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Pathology Block 12 > Nervous System And Neuromuscular Pathology > Flashcards

Nervous System And Neuromuscular Pathology Flashcards

1
Q

How does the pupillary light reflex go

A

In on 2 and out on 3

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2
Q

How do you test the pupillary light reflex

A

Dim lighting

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3
Q

Shining light into the right eye

A

Activates sensory arc following optic tracts bilaterally or pretectal nucleus (area) in midbrain

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4
Q

What does the pretectal nucleus do once it is activated by light

A

Each pretectal nucleus sends axon projections bilaterally to the left and right edinger Westphal nucleus to activate pre ganglionic parasympathetic neurons

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5
Q

When the parasympathetic neurons are stimulated by the edinger westphal nucleus in the pupillary light reflex, what happens

A

Post ganglionic parasympathetic neurons in the left and right ciliary ganglion activate pupillary constrictor muscle in both eyes (direct and consensual)

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6
Q

Pupillary light reflex and damage to the right optic nerve

A
  • if light is shined into the left eye, there is a direct and consensual response because of the projections from the left optic nerve tot he right CNIII
  • if light is shined into the right eye, there is neither a direct or consensual response because no light can send any signal back to even get to the bilateral projections of CNIII
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7
Q

Pupillary light reflex and damage to the right optic tract

A
  • light shined into the left eye has a direct and consensual reasoned
  • light shined into the right eye induces a normal pupil constriction for both direct and consensual since it is past the optic chiasm and has bilateral projections
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8
Q

Which causes more of a problem, optic nerve lesion or an optic tract lesions

A

Optic nerve

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9
Q

Pupillary light reflex and damage to the right CN3

A
  • Light shined in the left eye induces normal direct response but no consensual pupillary constriction in the right eye
  • light shined in the right eye does not have a direct response In the right eye, but a normal consensual response in the left eye
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10
Q

Why is accommodation not a specificity test only of the midbrain

A

Reflex circuitry for acocmmodation is not yet well destablished: may involve visual cortex or unconscious visual processing in tectum

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11
Q

Motor arc of pupil constriction in accommodation is mediated by what

A

Parasympathetics from the edinger westphal via CN3 as with light induced constriction

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12
Q

Pupils are abnormally asymmetrical in size

A

Anisocoria

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13
Q

What are the questions you need to ask when you see unequal pupil size

A
  • is it due to impaired pupillary constriction in the larger pupil?
  • is the asymmetry due to impaired pupillary dilation in the smaller pupil
  • does the asymmetry remain the same after testing for dilation and light reflex?
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14
Q

Left afferent pupillary defect

A
  • light not getting through the left eye
  • light shined into left eye will not elicit direct or consensual response
  • light shined in right eye will elicit a direct and consensual
  • this is called Marcus Gunn Pupil
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15
Q

Opiate drugs and the pupils

A

Inhibit sympathetic and cause pin point pupils

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16
Q

Afferent pupillary defect, aka “Marcus Gunn pupil”

A
  • impaired sensory arc of the reflex such that both the direct and consensual response are impaired to light on the side of the causal lesion
  • requires verification in intact motor arc on both sides
  • afferent pupillary defect refers to this finding of a sensory arc defect, but can result from a variety of lesions: retina, or optic nerve damage
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17
Q

Acute Adie’s pupil

A

-impaired constriction response to light and accommodation due to impaired motor component. Specific cause is not proven but involves partial degeneration of ciliary ganglion or post-ganglionic parasympathetic projections. Pattern of denervation in iris is segmental (partial). Possibly due to inflammatory damage

MOTOR

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18
Q

Chronic Adie’s tonic pupil

A

-involves ectopic re-innervation of iris by parastympathetic projections that would normally target the ciliary body. Thus, light reflex remains impaired, but accommodation testing shows improved pupil constriction response with delayed reversal to baseline pupil size, hence the term Adie’s tonic pupil or Adie’s myotonic pupil

Nerves regenerate, but some go to iris instead of to the ciliary body

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19
Q

Impairment in light reflex but with preserved accommodation response

A

Light-near dissociation

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20
Q

What are some conditions in which light-near dissociation occurs

A
  • Adie’s tonic pupil
  • neusosyphillis, accompanied by irregular shaped pupils, called Argyll-Robertson pupil
  • some diabetics
  • can occur in parinaud syndrome: dorsal midbrain compression (pineal tumor)
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21
Q

Pupillary motor arc is mediated by

A

Sympathetic NS

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22
Q

When the sympathetic to the head are damaged, what pupillary defect do we get

A

Horners syndrome

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23
Q

Emotional pupillary response

A

Starts in the hypothalamus and goes down to T1 and T2 and then back up the sympathetic

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24
Q

Things that can lead to horners

A

Lateral pons infarct

Lateral medulla infarct

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25
Q

Anterior ischemic optic neuropathy (AION)

A

Ischemia of anterior optic nerve (portion in the orbit) is a common cause of sudden vision loss, especially >50 y/o

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26
Q

What is the blood supply that supplies the anterior optic nerve that is involved in a tier or ischemic optic neuropathy

A

Short ciliary arteries derived from ophthalmic artery

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27
Q

Arteritis AION

A

In temporal arteritis, inflammatory process concludes arteries, treatable with glucocorticoids

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28
Q

What are some things that could cause AION

A

Atherosclerosis, HTN, diabetes, smoking, nocturnal hypotension (vision loss on waking)

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29
Q

Presentation of AION

A

Painless, visual field loss may be total, sector, or scotoma

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30
Q

What will you see on ophthalmic exam in AION

A

Reduced cup-to-disc ratio

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31
Q

What is a common precursor to MS

A

Optic neuritis

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32
Q

Optic neuritis

A

-inflammatory de-myelination of the optic nerve(s)

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33
Q

Etiology of optic neuritis

A
  • inflammatory process triggered during or after resolution of viral infection
  • pro-inflammatory chemical exposure
  • vitamin B12 deficiency
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34
Q

Onset of optic neuritis

A

30-45 years but can be later

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35
Q

Incidence of females to males in optic neuritis

A

2:1

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36
Q

___% of patients with optic neuritis later develop multiple sclerosis

A

50

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37
Q

Presentation of optic neuritis

A

Monocular vision loss, eye pain especially during eye movements

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38
Q

Visual loss in optic neuritis

A

Central scotoma, reduced acuity around scotoma, impaired color detection. Can be complete monocular vision loss

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39
Q

Ophthalmic exam for optic neuritis

A

-depends on whether inflammation extends to optic disc or is limited to retro-bulbar segment of optic nerve. Thus optic disc can be swollen and inflamed or normal. Prior episodes can lead to optic disc pallor

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40
Q

Additional diagnostic testing for optic neuritis

A

Afferent pupillary defect, VEP

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41
Q

VEP in optic neuritis

A
  • EEG recordings of primary visual cortex responding to alternating checkerboard stimulus
  • abnormally long latency of cortical response with normal amplitude consistent with de-myelination (atonal degeneration would result in reduced amplitude of the evoked response)
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42
Q

Temporal profile of optic neuritis

A
  • onset variable
  • acute, subacute, chronic
  • Duration <2 weeks followed by full or partial recovery
  • recovery can take 6 weeks to months
  • 1/3 of patients have 1 or mote recurrences
  • repeat episodes are more likely to yield residual damage and deficits
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43
Q

Is optic neuritis usually permanent

A

No

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44
Q

Reasons to suspect a different diagnosis from optic neuritis

A
  • over the age of 45
  • absence of associated eye pain (argues against inflammatory pathology)
  • bilateral visual loss
  • 1st episode and visual loss lasting more than 2 weeks, absence of recovery
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45
Q

DDx for optic neuritis

A 
Glaucoma 
Retinal artery occlusion
Optic nerve ischemia 
Compressive lesion
CNS infection
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46
Q

Radiological evidence of optic neuritis

A

MRI showing de-myelination lesions

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47
Q

Short term treatment for optic neuritis

A

Glucocorticoids

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48
Q

Pathophysiology of MS

A

-autoimmune de-myelinating disorder of the CNS only

NO PNS INVOLVEMENT!

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49
Q

Specific mechanisms of MS

A

Involves autoimmune attack against oligodendrocytes by T lymphocytes
-could target myelin basic protein or other components of the myelin sheath or other antigens on aoligodendrocytes. Axons are not directly affected

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50
Q

Presentation of MS

A

Multi-focal distribution for 2 or more focal lesions within CNS
-2 or more “attacks” separated in time (like one month apart)

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51
Q

If someone has a single lesion could that habe MS

A

No

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52
Q

Epidemiology of MS

A 
1 per 1000
2x as many females 
20-40 years 
Caucasians
Higher altitude
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53
Q

Original hypothesis of MS

A
  • small breaches of blood Brian barrier
  • Ab against myelin basic protein
  • followed by direct T cell attack
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54
Q

Newer hypothesis of MS

A
  • inflammation triggered by microglia
  • T cell invasion of CNS from blood
  • release cytokines that are toxic to oligos
  • following oligo cell death, macrophages attack debris and myelin sheath
  • astrocytes form glial scar around zone of damage
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55
Q

Genetic risks of MS

A
  • siblings 2.6% risk
  • 25% concordance in identical twins
  • 2.5% concordance in Sam sex fraternal twins
  • mutations in IL-2 and IL-7
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56
Q

MRI evidence of MS

A

2 or more white matter lesions (plaques)

  • plaques can be distributed anywhere at differnt levels
  • often appear as fingers extending from periventricular zones
  • MRI with contrast can highlight plaques
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57
Q

CSF analysis in MS

A
  • oligoclonal bands
  • presence of bands at specific molecule weights
  • 85% sensitivity for MS (not found in all MS pateints)
  • 92% specificity for MS (present in some other diseases)
  • elevates lymphocyte count
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58
Q

Mental status in MS

A
  • specific conginitive defects (visual defects, working memory deficits
  • psychiatric symptoms: depression, fatigue, manic
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59
Q

Cranial nerves and MS

A 
Oculomotor deficits (inter nuclear ophthalmoplegia) 
-lesion at the MLF causing the abducens and CNIII to not communicate properly
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60
Q

Cerebellum and MS

A

Poor coordination

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61
Q

Motor exam in MS

A

Weakness

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62
Q

Sensory exam in MS

A

Sensory loss, Lhermitte’s sign (flexing neck induces electrical shock running down back into legs

63
Q

Autonomic implications of MS

A

Sweating, bladder/bowl/sexual dysfunction

64
Q

Temporal profile of MS

A
  • 1st attack and medical eval often revels evidence for prior episodes
  • 50% have prior episode of optic neuritis
  • relapsing-remitting cycle
  • can become chronic and progressive
65
Q

Short term MS treatment

A

Glucocorticoids

66
Q

Long term Tx for MS

A

Immunomodulatory agents

-interferons

67
Q

Factors that can trigger or transiently intensify an attack

A
  • infection
  • over heating
  • dehydration
  • sleep deprivation
68
Q

Neuromyelitis optica (NMO)

A

MS look alike disorder

  • devic syndrome
  • de-myelination of the optic nerves and spinal cord (2 lesions)
69
Q

Presentation of neuromyelitis Optica

A

Bilateral visual loss, level-down sensory and motor deficits

70
Q

Distribution of neuromyelitis optica

A

Multi-focal (hence resembling MS)

71
Q

Pathophysiology of neuromyelitis optica

A

Auto-immune attack involving Ab to aquaporin 4

72
Q

Diagnosis of neuromyelitis optica

A

Aquaporin-4 AB

73
Q

Temporal profile of neuromyelitis optica

A

Acute and stable

74
Q

Pathophysiology of progressive multifocal leukoecephalopathy

A
  • multiple cocci of white matter de-myelination and damage in the CNS
  • viral infection of oligodendrocytes
  • infection is rarely symptomatic, but can lead to leukoencephalopathy
  • usually occurs in immunosuppressed patients
  • usually co-morbid
75
Q

Onset and course of progressive multifocal leukoencephalopathy

A

Subacute and progresive

76
Q

Progression of progressive multifocal leukoencephalopathy

A

Can be fatal, treatment is anti-retroviral Rx

77
Q

Neurological deficits in progressive multifocal leukoencephalopathy

A

Varies depending on the location of lesions

78
Q

What can progressive multifocal leukoencephalopathy progress too

A

Dementia (differs from MS)

79
Q

Pain in progressive multifocal leukoencephalopathy

A

None

80
Q

Presentation of lesions in progressive multifocal leukoencephalopathy compared to MS

A

In MS they are periventricual, in PML they are adjacent to cortical gray matter

81
Q

Differences between leukoencephalopathy and leukodystrophy

A

leukoencephalopathy has lesions that develop and damage structures

Leukodystrophy is a disorder that involves defects in myelin structure and function

  • can be genetic or acquired
  • myelin formation is impaired or the myelin is structurally and functionally defective
  • present during 1-2 years of life but can emerge as last as early adulthood
82
Q

Inflammatory damage to white and grey matter, mimics MS or stroke

A

Acute disseminated encephalomyelitis (ADEM)

83
Q

Inflammatory de-myelination in CNS, often with gray matter damage, typically 1-2 weeks after an infection (bacterial or viral) or after a vaccination (adverse reaction)

A

Acute disseminated encephalomyelitis (ADEM)

84
Q

Distribution of acute disseminated encephalomyelitis

A

Multifocal or diffuse

85
Q

Pathophysiology of ADEM

A

Inflammatory and rapid onset

86
Q

Diagnosis of ADEM

A

Lesions in white matter and gray matter

87
Q

Presentation of ADEM

A

Typically non-localizing signs, HA, lethargy, stupid, coma
-however, initial presentation can be focal, thus mimicking stroke except that localization does not conform to a single vascular territory

88
Q

Temporal profile of ADEM

A

Acute to subacute, rapid onset confers similarity to stroke

89
Q

Treatment of ADEM

A

Glucocorticoids

90
Q

Headaches and the dura

A

The Dura lines everything and is innervated all over and can cause headaches

91
Q

Acute onset headaches

A
  • last several minutes to hours
  • urgent/emergency likely
  • hemorrhage’s
  • meningitis or encephalitis
  • ophthalmic events (glaucoma, iritis)
92
Q

Subacute onset headaches

A
  • hours to days ago

- non emergent

93
Q

Chronic onset headaches

A
  • occurrence began weeks, months years ago
  • tension type
  • cluster type
  • migraine
94
Q

Temporal pattern of migraines

A

Spells, random pattern

95
Q

Temporal pattern of tension headache

A

Musculoskeletal, presistnant

96
Q

Cluster headache temporal pattern

A

Spells, a lot on a daily basis and Long spells without

97
Q

Brain tumor temporal pattern

A

Steady ramp over time

98
Q

Unilateral pain on headache

A

Cluster

-sometimes migraine

99
Q

Ocular or retro-orbital pain in headache

A

Ocular or neuro-ophthalmic causes

100
Q

Focal pain headache

A

Signal intracranial mass

101
Q

Diffuse or band like pattern headache

A

Tension headache (scalp)

102
Q

Cause of tension head

A

Not known

103
Q

Hypothesis of tension headache cause

A

MUsuloskeletal, excess muscle tone

-occipitopfrontalis or suboccipital triangle uncles, activates local pain fibers

104
Q

How to treat tension headache

A

Common Rx and osteopathic manipulative techniques

105
Q

Presentation of cluster headache

A
  • unilateral
  • non-pulsating
  • transient
  • minutes to hours
  • will wake the patient
  • extend remission periods
106
Q

Localization of cluster headaches

A

Periorbital region

-or along path of vessels and nerve branches

107
Q

Who gets cluster headaches more

A

Men

108
Q

Rx for cluster HA

A

Serotonin agent that acts on the blood vessels (sumatriptan)

  • constricts intracranial vessels
  • lidocain
109
Q

Migraine presentation

A
  • minutes to hours
  • <1 week
  • auras
  • nausea.vomitting
110
Q

Who is more likely to get a migraine

A

Women

111
Q

Localization of migraines

A

Hemi cranial but can be bilateral

112
Q

Causes of migraines

A
  • dietary, environmental factors

- possibly due to autonomic dysregulation of vasoconstriction and dilation, stimulating local pain fibers

113
Q

RX for migraines

A

Serotonin agents
CCB
Tricyclics anti-depressants

114
Q

Tumor origin is in CNS

A

Primary

115
Q

Tumor origin is outside the DNS

A

Secondary/metastatic

116
Q

Which is more common, primary or secondary intracranial tumors

A

Secondary

117
Q

Where do primary intracranial tumors come from

A

Glia. Meninges, pituitary

118
Q

Most common forms of secondary/metastatic tumors

A

Lung, breast, melanoma, prostate

119
Q

Primary tumor growth

A

Remains intracranial, but presence and growth can lead to seizures, compression and focal or diffuse neurological deficits, brain herniation syndromes

120
Q

Pain in intracranial tumor

A

Dull and focal or diffuse

121
Q

Intracranial histological structure (tumor)

A

Encapsulated, surgically removed
-diffuse and poorly circumscribed not able to be removed
-secondary typically well circumscribed and multifocal
-

122
Q

Which type of intracranial tumor is more likely to be diffuse and poorly circumscribed. I totally they are focal and well-circumscribed, but recurrences after surgical removal tend to be diffuse and not operable

A

Primary tumors

123
Q

How do you identify intracranial tumors

A

Neuroimaging and biopsy analysis

124
Q

How do you grade a intracranial tumor

A

1-4 based on histology and growth potential

125
Q

Tumors develop from cell types that

A

Can undergo mitosis

126
Q

Post-natal CNS neurons and mitosis

A

With very few exception, can NOT enter mitosis

-glia remains the ability to do so

127
Q

Most brain tumor types are derived from

A

Glia, choroid plexus, or meninges

128
Q

Rare type of brain tumor

A

Primary CNS lymphoma, few lymphocytes in brain, no lymphatic

129
Q

Neuroblastoma

A

From pre-natal neural stem cells

130
Q

Medulloblastoma

A

In developing cerebellum

NOT MEDULLA

131
Q

Neuromas

A

Schwann cells form these on nerves )acoustics neuroma)

132
Q

Oligodendroglioma

A

Cerebral white matter

133
Q

Astrocytoma or glioblastoma

A

Astrocytes

134
Q

Ependymomas

A

Ependymal cells

135
Q

What kind of tumors can choroid plexus form

A

Benign or malignant tumors (papilloma or carcinoma)

136
Q

Meningiomas

A

Several common hot-spots

137
Q

What are the implications of a space-occupying lesion

A

Brain compression and herniations

138
Q

Amyotrophic lateral sclerosis

A

UMN and LMN cell death

139
Q

Spinal muscular atrophy

A

LMN death

140
Q

Polio and post polio syndrome

A

LMN cell death

UMNs often spared

141
Q

Peripheral neuropathies

A
  • diabetic neuropathy
  • Guillain-barre
  • genetic
  • de-myelinating vs axonopathy
  • diagnostic methods
142
Q

Pathology of the NMJ

A

MG

143
Q

Pathophysiology of MG

A

Abs generated against nicotine ACH receptors, induced receptor internalization
-can also involve Abs against muscle-specific tyrosine kinase (MuSK) which normally acts to cluster nACHRs in synapse

144
Q

Presentation of MG

A

Fatiguable weakness

145
Q

Diagnostic tests for MG

A

Tensilon test

-edrophonium to see if they respsone

146
Q

Presentation of MG

A
  • diffuse
  • EOM weakness
  • includes weakness of levator palpebrae
  • pupillary light reflex spared (iris is smooth muscle)
  • other cranial motor weakness possible
147
Q

Temporal profile fo MG

A 
Any age 
Progressive 
Relapsing-remitting pattern
More in women 
After an infection
148
Q

Lambert-Eaton syndrome

A

Ab mediated auto-immune attack against Ca channels

  • Ab produced due to paraneoplastic syndrome (Secondary to tumor)
  • limbs effected but EOMs usually spared
  • AChase inhibitors not effective
  • use immunosuppresive agents nad plasma phoresis
149
Q

Difference between MG and lambert-Eaton syndrome

A

MG: Ab bind and block the nictoinic Ach receptors

LE: Ab bind calcium channels

150
Q

Oculomotor myopathies

A

Weakness most often with eye and lid elevation, often diplopia occurs

Major etiologies: hyperthyroidism, mitochondrial DNA mutations

151
Q

Duchenne musculat dystrophy

A
  • mutation in dystrophin, maintenance of sarcomere
  • pediatric disorder with progressive diffuse weakness, wheel chair bound
  • proximal limbs most affected
  • toe-walking, waddling gait, Gower’s sign (pushing off of legs with arms to stand upright)
152
Q

Bipolar disorder

A
  • inflated self esteem, decreased need for sleep, more talkative, flight of ideas, distractability
  • mood disturbances impair social and occupational functioning
  • psychotic features
  • not attributable to the psychological effects of substance abuse
  • followed by a very low depressive period
153
Q

How do we treat bipolar disorder

A

Lithium

154
Q

Lithium as a treatment for bi polar

A

Not sure why it works

  • must be maintained within a precise blood concentration
  • think it may stabilize amount of signaling through Ca channels

Pathology Block 12 (7 decks)

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