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PSBIM > NEUROLOGY > Flashcards

NEUROLOGY Flashcards

1
Q

An acute, frequently severe, and fulminant polyradiculoneuropathy that is autoimmune in nature

A

GBS

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2
Q

Manifests as a rapidly evolving areflexic motor paralysis with or without sensory disturbance.

A

GBS

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3
Q

Usual pattern of paralysis in GBS

A

ascending paralysis that may be first noticed as rubbery legs

legs > arms
facial diparesis – 50%
bulbar weakness

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4
Q

T or F. Fever and constitutional symptoms are usually present at the onset of GBS

A

False. Fever and constitutional symptoms are absent at the onset and, if present, cast doubt on the diagnosis

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5
Q

T or F. Bladder dysfunction is a usual presentation of GBS

A

False. Bladder dysfunction may occur in severe cases but is usually transient. If bladder dysfunction is a prominent feature and comes early in the course or there is a sensory level on examination, diagnostic possibilities other than GBS should be considered, particularly spinal cord disease

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6
Q

T or F. Autonomic involvement is common in GBS

A

True. The usual manifestations are loss of vasomotor control with wide fluctuations in blood pressure, postural hypotension, and cardiac dysrhythmias

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7
Q

Description of pain in GBS

A

Deep aching pain may be present in weakened muscles that patients liken to having overexercised the previous day

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8
Q

The most common variant of GBS

A

acute inflammatory demyelinating polyneuropathy (AIDP)

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9
Q

2 axonal variants of GBS that are often clinically severe

A

Acute motor axonal neuropathy (AMAN)

Acute motor sensory axonal neuropathy (AMSAN)

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10
Q

GBS variant which presents as rapidly evolving ataxia and areflexia of limbs without weakness, and ophthalmoplegia, often with pupillary paralysis.

A

Miller Fisher syndrome

accounts for ~5% of all cases

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11
Q

MFS is strongly associated with antibodies to the

A

ganglioside GQ1b

found in >90% of patients with MFS

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12
Q

Approximately ____ of cases of GBS occur 1–3 weeks after an acute infectious process, usually respiratory or gastrointestinal.

A

70%

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13
Q

T or F. Some vaccines may increase the risk of GBS.

A

True. The swine influenza vaccine, administered widely in the United States in 1976, is the most notable example

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14
Q

Aside from prior infection and vaccinations, risk of GBS is also increased in these group of patients (3)

A
  1. lymphoma (including Hodgkin’s disease)
  2. HIV-seropositive individuals
  3. Systemic lupus erythematosus (SLE)
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15
Q

These antibodies are common in GBS (20–50% of cases), particularly in AMAN and AMSAN and in those cases preceded by C. jejuni infection

A

Antiganglioside antibodies, most frequently to GM1

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16
Q

In the demyelinating forms of GBS, the basis for flaccid paralysis and sensory disturbance is

A

conduction block

axonal connections remain intact

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17
Q

______ after the first motor symptoms, it is not known whether immunotherapy is still effective for GBS

A

~2 weeks
If the patient has already reached the plateau stage, then treatment probably is no longer indicated, unless the patient has severe motor weakness and one cannot exclude the possibility that an immunologic attack is still ongoing

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18
Q

Management of GBS (2)

A

High dose IVIg
Plasmapheresis

Equally effective

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19
Q

Dose of IVIg in GBS

A

five daily infusions for a total dose of 2 g/kg body weight

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20
Q

Dose of plasmapheresis in GBS

A

~40–50 mL/kg PE 4–5 times over 7–10 days

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21
Q

T or F. Glucocorticoids is used as treatment in GBS.

A

False. Glucocorticoids have not been found to be effective in GBS .

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22
Q

Approximately ____ of patients with GBS achieve a full functional recovery within several months to a year, although minor findings on examination (such as areflexia) may persist and patients often complain of continued symptoms, including fatigue

A

85%

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23
Q

Mortality rate of GBS in an optimal setting

A

< 5%

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24
Q

T or F. CIDP responds to glucocorticoids

A

True

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25
Q

Criteria used in diagnosis of GBS and MFS

A

Brighton criteria

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26
Q

T or F. Virtually every possible type of focal neurologic disturbance has been reported in viral encephalitis

A

True

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27
Q

An inflammation of the brain caused either by infection or from a primary autoimmune process

A

Encephalitis

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28
Q

Most commonly identified viruses causing sporadic cases of acute encephalitis in immunocompetent patients

A

Herpesviruses

HSV, VZV, and EBV

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29
Q

A member of the Paramyxoviridae family that caused outbreak of encephalitis in Southest Asia

A

Nipah virus

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30
Q

T or F. Not all patients with suspected viral encephalitis should have CSF examination

A

False. Should be performed in all patients with suspected viral encephalitis unless contraindicated by the presence of severely increased intracranial pressure (ICP).

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31
Q

In CSF examination, how many mL of CSF must be collected?

A

at least 20 mL

5–10 mL stored frozen for later studies as needed

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32
Q

Atypical lymphocytes in the CSF is seen what infection?

A

EBV

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33
Q

RBCs in the CSF (>500/μL) is seen in 20% of patients with nontraumatic tap. This is most often caused by

A

HSV

Hemorrhagic encephalitis

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34
Q

Primary diagnostic test for CNS infections caused by CMV, EBV, HHV-6, and enteroviruses

A

CSF PCR

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35
Q

Nearly 80% of patient with HSV encephalitis will have abnormalities in the _____ lobe in MRI

A

Temporal

10% has abnormalities in the extratemporal regions
10% - normal MRI

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36
Q

Periodic, stereotyped, sharp-and-slow complexes originating in one or both temporal lobes and repeating at regular intervals of 2-3 s is a distinctive EEG pattern of

A

HSV encephalitis

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37
Q

Primary amebic meningoencephalitis cause

A

Naegleria fowleri

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38
Q

Causes of subacute or chronic granulomatous amebic meningoencephalitis

A

Acanthamoeba and Balamuthia

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39
Q

The major diagnostic challenge in management of viral encephalitis

A

To distinguish HSV from other viruses that cause encephalitis

Important to distinguish because HSV can be treated effectively with antiviral therapy

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40
Q

Empiric treatment of viral encephalitis with dose

A

Acyclovir 10 mg/kg IV every 8 h (30 mg/kg per day total dose) for 21 days

Each dose should be infused slowly over 1 h

Discontinued if proven to be not HSV encephalitis but may be continued with severe VZV or EBV

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41
Q

Treatment of CMV-related CNS infections

A

Ganciclovir and foscarnet

Alternative: cidofovir
Valganciclovir – oral drug

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42
Q

Dose of ganciclovir in CMV-related CNS infections

A
  • Induction therapy dose: 5 mg/kg q12h IV at a constant rate over 1 h
  • Maintenance therapy: 5 mg/kg per day for an indefinite period
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43
Q

Multifocal areas of demyelination of varying size distributed throughout the brain but sparing the spinal cord and optic nerves. This is seen in what condition

A

Progressive Multifocal Leukoencephalopathy

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44
Q

Most common visual defect in Progressive Multifocal Leukoencephalopathy

A

Homonymous hemianopia

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45
Q

80% of Progressive Multifocal Leukoencephalopathy patients has this comorbid

A

AIDS

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46
Q

5-HT2a receptor antagonist that may have potential beneficial effects because it may inhibit binding of JCV to its receptor on oligodendrocytes in patients with PML

A

Mirtazapine

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47
Q

A rare, chronic, progressive demyelinating disease of the CNS associated with a chronic nonpermissive infection of brain tissue with measles virus

A

Subacute sclerosing panencephalitis (SSPE)

Some 85% of patients are between 5 and 15 years old at diagnosis

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48
Q

Extremely rare disorder that primarily affects males with congenital rubella syndrome

A

Progressive Rubella Panencephalitis

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49
Q

The best test for WNV encephalitis is the

A

CSF IgM antibody test

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50
Q

A neuromuscular junction (NMJ) disorder characterized by weakness and fatigability of skeletal muscles

A

Myasthenia gravis (MG)

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51
Q

Decrease in the number of available acetylcholine receptors (AChRs) at NMJs due to an antibody-mediated autoimmune attack

A

Myasthenia gravis (MG)

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52
Q

Binding subunit of AChR

A

α subunit

AChR has 5 subunits: 2α, 1β, 1δ, 1γ, or ε

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53
Q

The amount of the ACh released per pulse normally declines on repeated activity. This phenomenon is called

A

Presynaptic rundown

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54
Q

Decreased efficiency of the neuromuscular transmission plus the normal rundown results in the activation of fewer and fewer muscle fibers by successive nerve impulses hence increasing weakness causes this clinical manifestation

A

Myasthenic fatigue

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55
Q

Antibodies that are present in 10% of patients with MG

A

Anti- muscle-specific kinase (MuSK)

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56
Q

Thymus is abnormal in ___ of patients with MG

A

~75%

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57
Q

Most common thymic abnormality in MG

A

Hyperplasia – 65%

Thymoma in 10%

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58
Q

Muscle-like cells in the thymus that may serve as a source of autoantigen and trigger the autoimmune reaction within the thymus gland in MG patients

A

Myoid cells

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59
Q

Peak incidence of MG in men and women

A
  • Women in their 20s and 30s
  • Men in their 50s and 60s

Women > men – 3:2

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60
Q

Cardinal features of MG (2)

A
  • Weakness

* Fatigability

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61
Q

Characteristic of weakness in MG

A

Weakness increases during repeated use or late in the day and may improve following rest or sleep

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62
Q

Common initial complaints in MG

A

Diplopia and ptosis

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63
Q

Facial weakness in MG is described as

A

“snarling” expression when patient attempts to smile

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64
Q

Characteristic of speech in MG

A

Nasal speech - weakness of the palate

Dysarthric “mushy” quality of voice – due to tongue weakness

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65
Q

Bulbar weakness is prominent in what subset of MG patients

A

MuSK antibody-positive

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66
Q

T or F. If MG isrestricted to EOM for 1 year, it is likely that weakness will not be generalized

A

False. 3 years.

Ocular MG

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67
Q

Effect of Ice Pack Test in MG

A

Improvement of ptosis

Less depletion of the AChR in the cold and reduced activity of AChE

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68
Q

Antibodies that is detected in ~85% in all MG patents

A

Anti AChR antibodies

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69
Q

Autoantibodies associated with MG (5)

A
  1. Anti AChR antibodies
  2. Anti MuSK antibodies
  3. Anti LRP4 antibodies
  4. Anti Agrin Antibodies
  5. Anti-striated muscle antibodies
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70
Q

Anti-AChE medication should be stopped _____ before electrodiagnostic testing

A

6-12 h

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71
Q

Normal response in electrodiagnostic testing

A

AP does not change by >10%

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72
Q

MG response in electrodiagnostic testing

A

Rapid reduction of >10% in the amplitude of the evoked responses

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73
Q

Anticholinesterase that is most commonly used for diagnostic testing

A

Endrophonium

  • Rapid onset – 30 s
  • Short duration – 5 mins
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74
Q

Dose of edrophonium in anticholinesterase test

A

Initial IV dose of 2mg endrophonium

Additional 8mg IV may be given if no response

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75
Q

Positive response in anticholinesterase test for MG

A

Improvement of weakness

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76
Q

In patients with adverse effects during anticholinesterase test, what may be given?

A

Atropine 0.6 mg

ADRs: nausea, diarrhea, salivation, fasciculations, and rarely, syncope or bradycardia

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77
Q

Anticholinesterase test may be false positive for MG if with this condition

A

ALS

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78
Q

Rare heterogenous group of disorders of the NMJ that are not autoimmune and is due to genetic mutations in which virtually all component of the NMJ may be affected

A

Non-autoimmune congenital myasthenia

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79
Q

Most common mutation in AChR in congenital myasthenia is seen in what subunit?

A

Mutation of ε subunit of the AChR - ~50% of the cases

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80
Q

Non-autoimmune congenital myasthenia that worsens with AChE inhibitors (3)

A
  1. Slow channel syndrome
  2. AChE deficiency
  3. DOK-7 related CMS
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81
Q

Drug-induced MG may be caused by (2)

A
  1. Penicillamine

2. Checkpoint inhibitors for cancer

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82
Q

Presynaptic disorder of the NMJ that mostly involves the proximal muscles of the lower limbs

A

Lambert-Eaton Myasthenic Syndrome (LEMS)

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83
Q

Difference of Lambert-Eaton Myasthenic Syndrome (LEMS) with MG

A

Have depressed or absent reflexes and experience autonomic changes such as dry mouth and impotence

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84
Q

Lambert-Eaton Myasthenic Syndrome (LEMS) is caused by autoantibodies directed against the

A

P/Q-type Ca channels at the motor nerve terminals

Impair the release of ACh from nerve terminals

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85
Q

Most common cancer associated with Lambert-Eaton Myasthenic Syndrome (LEMS)

A

Small-cell Lung Cancer

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86
Q

Treatment of Lambert-Eaton Myasthenic Syndrome (4)

A

Plasmapheresis
Immunotherapy
3,4 DAP
Pyridostigmine

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87
Q

Treatment of LEMS that blocks K channels prolonging depolarization of the motor nerve terminals, thus enhancing ACh release

A

3,4 DAP

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88
Q

Myasthenia-like fatigue syndrome without an organic basis

A

Neurasthenia

Subjective symptoms of weakness and fatigue
Muscle testing reveals “give-away weakness”

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89
Q

T or F. Thyroid function test must be obtained in all patients suspected to have MG

A

True. Hyperthyroidism or hypothyroidism may be present in MG patients or may aggravate myasthenic weakness

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90
Q

Most common autoimmune disorders that coexist with MG (2)

A

SLE and RA

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91
Q

Most widely used anticholinesterase drugs for MG

A

Pyridostigmine

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92
Q

Dose of pyridostigmine for MG

A

Initial dose: 30-60 mg 3-4 x a day

Max dose: 300 mg daily

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93
Q

T or F. Pyridostigmine is less beneficial for anti-MuSK MG

A

True. May actually worsen

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94
Q

Immunosuppressive treatment for MG if immediate improvement is essential

A

IVIg or plasmapheresis

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95
Q

Intermediate term immunosuppressive treatment for MG

A

glucocorticoids and cyclosporine or tacrolimus (provides improvement within 1-3 months)

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96
Q

Long term immunosuppressive treatment for MG

A

azathioprine and mycophenolate mofetil

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97
Q

Immunotherapy for MG that inhibits purine synthesis by the de novo pathway

A

Mycophenolate mofetil

Lymphocyte only have the de novo pathway and not the salvage pathway that is present in other cells

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98
Q

Azathioprine must not be used with this drug because it may cause severe bone marrow suppression due to common degradation pathway

A

Allopurinol

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99
Q

Calcineurin inhibitors used as immunosuppressive therapy for MG (2)

A

Cyclosporine

Tacrolimus

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100
Q

Monoclonal antibody that is effective in MuSK antbody positive MG

A

Rituximab

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101
Q

Treatment for rare refractory MG patients that reboots the immune system

A

High-dose cyclophosphamide

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102
Q

Dose of plasmapheresis in MG

A

5 exchanges (3-4 L per exchange) for 10-14 days

Short-term reduction in anti-AChR antibodies

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103
Q

Dose of IVIg in MG

A

2g/kg for >2-5 days

Short-term reduction in anti-AChR antibodies

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104
Q

An exacerbation of weakness sufficient to endanger life with ventilatory failure caused by diaphragmatic and intercostal muscle weakness

A

Myasthenic crisis

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105
Q

Deterioration in MG due to excessive AChE inhibitors

A

Cholinergic crisis

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106
Q

Most common cause of crisis in MG

A

Intercurrent infection

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107
Q

Subset of MG that does not typically experience crisis but are more difficult to treat

A

Anti MuSK positive MG

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108
Q

Antibiotics that may exacerbate MG (3)

A

Aminoglycosides
Macrolides
Quinolones

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109
Q

Most common causes of SAH (2)

A
  • Head trauma

* Rupture of a saccular aneurysm

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110
Q

Mortality rate of SAH secondary to saccular “berry” aneurysm over the next month after the rupture:

A

45% (for patients who arrive alive at hospital)

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111
Q

Of those who survive rupture of saccular aneurysm, more than half are left with major neurologic deficits as a result of (3)

A
  • Initial hemorrhage
  • Cerebral vasospasm with infarction
  • Hydrocephalus
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112
Q

If saccular aneurysm is not obliterated, rate of rebleeding in the first 2 weeks

A

20%

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113
Q

If saccular aneurysm is not obliterated, rate of rebleeding in the first month

A

30%

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114
Q

If saccular aneurysm is not obliterated, rate of rebleeding per year

A

3%

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115
Q

Berry aneurysms <10 mm in size has a ____ annual risk of rupture

A

0.1%

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116
Q

Berry aneurysms >10 mm in size has a ____ annual risk of rupture

A

~0.5–1%

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117
Q

Location of saccular aneurysm with the highest risk of bleeding

A

Basilar bifurcation aneurysms

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118
Q

Giant saccular aneurysms is ____ in diameter

A

> 2.5 cm

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119
Q

3 most common locations of giant saccular aneurysms

A
  • Terminal internal carotid artery
  • Middle cerebral artery (MCA) bifurcation
  • Top of the basilar artery
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120
Q

Usual location of mycotic aneurysm

A

distal to the first bifurcation of major arteries of the circle of Willis

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121
Q

This result from infected emboli due to bacterial endocarditis causing septic degeneration of arteries and subsequent dilation and rupture

A

Mycotic aneurysms

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122
Q

Usual locations of berry aneurysm

A

bifurcations of the large- to medium-sized intracranial arteries

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123
Q

Approximately 85% of saccular aneurysms occur in the _____ circulation

A

Anterior

Mostly on the circle of Willis

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124
Q

About ____ of patients have multiple brain aneurysms

A

20%

Many at mirror sites bilaterally

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125
Q

Features of aneurysm that are important factors in planning neurosurgical obliteration or endovascular embolization (2)

A

Length of the neck and size of the dome

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126
Q

Part of saccular aneurysm that is the most often site of rupture

A

Dome

Wall thins

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127
Q

Factors for greater risk of rupture of saccular aneurysm (3)

A
  • > 7 mm in diameter
  • At the top of the basilar artery
  • At the origin of the posterior communicating artery
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128
Q

Presenting complaint in ~45% of cases of rupture of aneurysm

A

Severe headache associated with exertion

“the worst headache of my life”

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129
Q

The most important characteristic of the headache of ruptured aneurysm

A

Sudden onset

Generalized headache, often with neck stiffness and vomiting

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130
Q

The hallmark of brain aneurysmal rupture

A

Sudden headache in the absence of focal neurologic symptoms

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131
Q

Bleeding of aneurysm in this sites will cause hemiparesis, aphasia, and mental slowness (abulia) (2)

A
  1. Anterior communicating artery

2. MCA bifurcation aneurysms

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132
Q

Aneurysm in this sites will cause third cranial nerve palsy (2)

A
  1. junction of the posterior communicating artery

2. internal carotid artery

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133
Q

Aneurysm in this site will cause 6th cranial nerve palsy

A

cavernous sinus

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134
Q

Aneurysm in this site will cause visual field defects (2)

A
  1. supraclinoid carotid

2. anterior cerebral artery (ACA) aneurysm

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135
Q

Aneurysm in this site will cause occipital and posterior cervical pain (2)

A
  1. posterior inferior cerebellar artery

2. anterior inferior cerebellar artery

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136
Q

Aneurysm in this site will cause pain in or behind the eye and in the low temple (2)

A

Expanding MCA aneurysm

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137
Q

A variant of migraine that simulates an SAH

A

Thunderclap headache

A definitive workup for aneurysm or other intracranial pathology is required

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138
Q

Small ruptures of brain aneurysm and leaks of blood into the subarachnoid space

A

Sentinel bleeds

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139
Q

Grade the initial clinical manifestations of SAH

A

Hunt-Hess

Or World Federation of Neurosurgical classification schemes

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140
Q

4 major causes of delayed neurologic deficits in aneurysmal rupture

A
  1. Rerupture
  2. Hydrocephalus
  3. Delayed cerebral ischemia
  4. Hyponatremia
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141
Q

Incidence of rerupture of an untreated aneurysm in the first month following SAH is ____, with the peak in the first ____

A

~30%,

7 days

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142
Q

Narrowing of the arteries at the base of the brain following SAH

A

Vasospasm

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143
Q

Delayed cerebral ischemia in aneurysmal rupture is secondary to

A

Vasospasm

May cause symptomatic ischemia and infarction in ~30%

Result from direct effects of clotted blood and its breakdown products on the arteries within the subarachnoid space

The more blood that surrounds the arteries, the greater chance of symptomatic vasospasm

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144
Q

Major cause of delayed morbidity and death in aneurysmal rupture

A

Vasospasm

Often preceded by a decline in mental status

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145
Q

Vasospasm appear ____ after the SAH, most often at _____

A

4-14 days

7 days

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146
Q

Cerebral salt-wasting syndrome in SAH is due to (2)

A

Natriuresis
Volume depletion

hyponatremia and hypovolemia

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147
Q

Laboratory hallmark of aneurysmal rupture

A

blood in the CSF

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148
Q

Based on high-quality non-contrast CT scan, high incidence of symptomatic vasospasm in MCA and ACA (2)

A
  • Subarachnoid clots >5 x 3 mm in the basal cisterns

* Layers of blood > 1 mm thick in cerebral fissures

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149
Q

Yellow spinal fluid in SAH

A

Xanthochromic spinal fluid

Due to lysis of RBCs and subsequent conversion of hemoglobin to bilirubin

within 6-12 hrs

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150
Q

ECG changes sec to intracranial hemorrhage (4)

A
  1. Prolonged QRS
  2. Increased QT
  3. Prominent “peaked” T wave
  4. Deeply inverted symmetric T waves
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151
Q

Aneurysmal repair may be via (2)

A
  1. Clipping of aneurysm (metal clip across the aneurysmal neck)
  2. Endovascular coiling (Placing of platinum coils or other embolic material within the aneurysm)
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152
Q

If patient with SAH is alert, systolic BP must be maintained

A

below 160 mmHg

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153
Q

If patient with SAH has depressed sensorium, systolic BP must be maintained based on

A

CPP targeted at 60-70 mmHg

154
Q

Management of vasospasm and delayed cerebral ischemia in aneurysmal rupture

A

Nimodipine 60 mg PO every 4 hours

155
Q

This drug prevent ischemic injury rather than reducing the risk of vasospasm in aneurysmal rupture

A

Nimodipine

Ca-channel antagonist

156
Q

Pharmacologic vasodilators that may be used in vasospasm of aneurysmal rupture (2)

A

Verapamil and nicardipine

157
Q

For DVT prophylaxis, unfractionated heparin can be initiated within ____following coiling or clipping

A

1–2 days

158
Q

T or F. Seizure is uncommon at the onset of aneurysm rupture

A

True

Quivering, jerking, and extensor posturing – may be related to increased ICP and not the seizure

159
Q

Why is free water restriction contraindicated in management of SAH?

A

May cause hypovolemia and hypotension  cerebral ischemia

160
Q

Hunt and Hess I

A

Mild headache, normal mental status, no cranial nerve or motor findings

161
Q

Hunt and Hess II

A

Severe headache, normal mental status, may have cranial nerve deficit

162
Q

Hunt and Hess III

A

Somnolent, confused, may have cranial nerve or mild motor deficit

163
Q

Hunt and Hess IV

A

Stupor, moderate to severe motor deficit, may have intermittent reflex posturing

164
Q

Hunt and Hess V

A

Coma, reflex posturing or flaccid

165
Q

The most common form of suppurative CNS infection

A

Acute meningitis

166
Q

Most common organisms causing community-acquired bacterial meningitis (in order)(5)

A 
Streptococcus pneumoniae (~50%)
Neisseria meningitidis (~25%)
Group B streptococci (~15%)
Listeria monocytogenes (~10%)
Haemophilus influenzae type b  (<10%)
167
Q

Causative organism of recurring epidemics of meningitis every 8–12 years

A

Neisseria meningitidis

168
Q

The most common cause of meningitis in adults >20 years of age

A

S. pneumoniae

169
Q

Most important risk factor in acute meningitis caused by S. pneumoniae

A

Pneumococcal pneumonia

170
Q

Why is there incidence of meningitis caused by N meningitidis even in patients vaccinated against the organism?

A

Usual vaccine does not contain serogroup B (responsible for 1/3 of cases of meningococcal disease)

Serogroup B meningococcal (MenB) vaccine must be given to aged 16-23 y.o.

171
Q

Important clue to the diagnosis of meningococcal infection

A

Petechial or purpuric skin lesions

172
Q

Initial infection in acute meningitis caused by N. meningitidis

A

Nasopharyngeal colonization

173
Q

Gram-negative bacilli cause meningitis in individuals with

A

chronic and debilitating diseases

diabetes, cirrhosis, or alcoholism and in those with chronic urinary tract infection

174
Q

Previously responsible for meningitis predominantly in neonates

A

Group B Streptococcus (i.e. Streptococcus agalactiae)

Increasing frequency in aged >50 years

175
Q

Causative agent of meningitis acquired by ingesting contaminated foods (coleslaw, milk, soft cheeses, and several types of “ready-to-eat” foods)

A

L. monocytogenes

176
Q

Important causes of meningitis that occurs following invasive neurosurgical procedures (i.e. shunting procedures) or as a complication of the use of subcutaneous Ommaya reservoirs for administration of intrathecal chemotherapy

A

S. aureus and coagulase-negative staphylococci

177
Q

T or F. Many of the neurologic manifestations and complications of bacterial meningitis result from the direct bacteria-induced tissue injury

A

False.

Many of the neurologic manifestations and complications of bacterial meningitis result from the immune response to the invading pathogen rather than from direct bacteria-induced tissue injury

178
Q

These 2 cytokines act synergistically to increase the permeability of the blood-brain barrier

A

TNF-α and IL-1β

179
Q

Classic clinical triad of acute meningitis

A
  • Fever
  • Headache
  • Nuchal rigidity
180
Q

Pathognomonic sign of meningeal irritation

A

Nuchal rigidity

181
Q

Decreased level of consciousness occurs in ____ of patients with meningitis

A

> 75%

lethargy to coma

182
Q

Elicited with the patient in the supine position and thigh is flexed on the abdomen, with the knee flexed. Positive response is noted when patient’s attempt to passively extend the knee elicit pain

A

Kernig’s sign

183
Q

Elicited with the patient in the supine position and is positive when passive flexion of the neck results in spontaneous flexion of the hips and knees

A

Brudzinski’s sign

184
Q

Major cause of obtundation and coma in acute meningitis

A

Raised ICP

185
Q

More than 90% of patients with acute meningitis will have a CSF opening pressure

A

> 180 mmH2O

186
Q

Cushing reflex is a sign of

A

Raised ICP

187
Q

Cushing reflex (3)

A
  • Bradycardia
  • Hypertension
  • Irregular respirations
188
Q

The most disastrous complication of increased ICP

A

Cerebral herniation

189
Q

CSF analysis is bacterial meningitis in terms of:

Cell count and differential
Glucose
CSF/serum glucose
Protein
Opening pressure
A 
Cell count and differential: 10-10000 cells/ neutrophilic predominance
Glucose: <2.2 mmol/L (<40 mg/dl)
CSF/serum glucose: <0.4
Protein: 0.45 g/L (>45 mg/dL)
Opening pressure: >180 mmH2O
190
Q

A rapid diagnostic test for the detection of gram-negative endotoxin in CSF and thus for making a diagnosis of gram-negative bacterial meningitis

A

Limulus amebocyte lysate assay

191
Q

Preferred imaging for acute meningitis

A

MRI

Diffuse meningeal enhancement – not diagnostic of meningitis but occurs in any CNS disease associated with increased blood-brain barrier permeability

192
Q

Rocky Mountain spotted fever (RMSF) is caused by the bacteria

A

Rickettsia rickettsia

transmitted by a tick bite

193
Q

Characteristic rash within 96 h of the onset of symptoms is initially a diffuse erythematous maculopapular rash that may be difficult to distinguish from that of meningococcemia, which progresses to a petechial rash, then to a purpuric rash, and if untreated, to skin necrosis or gangrene

A

Rocky Mountain spotted fever (RMSF)

194
Q

Goal in empirical antimicrobial therapy of acute meningitis

A

antibiotic therapy within 60 min of a patient’s arrival in the emergency room

195
Q

Empiric antimicrobial therapy for hospital-acquired meningitis (usually following neurosurgical procedures):

A

Vancomycin + ceftazidime/meropenem

Staphylococci and gram-negative organisms including P. aeruginosa are the most common etiologic organisms

196
Q

Antibiotic of choice for meningococcal meningitis

A

Pen G

7-day course – if uncomplicated

197
Q

Chemoprophylaxis for meningococcal meningitis

A

Rifampin 600 mg q12h for 2 days in adults

Alternative: azithromycin 500 mg single dose or ceftriaxone 250 mg IM single dose

Close contacts: contact with oropharyngeal secretions (e.g. kissing or by sharing toys, beverages, or cigarettes)

198
Q

Antibiotic of choice for pneumococcal meningitis

A

Cephalosporin (ceftriaxone, cefotaxime, or cefepime) + vancomycin

2-week therapy

199
Q

Ideally, when must LP be repeated after the initiation of antimicrobial therapy to document sterilization of CSF

A

24-36 h

Failure to strerilize CSF – presumptive evidence of antibiotic resistance

200
Q

Antibiotic of choice for Listeria meningitis

A

Ampicillin for at least 3 weeks

Gentamicin is added in critically ill patients
2 mg/kg loading dose, then 7.5 mg/kg per day given every 8 h and adjusted for serum levels and renal function

Alternative for penicillin-allergic patients: Co-trimoxazole (trim 10–20 mg/kg per day and sulfa 50–100 mg/kg per day) given every 6 h

201
Q

The drug of choice for MRSA and for patients allergic to penicillin

A

Vancomycin

202
Q

Antibiotic of choice for gram-negative bacillary meningitis

A

Third-generation cephalosporins for 3 weeks

203
Q

Dexamethasone exerts its beneficial effect in acute meningitis therapy by (3)

A
  • Inhibiting the synthesis of IL-1β and TNF-α at the level of mRNA
  • Decreasing CSF outflow resistance
  • Stabilizing the blood-brain barrier
204
Q

In acute meningitis management, Dexamethason must be given ____ before antibiotic therapy. Give the rationale.

A

20 min

Dexamethasone inhibits the production of TNF-α by macrophages and microglia only if it is administered before these cells are activated by endotoxin. It does not alter TNF-α production once it has been induced

205
Q

Dose of dexamethasone in acute meningitis

A

10 mg IV 15-20 mins before 1st dose of antimicrobial agent, then q6h for 4 days

206
Q

Management of increased ICP (4)

A
  • Elevation of the patient’s head to 30–45°
  • Intubation
  • Hyperventilation (PaCO2 25–30 mmHg)
  • Mannitol
207
Q

Mortality rates for acute meningitis caused by H. influenzae, N. meningitidis, or group B streptococci

A

3–7%

208
Q

Mortality rates for acute meningitis caused by L. monocytogenes

A

15%

209
Q

Mortality rates for acute meningitis caused by S. pneumoniae

A

20%

210
Q

CSF values that is predictive of increased mortality and poorer prognosis in acute meningitis (2):

A
  1. Decreased CSF glucose concentration (<2.2 mmol/L [<40 mg/dL])
  2. Markedly increased CSF protein concentration (>3 g/L [> 300 mg/dL])
211
Q

Characteristic of headache in viral meningitis

A

frontal or retroorbital

Associated with photophobia and pain on moving the eyes

212
Q

Which HSV more commonly cause the viral meningitis?

A

HSV 2 > HSV 1

HSV-1 – 90% of HSV encephalitis

213
Q

Most important laboratory test in the diagnosis of viral meningitis

A

CSF Examination

214
Q

CSF analysis is viral meningitis in terms of:

Cell count and differential
Glucose
Protein
Opening pressure

A

Cell count and differential: 25-500/μL; lymphocytic predominance
Glucose: normal
Protein: normal or sl. elevated
Opening pressure: 100-350 mmH2O

215
Q

The single most important method for diagnosing CNS viral infections

A

PCR amplification of viral nucleic acid

216
Q

Diagnostic procedure of choice for both enteroviral and HSV infections of the CNS

A

CSF PCR

217
Q

Most common cause of viral meningitis (>85% of cases)

A

Enteroviruses

218
Q

Viral infection that caused large epidemics of neurologic disease in Southeast Asia

A

Enterovirus 71

219
Q

Major cause of viral meningitis in adults

A

HSV meningitis

220
Q

Second most common cause of viral mengitis

A

HSV meningitis

221
Q

Most common cause of recurrent viral or “aseptic” meningitis

A

HSV meningitis

222
Q

Presence of atypical lymphocytes in the CSF or peripheral blood

A

EBV meningitis

223
Q

Cranial nerve palsies is more common in what viral meningitis as compared with other viral infections

A

HIV meningitis

224
Q

Most commonly involved cranial nerves in HIV meningitis (3)

A

V, VII, or VIII

225
Q

Meningitis associated with history of exposure to house mice (Mus musculus), pet or laboratory rodents (e.g., hamsters, rats, mice), or their excreta; some patients have an associated rash, pulmonary infiltrates, alopecia, parotitis, orchitis, or myopericarditis

A

LCMV infection

226
Q

Most common pathogen causing fungal meningitis

A

C. neoformans

227
Q

Most frequently involved cranial nerves in neurosyphilis (2)

A

Cranial nerves VII and VIII

228
Q

Most common causes of subacute meningitis (5)

A
  1. M. tuberculosis
  2. C. neoformans
  3. H. capsulatum
  4. C. immitis
  5. T. pallidum
229
Q

The combination of unrelenting headache, stiff neck, fatigue, night sweats, and fever with a CSF lymphocytic pleocytosis and a mildly decreased glucose concentration is highly suspicious for

A

tuberculous meningitis

230
Q

In the LP procedure, this is the best tube to send for a smear for acid-fast bacilli (AFB)

A

Last tube

231
Q

Positive AFB smears is seen in only ____ of cases of tuberculous meningitis in adults

A

10–40%

232
Q

The gold standard to make the diagnosis of tuberculous meningitis

A

Cultures of CSF

take 4–8 weeks

233
Q

In the evaluation of subacute meningitis, if spinal fluid examined by LP on two separate occasions fails to yield an organism, CSF should be obtained by

A

high-cervical or cisternal puncture

234
Q

A highly sensitive and specific test for cryptococcal meningitis

A

Cryptococcal polysaccharide antigen test

Reactive test establishes the diagnosis

235
Q

Specificity of 100% and a sensitivity of 75% for coccidioidal meningitis

A

CSF complement fixation antibody test

236
Q

Treatment of TB meningitis with dose and duration

A
  • Isoniazid (300 mg/d)
  • Rifampin (10 mg/kg per day)
  • Pyrazinamide (30 mg/kg per day in divided doses), iscontinued after 8 weeks
  • Ethambutol (15–25 mg/kg per day in divided doses), may be discontinued once isolate antimicrobial sensitivity is known

6 month course

237
Q

Dexamethasone dose in TB meningitis

A

12–16 mg/d for 3 weeks then tapered over 3 weeks

238
Q

Treatment of meningitis due to C. neoformans in non-HIV, nontransplant patients

A

Induction therapy: Amphotericin B (AmB) (0.7 mg/kg IV per day) plus flucytosine (100 mg/kg per day in four divided doses) for at least 4 weeks if CSF culture results are negative after 2 weeks of treatment; Extended to 6 weeks if with neurologic complications

Consolidation therapy: Fluconazole 400 mg/d for 8 weeks

239
Q

Treatment of meningitis due to C. neoformans in transplant recipients:

A

Liposomal AmB (3–4 mg/kg per day) or AmB lipid complex (ABLC) 5 mg/kg per day plus flucytosine (100 mg/kg per day in four divided doses) for at least 2 weeks or until CSF culture is sterile

Followed by an 8- to 10-week course of fluconazole (400–800 mg/d [6–12 mg/kg] PO). If the CSF culture is sterile after 10 weeks of acute therapy, the dose is decreased to 200 mg/d for 6 months to a year

240
Q

Treatment of meningitis due to C. neoformans in HIV patients:

A

AmB or a lipid formulation plus flucytosine for at least 2 weeks

Followed by fluconazole for a minimum of 8 weeks

May require indefinite maintenance therapy with fluconazole 200 mg/d

241
Q

Treatment of meningitis due to H. capsulatum:

A

AmB (0.7–1.0 mg/kg per day) for 4–12 weeks; total dose of 30 mg/kg is recommended; not discontinued until fungal cultures are sterile

Maintenance therapy: itraconazole 200 mg two or three times daily for at least 9 months to a year

242
Q

Treatment of meningitis due to C. immitis:

A

High-dose fluconazole (1000 mg daily) as monotherapy

IV AmB (0.5–0.7 mg/kg per day) for >4 weeks

Lifelong therapy with fluconazole (200–400 mg daily) to prevent relapse

243
Q

Most common complication of fungal meningitis

A

Hydrocephalus

244
Q

Treatment of meningitis secondary to syphilis

A

Aqueous penicillin G in a dose of 3–4 million units intravenously every 4 h for 10–14 days

Alternative regimen: 2.4 million units of procaine penicillin G IM daily with 500 mg of oral probenecid four times daily for 10–14 days

Followed with 2.4 million units of benzathine penicillin G IM once a week for 3 weeks

245
Q

In meningitis secondary to syphilis, CSF should be reexamined at

A

6-month intervals for 2 years

246
Q

Empiric therapy of acute meningitis in immunocompetent children >3 months and adults <55

A

Cefotaxime, ceftriaxone, or cefepime + vancomycin

247
Q

Empiric therapy of acute meningitis in adults >55 and adults of any age with alcoholism or other debilitating illnesses

A

Ampicillin + cefotaxime, ceftriaxone or cefepime + vancomycin

248
Q

Empiric therapy of acute meningitis in hospital-acquired meningitis, posttraumatic or postneurosurgery meningitis, neutropenic patients, or patients with impaired cell- mediated immunity

A

Ampicillin + ceftazidime or meropenem + vancomycin

249
Q

Glucocorticoid therapy for mild, moderate and severe MG

A

Mild or moderate weakness – 15-25 mg/d

Severe – high dose. Patients are maintained on the dose that seems to control their weakness for about a month, and then slowly tapered. Tapering is no faster than 10 mg a month until 20 mg daily and then 2.5-5 mg a month

250
Q

Chronic meningitis neurologic syndrome exists for how long?

A

> 4 week

251
Q

Five most common causes of chronic meningitis:

A
  1. Meningeal infections
  2. Malignancy
  3. Autoimmune inflammatory disorders
  4. Chemical meningitis
  5. Parameningeal infections
252
Q

Cardinal features of chronic meningitis (may occur alone or in combination)(6)

A
  1. Persistent headache
  2. Hydrocephalus
  3. Cranial neuropathies
  4. Radiculopathies
  5. Cognitive changes
  6. Personality changes
253
Q

Cerebrospinal fluid is produced by the ______ of the cerebral ventricles, then exits through narrow foramina into the _____ surrounding the brain and spinal cord, circulates around the _______ and over the _______, then resorbed by ______ projecting into the _____

A 
Choroid plexus
subarachnoid space
base of the brain
cerebral hemispheres
superior sagittal sinus

Pathway provides rapid spread of infectious and other infiltrative processes over the brain, spinal cord, cranial, and spinal nerve roots

254
Q

Arachnoid cuffs that surround the blood vessels that penetrate the brain tissue and may be a pathway of spread from the subarachnoid space into the brain parenchyma

A

Virchow-Robin spaces

255
Q

Thickening of the meninges caused by clumping of the lower nerve roots due to chronic inflammation

A

Pachymeningitis

256
Q

Major concern of chronic meningitis in the immunosuppressed patient (e.g. HIV patients)

A

chronic meningitis may present without headache or fever

257
Q

Two clinical forms of chronic meningitis

A
  1. Chronic and persistent symptoms

2. Recurrent, discrete episodes of illness

258
Q

Recurrent meningitis that is most often due to herpes simplex virus (HSV) type 2

A

Mollaret’s meningitis

259
Q

Recurrent meningitis that is due to episodic leakage from an epidermoid tumor, craniopharyngioma, or cholesteatoma into CSF

A

Chemical meningitis

260
Q

Meningitis wherein fatal levels of raised ICP can occur without enlarged ventricles

A

Cryptococcal meningitis

261
Q

This cells usually predominate in the CSF in most categories of chronic (not recurrent) meningitis

A

Mononuclear cells

262
Q

Nonencapsulated brain abscess

A

Cerebritis

263
Q

In up to 25% of cases of brain abscess, no obvious primary source of infection is apparent

A

cryptogenic brain abscess

264
Q

Otogenic abscesses occur predominantly in the(2)

A

temporal lobe (55–75%) and cerebellum (20–30%)

265
Q

In some series, up to 90% of cerebellar abscesses are

A

Otogenic

266
Q

Abscesses that develop as a result of direct spread of infection from the frontal, ethmoidal, or sphenoidal sinuses and those that occur due to dental infections are usually located in the

A

frontal lobes

267
Q

Hematogenous brain abscesses show a predilection for the

A

territory of the middle cerebral artery (i.e., posterior frontal or parietal lobes)

268
Q

T or F. for bacterial invasion of brain parenchyma to occur, there must be preexisting or concomitant areas of ischemia, necrosis, or hypoxemia in brain tissue

A

True. The intact brain parenchyma is relatively resistant to infection

269
Q

Stage of cerebritis that is characterized by a perivascular infiltration of inflammatory cells, which surround a central core of coagulative necrosis

A

early cerebritis stage (days 1–3)

270
Q

Cerebritis stage characterized by pus formation that leads to enlargement of the necrotic center, which is surrounded at its border by an inflammatory infiltrate of macrophages and fibroblasts.

A

late cerebritis stage (days 4–9)

A thin capsule of fibroblasts and reticular fibers gradually develops, and the surrounding area of cerebral edema becomes more distinct than in the previous stage

271
Q

Cerebritis stage characterized by the formation of a capsule that is better developed on the cortical than on the ventricular side of the lesion

A

third stage, early capsule formation (days 10–13)

272
Q

This stage of cerebritis correlates with the appearance of a ring-enhancing capsule on neuroimaging studies

A

third stage, early capsule formation (days 10–13)

273
Q

Cerebritis stage defined by a well-formed necrotic center surrounded by a dense collagenous capsule

A

final stage, late capsule formation (day 14 and beyond)

The surrounding area of cerebral edema has regressed, but marked gliosis with large numbers of reactive astrocytes has developed outside the capsule. This gliotic process may contribute to the development of seizures as a sequela of brain abscess

274
Q

The classic clinical triad of brain abscess

A

headache, fever, and a focal neurologic deficit

present in <50% of cases

275
Q

The most common symptom in patients with a brain abscess is

A

Headache

occurring in >75% of patients
constant, dull, aching sensation, either hemicranial or generalized, and it becomes progressively more severe and refractory to therapy

276
Q

T or F. Fever is present in all patients of brain abscess.

A

False.

277
Q

the most common localizing sign of a frontal lobe abscess

A

Hemiparesis

278
Q

the most common localizing sign of a temporal lobe abscess

A

disturbance of language (dysphasia) or an upper homonymous quadrantanopia

279
Q

the most common localizing sign of a cerebellar abscess

A

Nystagmus and ataxia

280
Q

Imaging of choice for brain abscess

A

MRI

Better than CT for demonstrating abscesses in the early (cerebritis) stages and is superior to CT for identifying abscesses in the posterior fossa

281
Q

T or F. LP should be performed in patients with suspected focal intracranial infections such as abscess or empyema.

A

False. CSF analysis contributes nothing to diagnosis or therapy, and LP increases the risk of herniation

282
Q

Blood cultures are positive in ~10% of brain abscess cases overall but may be positive in >85% of patients with abscesses due to

A

Listeria

283
Q

Empirical therapy of community-acquired brain abscess in an immunocompetent patient

A

third- or fourth-generation cephalosporin (e.g., cefotaxime, ceftriaxone, or cefepime) and metronidazole

284
Q

In brain abscess patients with penetrating head trauma or recent neurosurgical procedures, treatment should include

A

ceftazidime and vancomycin

Meropenem plus vancomycin also provides good coverage in this setting

285
Q

Medical therapy alone is not optimal for treatment of brain abscess and should be reserved for patients whose abscesses are: (4)

A
  1. neurosurgically inaccessible
  2. small (<2–3 cm)
  3. nonencapsulated abscesses (cerebritis)
  4. For patients whose condition is too tenuous to allow performance of a neurosurgical procedure
286
Q

T or F. Brain abscess patients should receive prophylactic anticonvulsant therapy because of the high risk (~35%) of focal or generalized seizures

A

True. Anticonvulsant therapy is continued for at least 3 months after resolution of the abscess, and decisions regarding withdrawal are then based on the EEG

287
Q

When do you give glucocorticoids in patients with brain abscess and what dose?

A

IV dexamethasone therapy 10 mg every 6
For patients with substantial periabscess edema and associated mass effect and increased ICP
Dexamethasone should be tapered as rapidly as possible to avoid delaying the natural process of encapsulation of the abscess

288
Q

The most common parasitic disease of the CNS worldwide

A

Neurocysticercosis

289
Q

Cause of neurocysticercosis

A

T. solium

290
Q

The most common manifestation of neurocysticercosis

A

new-onset partial seizures with or without secondary generalization

291
Q

Part of the T. solium that can often be visualized on MRI

A

Scolex

292
Q

most common finding and evidence that the neurocysticercosis parasite is no longer viable

A

Parenchymal brain calcifications

293
Q

Treatment of neurocysticercosis (3)

A

Albendazole 15 mg/kg per day in two doses for 8 days or praziquantel 50 mg/kg per day for 15 days

Prednisone or dexamethasone

Only cysts in the vesicular stage, where the cyst contains living larva (scolex seen on CT or MRI), and cysts in the colloidal stage as the larva degnerates (edema surrounds the lesion), are treated with anticysticidal therapy

There is universal agreement that calcified lesions do not need to be treated with anticysticidal therapy

294
Q

Treatment of CNS toxoplasmosis

A

combination of sulfadiazine, 1.5–2.0 g orally qid, plus pyrimethamine, 100 mg orally to load, then 75–100 mg orally qd, plus folinic acid, 10–15 mg orally qd

Folinic acid is added to the regimen to prevent megaloblastic anemia

Therapy is continued until there is no evidence of active disease on neuroimaging studies, which typically takes at least 6 weeks, and then the dose of sulfadiazine is reduced to 2–4 g/d and pyrimethamine to 50 mg/d

Alternative: Clindamycin plus pyrimethamine

295
Q

A collection of pus between the dura and arachnoid membranes

A

subdural empyema

296
Q

The most common predisposing condition of subdural empyema

A

Sinusitis and typically involves the frontal sinuses

297
Q

Sinusitis-associated subdral empyema has a striking predilection for

A

young males

possibly reflecting sex-related differences in sinus anatomy and development

298
Q

The most common causative organisms of sinusitis-associated SDE

A

Aerobic and anaerobic streptococci, staphylococci, Enterobacteriaceae, and anaerobic bacteria

299
Q

The most common causative organisms of SDE secondary to neurosurgical procedures

A

Staphylococci and gram-negative bacilli

300
Q

SDE is often associated with other intracranial infections such as (3)

A
  1. epidural empyema (40%)
  2. Cortical thrombophlebitis (35%)
  3. Intracranial abscess or cerebritis (>25%)
301
Q

This condition should always be suspected in a patient with known sinusitis who presents with new CNS signs or symptoms

A

Subdural empyema

302
Q

The most common complaint at the time of presentation of subdural empyema

A

Headache

303
Q

The most common focal neurologic deficit of SDE

A

Contralateral hemiparesis or hemiplegia

Can occur from the direct effects of the SDE on the cortex or as a consequence of venous infa

304
Q

The definitive step in the management of this SDE

A

Emergent neurosurgical evacuation of the empyema, either through craniotomy, craniectomy, or burr-hole drainage

305
Q

Empirical antimicrobial therapy for community-acquired SDE should include a combination of

A

third-generation cephalosporin (e.g., cefotaxime or ceftriaxone), vancomycin, and metronidazole for a minimum of 3–4 weeks after SDE drainage

same with epidural abscess. Ceftazidime or meropenem should be substituted for ceftriaxone or cefotaxime in neurosurgical patients

306
Q

A suppurative infection occurring in the potential space between the inner skull table and dura

A

Cranial epidural abscess

307
Q

This CNS suppurative infection may develop contiguous to an area of osteomyelitis, when craniotomy is complicated by infection of the wound or bone flap

A

Epidural abscess

308
Q

T or F. Cranial epidural abscesses may result from hematogenous spread of infection from extracranial primary sites

A

False

309
Q

Usual causative organism of an epidural abscess that develops as a complication of craniotomy or compound skull fracture

A

Staphylococci or gram-negative organisms

310
Q

Periorbital edema and Pott’s puffy tumor may be present in this CNS suppurative infection

A

Epidural abscess

Reflecting underlying associated frontal bone osteomyelitis
Present in ~40%

311
Q

The diagnosis should be considered when fever and headache follow recent head trauma or occur in the setting of frontal sinusitis, mastoiditis, or otitis media

A

Epidural abscess

Other CNS suppurative infections may also be considered

312
Q

Procedure of choice to demonstrate a cranial epidural abscess

A

Cranial MRI with gadolinium enhancement

313
Q

septic venous thrombosis of cortical veins and sinuses that may occur as a complication of bacterial meningitis; SDE; epidural abscess; or infection in the skin of the face, paranasal sinuses, middle ear, or mastoid

A

Suppurative intracranial thrombophlebitis

314
Q

largest of the venous sinuses

A

superior sagittal sinus

It receives blood from the frontal, parietal, and occipital superior cerebral veins and the diploic veins, which communicate with the meningeal veins

315
Q

the most common sites of primary infection resulting in septic cavernous sinus thrombosis (2)

A

sphenoid and ethmoid sinuses

316
Q

A transverse sinus thrombosis may also present with otitis media, sixth nerve palsy, and retroorbital or facial pain, a syndrome called

A

Gradenigo’s syndrome

317
Q

T or F. The presence of a small intracerebral hemorrhage from septic thrombophlebitis is an absolute contraindication to heparin therapy

A

False. Not an absolute contraindication

318
Q

Recent clinical trials have shown that systolic blood pressure (SBP) can be safely lowered acutely and rapidly to _____ in patients with spontaneous ICH whose initial SBP was 150–220 mmHg

A

<140 mmHg

319
Q

a large phase 3 clinical trial to address the effect of acute blood pressure lowering on ICH functional outcome that revealed that there was a significant shift to improved outcomes in the lower blood pressure arm, whereas both groups had a similar mortality

A

INTERACT2 trial

INTERACT2 randomized patients with spontaneous ICH within 6 h of onset and a baseline SBP of 150–220 mmHg to two different SBP targets (<140 and <180 mmHg). In those with the target SBP <140 mmHg, 52% had an outcome of death or major disability at 90 days compared with 55.6% of those with a target SBP <180 mmHg (p = .06).

320
Q

clinical trial to address the effect of acute blood pressure lowering on ICH functional outcome that demonstrated no difference in outcome between low and high BP

A

ATACH2

321
Q

In patient with intracerebral hemorrhage, the recommended CPP that should be maintained is

A

50–70 mmHg

322
Q

CPP is calculated by

A

MAP – ICP

323
Q

ICH accounts for ____ of all strokes, and about _____ of patients die within the first month

A

~10%

35–45%

324
Q

Most common causes of ICH (4)

A
  1. Hypertension
  2. Coagulopathy
  3. Sympathomimetic drugs (cocaine, methamphetamine)
  4. Cerebral amyloid angiopathy (CAA)
325
Q

Hypertensive ICH usually results from spontaneous rupture of a ______ deep in the brain

A

small penetrating artery

326
Q

Most common sites of hypertensive ICH (4)

A
  1. basal ganglia (especially the putamen)
  2. thalamus
  3. cerebellum
  4. pons
327
Q

Most hypertensive ICHs initially develop over_____, whereas those associated with anticoagulant therapy may evolve for as long as _____

A

30–90 min

24–48 h

However, it is now recognized that about a third of patients even with no coagulopathy may have significant hematoma expansion with the first day

328
Q

Within____, macrophages begin to phagocytize the blood in ICH at its outer surface

A

48 h

329
Q

After_______, the ICH is generally resolved to a slitlike cavity lined with a glial scar and hemosiderin-laden macrophages

A

1–6 months

330
Q

most common site for hypertensive hemorrhage

A

Putamen

adjacent internal capsule is usually damaged

331
Q

Sentinel sign of hypertensive ICH

A

Contralateral hemiparesis

332
Q

A prominent sensory deficit involving all modalities is usually present in this hypertensive ICH

A

Thalamic hemorrhages

Aphasia, often with preserved verbal repetition, may occur after hemorrhage into the dominant thalamus, and constructional apraxia or mutism occurs in some cases of nondominant hemorrhage

333
Q

Thalamic hemorrhages cause several typical ocular disturbances by extension inferiorly into the

A

upper midbrain

deviation of the eyes downward and inward so that they appear to be looking at the nose, unequal pupils with absence of light reaction, skew deviation with the eye opposite the hemorrhage displaced downward and medially, ipsilateral Horner’s syndrome, absence of convergence, paralysis of vertical gaze, and retraction nystagmus

334
Q

chronic, contralateral pain syndrome that occur later in thalamic hemorrhages

A

Déjérine-Roussy syndrome

335
Q

deep coma with quadriplegia often occurs over a few minutes in this hypertensive ICH

A

pontine hemorrhages

prominent decerebrate rigidity and “pinpoint” (1 mm) pupils that react to light

336
Q

impairment of reflex horizontal eye movements evoked by head turning (doll’s-head or oculocephalic maneuver) or by irrigation of the ears with ice water is usually seen in what hypertensive ICH

A

pontine hemorrhages

337
Q

Most patients with deep coma from pontine hemorrhage ultimately die, or develop a______ , but small hemorrhages are compatible with survival and significant recovery

A

locked-in state

338
Q

Hypertensive ICH that develop over several hours and are characterized by occipital headache, repeated vomiting, and ataxia of gait

A

Cerebellar hemorrhages

In mild cases, there may be no other neurologic signs except for gait ataxia. Dizziness or vertigo may be prominent

There is often paresis of conjugate lateral gaze toward the side of the hemorrhage, forced deviation of the eyes to the opposite side, or an ipsilateral sixth nerve palsy

339
Q

The major neurologic deficit with an occipital hemorrhage

A

hemianopsia

340
Q

The major neurologic deficit with a left temporal hemorrhage

A

aphasia and delirium

341
Q

The major neurologic deficit with a parietal hemorrhage

A

hemisensory loss

342
Q

The major neurologic deficit with a frontal hemorrhage

A

arm weakness

343
Q

A disease of the elderly in which arteriolar degeneration occurs and amyloid is deposited in the walls of the cerebral arteries

A

Cerebral amyloid angiopathy

It accounts for some intracranial hemorrhages associated with IV thrombolysis given for myocardial infarction

344
Q

the most common cause of lobar hemorrhage in the elderly

A

Cerebral amyloid angiopathy

345
Q

This disorder can be suspected in patients who present with multiple hemorrhages (and infarcts) over several months or years or in patients with “microbleeds” in the cortex, seen on brain MRI sequences sensitive for hemosiderin (iron-sensitive imaging)

A

Cerebral amyloid angiopathy

346
Q

definitively diagnosed by pathologic demonstration of Congo red staining of amyloid in cerebral vessels

A

Cerebral amyloid angiopathy

347
Q

associated with increased risk of recurrent lobar hemorrhage and may therefore be markers of amyloid angiopathy

A

ε2 and ε4 allelic variations of the apolipoprotein E gene

348
Q

Definitive diagnostic test for CAA

A

Cerebral biopsy

349
Q

Drugs that are frequent causes of stroke in young (age <45 years) patients (2)

A

Cocaine and methamphetamine

The mechanism of sympathomimetic-related stroke is not known, but cocaine enhances sympathetic activity causing acute, sometimes severe, hypertension, and this may lead to hemorrhage

350
Q

The common sites of ICH secondary to head injury (5)

A 
Temporal lobe
Inferior frontal lobe
Subarachnoid
Subdural
Epidural spaces
351
Q

Anticoagulant-related ICHs may occur at any location, but they are often

A

lobar or subdural

ICH associated with hematologic disorders (leukemia, aplastic anemia, thrombocytopenic purpura) can occur at any site and may present as multiple ICHs

352
Q

Most common metastatic tumors associated with ICH (4)

A

Choriocarcinoma
Malignant melanoma
Renal cell carcinoma
Bronchogenic carcinoma

353
Q

_______ in adults and ______ in children may have areas of ICH associated with the neoplasm

A

Glioblastoma multiforme

Medulloblastoma

354
Q

Complication of malignant hypertension that present as headache, nausea, vomiting, convulsions, confusion, stupor, and coma

A

Hypertensive encephalopathy

There are retinal hemorrhages, exudates, papilledema (hypertensive retinopathy), and evidence of renal and cardiac disease

355
Q

MRI brain imaging of hypertensive encephalopathy shows a pattern of typically (posterior/anterior?) edema that is (reversible or irreversible?) and termed ______

A

posterior (occipital > frontal) brain

reversible

reversible posterior leukoencephalopathy

356
Q

Distinguishing hypertensive encephalopathy with ICH from hypertensive ICH is important since aggressive lowering of SBP to 140–180 mmHg acutely is usually considered in ____ but less aggressive measures should be used in _____

A

hypertensive ICH

hypertensive encephalopathy

Having no alteration in mental status or other prodrome prior to the ICH favors hypertensive ICH as the disease

357
Q

Hemorrhages into the spinal cord are usually the result of (3)

A

AVM
Cavernous malformation
Metastatic tumor

358
Q

A validated clinical grading scale that is useful for stratification of mortality risk and clinical outcome of ICH

A

ICH Score

359
Q

A monoclonal antibody to dabigatran and the administration of two doses reverses the anticoagulation effect of dabigatran quickly

A

Idarucizumab

360
Q

T or F. You may do platelet transfusion of ICH without thrombocytopenia but with intake of antiplatelet drugs

A

False. A recent clinical trial of platelet transfusions in patients with ICH and without thrombocytopenia who are taking antiplatelet drugs suggested no benefit and possible harm.

361
Q

Trial that randomized patients with supratentorial ICH to either early surgical evacuation or initial medical management and no benefit was found in the early surgery arm

A

International Surgical Trial in Intracerebral Haemorrhage (STICH)

although analysis was complicated by the fact that 26% of patients in the initial medical management group ultimately had surgery for neurologic deterioration

362
Q

Trial that revealed that surgery within 24 h of lobar, supratentorial hemorrhage did not improve overall outcome, but might have a role in select severely affected patients

A

STICH-II

Therefore, existing data do not support routine surgical evacuation of supratentorial hemorrhages in stable patients. However, many centers still consider surgery for patients deemed salvageable and who are experiencing progressive neurologic deterioration due to herniation

363
Q

most cerebellar hematomas ____ in diameter will require surgical evacuation

A

> 3 cm

Patients with hematomas between 1 and 3 cm require careful observation for signs of impaired consciousness, progressive hydrocephalus, and precipitous respiratory failure

If the patient is alert without focal brainstem signs and if the hematoma is <1 cm in diameter, surgical removal is usually unnecessary

364
Q

T or F. Hyperventilation is one of the management of increased ICP in ICH

A

True, but limited to acute rescucitation only.

hyperventilation may actually produce ischemia by cerebral vasoconstriction

365
Q

T or F. Glucocorticoids are helpful for the edema from intracerebral hematoma

A

False

366
Q

congenital shunts between the arterial and venous systems that may present with headache, seizures, and intracranial hemorrhage

A

True AVMs

367
Q

AVMs occur in all parts of the cerebral hemispheres, brainstem, and spinal cord, but the largest ones are most frequently located in the _____, commonly forming a wedge-shaped lesion extending from the cortex to the ventricle.

A

posterior half of the hemispheres

368
Q

Familial AVM may be a part of the autosomal dominant syndrome of hereditary hemorrhagic telangiectasia syndrome called ______, which is due to mutations in either endoglin or activin receptor-like kinase 1, both involved in transforming growth factor (TGF) signaling and angiogenesis

A

Osler-Rendu-Weber syndrome

369
Q

Most common involvement of ICH secondary to AVM

A

intraparenchymal

with extension into the subarachnoid space in some cases

370
Q

Unlike primary subarachnoid hemorrhages, blood from a ruptured AVM is usually not deposited in the basal cisterns, and _______ is rare

A

symptomatic cerebral vasospasm

371
Q

The risk of AVM rupture is strongly influenced by a

A

history of prior rupture

372
Q

The AVM may be large enough to steal blood away from adjacent normal brain tissue or to increase venous pressure significantly to produce venous ischemia locally and in remote areas of the brain. This is seen most often with large AVMs in the

A

territory of the middle cerebral artery.

373
Q

Large AVMs of the ______ may be associated with a systolic and diastolic bruit (sometimes self-audible) over the eye, forehead, or neck and a bounding carotid pulse

A

anterior circulation

374
Q

Initial imaging of choice for cerebral AVM

A

MRI

although noncontrast CT scanning sometimes detects calcification of the AVM and contrast may demonstrate the abnormal blood vessels

375
Q

gold standard for evaluating the precise anatomy of the cerebral AVM

A

conventional x-ray angiography

376
Q

T or F. Venous anomalies in the brain are of little clinical significance and should be ignored if found incidentally on brain imaging studies

A

True

Surgical resection of these anomalies may result in venous infarction and hemorrhage. Venous anomalies may be associated with cavernous malformations (see below), which do carry some bleeding risk.

377
Q

true capillary malformations that often form extensive vascular networks through an otherwise normal brain structure

A

Capillary telangiectasias

378
Q

Typical locations of capillary telangiectasias (2)

A

pons and deep cerebral white matter

these capillary malformations can be seen in patients with hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber) syndrome

379
Q

tufts of capillary sinusoids that form within the deep hemispheric white matter and brainstem with no normal intervening neural structures

A

Cavernous angiomas

The pathogenesis is unclear. Familial cav- ernous angiomas have been mapped to several different genes: KRIT1, CCM2, and PDCD10

380
Q

acquired connections usually from a dural artery to a dural sinus

A

Dural arteriovenous fistulas

381
Q

In this acquired brain vascular lesion, patients may complain of a pulse-synchronous cephalic bruit (“pulsatile tinnitus”) and headache

A

Dural arteriovenous fistulas

382
Q

Clinical and imaging factor and their in ICH scoring (5)

A
  1. Age

<80 years – o
≥ 80 years – 1

  1. Hematoma volume

<30 cc – 0
≥ 30 cc – 1

  1. Intraventricular hemorrhage present

No – 0
Yes – 1

  1. Infratentorial origin of hemorrhage

No – 0
Yes – 1

  1. GCS score

13-15 – 0
5-12 – 1
3-4 – 2

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