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8. CMS > Lecture day 2 > Flashcards

Lecture day 2 Flashcards

1
Q

What does ALS stand for?

A

Amyotrophic lateral sclerosis

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2
Q

What is the median survival for someone with ALS?

A

24-50 months

10% of patients will live for 10 years

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3
Q

What is the median age of onset for ALS?

A

51-66

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4
Q

What is the pathophysiology of ALS?

A

TDP-43 cytoplasmic aggregates

Normally resides in nucleus. In ALS, this will move to cytoplasm and aggregate

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5
Q

What is the most common genetic link in ALS?

A

C9ORF72

ALS lies on the spectrum with frontotemporal dementia

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6
Q

How does ALS affect UMN and LMN?

A

Classical ALS is a combination of UMN and LMN impairment

In upper motor neuron (corticospinal tract) → impairment

  1. Spasticity
  2. Hyper-reflexia
  3. Babinski reflex
  4. Weakness

Lower motion neuron (anterior horn cell)

  1. Atrophy
  2. Fasciculations
  3. Hypo-reflexia
  4. Weakness
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7
Q

What are clinical signs of ALS?

A
  1. Atrophy of thenar eminences and first dorsal web spaces
  2. Atrophy of the tongue
  3. Upper limb fasciculation
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8
Q

What is the disease heterogeneity in onset in ALS?

A

1/3 starts as bulbar
1/3 starts lower limb
1/3 starts with upper limb

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9
Q

What are typical presenting symptoms for ALS?

A
  1. Speech slurring or hypophonia
  2. Clumsiness of hands
  3. Foot drop
  4. Asymmetric at onset
  5. Absence of major sensory symptoms
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10
Q

What are associated features of ALS?

A
  1. Fasciculations
  2. Cramps
  3. Gait imbalance
  4. Falls
  5. Emotional lability
  6. Weight loss
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11
Q

What guidelines would you use to diagnose ALS?

A

El Escorial

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12
Q

How long does it often take to go to onset of symptoms to diagnosis of ALS?

A

12 months

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13
Q

What investigations can you do for ALS?

A

Needle electromyography: mixed pattern of acute and chronic denervation

Diagnosis remains clinical - imaging excludes mimics

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14
Q

What are features of acute denervations?

A

Fibrillations, positive sharp waves and fasciculations (more precisely a sign of neuronal hyperexcitability)

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15
Q

What are features of chronic denervations?

A

Large, long, polyphasic motor unit action potentials (indicating compensatory reinnervation)

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16
Q

What are differential diagnoses for ALS?

A

Very few conditions cause mixed UMN and LMN damage

Syphilis is the great imitator

Sometimes vit B12 deficiency

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17
Q

What diseases mimic LMN impairments?

A 
Spinal degenerative disorder
Multifocal motor neuropathy 
Myasthenia graves 
HIV
Vitamin B12 deficiency
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18
Q

What diseases mimic UMN impairments?

A 
Stroke
MS
Neurosyphilis 
hereditary spastic paraplegia 
Leukodystrophies 
Vitamin B12 deficiency
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19
Q

What are established treatment options?

A

Mainly riluzole

Some symptomatic treatments

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20
Q

What are the benefits of Riluzole?

A

Glutamate antagonist which improves survival by 20%

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21
Q

What are primary headaches?

A

Migraine
Tension-type headache
Trigeminial autonomic cephalalgias

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22
Q

What are secondary headaches?

A
  1. Trauma or injury to the head
  2. Cranial or cervical vascular
  3. Intracranial non-vascular
  4. Substances
  5. Infection
  6. Homeostasis
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23
Q

What are the characteristics of a migraine?

A

Typically lasts 4-72 hours

Unilateral, pulsating, moderate to severe, aggravated by daily activity

Nausea/vomiting or photophobia and phonophobia

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24
Q

What are the characteristics of a cluster headache?

A

5-180 minutes

Severe or very severe unilateral orbital or temporal

Often with infection, eyelid oedema, nasal congestion, forehead fo facial sweating, mitosis or ptosis

Between 8 per day to one every other day

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25
Q

What are red flags for headaches?

A
  1. Systemic symptoms (fever or weight loss)
  2. Altered consciousness
  3. Age over 50 (unusual to have sudden onset headaches - more likely to be secondary)
  4. Postural or positional (CSF venus fistulla)
  5. Precipitated: Valsalva, exertion, sex
  6. Papilloedema
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26
Q

What are the differentials for a thunderclap headache?

A
  1. Subarachnoid haemorrhage
  2. Intracerebral haemorrhage
  3. Cerebral venous thrombosis
  4. Arterial dissection
  5. Reversible cerebral vasoconstriction syndrome
  6. Pituitary apoplexy
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27
Q

What are the characteristics of a raised ICP headache?

A
  1. Worse in morning
  2. Better in upright
  3. Worse with Valsalva
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28
Q

What are the characteristics of a lower ICP headache?

A

Worse as day goes on

Better recumbent

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29
Q

What are the characteristics of idiopathic intracranial hypertension?

A

Persistent, dull, pressing bilateral headache. Aggravated by coughing, pressing and physical activity. Potential nausea

Visual disturbances: decrease in acuity, increase in blind spot, papilloedema

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30
Q

How would you treat migraine?

A
  1. NSAIDs
  2. Triptans (use when patient is not pain free after 2 hours on NSAIDs)
  3. Antiemetics (occasionally, but not often)
    1. Metoclopramide
    2. Domperidone

Preventive treatment (use when around 7 migraines per month)

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31
Q

What preventative treatment could you give for migraines?

A

Metoprolole
Valproate
Flunarizine

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32
Q

What is a medication overuse headache?

A
  • Headache occurring on ≥ 15 days/month in a patient with a pre-existing headache disorder
  • Regular overuse for > 3 months of one or more drugs that can be taken for the acute and/or symptomatic treatment of headache
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33
Q

How would you manage a cluster headache?

A
  1. 100% oxygen (12-15 l/min) (after 10 minutes the headache is gone)
  2. Triptans (sc or nasal)
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34
Q

When would you give preventative treatment in a cluster headache?

A

ALWAYS

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35
Q

What are the preventative treatments for cluster headaches?

A
  1. Verapamil (works most of the time)

2. Topiramate, lithium

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36
Q

What are possible causes of tingling limbs?

A
  1. Stroke or TIA
  2. Spinal cord pathology
  3. Spinal nerve compression
  4. Peripheral nerve compression
  5. Nerve damage due to trauma
  6. MS
  7. Endocrine
  8. Vitamin deficiency
  9. Nerve toxicity
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37
Q

What can cause spinal cord compression?

A

metastatic malignancy, herniated disc

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38
Q

What can cause peripheral cord compression?

A

Tumour, enlarged blood vessels, infection

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39
Q

What endocrine disturbances can cause tingling limbs?

A

Diabetes

Hypothyroidism

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40
Q

What vitamin deficiencies can cause tingling limbs?

A

Vitamin B12

Thiamine

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41
Q

What substances can cause nerve toxicity?

A

Alcohol

Lead

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42
Q

What is hyperpathia?

A

Heightened noxious sensation

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43
Q

What is allodynia?

A

Noxious response to non-noxious stimuli

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44
Q

What is the MRC scale?

A

Muscle Power Scale

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45
Q

What are the grades of the MRC scale?

A

Grade 0 - no muscle movement

  1. Grade 1 = flicker or trace of muscle movement
  2. Grade 2 - active movement with gravity
  3. Grade 3- active movement against gravity
  4. Grade 4 = active movement against gravity and resistance
  5. Grade 5 = normal power
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46
Q

What kind of lesions would result in muscle atrophy?

A

UMN

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47
Q

What kind of lesions would result in muscle wasting?

A

LMN

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48
Q

What kind of lesions would result in Babiski sign?

A

UMN

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49
Q

What kind of lesions would result in hyperreflexia?

A

UMN

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50
Q

What kind of lesions would result in hyporeflexia?

A

LMN

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51
Q

What kind of lesions would result in a foot drop?

A

LMN

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52
Q

What kind of lesions would result in fasciculations?

A

LMN

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53
Q

What muscle, nerve and root are responsible for shoulder abduction?

A

Deltoid
Axillary
C5

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54
Q

What muscle, nerve and root are responsible for elbow flexion?

A

Biceps
Musculocutaneous
C5, C6

Brachioradialus
Radial
C6

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55
Q

What muscle, nerve and root are responsible for elbow extension?

A

Triceps
Radial
C7

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56
Q

What muscle, nerve and root are responsible for radial wrist extension?

A

Extensor carpi radialis longus
Radial
C6

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57
Q

What muscle, nerve and root are responsible for finger extension?

A

Extensor digitorum communis
Posterior interosseeous nerve
C7

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58
Q

What muscle, nerve and root are responsible for finger flexion?

A

Flexor pollicis longus
Anterior interosseous
C8

Median nerve C8

Flexor digitorum profundus
Ulnar (ring and little finger)

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59
Q

What muscle, nerve and root are responsible for finger abduction?

A

First dorsal interosseous and abductur digiti minimi
Ulnar
T1

Abductor pollicis brevis
Median
T1

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60
Q

What muscle, nerve and root are responsible for hip flexion?

A

Iliopsoas

L1 L2

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61
Q

What muscle, nerve and root are responsible for hip adduction?

A

Adductors of the hip
Obturator
L2, L3

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62
Q

What muscle, nerve and root are responsible for hip extension?

A

Gluteus maximus
Sciatic
L5, S3

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63
Q

What muscle, nerve and root are responsible for knee flexion?

A

Hamstring
Sciatic
S1

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64
Q

What muscle, nerve and root are responsible for knee extension?

A

Quadriceps
Femoral
L3, L4

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65
Q

What muscle, nerve and root are responsible for ankle dorsiflexion?

A

Tibialis anterior
Deep peroneal
L4

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66
Q

What muscle, nerve and root are responsible for ankle eversion?

A

Peronei
Superficial peroneal
L5, S1

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67
Q

What muscle, nerve and root are responsible for ankle plantar flexion?

A

Gastrocnemius, soleus
Tibial
S1, S2

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68
Q

What muscle, nerve and root are responsible for big toe extension?

A

Extensor hallucis longus
Deep peroneal
L5

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69
Q

What investigations would you do for tingling limbs?

A
  1. Blood tests
  2. HIV test
  3. Environmental exposure
  4. Nerve conduction studies
  5. EMG
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70
Q

What is the function and velocity of type alpha fibres?

A

Proprioception, somatic motor

70-120 m/s

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71
Q

What is the function and velocity of type beta fibres?

A

Touch and pressure

30-70 m/s

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72
Q

What is the function and velocity of type gamma fibres?

A

Motor to spindle muscles

15-30 m/s

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73
Q

What is the function and velocity of type delta fibres?

A

Pain, cold, touch

12-30 m/s

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74
Q

What is the function and velocity of type B fibres?

A

Preganglionic automatic

3-15 m/s

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75
Q

What is the function and velocity of type C dorsal root fibres?

A

Pain, temperature, mechanoreception

0.5-2 m/s

76
Q

What is the function and velocity of type C sympathetic fibres?

A

Postganglionic sympathetic

0.7-2.3 m/s

77
Q

What are key features of length dependent neuropathies?

A
  1. Symptoms start distally (often fingers)
  2. Often diabetes
  3. Usually symmetrical
  4. Motor signs: loss of reflexes and wasting
  5. Sensor signs: reduced pain, temp, vibration and proprioception
78
Q

What investigations would you do for length dependent neuropathies?

A

Full blood
ANA, HIV, ANCA, anti-neuronal antibodies

EMG
Microneuropathy
Nerve biopsy

79
Q

What are key features of entrapment neuropathies?

A
  1. Common world-wide and occupation related
  2. Mechanical or dynamic compression of the nerve
  3. Symptoms progress slowly and include pain, sensory loss, tingling and motor loss
  4. Treatment includes splinting, steroids, surgery
80
Q

What is neuropraxia?

A

Loss of myeline

81
Q

What are key facts about carpal tunnel?

A

Often due to pregnancy, myxoedema, wrist injury or genetics

Symptoms in the expected distribution of median nerve

Relieved by movement, worse in the morning

82
Q

How would you treat carpal tunnel syndrome?

A
  1. Splinting
  2. Steroid
  3. Surgery
83
Q

What are the main differentials besides carpal tunnel?

A

C8 radiculopathy

C8 plexopathy

84
Q

If the ulnar intrinsic muscles are involved, where is the problem?

A

Ulnar nerve: wrist or elbow

85
Q

If the ulnar intrinsic AND ulnar forearm muscles are involved, where is the problem?

A

Elbow

86
Q

If the ulnar intrinsic AND ulnar forearm AND median intrinsic muscles are involved, where is the problem?

A

C8 or T1 radiculopathy or brachial plexus lesion

87
Q

If there is a sensory abnormality in the terminal digits only, where is the problem?

A

Wrist or elbow

88
Q

If there is a sensory abnormality in the terminal digits AND palmar cutenaeous/dorsal ulnar cutaneous, where is the problem?

A

Elbow

89
Q

If there is a sensory abnormality in the terminal digits AND palmar cutenaeous/dorsal ulnar cutaneous AND inner forearm, where is the problem?

A

C8 or T1 radiculopathy or brachial plexus lesion

90
Q

What are causes of ulnar neuropathy?

A
  1. Trauma
  2. Elbow bony deformity
  3. External pressure (leaning on elbow)
91
Q

What muscles are involved in foot drop?

A

Dorsiflexors

Common peroneal nerve palsy at the fibular head

92
Q

How would you manage foot drop?

A

Conservatively

93
Q

What are differentials for foot drop?

A

Common peroneal nerve palsy at the fibular head

L5 radiculopathy post partum
UMN lesions

94
Q

What are the clinical findings of common peroneal palsy?

A

Weakness of foot dorsiflexion, eversion, and toe extension

Sensory loss of lateral lower leg and dorsum of the foot

95
Q

What are the clinical findings of lumbar plexopathy?

A

Weakness of hamstrings, glutei, foot inversion

Sensor loss is variable and difficult to delineate

96
Q

What are the clinical findings of lumbrosacral trunk of the plexus?

A

Weakness of hamstrings, glutei, foot inversion

Patch sensory loss

97
Q

What are the clinical findings of sciatic neuropathy (L4-S1)?

A

Mimics peroneal palsy

Sensory loss of the dorsum of the foot and lateral side of lower leg

98
Q

What are the clinical findings of peripheral neuropathy?

A

Stronger dorsiflexion than plantar flexion (heel toe test)

Length dependent pattern of sensory loss

99
Q

What are the clinical findings of L4/L5 radiculopathy?

A

Pain in L5 dermatome

Weakness of EHL, toes extensor, foot eversion, hip abduction

100
Q

What are the clinical findings of L5/S1 radiculopathy?

A

VERY common

Pain in back of leg and sole of foor

Ankle jerk reduced, weakness of plantar flexion may be present

101
Q

What can be a precipitating factor for radiculopathy?

A

Acute pain

102
Q

What are findings for radiculopathy?

A

Weakness of muscles innervated by the root

Absent or reduced reflexes

Dermatomal sensory loss

103
Q

What investigations would you do for radiculopathy?

A

Usually none

For atypical one: MRI

104
Q

How would you treat radiculopathy?

A

Conservatively

Physio, bed rest, analgesia

Takes 6 weeks to settle

105
Q

When would you consider surgery for radiculopathy?

A

Unremitting pain
Progressive signs

Fix with root decrompression

106
Q

What are symptoms and signs of Cauda Equina?

A
  1. Leg weakness and perineal numbness
  2. Loss of bladder and erectile functions
  3. Change in bowel function
  4. Lower motor flaccidity, weakness and areflexia
107
Q

What are causes of extrinsic cord lesions?

A

Tumour, compression

108
Q

How do signs and symptoms progress in extrinsic cord lesions?

A

Motor symptoms and signs tend to predominate and come early

Sensory signs may evolve later and develop rapidly

Bladder and bowel often involved LATE

109
Q

How do signs and symptoms progress in intrinsic cord lesions?

A

Bladder and bowel often involved EARLY

Causes spontaneous pain

110
Q

What are inherited neuropathies?

A

CMT: demyelinating (CMT1) or axonal (CMT2)

111
Q

What are key facts of CMT1?

A

Duplication of PMP22 gene on chromosome 17

Length depending neuropathy: wasting of peronei

Distal weakness

112
Q

What is meralgia paraesthetica?

A

Entrapments of the lateral cutaneous nerve of the thigh, often in obesity, diabetes and ageing population

113
Q

How does meralgia paraesthetica present?

A

Pain, allodynia and numbness

Sensory loss lateral to midline of the thigh, no motor findings

Clinical diagnosis

114
Q

How would you manage meralgia paraesthetica?

A

Weight loss

Remits over time

115
Q

What are differential diagnosis for wrist drop?

A

Posterior interosseous nerve at the arcade of Frohse

Causes finger weakness and no sensory signs!!

116
Q

What is Churg Strauss syndrome?

A

The disorder is characterised by the abnormal hypereosinophilia in the blood and tissues and vasculitis

Presents with asthma, hayfever, rash and sinusitis

117
Q

How does Churg Strauss syndrome present?

A

Eosinophilia: fevers, weight loss, arthralgia, breathlessness, neurological signs

Patients often left with significant neurological impairments

118
Q

How would you manage Churg Strauss syndrome?

A

Treatment of vasculitis and intensive suppression of the immune system

119
Q

How does sudden sensorineural hearing loss present?

A
  1. Tinnitus
  2. Sudden onset
  3. Feeling of fullness in ears
  4. Unilateral
  5. Sensorineural based on tuning fork test
120
Q

How would you manage sensorineural hearing loss?

A

1mg/kg prednisolone per day

  • Start within three days of onset
  • Refer to ENT emergency clinic
121
Q

What is the most dangerous foreign body?

A

Battery

122
Q

How would you remove an insect from the ear?

A

OIL ! Kills it

123
Q

What is the main problem with foreign bodies in the ear?

A

Main danger is clumsy attempt at removing it

A large foreign body may cause temporary hearing loss

124
Q

How does otitis externa present?

A
  1. Pain (severe)
  2. Discharge

Often in swimmers or after local trauma?

125
Q

How would you manage otitis externa?

A
  • Topical antibiotic/steroid drops
  • Keep water out!
  • Refer if doesn’t resolve
126
Q

What is acute otitis media often caused by?

A
  • H influenzae

- S pneumoniae

127
Q

How does acute otitis media often present?

A

Acute inflammation of the middle ear

  1. Pain
  2. Discharge

In children

128
Q

What are the complications of acute otitis media?

A
  1. Meningitis
  2. Abscesses
  3. Venous thrombosis

If left untreated it can cause perforation

129
Q

What are causes of facial nerve palsy?

A
  • Congenital
  • Inflammation
  • Acute otitis media
  • Bell’s palsy
130
Q

What are classic symptoms of Bell’s palsy?

A
  • Inability to close eye
  • Downwards angle of mouth
  • Disordered movement of the muscles that control facial expressions, such as smiling, squinting, blinking, or closing the eyelid
  • Drooling
  • Loss of feeling in the face.
  • Loss of the sense of taste on the front two-thirds of the tongue.
  • Asymmetrical smile
  • No muscle tone in cheek
  • Cannot furrow brow
131
Q

How would you treat Bell’s palsy?

A
  1. Steroids (oral corticosteroids)

2. Eyecare

132
Q

If you think something is Bell’s palsy, but it’s not. What can it be?

A
  1. Granulomatous disease – WG, Sarcoid, TB
  2. Parotid malignancy – adenoid cystic Ca
  3. Malignant OE (skull base osteomyelitis)
  4. Ramsey Hunt Syndrome
  5. Lyme disease
  6. HIV
  7. Facial neuroma
  8. Vestibular Schwannoma
133
Q

What are signs of skull base fracture?

A
  • Bruising behind the ears
  • Bruising around the eyes
  • Blood behind the ear drum

Types include anterior, central and posterior. Due to severe head injury

134
Q

What are complications of skull base fracture?

A
  • Cerebrospinal fluid leak
  • Facial fracture
  • Meningitis
135
Q

What causes temporal bone fracture?

A

Traumatic head injury
Penetrating injury
Falls

136
Q

What are signs of temporal bone fractures?

A

Anterior: raccoon eyes, halo signs, partial loss of vision and smell, eye movement defects

Middle: damage to carotid, hearing loss, loss of balance, battler sign

Posterior: cervical spine injury, vertebral injury, damage to lower cranial nerves

137
Q

How would you diagnose temporal bone fractures?

A

Physical exam
Glasgow coma scale
Neurological examination
CT

138
Q

What is the nasal blood supply?

A
  1. External carotid
    1. Sphenopalatine artery
    2. Greater palatine artery
    3. Ascending pharyngeal artery
    4. Posterior nasal artery
    5. Superior labial artery
  2. Internal carotid
    1. Anterior ethmoid artery
    2. Posterior ethmoid artery
139
Q

What do you know about anterior versus posterior nose bleed?

A
  1. Anterior
    • Most common (over 90%)
    • Usually in younger patients
    • Usually septal
    • Typically less severe
  2. Posterior
    • Older population
    • Usually Woodruff’s plexus
    • Typically more serious
140
Q

What are causes of nosebleed?

A
  1. Local: trauma, foreign bodies, neoplasms, idiopathic

2. Systemic: medications, ethanol, HHT, coagulapathy

141
Q

What are non-surgical ways to treat nosebleeds?

A
  1. Control hypertension
  2. Correct coagulopathies/thrombocytopenia
  3. Expel clots
  4. Topical decongestants or vasoconstrictors
  5. Cautery
  6. Nasal packing
142
Q

What are surgical ways to treat nosebleeds?

A
  1. Endoscopic sphenopalatine artery ligation
  2. Transmaxillary maxillary artery ligation
  3. Anterior/posterior ethmoid artery ligation
  4. External carotid artery ligation
  5. Embolization
143
Q

What are signs of Acute rhino-sinusitis?

A
  • Pain exacerbated by bending forwards
  • No cheek swelling
  • Fever
  • Nasal purulence
  • Raised CRP
144
Q

How would you manage Acute rhino-sinusitis?

A
  • Analgesia
  • Steam inhalation
  • Decongestants
    • ephidrine
    • Otrivine
  • Antibiotics
145
Q

How would you treat a complicated Acute rhino-sinusitis?

A
  1. Urgent CT with contrast
  2. Orbital collections and urgent drainage
  3. Intracranial collection, urgent neurosurgical drainage
  4. Antibiotics, decongestants, washout sinuses
146
Q

What are complications of sinusitis?

A
  1. Orbital cellulitis
  2. Frontal osteomyelitis
  3. Meningtitis
  4. Cerebral abscess
  5. Cavernous sinus thrombosis
147
Q

Where would you do a cricothyroidotomy?

A

Through cricothyroid membrane between cricoid and thyroid cartilage

148
Q

What are indications for cricothyroidotomy?

A
  • Inability to intubate
  • Inability to ventilate
  • Inability to maintain SpO2 >90%
149
Q

How would you lower intracranial pressure?

A
  1. Elevate head of bed to 30 degrees
  2. Discontinue cervical collar
  3. Straightedges head and neck to neutral position
  4. Remove ties around neck
  5. Treat fever
150
Q

What are the brainstem reflexes that are tested to confirm brainstem death?

A
  1. Pupil response
  2. Corneal reflex
  3. Oculovestibular reflex
  4. Apneic test
151
Q

How would you confirm brainstem death?

A
  1. Comatose patient dependent on mechanical ventilation
  2. Irreversible brain damage of known aetiology
  3. Exclusion of reversible causes of coma and apnea: drugs, hypothermia, CVD/metabolic/endocrine disturbances
  4. Absent brain stem reflexes, absent motor reflexes in cranial nerves
  5. Confirm death
152
Q

What does space occupation in the CNS lead to?

e.g. tumour, blood, swelling

A
  1. Focal deficits
  2. Seizures
  3. Raised ICP
153
Q

Who can you use brain US for?

A

Used in neonatal setting for many years for brain and spine due to open fontanelles

Increasing use intraoperatively

154
Q

What are the different types of hydrocephalus?

A
  • Communicating (post-haemorrhagic; post-infection)
  • Obstructive (aqueduct stenosis; obstruction at the outlets of the
    4th ventricle; foramina of Monro; tumour; blood; infection; membranes and cystic lesions)
155
Q

How does hydrocephalus present in children?

A
  1. Increasing head circumference
  2. Full and tense fontanelle
  3. Dilated scalp veins
  4. Loss of upgaze
  5. Irritability
  6. Vomiting
  7. Drowsiness, reduced conscious level
156
Q

How does hydrocephalus present in adults?

A
  1. Headaches
  2. Nausea and vomiting
  3. Visual blurring
  4. Drowsiness, reduced conscious level
157
Q

How would you manage hydrocephalus?

A
  1. CSF diversion
  2. Temporary → reservoir or VSGS
  3. Definitive → shunt, ETV
158
Q

How would you classify trauma based on GCS?

A
  • Mild (13-15)
  • moderate (9-12)
  • severe (3-8)
159
Q

What are contusions?

A

Traumatic intracerebral haematomas

Multiple small contusions (petechial haemorrhages) are one of the signs of diffuse axonal injury

160
Q

What are risk factors for a subarachnoid haematoma?

A

Smoking, HTN, family history, connective tissue disorder

161
Q

How would you manage a subarachnoid haematoma?

A

Endovascular coiling and neurosurgical clipping

Urgent !

162
Q

What is a cavernoma?

A

Cluster of abnormal blood vessels, usually found in the brain and spinal cord

163
Q

How do cavernoma often present?

A

Seizures, bleeds

164
Q

What are causes of spine injury?

A
  1. Degenerative (UMN, radiculopathy, spine degeneration)
  2. Tumour
  3. Trauma
165
Q

How would you grade spinal lesions?

A

Grade A: complete: no sensory or motor function

Grade B: incomplete. Sensory but no motor function

Grade C: incomplete. Motor function is preserved below the neurological level

Grade D: incomplete. Similar to C but more preserved muscles

Grade E: normal

166
Q

What is pituitary apoplexy?

A

Expansion of pituitary adenoma due to haemorrhage or ischaemic necrosis

167
Q

How does pituitary apoplexy present?

A

Sudden and rapid onset of severe headache, nausea, vomiting and meningism

Visual loss (bilateral hemianopia and/or VA reduced

Hypothalamic dysfunction

168
Q

How would you manage pituitary apoplexy?

A

Cortisol

169
Q

How would you manage a prolactinoma (pituitary tumour)?

A

Dopamine agonists: cabergoline, bromocriptine

170
Q

How would you manage acromegaly (pituitary tumour)?

A 
Dopamine agonists 
Somatostatin analogues (octreotide)
GH antagonists (pegvisomant)
171
Q

How would you manage a Cushing’s?

A

Adrenal steroid blockers (ketoconazole, metyrapone)

172
Q

How does prolactinoma present?

A

Galactorrhoea, amenorrhoea in women

Impotence, loss of libido and fertility in men

173
Q

How does a GH secreting tumour present?

A

Gigantism in prepubertal children

Acromegaly in adults

Skeletal overgrowth and soft tissue swelling

Glucose intolerance, peripheral nerve entrapment syndrome, headaches, excessive perspiration, sleep apnoea, fatigue

174
Q

What are key facts about acoustic neuroma?

A

Unilateral sensorineural hearing loss

Bilateral tumours in type 2 neurofibromatosis

Surgery

175
Q

When would you consider surgery for epilepsy?

A

After two trials for anticonvulsants

176
Q

What diseases can you use deep brain stimulation for?

A
  1. Parkinson’s
  2. Dystonia
  3. Tremor
177
Q

What are chair malformations?

A

a condition in which brain tissue extends into the spinal canal

178
Q

What is the difference between type 1 and 2 chiari malformations?

A

Type 1 Chiari malformation symptoms and signs can show up in infants, children, teens or adults.

Type 2 Chiari malformation is associated with spina bifida and is present at birth

179
Q

What are symptoms of type 1 chiari malformations?

A

Suboccipital headaches
Bilateral hearing loss
Dizziness, vertigo, disturbance of hearing

Problems of the spinal cord present in about 95% of patients with syringomyelia and two thirds of those without it. Symptoms include central cord syndrome, impaired sensation, impaired motor control, gait disturbance, torticollis, bowel and/or bladder symptoms, neuropathic joints, trophic phenomena and pain

180
Q

What are symptoms of type 2 chiari malformations?

A 
Inspiratory stridor.
Dysphagia or nasal regurgitation.
Aspiration from bilateral abductor vocal cord paralysis or central neural dysfunction, or both.
Respiratory distress.
Episodes of apnoea.
Weak cry.
Scoliosis.
Quadriparesis.
181
Q

What investigations would you do for chair malformations?

A

MRI

182
Q

What is the management for Chiari?

A

Surgery

183
Q

What are the different types of neural tube defects?

A
  1. Open: spina bifida and myelomeningocoele

2. Closed: fatty film, dermal sinus tract, lipoma, neurenteric cyst

184
Q

How would you manage open neural tube defects?

A

Repaired surgically

185
Q

How would you manage closed neural tube defects?

A

Only intervene when symptomatic

8. CMS (21 decks)

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