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Neuro Flashcards

1
Q

What is the presentation of intracranial bleeds?

A

Sudden onset headache

Seizures
weakness
Vomiting
Reduced consciousness

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2
Q

What are subdural haemorrhages?

A

Occur between dura mater and arachnoid mater

CT: crescent shape and not limited by suture lines

More common in elderly or alcoholic patients

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3
Q

What are extradural haemorrhages?

A

Rupture of middle meningeal artery

CT: bi-convex shape and limited by suture lines

E.g. young patient with trauma and ongoing headache, period of improvement then decline

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4
Q

What is a subarachnoid haemorrhage?

A

Bleeding into the subarachnoid space where CSF is due to ruptured cerebral aneurysm

Thunderclap headache

Associated with cocaine and sickle cell anaemia

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5
Q

What is the management of an intracranial bleed?

A

Immediate CT head to establish diagnosis

Check FBC and clotting

Admit to specialist stroke unit

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6
Q

What are the tracts affected and presentation of Brown-Sequard syndrome (spinal cord hemisection)

A

Tracts:

  1. Lateral corticospinal tract
  2. dorsal columns
  3. Lateral spinothalamic tract

Features:

  1. ipsilateral spastic paresis below lesion
  2. ipsilateral loss of proprioception and vibration sensation
  3. Contralateral loss of pain and temp sensation
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7
Q

What are the tracts affected and presentation of subacute degeneration of the spinal cord (Vit B12 and E deficiency) and Friedrich’s ataxia?

A

Tracts:

  1. Lateral corticospinal tracts
  2. Dorsal columns
  3. Spinocerebellar tracts

Features:

  1. Bilateral spastic paresis
  2. Bilateral loss of proprioception and vibration sensation
  3. Bilateral limb ataxia

Friedrich’s ataxia also has intention tremor

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8
Q

What are the tracts affected and presentation of anterior spinal artery occlusion

A
  1. Lateral corticospinal tracts
  2. Lateral spinothalamic tracts

Features:

  1. Bilateral spastic paresis
  2. Bilateral loss of pain and temp sensation
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9
Q

What are the tracts affected and presentation of syringomyelia

A

Tracts:

  1. Ventral horns
  2. Lateral spinothalamic tract

Features:

  1. Flacid paresis (intrinsic hand muscles)
  2. Loss of pain and temp sensation
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10
Q

Define TIA

A

transient neurological dysfunction secondary to ischaemia without infarction.

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11
Q

What is the presentation of a stroke?

A 
Asymmetrical:
Sudden weakness of limbs
Sudden facial weakness
Sudden onset dysphasia
Sudden onset visual or sensory loss
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12
Q

What is the management of stroke?

A

Admit patient to specialist stroke centre
Exclude hypoglycaemia
Immediate CT brain
Aspirin 300mg and continue for 2 weeks

Thrombolysis with alteplase

Thrombectomy (before 24hr)

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13
Q

What is the management of TIA?

A

Aspirin 300mg daily
Start secondary prevention measures
Seen within 24hr by stroke specialist

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14
Q

What is the gold standard imaging in stroke?

A

Diffusion-weighted MRI

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15
Q

What is the secondary prevention of stroke?

A

Clopidogrel 75mg/day
Atorvastatin 80mg but not started immediately
Carotid endarterectomy or stenting
Treat modifiable risk factors

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16
Q

What is vasovagal episodes?

A

Caused by a problem with the autonomic nervous system. When the vagus nerve receives a strong stimulation, it can stimulate the parasympathetic nervous system. This leads to hypoperfusion of the brain tissue causing patient to faint,

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17
Q

What are the causes of vasovagal syncope?

A

Primary:
Dehydration
Missed meals
Extended standing in a warm environment

Secondary:
Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
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18
Q

What is the difference between syncope and seizures?

A

Syncope:
Return of consciousness shortly after falling
No prolonged post-ictal period

Seizures:
Return of consciousness lasts more than 5 minutes
Prolonged post-ictal period

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19
Q

Describe the presentation of bell’s palsy?

A

Unilateral lower motor neurone facial nerve palsy:

  • forehead affected
  • drooping of eyelid
  • loss of nasolabial fold
  • loss of lacrimation
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20
Q

What is the prognosis of Bell’s palsy?

A

Majority of patients fully recover over several weeks but may take upto 12 months

1/3 are left with residual weakness

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21
Q

What is the management of Bell’s palsy?

A

If patient presents within 72 hours, consider prednisolone as either:
50mg for 10 days
60mg for 5 days followed by 5-day reducing regime of 10mg a day

Lubricating eye drops and tape

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22
Q

What is Ramsay-Hunt syndrome? Give the cause, presentation and treatment

A

Caused by varicella zoster virus.

Presents with unilateral lower motor neurone facial nerve palsy.

Painful vesicular rash in the ear canal, pinna and around the ear. Rash can extend to anterior 2/3 of tongue and hard palate

Treatment should be within 72 hours:
Prednisolone, aciclovir and lubricating eye drops.

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23
Q

What is cerebral palsy?

A

Permanent neurological problems resulting from damage to the brain at the time of birth. Not progressive.

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24
Q

What are the causes of cerebral palsy?

A

Antenatal:
Maternal infections
Trauma during pregnancy

Perinatal:
Birth asphyxia
Pre-term birth

Postnatal:
Meningitis
Severe neonatal jaundice
Head injury

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25
Q

What are the types of cerebral palsy?

A

Spastic (Pyramidal)
Dyskinetic (Extrapiramidal)
Ataxic
Mixed

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26
Q

What is the signs and symptoms of cerebral palsy?

A 
Failure to meet milestones
Increased or decreased tone
Hand preference below 18mths
Problems with coordination, speech  and walking
Feeding or swallowing problems
Learning difficulties
Upper motor neurone llesion signs
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27
Q

What is the difference between upper motor neurone and lower motor neurone lesion presentations?

A 
UPN:
Muscle bulk preserved
Hypretonia
Slightly reduced power
Brisk reflexes
LMN:
Reduced muscle bulk with fasciculation
Hypotonia
Dramatically reduced power
Reduced reflexes
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28
Q

What is the management of cerebral palsy?

A

Cannot be cured

Physiotherapy and other MDT
Muscle relaxants
Anti-epileptic
Glycopyrronium bromide

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29
Q

What are the symptoms of cluster headaches?

A 
Red, swollen and watering eye
Pupil constriction
Eyelid drooping
Nasal discharge
Facial sweating
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30
Q

What are the treatment options for cluster headaches?

A

ACUTE:
Triptans (e.g. sumatriptan 6mg IM)
High flow oxygen for 15-20mins

PROPHYLAXIS:
Verapamil
Lithium
Prednisolone (2-3wks)

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31
Q

What is multiple sclerosis?

A

Chronic and progressive condition that involves demyelination of the myelinated neurones in the CNS. Caused by an inflammatory process involving the activation of immune cells against the myelin.

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32
Q

What is the pathophysiology behind multiple sclerosis?

A

Schwann cells in PNS
Oligodendrocytes in CNS

MS typically only affects CNS (Oligodendrocytes)

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33
Q

What are the causes of Multiple sclerosis?

A 
Multiple genes
EBV
Low vitamin D
Smoking
Obesity
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34
Q

What are the signs and symptoms of multiple sclerosis?

A 
Optic neuritis
Eye movement abnormalities 
Focal weakness
Focal sensory symptoms 
Ataxia
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35
Q

What is relapsing-remitting MS?

A

Most common pattern at initial diagnosis.

Active: new symptoms are developing
Not active: no new symptoms
Worsening: overall worsening of disability over time
Not worsening: no worsening over time

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36
Q

What is secondary progressive MS?

A

Where there was relapsing-remitting disease at first but now there is progressive worsening of symptoms with incomplete remissions

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37
Q

What is primary progressive MS>

A

Where there is a worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions

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38
Q

What is the diagnosis of MS?

A

Made by neurologist based on clinical picture and symptoms suggesting lesions that change location over time.

Symptoms have to be progressive over 1 year period

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39
Q

What are the investigations in MS?

A

MRI scan with contrast
LP shows oligoclonal bands in CSF

CT for tinitus and other hearing problems

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40
Q

What is the presentation of optic neuritis?

A

Unilateral reduced vision developing over hours to days

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

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41
Q

What is the treatment for MS?

A

MDT

Methylprednisolone for relapses 500mg orally daily for 5 days

Symptomatic treatments

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42
Q

What is motor neurone disease?

A 
Umbrella term for progressive, ultimately fatal condition where motor neurones stop functioning but sensory neurones are spared. E.g:
ALS
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis
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43
Q

What is the presentation of motor neurone disease?

A 
Late middle aged patient
Insidious progressive weakness of muscles
Weakness first noticed in upper limbs
Increased fatigue when exercising 
Clumsiness
Dysarthria
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44
Q

What is the diagnosis of motor neurone disease?

A

Clinical presentation and excluding other conditions

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45
Q

What is the management of motor neurone disease?

A

Riluzole can slow progression in ALS

Edaravone (only in US)

Non invasive ventilation

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46
Q

What is parkinson’s disease?

A

Progressive reduction of dopamine in the basal ganglia leading to disorders of movements. Asymmetrical symptoms with one side affected more than the other.

Triad:
Resting tremor
Rigidity
Bradyinesia

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47
Q

What is the diagnosis of Parkinson’s disease?

A

Clinically based on symptoms and examinations by a speciailst

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48
Q

What is the management of Parkinson’s disease?

A

No cure

Levodopa and bensarazide
or Levodopa and carbidopa

Dopamine agonists e.g. bromocryptine, pergolide and cabergoline

Monamine oxidase B-inhibitor. E.g. selegiline and rasagiline

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49
Q

What are the side effects of dopamine?

A

Dyskinesias. E.g.:

Dystonia, chorea, athetosis

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50
Q

What are the treatments for neuropathic pain?

A
  1. Amitriptyline
  2. Duloxetine
  3. Gabapentin
  4. Pregabalin
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51
Q

What is the treatment for trigeminal neuralgia?

A

Carbamazepine

If that doesn’t work then refer to specialist

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52
Q

Which cancers metastasise to the brain?

A

Lung
Breast
Renal cell carcinoma
Melanoma

53
Q

What are the Gliomas and the different types?

A

Tumours of the glial cells

Astrocytoma (most common)
Oligodendroglioma
Ependymoma

54
Q

What are meningiomas?

A

Tumours growing from the cells of the meninges. Usually benign however can lead to raised ICP

55
Q

What are pituitary tumours?

A

Tend to be benign but can grow large enough to press on optic chiasm causing bitemporal hemianopia.

Can also cause hypopituitarism leading to:
acromegaly
hyperprolactinaemia
cushing's disease
thyrotoxicosis
56
Q

What is an acoustic neuroma?

A

Also known as vestibular schwannoma

Tumours of the schwann cells surrounding the auditory nerve that innervates the inner ear.

They occur around cerebellopontine anglle

Classic symptoms are: hearing loss, tinnitus and balance problems

57
Q

What are the features of a benign essential tremor?

A 
Fine tremor
Symmetrical
More prominent on voluntary movement
Worse when tired, stressed or after caffeine
Improved by alcohol
Absent during sleep
58
Q

What medications can improve essential tremor?

A

Propranolol

Primidone

59
Q

What is Huntington’s chorea?

A

Autosomal dominant genetic condition that causes progressive deterioration in the nervous system.

Trinucleotide repeat disorder that involved mutation in HTT gene on chromosome 4

60
Q

What is genetic anticipation?

A

Feature of trinucleotide repeat disorders where successive generations have more repeats in the gene resulting in:
Earlier age of onset
Increased severity of disease

61
Q

What is the presentation of Huntington’s Chorea?

A

Insidious progressive worsening of symptoms. Typically begins with cognitive, psychiatric or mood problems. Followed by:

Chorea
eye movement disorders
Speech difficulties
Swallowing difficulties

62
Q

What is the diagnosis of huntington’s chorea?

A

Genetic testing

63
Q

What is the management of huntington’s?

A

Symptomatic treatment

64
Q

What is myaesthenia graves and what is it linked with having?

A

Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest

Women under 40 and med over 60

Linked with having a thymoma

65
Q

What is the pathophysiology of myaesthesia graves?

A

Acetylcholine receptor antibodies created by the immune system

Antibodies again MuSK

Antibodies against LRP4

66
Q

What is the presentation of myaesthenia graves/

A 
Diplopia
Ptosis
Weakness in facial movements
Difficulty with swallowing
Fatigue in jaw when chewing
Slurred speech
Progressive weakness with repetitive movements
67
Q

What is the diagnosis of myaesthenia graves?

A

Testing for relevant antibodies:
ACh-R antibodies
MuSK antibodies
LRP4 antibodies

CT or MRI of the thymus to look for thymoma

Edrophonium test

68
Q

What is the management of myaesthenia graves?

A

Reversible acetylcholinesterase inhibitors (pyridostigmine or neostrigmine)

Immunosuppression

Thymectomy

Monoclonal antibodies (Rituximab, Eculizumab)

69
Q

What is cauda equina syndrome?

A

Rare but serious condition in which lumbosacral nerve roots that extend below the spinal cord are compressed

70
Q

What are the possible presenting features of cauda equina syndrome?

A 
Low back pain
Bilateral sciatica
Reduced sensation/pins and needles in perianal region
Decreased anal tone
Urinary dysfunction
71
Q

What is the investigation and management of cauda equina syndrome?

A

Urgent MRI

Surgical decompression

72
Q

What are the associations to tension headaches?

A 
Stress
Depression
Alcohol
Skipping meals
Dehydration
73
Q

What is the presentation of trigeminal neuralgia?

A

Intense facial pain that comes on spontaneously and last between seconds to hours.

Feels like electric shocks

Attacks worsen over time

74
Q

What is the most common cause of encephalitis?

A

HSV 1 in children

HSV 2 in neonates

75
Q

What is the presentation of encephalitis?

A 
Altered consciousness
Altered cognition
unusual behaviour
Acute onset of focal neurological symptoms
Acute onset of focal seizures
Fever
76
Q

What is the diagnosis of encephalitis?

A 
LP (or CT if contraindicated)
MRI
EEG
Swabs
HIV
77
Q

What is the management of encephalitis?

A

IV aciclovir treats HSV and VZV

IV ganciclovir treats CMV

78
Q

What are the most common bones to be affected by osteosarcoma?

A

Femur
Tibia
Humerus

79
Q

What is the presentation of an osteosarcoma?

A 
Persistent bone pain
Worse at night time
Bone swelling
Palpable mass
Restricted joint movements
80
Q

What is the diagnosis of an osteosarcoma?

A

X-ray within 48hrs shows sun-burst appearance

Blood tests: high ALP

81
Q

What is the management of a sarcoma?

A

Surgical resection of lesion with limb amputation and adjuvant chemo

82
Q

Where does Ewing’s sarcoma typically affect?

A

Pelvis
Femur
Shoulder girdle
Ribs

83
Q

What is hydrocephalus?

A

CSF build up within the brain and spinal cord either due to overproduction or a problem with draining and absorbing (arachnoid granulations)

84
Q

What are the causes of hydrocephalus?

A

Most common: aqueductal stenosis. The cerebral aqueduct that connects the 3rd and 4th ventricle is stenosed so blocks normal flow of CSF

Other causes:
Arachnoid cysts
Arnold-chiari malformations 
Chromosomal abnormalities
Congenital malformaitons
85
Q

What is the presentation of hydrocephalus?

A 
Babies:
Bulging anterior fontanelle
Poor feeding and vomiting
Poor tone
Sleepiness
86
Q

What is the treatment for hydrocephalus/

A

Placing a ventriculoperitoneal shunt that drains CSF from ventricles into peritoneal cavity is used.

87
Q

What is idiopathic intracranial hypertension?

A

Condition classically seen in young overweight females

88
Q

What are the risk factors for idiopathic intracranial hypertension?

A

Obesity
Female sex
Pregnancy
Drugs (COCP, steroids, tetracyclines, Vit A and lithium)

89
Q

What is the presentation of idiopathic intracranial hypertension?

A 
Headache
Blurred vision
Papilloedema
Enlarged blind spot
6th nerve palsy
90
Q

What is the management of idiopathic intracranial hypertension?

A 
Weight loss
Diuretics (acetazolamide)
Topiramate
LP
Surgery
91
Q

What is the presentation of a migraine?

A 
Pounding or throbbing in nature
Usually unilateral
Photophobia
Phonophobia
With/without aura
N+V
92
Q

What is a hemiplegic migraine?

A

Mimic stroke:
Sudden or gradual onset hemiplegia, ataxia and changes in consciousness

plus normal migraine symptoms

93
Q

What is the acute management of migraines?

A

Paracetamol
Triptans
NSAIDs
Antiemetics

94
Q

What is the prophylaxis for migraines?

A

Propranolol
Topiramate
Amitriptyline

95
Q

What is charcot-marie-tooth disease?

A

Inherited disease that affects peripheral motor and sensory nerves. (usually autosomal dominant)

96
Q

What is the presentation of charcot-marie-tooth?

A 
High foot arches
Distal muscle wasting
Weakness in lower legs - loss of ankle dorsiflexion
Weakness in hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss
97
Q

What are the causes of peripheral neuropathy?

A 
Alcohol
B12 deficiency
Cancer and Chronic kidney disease
Diabetes and Drugs (isoniazide, amiodarone and cisplatin)
Every vasculitis

ABCDE

98
Q

What is the management of charcot-marie-tooth?

A

Supportive

99
Q

What is gullain-barre syndrome?

A

Acute paralytic polyneuropathy that affects the peripheral nervous system. Triggered by an infection i.e. campylobactor jejuni, CMV and EBV

100
Q

What is the presentation of gullain-barre syndrome?

A

Symmetrical ascending weakness (starting at feet)
Reduced reflexes
Peripheral loss of sensation or neuropathic pain
May progress to cranial nerves and cause facial nerve weakness

101
Q

What is the diagnosis of guillain-barre syndrome?

A

Brighton criteria

Nerve conduction studies
LP for high CSF

102
Q

What is the management of Guillian-Barre syndrome?

A

IV immunoglobulins
Plasma exchange
Supportive care
VTE prophylaxis

103
Q

What is neurofibromatosis?

A

Genetic condition that causes nerve tumours (neuromas) to develop throughout nervous system.

Type 1 is more common that type 2

104
Q

What causes neurofibromatosis type 1?

A

NF1 gene is found on chromosome 17.

Codes for a tumour suppressor protein.

Autosomal dominant

105
Q

What is the diagnostic criteria for neurofibromatosis type 1?

A

At least 2 of the 7 to indicate diagnosis. CRABBING:

Cafe-au-lait spots
Relative with NF1
Axillary or inguinal freckles
Bony dysplasia such as Bowing of a long bone
Iris hamartomas (yellow brown spots on iris)
Neurofibromas
Glioma of optic nerve

106
Q

What are the investigations and management of neurofibromatosis type 1?

A

None needed for diagnosis but can do genetic testing, Xrays and other imaging to confirm or if unsure

No treatment for underlying disease - supportive

107
Q

What is the cause of neurofibromatosis type 2?

A

NF2 gene found on chromosome 22 and codes for protein called merlin which is a tumour suppressor protein important for schwann cells.

Autosomal dominant

108
Q

What is the presentation of neurofibromatosis type 2?

A

Acoustic neuromas - (hearing loss, tinnitus, balance problems)

109
Q

What is the management of neurofibromatosis type 2?

A

Surgery to resect tumours

110
Q

What is Wenicke’s encephalopathy?

A

Neuropsychiatric disorder caused by thiamine deficiency most commonly seen in alcoholics.

111
Q

What is the presentation of Wernicke’s encephalopathy>

A

Opthalmoplegia/nystagmus
Ataxia
Confusion

112
Q

What is the investigation and treatment of Wernicke’s encephalopathy?

A

Investigations:
Decreased red cell transketolase
MRI

Treatment is with urgent replacement of thiamine (B1)

113
Q

What are some features of fronto-temporal dementia?

A 
Lack of attention to personal hygiene
Repetitive behaviour
Hoarding/criminal behaviours
New eating habits
Lack of empathy
Change in social behaviours
114
Q

What is the treatment for subdural haemorrhages?

A

Burr hole drainage

115
Q

What medication in alzheimers disease to help with sleep?

A

Trazadone

116
Q

Which nerves control eye muscles?

A

Optic nerve does all except

SO4 and LR6
Superior oblique - Trochlear
Lateral rectus - Abducens

117
Q

What is Creutzfelt-Jakob disease?

A

Rapidly progressive neurological condition caused by prion proteins.

118
Q

What are the features of Creutzfelt-Jakob disease?

A

Dementia (rapid onset)

Myoclonus

119
Q

What are the investigations in Creutzfelt-Jakob disease?

A

CSF normal
EEG: biphasic, high amplitude sharp waves
MRI: hyperintense signals in basal ganglia and thalamus

120
Q

What is the presentation of coronary artery dissection?

A

Horner’s syndrome

121
Q

Difference between Lambert eaton and Myasthenia gravis?

A

MG: fatigue with effort
LE: Easier with effort

122
Q

What is first line for micro and amcroprolactinomas?

A

Cabergoline

123
Q

What is the triad of presentation for cerebellar stroke?

A

Headache
Nausea/Vomiting
Ataxia

124
Q

Which pathway blockage causes galactorrhoea?

A

Tuberoinfundibular pathway

125
Q

When can you drive after a TIA or stroke?

A

4 weeks for cars

1 year for Lorry’s

126
Q

Which test is abnormal during delirium regardless of the cause?

A

EEG shows diffuse slowing

127
Q

Difference between vestibular migraine and vestibular neuronitis?

A

Migraine is recurrent whereas neuronitis is a single episode

128
Q

Which type of dementia is most attributed to hallucinations?

A

Lewy body’s

129
Q

Which heart condition does subarachnoid haemorrhage lead to?

A

Torsades de pointes

Finals (20 decks)

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