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► Med Misc 06 > Neurology Falcon Review 2 > Flashcards

Neurology Falcon Review 2 Flashcards

1
Q

What are the types of parenchymal injuries

A

Concussion
contusion
diffuse axonal injury

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2
Q

Define concussion

A

Clinical syndrome of altered mental status secondary to head injury typically brought about by a change in momentum of the head

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3
Q

What are some of the symptoms of a concussion

A

Instantaneous onset of transient neurologic dysfunction, including loss of consciousness, temporary respiratory arrest, and loss of reflexes

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4
Q

Define contusion

A

Direct parenchymal injury to brain

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5
Q

What are the two types of contusions

A

Coup injury

Contracoup injury

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6
Q

What is a coup injury

A

Cerebral injury at point of direct contact

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7
Q

What is a Contracoup injury

A

damage to brain surface opposite to point of impact

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8
Q

What is a diffuse axonal injury

A

Injury to white matter due to acceleration and deceleration
– generally located in the corpus callosum, periventricular white matter, and hippocampus
– cerebral and cerebellar peduncle

typically associated with axonal swelling of white matter and is associated with a poor prognosis

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9
Q

What is the most common cause of an epidural hematoma

A

Trauma to skull causing an epidural artery tear (middle meningeal artery)
– patient may experience a lucid interval lasting upto a few hours

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10
Q

What are the deficits associated with an epidural hematoma

A

– Contralateral hemiparesis

– ipsilateral pupillary dilation

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11
Q

What is the most common cause of a Subdural hematoma

A

Tearing of bridging veins
– most common intracerebral lesions and dramatic brain injury

greatest risk is involved with:
– brain atrophy
– coagulopathy (alcoholics)

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12
Q

Do epidural hematomas require drainage

A

Always

– subdural hematomas to not always require drainage

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13
Q

What are the symptoms of a spinal cord transection

A

– Upper motor neuron signs below the level of the lesion
– complete sensory loss below the level
– bowel and bladder dysfunction
– may see lower motor neuron signs at the level of the lesion

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14
Q

What is a brown-Sequard syndrome

A

– Ipsilateral-weakness, joint positions sensory loss
– contralateral-pain and temperature loss
– bowel and bladder dysfunction is rare

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15
Q

What are the causes for central cord syndrome

A

Tumor

syringomyelia

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16
Q

What is syringomyelia

A

– Fluid filled cavity within the spinal cord
– most commonly occur in the cervical cord
– can occur after trauma
– can occur in conjunction with chiari malformation

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17
Q

What is the symptoms of a central cord syndrome

A

– Loss of pain and temperature in a cape like distribution
– lower motor neuron signs and arms
– upper motor neuron signs of lower extremities
– generally spares the dorsal columns

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18
Q

Discuss an anterior spinal artery syndrome

A

– Rear
– infarction of anterior two thirds of cord
–affects spinothalamic and corticospinal tracts, sparing dorsal columns
– results in spastic paralysis and loss of pain and temperature sensation with intact joint position since and vibration

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19
Q

what cranial nerves are associated with pain sensitive fibers

A

V
IX
X

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20
Q

Does the brain parenchyma have pain fibers

A

No

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21
Q

What is the most useful symptom regarding clinical approach to headaches

A

Time course is the most useful

– quality, severity and location have significant overlap between headache etiologies

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22
Q

What are the signs and symptoms of a subarachnoid hemorrhage

A

– Thunderclap headache - instantaneous onset, with maximal intensity within minutes
– worst headache of my life
– severe nausea and vomiting is common
– altered level of consciousness is frequent
– may have focal neurologic deficits

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23
Q

Discuss intraparenchymal hemorrhage

A

Acute onset
focal deficits commonly occur simultaneously
altered level of consciousness is related to the location and size of the bleed

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24
Q

how does a headache associated with meningitis typically present

A

Bacterial meningitis:
– headache is usually diffuse
– fever and meningismus are typical

viral meningitis
– diffuse headache usually has developed over several days
– associated symptoms of fatigue and myalgias are common

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25
Q

How is the headache associated with temporal arteritis

A

– headache is typically intermittent, unilateral, and temporal at first, then bilateral temporal, then continuous
– Pain is often throbbing in nature, but also described as aching or burning
– tenderness of the scalp

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26
Q

What is the typical patient presentation for a headache associated with temporal arteritis

A

Usually women over the age of 60
firm and tender superficial temporal artery
elevated ESR

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27
Q

What is the treatment for temporal arteritis

A

Steroids until biopsy is negative

– may be continued for years to prevent recurrence

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28
Q

how will a patient with a headache due to hypertensive urgency present

A

Dull, bilateral ache and pain
no focal deficits
usually seen with BP >170/110

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29
Q

What is RPLS

A

Reversible posterior leukoencephalopathy

– high blood pressure leading to posterior demyelination in the brain

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30
Q

Discuss cluster headaches

A

Typically abrupt and onset, peeking over 5 to 10 minutes.
Persist for 45 minutes to 2 hours
clusters over days two weeks
consistently unilateral, orbital location

Nausea and vomiting are atypical

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31
Q

Who is generally affected by cluster headaches

A

Typically young adult men onsets in the third decade

male-female ratio 5:1

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32
Q

What is a treatment for cluster headache

A 
Abortive therapy is often ineffective but can use:
– sumatriptan
– DHE
– oxygen
– intranasal lidocaine

Prophylactic therapy
– lithium
– valproic acid
– amitriptyline

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33
Q

Describe the headache that is associated with a venous sinus thrombosis

A

An abrupt onset headache that lingers

often diffuse, may localize near the vertex

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34
Q

What is the diagnosis and management of venous sinus thrombus

A

MRI to define

IV heparin followed by oral anticoagulation

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35
Q

What is the major difference between a classic migraine in common migraine

A

A classic migraine has a preceding neurologic symptom (aura)

common migraines or more likely to be bilateral

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36
Q

What is the treatment for migraine

A 
Abortive therapy
– triptans
– IV ergotamine (status migrainnosis)
– caffeine
– NSAIDs

Preventive therapy
– avoid triggers
– treat attacks early
– tricyclic antidepressants

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37
Q

What is the mechanism of triptan’s

A

Serotonin 5 HT-1D antagonists

– may cause chest pain and facial flushing

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38
Q

What is the pseudotumor cerebi

A

A.k.a. idiopathic intracranial hypertension
– headache is described as a diffuse, dull, ache or pressure sensation
– onset is gradual but often progressive
– worsened by laying down in my physical activity
– horizontal diplopia is occasionally seen

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39
Q

Discuss the epidemiology of pseudotumor cerebri

A

75% of patients are female
20 to 40 years of age
majority are obese
can be associated with drugs (steroid, vitamin A toxicity, tetracycline)

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40
Q

How’s a diagnosis pseudotumor cerebri made

A

Imaging to rule out mass lesion

LP to document opening pressure (elevated)

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41
Q

What is the treatment for pseudotumor cerebri

A

Lumbar puncture
weight loss
carbonic anhydrase inhibitor
shunts

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42
Q

How do carbonic anhydrase inhibitors (acetazolamide) benefit pseudotumor cerebri

A

Decreased CSF production

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43
Q

how are headaches associated with brain tumors

A

No classic headache syndrome defines a tumor
usually insidious onset
worse in the morning or wakens patient at night due to raised ICP

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44
Q

Discuss tension headaches

A

Most common variant of headaches
– May limits, but not prohibit activities
– usually bilateral, within a occipital-temporal-frontal “band like” distribution
– tenderness in the cervical paraspinals and temporalis muscles
– typically respond to OTC analgesics

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45
Q

Was the prophylactic treatment for tension headaches

A

Tricyclic antidepressants arefirst line

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46
Q

What is chronic daily headaches

A

Typically involves out of tension type headaches associated with analgesic abuse
– cessation of analgesic use as first line treatment followed by tricyclic antidepressants

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47
Q

What is trigeminal neuralgia

A

Tic doulaureaux
– electric, shooting pain lasting seconds
– neuralgia of cranial nerve V
– triggered by non-noxious sensory stimuli to the affected face

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48
Q

What headaches are associated with an increased risk of suicide

A

Cluster headaches

trigeminal neuralgia

49
Q

What is the treatment for trigeminal neuralgia

A

Carbamazepine or oxcarbamazepine
– may be combined with baclofen
surgical intervention
– decompression of trigeminal nerve

50
Q

What are the AHS guidelines for imaging for headaches

A

– New onset headache inpatient over 40
– headache with abnormal neurologic exam
– reassure and anxious patient

CT useful only in ER situations suspected of SAH

MRI brain is the study of choice to rule out tumor

51
Q

What is epilepsy

A

Tendency to experience recurrent unprovoked seizures
– 10% of the population will have a seizure in their lifetime. 30% chance of a future second seizure
– 1% have epilepsy

52
Q

What are generalized seizures

A

A seizure which affects the entire brain at once
– primary generalization
– secondary generalization (begins locally then spreads to entire brain)

53
Q

What is a partial seizures

A

A seizure which originates in one area of the brain. May secondarily generalized

54
Q

What differentiates a simple partial seizure from a complex partial seizure

A

Simple partial seizures have no loss of consciousness. Associated with positive neurologic symptoms

Complex partial seizures has impaired consciousness. Associated with automatism’s

55
Q

What is a generalized tonic clonic seizure

A

Grand mal seizure
– tonic extension of all four extremities followed by chronic jerking
– Todd’s paralysis is common

56
Q

What is an absence seizure

A

Generalized seizure characterized by unresponsive staring lasting several seconds followed by immediate recovery
– typically seen in childhood

57
Q

Discuss febrile seizures

A

Most common cause of new onset seizures in children
– six months to five years of age
– occur in the setting of a febrile illness without evidence of intracranial infection
– typically generalized at onset
– generally are benign

58
Q

What is done in the workup for a first non-febrile seizure

A

History and physical
EEG
lab work
neuroimaging

59
Q

What is benign Rolandic epilepsy

A

– childhood onset

– Simple partial seizure involving mouth and face, maybe generalized tonic clinic

– Nocturnal preponderance of seizures

– EEG findings: Centrotemporal spikes

– Treatment: generally no treatment needed, carbamazepine if necessary

60
Q

What is Lennox-Gastaut syndrome

A

– childhood to early adolescence

– All types of seizures

– Associated with mental retardation

– EEG findings: slow (1 to 2 Hz spike and wave), proximal fast activity, multifocal spikes

– All anti-epileptic drugs

61
Q

What is Absence Epilepsy

A

– childhood and adolescence

– Absence, may generalized tonic clonic

– Hyperventilation’s often a trigger. May outgrow seizures

– EEG findings: 3 Hz spike-and-wave

– Treatment ethosuximide; valproate if it generalizes

62
Q

What is juvenile myoclonic epilepsy (JME)

A

– adolescents and young adults

– Myoclonic, absence, generalized tonic clonic seizures

– Early-morning predominance of seizures. Triggers include sleep deprivation and alcohol use

– EEG findings: 4 to 6 Hz spike-and-wave. Frequent photo paroxysmal response (strobe light activation of seizures)

63
Q

Was the most common cause of adult epilepsy

A

Adults
– idiopathic is most common
– medial temporal lobe sclerosis
– tumors are more common cause in adults than in children

Elderly
– stroke is the most common
– metabolic disturbances (calcium, sodium, magnesium)
– UTI
– medication related (benzodiazepine withdrawal)

64
Q

When this treatment indicated for seizures

A

After the second unprovoked seizure

65
Q

Were the common anti-epileptic drugs

A 
Phenytoin
carbamazepine
valproic acid
phenobarbital
ethosuximide
gabapentin
lamotrigine
tiagabine
topiramate
zonisamide
felbamate
levetiracetam
66
Q

Discuss phenytoin

A

– Na channel blocker

– Used for partial, generalized seizures

– Side effects: gingival hyperplasia, coarsening of facial features

67
Q

Discuss carbamazepine

A

– Na channel blocker

– used for Partial, generalized seizures. May worsen myoclonus and absence seizures

– Side effects: hyponatremia, agranulocytosis

68
Q

discuss valproic acid

A

– Na channel blocker, GABA receptor agonist

– Used for partial, generalized, absence

– Side effects: weight gain, tremor, hair loss, hepatotoxicity, thrombocytopenia

69
Q

Discuss phenobarbital

A

– GABA receptor agonist

– Used for partial, generalized seizures

– Side effects: sedation, mild addiction potential

70
Q

Discussed ethosuximide

A

– T type Ca channel blocker

– Used for absence seizures

– Side effects: G.I. symptoms

71
Q

Discuss gabapentin

A

– manipulates GABA pathway

– Used for partial seizures

– Side effects: sedation, ataxia, weight gain at high doses

72
Q

Discuss lamotrigine

A

– Na channel blocker, glutamate receptor antagonist

– Use for partial, generalized seizures

– Side effects: Stevens-Johnson’s syndrome with rapid titration

73
Q

Discuss tiagabine

A

– GABA reuptake inhibitor

– Used for partial seizures

– Side effects: sedation

74
Q

Discuss topiramate

A

– mechanism unknown

– Used for partial, generalized seizures

– Side effects: weight loss, cognitive difficulty, renal stones (skinny and stupid)

75
Q

Discuss zonisamide

A

– T-type Ca channel blocker, inhibits glutamate release

– Used for partial, generalized seizures

– Side effects: weight loss, drowsiness, ataxia at high doses, renal stones

76
Q

Discuss felbamate

A

– unknown mechanism

– Used for partial, generalized seizures

– Side effects: weight loss, insomnia, aplastic anemia, liver failure

77
Q

Discuss levetiracetam

A

– Unknown mechanism

– Used for partial, generalized seizures

– Side effects: somnolence, asthenia, dizziness, akasthesia

78
Q

What is the problem with epilepsy in pregnancy

A

Untreated women have a higher risk of birth defects

All AED’s are potentially teratogenic. Risk can be minimized by taking 1 mg folate PO Q day

79
Q

What is the treatment for status epilepticus

A
  1. ABCs, ABG, IV access
  2. Benzodiazepines
  3. Phenytoin if status continues
  4. Intubate, phenobarbital 20 MG/KG IV to induce a coma
80
Q

What is meningitis

A

Inflammation of the leptomeninges and cerebrospinal fluid within subarachnoid space

81
Q

What is meningoencephalitis

A

Inflammation of the meninges and the brain parenchyma

82
Q

What are the causes of meningitis

A
  1. Infectious
    – bacterial, viral, mycobacterial, spirochete, fungal, parasitic
  2. Chemical
  3. Neoplastic
83
Q

With the CSF findings for acute bacterial meningitis

A

Wbc’s >1000
neutrophils >50
glucose 100

84
Q

Where the CSF findings for acute fungal or viral meningitis

A

Wbc’s 100-500

neutrophils

85
Q

What a CSF findings for acute HSV encephalopathy

A

Wbc’s 10-1000
neutrophils 30
protein >75

86
Q

What are the common bacterial pathogens for meningitis in a patient less than one month

A

Group B strep
E. coli
Listeria
Klebsiella

87
Q

What is the treatment for bacterial meningitis in a patient less than one month

A

Ampicillin + cefotaximine

88
Q

Were the common bacterial pathogens for meningitis in a patient 1 month to 23 months of age

A 
Strep pneumonia
N. meningitidis
group B strep
H influenza
E. coli
89
Q

What is the treatment for bacterial meningitis in a patient’s 1 month to 23 months of age

A

Vancomycin and a third-generation cephalosporin

90
Q

Were the common bacterial pathogens for bacterial meningitis in a patient 2-50 years old

A

N. Meningitidis

strep pneumoniae

91
Q

What is the treatment for bacterial meningitis in a patient’s 2-50 years old

A

Vancomycin plus a third-generation cephalosporins

92
Q

What are the common bacterial pathogens for meningitis in a patient >50 years old

A

Strep pneumoniae
N. Meningitidis
Listeria
aerobic gram-negative bacilli

93
Q

What is the treatment for bacterial meningitis in a patient’s >50 years old

A

Vancomycin plus third-generation cephalosporin plus ampicillin

94
Q

What are the etiologies associated with acute viral meningitis

A

Non-polio enteroviruses (85%)
– Echovirus
– coxsackievirus

Arboviruses (5%)
– Eastern equine encephalitis
– Western equine encephalitis
– St. Louis encephalitis

Herpes family viruses (4%)

95
Q

For the spirochetes that can cause meningitis

A

Treponema
Borrelia
Leptospira

96
Q

What is the Argyle-Robertson pupil

A

No direct or consensual light response, but pupils constrict with accommodation

97
Q

What diagnostic testing is done for neurosyphilis

A

Non-Treponema antigen test
– R PR or VDRL

Treponema antigen test
– FTA-ABS

98
Q

What diseases caused by the spirochete Borrelia burgdorferi

A

Lyme disease

99
Q

What is the treatment for Lyme disease

A

Amoxicillin or doxycycline

100
Q

Were the common fungal organisms associated with meningoencephalitis

A 
Cryptococcus neoformans
coccidoides immitis
Candida albicans
Mucor
Aspergillus fumigatus
Histoplasma capsulatum
Blastomyces dermatiitidis
101
Q

What is the most common fungal infection of the CNS

A

Cryptococcus meningoencephalitis

102
Q

Discuss Cryptococcus meningoencephalitis

A

– typically in the immuno compromised
– inhalation of spores from soil and pigeon excrement
– increased intracranial pressure leading to a protean headache
– CSF: very low glucose, elevated protein

103
Q

What is the treatment for Cryptococcus meningoencephalitis

A

Amphotericin B, flucytosine, fluconazole

104
Q

Were the common parasitic organisms that lead to meningoencephalitis

A 
Toxoplasmosis
Cysticercosis and echinococcosis
malaria
amebiasis
trypanosomiasis
105
Q

What was CT and MRI demonstrate for a patient with cerebral toxoplasmosis

A

Multiple ring enhancing lesions
– similar findings with CNS lymphoma, tuberculosis, or fungal infections

Toxois the most common calls for a cerebral mass lesion in a patient with AIDS

106
Q

What is the treatment for toxoplasmosis

A

Pyrimethamine, sulfadiazine and folinic acid

107
Q

What is the most common parasitic infection of the CNS worldwide

A

Neuro-cysticercosis
– caused by the pork tapeworm Taenia solum
– brain involvement in 50 to 70% of cases

108
Q

What will imaging demonstrated for Neuro cysticercosis

A

Ring enhancing cystic lesions (active cyst)

Parenchymal calcifications (old cyst)

Vasogenic edema

109
Q

What is the treatment for Neuro cysticercosis

A

Albendazole to kill the parasite

110
Q

What is leptomeningeal carcinomatosis

A

Diffuse seating of leptomeninges with metastatic tumor cells

Occurs in breast cancer, small cell lung cancer, melanoma, medulloblastoma, PNET tumors (primary Neuro ectodermal tumors)

111
Q

What is encephalitis

A

Infection of the brain parenchyma

– leads to confusion, delirium, focal neurologic deficits, seizures and coma

112
Q

What are the common etiologies to encephalitis

A

Arboviruses
Enteroviruses
herpes simplex virus
CMV, EBV, VZV

113
Q

Discuss HSV encephalitis

A

Most common in children and young adults
– presents with alteration in mood, memory, and behavior
– involves inferior and medial regions of temporal lobes and orbital gyri of frontal lobes
– often hemorrhagic
– Cowdrey intra-nuclear viral inclusion bodies

114
Q

What is the most accurate diagnostic procedure for HSV encephalitis

A

CSF HSV PCR

115
Q

What is progressive multifocal leukoencephalopathy

A

A viral encephalitis caused by polyomavirus (JC virus)
– virus preferentially infects oligodendrocytes which leads to demyelination
– PML does not enhance on MRI

116
Q

What are the transmissible spongiform encephalopathies

A 
Creuzfeldt-Jakob disease
– new variant CJD (mad cow)
Gerstmann-Straussler-Scheinker syndrome
fatal familial insomnia
Kuru

All associated with abnormal forms of a specific protein (prion protein) which is infectious and transmissible

117
Q

Discuss the pathogenesis of prion diseases

A

– Prion protein is usually a normal protein in neurons.
– The prion protein undergoes conformational change from Alpha helix to beta pleated sheet
– prion protein acquires relative resistance to digestion with proteases
– infectious nature comes from ability to corrupt the integrity of normal cellular components
– leads to a buildup in neurons

118
Q

What are the clinical features of Creufeldt-Jakob disease

A

– Rapidly progressive dementia
– peak incidence in seventh decade
– iatrogenic transmission possible with transplants
– subtle changes in memory and behavior followed by rapidly progressive dementia with involuntary jerking muscle contractions (myoclonus)

► Med Misc 06 (27 decks)

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