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Medicine Finals > Neurology > Flashcards

Neurology Flashcards

1
Q

Headaches:

Red flags?

A
  • Fever
  • Focal neurological deficits
  • Seizures
  • Meningism
  • Signs of โ†‘ICP e.g. papilloedema
  • Reduced consciousness level
  • Age >50
  • Progressively worsening headache
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2
Q

Headaches:

Tension headache features?

A
  • F > M
  • 30mins to a few days
  • Whole head/frontal
  • Constant, like a band around the head
  • Often associated with neck tightness
  • May be triggered by stress/lack of sleep
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3
Q

Headaches:

Tension headache management & prophylaxis?

A
  • Acute management: NSAIDs and paracetamol

- Prophylaxis: acupuncture

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4
Q

Headaches:

Migraine headache features?

A
  • F > M
    Features = ๐—ฃ๐—ข๐—จ๐—ก๐——๐—ฆ
  • ๐—ฃulsatile
  • ๐—ขne to three days (4-72hrs) in duration
  • ๐—จnilateral pain (often bilateral in children)
  • ๐—กausea ยฑ vomiting
  • ๐——isabling intensity (moderate-severe, worse with movement)
  • ๐—ฆensitive to sound and light (photo-/phonophobia)
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5
Q

Headaches:

Migraine headache management & prophylaxis?

A
  • Acute management: oral triptan + paracetamol/ibuprofen
  • Prophylaxis: propranolol or topiramate (teratogenic so contraindicated in pregnant women)

(Other treatment options can be started at a specialist headache clinic)

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6
Q

Headaches:

Cluster headache features?

A
  • M > F (only headache commoner in males)
  • Last 15mins - 3hrs
  • Occur in clusters, 1 - 3 per 24hrs
  • Retro-orbital/temporal, burning/piercing pain
  • Associated with lacrimation, ptosis & miosis, suicidal ideation
  • Can be triggered by drinking alcohol
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7
Q

Headaches:

Cluster headache management & prophylaxis?

A
  • Acute management : High flow 100% FiOโ‚‚ oxygen & subcutaneous sumatriptan
  • Prophylaxis: verapamil
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8
Q

Headaches:
Causes of secondary headaches?
(Dozens, name a few)

A
  • Meningitis
  • Intracerebral haemorrhage
  • Subarachnoid haemorrhage
  • Subdural haematoma
  • Epidural haematoma
  • Cerebral venous sinus thrombosis
  • Giant cell arteritis
  • Hypertensive crisis
  • Medication overuse headache
  • Trigeminal neuralgia
  • Space-occupying lesion

etcโ€ฆ.

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9
Q

Headaches:

Typical patient with idiopathic intracranial hypertension?

A

Obese woman aged 15-35

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10
Q

Headaches:

Risk factors for idiopathic intracranial hypertension?

A
  • Female sex
  • Obesity
  • Drugs: tetracyclines, retinoids, lithium, nitrofurantoin
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11
Q

Headaches:

Features of idiopathic intracranial hypertension?

A
  • Diffuse headaches
  • Visual symptoms (transient vision loss, photopsia)
  • Cranial nerve VI dysfunction โ†’ double vision
  • No changes in consciousness
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12
Q

Headaches:

Diagnosis of idiopathic intracranial hypertension?

A
  • MRI โ†’ rules out other causes of raised ICP
  • Fundoscopy โ†’ bilateral papilloedema
  • Lumbar puncture โ†’ increased opening pressure (โ‰ฅ20cmHโ‚‚O), normal CSF
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13
Q

Headaches:

Management of idiopathic intracranial hypertension?

A

Conservative measures:

  • Weight loss
  • Withdraw any causative drugs

Medical management:

  • Acetazolamide
  • Add furosemide if insufficient
  • Alternative = indomethacin

Surgery:

  • Optic nerve sheath fenestration (pierces holes in dura mater surrounding optic nerve to allow CSF drainage)
  • CSF shunt
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14
Q

Headaches:

Prognosis of idiopathic intracranial hypertension?

A
  • May be self-limiting, but recurs in roughly 20%
  • Permanent, severe vision loss/blindness in 10%
  • Life expectancy normal
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15
Q

Headaches:

Features of trigeminal neuralgia?

A
  • Unilateral, paroxysmal facial pain
  • Severe shooting/stabbing pain (like an electric shock)
  • Lasts several seconds and may occur 100 times per day
  • Triggered by movements like chewing or by touch
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16
Q

Headaches:

Diagnosis of trigeminal neuralgia?

A

Diagnosed clinically

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17
Q

Headaches:

Management of trigeminal neuralgia?

A
  • Carbamazepine first line

- Failure to respond or atypical features (e.g. under-50) should prompt referral to neurology

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18
Q

Seizure disorders:

Causes of provoked seizures?

A
  • Traumatic brain injury
  • Stroke
  • CNS infection (e.g. meningitis, encephalitis)
  • Alcohol withdrawal
  • Metabolic disturbances (e.g. hyponatraemia)
  • Recreational drug use
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19
Q

Seizure disorders:

Classification of epileptic seizures?

A

Depends on three criteria:

  • Where the seizure originated (focal/generalised)
  • The patientโ€™s level of awareness during the seizure (aware/impaired awareness)
  • Other features of the seizure (pattern of evolution/change)
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20
Q

Seizure disorders:

Localising features of temporal lobe seizures?

A
  • Automatisms (usually lip smacking, chewing, may also be plucking/grabbing movements)
  • Dysphasia
  • Dรฉjร  vu or jamais vu
  • Emotional disturbances (e.g. sudden terror, anger, or derealisation)
  • Hallucinations
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21
Q

Seizure disorders:

Localising features of frontal lobe seizures?

A
  • Motor features such as dystonic posturing
  • Jacksonian march
  • Motor arrest
  • Dysphasia or speech arrest
  • Toddโ€™s palsy (post-ictal weakness and paralysis of the face and/or limbs, may last minutes or hours)
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22
Q

Seizure disorders:

Localising features of parietal lobe seizures?

A
  • Sensory disturbances - tingling, numbness, pain (rare)

- Motor disturbances (seizure spreads to primary motor cortex)

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23
Q

Seizure disorders:

Localising features of occipital lobe seizures?

A
  • Visual phenomena such as spots, lines, and flashes
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24
Q

Seizure disorders:

Types of generalised seizures?

A

Motor onset

  • Tonic-clonic seizure
  • Clonic seizure
  • Tonic seizure
  • Myoclonic seizure
  • Atonic seizure

Nonmotor (absence seizures)

  • Typical - blank stare, unresponsive
  • Atypical - may be responsive
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25
Q

Seizure disorders:

Management of first seizure episode (unprovoked)?

A
  • Refer to โ€œfirst fitโ€ clinic
  • Patient education and advice (e.g. film/note description of any future events)
  • Long-term medical management NOT typically needed
  • Advise patient not to drive for 6 months, inform DVLA
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26
Q

Seizure disorders:
Pharmacological management of epilepsy?
(Focal seizures)

A

1st line = carbamazepine or lamotrigine

2nd line = levetiracetam (Keppra) or sodium valproate

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27
Q

Seizure disorders:
Pharmacological management of epilepsy?
(Tonic-clonic seizures)

A

1st line = sodium valproate

2nd line = carbamazepine or lamotrigine

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28
Q

Seizure disorders:
Pharmacological management of epilepsy?
(Absence seizures)

A

Sodium valproate or ethosuximide

Carbamazepine may worsen absence seizures

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29
Q

Seizure disorders:
Pharmacological management of epilepsy?
(Myotonic/clonic seizures)

A

1st line = sodium valproate

2nd line = lamotrigine or clonazepam

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30
Q

Seizure disorders:

When can you drive after having a seizure?

A
  • First unprovoked seizure = 6 months
  • Epilepsy = 12 months
  • If epilepsy is controlled (no seizures) for 5 years, may apply for a normal โ€˜til 70 driving license
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31
Q

Seizure disorders:

What is status epilepticus?

A

Either:
- Continuous seizure activity lasting >5 mins without stopping
OR
- โ‰ฅ2 seizures occurring within 5 minutes without the patient returning to normal in between

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32
Q

Seizure disorders:

How do you manage status epilepticus?

A
  • ABCDE approach as it is a medical emergency, then:
  • Stage 1 - IV lorazepam, if no access โ†’ rectal diazepam. Repeat after 10-20 minutes
  • Stage 2 (established S.E.) - IV phenytoin or fosphenytoin
  • Stage 3 (refractory S.E.) - induction of coma (IV propofol/thiopental/phenobarbital)
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33
Q

Seizure disorders:

Consequences of status epilepticus if not promptly managed?

A
  • Cerebral oedema
  • Hyperthermia
  • Rhabdomyolysis
  • Cardiovascular failure
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34
Q

Seizure disorders:

What is West syndrome (aka infantile spasms)?

A
  • A condition of epileptic spasms with an onset within the first year of life
  • Typically accompanied by a global developmental delay.
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35
Q

Seizure disorders:

Features and diagnosis of West syndrome?

A
  • Sudden, synchronous spasms, in clusters of 5-10

- Diagnosed with EEG, showing ๐—ต๐˜†๐—ฝ๐˜€๐—ฎ๐—ฟ๐—ฟ๐—ต๐˜†๐˜๐—ต๐—บ๐—ถ๐—ฎ

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36
Q

Seizure disorders:

Management of West syndrome?

A
  • 1st line = vigabatrin
  • 2nd line = ACTH
  • Poor prognosis (33% mortality by 1 year old)
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37
Q

Seizure disorders:

What is Lennox-Gastaut syndrome?

A

A rare, complex childhood epilepsy syndrome characterised by a variety of different seizure types, with a significant cognitive dysfunction

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38
Q

Seizure disorders:

Diagnosis of Lennox-Gastaut syndrome?

A
  • History: multiple seizure types, 50% have history of West syndrome
  • EEG: ๐˜€๐—น๐—ผ๐˜„ ๐˜€๐—ฝ๐—ถ๐—ธ๐—ฒ-๐˜„๐—ฎ๐˜ƒ๐—ฒ ๐—ฝ๐—ฎ๐˜๐˜๐—ฒ๐—ฟ๐—ป
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39
Q

Seizure disorders:

Management of Lennox-Gastaut syndrome?

A
  • Antiepileptics
  • Ketogenic diet may help
  • Poor prognosis (high mortality, only 10% have controlled symptoms)
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40
Q

Seizure disorders:

Symptoms of a simple febrile seizure?

A
  • Symmetrical, generalised tonic-clonic seizure
  • Lasts < 15 mins
  • Short post-ictal phase (full recovery by 1 hour)
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41
Q

Seizure disorders:

Symptoms of a complex febrile seizure?

A

Any of:

  • Focal onset
  • Lasts > 15 mins
  • Asymmetrical generalised seizure
  • Multiple seizures within 24hrs
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42
Q

Seizure disorders:

Management of a febrile seizure?

A
  • All complex seizures should be referred to a specialist

- May be diagnosed clinically if obvious, refer to first fit clinic wherever there is any doubt

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43
Q

Seizure disorders:

Prognosis of febrile seizures?

A
  • 33% will have another febrile seizure
  • Risk of epilepsy increases if: family history, complex febrile convulsion, history of neurodevelopmental delay
  • Advise parents to call ambulance if seizure lasts >5 minutes
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44
Q

Seizure disorders:

Side effects of phenytoin?

A 
๐—ฃ-450 inducer (phenyto-in-ducer)
๐—›irsutism
๐—˜nlarged gums (gingival hyperplasia)
๐—กystagmus
๐—ฌellow-brown skin (melasma)
๐—งeratogenic
๐—ขsteomalacia
๐—œnteracts with folate
๐—กeuropathy
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45
Q

Seizure disorders:

Side effects of valproate?

A 
๐—ฉomiting & nausea
๐—”norexia
๐—Ÿiver toxicity
๐—ฃancreatitis
๐—ฅetaining weight
๐—ขedema
๐—”lopecia
๐—งeratogenic
๐—˜nzyme inhibitor
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46
Q

Brain tumours:

Commonest brain tumours in children?

A

Most are primary tumours:

  • Pilocytic astrocytoma (commonest benign)
  • Medulloblastoma (commonest malignant)
  • Ependymoma
  • Craniopharyngioma
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47
Q

Brain tumours:

Commonest brain tumours in adults?

A

Most are metastatic

Brain primaries account for around 2% of adult cancers:

  • Glioblastoma multiforme (commonest malignant)
  • Meningioma (commonest benign)
  • Schwannoma
  • Oligodendroglioma
  • Pituitary adenoma
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48
Q

Brain tumours:

Commonest sources of brain metastases?

A
  • Lung cancer (commonest)
  • Breast cancer
  • Renal cell carcinoma
  • Colorectal cancer
  • Malignant melanoma
  • Prostate cancer
  • Testicular cancer
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49
Q

Brain tumours:

Presentation of brain tumours?

A
  • Often asymptomatic, especially when small
  • Focal neurological deficits when they grow larger, dependant on the type and location of the tumour
  • May also show signs and symptoms of raised ICP
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50
Q

Brain tumours:

Features of raised intracranial pressure?

A

Symptoms:

  • Progressive headache, worst when lying down and worsened by Valsalva manoeuvre
  • Nausea and vomiting

Signs:

  • Papilloedema
  • Cushingโ€™s triad (bradycardia, wide pulse pressure, irregular breathing)
  • Reduced consciousness
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51
Q

Brain tumours:
What is a glioblastoma multiforme (GBM)?
How is it diagnosed, and what is the prognosis?

A
  • Fast-growing, malignant brain tumour
  • Arises from astrocytes
  • Ring enhancing lesion with perifocal oedema on CT
  • Incurable
  • Rapid death after onset of symptoms (often within wks)
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52
Q

Brain tumours:
What are acoustic neuromas (aka vestibular schwannomas)?
What does the presence of bilateral acoustic neuromas indicate?

A
  • Tumours arising from Schwann cells, predominantly those in the vestibular portion of CN VIII
  • Bilateral acoustic neuromas is highly suggestive of neurofibromatosis type 2 (NF2)
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53
Q

Brain tumours:

Features of acoustic neuromas?

A
  • Unilateral sensorineural hearing loss (commonest symptom)
  • Tinnitus
  • Vertigo

In later stages they can compress CN V and CN VII at the cerebellopontine angle, causing facial numbness and facial paralysis

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54
Q

Brain tumours:

Diagnosis of acoustic neuromas?

A

Cranial nerve testing:

  • Rinneโ€™s test (air > bone conduction)
  • Weberโ€™s test (lateralises to normal ear)
  • Audiometry

Imaging
- MRI of the cerebellopontine angle (gold standard for dx)

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55
Q

Brain tumours:

Treatment and prognosis of acoustic neuromas?

A
  • If small and asymptomatic or in an especially elderly patient, can be managed expectantly with regular MRI screening
  • If significantly large or symptomatic, surgery or radiation therapy are most appropriate

Good prognosis: neuromas are WHO grade 1 and have <5% rate of recurrence

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56
Q

Brain tumours:

What are the main types of pituitary adenoma (i.e. what do they secrete)?

A
  • Prolactinoma (prolactin, 40% of pituitary adenomas)
  • Somatroph (growth hormone โ†’ acromegaly, 10-15%)
  • Corticotroph (ACTH โ†’ Cushingโ€™s disease, 5%)
  • Thyrotroph (TSH, 1%)
  • Gonadotroph (FSH & LH, rare)
  • โˆผ35% are non-secretory โ€œincidentalomasโ€
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57
Q

Brain tumours:

Symptoms of a prolactinoma?

A

Women:

  • Glactorrhoea
  • Amenorrhoea
  • Reduced bone density due to suppression of oestrogen

Men:

  • Gynaecomastia
  • Reduced libido
  • Infertility

All macroadenomas can cause a bitemporal hemianopia

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58
Q

Brain tumours:

Management of pituitary adenomas?

A
  • Prolactinoma = bromocriptine 1st line, surgery 2nd line
  • All other macroadenomas = trans-sphenoidal surgery
  • Octreotide = 2nd line for GH secreting adenomas
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59
Q

Brain tumours:

An important complication of pituitary adenomas?

A

Pituitary apoplexy: infarction of the pituitary resulting from ischaemia/haemorrhage

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60
Q

Meningitis:

Commonest organisms in children aged <1 month?

A
  • ๐—š๐—ฟ๐—ผ๐˜‚๐—ฝ ๐—• ๐˜€๐˜๐—ฟ๐—ฒ๐—ฝ๐˜๐—ผ๐—ฐ๐—ผ๐—ฐ๐—ฐ๐—ถ (commonest cause in neonates aged โ‰ค72h)
  • Listeria monocytogenes
  • Gram-negative bacilli (e.g. E. coli)
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61
Q

Meningitis:

Commonest organisms in children aged between 1 month and 2 years?

A
  • ๐—ฆ๐˜๐—ฟ๐—ฒ๐—ฝ๐˜๐—ผ๐—ฐ๐—ผ๐—ฐ๐—ฐ๐˜‚๐˜€ ๐—ฝ๐—ป๐—ฒ๐˜‚๐—บ๐—ผ๐—ป๐—ถ๐—ฎ๐—ฒ
  • Neisseria meningitidis
  • Group B strep (e.g. S. agalactiae)
  • Haemophilus influenzae B (if not vaccinated)
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62
Q

Meningitis:

Commonest organism in teenagers aged 11 - 17?

A
  • ๐—ก๐—ฒ๐—ถ๐˜€๐˜€๐—ฒ๐—ฟ๐—ถ๐—ฎ ๐—บ๐—ฒ๐—ป๐—ถ๐—ป๐—ด๐—ถ๐˜๐—ถ๐—ฑ๐—ถ๐˜€ (gram-negative diplococci)
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63
Q

Meningitis:

Commonest organisms in adults?

A
  • ๐—ฆ๐˜๐—ฟ๐—ฒ๐—ฝ๐˜๐—ผ๐—ฐ๐—ผ๐—ฐ๐—ฐ๐˜‚๐˜€ ๐—ฝ๐—ป๐—ฒ๐˜‚๐—บ๐—ผ๐—ป๐—ถ๐—ฎ๐—ฒ
  • E. coli
    (+ ๐—Ÿ๐—ถ๐˜€๐˜๐—ฒ๐—ฟ๐—ถ๐—ฎ ๐—บ๐—ผ๐—ป๐—ผ๐—ฐ๐˜†๐˜๐—ผ๐—ด๐—ฒ๐—ป๐—ฒ๐˜€ in >50s)
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64
Q

Meningitis:

Commonest organisms in immunocompromised patients?

A
  • ๐—Ÿ๐—ถ๐˜€๐˜๐—ฒ๐—ฟ๐—ถ๐—ฎ ๐—บ๐—ผ๐—ป๐—ผ๐—ฐ๐˜†๐˜๐—ผ๐—ด๐—ฒ๐—ป๐—ฒ๐˜€
  • ๐—ฆ๐˜๐—ฟ๐—ฒ๐—ฝ๐˜๐—ผ๐—ฐ๐—ผ๐—ฐ๐—ฐ๐˜‚๐˜€ ๐—ฝ๐—ป๐—ฒ๐˜‚๐—บ๐—ผ๐—ป๐—ถ๐—ฎ๐—ฒ
  • ๐—›๐—ฎ๐—ฒ๐—บ๐—ผ๐—ฝ๐—ต๐—ถ๐—น๐˜‚๐˜€ ๐—ถ๐—ป๐—ณ๐—น๐˜‚๐—ฒ๐—ป๐˜‡๐—ฎ๐—ฒ ๐—•
  • E. coli
  • Salmonella
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65
Q

Meningitis:
Commonest viral causes?
(Typically cause meningoencephalitis)

A
  • Enteroviruses e.g. coxsackievirus
  • Herpesviruses (mostly HSV2)
  • HIV
  • West Nile virus
  • JC virus (progressive multifocal leukencephalopathy_
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66
Q

Meningitis:

Incubation period of bacterial meningitis?

A

3 - 7 days

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67
Q

Meningitis:

Features of neonatal meningitis?

A

Typically vague, without the classic triad:

  • Lethargy
  • Hypotonia
  • Vomiting
  • Hypo-/hyperthermia
  • Bulging anterior fontanelle (late sign)
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68
Q

Meningitis:

Features of meningitis in children and adults?

A

Classic triad:

  • Fever
  • Headache
  • Nuchal rigidity

Also:

  • Altered mental status
  • Photophobia
  • N&V
  • Seizures
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69
Q

Meningitis:

Two classical signs of meningitis?

A

Kernigโ€™s sign: with a flexed hip, extension of the knee yields pain and resistance
Brudzinskiโ€™s sign: flexion of the neck causes involuntary flexion of the hips and knees

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70
Q

Meningitis:

Additional sign for haematogenous infection (meningococcal septicaemia)?

A
  • Petechial rash

N.B. a maculopapular rash is not uncommon in viral meningitis

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71
Q

Meningitis:

Investigations in suspected meningitis?

A

โ—Management should be initiated immediately with empirical drug therapy, and should not be delayed for investigationsโ—

  • Blood cultures
  • Diagnosis confirmed with LP and CSF analysis
  • CT or MRI with contrast in high-risk patients (e.g. immunocompromised)
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72
Q

Meningitis:

Contraindications to lumbar puncture?

A

Signs of raised ICP (may cause coning)

  • Papilloedema
  • Bulging anterior fontanelle
  • Focal neurological deficit
  • etc.

Petechial rash (septicaemia) - risks worsening/introducing infection in CSF

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73
Q

Meningitis:

What is cerebral coning?

A
  • Coning is when removal of CSF from the spinal cord (e.g. by LP) causes cerebral herniation
  • In inflammatory or neoplastic causes of raised ICP, diagnostic LP creates an acute pressure gradient resulting in the downward displacement of the cerebrum and brainstem. Although rare, this is usually terminal.
  • Hence, LP is contraindicated whenever there is a raised ICP*

*The exception to this rule is where the raised ICP is due to increased CSF production, such as in idiopathic intracranial hypertension, where LPs are therapeutic

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74
Q

Meningitis:
Findings of CSF analysis in bacterial meningitis?
(Normal values in brackets)

A 
Appearance: cloudy, purulent fluid
White cell count: >1000/mmยณ  (< 5)
Opening pressure: โ†‘โ†‘   (5-18cmHโ‚‚O)
Protein: โ†‘    (15-45mg/dL)
Glucose: โ†“    (40-75mg/dL)
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75
Q

Meningitis:
Findings of CSF analysis in viral meningitis?
(Normal values in brackets)

A 
Appearance: clear fluid
White cell count: โ†‘ lymphocytes
Opening pressure: -/โ†‘   (5-18cmHโ‚‚O)
Protein: -/โ†‘   (15-45mg/dL)
Glucose: normal (15-45mg/dL)
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76
Q

Meningitis:

Empirical antibiotic therapy in patients aged < 3 months?

A
  • IV cefotaxime + amoxicillin (or ampicillin)
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77
Q

Meningitis:

Empirical antibiotic therapy in patients aged between 2 months and 50 years?

A
  • IV cefotaxime (or ceftriaxone)
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78
Q

Meningitis:

Empirical antibiotic therapy in patients aged > 50 years?

A
  • IV cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin)
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79
Q

Meningitis:

Antibiotic therapy in meningococcal meningitis?

A
  • IV benzylpenicillin OR cefotaxime OR ceftriaxone
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80
Q

Meningitis:

Antibiotic therapy in meningitis caused by listeria?

A
  • IV amoxicillin OR ampicillin OR gentamicin
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81
Q

Meningitis:

What can be given to reduce the risk of neurological complications?

A
  • IV dexamethasone

withhold in septicaemia, sepsis or if immunocompromised

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82
Q

Meningitis:

Prophylaxis for close contacts of patients with bacterial meningitis?

A
  • Offer if close contact within 7 days before onset

- Oral ciprofloxacin or rifampicin

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83
Q

Meningitis:

Management of tuberculous meningitis?

A
  • Same as for pulmonary tuberculosis

- R.I.P.E.

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84
Q

Meningitis:

Complications of meningitis?

A
  • Sensorineural hearing loss (most common)
  • Seizures
  • Cognitive impairment
  • Focal neurological deficit
  • Brain abscess
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85
Q

Meningitis:
Complication of meningococcal septicaemia?
What is it and who does it affect?

A
  • Waterhouse-Friederichson syndrome
  • Intra-adrenal haemorrhage โ†’ hypovolaemic shock
  • Seen almost exclusively in children/asplenic patients
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86
Q

Brain abscess:

Clinical features?

A
  • Dull, persistent headache
  • Focal neurological deficit (usually CN III / CN VI palsies due to raised ICP)
  • Fever
  • Seizures
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87
Q

Brain abscess:

Commonest organisms?

A

Aetiology important:

  • Strep viridans (often secondary to sinusitis)
  • S. aureus
  • If immunocompromised โ†’ ๐˜๐—ผ๐˜…๐—ผ๐—ฝ๐—น๐—ฎ๐˜€๐—บ๐—ผ๐˜€๐—ถ๐˜€
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88
Q

Brain abscess:

Diagnosis?

A

Blood tests:

  • โ†‘CRP
  • โ†‘WCC

Imaging (CT/MRI):

  • Best initial test
  • Shows necrotic core & peripheral ring enhancement

Biopsy:

  • Confirms diagnosis
  • Can be used for M, C & S
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89
Q

Brain abscess:

Management?

A

Surgery:
- Craniotomy โ†’ incision and drainage

Antibiotic therapy (< 2.5cm, no raised ICP):
- IV ceftriaxone and metronidazole

Management of ICP if raised:
- IV dexamethasone

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90
Q

Herpes simplex encephalitis:

Clinical features?

A

Prodromal phase (N&V, headache, fever)

Acute encephalitis:

  • Reduced consciousness
  • Seizures
  • Focal neurological deficits (e.g. ataxia, memory loss, changes in smell and loss of vision)

N.B. may present similarly to meningitis, although the triad above is more common in HSV encephalitis

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91
Q

Herpes simplex encephalitis:

Diagnosis?

A

โ—Progressses very rapidly and diagnosis should not delay management if suspectedโ—

  • CSF PCR for HSV-1 and HSV-2 = gold standard initial test
  • MRI head = most specific and sensitive test (shows hyperintense temporal lobe lesions)
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92
Q

Herpes simplex encephalitis:

Management?

A

Immediate IV aciclovir

- Monitor for nephrotoxicity, keep the patient hydrated

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93
Q

Toxoplasmosis:

Clinical manifestations?

A

Immunocompetent patient
- Typically asymptomatic

Immunocompromised patient
- Cerebral toxoplasmosis (most common neurological AIDS-defining illness)

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94
Q

Cerebral toxoplasmosis:

Clinical features?

A
  • Fever
  • Headache
  • Change in level of consciousness
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95
Q

Cerebral toxoplasmosis:

Diagnosis?

A

CT or MRI with contrast:

- MULTIPLE, ring-enhancing lesions

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96
Q

Cerebral toxoplasmosis:

Management?

A

Toxo๐—ฃ๐—Ÿa๐—ฆmosis

  • ๐—ฃyrimethamine
  • ๐—Ÿeucovorin
  • ๐—ฆulfadiazine
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97
Q

Tetanus:
Whatโ€™s the causative organism?
How does infection occur?

A
  • Clostridium tetani

Wounds with compromised blood supply create anaerobic conditions for growth, such as:

  • Deep penetrating wounds
  • Open fractures
  • Burns
  • Surgical wounds
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98
Q

Tetanus:

Pathophysiology?

A
  • C. tetani produces tetanospasmin, a toxin
  • This travels retrograde up axons, preventing GABA transmission in the spinal cord
  • This lack of inhibition causes constant firing of motor neurones
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99
Q

Tetanus:

Clinical features?

A

Generalised tetanus; painful muscle spasms and rigidity

  • Trismus (lockjaw)
  • Abnormal facial expressions (called risus sardonicus)
  • Arched back

Life-threatening complications:

  • Laryngospasm
  • Autonomic dysfunction
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100
Q

Tetanus:

Diagnosis?

A

Clinical - presence of classical muscle spasms associated with a possible entry point for bacteria

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101
Q

Tetanus:

Prevention and management?

A
  • Childhood vaccination
  • Wound cleaning and debridement

Consider need for tetanus vaccine or immunoglobulin:
- If patient has had a full course of vaccination with last dose within 10 years:
โ€ข no vaccine or Ig is needed, regardless of wound severity

  • Patient has had full course of vaccines, last dose >10 years ago:
    โ€ข high-risk wound โ†’ vaccine & immunoglobulin
    โ€ข medium-risk โ†’ vaccine
  • Patient not had vaccines/vaccination status unknown:
    โ€ข vaccine regardless of wound severity
    โ€ข for medium and high-risk wounds give Ig too
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102
Q

Rabies:

How is it transmitted and how does it spread through the CNS?

A
  • Expressed by salivary glands in affected animals
  • Transmitted through bites, most commonly from dogs and bats
  • Binds to ACh receptor of peripheral nerves in the bite wound โ†’ migrates retrogradely up axons โ†’ infects the brain
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103
Q

Rabies:

Incubation period?

A

4 - 12 weeks average

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104
Q

Rabies:

What are the two types?

A
  • Encephalitic (furious) rabies

- Paralytic rabies

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105
Q

Rabies:

Features of encephalitic rabies?

A
  • ๐—›๐˜†๐—ฑ๐—ฟ๐—ผ๐—ฝ๐—ต๐—ผ๐—ฏ๐—ถ๐—ฎ (involuntary, painful pharyngeal contractions when the patient attempts to drink water)
  • CNS symptoms (e.g. anxiety, confusion, photophobia)
  • Hypersalivation
  • Coma and death occur within days to weeks of neurological symptom onset
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106
Q

Rabies:

Features of paralytic rabies?

A
  • Flaccid paralysis
  • Paraplegia
  • Respiratory failure and death
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107
Q

Rabies:

Diagnosis?

A
  • Clinical features after an animal bite

- Usually diagnosed in post-mortem

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108
Q

Rabies:

Management?

A
  • Assess risk (find and test animal if possible)
  • Clean and debride wound
  • Initiate PEP (rabies immunoglobulin AND vaccine)
109
Q

Shingles:

What is it?

A

Reactivation of herpes zoster that was dormant in a dorsal root ganglion

110
Q

Shingles:

Clinical features?

A

Dermatomal distrubution of:

  • Burning/stabbing pain & hyperesthesia
  • Erythematous maculopapular rash โ†’ vesicular rash
111
Q

Shingles:

Treatment?

A
  • Oral acyclovir (IV if immunocompromised)

- Neuropathic painkillers if needed

112
Q

Shingles:

Complications?

A
  • Post-herpetic neuralgia

- Herpes zoster encephalitis

113
Q

Neurosyphilis:

What is it?

A

Invasion of the CNS by syphilis, causing inflammation of the meninges and cortex

114
Q

Neurosyphilis:

Signs and symptoms?

A

General symptoms:

  • Personality changes and memory loss
  • Neuro symptoms e.g. tremor, dysarthria and hypotonia

Signs:
- Argyll-Robertson pupil - absent light reflex, but constrict with accommodation (looking at a near object)

Tabes dorsalis:

  • Late-stage manifestation
  • Demyelination of the dorsal columns
  • Causes wide, ataxic gait, loss of proprioception and vibration sense, and absent reflexes
115
Q

Vertigo:

What is benign paroxysmal positional vertigo (BPPV)?

A
  • Idiopathic condition
  • Dysfunction of the semicircular canals due to the presence of canaliths (crystals)
  • Changes in head position โ†’ abnormal vestibulocochlear nerve stimulation โ†’ severe vertigo lasting seconds
116
Q

Vertigo:

BPPV features?

A
  • Episodic, severe vertigo
  • Stimulated by changing head position
  • Lasts several seconds (โ‰ค 1 minute)
  • Transient horizontal nystagmus

DOES NOT cause hearing loss or tinnitus

117
Q

Vertigo:

BPPV diagnosis?

A
  • Can be diagnosed clinically

- Diagnosis made if symptoms provoked by Dix-Hallpike manoeuvre

118
Q

Vertigo:

BPPV management?

A
  • Teach the patient repositioning measures (Epley manoeuvre) - successful in 80%
  • Vestibular suppressants are of limited use, and if used long-term inhibit central compensation, worsening sx
119
Q

Vertigo:

Meniereโ€™s disease pathophysiology?

A

Impaired endolymph absorption from endolymphatic sac โ†’ โ€˜endolymph hydropsโ€™ โ†’ compresses semicircular canals

120
Q

Vertigo:

Meniereโ€™s disease features?

A

Classic triad:

  • Vertigo
  • Tinnitus
  • Asymmetrical, fluctuating sensorineural hearing loss

Other symptoms:

  • Feeling of fullness in the ear
  • N&V
  • Spontaneous horizontal nystagmus
121
Q

Vertigo:

Meniereโ€™s disease diagnosis?

A

Diagnosed clinically, should be confirmed by ENT specialist

122
Q

Vertigo:

Meniereโ€™s disease treatment?

A
  • Symptom prevention: betahistine and vestibular rehabilitation exercises
  • Acute flares: buccal or IM prochlorperazine
123
Q

Vertigo:

Vestibular neuronitis features?

A

Symptoms arising after URTI:

  • Severe, sudden-onset vertigo
  • N&V
  • Gait instability
  • Nystagmus

Typically lasts 1 - 2 days, can be milder but last for months

NO tinnitus/hearing loss

124
Q

Vertigo:

Vestibular neuronitis management?

A
  • Vestibular rehabilitation exercises if chronic symptoms

Acute symptoms:

  • Buccal/intramuscular prochlorperazine if severe
  • Oral prochlorperazine/antihistamines if mild
125
Q

Vertigo:

Labyrinthitis features?

A
  • Inflammation of the vestibular nerve and labyrinth occurring secondary to a URTI

Acute onset of:

  • Vertigo, worsened by, but not triggered by movement
  • Hearing loss
  • Tinnitus
  • N&V
  • Horizontal nystagmus
126
Q

Vertigo:

Labyrinthitis management?

A
  • Episodes are usually self-limiting

- Symptom control with prochlorperazine or antihistamines

127
Q

Alzheimerโ€™s disease:

Pathological changes?

A

Macroscopic:
- Widespread cerebral atrophy, especially of the cortex and hippocampus

Microscopic:

  • ฮฒ-amyloid plaques
  • Neurofibrillary tangles (hyperphosphorylated tau protein โ†’ unstable microtubules)

Biochemical:
- โ†“ACh secondary to forebrain atrophy

128
Q

Alzheimerโ€™s disease:

Clinical features?

A

Cognitive:

  • Short-term memory impairment
  • Insidious onset, slow progression
  • Language impairment
  • Visuospatial disorientation

Non-cognitive:

  • Behavioural changes (apathy, agitation)
  • Depression
  • Urinary incontinence
129
Q

Alzheimerโ€™s disease:

Diagnosis?

A
  • Neuropsychological testing e.g. MMSE
  • CT/MRI will show generalised cerebral atrophy (narrow gyri, widened sulci, enlarged ventricles)
  • Rule out reversible causes of dementia e.g. normal pressure hydrocephalus
130
Q

Alzheimerโ€™s disease:

Non-pharmacological management?

A
  • Offer a range of activities to promote wellbeing
  • Offer group cognitive stimulation therapy
  • Consider options like group reminiscence therapy, cognitive rehabilitation
131
Q

Alzheimerโ€™s disease:

Pharmacological management?

A

Mild-moderate:

  • Acetylcholinesterase inhibitors
  • Donepezil, rivastigmine, galantamine recommended

Moderate-severe:

  • Memantine
  • NMDA receptor antagonist
  • Can be monotherapy or used with ACh-ase inhibitors
132
Q

Alzheimerโ€™s disease:

Management of non-cognitive symptoms?

A

Depression:
- NICE does not recommend antidepressants for mild to moderate depression (SSRIs if severe - avoid TCAs)

Psychosis:
- Only use antipsychotics (e.g. risperidone) if patient is at risk of harm or severely distressed

133
Q

Alzheimerโ€™s disease:

Complications and prognosis?

A
  • Infections
  • Malnourishment/dehydration
  • Intracerebral haemorrhage (โ†‘risk due to amyloid deposits)
  • Mean survival time is 3-10 years after diagnosis
134
Q

Vascular dementia:
Risk factors for vascular dementia?
(Same as stroke risk factors)

A 
๐—ฉascular disease hx e.g. stroke/TIA
๐—”trial fibrillation
๐—ฆmoking
๐—–oronary heart disease
๐—จnderlying genetic predisposition (e.g. thrombophilia)
๐—Ÿipids (hyperlipidaemia)
๐—”ge
๐—ฅaised BP/glucose (hypertension & diabetes)
135
Q

Vascular dementia:

What is it?

A
  • Gradual cognitive decline caused by small or large vessel disease.
  • Large vessel disease โ†’ thrombosis โ†’ localised infarction
  • Small vessel disease โ†’ more diffuse lesions
136
Q

Vascular dementia:

Clinical features?

A
  • ๐—ฆ๐˜๐—ฒ๐—ฝ๐˜„๐—ถ๐˜€๐—ฒ deterioration
  • Often present after months/years

Symptoms vary, but may include:

  • Memory disturbance
  • Gait disturbance
  • Memory disturbance
  • Focal neurological abnormalities e.g. visual change, sensory and/or motor symptoms
137
Q

Vascular dementia:

Diagnosis?

A
  • Can be diagnosed clinically, with use of MMSE and history & examination
  • Diagnosis confirmed with MRI, showing multiple cortical/subcortical infarcts and white matter lesions
138
Q

Vascular dementia:

Treatment?

A
  • Detect and address vascular risk factors to slow/halt progression

Non-pharmacological:
- Offer cognitive stimulation e.g. music & art therapy

Pharmacological:

  • No specific treatment approved
  • ACh-ase inhibitors or memantine can be used in mixed (AD & vascular) dementia
139
Q

Frontotemporal lobar degeneration:

What is it?

A

A varied group of syndromes involving degeneration of frontal, insular, and/or temporal cortices

140
Q

Frontotemporal lobar degeneration:

Epidemiology & onset?

A
  • Typically affects younger people than Alzheimerโ€™s disease

- Insidious, slow onset

141
Q

Frontotemporal lobar degeneration:

Commonest variety?

A

Pickโ€™s disease (frontotemporal dementia)

142
Q

Frontotemporal dementia:

Pathophysiology?

A

Intracellular inclusion bodies (Pick bodies) caused by mutations in tau proteins

143
Q

Frontotemporal dementia:

Clinical features?

A

Early changes in personality and behaviour:

  • ๐—”๐—ฝ๐—ฎ๐˜๐—ต๐˜†
  • ๐——๐—ถ๐˜€๐—ถ๐—ป๐—ต๐—ถ๐—ฏ๐—ถ๐˜๐—ถ๐—ผ๐—ป and hypersexuality

Changes in cognition:

  • ๐—”๐—ฝ๐—ต๐—ฎ๐˜€๐—ถ๐—ฎ
  • Intelligence, memory and orientation initially preserved

Motor deficits:
- ๐—ฃ๐—ฎ๐—ฟ๐—ธ๐—ถ๐—ป๐˜€๐—ผ๐—ป๐—ถ๐˜€๐—บ (later stages)

144
Q

Frontotemporal dementia:

Diagnosis?

A

Clinical diagnosis based on classic features.

CT/MRI:

  • Rule out other pathology
  • Atrophy of frontal and/or temporal lobes
  • โ€œKnife-bladeโ€ appearance of frontal gyri
145
Q

Frontotemporal dementia:

Management?

A

Non-pharmacological management:

  • Supportive care
  • Group therapy

Pharmacological management:

  • Dementia: AChE inhibitors and memantine NOT effective
  • Agitation: benzos, atypical antipsychotics as last resort
  • Depression: SSRIs
146
Q

Frontotemporal lobar degeneration:

What are the two other types?

A
  • Progressive non-fluent aphasia

- Semantic dementia

147
Q

Normal pressure hydrocephalus:

What is it?

A

A ๐—ฟ๐—ฒ๐˜ƒ๐—ฒ๐—ฟ๐˜€๐—ถ๐—ฏ๐—น๐—ฒ cause of ๐—ฑ๐—ฒ๐—บ๐—ฒ๐—ป๐˜๐—ถ๐—ฎ, due to a chronic ๐—ฐ๐—ผ๐—บ๐—บ๐˜‚๐—ป๐—ถ๐—ฐ๐—ฎ๐˜๐—ถ๐—ป๐—ด ๐—ต๐˜†๐—ฑ๐—ฟ๐—ผ๐—ฐ๐—ฒ๐—ฝ๐—ต๐—ฎ๐—น๐˜‚๐˜€ with normal (or episodic increase in) ICP

148
Q

Normal pressure hydrocephalus:

Clinical features?

A

Clinical triad:

  • Wet (urinary incontinence)
  • Wacky (dementia)
  • Wobbly (ataxic, โ€˜magneticโ€™ gait)
149
Q

Normal pressure hydrocephalus:

Diagnosis?

A

MRI:
- Ventriculomegaly without widened sulci

LP confirms dx:

  • Normal opening pressure
  • Symptoms improve after CSF removal
150
Q

Normal pressure hydrocephalus:

Management?

A

Insertion of a ventriculoperitoneal (VP) shunt

151
Q

Creutzfelt-Jakob disease:

What is it?

A
  • A neurodegenerative condition caused by misfolded protein particles, called ๐—ฝ๐—ฟ๐—ถ๐—ผ๐—ป๐˜€.
  • Some prions exist in ๐—ฎ๐—น๐—ฝ๐—ต๐—ฎ-๐—ต๐—ฒ๐—น๐—ถ๐—ฐ๐—ฎ๐—น structures to protect the brain from oxidative radicals
  • When these ๐—บ๐—ถ๐˜€๐—ณ๐—ผ๐—น๐—ฑ ๐—ถ๐—ป๐˜๐—ผ ๐—ฏ๐—ฒ๐˜๐—ฎ-๐—ฝ๐—น๐—ฒ๐—ฎ๐˜๐—ฒ๐—ฑ ๐˜€๐—ต๐—ฒ๐—ฒ๐˜๐˜€, they become insoluble and ๐—ฝ๐—ฟ๐—ผ๐˜๐—ฒ๐—ฎ๐˜€๐—ฒ-๐—ฟ๐—ฒ๐˜€๐—ถ๐˜€๐˜๐—ฎ๐—ป๐˜. They induce other prions to misfold, progressing to ๐˜€๐—ฝ๐—ผ๐—ป๐—ด๐—ถ๐—ณ๐—ผ๐—ฟ๐—บ ๐—ฒ๐—ป๐—ฐ๐—ฒ๐—ฝ๐—ต๐—ฎ๐—น๐—ผ๐—ฝ๐—ฎ๐˜๐—ต๐˜†.
152
Q

Creutzfelt-Jakob disease:

What is variant CJD?

A
  • Cows can develop a prion disease called bovine spongiform encephalopathy (aka โ€œmad cow diseaseโ€)
  • People get infected by eating beef containing prions
153
Q

Creutzfelt-Jakob disease:

Clinical features?

A
  • ๐—ฅ๐—ฎ๐—ฝ๐—ถ๐—ฑ๐—น๐˜† ๐—ฝ๐—ฟ๐—ผ๐—ด๐—ฟ๐—ฒ๐˜€๐˜€๐—ถ๐—ป๐—ด ๐—ฑ๐—ฒ๐—บ๐—ฒ๐—ป๐˜๐—ถ๐—ฎ (weeks-months)
  • ๐— ๐˜†๐—ผ๐—ฐ๐—น๐—ผ๐—ป๐˜‚๐˜€
  • Cerebellar disturbances (e.g. ataxia)
  • Autonomic dysfunction
154
Q

Creutzfelt-Jakob disease:

Diagnosis?

A

CSF analysis:
- โ†‘ 14-3-3 protein

Imaging:
- MRI shows hyperintensity in the basal ganglia

EEG:
- Sharp wave complexes

Diagnosis can only be confirmed by biopsy/autopsy

155
Q

Creutzfelt-Jakob disease:

Management?

A
  • Typically leads to death within a year of symptom onset

- Symptom management and palliation

156
Q

Stroke:

Define stroke

A

Acute neurological injury and cerebral infarction caused by ischaemia or haemorrhage

157
Q

Stroke:

Define transient ischaemic attack

A

Temporary, focal ๐—ถ๐˜€๐—ฐ๐—ต๐—ฎ๐—ฒ๐—บ๐—ถ๐—ฎ, ๐˜„๐—ถ๐˜๐—ต๐—ผ๐˜‚๐˜ ๐—ถ๐—ป๐—ณ๐—ฎ๐—ฟ๐—ฐ๐˜๐—ถ๐—ผ๐—ป or permanent loss of function

158
Q

Stroke:

Types?

A

Ischaemic (85%)

  • Thrombotic
  • Embolic

Haemorrhagic (15%)

  • Intacerebral haemorrhage
  • Subarachnoid haemorrhage
159
Q

Stroke:

Risk factors?

A 
๐—ฉascular disease hx e.g. stroke/TIA
๐—”trial fibrillation
๐—ฆmoking
๐—–oronary heart disease
๐—จnderlying genetic predisposition
๐—Ÿipids (hyperlipidaemia)
๐—”ge
๐—ฅaised BP/glucose (hypertension & diabetes)
160
Q

Ischaemic stroke:

What kind of infarct occurs with systemic hypoperfusion?

A
  • Watershed infarct

- Common during cardiac surgery

161
Q

Ischaemic stroke:
What areas are most vulnerable to hypoxia?
(Sorry for the stupid mnemonic)

A

Remember that ๐—›๐—ถ๐—ฝ๐—ฝ๐—ผs ๐—ก๐—ฒed ๐—ฃ๐˜‚๐—ฟe ๐—ช๐—ฎ๐˜๐—ฒ๐—ฟ:

  • ๐—›๐—ถ๐—ฝ๐—ฝ๐—ผcampus
  • ๐—ก๐—ฒocortex
  • ๐—ฃ๐˜‚๐—ฟkinje fibres (cerebellum)
  • ๐—ช๐—ฎ๐˜๐—ฒ๐—ฟshed areas
162
Q

Ischaemic stroke:

Initial assessment and stablisiation?

A
  • Primary survey
  • Neurological examination

Investigations:

  • Check glucose
  • Arrange emergency non-contrast CT head to rule out intracranial haemorrhage
  • Treatment should not be delayed for any other investigations
  • Other investigations include ECG and carotid artery doppler ultrasound
163
Q

Ischaemic stroke:

Findings on non-contrast CT head?

A

May be normal or show evolving change over time:

  • Hyperacute โ†’ hyperdense occluded vessels
  • Later on all that remains is hypodense parenchyma
164
Q

Ischaemic stroke:

Most sensitive imaging?

A
  • MRI with diffusion-weighted imaging (DWI)
165
Q

Ischaemic stroke:

Management?

A
  • Maintain vital signs within normal levels (avoid rapid lowering of BP โ†’ ischaemia)
  • Aspirin 300mg orally ASAP once haemorrhagic stroke excluded
  • Reperfusion therapy if indicated
166
Q

Ischaemic stroke:

Indications for thrombolysis?

A

IV altiplase if:

  • Administered within ๐Ÿฐ.๐Ÿฑ ๐—ต๐—ผ๐˜‚๐—ฟ๐˜€ of ๐˜€๐˜†๐—บ๐—ฝ๐˜๐—ผ๐—บ ๐—ผ๐—ป๐˜€๐—ฒ๐˜
  • Haemorrhage has been excluded with imaging
167
Q

Ischaemic stroke:

Absolute contraindications for thrombolysis?

A

Any of the following means ๐—ก๐—ข alte-/tenecte๐—ฃ๐—Ÿ๐—”๐—ฆ๐—˜:

  • ๐—กeoplasm (intracranial)
  • ๐—ขesophageal varices
  • ๐—ฃregnancy
  • ๐—Ÿumbar puncture in last 7 days
  • ๐—”ctive bleeding
  • ๐—ฆtroke/TBI in last 3 months
  • ๐—˜pileptiform seizure at stroke onset (โ†’SAH)
168
Q

Ischaemic stroke:

Indications for thrombectomy?

A

Offer ASAP:

  • Within ๐Ÿฒ ๐—ต๐—ผ๐˜‚๐—ฟ๐˜€ of ๐˜€๐˜†๐—บ๐—ฝ๐˜๐—ผ๐—บ ๐—ผ๐—ป๐˜€๐—ฒ๐˜
  • Confirmed occlusion of ๐—ฝ๐—ฟ๐—ผ๐˜…๐—ถ๐—บ๐—ฎ๐—น ๐—ฎ๐—ป๐˜๐—ฒ๐—ฟ๐—ถ๐—ผ๐—ฟ ๐—ฐ๐—ถ๐—ฟ๐—ฐ๐˜‚๐—น๐—ฎ๐˜๐—ถ๐—ผ๐—ป on angiography

OR

  • Within ๐Ÿฎ๐Ÿฐ ๐—ต๐—ผ๐˜‚๐—ฟ๐˜€ of ๐˜€๐˜†๐—บ๐—ฝ๐˜๐—ผ๐—บ ๐—ผ๐—ป๐˜€๐—ฒ๐˜
  • With ๐—ฝ๐—ฟ๐—ผ๐˜…๐—ถ๐—บ๐—ฎ๐—น ๐—ฎ๐—ป๐˜๐—ฒ๐—ฟ๐—ถ๐—ผ๐—ฟ ๐—ฐ๐—ถ๐—ฟ๐—ฐ๐˜‚๐—น๐—ฎ๐˜๐—ถ๐—ผ๐—ป occlusion
  • With a salvagable ๐˜ฑ๐˜ฆ๐˜ฏ๐˜ถ๐˜ฎ๐˜ฃ๐˜ณ๐˜ข around the infarct core
169
Q

Ischaemic stroke:

Secondary prevention?

A
  • Antiplatelet (clopidogrel 1st line, aspirin + dipyridamole 2nd)
  • Carotid endarterectomy only if severe carotid stenosis
170
Q

Ischaemic stroke:

What stroke syndromes are classified in the Bamford Classification system (aka Oxford Stroke Classification)?

A
  • Total anterior circulation infarcts (TACI, 15%)
  • Partial anterior circulation infarcts (PACI, 25%)
  • Lacunar infarcts (LACI, 25%)
  • Posterior circulation infarcts (POCI, 25%)
171
Q

Ischaemic stroke:

What are the symptoms of an anterior circulation infarct, and how do you differentiate a TACI from a PACI?

A
  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction (e.g. dysphasia)
TACI = all 3
PACI = 2/3
172
Q

Ischaemic stroke:

What vessels are involved in TACI and PACI?

A 
TACI = MCA & ACA
PACI = small divisions of MCA & ACA
173
Q

Ischaemic stroke:
Features of lacunar infarcts?
What vessels are affected?

A

Presents with one of:

  1. Pure motor stroke (commonest)
  2. Pure sensory stroke (rare)
  3. Sensorimotor stroke
  4. Ataxic hemiparesis

Affects perforating branches of MCA

174
Q

Ischaemic stroke:
Features of POCI?
What vessels are affected?

A

One of:

  1. Cerebellar syndromes
  2. LOC
  3. Isolated homonymous hemianopia (with macular sparing)

Involves vertebrobasilar arteries

175
Q

Epidural haematoma:

What is it?

A

Bleeding in the epidural space, typically due to damage of the middle meningeal artery which underlies the pterion (weakes part of the skull)

176
Q

Epidural haematoma:

Clinical features?

A
  1. Head trauma โ†’ LOC
  2. Temporary recovery (๐—น๐˜‚๐—ฐ๐—ถ๐—ฑ ๐—ถ๐—ป๐˜๐—ฒ๐—ฟ๐˜ƒ๐—ฎ๐—น)
  3. Rapid decline in neurological status due to โ†‘ICP
177
Q

Epidural haematoma:

Diagnosis?

A

Non-contrast CT head:

  • ๐—•๐—ถ๐—ฐ๐—ผ๐—ป๐˜ƒ๐—ฒ๐˜… ๐—ต๐˜†๐—ฝ๐—ฒ๐—ฟ๐—ฑ๐—ฒ๐—ป๐˜€๐—ฒ lesion
  • Limited by suture lines
  • Possible skull fracture
178
Q

Epidural haematoma:

Management?

A
  • ๐—จ๐—ฟ๐—ด๐—ฒ๐—ป๐˜ ๐—ฐ๐—ฟ๐—ฎ๐—ป๐—ถ๐—ผ๐˜๐—ผ๐—บ๐˜† โ†’ haematoma/clot evacuation โ†’ vessel ligation
179
Q

Subdural haematoma:

What is it?

A

Bleeding into the subdural space (between dura and arachnoid mater), caused by damage to bridging veins

180
Q

Subdural haematoma:

Whoโ€™s at risk, and why?

A
  • Elderly/alcoholic patients โ†’ cerebral atrophy โ†’ bridging veins are fragile
  • Babies โ†’ weak neck muscles and underdeveloped brains โ†’ fragile bridging veins & stronger impact โ†’ โ€˜shaken baby syndromeโ€™
181
Q

Subdural haematoma:

Clinical features?

A
  • Headache
  • Confusion
  • Pupil signs (e.g. CN III palsy)
  • Focal neurological deficits

Can be chronic, with recurrent headaches and declining mental function, eventually progressing to coma

182
Q

Subdural haematoma:
Diagnosis?
(Acute vs. chronic)

A

Non-contrast CT head

  • ๐—ฐ๐—ผ๐—ป๐—ฐ๐—ฎ๐˜ƒ๐—ฒ, ๐—ฐ๐—ฟ๐—ฒ๐˜€๐—ฐ๐—ฒ๐—ป๐˜-๐˜€๐—ต๐—ฎ๐—ฝ๐—ฒ๐—ฑ lesion
  • crosses suture lines, but not midline
Acute = ๐—ต๐˜†๐—ฝ๐—ฒ๐—ฟ๐—ฑ๐—ฒ๐—ป๐˜€๐—ฒ
Chronic = ๐—ต๐˜†๐—ฝ๐—ผ๐—ฑ๐—ฒ๐—ป๐˜€๐—ฒ

N.B. this is the other way round on T2-weighted MRI imaging

183
Q

Subdural haematoma:

Management?

A
  • Small subdurals can be observed

Acute:
- If โ†‘ICP then craniectomy

Chronic:
- If symptomatic then burr hole decompression

184
Q

Subarachnoid haemorrhage:

What is it?

A

Bleeding into the subarachnoid space, typically due to trauma or a ruptured berry aneurysm

185
Q

Subarachnoid haemorrhage:

Features?

A
  • Occipital, โ€˜thunderclapโ€™ headache (very severe and sudden)
  • Meningism (Kernigโ€™s & Brudzinskiโ€™s)
  • Reduced consciousness
  • Seizures
186
Q

Subarachnoid haemorrhage:

Complications?

A
  • Cerebral vasospasm (can cause ischaemic stroke)
  • Hydrocephalus
  • SIADH
  • Lengthens QT โ†’ TdP
187
Q

Subarachnoid haemorrhage:

Diagnosis?

A

Non-contrast CT head:

  • Hyperdense blood in star shaped pattern
  • Normal in 7%

Lumbar puncture:

  • 12 hours after symptom onset
  • Xanthochromia from blood breakdown
  • โ†‘/- opening pressure
188
Q

Subarachnoid haemorrhage:

Management?

A
  • Immediate neurosurgical referral
  • Identify cause
  • Typically treated by coiling
  • Some may require craniotomy and clipping
  • Nimodipine to prevent vasospasm
189
Q

Stroke syndromes:

Where do the cranial nerves arise from? (The rule of 4โ€™s)

A
  • 1-4 from the midbrain*
  • 5-8 from the pons
  • 9-12 from the medulla

Good video on YouTube about the rule of 4โ€™s by Dirty Medicine

190
Q

Stroke syndromes:
Features of lateral medullary syndrome?
What vessels are affected?
(Aka Wallenberg syndrome)

A

๐—Ÿateral ๐— edullary = ๐—Ÿend ๐— e a ๐—›๐—”๐—ก๐——

  • ๐—›ornerโ€™s syndrome
  • ๐—”taxia
  • ๐—กystagmus
  • ๐——๐˜†๐˜€๐—ฝ๐—ต๐—ฎ๐—ด๐—ถ๐—ฎ (key feature)

Caused by occlusion of the vertebral and posterior inferior cerebellar arteries (PICA)

N.B. Can be remembered as Pikachu - PICA occlusion โ†’ canโ€™t chew (dysphagia)

191
Q

Stroke syndromes:
What is locked-in syndrome?
What vessels are affected?

A
  • Bilateral, ventral (anterior) pontine stroke
  • Also caused by demyelination
  • Causes quadriplegia with preserved use of ocular muscles

Occlusion of the ๐—ฏ๐—ฎ๐˜€ilar artery

Think โ€˜locked-in the ๐—ฏ๐—ฎ๐˜€ementโ€™

192
Q

Stroke syndromes:
What are the features of medial medullary syndrome?
What vessels are affected?

A
  1. Contralateral arm and leg weakness
  2. Contralateral vibration & proprioception loss
  3. Tongue deviation towards lesion

Caused by anterior spinal artery occlusion

193
Q

Stroke syndromes:
What are the features of Weberโ€™s syndrome?
What vessels are affected?
(Midbrain lesion)

A
  1. Contralateral hemiplegia
  2. Ipsilateral CN III palsy

Caused by posterior cerebral artery occlusion

194
Q

Stroke syndromes:
Features of Hornerโ€™s syndrome?
What is it caused by?

A
  1. Partial ptosis
  2. Miosis
  3. Hemifacial anhidrosis (loss of sweating)

Caused by compression/damage to the cervical sympathetic chain

195
Q

Spinal cord syndromes:

What is Brown-Sรฉquard syndrome? How does it present?

A
  • Hemisection of the spinal cord

At the level of the lesion:

  • Loss of all modalities of sensation
  • LMN signs (e.g. flaccid paralysis)

Below lesion, ipsilateral:

  • Loss of proprioception, vibration, and fine-touch sensation
  • UMN signs (e.g. spastic paralysis)

Below lesion, contralateral:
- Loss of pain, temperature and crude touch sensation

196
Q

Spinal cord syndromes:

What is syringomyelia?

A

Compression of the central spinal cord due to the presence of a fluid-filled syrinx

197
Q

Spinal cord syndromes:

Clinical features of syringomyelia?

A
  • โ€œ๐—–๐—ฎ๐—ฝ๐—ฒ-๐—น๐—ถ๐—ธ๐—ฒโ€ loss of ๐—ฝ๐—ฎ๐—ถ๐—ป ๐—ฎ๐—ป๐—ฑ ๐˜๐—ฒ๐—บ๐—ฝ๐—ฒ๐—ฟ๐—ฎ๐˜๐˜‚๐—ฟ๐—ฒ sensation

- Can be LMN signs too e.g. wasting

198
Q

Spinal cord syndromes:

Diagnosis of syringomyelia?

A

Can be diagnosed clinically, confirmed with MRI

199
Q

Spinal cord syndromes:

Features of spinal stenosis?

A

Depends on level of narrowing:

  • Lumbar spinal stenosis โ†’ lower back pain and claudication pains
  • Cervical spinal stenosis โ†’ neck pain
200
Q

Spinal cord syndromes:

Diagnosis of spinal stenosis?

A

MRI spine โ†’ narrowing of spinal canal ยฑ compression

201
Q

Spinal cord syndromes:

Management of spinal stenosis?

A
  • Conservative management with NSAIDs and physio

- Surgical decompression if poor response

202
Q

Spinal cord syndromes:

What is autonomic dysreflexia? What condition is it usually seen in?

A
  • Typically seen in complete trans-section of the spinal cord, usually at or above the level of T6
  • Excessive sympathetic and parasympathetic nervous system activation following a stimulus below the level of injury e.g. catheterisation
203
Q

Spinal cord syndromes:

At what level does the cauda equina arise?

A

L1-L2

204
Q

Spinal cord syndromes:

What is cauda equina syndrome?

A

Damage to or compression of the cauda equina with nerve fibres of L3-S5

205
Q

Spinal cord syndromes:

Features of cauda equina syndrome?

A
  • Saddle anaesthesia
  • Asymmetrical flaccid paralysis of the legs
  • Loss of anal sphincter tone โ†’ faecal incontinence
  • Urinary retention
206
Q

Spinal cord syndromes:

Diagnosis of cauda equina syndrome?

A

Urgent MRI

207
Q

Spinal cord syndromes:

Management of cauda equina syndrome?

A

Urgent neurosurgical referral for decompression

208
Q

Spinal cord syndromes:

What is conus medullaris syndrome? How does it differ from cauda equina syndrome?

A

Compression of the conus medullaris at the spinal level of the L1 vertebra

The presentation tends to be more acute onset, with bilateral symptoms, and UMN signs. It is still a medical emergency!

209
Q

Spinal cord syndromes:

Diagnosis and management of conus medullaris syndrome?

A

Same as cauda equina syndrome:

  • Urgent MRI for diagnosis
  • Urgent surgical decompression to prevent permanent damage
210
Q

Spinal cord syndromes:

Features of degenerative cervical myelopathy (DCM)?

A
  • LMN signs in the upper limbs
  • Bilateral, progressive carpal-tunnel-like symptoms
  • Loss of balance and proprioception in the lower limbs
211
Q

Spinal cord syndromes:

Diagnosis and management of DCM?

A
  • MRI spine (x-rays not sufficient)

- Neurosurgical referral for decompression

212
Q

Parkinsonโ€™s disease:

Pathophysiology?

A
  • Progressive depletion of dopaminergic neurones in the substantia nigra โ†’ hypoactivity of the direct pathway
  • Depletion of dopamine in the striatum โ†’ โ†“D2 receptor activation โ†’ hyperactivity of the indirect pathway

Overall effect is more inhibition of the motor cortex with less stimulation โ†’ motor syptoms of Parkinsonโ€™s

213
Q

Parkinsonโ€™s disease:

Features?

A

Classic triad:

  • Bradykinesia - short, shuffling steps with โ†“ arm swing
  • Tremor - asymmetrical, 3-5Hz, โ€œpill-rollingโ€, worse at rest
  • Rigidity - lead-pipe, with cogwheeling

Other features:

  • Micrographia
  • Depression develops in 40%
  • Poor REM sleep and fatigue
  • Postural hypotension (later feature)
214
Q

Parkinsonโ€™s disease:

Diagnosis?

A
  • Should be diagnosed by a specialist
  • Diagnosis is usually made clinically
  • Imaging is NOT routinely used
215
Q

Parkinsonโ€™s disease:

What are Lewy Bodies? What are they seen in?

A
  • ฮฑ-synuclein deposits seen in brainstem, substantia nigra, and cortex
  • Seen in Parkinsonโ€™s disease and dementia with Lewy Bodies
216
Q

Parkinsonโ€™s disease:

Management of motor symptoms?

A
  • Should be initiated and coordinated by a Parkinsonโ€™s specialist

First line:

  • Motor symptoms impacting patientโ€™s QOL โ†’ levodopa
  • Motor symptoms not impacting patientโ€™s QOL โ†’ levodopa, MAO-B inhibitor (e.g. selegiline), COMT inhibitor (e.g. entacapone) or dopamine agonist (e.g. ropinirole/apomorphine)
217
Q

Parkinsonโ€™s disease:

Management of sickness?

A
  • Common exam question
  • Donโ€™t use a D2 receptor antagonist that crosses the BBB (e.g. metoclopramide, prochlorperazine)
  • Domperidone can be used as it doesnโ€™t cross the BBB
  • Other options include ondansetron, promethazine, or cyclizine
218
Q

Parkinsonโ€™s disease:

Management option for severe Parkinsonโ€™s disease?

A

Deep Brain Stimulation (DBS)

219
Q

Parkinsonโ€™s-plus syndromes:

Give some examples

A
  • Multi-system atrophy (MSA)
  • Progressive-supranuclear palsy (PSP)
  • Corticobasal degeneration
220
Q

Parkinsonโ€™s-plus syndromes:

Key features of MSA? (other than parkinsonism)

A
  1. Autonomic dysfunction (orthostatic hypotension, erectile dysfunction, urinary incontinence/retention)
  2. Cerebellar symptoms (DANISH)
221
Q

Parkinsonโ€™s-plus syndromes:

Key features of PSP? (other than parkinsonism?)

A
  1. Vertical gaze palsy (especially downward gaze)

2. Frontal lobe abnormalities (disinhibition, apathy)

222
Q

Parkinsonโ€™s-plus syndromes:

Key features of corticobasal degeneration? (other than parkinsonism)

A
  • Asymmetrical motor abnormalities โ†’ โ€œ๐—ฎ๐—น๐—ถ๐—ฒ๐—ป ๐—น๐—ถ๐—บ๐—ฏ ๐—ฝ๐—ต๐—ฒ๐—ป๐—ผ๐—บ๐—ฒ๐—ป๐—ผ๐—ปโ€ - the perception that the affected limb does not belong to them
223
Q

Huntingtonโ€™s disease:

Gene mutation? How is it inherited?

A
  • CAG trinucleotide repeat on chromosome 4

- Autosomal dominant, with anticipation (each subsequent generation is affected more severely)

224
Q

Huntingtonโ€™s disease:

Pathophysiology?

A
  • Neuronal loss in the striatum (esp. caudate nucleus)
  • Reduced indirect pathway activity and increased direct pathway activity
  • Impaired motor inhibition and increased motor excitation
225
Q

Huntingtonโ€™s disease:

Clinical features?

A

Early:

  • Chorea
  • Athetosis (involuntary writhing movements)

Later:

  • Parkinsonism
  • Akinetic mutism (canโ€™t move or talk)
  • Dementia
  • Depression
226
Q

Huntingtonโ€™s disease:

Management?

A
  • MDT, co-ordinated by specialist neurologist
227
Q

Cerebral palsy:

What is it?

A

Non-progressive, perinatal hypoxic brain injury

228
Q

Cerebral palsy:

Clinical features?

A

All types:

  • Neurodevelopmental delay
  • Intellectual disability
  • Joint contractures

Spastic CP: (70%)

  • โ†‘ muscle tone in one or more limbs
  • โ†‘ deep tendon reflexes
  • scissor gait

Non-spastic CP (dyskinetic or ataxic)

  • Dysarthria and dysphagia
  • Ataxia

N.B. Hand preference BEFORE the age of 1 indicates one-sided muscle weakness and should be investigated

229
Q

Cerebral palsy:

Management?

A
  • MDT approach
  • Treatments for spasticity (e.g. baclofen, Botulinum Toxin-A)
  • Orthopaedic surgery
230
Q

Friedrichโ€™s ataxia:

Clinical features?

A
  • Progressive ataxia
  • Spastic paralysis
  • Scoliosis
  • Hypertrophic cardiomyopathy (main cause of death)
231
Q

Multiple sclerosis:

Pathophysiology?

A
  • Autoimmune inflammation, demyelination and axonal degeneration
  • Only affects oligodendrocytes (CNS), not Schwann cells (PNS)
232
Q

Multiple sclerosis:

Presentation?

A

Can present with a diverse range of symptoms, typically coming in bouts lasting a few weeks at a time.

Optic neuritis:

  • Most common manifestation
  • Painful (esp. on movement)
  • Relative afferent pupillary defect (RAPD) (light reflex absent, but concentric constriction intact)

Internuclear ophthalmoplegia:

  • Demyelination of the medial longitudinal fasciculus (MLF)
  • Good video by HippocraTV on YouTube
  • Disconjugate, lateral gaze nystagmus in contralateral eye

Other symptoms include:

  • Demyelination of the pyramidal tracts โ†’ Lhermitte sign, UMN signs, loss of fine touch & vibration sensation, ataxia
  • Cerebellar involvement
  • Cranial nerve palsies
  • Symptoms worse in the head (Uhthoff phenomenon)
233
Q

Multiple sclerosis:

How can MS be categorised based on its clinical course?

A
  • Relapsing-remitting (RR-MS)
  • Primary progressive (PP-MS)
  • Secondary progressive (SP-MS)
234
Q

Multiple sclerosis:

Diagnosis?

A

MRI ๐˜„๐—ถ๐˜๐—ต ๐—ฐ๐—ผ๐—ป๐˜๐—ฟ๐—ฎ๐˜€๐˜:
- Multiple white-matter lesions disseminated in time and space

Lumbar puncture:
- Oligoclonal bands

235
Q

Multiple sclerosis:

Management of an acute relapse?

A
  • High dose steroids (oral or IV methylprednisolone)
  • Shortens the course of relapse but doesnโ€™t improve long-term recovery
  • 2nd line = plasmapheresis
236
Q

Multiple sclerosis:

Maintaining relapse?

A
  • Beta-interferon - reduces relapse rate by 30%
  • Glatiramer acetate
  • Natalizumab
237
Q

Guillain-Barrรฉ syndrome:

Pathophysiology?

A
  • โ…” have URTI or diarrhoeal illness 1 - 4 weeks prior
  • Most commonly associated with Campylobacter jejuni
  • Immune system activation โ†’ makes cross-reactive antibodies that work against Schwann cells (molecular mimicry) โ†’ axonal degeneration of motor and sensory fibres in peripheral nervous system
238
Q

Guillain-Barrรฉ syndrome:

Features?

A
  • ๐—ฃ๐—ฟ๐—ผ๐—ด๐—ฟ๐—ฒ๐˜€๐˜€๐—ถ๐˜ƒ๐—ฒ, ๐˜€๐˜†๐—บ๐—บ๐—ฒ๐˜๐—ฟ๐—ถ๐—ฐ๐—ฎ๐—น ๐˜„๐—ฒ๐—ฎ๐—ธ๐—ป๐—ฒ๐˜€๐˜€ ๐—ผ๐—ณ ๐—ฎ๐—น๐—น ๐˜๐—ต๐—ฒ ๐—น๐—ถ๐—บ๐—ฏ๐˜€ ๐˜„๐—ถ๐˜๐—ต ๐—ต๐˜†๐—ฝ๐—ผ๐—ฟ๐—ฒ๐—ณ๐—น๐—ฒ๐˜…๐—ถ๐—ฎ
  • Weakness is ascending i.e. legs are affected first
  • Sensory symptoms tend to be mild e.g. distal paraesthesia
239
Q

Guillain-Barrรฉ syndrome:

Diagnosis?

A

Lumbar puncture:

  • Raised protein with normal white cell count
  • called โ€˜albuminocytologic dissociationโ€™

Nerve conduction studies can be performed showing decreased conduction velocity

240
Q

Guillain-Barrรฉ syndrome:

Treatment?

A
  • Supportive care (in some cases intubation and ITU may be needed)
  • Intravenous Immunoglobulin
  • Plasmapheresis
241
Q

Motor neurone disease:

What are the types?

A
  • Amyotrophic lateral sclerosis (ALS)
  • Progressive bulbar palsy (PBP)
  • Pseudobulbar palsy
  • Progressive muscular atrophy (PMA)
  • Primary lateral sclerosis (PLS)

There are others, but they are exceedingly rare.

242
Q

Motor neurone disease:

Clinical features of ALS?

A
  • ๐— ๐—ถ๐˜…๐—ฒ๐—ฑ ๐˜‚๐—ฝ๐—ฝ๐—ฒ๐—ฟ ๐—ฎ๐—ป๐—ฑ โ€‹๐—บ๐—ผ๐˜๐—ผ๐—ฟ ๐—ป๐—ฒ๐˜‚๐—ฟ๐—ผ๐—ป๐—ฒ ๐˜€๐—ถ๐—ด๐—ป๐˜€
  • ๐—™๐—ฎ๐˜€๐—ฐ๐—ถ๐—ฐ๐˜‚๐—น๐—ฎ๐˜๐—ถ๐—ผ๐—ป๐˜€
  • Progresses from typically starting in one limb to affect all skeletal muscle in the body

Late symptoms:

  • Cognitive impairment
  • Dysphagia
  • Respiratory failure โ†’ death
243
Q

Motor neurone disease:

Diagnosis?

A
  • History and examination findings
  • Electromyography โ†’ denervation
  • Nerve conduction studies โ†’ usually normal
  • Bedside swallowing test to screen for dysphagia
244
Q

Motor neurone disease:

Treatment?

A
  • Riluzole: prevents glutamate release, prolongs life by โˆผ3 months
  • NIV: use of BiPAP at home prolongs life by โˆผ 7 months

Prognosis is poor, roughly 50% mortality at 3 years

245
Q

Poliomyelitis:

What is polio? How is it treated?

A

Anterior horn cell disease caused by poliovirus, causing progressive LMN signs and eventually respiratory failure

Treatment is supportive, with analgesia and mechanical ventilation

246
Q

Myasthenia gravis:

Pathophysiology?

A

Autoimmune antibodies against post-synaptic acetylcholine receptors โ†’ ACh receptor decay โ†’ fatiguability

247
Q

Myasthenia gravis:

Clinical features?

A
  • Eye muscle weakness โ†’ diplopia, ptosis, blurred vision
  • Bulbar muscle weakness โ†’ slurred speech
  • Proximal muscle weakness โ†’ difficulty standing from chair
  • Respiratory muscle weakness โ†’ dyspnoea

Weakness gets worse throughout the day

248
Q

Myasthenia gravis:

Investigations and diagnosis?

A
  • Diagnosis usually confirmed by EMG and AChR antibody screening
  • Chest CT to rule out thymoma (commonly associated)
  • Edrophonium test (tensilon test) โ†’ administration of short acting acetylcholinesterase inhibitor rapidly improves symptoms
249
Q

Myasthenia gravis:

Long-term management:

A
  • 1st line = pyridostigmine
  • Immunosuppression can be added: prednisolone first, then azathioprine/ciclosporin if not sufficient
  • Thymectomy
250
Q

Myasthenia gravis:

Management of myasthenic crisis?

A
  • Intravenous immunoglobulins

- Plasmapheresis

251
Q

Facial nerve palsy:

Clinical features of Bellโ€™s palsy?

A
  • Lower motor neurone facial palsy (forehead not spared)
  • Dry eyes
  • Altered taste
  • Hyperacusis
252
Q

Facial nerve palsy:

Diagnosis of Bellโ€™s palsy?

A

Itโ€™s a diagnosis of exclusion; other causes of facial nerve palsy should be ruled out first

253
Q

Facial nerve palsy:

Management of Bellโ€™s palsy?

A
  • Prescribe prednisolone (ideally within 72 hours of symptom onset)
  • Prescribe artificial tears and eye lubricants
  • Antivirals (e.g. aciclovir) may be used, with a small improvement. in symptoms, though this is not yet NICE guidance
  • If no improvement by 3 weeks then refer urgently to ENT
254
Q

Facial nerve palsy:

Clinical features of Ramsay-Hunt syndrome?

A
  • Auricular pain (often first feature)
  • Facial nerve palsy
  • Vesicular rash around the ear
  • Other symptoms include tinnitus and vertigo
255
Q

Facial nerve palsy:

Management of Ramsay-Hunt syndrome?

A
  • Oral prednisolone and aciclovir
256
Q

Wernicke-Korsakoff syndrome:

Pathophysiology of Wernickeโ€™s encephalopathy?

A
  • Chronic alcoholism downregulates intestinal B1 (thiamine) absorption channels โ†’ B1 deficiency
  • Thiamine pyrophosphate (TPP) is the active form of B1
  • TPP is involved in glycolysis, acting as a coenzyme for pyruvate dehydrogenase
  • Therefore low B1 โ†’ impaired/absent aerobic respiration โ†’ neuronal injury
257
Q

Wernike-Korsakoff syndrome:

Pathophysiology of Korsakoff syndrome?

A
  • Long term B1 deficiency โ†’ permanent damage to the limbic system (e.g. mamillary bodies)
  • Destruction of these components โ†’ memory loss, apathy and emotional dysregulation
258
Q

Wernicke-Korsakoff syndrome:

Clinical features?

A

Classic triad:

  1. Confusion
  2. Oculomotor dysfunction (most commonly nystagmus/conjugate gaze palsy)
  3. Gait ataxia
259
Q

Wernicke-Korsakoff syndrome:

Clinical features?

A
  1. Confabulation
  2. Anterograde and retrograde amnesia
  3. Personality change
260
Q

Wernicke-Korsakoff syndrome:
What are the differences between Wernickeโ€™s encephalopathy and Korsakoff syndrome?
(In terms of onset and prognosis)

A 
Wernicke's = acute, reversible
Korsakoff = chronic, irreversible
261
Q

Wernicke-Korsakoff syndrome:

Diagnosis?

A
  • Usually a clinical diagnosis (features are quite distinctive)
  • Laboratory tests โ†’ low serum B1
  • Brain MRI โ†’ periventricular haemorrhage/๐—ฎ๐˜๐—ฟ๐—ผ๐—ฝ๐—ต๐˜† ๐—ผ๐—ณ ๐˜๐—ต๐—ฒ ๐—บ๐—ฎ๐—บ๐—ถ๐—น๐—น๐—ฎ๐—ฟ๐˜† ๐—ฏ๐—ผ๐—ฑ๐—ถ๐—ฒ๐˜€ and dorsomedial nuclei of the thalamus
262
Q

Wernicke-Korsakoff syndrome:

Management?

A

Wernickeโ€™s encephalopathy:

  • Urgent thiamine replacement
  • Glucose replacement if needed (MUST be after thiamine replacement or glucose accumulates โ†’ cerebral oedema)
  • Abstinence from alcohol

Korsakoff syndrome:

  • Treatment aimed at halting the progression
  • Long-term thiamine supplementation
  • Abstinence from alcohol
263
Q

Neurocutaneous disorders:

Neurofibromatosis 1 mutation?

A
  • NF1 gene
  • Chromosome 17
  • Encodes neurofibromin (tumour suppressor factor)
  • 100% penetrance
264
Q

Neurocutaneous disorders:

Neurofibromatosis 1 features?

A

The main cutaneous feature is the presence of โ€œcafรฉ au lait spotsโ€. To remember the features think of the mnemonic ๐—–๐—”๐—™๐—˜ ๐—ฆ๐—ฃ๐—ข๐—ง๐—ฆ:

๐—–afรฉ au lait spots (โ‰ฅ6, 15mm in diameter)
๐—”xillary/groin freckles
๐—™ibromas (neurofibromas)
๐—˜ye nodules (iris hamartomas - โ€œLisch nodulesโ€)

๐—ฆkeletal abnormalities (e.g. scoliosis, sphenoid dysplasia)
๐—ฃhaeochromocytoma โ†’ high blood pressure
๐—ขptic ๐—งumour (optic nerve glioma)
๐—ฆhort stature

265
Q

Neurocutaneous disorders:

Neurofibromatosis 2 mutation?

A
  • NF2 gene
  • Chromosome 22
  • Encodes neurofibromin 2 (more commonly called Merlin; also a tumour suppressor protein)
266
Q

Neurocutaneous disorders:

Neurofibromatosis 2 features?

A
  • Bilateral acoustic neuromas
  • Bilateral cataracts
  • Multiple cerebral and spinal tumours
  • Epilepsy
  • Skin lesions
267
Q

Neurocutaneous disorders:

Tuberous sclerosis mutation?

A

Either:

  • TSC1 gene encoding tuberin
  • TSC2 gene encoding hamartin
  • Both are tumour suppressor genes, so mutations cause unchecked growth
268
Q

Neurocutaneous disorders:

Tuberous sclerosis features?

A

Skin manifestations: (KEY)

  • ๐—”๐˜€๐—ต ๐—น๐—ฒ๐—ฎ๐—ณ ๐—บ๐—ฎ๐—ฐ๐˜‚๐—น๐—ฒ๐˜€ (hypopigmented)
  • ๐—ฆ๐—ต๐—ฎ๐—ด๐—ฟ๐—ฒ๐—ฒ๐—ป ๐—ฝ๐—ฎ๐˜๐—ฐ๐—ต (thickened, scaly patch over lower back)
  • ๐—”๐—ฑ๐—ฒ๐—ป๐—ผ๐—บ๐—ฎ ๐˜€๐—ฒ๐—ฏ๐—ฎ๐—ฐ๐—ฒ๐˜‚๐—บ (angiofibromas on face, often misdiagnosed as acne)
  • Subungual fibroma (under the nail)
  • Cafรฉ au lait spots (hyperpigmented) may be seen

Neurological manifestations:

  • Developmental delay
  • Treatment-resistant epilepsy

Other:

  • Polycystic kidneys
  • Rhabdomyomas of the heart
  • ๐—ฅ๐—ฒ๐˜๐—ถ๐—ป๐—ฎ๐—น hamartomas (these affect the iris in NF1)

Medicine Finals (18 decks)

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