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Patho > Pathology of the Central Nervous System > Flashcards

Pathology of the Central Nervous System Flashcards

1
Q

Nervous system is largely comprised of

A

Permanent cells (neurons) and stable cells (glia)

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2
Q

Do the CNS have an ability for. exansion

A

CNS exists within a physically unyielding and restrictive environment (the skull and spinal canal) with little ability for expansion
- Increased intracranial pressure is an event common to many pathological conditions

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3
Q

Human brain damage

A

Human brain exhibits remarkable regional specialization of function; clinical loss of function may result from damage to extremely small and specific regions
- Many diseases are the result of dysfunction at the level of receptors and transmitters, without apparent morphological changes

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4
Q

Blood-Brain-Barrier

A

Physico-chemical system regulating movement of nutrient and chemical into and out of the CNS
- BBB includes transporter that prevent surges of nutrients/AAs and neurotransmitter
- Primary BBB resides at the level endothelial cells, joined by tight junction to prevent promiscuous entry
- Astrocytes provide secondary BBB, fluid volume control

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5
Q

Where do BBB resides at?

A

The level of endothelial cells, joined
by tight junctions to prevent promiscuous entry

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6
Q

What provides secondary BBB

A

Astrocytes; fluid volume control

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7
Q

Cerebral Spinal Fluid

A

Transudate of blood formed by specialized cells (choroid plexus) within ventricles
- 600mL of CSF formed daily. 125-150mL in ventricles at any one time
- CSF replaced multiple times at each day
- CSF contains 0-6 WBCs/mL, 50-75mg/dL glucose (60% of serum glucose levels)
- CSF pressure is 80-180 mm water (5-14 mmHg) recumbent

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8
Q

CSF may be sampled

A

by Lumbar puncture

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9
Q

Where is transudate of blood formed

A

by specialized cells (choroid plexus) within ventricles

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10
Q

What do each part of the brain

A

Frontal Lobe
Parietal Lobe
Occipital Lobe
Temporal Lobe
Cerebellum
Brain Stem

Screen Shot

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11
Q

Frontal Lobe

A
  • Problem solving
  • Speaking
  • Emotional traits
  • Reasoning
  • Voluntary motor activity
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12
Q

Brain Stem

A
  • Breathing
  • Temp
  • Digestion
  • Sleep/Alertness
  • Swallowing
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13
Q

Cerebellum

A
  • Balance
  • Coordination and control of voluntary movement
  • Fine muscle control
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14
Q

Temporal Lobe

A
  • Understanding language
  • Behavior
  • Memory
  • Hearing
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15
Q

Occipital Lobe

A
  • Vision
  • Color perception
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16
Q

Parietal Lobe

A
  • Knowing right from left
  • Sensation
  • Reading
  • Body orientation
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17
Q

Somatic Sensory Nuclei

A

Gets information by afferent sensory information

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18
Q

Somatic motor nuclei

A

Sends efferent signals to muscle and glands via the ventral root

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19
Q

Pattern of Pyramidal Motor Neuron Injury

A
  • Upper motor neuron injury (‘brain injury’)
  • Lower motor neuron injury (‘cord injury’)
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20
Q

Upper motor neuron injury (‘brain injury’)

A
  • Primarily contralateral involvement
  • Spastic paralysis, contractures
  • Muscle is hypertonic
  • Minimal atrophy
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21
Q

Lower motor neuron injury (‘cord injury’)

A
  • Flaccid paralysis
  • Prominent atrophy
  • Contractures
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22
Q

Extrapyramidal Motor System

A

Function to fine tune and adjust action of the pyramidal system to enhance their precision and maintain muscle tone and posture
- Control automatic voluntary movements (eg. walking, riding a bicycle); inhibits involuntary movements
- Actions are involuntary and capable of great speed and precision

Input arises from deep brain nuclei, including the striate ganglia, substantia nigra, red nucleus
- Acts on ipsi and contralateral motor functions
- Damage causes increased muscle tone and rigidity or chorea (sudden involuntary movements)

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23
Q

Where do the extrapyramidal motor system input arises from?

A

Input arises from deep brain nuclei, including the striate ganglia, substantia nigra, red nucleus

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24
Q

What do Extrapyramidal Motor System do?

A

Functions to ‘fine-tune and adjust’ actions of the pyramidal system to enhance their precision, and maintains muscle tone and posture
- Controls automatic voluntary movements (eg. walking, riding a bicycle); inhibits involuntary movements

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25
Q

Cerebellar Dysfunctions

A

Ataxia:
- Disturbance of posture and gait which doens’t get worse when patient closes his/her eyes
- Patient will swerve or fall to injured side
- Decompensation of movement
- Dysmetria: inability to stop movement (past-pointing)
- adiadochokinesia
- scanning speech

Tremor
- Intention tremor that is absent at rest

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26
Q

Fine Touch Proprioception Vibration

A

(Primary Sensory) neuron synapses in the medulla ==> (Secondary sensory) neuron crosses midline of body in medulla ==> (Synapse with) tertiary sensory neuron in the THALAMUS ==> (Tertiary sensory) neuron terminates in somatosensory cortex

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27
Q

Irritants, Temperature, Coarse Touch

A

(Primary Sensory) neuron synapses in dorsal horn of spinal cord ==> (Secondary sensory) neuron crosses midline of body in spinal cord ==> (Synapse with) tertiary sensory neuron in the THALAMUS ==> (Tertiary sensory) neuron terminates in somatosensory cortex

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28
Q

Sensory and Proprioceptive Functions

Loss of it will cause

A
  • Inability to assess limb position
  • Astereognosis
  • Loss of two point discrimination
  • Loss of vibratory sense
  • Loss of pain, pressure, heat sensation
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29
Q

Cells of CNS

A

Neurons
Astrocyte
Oligodendroglia
Microglia
Ependyma

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30
Q

Neurons

A

Parenchymal unit of CNS

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31
Q

Astrocyte

A
  • Supporting glial cell
  • provides trophic maintenance of neurons
  • Contributes to BBB
  • 10:1
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32
Q

Oligodendroglia

A
  • Cell membrance supplies myelin to multiple axons in CNS
  • Myelin in PNS is provided by Schwann cells
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33
Q

Microglia

A
  • Immune cell of CNS
  • Derived from circulating monocytes
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34
Q

Ependyma

A
  • Line the CSF-containing ventricular system
  • Modified ependyma (choroid plexus) forms CSF
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35
Q

Diseases of the Nervous System

A
  • Developmental Disorders
  • Vascular Pathology and Trauma
  • Tumors
  • Demyelinating Disease
  • Degenerative Conditions
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36
Q

Developmental Neuropathology

A

1-5% of newborns have a CNS anomaly
May be caused by
- genetic defects
- drugs
- toxin/toxicants (often via maternal behavior)
- nutritional abnormalities,
- Infections (TORCH: Toxoplasmosis, Rubella, CMV, Herpes, Zika)
- Perinatal injury
- Most congenital defects are idiopathic

Consequences usually permanent

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37
Q

When is CNS most vulnerable?

A

During early gestation
- Early lesions are more severe
- Consequences usually permanent

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38
Q

Window of Vulnerability in Brain Morphogenesis

A

Initial Morphogenesis
Normal Differentiation
Neural Stabilization

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39
Q

Initial Morphogenesis

A
  • Neural Induction/commitment
  • Cell Proliferation
  • Dysraphism (1st trimester)
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40
Q

Normal Differentiation

A
  • Migration
  • Aggregation
  • Migration Disorders (2nd trimester)
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41
Q

Neural Stabilization

A
  • Cytodifferentiation
  • Synapse formation
  • Differentiation disorders (3rd trimester)
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42
Q

Neural Tube Fusion

A

Lead to Fetal death and dysraphisms (NTDs)

Can be caused by:
- Carcinogens
- Heavy metals
- Hormones
- Antimitotic agents
- Vitamin A excess
- Folic acid deficiency

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43
Q

Craniorachischisis Totalis

A
  • Failure of neural tube closure along it’s full length
  • Absence of mature neural tissue and related structures (eg. calvarium)

Incompatible with life

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44
Q

Encephalocele

A
  • Failure of anterior neural tube to fuse
  • Incomplete formation of brain and calvarium
  • Formation of CSF-filled sac
  • Lesions is very severe

Lesser encephaloceles may be compatible with life

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45
Q

Meningocele

A

Meningoceles contain meninges and CSF, but no formed portion of brain
- Lesions vary widely in severity. If large the likelihood of rupture or infection is substantial
- Moderate lesions may be surgically repaired with survival
- Alpha-fetoprotein is elevated in ALL DYSRAPHISMS
– Test is used in prenatal screening

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46
Q

What do they for in prenatal screening for Meningocele

A

Alpha-fetoprotein is elevated
in all dysraphisms

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47
Q

Types of Spina Bifida

A

Spina Bifida Occulta (less sever)
Meningocle (sever)
Myelomeningocele (most sever)

48
Q

Neuronal Migration

A

It causes Structural abnormalities (eg. microcephaly, agyria), Heterotopias, and Seizure disorders

Can be caused by
- Antimicrotuble agents
- Heavy metals
- Alcohol
- Pharmaceutical
- Pesticides
- Polychlorinated biphenyls

49
Q

Differentiation

A

Causes:
- Structureal abnormalities (subtle)
- Pathway deficits
- Psychomotor deficits
- Epilepsy
- Delayed neurotoxicity

Caused by:
- Alcohol
- Pharmaceuticals
- Heavy metals
- Drugs of abuse
- Dietary deficiency
- Polychlorinated biphenyls

50
Q

Hydrocephalus

A

An abnormal buildup of fluid in the ventricles (cavities) deep within the brain.

51
Q

Synaptogenesis

A

Casues
- Discrete neurological expression
- Psychomotor retardation
- Delayed neurotoxicity

Caused by
- Alcohol
- Heavy metal
- Industrial pollutants
- Pharmaceuticals
- Drugs of abuse
- Pesticides

52
Q

Crouzon’s Disease

A

genetic syndrome in which the seams of the skull fuse in abnormally

53
Q

Brain Vasculature

A

Brain is 2% of body weight but receives 15-25% of cardiac output, consumes 20% of oxygen used by body
- Brain blood flow is relatively constant over wide systolic pressures due to autoregulation but shows regional variation of flow according to activity
- Autoregulation fails when systolic BP <50mm Hg
- Arterial supply enter from outside-in
- Arterial vessel reduces diameter rapidly upon entering cortex; may events such as deposition of metastase occur at the gray-white junction
- BBB resides primarily at brain vascular endothelium
- Brain possesses little extracellular space

54
Q

Where is BBB

A

resides primarily at the brain
vascular endothelium

55
Q

Where do the arterial supply enter from?

A

Outside in
- Autoregulation fails when systolic BP <50mm Hg

56
Q

What do autoregulation do for the brain?

A

Keeps the Brain blood flow relatively constant over wide systolic pressures
- shows regional variation of flow according to activity

56
Q

What do autoregulation do for the brain?

A

Keeps the Brain blood flow relatively constant over wide systolic pressures
- shows regional variation of flow according to activity

57
Q

Vasucular Disease of the CNS

A
  • Intracranial Pressure
  • Vessel distribution/Circle of Willis

caused by
Aneurysms
Atherosclerosis
Strokes and CVAs
Intracranial pressure
Hematomas and traumatic events
- epidural (middle meningeal artery)
- Subdural (bridging veins)

58
Q

Aneurysms

3mm-1cm

A

Most common in the Circle of Willis
- Most common (80%) at branch point of internal carotid artery
- Berry (saccular) aneurysm is rarely congenital; is. acquired with maturity and is present in 2% of adult population
- Atherosclerotic aneurysm are fusiform and commonly involve the basilar artery
- Rupture of either type is commonly fatal (25-50% die with first bleeding); next bleeds are worse
- 3-% of rupture occure with acute increases of intracranial pressure

Most common cause of non-traumatic subarachnoid beeding

59
Q

What causes the Thunderclap headaches

A

Aneurysms

60
Q

Aneurysm is the most common cause of

A

non traumatic subarachnoid bleeding

61
Q

Atherosclerotic aneurysms are

A

Fusiform and commonly involve basilar artery

62
Q

Cerebral Artery Aneurysm Treatment

A

Clip placed on the neck of the aneurysm
- Need surgury

Platinum wire is inserted into aneurysm until it is filled with coils => forced thrombus
- No breaking of skull is needed
- Leaking is possible

Flow Diversion Stent

63
Q

Cerebrovascular Atherosclerosis

A

Involves larger vessels such as carotid, middle cerebral, basilar arteries
- Embli arising in atherosclerosis is a primary source of cerebral vascular accidents (stoke)
- With advanced therosclerosis, patients suffering a drop in BP may develop infarcts in the absence of occlusion (watershed infarcts)
- Chronic vascular insufficiency contributes to development of dementia (eg,. sleep apnea)
- Small emboli/platelet clots may cause transient ischemic attacks (TIAs); doesn’t cause neuronal death
– anticipate full stoke within several months of TIA

64
Q

What vessels Cerebrovascular Atherosclerosis involve?

A

Larger vessels like carotid, middle cerebral, basilar arteries

65
Q

An advanced atherosclerosis + drop in BP

A

May develop infarcts in the absence of occlusion (watershed infarcts)
- means blood flow drops

66
Q

What is the primary source of cerebral vascular accidents (stokes)

A

Emboli arising in atherosclerosis a primary source of cerebral vascular accidents

67
Q

What do chronic vascular insufficiency contributes to?

A

Development of dementia

68
Q

Stroke

A
  • 65% of stokes (CVA) are ischemic, arising from thrombi or thrombo-emboli from atherosclerosis in brain or heart (valces, atrial fibrillation or vessels)
  • Emboli&raquo_space;> thrombi
  • 20% of strokes are hemorrhagic, usually involving the lenticulostriate branch of the middle cerebral artery (MCA)
  • hemorrhages stokes result from hypertension; often occuring while straining at stool or during sexual activity
  • Hemorrhages may be associated with use of thrombolytic drugs or anticoagulant
  • Causes upper motor neuron syndorm
  • Acute event involve impairment of BBB and edema
69
Q

What is more serious for stoke Emboli or thrombi

A

Emboli

70
Q

What do hemorrhagic stokes involves

A

lenticulostriate branch of the middle cerebral artery (MCA)

71
Q

Hemorrhagic stoke result from? associated with?

A
  • Usually result from hypertension; often occur while straining at stool or during sexual activity
  • Hemorrhages may be associated with use of
    thrombolytic drugs or anticoagulant therapy
72
Q

What do stokes causes

A

upper motor neuron syndrome

73
Q

Ischemic stroke Treatment

A

Drug management to lyse clot must begin <3.0—4.5 hrs into the event (control lipids)
- TPA iv; aspirin if emergent setting (need to be sure of the type)
- May require carotid endarterectomy or angioplasty/stenting

74
Q

Hemorrhagic Stoke Treatment

A

Goal is to control intracranial bleeding and pressure
- Discontinue any blood thinning (Coumadin, Plavix),
- Administer anti-pressor, and drugs to reverse anticoagulant
- May require surgery if bleeding continues and/or damaged vessel identified
- REHAB as early and aggressively as patient can manage

75
Q

t-Pa causes

A

Vessels to represses in the cold zone

76
Q

Ischemic Stroke can be identified through

A

Radioactive glucose dye
- Blood shunted according to activity and shows the cold zone

77
Q

Hemorrhagic Stroke; inside

A

Neurons going to die => liquified necrosis and removed

78
Q

Neural Trauma

A

Common cause of death and long term disability (25% of accidental death is due to head trauma)
- Among survival, >20% suffer permanent disability; 5% remain permanently vegetative

Underlying events include
- Hemorrhage
- Movement of brain inside skull with resulting concussion (coup/contre-coup)
- Diffuse axonal injury (DAI; tear axons)
- Infection and EDEMA from altered BBB

BBB disruption may be long standing

79
Q

Combat or sport injury

A

(‘closed-head’ injury)

80
Q

In U.S., most traumatic brain injury results from

A

vehicular accidents, falls and collisions with objects, criminal assault including child abuse (‘shaken-baby syndrome’)

81
Q

BBB disruption

A

may be long standing

82
Q

Diffuse Axonal Injury

A

Consequence of acceleration or deceleration of brain, with stretching and/or tearing of axons
- Result in SCATTERED LESIONS both in white and grey matter
- Injury develop over a period of hours to weeks; it is progressive and irreversible
- Occures in 50% of sever head trauma
- 90% of patients with sever head trauma never regain consciousness
- Seen in shaken baby syndrome, TBI, vehicular truama fall, ..
- Difficult to diagnose by imagining

83
Q

DAI result in

A

scattered lesions in both white and grey matter

84
Q

Can DAI recover

A

Injury develops over a period of hours to weeks; is progressive and irreversible

85
Q

Epidural Hemorrhage

A

Middle meningeal artery
- Generally acute, posttraumatic with skull fracture; Rapidly symptomatic
- A medical emergency

86
Q

Subdural Hemorrhage

A

Bridging veins
- Generally slow in onset, may become chronic
- May be spontaneous or result of minor trauma
- Most common in elderly

  • Headache (‘bursting’)
  • Projectile vomiting w/o nausea
  • Papilledema
  • High mortality without treatment
87
Q

Which hemorrhage happen posttraumatic event; Acute

A

Epidural

88
Q

Which hemorrhage happen in the middle of the meningeal artery

A

Epidural

89
Q

Which hemorrhage can become chronic

A

Subdural

90
Q

Which hemorrhage happen in the bridging veins

A

Subdural

91
Q

Intracranial Pressure (ICP)

A

Common in any space occupying condition:edema, tumor, hemorrhage, obstruction of CSF, trauma, Infections, etc.
- The higher the ICP the less promising the outcome
- Normal ICP 7-15 mmHg in supine adult; 20-25 mmHg may require treatment

Signs:
- Headache (made worse by coughing, sneezing, bending)
- Vomiiting w/o nausea
- Ocular effects (papilledema)
- Change in consciousness (ICP>50)
- Cheyne-Stokes respiration
- Reflex bradycarida (esp. in children)

Consequences:
- Increased CSF pressure
- Decreased cerebral perfusion
- Ischemia/necrosis
- Brain displacement
- Herniation

Treatment: aggressive
- Must maintain respiration and circulation, diruretics, hyperosmotic agents

92
Q

ICP Signs

A

Signs:
- Headache (made worse by coughing, sneezing, bending)
- Vomiiting w/o nausea
- Ocular effects (papilledema)
- Change in consciousness (ICP>50)
- Cheyne-Stokes respiration
- Reflex bradycarida (esp. in children)

93
Q

ICP Consequences and treatment

A

Consequences:
- Increased CSF pressure
- Decreased cerebral perfusion
- Ischemia/necrosis
- Brain displacement
- Herniation

Treatment: aggressive
- Must maintain respiration and circulation, diruretics, hyperosmotic agents (draw fluid out of brain)

94
Q

Unique Features of CNS Tumors

A
  • Do not have morphologically evident premalignant or in situ stages
  • Low-grade lesions may infiltrate large areas of brain, with serious clinical consequences, inability to be resected, and poor prognosis
  • Anatomic site can influence outcome independent of histological classification (eg. positional malignancy)
  • Even highly malignant gliomas rarely spread outside the CNS
95
Q

CNS Neoplasia

A
  • Meningioma (benign)
  • Astrocytoma (malignant)
  • Glioblastoma multiforme (malignant)
  • Oligodendroglioma
  • Medulloblastoma
  • Metastasis (most common)
96
Q

Rule of 70’s

A
  • 70% of primary brain tumors in children are located in the posterior fossa
  • 70% of posterior fossa tumors are astrocytomas
  • 70% of primary brain tumors in adults are in cerebrum
  • 70% of primary brain tumors in adults are glioblastoma multiforme
97
Q

Signs/Symptoms of Brain Tumors

A
  • Headaches
  • Seizures
  • Cognitive/personality changes
  • Eye weakness
  • Nausea/vomiting
  • Speech disturbance
  • Memory loss
98
Q

70% of posterior fossa tumors

A

astrocytomas

99
Q

70% of primary brain tumors in children

A

are located in the posterior fossa

100
Q

70% of primary brain tumors in adults

A

glioblastoma multiforme

101
Q

70% of primary brain tumors in adults are in

A

cerebrum

102
Q

Clinical Features of Brain Tumors

A
  • Elevated intracranial pressure/compression due to space-occupying lesion
  • Cerebral edema
  • Irritative effects
  • Destruction of local tissue
  • Localizing signs reflecting areas of involvement ‘Positional malignancy’
  • Hydrocephalus
  • Rarely metastasize outside neuroaxis
103
Q

Meningioma

A

Arises from the meningeal layer (mostly from the dura mater): Most common benign (90%) intracranial tumor
- 1:1000 individuals, F>M: 40-70 years of age
- Mostly sporadic, some related to radiation to head

104
Q

Meningioma Signs and treatment

A

Signs/symptoms of elevated intracranial pressure.
- Most are clinically silent and slow growing

Treatment surgical, when location permits.
- Pre-surgical management includes trans-arterial embolization.
- Chemo not useful due to slow growth.
- Proton beam may be useful

105
Q

Where do Meningioma arise from

A

from the meningeal layer (mostly from the dura mater)

106
Q

What is the most common benign intracranial tumor

A

Meningioma

107
Q

Medulloblastoma

A
  • Predominantly in children
  • Exclusively cerebellar, may ‘seed’ along the CSF pathway
  • Highly malignant
  • Highly radiosensitive
  • With proper treatment, 5-year survival ~75%
  • Arises from neurons of the forming cerebellum
108
Q

A brain tumor that is most common in 40-70

A

Meningioma

109
Q

A brain tumor that is highly malignant

A

Medulloblastoma

110
Q

A brain tumor that arises from neurons

A

Medulloblastoma
- Arises from neurons of the forming cerebellum

111
Q

Glioblastoma Multiforme

A
  • Arises from astrocytes (astrocytoma GradeIV)
  • More common in males; over 50 years of age
  • No know cause
  • May arise from progression of lower grade astrocytoma or as full GM
  • Survival w/o treatment is <6 months
  • Survival w treatment ~14 months

Treatment is surgery + radiation; tumor is very resistant to conventional therapy

112
Q

Brain Metastasis

A

Account for ~50% of intracranial tumors

Common sites of primary tumor
- lung
- breast
- melanoma
- GI
- Kidney

Often occur at gray-white junction
- May present with paraneoplastic syndromes

Often treated with focused-beam radiation; palliative effect

113
Q

A brain tumor that arises from astrocytes

A

Glioblastoma Multiforme

114
Q

A brain tumor that is more common in adult men

A

Glioblastoma Multiforme

115
Q

a brain tumor with unknown cause

A

Glioblastoma Multiforme

116
Q

A brain tumor with 75% survival (5 years)

A

Medulloblastoma

Patho (17 decks)

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