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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
# Neurology How does **Guillian-Barre syndrome** present?
* 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
26
# Neurology How is **Guillian-Barre syndrome** diagnosed?
**CSF**: cyto-protein dissociation/pleocytosis, elevated protein, few or no cells **EMG**: slow nerve conduction velocities
27
# Neurology What are the **complications** of **Guillian-Barre syndrome**?
Severe weakness Aspiration Respiratory failure Autonomic instability: major cause of death, severe sudden hypotension and cardiac arrhythmia
28
# Neurology How is **Guillian-Barre syndrome** managed?
* 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
# Neurology How does an **upper motor neurone** lesion present on examination?
Bulk: normal Tone: increased Strength: decreased Fasculations: absent Reflexes: increased
30
# Neurology How does a **lower motor neurone** lesion present on examination?
Bulk: reduced (wasting) Tone: normal or decreased Strength: decreased Fasciculations: may be present Reflexes: decreased or absent
31
# Neurology How is **damage to the peripheral nerves** classified?
Polyneuropathy Mononeuritis multiplex: at least two nerves Mononeuropathy: one single nerve
32
# Neurology How does **polyneuropathy** present?
Affects peripheral nerves Usually chronic and slowly progressive Starts in the legs and longer nerves Sensory, motor or both
33
# Neurology What causes **peripheral neuropathy** with predominantly **motor** loss?
* 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
# Neurology What causes **peripheral neuropathy** with predominantly **sensory** loss?
Deficiency states e.g., B12/folate Diabetes Alcohol/toxins/drugs Metabolic abnormalities e.g., uraemia Leprosy Amyloidosis
35
# Neurology What is **mononeuritis multiplex** and how does it **present**?
Painful, asymmetrical sensory and motor neuropathy * Subacute presentation * Inflammatory/immune mediated
36
# Neurology What are the **causes** of **mononeuritis multiplex**?
Vasculitides e.g., Churg Strauss Connective tissue disorders e.g., Sarcoid
37
# Neurology What are some examples of **mononeuropathy**?
Median nerve entrapment at the wrist (carpal tunnel syndrome) Ulnar nerve at elbow Radial nerve in axilla Common peroneal nerve in leg
38
# Neurology What **investigations** should be performed for **neuropathy**?
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
# Neurology What is the **management** of **neuropathy**?
* 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
# Neurology What is **myasthenia gravis**?
An autoimmune disorder, antibodies against nicotinic acetylcholine receptors
41
# Neurology How does **myasthenia gravis** present?
* 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
# Neurology What conditions is **myasthenia gravis** associated with?
Other autoimmune diseases e.g., thyroid, pernicious anaemia, rheumatoid, SLE Thymomas in 15% Thymic hyperplasia in 50-70%
43
# Neurology What **investigations** should be performed for **myasthenia gravis**?
Tensilon test: allow accumulation of ACh in the neuromuscular junction AChR antibodies EMG (single fibre) CT thorax to exclude thymoma Creatinine kinase: normal
44
# Neurology How is **myasthenia gravis** managed?
If symptomatic: acetylcholine esterase inhibitors (pyridostigmine) Immunosuppresants: steroids, azathioprine/methotrexate/mycophenolate Thymectomy
45
# Neurology What is **myasthenic crisis**?
Severe weakness including respiratory muscles
46
# Neurology What are the **causes** of **myasthenic crisis**?
Infection Natural cycle of disease Under-dosing or overdosing of medication
47
# Neurology What is the **management** of **myasthenic crisis**?
Urgent review by neuro ABCDE, monitor breathing Anaesthetist review Plasmapherisis IV Ig
48
# Neurology What is **motor neurone disease**?
Degeneration of motor neurons in the motor cortex and anterior horns of the spinal cord
49
# Neurology How does **motor neurone disease** present?
* 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
# Neurology What **investigations** should be performed when **MND** is suspected?
Clinical diagnosis, investigations rule out other conditions LP NCS/EMG MRI
51
# Neurology What are some examples of c**ommon muscle disorders**?
Steroid myopathy Statin myopathy Metabolic and endocrine myopathies Myotonic dystrophy
52
# Neurology What are some examples of **uncommon muscle disorders**?
Most muscular dystrophies: Duchenne, Becker, Facioscapulohumeral Inflammatory muscle disease: Polymyositis, dermatomyositis Mitochondrial disorders
53
# Neurology How do **muscle disorders** present?
* 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
# Neurology What **investigations** should be performed for **muscle disorders**?
Creatinine kinase EMG ESR/CRP Genetics Biopsy
55
# Neurology What is the **management** of **muscle disorders**?
Remove causal agent Supportive: occupational therapy, physio, back, renal, diet Immunosuppress if inflammatory
56
# Blackouts How does **syncope** present?
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
# Blackouts How does **vasovagal syncope** present?
Triggered by pain, prolonged standing, emotional stress, instrumentation
58
# Blackouts How does **situational syncope** present?
Micturition, swallow, defecation, cough, sneeze, post-exercise, laughing
59
# Blackouts How does **carotid sinus syndrome** present?
Loss of consciousness while turning head to one side, particularly in men >50 years old
60
# Blackouts What is **orthostatic hypotension** caused by?
**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
# Blackouts How does **epilepsy** present?
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
# Blackouts How does **non-epileptic attack disorder** present?
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
# Blackouts What **investigations** should be performed for **loss of consciousness**?
BP lying/standing heart sounds ECG If cardiac suspected: prolonged ECG and echo If epilepsy suspected: MRI and/or EEG
64
# Blackouts What is the **management** of **syncope**?
Vasovagal: advice Orthostatic: review drugs, advice, compression stockings, raise head of bed
65
# Blackouts What is the **management** of **NEAD**?
Explanation/advice/support Psychotherapy

Phase 3a (10 decks)

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