Neurological Emergancies Flashcards

1
Q

What are the signs and symptoms of meningitis?

A
  • generalised headache, gradual onset
  • vomiting, neck stiffness, fever, photophobia, altered consciousness
  • Kernig’s sign - difficult to bend knee
  • non-blanching rash
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2
Q

What the main risk factors for menginitis?

A
  • extremes of age
  • diabetes
  • immunosuppression
  • splenectomy
  • alcoholism
  • contagious infection
  • defects in dura mater
  • IV drug abuse
  • ## malignancy
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3
Q

What are the most common causative organisms for bacterial meningitis?

A
  • S.pneumoniae
  • N. meningitides
  • If pregnant or over 60 its more likely to be L. monocytogenes
  • recently had surgery = S.aureus
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4
Q

What is the essential treatment if bacterial meningitis is suspected?

A
  • start benzylpenicllins in case its meningococcus
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5
Q

What are the diagnostic tests for meningitis?

A
  • CT indicated if impaired conciousness or focal neurological deficit
  • LP to diagnose
  • blood tests to look for DIC
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6
Q

What the CSF findings for bacterial meningitis?

A
  • marked elevation of WBCs, mainly polymorphs
  • usually elevated protein
  • reduced glucose by 50%
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7
Q

What are the CSF findings for viral meningitis?

A
  • WBC elevated, usually lymphocytes
  • protein elevated
  • normal glucose
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8
Q

What are the CSF findings for TB meningitis?

A
  • elevated WBCs, mixed,
  • usually very high protein
  • reduced glucose
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9
Q

Malignant CSF findings

A

WBCs elevated

  • often elevated protein
  • reduced glucose
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10
Q

How does TB meningitis present?

A
  • insidious onset, however acute presentation can occur if it is complicated by hydrocephalus or vasculitis
  • often presents with mild heachace, lesions of CN 6, 3 and 4
  • papilloemea, and optic nerve damage
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11
Q

How is TB meningitis treated?

A
  • rifampicin
  • isoniazid
  • pyrazinamide
  • ethambutol
    + steroid over two months
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12
Q

How is viral meningitis treated?

A
  • antipyretics and support until full recovery occurs
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13
Q

What is the treated of the following causes of bacterial meningitis?

  • unknown
  • meningococcus
  • pneumococcus
  • s.aureas
A
  • unknown = cefotaximine
  • meningococcus = cefotaximine/benzylpenicillin, if allergic chloramphenicol can be used, also give dexamethasone
  • pneumococcus = cefotaximine
  • s.aureas = rifampicin
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14
Q

What is encephalitis?

What are the symptoms?

A
  • inflammation of the brain parenchyma

- symptoms include headache, fever, focal neurological deficit (dysphagia, weakness), seizures, and encephalopathy

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15
Q

What is the typical cause of encephalitis?

A
  • typically viral in cause, usually HSV and other human herpesvirus
    , but can also be due to bacteria such as listeria. Additionally autoimmune is increasing in prevelance
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16
Q

How should HSV encephalitis be treated?

A
  • if suspected acyclovir should commence before investigation
17
Q

What are the investigations for encephalitis?

A
  • MRI, EEG, LP to culture virus
18
Q

In all episodes of acute and sub-acute flaccid weakness it is important to…

A
  • monitor respiration in all causes using FVC
19
Q

What are the causes of acute and subacute neuromuscular failure?

A
  • Nerve lesions include Guillain Barre
  • Muscle disease such as inflammatory dermatomyositis and metabolic disorders such as acid maltase
  • NMJ pathology includes myasthenia graves and botulism
20
Q

What are the features of Guillain Barre?

A

most common cause of acute NMJ weakness, leading to inflammatory polyradiculopathy
- it normally is preceded by respiratory tract infection, generating antibodies that then cross-react with the myelin sheath of neurones

21
Q

What are the symptoms of GBS?

A
  • parastheisa but little sensory loss, back pain is common
  • distal upper and proximal lower limb weakness, facial and bulbar involvement
  • respiratory muscles may be involved
22
Q

What are the investigations for GBS?

A
  • LP, CSF will show elevated protein, and nerve conduction studies
23
Q

Prognosis in GBS is poor if it is caused by …….. . Why?

Treatment?

A

campylobacter
- axonal loss, and the time to nadir is short-
Treatment - plasma exchange and IV Ig to accelerate recovery

24
Q

What is MG?

A
  • an autoimmune condition characterised by the presence of AChR antibodies that block the post-synaptic receptor at the NMJ
  • this will present with fatiguable weakness of muscle function with no autonomic features
25
Q

What are the investigations for MG?

A
  • the ice test (placing ice over brow will decrease ptosis), the tenilson test (give a short active acetyl- cholinesterase inhibitor will increase function) and repetitive stimulate EMG
  • blood test should shoe AChR antibodies and/or MuSK antibodies
  • CXR and CR thorax can show thymoma
26
Q

What is the treatment for MG?

A

Treatment is both symptomatic and immunosuppressive

  • long acting acetyl-cholinesterase inhibitors such as pyridostigmine and steroids such as methotrexate and prednisolone
  • thymectomy may be indicated
  • in acute cases, plasma exahcnage and IV Ig
27
Q

What is status epilepticus?

A
  • continuous seizures for 30 minutes or serial seizures over 30 minutes without regaining conciseness
28
Q

What are the causes of status epilepticus?

A
  • non-compliance to anti-epileptics
  • alcohol
  • drug overdose
  • metabolic disorders
  • hypoxia
  • tumour
  • trauma
29
Q

How is status epilepticus traeted?

A
  • manage ABCDE
  • cause of precipitating factor should be addressed, this include 50ml of 20% IV glucose if BM is kit
  • 1-2mg lorazepam
  • if not effective then phenytoin and fosphentoin can be used
  • if the patient remains in status they need to be paralysed using thiopentone/propofol and supported in ITU
30
Q

How should status epileptics be investigated?

A

urgent biochemistry, haematology, BMs,
- AED, calcium and Mg levels measured
- blood gases taken
CT scanning, LP, EEG monitoring

31
Q

What are the causes of coma?

A

Neurological - infection, neoplasm
Systemic - metabolic, endocrine, infection
Extrinsic - drugs, toxins

32
Q

What is the difference in signs and symptoms between cord compression and cauda equina compression?

A
  • cord compression - weakness is asymmetrical and reflexes are absent
  • cauda equina - weakness is equal and bilateral and reflexes are brisk