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Neurosciences Flashcards

MLA conditions: Meningitis, encephalitis, brain abscess. Describe causes, diagnosis, and management.

1
Q

Why does meningitis cause headaches?

A

Cerebral odedma/raised ICP

Pathogens invade the meninges, releasing toxins and triggering an inflammatory response > increased permeability of the blood-brain barrier.

Inc number of WBC and proteins, results in cerebral oedema and raised ICP.

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2
Q

What are the 3 most common bacteria that cause meningitis?

Which is the most common?

A

1. Streptococcus pneumoniae
2. Neisseria meningitidis
3. Haemophilus influenzae.

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3
Q

What are the 3 most common viruses that cause meningitis?

A
  1. Enteroviruses,
  2. herpes simplex virus, and
  3. mumps virus.

Cancer (meningeal involvement such as leukaemia),
SLE, certain drugs, or head injury can also cause meningitis. But less acute.

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4
Q

A food-borne virus that is a facultative, gram-positive rod. Can cause severe sympotms (N/V+D, myalgia, meningitis)

A

Listeria monocytogenes

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5
Q

Classic triad of meningitis

A

Fever, headache, neck stiffness (classic triad in adults),

Plus photophobia, nausea/vomiting, altered mental status e.g. drowsiness, and sometimes a rash (in meningococcal meningitis).

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6
Q

What are signs that indicate meningococcal septicaemia?

A

Signs include a non-blanching purpuric rash, hypotension, tachycardia, cold extremities, and multi-organ failure.

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7
Q

Which 2 clinical tests are specific but not sensitive to bacterial meningitis?

A

Kernig’s sign and Brudzinski’s sign (specific but not sensitive)

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8
Q

If you suspect meningitis in the community, what should be your first step?

A

Immediate transfer to the hospital.

For people with strongly suspected meningococcal disease, give intravenous or IM ceftriaxone or benzylpenicillin

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9
Q

When should treatment be started for suspected meningitis and encephalitis ?

A

Immediately upon clinical suspicion, due to potentially life-threatening consequences e.g. coma, extensive damage and death.

Admit to hospital if not already.

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10
Q

If bacterial meningitis is strongly suspected e.g. patient very unwell, having non-blanching purpura, what should you do before any investigations?

A

Take a blood culture and give empiric antibiotics (broad-spectrum e.g. ceftriaxone).

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11
Q

How do pathogens reach the meninges? List 3 ways

A
  • bloodstream/septicaemia (hematogenous spread),
  • direct extension from nearby infections (e.g., sinusitis, otitis media), or
  • through a breach in the skull or spinal column connecting the nasopharynx and the meninges.
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12
Q

List 5 domains in a lumbar puncture that you should look for in diagnosis of meningitis.

A
  • Opening pressure/appearance (often increased, cloudy)
  • WBC: number and type
  • glucose
  • protein
  • culture (and gram staining)
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13
Q

What are the typical cerebrospinal fluid (CSF) findings in bacterial versus viral meningitis?

A

Bacterial: Cloudy CSF, elevated WBC (predominantly neutrophils), low glucose, high protein.

Viral: normal/elevated WBC count (predominantly lymphocytes), normal glucose, moderately elevated protein.

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14
Q

When should imaging e.g. CT be considered before a lumbar puncture? What are some symptoms that?

A

Imaging is recommended if there are signs of increased ICP:

  • focal neurological deficits,
  • pupil abnormality,
  • rapidly dropping GCS
  • new-onset seizures,

or immunocompromised state to rule out mass effect or other contraindications.

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15
Q

What are the first-line antibiotics used in the treatment of bacterial meningitis? What additional antibiotic may be used in immunocompromised/elderly people?

A

Ceftriaxone or cefotaxime

Vancomycin for strep. pneumoniae
Amoxicillin/ampicillin to treat Listeria

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16
Q

What is the role of corticosteroids in the management of meningitis?

A

Corticosteroids, such as dexamethasone, are used to reduce inflammation and prevent neurological complications, particularly in cases of pneumococcal meningitis.

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17
Q

How should close contacts of a patient with meningococcal meningitis be managed?

What is the most common antibiotic of choice?

A

Close contacts should receive prophylactic antibiotics.

Ciprofloxacin: Single dose, more commonly used.

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18
Q

What vaccines are available to prevent meningitis?

A

Vaccines include the Haemophilus influenzae type b (Hib) vaccine, pneumococcal vaccines (PCV13, PPSV23), and meningococcal vaccines (MenACWY, MenB).

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19
Q

What is a lifestyle RF for developing meningitis?

A

Living in close quarters (e.g., uni students living in dormitories, military barracks)

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20
Q

Is bacterial meningitis a notifiable disease?

A

Yes

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21
Q

Co-occurring meningitis and encephalitis is called –?

A

Meningoencephalitis

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22
Q

What is the most common cause of encephalitis?

A

HSV-1
Herpes simplex virus

Other viruses: Varcella-zoster virus, CMV, EBV

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23
Q

How does HSV-1 enter the brain?

A

Through the olfactory nerve or other mucosal surfaces.

Leading to viral replication and inflammation in the brain tissue.

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24
Q

What are the treatment options for viral encephalitis?

A
  • Acyclovir for HSV —started empirically for a suspected case,
  • supportive care,
  • management of complications e.g. as seizures and increased intracranial pressure (anti-epileptics, IV mannitol)
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25
Q

Which brain region does HSV-1 affect? As a result, what symptoms are caused?

A

Temporal lobes of the brain, including the hippocampus and amygdala.

These areas are crucial for memory and emotional processing, explaining the cognitive and behavioral symptoms often seen in HSE patients.

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26
Q

What are some arboviruses that can cause encephalitis?

A

West Nile virus, Japanese encephalitis virus, tick-borne encephalitis virus

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27
Q

What may precipitate encephalitis?

A

Recent infection

Post-Infectious Encephalitis: occurs after the body has fought off an initial infection, leading to demyelination and white matter damage.

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28
Q

How does encephalitis generally present?

Think neuropsychiatry

A

Acute onset of psychiatric symptoms/altered mental state such as confusion/agitation/hallucinations/behavioural changes + seizures/ focal neurological signs e.g. hemiparesis, hyperrefleia, weakness, aphasia

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29
Q

If a patient comes in with a few days of headache, low-grade fever, and neck stiffness, nausea, and some weakness in one limb, following an unresolving ear infection. What would you suspect? How would you confirm it?

A

Brain abscess. Cofirmed through CT - ring enhancing lesion with hypodense centre ( inflammed then necrotic)

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30
Q

Pathophysiology of myasthenia gravis.

A

It is an autoimmune neuromuscular disorder characterised by weakness and fatigueability of voluntary muscles caused by autoantibodies targeting the NMJ endplate.

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31
Q

Clinical presentation of myasthenia gravis— list 4 locations that are commonly affected.

What are two major risks associated with it that may be life-threatening?

A
  • Ocular: Ptosis and diplopia are often the initial and most common symptoms.
  • Bulbar: Dysphagia, dysarthria, and difficulty chewing, neck weakness.
  • Limb: Symmetrical proximal muscle weakness affecting the arms more than the legs.
    Patients report difficulty getting out of chairs, climbing stairs etc.
  • Respiratory: Severe cases can lead to respiratory muscle involvement and myasthenic crisis.
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32
Q

First line diagnostic investigations for myasthenia gravis.

A
  1. Acetylcholine receptor (AChR) Antibody: Detectable in 80-90% of patients.
  2. Muscle Specific Tyrosine Kinase (MuSK) Antibody: Detectable in 70% of patients that are seronegative for AChR antibodies.
  3. Serial Pulmonary Function Tests: Will be considered for patients with myasthenic respiratory compromise.

Second-line: nerve conduction studies/ single fibre EMG

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33
Q

What are tips of examining a patient with myasthenia gravis? Especially if they don’t present with any symptoms?

A

Ask them to stare up for a minute. Notice ptosis or diplopia.

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34
Q

Pharmacological management of myasthenia gravis

A

For those with AchR antibodies: Anticholinesterase Inhibitors (Pyridostigmine).

Corticosteroids (e.g. prednisolone): Low dose then gradually increased

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35
Q

What is a myasthenia crisis?

A

A life-threatening exacerbation of myasthenia gravis, characterised by severe muscle weakness leading to respiratory failure, requiring immediate medical intervention.

How it occurs:
- Happens in MG patients with an exacerbating factor e.g. Infection, surgery, certain medications (e.g., antibiotics, beta-blockers), emotional stress, or abruptly stopping anticholinesterase medications.)
- Manage with ITU/ventilatory support. Immune support e.g. IVIG

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36
Q

Which muscles do neuromuscular auto-immune conditions tend to affect?

A

Muscles that are larger and have higher activity, e.g. shoulders, thigh, cardiac, and eye muscles (Myathenia!)

37
Q

What is a condition that presents with descending paralysis and autonomic symptoms (e.g., dry mouth, blurred vision).

A

Botulism

38
Q

The excision of which other organ is considered for patients with myasthenia gravis?
» especially if they are younger e.g. 18-50 years old?

A

Thymectomy (due to risk of malignany transformation of thymoma)

39
Q

What is myasthenia gravis called when it just affects the eyes/an eye?

A

Ocular myasthenia

40
Q

List a group of congential conditions that cause progressive, ascending muscle weakness, including the Gower’s sign.

A

Muscular dystrophy (MD)

A group of genetic disorders characterised by progressive muscle weakness and degeneration.

The most common types include Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD).

DMD: lack of functional dystrophin. Severe, in early childhood (around ages 2-5).

BMD: some functional dystrophin results, often starts during adolescence or adulthood.

41
Q

What is the inheritance of muscular dystrophies?

A

X-linked inheritance – affected males of carrier mothers.

42
Q

What is the role of muscle biopsy in DMD/BMD.

A

To examine dystrophin level.

Investigaton/diagnosis:
* genetic testing to identify mutations in the DMD gene,
* muscle biopsy
* elevated serum creatine kinase (CK) levels indicating muscle damage.

43
Q

What is the role of corticosteroids in the management of Duchenne muscular dystrophy (DMD)?

A

Slow the progression of muscle weakness and improve muscle strength and function.

44
Q

What are some potential complications associated with muscular dystrophy?

  • impact in quality of life, reduced life expectancy
A

Complications can include respiratory failure, cardiomyopathy, scoliosis, and contractures.

Regular monitoring and supportive care are essential to manage these complications.

45
Q

What is Guillain-Barré Syndrome (GBS)? What is it characterised by?

A

An acute, immune-mediated polyradiculoneuropathy (affecting nerve roots and peripheral nerves), often triggered by an infection.

46
Q

What are the two common initial symptoms of Guillain-Barré Syndrome?

A
  • Paresthesia
  • Weakness
  • Symmetrical, ascending pattern from lower limbs

affects sensory and motor nervous system

47
Q

What is a major complication of Guillain-Barre Syndrome?

A

Respiratory failure (restrictive)

48
Q

Two tests to confirm Guillain-Barré Syndrome diagnosis.

A
  • Nerve conduction studies (slower transmission) and
  • LP: elevated protein levels with normal white cell count.
  • MRI to rule out
49
Q

What are the main treatment options for Guillain-Barré Syndrome?

A
  • IVIG and plasmapheresis,
  • Steroids may be added.
50
Q

How long does Guillain-Barré Syndrome usually take to resolve?

A

Slow (takes a few weeks - gets to the worst point, then improves.)

Prognosis - generally good. Most patients recover fully, but some may have residual weakness or other neurological deficits.

51
Q

What is the most common trigger for Guillain-Barre Syndrome?

A

Campylobacter jejuni

52
Q

Pathophysiology of Guillain-Barre Syndrome.

A

Molecular mimicry: antibodies mistakenly target the myelin sheath or axons of peripheral nerves following infection

Causing an acute inflammatory demyelination and motor axonal damage

53
Q

Apart from peripheral motor and sensory symptoms, what other problems may Guillain-Barré Syndrome patients experience?

A

Autonomic dysfunction and cranial nerve involvement.

Fluctuations in BP, bowel and bladder dysfunction. Cranial nerve involvement e.g. bilateral facial weakness, difficulty swallowing, impaired eye movements.

54
Q

What exam findings might you find in Guillain-Barré Syndrome?

A
  • Weakness/ paralysis
  • Reduced sensation in a gloves-stocking distribution
  • reduced reflexes
55
Q

What is a chronic, fluctuating form of Guillain-Barré Syndrome?

A

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)

GBS= AIDP

56
Q

First-line medication for preventing cerebral vasospasm in SAH patients.

A

Nimodipine

57
Q

Two options for resolving SAH.

A

Coiling
Clipping

58
Q

Typical age group for SAH occurrence.

A

35-65

59
Q

Most common cause of SAH. Common sites.

A

Berry aneurysm rupture (80%). Common sites: junctions of posterior communicating artery with the internal carotid OR anterior communicating artery with the anterior cerebral OR bifurcation of the middle cerebral.

60
Q

SAH differentials.

A

1) Meningitis
2) Migraine
3) Intracerebral bleed
4) Cortical vein thrombosis
5) Vertebral or carotid artery dissection
6) Benign thunderclap headache (triggered by Valsalva manoeuvre, cough, or coitus).

61
Q

SAH management.

A

Refer all proven SAH to neurosurgery immediately.

> Re-examine CNS chart often; chart BP, pupils, and GCS. Repeat CT if deteriorating.

> Maintain cerebral perfusion by keeping the patient well hydrated, but aim for SBP <160 mm/Hg.

> Nimodipine (60mg/4h PO for 3 weeks, or 1mg/hr IVI).

> Surgery: coiling vs clipping— the decision depends on accessibility and size of aneurysm. Do catheter or CT angiography to identify single vs multiple aneurysms before intervening.

Note: Newer techniques, such as balloon remodelling and flow diversion, can be helpful in anatomically-challenging aneurysms.

62
Q

Investigations for suspected SAH.

A

> Urgent CT (within first 24hrs).

> Consider LP if CT is negative but the history is very suggestive of SAH and there are no CI. This needs to be done >12hr after headache onset to allow breakdown of RBCs, so that a positive sample is xanthochromic (differentiates from ‘bloody tap’).

63
Q

Complications of SAH.

A

1) Rebleeding (most common cause of death— occurs in 20%, often within first few days).

2) Cerebral ischaemia: due to vasospasm— may cause permanent CNS deficit, and is the most common cause of morbidity). If this happens, surgery is not helpful at the time but may be so later.

3) Hydrocephalus: due to blockage of arachnoid granulations— requires a ventricular or lumbar drain.

4)Hyponatraemiais common but should not be managed with fluid restriction (seek expert advice).

64
Q

When does most mortality occur in SAH patients?

A

Within the 1st month.

Note: 90% of survivors of the 1st month survive >1yr.

65
Q

Risk factors for SAH.

A

> Previous aneurysmal SAH (new aneurysms form, old ones get bigger).

> Smoking.

> Alcohol misuse.

> Hypertension.

> Bleeding disorders.

> Subacute bacterial endocarditis (mycotic aneurysm).

> Family history (3-5* increased risk in close relatives).

> Polycystic kidney disease, aortic coarctation, and EDS are all associated with berry aneurysms.

66
Q

Symptoms of SAH.

A

Sudden excruciating headache (worst headache ever/thunderclap). This headache is typically occipital.

Vomiting, collapse, seizures, and coma often follow.

Coma/drowsiness may last for days.

Some patients report a preceding ‘sentinel’ headache (perhaps due to a small leak from the offending aneurysm).

67
Q

Signs of SAH.

A

Meningism— Kernig’s sign may be present (may take 6hrs to develop).

Eye involvement: Retinal, subhyaloid, and vitreous bleeds (Terson syndrome).

Focal signs at presentation may suggest site of aneurysm (e.g. pupil changes indicating a 3rd CN nerve palsy due to posterior communicating artery aneurysm) or intracerebral haematoma. Later deficits suggest complications.

68
Q

Subdural haematoma signs and symptoms.

A

Symptoms: Fluctuating level of consciousness (seen in 35% of patients) +/- insidious intellectual or physical slowing, sleepiness, headache, personality change, and unsteadiness.

Signs: increased ICP, seizures, localising neurological symptoms (e.g. unequal pupils, hemiparesis) occur late, often >1 month after injury.

69
Q

Subdural haematoma imaging findings.

A

CT/MRI shows clot +/- midline shift (but beware bilateral isodense clots).

Crescent-shaped collection of blood over one hemisphere.

70
Q

Management of subdural haematoma.

A

Reverse clotting abnormalities urgently.

Surgical management depends on the size of clot, its chronicity, and clinical picture (generally those >10mm or with midline shift of >5mm need evacuating— via craniotomy or burr hole washout).

Address cause of trauma (e.g. falls or abuse).

71
Q

Extradural haematoma cause.

A

Suspect after any traumatic skull fracture. Often due to a fractured temporal or parietal bone causing laceration of the middle meningeal artery or vein (typically after trauma to a temple just lateral to the eye).

Any tear to a dural venous sinus will also produce an extradural bleed.

72
Q

Extradural haematoma differentials.

A

Epilepsy
Carotid artery dissection
CO poisoning

73
Q

Management of extradural haematoma.

A

Stabilise and transfer urgently to a neurosurgical unit for clot evacuation +/- ligation of bleeding vessel.

Maintain airway.

Reduce ICP.

Intubation and mechanical ventilation are often required.

Mannitol IVI.

74
Q

What are dural venous sinuses? Where do they drain to?

A

Dural Venous Sinuses are endothelium-lined venous channels located between the meningeal and periosteal dural layers in the brain (resistant to compression due to their position between rigid layers.)

**They collect blood from different intracranial venous systems (cerebrum, cerebellum, brainsteam) and drain into the internal jugular veins. **

75
Q

Most common form of dural venous sinus thrombosis.

A

Sagittal sinus thrombosis.

76
Q

List the types of dural venous sinus thrombosis.

A

1) Sagittal sinus thrombosis.
2) Transverse sinus thrombosis.
3) Sigmoid sinus thrombosis.
4) Inferior petrosal sinus thrombosis.
5) Cavernous sinus thrombosis.

77
Q

Features of each type of dural sinus thrombosis.

A

Sagittal: headache, vomiting, seizures, decreased vision, papilloedema.

Transverse: headache +/- mastoid pain, focal CNS signs, seizures, papilloedema.

Sigmoid: cerebellar signs, lower CN palsies.

Inferior petrosal: 5th and 6th CN palsies with temporal and retro-orbital pain (Gradenigo’s syndrome— suggests that otitis media is the cause).

Cavernous (often due to spread from facial pustules or folliculitis, causing headache, chemosis, oedematous eyelids, proptosis, painful ophthalmoplegia, and fever.

78
Q

What is cortical vein thrombosis?

A

Usually occurs with a sinus thrombosis as it extends into the cortical veins, causing infarction in a venous territory.

These infarcts give rise to stroke-like focal symptoms that develop over days. There are often seizures and an associated headache which may come on suddenly (thunderclap).

79
Q

A 42-year-old woman presents to the emergency department with severe headache, fever, and swelling around her left eye. She reports that the symptoms began 3 days ago with a mild headache and gradually worsened. She also mentions a recent history of a facial infection that was treated with antibiotics. On physical examination, the patient has periorbital edema, proptosis, and ophthalmoplegia of the left eye. Her temperature is 38.5°C (101.3°F), and she has tenderness over her left forehead and cheek. Neurological examination reveals left-sided sixth cranial nerve palsy.

What is the most likely diagnosis?

A

Cavernous sinus thrombosis.

80
Q

Causes of dural venous sinus thrombosis.

A

Numerous.

> Anything that produces a hypercoagulable state.

Common causes:

-Pregnancy
-COCP
-Head injury
-Dehydration
-Blood dyscrasias
-Tumours (local invasion/pressure)
-Extracranial malignancy (hypercoagulability)
-Recent LP

Other causes:
Infection
Drugs (antifibrinolytics, androgens)
SLE
Vasculitis
Crohn’s
UC

81
Q

Intracranial venous sinus thrombosis investigations.

A

Exclude SAH (if thunderclap headache present) and meningitis.

Bloods: thrombophilia screen.
Imaging: CT/MRI venography may show absence of a sinus though an absent transverse sinus can be a normal variant.
MRI T2-weighted gradient echo sequences can visualise thrombus directly and also identify haemorrhagic infarction.

CT may be normal initially, but show filling defect at ~1 week (delta sign).

LP (if no CI): raised opening pressure.
CSF may be normal or show RBCs and xanthochromia.

82
Q

Management of dural venous sinus thrombosis.

A

Seek expert help.

Treat underlying infection.

Anticoagulation with heparin or LMWH then warfarin (INR 2-3) may benefit even if there is secondary cerebral haemorrhage (unless otherwise CI).

If there is deterioration despite adequate anticoagulation, endovascular thrombolysis or mechanical thrombectomy may provide limited benefit (but not in those with large infarcts and impending herniation).

Increased ICP requires prompt attention. Decompressive hemicraniectomy may prevent impending herniation.

83
Q

What is the most common cause of Cavernous Sinus Thrombosis? What is usually a clue from the history?

A

Infection.

Facial or eye infection e.g. sinusitis may precede 5-10 days before presenting with CST symptoms e.g. headache and eye symptoms.

84
Q

How does infection typically spread to cause Cavernous Sinus Thrombosis?

A

Infection typically spreads from an extracranial location such as the orbit, paranasal sinuses, or the ‘danger zone’ of the face.

85
Q

What are common clinical features of Cavernous Sinus Thrombosis?

A

Common clinical features include severe headache, unilateral periorbital oedema, proptosis, photophobia/diplopia, and cranial nerve palsies.

Progressive and not-intermittent

86
Q

Which cranial nerve is most commonly affected in CST?

A

The abducens nerve (CN VI)

87
Q

What is the typical treatment for CST?

A

Treatment is typically with antibiotic therapy.

Heparin may be used to dissolve clot.

88
Q

What can happen if the cause of Cavernous Sinus Thrombosis is infection without prompt antibiotic treatment?

A

Meningitis.

89
Q

Predominant types of Multiple System Atrophy (MSA)

A
  1. MSA-P: Parkinson - predominantly parkinson symptoms e.g. bradykinesia, rigidity
  2. MSA-C: predominantly cerebellar type - ataxia/balance issues, coordination issues

PLUS autonomic sympoms e.g. postural hypotension, urinary incontinence.

Medical conditions (25 decks)

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