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Phase 1 Exam > Neuro > Flashcards

Neuro Flashcards

1
Q

Definition of trigeminal neuralgia

A
  • Facial nerve pain that occurs in one or more of the divisions of the trigeminal nerve - maxillary, opthalmic or mandibular
  • Characterised by sharp intense stabbing pain lasting up to 2 minutes and/or constant component of facial pain without neurological pain.
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2
Q

Aetiology of trigeminal neuralgia

A
  • Compression, demyelination or brain stem lesion
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3
Q

Risk factors of trigeminal neuralgia

A
  • Smoking, MS, increasing age, women and hypertension
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4
Q

Presentation of trigeminal neuralgia

A
  • Knife like pain
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5
Q

Investigations of trigeminal neuralgia

A
  • Clinical picture
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6
Q

Management of trigeminal neuralgia

A
  • Carbamazepine

- Gabapentin

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7
Q

Definition of cluster headache

A
  • Painful, unilateral headache

- Men, common and between 20 to 50.

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8
Q

Aetiology and risk factors of cluster headache

A
  • Unknown but risk factors include male, family history, head injury, smoking and heavy drinking
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9
Q

Presentation of cluster headache

A
  • Pain around the eye or temple, extruciating pain.
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10
Q

Investigations of cluster headache

A
  • Rule out of red flags and use of MRI/CT
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11
Q

Management of cluster headache

A
  • Acute attacks with triptans.
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12
Q

Definition of migraine

A
  • Recurrent headaches with visual and GI disturbances
  • Chronic and usually occur in patients with genetic predisposition
  • Women
  • Common
  • Mostly commonly before the age of 40
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13
Q

Aetiology of migraine

A
  • No known cause but due to genetic and abnormal brain activity
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14
Q

Presentation of migraine

A
  • Triggers - CHOCOLATE
  • Unilateral throbbing or pulsative headache with moderate to severe pain, usually lasting around 4 to 72 hours.
  • With or without aura including visual, sensory, motor or speech that lasts 5 to 60 minutes and is reversible
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15
Q

Investigations of migraine

A
  • Clinical
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16
Q

Management of migraine

A
  • Acute attacks = triptans with NSAIDs/paracetomol
  • Prophylaxis = beta blockers or anti epileptic medications
  • Remove triggers - ie OCP
  • Hot/cold compresses, sleep, dark rooms or acupuncture
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17
Q

Definition of tension type headaches

A
  • Chronic or episodic

- Most common type of headache and rarely disabling

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18
Q

Aetiology and risk factors of tension type headaches

A
  • Usually triggered by emotion or stress

- Females, 20 - 40, fatigue or analgesic overuse

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19
Q

Presentation of tension type headaches

A
  • Mild to moderate ‘band like’ headache
  • Bilateral and non pulsitile
  • Can be with or without scalp muscle tenderness
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20
Q

Investigations of tension type headaches

A
  • Clinical picture
  • Can classify episodic or chronic - less than 15 days a month is considered episodic where as more than 15 days a month for 3 month is chronic
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21
Q

Management of tension type headaches

A
  • Over the counter analgesics such as NSAIDs or paracetomol

- Accupuncture?

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22
Q

Definition of meningitis

A
  • Inflammation of the meninges

- Epidemiology varies due to widespread vaccination programme.

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23
Q

Aetiology of meningitis

A
  • Bacteria: N.meningitidis, S. penumonia
  • Viral: Enterovirus
  • Chronic: Myobacterium tuberculousis, syphilis
  • Neonates usually Listeria
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24
Q

Presentation of meningitis

A
  • Classically acute bacterial meningitis can present with fever, headache, neck stiffness - usually occurs over minutes and hours.
  • Viral meningitis - self limiting usually around 4 to 10 days.
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25
Q

Investigations of meningitis

A
  • Bacterial meningitis is a medical emergency.
  • Glasgow Coma Score
  • Blood cultures - as soon as possible
  • Lumbar puncture
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26
Q

Management of meningitis

A
  • Broad spectrum antibiotics such as Certifixone
  • Steroids such as IV dexamethasone
  • Contact tracing
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27
Q

Definition of ataxia

A
  • A neurological syndrome characterised by clumsy and uncoordinated movement of the limbs, trunk and cranial muscles.
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28
Q

Presentation of ataxia or cerebellar disease

A
  • It can affect any motor function - this includes slurring speech, difficulty swallowing, blurred vision, clumsiness due to loss of precision of movement, tremor, unsteadiness when walking, falls and cognitive movement
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29
Q

Investigations of ataxia or cerebellar disease

A
  • MRI
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30
Q

Definition of muscular dystrophies

A
  • Progressive, generalised disease of muscle.
  • Most often caused by a defective or specifically absent glycoprotein (Dystrophin)
  • Characterised by ongoing degeneration and regeneration of muscle fibres
  • Examples include Duchenne and Becker’s: X linked, most common males, rarely females but can be carriers
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31
Q

Presentation of muscular dystrophies

A
  • Duchenne presents in childhood usually around 18 month, with proximal muscle weakness.
  • The patient has hip and knee flexor and ankle planter flexers being stronger than the hip and knee extensors and ankle dorsiflexors.
  • Calf hypertrophy
  • Diminished muscle tone and deep tendon reflexes
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32
Q

Investigations of muscular dystrophies

A
  • Increased serum creatine kinase levels
  • Muscle biopsies
  • Genetics - Xp21
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33
Q

Management of muscular dystrophies

A
  • No cure

- Steroids delay progression

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34
Q

Definition of myasthenia gravis

A
  • Autoimmune disorder of neuromuscular junction transmission that is characterised by fatiguability and weakness of the proximal limb, bulbar and ocular muscles.
  • Most commonly seen in patients in their 30s or 60s and twice as likely in men than women.
35
Q

Aetiology of myasthenia gravis

A
  • Due to autoimmune antibodies in the post neurosynaptic junctions replacing the acetyl receptors leading to receptor loss.
36
Q

Presentation of myasthenia gravis

A
  • Weakness and fatiguiability in the proximal limb, ocular and bulbar muscle due to sustained or repeated activity that is relieved by rest.
  • Most commonly seen in ocular bulbar
37
Q

Investigations of myasthenia gravis

A
  • Anti AchR

- Nerve stimulation

38
Q

Management of myasthenia gravis

A
  • Anticholinestrase (mide)

- Immunosuppressentas

39
Q

Definition of encephalitis

A
  • Inflammation of the brain parenchyma

- Peak incidence is under 1 and over 65

40
Q

Aetiology of encephalitis

A
  • Most commonly viral

- HSV, VSV, EBV, MMR

41
Q

Presentation of encephalitis

A
  • Flu like illness in hrs or days prior to presenting with an altered GCS, fever, memory loss and seizures.
  • Serious presentations include focal signs, seizures and coma
42
Q

Investigations of encephalitis

A
  • MRI with/without EEG
  • Lumbar puncture with lymphocytic CSF and viral PCR
  • Check for HIV
43
Q

Management of encephalitis

A
  • Supportive management

- HSV or VSV can treat with 14 to 21 acyclovir.

44
Q

Definition of Parkinson’s Disease

A
  • Neurodegenrative disease developing predominatently in older people
  • Clinical features result from the loss dopamine producing cells with the substantia nigra
  • Usually presents around the age of 65
  • More common in men
45
Q

Aetiology of Parkinson’s Disease

A
  • Unknown
46
Q

Presentation of Parkinson’s Disease

A
  • Resting trauma, rigidity and bradykinesia developing over months or years with postural changes.
  • Usually unilateral initially with progressive development to bilateral
47
Q

Investigations of Parkinson’s Disease

A
  • Clinical diagnosis
48
Q

Management of Parkinson’s Disease

A
  • No cure but symptomatic treatment, all about compensating for the loss of dopamine within the brain
  • Levodopa, dopoamine agonist and monoaminoxidase b inhibitors.
49
Q

How does the brain deal with raised intracranial pressure and what are the consequences?

A
  • As volume and capacity within the brain increases, this leads to raised intracranial pressure. Over time the brain is able to compensate for this but eventually the pressure begins to rise so exponentially that is can leading to structures impacting other structures leading to symptoms and damage - ultimately the displacement of tissue.
50
Q

Definition of dementia

A
  • Clinical syndrome with multiple causes
  • Defined as the progressive acquired loss of higher mental function.
  • Most common = alzheminers, which is the accumulation of beta amyloid peptide within the brain leading to progressive neurological damage, neurofibirarly tangles and amyloid plaques.
  • Vascular: loss of blood to the brain, usually post multiple infarct
51
Q

Time course of dementia

A
  • Alzheimer’s - gradual onset with progressive neurodegeneration
  • Vascular - much more rapid onset with step wise deterioration so the patient has periods of stability.
52
Q

Presentation of dementia

A
  • Alzehimers is about memory loss, difficulty carrying out activities or events that require planning, confusion in terms of memory of places, famililar people and times, eventually loss of ability to carry out every day activites and changes in personality and mood.
  • Vascular: presents like a stroke
53
Q

Investigations of dementia

A
  • MMSE
  • MRI/CT
  • Bloods
  • PET Scan/Tau imaging
54
Q

Management of dementia

A
  • No cure, about symptoms management
  • Acetylholinesteraise inhibitors initially and then if these fail to work then Mematine
  • Vascular is about managing the predisposing factors.
55
Q

How are brain tumours classified?

A
  • Depending on the region of the brain that they’re found in.
  • Tumours of the meninges = meningiomas
  • Tumours of the glial cells = gliomas
  • Including cells such as oligodendricties and astrocytic cells.
  • In paeds, tumours of the germ cell line and Stellar region.
56
Q

What cancers can cause secondary or metastasis brain tumours?

A
  • Breast, lung, colorectal, testicular, renal cell and malignant melanomas
  • Breast and lung are most common
57
Q

How are glioma cells classified?

A
  • WHO classification system
  • Grade I and II - low grade, slow growing tumour, usually presents around the age of 35.
  • Grade III and IV - high grade, usually present between 45 and 60
58
Q

Presentation of brain tumours

A
  • Classically headaches, seizures, focal and non focal symptoms.
  • Headache can be due to raised ICP - patient is woken with a severe headache, its worse in the morning and when lying down, associated with nausea and vomiting and made worse by coughing, sneezing and dizziness.
  • Papillodema
  • Non focal symptoms include personality changes, memory disturbances and confusion.
59
Q

Investigations of brain tumours

A
  • MRI/CT

- Biopsy

60
Q

Management of brain tumours

A
  • Steroids, resection radiotherapy
61
Q

How are brain tumours classified?

A
  • Type (Blunt or non missile), distribution (focal or dissue) and their time course (primary or secondary)
62
Q

Definition of epilepsy/seizures

A
  • Seizures = convulsion or transient abnormal events caused by paroxysmal discharge of cerebral neurons.
  • Epilepsy = continued tendency to have seizures
  • Under the age of 20 or over the age of 60
63
Q

Aetiology of epilepsy/seizures

A
  • Flashing lights/flickering tv

- Cerebrovascular disease, tumours, alcohol, post head injury

64
Q

Pathophysiology of epilepsy/seizures

A
  • About changes in membrane potential that lead to hypersensitivity or over activity of the cells.
  • Focal = one part of the brain - usually associated with underlying health conditions.
  • Generalised = all of the brain - bilateral presentation and associated with loss of consciousness/awareness
65
Q

Presentation of epilepsy/seizures

A
  • Temporary confusion, storing spell, uncontrolled jerking of arms and legs, loss of consiousness/awareness, cognitive or emotional symptoms
66
Q

Investigations of epliepsy/seizures

A
  • EEG, neurological examinations, bloods, lumbar puncture, CT/MRI/PET
67
Q

Management of epilepsy/seizures

A
  • Anticonvulsants = carbamezepine for focal and sodium valproate for generalised
68
Q

Defintion of MS

A
  • Chronic disabling autoimmune condition thats due to multiple plaques found in the CNS.
  • Usually women between the ages of 20 and 40
69
Q

Aetiology of MS

A
  • Inflammation of the white matter in the brain and spinal cord mediated B cells and CD4 T cells.
  • Risk factors include autoimmune diseases, EBV, vit D deficiency, northern latitude.
70
Q

Pathogenesis of MS

A
  • Inflammation, demyelination and axonal loss.
71
Q

Presentation of MS

A
  • Typically a young adult with 2 or more distinct episodes of CNS dysfunction followed by a period of remission of the signs and symptoms within weeks - due to inflammatory oedema and partial remyelination.
  • Optic neuropathy = blurred vision and unilateral eye pain.
  • Brainstem demyelination = dysphagia, dysarthria and facial weakness
  • Spinal cord = pins and needles and numbness
  • 4 patterns = repalpsing/remitting, primary progressive, secondary progressive or progressive relapsing/remitting
72
Q

Investigations of MS

A
  • MRI
  • CSF
  • Electrophyiscal
73
Q

Management of MS

A
  • Steroids
  • Interferon B
  • Glatirsmar agents
74
Q

Definition of ischaemic stroke

A
  • A rapid onset of neurological deficit that last for more than 24 hours due to vascular lesions that lead to infarction of the central nervous tissue. A complete stroke is when the neurological deficit is at the maximum, usually within 6 hours.
  • TIA is a transient ischaemic attack - transient ischaemic dysfunction that leads to deficit within the frontal lobe, retinal lesion or brain stem for less than 24 hours.
75
Q

Aetiology of ischaemic stroke

A
  • Is a syndrome that occur due to reduced blood flow to an area of the brain.
  • TOAST classification
76
Q

Risk factors of ischaemic stroke

A
  • atheroma, obesity, AF, OCP, cocaine
77
Q

Presentation of ischaemic stroke

A
  1. ACA = leg, hip and trunk symptoms including leg weakness and sensory loss, ataxia and incontinence.
  2. MCA = most devastating, includes internal capsule. Presents with contralateral arm and leg weakness and sensory loss, aphasia, heminopia, dysphagia and facial droop.
  3. PCA = visual issues
    - Posterior circulation affects the cerebellum and posterior cranial fossa.
78
Q

Investigations of ischaemic stroke

A
  • CT to distinguish between ischaemic or haemographic
  • MRI
  • ECG
79
Q

Management of ischaemic stroke

A
  • Thromboyltic treatment
  • Aspirin 300mg
  • Risk assessment - statin, platelet therapy, statins, BP meds.
80
Q

What is motor neurone disorder?

A
  • A condition affecting the brain and nerves causing weakness that gets worse overtime.
81
Q

Definition of motor neurone disease

A
  • Rentless and unexplained destruction of upper motor neurones and anterior horn cells in the brain and the spinal cord.
  • Middle age, men
  • Mostly sporadic
  • Death within 3 years.
82
Q

Presentation of motor neurone disease

A
  • Progressive muscular atrophy - weakness, wasting and fasciculation in hands and arms.
  • Tetraparesis and paraperesis
  • Progressive bulbar and pseudobulbar pasly - dysarthria, dysphagia with wasting and fasciculation of the tongue.
83
Q

Investigation and management of motor neurone disease

A
  • Clinical

- Sodium channel block - Rizole

Phase 1 Exam (25 decks)

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