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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

Emergencies

How is coma measured?

A

On the Glascow Coma Scale

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2
Q

Emergencies

What are criteria for a coma?

A

GCS <8

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3
Q

Emergencies

List the eye responses and their grading on the GCS

A
  1. No eye opening
  2. Opens to painful stimulus
  3. Opens to voice
  4. Spontaneously open
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4
Q

Emergencies

List the voice responses and their grading on the GCS

A
  1. No speech
  2. Incoherent speech
  3. Inappropriate words
  4. Confused
  5. Orientated
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5
Q

Emergencies

List the motor responses and their grading on the GCS

A
  1. No movement
  2. Extending
  3. Flexing
  4. Withdraws from painful stimulus
  5. Localises to painful stimulus
  6. Obeys commands
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6
Q

Emergencies

What are the common causes of coma?

A

Drugs, toxins (opiates, alcohol)
Head injury
Metabolic (Hypoglycaemia, DKA, hepatic encephalopathy, uraemia)
Seizures
Anoxia (post arrest)
Mass lesions (bleeds, abscess)
Infections (HSE, bacterial meningitis)
Infarcts (brainstem)
SAH

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7
Q

Neurology

What might purposeful eye movement indicate in a patient who is otherwise unresponsive?

A

A psychogenic cause e.g., catatonia or locked-in syndrome

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8
Q

Neurology

What might blood or clear fluid in the ears indicate in an unresponsive patient?

A

Blood or leakage of CSF in the ears can indicate a fracture at the base of the skull

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9
Q

Neurology

What may periorbital bruising or bruising around the mastoid process indicate in a patient who is unresponsive?

A

Basilar skull fracture

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10
Q

Neurology

What investigations should be performed for a patient that has reduced GCS?

A

Depending on suspected causes
Basic bloods including glucose (FBC, U&E, LFTs)
If indicated:
* ABG
* Imaging (CT or MRI)
* Lumbar puncture
* EEG
* Toxilogy and alcohol levels

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11
Q

Neurology

How does herpes simplex encephalitis present?

A

Affects temporal lobes
* Fever
* Headache
* Psychiatric symptoms
* Seizures
* Vomiting
* Focal features e.g., aphasia

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12
Q

Neurology

What investigations should be performed for suspected herpes simplex encephalitis?

A

CSF: lymphocytosis, high protein
PCR for HSV
CT: medial temportal and inferior frontal changes, no changes in a third of patients
MRI more reliable
EEG: lateralised periodic discharges at 2Hz

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13
Q

Neurology

What is the treatment for herpes simplex encephalitis?

A

IV aciclovir

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14
Q

Neurology

What is status epilepticus?

A

Seizure lasting:
* 5 minutes for generalised tonic-clonic seizures
* 10 minutes for focal seizures
* 10-15 minutes for absence seizures

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15
Q

Neurology

What are the complications of status epilepticus?

A
  • Increased CNS metabolic consumption
  • Rhabdomyolysis
  • Renal failure
  • Metabolic acidosis
  • Hyperthermia
  • Heart and other organ effects
  • End organ damage due to lack of oxygen
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16
Q

Neurology

What is the management of status epilepticus?

A
  1. Benzodiazepam if fitting >5mins
  2. Second dose of benzodiazepam after 10 minutes
  3. Phenytoin or levetiracetam or sodium valproate + inform ICU
  4. General anaesthesia with intubation and ventilation
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17
Q

Neurology

How does third nerve palsy present?

A

Ptosis with diplopia on upward gaze
Eye deviated ‘down and out’
Pupil may be dilated

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18
Q

Neurology

What is associated with sudden onset headache + CN III palsy OR painful CN III palsy?

A

Sub-arachnoid haemorrhage

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19
Q

Neurology

What are the causes of SAH?

A

Most commonly ruptured saccular aneurysms
Non-aneurysmal:
* trauma
* cranial or spinal vascular malformations
* dissection of an intracranial artery
* illicit drug use
* cerebral venous thrombosis

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20
Q

Neurology

How does SAH present?

A
  • ‘Thunderclap’ headache - within one minute, very severe
  • Transient loss of consciousness
  • Vomiting
  • Meningism (neck pain or stiffness)
  • Altered neurology, seizures or focal neurological deficit
  • Sentinel headache (previous sudden severe headache)
  • O/E: CN III palsy, subhyaloid haemorrhage, may have bilateral extensor plantar responses
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21
Q

Neurology

What investigations should be performed for SAH?

A

CT head
CT angiogram or MRI/MR angiogram
Lumbar puncture 12 hours after the event - high red cell count,

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22
Q

Neurology

What is an aneurysm?

A

Ballooning at a weak spot in an artery wall

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23
Q

Neurology

What is the investigation for aneurysms?

A

Angiography

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24
Q

Neurology

What is the definitive management of aneurysms?

A

Endovascular coiling or neurosurgical clipping

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25
Q

Neurology

How does Guillian-Barre syndrome present?

A
  • acute or subacute
  • demyelinating > axonal
  • immue-mediated, post infectious (resp or GI common)
  • multifocal polyradiculo-neuritis
  • numbness starts distally
  • progressive ascending weakness
  • bifacial weakness and other cranial neuropathies
  • flaccid tetra/para paresis
  • areflexia
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26
Q

Neurology

How is Guillian-Barre syndrome diagnosed?

A

CSF: cyto-protein dissociation/pleocytosis, elevated protein, few or no cells
EMG: slow nerve conduction velocities

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27
Q

Neurology

What are the complications of Guillian-Barre syndrome?

A

Severe weakness
Aspiration
Respiratory failure
Autonomic instability: major cause of death, severe sudden hypotension and cardiac arrhythmia

28
Q

Neurology

How is Guillian-Barre syndrome managed?

A
  • Hospital admission
  • ITU care: <1 vital capacity OR sniff pressures, counting in one breath
  • DVT prophylaxis
  • BP
  • ECG
  • Monitor swallow: NG feeding may be needed
  • Treatment: IV Ig or plasma exchange
29
Q

Neurology

How does an upper motor neurone lesion present on examination?

A

Bulk: normal
Tone: increased
Strength: decreased
Fasculations: absent
Reflexes: increased

30
Q

Neurology

How does a lower motor neurone lesion present on examination?

A

Bulk: reduced (wasting)
Tone: normal or decreased
Strength: decreased
Fasciculations: may be present
Reflexes: decreased or absent

31
Q

Neurology

How is damage to the peripheral nerves classified?

A

Polyneuropathy
Mononeuritis multiplex: at least two nerves
Mononeuropathy: one single nerve

32
Q

Neurology

How does polyneuropathy present?

A

Affects peripheral nerves
Usually chronic and slowly progressive
Starts in the legs and longer nerves
Sensory, motor or both

33
Q

Neurology

What causes peripheral neuropathy with predominantly motor loss?

A
  • Guillian Barre syndrome
  • Chronic Inflammatory demyelinating polyneuropathy (CIDP, chronic version of GBS)
  • Hereditary sensorimotor neuropathies (HSMN) e.g., Charcot-Marie-Tooth disease
  • Diptheria
  • Porphyria
34
Q

Neurology

What causes peripheral neuropathy with predominantly sensory loss?

A

Deficiency states e.g., B12/folate
Diabetes
Alcohol/toxins/drugs
Metabolic abnormalities e.g., uraemia
Leprosy
Amyloidosis

35
Q

Neurology

What is mononeuritis multiplex and how does it present?

A

Painful, asymmetrical sensory and motor neuropathy
* Subacute presentation
* Inflammatory/immune mediated

36
Q

Neurology

What are the causes of mononeuritis multiplex?

A

Vasculitides e.g., Churg Strauss
Connective tissue disorders e.g., Sarcoid

37
Q

Neurology

What are some examples of mononeuropathy?

A

Median nerve entrapment at the wrist (carpal tunnel syndrome)
Ulnar nerve at elbow
Radial nerve in axilla
Common peroneal nerve in leg

38
Q

Neurology

What investigations should be performed for neuropathy?

A

Neuropathy screen: FBC, ESR, U&E, glucose, TFT, CRP, serum electrophoresis, B12, Folate, Anti-Gliadin, TPHA, HIV
Vasculitic screen: FBC, ESR, U&E, Creatinine, CRP, ANA, ANCA, anti dsDNA, RhF, complement, cryoglobulins
EMG/NCS
CSF study
Imaging/nerve biopsy

39
Q

Neurology

What is the management of neuropathy?

A
  • 20% idiopathic - neuropathic analgesia (gabapentin, pregabalin, amitriptyline)
  • Treat/remove underlying cause
  • Inflammatory: prednisolone with steroid sparing agents e.g., azathioprine
  • Vasculitic: prednisolone with immunosuppresant e.g., cyclophosphamide
40
Q

Neurology

What is myasthenia gravis?

A

An autoimmune disorder, antibodies against nicotinic acetylcholine receptors

41
Q

Neurology

How does myasthenia gravis present?

A
  • More common in women
  • Muscle fatigability - progressively weaker after activity and improves with rest
  • Extraocular muscle weakness: diplopia
  • Proximal muscle weakness: face, neck, limb girdle
  • Ptosis
  • Dysphagia (bulbar symptoms) - especially in elderly
  • Proximal limbs weakness
42
Q

Neurology

What conditions is myasthenia gravis associated with?

A

Other autoimmune diseases e.g., thyroid, pernicious anaemia, rheumatoid, SLE
Thymomas in 15%
Thymic hyperplasia in 50-70%

43
Q

Neurology

What investigations should be performed for myasthenia gravis?

A

Tensilon test: allow accumulation of ACh in the neuromuscular junction
AChR antibodies
EMG (single fibre)
CT thorax to exclude thymoma
Creatinine kinase: normal

44
Q

Neurology

How is myasthenia gravis managed?

A

If symptomatic: acetylcholine esterase inhibitors (pyridostigmine)
Immunosuppresants: steroids, azathioprine/methotrexate/mycophenolate
Thymectomy

45
Q

Neurology

What is myasthenic crisis?

A

Severe weakness including respiratory muscles

46
Q

Neurology

What are the causes of myasthenic crisis?

A

Infection
Natural cycle of disease
Under-dosing or overdosing of medication

47
Q

Neurology

What is the management of myasthenic crisis?

A

Urgent review by neuro
ABCDE, monitor breathing
Anaesthetist review
Plasmapherisis
IV Ig

48
Q

Neurology

What is motor neurone disease?

A

Degeneration of motor neurons in the motor cortex and anterior horns of the spinal cord

49
Q

Neurology

How does motor neurone disease present?

A
  • Both upper and lower motor neurone symptoms
  • fasciculations
  • absence of sensory signs/symptoms
  • wasting of small hand muscles/tibialis anterior
  • not affecting external ocular muscles
  • no cerebellar signs
  • asymmetric weakness
  • no visual involvement
  • bulbar or limb onset
50
Q

Neurology

What investigations should be performed when MND is suspected?

A

Clinical diagnosis, investigations rule out other conditions
LP
NCS/EMG
MRI

51
Q

Neurology

What are some examples of common muscle disorders?

A

Steroid myopathy
Statin myopathy
Metabolic and endocrine myopathies
Myotonic dystrophy

52
Q

Neurology

What are some examples of uncommon muscle disorders?

A

Most muscular dystrophies: Duchenne, Becker, Facioscapulohumeral
Inflammatory muscle disease: Polymyositis, dermatomyositis
Mitochondrial disorders

53
Q

Neurology

How do muscle disorders present?

A
  • Stairs, chairs and hairs
  • Wasting
  • Facial weakness in some e.g., facioscapulohumeral dystrophy
  • Neck weakness
  • Contractures
  • Scoliosis especially in Duchenne
  • Eye movement disorders rare, seen in mitochondrial disorders
54
Q

Neurology

What investigations should be performed for muscle disorders?

A

Creatinine kinase
EMG
ESR/CRP
Genetics
Biopsy

55
Q

Neurology

What is the management of muscle disorders?

A

Remove causal agent
Supportive: occupational therapy, physio, back, renal, diet
Immunosuppress if inflammatory

56
Q

Blackouts

How does syncope present?

A

Before:
* prodrome/precipitant/posture
* minor warning
* standing/hot room/vagal maneuvers
* looked grey/sweaty/clammy
* chest pain/exertion
* sudden startle in long QT syndrome

During:
* rapid onset
* minimum twitching

After:
* rapid recovery
* no confusion

Others:
* previous events
* known low BP
* cardiac drugs
* drugs that cause ECG changes
* family history of cardiac disease

57
Q

Blackouts

How does vasovagal syncope present?

A

Triggered by pain, prolonged standing, emotional stress, instrumentation

58
Q

Blackouts

How does situational syncope present?

A

Micturition, swallow, defecation, cough, sneeze, post-exercise, laughing

59
Q

Blackouts

How does carotid sinus syndrome present?

A

Loss of consciousness while turning head to one side, particularly in men >50 years old

60
Q

Blackouts

What is orthostatic hypotension caused by?

A

Drug induced: vasodilators, diuretics, phenothiazine, antidepressants
Volume depletion: haemorrhage, diarrhoea, vomiting
Primary autonomic failure/neurogenic: pure autonomic failure, multiple system atrophy, Parkinson’s, dementia with Lewy bodies
Secondary autonomic failure/neurogenic: diabetes, amyloidosis, spinal cord injuries, auto-immune autonomic neuropathy, paraneoplastic autonomic neuropathy, kidney failure
Other causes: adrenal insufficiency, cardiac impairment, vasodilation

61
Q

Blackouts

How does epilepsy present?

A

Before:
* no precipitant
* from sleep/sleep deprivation/alcohol withdrawal

During:
* no warning/aura
* posturing of limbs, head turning, eye gaze, groaning/grunting
* tonic then clonic
* very rhythmic shaking then gradually eases off
* no stopping and starting
* short duration <5mins
* eyes open, gaze may be deviated

After:
* confused
* tongue biting, incontinence urine and faeces

Other:
* brain injury/illness
* minor seizures
* family history of epilepsy

62
Q

Blackouts

How does non-epileptic attack disorder present?

A

Before:
* precipitant (often repeated)
* prodrome (patient can’t describe)

During:
* may collapse or shake
* may be prolonged up to 45mins
* wax and wane
* inconsistent
* irregular
* respond during attack
* vary in features
* eyes closed/resisting opening

After:
* quick or slow recovery
* may be emotional

Other:
* patient unable to describe attack but able to describe consequences

63
Q

Blackouts

What investigations should be performed for loss of consciousness?

A

BP lying/standing
heart sounds
ECG
If cardiac suspected: prolonged ECG and echo
If epilepsy suspected: MRI and/or EEG

64
Q

Blackouts

What is the management of syncope?

A

Vasovagal: advice
Orthostatic: review drugs, advice, compression stockings, raise head of bed

65
Q

Blackouts

What is the management of NEAD?

A

Explanation/advice/support
Psychotherapy

Phase 3a (10 decks)

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