Cellular Neuropathology

Question 1

Selective Vulnerability

Answer 1

is the variation in neuronal damage in different pathological states. Neurons differ grately in their interconnections, neurotransmitters, levels of electrical activity and metabolic requirements

Question 2

______ areas of the CNS are vulnerable to hypoxic encephalopathy. Describe the morphologic changes.

Answer 2

Sommer’s sector of the hippocampus (CA1), purkinje cells of the cerebellum, and the deeper layers of the cerebral cortex
*Morphological changes: The neurons become eosinophilic (dead and red) because of the disintegration of Nissl substance. The red appearance is accompanied by nuclear pyknosis and/or karyolysis (fading chromatin) indicative of cell death.

Question 3

Laminar necrosis

Answer 3

Macrophages here, line of necrosis in the deeper layer of the cortex

Question 4

Parkinson’s disease has ______.

Answer 4

Lewy Body, protein is misfolded, can form inclusions

Question 5

Gliosis vs. Fibrosis

Answer 5

Gliosis is when astrocytes react to injury similar to fibroblasts in other tissue. They proliferate and elaborate numerous processes containing glial filaments. Fibrosis (the production of a fibrous connective tissue scar by fibroblasts) is rare in the CNS and only occurs in rare situations such as trauma and around organizing abscess

Question 6

Gemistocytic astrocytes

Answer 6

Large pink cytoplasm, glassy, involved in trauma/injury, processes coming out, resident histiocytes

Question 7

Macrophages morphology

Answer 7

very well circumscribed cell border

Question 8

Multiple Sclerosis

Answer 8

A disease of oligodendrocytes, demyelinating, periventricular white matter plaques-lost the myelin. Variable involvement of areas of the CNS over time and variable changes within the lesions explains the variable clinical course. Episodes, separated with some recovery. The processes are continuing but the myelin is gone (axons are preserved). Lots of macrophages come in to clean up the myelin debris.

Question 9

progressive multifocal leukoencephalopathy

Answer 9

opportunistic infection caused by reactivation of latent JC virus. Virus invades and replicates in oligodendrocytes (tropism). Destruction of oligodendrocytes leads to demyelination. Virus also invades astrocytes producing atypical astrocytic morphology. This is not episodic, patients usually die within a year

Question 10

Leukodystorphy

Answer 10

Not a normal formation of myelin. Leukodystrophy is one of a group of disorders characterized by degeneration of the white matter in the brain.[1] The word leukodystrophy comes from the Greek roots leuko, “white”, dys, “lack of”, and troph, “growth”. The leukodystrophies are caused by imperfect growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fibers.

Question 11

Vasculitis

Answer 11

Fibrinoid necrosis, can be seen on peripheral nerve biopsy, it’s an autoimmune disorder

Question 12

Axon Degeneration

Answer 12

primary destruction of the axon. Transection will result in distal degeneration. Distal end may sprout and regenerate. Damage to the cell body-dying back neuropathy.

Question 13

Segmental Demyelination

Answer 13

Inflammatory demyelinating polyradiculoneuropathy. Acute: AIDP (Guillain-Barre) Chronic: CIDP, Genetic disease, diabetes, acromegaly, hypothyroidism

Question 14

Guillian Barre Syndrome

Answer 14

Acute inflammatory demyelinating polyradiculopathy, ascending paralysis, commonly preceded by an acute flu-like illness which leads to a t-cell hypersensitivity reaction. Sural nerve biopsy often negative because it involves more proximal parts of the nerve. This would be in dorsal roots or ventral roots.

Question 15

Chronic demyelinating polyradiculoneropathy-

Answer 15

Relapses and remissions over several years. Repeated demyelination and remyelination. Redundant Schwann cell processes: onion bulb formation.

Question 16

Diabetic Neuropathy

Answer 16

Axonal degeneration and reduplication of capillary basement membranes.