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Neurology Flashcards

1
Q

What are the features of narcolepsy?

What is the diagnostic test?

A

Hypersomnolence

Cataplexy

Sleep paralysis

Hallucinations upon waking

Test:
- Multiple sleep latency EEG

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2
Q

Which antibiotics can induce idiopathic intracranial hypertension?

A

Tetracycline antibiotics

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3
Q

What is a major diagnosis that needs to be ruled out for a TIA?

A

Hypoglycemia

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4
Q

What is the time frame for thromboectomy?

A

Within 6 hours

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5
Q

What is thiamine?

A

Vitamin B1

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6
Q

Optic chiasm tumours cause bitemporal hemianopias, but they usually affect a quadrant, how does this vary?

A

Inferior Optic chiasm compression (pituitary tumour) causes:
- Upper quadrant defect

Superior optic chiasm compression (Craniopharyngioma) causes:
- lower quadrant defect

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7
Q

What are the treatment options for neuropathic pain?

A

Rescue therapy: Tramadol
- exacerbations

1st line are:

  • amitriptyline
  • duloxetine
  • gabapentin

capsaicin - can be trialed for post-herpatic pain

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8
Q

What are the two most important causes of status epilepsy to be ruled out?

A

Hypoxia

Hypoglycaemia

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9
Q

If a patient develops diplopia when looking to the right, which side is the palsy?

A

Right side.

the symptoms (diplopia) gets worse the more you look to that side

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10
Q

If some experiences double vision when looking down, say when reading. Where is the palsy?

A

4th nerve
- trochlear

They get vertical diplopia

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11
Q

Which nerve provides motor innervation to the tongue? What happens if there is damage?

A

12th

Deviates towards side of lesion

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12
Q

If you had defects in III, IV, V and VI cranial nerves, where may there be a lesion?

A

Cavernous sinus

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13
Q

What nerves pass though the jugular foramen?

A

IX, X, XI

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14
Q

What nerves are affect in balbar palsy?

A

IX, X, XI, XII

  • these nerves are within the medulla.
  • *it is called bulbar because the medulla means bulb because it looks like a bulb, hence the term “bulbar”
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15
Q

What nerves are associatted with the cerebellopontine angle?

A

V, VII, VIII

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16
Q

If you had a lesion over the internal capsule where anatomically would you expect to see defects?

A

Almost entirely across the contralateral side

- since all the fibres filter through this area

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17
Q

What are the signs of an UMN lesion?

A 
Increased tone 
Spastic weakness 
Brisk reflexes 
Clonus - if ankle 
Up going planters 
Minimal atrophy *some occurs due to disuse

*UMN signs can take weeks to develop

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18
Q

What is the most commonly inherited neuropathy?

A

Charcot marie tooth

AD

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19
Q

If there is a lesioni the thalamus, what signs and symptoms would you expect?

A

Hemi -sensory changes

Drowsiness

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20
Q

If there is weakness on right side of the face, and weakness on the left side of the body, what is this called and where is the lesion likely to be?
What investigation would be most suitable for this?

A

Crossed sign

  • where there is ipsilateral signs on side of lesion on face (distrubution of cranial nerves)
  • contralateral weakness/ signs on opposite of body

Lesion will be within the brainstem.

**because certain fibres such as corticospinal tracts haven’t cross over yet. making it contralateral

MRI is needed for investigations. More sensitive than CT

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21
Q

In Brown - Sequard Syndrome - what would you expect the reflexes to be?

A

Brisk on the ipsilateral side.
- these are controlled via descending fibres on the same side

*plantars will also be up going in these

22
Q

Which clinical test can be done to differentiate between sensory and cerebellar ataxia and explain how:

A

Romberg’s test

  • in sensory ataxia there will be a postive romberg’s.
  • the patient will fall or become unsteady when eyes are shut as they have no tactile sensory input they were relying on their vision.
23
Q

Name an important neoplastic condition that must be screened for when someone presents with length depentant neuropathy:

A

Multiple myeloma.

Electrophresis should be conducted in those who present with length depentent axonal neuropathy

24
Q

Highlight some typical tests that may be carried out in someone presenting with peripheral neuropathy:

A

Bloods:

  • Glucose/ OGTT
  • FBC
  • U&Es
  • B12
  • LFTs
  • TFTs
  • Electrophoresis
25
Q

What are the main investigation modalities used in neurophysiology? Which are used for central neuropathies?

A

EEG
- Recording electrical activity within the cortex

EMG
- used to specifically locate the lesion area. i.e. myopathy or neuronal death to the muscle

Nerve conduction studies

Evoked Potentials
- used in MS, usually visual evoked potentials

Central:

  • EEG
  • EP
26
Q

In nerve conduction studies, what findings would you expect to see in axonal damage and mylinated damage?

A

Axonal = low amplitude
- less axons being stimulated

Mylinatation damage = slow wave form

27
Q

In a peroneal injury what type of paralysis would you expect, how does this differ from sciatic lesion?

A

Distal (peroneal) - dorsiflexion and eversion is only affected

Proximal (sciatic) - inversion is affected as well

28
Q

What nerve conduction study is used to diagnose myasthenia gravis and what is the characterstic finding?

A

Myasthenia repetitive stimulation
or
Single fibre EMG

normally the amplitude remains the same.
in MG the level reduces with continual stimulation
- decreament

29
Q

What can be done during an EEG and video recording to potentially bring about a non-epileptic event?

A

Hyperventilation

Photostimulation

30
Q

Outwith seizures when else is EEG useful?

A 
Coma 
Encephalitis 
CJD 
Dementia (only useful in rare Scenarios)  
Prognosis of hypoxic brain injury
31
Q

When doing an EEG on someone in a coma or reduced GCS, what is one of the main things that are being assessed for?

A

Non- Convulsive status epilepticus

32
Q

In a patient with bilateral leg pain what question do you want to ask?

A 
Time line 
Distribution
Bladder/ Bowel issues 
Saddle paraesthesia 
Lack of sensation on going to toilet 
Neurological sign in lower limbs
33
Q

Would you expect LMN or UMN signs in cauda equina syndrome?

A

LMN

if LMN are present then re-consideration of diagnosis is advised

34
Q

What clinical examination should be conducted on suspected cauda equina syndrome?

and what is an important bedside test that must be done?
and whats the definitve test?

A

Lower limb sensation/ motor control

Saddle sensation with pinprick (may trigger anal reflex)

Anal tone (either absent or present)

Anal wink reflex / catheter tug sensation

Test:

  • Post-void bladder scan. Assess to see if they were sufficient at emptying it.
  • remember to address pain or medication that may be causing the urinary retention

Definitive test:
- MRI lumbar with contrast T2 weighted

35
Q

What is the history of cauda equina syndrome:

A

Suspected/ CESS:

  • bilateral leg pain
  • progressive neurology
  • bladder and bowel are fine

Incomplete/ CESI:

  • Sphincter involvement but still got tone
  • difficult passing urine but not in retention
  • prompt MRI and Decompression
  • *can get recovery from here

Claude Equina syndrome with retention/ CESR

  • complete loss of urinary bladder and bowel
  • usually >48 hours
  • poor prognosis
36
Q

When might thrombolytic agents be used >4.5hours after a stroke?

A

If there is a penumbra area

This is detected via a CT perfusion scan which allows for salvageable penumbra area to be seen.

37
Q

Who does the coiling in patients with a SAH? and how do you follow up a coiling?

A

Interventional radiology

Follow up via MRI

38
Q

In the diagnosis of MS, using macdonald’s criteria explain how these physcially appear:

A

Dissemination in space:
- a lesion will be present in more than one brain area, i.e. paraventricular, subcortial, spinal cord, sub-tentorium

Dissemination in time:
- one will light up with gadolinium (active) one will not light up (old)

39
Q

Other than follow up of disease why else might a MS patient be followed up?

A

Assessing for JC reactivation

- progressive multifocal leukoencepalopathy

40
Q

What are the symptoms of encephalitis, most common organisms and how will you investigate and treat?

A 
Bizzare behaviour 
reduced GCS 
Fever 
Headache 
Focal neurology 
*evidence of previous infections with fever, lymphadenopathy etc

Organisms:

  • HSV-1
  • VZV
  • CMV
  • EBV

Investigations:

  • Bloods cultures
  • PCR for viral cultures
  • Toxoplasmosis screen

Head CT- bilateral involvement
*involvement of bilateral temporal involvement is highly suggestive of HSV-1

Treatment:

  • Aciclovir immediately.
  • toxoplasmosis treatment is toxoplasmosis
41
Q

What is meant be fatigable weakness?

A

Change in muscle power with exertion

- power that dimishes throughout the day

42
Q

Highlight some key characteristics of Lambort Eaton syndrome:

A

Proximal limb and trunk weakness

Get stronger with exertion

Hyporeflexia
- which improves with repeated contraction of muscle

43
Q

What do the antibodies in Lambort Eaton syndrome affect?

what is it associatted with?

A

Voltage gated calcium channel ion receptor on the pre-synaptic neuron

Small cell carcinoma
- therefore CXR is needed

44
Q

What is the treatment of Lambort Eaton syndrome?

A

3,4 Diaminopyridine

Immunotherapy
- IV IgG

Tumour
- treatment if tumour is present

45
Q

What are the drugs that can make MG worse and what is the most important one not to give?

A

Ineffective doses of pyridostigmine (too much or too little)

Gentamcin

Opioids

Beta blockers

Quinine

Tetracyclines

**gentamicin absolutely must not be given

46
Q

What can you asked the patient to do clinically to worsen a parkinsomism tremor?

A

Ask them to count backwards

- co-activation makes it worse

47
Q

There are 3 major types of wave forms seen in ICP, what are they?

A

A wave

  • consistently high pressure, usually above 50mmHg
  • tumours, Haematomas, Abscess, brain trauma

B wave

  • consistently high but not as high as A wave.
  • usually due to non compliant brain tissue

C- wave
- various in pressure

48
Q

What is the cerebral blood flow equation, and how is it regulated and what is the doctrine of compensation that takes place?

A

Cerebral blood flow = Cerebral perfusion pressure / Cerebral vascular resistance

**cerebral perfusion pressure = mean arterial pressure - intracranial pressure

Chemoregulation

  • pCO2
  • pO2
  • pH
  • metabolic products

Autoregulation
- Smooth muscle in response to systemic blood pressure

Munro- Kellie Doctrine
- for compensatory mechanisms

49
Q

What compensatory mechanisms are available to cope with raised ICP, and what additional mechanisms do children have?

A

Reduce CSF
Reduce venous blood
Reduce extracellular fluid

Children

  • expand fontanelle
  • skull suture expansion
50
Q

What is the medical treatment of raised ICP?

A

Dexamethasone
*condraindicated in traumatic brain injury

Mannitol

  • allows for 4-6 hours decreased pressure
  • useful when transporting for surgery

Ventilation to reduce CO2

Sedation
- propofol

Craniectomies

  • traumatic brain injuries
  • extensive ischmic stroke
  • intracerebral haemorrhage

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