clot goes from white-> grey with time

Mid-line shift

?SDH

597

SDH

598

Mx of SDH

1st line: irrigation/evacuation via burr-hole craniostomy

2nd line: craniotomy

Address causes of trama

599

DDx SDH

Stroke

Dementia

SOL

600

Def: EDH

Often due to # temporal or parietal bone leading to MMA and vein laceration

Blood between bone and dura

Suspect if after head inury GCS falls, is slow to improve or there is a lucid interval

601

Deterioration of GCS after head injury that caused no LOC or following initial improvements in GCS

Can last hrs or days

EDH

602

Lucid Interval

Symptoms of raised ICP

Brainstem compression

?EDH

603

Headache

Vomiting

Confusion-> coma

Fits

Ipsilateral blown pupil (surgical 3rd nerve palsy)

+/- hemiparesis with upgoing plantars and reflexes

?Raised ICP

604

Symptoms of brainstem compresion?

Deep irregular breathing

Cushing response: raised BP, reduced HR is late

Death by cardiorespiratory arrest

605

Lens-shaped haematoma

Skull #

?EDH

606

Mx of EDH

Neuroprotective ventilation: O2 >100, Co2 35-40

Consider mannitol (1g/kg IV via central line)

Craniectomy for clot evacuation and vessel ligation

607

EDH

608

Features of intracranial venous thrombosis

Symptoms come on gradually over days-weeks

Sinus thrombosis may extend into cortical veins

609

Types of intracranial dural venous sinus thrombosis

Saggital sinus

Transverse

Sigmoid 

Inferior petrosal

Cavernous sinus

610

Features of saggital sinus thrombosis

45% of IVT

Often co-exists if other sinuses are thrombosed

Headache, vomiting, seizures, altered vision, papilloedema

611

Features of transverse sinus thrombosis

35% of IVT

Headache +/- mastoid pain, focal neurology, seizures, papilloedema

612

Features of sigmoid sinus thrombosis

Cerebellar signs

Lower CN palsies

613

Features of inferior petrosal sinus thrombosis

5th and 6th CN palsies

614

Gradenigo's syndrome

Gradenigo's syndrome, also called Gradenigo-Lannois syndrome[1][2] and petrous apicitis, is a complication of otitis mediaand mastoiditis involving the apex of the petrous temporal bone. It was first described by Giuseppe Gradenigo in 1904 when he reported a triad of symptoms consisting of periorbital unilateral pain related to trigeminal nerve involvement, diplopia due to sixth nerve palsy and persistent otorrhea, associated with bacterial otitis media with apex involvement of the petrous part of the temporal bone (petrositis). The classical syndrome related to otitis media has become very rare after the antibiotic era.

Symptoms[edit]

615

Features of cavernous sinus thrombosis

Spread from facial pustules of folliculitis

Headache, chemosis, eyelid oedema, proptosis, painful opthalmoplegia, fever

616

Often-> venous infarcts with stroke-like focal symptoms evolving over days

Thunderclap headache

Focal seizures

?Cortical vein thrombosis

617

DDx for intracranial venous thrombosis

SAH

Meningitis

Encephalitis

Intracranial abscess

Arterial stroke

618

Common causes of intracranial venous thrombosis

Pregnancy/puerperium

OCP

Head injury

Dehydration

Intracranial/extracranial malignancy

Thrombophilia

619

Ix in intracranial venous thrombosis

Exclude SAH and meningitis

CT/MRI venography: absence of a sinus

LP: raised pressure, may show RBCs and xanthochromia

620

Mx of intracranial venous thrombosis

LMWH-> warfarin (INR 2-3)

Fibrinolytics e.g. streptokinase can be used via selective catheterisation

Thrombophilia screen

621

Outline the features of the dural venous sinuses

Lie between the periosteal and meningeal layers of the dura mater

All ultimately drain into the internal jugular vein. 

11 sinuses in total. 

Straight, superior and inferior saggital sinuses are found in the falx cerebri of the dura mater. They converge at the confluence of sinuses (overlyling the internal occipital protruberance). 

The straight sinus is a continuation of the great cerebral vein and the inferior sagittal sinus.

From the confluence, the transverse sinus continues bilaterally and curves into the sigmoid sinus to meet the opening of the IJV

Cavernous sinus drains the ophthalmic veins and is found either side of the sella turcica. 

Blood returns to the IJV via the superior or inferior petrosal sinuses.  

 

622

623

What is Trolard?

The superior anastomotic vein that connects the superficial middle cerebral vein to the superior sagittal sinus

624

What is the Labbe

Connects the superficial middle cerebral vein to the transverse sinus

625

What is the vein of Galen?

The great cerebral vein

626

Who was Galen

Aelius Galenus or Claudius Galenus (/ɡəˈliːnəs/;[1] Greek: Κλαύδιος Γαληνός; September 129 AD – c. 200/c. 216), often Anglicized as Galenand better known as Galen of Pergamon (/ˈɡeɪlən/),[2] was a prominentGreek physician, surgeon and philosopher in the Roman Empire.[3][4][5]Arguably the most accomplished of all medical researchers of antiquity, Galen influenced the development of various scientific disciplines, including anatomy,[6] physiology, pathology,[7] pharmacology,[8] andneurology, as well as philosophy[9] and logic.

 

Vein of Galen

627

How can the features of meningitis be classified?

Meningitic

Neurological

Septic

628

Meningitic features

Headache

Neck stiffness: Kernig's and Brudzinski's

Photophobia

N+V

629

Neurological features of meningitis?

Reduced GCS-> coma

Seizures (20%)

Focal neurology (20%) e.g. CN palsies

630

Clinically septic

Fever

Reduced BP, Increaed HR

Increased CRT

(purpuric rash)

DIC

631

Abx management of meningitis in the community

Admit to hospital as emergency

 

IM benzylpenicillin 1200mg Adults dose

632

Children <1y meningitis in the community benpen dose

300mg

633

Children <10 >1 meningitis in community benpen dose

600mg

634

Adult/children >10 meninigits in the community, benpen dose

1200mg

635

Abx therapy in hospital meningitis

<50

Ceftriaxone 2g IVI/IM BD

636

Abx therapy in hospital setting meningitis

>50

Ceftriaxone and ampicillin 2g IVI/4h

637

Viral causes of meningitis

Enteroviruses (coxsackie, echovirus)

HSV2

638

If ?HSV meningitis

Aciclovir

639

Bacterial causes of meningitis

Meningococcus

Pneumococcus

Listeria

Haemophilus

TB

Cryptococcus

640

Sepsis 6

Administer high flow O2 to maintain target O2 saturations greater than 94%

Take blood cultures

Give IV Abx

Start IV fluid resuscitation (fluid bolus)

Check lactate

Monitor UO

641

Mx of mainly septicaemic meningococcal infection

Don't attempt LP

Ceftriaxone 2g IVI

Consider ITU if shocked

642

Mx of mainly meningitic meningococcal infection

If no shock or CIs- LP

Dexamethasone 0.15mg/kg IV QDS

Ceftriaxone 2g IVI post-LP

643

Continuing management of meningitis

Ceftriaxone 2g BD IVI

Meningococcus: 7d IV then review

Pneumoccus: 14d IV then review

 

Maintenance fluids:

UO >30ml/h

SBP >80mmHg

 

If response is poor consider intubation +/- inotropic support

 

Rifampicin prophylaxis for household contacts

644

Contraindications to LP

Try LP Unless ContraINdicated

Thrombocytopenia

Lateness (i.e. delaying Abx administration)

Pressure (signs of raised ICP)

Unstable (cardio and respiratory systems)

Coagulation disorder

Infection at LP site

Neurology (focal neurological signs)

645

Infectious prodrome: fever, rash, LNs, cold sores, conjunctivitis, meningeal signs

Bizzare behaviour or personality change

Confusion

Reduced GCS-> coma

Fever

Headache

Focal neurology

Seizures

Hx of travel or animal bite

?Encephalitis

646

Viral causes of encephalitis

HSV 1.2

CMV, EBV, VZV

Arboviruses

HIV

647

Ix for causes of encephalitis

Bloods: cultures, viral PCR, malaria film

Contrast CT: focal bilateral temporal involement suggests HSV

LP: raised CSF proteins, lymphocytes, PCR

EEG: shows diffuse abnormalities, may confirm Dx

648

Encephalitis with focal bilateral temporal involvement on contrast CT

Suggests HSV encephalitis

649

Ix in meningitis

Bloods: FBC, U+Es, clotting, glucose, ABG

Blood cultures

LP: MCS, glucose, virology/PCR, lactate

650

Mx of encephalitis

Aciclovir STAT: 10mg/kg/8h IV over 1h for 14/7

Supportive measures in HDU/ITU

Phenytoin for seizure control

651

Encephalitic symptoms without fever, consider

Encephalopathy

652

Causes of encephalopathy (non-infective)

Reduced glucose

Hepatic

DKA

Drugs

SLE

Uraemia

Hypoxic brain injury

Beri-Beri

653

Pre-disposing factors to cerebral abscess

Infection: ear, sinus, dental or periodontal

Skull #

Congenital heart disease

Endocarditis

Bronchiectasis

Immunosuppression

654

Organisms causing frontal sinus/teeth infection-> cerebral abscesss

Strep. Milleri, oropharyngeal anaerobes

655

Organisms causing ear infection -> cerebral abscess

Bacteroides

Other anaerobes

656

Seizures

Fever

Localising signs

Signs of raised ICP

Signs of infection elsewhere

 

Ring-enhancing lesion on CT/MRI

?Cerebral abscess

657

Cerebral abscess

 

In patients with suspected intraparenchymal sepsis, pre- and postcontrast scans should be obtained, unless the plan is to proceed to MRI regardless of the CT findings. Typical appearances include:

ring of iso- or hyperdense tissue, typically of uniform thickness

central low attenuation (fluid/pus)

surrounding low density (vasogenic oedema) 

ventriculitis may be present, seen as enhancement of the ependyma

obstructive hydrocephalus will commonly be seen when intraventricular spread has occurred

658

What is the most sensitive and specific imaging modality for cerebral abscess

MRI (DW-MRI especially)

659

Mx of cerebral abscess

Neurosurigcal referral

Abx e.g. ceftriaxone

Treat raised ICP

660

Def: epilepsy

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures

661

What proportion of epilepsies are idiopathic?

2/3

662

What are the congenital causes of epilepsy

NF

Tuberous Sclerosis

TORCH

Perinatal anoxia

663

What are the acquired causes of epilepsy

Vascular: CVA

Cortical scarring: trauma, infection

SOL

Other: SLE, PAN, MS, sarcoid

664

What are the different types of non-epileptic/provoked seizures

Withdrawal: EtOH, opiates, benzos

Metabolic: glucose, Na, Ca, urea, NH3

Raised ICP: trauma, haemorrhage, cortical venous thrombosis

Infection: meningitis, encephalitis, cycticercosis, HIV

Eclampsia

Pseudoseizures

665

What is the recurrence rate of provoked seizures vs unprovoked seizures

3-10% vs 30-50%

666

What are the terms to describe seizures?

Prodrome

Aura

Partial (focal)

Generalised

Simple

Complex

Secondary generalised

667

Epilepsy descriptive terms:

Prodrome

 

Patient or others may notice change in mood or behaviour lasting hours-days

Not part of seizure

668

Epilepsy descriptive terms:

Aura

A simple partial seizure (usually temporal) which may precede other manifestations

Experienced as strange feeling:

Epigastric rising

deja/jamais vu

Automatism

Smells, lights, sounds

669

Epilepsy descriptive terms:

Partial (focal)

Features referable to part of one hemisphere

670

Epilepsy descriptive terms:

Simple

Awareness unimpaired

671

Epilepsy descriptive terms:

Complex

Awareness impaired

672

Epilepsy descriptive terms:

Secondary generalised

Focal seizure-> generalised

Aura-> tonic-clonic

673

What are the diagnostic pointers towards epilepsy?

Aura

Specific trigger e.g. flashing lights

Lateral tongue biting (> incontinence)

Typical movements e.g. tonic clonic

Cyanosis

Post-ictal phase

674

Focal motor, sensory, autonomic or pyschic symptoms

Simple partial seizure

675

What are the 5As of complex partial seizures?

Aura

Autonomic: change in skin colour, temperature, palpatations

Awareness lost: motor arrest, motionless stare

Automatisms: lip-smacking, fumbling, chewing, swallowing

Amnesia

 

Usually arise from temproal lobe

676

Features of ABSENCES seizures

ABrupt onset and offest

Short: <10s

Eyes: glazed, blank stare

Normal: intelligence, examination, brain scan

Clonus or automatisms may occur

EEG: 3Hz spike and wave

Stimulated by hyperventilation and photics

677

Features of tonic-clonic seizure

LOC

Tonic: limbs stiffen

Clonic: rhythmic jerking of limbs

+/- cyanosis, incontinence, tongue biting (lateral)

Post-ictal confusion and drowsiness

678

Sudden jerk of limb, face or trunk

Myoclonic seizure

679

Sudden loss of muscle tone-> fall

No LOC

Atonic (akinetic seizure)

680

Clusters of head nodding and arm jerks

EEG showing hypsarrhythmia

Children

West Syndrome/ infantile spasms

 

681

What are the localising features of a temporal seizure

Automatisms: lip-smacking, chewing, fumbling

Deja/jamais vu

Delusional behaviour

Abdominal: rising, n/v

Emotional disturbance: terror, panic, anger, elation

Tastes/smells

682

Localising features in epilepsy:

Frontal

Arrest

Jacksonian march

Todd's palsy

683

Jacksonian March

Jacksonian march or Jacksonian seizure is a phenomenon where a simple partial seizure spreads from the distal part of the limb toward the ipsilateral face (on same side of body). They involve a progression of the location of the seizure in the brain, which leads to a "march" of the motor presentation of symptoms

Partial seizure

684

Localising features in epilepsy:

Parietal

Sensory disturbance: tingling, numbness

685

Localising features in epilepsy:

Occipital

Visual phenomena: spots, lines, flashes

686

General principles in investigation and management of epilepsy

After any seizure, advise against driving, swimming etc until a Dx is established

Don't diagnose epilepsy from a single seizure

Diagnosis should be made by a specialist

After Dx, cannot drive until seizure-free for >1y

687

Ix in ?epilepsy

Bloods: FBC, U+Es, glucose

Se prolactin raises 10 minutes after fit

Se AED levels

Urine toxicology

ECG

688

EEG in epilepsy

Use to support Dx: cannot exclude or prove

Helps classification and prognosis

Use with hyperventilation and photic stimulation

689

Indications for neuroimaging in epilepsy

Not routine for idiopathic generalised epilepsy

 

Developed epilepsy as an adult

Any evidence of focal onset

Seizures continue despite first line Rx

690

Mx of focal seizures

1st line:

Lamotrigine

 

2nd line:

CBZ

 

 

691

Rx in tonic-clonic seizures

1st line

Valproate

 

2nd line

Lamotrigine

692

Rx in absence seizures

1st line

Valproate or ethosuximide

 

2nd line:

Lamotrigine

693

Rx in tonic, atonic or myoclonic seizures

Valproate

 

Levetiracetam

694

AEDs in pregnancy

Avoid valproate: take lamotrigine or CBZ

5mg folic acid

695

Alternatives to AEDs

Neurosurgical resection can be an option if a single epileptogenic focus is identified

Vagal nerve stimulation can reduce seizure frequency and severity in 33%

696

Which AEDs are enzyme inducers?

CBZ, PHE and barbiturates

697

Which AEDs are enzyme inhibitors?

VPA

698

Side effects of lamotrigine

Skin rash-> SJS occurs within 1st 8w

Rash may be associated with hypersensitivity-> fever, raised LFTs, DIC

Diplopia

Levels affected by enzyme inhibitors/inducers

699

Skin rash-> SJS occurs within 1st 8w

Rash may be associated with hypersensitivity-> fever, raised LFTs, DIC

Diplopia

Levels affected by enzyme inhibitors/inducers

LTG

700

Side effects of VPA

V-ALPROATE

Appetite increased- weight gain

Liver failure: monitor LFTs over 1st 6mo

Pancreatitis

Reversible hair loss

Oedema

Ataxia

Teratogenicity, tremor, thrombocytopenia

Encephalopathy due to raised ammonia

701

Side effects of CBZ

Leukopenia

Skin reactions

Diplopia, blurred vision

SIADH-> hyponatraemia

702

Leukopenia

Skin reactions

Diplopia, blurred vision

SIADH-> hyponatraemia

CBZ

703

Appetite increased- weight gain

Liver failure: monitor LFTs over 1st 6mo

Pancreatitis

Reversible hair loss

Oedema

Ataxia

Teratogenicity, tremor, thrombocytopenia

Encephalopathy due to raised ammonia

Valproate

704

Side effects of Phentyoin

Gingival hypertrophy

Hirsutism

Cerebellar syndrome: ataxia, nystagmus, dysarthria

Peripheral sensory neuropathy

Diplopia

Tremor

705

Gingival hypertrophy

Hirsutism

Cerebellar syndrome: ataxia, nystagmus, dysarthria

Peripheral sensory neuropathy

Diplopia

Tremor

Phenytoin

706

Definition of status epilepticus

Seizure lasting >30 minutes or

Repeated seizures without intervening consciousness

707

Ix in status epilepticus

BM

Bloods: glucose, ABG, U+E, FBC, Ca

ECG, EEG

Consider: AED levels, tox screen, LP, beta HCG, CT

708

Lorazepam in status epilepticus

2-4mg IV bolus over 30 seconds

2nd dose if no response within 2 minutes

Alternatives: diazepam 10mg IV/PR (20mg max)

Midazolam 10mg buccal

709

Phenytoin in status epilepticus

18mg/kg IVI @50mg/min

100mg/6-8h maintenance

Monitor ECG and BP

CI: bradycardia or heart block

710

Features of diazepam infusion in status epilepticus

100mg in 500ml 5% dex @40ml/hour (3mg/kg/24h)

711

Dexamethasone

10mg IV if vasculitis/cerebral oedema (tumour) possible)

712

Acute management of status epilepticus overview

ABC

IV access and bloods

Reverse potential causes

Slow IV bolus phase

IV infusion phase

RSI phase

713

ABC phase in status epilepticus

Oral/nasal airway, intubate

Suction

100% O2

CBG

714

IV access + bloods phase in status

U+E, LFT, FBC, glucose, Ca

AED levels

Tox screen

715

Reversing potential causes phase in status

Thiamine 250mg IV if EtOH

100ml 20% glucose unless glucose known to be normal

716

Slow IV bolus phase in status

Lorazepam 2-4mg IV

2nd dose if no response within 2 minutes

717

Iv infusion phase in status

Phenytoin 18mg/kg IVI then 100mg(6-8h)

Or diazepam 100mg in 500ml 5% dextrose IV

718

RSI phase in status

Never spend >20 minutes with someone in status without getting an anaesthetist

719

Initial Mx of head injury

1o survey

2o survey

Hx if possible

720

Features of 1o survery in Head injury

A: ?intubation, immobilise C-spine

B: 100% O2, RR

C: IV access, BP, HR

D: GCS, pupils

 

Treat seizures:

Lorazepam 2-4mg IV

Phenytoin 18mg/kg IVI then 100mg/6-8h

 

E: expose pt and look for other obvious injuries

721

Features of 2o survery in head injury

Look for:

Lacerations

Obvious facial/skull deformity

CSF leak from nose or ears

Battle's sign

Racoon eyes

Blood behind TM

C-spine tenderness +/- deformity

 

Head to toe examination for other injuries

 

Log roll

722

Battle's sign

In medical terminology, Battle's sign, also mastoid ecchymosis, is an indication of fracture of posterior cranial fossa of the skull, and may suggest underlying brain trauma.

723

Battle's sign

724

Racoon eyes

725

Racoon eyes

periorbital ecchymosis is a sign of basal skull fracture or subgaleal hematoma, a craniotomy that ruptured the meninges, or (rarely) certain cancers.[1][2] Bilateral hemorrhage occurs when damage at the time of a facial fracture tears the meninges and causes the venous sinuses to bleed into the arachnoid villi and the cranial sinuses. In layman's terms, blood from skull fracture seeps into the soft tissue around the eyes. Raccoon eyes may be accompanied by Battle's sign, an ecchymosis behind the ear. These signs may be the only sign of a skull fracture, as it may not show on anX-ray. They may not appear until up 2–3 days after the injury.[3] It is recommended that the patient not blow theirnose, cough vigorously, or strain to prevent further tearing of the meninges

726

Hx in head injury

How and when?

GCS and other vitals immediately after injury

Headache, fits, vomiting, amnesia, EtOH

727

Ix in head innjury

Bloods: FBC, U+Es, glucose, clotting, EtOH level, ABC

?CT head + spine

728

Rx in Head injury

Neurosurgical opinion if signs of raised ICP, CT evidence of intracranial bleed or significant skull #

 

Criteria for admission:

Abnormalities on imaging

Difficult to assess: EtOH, post-ictal

Not returned to GCS 15 after imaging

CNS signs: vomiting, severe headache

 

Neuro-obs half hourly until GCS 15

729

Components of neuro-obs

GCS

Pupils

HR, BP

RR, SpO2

Temperature

730

Discharge advice post head injury

Stay with someone for 48h

Return if

Consfusion, drowsiness, unconsciousness

Visual problems

Weakness

Deafness

V. painful headache that won't go away

Vomiting

Fits

731

Indications for intubation following head injury

GCS <8

PaO2< 9kPA on air/ <13kPa on O2 or PCO2 >6kPa

Spontaneous hyperventilation: PCO2 <4kPa

Respiratory irregularity

732

CT head guidelines

BANGS LOC

 

Break: open, depressed or base of skull

Amnesia: >30 min retrograde

Neuro deficit or seizure

GCS <13 at any time or <15 2h after injury

Sickness: vomited > once

LOC or any amnesia and any of:

Dangerous mecahnism: RTA, great height

Age >65

Coagulopathy (inc warfarin)

733

Risk of intracranial haematoma in adults

Fully conscious, no skull #: <1:1000

Confused, no skull#: 1:100

Fully conscious, skull # 1:30

Confused, skull #: 1:4

734

Components of GCS

 

E: 4

V: 5

M: 6

735

Eyes in GCS

4: spontaneous eye opening

3: open to voice

2: open to pain

1: no opening

736

Verbal in GCS

5: orientated conversation

4: confused conversation

3: inappropriate speech

2: incomprehensible sounds

1: no speech

737

Motor in GCS

6: obeys commands

5: localises pain

4: withdraws to pain

3: decorticate posture: flexor

2: decerebrate posutre: extensor

1: no movement

738

Decorticate posutring

739

Decerebrate posturing

740

Presentation of SOL

Raised ICP

Seizures: exclude SOL in adult-onset seizures, especially with localising aura or post-ictal weakness

Evolving focal neurology e.g. false localising (CN6 palsy)

Subtle personality change

741

Causes of SOL

Vascular: chronic SDH, AVM, aneurysm

Infection: abscess, cyst (cysticerosis)

Neoplasm: 1o or 2o

Granuloma: TB, sarcoid

742

Tumours causing SOL

30% metastatic: breast, lung, melanoma

Astrocytoma

GBM

Ependyoma

Meningiomas

Cerebellar haemangioblastoma

CNS lymphoma

743

DDx for SOL

Vascular: Stroke, DVST

TBI

Infection: encephalitis

Inflammation: vasculitis, MS

Metabolic distrubance

Idiopathic intracranial hypertension

744

Ix in SOL

CT or MRI (better for posterior cranial fossa)

Consider biopsy

745

Obese female

Raised ICP, headache, papilloedema

Blurred vision

6th CN palsy

Enlarged scotoma

?Idiopathic intracranial HTN

746

Causes of idiopathic intracranial HTN

Usually idiopathic

May be 2o to venous sinus thrombosis or drugs

747

Mx of idiopathic intracranial hypertension

Weight loss

Acetazolamide

Loop diuretics

Prednisolone

Lumbar-peritoneal shunt may be necessary if drugs fail and visual loss deteriorates

748

Px of idiopathic intracranial HTN

Usually self-limiting

Permanent visual loss in 10%

749

What are the different types of cerebral oedema

1. Vasogenic: increased capillary permeability- trauma, tumour, ischaemia, infection

2. Cytotoxic e.g. from hypoxia

3. Interstitial e.g. obstructive hydrocephalus, reduced Na

750

Causes of raised ICP

Haemorrhage

Tumours

Infection: meningitis, encephalitis, abscess

Hydrocephalus

Status

Cerebral oedema

751

Headache

N+V

Seizures

Drowsiness-> coma

Cushing's reflex

6th CN palsy

Cheynes-Stokes respiration

Pupils: constriction-> dilatation

Papilloedema, loss of venous pulsation at disc

?Raised ICP

752

Cushing's reflex

Raised BP

Reduced HR

Irregular breathing

753

 an abnormal pattern ofbreathing characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease that results in a temporary stop in breathing called an apnea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes.[1] It is an oscillation of ventilation between apnea and hyperpnea with a crescendo-diminuendopattern, and is associated with changing serum partial pressures ofoxygen and carbon dioxide

Cheynes Stokes respiration

754

Causes of Cheynes-Stokes respiration

Heart failure

Stroke

TBI

Brain tumour

Hyponatraemia

Toxic metabolic encephalopathy

CO poisoning

Seen after morphine administration

755

Acute management of raised ICP

ABC

Treat seizures and correct hypotension

Elevate bed to 40 degrees

Neuroprotective ventilation

Mannitol or hypertonic saline

756

Features of neuroprotective ventilation

PaO2 >13kPa

PCO2: 4.5kPa

Good sedation +/- NM blockade

757

Mannitol or hypertonic saline to treat raised ICP

Reduce ICP but there may be an ICP rebound later

Mannitol 1g/kg

Hypertonic saline 20% at 5ml/kg

758

Increased pressure in posterior fossa-> displacement of cerebellar tonsils through foramen magnum

Leads to compression of brainstem and cardiorespiratory centres in medulla

May see a CN6 palsy, upgoing plantars-> irregular breathing-> apnoea

Infratentorial

Tonsillar herniation (coning)

759

Tonsillar herniation

760

Lateral supratentorial mass-> compression of ipsilateral inferomedial temporal lobe (uncus) against free margin of tentorium cerebelli

Ipsilateral CN3 palsy: mydriasis then down and out

Ipsilateral corticospinal tract: contralateral hemiparesis

May-> compression of contralateral corticospinal tracts-> ipsilateral hemiparesis

Transtentorial/uncal herniation

761

762

Kernohan's notch

Kernohan's notch is a cerebral peduncle indentation associated with some forms of transtentorial herniation (uncal herniation).[1][2] It is a secondary condition caused by a primary injury on the opposite hemisphere of the brain.[3]Kernohan's notch is an ipsilateral condition, in that a left-sided primary lesion (in which Kernohan's notch would be on the right side) evokes motor impairment in the left side of the body and a right-sided primary injury evokes motor impairment in the right side of the body.[4] The seriousness of Kernohan's notch varies depending on the primary problem causing it, which may range from benign brain tumors to advanced subdural hematoma.

763

764

Frontal mass

Displacement of cingulate gyrus (medial frontal lobe) under falx cerebri

Compression of ACA-> stroke

Contralateral motor/sensory loss in legs>arms

Abulia (pathological laziness)

Subfalcine herniation

765

What are the dural reflections and what is their orientation?

Vertical reflections:

falx cerebri

falx cerebelli

 

Horizontal reflections:

Tentorium cerebelli

Diaphragma sellae

766

What is the function of the falx cerebri/falx cerebelli

Separate the right and left hemisphere

767

What is the function of the tentorium cerebelli

Separates cerebellum and brainstem from the cerebrum

Falx cerebri is attached to the tentorium cerebelli and pulls it up

768

What is the function of the diaphragma sellae

Partially covers the pituitary gland allowing the infundibulum and vessels 

769

770

What are the causes of Parkinsonism?

Degenerative:

PD

Parkinson's plus syndrome

 

Infection:

Syphilis, HIV, CJD

 

Vascular: multiple infarcts in SN

 

Drugs: antipsychotics, metoclopramide

 

Trauma: dementia pugilistica


Genetic: Wilson's

771

What are the Parkinson's plus syndrome?

Basal ganglia degeneration + other system

MSA/ Shy-Drager

PSP

Corticobasilar degeneration

LBD

772

Autonomic dysfunction: postural hyptension, bladder dysfunction

Cerebellar and pyramidal signs

Parkinsonism: Rigidity>Tremor

MSA/ Shy-Drager

773

Postural instability-> falls

Speech disturbance (+ dementia)

Palsy: vertical gaze

Parkinsonism

Progressive supranuclear palsy

774

Aphasia, dysarthria, apraxia

Akinetic rigidity in one limb

Astereognosis (cortical sensory loss)

Alien limb phenomenon

Parkinsonism

Corticobasilar degeneration

775

Fluctuating cognition

Visual hallucinations

Parkinsonism

LBD

776

Cardinal symptoms of parkinsonism

Tremor

Rigidity

Bradykinesia

Gait disturbance

777

Parkinsonian tremor

Worse at rest

Exacerbated by distraction

4-6Hz, pill rolling

778

Rigidity in Parkinsonism

Increased tone in all muscle groups: lead-pipe rigidity

Rigidity + tremor: cog-wheel rigidity

779

Spasticity vs rigidity

https://www.youtube.com/watch?v=gLZoYLxdXCQ

 

Increased resistance to movement: rigidity vs spasiticity

Spasticity: weak extremity, resistance in one direction is different to resistance in the other direction. 

Spasticity is velocity dependant, faster you go more spastic  

 

Rigidity: extremity not weak. Resistance is the same in both directions. No characteristic postures, not velocity dependant. 

780

Clasp-knife response

UMN lesion

781

Features of bradykinesia in parkinsonism

Slow initiation of movement with reduction of amplitude on repetition

Expressionless face

Monotonous voice

Micrographia

782

Gait in parkinsonism

Reduction in arm swing

Festinating

Freezing, especially in doorways

783

Epidemiology parkinson's

Mean onset 65y

2% prevalence

784

Pathophysiology of PD

Destruction of dopaminergic neurones in pars compacta of susbstantia nigra

beta-amyloid plaques

NFTs: hyperphosphorylated tau

785

Features of PD

A TRAPPS PD

Asymmetric onset: side of onset remains worst

 

Tremor: increased by stress, decreased by sleep

Akinesia: slow initiation, difficulty with repetitive movement, micrographia, monotonous voice, mask like face

Postural instability: stoop gait with festination

Postural hypotension + other autonomic dysfunction

Sleep disorders: insomnia, EDS, OSA, RBD

Psychosis: esp. visual hallucinations

 

Depression/Dementia/ Drugs SEs

786

Sleep disorder in PD

Affects 90% of PD patients

787

Excessive Daytime Sleepiness in PD?

Insomnia and frequent waking-> EDS

Inability to turn

Restless legs

Early morning dystonia

Nocturia

OSA

788

REM behavioural sleep disorder in PD

Loss of muscle atonia during REM sleep

Violent enactment of dreams

789

Apart from EDS and RBD what else contributes to sleep disorder in PD?

DA side effects: insomnia, drowsiness, EDS

790

Autonomic dysfunction in PD consequence of?

Combined effects of drugs and neurodegeneration

791

Features of autonomic dysfunction

Hypersalivation-> dribbling

Hyperhidrosis

Postural hypotension

Constipation

Urgency, frequency, nocturia

ED

 

792

Side effects of L-DOPA

DOPAMINE

Dyskinesia

On-off phenomena= motor fluctuations

Psychosis

Reduced arterial BP

Mouth dryness

Insomnia

N+V

EDS

793

Motor fluctuations in PD treatment

End of dose: deterioration as dose wears off with progressively shorter benefit

On-off effect: unpredictable fluctuations in motor performance unrelated to timing of dose

794

DDx for PD

Parkinson +

Multiple infarcts

Drugs: neuroleptics

Inherited: Wilson's

Infection: HIV, syphillis, CJD

Dementia pugilistica

795

Ix in PD

Clinical diagnosis (UK Parkinson's Society Brain Bank Diagnostic Criteria)

can use DaTSCAN

796

Mx of PD

MDT: neurologist, PD nurse, physio, OT, social worker, GP and carers

Assess disability: UPDRS

PT: postural exercises

Depression screening

797

What can be used to assess disability in PD?

UPDRS

Unified Parkinson's Disease Rating Scale

798

Medical management of PD in young onset +/- biologically fit

1. Da agonists: ropinirole, pramipexole

2, MAO-B inhibitors: rasagiline, selegiline

3. L-DOPA: co-careldopa or co-beneldopa

799

Medical management of PD in biologically frail +/- comorobidities

1. L-DOPA

2. MAO-B inhibitors

800

Tolcapone, entacapone

Drug class

Use

COMT inhibitor

Lessen end-of-dose effect in PD

801

Apomorphine

Drug class

Use

Potent Da agonist

SC rescue pen for sudden "off" freezing in PD

802

Amantadine

Drug class

Use

Weak Da agonist (and also licensed antiviral)

Rx of drug induced dyskinesias

803

Use of atypical antipsychotics in PD

Disease-induced psychosis

e.g. quetiapine

 

804

Use of SSRIs in PD

Sertraline, citalopram

Depression

805

Ropinirole, pramipexole

Drug class

Da agonists

806

Rasageline

Selegiline

Drug calss

MOA-B inhibitors

 

807

Co-careldopa or co-beneldopa

Drug class

L-DOPA

808

Draw the rationale for PD treatments

809

Surgical options for PD

Interrupt BG

Deep brain stimulation

810

Px in PD

Increased mortality

Loss of response to L-DOPA within 2-5y

811

DDx in PD

Parkinson+

Multiple infarcts

Drugs e.g. neuroleptics

Inherited: Wilson's

Infection: HIV, syphilis, CJD

Dementia pugilistica

812

Def: MS

Chronic inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in time and space

813

Epidemiology of MS

Lifetime risk: 1/1000

Age: mean @ onset = 30y

F>M 3:1

Rarer in blacks

814

What HLA polymorphism is assocaited with MS?

HLA-DRB1

815

Pathophysiology in MS

CD4 cell-mediated descrution of oligodendrocytes-> demyelination and eventual neuronal death

816

What are the different MS subtypes?

Relapsing-remitting: 80%

Secondary progressive

Primary progressive 10%

Progressive relapsing

817

818

Tingling

Eye: reduced central vision and pain on eye movement

Ataxia and other cerebellar signs

Spastic paraparesis

?MS

819

Presentation of MS

TEAM

Tingling

Eye: optic neuritis

Ataxia and other cerebellar signs

Motor: usually spastic paraparesis

820

What are the sensory features of MS?

Dys/paraesthesia

Reduced vibration sense

Trigeminal neuralgia