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Clinical > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the components of GCS?

A

Eye Opening: spontaneous (4), to speech (3), to pain (2), no response (1)
Verbal response: orientated (5), confused (4), inappropriate words (3), incoherent words (2), no response (1)
Motor Response: obeys commands (6), localises pain (5), withdraws from pain (4), flexes to pain (3), extends to pain (2), no response (1).

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2
Q

How is delirium tremens managed?

A

Chlordiazepoxide for anxiety and seizure prevention, fluids, antiemetics, pabrinex for vitamin B+C deficiency,

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3
Q

What causes delirium tremens? How does it present? When does it onset? Which neurotransmitter is unopposed?

A

Withdrawal from alcohol causing confusion, hallucinations, sweating, HeTN, seizures, etc.
Usually begins around 72 hours after last drink and peaks 4/5 days after.
Unopposed glutamate activity.

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4
Q

What are the characteristics of normal pressure hydrocephalus? How is it managed?

A

Wet (incontinence), wacky (dementia), and wobbly (ataxic).
Ventriculo-peritoneal shunt.

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5
Q

Why might you want to hyperventilate someone with an intracranial bleed?

A

Hyperventilation = reducing CO2 levels,
Less CO2 = vasoconstriction,
Vasoconstriction reduces bleeding and prevents raised ICP.

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6
Q

What is Cushing’s triad? Why is it dangerous?

A

HeTN, bradycardia, and irregular breathing/apnoea.
Causes cerebral hypoperfusion, which can cause death.

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7
Q

What are the conditions for CT head <1hour?

A
  • GCS <13 1 hour after injury
  • GCS <15 2 hours after injury
  • suspected skull base fracture or depressed skull fracture
  • seizure
  • focal neurological deficit (weakness, paralysis, loss of reflexes, etc)
  • > 1 episode of vomiting (>3 in children)
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8
Q

What is deficient in Wernicke’s encephalopathy? What are the sx?

A

thiamine deficiency - confusion, ataxia, and ophthalmoplegia - doesn’t necessarily mean all three will be present.

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9
Q

What develops in someone who has prolonged/untreated Wernicke’s encephalopathy?

A

Korsakoff’s Syndrome:
Chronic, irreversible retrograde and anterograde amnesia with confabulation due to prolonged thiamine deficiency/Wernicke’s encephalopathy.

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10
Q

What are the symptoms of cauda equina? What invx is needed?

A

Saddle anaesthesia, loss of bowel/urinary continence, numbness/paraesthesia down legs.
MRI!!!

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11
Q

What are the signs of signs of a cerebellar neoplasia?
What complication might make it present emergently?

A

DANISH and signs of space occupying lesion:
- headache,
- night sweats,
- raised ICP, etc
Might present with coning (tonsillar herniation syndrome) due to it being a posterior lesion:
- HeTN/BP instability
- cranial nerve palsies
- Decreasing conciousness
- Flaccid paralysis
- N+V, headache, neck stiffness

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12
Q

How does autoimmune encephalitis present? How is this managed? What are the types?

A
  • Confusion/reduced conciousness/cognitive impairement
  • Behavioural changes/emotional lability/psychosis,
  • Seizures,
  • Movement disorders,
    Mx: methylprednisolone (steroids), IV Ig
    Types:
  • Anti-NMDA encephalitis
  • Hashimoto’s.
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13
Q

A pt presenting with abnormal sensation and paralysis which started in the feet and has moved more proximal on a background of gastroenteritis is what?

A

Guillain-Barre (associated with campylobacter).

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14
Q

How do you investigate for/montior GBS? How do you manage Guillain-Barre?

A

Inx- isolated, raised CSF protein (>5.5), nerve conduction studies, monitor FVC (effect on respiratory system)
Mx: IV Ig and plasmapheresis - monitor FVC to know affect on respiratory system.

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15
Q

Which nerve is affected in Bell’s palsy? How does it present? How is it managed?

A

LMN CN VII (facial).
- Unilateral facial paralysis: ptosis, facial droop which including forehead
- Taste bud impairment,
- Excessive tearing (epiphroa) OR dry eyes.
Mx - oral pred and artificial tears.

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16
Q

Keratcoconjunctivitis Sicca is a complication of what palsy?

A

Bells’ - dry eyes cause failure of lid to close properly leading damage to the eye - eyedrops prevent this.

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17
Q

What is Trigeminal Neuralgia? How can it be managed?

A

Severe shooting/stabbing pains in the distribution of the trigeminal nerve divisions. Worsened by touching face, brushing hair and teeth, etc.
Mx - Carbamazepine and refer for MRI if no discernible cause.

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18
Q

Which way does the tongue deviate in a hypoglossal nerve palsy?

A

Deviation of tongue to side of lesion on protrusion.

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19
Q

What are medical vs surgical causes of CN III palsy? What is the characteristic appearance of the eye?

A

Medical- vasculopathic ischaemia (e.g., diabetes), these always spare the pupil.
Surgical- compression (e.g., aneurysm, tumour, etc), this always involve the pupil (e.g., anisocoria).

Both show ‘down and out’ appearance of the eye.

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20
Q

What is meralgia paraesthesia?

A

compression of the lateral cutaneous nerve of the thigh, causing sensitivity to heat and touch, paraesthesia, and numbness.

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21
Q

What are dissociative/psychogenic seizures?

A

non-epileptic, involuntary movements (e.g., limb/trunk jerking) and behaviours due to psychological distress.

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22
Q

What is 1st line for myoclonic seizures?

A

Sodium valproate

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23
Q

Temporal lobe seizures are usually preceeded by what? What do the seizures look like?

A

Preceded by aura, followed by weakness/blankness, automatisms (e.g., lip smacking).

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24
Q

What is a complication of recurrent temporal lobe seizures?

A

Damage to the hippocampus (memory learning and emotions problems) and mesial temporal lobe (memory,emotion, social behaviour problems).
Most commonly see memory problems.

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25
Q

What do parietal lobe seizures usually look like?

A

Sensory symptoms (e.g., pins and needles)

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26
Q

What is the difference between a simple and complex febrile seizure?

A

Simple is <5minutes and singular event,
Complex >5minutes or recurrent in a short space of time.

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27
Q

What is serotonin syndrome?

A

Results from serotonin increasing drugs such as SSRIs.
- Restlessness,
- Diaphoresis (sweating) and hyperthermia
- Clonus and hypertonia,
- Hyperreflexia.

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28
Q

What is Neuroepileptic malignant syndrome? What is the classic tetrad? What blood result is usually elevated?

A

Reaction to starting/increasing antipsychotic drugs such as risperidone (most commonly 1st gens), usually within weeks.
Tetrad - hypertonia, hyperthermia, autonomic instability, mental state change.
CK usually elevated - can get muscle necrosis and rhabdomyolysis (and ATN) if severe.

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29
Q

What is 1st line pharmacological agent for ADHD?

A

Methylphenidate

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30
Q

What are the pharmacological options for Alzheimer’s?

A

1) Donepezil - cholinesterase inhibitor
2) Memantine - glutamate receptor antagonist

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31
Q

How does fronto-temporal dementia usually present? What investigation is used and what does it show?

A

Youngish (50s) pts with memory problems, personality changes, and constructional apraxia (inability to complete moves]ments related to specific complete tasks).
MRI shows atrophy of frontal and temporal lobes.

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32
Q

Wallenberg Syndrome (aka lateral medullary syndrome) is an infarct of what vessel? What does it cause?

A

Posterior inferior cerebellar artery affecting medulla oblongata…
- Autonomic dysfunction e.g., Ipsilateral Horner’s,
- Vestibulocerebellar sx e.g., vertigo, diplopia, multidirectional nystagmus
- Sensory symptoms: contalateral loss of pain/temp senation
- Bulbar weakness: hoarsness, dysphagia, dyshonia

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33
Q

Lateral pontine syndrome is an infarct where? What does it cause?

A

Anterior inferior cerebellar artery.
Wallenberg’s sx + involvement of cranial nerve nuclei.

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34
Q

Basilar artery occlusion causes what?

A

Locked in syndrome (quadriparaesis with sustained consciousness and ocular movements), complete loss of consciousness or death.

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35
Q

What is Weber’s Syndrome?

A

Medial midbrain stroke:
- Ipsilateral oculomotor palsy (diplopia and ptosis)
- Contralateral hemiparesis.

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36
Q

A total anterior cerebral infarction (TACI) causes what?

A
  • Contralateral homonymous hemianopia,
  • Contralateral hemiplegia,
  • Higher cognitive dysfunction (hemispatial neglect, dysphagia, etc)
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37
Q

What is a partial anterior cerebral infarction (PACI)?

A

2 of TACI components or just higher cognitive dysfunction.

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38
Q

What symptoms do you get from a posterior circulation stroke?

A

DANISH

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39
Q

What is Amaurosis Fugax?

A

TIA affecting the eye - loss of vision that suddenly returns.

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40
Q

What is a Lacunar Infarct?

A

Occlusion of a single branch of a large cerebral artery often in basal ganglia, thalamus, or internal capsule.
Sx can be purely motor, purely sensory, sensorimotor, ataxic hemiparesis, dysarthria-clumsy hand syndrome.

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41
Q

What is the underlying pathology of cerebral amyloid angiopathy? What is the most common clinical manifestation and how is it seen on MRI?

A

Amyloid-beta deposits in the walls of…
- leptomeningeal arteries,
- cortical arteries,
- and cortical capillaries.
Spontaneous lobar intracerebral haemorrhage.
Cortical superficial siderosis and lobar microbleeds on MRI.

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42
Q

What sx are associated with intracranial venous thrombosis? What is seen on CT?

A

Headache, N+V, and other non-specific sx.
Hyperdensity in affected sinus - contrast shows filling defect (empty delta sign).

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43
Q

What is the most important management of haemorrhagic stroke?

A

BP control - should be <140 systolic within 1 hour of admission.

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44
Q

What are the symptoms associated with a subdural haematoma?

A

Vomiting, weakness of one side (if unilateral haemorrhage), variable confusion.

45
Q

How do you know the difference between acute and chronic subdural haemorrhage?

A

CT:
Acute - bright white
Chronic - dark

46
Q

What are the risk factors for a subdural haemorrhage?

A

Old age, chronic alcohol use, trauma, anticoagulant use.

47
Q

How do you manage cauda equina?

A

1) 16 mg dex stat, 8 mg BD thereafter.
2) Surgical decompression.

48
Q

Devic’s Disease (neuromyelitis optica) is characterised by inflammation where? What antibodies is it associated with?

A

Transverse myelitis (inflammation of the spinal cord), and optic myelits (inflammation of the optic nerve).
+ve NMO-IgG antibodies (against aquaporin 4).

49
Q

What is Miller-Fisher Syndrome? What antibodies are associated? What is the sx?

A

Rare form of Guillain-Barre that starts proximally such as at the eyes instead of distally.
Associated with GQ1B antibodies.
Weakness, ataxia, areflexia, opthalmoplegia.

50
Q

Autoimmune encephalitis can be put into what two categories? How does it present?

A

Anti-NMDA or Hashimoto’s encephalitis.
Seizures, confusion, movement disorders, behavioural change, cognitive impairment.

51
Q

What do you get on CSF analysis of autoimmune encephalitis? How is it manged?

A

CSF shows raised lymphocytes.
Mx - steroids and IV Ig 1st line, immunosuppressants may be considered 2nd line.

52
Q

What are the symptoms of myasthenia gravis? What time of day are they worse? Wht improves symptoms? What antibodies are associated? What is the management?

A
  • Ptosis and double vision,
  • Dysarthria/bulbar muscle weakness (hoarsness, dysphonia),
  • skeletal weakness,
    Sx often worse at the end of the day but improves with rest.
    80% have anti-AchR, can also be associated with muscle specific tyrosine kinase abs.
    Mx - steroids, anticholinesterases such as pyridostigmine, and possibly IV Ig acutely.
53
Q

What is the underlying pathology of MS?

A

Autoimmune disease of the CNS, demyelination and axonal loss of neurons.

54
Q

What are the clinical manifestations of MS?

A
  • Optic neuritis: blurred/loss of coloured vision
  • Internuclear ophthalmoplegia: failure of ipsilateral abduction and contralateral nystagmus (lesion at the medial longitudinal fasciculus)
  • Marcus-Gunn pupil: swinging torch elicits bilateral pupil dilation
  • Sensory disease
  • Cerebellar ataxia
  • Spastic paraparesis (weak/stiff legs)
55
Q

How do you diagnose MS? How is it managed?

A

Clinical examination, MRI (white matter lesions), CSF analyses (oligoclonal bands).
Mx - acute attacks with steroids, plasma exchange may also be used.
Beta-interferon may be used for relapsing-remitting MS.
Modafinil and amantadine may be used to manage fatigue sx.

56
Q

How does bacterial/viral encephalitis present? How is it manged?

A

Fever, change in mental state, flu-like sx, seizures, and temporal lobe involvement in the case of HSV encephalitis.
Mx - ceftriaxone and acyclovir.

57
Q

What are Kernig and Brudzinski signs?

A

Kernig - pain on knee extension
Brudzinski - pain on neck flexion

58
Q

How do viral and bacterial meningitis show on CSF?

A

Viral: clear appearance, increased protein, normal glucose, predominantly lymphocytes.
Bacterial: turbid appearance, increased protein, decreased glucose, predominantly leukocytes.

59
Q

How do you manage cryptococcal meningitis? How do you identify it?

A
  • 2 weeks IV amphotericin B and oral flucytosine. Followed by 8 weeks oral fluconazole and then long term maintenance therapy with low dose fluconazole.
  • Immunocompromised pts, subacute onset, raised opening pressure on LP (poor prognostic sign).
60
Q

How is bacterial and viral meningitis managed?

A

Bacterial: in primary care IM ben-pen, secondary care IV ceftriaxone with added amoxicillin for listeria cover in age extremeties.
Viral: acyclovir

61
Q

What is waterhouse-friderichsen syndrome?

A

Meningococcal sepsis - DIC - bleeding into adrenal glands - adrenal failure.
Very poor prognosis.
Hypotension, altered mental status, multi-organ dysfunction.

62
Q

What causes a pseudobulbar palsy?

A

Demyelination of corticobulbar and white matter tracts (UMN lesion) affecting muscles of speech and swallowing.
Relapsing and remitting disease pattern.

63
Q

What deficiency causes subacute combined degeneration of the spinal cord? How would it present?

A

B12 deficiency causing demyelination of lateral and posterior columns (dorsal and corticospinal)…
- Clumsiness/unsteady gait/falls
- Brisk reflexes
- Decreased vibration and proprioception sense
- Decreased vision
- Cognition and memory problems
- Depression
- Sleepiness

64
Q

What is the triad of Parkinson’s? What is the underlying pathology?

A

Bradykinesia, rigidity, intention tremor.
Death of neurones of substantia nigra.

65
Q

What pharmacological agent is primarily used in Parkinson’s? What are the SEs?

A

Levadopa…
SEs - N+V, postural hypotension, hallucinations, dyskinesia, confusion, psychosis).

66
Q

What are the hallmarks of PSPS (progressive supranuclear palsy)?

A

Intention tremor, hypertonia (rigidity), bradykinesia, and VERTICAL GAZE PALSY.
This is a parkinson’s plus syndrome.

67
Q

ALS (amyotrophic lateral sclerosis) is what type of disease?

A

It is the most common form of motor neurone disease.

68
Q

What mutation causes familial ALS?

A

SOD1 mutation

69
Q

What are the sx of ALS?

A

UMN - hyperreflexia and increased tone
LMN - fasciculations and muscle atrophy

70
Q

Myotonic dystrophy is caused by inheritance pattern?

A

Autosomal dominant trinucleotide repeat disorder causing dysfunction of muscle specific chloride channels.

71
Q

What are the features of myotonic dystrophy?

A

Face: frontal balding, catarcats, bilateral ptosis, long, thin face.
Speech: dysarthria
Neck: STCLM wasting
Hands: percussion myotonia, distal wasting, slow relaxing grip
Internal: metabolic syndromes and insulin intolerance, testicular atrophy, cardiomyopathy/cardioarrhythmias

72
Q

What is Charcot-Marie Tooth Disease?

A

Hereditary motor and sensory peripheral neuropathy.
Often presents in puberty in feet and slowly progresses to upper limbs.

73
Q

How can we diagnose Charcot-Marie Tooth Disease? What are some signs?

A

Nerve conduction studies (velocity reduced in type 1), clinical examination, and genetic testing.
Signs..
- Enlargement and thickening of nerves
- Symmetrical muscular atrophy causing ‘champagne bottle’ legs and claw hand.
- Pes cavus (high-arched feet)

74
Q

What is the inheritance of Huntington’s disease?

A

Autosomal dominant - CAG trinucleotide repeat with anticipation through spermatogenesis.

75
Q

What are the characteristics of Huntington’s? What do you see on MRI? What is the prognosis?

A

Choreoathetosis (unpredictable, writhing movements) and dementia.
MRI - atrophy of caudate nucleus and putamen.
Death within 10 years of sx onset.

76
Q

Where is the lesion in cerebral palsy?

A

UMN lesion in pyramidal tracts.

77
Q

A unilateral sudden onset extreme pain often around the eye, happening in groups and then disappearing for a while before returning is what type of headache? How is it mx?

A

Cluster headache - sumitriptan.

78
Q

A unilateral headache, associated with photophobia, often preceded with aura is what? Mx?

A

Migraine - propranolol prophylactically, acute mx with triptans.

79
Q

Who is CI to triptans e.g., sumatriptan?

A

HeTN, previous stroke, angina, PVD

80
Q

What extra sx might be associated with basilar migraine? Mx?

A

Vertigo, diplopia, dysarthria, tinnitus, bilateral visual sx, and bilateral paraesthesia.
Mx - simple analgesics (NSAIDs, paracetamol).

81
Q

What is Gerstmann Syndrome? Where is the lesion?

A

Finger agnosia, acalculia, agraphia, R/L discrimination disorder.
Lesion in the dominant angular gyrus (posterior inferior parietal lobe).

82
Q

What are the characteristics of Brown-Sequard syndrome?

A

Hemi-lesion of the spinal cord…
- ipsilateral paralysis, hyperreflexia, loss of vibration/position sense
- Contralateral loss of pain/temperature sense

83
Q

A lesion in karea causes what?

A

language comprehension disorder

84
Q

A lesion in Broca’s area causes what?

A

Problems with speech production.

85
Q

What is Todd’s paresis?

A

Weakness following a seizure.

86
Q

What are examples of autonomic dysfunction someone with Parkinson’s may experience?

A

Changes in bowel habit, ED, sleep disturbance, low mood.

87
Q

Ankle, knee, bicep, and tricep reflexes come from whish nerve roots?

A

S1 and 2 = ankle (buckle my shoes)
L3 and 4 = knee jerk (kick down the door)
C5 and 6 = bicep (pick up the sticks)
C7 and 8 = tricep (keep them straight)

88
Q

What are the cerebellar signs? How do you test for them?

A
  • Dysdiadochokinesis (hand flip = slow, difficult movement)
  • ataxia (walk)
  • nystagmus (follow the finger)
  • intention tremor (finger-nose test fully outstretched)
  • slurred speech (red lorry yellow lorry)
  • hypotonia (complete flaccidity)
89
Q

What are requirements for a diagnosis of MS?

A

Evidence of damage in both time and space.

90
Q

By what way does vascular dementia usually progress?

A

Stepwise progression.

91
Q

How do you differentiate between Dementia with Lewy Bodies and Parkinson’s Dementia?

A

If the movement disorder and dementia occur within a year of each other then it is Dementia with Lewy bodies. If they occur greater than 1 year apart, this is Parkinson’s disease dementia.

92
Q

What is the triad associated with Juvenile myoclonic epilepsy?

A
  • absence seizures
  • myoclonic seizures (often making them drop things)
  • tonic-clonic seizures
    Seizures often occur in the morning.
93
Q

What management can help prolong life in ALS?

A

Riluzole (anti-glutamatergic which reduces motor neurone firing)

94
Q

What can be given to manage choreoathetosis in Huntington’s disease?

A

Tetrabenazine (reduces monoamine release such as dopamine to reduce sx)

95
Q

What is the first line medication for absence seizures?

A

Ethosuximide

96
Q

What is first line for focal seizures?

A

Lamotrigine or levetiracetam

97
Q

Which seizure medication can make myoclonic seizures worse?

A

Carbamazepine

98
Q

What is idiopathic intracranial hypertension? Mx?

A

Tends to affect young, obese women, causing pulsatile, bilateral headaches, visual disturbance and papilledema.
Mx- acetazolamide to reduce CSf.

99
Q

What visual defect occurs in Idiopathic Intracranial Hypertension?

A

Enlarged blind spots and constricted visual fields.

100
Q

Which part of the brain is damaged to cause a conduction aphasia? How is this seen in a patient?

A

Articulate fasciculus (joins Wernicke’s and Broca’s).
Inability to repeat words back, and substitution errors.

101
Q

Damage to which part of the brain causes difficulty with language comprehension?

A

Wernicke’s area- Superior temporal gyrus.

102
Q

Damage to which part of the brain causes poor speech production?

A

Broca’s area- lower frontal gyrus

103
Q

What can be used to manage the symptoms of vascular dementia?

A

ACH esterase inhibitors such as donepezil.

104
Q

What antibiotic is given to close contacts of someone with bacterial meningitis as prophylaxis?

A

Oral rifampicin or ciprofloxacin.

105
Q

Which familial gene mutation is associated with both frontotemporal dementia and ALS?

A

C9orf72: hexanucleotide repeat gene

106
Q

What is multi-systems atrophy (MSA)?

A

Parkinson’s plus syndrome demonstrating rigidity, bradykinesia, and resting tremor alongside urinary and bowel disturbance, orthostatic hypotension, erectile dysfunction, and sweating abnormalities.

107
Q

What is hemiballismus? Where is the lesion?

A

Unilateral flinging movements.
Contralateral subthalamic nucleus.

108
Q
A

Clinical (27 decks)

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