Basic neuropathology

• 1) H&E = pink w/ blue dots
• 2) Cresyl violet- nissl substance
• - Luxol fast blue - glia
• 3) Bielschowkys silver- fiber neurons
• 4) GFAP- immunohistochemistry (glia tumors)

• Neuronal reaction
• acute axon injury -> perikaryon -> swelling & peripheral displacement of nucleus & nissl substance
• Regeneration of the axon

Caused by: acute infection, toxic, vascular, or metabolic changes

Neuronal reaction after acute injury that leads to necrosis or apoptosis.

• shrinkage, pyknosis of nucleus(dense chromatin), triangular, cytotoxic edema, eosinophilia, loss of nissl bodies
• H & E stain 12 -24 hours after irreversible hypoxic insult.
• WHERE: hippocampus, neocortex, purkinje cells

• Neuronal reaction
• cork screw axons with microglia infiltration

• acidophilic neurons, vascular proliferation
• neurophagy via scavenger cells -> microglia scar & iron deposition

• Neuronal reaction
• end stage
• accumulation of lipfuscin, distortion, dead neuron
• If seen histologically = prolonged death

>30% depopulation in a given section

• neuronal reaction (neuronal atrophy)
• dendrite degeneration -> loss of afferent connection
• WHERE: lat geniculate bodies (optic nerve damage)
• - mammillary bodies (degen of fornix)
• - neurons of gracile & cuneate (degen of post spinal cord)

• Microscopically: binuclear nueron
• - fenestrated neuron

• Neuronal reaction (trans-synaptic finding)
• binuclear
• neurofibrillary degeneration
• fenestrated neuron

• Iron deposit
• SEEN IN:
• Chronic trauma(boxers)
• Old infarcts
• Stage III syphilis

• CMV inclusion
• Herpes cowdry bodies
• oligodendrocytes with viral intranuclear inclusions
• intracytoplasmic negri (rabies)

• Intracyoplasmc inclusions and highly resistant to degradation.
• Alzheimers- neurofibrillary tangles
• Parkinsons - Lewy bodies
• Creutzfeldt-Jakob disease- vacuolization of perikaryon & neuronal cell processes in the neuropil

• Neurolipid accumulation
• Ganglioside

• Neurolipid accumulation
• sphingomyelin

• Neurolipid accumulation
• Glucocerbroside

local proliferation of astrocytes which leads to hypertrophy and hyperplasia

• Protoplasmic = intial repair
• fibrous = later repair

• Anisomorphic = cortical scars
• Isomorphic = white matter

• Reactive gliosis:
• Hypertrophy of cytoplasmic processes
• inc production of GFAP

• Astrocytic gliosis:
• hypertrophy and hyperplasia of astrocytes

Bright pink, somewhat irregular swath around an eccentric nucleus, from which emerge numerous stout, ramifying processes.

• Found near tumors or areas of necrosis
• or in tissue destruction & repair

• Glucose polymers inclusion of astrocytes
• Located in subpial, subependymal, and perivascular, and olfactory tracts.

• Astrocytes cytoplasmic inclusion bodies.
• densely compacted glial intermediate filaments with entrapped cytosolic proteins and form in long standing astrogliosis.

• Viral inclusion in progressive multifocal leukoencephalopathy.
• Multiple system atrophy- glial cytoplasmic inclusions composed of a-synulein.

• Lines ventricles.
• Disruption leads to prolferation of subependymal astrocytes --> irregularities of ventricular surface.
• CMV is a cause

Type I (astrocytes) - multinucleated, eosinophilic, giant cells. WHERE: white matter

Type II (liver glia)- nuclei > 20Mm & liver disease related(chronic liver disease, Wilsons disease, or hereditary metabolic disorder of urea cycle. Lobular nucleus & thick membrane

Type III glia - devoid of cytoplasm. naked nuclei glia.

• activated into rod cells - lipid accumulation -> foamy cells
• Also form microglial nodules (aggreagates around tissue necrosis)
• neuronophagia (congregation around cell bodies of dying neurons)

• Vasogenic
• cytotoxic
• interstitial

• BY: no lymphatic drainage & damage to BBB
• CAUSES: ischemia & herniation

Unilateral

Widened gyri, engorged veins, compressed sulci.

• Traumatic brain injury
• disruption of brain functions with 1 or more:
• LOC
• loss of memory
• AMS
• Focal neurological changes

• Primary: trauma is the main cause
• results in Diffuse axonal injury
• Secondary: Blunt trauma leads to something else that causes brain problems
• - Intracranial hematoma, edema, herniation, infection, infarction

• Functional impairments related to site of injury
• Spinal cord transection or crush injury

• Small hemorrhagic lesions & diffuse damage to axons
• No fracture involved
• Microscopically: axon is swollen & looks like neuron (retraction ball) Present 12-24 hours later

• Grade I = DAI
• Grade II = DAI & hemorrhage in corpus callosum
• Grade III = DAI, hemorrhage in corpus callosum & lesions to DLR brainstem

• altered consciousness after blunt head trauma
• Presents with:
• Transient LOC
• Paralysis
• Siezures
• Recovery can take hours to days

• Blunt trauma with microhemorrhage without cavity formation
• No hematoma present and continuity is preserved
• Clincal:
• LOC
• transient --> permanent focal neurological defect
• INC ICP
• Coup vs countercoup

• DAI- 24 hours
• Cerebral edema - 3 days
• Delayed subdural hematoma ischemic injury- years

• Pathology of concussion
• Involves: Dysfx of reflexes
• altered consciousness
• widespread depolarization
• no morphological findings

• Epidural hematoma caused by middle meningeal artery ->inc ICP -> mass effect
• Course: drowsy-> coma-> death

• small trauma -> veins damaged -> fibroblastic organization or cyst formation -> attracts water -> edema -> Inc ICP -> herniation or cerebral ischemia
• Clinical: Biphasic LOC

• headache
• irritability
• dizziness
• dec concentration
• memory problems
• fatigue
• visual disturbance
• Noise sensitivity
• judgement problems
• anxiety & depression

• Birth Injury
• Between skin & epicranial aponeurosis
• Crosses midline
• asymptomatic
• gradually resolves

• Birth injury
• collection of blood between Periosteum and skull
• Common over parietal or occipital bones
• limted by skull sutures -> does not cross midline
• may lead to anemia or jaundice
• gradually resolves

• Birth injury
• Collection of blood between epicranial aponeurosis & periosteum of skull

• Intracerebral bleeding from dural sinuses or brain substances
• devastating

• Holes in white matter surrounding the ventricle.
• Caused by change in blood flow or infection.

Formation of large multicoular cavities throughout the cerebral hemispheres