Difference between revisions of "Neuropathology"
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*+/-Headache. | *+/-Headache. | ||
*+/-Decreased level of consciousness. | *+/-Decreased level of consciousness. | ||
CSF findings: | |||
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! Type | |||
! Glucose | |||
! Protein | |||
! Cells | |||
|- | |||
| Bacterial, acute | |||
| low | |||
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| neutrophils | |||
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====Etiology==== | ====Etiology==== | ||
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===Microscopic=== | ===Microscopic=== | ||
Features: | Features: | ||
*Inflammation of the meninges. | *Inflammation of the meninges: | ||
* | **+/-[[Neutrophil]]s. | ||
** | **+/-Lymphocytes. | ||
**+/-[[Plasma cell]]s. | |||
*+/-Microorganisms (infectious meningitis): | |||
**Bacteria. | |||
**[[Fungi]], e.g. [[aspergillosis]] (may be intravascular). | |||
Image: | Image: |
Revision as of 15:06, 4 May 2012
Neuropathology is the bane of many anatomical pathologists in teaching hospitals... 'cause they have to fill in for the neuropathologist when he or she is on vacation.
This article is an introduction to neuropathology. There are separate articles for brain tumours, the pituitary gland, the spine, the eye, muscle pathologies, neurohistology and neuroanatomy.
Neuroanatomy
This is a large topic. It covered in a separate article, that also covers grossing.
Neuroradiology
Enhancing vs. non-enhancing:
- If it is tumour... enhancing usu. high grade, non-enhancing usu. low grade.
Ring enhancing lesions
In HIV/AIDS patients... mass on CT if infection:
- Toxoplasmosis - most common.[1]
Ring enhancing lesion (DDx) - mnemonic MAGICAL DR:[2]
- Metstasis.
- Abscess.
- Glioblastoma.
- Infarct.
- Contusion.
- AIDS-related.
- Lymphoma + HIV assoc. disease (toxoplasma).
- Demyelination (e.g. multiple sclerosis).
- Resolving hematoma.
Grossing
This is covered in the neuroanatomy article.
Gross pathology
The gross usually useless for arriving at a definitive diagnosis.
Exceptions:[3]
- Sausage shape lesion of filum terminale = myxopapillary ependymoma.
- Soft & tan colour = pituitary adenoma.
Normal histology
This is a big topic. It is covered in a separate article called neurohistology.
Histopathology
Neuronal changes
Anoxic neurons
- AKA red neurons.
Features:
- Intensely red cytoplasm.
- Pyknosis = nuclear shrinkage + darker staining.
Images:
Central chromatolysis
Features:[5]
- Central clearing.
- Nucleus and Nissl substance are pushed to cell periphery.
DDx:
Images:
- Central chromatolysis - intermed. mag. (WC).
- Central chromatolysis - NF stain - very high mag. (WC).
Axonal swellings
H&E:
- Eosinophilic (light pink) - ground glass-like appearance.
- Shape:
- Round if sectioned perpendicular to axis of axon.
- Bound by cell membrane.
- Large ~ typically 2-4x RBC diameter.
- Sausage-shaped if cut in along axis.
- Round if sectioned perpendicular to axis of axon.
Images:
IHC
- APP.
Image:
Glial changes
Astrocyte changes
Reactive astrocytes:
- Approximately equally-spaced; distance between neighbouring astrocytes is ~2x (or more) the cell size.
- Well-defined cell border.
- Eosinophilic cytoplasm with many branching processes.
- Classically described as "funnel-shaped" in benign astrocytes.[10]
- Peripheral nucleus.
- Image: Reactive astrocytes - high mag. (WC).
Alzheimer type II astrocyte:[11]
- Large cleared nucleus - key feature.
- Indistinct cytoplasm.
- Found in the context of hepatic encephalopathy in basal ganglia and lower layers of cortex.[12]
- Images:
Creutzfeldt cell:[13]
- Astrocyte that mimics a mitoses; has moderate (identifiable) cytoplasm.
- Finding associated with demyelinating disease.
- Image: Crutzfeldt cell (upmc.edu).[14]
Gemistocytic astrocytes:[15]
- Distinct eosinophilic cytoplasm - with ground-glass appearance.
Tufted astrocytes:[16]
- Cellular processes loaded with tau protein (as may be seen with tau IHC or Gallyas silver stain); Parisian-star-like appearance with special stain.
- +/-Multinucleated.
- A classic feature of progressive supranuclear palsy.
Other glial
Bergmann gliosis (in the cerebellum):[13]
- Thin layer of cells (2-3 cells) with open nuclei that are larger than granular cell layer nuclei; seen with Purkinje cell loss.
Reactive change vs. malignancy
Reactive changes vs. malignancy (mnemonic MIMICS):[17]
- MIcrovesicular pattern.
- Mitoses.
- Irregular spacing.
- Calcifications.
- Satellitosis, perineuronal.
- Large "crowds" of glial cells associated with nuclei.
Inflammatory
DDx:
- Autoimmune - Multiple sclerosis.
- Neoplastic - CNS lymphoma.
- Infectious - HSV.
Encephalitis
General
DDx:
- Viral encephalitis.
- Paraneoplastic syndromes.
Microscopic
Features:[18]
- Perivascular inflammation.
- Microglia.
- +/-Neuronophagia.
- Phagocytosis of neurons.[19]
- +/-Viral cytopathic changes.
- +/-Perineuronal inflammation.
Notes:
- Hemorrhage[20] and necrosis - characteristic of HSV encephalitis.
Image:
IHC
IHC stains for:
- Viral etiologies, e.g. HSV, CMV.
- Parasites, e.g. toxoplasma.
- Fungi, e.g. PASD.
Architecture
Rosettes
- Rosette = circular/flower-like arrangement of cells.[22]
- Perivascular pseudorosette = circular/flower-like arrangement of cells with blood vessel at the centre.[22]
- Homer-Wright rosette = (circular) rosette with a small (~100 micrometers ???) meshwork of fibers (neuropil) at the centre.[22]
- Medulloblastoma.
- Image: Medulloblastoma (ouhsc.edu).[23]
- PNET (can be thought of as a supratentorial medulloblastoma) .
- Medulloblastoma.
- Flexner-Wintersteiner rosette = rosette with empty centre (donut hole).[22]
- Retinoblastomas.
- Pineoblastomas.
- Medulloepitheliomas.
- True ependymal rosette = surrounds a space.[22]
- Pineocytomatous/neurocytic rosette = irregular rosette with a large meshwork of fibers (neuropil) at the centre.[22]
- Similar to Homer-Wright rosette.
- Pineocytoma.
- Neurocytoma.
Other
- Rosenthal fibres = worm-like or corkscrew-like (brightly) eosinophilic bodies; 10-40 micrometers.
- Key feature: variable thickness; helps separate from RBCs.
- Well-seen on trichrome stains.
- Images: Rosenthal fibres (WP), Rosenthal fibres - smear (WC/AFIP).
- Eosinophilic granular bodies = related to Rosenthal fibres; round cytoplasmic hyaline droplets in astrocytes.[24]
- Image: EGBs (WC/AFIP).
- Pseudopalisading - picket fence-like alignment of cells; long axis of cells perpendicular to interface with other structures/cells.
- Pseudopalisading of tumour cells (around necrotic regions) is seen in glioblastoma.
Note:
- Good set of articles: Neuropathology for radiologists (ncbi.nlm.nih.gov).
Inclusion bodies
- Negri bodies.
- Cytoplasmic inclusions; classically in Purkinje cells of the cerebellum, pyramidal cells of Ammon's horn.
- Rabies.
- Image: Negri bodies (WC/CDC).
- Lewy bodies.
- Eosinophilic cytoplasmic inclusion - composed mostly of alpha-synuclein.[25]
- Image: Lewy body (WC).
Table of inclusions
Feature | Appearance | Associated disease | Comment | Image |
Grumous bodies AKA granular bodies |
granular and eosinophilic ~50 micrometers | neurodegenerative disease, neuroaxonal dystrophies, aging | ?Comment | ?Image |
Cowdry type 1 AKA Cowdry type A |
eosinophilic & round + halo | herpes simplex virus | can be confused with Lewy body, Marinesco body |
?Image |
Lewy body | round cytoplasmic eosinophilic body +/- pale halo |
Parkinson disease, dementia with Lewy bodies | morphology dependent on location in brain; +ve for alpha-synuclein, alpha-B crystallin, ubiquitin |
[1], [2] |
Lafora body | round | myoclonic epilepsy | look like corpora amylacea; location: dentate nucleus, liver, skeletal muscle, sweat glands | ?Image |
Lipofuscin | yellow & granular | aging | olive, dendate | ?Image |
Negri body | small eosinophic bodies | rabies | found in hippocampal neurons and Purkinje cells | [3] |
Hirano body | concentric calcification/rod-shaped bright eosinophilic; overlap edge of neuron | Alzheimer disease, Pick disease[26] | actin crystals, may look like capillaries; location: CA1 of hippocampus | [4][27] |
Neurofibrillary tangles | flame-shaped cytoplasmic thingy ~30 micrometers |
aging, Alzheimer's disease | seen with silver stain | Schematic[27], [5][28] |
Granulovacuolar degeneration | cytoplasmic vacuoles 4-5 micrometers | ageing, Alzheimer's disease, Pick's disease |
main found in Ammon horn[26] | [6][28] |
Pick bodies | round, homogenous, intracytoplasmic, ~10 micrometers | Pick's disease | pyramidal neurons, dentate granule cells (hippocampus); +ve for tau, tubulin, ubiquitin |
[7] |
Bunina body | size of Nissl granules, eosinophilic | amyotrophic lateral sclerosis (ALS) | EM: membrane-bound bodies; ubiquitin +ve | [8] |
Image collection: Inclusion bodies (photobucket.com).
Immunohistochemistry
General
- S-100.
- Sensitive... but non-specific, e.g. also stains melanoma.
Glial
- GFAP (glial fibrillary acidic protein) - should stain perikaryon.
Glial tumours
Standard work-up:
- GFAP.
- p53.
- Ki-67.
Neuronal
- Synaptophysin.
- Chromogranin.
Carcinoma vs. glial tumours
- AE1/AE3 often +ve in glial tumours (e.g. astrocytomas, oligodendrogliomas); CAM5.2 is usu. -ve in glial tumours.[29]
Others
- APP (amyloid precursor protein) - detects axonal swellings.
- NF (neurofilament) - detects axonal swellings.
Brain tumours
Tumours are a big part of neuropathology. The most common brain tumour is a metastasis. The most common primary tumour (in adults) is glioblastoma which has a horrible prognosis.
Non-tumour
Cerebral hemorrhage
- See: Intracranial hematoma for intracranial bleeds
Includes discussion of:
Duret hematoma
- AKA Duret hemorrhage.
General
- Bleed in the upper brainstem (midbrain and pons).
- Thought to be due to transtentorial herniation secondary to supratentorial mass effect (e.g. supratentorial tumour, intracranial hemorrhage).[30]
- Often fatal.[31]
Gross
- Extravasated blood in midbrain and pons - usu. ventral (anterior) and paramedian (adjacent to the midline).[30]
Image:
Microscopic
Features:
- RBC extravasation.
- +/-Hemosiderin-laden macrophages.
- +/-Ischemic neurons.
Alcohol & CNS
Clinical
- Wernicke's encephalopathy
- Mnemonic WACO:
- Wernicke's.
- Ataxia.
- Confusion, confabulation -- Korsakoff.
- Ocular Sx (CN IV palsy).
- Cause: thiamine deficiency.
- Mnemonic WACO:
Pathology
Features:[33]
- Morel's laminar sclerosis = spongy degeneration and gliosis of the cerebral cortex[34] usu. prominent in the third layer of the cortex (outer pyramidal layer) and especially in the lateral-frontal cortex.[35]
- Central pontine myelinolysis (CPM).[36]
- Just what it sound like - myelin loss in the central pons.
- Classically associated with rapid correction of hyponatremia.[37]
- Mammillary body shrinkage.[38]
- Anterior cerebellar vermis atrophy; weak finding - as also age-related.[39]
- Vermis atrophy is also seen in schizophrenia.[40]
Marchiafava-Bignami Disease
- Rare.
- Demyelination of the corpus callosum.[35]
Wernicke's encephalopathy
General:
- Due to thiamine deficiency.
Features:
- Neurons preserved - key.
- Loss of myelin.
- Hemorrhage.
- Spongiosis.
- Reactive blood vessels.
Common non-specific findings
- Intracranial haemorrhage - due to trauma.
Meningitis
General
- Definition: inflammation of the meninges (pia mater, arachnoid membranes, dura mater).
Classic clinical presentation:
- Neck stiffness.
- Fever.
- +/-Headache.
- +/-Decreased level of consciousness.
CSF findings:
Type | Glucose | Protein | Cells |
---|---|---|---|
Bacterial, acute | low | high | neutrophils |
Viral | normal | slight elevation | lymphocytes |
Etiology
- Infectious.
- Bacterial.
- Viral.
- Parasitic
- Autoimmune.
- Toxic.
- Aseptic - see Mollaret's meningitis.
Bacterial meningitis - most probably cause by age:[41]
Age | Organism |
---|---|
Neonate | Escherichia coli, Group B Streptococcus |
Infants, children | Streptococcus pneumoniae |
Adolescents, young adults | Neisseria meningitidis |
Elderly | Streptococcus pneumoniae, Listeria monocytogenes |
Gross
Features:
- +/-Clouded appearance of the meninges.
- +/-Pus.
- +/-Petechiae.
- +/-Cerebral edema.
Image:
Microscopic
Features:
- Inflammation of the meninges:
- +/-Neutrophils.
- +/-Lymphocytes.
- +/-Plasma cells.
- +/-Microorganisms (infectious meningitis):
- Bacteria.
- Fungi, e.g. aspergillosis (may be intravascular).
Image:
Cerebral abscess
General
- May mimic malignancy clinically.
Microscopic
Features:
- Sheets of neutrophils surrounded by fibrosing brain.
- Fibrosing brain: pale (lighter pink than normal brain tissue), dense.
Images:
Neurodegenerative diseases
This is a hueueuge topic. It is covered its own article and includes a general discussion of dementia.
Epilepsy
Cerebrovascular accident
- Abbreviated CVA.
- AKA stroke.
General
- Very common.
- Leading cause of morbidity and mortality.
Clinical classification:
- Hemorrhagic stroke.
- Ischemic stroke.
Gross
- Soft/mushy brain.
- Older infarcts.
- A "roof" is present - a thin submeningeal layer is preserved by the CSF.[43]
- "Roof" is absent in trauma.
- Cavity - in older infarcts.
- Multiple sclerosis does not cavitate.
- A "roof" is present - a thin submeningeal layer is preserved by the CSF.[43]
- Laminar necrosis = (thin) chalky line replaces grey mater.[44]
DDx:
Microscopic
Features:
- Ischemic neurons.
- +/-Neuronal loss.
- +/-Microglial.
- +/-Thrombosis.
- +/-Atherosclerosis.
Hypoxic-ischemic encephalopathy
- Abbreviated HIE.
General
- Often due to cardiac arrest, i.e. global ischemia.
- Triple watershed area = parieto-occipital cortex, extrastriate occipital cortex.
Note:
- Hypoxia = blood decreased oxygen carrying capacity,[46] e.g. anemia.
- Ischemia = decreased blood flow.[46]
- Either or both = less oxygen delivery to tissue.
Microscopic
Features:
- Hippocampal ischemic changes (in adults):
- Loss of neurons in CA1, CA3 and CA4 +/- "cavitation".
- Neuronal loss: No blue (nuclei) where there should be some.
- Cavitation: bubbles/clear spaces where there should be none.
- CA2 neurons preserved/resistant.
- Loss of neurons in CA1, CA3 and CA4 +/- "cavitation".
- Purkinje cell loss in the cerebellum and Bergmann gliosis.
- "Anoxic neurons".[47]
- Shrunken neurons with intensely eosinophilic cytoplasm and pyknotic (shrunken) nuclei.
- Pseudolaminar necrosis - (uncontrolled) cell death in the cerebral cortex in a band-like pattern,[48] with a relative preservation of cells immediately adjacent to the meninges.
Images:
- Anoxic neurons:
- Hippocampal ischemic changes:
- Pseudolaminar necrosis:
Notes:
- Neurons of subiculum in adults - usu. normal (as they are resistant to ischemic changes).
Multiple sclerosis
- Abbreviated MS.
General
- A bread 'n butter disease of neurology in Canada.
Clinical:
- CSF: oligoclonal bands of immunoglobulin.[51]
Radiologic/Gross
Features:[52]
- White matter lesions.
- Cerebrum (classically): periventricular distribution.
- Optic nerves (optic neuritis) - classic presentation.
Microscopic
Features:[53]
- Perivascular inflammation.
- Demyelination.
- Subcortical myelinated fibers are often spared.
Classification of MS lesions:
- Early active.
- Inactive.
- Early remyelinating.
- Late remyelinating.
DDx:
Images:
- Multiple sclerosis masquerading as a diffuse astrocytoma - several images (upmc.edu).
- Tumefactive multiple sclerosis - several images (upmc.edu).
IHC
- HAM-56 - macrophages.
- CD8 - lymphocytes.
Cerebral amyloid angiopathy
General
- Abbreviated CAA.
- Disease of the old.
- Strong association with lobar haemorrhage (bleeds of the cerebellar cortex and cerebral cortex).[54]
Etiology:
- Amyloid deposition in the basal lamina of smooth muscle (in the cerebellar cortex and cerebral cortex).
Gross
- Bleeds typically superficial (cortex and subcortical white matter) and in the frontal lobe or parietal lobe.[55]
Microscopic
Features:
- Amorphous, acellular eosinophilic material within walls of small arteries.
- This is a high power diagnosis with congo red staining.
Notes:
- Amyloidosis is seen in all individuals with Alzheimer's disease; the amount of amyloid is what differs -- in CAA it is lots and lots.
- The white matter is typically spared by CAA.[56]
Images:
- CAA - congo red - very high mag. (WC).
- CAA - congo red - low mag. (WC).
- CAA - beta-amyloid - high mag. (WC).
Stains
IHC
- Abeta-amyloid (AKA beta-amyloid).
Central pontine myelinolysis
- Abbreviated CPM.
- AKA pontine myelinolysis.
General
- Classically in the pons, ergo "pontine" is in the name.
- Classically midline, ergo "central" is in the name.
- May occur elsewhere -- known as extrapontine myelinolysis.
Etiology:
- Rapid correction of hyponatremia.[57]
- Tacrolimus post-liver transplant.[58]
- Associated with alcoholism and malnourishment.
Clinical:[59]
- Decreased level of consciousness - most common.
- Quadriplegia.
- Poor prognosis.
Microscopic
Features:[60]
- Myelin loss.
- No inflammation.
- Relative preservation of neurons.
Images:
Vascular malformations
Types:[61]
- Arteriovenous malformation.
- Most important clinically - highest risk of bleeding.
- Varix.
- One large (dilated) vein.
- Venous angioma.
- Many small veins.
- Caverous malformation.
- Vessels are back-to-back (no intervening parenchyma).
Also see: Sturge-Weber syndrome.
Cysts
General
- All are "benign", but some may be fatal due to spatial constraints.
List of cysts
- Colloid cyst.
- Columnar epithelium.
- Arachnoid cyst - considered precursor of meningioma.
- Psammoma bodies.
- Clumps of cells.
- Whorled pattern.
- Dermoid cyst.
- Skin + adnexal structures.
- ... think of ovarian dermoid.
- Epidermoid cyst.
- Choriod cyst.
- Neuroenteric cyst.
- Foregut cyst with connection to dura.[62]
- Gastrointestinal tract epithelium.
- Usually seen with vertebral anomalies.
- Foregut cyst with connection to dura.[62]
- Epithelial cyst.
- Others.
Colloid cyst
General
Classic presentation:[63]
- Headache - may be relieved by lying down.
- Can cause sudden natural death.[64]
Gross
- Classically in the third ventricle.
Microscopic
Features:[65]
- Simple epithelium with ciliated cells and goblet cells.
Images:
Paediatric pathology
Kernicterus
General
- Due to hyperbilirubinemia.[66]
Gross
- Yellow staining of the basal ganglia.[67]
Note:
- May not be specific.[66]
Image:
Joubert syndrome
- Malformation of the cerebellar vermis.[68]
Epidemiology
- Autosomal recessive - mutation in a number of genes including NPHP1, AHI1, and CEP290.[68]
Weird stuff
Acute disseminated encephalomyelitis
- Abbreviated ADEM.
General
- Thought to be autoimmune; often associated with/preceded by by viral illness.[69]
- May mimic multiple sclerosis.
Treatment:
- Steroids.
- Plasmapheresis.
Diagnosis:
- Need to r/o infection (with lumbar puncture).
- No old plaques on imaging (MRI).
An acute form exists known as acute hemorrhagic leukoencephalitis[70] (AKA acute necrotizing hemorrhagic encephalomyelitis).
Microscopic
Features:[71]
- Myelin loss with sparing of axons.
- Inflammation:
- Early: neutrophils.
- Late: mononuclear cells (lymphocytes, plasma cells).
- Lipid-laden macrophages.
DDx:
- Multiple sclerosis.
- Age of the lesions differ.
- Acute necrotizing hemorrhagic encephalomyelitis (ANHE) - if one considers this a separate entity.
- Acute necrotizing encephalopathy.[72]
Neuromyelitis optica
- Abbreviated NMO.
General
- Rare autoimmune disease - once considered a variant of multiple sclerosis.
- Autoantibodies directed at aquaporin-4.[73]
Diagnosis:
- NMO-IgG.
Clinical - preferentially:
- Eye (optic neuritis).
- Spinal cord (myelitis).
Microscopic
Features:
- Inflammation - lymphocytes, macrophages.
- Reactive astrocytes.
Images:
IHC
- Mixed lymphocyte population with CD3 > CD20.
- Aquaporin-4 loss.
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
- Commonly abbreviated CADASIL.
General
- Autosomal dominant disorder - as the name implies.[74]
- Causes strokes in 40-50 year-old.
- Cerebral microbleeds - common.
- Associated with increased risk of intracerebral hemorrhage.[75]
- Characteristic MRI findings - present in asymptomatic individuals with mutation.
- Increased risk of myocardial infarction.[76]
Note:
- There is also an autosomal recessive form - CARASIL.[77]
Etiology
- Mutation of Notch 3 gene.[78]
- Diagnosis: proven Notch 3 mutation.
Microscopic
Features:
- +/-Subcortical infarcts.
- Patches of (non-myelinated) tissue within the white matter deep to the cortex with abundant macrophages.
- Blood vessels typically have a basophilic granularity.[79]
IHC
- Notch 3: smooth muscle and pericytes punctate +ve.[76]
Image: Notch 3 staining in CADASIL (WC).
Notes:
- No cortical involvement -- this is unlike multiple sclerosis.
DDx:
- Amyloidosis.
- Binswanger's disease - multi-infarct dementia affecting subcortical white matter.
- Often diagnosed as Alzheimer's disease in the past.
Skin biopsy diagnosis
- Can be diagnosed on a skin biopsy.[80]
Electron microscopy
- Granular osmiophilic material (GOM).
Progressive multifocal leukoencephalopathy
- Abbreviated PML.
General
- Caused by JC virus (a type of polyomavirus[81]) in the context of immunodeficiency; usu. in the setting of HIV infection.[82]
- Suspected cases are biopsied - unlike other demyelinating diseases.[84]
Gross
- Multifocal - as the name suggests.
DDx:
Microscopic
Features:[85]
- Perivascular inflammatory cells.
- Foamy histiocytes.
- Abnormal appearing glial cells:[86]
- Reactive astrocytes.
- Oligodendrocytes with nuclear enlargement and glassy magenta chromatin - key feature.
- Atypical mitoses - known as Creutzfeldt cell.
Images:
- PML - case 1 (upmc.edu).
- PML - case 1 (upmc.edu).
- Crutzfeldt cell - case 2 (upmc.edu).[87]
- PML oligodendrocyte (ucsf.edu).[86]
- PML oligodendrocyte (psychiatryonline.org).[88]
IHC
- SV40 +ve.[89]
See also
References
- ↑ MUN. Feb 3, 2009.
- ↑ TN2005 NS7.
- ↑ R. Kiehl. 8 November 2010.
- ↑ URL: http://moon.ouhsc.edu/kfung/iacp-olp/apaq-text/N1-MS-01-16-Ans.htm and http://moon.ouhsc.edu/kfung/iacp-olp/apaq-text/n1-ms-01.htm. Accessed on: 31 October 2010.
- ↑ URL: http://www.neuropathologyweb.org/chapter1/chapter1aNeurons.html. Accessed on: 22 December 2010.
- ↑ Holland GR (1996). "Experimental trigeminal nerve injury". Crit. Rev. Oral Biol. Med. 7 (3): 237–58. PMID 8909880.
- ↑ Piercecchi-Marti MD, Pélissier-Alicot AL, Leonetti G, Tervé JP, Cianfarani F, Pellissier JF (December 2004). "Pellagra: a rare disease observed in a victim of mental and physical abuse". Am J Forensic Med Pathol 25 (4): 342–4. PMID 15577526.
- ↑ URL: http://frontalcortex.com/?page=oll&topic=24&qid=602. Accessed on: 3 November 2010.
- ↑ Finnie JW, Manavis J, Blumbergs PC, Kuchel TR (November 2000). "Axonal and neuronal amyloid precursor protein immunoreactivity in the brains of guinea pigs given tunicamycin". Vet. Pathol. 37 (6): 677–80. PMID 11105962. http://vet.sagepub.com/content/37/6/677.full.
- ↑ MUN. 15 November 2010.
- ↑ URL: http://www.neuropathologyweb.org/chapter1/chapter1bAstrocytes.html. Accessed on: 2 July 2010.
- ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 202. ISBN 978-1416002741.
- ↑ 13.0 13.1 Perry, Arie; Brat, Daniel J. (2010). Practical Surgical Neuropathology: A Diagnostic Approach: A Volume in the Pattern Recognition series (1st ed.). Churchill Livingstone. pp. 18. ISBN 978-0443069826.
- ↑ URL: http://path.upmc.edu/cases/case336.html. Accessed on: 15 January 2012.
- ↑ URL: http://www.neuropathologyweb.org/chapter1/chapter1bAstrocytes.html. Accessed on: 7 November 2010.
- ↑ Gray, Francoise; Poirier, Jacques; De Girolami, Umberto (2003). Escourolle and Poirier's Manual of Basic Neuropathology (4th ed.). Churchill Livingstone. pp. 173. ISBN 978-0750674058.
- ↑ Weedman Molavi, Diana (2008). The Practice of Surgical Pathology: A Beginner's Guide to the Diagnostic Process (1st ed.). Springer. pp. 254. ISBN 978-0387744858.
- ↑ Takei, H.; Wilfong, A.; Malphrus, A.; Yoshor, D.; Hunter, JV.; Armstrong, DL.; Bhattacharjee, MB. (Aug 2010). "Dual pathology in Rasmussen's encephalitis: a study of seven cases and review of the literature.". Neuropathology 30 (4): 381-91. doi:10.1111/j.1440-1789.2009.01079.x. PMID 20051019.
- ↑ URL: http://medical-dictionary.thefreedictionary.com/neuronophagia. Accessed on: 11 April 2012.
- ↑ Vossough, A.; Zimmerman, RA.; Bilaniuk, LT.; Schwartz, EM. (Apr 2008). "Imaging findings of neonatal herpes simplex virus type 2 encephalitis.". Neuroradiology 50 (4): 355-66. doi:10.1007/s00234-007-0349-3. PMID 18246335.
- ↑ URL: http://neuropathology-web.org/chapter5/chapter5dViruses.html. Accessed on: 27 January 2012.
- ↑ 22.0 22.1 22.2 22.3 22.4 22.5 Wippold FJ, Perry A (March 2006). "Neuropathology for the neuroradiologist: rosettes and pseudorosettes". AJNR Am J Neuroradiol 27 (3): 488–92. PMID 16551982.
- ↑ URL: http://moon.ouhsc.edu/kfung/IACP-OLP/APAQ-Text/N1-TU-01.htm#17. Accessed on: 3 December 2010.
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