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Neuro > Intoxications and infections of the NS > Flashcards

Intoxications and infections of the NS Flashcards

1
Q

how does tetanospasmin (the tetanus toxin) affect the nervous system

A

binds to cortical, brain stem, and spinal interneurons, preventing the release of the inhibitory neurotransmitters glycine and GABA

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2
Q

what symptoms does tetanus cause

A

Severe, prolonged, painful muscle spasms (may be localized or diffuse), if the toxin enters the blood stream there are generalized convulsive seizures. Trismus or lockjaw, grimacing smile (risus sardonicus) and arching back (opisthotonus)

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3
Q

how is tetanus treated

A

ICU care with mechanical ventilation, sedation, pharmacological neuromuscular blockade and anticonvulsants. human tetanus immune globulin may neutralize any remaining tetanospasmin

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4
Q

where do patients commonly get botulism from

A

improperly canned or contaminated food (destroyed with proper cooking)

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5
Q

how does the botulism toxin affect the nervous system

A

the exotoxin binds to presynaptic nerve terminals and prevents the release of ACh from LMNs and parasympathetic nerves. Resulting in paralysis of skeletal muscle, bowel, bladder and salivary glands. Severity depends on how much toxin in consumed

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6
Q

what are the symptoms seen with botulism toxin

A

ptosis, diplopia, and pupillary paralysis, followed by dysphagia, facial and limb weakness, and possibly respiratory paralysis

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7
Q

what antitoxin is available for botulism toxin

A

guanidine to help facilitate ACh release

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8
Q

what is the prognosis for botulism toxin

A

gradual spontaneous recovery after days to weeks given good supportive care

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9
Q

how does lead poisoning present in adults

A

peripheral neuropathy often with prominent focal neuropathies like wrist drop

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10
Q

how does lead poisoning present in children

A

encephalopathy and abdominal pain

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11
Q

how is lead poisoning treated

A

chelating agents

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12
Q

what does organic solvent exposures cause

A

peripheral neuropathy or encephalitis

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13
Q

what are some environmental exposures to consider when a patient presents with peripheral neuropathies

A

lead poisoning, organic solvents, carbon monoxide

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14
Q

what are early symptoms of CO poisoning

A

headache, vomiting, and blurry vision that can progress to coma, seixures and cardiopulmonary arrest

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15
Q

how do you treat CO poisoning

A

100% oxygen or a hyperbaric chamber

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16
Q

what may happen after a CO poisoning (lasting effects)

A

memory or cognition deficits and a few may get parkinsonism symptoms after a few weeks (basil ganglion is very sensitive to CO)

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17
Q

what should be a consideration when stroke symptoms are seen in a young, otherwise healthy patient

A

drug induced vasoconstiction or hypertension leading to ischemic infarction or brain hemorrhage – cocaine is the most common culprit

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18
Q

what are symptoms of an alcohol withdrawal syndrome

A

initially hypersympathic stage - tremulousness, sweating, tachycardia and jitteriness, cluster of generalized tonic-clonic seizures

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19
Q

what kind of seizure should raise suspicion for a focal brain lesion in a patient undergoing alcohol withdrawal

A

any aura or partial seizure since seizures due to withdrawal should be generalized and diffuse

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20
Q

when are delirium tremors seen in an alcoholic patient

A

3-4 days after alcohol cessation

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21
Q

what are delirium tremors

A

fluctuating motor and autonomic activity, confusion, and hallucinaitons - must be treated or may become fatal

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22
Q

what drug may be given to a patient undergoing alcohol withdrawal for seizure control

A

benzodiazepines - provide sedation and seizure control

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23
Q

what causes Wernicke-Korsakoff syndrome

A

Thiamine (B1) deficiency - common in alcoholic

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24
Q

what does Wernicke’s encephalopathy refer to

A

acute phase of the Wernicke-Korsakoff syndrome consisting of nystagmus, ophthalmoplegia, gait ataxia, and confusion - resolves with thiamine administration

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25
Q

what causes Korsakoff’s psychosis

A

persistant, severe, or recurrent thiamine deficiency

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26
Q

how does Korsakoff’s psychosis present

A

chronic memory deficit or amnestic syndrome with frequent confabulation (story telling- to fill in memory gaps)

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27
Q

what is seen pathologically in Korsakoff’s psychosis

A

petechial hemorrhages and gliosis in the vicinity of the third and fourth ventricles and connecting aqueduct - involving the mammillary bodies, fornix and dorsomedial thalamus

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28
Q

what structure does Alcoholic Cerebellar degeneration affect

A

anterior-superior vermis

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29
Q

what symptoms does Alcoholic Cerebellar degneration

A

ataxic gait and dysmetria of the lower limbs

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30
Q

who gets central pontine myelinolysis

A

occurs in alcoholics and patients who undergo an overly rapid correction of severe hyponatremia (low to high the pons will die)

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31
Q

what is central pontine myelinolysis

A

demyelination of the corticospinal and corticobulbar tracts in the pons

32
Q

how can menengitis spread

A

either from the blood stream or directly from an otitis or sinusitis

33
Q

what are symptoms of acute menengitis

A

fever, headache, stiff neck, malaise, lethargy, nausea, and vomiting = medical emergency

34
Q

what are the signs seen in meningitis due to nuchal rigidity

A

Kernig or Brudzinski

35
Q

what kind of meningitis is associated with a petechial rash

A

N. meningitidis - meningococcal

36
Q

what is common initial antibiotics used for meningitis

A

newer cephalosporin such as ceftriaxone plus vancomycin for any pneumococci resistant to pcn + ampicillin for elderly or neonates to cover listeria

37
Q

what can be given with antibiotics to reduce neurological complications

A

IV dexamethasone (reduces complications of deafness and cognitive deficits and lowers mortality)

38
Q

what are complications of bacterial meningitis

A

hydrocephalus due to pus obstructing the CSF pathways. inflammation and edema of the cortex itself, or infarction of the brain due to inflammation of superficial blood vessels

39
Q

what are common causes of meningitis in a neonate

A

Group B strep
E. coli
listeria

40
Q

what are common causes of meningitis in children

A

N. meningitidis

S. pneumo

41
Q

what are common causes of meningitis in adults

A

S. pneumo
N. meningitis
E. coli

42
Q

when should a lumbar puncture be postponed

A

if the patient has elevated ICP (unconscous state, papilledema) or an intracranial mass with edema

43
Q

what is the typical CSF profile for bacterial meningitis

A

Predominantly PMN WBS, low CSF glucose and high protein

44
Q

what is the typical CSF profile for viral meningitis

A

lymphocytes, normal protein, normal glucose

45
Q

what is the typical CSF profile for fungal meningitis

A

lymphocytes, high protein, low glucose

46
Q

who is at risk for chronic meningitis

A

the elderly, malnourished or immunocompromised

47
Q

what is encephalitis

A

when the brain (not the subarchnoid space) is the primary site of infection and inflammation

48
Q

what is the usual cause of encephalitis

A

viruses

49
Q

what is the onset and symptoms associated with encephalitis

A

symptoms evolve over hours to days and involve fever and headache, seizures, focal neurological deficits, behavioral changes and impairment of consciousness

50
Q

what happens pathologically in encephalitis

A

patchy demyelination, edema and tiny, petechial hemorrhages

51
Q

what can be seen microscopically in encephalitis

A

neuronal destruction by microglia, perivascular lymphocytes and viral inclusions within neurons or glia

52
Q

what does the CSF show in encephalitis

A

it looks similar to viral meningitis with lymphocytes and normal or slightly decreased glucose

53
Q

what should you look for in a patient with encephalitis

A

antibody titres to suspected viruses and HSV-1 via PCR

54
Q

what is the treatment for encephalitis

A

acyclovir if due to herpes virus. treat the increased ICP, anticonvulsants and sedatives

55
Q

where does HSV-1 usually infect

A

frontal and medial temporal lobes - often bilaterally and symmetrically

56
Q

what signs and symptoms are indicative of herpes simplex encephalitis

A

aphasia, behavioral changes, and memory deficits

57
Q

what treatment is important when there is suspicion for herpes simplex encephalitis

A

Acyclovoir (decreases mortality from > 40% to 20%)

58
Q

what is unique to west nile encephalitis

A

causes significant weakness by affecting peripheral nerves or anterior horn cells

59
Q

what areas does polio affect

A

viral invasion and destruction of anterior horn cells and brain stem motor nuclei

60
Q

what does the varicella-zoster virus cause

A

shingles

61
Q

how does shingles present

A

eruption of a vesicular rash with severe neuralgic pain on one or two adjacent dermatomes or on the torso or limbs

62
Q

what treatment can be given for shingles

A

acyclovoir

63
Q

what is destroyed by the HIV-1 virus

A

T4 helper cells

64
Q

what kind of brain tumor is most commonly associated with AIDS patents

A

Primary cerebral lymphoma

65
Q

what opportunistic infections of the CNS are most often associated with AIDS patients

A

cerebral toxoplamosis, cryptococcal meningitis and CMV retinitis or encephalitis, PML

66
Q

in addition to bacterial infections causing abscesses in the immunocompromised what else do you need to consider

A

fungal and parasitic

67
Q

what symptoms are seen with abscess

A

headache and fever the patient may be severely ill from a systemic infection. a cerebral abscess may cause seizures and focal neurological signs dependent on its location or it could cause brain edema with mass effect and increased ICP

68
Q

what results when a brain abscess ruptures

A

it can produces meningitis

69
Q

how do prions cause disease

A

they are misfolded proteins that induce other proteins to convert into a misfolded state as well

70
Q

what is unique about how prions cause disease

A

they don’t have nucleic acid and they don’t invoke an inflammatory response

71
Q

what is the most common prion disease

A

Creutzfeldt-Jakob dementia (CJD)

72
Q

what is Creutzfeldt-Jakob dementia

A

a very rapidly progressive dementia with cerebellar, corticospinal, lower motor neuron, or extrapyramidal signs and symptoms

73
Q

what is the prognosis of Creutzfeldt-Jakob dementia

A

it progressives to death within weeks to months and has no cure

74
Q

what is seen on biopsy of someone with Creutzfeldt-Jakob dementia

A

spongiform changes which are cytoplasmic vacuoles in neurons and astrocytes and neuronal loss without inflammation.

75
Q

what may be detected on an EEG of someone with Creutzfeldt-Jakob dementia

A

periodic sharp wave discharges

76
Q

what is the variant of Creutzfeldt-Jakob dementia that causes a slower progressing disease with more psychiatric and behavioral symptoms

A

Mad Cow disease

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