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Pathology > Cns1 > Flashcards

Cns1 Flashcards

1
Q

Neuron

A

• Cell body
– Nucleus
– Cytoplasm

• Axon

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2
Q

Cortical Architecture

A

• Sixlayersparalleltosurface
– I. Molecular: glia, few small neurons
– II. External granular: small neurons with short axons
– III. Outer pyramidal: medium and large neurons
– IV. Inner granular: small stellate neurons
– V. Inner pyramidal: medium neurons, Beta cells
– VI. Polymorphic layer

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3
Q

Patterns of Injury in the Nervous System: Neuronal Injury

A

• Within 12 hrs. of an irreversible hypoxic- ischemic injury:

– Acute neuronal injury becomes evident – H&E staining
• Shrinkage of the cell body
• Pyknosis of nucleus
• Disappearance of the nucleolus
• Loss of Nissl substance
• Intense eosinophilia of cytoplasm
• Axonal swelling and disruption of axonal transport

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4
Q

Normal Cells
• Neurons

A

– Topographically organized
• Nuclei, ganglia, columns
– Functional domains have been assigned to many anatomic regions

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5
Q

Morphologic Patterns of Neuronal Injury

A
  • Coagulation necrosis
    – Hypoxic-ischemic injury
  • Apoptosis
    – Normal development
    – Some hypoxic-ischemic injury
    – Certain toxic agents
    – ? Aging and some neurodegenerative diseases
  • Chromatolysis
  • Cytoplasmic inclusions
    – Infections
    – Neurodegenerative disorders
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6
Q

Morphologic Patterns of Neuronal Injury

A
  • Axonal injury
    – Leads to cell body enlargement
    – Peripheral displacement of the nucleus
    – Enlargement of the nucleolus
    – Peripheral displacement of the Nissl substance
  • Acute injuries often result in a loss of the blood-brain barrier
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7
Q

Astrocytes in Injury and Repair

Principal cell responsible for repair and scar formation in the CNS

A

– Gliosis

Astrocytes undergo both hypertrophy and hyperplasia
– Fibroblasts play a limited role in repair following brain injury
– In long-standing gliosis:
• Astrocytic cytoplasm shrinks
• Cellularprocessesbecometightlyinterwoven
• Rosenthal fibers(thick,elongated,eosinophilicprotein aggregates in chronic gliosis and some low-grade gliomas

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8
Q

Oligodendrocytes

A

• Most common cells in white matter
• Smaller than astrocytes
• Production and maintenance of CNS myelin

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9
Q

Ependyma

A
  • Lines ventricular walls and central canal of spinal cord

* May be the target of infectious agents – CMV

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10
Q

Microglial Cells

A

• Derived from the bone marrow
• Function as the resident phagocytic cell of the CNS
• When activated by injury, infection, or trauma – Proliferate
– Take on the appearance of activated macrophages in areas of demyelination, organizing infarct, or hemorrhage

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11
Q

Features Unique to the Brain

A

• Function is localized within the nervous system
– It is inherently vulnerable to small focal lesions
– A given type of lesion produces different clinical symptoms when occurring in different parts of the CNS
– Different pathologic lesions can produce similar clinical symptoms when occurring in the same area of the brain

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12
Q

Features Unique to the Brain

A

• The brain has a number of unique anatomic features which offer protection against one form of pathologic insult while rendering it more vulnerable to another

– Blood-brain barrier
– Skull
– CSF (shock absorp)
– Selective vulnerability of some areas/neurons

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13
Q

Features Unique to the Brain

A

• Similar symptoms or clinical findings can be produced by different pathologic mechanisms
– Example:
• Papilledema
– Hydrocephalus
– Meningitis
– Tumor
– Abscess
– Other

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14
Q

Features Unique to the Brain

A

• Certain diseases are unique to neuropathology

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15
Q

Increased Intracranial Pressure

A

Cerebral Edema
Herniation
Hydrocephalus

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16
Q

Increased Intracranial Pressure

A

• Increase in mean CSF pressure above 200 mm H2O with patient recumbent

• Associated conditions:
– Mass effect:
• Diffuse: generalized edema
• Focal: localized edema, tumor, abscess, hemorrhage

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17
Q

Cerebral Edema

A

• Technically brain parenchyma edema
• May be caused by a number of diseases
• Major categories:
– Vasogenic edema
– Cytotoxic edema

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18
Q

Vasogenic Edema

A
  • Disruption of normal blood-brain barrier
  • Fluid escapes into the intercellular space
    – Brain has few lymphatics
    – Poor resorption of excess intercellular fluid
  • May be localized or generalized
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19
Q

Cytotoxic Edema

A

• Increased intracellular fluid
• Secondary to cellular injury
• In conditions associated with generalized edema, one frequently finds elements of both cytotoxic and vasogenic edema

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20
Q

Edema: Morphology

A

• Soft parenchyma
• Herniation may be a complication • In generalized edema:
– Gyri are flattened
– Sulci are narrowed
– Ventricular cavities compressed

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21
Q

Hydrocephalus

A

• Increased CSF causing enlargement of the ventricles
• Two types:
– Communicating: blockage outside the ventricular system
– Noncommunicating: blockage anywhere along the ventricular system

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22
Q

Hydrocephalus

A

• caused by decreased resorption of CSF
• Rarely caused by increased production
• Hydrocephalus ex vacuo: brain atrophy with compensatory expansion of ventricular system

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23
Q

Herniation: Types

A
  • Subfalcine
    – Cingulate gyrus under the falx cerebri
  • Transtentorial
    – Displacement of the uncus over the free edge of the opening of the tentorium
  • Tonsillar
    – Displacement of the cerebellar tonsils into the foramen magnum
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24
Q

Malformations

Neural Tube Defects

A

• Anencephaly: absence of the brain and calvarium
• Encephalocele: diverticulum of CNS tissue through a defect in the cranium
• Myelomeningocele: extension of CNS tissue through a defect in the vertebral column
• Meningocele: only meningeal extrusion

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25
Neural Tube Defects
• Spina bifida: may be asymptomatic bony defect or severe malformation
26
Forebrain Abnormalities
• Polymicrogyria: small, unusually numerous gyri • Megalencephaly & microencephaly: abnormally large or small volumes of brain • Lissencephaly: absence of gyri • Holoproprosencephaly: incomplete separation of cerebral hemisheres • Agenesis of the corpus callosum
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Neurons
Topographically organized - nuclei, ganglia, columns Functional domains have been assigned to many anatomic regions
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Posterior Fossa Abnormalities
* Arnold-Chiari malformation: small posterior fossa, malformed cerebellum with extension of the fermis through the foramen magnum, hydrocephalus, lumbar meningomyelocele * Dandy-Walker malformation: enlarged posterior fossa, absent or rudimentary cerebellar vermis, midline ependymal cyst
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Perinatal Brain Injury
* Cerebral palsy: any nonprogressive neurologic motor deficit attributable to injury in the prenatal or perinatal period * Intraparenchymal hemorrhage: premature infants
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Trauma
• Anatomic location of the lesion and the brain’s limited capacity for repair have great significance
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Blows to Head
• Penetrating • Blunt • Open • Closed • Repetitive episodes of trauma can lead to later development of neurodegenerative disorders – Alzheimer disease – Chronic traumatic encephalopathy
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Skull Fractures
* Displaced skull fracture – A fracture in which bone is displaced into the cranial cavity by a distance greater then the thickness of the bone * Diastatic – When the kinetic energy that causes a fracture is dissipated at a fused suture. – The fracture crosses sutures
33
Traumatic Parenchymal Injuries Concussion Contusion
* Concussion: clinical syndrome of alteration in consciousness. Usually includes sudden onset of transient neurologic dysfunction with complete recovery * Contusion: caused by rapid displacement, disruption of vascular channels, and subsequent hemorrhage, injury, and edema – Coup lesion: injury underlying the point of contact – Contracoup lesion: injury opposite the point of contact
34
Traumatic Parenchymal Injuries
• Laceration: penetration of an object with tearing of tissue • Diffuse axonal injury: axonal swelling in white matter. Result of angular deceleration or acceleration
35
Traumatic Vascular Injury • Epidural Hematoma
– Blood between dura & periostium of the skull – Caused by laceration of the middle meningeal artery – Patients may be lucid for hours between the moment of trauma & the development of neurologic symptoms – Neurosurgical emergency
36
Traumatic Vascular Injury • Subdural hematoma
– Blood between the dura mater and the arachnoid layer of the leptomeninges – Tearing of bridging veins – Most common over the lateral aspects of the cerebral hemispheres – Most often become clinically manifest within the first 48 hrs after injury
37
Subdural Hematoma Acute- Chronic-
* Acute: – Clear history of trauma | * Chronic: – Less frequently associated with well defined history of trauma – May be associated with brain atrophy
38
Traumatic Vascular Injury: Morphology
* Acute – Freshly clotted blood – Underlying brain parenchyma compressed * Chronic – Granulation tissue contracts – Rebleeding may be a problem
39
Sequelae of Brain Trauma
* Post-traumatic dementia • Post-traumatic hydrocephalus | * Epilepsy • Psychiatric disorders • Infectious disease
40
Hypoxia, Ischemia, and Infarction Vascular Disease
* Brain normally receives – 15% of cardiac output – ~20% of O2 consumed by the body – Requires a constant supply of glucose * Interruption of normal blood flow may produce irreversible injury (parenchymal)
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Vascular disease | • Autoregulation
– The brain is exquisitely sensitive to changes in blood flow – It is capable of regulating blood flow over a wide range of perfusion pressures
42
Hypoxia: Categories Functional hypoxia Ischemia Permanent
• Functional hypoxia – Low inspired PO2 – Impaired oxygen-carrying capacity of blood (anemia, hemog) – Inhibition of oxygen use by tissue • Ischemia – Transient • Interruption o fbloodflow – Permanent • Cessation of bloodflow
43
Principle Types of Acute Ischemic Injury
• Globalcerebralischemia(ischemic/hypoxic encephalopathy) – Results in generalized reduction in cerebral perfusion (shock) * Focalcerebralischemia – Reduction or cessation of blood flow to a localized area of the brain (clot) * Hemorrhage – Within the brain parenchyma or subarachnoid space
44
Global Cerebral Ischemia
• Outcome of severe hypotensive episode • Autoregulatory mechanisms unable to compensate – Systolic pressures fall below 50 mm/Hg • Outcome varies with severity and duration of insult
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Hypoxia / Ischemia
• Hypoxia: decrease in oxygen available to the tissues • Ischemia: decreased tissue perfusion
46
Sensitivity of CNS Cells to Hypoxic/Ischemic
• Neurons>glial cells • Pyramidal cells of the hippocampus • Purkinje cells of the cerebellum • Areas of the brain located at the junction of arterial territories (arterial border zones) – Wedge shaped infarcts
47
Morphology • Immediately after event: may appear normal
* In those surviving: softened, edematous * Early changes: 12 – 24 hrs. – Acute neuronal cells change (red neurons) – Similar changes in astrocytes and oligodendroglia
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Morphology • Subacute changes: 24 hrs. to 2 wks. – Necrosis of tissue – Influx of macrophages – Vascular proliferation – Reactive gliosis
• Repair – After 2 weeks – Removal of necrotic tissue and gliosis – Loss of normal CNS structure
49
Morphology •Neurons most susceptible to irreversible injury: – Pyramidal cells of Sommer’s sector of the hippocampus, Purkinje cells of the cerebellum, and pyramidal neurons in the neocortex
* Laminar necrosis of the neocortex | * Watershed Infarcts: – Wedge-shaped lesions in areas between major arterial distribution (border zone)
50
Hypoxic/Ischemic Injury: Clinical Features • May occur in the following circumstances: – Anything which results in a global decrease in the amount of oxygenated blood available to the brain
• Cardiac dysrythmias, shock, increase in intracranial pressure – Factors modifying the parenchymal injury • Age • Temperature • Duration
51
Focal Cerebral Ischemia: Infarction
•Cerebralarterialocclusionmayleadtoischemiaor infarction • Anatomiclocationofthelesiondeterminesthe symptoms • Caused by in situ thrombosis (atherothrombus) or embolization – Embolic infarct more common than thrombotic • Maybehemorrhagicornonhemorrhagic • Mostcommonformofcerebrovasculardisease
52
Cerebral Infarction: Nonhemorrhagic
* Usually associated with emboli (thrombus less common) – Mural cardiac thrombus, MI, valvular disease, atrial fibrillation, atherosclerosis, arteritis, * In first 6 hours, no change in macroscopic appearance * By 48 hrs., area is swollen, pale, indistinct corticomedullary junction
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Cerebral Infarction: Nonhemorrhagic
• 2 to 3 weeks: there is neutrophilic emigration followed by mononuclear phagocytic cell emigration • Macrophages containing myelin or red cell breakdown products cam be preset for months to years • The process of liquefaction proceeds with astrocytic reaction around the edges
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Cerebral Infarction: Hemorrhagic
• Results from reperfusion of ischemic tissue – Collaterals – After dissolution of emboli • The evolution parallels that of nonhemorrhagic infarction with the addition of blood extravasation and resorption
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Infarction: Clinical S&S
• Typically sudden • May be preceded by transient ischemic attacks (TIA’s) • Neurologic deficits related to: – Location – Amount of tissue damage • Occur most commonly in area supplied by the middle cerebral artery
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Intracranial Hemorrhage (in brain parenchyma) • Associated with:
– Hypertension and other diseases leading to vascular wall injury – Structural lesions (arteriovenous and cavernous vascular malformations) – Tumors
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Primary Brain Parenchymal Hemorrhage | • Most important predisposing factor: hypertension
– Accounts for >50% of clinically significant hemorrhage – Brain hemorrhage accounts for ~15% of deaths among those with HTN (chronic) • Hyalin arteriolosclerosis – Weaker walls – Chracot-Bouchard microaneurysms
58
Intraparenchymal Hemorrhage (Nontraumatic)
• Hypertensive hemorrhages most often involve the putamen, thalamus, pons, and cerebellar hemispheres • Clinical outcome depends on the size and location of the lesion
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Intraparenchymal Hemorrhage (Nontraumatic) • Cerebral Amyloid Angiopathy (CAA)
– A condition in which amyloidogenic peptides (typically the same ones found in Altzheimer disease, deposit in the walls of medium and small-caliber meningeal and cortical vessels – Can result in weakening of the vascular wall – Is a relationship between a polymorphism in the gene that encodes apolipoprotein E and the risk of disease
60
Vascular Malformations • Classified into four types:
– Arteriovenous (AVM) – Cavernous – Capillary telangiectasias – Venous angiomas
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AVM
• Most common type of vascular malformation • M>F (2:1) • Frequently between the ages of 10 to 30 years • Clinical – Siezures, intracerebral hemorrage or subarachnoid hemorrhage
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Intraparenchymal Hemorrhage: Clinical S&S
* Abrupt onset * Evidence of increased intracranial pressure – Headache, vomiting, rapid loss of consciousness – Nuchal rigidity infrequent * Localizing signs may be present – Hemiparesis, slurred speech
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Clinical S&S
• Progression may lead to herniation and brain stem compression • Large and medium -sized cerebral clots – Grave prognosis • Location as well as size are important in considering prognosis
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Laboratory Studies • CT scan – Provides for rapid diagnosis on intracerebral hemorrhage
* MRI – Useful in demonstrating brainstem hemorrhages and residual hemorrhages * Lumbar puncture – Not advised, may precipitate herniation
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Treatment • If coma is present – Maintenance of adequate ventilation – Monitor ICP – Selective acute use of controlled hyperventilation
* Supratentorial hemorrhage – Surgical evacuation does not improve outcome * Cerebellar Hemorrhages – Surgical evacuation is a generally accepted Tx.
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Spinal Cord
Infarction | Trauma
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Spinal Cord Infarction • Pathogenesis
– Occurs most commonly in the territory of the anterior spinal artery • Supplies the anterior 2/3 of the cord • Is supplied by only a limited number of feeding vessels • Well supplied in the cervical region, so tends to occur caudally
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Spinal Cord Infarction • Causes
– Trauma – Dissecting aortic aneurysm | – Aortography – Polyarteritis nodosa – Hypotensive crisis
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Spinal Cord Infarction • Typical clinical presentation
– Acute onset of flaccid, areflexic paraparesis – As the spinal shock wears off —evolves into a spastic paraparesis • Brisk tendon reflexes and extensor plantar responses • Dissociated sensory impairment – Pain and temperature lost – Vibration and proprioception spared
70
Spinal Cord Trauma • Normally protected within the bony vertebral canal – Vulnerable to trauma from its skeletal encasement
• Most injuries that damage the cord are associated with displacement of the vertebral colum
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Spinal Cord Trauma
• Level of cord injury determines the extent of neurologic manifestations
72
Spinocerebellar Degenerations
Spinocerebellar Ataxia | Friedreich Ataxia
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Spinocerebellar Ataxias
• A group of genetically distinct diseases • Characterized by signs and symptoms referable to the cerebellum, brainstem, spinal cord, and peripheral nerves • Other brain regions may be affected in different subtypes
74
Spinocerebellar Ataxias: Molecular Genetics
• At least 29 distinct entities • Autosomal dominant • Three distinct types of mutations – Polyglutaminde diseases linked to expansion of a CAG repeat – Expansion of non-coding region repeats – Other types of mutations
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Friedreich Ataxia • A distinctive spinocerebellar degeneration • Autosomal recessive • Progressive:
– Begins in the first decade of life with gait ataxia – Followed by hand clumsiness and dysarthria – Depressed or absent deep tendon reflexes – Proprioception and vibratory sense are impaired – Some loss of light touch, pain and temperature sensation
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Friedreich Ataxia • Other clinical findings:
– Pes cavus and kyphoscoliosis – High incidence of cardiac arrhythmias and CHF – Wheelchair bound within 5 years of onset – Cause of death: pulmonary infection and cardiac disease
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Friedreich Ataxia: Pathophysiology
* Expansion of GAA trinucleotide repeat in the first intron of a gene on chromosome 9q13 * Encodes a protein called frataxin – Affected individuals have very low levels of this protein
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Friedreich Ataxia: Pathophysiology | • Frataxin normally localizes to the inner mitochondrial membrane:
– May have a role in regulating iron levels – Iron is essential for many of the complexes in oxidative phosphorylation – Mutations in frataxin cause mitochodrial dysfunction
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Friedreich Ataxia: Morphology | • Spinal Cord:
– Loss of axons and gliosis in the posterior columns, the distal portions of the corticospinal tracts, and the spinocerebellar tracts – Degeneration of neurons in the spinal cord, brainstem, cerebellum, and the Betz cells of the motor cortex
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Friedreich Ataxia: Morphology | • Large dorsal root ganglion neurons are also decreased in number, with secondary degeneration of their axons
• Heart – Enlarged – Multifocal destruction of myofibers with inflammation and fibrosis

Pathology (15 decks)

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