Nervous System Disorders

Question 1

Pathological responses from CNS features

Answer 1

Protection by bony enclosures
Metabolic requirements
Absence of central lymphatics
Cirrculation of CSF
Distinctive pattern of wound healing?

Question 2

Ways that neurons differ from one another

Answer 2

function
distribution of connections
Use of neurotransmitters
Metabolic requirements

Question 3

Selective vulnerability

Answer 3

A group of functionally related neurons may be damaged as a result of specific injury

Question 4

exposure to limited hypoglycemia and hypoxia

Answer 4

Cause greatest damage to portions of teh hippocampus, pyramidal cells of the cortex, purkunje cells of the cerebellum and the basal ganglia

Question 5

hippocampus is affected most extensibly in

Answer 5

Alzheimer’s disease

Question 6

______ are most susceptible to the effects of mercury

Answer 6

cerebellar granular neurons

Question 7

_______ selectively infects and destroys anterior horn cells

Answer 7

Poliomyelitis

Question 8

Reactions of neurons to injury

Answer 8

Acute neuronal injury (red neurons)
Axonal reaction
atrophy and degeneration of nerve cells in chronic progressive degenerative diseases
Intraneuronal deposits may appear with certain neurodegenerative disorders

Question 9

Acute Neuronal Injury

Answer 9

Contributing causes include ischemia, overwhelming infections, toxicity, and others that lead to neuronal death
Alterations characterized by loss of Nissl, increased angularity, and nuclear pyknosis appear after 12-24
hours of irreversible injury

Fragmentation occurs

Question 10

Pyknosis

Answer 10

Irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is followed by karyorrhexis, or fragmentation of the nucleus.

Question 11

Axonal reaction

Answer 11

Reactions in the cell bod that accompany axonal regenration
Associated with synthesis of proteins and sprouting of axons

Causes: Axon trauma, hypoxia, conditions that prevent a cell from maintaining its axon

Perikaryon swells and rounds up and nissl substance disappears from the central portions of the cell body and nucleus moves to the periphery

Wallerian degenration of distal axon

Question 12

Atrophy and degeneration of nerve cells in

chronic progressive degenerative diseases and aging

Answer 12

Reduction in size, lipofuscin deposits, neuronal death and necrosis
Progressive loss of neurons results in loss of functionally associated neurons and gliosis (though singular loss does not produce this effect)

Question 13

Transynaptic degenration occurs in

Answer 13

Communicating neurons (ex. visual pathways)

Question 14

Neurofibrillary tangles

Answer 14

composed of twisted cytoskeletal filaments (stainable with silver)
Contains ubiquitin which tags abnormal proteins for removal

Alzheimer’s disease, postencephalitic parkinsonism, parkinson’s dementia, boxer’s dementia

Question 15

Lewy bodies

Answer 15

pink staining spheroids made largely of ubiquitin typical of idiopathic Parkinson’s (loss of substantia nigra) and lewy body dementia (affects cortex)

Question 16

Inclusion bodies (virus particles)

Answer 16

Appear in infected cells in polio and viral encephelitis

in rabies these structures are known as Negri bodies

Question 17

Lipofuscins

Answer 17

(wear and tear pigment)

Accumulate in neurons under the of old age and chronic hypoxia

Question 18

Metabolic storage diseases

Answer 18

Contribute to accumulated intraneuronal deposits of complex lipids
Degenration of neuronal elements contribute to a cherry red spot in the fovea

Question 19

Myelin loss only leads to neuronal degeneration if the loss is _____

Answer 19

Extensive or prolonged

Question 20

The most sensitive glial elements

Answer 20

Oligodendrocites

Question 21

Most resilient glial element

Answer 21

Astrocytes

Survive all but the most prolonged and severe hypoxia

Question 22

Astrocytes and neuronal injury

Answer 22

Participate in repair and produce glial scars (other types of scars are less common in the CNS)
With a penetrating injury the astrocytic scars may cause distortion of the cortex and lead to seizures

Prolonged mild ischemia may cause necrosis of astrocytes

Question 23

Microglia and neuronal injury

Answer 23

Mesodermal cells functioning as phagocytes of the CNS, numbers may increase in response to injury and infection of components of the CNS

Question 24

Oligodendrocytes

Answer 24

Wrap myelin around several neurons
Most vulnerable to injury and swell when stressed

Multiple sclerosis and other disease that affect myelination affect oligodendrocytes
replaced by astrocytic scars

Question 25

Increased intracranial pressure can occur due to

Answer 25

Space occupying lesions Swelling and edema Hydrocephaly

Question 26

Edema and swelling of the CNS

Answer 26

Vascular (Vasogenic) Associated with increased vascular permeability Most common cause of brain edema Cellular (cytotoxic) Increased cell water indicates injury

Question 27

Hydrocephalus

Answer 27

Volume of CSF is increased causing the ventricles to dilate Can be caused by: If this follows brain atrophy then then CSF does not increase and this condition is known as hydrocephaly ex vacuo An imbalance of the production and the drainage of CSF Vascular tears and hemorrhage Trauma Infection of the CNS

Question 28

Obstructive (non-communicating) hydrocephalus

Answer 28

CSF does not reach the subarachnoid space because it's path is blocked internally. results from: congeinital causes, tumors, scarring in the ventricular system, obstruction at the foramina of magdenie or luschka

Question 29

Communicating hydrocephalus

Answer 29

CSF enters the subarachnoid space but the circulation or absorption is interrupted Causes: scars of the arachnoid granulations (following inflammation or hemorrhage) and/or in the meninges. Thrombi, neoplasms, and other obstructions of cerebral (dural) cenous sinuses and associated veins Severe CHF leads to venous congestion and pooling

Question 30

Sites of narrowing that are vulnerable for obstruction

Answer 30

Aqueduct of Silvius Foramina of Magendie and Luschka Subarachnoid space between the forebrain and midbrain

Question 31

Manifestation of hydrocephaly

Answer 31

Early features of increased intercranial pressure include headache, mental dullness, nausea, and vomiting Papilledema Herniation

Question 32

Hydrocephaly herniation

Answer 32

Rigid skull and dural reflections force the brain to be squeezed through the openings and around the partitions like putty when it is displaced or undergoes swelling or expansion Common examples include cingulate (subfalcine), uncal (trans-tentorial), and tonsillar (cerebellar, “coning”) herniation Tonsillar herniation may lead to compression of the medulla at the foramen magnum and is a common mechanism of death in brain swelling

Question 33

Trauma leading to hydrocephaly

Answer 33

Penetrating and crushing injuries: Distortion of cranial vault and vertebral column Brain trauma with no damage to cranium (Contusion, laceration, concussion, shearing forces from rotation, contrecoup injury {damage to part of the brain opposite the side of impact]) Cord trauma: displacement or distortion of vertebral elements damage cord. Vertebral dislocations.

Question 34

Meningitis

Answer 34

Infection of meninges and CSF Systemic signs of infection in addition to stiff neck, headaches, photophobia, rash and fevers leads to scarring and obstruction of the CSF

Question 35

Bacterial meningitis

Answer 35

Pyogenic characterized by pus in the meninges Acute in course with a high risk for death

Question 36

Causes of bacterial meningitis

Answer 36

Neissaria (Meningococcus) - most common epidemic form | E Coli., H. Influenza, strep. pneumonia and oppurtunistic infections in the immune compromised

Question 37

CSF findings of bacterial meningitis

Answer 37

Increased turbidity, increased polymorphonuclear leukocytes, and bacteria Elevated protein and reduced glucose

Question 38

Meningococcal septicemia

Answer 38

Gives rise to purpurric lesions, high fever, and potentially shock Consequence of severe infection and skin and organ hemmorhage and mucousal bleeding are common

Question 39

Types of meningitis

Answer 39

Bacterial ``` Acute lymphatic (Vral, "aseptic") More common with milder clinical effects, increased lymphocytes in CSF, milder inflammation ``` Chronic insidious origin Causes include TB, fungi, and brucellosis

Question 40

Viral encephalitis

Answer 40

Most common general features include an increased number of iniltrates of lymphocytes and macrophages called "inclusion bodies" in infected cells and glial cell reactions Delayed symptoms is common Herpes encephalitis, post measeles, congenital malformation (if the mother has rubella), postencephalitic parkinson's after influenza

Question 41

Selectivity of encephalitis

Answer 41

Tropism May choose a specific are or type of cell may also be diffuse

Question 42

Viral encephalitis causes

Answer 42

Arbor viruses from insect and animal hosts Chuldhood infectiosn such as measles Herpes Simplex I and II Polio, rabies HIV (60% of AIDS patients have symptoms leading to viral encephalitis)

Question 43

Slow virus diseases

Answer 43

Infectiosn characterized by long periods of latency Subacute Sclerosing Panencephalitis: Associated with infection of measles virus and is fatal in 2-3 years

Question 44

Hallmarks of prion diseases of encephalopathies

Answer 44

Proteinaceous transmittable agents - NO DNA Affect nerve tissue in humans and animals Hallmarks: Vacuolization (hole formation) of brain tissue and accumulation of prion proteins

Question 45

Prion protein

Answer 45

Membrane glycoprotein that becomes changed by misfolding Acquired through sporadic or inheireted mutations or infected animal tissue, iatrogenic effects (surgery, etc.), exposure to infected humans

Question 46

Creutzfeldt-Jacob disease (encephalopathy)

Answer 46

Human-human transmission from breathing and certain medical procedures

Question 47

Scrapie in sheep and mad cow disease

Answer 47

Concern for transmission to humans that eat or handle infected meats Leads to variant CJD

Question 48

Abscesses

Answer 48

Focal infection that is usually bacterial During acute stage local destruction and swelling may cause symptoms CSF findings are variable Repair is associated with vascularized collagenous tissue and cortical adhesions may occur

Question 49

Granulomas

Answer 49

From tuberculosis Focal nodular infections consisting of macrophages, giant cells, etc. Causes local destruction and expansion

Question 50

Pott's disease

Answer 50

Causes a collapse of vertebral bodies that makes a gibbous deformity in the spinal cord

Question 51

Sources of CNS infections

Answer 51

Extension from middle ear and sinus infections Hematogenous disemmination Direct invasion - trauma, congenital defects, iatrogenic Extension along peripheral nerves (rabies, encephelitis)

Question 52

Stroke (cerebral vascular accident)

Answer 52

Focal loss of neurological function of vascular origin which lasts more than 24 hours spontaneous in onset due to underlying CV disease 3rd leading cause of death 40-50% of death following the first month defecits persist in 60%

Question 53

Transient Ischemic Attacks

Answer 53

Spontaneous focal reversible neurological disturbance slasting less than 24 hours and results from disruption of blood supply Most caused by emboli Risk for stroke is 5% per year

Question 54

Causes of stroke

Answer 54

Focal ischemic infarcts - thrombi - emboli

Question 55

Types of stroke

Answer 55

Hemorrhagic - bleeding | Ischemic - obstruction

Question 56

Focal ischemic stroke

Answer 56

75-90% of strokes Atherosclerosis is most common underlying factor (emboli) inflammatory arthretitis Arterial spasms Dissecting aneurysms 3-5 minutes before damage

Question 57

F-A-S-T

Answer 57

Face droopin Assymetrical movement Slurred speech Time call 911 TO RECOGNIZE STROKE

Question 58

Ischemic encephalopathy

Answer 58

Cause of stroke Generally caused by ischemia of the entire brain. Hypotension can contribute to this Effects change from reversible confusion to infarction May also be limited to watershed regions of the brain and spinal cord

Question 59

Morphology of infarction

Answer 59

6-12 hours: discoloration and softening, petechiae may appear in the margin of teh affected area 2-3 Days: Cerebral tissue becomes soft and begins to break up. edema is common and may cause a herniation and exacerbates neurological symptoms but it gets better Several months: Residual cavity surrounded by astrocytes or a collapsed scar

Question 60

Spontaneous hemorrhage types

Answer 60

Intracerebral | subarachnoid

Question 61

Intracerebral hemorrhage

Answer 61

peak at 60 years Rupture of small intraparenchymal arteries Effects: dissection of nerve tissue, mass effects, and disruption of blood supply blood may reach the subarachnoid space or ventricles Arises suddenly and progresses slowly

Question 62

CNS effects of hypertension

Answer 62

Accounts for 50% of brain hemorrhage arteriole sclerosis with occlusion of small lesions known as lacunar infarcts Rupture of small penetrating arteries may give rise to slit hemorrhages Multi-infarct dementia: characterized by accumulated effects of repeated brain infarcts due hypertensive arteriosclerotic disease Exertion may contribute to onset

Question 63

Subarachnoid hemorrhage

Answer 63

Rupture of congenital berry aneurysms is most common (other causes include other types of aneurysms, clotting defects, traumatic injury, etc.) Onset: sudden with signs of meningeal irritation (e.g. severe headaches) CSF findings • 1-24 hours: blood "stained" • >24 hours: xanthochromia (yellow discoloration of CSF)