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FINALS > Neurology > Flashcards

Neurology Flashcards

1
Q

Features of Trigeminal Neuralgia

A

Sharp stabbing facial pain along distribution of trigeminal nerve

Episodic
No associated neurological deficit

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2
Q

Management of trigeminal neuralgia

A
  1. Anti-epileptics: CARBAMAZEPINE
  2. Gabapentin, pregabalin, amitriptyline

Medication resistant: ablative surgery / microvascular decompression

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3
Q

Management of status epilepticus

A

A-E approach
Call for help if >5mins

4mg Lorazepam /2 mins
Repeat after 5 mins

IV phenytoin 20mg/kg at <50mg/min

Transfer to ITU if >40 mins

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4
Q

Life threatening causes of seizures

A

Hypoxia
Meningitis/encephalitis
Hypoglycaemia
Metabolic (Ca/Na)
Trauma
Raised ICP
Toxins/OD
Hypertension/eclampsia

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5
Q

Management of raised intracranial pressure

A

Treat underlying cause
Head elevation to 30 degrees
IV MANNITOL
Controlled hyperventilation
Removal of CSF, from:
- intraventricular monitor
- LP (repeated)
- VP shunt (hydrocephalus)

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6
Q

Causes of raised ICP

A

Idiopathic intracranial HTN
Traumatic head injury
Infection (meningitis)
Tumours
Hydrocephalus

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7
Q

Treatment of a medication overuse headache

A

Stop simple analgesia / triptans abruptly (may initially worsen headache)
Opioid analgesia should be gradually withdrawn

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8
Q

What is Kernig’s test ?

A

To demonstrate symptoms of meningitis

Pt supine with hips and knee flexed to 90 degrees

Extend knee slowly

Resistance/pain and inability to fully extend knee is a positive kernig’s sign

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9
Q

What is Brudzinski’s test?

A

Demonstrates symptoms of meningitis

Patient supine
Hold behind patients head with one hand, other hand on patients chest
Gently flex the neck bringing chin to chest

Positive test = involuntary flexing of hips and knees (reaction to lessen stretch on inflamed meninges)

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10
Q

Criteria for CT head < 1 hour

A

GCS <13 on inital assessment
GCS <15 2 hours after injury
Focal neurological deficit
Suspected open or depressed skull fracture
Signs of basal skull fracture
Post-traumatic seizure
Vomiting more then once

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11
Q

Risk factors for subdural hemorrhage

A

Age = older
Alcoholism
Anticoagulation
Falls (alcoholism / epileptics)

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12
Q

Between what layers does a subdural form

A

Between dura and arachnoid

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13
Q

Causes of subdural haemorrhage

A

The majority of acute SDH occurs due to TRAUMA
Although can occur in absence of trauma (e.g. decreased ICP, dural metastases)
or the trauma may have been forgotten as it was so minor/a while ago

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14
Q

Consequences of raised ICP as a result of a subdural haemorrhage

A

SDH is associated with a gradual rise in ICP

  • Shift of midline structures
    if left untreated
  • herniation / coning
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15
Q

Pathophysiology of a subdural haematoma

A

Tearing of the bridging veins that cross from the cortex to the dural venous sinuses

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16
Q

Imaging for a SDH and characteristic appearance

A

Non-contrast CT

Crescent-shaped collection of blood over one hemisphere
+/- midline shift

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17
Q

Most common location for a spontaneous intracranial haemorrhage

A

Basal ganglia

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18
Q

What form of amnesia following head injury is an indication for CT scan <8hours

A

Retrograde amnesia >30 mins
- memory problem of events before incident

NOT anterograde amnesia (memory problems since the incident)

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19
Q

pupillary findings in head injuries:

Unilaterally dilated
Light response: Sluggish or fixed

A

CN III compression
Secondary to tentorial herniation

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20
Q

pupillary findings in head injuries:

Bilaterally dilated
Light response: Sluggish or fixed

A

Poor CNS perfusion
Bilateral 3rd nerve palsy

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21
Q

pupillary findings in head injuries:

Bilaterally constricted

A

Opiates
Pontine lesions
Metabolic encephalopathy

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22
Q

pupillary findings in head injuries:

Unilaterally constricted
Preserved light response

A

Sympathetic pathway disruption

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23
Q

pupillary findings in head injuries:

Unilaterally dilated or equal
Relative afferent pupillary defect (RAPD)

A

Optic nerve injury

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24
Q

Minimum cerebral perfusion pressure (adults)

A

70 mmHg

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25
Q

What are brain arteriovenous malformations?

A

defects in the vascular system of the brain
Absence of a true capillary bed
Arteries –> directly to venous drainage system

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26
Q

What is cerebral contusion?

A

Form of focal traumatic brain injury = “bruise of brain tissue”
Type of intracerebral hemorrhage

Occur from coup-contrecoup injury (rapid deceleration)

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27
Q

Features of a stroke syndrome

A
  1. Sudden onset
  2. Focal (only the neurovascular units within vascular territory affected)
  3. Predominantly negative (loss of function)
  4. Vascular territory hypoperfusion can explain the collection of symptoms
  5. Symptoms do not typically migrate
  6. Episodes do not stereotype
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28
Q

Clinical features of a lacunar syndrome stroke

A

No cortical dysfunction or hemianopia

Pure motor/pure sensory (or sensorimotor)
Involving at least 2 contiguous somatic areas
(Face/arm/leg or face/arm or arm/leg)

29
Q

Trigeminal Neuralgia - Red flag features

A

Sensory changes
Ear problems/deafness
Bilateral
Pain only in ophthalmic division (eye socket, forehead, nose)
Optic neuritis
FHx of MS
Age of onset < 40 yrs

  • These warrant urgent referral to specialist
30
Q

Vascular region involved in Lacunar syndrome stroke

A

End arteries supplying white matter
- usually lenticulostriate branches of MCA

31
Q

Clinical features of a Total anterior circulation syndrome (TACS)

A

Hemiparesis AND
Higher cortical dysfunction (dysphagia or visuospatial neglect) AND
Homonymous Hemianopia

32
Q

Vascular region involved in TACS

A

Internal carotid artery or proximal Middle cerebral artery (MCA)

A large cortical stroke affecting the areas of the brain supplied by both the middle and anterior cerebral arteries

33
Q

Clinical features of a Partial Anterior Circulation Syndrome (PACS)

A

Isolated higher cortical dysfunction
OR, any 2 of:
Hemiparesis
Higher cortical dysfunction
Hemianopia

34
Q

Vascular region involved in PACS

A

Usually branch of MCA
- Upper or lower divisions of MCA

35
Q

Clinical features of Posterior circulation syndrome (POCS)

A

Isolated homonymous hemianopia
OR
Brain stem / cerebellar signs / cranial nerve syndromes

36
Q

Vascular territories involved in POCS

A

Occlusion in vertebral, basilar or posterior cerebral artery

37
Q

What is lateral medullary syndrome? (i.e. Wallenburgs)

A

Damage to lateral portion of medulla oblongata

Typically due to ischaemia from a vertebral artery or posterior inferior cerebellar artery

38
Q

Clinical features of lateral medullary syndrome (i.e. wallenburgs)

A

Ipsilateral: ataxia, nystagmus, dysphagia, CN palsy, facial numbness

Contralateral: Limb sensory loss

39
Q

What is Webers syndrome and clinical features?

A

ie. midbrain stroke

Ipsilateral CN III palsy
Contralateral hemiparesis

40
Q

Stroke syndromes that give the appearance of stereotyping

A

Capsular warning syndrome
Intracranial stenosis

41
Q

Group 1 stroke mimics

A

Readily identifiable on standard imaging

e.g. Subdural haematoma, brain tumour, multiple sclerosis, brain abscess

42
Q

Group 2 Stroke mimics

A

Sydromically distinguishable from stroke syndrome on clinical grounds (shouldn’t be a mimic in capable hands!)

e.g. Syncope syndrome, BPPV, vestibular neuritis, transient global amnesia, bells palsy etc

43
Q

Group 3 stroke mimics

A

Exclusion of stroke syndrome requires specialist stroke assessment incl. brain imaging

e.g. migraine with aura, focal seizures, functional syndrome

44
Q

What is Transient global amnesia?

A

Dysfunction of episodic memory with preservation of other types of memory e.g. procedural (making tea, driving) bibliographic memory
Gap in memory during TGA episode

45
Q

Features of migraine with aura

A

Cortical spreading depression
Gradual
Separate auras evolve sequentially as CSD spreads from one brain region to another

46
Q

How is cortical spreading depression different from TIA?

A
47
Q

Widespread ‘global’ T wave inversion - cause?

A

Think non-cardiac cause - if not fitting with a coronary artery territory
Think ‘cerebral T waves’

48
Q

What can cause osmotic demyelination syndrome?

A

Aka central pontine myelinolysis –> Locked in syndrome

Over-correction/rapid correction of severe hyponatremia

symptoms usually occur after 2 days and are usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma

49
Q

Main differentiating feature of Ramsay Hunt syndrome and Bell’s palsy

A

Ramsay Hunt syndrome:
- often have more severe paralysis at onset and are less likely to recover completely.

50
Q

What is Amaurosis fugax?

A

a transient loss of vision in one or both eyes

Often a symptom of a TIA affecting the retinal/ophthamlic artery

51
Q

Visual impairment associated with posterior cerebral artery stroke? and why?

A

homonymous hemianopia with macular sparing and visual agnosia

Occipital pole (where the macula is represented) receives a dual blood supply from the PCA and the MCA. Visual agnosia is an inability to recognise visually presented objects because of damage to the connections between the occipital and temporal lobes. There is no prosopagnosia (face blindness) as this information is stored in the temporal lobe of the brain which is not supplied by the PCA.

52
Q

Nerve lesion that causes thenar muscle wasting

A

Median Nerve (C5-T1)

53
Q

Nerve lesion that causes wrist drop

A

Radial Nerve (C5-T1)

54
Q

Nerve lesion that causes deltoid wasting

A

Axilliary nerve (C5-C6)

55
Q

Nerve lesion that causes foot drop

A

Common peroneal nerve (L4-S2)

56
Q

What is the corticobulbar tract?

A

Motor tract involved in movement of face and neck
Originates in motor cortex
Terminates in brainstem and synapses with cranial nerves

57
Q

What are the 3 ascending spinal cord tracts and what are their functions

A

Dorsal column medial lemniscus (DCML)
- fine touch, vibration, proprioception
- contralateral side

Spinothalamic
- pain and temperature
- contralateral side

Spinocerebellar
- unconscious proprioception
- ipsilateral side

58
Q

What are the descending spinal tracts

A

Corticospinal
Corticobulbar

59
Q

Which tract decussates in medullary pyramids

A

Corticospinal

60
Q

What is Brown Sequard syndrome

A

Lesion in one half of the spinal cord (due to hemisection or unilateral cord lesion)

Causing:
- Ipsilateral UMN weakness below the lesion (severed corticospinal tract)
- Ipsilateral loss of proprioception and vibration (DCML)
- contralateral loss of pain and temperature sensation (severed spinothalamic tract which has crossed over)

61
Q

The corticobulbar tract innervates each CN BILATERALLY except for which cranial nerves

A

Facial nerve (CN VII)
- forehead = bilateral
- Lower face = unilateral
- So UMN lesion causes forehead sparing

Hypoglossal nerve (CN XII)
- each half of tongue supplied by contralateral corticobulbar tract
- tongue deviates towards the weak side

62
Q

LMN lesion of the hypoglossal nerve (CN XII) - which way does the tongue deviate

A

“Licks the lesion” - toward the lesion

63
Q

Contraindications to Lumbar puncture

A

Suspected raised intracranial pressure (will cause coming)
Pt at increased bleeding risk
Intracranial abscess
Severe septic features
Meningococcal rash

64
Q

Conditions that cause a raised opening pressure on Lumbar puncture

A

Bacterial/viral infection
Cerebral haemorrhage
Idiopathic intracranial hypertension
Venous sinus thrombosis

65
Q

Diagnostic test for Multiple Sclerosis

A

Mainly clinical suspicion

MRI - hypertense lesions in periventricular white matter

LP & CSF analysis
- Oligoclonal bands on electrophoresis
- normal cell and protein counts

66
Q

Migraine management

A

Acute: Combination therapy - oral triptan + NSAID or Oral triptan + paracetamol
(young people 12-17 consider nasal triptan not oral)

Prophylaxis: propranolol or topiramate or amitriptyline

67
Q

Features of Wernicke’s encephalopathy

A

CANON

C- Confusion
A - Ataxia
N - Nystagmus
O - Opthamoplegia
N - Neuropathy (peripheral)

68
Q

Features of Korsakoff syndrome

A

Retrograde Amnesia (cant remember)
Anterograde amnesia (cant make new memories)
Confabulation
Korsakoff’s psychosis

FINALS (19 decks)

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