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Neuro path Flashcards

0
Q

What is anterior cord syndrome?

A

Dorsal columns are spared

UMN paralysis and loss of pain / temp below lesion

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1
Q

What is Brown-Sequard and what are its symptoms?

A

Hemisection of the spinal cord

  • UMN paralysis: ipsilateral below level of lession
  • Ipsilateral pain / temp sensory loss below level of lesion
  • CONTRALATERAL pain / temp sensory loss below level of lesion
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2
Q

What are the symptoms of central cord syndrome?

A

Bilateral loss of spinothalamic tracts below lesion
UMN paralysis of upper limbs more than lower limbs
Assoc. w/ cervical injury, often -> bladder dysfunction

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3
Q

Cauda Equina syndrome

A

Saddle distribution of sensory loss

LMN paralysis below lesion

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4
Q

What causes superior quadrantopia?

A

lesion of Meyer’s loop: ventral projection from LGN. contains fibers representing superior visual field

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5
Q

Why is there macular sparing in an infarct of PCA?

A

Macular area of visual cortex receives dual blood supply from PCA and MCA

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6
Q

What is Weber’s syndrome (superior alternating hemiplegia)?

A

Lesion of rostral midbrain affecting crus cerebri and CNIII
Contralateral UMN syndrome
Ipsi CNIII palsy
Loss of consensual response when light shone in contra eye

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7
Q

What is Foville’s syndrome? cause?

A

Lesion of caudal pons
CN VI and VII affected: Ipsi loss of lateral eye movement, facial expression
MLF: internuclear opthalmoplesia
Pyramidal tract: contralateral hemiparesis
Medial lemniscus: contralateral fine touch, conscious proprio, deep pressure

thrombosis of basillar artry, pontine tumor

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8
Q

What is Millard-Gubler?

A

Lesion of CN VI, VII and corticospinal tract (pons)

thrombosis of paramedian branches of basillar artery

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9
Q

What is Wallenberg’s syndrome?

A

Occlusion of PICA - mid medulla
Ipsi: loss of pain / temp in face (CN V)
Ipsi: Horner’s (sympathetic damage)
Ipsi: Soft palate, phraygeal paralysis, dysphagia (nucleus ambiguous of CN X)
Contra: loss of pain / temp in body (spinothalamic)

spinocerebellar tract: ataxia

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10
Q 
The following are indications of damage to what brain regions?
Large fixed pupils
Unilateral dilated pupil
Mid position fixed pupil
Pinpoint pupil 
Small pupil with ptosis and anhydrosis
A

Large fixed pupils : tectum (dorsal midbrain)
Unilateral dilated pupil: CN III paralysis
Mid position fixed pupil: midbrain
Pinpoint pupil : pons
Small pupil with ptosis and anhydrosis : sympathetic lesion (Horner’s syndrome)

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11
Q

What functions are intact in a persistent vegetative state?

A

Sleep-wake

brainstem function

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12
Q

When should a neurologic exam to determine brain death be performed?

A

More than 24-48 hrs. post MI or severe brain injury

24 hrs after withdrawal of sedative drugs or those that could contribute to comatose state

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13
Q

What are the 2 main types of astrocytoma?

A
  1. Diffuse
    • astrocytoma (WHO II)
    • anaplastic astrocytoma (WHO III)
    • glioblastoma multiforme (WHO IV)
  2. Pilocytic (WHO I)
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14
Q

Distinguishing feature of pilocytic astrocytoma

A

Occurs in children
Macroscopic cysts
Rosenthall fibers in tumor cells (composed of alpha B crystallin)

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15
Q

What is PNET? Most common form?

A

Primitive Neuroectodermal tumors

Medulloblastoma (WHO IV) is most common, usually cerebellar tumor in children.

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16
Q

From what cells do mengiomas typically arise?

A

Cells of arachnoid layer - may become attached to dura

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17
Q

What is the viral association with primary CNS lymphoma?

A

EBV in patients with HIV / AIDS

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18
Q

Example of germ cell tumors and common locations

A 
Generally arise in pineal or hypothalamus
Teratoma - benign
Germinoma
Embryonal carcinoma
Yolk sac tumor (AFP)
Choriocarcinoma (HCG)
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19
Q 
Genetic factors associated w/ the following:
Astrocytoma
Oligodendroglioma
Medulloblastoma
Meningioma
A

Astrocytoma: TP53 ; IDH 1
Oligodendroglioma: 1p and 19q
Medulloblastoma: 17p loss ; PTCH 1
Meningioma: 22 mutation

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20
Q

What is the timeframe for maximal post-infarct cerebral edema?

A

4-7 days

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21
Q

What is encephalomalacia?

A

liquefaction of brain tissue following infarct: “brain softening”

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22
Q

Where do lacunar infarcts most commonly occur?

A

Basal ganglia, thalamus, white matter

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23
Q

What area of the hippocampus is particularly vulnerable to ischemic damage?

A

CA1: Sommer’s sector

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24
Q

possible CNS effects of chronic HTN

A
  1. lacunar infarcts: usually basal ganglia, <1cm
  2. Charcot-Buchard aneurisms: small vessel aneurisms, often in BG
  3. Etat-Crible: loss of tissue w/o infarction around small BVs
    * chronic hypertensive encephalopathy / multi-infarct dementia*
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25
Q

In diffuse hypoxic / ischemic injury what cell populations are injured first?

A
  1. Hippocampus (CA1)
  2. Cerebral cortex (laminar necrosis - middle cortical layers 3-4)
  3. Watershed zones
  4. Purkinje cells of cerebellum
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26
Q

What is the most common type of head injury?

A

Blunt trauma

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27
Q

What is a diastatic fracture?

A

Separation along a suture line

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28
Q

What is a commuted skull fracture?

A

One w/ many small fragments

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29
Q

What is pneumocephalus?

A

Ingress of air into brain enclosure following skull fracture

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30
Q

What are symptoms of diffuse axonal injury?

A

LOC
Concussion
Coma, PVS, severe disability (long term)

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31
Q

What neuronal protein is upregulated following injury (DAI)?

A

B-APP (beta-amyloid precursor protein)

Believed to be involved in synaptic reformation / repair

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32
Q

What is a microscopic marker of DAI?

A

Axonal spheroids: Spherical enlargements of disrupted axons

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33
Q

What is the prototypical cause of epidural hematoma?

A

Middle meningeal artery rupture w/ skull fracture

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34
Q

3 classifications of missile head injury

A

Depressed: Depressed fracture w/o penetration
Penetrating: missile enters cranial cavity
Perforating: In and out

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35
Q

What is the cause of post-traumatic hydrocephalus?

A

Blockage of arachnoid granulations

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36
Q

What is ABCD2 criteria?

A

Used to identify TIA patients with elevated risk of stroke
A: Age: 1 pt if 60+
B: BP: 1pt. for HTN (>140/90)
C: Clinical: 2 pts. for weakness; 1pt. for speech disturbance w/o weakness
D: Duration: 1 pt. for 10-59 min; 2pt. for 60+
D: Diabetes: 1pt. if pos
Score of 4+: justify 24-48 hr. admission

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37
Q

Signs/ Symptoms of stroke

A 
Sudden (10 seconds) onset of:
Weakness
Numbness
Confusion
Speech
Vision
Headache
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38
Q

What is the time target for treatment of a patient presenting w/ stroke?

A

w/in 60 mins of arrival

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39
Q

What is the time frame goal for a patient presenting w/ stroke to see a doctor and get a CT?

A

Door - doctor: 10 mins
Door - CT: 25 mins
Door - CT read: 45 mins

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40
Q

basic criteria for T-PA consideration

A 
18+
Ischemic stroke w/ measurable deficit
80
taking oral anticoagulants
baseline stroke scale >25
Hx of previous stroke AND diabetes
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41
Q

In what patient population is prophylactic anticoagulant therapy preferred to aspirin?

A

Afib

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42
Q

What is the INR goal for patients taking anticoagulant?

A

2.0-3.0

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43
Q

What patients has the FDA approved for carotid angioplasty and stenting?

A

High risk patients with symptomatic high-grade carotid stenosis.

Stenting carries 2x greater risk for in-hospital stroke in non-symptomatic patients copared to endarterectomy

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44
Q

What patients are candidates for CEA or CAS?

A

Asymptomatic: if >80% occlusion
Symptomatic: If >69% occlusion (possibly if >50%)

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45
Q

What is leptomeningitis?

A

Inflammation of subarachnoid space

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46
Q

What is Waterhouse - Friderichsen syndrome?

A

Associated with N. meningitidis meningitis

Adrenal hemmorhage and insufficiency, purpura, septic shock (hypotension)

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47
Q

What are some causes of chronic meningitis? where is the inflammation usually concentrated?

A

TB, syphilis, sarcoidosis, low-grade tumor, foreign bodies

*usually Basal Meningitis - base areas of brain more than hemispheres

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48
Q

What is a serious complication of chronic meningitis?

A

Brain Stem infarction due to stenosis / thrombosis of basilar artery branches

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49
Q

How does HSV gain access to the CNS and what tissue tropism does it display?

A

access via olfactory tract

Tropism for temporal lobe (hemorrhagic necrosis of medial temporal lobes)

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50
Q

What are Cowdry type A inclusions?

A

Nuclear inclusions of HSV particles

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51
Q

What are 4 types of chronic viral encephalitis and causative agents?

A

HIV encephalopathy: HIV
Progressive Multifocal Leukoencephalopathy: JC papovirus
Subacute Sclerosing Panencephalitis: Measles
Tropical Spastic Paraparesis: HTLV-1

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52
Q

What characterizes primary HIV encephalitis?

A

Perivascular monocytic inflammation -> white matter damage and myelin loss
Formation of multinucleated giant cells common, though in AIDS dementia may be brain atrophy and demyelination w/o inflammatory cells

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53
Q

CSF findings in acute leptomeningitis

A

Opening pressure: 200-500 mm H2O (50-180 N)
Elevated protien: >50 mg/dL (15-45 N)
Low glucose: <40 mg/dL (40-85 N)
Leukocytosis (PMN)

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54
Q

When in the course of movement execution is the Basal Ganglia active?

A

active in preparation and execution - even in imagined movements
Act to “filter” motor program - integration of sensory and other input
have no bearing on motor decisions or basic parameters of movement

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55
Q

What are the relative roles of the Putamen and Caudate nuclei of the basal ganglia?

A

Putamen is motor center: innervated by somatosensory and motor cortex (clinical correlate: degenerates in Parkinson’s)
Caudated is innervated by PFC: planning, memory based, psychological (early degeneration in Huntington’s: cognitive and eye movement abnormalities

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56
Q

What are striosomes and matrisomes?

A 
Cell groupings in striatum of BG. 
Striosome:  emotional and behavioral over movement (caudate)
-proj to SNc
-Substance P and Dynorphin
-GABAergic w/ D1 and D3 receptors
Matrisome:  movement (putamen)
-project to direct and indirect pathways
-Enkephalin
-GABAergic w/ D2 receptors
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57
Q

What are the main neuron type involved in striatal output? Subtypes?

A

Medium Spiny Neurons - GABAergic, silent at rest.
Classified by DA receptor type:
D1: subs. P and dynorphin. to SNr and GPi. mostly striosomal
D2: Enkephalin. To GPe. Mostly matrosomal
D3: function ???

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58
Q

What are the D1 and D2 receptor families?

A

D1 family: D1, D5: DA is excitatory, pos. coupling to cAMP

D2 family: D2,3,4: DA is inhibitory. neg. coupling to cAMP

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59
Q

What nucleus is disrupted in hemibalism? Huntington’s?

A

Hemibalism: Subthalamic nucleus
Huntington’s: connection from striatum -> GPe
-> decreased inhibitory input to motor cortex: HYPERKINETIC

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60
Q

Is Huntington’s Disease AD or AR? What is the genetic change?

A

AD
CAG repeat (>30) on chromosome 4
-> caudate nucleus atrophy

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61
Q

What is Sydenham’s chorea?

A

hypokinetic disorder associated with rheumatic fever (GAS infection)

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62
Q

Name 3 genetic dystonias

A

DYT1: Early onset generalized torsion dystonia 9q34, AD. Torsin-A.
DYT5 / 14: DOPA sensitive (AD: 14q22); segawa (AR: 11p15). DA deficiency.
DYT8: Paroxysmal nonkinesigenic dyskinesia 2q35 (AD) MR1

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63
Q

What is blepharospasm?

A

dystonic eye closure - idiopathic

64
Q

3 features in classifying a tremor

A
  1. Rhythm: must be regular, rate: fast / slow
  2. Morphology: flex, extend, pill-roll
  3. Circumstance: rest, w/ movement, postural
65
Q

What kind of tremor is essential tremor? Genetics?

A

Postural tremor, 8-12 Hz

Often AD

66
Q

What are some treatments for essential tremor?

A 
Primidone
B-blocker
Topiramate
Alprazolam
Gabapentin
DBS
67
Q

What gene is associated with Wilson’s disease?

A

13q14.3 - q21.1
Autosomal Recessive
Enccodes ATP7B: hepatic B-type ATPase

68
Q

How do Ceruloplasmin levels correspond to Wilson’s disease?

A

Low in 73% of cases

Not always reduced and reduction does not correlate to disease severity

69
Q

What other disorders are linked to Tourettes?

A

OCD: genetic link
ADHD: often co-occurrance

70
Q

With what conditions is myoclonus associated?

A

Toxic and metabolic encephalopathy

71
Q

What are the cardinal motor signs of Parkinsons?

A 
Must display 2 for diagnosis:
cog-wheel rigidity
bradykinesia
hypokinesia
resting tremor (4-6 Hz, pill-rolling)
postural instability:  flexed posture, festination and retropulsion
72
Q

What cells are lost in Parkinson’s and how many must be lost before symptoms manifest?

A

DA producing cells of SNc

50% loss -> motor symptoms

73
Q

What nuclei other than SNc are affected in Parkinson’s? (6 locations of Lewy Body formation)

A
  1. SNc: DA
  2. Nucleus Paranigralis: DA
  3. Vagal Dorsal Motor Nucleus: NE
  4. Locus Ceruleus: NE
  5. Nucleus Basalis: Ach
  6. Nucleus Accumbens: Serotonin
74
Q

What are the first areas of the brain affected in Parkinson’s? According to Braak staging, when do symptoms appear?

A

a-synuclein changes first affect medullary structures: Dorsal motor nuclei of CN IX and X and anterior olfactory nucleus with destruction ascending to meso and neocorteces

Midbrain DA symptoms at Braak stage 3 (anosmia, constipation, depression))

75
Q

Where is the familial Parkinson’s gene located?

A

chromosome 4

atypical Parkinson’s disease

76
Q

What is the major component of Lewy Bodies? what is its function?

A

alpha-synuclein (chr. 4): 2 mutations noted. AD inheritence.
Associated with early onset (40s) and rapid progression
Complexes w/ presynaptic DA transporter enhancing DA uptake.
Overexpression may -> increased transporters

77
Q

What protein is associated with early onset of Parkinson’s and a slow disease progression?

A

Parkin: disease onset in 20’s w/ slow progression
AR inheritence, chr 6. (E3 ubiquitin ligase, protosome regulator)
No Lewy Bodies

78
Q

What gene is the most common cause of inherited Parkinson’s Disease?

A

LRRK-2 (Leucine Rich Repeat Kinase-2)
AD pattern, but only 30-40% penetrance in some mutations
Mutations of GTPase and Kinase regions of protein
Indistinguishable from idiopathic PD

79
Q

What is the MOA of Levodopa? What is it given with?

A 
Crosses BBB (DA does not) 
Converted to DA by Dopa Decarboxylase (DDC) in dopaminergic nerve terminals
* Given w/ Carbidopa:  inhibits peripheral DDC*
80
Q

What is the levodopa + carbidopa combination drug?

A

Sinemet

81
Q

What is a dietary concern for people taking Sinemet?

A

Protein hinders absorption

82
Q

How does the effect of levodopa change with progression of PD?

A

Therapeutic window narrows -> increased incidence of dyskenesias and shorter period of drug effectiveness

83
Q

What transporter allows levodopa to cross the BBB?

A

Large neutral amino acid transporter (LAAN)

84
Q

3 dopaminergic side effects associated with PD therapy (levodopa)

A

Dyskinesia
Hallucination (treat with clozapine or quetiapine - atypical antipsychotics)
Hedonistic Homeostatic Dysregulation: gambling, hypersexual, long walks, shopping, etc. (more in young men (early onset))

85
Q

What is “on-off” effect seen in levodopa therapy for PD and how is it handled?

A

Unpredictable fluctuations in mobility and parkinsonian symptoms. not related to dose timing.
Treat: DA agonist (Apomorphine) - rapid relief
-increase frequency of doses

86
Q

What are 2 DA antagonists that are contraindicated in PD therapy?

A

Metoclopramide (Reglan)

Phenothiazine

87
Q

Disadvantages of DA agonists compared to levodopa

A 
More cognitive (hallucinations) and adverse events than l-dopa
Contraindicated w/ angina or recent MI
CYP450 interactions
88
Q

What should be administered w/ apomorphine?

A

antiemetic

very high incidence of N/V

89
Q

What drugs can be given to PD patients that enable lowering L-dopa dose?

A

COMTi

MAO-Bi

90
Q

Possible advantages of MAO-Bi therapy for PD?

A

Lower L-dopa dose
delay starting l-dopa
may reduce oxidative stress - neuroprotective? not proven

91
Q

What is Gerstmann’s Syndrome?

A

Tetrad of dominant parietal lobe lesion:

1) L - R disorientation
2) Finger agnosia (difficulty naming fingers)
3) Acalcula / Anarithmetria
4) Agraphia

92
Q

What is Anton’s syndrome?

A

Cortical blindness w/ anosagnosia.

May resolve via Balint’s syndrome (oculomotor apraxia)

93
Q

What is Balint’s syndrome?

A

Lesion of occipital - parietal connection ->
occulomotor apraxia, visual ataxia, visual inattention, and sometimes facial recognition problems. Color info better preserved.

Anton may -> Balint

94
Q

What part of the brain is affected in achromatopsia?

A

Inferior parietal / occipital lobe lesion

Loss of color vision

95
Q

What part of the brain is damaged in alexia w/o agraphia?

A

posterior dominant hemisphere - occipital and splenium of corpus callosum.
Associated with homonymous hemianopsia, color anomia, achromatopsia

96
Q

What is Amnestic Syndrome?

A

Bilateral limbic system lesion (medial temporal and thalamus)-> mixed anterograde / retrograde amnesia

97
Q

What is a tool that can be used to differentiate vascular from other dementias?

A

Modified Hachinski Ischemic score

7: probably vascular

98
Q

Requirements for a diagnosis of dementia

A

Memory impairment plus one of:

language, judgement, abstract thought, praxis, constructional ability, visual recognition

99
Q

How would early Alzheimer’s and Diffuse Lewy Body disease appear different on a PET scan?

A

AD: decreased glucose utilization in posterior cingulate gyrus and parietal cortex

DLD: decreased glucose utilization in anterior cingulate gyrus

100
Q

Key microscopic findings in Alzheimer’s disease

A
  1. Neurofibrillary tangles: intracellular. Tau, neurofillament, B amyloid
  2. Senile plaques: extracellular - disrupted neuropil and distended axons. B-amyloid core
101
Q

What is Khachaturian criteria for diagnosis of AD?

A

Count number of plaques in areas of brain most affected by AD (entorhinal, parietal, insular cortices and amygdala)
55: 15+

102
Q

What brain areas are first affected in the Cholinergic theory of AD?

A

Nucleus Basalis

Locus Cerulius

103
Q

What fragments of APP can form amyloid?

A

I-40 and I-42

104
Q

Major genes involved in Alzheimer’s pathology

A 
B-APP:  21:  early onset
APO E4:  19:  assoc.
APO E2:  19:  protective
PS1:  14 ; PS2:  1:  GOF -> increased amyloid production
MAPT:  17:  NFT
105
Q

4 possible protective therapies against Alzheimers

A

Smoking and moderate alcohol use
NSAIDs
Estrogen replacement
Statins

106
Q

Average survival in CJD after onset

A

8mos

107
Q

What are the characteristic features of Crutzfeldt Jakob Disease?

A

Myoclonus, ataxia, visual disturbances
EEG: periodic sharp waves
MRI: signal abnormalities in Basal Ganglia
CSF: 14-3-3 protein (not specific)

108
Q

What protein is involved in prion disease, what gene codes it and where is it found?

A

Chromosome 20
PRNP gene
PrP protein: PrP(c) is normal PrP(Sc) or (Res) is seen in disease

109
Q

Using ATPase staining, how do Type I and II muscle fibers stain?

A

Type I: (non-fatigable, low glycogen, high lipid) light staining
Type II: (fatigable, high glycogen, low lipid) dark staining

110
Q

Upon what muscular structure is the myotactic reflex arc dependent?

A

Muscle spindle (intrafusal fibers): encapsulated group of fibers with sensory and motor innervation. rapids stretch -> reflex contraction

111
Q

What are the effects of strength training and aerobic training on muscle composition?

A

Strength: Type 2 (fatigable) fiber hypertrophy
Aerobic: Increased oxidative capacity of muscle
Disuse -> Type 2 atrophy

112
Q

3 neurogenic muscle disorders that affect Anterior Horn Cells

A
  1. poliomyelitis
  2. amyotrophic lateral sclerosis
  3. hereditary spinal muscle atrophies
113
Q

What are the basic mechanisms of polymyositis and dermatomyositis?

A

PM: CD8+ cells attack muscle cells
DM: antibody or immune complex mediated microangiopathy -> muscle damage

114
Q

What is the mechanism of steroid induced myopathy?

A

Probably insulin intolerance and protein catabolism -> atrophy of type 2 fibers

115
Q

Nerve fiber classifications

A

a: extrafusal muscle fibers
Aa: vibration, proprioception, soft touch
gamma: intrafusal fibers
AB, Ad: sharp pain, temperature, pressure
C: pain, autonomic

116
Q

What do increased or reduced reflexes indicate in a case of muscle weakness

A

Increased reflex: central lesion

Decreased reflex: neuropathy or problem at NMJ

117
Q

How is a demyelinating disease differentiated from an axonal disorder?

A

Nerve conduction studies or biopsy

118
Q

With what disease is connexin-32 involved and how does it present?

A

Charcot-Marie-Tooth X
presents differently in men vs. women
Male: demyelinating neuropathy w/ intermediate conduction
Female: axonal neuropathy w/ near normal conduction

119
Q

What is P0 associated with?

A

mutation may -> either demyelinating or axonal neuropathies

120
Q

What diseases is GDA-P1 associated with?

A

Demyelinating: CMT4A
Axonal: CMT w/ hoarsness

121
Q

2 examples of periodic paralysis disorders and cause of each.

A

Periodic paralysis: results from voltage-gated ion channel disorders

  1. Hyperkalemic periodic paralysis: Na+ channel mutation
  2. Hypokalemic periodic paralysis: Ca++ channel mutation
122
Q

Infectious causes of myositis

A

Viral: Flu A and B, parainfluenza, coxsackie, echo, adeno
Bacterial: S. aureus, S. pyogenes (GAS)
Parasitic: toxoplasmosis, cysticercosis (taenia solium), trichinosis

123
Q

What are some drugs known for causing myositis?

A 
D-Penicillamine
Procainamide
Cimetidine
Ranitidine
Statins
Fibrates
124
Q

What gene is affected in muscular dystrophy?

A

Xp21: dystrophin gene (X-linked)
Duchene: dystrophin is absent or severely reduced (<3% normal)
-onset in 2nd year, wheelchair by 12, death in 3rd decade.
Becker: reduced dystrophin, less severe, generally no contractures

125
Q

What is the most common muscular dystrophy in adults?

A

Myotonic dystrophy (AD)
CTG repeat on 19 and another form w/ mutation on 3q
myotonia, muscular dystrophy, cataracts, frontal balding, EKG changes
Reduction in IQ

126
Q

What is one mechanism by which corticosteroid therapy helps Myasthenia Gravis?

A

Increases expression of Ach receptors

127
Q

What is neonatal myasthenia?

A

Transfer of maternal anti-Ach R antibodies to infant -> myasthenia gravis symptoms

128
Q

What are 2 bedside tests that can be done to aid in diagnosis of Myasthenia Gravis?

A

1) Arm abduction: if held < 5 minutes, demonstrates fatigability
2) Edrophonium: anti-cholinesterase - alleviates symptoms
- have Atropine on hand in case of CV effects

129
Q

2 antibodies involved in Myasthenia Gravis

A

1) anti-AchR (specific: 80-90% of pts)

2) anti- Muscle specific Tyrosine Kinase (40% of those w/o anti-AchR)

130
Q

Two EMG findings in myasthenia gravis

A

1) : CMAP: progressive decrement w/ repeat stim due to decreased Ach release. decrease of 10% between 1st and 5th at 3Hz
2) SFEMG: Jitter: variable synaptic transmission

131
Q

2 causes of myasthenia gravis

A

Thymoma
Penicllamine
no identified bacterial or viral causes

132
Q

4 treatments for myasthenia gravis

A

1) Pyridostygmine: enhanced cholinergic transmission
2) prednisone / prednisolone: alternate day dosing reduces side effects
3) thymectomy
4) plasmaphoresis

133
Q

What is Lambert Eaton?

A

Autoimmune disorder affecting Ach transmission
Antibodies against voltage gated Ca++ channel (VGCC)
Gait affected, autonomic dysfunciton
60% assoc. w/ small cell lung cancer

134
Q

What occurs in lambert eaton w/ EMG?

A

repetitive stim -> increased response due to increased [Ca++]

135
Q

What illnesses have been associated with Guillan-Barre

A

Campylobacter jejuni, Mycoplasma pneumoniae, CMV

136
Q

What is Fisher syndrome?

A

Variant of Guillain-Barre
Ataxia, areflexia, opthalmoplegia
Anti-GQ1b ganglioside : found on oculomotor fibers and sensory ganglia

137
Q

What is multifocal motor neuropathy (MMN)?

A

Autoimmune motor neuron disease
Asymmetric, slowly progressive weakness, begins in arms
anti GM1 ganglioside Ab
similar to ALS, but no UMN symptoms - also more treatable
Treatment: IVIg - not plasmaphoresis or steroids

138
Q

Name 3 paraneoplastic neuromuscular syndromes

A

1) Paraneoplastic Cerebellar Degeneration: anti-Yo. Breast, ovarian, uterine cancers.
2) Paraneoplastic Opsoclonus - myoclonus: dancing eyes and dancing feet. anti - Ri. Childhood neuroblastoma, multiple adult tumors.
3) Paraneoplastic encephalopathy and sensory neuronopathy: anti - Hu. Small cell carcinoma

139
Q

How is motor nerve conduction velocity calculated?

A 
Using CMAP (compound motor nerve action potential)
2 stimulus points along motor nerve - timed from stimulus to muscle reaction.
Distance between 2 sites divided by difference between the 2 latencies = nerve conduction velocity
140
Q

How is sensory nerve conduction velocity measured?

A

Distance between stim and recording site divided by latency

141
Q

What is the H-response and what nerve is used?

A

H-response evaluates reflex pathway

Only tibial nerve is used - ankle jerk reflex

142
Q

What is F-response?

A

Motor nerve stimulated - antidromic conduction -> motor nucleus
~5% of motor neurons re-stimulated to send AP back down nerve -> muscle.
Delay in addition to conduction velocity / distal latency is attributed to activity in / out of spinal cord.

143
Q

What is a test that can be done for Benign Paroxysmal Positional Vertigo?

A

Hallpike-Dix maneuver
turn 45 deg. in one direction, extend neck, then quickly go to lying position
If vertigo -> nystagmus

144
Q

Differential for vertigo lasting 1 hour or less

A

TIA
Migraine
Panic attack

145
Q

What is a concern in long lasting (hours to days) vertigo?

A

Mentrier’s Syndrome: increased endolymphatic pressure

Untreated -> low frequency hearing loss

146
Q

How is Multiple Sclerosis diagnosed?

A

History - multiple lesions in space and time
CSF: pleocytosis during acute attack, increased protein (IgG), oligoclonal bands
MRI: multiple lesions

147
Q

How does MS risk correlate with location?

A

Risk correlates with geographic location of residence prior to age 15.
Risk increases with increasing Northern Latitude

148
Q

What is the genetic association with Multiple Sclerosis?

A 
MHC locus on chr. 6
class II HLA-DR2, DR5, DQ6
149
Q

What is Neuromyelitis Optica?

A

Severe form of MS that selectively affects optic nerves and spinal cord
Marker: NMO IgG : binds aquaporin 4 in astrocytic foot processes forming BBB

150
Q

What is central pontine myelinolysis?

A

Myelin destruction in central pons due to overly rapid correction of hyponatremia
Avoidable!
Marked by rapid onset of quadriplegia due to bilateral damage to corticospinal tract myelin

151
Q

What is prevention for post-herpetic neuralgia?

A

Preventative: Zostavax vaccine (also varivax, but not studied)

Steroids and early antivirals w/ incidence of shingles may decrease severity

152
Q

1st and 2nd line treatments for trigeminal nerve pain

A

1st: Carbamazepine: VGNaC blocker. P450 inducer. induces own metabolism.
2nd: Gabapentin, Pregabalin, Tramadol, Opioids (all +/- carbamazepine)

153
Q

What is the pathogenesis of Diabetic neuropathy?

A

Elevated blood glucose -> increased sorbitol production via aldose reductase -> oxidative stress -> ion channel damage and axonal shrinkage

abnormal sensory function and pain

154
Q

What is the tiered approach to treatment of neuropathic pain?

A

1: Gabapentin, pregabalin, lidocaine patch
2: TCA, venlafaxine, opioids
3: other: capsaicin, topiramate, lamotrigine, valproic acid

155
Q

List risk factors for failure of ventral induction of CNS

A

Trisomies 13 and 18
Maternal diabetes
ETOH
Maternal infections (toxoplasmosis, rubella, syphillis)

156
Q

Drug of choice for absence seizures

A

Ethosuximide

Alternative: Clonazepam

157
Q

Drug of choice / alterantives for partial seizures

A

DOC: Carbamazepine or Levetiracetam or Phenytoin

Alt: Valproic acid, Phenobarbital

158
Q

Drug of choice for generalized seizures

A

Valproic acid

Levetiracetam

M2 (19 decks)

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