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MSRA Content > Neurology - Level 2 > Flashcards

Neurology - Level 2 Flashcards

1
Q

Investigations to perform in first fit?

A

o Consider alcohol/drugs, withdrawal states, hypoglycaemia, arrhythmias, head injury, SAH, TIA/stroke, infection, metabolic
o Investigations
 BMG
 Bloods – glucose, FBC, U&Es, cultures if pyrexial
 ECG
 CXR if signs
 Urine pregnancy test
 CT scan if:
• Focal signs, head injury, known HIV, suspected intracranial infection, bleeding disorder or conscious level does not improve

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2
Q

Discharge advice to patient with first fit?

A

 Accompanied by adult if normal neurological and CV examination, ECG and electrolytes are normal
 Make appointment with epilepsy specialist in coming week
 Do not drive or use heavy machinery
 Supervision when performing swimming/bathing

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3
Q

Admit patient with first fit if?

A

 More than one seizure in day

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4
Q

Definition of status epilepticus?

A
  • Continuous generalised seizure for 5 minutes or longer, or recurrent seizures one after the other without recovery in between
  • Mortality and risk of permanent brain damage increase with length of attack
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5
Q

Risk factors of status epilepticus?

A

o Under 5 or elderly age

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6
Q

Precipitants of status epilepticus?

A

Cerebral infarction, trauma, CVA, metabolic disturbances, febrile seizures

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7
Q

Symptoms of status epilepticus?

A
  • Tonic-clonic easy to distinguish, non-convulsive states harder to spot
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8
Q

Community management of status epilepticus? Drugs if over 5 minutes long

A

o Buccal midazolam 10mg 1st line
o Alternative: rectal diazepam 10-20mg, IV lorazepam (if IV access)
o Call ambulance if still fitting 5 minutes after medications, concerns about ABC

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9
Q

Initial management of status epilepticus?

A

o Time the seizure
o Position patient to avoid injury
o Open and maintain airway, lay in recovery position - Remove false teeth, insert Guedel/Nasopharyngeal airway
o High flow oxygen 15L/min via NRB mask + suction
o IV access and take blood (FBC, U&Es, LFTs, glucose, Ca, Mg, VBG, toxicology screen)
o Blood cultures if septic
o Check BM glucose
o Assess cardiac and respiratory function

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10
Q

Drug management (after 5 minutes) in status epilepticus?

A

o IV lorazepam 4mg slowly
o Repeat IV lorazepam after 10 minutes if seizures fail to respond or recur
 Alternative: IV diazepam
 If no IV access, buccal midazolam or rectal diazepam

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11
Q

Drug management in status epilepticus if alcohol abuse suspected?

A

o If alcohol abuse – IV thiamine 250mg over 30 mins

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12
Q

Drug management in status epilepticus if hypoglycaemic?

A

o Treat hypoglycaemia with 50ml of 20% dextrose (10g)

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13
Q

Further drug management (if fails to respond after 25 minutes)?

A

o Phenytoin 15-20mg/kg IVI at rate of 50mg/minute – if fails to respond after 25 minutes
 Alternative diazepam infusion until seizures respond

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14
Q

Monitoring of status epilepticus?

A
  • Monitor ECG and BP
  • Anaesthetic help
    o May need ICU and ventilation
    o RSI – propofol, thiopental, miadazolam and tracheal intubation
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15
Q

Olfactory nerve lesion - anatomy?

A

olfactory cells are bipolar neurones passing through cribiform plate to olfactory bulb

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16
Q

Olfactory nerve lesion - symptoms?

A

reduced taste and smell but not to ammonia which stimulates the pain fibres carried in trigeminal nerve

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17
Q

Olfactory nerve lesion - causes?

A

Trauma, frontal lobe tumour, meningitis

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18
Q

Optic nerve lesion - symptoms - visual field defects?

A

 Scotomas

 Monocular blindness – MS, GCA

 Bilateral blindness – methyl alcohol, tobacco, neurosyphilis

 Bitemporal hemianopia – optic chiasm compression (internal carotid artery aneurysm, pituitary adenoma, craniopharyngioma)

 Homonymous hemianopia (loss of same half of visual field in both eyes on opposite side of lesions e.g. right sided lesion causes loss of left side of visual field) - lesions behind optic chiasm in optic tract/lateral geniculate nucleus/optic radiations including tumour, stroke, abscess

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19
Q

Optic nerve lesion - symptoms - optic neuronitis?

A

Pain on moving eye, loss of central vision, afferent pupillary defect, papilloedema

MS, syphilis, sinusitis

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20
Q

Optic nerve lesion - symptoms - optic atrophy?

A

Pale optic discs and reduced acuity

MS, frontal tumours, Friedreich’s ataxia, syphilia, glaucoma, optic nerve compression

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21
Q

Optic nerve lesion - symptoms - papilloedema?

A

 Raised ICP (tumour, abscess, encephalitis, hydrocephalus, benign intracranial hypertension)
 Inflammation (optic neuritis)
 Ischaemia (accelerated hypertension)

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22
Q

Symptoms of oculomotor nerve lesion?

A
  • Fixed dilated pupil
  • Ptosis
  • Down and outward deviation of eye
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23
Q

Causes of oculomotor nerve lesion?

A
  • DM
  • GCA
  • Syphilis
  • PCA aneurysm
  • Raised ICP
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24
Q

Symptoms of trochlear nerve lesion?

A
  • Diplopia due to weak down and in eye movements
  • Eye up and outwards
  • Patient tilts head away from affected side
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25
Q

Causes of trochlear nerve lesion?

A
  • Trauma to orbit
  • DM
  • Infarction
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26
Q

Symptoms of trigeminal nerve lesion?

A
  • Reduced sensation over affected area

* Weakness of jaw clenching and side-to-side movement

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27
Q

Causes of trigeminal nerve lesion?

A

Sensory- trigeminal neuralgia, herpes, nasopharyngeal carcinoma

Motor – bulbar palsy, acoustic neuroma

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28
Q

Symptoms of abducens nerve lesion?

A

• Eye deviated medially due to unopposed action of medial rectus (LR paralysed)

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29
Q

Causes of abducens nerve lesion?

A
  • MS

* Pontine CVA

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30
Q

Symptoms of facial nerve lesion?

A
  • Facial weakness
    • If LMN – forehead paralysed too
    • If UMN – forehead spared due to crossing over of pathways
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31
Q

Cause of facial nerve lesion?

A
  • LMN – Bell’s palsy, polio, otitis media, skull fracture, cerebellopontine angle tumur, parotid tumour, herpes (Ramsay hunt syndrome), Lyme disease
  • UMN – stroke, tumour
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32
Q

Symptoms of vestibulocochlear nerve lesion?

A

• Unilateral sensorineural hearing loss, tinnitus

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33
Q

Symptoms of vestibulocochlear nerve lesion?

A

• Loud noise, Paget’s disease of bone, Menieres’ disease, herpes, acoustic neuroma, brainstem CVA, furosemide, aspirin

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34
Q

Symptoms of vagus nerve lesion?

A

• Palatal weakness, nasal speech, uvula moves asymmetrically (away lesion) when say ahh

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35
Q

Cause of vagus nerve lesion?

A

• Trauma, brainstem lesion, cerebellopontine angle tumour, polio, GBS

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36
Q

Symptoms of accessory nerve lesion?

A

• Weakness to sternocleidomastoid and trapezius

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37
Q

Causes of accessory nerve lesion?

A

• Trauma, brainstem lesion, cerebellopontine angle tumour, polio, GBS

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38
Q

Symptoms of hypoglossal nerve lesion?

A
  • LMN lesion – wasting of ipsilateral side of tongue, fasciculations and protrusion of tongue deviates to side of lesion
  • If UMN lesions – deviates away from lesion but tongue wont be wasted
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39
Q

Causes of hypoglossal nerve lesion?

A

• Polio, syringomelia TB

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40
Q

Lesions of cerebellopontine angle tumour?

A

CN 7, 8 then 10 and 9

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41
Q

Innervation of ulnar nerve?

A
  • C7-T1
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42
Q

Pathology of ulnar nerve palsy?

A
  • Vulnerable to elbow trauma – humeral fracture
  • Most often damaged at epicondylar groove or in cubital tunnel
  • Compression at wrist in Guyon’s canal
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43
Q

Symptoms and sign of ulnar nerve palsy?

A
  • Weakness/Wasting of medial (ulnar side) wrist flexors
  • Interossei (cannot cross fingers)
  • Medial two lumbricals (claw hand) – cannot extend 4/5th fingers
  • Hypothenar eminence wasting
  • Sensory loss over medial 1 ½ fingers and ulnar side of hand
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44
Q

Management of ulnar nerve palsy?

A 
•	Rest
•	NSAIDs
•	Night-time soft elbow splinting for 6 months
•	Surgery
	Decompression
	Epicondylectomies
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45
Q

Innervation of median nerve?

A

• C6-T1

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46
Q

Definition of median nerve palsy?

A
  • Compression of median nerve in carpal tunnel
  • Carpal tunnel= bounded by carpal bones and transverse carpal ligament
  • Reduction in dimensions cause pressure, ischaemia of median nerve and impairs conduction
  • If continued, leads to segmental demyelination with more constant symptoms
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47
Q

Causes of median nerve palsy?

A 
•	Entrapment
	Hypothyroidism, DM, acromegaly, neoplasms, lipoma, OA, RA, amyloidosis, pregnancy, sarcoidosis
•	Excessive use of wrist
•	Tenosynovitis
•	Obesity
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48
Q

Symptoms and signs of median nerve palsy?

A

• Intermittent tingling, numbness or altered sensation
• Burning or pain in median nerve distribution (radial 3 ½ fingers and palm)
 Worse at night and can disrupt sleep
 Relieved by shaking it
• Loss of grip strength
• Atrophy of thenar eminence

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49
Q

Tests of median nerve palsy?

A

• Phalen’s Test
 Flex wrist for 60s and brings on symptoms

• Tinnel’s Test
 Tapping lightly over median nerve produces paraesthesia or pain in median nerve distribution

• If alternative cause:
 Bloods (hypothyroidism)
 US (ganglion)

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50
Q

Management of median nerve palsy - when to refer to specialist?

A

 Symptoms severe or ADLs reduced
 Symptoms recur following carpal tunnel surgery
 Patient requests
 Conservative management in primary care has failed

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51
Q

Management of median nerve palsy - primary care management?

A

 Wrist splinting in neutral position – purchase at pharmacy
 Corticosteroid injection
 Specialist – Decompression surgery
 DO NOT PRESCRIBE NSAIDs or DIURETICS

52
Q

Innervation of radial nerve?

A
  • C5-T1
53
Q

Causes of radial nerve palsy?

A

• Compression against humerus
• Saturday night palsy – sleeping with arm over back of chair
 Compression of lower brachial plexus
• Fracture or dislocation of head of humerus
• Shoulder crutches

54
Q

Symptoms of radial nerve palsy?

A
  • Wrist and finger drop

* Sensory loss variable – dorsal aspect of root of thumb (snuff box)

55
Q

Investigations of radial nerve palsy?

A
  • Nerve conduction studies
  • US
  • MRI
56
Q

Management of radial nerve palsy?

A
  • Usually recover spontaneously
  • NSAIDs
  • Entrapments requires surgical decompression
57
Q

Innervation of phrenic nerve?

A

C3-C5

58
Q

Causes of phrenic nerve palsy?

A 
Malignancy
Trauma
Central lines
Inflammation (pneumonia, empyema, pleurisy)
AAA
59
Q

Symptoms of phrenic nerve palsy?

A

If unilateral – asymptomatic
SOB and orthopnoea
Respiratory function tests – restrictive pattern

60
Q

Management of phrenic nerve palsy?

A

Phrenic nerve stimulation

Direct muscular stimulation

61
Q

Innervation of laternal cutaneous nerve of thigh?

A
  • L2-L3
62
Q

Symptoms of laternal cutaneous nerve of thigh palsy?

A
  • Meralgia paraesthesia – anterolateral burning thigh pain from entrapment under inguinal ligament
  • Pain reproduced by palpation under ASIS
  • No motor weakness
63
Q

Innervation of common peroneal nerve?

A
  • L4-S1
64
Q

Causes of common peroneal palsy?

A
  • Trauma
  • Sitting cross-legged
  • Pressure to lateral leg as winds around fibular head
65
Q

Symptoms and signs of common peroneal palsy?

A
  • Foot drop
  • Weak ankle dorsiflexion and eversion
  • Inability to extend toes
  • Sensory loss over dorsum of foot
66
Q

Management of common peroneal palsy?

A
  • Rest
  • NSAIDs
  • Aluminium night-shoe at night
  • Ankle-foot orthoses in the day
67
Q

Innervation of tibial nerve?

A

L4-S3

68
Q

Causes of tibial nerve palsy?

A
  • Ankle sprains and fractures
  • Ill-fitting footwear
  • Cysts
  • Ganglia
  • Arthritis
69
Q

Symptoms of tibial nerve palsy?

A
  • Inability to stand on tiptoe (plantarflexion), invert foot or flex toes
  • Sensory loss of sole
70
Q

Management of tibial nerve palsy?

A
  • Rest

* NSAIDs

71
Q

Definition of Guillain-Barre Syndrome?

A
  • Acute inflammatory demyelination causing ascending and progressive polyneuropathy
  • Trigger causes antibodies which attack nerves
  • Peak ages 15-35 and 50-75
72
Q

Triggers of Guillain-Barre Syndrome?

A
  • Campylobacter jejuni
  • CMV
  • Mycoplasma
  • Zoster
  • HIV
  • EBV
  • Vaccinations
73
Q

Pattern of Guillain-Barre Syndrome?

A
  • 1-3 weeks after infection a symmetrical ascending muscle weakness starts
  • Progressive phase up to 4 weeks, followed by recovery
74
Q

Symptoms of Guillain-Barre Syndrome?

A

• Weakness
 Ascending progressive symmetrical weakness starting in lower extremities
 Facial weakness, dysphasia and dysarthria may develop
 Severe cases leads to weakness in respiratory muscles
• Pain in legs common
• Paraesthesia and sensory loss starting in lower extremities
• Autonomic dysfunction – sweating, tachycardia, BP changes

75
Q

Investigations of Guillain-Barre Syndrome?

A
  • Bloods – U&E, LFTs
  • LP - Protein high, normal WCC
  • Spirometry – FVC determines needs to ITU admission and intubation
  • Nerve conduction studies – slowed, repeat after 2 weeks if normal
76
Q

Management of Guillain-Barre Syndrome?

A

• Respiratory involvement – need ITU transfer
 FVC every 4 hours
 Ventilate when FVC<1.5L, PaO2 <10kPa, PaCO2 >6kPa
• IV immunoglobulin 0.4g/kg/24h for 5d
• Plasma Exchange
• Neuropathic analgesia – gabapentin, carbamazepine
• VTE prophylaxis essential

77
Q

Complications of Guillain-Barre Syndrome?

A
  • Persistent paralysis
  • Respiratory failure
  • Hypo/Hypertension
  • Pneumonia
  • Urinary retention
  • Depression/Anxiety
78
Q

Prognosis of Guillain-Barre Syndrome?

A
  • Good, 85% make complete or near-complete recovery

* Mortality 10%

79
Q

Causes of head injury?

A 
o	RTAs
o	Falls
o	Assaults
o	Sporting/Leisure injuries
o	Workplace injuries
80
Q

Symptoms of raised ICP?

A 
o	Changes or LOC
o	Headache
o	Vomiting
o	Eyes – papilloedema, dilated pupils, impaired eye movements
o	Aphasia
o	Seizures
o	Cushing’s triad – hypertension, bradycardia, bradypnoea (Cheyne-Stokes breathing)
o	Coning
81
Q

When to refer head injury to hospital?

A 
o	Impaired conscious level
o	Amnesia
o	Neurological symptoms
o	Skull fracture
o	Worrying mechanism of injury
82
Q

Examination of patient with head injury?

A

o Vital Signs
o BMG
o GCS
o Neurological assessment
o Evaluate lacerations and note skull/facial fractures
 Basal skull # - haemotympanum, Panda eyes, CSF leakage, Battle’s sign
o Check for CSF leak

83
Q

Investigations in head injury?

A

o U&Es, glucose, FBC, blood alcohol, toxicology screen, ABG, clotting
o CT scan
 Skull fractures
 Intracranial haematomas – midline shift
 Extradural haematoma – high density lens shaped lesions
 Subdural conform more to surface of brain
 Contusions are low density
 Cerebral swelling may shrink ventricles

84
Q

Management of head injury - initial management?

A

o Oxygen if hypoxic, intubate if GCS<9
o Immobilise C-spine until excluded
o IV access, stop blood loss and treat shock
o Bloods – FBC, U&Es, clotting, cross-match, glucose
o Seizures – IV lorazepam +/- phenytoin
o Assess need for tetanus toxoid

85
Q

Management of head injury - pain management?

A

o Splintage of limb fractures
o Catheterisation of full bladder
o IV opioids titrated against clinical response

86
Q

Management of head injury - when to CT adult within 1 hour?

A 
GCS <13 on initial assessment
GCS<15 at 2 hours after injury
>1 vomit
Suspected open or depression skull fracture
Sign of basal skull fracture
Post-trauma seizure
Focal neurological deficit
87
Q

Management of head injury - when to CT adult within 8 hours?

A

If LoC or amnesia since head injury + 1 of:

Age>65
History of bleeding disorder
Dangerous mechanism of injury (>1 metre/5 stair fall, pedestrian struck by vehicle, occupant ejected from car)
>30 mins retrograde amnesia of events before head injury

88
Q

Management of head injury - when to CT child within 1 hour?

A 
GCS<14 or <15 for <1-year olds
GCS<15 at 2 hours post-injury
>5cm bruise on head of <1 year old
LOC >5 mins, drowsiness, >2 vomits, dangerous mechanism of injury, amnesia >5 mins
Non-accidental
Post-traumatic seizure
Suspected open or depression skull fracture
Sign of basal skull fracture
Focal neurological deficit
89
Q

Management of head injury - when to CT on warfarin?

A

 CT within 8 hours if no indication for earlier

90
Q

Management of head injury - when to perform 3-view XR of C-spine within 1 hour?

A

o If cannot assess or patient cannot rotate neck to 45o to left and right

91
Q

Management of head injury - referral to neurosurgery?

A 
o	GCS 8 or less after initial resus
o	Confusion >4 hours
o	Deteriorating GCS
o	Progressive focal neurological signs
o	Seizure without full recovery
o	Penetrating injury
o	CSF leak
92
Q

Management of head injury - when to admit into hospital?

A

o Abnormal imaging, GCS<15, persistent vomiting, severe headaches, intoxicated or other concerns

93
Q

Monitoring in head injury - what and how often?

A

 GCS, pupil size, reactivity, limb movements, RR, HR, BP, temperature, O2 sats
 Half-hourly until GCS 15
 When GCS 15: half hourly for 2 hours, 1-hourly for 4 hours and 2-hourly thereafter

94
Q

When to discharge person with head injury?

A

o When GCS 15 with somebody suitable at home to supervise for 24h

95
Q

Advice given in head injury on discharge?

A 
	Rest for 24h
	Analgesia when required
	DO NOT drink alcohol for 24 hours, take sleeping tablets or tranquilisers
	DO take your normal medications
	If any of the following occur, return to hospital:
•	Headache not relived by painkillers
•	Vomiting
•	Vision disturbances
•	Balance problems
•	Fits
•	Unarousable
96
Q

Pathology of subdural haematoma?

A

o Bleeding is from bridging veins between cortex and venous sinuses (vulnerable to deceleration injuries), haematoma between dura and arachnoid
o Leads to raised ICP, midline shift and eventually tentorial herniation and coning

97
Q

Risk factors of subdural haematoma?

A

elderly, falls (epileptics, alcoholics), anticoagulation

98
Q

Symptoms of subdural haematoma?

A

fluctuating consciousness, insidious physical or intellectual slowing, sleepiness, headache, personality change

99
Q

Signs of subdural haematoma?

A

Raised ICP, seizures, localising symptoms occur late (unequal pupils, hemiparesis)

100
Q

Investigations of subdural haematoma?

A

CT (crescent shaped collection of blood over 1 hemisphere, sickle-shaped)

101
Q

Management of subdural haematoma?

A

Irrigation (Via burr twist drill and craniostomy), craniotomy

102
Q

Pathology of extradural haematoma?

A

o Due to fractures temporal or parietal bone causing laceration to middle meningeal artery and vein, typically after trauma to temple
o Also tears in dural venous sinus
o Blood accumulates between bone and dura mater

103
Q

Symptoms of extradural haematoma?

A

o Deteriorating consciousness after head injury, lucid period (LOC and then recovery before LOC when haematoma expands enough), increasing severity of headaches, vomiting, confusion and fits
o May have upgoing plantars, brisk reflexes, hemiparesis, ipsilateral pupil dilates, irregular breathing

104
Q

Investigations of extradural haematoma?

A

CT (lens-shaped haematoma, tough dura mater keeps it localised), Skull XR (fractures)

105
Q

Management of extradural haematoma?

A

Stabilise and transfer to neurosurgical unit urgently, clot evacuation and ligation of bleeding vessel, may need mannitol, ventilation and intubation

106
Q

Definition of multiple sclerosis?

A
  • Acquired, chronic, immune-mediated inflammatory condition of CNS affecting brain, brain stem and spinal cord
  • Inflammation causes demyelination, gliosis and neuronal damage (cell loss) throughout CNS
  • T-cell mediated attack of oligodendrocytes
107
Q

Nerves affected in multiple sclerosis?

A
  • Optic nerve, periventricular white matter, brainstem and cerebellum
  • Peripheral nerves never affected
108
Q

Definition of relapse of multiple sclerosis?

A

• Relapse is onset of new symptoms, or worsening, lasting >24 hours in absence of cause

109
Q

Epidemiology of multiple sclerosis?

A
  • Prevalence directly related to distance from equator

- About 1 in 2000, mean age 30 years, Women 3>1 Men

110
Q

Types of multiple sclerosis?

A

Relapsing-Remitting
• Episodes or exacerbations of symptoms followed by recovery and periods of stability

Secondary progressive
• Onset of MS is of RRMS but at some point, disease course changes and neurological function worsens with or without relapses
• 25% of RRMS progress to SPMS within 6 years

Primary Progressive
• Steady progression and worsening from disease onset without remissions

111
Q

Risk factors of multiple sclerosis?

A
  • Genetics
  • Smoking
  • Obesity
  • EBV exposure
  • Vitamin D is PREVENTATIVE
112
Q

Symptoms of multiple sclerosis?

A

Two or more distinct episodes of CNS dysfunction followed by remission

• Optic neuropathy
 Unilateral optic neuritis
 Partial or total unilateral visual loss developing over few days
 Eye pain behind eye, particularly on eye movement
 Reduced acuity with scotoma, disc swelling and atrophy

• Transverse Myelitis
 Numbness/weakness/tingling in legs, trigeminal neuralgia, erectile dysfunction, urinary symptoms

• Brainstem demyelination
 Diplopia, vertigo, dysphagia, nystagmus, ataxia

113
Q

Relapse triggers in multiple sclerosis?

A

• Triggered by stress, heat, exercise

114
Q

Investigations before referral in multiple sclerosis?

A

• FBC, CRP, ESR, LFT, U&E, calcium, glucose, TFT, VitB12, HIV

115
Q

Investigations by neurologist in multiple sclerosis?

A

MRI – plaques in area of MS

CSF – IgG in CSF and not blood suggest inflammation

116
Q

When to refer to neurologist in multiple sclerosis?

A
  • If suspected MS or isolate optic neuritis confirmed by ophthalmologist
  • Diagnosis made by consultant neurologist using McDonald Criteria
  • Follow up within 6 weeks after diagnosis
117
Q

Criteria used in diagnosis of multiple sclerosis?

A

McDonald Criteria

118
Q

Management of multiple sclerosis - general management?

A
  • Encourage stress free life
  • Regular exercise and stop smoking
  • Give vitamin D if low levels
119
Q

Management of multiple sclerosis - symptom management?

Fatigue
Emotionally labile
Oscillopsia
Spasticity
Tremor
Urgency
A

Fatigue
- Offer amantadine or CBT

Emotionally labile – amitriptyline

Oscillopsia – gabapentin (memantine)

Spasticity - Baclofen/gabapentin/tinzanidine

Tremor - Physiotherapist or OT, Botulinum toxin type A

Urgency – Intermittent self-catheterisation, tolterodine

120
Q

Management of multiple sclerosis - rehab?

A
  • Physio and OT management
  • Walking Aids
  • Alter home, garden, carers
  • Benefits
121
Q

Management of multiple sclerosis - acute relapse - what to rule out?

A

Rule out infection and make sure it is not disease progression

122
Q

Management of multiple sclerosis - acute relapse - diagnose relapse when?

A

 Worse or new symptoms lasting >24 hours in absence of infection after 1 month stable period

123
Q

Management of multiple sclerosis - acute relapse - drug management?

A

 Methylprednisolone 0.5g daily PO for 5 days

- Consider IV 1g if oral steroids failed or need admitting for severe relapse

124
Q

Management of multiple sclerosis - Disease modifying agents in relapsing remitting MS?

A

 Interferon 1A&1B
 Alemtuzumab/Natalizumab
 Glatiramer
 Azathioprine (instead of interferon)

125
Q

Management of multiple sclerosis - Disease modifying agents in secondary progressive?

A

 Interferon Beta 1B

126
Q

Management of multiple sclerosis - Disease modifying agents in primary progressive?

A

 No effective treatment

127
Q

Complications of MS?

A
  • Fatigue
  • Spasticity
  • Ataxia and tremor
  • Optic Neuritis
  • Diplopia
  • Reduce mobility
  • Pain
  • Bladder dysfunction
  • Sexual dysfunction

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