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Pathology II > Nervous System > Flashcards

Nervous System Flashcards

1
Q

5 Unique pathological response features to the nervous system

A
  1. Protection by bony enclosures
  2. Metabolic requirements
  3. Absence of central lymphatics
  4. Circulation of CSF
  5. Distinctive patterns of wound healing
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2
Q

Neurons differ from each other in 4 ways

A
  1. Function
  2. Distribution of connections
  3. Neurotransmitters used
  4. Metabolic requirements
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3
Q

Definition: Selective Vulnerability

A

a group of functionally related neurons may be selectively damaged due to a particular insult

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4
Q

Example of Selective Vulnerability

A
  1. Exposure to limited hypoxia or hypoglycemia will cause the greatest damage to portions of the hippocampus, the pyramidal cells of the cortex, the purkinje cells of the cerebellum, and the basal ganglia
  2. The hippocampus is affected most extensively in Alzheimer’s disease
  3. Cerebellar granular neurons are most susceptible to the effects of Hg
  4. Poliomyelitis selectively infects and destroys anterior horn cells
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5
Q

Repair of injured nerve processed is predominantly limited to which part of the nervous system?

A

the PNS

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6
Q

4 Reactions of neurons to injury include:

A
  1. Acute Neuronal Injury
  2. Axonal Reaction
  3. Atrophy
  4. Intra-neuronal Deposits (inclusions)
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7
Q

Causes: Acute neuronal injury (red neurons)

A
  1. Contributing causes include ischemia, overwhelming infections, toxicity, and others that lead to neuronal death
  2. Alterations characterized by loss of Nissl, increased angularity, and nuclear pkynosis appear after 12-24 hours of irreversible injury
  3. Ultimately fragmentation occurs (karyolysis!)
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8
Q

Definiton: Axonal Reaction (Central Chromatolysis)

A

refers to reactions in the cell body that accompany axonal regeneration. The reactive processes are associated with synthesis of proteins and sprouting of axons.

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9
Q

Causes: Axonal Reaction (Central Chromatolysis)

A
  1. axon trauma, hypoxia, and other conditions that compromise the capacity of a neuron to maintain its axon and other neuronal “crises”
  2. the perikaryon swells and rounds up, Nissl substance disappears from the central portions of the cell body and the nucleus moves to the periphery.
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10
Q

What is Wallerian Degeneration?

A

Axonal reaction; changes that occur in the distal axon

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11
Q

Effects: Atrophy

A
  1. Reduction in size, possible lipofuscin deposits, and in severe cases, may progress to neuronal death and necrosis
  2. Loss of a single neuron produces no reaction in the glia, however, progressive degenerative diseases are characterized by selective loss of functionally related neurons (ALS) and reactive gliosis
  3. Sometimes, “trans-synaptic degenration” of communicating neurons occur (visual pathway lesions)
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12
Q

What are the 5 types of Intra-neuronal deposits?

A
  1. Neurofibrillary tangles
  2. Lewy bodies
  3. Viruses
  4. Lipofuscins
  5. Metabolic storage diseases
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13
Q

What are Neurofibrillary tangels?

A
  1. Structures composed of twisted cytoskeletal filaments, stainable with silver
  2. Contain ubiquitin and other proteins
  3. Typical of Alzheimer’s disease, post-encephalitic Parkinsonism, Parkinson-dementia complex of guam, dementia of boxers, etc.
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14
Q

Lewy Bodies are?

A

Pink staining spheroids made largely of ubiquitin, most typical of idiopathic Parkinson’s disease (substantia nigra) and Lewy-body dementia (cortex)

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15
Q

Viruses are?

A

intracellular inclusion bodies (virus particles) appear in infected cells as in polio and viral encephalitis. in rabies, these structures are known as negri bodies

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16
Q

When do Lipofuscins accumulate?

A

accumulate within neurons under conditions that include old age and chronic hypoxia

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17
Q

Metabolic Storage Diseases

A
  1. These conditions contribute to accumulated inraneuronal deposits of complex lipids
  2. In the retina, degeneration of neuronal elements contributes to a cherry red spot in the fovea (vascularized choroid shows through thinned macula)
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18
Q

Myelin loss leads to?

A
  1. Death of neuron or loss of axon always leads to myelin degeneration
  2. Myelin loss does not necessarily lead to neuronal degeneration unless this condition is extensive or prolonged (chronic demyelinating disease, chronic injury)
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19
Q

What do Glial cells do, and what are the 4 types?

A
  1. maintain and support nerve cells and fibers within the CNS and are generally less sensitive than neurons to injury
  2. different forms of glia also vary in sensitivity to injury
    2a. oligodendrocytes are the most sensitive to hypoxia
    2b. astrocytes are capable of withstanding all but the most severe and prolonged hypoxia
    2c. microglia is also likely to be very resistant to hypoxic injury
    2d. ependymal cells are moderately sensitive to hypoxia
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20
Q

What do Astrocytes participate in and produce?

A
  1. Participate in repair, produce glial scars
  2. Astrocytic scars may distort the cortex and contribute to seizures
  3. Prolonged mild ischemia may cause necrosis of some astrocytes
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21
Q

What are Microglia? What would increase their numbers?

A
  1. Mesodermal cells functioning as phagocytes of the CNS

2. Numbers may increase in response to injury and infection of components of the CNS

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22
Q

What are Oligodendrocytes responsible for? What happens when stressed?

A
  1. Responsible for the production of myelin, unlike the Schwann cell, ann oligodendrocyte ay wrap around several axons
  2. Most vulnerable of glial cells to injury and may swell when stressed
  3. Diseases of oligodendrocytes and myelin are replaced by astrocytic scars
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23
Q

Diseases of the CNS; list of 11

A
  1. Increased intracranial pressure
  2. Vascular tears and hemorrhage
  3. Trauma
  4. Infections of the CNS
  5. Cerebrovascular disease
  6. Traumatic vascular injury
  7. Degenerative disease
  8. Syringomyelia
  9. Multiple Sclerosis
  10. Neruosyphilis
  11. Tumors of CNS
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24
Q

Increased intracranial pressure

A

recumbent SF pressure exceeds 200mm water

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25
Q

Are you with me?

A

No.

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26
Q

Causes: Increased intracranial pressure

A
  1. Space occupying lesions
  2. Edema and swelling
  3. Hydrocephaly
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27
Q

2 types of edema and swelling when pertaining to increased intracranial pressure

A
  1. Vascular (vasogenic), most common cause of brain edema, associated with increased vascular permeability
  2. Cellular (cytotoxic), increased cell water indicates injury
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28
Q

Hydrocephalus: definition

A

the volume of CSF is increased, the ventricles are dilated

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29
Q

Hydrocephaly ex vacuo: definition

A

the ventricles are expanded secondary to atrophy of the brain, therefore there is not an increase in CSF pressure

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30
Q

Pathogenesis of hydrocephalus

A

an imbalance exists between the rates of production (choroid plexus) and absorption (arachnoid granulations)

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31
Q

Causes of hydrocephalus

A
  1. Overproduction of CSF

2. Decreased transport and/or absorption of CSF

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32
Q

Obstructive (non-communicating) hydrocephalus: causes and effects

A
  1. CSF does not reach the subarachnoid space since its circulation is blocked internally
  2. Congenital anomalies
  3. tumors, abscesses and other SOL’s
  4. Scarring in the ventricular system, obstruction at foramina of Magendie and Luschka
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33
Q

Communicating Hydrocephalus: causes and effects

A
  1. CSF enters the subarachnoid space but the circulation or its absorption is blocked
  2. Scars of the arachnoid granulations and/or in the meninges (bacterial meningitis, hemorrhages)
  3. Thrombi, neoplasms, and other obstructions of cerebral (dural) venous sinuses and associated veins
  4. Severe CHF -> venous congestion and pooling
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34
Q

Sites of narrowing that are vulnerable to obstruction

A
  1. Cerebral Aqueduct of Sylvius
  2. Foramina of Magendie and Luschka
  3. The subarachnoid space between the midbrain and the forebrain
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35
Q

Scarring following inflammation or hemorrhage may

A

block absorption of CSF in the arachnoid granulations

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36
Q

Are you with me?

A

maybe…

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37
Q

Manifestations of hydrocephaly

A
  1. Papilledema (‘chocked disc”)
  2. Herniation: the rigid skull and dural reflections force the brain to be squeezed through openings and around partitions like putty when it is displaced or undergoes sufficient swelling or expansion.
    2a. Cingulate (subfalcine)
    2b. Uncal (trans-tentorial)
    2c. Tonsillar (cerebellar, “coning”) - may lead to compression of the medulla at the foramen magnum and is a common mechanism of death in swelling of the brain
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38
Q

Early features of increased intracranial pressure

A
  1. Headache
  2. Mental Dullness
  3. Nausea
  4. Vomiting
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39
Q

Early features of SARS

A
  1. Drooling
  2. Squinty eyes
  3. Forgetting green water bottle places
  4. Frustration with fantasy NHL
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40
Q

Trauma

A
  1. Penetrating and crushing injuries associated with distortion of cranial vault and cerebral column
  2. Trauma without damage to cranium
  3. Cord trauma
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41
Q

Brain trauma with no damage to cranium

A
  1. Contusion
  2. Laceration
  3. Concussion
  4. Rotary motion
  5. Contrecoup injury
  6. SUBLUXATION
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42
Q

Contusion

A

interstitial bleeding due to blunt trauma (bruise)

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43
Q

Why do squirrels swim on their backs?

A

To keep their nuts dry!

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44
Q

Laceration are associated with?

A

associated with tearing (damage) of brain surface with bleeding into surrounding region (CSF), trauma also contributes to edema and swelling of affected components

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45
Q

Concussion: definition, effects, pathogenesis, and prognosis

A
  1. A clinical syndrome associated with a closed head injury, usually in the absence of bleeding
  2. Effects include loss of consciousness, possible alterations in reflexes
  3. The pathogenesis is unclear but may be associated with disturbances to the midbrain reticular activating system
  4. Severity is variable but recovery is common
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46
Q

Rotary Motion creates?

A

shearing effects

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47
Q

Contrecoup injury

A

head trauma causes damage to parts of the brain opposite the site of impact

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48
Q

Why does Jake swim breaststroke?

A

Doesn’t need to worry about wet nuts, Kayla’s got them.

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49
Q

Cord Trauma

A
  1. Penetrating and crushing injuries: displacement or distortion of vertebral elements damage cord
  2. vertebral dislocations
  3. SUBLUXATION
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50
Q

Effects of cord trauma can be exaggerated with

A
  1. stenosis of the vertebral canal

2. similar skeletal changes

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51
Q

Two major classes of CNS infections

A
  1. Meningitis

2. Encephalitis

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52
Q

Meningitis: definition

A

infection of the meninges and CSF

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53
Q

General features of Meningitis

A
  1. infection of meninges and CSF
  2. when severe, may present with systemic signs of infection in addition to localizing signs; stiff neck, headaches, photophobia
  3. in survivors, meningeal scarring and obstruction of CSF flow may produce complications
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54
Q

3 Types of meningitis

A
  1. Acute pyogenic (bacterial)
  2. , Acute lymphocytic (viral)
  3. Chronic
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55
Q

Acute pyogenic meningitis: definition and causes

A

characterized by purulent exudates in meninges

  1. Generally acute clinical course with high mortality
  2. Bacterial cause
  3. Increased turbidity in CSF
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56
Q

Definition: Purulent

A

consisting of, containing, or discharging pus

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57
Q

Causative agents of Acute Pyogenic Meningitis

A
  1. N. meningitidis (meningococcus) - most common in adolescents and young adults, especially during epidemics
  2. E. coli, H. influenzae, S. pneumoniae and other opportunisitc infections in young and immunodeficients
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58
Q

CSF findings in Acute Pyogenic Meningitis

A
  1. Elevated polys
  2. Elevated protein
  3. Reduced glucose
  4. Bacteria present
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59
Q

Acute lymphocytic meningitis: course, cause, and effect

A
  1. More common, course is less severe
  2. Microbial causes
  3. CSF changes
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60
Q

Causative agents of Acute Lymphocytic Meningitis

A
  1. Mumps
  2. ECHO viruses
  3. Epstein-Barr
  4. Herpes simplex (type II)
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61
Q

CSF findings in Acute Lymphocytic Meningitis

A
  1. Elevated Lymphocytes
  2. Moderately elevated protein
  3. Normal glucose
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62
Q

Chronic Meningitis: course, cause, and effect

A
  1. Course may have insidious origin, progressive headaches, malaise, vomiting, etc.
  2. Microbial causes:
    - Tuberculosis
    - Fungi
    - Brucellosis
  3. Subarachnoid space is often filled with exudates or becomes fibrotic
  4. CSF: increased “mononuclear” cells, markedly elevated protein
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63
Q

Encephalitis: definition

A

infection of brain parenchyma

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64
Q

General features of Viral Encephalits

A
  1. Mononuclear cell infiltrates - interstitial, perivascular
  2. Intracellular inclusion bodies - proliferation of viruses
  3. Latency is common
  4. “Tropism” (selectivity) determines which neurons or parts of the brain are affected
  5. Effects range from mild to lethal according to cause and resistance in the host
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65
Q

Examples of Viral Encephalitis

A
  1. Arbor viruses
  2. Childhood infections
  3. Herpes simplex types I and II
  4. Poliomyelitis
  5. Rabies
  6. HIV
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66
Q

Arbor viruses: definition

A

arthropod borne, most common epidemic forms

also includes equine types (reservoir is birds not horses)

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67
Q

Childhood infections

A

MMR

CNS if likely associated with immune mechanisms

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68
Q

Herpes simplex types I and II: where it affects

A

generally affect peripheral nerves but the infection spreads centrally along nerve fibers and reaches the brain on occasion

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69
Q

Poliomyelitis: history

A

nearly eradicated in the western hemisphere, but carriers (canadians) for the disease exist

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70
Q

Rabies: how you get it, pathogenesis, morbidity

A

acquired from animal bites, virus follows nerves to brain - 40k deaths/year

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71
Q

HIV: what percent develop neurologic complications, and what types

A

60% AIDS patients develop neurologic complications - cognitive and motor dysfunction

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72
Q

“Slow Virus” Encephalitis: characteristics

A

characterized by long incubation period and prolonged relentless illness

  1. SSPE
  2. Progressive multifocal leukoencephalopathy
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73
Q

Subacute Sclerosing Panencephalitis SSPE may follow _________ and give rise to ________.

A
  1. may follow childhood measles

2. gives rise to dementia and motor disturbances leading to death over a few years

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74
Q

Progressive Multifocal Leukoencephalopathy is due to infected ________ in ___________ patients

A
  1. In immunosuppressed patients

2. Oligodendroglia infected

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75
Q

“Unconventional Agent Encephalopathies”

A
  1. Primarily affect the nervous system of humans and animals
  2. Microscopic vacuolization of the brain tissue (spongiform degeneration) and the accumulation of abnormal forms of prion proteins (PrP)
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76
Q

3 Types of “Unconventional Agent Encephalopathies”

A
  1. Creutzfeldt Jacob disease
  2. Kuru
  3. FFI/MCD
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77
Q

Creutzfeldt Jacob disease

  1. DDX
  2. S/Sx
  3. Incidence
A
  1. “Subacute Spongiform Encephalopathy” - involved areas of gray matter undergo extensive atrophy
  2. Initial effects include subtle changes in behavior and memory followed by rapidly progressive dementia (7 months duration)
  3. Incidence: 1/1 million. Conrtibutuing factors include spontaneous and hereditary mutations and transmission
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78
Q

Creutzfeldt Jacob Dis-ease exposure vectors (6)

A
  1. Corneal transplants
  2. Pituitary extracts
  3. Ocular instrumentation
  4. Cranial surgery
  5. Electrode implants
  6. Contact with infected tissue
79
Q

Kuru

  1. Region and transmission
  2. causative agent
  3. clinical presentation
A
  1. Described in the highlands of New Guinea and appears to have been transmitted by cannibalism of infected human brains
  2. causative agent and lesions appear to be similar to those observed in Creutzfeldt Jacob disease except that degeneration is most prominent in the cerebellum and corpus striatum
  3. Clinical: ataxia leads to motor incapacity and death within one year
80
Q

Other “Unconventional Agent Encephalopathies” (3)

A
  1. Fatal familial insomnia - human and scrapie in sheep
  2. Chronic wasting disease - deer and elk
  3. Mad Cow Disease - bovine spongiform encephalopathy (BSE), possibly transmission to humans through handling and consuming body parts from infected animals
81
Q

PrP (Prion Protein): Definition

A

normal membrane glycoprotein that becomes changed to an abnormal isoform in disease; change from a normal alpha-helix to a beta-pleated sheet pattern. abnormal molecules seem to propagate by making contact with normal molecules and inducing them to “refold” into the pathologic configuration. Accumulation of this material appears to be the cause of disease but how this contributes to neuronal damage and eventual cell death is unclear
- abnormal proteins are generaly resistant to many agents that normally inactivate viral DNA. These molecules are also more resistant to digestion with proteases but it is reported that phenol and certain other treatments may render this material non-infectious.

82
Q

Changes in PrP may occur spontaneously at extremely low rates or more frequently with mutation in the regulatory gene contributing to familial forms. What about abnormal PrP?

A

Abnormal PrP is transmissible and infectious when inoculated into appropriate hosts
Abnormal PrP infects any species that has the gene for PrP
Eliminating the gene results in no infection

83
Q

Sources of infection: for example, Creutzfeldt-Jacob disease may be acquired through any of the following

  1. Genetic
  2. Environmental
A
  1. Genetic: hereditary and sporadic mutations of the PrP regulatory gene
  2. Environmental: exposure to infected individuals; respiratory dissemination, neurosurgery; or contaminated material; nerve tissue in animal parts, brain tissue, pituitary ext rats, ocular and CNS instrumentation, corneal transplants, etc.
84
Q

Other CNS infections

A
  1. Abscess

2. Granulomas

85
Q

Abscess: Definition, causes, effects, clinical findings

A
  1. Focal, usually bacterial infection
  2. Causes include hematogenous dissemination and local extension
  3. during acute stages local destruction and swelling may produce symptoms
  4. CSF findings are variable dependent upon location, size, and extension of the infection
  5. Repair is associated with vascularized collagenous tissue with risk for adhesions
86
Q

Granulomas: Definition, causes, effects, clinical findings

A

focal nodular infections consisting of macrophages, giant cells, etx

  1. give rise to locally destructive and expansile lesions
  2. Causes include TB and Fungi; may extend to meninges
87
Q

Sources of CNS infections

A
  1. Extension from sinus and middle ear infections
  2. Hematogenous dissemination
  3. Direct invasion: trauma and congenital defects
  4. Peripheral nerves: Rabies and Herpes Encephalitis
88
Q

Cerebrovascular disease 2 types

A
  1. Stroke

2. Transient Ischemic Attacks

89
Q

Definition: Stroke

A
  1. Focal loss of neurological function of vascular origin which lasts more than 24 hours or leads to death
  2. Spontaneous onset due to underlying CV disease
90
Q

Morbidity and mortality of a stroke

A
  1. 3rd leading cause of death in industrialized societies
  2. the overall mortality during the first month is generally 40-50%
  3. neuroligical deficits persist in 60% of survivors
91
Q

Transient Ischemic Attacks (TIA)

A
  1. Sudden focal and reversible neurological disturbances due to disruption of blood supply which last less than 24 hours.
  2. Most of these events are caused by emboli and the risk for stroke in these subjects is about 5%/yr
92
Q

Causes of stroke

A
  1. Focal Ischemic Infarcts due to local obstruction of blood supply
  2. Spontaneous hemorrhage
93
Q

Causes of Ischemic Infarcts

A
  1. Account for 75-90% strokes
  2. Most are caused by atherosclerotic disease
  3. other causes or reduced perfusion include inflammatory arteritis, arterial spasms, and dissecting aneurysms
  4. neurons can tolerate up to 3-5 minutes of poor vascular perfusion before permanent damage occurs; however, recent reports describe neuronal deficits during much shorter periods of hypoxia
94
Q

Thrombi

A
  1. commonly associated with atherosclerotic lesions

2. frequent locations include carotids, basilar and proximal middle cerebral arteries

95
Q

Emboli

A
  1. Thrombi, fragments of athersclerotic plaques
  2. Important sources include the arterial supply of the brain and lesions/dysfunction of the left side of the heart
  3. Emboli are usually carried into smaller vessels; branches of the middle cerebral artery
96
Q

Ischemic Encephalopathy and “boundary zone” infarcts

A
  1. ischemia of the entire brain; hypotensive events
  2. reversible mental confusion to infarction, may involve the entire brain (vegetable state) or may be limited to more susceptible parts or in the “watershed” regions of the brain and spinal cord
97
Q

Morphology of infarction: 6-12 hours

A

discoloration and softening, petechiae may appear in the margins of the affected region

98
Q

Morphology of infarction: 2-3 days

A
  1. Cerebral tissue becomes very soft and begins to break up
  2. Edema is also common and when severe, may cause herniation
  3. Edema often exacerbates early neurological symptoms but as it diminishes during recovery, function often improves
99
Q

Morphology of infarction: Several Months

A

residual cavity (cyst) surrounded by astrocytes or a collapsed scar is common

100
Q

Spontaneous Hemorrhage (non-traumatic)

A
  1. Intracerebral

2. Subarachnoid

101
Q

Intracerebral

A

bleeding withing brain

  1. peak incidence: 60 yrs
  2. Most cases are due to rupture of small intraparenchymal arteries
102
Q

Effects of Intra-cerebral rupture of small intra-parenchymal arteries

A
  1. effects of intersititial hemorrhage include dissection of nerve tissue, mass effects, disruption of blood supply
  2. Sometimes blood may reach the subarachnoid space or the ventricles
  3. Usually arises suddenly, progression is rapid
103
Q

Hypertension >50% cases of brain hemorrhage. Other CNS effects include:

A
  1. Arteriolar sclerosis with occlusion os small “penetrating” arteries and arterioles give rise to small lesions known as lacunar infarcts. depending upon location, neurologic symptoms range from absent to severe
  2. Rupture of small penetrating arteries may give rise to “slit hemorrhages”
  3. Acute hypertensive encephalopathy: diffuse cerebral dysfunction caused by elevated intracranial pressure that requires immediate intervention
  4. Multi-infarct dementia: characterized by accumulated effects of repeated brain infarcts due to hypertensive arteriosclerotic disease
104
Q

Subarachnoid hemorrhage

A
  1. rupture of congenitial berry aneurysms
  2. sudden onset with signs of meningeal irritation
  3. CSF findings
    1-24 hours: blood “stained”
    >24 hours: xanthochromia
105
Q

Traumatic Vascular Injury

A
  1. Epidural hematoma
  2. Subdural hematoma
  3. Head trauma and spinal injury
106
Q

Dx: Epidural hematoma

A

Cz: rupture or lacerations of the middle meningeal artery
Sx: Neurological manifestations are commonly absent during the first few hours - “lucid interval”
As hemorrhage progresses an expanding hematoma is produced within a few hours and symptoms associated with elevated intracranil pressure and brain displacement develop.
Tx: Immediate surgical intervention is required

107
Q

Dx: Subdural hematoma

A

Cz: rupture of small communicating veins that course between cortex and the dural venour sinuses, blood accumulates in a “potential space” between the dura and arachnoid
Trauma is a common cause; brain atrophy for any reason may lead to stretching of the cerebral veins with an increased vulnerability for rupture.
Sx: appear within 48hrs of trauma but are slowly progressive; clinical symptoms are often vaguely localized and include headache and mental confusion

108
Q

Head trauma and Spinal injury may cause

A

contusions and lacerations of the brain and spinal cord

109
Q

Degenerative Diseases

A
  1. Parkinsonism
  2. Dementia
  3. Degenerative motor neuron disease
110
Q

Parkinsonism Sx:

A
  1. Stooped posture
  2. festinating gait
  3. “cogwheel rigidity” of the limbs
  4. sluggish voluntary movement
  5. a “Pill-rolling” tremor at rest
  6. Rigid and expressionless facial expression
111
Q

Parkinsonism Associated Causes:

A

degeneration of the dopamine-producing pigmented neurons of the substantia nigra and locus ceruleus

112
Q

Parkinsonism pathology:

A
  1. Lewy bodies consisting of filamentous deposits appear in degenerating neurons
  2. in H&E stained tissue, these bodies are homogenous and pink in appearance and exhibit a pale halo
  3. In Parkinsonism, the pigmented neurons of the substantia nigra are predominantly affected
113
Q

Although parkinsonism is not familial, it may be associated with

A
  1. An autosomal dominant gene defect associated with regulation of synuclein - a presynaptic protein. One extra copy leads to parkinsonism w/o dementia, two leads to parkinsonism with lewy body dementia
  2. An autosomal recessive gene regulates parkin, an agent that serves to “upiquinate” products associated with synuclein
114
Q

Classification for parkinsonism

A
  1. Idiopathic Parkinson’s Disease (Paralysis Agitans)
  2. Secondary to encephalitis (Influenza), exposure to dopamine antagonists and other agents, vascular disease, multiple head trauma
  3. Diffuse Lewy body disease (DLBD)
115
Q

Paralysis Agitans

A
  1. Spontaneouls onset; 50-60 years
  2. Pigmented neurons in the substantia nigra and locus ceruleus undergo degeneration with Lewy bodies
  3. Cognitive functions usually preserved except ina subset of Parkinson’s
116
Q

Secondary to encephalitis (Influenza), exposure to dopamine antagonists and other agents, vascular disease, multiple head trauma

A
  1. More common in younger subjects

2. Less distinctive, depletion of substantia nigra with formation of neurofibrillary tangles is common

117
Q

Diffure Lewy body disease

A

associated with degeneration of cortical neurons in addition to the substantia nigra with dementia and Parkinsonism

118
Q

Parkinsonism Tx:

A

L-dopa provides symptomatic improvement

Severity of parkinsonism is proportional to dopamine deficiency

119
Q

Dementia is associated with:

A
  1. Diseases of the cortex
  2. Mental incompetency in previously normal subjects
  3. Effects include memory loss, poor judgment, “delusions of grandeur”, disorientation
120
Q

Known causes of dementia

A
  1. CVA
  2. Hydrocephalous
  3. Encephalitis
  4. Metabolic Disturbances
  5. Slow viruses
121
Q

Idiopathic Dementia, Alzheimers

A
  1. Senile and Presenile patterns
  2. Progressive brain atrophy
  3. Loss of cortical functions lead to profound dementia, 5-7 years. loss of motor function leads to death
122
Q

Characteristic features

A
  1. Cerebral atrophy (frontal, temporal, parietal)
  2. Increased number of neuritic plaques
  3. Neurofibrillary tangles
  4. Amyloid Angiopathy
  5. Granulovacuolar degeneration
123
Q

Neuritic Plaques

A
  1. Composed of tortuous neuronal processes containing abnormal “tau-proteins” that surround a central amyloid core. The amyloid core consists of small peptides, alipoprotein, and other elements.
124
Q

Alzheimer’s (AD) pathology

A
  1. A-beta appears to be neurotoxic or enhances neurotoxicity of some other agent. Amyloid deposits appear to stimulate inflammation, antibodies against amyloid fragments appear to clear away the plaques and proteins against disease
  2. Genetic defects in presinilins lead to early onset AD. Presinilins modify activity of one or more of the enzymes that degrade A-beta.
  3. Alipoprotein E is a risk factor for late onset AD. APOE accumulates in senile plaques, blood vessels and it seems to contribute to “tangling” of nerve prcesses and serves as a template for beta-pleating.
125
Q

Dementia Pathogenesis:

A
  1. Unknown
  2. Aluminum toxicity, slow viruses, prions, hereditary factors
  3. Familial defects on chromosomes 21, 1, 14, 19
  4. Individuals with Down’s syndrome exhibit cortical changes identical to AD
126
Q

Degenerative motor neuron disease varients

A
  1. UMN
  2. LMN
  3. Combined
127
Q

Amyotrophic Lateral Sclerosis (ALS); Lou Gehrig’s Disease

A

Most common motor neuron disorder, affects both upper and lower motor neurons; sensory elements are generally not affected

128
Q

ALS Morphology

A
  1. Loss of motor neurons in the anterior horn cells of the spinal cord, may also involve cranial motor nuclei and UMN (Betz cells)
  2. Loss of anterior horn cells leads to muscle atrophy in the hand and other locations
  3. Loss of UMNs lead to lateral column degeneration with gliosis
129
Q

Etiology of ALS

A
  1. Unknown
  2. Suspected factors include viruses and metabolic disorders
  3. A hereditary form associated with a defective superoxide dismutase gene on chromosome 21 in 10%
130
Q

Definition: Syringomyelia

A

cystic expansion of central canal of spinal cord affects “crossing fibers” with segmental motor and sensory deficits

131
Q

Multiple Sclerosis; Incidence

A
  1. MS is the most common of acquired and inherited conditions that affect myelin in the CNS
    a. US - 250k-500k
    b. Peak onset 20-40 years of age
    c. Women 2x
    d. Most common in Caucasian population
132
Q

MS; Etiology and pathogenesis

A
  1. Host susceptibility - risk 15x greater in 1st order relatives of patients
  2. Exposure to certain infectious agents is suggested and populations living in higher temperate latitudes seem to be at greatest risk
    a. childhood exposure to infections
    b. most clear in Europe and North America… yes even Canada
133
Q

MS; Autoimmunity

A

Autoimmunity to components of the myelin sheath contributes to damage. This is associated with patchy demyelinization and glial scarring within the CNS. T and B cell mechanisms implicated

134
Q

MS; Morphology

A
  1. Distinct demyelinated plaques originate around venules and veins and progress to reach macroscopic size
135
Q

MS; Locations

A
  1. Optic nerve and chiasm - may cause ocular pain, retinal changes and visual disturbances
  2. Periventricular white matter
  3. Brain Stem
  4. Cerebellar peduncles, dorsal columns of spinal cord
136
Q

MS; Sx

A
  1. Increased fatigability
  2. Paresthesia
  3. Visual losses and other optic disturbances
  4. Locomotor disturbances
  5. Depression
137
Q

MS; Clinical Variants

A
  1. Acute progressive - 10-20 months survival

2. Chronic progressive - 20-30 years survival

138
Q

MS; Remitting-relapsing form

A
  1. Typical MS
  2. Characterized by episodic periods of remission and exacerbation; loss of function progresses with each episode
  3. Long survival
139
Q

MS; Dx

A
  1. Sypmtoms
  2. CSF
  3. CT/MRI
  4. Nerve conduction studies
140
Q

MS; Exacerbations

A
  1. Brought on by stress or other illness, increasing body temperatures
  2. Stress management therapy, exercise, dietary management
  3. Medicinal to “desensitize” and control anti-myelin reations
141
Q

MS; Px

A

65% are “functional” at 10 years, and 35-30% after 20 years

142
Q

Neurosyphilis; CNS effects of the tertiary stage. Manifestations

A
  1. Paresis
  2. Tabes dorsalis
  3. Meningeo-vascular lesions
143
Q

Paresis

A
  1. Progressive neuronal loss with cerebral atrophy

2. Clinical effects: dementia, changes in behavior, tremor, memory loss, Argyll-Robertson pupil

144
Q

Tabes Dorsalis; Locomotor Ataxia

A
  1. Fibrosis and gliosis of posterior columns of spinal cord
  2. Pathogenesis: poorly defined
  3. Sx: variable
145
Q

Tabes Dorsalis; Sx

A
  1. lightning pains, painful paresthesias
  2. ataxia, loss of DTR
  3. Visceral effects include bladder dysfunction, episodic abdominal pain and vomiting
146
Q

Meningeo-vascular lesions

A

chronic meningitis with thickening, obliterative arteritis - gummas may extend into cortex, brain stem or cord

147
Q

Tumors of the CNS; General Features

A
  1. Primary Tumors - derivatives of glial elements most common
  2. All primary neoplasms arising within the substance of the CNS are potentially life threatening because of their critical location. Also, morphologic distinctions between benign and malignant CNS tumors are often vague and some may change from to a malignant course spontaneously
148
Q

Incidence of intercranial tumors - secondary

A

secondary (metastatic) - includes 25-30% of intracranial tumors, recent reports suggest closer to 50%

  1. tends to be multiple
  2. most commonly associated with metastasis of malignant melanoma as well as from primary tumors of breast and lung
149
Q

Incidence of intercranial tumors - primary

A
  1. Extra-axial tumors
  2. arise outside the CNS
  3. cause compression and are more easily removed than those originating within the brain or spinal cord
150
Q

Incidence of intercranial tumors - primary locations

A
  1. Meninges and epidural structures
  2. Nerve sheaths
  3. Pituitary
  4. Craniopharyngiomas and pineal gland tumors
151
Q

Incidence of intercranial tumors - intra-axial

A
  1. arise within the CNS
  2. 70% adult within the cerebral hemispheres
  3. 70% children in cerebellum
152
Q

Gliomas: 40-60% of CNS tumors

A
  1. Astrocytoma
  2. Glioblastoma multiforme
  3. Ependymoma
  4. Oligodendroglioma
153
Q

Astrocytoma

A

located in cerebrum, also in cerebellum, brain-stem, and spinal cord

154
Q

Glioblastoma multiforme

A

a poorly differentiated, invasive glial cell tumor

155
Q

Ependymoma

A

derived from the lining of the ventricular system of the brain and the central canal of the spinal cord

156
Q

Oligodendroglioma

A

uncommon, in some cases the lesions may calcify

157
Q

Medulloblastoma

A
  1. Most common in children 2-4 yrs

2. Composed of small, poorly differentiated cells seen most commonly in the crebellum

158
Q

Neurocyte and neuroblastomas

A
  1. Retinoblastoma - chromosome 13 defect

2. Neuroblastic tumors - Adrenal medulla, peripheral ganglia, may give rise to intra-axial tumor

159
Q

Peripheral Nerve Disorders

A
  1. Regeneration
  2. Neuropathy
  3. Neuralgia
160
Q

Regeneration

A

Limited to peripheral fibers and is dependent upon preservation of the neuriemmal tube

161
Q

Neuropathy

A

functional/pathological disturbances of peripheral nerves

  1. Pathogenesis
  2. Distribution
  3. Symptoms
  4. Etiology
162
Q

Pathogenesis

A

Mechanisms that cause the degeneration of axons and/or loss of myelin

  1. Wallerian Degeneration
  2. Axonal Degeneration
  3. Segmental Demyelination
163
Q

Wallerian Degeneration

A
  1. Occurs in distal segment of injured peripheral nerve
  2. Typical response to mechanical injury
  3. Debris is removed prior to regeneration of peripheral fiber
  4. Perikaryon of the injured nerve undergoes swelling, chromatolysis and other acute neuronal stress reaction; recovery depends upon survifval of neuron and a maintained continuity of the neurilemma
164
Q

Axonal Degeneration

A
  1. “Dying back” of affected nerve fibers
  2. Seems to reflect an inability of a neuron to maintain its axons
  3. Potential causes include metabolic and ischemic conditions that affect the neuron and/or axons
  4. Recovery depends upon survival of the neuron and neurilemma
165
Q

Segmental Demyelination

A
  1. Underlying axon is initially preserved
  2. Underlying processes appear to be related to metabolic, inflammatory or toxic injurt to the neurilemma
  3. The injury is reversible but if repeated or prolonged excessively, the underlying axons will also degenerate
166
Q

Neuropathy Distribution

A
  1. Polyneuropathy

2. Mononeuropathy

167
Q

Polyneuropathy

A
  1. Affects multiple nerves in a wide pattern
  2. Causes tend to be “systemic” in nature
  3. Tends to affect the longest neurons most greatly and initially in a symmetrical and peripheral pattern
168
Q

Mononeuropathy

A
  1. Affects single or isolated group of neurons

2. Causes include localized mechanical factors and other forms of isolated pathology

169
Q

Neuropathy Symptoms

A
  1. Peripheral Somatic Nerves

2. Autonomic Nerves

170
Q

Peripheral Somatic Nerve Symptoms

A
  1. Motor and sensory nerves may be affected selectively or concurrently
  2. Affects include motor weaknesses, paralysis, sensory loss and or paresthesia
171
Q

Autonomic Nerve Symptoms

A

When affected, may contribute to bowel, bladder, and CV disturbances

172
Q

Neuropathy Etiology

A
  1. Trauma
  2. Nutritional deficiencies
  3. Systemic Disease
  4. Toxins
  5. Inflammatory Mechanisms
173
Q

Mechanical Trauma

A

includes compression and entrapment

1. Demyelination seems to occur initially, followed by axonal degeneration

174
Q

Causes of mechanical trauma

A
  1. Spinal nerve compression at IVF
  2. Radial nerve injury
  3. Peroneal nerve injury
  4. Ulnar nerve entrapment
  5. Carpal tunnel syndrome
175
Q

Nutritional deficiencies

A

Beriberi - B1

causes myelin degeneration and loss of axons, usually starts in legs

176
Q

Systemic Dis-ease

A
  1. Diabetes

2. Amyloidosis

177
Q

Diabetes

A

neuropathy in 50% when the disease has been present for 25 years or more

  1. Peripheral vascular disease and hyperglycemia - related metabolic factors
  2. Distribution of neurologic manifestations
178
Q

Distribution of neurologic menifestations in diabetes

A
  1. Sensory fibers affected most greatly; particularly those of greatest length: somatic motor fibers may also be ultimately affected
  2. Autonomic fibers affected in 20-40% chronic diabetics - contribute to bladder, bowel, and CV disturbances, visceral pain and sweating anomalies
179
Q

Toxins

A
  1. Diphtheria
  2. Lead
  3. Other agents
180
Q

Diphtheria

A

Endotoxin damages nerves

181
Q

Lead

A

affects include dysfunction of radial and peroneal nerves; wrist and foot drop

182
Q

Other Toxins

A

Hg, Uremia, arsenic, etc.

183
Q

Inflammatory Mechanisms

A
  1. Bell’s Palsy

2. Guillain-Barre Syndrome

184
Q

Bells Palsy

A
  1. Inflammatory swelling of CN VII of uncertain origin

2. Leads to nerve compression and weakness of facial muscles - usually lasts 4-8 weeks 75% recovery

185
Q

Guillain-Barre Syndrome

A
  1. Most common acute paralytic disease of young adults in US
  2. Pathogenesis uncertain but immunological mechanisms are implicated in most cases
    About 2/3 follow acute flu-like illness
    EBV, vaccination, HIV, surgery, lymphomas
186
Q

Guillain-Barre Syndrome Morphology

A
  1. Inflammatory cells and segmental demyelination; lymphocytes and monocytes, axonal degeneration
  2. Large nerves affected most extensively; spinal roots, plexuses, nerve trunks
187
Q

Guillain-Barre Syndrome Onset

A

Usually acute with rapid progression of weakness from distal to proximal muscle groups

  1. Dominated by ascending paralysis of lower extremities, may progress to variably affect trunk, arm, and facial muscles
  2. When severe, respiration, swallowing, and visceral autonomics may be affected - 2-5% die of complications
  3. Paresthesia is also common but is less dominating
  4. Recovery begins within 2-4 weeks, 85% are ambulatory at 6 months
188
Q

Neuralgia

A

Pain

  1. Nerve Trauma or Compression
  2. Inflammation (neuritis)
  3. Idiopathic: tix douloureux <- what a canadian word!
189
Q

Inflammation

A
  1. Shingles (Herpes Zoster)

2. Herpes Simplex

190
Q

Shingles

A

Herpes Zoster

  1. Associated with latent infection of DRG
  2. Episodic flare-ups with painful segmental cutaneous vesicular eruptions
191
Q

Herpes Simplex

A
  1. Type I (above waist) - cold sores
  2. Type II - genital herpes
  3. Leads to vesicular lesions in skin and mucus membranes at site of initial exposure and infects neurons that innervate these locations
192
Q

Herpes Simplex Lesions

A
  1. Epithelial lesions heal
  2. Infection remains latent in neurons and may be episodically reactivated and produce more lesions
  3. Type I commonly localizes in sensory component of CN V, involvement of opthalmic division may cause corneal lesions. In infants and immunosuppressed, control is reduced and the infection may follow nerve fibers into the brain and cause encephalitis
193
Q

Idiopathic: tic douloureux

A
  1. Spontaneous episodes of lightning pain affecting one or more divisions of CN V
  2. Tx include sectioning portions of the CN V or its sensory pathways, relief of compression and certain drugs
194
Q

Lightning Pain on CN V

A
  1. Attacks may be precipitated by light stimulation of skin of face or in mouth - touching, brushing, talking, and eating - episodes may last a few seconds at a time and may be extremely painful
  2. Underlying cause unclear
    a. compression of portions of V seen in some, ganglion tumors may be responsible in others
    b. Structural lesions are not always seen.

Pathology II (3 decks)

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