Week 2 Overview of Neuropathology (NS Response to Injury)

Question 1

Developmental

Answer 1

Onset: At birth

Duration: Static

Focality:

Cellular changes: Neuralation or neuronal migration abnormalities

Other Clues: Folate deficiency (valproate)

Question 2

Trauma

Answer 2

Onset:

Duration: Static

Focality: Yes

Cellular changes: Tissue disruptio, axonal spheroids , petechial hemorhhage (contusion); cell death

Other Clues: Trauma history, suspicious history for pediatric non-accidental trauma

Question 3

Cerebro-Vasular

Answer 3

Onset: Acute

Duration: Static

Focality: Vascular distribution

Cellular changes: Ischemia and or hemorrhage neurons > neutrophils > macrophages (cavitation)

Other Clues: Risk factors, cardiac arrythmias, atheroscleorisis, hypertension

Question 4

Toxic metabolic

Answer 4

Onset: subacute

Duration:

Focality: usually global (rarely focal or systemic)

Cellular changes: Alzheimer’s tyoe II astricytes with hepatic encephalopathy

Other Clues: Drugs, vitamin deficiency

Question 5

Neoplastic

Answer 5

Onset: subacute

Duration: progressive

Focality: usually focal (or regionally infiltrative)

Cellular changes: Atypia, mitoses

Other Clues: Imaging

Question 6

Infectious

Answer 6

Onset: subacute

Duration: progressive

Focality: sometimes

Cellular changes: Inflammatory cells, organisms and inclusions (viral)

Other Clues: CSF, fever, history

Question 7

Neurodegenerative

Answer 7

Onset: chronic

Duration: progressive

Focality: Systems (ie motor; extrapyramidal; cognitive)

Cellular changes: Neuronal loss, gliosis, includions

Other Clues: protein abnormality in cells, genetic risk factors

Question 8

Amytrophic lateral sclerosis clues

Answer 8

Symptoms would be related to the motor system (corticospinal tracts)

onset and duration would be slowly progressive

pathologic changes including neuronal loss and gliosis would be degenerative

Question 9

Middle cerebral artery stroke clues

Answer 9

Symtoms would be focal (ie MCA distribution)

onset would be abrupt

pathologic changes would be ischemic

Include shrunken eosinophilic neurons acutely and later macrophages and gliosis

Question 10

Neuron

Answer 10

most vulnerable cell

limited regeneration

Question 11

Astrocyte

Answer 11

Major reactive cell of CNS (infarcts, neurodegenerative, infectious, ext)

proliferative

Question 12

Oligodendrocyte

Answer 12

myelinated axonal processes

highly vulnerable (ie multiple sclerosis)

limited proliferation

Question 13

Ependymal cell

Answer 13

lines ventricles

vulnerable

limited regeneration

Question 14

Vascular disease cellular response

Answer 14

atherosclerosis, thrombosis, infarction/ eosinophilic neuronal necrosis

Red is dead = hypoxic, ischemic changes

Question 15

Neoplastic cellular response

Answer 15

Unregulated proliferation of atypical cells due to tumor suppressor gene mutation

Question 16

Neurodegenerative cellular response

Answer 16

Neuronal loss

gliosis

specific or non-specific inclusions (ie fibillary phosphotau positive inclusions; alzheimers or other neurodegenerative tauopathy)

Question 17

Neurodegenerative cellular response 2

Answer 17

neuronal loss

subsequent loss of myelinated fibers in corticospinal tracts

ALS

Question 18

Normal physiology

Answer 18

neuromelanin pigment

normal findings sumstantia migra/ locus ceruleus

Question 19

Congenital inborn errors of metabolism cellular response

Answer 19

abnormal material within cytoplasm of neurons

neuronal storage diseases

Question 20

Autoimmune cellular response

Answer 20

T cell inflammation

demyelination

macrophages

multiple sclerosis

Question 21

Trauma cellular response

Answer 21

diffuse axonal injury shearing of axons/ vessels

axonal spheroids

hemorrhage

Question 22

Toxic/ metabolic cellular response

Answer 22

alzheimers type II astrocytosis = hepatic encephalopathy

Question 23

Infectious cellular response

Answer 23

Bacterial = neutrophils

Viral = microglial nodules/ lymphocytes

fungal = granulomas

Question 24

rosenthal fibers

Answer 24

an be reactive (ie wall of a syrinx) or related to a pilocytic astrocytoma (pediatric tumor)

Question 25

Causes of increased intercranial pressure

Answer 25

increased tissue: tumors

increased blood : hemorrhage, venous comgestion

increased water: hydrocephalus, cerebral edema (ie with infarction)

Question 26

Types of hermiation

Answer 26

1) subfalcine (cingulate)
2) transtentorial (uncal)
3) tonsillar (foramen magnum) and upward cerebellar herniation
4) extracranial = transcalvarial = external herniation

Question 27

Consequences of increased intercranial pressure

Answer 27

headache

herniation

pupillary dilation (uncal herniation)

duret hemorrhage

death

Question 28

non communicating hydrocephalus

Answer 28

Obstruction to CSF flow hinders the free passage of CSF through the ventricular system and subarachnoid space (eg stenosis of the cerebral aqueduct or obstuction if interventricular foramina)

secondary to tumors, hemorrhages, infections or congential malformations

can cause increases in CNS pressure

Question 29

Communicating hydrocephalus

Answer 29

non obstructive hydrocephalus

caused by impaired CSF reabsorption in the abswence of any CSF flow obstruction between the ventricles and subrachnoid space

it has been theorized that this is due to functional impairment of the arachnoidal granulations which are located alone the superior sagital sinus and is the site of the CSF resorption back into the venous system

Various neurologic conditions