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Flashcards in CNSI Deck (182)
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1
Q

What proportion of patients with active TB meningitis would also have TB elsewhere?

A

2/3

2
Q

How does TB affect the spine?

A
  1. Compression of spinal roots and cord
  2. Direct parenchymal invasion
  3. Osteomyelitis causing an epidural abscess
  4. Osteomyelitis causing bone deformity affecting spine
  5. Arteritis causing cord infarct
3
Q

Dose of anti tb meds?

A

5mg per kg H
10 R
15 E
20 Z

4
Q

What cell is dysfunctional in patients with fungal meningitis?

A

T cells

5
Q

T or F: Fungal meningitis presents with multiple cranial nerve involvement, arteritis with thrombosis, brain infarction, microabscesses and HCP?

A

True. much like TB

6
Q

T or F CALAS is sensitive

A

T. 90% reliability to exclude the disease

7
Q

How to grow crypto in the lab?

A

Saboraud agar at 37 deg cel

8
Q

T or F In patients with AIDS, an elevated Toxo IgG titer + clinical syndrome + MRI findings are diagnostic of toxoplasmosis?

A

F. EXCEPT AIDS because they do not display an elevation of titers.

9
Q

Antitbiotics for Toxoplasmosis?

A

Sulfadiazine and pyrimethamine

10
Q

Treatment for Cysticercosis and Schistosomiasis

A

Praziquantel 20mg per kg

11
Q

What do cerebral lesions of schistosomiasis look like?

A

Mixed necrotizing and ischemic parenchymal foci infiltrated with eosinophils and giant cells

12
Q

Where is schistosomiasis endemic in the Philippines?

A

Mindoro Oriental and Sorsogon in Southern Luzon; the provinces of North, East and Western Samar; Leyte; and Bohol in Eastern Visayas, and all the provinces of Mindanao with the exception of Misamis Oriental, Davao Oriental and Maguindanao.

13
Q

What are the most common cauasative organisms of septic thrombophlebitis?

A

Staph and strep

14
Q

What are the CSF findings in septic cavernous sinus thrombophlebitis?

A

May be normal

15
Q

What bacterial type of meningitis may take the form of a rhombencephalitis?

A

Listeria monocytogenes or burkholderia psuedomallei

16
Q

What bacteria is responsible for Whipple Disease?

A

Tropheryma whipplei

17
Q

Treatment for:
Listeria
Legionella
Mycoplasma

A

Legionella Levofloxacin, azithromycin
Listeria Ampicillin Gentamicin
Mycoplasma Azithromycin and Clarithromycin

18
Q

Subdural empyema of sinus origin is due to?

A

Streptococci, non-hemolytic + viridans

19
Q

What is the usual precedent of epidural abscess?

A

Osteomyelitis

20
Q

What is the likely bac men pathogen in:

  1. Petechial and purpuric rash
  2. Alcoholics
  3. Splenectomized patients
A
  1. Meningococcal meningitis

2-3. Pneumococcal meningitis

21
Q

What is the usual number of WBC in bacterial meningitis?

A

1000-10000

22
Q

What bacterial meningitis presents with bloody CSF?

A

Anthrax

23
Q

90% of bacterial meningitis patients will have a protein higher than?

A

45mg dl

24
Q

What CSF value can distinguish between bacterial or fungal from viral meningitis?

A

Lactic acid is greater than 35mg dl in bacterial or fungal

25
Q

Cultures of spinal fluid are positive in how many cases of bacterial meningitis?

A

70-90%

26
Q

What are the 3 tests that can be used to determine if nasal fluid is of central origin?

A
  1. beta 2 transferrin test
  2. Protein hanky test if does not stiffen must be sf
  3. Glucose if 2/3 serum must be csf
27
Q

What causes Mollaret meningitis?

A

Herpes simplex

28
Q

What syndrome? Iridiocyclitis, poliosis, vitiligo and recurrent meningitis

A

Vogt Koynagi Harada

29
Q

How to give dexamethasone to adults?

A

Dexa 10mg just before the first dose of antibiotics

30
Q

Waterhouse Friedrichsen syndrome (adrenocortical hemorrhages) is associated with what kind of meningitis?

A

Meningococcimia. N meningitidis

31
Q

What is osler triad?

A

Endocarditis, pneumococcal meningitis, pneumonia

32
Q

What meningitis is frequently associated with hearing loss?

A

Pneumococcal meningitis

33
Q

What is the common csf picture in aseptic meningitis?

A

Normal CHO with lymphocytic pleocytosis

34
Q

What is the most common cause of viral meningitis?

A

Enterovirus: echo and coxsackie followed by HSV-2

35
Q

The lymphocytic choriomeningitis virus is commonly acquired from what animal?

A

Hamsters/ rats

36
Q

What drugs can causes aseptic meningitis?

A

IVIG, NSAIDS, antibiotics (Bactrim and Amoxicillin)

37
Q

What is the most common cause of acute encephalitis?

A

HSV

38
Q

What is the serogroup of Japanese encephalitis?

A

Flaviviruses

39
Q

What are the neurologic complications of EBV (Infectious mononucleosis)?

A

Meningitis, Encephalitis, Facial palsy, polyneuritis of GBS type

40
Q

CSF in herpes simplex encephalitis ALWAYS shows?

A

pleocytosis usually in the range of 10-200 lymphocytes

41
Q

What is the incubation period of rabies?

A

20-60 days

42
Q

Babes nodules and negri bodies are found in what disease/s?

A

Rabies.
babes- focal collections of microglia
negri- eosinophilic cytoplasmic inclusions mostly in the pyramidal cells of the hippocampus

43
Q

What cleanser should be used for dog bites to avoid rabies?

A

Ammonium chloride

44
Q

What is the mean latency of infection and AIDS?

A

8-10 years

45
Q

What test is most sensitive for the early stages of AIDS dementia?

A

Trail making

46
Q

What are imaging findings in AIDS dementia?

A

Widening of sulci, enlargement of ventricles and diffuse white matter changes with ill defined margins

47
Q

What is the first proven viral polyneuritis in humans?

A

AIDS peripheral neuropathy

48
Q

What AIDS medication is purported to cause a myopathy?

A

Zidovudine

49
Q

Treatment for Toxoplasmosis?

A

Pyrimethamine and sulfonamide

50
Q

What is the clinical picture of CMV encephalitis?

A

Acute confusional state + Cranial nerve signs

C for C! CMV with cranial nerve signs

51
Q

A special result of HIV treatment may induce an intense inflammatory reaction to a coexistent infection called?

A

Immune reconstitution inflammatory syndrome. IRIS.

52
Q

How long is the asymptomatic period after an infection with measles before SSPE happens?

A

6-8 years!

53
Q

What is the EEG pattern of SSPE?

A

EEG of periodic 5 to 8 second bursts of 2-3/s high voltage waves followed by a relatively flat pattern

54
Q

What part of the brain is usually spared in SSPE?

A

Cerebellum

55
Q

What is the most common kind of sporadic CJD?

A

MM1

56
Q

What are the variants of CJD?

  1. Prominent cerebellar ataxia
  2. Prominent visual distubance
A
  1. Brownell-Oppneheimer variant
  2. Heidenhain variant

Heiden is blind!
Brownell is dancing with oppenheimer!

57
Q

What are the EEG findings in CJD?

A

Diffuse non-specific slowing –> stereotyped high voltage slowing + sharp wave complexes on low voltage background and slow

May also exhibit pseudoperiodicity

58
Q

What are the MRI findings of CJD?

A

Hyperintensity of lenticular nuceli, cortex and basal ganglia on T2 and DWI.

59
Q

What movement disorder is characteristic of CJD?

A

Myoclonus

60
Q

How to differentiate SSPE and CJD based on CSF?

A

SSPE: CSF with elevated IgG
CJD: NORMAL

61
Q

What can kill cjd prion?

A

autoclave 132 degrees celsius at 15lb/in2 OR 5% sodium hypochlorite immersion

62
Q

Kuru plaques are predominantly in which part of the brain?

A

Cerebellum

63
Q

What is a prion?

A

A proteinacious infectious particle that is devoid of nucleic acid resists the action of enzymes that destroy RNA and DNA

Normal prion protein PrP is normally encoded by a gene on the short arm of chromosome 20 in humans

64
Q

Creutzfeldt-Jakob Disease is aka?

A

Subacute spongiform encephalopathy

65
Q

What prior disease caused the mini 1986 epidemic called mad cow disease?

A

variant Creutzfeldt-Jakob Disease

Prion is identical to prions seen in bovine spongiform encephalopathy

66
Q

What is the conformational change that PrPc being transformed to PrPsc goes through?

A

Helix to beta pleated sheets

67
Q

What ist he most common type of isoform of the prion of CJD?

A

MM1 present in 2/3 of sporadic cases

68
Q

What is the order of development of sxs in CJD?

A

Behavioral change
Ataxia
Visual disturbances
Myoclonus

RAPIDLY progressive over weeks

69
Q

What sequences show hyperintensity in the lenticular nuclei and cortex (long contiguous segments) in CJD?

A

T2 and DWI

70
Q

What is the Sn and Sp of 14-3-3 immunoassay of peptide fragments? For Creutzfeldt-Jakob disease

A

92

80

71
Q

Re CJD: What is the histopathologic substrate of myoclonus and positive sharp waves in the EEG?

A

Loss of certain inhibitory neurons in the thalamic reticular nuclei

Microscopic vacuoles of the cytoplasmic processes of the glia give rise to the spongy appearance of the brain

NO EVIDENCE OF INFLAMMATION!!! One of the key pathologic features

72
Q

Intoxication with what element can results in dementia and myclonus similar to CJD?

A

Lithium

Other DDX: SSPE, Hashimoto encephalopathy, carcinomatous meningitis

73
Q

What characteristics of these prion diseases differentiate them from CJD:

  1. Gerstmann-Straussler-Scheinker Syndrome
  2. Fatal insomnia
  3. Kuru
A
  1. Gerstmann-Straussler-Scheinker Syndrome: Familial rather than sporadic, minimal dementia, presents with cerebellar ataxia
  2. Fatal insomnia: Insomnia, Sympathetic overactivity, no evidence that infected brain can transmit
  3. Kuru: Presents with ataxia, transmitted by cannibalism in the natives of New Guinea
74
Q

Subacute sclerosing panencephalitis

  1. Infectious agent
  2. Presenting signs
  3. Prognosis
A
  1. Infectious agent: Chronic measles virus
  2. Presenting signs: Behavioural change, intellectual decline, loss of interest in activities –> Myoclonus, ataxia
  3. Prognosis: Death in 1-3 years while in decorticate posturing
75
Q

SSPE diagnostics

EEG?
CSF?
Biopsy?

A

EEG: high voltage periodic bursts lasting 2-3s
CSF: No cells but CHON increased and there are Ogc bands
Biopsy: Degeneration of white matter axons and myelin with perivascular cuffing with mononuclear cells and fibrous gliosis WITH EOSINOPHILIC INCLUSIONS IN THE NUCLEUS AND CYTOPLASM of neurons and glia

76
Q

What do the glia of PML brains look like?

A

Gigantic with deformed and bizarre shaped nuclei and mitotic figures– a feature that is otherwise only seen in malignant glial tumors

77
Q

What percentage

of HIV patients have PML
of PML patients have HIV

A

5

75

78
Q

What virus causes PML?

A

Polyoma virus, JC virus

70% of normal adult population will antibodies for it dormant in the kidney and marrow until immunosuppression allows for activation

79
Q

In encephalitis lethargica (von Economo Disease, Sleeping Sickness) that was discovered in the wake of the influenza pandemic of World War 1, what is the terminal movement disorder seen?

A

Starts with ophthalmoplegia and pronounced somnolence

after a few weeks or months a parkinsonian syndrome supervenes

80
Q

What are the two families of retroviruses known to infect humans? Where does HIV belong?

A
  1. Lentiviruses, HIV

2. Oncornaviruses, HTLV

81
Q

What percentage of untreated AIDS patients will have neurologic abnormalities?

A

1/3 clinically

Autopsy all

82
Q

What is the interval between infection and development of AIDS in adults?

A

Several months to 15 years

8-10 years mean latency time

83
Q

What percentage of AIDS patient with present with HAND? HIV associated neurocognitive disorders?

A

3%

but 2/3 will have HAND once AIDS is established already.

Survival after dementia is 3-6 months

Quickly progressive over weeks to months only IF UNTREATED

84
Q

What does the MRi of a HAND patient look like?

A

Widened sulci, enlarged ventricles, patchy but confluent or diffuse white matter changes with ill defined margins

85
Q

What is the most common peripheral neuropathy pattern in AIDS?

A

Distal symmetrical, axonal polyneuropathy, predominantly sensory and dysesthetic dtype

Can also have mononeuropathy multiplex from vasculitis

86
Q

The absence of IgG antibodies to toxoplasma should shift management in an HIV brain mass to addressing which pathology?

A

Primary CNS lymphoma

87
Q

CMV CNS infection in HIV patients is characterised by the preponderance of which symptoms?

A
Opthalmoparesis
Nystagmus
Ptosis
Facial nerve palsy
Deafness

Starts with delirum and CN deficits

88
Q

Tropical spastic paraparesis is due to what virus?

A

HTLV-1

89
Q

How is polio transmitted?

A

Fecal oral

95-99% of infected patients are asymptomatic or experience only a non-specific febrile illness

90
Q

Besides the central chromatolysis that occurs in the anterior horn of the spinal cord what other structures are affected in polio?

A

Brainstem nuclei! usually for muscles of swallowing and deglutition

Inflammatory lesions in the meninges accounting for meningitis, lesions in the dorsal root and ganglia accounting for muscle pain and paresthesia in parts that later become paralyzed, abnormalities of autonomic functions

Loss of respiration centers in the brainstem resulted in the use of an IRON LUNG

91
Q

What cells in the brain are selectively damaged by the JC virus?

A

Oligodendrocytes leading to PML

92
Q

T or F: Kernig’s and babinski is usually absent in viral meningitis?

A

T

93
Q

what is the CSF glucose of viral meningitis?

A

Usually normal. NEVER BELOW 25mg per dl

94
Q

What viruses make up the majority of acute aseptic meningitis?

A

Echovirus and coxsackie virus

Followed by HSV2 in adults

95
Q

What viral infections can cause orchitis?

A

Mumps virus,
group B coxsackie virus infections,
infectious mononucleosis,
lymphocytic choriomeningitis (LCM virus FROM THE HOUSE MOUSE!!)

96
Q

Contraction of the parvovirus that causes fifth disease in children by an adult will cause what type of neuro manifestation?

A

Brachial neuritis! Some with meningitis and encephalitis

97
Q

What are ddx for NON viral causes of aseptic, chronic and recurrent meningitis?

A
  1. Parameningeal infectious such as an abscess
  2. Fungal or TB
  3. Neoplastic (carcinomatous meningitis)
  4. Granulomatous such as sarcoidosis
  5. Partially treated bac men
  6. Chemical meningitis such from when a craniopharyngioma ruptures
  7. Allergic: NSAIDs, IVIG
98
Q

Besides presenting as chronic recurrent meningitis, what are other clues that will point towards the following diseases?

  1. Vogt Koyanagi Harada syndrome
  2. Mollaret recurrent meningitis
A
  1. Vogt Koyanagi Harada syndrome: iridocyclitis, depigmentation of a thick swath of hair, deafness, vitiligo near the eye, no lashes – looks like rogue!!!
  2. Mollaret recurrent meningitis, associated with HSV, 2 week episodes of the headache and fever recurring over several months or years
99
Q

What is the mortality/ neuro deficit rate for patients with HSV encephalitis?

A

50%

100
Q

What is the CSF picture of Herpes simplex encephalitis?

A

May be normal in the first few days but will invariably show pleocytosis– 10-200 lymphocytes

Increased CHON

Glucose usually normal rarely slightly less than 40mg per dl

101
Q

Re: Herpes simplex encephalitis

  1. EEG picture
  2. MRI/CT
  3. When will HSV PCR of the CSF have a false negative?
  4. What is the dose for the medication?
A
  1. Lateralized periodic high voltage sharp waves in the temporal regions and slow wave complexes at regular 2-3 per second intervals
  2. CT 2/3 with hypodensity in temporal lobe; MRI signal change in almost all HSE patients in T2; with lesions that almost always enhance… T1 with hypointensity with edema
  3. First 48 hours of the illness
  4. 30mg per kg/day for 10-14 days
102
Q

What is the prognosis of Herpes simplex encephalitis if treatment with begun within 4 days of onset of illness in an awake patient?

A

90% survival

103
Q

Re: Rabies

  1. Length of incubation period?
  2. Pathology location in dumb rabies
  3. Diagnostic finding in histopathology?
A
  1. Length of incubation period? 20-60 days
  2. Pathology location in dumb rabies: spinal cord
  3. Diagnostic finding in histopathology? Negri bodies are eosinophilic cytoplasmic includsions AND Babes nodules which are focal collections of microglia
104
Q

What should be used to cleanse rabies wounds?

A

Ammonium chloride shown to inactivate the virus

105
Q

What is the regimen for post exposure prophylaxis for rabies?

A
  1. Human rabies immunoglobulin: 20U per kg of body weight (1/2 around wound 1/2 IM) effective for 20 days to give time for the HDCV to take effect
  2. Human diploid cell vaccine 1ml injections D0 D3 D7 D14 D28
106
Q

Acute cerebellitis or acute ataxia of childhood is most related to which virus?

A

Chickenpox, Varicella

107
Q

Chickenpox and herpes zoster is caused by what DNA virus?

A

Varicella

Similar structure to herpes simplex virus

108
Q

Where is varicella virus usually located?

A

In the trigeminal and thoracic ganglion cells (T5-T10)

After initial chickenpox infection the virus is latent only to be awoken by immunosuppressive states such as: radiation, chemo, aids, lymphomas, elderly

10% of patients with lymphoma
25% of those with hodgkin disease

109
Q

What is the Ramsay hunt syndrome?

Why is ophthalmic herpes scary?

A

Herpetic eruption of the EAM WITH FACIAL PALSY

Can cause involvement of the cornea and conjunctiva resulting in corneal anesthesia and scarring

110
Q

How soon should acyclovir be given in herpes zoster (shingles)?

A

within 48 hours to shorten the duration of acute pain and speed up the healing of vesicles

111
Q

Post herpetic neuralgia follows in 5-10 percent of shingles patients often in the elderly. What drug can ameliorate pain?

A

Amitriptyline

112
Q

Which rickettsial disease?

  1. Confined to eastern and southeastern Asia transmitted by mites from infected rodents or humans
  2. Due to inhalation of materials infected with coxiella burnetti
  3. Transmitted by lice to humans and from person to person– in underdeveloped parts of the world only
A
  1. Confined to eastern and southeastern Asia transmitted by mites from infected rodents or humans; with necrotic ulcer and eschar at the site of attachment of the infected mite: Scrub typhus/ tsutsugamushi fever
  2. Due to inhalation of materials infected with coxiella burnetti: Q fever
  3. Transmitted by lice to humans and from person to person– in underdeveloped parts of the world only: Epidemic typhus
113
Q

What are the the neurologic manifestations of typhus?

A

Starts with fever headache with a macular rash on the 4th febrile day –>

Delirium, stupor, optic neuritis

Brain shows swelling and proliferation of endothelial cells of small vessels and a microglial reaction with typhus nodules

114
Q

What is the treatment for all rickettsial disease?

A

Doxycycline OR chloramphenicol

115
Q

Re Toxoplasma: What is the mode of transmission?

A

Raw beef and cat feces

116
Q

What are the manifestations of congenital infections in toxoplasma?

A
  1. Microcephaly
  2. Calcificaitons
  3. HCP
  4. Chorioretinitis
117
Q

What can a presumptive diagnosis of toxoplasma be made?

A
  1. Rising serum antibody titers
  2. Positive IgM indirect fluorescent antibody

PATIENTS WITH AIDS USUALLY DO NOT DISPLAY AN ANTIBODY RESPONSE!!

118
Q

What is the standard treatment for toxoplasmosis?

A

Oral sulfadiazine and pyrimethamine with leucoverin

119
Q

What does the CSF of amebic meningitis look like?

A

Like bac men: High PMNs, NOT EOSINOPHILS, high protein and low glucose

Trophozoites

Treatment: Amphotericin B BUT STILL POOR PROG

120
Q

What is the histopath of cerebral malaria?

A

Vessels packed with parasitized erythrocytes: small foci of necrosis surrounded by glia

Retinopathy signals severe malaria

121
Q

When do neuro sypmtoms appear in a malaria infection?

A

second or third week

122
Q

Treatment for cerebral malaria

A

Quinine and artesunate

123
Q

What are the neurologic manifestations of trypanosomiasis?

A
  1. Kerandel hyperesthesia– Prounounced pain at sites of minor injury
  2. Diffuse meningoencephalitis at the second year of the infection– stupor, dysarthria, seizures, ophthalmoplegia
  3. Winterbottom sign– Posterior cervical adenopathy
124
Q

Identify which parasite/ worm?

  1. Chitinoma, large fluid filled cyst:
  2. Cyst with scolex and late calcification:
  3. Severe myositis, nematode:
  4. Granuloma with a migrating track, nematode roundworm:
  5. Myelopathy, swimmer’s itch, trematode, single granuloma that may be large:
A
  1. Chitinoma, large fluid filled cyst: Hydatid disease (echinococcus)
  2. Cyst with scolex and late calcification: Cysticercosis (taenia solium)
  3. Severe myositis, nematode: Trichinosis
  4. Granuloma with a migrating track: Angiostrongyloidiasis
  5. Myelopathy, swimmer’s itch, trematode, single granuloma that may be large: Schistosomiasis
125
Q

What is the source of trichinella spiralis? And what neurologic manifestations do they cause? Treatment?

A

Raw pork
Myopathy and rarely encephalitis with seizures

Tx: Prednisone and albendazole

126
Q

What does the neuroimaging of a patient with neurocysticercosis look iike?

What tapeworm is responsible?

A

Initial: Scolex can be seen

Months later: Degeneration and calcification of multiple of the larvae in the parenchyma and subarachnoid space

Symptomatic/ malignant form: Similar to TB– hydrocephalus, vasculitis and stroke and CN palsies

Taenia solium

Tx: Prednisone and albendazole

127
Q

What type of schistosoma usually invades the nervous system?

A

Brain: S. japonicum
Cord: S. mansoni

Puro J ang nasa isip! A man down there.

128
Q

What is the treatment for schistosomiasis?

Pathology?

Dfx from cysticercosis via CT

A

Praziquantel

Mixed necrotizing and ischemic lesions infiltrated with esosinophils and giant cells.

Schistosomiasis lesions DO NOT CALCIFY. Unlike taenia cysticercosis lesions

129
Q

What proportion of TB meningitis patients will have TB in another part of their body?

A

2/3

130
Q

How long before a person with untreated TB med dies?

A

4-8 weeks

131
Q

CSF profile of TB men?

A

50-500 WBC 50-50 PMN and lymphocytes early on –> lymphocytes predominate

CHON 100-200mg per dl bUT CAN BE HIGHER IF THERE IS FLOW BLOCK

CHO less than 40mg per dl

132
Q

What is the Se of TB PCR in the CSF? False + rate?

A

80%

10%

133
Q

Which among the TB meds have the highest CNS penetration?

In the case of multi-drug resistance what can be added as a fifth drug?

Doses?

A

INH and PZA

Ethionamide

Treat for 9-12 months

INH: 5mg/kg
give with 50mg pyridoxine daily to prevent neuropathy

RMP: 10mg/kg

ETA: 15mg/kg can cause optic neuropathy– red green color discrimination

PZA: 20mg/kg

134
Q

AE of INH and ETA for TB treatment?

A

ETA: 15mg/kg can cause optic neuropathy– red green color discrimination

INH: 5mg/kg
give with 50mg pyridoxine daily to prevent neuropathy
also WOF abnormal liver test

135
Q

In the classic Thwaites et al. study in Vietnam (2004), what was the benefit of giving dexamethasone and the dose at which it was given?

What was the population?

A

Outcomes: Decrease in mortality from 41.3 to 31.8%

Population: 14 years old and above with or without AIDS

BMRC grade 2 and 3
(0.4 mg per kilogram per day
for week 1, 0.3 mg per kilogram per day for week 2,
0.2 mg per kilogram per day for week 3, and 0.1 mg
per kilogram per day for week 4) and then oral treatment
for four weeks, starting at a total of 4 mg per
day and decreasing by 1 mg each week.

BMRC grade 1
Therefore, patients with grade
I disease received two weeks of intravenous therapy
(0.3 mg per kilogram per day for week 1 and 0.2
mg per kilogram per day for week 2) and then four
weeks of oral therapy (0.1 mg per kilogram per day for week 3, then a total of 3 mg per day, decreasing
by 1 mg each week)

136
Q

How to grade the severity of TB meningitis?

A

MODIFIED British Medical Research Council criteria:
Grade I disease had
a score on the Glasgow Coma Scale of 15 with no focal neurologic signs;
Grade II had a score of either 11 to 14, or of 15 with focal neurologic signs
Grade III had a score of 10 or less.

Modified Vellore grading of tuberculous meningitis
and hydrocephalus
Grade I: GCS 15
Headache, vomiting, fever ± neck stiffness
No neurological deficit
Grade 2: II GCS 15
Neurological deficit present
Grade 3: GCS 9-14
Neurological deficit may or may not be present
Grade 4: GCS 3-8
Neurological deficit may or may not be present

137
Q

What percentage of Sarcoidosis patients will have clinically significant neurologic deficits?

What is the most common CN affected by sarcoidosis?

A

5%

CN7

138
Q

What is elevated in the serum of patients with pulmo sarcoid?

A

ACE levels elevated in 2/3

1/5 in those with chronic disease (not necessarily pulmo)

139
Q

Why is there a dilemma in giving prednisone to sarcoidosis patients?

A

1/2 of them will remit anyway

140
Q

Re: Syphillis

  1. How long before CNS is invaded after initial inoculation
  2. Initial neuro event in 25%
  3. What are later events in neurosyphilis
A
  1. How long before CNS is invaded after initial inoculation: 3 months
  2. Initial neuro event in 25%: Meningitis onset at about 2 years
  3. What are later events in neurosyphilis: Meningovascular (secondary syphillis)
    - -> Paretic (tertiary syphillis) –> tabetic

IMPORTANT: TREAT DURING AYSMPTOMATIC SYPHILITIC MENINGITIS STAGE– may just have argyll robertson pupils accomodate but NO reaction to light

141
Q

CSF picture of syphilllis?

What is in common with MS?

A

Cells up to 100 lymphocytes
CHON 40-200mg/dl
Positive serology
CHO normal

POSITIVE OLIGOCLONAL BANDS

142
Q

With treatment what is the pattern of normalization in syphillitic meningitis?

A

Cells –> CHON –> gamma globulin –> serologic tests

Re serology:

Nontreponemal (reagin) VDRL test/ Kolmer
antibodies if in CSF is ALREADY DIAGNOSTIC OF NEUROSYPHILLIS

FTA-ABS is the specific treponemal test will always be positive if there is neurosyphillis

143
Q

The absence of what clinical symptom will distinguish meningeal syphilis from TB meningitis?

A

FEVER. They also have headhache, papilledema, cranial nerve deficits, convulsions BUT THE PATIENT IS AFEBRILE

144
Q

What is the most common manifestation of neurosyphillis accounting for 35% or NS syndrome? When does it manifest?

A

Meningovascular syphililis
6-7 years
range 9 months to 10-12 years

145
Q

What is the pathology of meningovascular syphillis?

A

Heubner arteritis (fibrosis of small articles) Usually of medium to small caliber lenticulostriate arteries

Characteristic lesion is an internal capsular lesion with extending to the adjacent basal ganglia

146
Q

What disease entity should be kept in mind for a 35-50 year old presenting with dementia and paresis? Dementia paralytica

A

Tertiary/ Parteic Neurosyphillis

147
Q

Besides the nervous system what else is affected in tabes dorsalis?

A

Visceral crises

Gastric: Pain, constricting feeling, nausea vomiting pylorospams

May also happen to rectal crisis, laryngeal crises, genitourinary crises

148
Q

What is the histopath of tabes dorsalis?

A

Inflammation along the posterior root usually of the lumbosacral region with secondary involvement of the posterior column causing thinning of the cord and slkight dorsal ganglion cell loss

149
Q

What is the treatment regimen for neurosyphilis?

When to test again?

A

Penicillin G given at 18-24 million units daily for 14 days

Re-examine the patient every 3-6 months after treatment. CSF re test at 6 months– treat again based on CSF

150
Q

What is the causative spirochete in erythema chronicum migrans?

A

Borrelia burgdorferi in the ixodid tick

THIS IS LYME DISEASE

151
Q

What is the order by which the clinical manifestations of Lyme disease progress?

A

Ring erythematous lesion
Flu: Myalgia arthralgia headache

Neurologic:

Mengingoradiculitis especially in the Bannwarth syndrome of the Euro variant

Peripheral neuritis

152
Q

In lyme disease what percentage will manifest neurologic and cardiac symptoms

A

15% and 8%

153
Q

What is the most usual type of CN involvement with lyme disease?

A

CN 7 unilateral or bilateral similar to sacroidosis

154
Q

How to detect lyme disease?

Treatment?

A

ELISA IgM and IgG for recent
IgG for later caes

90% of patients with acute or convalescent will be positive for IgM

Oral doxycycline 100mg BID for 14 days
Alt: Amoxicillin, Cefuroxime

IF WITH Menigeal, CNS, PNS involvement– most effective is CEFTRIAXONE 2g daily

155
Q

When macrophages encounter the endotoxins from the bacteria what two cytokines are released that stimulate the local immune response?

A

Tumor necrosis factor

Interleukin-1

156
Q

What subacute form of meningitis should be considered in a child with improved CSF picture but still drowsy, vomiting, refusing to eat?

A

Subdural effusion

157
Q

What are the 2 pathophysiologies for CN involvement in bacterial meningitis?

A
  1. ACUTE: Inflammatory or vascular involvement of cranial nerve roots
  2. CHRONIC/ LATE: Meningeal fibrosis around optic nerves and spinal cord roots
158
Q

Which age group (bac men)

E. coli and group B streptococcus?

A

Newborns

159
Q

Top 4 bac men

A

N. meningitidis
H. influenzae
S. pneumoniae
L. monocytogenes

160
Q

Which bacterial meningitis pathogen?

  1. Rapid, petechial or purpuric rash, large ecchymoses and lividity or the skin of the lower parts of the body when there is circulatory shock– 50% will have rash!
  2. Preceded by lung ear heart infection. Alcoholic, splenectomized patients, basilar skull fx.
  3. Follows URTI and ear infection in a child; seizures encountered most often here
A
  1. Rapid, petechial or purpuric rash, large ecchymoses and lividity or the skin of the lower parts of the body when there is circulatory shock– 50% will have rash!: Meningococcal meningitis
  2. Preceded by lung ear heart infection. Alcoholic, splenectomized patients, basilar skull fx.: Pneumonoccal
  3. Follows URTI and ear infection in a child: H. influenzae
161
Q

What is the definition for elevated CSF for bac men?

Counts?

A

More than 18 cm H2O

250-100,000 85% neutrophils

CHON more than 45mg dl– 100-500 usually

CHO less than 40mg per dl or less than 40% of blood glucose concentration

162
Q

What type of meningitis will have bloody csf?

In bac men what are the levels of
Cl
Lactate dehydrogenase
Lactic acid

A

Anthrax
Dengue
Ebola

Cl Low reflecting dehydration
Lactate dehydrogenase fractions 4 and 5 show a rise in bac men
Lactic acid elevated in bacterial and fungal more than 35mg dl

163
Q

What percentage of bacterial meningitis patients will have positive blood culture

A

40-60%

164
Q

How to know if rhinorrhea is csf vs mucous?

A

beta2 transferrin is found in CSF

High protein mucous makes hanky stiff

165
Q

What antibiotics are indicated for the 0-4week bac men?

4-12 week

A

Cefotaxime with ampicillin
3rd gen with ampicillin PLUS dexamethasone

Dexa reduces incidence of deafness in h influenzae

AMPICILLIN IS FOR LISTERIA COVERAGE

Always add ampicillin for ICC patients

166
Q

What antibiotics for bac men

3 months to 50 years old

A

3rd gen plus vancomycin

ABOVE 50 add ampicillin again

167
Q

What antibiotics for basilar skull fracture

Head trauma/ csf shunt

A

3rd gen plus vancomycin

Vancomycin plus ceftazidime (for pseudomonal coverage)

168
Q

Does of dexa for bac men in children 0.15mg per kg QID for 4 days

In adults

A

For H. influenzae sensorineural deafness

10mg IV before antibiotics then q6 for 4 days to decrease mortality, seizures and coma

169
Q

What is prophylaxis for meningococcal exposure?

A

Single dose of ciprofloxacin

170
Q

What is Osler triad?

A

Pneumococcal meningitis
Pneumonia
Endocarditis

high fatatlity rate

171
Q

Why do bac men patients develop deafness?

A

Suppurative Cochlear destriction OR aminoglycoside use

172
Q

What are the common bacteria that can cause an encephalitis?

Give their treatments.

A

Mycoplasma pneumoniae– Macrolides: Azithromycin

Listeria monocytogenes: Ampicillin with gentamicin

Legionella: Levofloxacin or azithromycin

173
Q

What is the clinical picture of a Listeria encephalitis?

A

Rhombencephalitis– typical meningitis symptoms followed by asymmetric cranial nerve palsies and signs of cerebellar dysfunction

174
Q

What bacteria is responsible for: Encephalitis with seizures following a cat scratch and adenopathy?

A

Bartonella henslae

175
Q

What is the characteristic feature of Bacillus anthracis infection?

A

Hemorrhagic meningoencephalitis

only in 5% is the CNS involved

176
Q

What are the 3 cardinal features of whipple disease? What is the causative organism?

A
  1. Cognitive changes with psychiatric features
  2. Myoclonus
  3. Ataxia
  4. Oculomasticatory and skeletal myorhythmias

Tropheryma whipplei

177
Q

What is the most common organism in subdural empyema?

A

Streptococcus (nonhemolytic and viridans)

178
Q

What is the route of the majority of brain abscesses to the brain?

What % do not have a known focus?

A

Hematogenous

20%

179
Q

What does an early abscess look like on MRI?

A

Restricted diffusion
T1 hypointense
T2 capsule hypointense
Capsule is THINNER on the side directed to the lateral ventricle

Cerebritis: Dot sized areas of decreased density that enhance with Gad

180
Q

What % of patients with congenital heart disease will also develop a brain abscess?

A

5%

181
Q

What is empiric treatment for an abscess?

A

Vancomycin
3rd Cephalosporin
Meropenem/metronidazole

182
Q

What is the duration of treatment of the following pathogens for bacterial meningitis? (days)

Neisseria meningitidis
H. influenzea
S. Pneumoniae
S. agalactiae
Gram negative bacilli
Listeria monocytogenes
A
Neisseria meningitidis 7
H. influenzea 7
S. Pneumoniae 10-14
S. agalactiae 14-21
Gram negative bacilli 21 days or two weeks beyond the first sterile CSF culture in neonates
Listeria monocytogenes 21 days or longer