Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Special Senses > Neuro > Flashcards

Neuro Flashcards

1
Q

Define transient ischaemic attack

A

Symptoms of a stroke resolving within 24 hours, secondary to ischaemia without infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Crescendo TIA

A

2 or more TIAs in one week, high risk for future stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presentation of stroke

A

Sudden onset asymmetrical symptoms
Sudden weakness of limbs
Sudden facial weakness
Sudden onset dysphasia
Sudden onset visual/sensory loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Risk factors for stroke

A

Pre-existing cardiovascular disease
Previous stroke / TIA
Atrial fibrillation
Carotid artery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
COCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical scoring tool to recognise stroke

A

ROSIER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Management of stroke

A

Immediate CT brain to exclude haemorrhage
Aspirin 300mg STAT (continue for 2 weeks)
Thrombolysis with alteplase if within 4.5hrs
Thrombectomy if within 6 hours
Clopidogrel 75mg after aspirin for life
Admit to stroke centre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management of TIA

A

Aspirin 300mg
Secondary prevention for CVD
Stroke specialist within 24hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Gold standard imaging for stroke

A

Diffusion-weighted MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Secondary stroke prevention

A

Clopidogrel 75mg
Atorvastatin 80mg
Carotid endarterectomy or stenting if carotid artery
Treat modifiable risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Major stroke categories

A

Ischaemic stroke
Haemorrhagic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mechanisms of ischaemic stroke

A

Embolism
Thrombosis
Systemic hypoperfusion
Cerebral venous sinus thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which area of the brain is supplied by the anterior cerebral arteries

A

Anteromedial cerebrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which area of the brain is supplied by the middle cerebral arteries

A

Lateral cerebrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which area of the brain is supplied by the posterior cerebral arteries

A

Medial & lateral areas of the posterior cerebrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the Bamford classification of strokes

A

Total anterior circulation (TACS)
Partial anterior circulation (PACS)
Posterior circulation (POCS)
Lacunar (LACS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Criteria for TACS

A

Unilateral weakness and/or sensory deficit of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Criteria for PACS

A

TWO of:
- Unilateral weakness and/or sensory deficit of face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Criteria for LACS

A

ONE of:
- Pure sensory stroke
- Pure motor stroke
- Sensori-motor stroke
- Ataxic hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Criteria for POCS

A

ONE of:
- Cranial nerve palsy & contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Conjugate eye movement disorder
- Cerebellar dysfunction
- Isolated homonymous hemianopia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Risk factors for intracranial bleed

A

Head injury
Hypertension
Aneurysm
Ischaemic stroke
Brain tumour
Anticoagulant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Presentation of intracranial bleed

A

Sudden onset headache
Seizures
Weakness
Vomiting
Reduced consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which vascular structure is involved in subdural haemorrhage

A

Bridging veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Between which layers does a subdural haemorrhage occur

A

Dura mater & arachnoid mater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Appearance of subdural haemorrhage on CT

A

Crescent/banana

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which vascular structure is involved in extradural haemorrhage

A

Middle meningeal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Between which layers does extradural haemorrhage occur

A

Skull & dura mater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which injury is associated with extradural haemorrhage

A

Temporal bone fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Appearance of extradural haemorrhage on CT

A

Biconvex/lemon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Between which layers does a subarachnoid haemorrhage occur

A

Pia mater & arachnoid membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Presentation of subarachnoid haemorrhage

A

Sudden onset occipital headache
Strenuous activity
Neck stiffness
Photophobia
Neurological changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Management of intracranial bleed

A

CT head
Check FBC & clotting
Discuss with specialist neurosurgical centre
Consider escalation to ITU
Correct clotting abnormalities
Correct severe hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Risk factors for subarachnoid haemorrhage

A

Hypertension
Smoking
Excessive alcohol consumption
Cocaine use
Family history
Sickle cell anaemia
Connective tissue disorders
Neurofibromatosis
ADPKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

CSF findings in subarachnoid haemorrhage

A

Raised RCC
Xanthochromia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Pathophysiology of Multiple Sclerosis

A

Immune cell response causing demyelination of neurons of CNS neurons, reducing nerve impulse transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Potential causes of Multiple Sclerosis

A

Multiple genes
Epstein-Barr virus
Low vitamin D
Smoking
Obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Signs & symptoms of multiple sclerosis

A

Optic neuritis
Double vision
Conjugate lateral gaze disorder
Focal weakness
Trigeminal neuralgia
Paraesthesia
Lhermitte’s sign
Ataxia
Positive Romberg’s test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Patterns of multiple sclerosis

A

Relapsing-remitting
Primary progressive
Secondary progressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the most common pattern of multiple sclerosis

A

Relapsing-remitting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is secondary progressive multiple sclerosis

A

Started off as relapsing-remitting disease, but now there is progressive worsening of disease with incomplete remissions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is primary progressive multiple sclerosis?

A

Worsening of disease and symptoms from point of diagnosis, without any initial relapses or remissions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Investigations and findings for multiple sclerosis

A

MRI to visualise lesions
Oligoclonal bands in CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Presentation of optic neuritis

A

Central scotoma
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Management of multiple sclerosis

A

MDT input
Patient education
DMARDs
Biologics
Methylprednisolone for relapses
Tolterodine/oxybutynin for incontinence
Amitriptyline for neuropathic pain
Baclofen for spasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Types of motor neurone disease

A

Amyotrophic lateral sclerosis
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Features of amyotrophic lateral sclerosis

A

LMN signs in arms
UMN signs in legs
Family history - Ch21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Features of primary lateral sclerosis

A

UMN signs only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Features of progressive muscular atrophy

A

LMN signs only
Distal muscles affected before proximal
Carries best prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Features of progressive bulbar palsy

A

Loss of function of brainstem motor nuclei
Palsy of tongue and facial muscles
Progressive swallowing difficulty
Progressive talking difficulty
Worst prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

LMN signs

A

Muscle wasting
Reduced tone
Fasciculation
Hyporeflexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

UMN signs

A

Hypertonia
Spasticity
Brisk reflexes
Upgoing plantar response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Presentation of motor neurone disease

A

Late middle age (usually)
Insidious onset
Progressive weakness
Increased fatigue when exercises
Clumsiness
Trips and falls
Slurred speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Management of motor neurone disease

A

Irreversible
Riluzole can slow progression & extend survival
NIV
End of life care planning
Advanced directives
MDT involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Pathophysiology of Parkinson’s disease

A

Progressive reduction of dopamine in the basal ganglia due to reduced production by substantia nigra, leading to disorders of movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Classic triad of features on Parkinson’s disease

A

Resting tremor
Rigidity
Bradykinesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Signs and symptoms of Parkinson’s disease

A

Unilateral 4-6hz pill rolling tremor
Cogwheel rigidity
Micrographia
Shuffling gait
Facial masking
Difficulty turning
Depression
Sleep disturbance
Anosmia
Cognitive impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Features of Parkinsons tremor

A

Asymmetrical
4-6 hertz
Worse at rest
Improves with intentional movement
No change with alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Feature’s of benign essential tremor

A

Symmetrical
5-8 hertz
Improves at rest
Worse with intentional movement
Improves with alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Parkinson’s plus syndromes

A

Multiple system atrophy
Dementia with Lewy bodies
Progressive supranuclear palsy
Corticobasal degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Management of Parkinson’s disease

A

Co-careldopa’
Entacapone
Cabergoline
Bromocryptine
Selegiline
Rasagiline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Management of benign essential tremor

A

Propranolol
Primidone

61
Q

Types of seizure

A

Generalised tonic-clonic seizures
Focal seizures
Absence seizures
Atonic seizures
Myoclonic seizures
Infantile spasms

62
Q

Features of tonic clonic seizures

A

Loss of consciousness
Muscle tensing
Muscle jerking
Tongue biting
Incontinence
Groaning
Irregular breathing

63
Q

Management of tonic-clonic seizures

A

Sodium valproate
Lamotrigine/carbamazepine

64
Q

Features of temporal lobe seizures

A

Automatisms
Deja vu
Emotional disturbance
Auditory/gustatory/olfactory hallucinations

65
Q

Features of frontal lobe seizures

A

Jacksonian march
Localised muscle jerking
Dysphasia
Todd’s palsy

66
Q

Features of parietal lobe seizures

A

Tingling
Numbness
Motor symptoms

67
Q

Features of occipital lobe seizures

A

Spots & lines in visual field

68
Q

Management of focal seizures

A

Carbamazepine/lamotrigine
Sodium valproate/levetiracetam

69
Q

Features of absence seizures

A

Typically occur in children
Blankness
Staring into space
Very short

70
Q

Management of absence seizures

A

Sodium valproate/ethosuxamide

71
Q

Features of atonic seizures

A

“drop attacks”
Brief lapses in muscle tone
Usually last less than 3 minutes
Associated with Lennox-Gastaut syndrome

72
Q

Management of atonic seizures

A

Sodium valproate
Lamotrigine

73
Q

Features of myoclonic seizures

A

Sudden brief muscle contractions
Usually conscious
Typical of juvenile myoclonic epilepsy

74
Q

Management of myoclonic seizures

A

Sodium valproate
Lamotrigine/levetiracetam/topiramate

75
Q

Features of infantile spasms (west syndrome)

A

Clusters of full body spasms
1/3 die by age 25

76
Q

Management of West syndrome

A

Prednisolone
Vigabitran

77
Q

Notable side effects of sodium valproate

A

Teratogenic
Liver damage
Hair loss
Tremor

78
Q

Notable side effects of Carbamazepine

A

Agranulocytosis
Aplastic anaemia
P450 inducer so many drug interactions

79
Q

Notable side effects of Phenytoin

A

Folate & vitamin D deficiency
Megaloblastic anaemia
Osteomalacia

80
Q

Notable side effects of ethosuximide

A

Night terrors
Rashes

81
Q

Notable side effects of Lamotrigine

A

SJS
DRESS syndrome
Leukopenia

82
Q

Management of status epilepticus

A

Buccal midazolam / rectal diazepam
IV lorazepam 4mg (repeat after 10 minutes)
IV phenobarbital

83
Q

Branches of the facial nerve

A

Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical

84
Q

Functions of the facial nerve

A

Muscles of facial expression, stapedius, posterior digastric, stylohyoid and platysma muscles
Carries taste from anterior 2/3 of tongue
Parasympathetic supply to submandibular and sublingual salivary glands and lacrimal gland

85
Q

Which motor neurone lesion is forehead sparing

A

UMN

86
Q

What type of motor neuron is involved in Bell’s palsy

A

LMN

87
Q

Management of Bell’s palsy

A

Prednisolone for 20 days
Lubricating eye drops

88
Q

What causes Ramsey-Hunt syndrome

A

Varicella-zoster virus

89
Q

Features of Ramsey-Hunt syndrome

A

Unilateral LMN facial palsy
Painful & tender vesicular rash affected ear canal, pinna and around the ear

90
Q

Management of Ramsey-Hunt syndrome

A

Prednisolone
Aciclovir
Lubricating eye drops

91
Q

Causes of LMN facial nerve palsy

A

Otitis media
HIV
Lyme disease
Diabetes
Multiple Sclerosis
Guillain-Barre syndrome
Acoustic neuroma
Cholesteatoma
Nerve trauma
Basal skull fracture

92
Q

Causes of raised ICP

A

Brain tumours
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscess
Infection

93
Q

Red flags for headaches

A

Constant
Nocturnal
Worse on waking
Worse on coughing, straining or bending forward
Vomiting

94
Q

Presenting features of raised ICP

A

Altered mental state
Visual field defects
Seizures
Unilateral ptosis
3rd & 6th nerve palsies
Papilloedema

95
Q

Fundoscopic changes in papilloedema

A

Blurred optic disc margin
Elevated optic disc
Loss of venous pulsation
Engorged retinal veins
Haemorrhages around optic disc
Paton’s lines

96
Q

Types of brain tumour

A

Gliomas
Meningiomas
Pituitary tumour
Acoustic neuroma
Metastases

97
Q

Which cancers commonly metastasise to the brain

A

Lung
Breast
Renal cell carcinoma
Melanoma

98
Q

Types of glioma

A

Astrocytoma
Oligodendroglioma
Ependymoma

99
Q

Most malignant type of brain tumour

A

Glioblastoma

100
Q

Benign brain tumour

A

Meningioma

101
Q

Symptoms of pituitary tumours

A

Bitemporal hemianopia
Acromegaly
Hyperprolactinaemia
Cushing’s disease
Thyrotoxicosis

102
Q

Symptoms of acoustic neuroma

A

Hearing loss
Tinnitus
Balance problems
Facial nerve palsy

103
Q

What disorder is associated with bilateral acoustic neuromas

A

Neurofibromatosis type 2

104
Q

Treatment of pituitary tumours

A

Trans-sphenoidal surgery
Radiotherapy
Bromocriptine
Ocreotide

105
Q

Inheritance pattern of Huntington’s chorea

A

Autosomal dominant

106
Q

Type of mutation causing Huntington’s chorea

A

Trinucleotide repeat on Ch4

107
Q

Typical age of onset for Huntington’s chorea

A

30-50 yrs

108
Q

Presentation of Huntington’s chorea

A

Chorea
Eye movement disorders
Speech difficulties
Swallowing difficulties

109
Q

Management of Huntington’s chorea

A

No treatment to slow/stop disease
MDT involvement
SALT
Genetic counselling
Advanced directives
End of life care planning

110
Q

Which type of tumour has a strong link with Myasthenia Gravis

A

Thymoma

111
Q

Pathophysiology of Myasthenia Gravis

A

Acetylcholine receptor antibodies are produced which bind to postsynaptic neuromuscular junction receptors, blocking ACh from stimulating these receptors to trigger muscular contraction. Less ACh transmission gives less muscle contraction

112
Q

Presentation of Myasthenia Gravis

A

Proximal muscles & small muscles of head and neck most affected
Diplopia
Ptosis
Weakness in facial movement
Swallowing difficulty
Jaw fatigue when chewing
Slurred speech
Progressive weakness with repetitive movements

113
Q

Management of Myasthenia Gravis

A

Pyridostigmine/neostigmine
Prednisolone
Thymectomy if thymoma
Rituximab

114
Q

Important bedside test in Myasthenia Gravis

A

Spirometry for FVC

115
Q

Management of Myasthenic crisis

A

IV immunoglobulins
Plasma exchange

116
Q

Which type of cancer is associated with Lambert-Eaton myasthenic syndrome

A

Small cell lung cancer

117
Q

Presentation of Lambert-Eaton Myasthenic Syndrome

A

Insidious onset
Proximal leg muscle weakness
Diplopia
Ptosis
Dysphagia
Reduced tendon reflexes

118
Q

Management of lambert-eaton myasthenic syndrome

A

Investigate for small cell lung cancer
Amifampridine
Prednisolone
IV immunoglobulins
Plasmapheresis

119
Q

Inheritance pattern of Charcot-Marie-Tooth

A

Autosomal dominant

120
Q

Usual age of onset of Charcot-marie-tooth

A

Before age 10

121
Q

Classical features of Charcot-Marie-Tooth

A

High foot arches
Distal muscle wasting
Weakness of lower legs
Loss of ankle dorsiflexion
Weakness in hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

122
Q

Management of Charcot-Marie-Tooth

A

MDT involvement
Physiotherapy
Orthopaedic surgeons for joint deformity
Occupational therapy

123
Q

What infections are particularly associated with Guillian Barre Syndrome

A

Campylobacter jejuni
Cytomegalovirus
Epstein-Barr virus

124
Q

Presentation of Guillain-Barre Syndrome

A

Symmetrical ascending weakness
Reduced reflexes
Peripheral loss of sensation
Neuropathic pain
History of preceding infection

125
Q

Diagnostic investigations for suspected Guillian-Barre Syndrome

A

Nerve conduction studies
CSF - raised protein

126
Q

Management of Guillian-Barre Syndrome

A

IV immunoglobulins
Plasma exchange
Supportive care
VTE prophylaxis

127
Q

Prognosis of Guillian-Barre Syndrome

A

80% full recovery
15% with some persisting disability

128
Q

Inheritance pattern of Neurofibromatosis Type 1

A

Autosomal dominant

129
Q

Criteria for Neurofibromatosis Type 1

A

2 of:
- Cafe-au-lait spots
- Relative with NF1
- Axillary/inguinal freckles
- Bony dysplasia
- Iris hamartomas
- Neurofibromas
- Glioma of optic nerve

130
Q

Complications of neurofibromatosis type 1

A

Migraines
Epilepsy
Renal artery stenosis
Hypertension
Learning difficulties
Scoliosis
Vision loss
Gastrointestinal stromal tumour
Brain tumours
Leukaemia

131
Q

Inheritance pattern of neurofibromatosis type 2

A

Autosomal dominant

132
Q

Which tumour types are most associated with neurofibromatosis type 2

A

Acoustic neuromas

133
Q

Most common type of neurofibromatosis

A

Type 1

134
Q

Characteristic feature of Tuberous Sclerosis

A

Hamartomas

135
Q

Which genes can be mutated in Tuberous Sclerosis

A

TSC1 on Ch9
TSC2 on Ch16

136
Q

Skin signs in Tuberous Sclerosis

A

Ash leaf spots
Shagreen patches
Angiofibromas
Subungal fibromatoma
Cafe-au-lait spots
Poliosis

137
Q

Non-skin features in Tuberous Sclerosis

A

Epilepsy
Developmental delay
Rhabdomyomas
Gliomas
Polycystic kidneys
Retinal hamartomas

138
Q

Management of Tuberous Sclerosis

A

Supportive care
Monitor for & treat complications

139
Q

Differentials for headache presentation

A

Tension headache
Migraine
Cluster headache
Sinusitis
Giant cell arteritis
Glaucoma
Intracranial haemorrhage
Analgesic headache
Raised ICP
Meningitis
Encephalitis
Cervical spondylosis

140
Q

Headache red flags

A

Photophobia
Neck stiffness
New neurological symptoms
Visual disturbance
Worse on coughing or straining
Pain disturbs sleep
Vomiting
History of trauma
Pregnancy
Sudden onset occipital headache

141
Q

Causes of tension headache

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

142
Q

Migraine features

A

Moderate-severe intensity
Pounding/throbbing nature
Unilateral
Photophobia
Phonophobia
Aura
Nausea & vomiting

143
Q

Features of hemiplegic migraine

A

Typical migraine symptoms
Hemiplegia
Ataxia
Change in consciousness

144
Q

Common migraine triggers

A

Stress
Bright lights
Strong smells
Caffeine
Chocolate
Dehydration
Menstruation
Abnormal sleep patterns

145
Q

Actions of triptans in migraine

A

Serotonin receptor agonists
Vasoconstriction
Inhibit activation of pain receptors
Reduce CNS neuronal activity

146
Q

Migraine prophylaxis

A

Propranolol
Topiramate
Amitriptyline

147
Q

Symptoms of cluster headache

A

Red, swollen, watery eye
Pupil constriction
Ptosis
Nasal discharge
Facial sweating

148
Q

Acute management of cluster headache

A

Triptans
High flow 100% oxygen

149
Q

Cluster headache prophylaxis

A

Verapamil
Lithium
Prednisolone

Special Senses (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions