Neuro Flashcards

1
Q

What is a tension type headache (TTH)?

A

A tension-type headache (TTH) is the most common type of headache and is often described as a dull, aching pain or pressure around the forehead, temples, or back of the head

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2
Q

H&E of TTH

A
  • Bifrontal/occipital pain
  • Episodic in nature
  • Pressure/band-like tightness around head
  • Lasts a few hours
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3
Q

RF of TTH

A
  • Stress
  • Fatigue
  • Mental tension
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4
Q

Investigations of TTH

A

First investigation is clinical diagnosis (normal neuro exam) and diagnosis via exclusion

Consider (if headache is refractory or progressing):
- CT sinus : exclude sphenoid sinusitis
- MRI : exclude brain tumour
- Lumbar puncture : exclude infective causes, sinus venous thrombosis or pseudotumour cerebri

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5
Q

Management of TTH

A

Acute - simple analgesics (aspirin, paracetamol, ibuprofen or naproxen)

Chronic (> 7-9/month)
- antidepressant (amitriptyline or doxepin)
- muscle relaxant (tizanidine)
- consider non-drug therapies

Prophylactic acupuncture

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6
Q

What is a Stroke?

A
  • AKA Cerebrovascular Accident
  • Represents a sudden interruption in the vascular supply of the brain
  • Two types are haemorrhagic and ischaemic
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7
Q

H&E for Stroke

A
  • motor weakness
  • dysphagia
  • swallowing problems
  • homonymous hemianopia
  • balance problems

Cerebral Hemisphere infarcts

  • contralateral hemiplegia
  • contralateral sensory loss
  • homonymous hemianopia
  • dysphasia

Brainstem infarct

  • More severe symptoms including quadriplegia and lock-in syndrome

Lacunar infarct

  • small infarcts around basal ganglia, internal capsule, thalamus and pons
  • may result in pure motor, pure sensory, mixed signs or ataxia
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7
Q

What is Subdural Haemorrhage?

A

A collection of blood deep to the dural layer of the meninges

Blood is not within the substance of the brain and therefore is called an ‘extra-axial’ or ‘extrinsic’ lesion

Can be uni- or bi-lateral

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8
Q

How can Subdural Haemorrhage be classified?

A

Acute - most commonly caused by high-impact trauma, often underlying brain damage

Subacute

Chronic - present for weeks to month, rupture of the small bridging veins within subdural space that cause slow bleeding
Elderly and alcoholic patients are at risk since they have brain atrophy and therefore fragile and taut bridging veins

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9
Q

H&E of Subdural Haemorrhage

A

Key

  • Headache
  • Evidence of trauma
  • N + V
  • Low GCS
  • Confusion

Other

  • Loss of consciousness
  • Seizure
  • Loss of continence
  • Focal neurological deficits
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10
Q

RF for Subdural Haemorrhage

A
  • Recent trauma
  • Anticoagulant use
  • Alcoholism
  • Advanced age
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11
Q

Investigations for Subdural Haemorrhage

A

1st
- Non-contrast CT head

  • Shows fluid collection
  • Crescenteric collection, not limited by suture lines
  • Acute bleeds appear hyper dense, whereas chronic is hypo dense
  • Large acute haematomas will cause ‘mass effect’ - midline shift or herniation
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12
Q

Management of Acute Subdural Haemorrhage

A
  • If <10mm, <5mm midline shift and non-expansile without neurological dysfunction - conservative management
  • If >10mm, >5mm midline shift, expansile, or neurological dysfunction - craniotomy

Antiepileptics if seizures/risk of seizures (phenytoin/levetiracetam)

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13
Q

Management of Chronic Subdural Haemorrhage

A
  • Manage conservatively if small and no neurological deficit
  • If patient is confused, has neurological deficit or severe image findings - surgical decompression with burr holes

Antiepileptics if seizures/risk of seizures (phenytoin/levetiracetam)

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14
Q

What is spinal cord compression?

A

An oncological emergency and effects up to 5% of cancer patients

Extradural compression accounts for majority of cases, usually due to vertebral body mets

More common in patients with lung, breast and prostate cancer

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15
Q

H&E of Spinal Cord Compression

A
  • back pain - earliest and most common symptom, may be worse when prone or coughing
  • lower limb weakness
  • sensory changes : loss and numbness
  • neurological signs dependent on level of lesion
    • above L1 usually UMN signs in legs and a sensory level
    • below L1 usually LMN signs in legs and perianal numbness
    • tendon reflexes tend to be increased below level of lesion and absent at level of lesion
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16
Q

Investigations for Spinal Cord Compression

A
  • Urgent whole spine MRI within 24hrs of presentation
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17
Q

Management of Spinal Cord Compression

A
  • high dose oral dexamethasone
  • urgent oncological assessment for consideration or radiotherapy or surgery
18
Q

What is Bell’s palsy?

A
  • Type of facial paralysis that occurs due to the dysfunction of the facial nerve, usually due to inflammation or compression
  • MC cause of acute facial weakness
  • Can occur at any age but is more common between 15-60 years old
19
Q

H&E of Bell’s palsy

A
  • May present with sudden onset facial weakness or paralysis, usually unilateral
  • Drooping of mouth, inability to close the eye on the affected side, drooping of eyelid and altered taste sensation may present
  • Exam may reveal weakness or paralysis of muscle of facial expression as well as loss of corneal reflex and hyperacusis
20
Q

Investigations of Bell’s palsy

A
  • First-line is thorough history and exam to rule out other causes of facial nerve dysfunction
  • If diagnosis uncertain, further investigations such as EMG or imaging such as MRI or CT
21
Q

Management of Bell’s palsy

A
  • Corticosteroid therapy, initiated ASAP from onset of symptoms
    • High dose (50-60mg) prednisolone within 72 hours
    • Prednisolone 25mg orally once daily for 10 days for most patients
  • Antiviral therapy may also be considered in some cases if there is evidence of HSV
  • Eye care is essential to prevent corneal damage - artificial tears, ointments and eye patches
  • PT and facial exercises may be beneficial
  • Most patients recover in 3-6 months, although some may experience persistent or recurrent symptoms
22
Q

What is Myasthenia Gravis?

A

An autoimmune disorder resulting in insufficient functioning acetylcholine receptors

Antibodies to Ach receptors seen in 85-90% of cases

F>M

23
Q

Exacerbating factors of Myasthenia Gravis

A

MC factor is exertion resulting in fatiguability - hallmark feature

Exacerbating drugs:
- Penicillamine
- Quinidine, procainamide
- BBs
- Lithium
- Phenytoin
- Abx : gentamicin, macrolides, quinolones, tetracyclines

24
Q

H&E of Myasthenia Gravis

A

Key feature is muscle fatiguability - muscles become progressively weaker during rest periods of activity and slowly improve after rest

  • Extraocular muscles : diplopia
  • Proximal muscle weakness : face, neck, limb girdle
  • Ptosis
  • Dysphagia

Associated with :
- Thymomas in 15%
- Autoimmune conditions : pernicious anaemia, thyroid, rheumatoid, SLE
- Thymic hyperplasia in 50-70%

25
Q

Investigations for Myasthenia Gravis

A
  • Antibodies to Ach Receptors
    • +ve in 85-90%
    • in remaining patients, 40% positive for anti-muscle-specific tyrosine kinase antibodies
    • antibodies are less commonly seen in disease limited to ocular muscles
  • CK normal
  • CT thorax to exclude thymoma
  • single fibre EMG : high sensitivity (92-100%)
26
Q

Management on Myasthenia Gravis

A
  • Pyridostigmine (long-acting Ach-erase inhibitor)
  • Immunosuppression is usually not started at diagnosis but majority of patient will end up needing it
    • Prednisolone initially
    • Azathioprine, cyclosporine, mycophenolate, mofetil may also be used
  • Thymectomy
27
Q

Management of Myasthenia Gravis Crisis

A
  • Plasmapheresis
  • IV Immunoglobulins
28
Q

What is Trigeminal Neuralgia?

A

A type of chronic pain disorder that involves sudden attacks of severe facial pain

Occurs more often in women

Typical age of onset is 60-70yo

29
Q

H&E for Trigeminal Neuralgia

A
  • Unilateral stabbing, sharp facial pain
    • Involving one or more division of trigeminal nerve
    • Lasts seconds
    • Triggered by eating, laughing, talking or touching affected area
30
Q

RF for Trigeminal Neuralgia

A
  • Increasing age
  • Female
  • MS
31
Q

Investigations for Trigeminal Neuralgia

A

Clinical diagnosis

Other investigations to consider:
- Intra-oral XR - if dental cause suspected

  • MRI - if other pathology suggested
  • Trigeminal reflex testing - after diagnosis, early blink reflex or early masseter inhibitory reflex
32
Q

Management of Trigeminal Neuralgia

A
  • Anticonvulsant - carbemazepine
  • Refer to neurology if failure to respond to treatment or atypical features
33
Q

Red Flags for Trigeminal Neuralgia

A
  • Sensory changes
  • Deafness or other ear problems
  • Hx of skin or oral lesions that could be spread perineurally
  • Pain only in opthalmic division or bilaterally
  • Optic neuritis
  • FHx of MS
  • Age of onset before 40yo
34
Q

What is Wernicke’s Encephalopathy?

A

Neuropsychiatric disorder caused by thiamine deficiency, MC seen in alcoholics

Rarer causes include persistent vomiting, stomach cancer and dietary deficiency

Classic triad of opthalmoplegia/nystagmus, ataxia and encephalopathy may occur

Petechial haemorrhages occur in variety of structures in brain including mamillary bodies and ventricle walls

35
Q

H&E of Wernicke’s Encephalopathy

A

Occulomotor dysfunction
- nystagmus
- opthalmoplegia (lateral rectus palsy, conjugate gaze palsy)

Gait ataxia

Encephalopathy (confusion, disorientation, indifference, inattentiveness)

Peripheral sensory neuropathy

36
Q

Investigations of Wernicke’s Encephalopathy

A
  • Decreased red cell transketolase
  • MRI : areas of symmetrical inc. T2/FLAIR signal
37
Q

Management of Wernicke’s Encephalopathy

A

Treatment is with urgent replacement of Thiamine

  • Give Pabrinex (IV B/C vitamins) : replaces thiamine and prevents the condition from progressing to Korsakoff’s psychosis
38
Q

What is Korsakoff’s Syndrome?

A

If Wernicke’s Encephalopathy not treated, Korsakoff’s syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation (generation of false memories) in addition to the above symptoms.

39
Q

What is Chronic Fatigue Syndrome?

A

Diagnosed after 3 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain symptoms

MC in women
Past psychiatric Hx has not been shown to increase risk

40
Q

H&E of Chronic Fatigue Syndrome

A
  • Fatigue is central feature
  • Sleep problems
  • Muscle or joint pains
  • Headaches
  • Painful lymph nodes without enlargement
  • Sore throat
  • Cognitive dysfunction (brain fog e.g.)
  • Physical or mental exertion
  • General malaise
  • Dizziness
  • Nausea
  • Palpitations
41
Q

Investigations for Chronic Fatigue Syndrome

A

DO ALL TEST TO EXCLUDE OTHER PATHOLOGY
e.g. bloods, coeliac screening, urinalysis, hormones

42
Q

Management of Chronic Fatigue Syndrome

A
  • Refer to specialist CFS service
  • Energy management
  • Physical activity and exercise overseen by specialist
  • Cognitive behavioural therapy