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Theme III > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a TIA?

A

Transient ishcaemia with no infarct and no permanent neurological deficit. Lasts upto 24 hours, generally less than

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2
Q

What are further complication risks with TIA?

A

2% risk of stroke in 2months if treated within 72hrs.

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3
Q

How do you treat TIA?

A

Treat with clopidogrel 75mg/d, treat BP and lipids, modify SNAP and consider endarterectomy

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4
Q

What is a stroke?

A

If acute neurologic deficits persist beyond 24 hours or are interrupted by death within that timeframe.

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5
Q

How common is an ischaemic stroke and what are the causes?

A

87% - loss of focal reigon of the brain

  • Primary embolic - occlusion or critical stenosis. (carotid or cardiac in origin, artificial valves, CABG surg, DVT,, VSD, fat emboli, cncerm septic emboli (infective endocarditis)
  • Systemic hypoperfusion - shock or rapid lowering of BP - watershed areas are vulnerable
  • Central venous thrombosis
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6
Q

What is haemorrhagic transformation of stroke?

A

Bleeding into area of ischaemia - can occur in first few days of untreated stroke, often in first 24 hours in embolic stroke treated with coags

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7
Q

Risk factors for Cerebrovascular disease?

A

HTN (PmHx (TIA, CVD, PVD), DM, Smoking, obesity, HRT, Lipidaemia, Cancer, Old age, Male, Arrhythmia (AF)

10-25% of ischaemic strokes due to arrhythmia

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8
Q

What is the pathophysiology for Cerebrovascular disease?

A

Disease of blood vessels supplying the brain, with HTN as the most important cause – endothelial damage → collagen exposure → sustained prethrombotic state of carotid vessels → carotid atherosclerosis and stenosis. These vessels are now more sensitive to changes in BP – strokes when BP changes – ie waking up, excitation

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9
Q

Common site for carotid plaques?

A

Common/internal carotids – often at carotid bifurcation, Circle of Willis. Progressive atherosclerotic luminal stenosi

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10
Q

What does basal ganglia stroke present with? (what arteries are affected)

A

ICA → MCA → internal capsule, lenticulostriate arteries. These supply internal capsule white matter corticospinal efferents. Contralateral hemiparesis.

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11
Q

What is the ishcaemic cascade with hypoxia?

A

Excess glutamate released from tissue, lactic acid buildup, ↑apoptosis, oxygen free radicals released. Brain particularly vulnerable as it is completely reliant on aerobic metabolism.

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12
Q

What is the FAST acronym for patients having a stroke?

A 
F = Facial weakness (droop), 
A = Arm weakness (drift), 
S = Speech difficulty (slur), and 
T = Time to act (priority of intervention)
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13
Q

3 cardinal features of Stroke/TIA?

A

Sudden onset facial weakness, Arm drift, abnormal speech - aphasia/slurring

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14
Q

What is amaurosis fugax?

A

(TIA sign: dimming) –> transient loss of vision. Embolic obstruction of centrinal retinal artery.
Vital to treat carotid artery disease!

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15
Q

LOC + N/V + Headache - more likely to be haemorrhagic or ischaemic?

A

Haemorrhagic!

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16
Q

Which artery is affected?

  • Legs affected (contralateral lower limb), gait apraxia, personality changes (frontal lobe)
A

Anterior Cerebral artery!

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17
Q

Which artery is affected?

  • Contralateral arms, face and eyes. Dysphasia if affected side is the dominant hemisphere!
A

Middle cerebral artery!

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18
Q

Which artery is affected?

  • Eyes, vision loss
A

P (posterior) CA

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19
Q

Which artery is affected?

4S: Spinal nucleus of CNV, Spinothlamic, spinocerebellar, sympahetic (Horner’s)

A

Laterally medullary syndrome: PICA!

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20
Q

Which artery is affected?

4M’s: Ipslateral Tongue weakness, contralateral hemiplegia(medullary pyramid), Loss of discriminative touch - proprioception, vibration (Medial Laminiscus)

A

Anterior Spinal artery - Medial Medullary syndrome

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21
Q

What are the 4M’s:

A
  1. Motor pathway (corticospinal tract - contralateral weakness of arm and legs)
  2. Medial Meniscus - Contralateral loss of vibration and proprioception in the arm and leg
  3. Medial Longitudinal fasciculus -ipsilateral inter-nuclear ophthalmoplegia
    (failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally)
  4. Motor nucleus and nerve:
    ipsilateral loss of the cranial nerve that is affected (3, 4, 6 or 12)

Anterior Spinal artery

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22
Q

The 4’s (side structures):

A
  1. Spinothalamic pathway - contralateral alteration of pain and temperature affecting the arm, leg and rarely the trunk
  2. Spinocerebellar pathway - ipslateral ataxia of the arm and leg
    3.Sensory nucleus of the 5th cranial nerve -ipsilateral alteration of pain and temperature on the face in the distribution
    of the 5th cranial nerve
  3. Sympathetic pathway:
    ipsilateral Horner’s syndrome, that is partial ptosis and a small pupil (miosis)
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23
Q

What happens if damage to CN 9 - Glossopharyngeal nerve

A

Ipslateral loss of pharnygeal sensation

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24
Q

What would happen if damage to vagus nerve?

A

Ipslateral palatal weakness

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25
Q

What happens if damage to Spinal accessory nerve (CN 11)?

A

ipsilateral weakness of the trapezius and stemocleidomastoid muscles

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26
Q

What happens if damage to Hypoglossal nerve?

A

ipsilateral weakness of the tongue

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27
Q

What happens if damage to the Trigeminal nerve?

A

Ipsilateral alteration of SENSATIONS - pain, temperature and light touch on the face back as far as the anterior two-thirds of the scalp and sparing the angle of the jaw.

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28
Q

What happens if damage to the Abducent nerve?

A

Ipsilateral weakness of abduction (lateral movement) of the eye (lateral rectus)

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29
Q

What happens if damage to Facial nerve (CN VII)?

A

Ipslateral facial weakness

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30
Q

Are CN I and CNII in the midbrain?

A

NO.

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31
Q

T or F?:

Is the order: Medulla, Midbrain, Pons?

A

No! Brainstem = Midbrain, Pons, medulla

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32
Q

Palsy of trochlear nerve?

A

eye unable to look down when the eye is looking in towards the nose (superior oblique)

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33
Q

What happens if damage/occlusion to the Basilar artery?

A

Locked in syndrome - full awareness but can only move eyes

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34
Q

Signs of MCA stroke?

A

Supples most of the lateral surface of the hemisphere,
supplies Broca’s and Wernicke’s area, deep branches supply basal ganglia and the internal capsule.
 Contralateral hemiparesis  Contralateral hemianaesthesia  Contralateral homonymous hemianopia  Gaze preference to ipsilateral side  Dominant hemisphere: global aphasia  May have nominal aphasia, Broca’s, Wernicke’s

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35
Q

Differential Diagnosis for Stroke?

A

Hypoglycaemia coma (check BSL), CNS lymphoma (or tumour), Head injury, Abscess, ?SDH, Drug overdose, herpes encephalitis, seizure + post-ictal deficits, venous sinus thrombosis

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36
Q

Ix for Stroke like symptoms?

A

FBE, CRP, UEC, Lipids,, BSL - Hypo?, Tox screen -alco/drugs, Neuro exam, Head non-contrast CT

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37
Q

What is the importance of non-contrast CT in stroke/TIA?

What will acute CT show if ischaemic stroke?

A

Head non-contrast CT urgently if can treat (thrombolyse) or potential haemorrhage which needs evacuation, otherwise
within 24h. CT won’t show 40% within 3-6h, will show all in 24h.

–> However will show haemorrhage, so if no haemorrhage, midline shift, or tumour → yes,
thrombolyse

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38
Q

To detect source of emboli?

A
  • carotid doppler - >70% stenosis is significant
  • ECG - AF?
  • Thrombophilia screen if no identifiable cause
  • Check for AF post-stroke - if AF suitable for cardioversion?
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39
Q

Pharmacological Mx of stroke?

A
  • Prevention in AF patient with CHADSVASC of 1 warfarin, apixaban

Acute:

  1. NBM
  2. If decided not haemorrhage and >3hrs, aspirin 300mg
  3. If within last 3hrs, and imaging shows non-haemorrhagic stroke - alteplase (TPA) - can cause haemorrhage though. Continue with aspirin 24hrs later -300mg daily and supportive care (swallowing assessment, rehab support)
  • If haemorrhagic may require neurosurg consult
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40
Q

thrombolysis with tPA if

A

3

41
Q

Post stroke therapy:

A 
1. If ischaemic - lifelong clopidogrel monotherapy. If due to non-valvular AF - cardiovert or warfarin 
or Aspirin with dipyridamole 
2. Ace-i
3. Statin
4. ?carotid endarectomy
42
Q

When do you correct carotid stenosis?

A

Either when symptomatic or after 70%.

43
Q

What is involved in stroke rehabilitation?

A

– admit to stroke unit – speech/language, swallowing, physical therapy, OT, prevent pressure sores, hydrotherapy – help sufferer adapt to everyday life and maximize ADL capacity

44
Q

What is the definition of Epilepsy?

A

Chronic neurological condition characterised by 2 or more recurrent, unprovoked seizures by an excessive disorderly discharge of cortical nerve cells. Episodic abnormal electrical activity in the brain.

45
Q

Risk factors for Epilepsy/Seizures?

A

Acquired brain damage (trauma, stroke, brain lesion, substance abuse, substance withdrawal). family Hx, genetics, Electrolytes distrubances

46
Q

_______ lobe most commonly affected by focal/partial seizures

A

Temporal

47
Q

Difference between simple and complex seizure:

A

Simple - consciousness/awareness unaffected

48
Q

What are the features of an absence seizure?

A

Decreased consciousness, no motor disturbances for about 20 seconds. No aura/postictal state. Automisms

49
Q

What type of seizures are automisms related to (lip smacking, eye lid blinking)

A

Absence

50
Q

brief jerks of the body, resulting in falls –

A

Myoclonic epilepsy

51
Q

Differential diagnosis for seizure?

A

Epilepsy, Febrile convulsions, Hypoglycaemic seizure, Vasovagal episode (clear trigger and no post-ictal state), stroke, pscyhogenic non-epileptic syndrome

52
Q

Medications function to ________________ and are chosen based on the epileptic syndrome of the patient.

A

Medications function to increase the seizure threshold, and are chosen based on the epileptic syndrome of the patient.

53
Q

First line for partial seizure?

A

Carbamazepine

54
Q

First line for absent seizure?

A

Ethosuximide/Valproate

55
Q

First line for Tonic Clonic seizures?

A

Valproate

56
Q

Which drug is a neuronal T-type Calcium channel blocker?

A

Ethosuximide

57
Q

Which anti-epileptic drugs are involved in decreasing cell excitation

A

Phenytoin, Carbamazepine, Latotrigine, Ethosuximide

58
Q

Which anti-epileptic drugs are used to increase GABA inhibition?

A

Benzo, Barbiturates, Vigabatrin, Valproate

59
Q

What drugs act as CYP450 inducers and reduce the efficacy of COCP by increasing the metabolism of oestrogens in the pill in the liver?

A

Phenytoin, Carbamazepine, Phenobarbitone

60
Q

Acute management of stroke?

A
  1. Call ambo
  2. Stabilise patient - resusc
  3. Take BSL - if cannot giev dextrose with thiamine
  4. Give O2 and take EG
  5. Treat with IV lorazepam or diazepam → valproate /phenytoin. If neither of these work, phenobarbital (GABA agonist - barbiturate induced coma

Restrict driving

61
Q

What can happen if dextrose load is given alone in an alcoholic man?

A

Without thiamine - it can precipitate Wernicke-Korsakoff syndrome.

62
Q

Common side effects of Clonazepam?

A

Behavioural chnages and excess salivary and bronchial secretions

63
Q

Where is midazolam excreted?

A

The kidneys!

64
Q

Does Clozapine cause agranulocytosis?

A

Yes

65
Q

Which antibiotics inhibit Carbamazepine metabolism?

A

Erythromycin and Clarithromycin - they can lead to carbamazapine toxicity

66
Q

Side effects of Carbamazepine?

A

Sedation, CYP450 inducer, headache, diplopia, headache, nausea.
Can lead to reversible leukopenia

at high concentrations has an ADH like action - but the resulting hyponaetremia is usually mild and asymptomatic.
Can lead to steven johnson syndrome

67
Q

is Sodium valproate a CYP450 inducer or inhibitor?

A

Inhibitor!

68
Q

How does Gabapentin act?

A

Inhibiting Glutamate synthesis and hence increasing brain GABA levels

69
Q

How does Phenytoin work?

A

Blocks voltage dependent sodium channels - limiting the propagation of seizure discharges. It is high bound to albumin

70
Q

What are adverse effects of phenytoin?

A

Neurotoxic symptoms (drowsiness, dysarthria, tremor, ataxia, diplopia, cognitive difficulties), a lupus like syndrome, Stevens-Johnson Syndrome.

Long term use can give rise to a predominantly sensory peripheral neuropathy and cerebellar degeneration.

There may be other reversible changes like gum hypertrophy, acne, hirsutism, and facial coarsening

71
Q

What do you use for Absent seizures

A

Ethosuximide

72
Q

What do you use for focal seizures?

A

Carbamazapine

73
Q

What do you use for General seziures?

A

Valproate

74
Q

How to test for autonomic neuropathy?

A

Sweat test and tilt test

75
Q

Rapidly progressive wide spread weakness and sensory disturbances beginning in the legs …

A

Gullian Barre Syndrome

76
Q

In people with Dm, mononeuritis multiplex typically presents as…..

A

Acute, unilateral and severe thigh pain followed by anterior muscle weakness and loss of knee reflex

77
Q

neuropathy seen in DM?

A
  1. Autonomic neuropathy
  2. Peripheral neuropathy (Glove and stocking distribution)
  3. Mononeuropathy - nerve compression or infarct
78
Q

Infarction of Wernicke’s area leads to…. and which lobe

A

Receptive aphasia in the temporal lobe

79
Q

Infarction of broca’s area leads to _____ in which lobe

A

Expressive aphasia in the frontal lobe

80
Q

Xanthochromia on LP is indicative of ___

A

Haemorrhagic stroke - SAH

81
Q

Causes of SAH?

A

Rupture berry aneurysm, Aterovenous malformation and trauma

82
Q

Complications of SAH and what day do they arise (4 of them)?

A
  1. Seizures (Day 1)
  2. Rebleeding (Day 1-2)
  3. Vasospasm (Day 3)
  4. Hydrocephalus (Day 1 -7)
83
Q

Investigations for SAH?

A
  1. Non contrast Ct
  2. LP?
  3. Angiography?
84
Q

Intubate when the GCS < ____

A

8

85
Q

BP aim in SAH is ______

A

Systolic: 120-150

86
Q

Nimodipine is given after SAH because ______

A

To prevent vasospams

87
Q

How do you reduce ICP?

A

Mannitol, put bed at 30 degrees angle and consider a ventricular shunt

88
Q

headache after blunt trauma, loss of consciousness, ipslateral pupillary dilatation -

A

Epidural haematoma

89
Q

CT Brain shows: dense triangle from hyper dense thrombus within the superior sagittal sinus

A

Venous sinus thrombosis

90
Q

headache with excessive lacrimation, facial swelling and ptosis

A

Cluster headache

91
Q

Paroxysms of severe unilateral pain in the nerve along the face

A

Trigeminal neuralgia

92
Q

Acute eye and forehead pain with visual deficits and decreased acuity

A

Acute angle closure glaucoma

93
Q

Old female, unilateral blindness, tenderness to temporal area, flu like symtpoms, jaw claudication

A

Giant cell arteritis (Temporal arteritis) - perform doppler U/S of the temporal artery

94
Q

Causes of meningitis?

A
  • Strep pneumonia
  • Neisseria Meningitides
  • H. Influenzae
  • Listeria monocytogenes
95
Q

How does optic neuritis in MS present?

A

RAPD, Impaired coloured vision, Pain on eye movement, Pale optic disc,

96
Q

What medications are usedto prevent Migraines?

A
  1. BB or TCA

2. Anticonvulsants

97
Q

A sudural haematoma is between the ____ and _____

A

Dura and arachnoid mater.

98
Q

How do you treat trigeminal neuralgia?

A

carbamazepine

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