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Final year recaps/management > Neuro > Flashcards

Neuro Flashcards

1
Q

How is SAH confirmed

A

CT head

  • acute blood (hyperdense/bright on CT)
  • CT is negative for SAH in 7% of cases

LP used to confirm SAH if CT negative

  • perform at least 12 hours following onset of symptoms to allow the development of xanthochromia (helps distinguish true SAH from traumatic tap)
  • as well as xanthochromia, CSF findings consistent with subarachnoid haermorrhage include a normal or raised opening pressure.

REFER TO NEUROSURG as soon as SAH confirmed.

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2
Q

Tx of SAH

A

After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:

  • CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
  • +/- digital subtraction angiogram (catheter angiogram)

Most intracranial aneurysms are now treated with a coil, but a minority require craniotomy and clipping by neurosurgeon

Vasospasm is prevented using a 21 day course of nimodipine (CCB targeting brain vasculature)

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3
Q

What is Lambert Eaton syndrome

A

Seen in association with small cell lung cancer or as an autoimmune disorder.

Antibody against presynaptic voltage gated calcium channels in the PNS

  • repeated muscle contractions lead to increased muscle strength (as opposed to myaesthenia)
  • limb girdle weakness
  • hyporeflexia
  • autonomic symptoms

Tx - underlying cancer
- immunosuppression

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4
Q

Myaesthenia Gravis vs Lambert Eaton?

A

MG - increased fatiguability with exercise

LES - weakness improves with exercise

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5
Q

What is a vestibular schwannoma and how does it present?

How to investigate?

A

Also known as acoustic neuroma, is a cerebellopontine tumour that affects the (8th) vestibulocochlear nerve. may also affect the trigeminal and facial nerve during the late stages.

Unilateral sensorineural hearing loss (most common symptom), tinnitus and dizziness.
Trigeminal and facial nerve involvement may manifest as unilateral facial pain (absent corneal reflex too) and unilateral facial weakness respectively.

bilateral vestibular schwannomas are associated with Neurofibromatosis type 2

1st line Ix: audiogram and gadolinium-enhanced MRI head scan. urgent referral to ENT

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6
Q

Common adult brain tumours?

A

Metastases

  • often multiple and not treatable with surgical intervention
  • tumours that commonly spread to brain include: lung, breast, bowel, skin (melanoma), kidney

Meningioma - 2nd most common

  • typically benign
  • arise form the dura mater of the meninges, cause their symptoms via compression rather than invasion
  • CT will show contrast enhancement. Tx can be either observation, radiotherapy or surgical resection

GBM

  • most common primary tumour in adults
  • v poor prognosis
  • imaging: solid tumours with central necrosis and a rim that enhances with contrast. BBB disrupted to associated with vasogenic oedema
  • surgery with post op chemo/radio. dex for oedema
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7
Q

Acute and chronic management of migraine

A

Acute:
- oral triptan + NSAID or oral triptan + paracetamol

Prophylaxis: topiramate or propranolol

(in women of childbearing age propranolol is preferred as topiramate may be teratogenic)

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8
Q

Stroke management acutely

A

If <4.5 hours - thrombolysis (alteplase) AND thrombectomy

  • acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation
  • obvi exclude haemorrhagic

within 6 hours but >4.5 - thrombectomy

  • acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation
  • potential to salvage brain tissue

Within 24 hours of symptom onset, and once haemorrhagic excluded - 2 weeks aspirin 300mg then long term clopidogrel (aspirin + MR dipyridamole if aspirin not tolerated)

statin if cholesterol >3.5mmol (many delay 48 hours due to risk of haemorrhagic transformation)

don’t lower BP unless acute complications e.g. hypertensive encephalopathy

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9
Q

What nerve is at risk with fracture of surgical neck of humerus?

A

Axillary nerve winds around the bone at the neck of the humerus. The Axillary nerve is also at risk during shoulder dislocation

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10
Q

Erbs vs Klumpke palsy?

A

Erbs palsy - injury to upper group of arms nerves, specifically brachial trunks c5-6

Klumpke - involves brachial trunks C8-T1. involvement of T1 may cause a Horner’s syndrome

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11
Q

Localising features of focal seizures

A

Temporal - hallucinations, epigastric rising/emotional, automatisms (lip smacking, grabbing, plucking), deja vu/dysphasia post ictal)

Frontal (motor) - head/leg movements, posturing, post ictal weakness, jacksonian march

Parietal (sensory) - paraesthesia

Occipital (visual) - floaters/flashes

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12
Q

Cluster headache management

A

acute: 100% O2, subcut triptan
prophylaxis: verapamil

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13
Q

Neurofibromatosis vs tuberous sclerosis? what the hell is going on here please learn

A

no fucking clue mate

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14
Q

Investigations for mysathenia gravis?

A

single fibre electromyography
Ct thorax to exlude thymoma (present in 15%)
CK is normal
autoantibodies - to ACh in around 85-90%, in the remaining, 40% for anti-muscle-specific tyrosine kinase abs
Tensilon test (not commonly used)

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15
Q

Mx myasthenia Gravis

A

Long-acting acetylcholinesterase inhibitors - PYRIDOSTIGMINE is first line.

Prednisolone is added as adjunctive treatment if pyridostigmine does not resolve her symptoms well enough.

down the line - cyclosporine, mycophenolate mofetil
thymectomy

Crisis - plasmapharesis, IVIg

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16
Q

Stroke associated effects with the sites of the lesions

A

Anterior cerebral artery

  • contralateral hemiparesis and sensory loss
  • lower extremity > upper

Middle cerebral artery

  • Contralateral hemiparesis and sensory loss, upper extremity > lower
  • Contralateral homonymous hemianopia
  • Aphasia

Posterior cerebral artery

  • contralateral homonymous hemianopia with macular sparing
  • visual agnosia

Lacunar strokes

  • either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
  • strong association with hypertension
  • common sites - basal ganglia, thalamus, internal capsule
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17
Q

Guillain-Barre syndrome features

Ix

A

rapidly progressive peripheral neuropathy with lower motor neurone signs (hyporeflexia)

Often follows a diarrhoeal illness, esp campylobacter

  • around 65% patients get back/leg pain in initial stages
  • weakness is classically ascending
    proximal muscles usually affected before distal ones
  • reflexes reduced or absent
  • sensory symptoms tend ot be mild

IX:

  • LP: rise in protein + abnormal WCC in 66%
  • nerve conduction may be performed
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18
Q

Parkinson’s plus syndromes?

A

do this answer lol

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19
Q

Features and management of essential tremor?

A

Autosomal dominant condition which usually affects both upper limbs

Features
- postural tremor: worse if arms outstretched
improved by alcohol and rest
- most common cause of titubation (head tremor)

Management

  • propranolol is first-line
  • primidone is sometimes used
20
Q

What are the features, Ix and Mx of Wernicke’s encephalopathy?

A 
Neuropsych disorder caused by thiamine deficiency, seen in alcohlics. 
Classic triad of 
- nystagmus/opthalmoplegia
- ataxia 
- confusion/altered GCS 
Can get peripheral sensory neuropathy

Ix

  • decreased red cell transkelotase
  • MRI

Mx - urgently replace thiamine
- if untreated can lead to Korsakoff’s syndrome

21
Q

What is the relationship between Wernicke’s encephalopathy and Korsakoff’s syndrome?

A

Wernicke’s - nystagmus, opthalmoplegia, ataxia.

If untreated -> korsakoff’s
- addition of antero- and retrograde amnesia and confabulation in addition to above symptoms

22
Q

What is Bell’s palsy? How is it managed?

A

Acute, unilateral, idiopathic facial nerve paralysis.
Peak incidence is 20-40 years, more common in pregnany women.

It is a LOWER MOTOR NEURON facial palsy, therefore is forehead affecting

Patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis

Oral pred within 72 hours of onset

  • uptodate: add antivirals for severe facial palsy
  • eye care (artificial tears/eye lubes)
23
Q

How is status epilepticus defined

A

Single seizure >5mins
OR
>= 2seizures within a 5 min period without person returning to normal in between

Medical emergency. danger of irreversible brain damage if seizure activity is not terminated.

24
Q

Management of status epilepticus?

A

ABC

  • airway adjunct
  • oxygen
  • check BM

Benzo such as diazepam or lorazepam

  • prehospital setting, rectal diazepam may be given
  • IV lorazepam usually used in hospital

If ongoing
- phenytoin or phenobarbital infuson

If refractory status within 45 mins from onset - best to achieve seizure activity control with induction of GA

25
Q

Extradural haematoma features and imaging

A

Collection of blood between the skull and dura, almost always caused by trauma (typically low-impact e.g. blow to head or fall).

Collection is usually temporal region since thin skull at pterion overlies the MIDDLE MENINGEAL ARTERY - vulnerable to injury.

Classic presentation - initially pt loses then regains consciousness (lucid interval) then loses it again.

As haematoma expands - fixed and dilated pupil due to the compression of the parasympathetic fibres of cranial nerve 3

Imaging - biconvex (or lentiform), hyperdense collection around the surface of the brain. LIMITED BY SUTURE LINES.

26
Q

Which nerve is associated with mid shaft humeral fractures? How to test?

A

Radial nerve. Extend wrist.
Radial nerve palsy is associated with wrist drop.

Extending the elbow would test the radial nerve, but as the injury is at the shaft of the humerus, innervation of the triceps may arise proximal to a radial nerve injury. This would mean that a more distal injury could be missed.

27
Q

Features and management of neuroleptic malignant syndrome?

A

Can occur with antipsychotics or sudden stopping of dopaminergic drugs in e.g. parkinson’s

Typical features - pyrexia, muscle rigidity, autonomic lability, agitated delirium
- Raised CK in most cases. AKI in severe cases

Mx

  • stop antipsychotic
  • admit
  • IV fluids to prevent renal failure
  • bromocriptine - dopamine agonist - may be used
  • dantrolene in some cases
28
Q

Trigeminal neuralgia features and management

A

Severe unilateral pain, usually idiopathic but can be caused by compression of trigeminal roots by tumours or vascular problems

Electric shock like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve

Pain commonly evoked by light touch (washing, shaving, smoking, talking, teeth brushing etc)

Mx

  • carbamazepine first line
  • failure to respond or atypical features e.g. <50 years old should prompt referral to neurology
29
Q

Broca’s vs conduction aphasia

A

Broca’s - lesion of the inferior frontal gyrus. Speech is non-fluent, laboured and halting. Repetition is impaired

Conduction - usually stroke at the connection between Wernicke’s and Broca’s area. Speech is fluent but repetition is poor. aware of the errors they are making.

comprehension normal for both

30
Q

Management of degenerative cervical myelopathy

A

presentation of DCM is very variable. it is a progressive condition.

Leads to loss of fine motor function in both upper limbs. commonly misdiagnosed as carpal tunnel syndrome.

MRI of the cervical spine is the gold standard test where cervical myelopathy is suspected. It may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change.

Urgently refer to specialist spinal services as early treatment is important.
- decompressive surgery is the only effective treatment

31
Q

Visual field defects main points

A

Homonymous quadrantanopias - PITS

  • Parietal - Inferior
  • Temporal - Superior

Incongruous defects - optic tract lesion
Congruous defects - optic radiation lesion or occipital cortex

32
Q

How to differentiate between true seizure and pseudoseizure?

Factors favouring each?

A

Prolactin - elevates 10 to 20 min after an episode of a true epileptic seizure

True epileptic - tongue biting, raised serum prolactin

pseudoseizure - pelvic thrusting, family member with epilepsy, more common in females, crying after a seizure, don’t occur when alone, gradual onset

33
Q

What is thoracic outlet syndrome?

A

TOS is a disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet. Can be neurogenic (90% of cases) or vascular.

Happens when neck trauma occurs to individuals with anatomical predispositions - can be a single trauma or repeated stresses
- presence of cervical rib is a well known osseous anomaly

Clinical presentation of neurogenic TOS

  • painless muscle wasting of hands, pts complaining of hand weakness e.g. grasping
  • may have sensory symptoms such as numbness and tingling
  • if autonomic nerves involved may have cold hands, blanching or swelling
34
Q

Management of multiple sclerosis is focused at reducing frequency and duration of relapses as there is no cure. what are the treatments for specific problems such as spasticity?

A

Acute relapse
- high dose steroids e.g. oral or IV methylprednisolone for 5 days

Spasticity

  • baclofen and gabapentin first line. Other options include dizepam, dantorlene and tizanidine
  • physio is important
35
Q

Third nerve palsy features and causes

A

‘down and out’
ptosis
pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)

diabetes, vasculitis

36
Q

Typical cerebellar signs

A

DANISH

D - dysdiadochokinesia, dysmetria
A - ataxia
N - nystagmus 
I - intention tremor
S - slurred speech, staccato, scnaning dysarthria
H - hypotonia
37
Q

Management of neuropathic pain?

A

Causes - diabetic neuropathy, post-herpetic neuralgia, trigeminal neuralgia, prolapsed intervertebral disc

1st line - amitriptyline, duloxetine, gabapentin or pregabalin

  • if first does not work, try one of the other three
  • do not add, switch

tramadol may be used as ‘rescue therapy’ for exacerbations

topical capsaicin for localised neuropathic pain e.g. post herpetic

pain management clinic if resistant problems

38
Q

Tx of epilepsy

A

Following a first seizure, anti-epileptic drug treatment should only be started before specialist review in exceptional circumstances.

Most start tx after a 2nd epileptic seizure, unless pt has other neuro deficits, structural abnormality, EEG shows unequivocal epileptic activity

Sodium valproate first line for generalised and carbamazepine/lamotrigine for focal. (except no valproate in pregnancy for example)

39
Q

Features of motor neuron disease

A

unknown cause which can present with both upper and lower motor neuron signs. It rarely presents before 40 years and various patterns of disease are recognised including amyotrophic lateral sclerosis, progressive muscular atrophy and bulbar palsy.

  • fasciculations
  • absence of sensory signs/symptoms
  • mix of UMN and LMN signs
  • wasting of small hand muscles/tibialis anterior is common
  • doesn’t affect external ocular muscles
  • no cerebellar signs
40
Q

Features of a common peroneal nerve lesion

A

The sciatic nerve divides into the tibial and common peroneal nerves. Injury often occurs at the neck of the fibula

The most characteristic feature of a common peroneal nerve lesion is foot drop.

Other features include:

  • weakness of foot dorsiflexion
  • weakness of foot eversion
  • weakness of extensor hallucis longus
  • sensory loss over the dorsum of the foot and the lower lateral part of the leg
  • wasting of the anterior tibial and peroneal muscles
41
Q

Features of parkinsons

A

Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra
Classic triad - bradykinesia, tremor and rigidity
Symptoms classically ASYMMETRICAL

Bradykinesia

  • and poverty of movement also seen
  • short shuffling steps with reduced arm swinging
  • difficulty in initiating movement

Tremor

  • most marked at rest 3-5Hz
  • worse when stressed or tired, improves with voluntary movement
  • typically pill rolling

Rigidity

  • lead pipe
  • cogwheel due to superimposed tremor

Other characteristic features
- mask like facies, flexed posture, micrographia, drooling of saliva, psychiatric features (depression), dementia, sleep disturbances, fatigue, hypotension

42
Q

How is drug induced parkinsonism usually different to PD

A

Motor symptoms are generally rapid onset and bilateral

Rigidity and rest tremor are uncommon

43
Q

Chronic subdural haematoma characteristics

And what’s seen on imaging

A

Collection of blood within the subdural space that has been present for weeks to months usually due to rupture of the small bridging veins causing slow bleeding.

Affects elderly and alcoholics particularly due to brain atrophy making fragile or taut bridging veins.

Several week to month progression of either confusion, reduced consciousness or neurological deficit

Crescentic in shape, not restricted by suture lines. Hypodense compared to the substance of the brain (contrasts to acute subdural haematomas)

If incidental/small in size/no deficit - conservatively

If associated deficit or severe image findings - surgical decompression with burr holes

44
Q

What is normal pressure hydrocephalus and how to manage?

A

Wet, whacky, wobbly

Reversible cause of dementia seen in elderly patients.
Thought to be secondary to reduced CSF absorption at the arachnoid villi. These changes may be secondary to head injury, subarachnoid haemorrhage or meningitis

Classic triad

  • urinary incontinence
  • dementia and bradyphrenia
  • gait abnormality (may be similar to PD)

Imaging

  • hydrocephalus with an enlarged fourth ventricle
  • in addition there is typically an absence of substantial sulcal atrophy

Mx

  • ventriculoperitoneal shunting
  • around 10% of patients will get complications from this
45
Q

Acute subdural haematoma?

A

Collection of free blood within the subdural space and is most commonly caused by high-impact trauma

CT first line - crescentic collection not limited by suture lines, hyperdense in comparison to the brain.
- large acute subdural haematomas will push on the brain and cause midline hsift or herniation

Small or incidental acute subdurals can be observed conservatively. Surgical options include monitoring of intracranial pressure and decompressive craniectomy.

46
Q

Subacute combined degeneration of spinal cord?

A

due to vitamin B12 deficiency
dorsal + lateral columns affected
joint position and vibration sense lost first then distal paraesthesia
upper motor neuron signs typically develop in the legs, classically extensor plantars, brisk knee reflexes, absent ankle jerks
if untreated stiffness and weakness persist

Final year recaps/management (7 decks)

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