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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Opioid analgesia should be gradually withdrawn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
What are brain arteriovenous malformations?
defects in the vascular system of the brain Absence of a true capillary bed Arteries --> directly to venous drainage system
26
What is cerebral contusion?
Form of focal traumatic brain injury = "bruise of brain tissue" Type of intracerebral hemorrhage Occur from coup-contrecoup injury (rapid deceleration)
27
Features of a stroke syndrome
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
28
Clinical features of a lacunar syndrome stroke
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
Trigeminal Neuralgia - Red flag features
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
Vascular region involved in Lacunar syndrome stroke
End arteries supplying white matter - usually lenticulostriate branches of MCA
31
Clinical features of a Total anterior circulation syndrome (TACS)
Hemiparesis AND Higher cortical dysfunction (dysphagia or visuospatial neglect) AND Homonymous Hemianopia
32
Vascular region involved in TACS
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
Clinical features of a Partial Anterior Circulation Syndrome (PACS)
Isolated higher cortical dysfunction OR, any 2 of: Hemiparesis Higher cortical dysfunction Hemianopia
34
Vascular region involved in PACS
Usually branch of MCA - Upper or lower divisions of MCA
35
Clinical features of Posterior circulation syndrome (POCS)
Isolated homonymous hemianopia OR Brain stem / cerebellar signs / cranial nerve syndromes
36
Vascular territories involved in POCS
Occlusion in vertebral, basilar or posterior cerebral artery
37
What is lateral medullary syndrome? (i.e. Wallenburgs)
Damage to lateral portion of medulla oblongata Typically due to ischaemia from a vertebral artery or posterior inferior cerebellar artery
38
Clinical features of lateral medullary syndrome (i.e. wallenburgs)
Ipsilateral: ataxia, nystagmus, dysphagia, CN palsy, facial numbness Contralateral: Limb sensory loss
39
What is Webers syndrome and clinical features?
ie. midbrain stroke Ipsilateral CN III palsy Contralateral hemiparesis
40
Stroke syndromes that give the appearance of stereotyping
Capsular warning syndrome Intracranial stenosis
41
Group 1 stroke mimics
Readily identifiable on standard imaging e.g. Subdural haematoma, brain tumour, multiple sclerosis, brain abscess
42
Group 2 Stroke mimics
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
Group 3 stroke mimics
Exclusion of stroke syndrome requires specialist stroke assessment incl. brain imaging e.g. migraine with aura, focal seizures, functional syndrome
44
What is Transient global amnesia?
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
Features of migraine with aura
Cortical spreading depression Gradual Separate auras evolve sequentially as CSD spreads from one brain region to another
46
How is cortical spreading depression different from TIA?
47
Widespread 'global' T wave inversion - cause?
Think non-cardiac cause - if not fitting with a coronary artery territory Think 'cerebral T waves'
48
What can cause osmotic demyelination syndrome?
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
Main differentiating feature of Ramsay Hunt syndrome and Bell's palsy
Ramsay Hunt syndrome: - often have more severe paralysis at onset and are less likely to recover completely.
50
What is Amaurosis fugax?
a transient loss of vision in one or both eyes Often a symptom of a TIA affecting the retinal/ophthamlic artery
51
Visual impairment associated with posterior cerebral artery stroke? and why?
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
Nerve lesion that causes thenar muscle wasting
Median Nerve (C5-T1)
53
Nerve lesion that causes wrist drop
Radial Nerve (C5-T1)
54
Nerve lesion that causes deltoid wasting
Axilliary nerve (C5-C6)
55
Nerve lesion that causes foot drop
Common peroneal nerve (L4-S2)
56
What is the corticobulbar tract?
Motor tract involved in movement of face and neck Originates in motor cortex Terminates in brainstem and synapses with cranial nerves
57
What are the 3 ascending spinal cord tracts and what are their functions
Dorsal column medial lemniscus (DCML) - fine touch, vibration, proprioception - contralateral side Spinothalamic - pain and temperature - contralateral side Spinocerebellar - unconscious proprioception - ipsilateral side
58
What are the descending spinal tracts
Corticospinal Corticobulbar
59
Which tract decussates in medullary pyramids
Corticospinal
60
What is Brown Sequard syndrome
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
The corticobulbar tract innervates each CN BILATERALLY except for which cranial nerves
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
LMN lesion of the hypoglossal nerve (CN XII) - which way does the tongue deviate
"Licks the lesion" - toward the lesion
63
Contraindications to Lumbar puncture
Suspected raised intracranial pressure (will cause coming) Pt at increased bleeding risk Intracranial abscess Severe septic features Meningococcal rash
64
Conditions that cause a raised opening pressure on Lumbar puncture
Bacterial/viral infection Cerebral haemorrhage Idiopathic intracranial hypertension Venous sinus thrombosis
65
Diagnostic test for Multiple Sclerosis
Mainly clinical suspicion MRI - hypertense lesions in periventricular white matter LP & CSF analysis - Oligoclonal bands on electrophoresis - normal cell and protein counts
66
Migraine management
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
Features of Wernicke's encephalopathy
CANON C- Confusion A - Ataxia N - Nystagmus O - Opthamoplegia N - Neuropathy (peripheral)
68
Features of Korsakoff syndrome
Retrograde Amnesia (cant remember) Anterograde amnesia (cant make new memories) Confabulation Korsakoff's psychosis

FINALS (19 decks)

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