Exam 2: [Pathology Of The CNS] Flashcards

1
Q

Causes of Primary Diseases in the CNS & (%)

A

10% of Diseases
1) CVA
2) Epilepsy
3) Trauma
4) Tumors
5) Infections
6)Cerebral Edema
7) Hydrocephalus

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2
Q

Cause of Secondary Diseases in the CNA & (%)

A

90% of Diseases
1) Circulatory Failure
2) Cardiac Disease
3) Metobolic Causes
4) Chemical Causes

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3
Q

Manifestations of CNS Disease

A

1) Disturbances of Conciuosness
2) Increased Cranial Pressure
3) Focal Neurological Signs & Symptoms
4) Epilepsy

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4
Q

Causes of Increased Intracranial Pressure

A

1) Tumor
2) Infections
3) Hemorrhage or Hematoma
4) Infarction
5) Trauma
6) Cerebral Edema
7) Hydrocephalus
8) Pseudotumor Cerebri

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5
Q

Effects of Increased Intracranial Pressure

A

1) Headache
2) Vomiting
3) Papilledema - Optic Atrophy
4) Brain Herniations

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6
Q

Types of Brain Herniations

A

1) Mid-Line Shift
2) Tentorial Herniations
3) Tonsillar Herniations
4) Caudal Shift of Brain Stem

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7
Q

Types of Disturbances of Conciousness

A

1) Confusion (Disorientation)
2) Syncope
3) Lethargy
4) Stupor
5) Coma

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8
Q

Non-Communicating Hydrocephalus

A

Occurs when the flow of CSF is blocked along one or more of the narrow passages connecting the ventricles.

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9
Q

Communicating Hydrocephalus

A

CSF can still flow between the ventricles, which remain open

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10
Q

Causes of Hydrocephalus

A

Congenital

Acquired:
Trauma, Infection, Hemmorhage

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11
Q

Anencephaly

A

Serious birth defect in which a baby is born without parts of the brain and skull

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12
Q

Types of Spina Bifida

A

Occulta: Posterior Arch

Meningocele: CSF goes through Posterior Arch, Spinal Cord stays forward

Myelomeningocele: CSF & Spinal Cord go through the Posterior arch

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13
Q

Spina Bifida: Patient features

A

1) Acrania
2) Protruding Eyes
3) Long Arms

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14
Q

Syringomyelia (Syrinx)

A

Fluid-Filled Cyst forms in the Spinal Cord

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15
Q

Trisomy 21: Features

A

[Down Syndrome]
- Single Palmar Crease
- Intestinal Stenosis
- Hypotonia
- Umbilical Hernia
- Congenital HeartDefects
- Epicanthal Folds

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16
Q

Trisomy 18: Features

A

[Edwards Syndrome]
- Prominent back of head
- Low-set ears
- Cleft Palate/Small Mouth & Jaw
- Clenched Fist Hands
- Clubfeet w/ webbed or fused toes

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17
Q

Trisomy 13

A

[Patau Syndrome]
- Palm Crease
- Flat back of head
- Dental Abnormalities
- Congenital heart Disease
- Enlarged Colon
- Umbilical hernia
- Unilateral or Bilateral Absence of 1 Rib

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18
Q

Cerebral Palsy

A
  • Cognitive Impairment
  • Slurred Speech
  • Lack of Muscle Control
  • lack of Bowel Control
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19
Q

Neurofibromatosis

A
  • Tumors form on Nerve Tissue
    (Brain, Spinal Cord & Nerves)
  • Noncancerous
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20
Q

Neurofibromatosis Type 1

A

[Childhood - Chromosome 17]
- “Von Recklinghausen Disease”
- Multiple benign skin & peripheral nerve tumors
- Cafe-au-lait spots

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21
Q

Neurofibromatosis Type 2

A

[Early Adulthood - Chromosome 22]
- Central type, B/L Acoustic Neuromas (8th Nevre)
- Deafness
- 7th CN Compression

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22
Q

Trigeminal Neuralgia (Tic Douloureux)

A
  • Light touch = Painful
  • Trigger Zone on face or Intraoral
  • 45+ years old
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23
Q

Associated Lesion with Arnold-Chiari

A

Kinking of Dorsal Aspect of lower Medulla/Upper Cervical Cord

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24
Q

Sturge-Weber Syndrome: What is it?

A

Cavernous Hemangioma, Port-Wine Stain
Calcifications along Deep Layer of Cortex

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25
Q

Sturge-Weber Syndrome: Clinical Features

A

1) Mental Retardation
2) Hemiparesis
3) Associated with Seisures

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26
Q

CerebroVascular Accidents Types

A

Hemorrhagic Stroke

Ischemic Stroke

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27
Q

Hemorrhagic Stroke: General Info

A
  • Subarachnoid or Intracranial
  • 10% of all strokes
  • Most serious in Consequence
  • Loss of Conciousness
  • MCly Causes Death
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28
Q

Ischemic Stroke: General info

A
  • 90% of all Strokes
  • NO loss of Consciousness
  • May occur slowly
  • Global or Regional
  • Regional Preceded by TIA’s
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29
Q

Ischemic Stroke: [Global Ischemia] Cause & What is at Risk?

A

Cause: Widespread Hypoxia or Hypotension
At More Risk:
- Neurons > Glial Cells
- Pyrimidal cells of Sommers (Hippocampus
- Purkinjie cells (Cerebellum)
- Water-Shed Infarction
- Laminar Necrosis

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30
Q

Water-Shed Infarction: Arteries Involved

A

Anterior & Middle Cerebral Arteries

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31
Q

Laminar Necrosis: Cortex Layers Involved

A

4th & 6th Cortical Layers

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32
Q

Embolic Stroke

A

[Regional]

  • Thromboemboli, Gas Embolism, Fat Embolism etc
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33
Q

Thrombotic Stroke

A

[Regional]
- From Thrombi in the Cerebral Arteries themselves

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34
Q

Results of Ischemic Stroke

A

1) Loss of Neurons
2) Liquefactive Necrosis
3) Fluid-Filled Cyst in Brain

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35
Q

Congenital Berry Aneurysm

A
  • (Saccular) forms on Circle of Willis
  • Born w/ weakness in vessel @ bifurcation point
  • Rupture suddenly to produce subarachnoid hemorrhage
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36
Q

(%) of Aneuryms at MC Arteries

A

35% Internal Carotid Complex
30% Anterior Communicating Artery
30% Trifurcation
5% Other Sites

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37
Q

Atherosclerotic Aneurysm

A
  • Due to Weakening of vessel wall by atherosclerosis
  • Larger Arteries (Circle of Willis or its branches)
  • Larger Aneurysm may have symptoms (mass effect)
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38
Q

Charcot-Bouchard Aneurysm

A
  • Microaneurysm that develops on Striate Arteries of a damaged artery wall
  • Basal Ganglia or Internal/External Capsule
  • Prior Hx of Chronic Hypertension
  • Rupture -> Intracerebral Hemorrhage in brain tissue itself
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39
Q

What is a histological sign of previous hemorrhage?

A

Hemosiderin-Laden Macrophages

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40
Q

Arteriovenous Malformations: Etiology, Symptoms & Presentation

A
  • Congenital/Asymptomatic
  • Presentation: Spontaneous Hemorrhage
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41
Q

Arteriovennous Malformations: Effect after Rupture

A

Sudden Loss of Consciousness & Death in a young Individual in association with an episode of HBP

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42
Q

Types of Acquired CNS Diseases

A

1) Trauma
2) Circulatory
3) Infections
4) Demyelinating Disorders
5) Degenerative Diseases
6) Vitamin Deficiencies
7) Neoplasms

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43
Q

Coup vs. Countrecoup Contusion

A

Coup: contusions on the brain are directly below the point of trauma

Contrecoup: contusions on the brain are directly opposite the point of trauma.

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44
Q

Penetrating Injury: High velocity Bullet

A
  • Entry wound & Exit wound
  • Gases behind bullet expand immediately creating instantaneous increased pressure
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45
Q

Penetrating Injury: Low Velocity Bullet

A
  • Entry Wound only (bullet lodged in brain)
  • Hemorrhage along track of bullet & edema that cause increased pressure
  • Slower
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46
Q

Spinal Cord Hyperextension

A
  • Posterior Contusion
  • Rupture of Anterior Spinal Ligament
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47
Q

Spinal Cord Hyperflexion

A
  • Anterior Contusion
  • Teardrop Fracture Anterior Lip of Vertebrae
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48
Q

Hemisection of the Cord-Brown-Sequard

A
  • Ipsilateral Paralysis: Loss of fine touch, Vibration & Position Sense
  • Contralateral: Loss of Pain & Temperature
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49
Q

Complete Transection

A

Pressure that develops following the injury because of Inflammation

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50
Q

QQ: Dementia can be temporary state of loss of entail and intellectual function brought on by drugs, acid-base imbalances, infectious disease, or conditions brought on by dehydration. (T/F)

A

False

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51
Q

QQ: The Etiology of Cerebral Palsy is:

A

Mechanical

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52
Q

QQ: Which of the following pathological findings is not associated with Arnold Chiari Malformation?

A

Enlarged Occipital Fossa

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53
Q

QQ:Congenital obstructive hydrocephalus is usually associated with a decreased absorption of CSF at the Arachnoid Granulations. (T/F)

A

False

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54
Q

QQ: Which of the following is not a neuroglial cell of the CNS?
Astrocytes, oligodendrocytes, Microglial Cell, Schwann cell

A

Schwann Cell

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55
Q

QQ: All of the following are classic features of an increase in intracranial pressure, EXCEPT: papilledema, the presence of calcium soft tissue deposits, headaches, vomiting

A

The presence of calcium soft tissue deposits

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56
Q

QQ: A concussion is defined as a temporary loss of conscious awareness following head trauma with visible organic brain injury as evidenced on an MRI or other radiographic studies. (T/F)

A

False

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57
Q

QQ: The mononuclear phagocytic cell of the CNS is called a:

A

Microglial Cell

58
Q

QQ: Which one of the following changes within a cell is considered irreversible?
cloudy swelling, membrane bleb formation, pyknosis, hydropic change

A

Pyknosis

59
Q

QQ: Most of the causes of disease that eventually affect the CNS actually begin in the brain. (T/F)

A

False

60
Q

QQ: An atherosclerotic aneurysm is described as a ______ aneurysm.

A

Fusiform

61
Q

QQ: The type of CVA that most often causes loss of consciousness is an ischemic CVA. (T/F)

A

False

62
Q

QQ: Cerebral palsy in a premature infant most likely will eventually demonstrate:

A

Signs of Paraplegia

63
Q

QQ: The flaccid paralysis often associated with the neurological deficits of polio are described as a/an:

A

Lower motor neuron lesion

64
Q

QQ: A meningocele typically presents with the presence of a cyst protruding from the spine that contains CSF, spinal nerves, and a portion of the spinal cord. (T/F)

A

False

65
Q

QQ: Ruptured bridging veins from the surface of the brain produce an epidural hematoma. (T/F)

A

False
(Sub dural hematoma)

66
Q

QQ: Contrecoup injuries of the brain:

A

Are brain contusions that occur opposite the area of trauma to the head of a falling person.

67
Q

QQ: A progressively enlarging cyst in the spinal cord that begins in the posterior columns and presents with loss of sensation across the shoulders in a cape-like distribution is referred to as a Syringomyelia.
(T/F)

A

True

68
Q

All of the following are associated with Sturge-Weber syndrome, EXCEPT:
mental retardation, cavernous hemangioma, calcium deposition in the frontal lobes, Meningocele

A

Meningocele

69
Q

QQ: The mechanism of hydrocephalus caused by Arnold-Chiari malformation is:

A

Obstruction due to tonsillar herniation

70
Q

QQ: A Lewy body inclusion is associated with

A

Parkinson’s Disease

71
Q

QQ: The type of CVA that most often causes loss of consciousness is an ischemic CVA. (T/F)

A

False

72
Q

QQ: The most common cause of an acquired form of demyelination disease is multiple myeloma. (T/F)

A

False

73
Q

QQ: The rupture of bridging veins connecting to the dural venous sinuses produce:

A

a Subdural hematoma

74
Q

QQ: The most common site of primary tumors found in the CNS in children is:

A

Infratentorial

75
Q

QQ: The most common type of neoplasms found in the Central Nervous System are what?

A

Metastatic Tumors

76
Q

QQ: Perivascular cuffing is a classic feature seen in viral meningitis. (T/F)

A

False

77
Q

QQ: Cowdry bodies are a type of inclusion body observed in neural tissue associated with:

A

Herpes Simplex Virus

78
Q

QQ: Beta amyloid plaques are commonly associated with:

A

Alzheimer’s Disease

79
Q

QQ: General Paresis Neurosyphillis affects:

A

Frontal lobes of the brain

80
Q

Non-Mitotic Neuron

A

(Permanent)
No replacement if injured

81
Q

Parenchymal Cells

A

Function cells of the Nervous System

82
Q

Mature Neurons

A

Have No Neoplasms

83
Q

Injury to neurons may produce:

A

1) Chromatolysis, Pyknosis
2) Wallerian Degeneration
3) Neuronophagy
4) Inclusion Bodies: (cytoplasmic vs. intranuclear)

84
Q

Death of neurons produces:

A

Liquefactive Necrosis & in late stages formation of a Fluid-Filled Cyst

85
Q

Astrocytes: General Info

A
  • Most numerous in the NS
  • Major supporting cell in brain
  • Formation of blood-brain barrier
86
Q

MC cell that causes of Primary Neoplasms of the CNS

A

When ASTROCYTES after injury create gliosis
(Equivalent of fibrous scar somewhere else)

87
Q

Oligodendrocytes: Function & Damaged in What Diseases?

A
  • Myelination in the CNS
  • Damaged in Demyelinating diseases & Leukodystrophies
88
Q

Ependymal Cells: Location & Function

A
  • Single layer of cells lining ventricles of brain & central canal of spinal cord
  • Produce plasma ultrafiltrate (CSF)
89
Q

Ependymal Cells: Features

A

1) Cilia: keep CSF flowing
2) In some areas, Masses of capillaries derived from pia mater called Choroid Plexus

90
Q

Microglial Cells: Origin & What are They?

A
  • Origin: Blood Monocytes
  • Phagocytes of the CNS that form microglial nodules or take up lipid to form foamy macrophages known as “Gitter cells”
91
Q

What are Brain Herniations?

A
  • Increase in ICP leading to herniation of intracranial CNS structures
  • Eventually develop “false localizing signs”
92
Q

Subfalcine (cingulate gyrus) Herniation:

A

“Mid-line shift”
- MC cerebral hernia
- Pushes Ipsilateral cingulate gyrus down under flax cerebri

93
Q

Tentorial Herniation

A

Movement of brain tissue from one intracranial compartment to another (Like midbrain going down into brain stem area)
- Includes: Uncal, Central & Upward Herniations

94
Q

Tonsillar Herniation

A

Cerebellar tonsils through foramen magnum

95
Q

Caudal Shift of Brain Stem

A

“Transtentorial Herniation”
“Duret Hemorrhage”
- Brain stem falls through notch

96
Q

Sturge-Weber Syndrome: Radiology, Associated with, & Clinical Features

A
  • Calcify creating “Rail-Track” X-ray pattern
  • Associated with Seizures
  • Mental retardation & Hemipoesis
97
Q

Epidural Hemotoma

A
  • Between skull and outer most layer of meninges (dura mater) @ Sutures
  • Involves artery, so can occur faster
98
Q

Subdural hematoma

A
  • Between Dura Mater & Arachnoid Layer
  • Blood escapes forming a clot putting pressure on the brain
99
Q

Neoplasms of the Nervous System: Clinical Features

A

1) Compression causing Cerebral edema
2) Inefficient Ducts
3) Neovascularization
4) Hydrocephalus from interference of CSF flow

100
Q

Neoplasms of the Nervous System: Abnormal Stimulations

A
  • Sensory or Motor (smells, sights, sounds)
  • Jacksonian Epilepsy
101
Q

Jacksonian Epilepsy

A

Peripheral twitching of (opposite side) extremities progressive to proximal muscle

102
Q

MC Type of Glioma

A

Astrocytoma

103
Q

Astrocytoma

A
  • Low Grade (1), grow slowly but INFILTRATE, so hard to resect
  • 5 year survival rate (50% if Dx early)
  • Some response to radiation
104
Q

Glioblastoma Multiforme

A
  • Grade 4 Malignant Astrocytoma
  • 33% of all Gliomas
  • Forms butterfly tumor across mid-line -> Necrosis
  • 20% 1 year survival
105
Q

Juvenile Pilocytic Astrocytoma

A
  • 25% of al brain CA’s
  • Children under 10
  • Operable, Good Prognosis
106
Q

Oligodendroglioma

A
  • Mid-life tumor
  • 5-10 year post surgery survival
  • 90% have calcification on radiograph (Speckled)
  • Good prognosis
107
Q

Ependymoma

A
  • Brain: 60% in 4th Ventricle
  • Children & Young Adults
  • Mid-Life in Spinal Cord
108
Q

Medulloblastoma

A
  • Children & Young Adults
  • Cerebellum
  • Histological Rosette (characteristic sign)
  • Metastasize via CSF to Spinal Cord
  • 70% 5 Year Survival
109
Q

Meningioma

A
  • Tumor had Progesterone receptors
  • Well circumcised mass attached to Dura
110
Q

Meningioma: Microscopy

A
  • Psammoma Bodies(concentric laminated Ca2+ rich)
  • Whorled Pattern
  • Meningothelial Cells
111
Q

Lymphoma

A
  • Primary to Brain (PBL)
  • Transplant/AIDS patients (Immunocompromised)
  • B-Lymph variety
112
Q

Secondary Neoplasm

A
  • Metastasis to Brain
  • Meminges involved in Acute Leukemias
113
Q

Secondary neoplasms: Metastasis order

A

Lung, Breast, Skin, Kidney, GI Tract

114
Q

Craniopharyngioma: Embryonic

A
  • Remnant of foregut 5% of brain cancers
  • 2nd to 3rd decade of life
115
Q

Craniopharyngioma: What does it Form in the Body?

A
  • Encapsulated cyst with calcification around cholesterol crystals
  • Superior to Sella Turcica
116
Q

Craniopharyngioma: May Compress what Structures?

A

1) Hypothalamus (pituitary/growth retardation)
2) Optic Chiasm (visual defects)
3) 3rd Ventricle (hydrocephalus, headaches)

117
Q

Guillain-Barre Syndrome: Etiology

A
  • Follows Viral Infection, few after Immunization
  • Autoimmune Destruction
118
Q

Guillain-Barre Syndrome: Microscopy

A
  • Poly Radiculopathy
  • Demyelination of nerve roots/Cranial nerves
119
Q

Guillain-Barre Syndrome:Clinical features

A

[Ascending paralysis]
- Tingling/weakness in extremities (feet)
- Migrate superior in (2-4 week period)
- Severe: Facial paralysis & Respiratory Failure
- Improvement takes several months

120
Q

Guillain-Barre Syndrome: treatment

A

Supportive Physical therapy
Chiropractic Expedites Recovery

121
Q

Myasthenia Gravis: Etiology

A
  • Unknown, 15% have autoimmune diseases
  • Lupus, RA
122
Q

Myasthenia Gravis: Pathology

A

[Auto-Immune-Develops Antibody to ACh receptor]
Lymphocytic Infiltration
Thymus Hypertrophy (60-70% cases)

123
Q

Myasthenia Gravis: Clinical Aspects

A
  • 20 to 40 year olds
  • Eyes: ptosis, diplopia
  • weakening facial, pectoral girdle, neck flexor & respiratory muscles
124
Q

Myasthenia Gravis: Course of Time

A

5-20 years (symptoms waxing & waning throughout)

125
Q

Myasthenia Gravis: Treatment

A

Management: Anticholinesterase/Corticosteroid
- Prednisone
- Remove Thymus
- Limit activity in Summer Months

126
Q

Trigeminal Neuralgia (Tic Douloureux): Treatment

A
  • Anticonvulsant Drugs
  • Local Cauterization of receptor Asensory
  • Cryosurgery
127
Q

Facial Paralysis (Bell’s Palsy): Cause, Population, Onset

A

Cause: Unknown (post-viral inflammatory??)
Population: Adult
Onset: Acute (side exposed to cold air

128
Q

Facial Paralysis (Bell’s Palsy): Symptoms

A

1) Pain around Ear or in Mandible
2) Paralysis of unilateral facial muscles
3) Eye cannot close: biggest problem (no blink reflex)

129
Q

Facial Paralysis (Bell’s Palsy): Treatment & Recovery

A

Tx: Corticosteroid, PT, Artificial tears, Eyepatch
Recovery: 80% full recovery in a few weeks

130
Q

Diabetic Neuropathy: Pathogenic Hallmarks

A

1) Microangiopathy of Vasa Nervosum
2) Loss of Axons/Axonal Atrpohy
3) Demyelination

131
Q

Toxic Neuropathy: Pathological Features

A

[By drug ingestion/chemical abuse]
- Axonal Degeneration/Transport
- Myelin Damage
- Peripheriral Neuron energy Metabolism

132
Q

Schwannoma: Definition

A

Benign nerve sheath tumor arising from differentiated Schwann Cells

133
Q

Neurofibroma: Components

A

1) Transformed Schwann cells
2) Non-neoplastic Fibrous Component
3) Fibroblasts

134
Q

Toxic Neuropathy: Tissues Affected by Toxicity

A

1) Ranvier Node
2) Ion Channels
3) Small Fibers

135
Q

Schwannoma: Pathological Features

A
  • Encapsulated, well-circumcised
  • Zonal pattern (Antoni A)
  • Nuclear Palisading (verocay Bodies)
  • Hypocellular component (Antoni B)
136
Q

Schwannoma: Pathophysiology

A

Occur with: NF2, Carney Complex, Schwannomatosis
- Tumor Suppressor Gene “Schwannomin” dysfunc.

137
Q

Schwannoma: Microscopy

A

Biphasic, Nuclear Palisading around Verocay Bodies
- Narrow cells interspersed with collagen fibers
- Dense Chromatin
- Nuclear Atypia, Cystic Degeneration & Hemorrhage

138
Q

Neurofibroma: Essential Features

A

1) Elongated cells w/ dark wavy stained nuclei
2) Collagen Bundles & Mast Cells
3) Monomorphic Comma Shaped Nuclei

139
Q

Neurofibroma: Etiology

A
  • Caused by “Biallalic” Inactivation of Tumor Suppressor gene NF1
140
Q

Neurofibroma: Sites

A

[Benign]
Localized: Superficially Evenly on Body Surface
Diffuse: Head & Neck Region
Plexiform: Major Nerve Trunk