Neuro 1 - circulation, injury Flashcards
types of cells (4)
- neurons
- oligodendrocytes
- astrocytes
- microglia
3 circulatory disorders and injury to the CNS
- raised incracranial pressure
- circulatory disorders
- trauma
what can increased ICP lead to and why
head pressing due to edema
types of CNS circulatory disorders
- brain swelling and edema
- thrombosis, ischemia, infarcts
- hydrocephalus
what is increased ICP
limited potential for expansion due to the non-yielding nature of the cranial vault –> results in increased ICP
causes of increased ICP
- focally expanding mass (tumor, abscess)
- CSF accumulation (ventricular obstruction)
- vascular congestion (inflammation, trauma, toxin, etc)
- brain edema
list consequences of intacranial expanding lesion (swelling)/increased ICP
- local deformity (tumor), reduced CSF volume and brain distortion
- internal herniation
- ischemic brain necrosis
significance of internal brain herniation
results in hemorrhagic infarction of the herniated segment and/or the tissue compressed by the herniated segment
what happens in ischemic brain necrosis
- brain swelling compresses small caliber vessels, esp those entering from meningeal surfaces
- widespread endothelial damage
- even if severe swelling is reduced, reperfusion of damaged vessels will cause severe vasogenic edema
- greater degrees of vascular compression = ischemic brain necrosis
4 locations for brain herniation
- supracallosal subfalcine
- trantentorial
- foraminal
- transcalvarias
supracallosal subfalcine herniation
- falx cerebri (dural septium) –> permanent location
- falx cerebri = division between hemispheres (part of meninges)
- cingulate gyrus slips beneath it
- clinical signs aren’t as defined (seizures, loss of voluntary consciousness)
- 12:00 on drawing
transtentorial herniation
- tentorium cerebelli (dural septum + bone) –> permanent location
- occipital cortex slips beneath, compressing midbrain –> displaces it posteriorly
- 4:00 on drawin
foraminal herniation
- most common
- herniation of cerebellum may compress and thus disrupt function of respiratory centers in brain
- permanent location
- 6:00 on drawing
transcalvarias herniation
- from trauma
- location varies (2:00 on drawi6)ng)
what is brain swelling
increase in volume of all or part of the brain
what is brain swelling a potential complication of (6)
- head injury
- ischemia
- hemorrhage
- tumor
- infection
- metabolic disease
what is congestive brain swelling
enlargement of the brain resulting in elevated ICP caused by an increased diameter of the blood-containing vasculature (cerebrovascular dilation) –> localized or generalized
cause of congestive brain swelling
trauma
what is brain edema
increased brain tissue water content (of brain parenchyma) within the cell and within the intercellular space
types of brain edema (4)
- vasogenic edema
- cytotoxic edema
- hypo-osmoic edema
- hydrostatic edema
what is neuropil
everything in the brain that is not cell body, cell processes, or glia/neuron processes
BBB and permeability with edema
- separation of interendothelial tight junction
- increased vesicular transport and formation of transendothelial channels
- biochemical and structural alteration of the endothelial membrane –> increase in permeability
vasogenic edema
- most common
- from loss of BBB function
- distribution of edema depends on distribution of affected vessels (localized things like tumor/abscess/hematoma/trauma/infarct or generalized things like trauma/toxins)
cytotoxic edema
- intracellular fluid accumulation with normal vascular permeability
- damaged ATP-dependent ion pumps (hypoxia, bacterial exotoxin)
histologic changes in vasogenic edema
- polymicrocavitation change, fluid accumulation between cells
- vacuolization of neuropil
ultrastructural changes in cytotoxic edema
- accumulation of fluid within astrocyte (clear cytoplasm sparse chromatin, vacuolization of cytoplasm)
- toxin in astrocyte –> cytotoxic edema
hypo-osmotic edema
- rapid osmolarity shifts
- water intoxication, salt toxicity
- osmolarity of CSF slightly higher than plasma –> drink lots of water –> liquid moves into brain –> edema
hydrostatic edema
- interstitial edema
- elevated intraventricular hydrostatic pressure that accompanies hydrocephalus
- abnormal circulation of CSF
combination of vasogenic and cytotoxic edema (2 types)
- common
- primary endothelial injury –> vasogenic edema + decreased tissue perfusion –> tissue hypoxia –> cytotoxic component
- primary astrocytic insult –> cytotoxic edema + tissue volume expansion –> vascular compression/low flow –> endothelial injury from loss of laminar blood flow –> vasogenic component
status spongiosus
extracellular or intracellular edema of white matter affecting mostly oligodendrocytes
spongiform changes
-vacuolation observed in neurons and its processes in the transmissible spongiform encephalopathy (prion diseases)
intramyelinic edema
- histo: status spongiosus (white matter) –> holes
- uncommon, reflecting toxic insult to oligodendrocytes
- fluid accumulation within myelin lamella –> resultant vacuoles are sharply demarcated
what is it when you have increased water content in brain interstitium
brain edema
causes of hemorrhage in animals
- trauma
- infection and clotting disorders
- degeneration of the vascular wall
- arterio-venous malformations (uncommon)
- hypertention (only great apes)
- aneurysms (rare)
what happens in “brain vascular accident”
vessel rupture –> bleeding –> expansion –> edema, compression, necrosis
what is ischemia
reduction in blood flow to a region
metabolism of brain tissue and ischemia
- nervous tissue has high metabolic rate
- regional variations in metabolic rate (developing tissue/cell vulnerability) –> measure blood flow
selective vulnerability to ischemia and selective neuronal death
- specific neuron population
- not all cell types are equally vulnerable to ischemic insults
- neurons more susceptible than glia or vascular cells, some neurons more susceptible than others
neurons most susceptible to ischemia
- large pyramidal cells of layers 3, 5, 6 in cerebral cortex, hippocampal pyramidal cells, and purkinje cells in cerebellum
- neonate: more involvement of brain stem nuclei than in adult
time limit of ischemia
2-3 minutes of oxygen deprivation is all that neurons can tolerate (depends on energy sensitivity)
causes of diminished tissue perfusion
- embolism
- thrombosis (secondary to endothelial damage; vasculitis)
- trauma
- external compression
what is infarction
- territorial death of nervous tissue die to lack of blood supply
- gross appearance: red or pale (depends on whether reperfusion takes place)
causes of infarction
- thrombi
- emboli
- idiopathic
- feline ischemic encephalopathy
- septic emboli
- edema
major consequence of hemorrhage
-increased ICP due to space occupying nature of lesion and destruction of functional tissue
feline ischemic encephalopathy
- cause of infarction
- affects animals of all ages, both sexes
- acute onset with variable signs: ataxia (cerebellum), circling (ears), seizures, blindness, postural deficits
- mild improvement over first few days then typically remain stable
pathology of infarction
- usually unilateral ischemic necrosis, typically involving territory of middle cerebral artery
- boundary or border zone infarcts: distal regions of vascular territories particularly vulnerable to reductions in BP and blood flow
- can be bilateral, probably won’t be symmetric
ischemic changes over time
- 0-12hrs: no changes in routine light microscopy
- 12hrs: pink neurons
- 12-24hrs: neutrophils
- 1-3d: macrophages
- 1-2wks: reactive astrocytes
- months: cavitation
spinal cord infarction info
- fibrocartilaginous disc emboli
- dogs, cats, horses, swine, humans
- acute onset of sudden hemiparesis or flaccid paraplegia (signs depend on occlusion site)
- little recovery
- in dogs, more common in chondrodysplastic or large breeds
pathology of spinal cord infarction
- usually in lumbar and thoracic segments
- unilateral infarct of cord involving both gray and white matter
- sometimes can localize disc material within arteries and veins
- how the disc material gains access to vasculature is unclear
what is malacia
softness of nerve tissues
principal effect of vascular compressive spinal cord lesion
reduction of blood supply –> extent of injury function of rapidity in which mass compromises vascular supply and degree of compromise
nature of mass in vascular compression spinal cord lesions
- herniated interverterbral disc material
- epidural abscess/neoplasm
- displaced vertebral body (subluxation)
what part of the cord is usually compressed and why
since most of the compression of the spinal cord originates in the vertebral disc or body, most tend to compress the ventral aspect of the cord
what is wallerian degeneration
degeneration of distal part of axon (from compression) –> hallmark of the response of the nerve fiber to a compression (axon and myelin around axon degenerates, macrophages come to remove debris)
causes of extramedullary spinal cord compression (7)
- canine degenerative intervertebral disc disease
- equine cervical vertebral instability/stenotic myelopathy (young thoroughbreds)
- equine cervical static stenosis (QH)
- cranioventral malformation of arab
- canine lumbar discospondylitis (brucella canis)
- epidural abscesses
- spinal neoplasia
what is hydrocephalus
- consequence of a structural anomaly which is either acquired or heritable, congenital or post-natal in development
- underlying defect is increase in CSF volume reflecting imbalance in rate of production and resorption
2 types of hydrocephalus (list)
- communicating hydrocephalus
- noncommunicating hydrocephalus (internal hydrocephalus)
communicating hydrocephalus
- CSF may accumulate in subarachnoid space and ventricular system
- physical alteration of arachnoids granulations is such that CSF absorption occurs at a slower rate
- uncommon, generally acquired
noncommunicating hydrocephalus
- results from decreased CSF resorption (stuck in 1 chamber)
- most common congenital anomaly of dogs
- more commonly, accumulation may be restricted to venitricular system
- for CSF to reach arachnoid villi from origin in choroid plexus of lateral ventricles, efficient passage through 3 foramina/ducts must be unhindered (interventricular forames, mesencephalic aqueduct, lateral apertures of 4th ventricle)
interventricular foramen
- due to large size of opening, obstruction is uncommon
- causes are generally masses in the vicinity (ipsilateral choroid plexus, foramen thalamic neoplasm)
- unilateral or bilateral (symmetric or asymmetric)
mesencephalic aqueduct
- highly susceptible to alterations, decreasing CSF flow due to small diameter of channel and length
- hereditary malformations often result in congenital hydrocephalus
- inflammatory lesions where there is ependymal destruction
- reparative processes restrict the diameter of the duct (canine parainfluenza, FIP, mass)
consequences of hydrocephalus (3)
- hydrostatic edema
- herniation (cerebellum)
- atrophy
CNS trauma
- generally holds poor prognosis
- lack of neuron regenerative abilities
- hemorrhage increases ICP due to fixed volume of cranial vault and inability of CSF to compensate for space occupying lesions
- local hemorrhage –> vasoconstructive effect on brain vasculature –> infarction
concussion
- loss of consciousness following transient deformation of axonal processes (temporary)
- structural changes not present, reversible
- when structural changes are present, lesion is a diffuse axonal injury characterized by axonal degeneration and necrosis
contusion
- structural changes are present
- coup: stationary head is struck by moving object –> lesion on same side as trauma
- contrecoup: moving head strikes a stationary object –> lesion on opposite side of trauma
laceration/avulsion
- cutting or tearing of parenchyma; frequently involves fracture of bone encasement of the CNS
- displacement of bone fracture margins
- penetrating wound
- stretching/rupture of optic nerve
- contusion may have laceration component
