CENTRAL NERVOUS SYSTEMCENTRAL NERVOUS SYSTEM• neurocytology
a) cells include neurons, glia, meninges and cells composing vasculature• NEURONSNEURONS:
a) composed as either i) aggregates - such as nuclei or ganglia
ii) elongated columns - such as in spinal column or iii) layers - of cerebral cortex
b) vary in structure, size and cytoplasmic composition
c) features consistent to neurons are: i) microtubules
ii) neurofilamentsiii) Golgi apparatus and iv) rER
d) Mature neurons do not dividei) loss of neurons with ageii) neurons of CNS do not
regenerate over long distancesiii) infarcts that transect internal
capsule permanent motor deficits
e) CNS neurons do not remyelinatei) MS causes permanent deficits
• Anatomya) centrally, round nucleus contains prominent nucleolusb) cytoplasm is abundant
i) ribosome-studded ER forms prominent basophilic granules
known as Nissl bodiesii) some neurons, of the
substantia nigra and locus ceruleus contain pigment termed neuromelanin
Normal Neuron
Pigmented Neuron
neuromelaninneuromelanin
• Neurons react to injury in several ways:a) chromatolysis
i) injured neurons swell, cytoplasm expands and Nissl substances
disperse near the plasma membrane
ii) nucleus becomes eccentriciii) these processed (i and ii) are known as chromatolysis and is
common response to injury- may be reversible or progress to
irreversible damage
ChromatolysisChromatolysis1.Swollen2.Nissl margination3.Pale cytoplasm4.Eccentric nucleus
b) atrophyi) loss of neurons in brain – aging
processii) may be global or regionaliii) single neurons may shrivel and
become hyperchromatic (e.g., “Creutzfelt-Jacob disease”)
c) neuronophagia (phagocytic response)i) injuries that kill neurons create
debris and elicit phagocytosis by brain macrophages or microglial cells
Atrophy (Creutzfeld-Jacob disease)1.Injured neurons shrivel and2.Are hyperchromatic
Spongiform changes
d) intraneuronal inclusionsi) diverse neuronal and
cytoplasmic inclusions affect neurons (e.g., viral encephalitides and degenerative diseases)
- cytomegalovirus induces inclusions (both nucleus
and cytoplasm) (intranuclear) with prominent clear “halos”
- rabies encephalitis induce cytoplasmic “Negri
body”, which resemble RBC
cytomegalovirus
Negri Negri BodyBody
- Lewy bodies of Parkinsons disease
- Cowdry bodies as seen in herpetic infections
- Neurofibrillary tangles (intracytoplasmic)
AstrocytesAstrocytes
• Support neurons and promote repaira) star shaped glial cells
i) outnumber neurons throughout CNS
b) 2 prominent types:i) fibrillary astrocytes (white
matter)ii) protoplasmic astrocytes (grey
matter)iii) Glial Fibrillary Acidic Protein
(GFAP) or silver impregnation stain demonstrate processes
extending in all directions from cell body, some terminating as foot process on blood vessels
iv) proliferate locally in response to injury (trauma, abscess,
tumors, infarcts and hemorrhages). This process is referred to as
“astrocytosis” or “gliosis”
- most important histopathologic indicator of CNS injury, regardless of etiology
- evolves over hours to days and presence commensurate with severity of injury.
- result in “glial scar”
- Astrocytes undergo hypertrophy (e.g., cell swelling – edema)
and hyperplasia - cytoplasm expands to bright pink
(gemistocytic Astrocytes)- long standing gliosis associated
with Rosenthal fibers (bright, thick, elongated eosinophilic structures). Also associated with cerebellar pilocytic astrocytoma and reactive brain structures adjacent to craniopharyngioma
Astrocyte proliferation
GFAPGFAPSilver carbonateSilver carbonate
v) astrocytes may undergo neoplastic transformation resulting in most common primary brain tumor named “glioma” or “astrocytoma”
c) corpora amylaceai) 5-50 m basophils and
amorphous structures which accumulate with normal aging in the subpial and subependymal regions
- extracellular that evolve within processes of Astrocytes
ii) represent degenerative change in astrocyte
iii) composed of polyglucosan
Corpora amylaciaCorpora amylacia
d) Alzheimer type II Astrocytesi) unrelated to Alzheimer diseaseii) occurs most often in patients
with long standing:- hyperammonia (due to liver
disease) - Wilsons disease
- hereditary metabolic diseases of urea cycle
ii) GliaGlia- AstrocytesAstrocytes: found
throughout CNS (grey and white
matter).- act as BBB- metabolic buffers- repair and scar formation
iii) Oligodendrocytes- myelination ( on multiple
axons)- damage mediated via
acquired demyelination diseases (e.g., MS)
- may harbor viral inclusions iv) Ependymal cellsEpendymal cells
- line ventricular system
• Regulate fluid transport (CSF)a) single layer of cells line the four ventricular chambers, aquaduct
of Sylvius, central canal of spinal cord and filum termianle.
b) during gestation, some viral infectious target ependymal cells which
may result in congenital hydrocephalus
c) ependymomasi) usually arise within ventricles but may also appear in spinal cord
and filum terminale
Ependyma
v) MicrogliaMicroglia- primary function to serve as
fixed macrophages- proliferate with injury and develop elongated
nuclei (“rod cells”)• Reactions of neurons to injuryReactions of neurons to injury
a) several forms: degeneration and cell death (necrosis and apoptosis)
i) acute neuronal injury (redred neuron)
- result from acute CNS hypoxia/ischemia (12-
24 hrs)- or any insult which results in cellular death
MicrogliaMicroglia
- cell body atrophy- pyknosis of nucleus- loss of Nissl substance- intense eosinophilia of
cytoplasmii) Subacute and Chronic neuronal
injury (degeneration)- result of a progressive
disease- seen early as reactive gliosis (i.e., best early indicator) (early cell loss often difficult
to determine!!)
iii) Axonal reaction- refers to axonal
regeneration- associated with protein synthesis- extensively studied in motor neurons of experimental
animals