Neuropathology

melian.yates
Mind Map by , created almost 6 years ago

Doctorate Pathology (Systems Pathology) Mind Map on Neuropathology, created by melian.yates on 11/23/2013.

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melian.yates
Created by melian.yates almost 6 years ago
General Pathoanatomy Final MCQs (201-300)- 3rd Year- PMU
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melian.yates
General Pathoanatomy Final MCQs (301-400)- 3rd Year- PMU
Med Student
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Med Student
Neuropathology
1 Anatomy
1.1 Brain
1.1.1 Grey Matter (Outside)
1.1.1.1 Cerebral & Cerebellar cortex
1.1.1.1.1 Contains neuronal cell bodies
1.1.2 White Matter (Inside)
1.1.2.1 Contains axons, myelin sheaths, astrocyte fibers
1.1.3 Nuclei
1.1.3.1 Foci of grey matter also occur w/in the white matter
1.1.3.1.1 Ex. Olivary, red, cuneate, etc.
1.1.4 Meninges
1.1.4.1 Protect CNS
1.1.4.1.1 Encase CSF
1.1.4.1.1.1 Support blood vesels
1.1.4.2 Dura (Outside -thick (Packy)) -> Arachnoid -> Pia Matter (Inside - thin (Lepto))
1.1.4.2.1 Sunbarachnoid space (Blood vessels)
1.2 CNS Cell Types
1.2.1 1) Neurons
1.2.1.1 Response to Injury
1.2.1.1.1 Extremely vulnerable to injury
1.2.1.1.1.1 High metabolic rate
1.2.1.1.1.1.1 Little NRG storage
1.2.1.1.1.1.1.1 An Axon to care for
1.2.1.1.1.1.1.1.1 Axon has no Nissl (ribosomes)
1.2.1.1.1.1.1.1.1.1 Can't make protein
1.2.1.1.1.1.1.1.1.1.1 Can't dispose of own waste
1.2.1.1.1.1.1.1.2 Neurons CANNOT regenerate
1.2.1.1.2 Acute Necrosis
1.2.1.1.2.1 Most common response
1.2.1.1.2.2 Ischaemia
1.2.1.1.2.2.1 O2 required for oxidative phosphorylation
1.2.1.1.2.2.1.1 Cell's ATP drops & ion channels leak
1.2.1.1.2.2.1.1.1 Ca 2+ enters cells => membrane damage
1.2.1.1.2.2.1.1.1.1 Increased intracytoplasmic Ca2+ =>
1.2.1.1.2.2.1.1.1.1.1 ATPase => Decreased ATP
1.2.1.1.2.2.1.1.1.1.1.1 Phospholipase => Decreased phospholipids
1.2.1.1.2.2.1.1.1.1.1.1.1 Protease => Disruption of membrane & cytoskeletal proteins
1.2.1.1.2.2.1.1.1.1.1.1.1.1 Endonuclease => Nucleus chromatin damage
1.2.1.1.2.2.2 Red dead cells (Red cytoplasm)
1.2.1.1.2.2.2.1 Pyknosis
1.2.1.1.2.3 Hypoxia
1.2.1.1.2.4 Hypoglycaemia (toy breed puppies -> seizures)
1.2.1.1.2.5 Nutritional Deficiency (e.g. thiamine deficiency)
1.2.1.1.2.6 Toxins (e.g. Pb & Hg)
1.2.1.1.2.7 Laminar cortical necrosis
1.2.1.1.2.7.1 Polioencephalomalacia
1.2.1.1.2.7.1.1 Outer cortex "Melting" => Gelatinous material
1.2.1.1.2.7.1.2 Ruminants
1.2.1.1.2.7.2 Acute neuronal necrosis in a distinct pattern
1.2.1.1.2.7.3 Causes:
1.2.1.1.2.7.3.1 Salt poisoning (Pigs)
1.2.1.1.2.7.3.1.1 Water deprivation
1.2.1.1.2.7.3.1.1.1 Pb & Hg toxicity
1.2.1.1.2.7.3.1.1.1.1 Polioencephalomalacia
1.2.1.1.2.8 Polioencephalomalacia
1.2.1.1.2.8.1 Cerebrocortical necrosis (CCN)
1.2.1.1.2.8.2 Pathogenesis unclear
1.2.1.1.2.8.3 Thiamine deficiency vs. sulfide toxicity
1.2.1.1.2.8.3.1 Thiamine required for glucose metabolism => Hypoglycaemia
1.2.1.1.3 Chromatolysis
1.2.1.1.3.1 Swelling of the Neuron
1.2.1.1.3.1.1 Powdery appearence => Nissel substances dispersed ( unraveling ER)
1.2.1.1.3.2 NOT necrosis => Adaptive change
1.2.1.1.3.3 Dissolution of Nissel bodies
1.2.1.1.3.4 Ex. Equine dysautonomia (grass sickness)
1.2.1.1.4 Wallerian degeneration
1.2.1.1.4.1 Response of Axon to injury (Normally seen in white matter)
1.2.1.1.4.1.1 Healing => Axoplasm (Myelinated - built up at point of injury => swollen axon)
1.2.1.1.4.1.2 Neuroma => conglomeration of axons, axoplasm ("abortive attempt" at repair)
1.2.1.1.4.1.2.1 Ex. tail dock neuroma
1.2.1.1.4.1.3 No renegeration of basal lamina, inefficent clearance of debris & re-myelination (oligodendrocyte), inhibits axonal sprouting => Chances of repair low
1.2.1.1.4.2 Breakdown of the nerve fiber DISTAL to the point of initiating injury
1.2.1.1.4.2.1 Myelin sheath breaks up
1.2.1.1.5 Vacuolation
1.2.1.1.5.1 Transmissable spongioform encephalopathies (BSE, scrapie)
1.2.1.1.5.2 Common artefact (Not fixed properly)
1.2.1.1.5.3 Normal finding
1.2.1.1.5.4 Lysosomal storage disease
1.2.1.1.5.5 Early cell injury
1.2.1.1.5.6 Some toxins
1.2.2 2) Glial cells (Neural glue)
1.2.2.1 Astrocytes
1.2.2.1.1 " Star-shaped", multiple dendritic extensions
1.2.2.1.2 CNS equivalent of fibroblast
1.2.2.1.3 Functions:
1.2.2.1.3.1 Support
1.2.2.1.3.1.1 Insulating synapses
1.2.2.1.3.1.1.1 Detoxification
1.2.2.1.3.1.1.1.1 BBB
1.2.2.1.3.1.1.2 Produces cytokines
1.2.2.1.4 Response to Injury
1.2.2.1.4.1 Necrosis
1.2.2.1.4.2 Astrocytosis (astrocyte hyperplasia)
1.2.2.1.4.3 Astrogliosis (astrocyte hypertrophy & hyperplasia)
1.2.2.1.4.3.1 Starting to produce glial fibers ("Fibrosis")
1.2.2.2 Oligodendrocytes
1.2.2.2.1 Look like circular nuclei (Circular cells), Myelinate axons
1.2.2.2.2 Inefficient at re-myelinating in response to injury
1.2.2.2.3 Myelinate axons
1.2.2.2.3.1 Oligodendrocyte injury => De-myelination
1.2.2.3 Microglial cells
1.2.2.3.1 " Macrophage"
1.2.2.4 Ependymal cells
1.2.2.4.1 Line the ventricles
1.2.2.5 Choroid plexus epithelial cells
1.2.2.5.1 Produce CSF
1.2.3 Order of vulnerability to injury:
1.2.3.1 Neurons > Oligodendrocytes > Astrocytes > Microglia > Blood vessels
2 General Responses to Injury (CNS & PNS)
2.1 Oedema
2.1.1 Vasogenic
2.1.1.1 Most common form in animals
2.1.1.2 Follows vascular injury
2.1.1.3 Breaches BBB -> Increased permeability
2.1.1.4 Fluid is extracellular
2.1.1.5 Ex. Oedema disease in Pigs
2.1.1.5.1 E.coli (bacterial infection of GI tract)
2.1.1.5.1.1 Bacteria produce toxins in the intestine (endotoxaemia)
2.1.1.5.1.1.1 Toxin enters bloodstream => Brain => Vasculitis, Leaky vessels
2.1.2 Interstitial
2.1.2.1 Usually follows hydrocephalus
2.1.2.2 Ventricles dilate & increased hydrostatic pressure => Fluid forced into parenchyma
2.1.2.3 Fluid is Extracellular
2.1.3 Cytotoxic
2.1.3.1 ATP deficit & Failure of Na+/K+ pump => Na+ & H2O build up in cell
2.1.3.2 Fluid in Intracellular
2.1.3.3 Hypoxia, Ischaemia, toxins (anything that inhibits ATP production)
2.1.3.4 => Hydrophobic degeneration in other cells
2.1.4 Consequences
2.1.4.1 Brain swells, becomes compressed => Herniation
2.1.4.1.1 1) Through the Foramen Magnum
2.1.4.1.1.1 Most common
2.1.4.1.1.2 2) At Cingulate gyrus under the falx
2.1.4.1.1.2.1 3) Transtentorial herniation
2.1.4.1.2 Ex. Cerebellar herniation
2.1.4.1.2.1 Compresses Medulla (Resp. centers) => Sudden death
2.2 De-myelination
2.2.1 Primary: Myelin forms normally & then is selectively destroyed
2.2.1.1 Impaired maintenance (i.e. infectious destruction of oligodendrocytes)
2.2.1.1.1 Nutritional (Cu, Vit. B12)
2.2.1.1.1.1 Toxins (Cyanide)
2.2.1.1.1.1.1 Cytotoxic oedema
2.2.1.1.1.1.1.1 Immune mediated (i.e. multiple sclerosis, canine distemper (Most common))
2.2.1.1.1.1.1.1.1 Proposed Pathogenesis:
2.2.1.1.1.1.1.1.1.1 Oligodendrocytes die as a result of immune response against viral Ag on their surface
2.2.1.1.1.1.1.1.1.1.1 Molecular mimicry
2.2.1.1.1.1.1.1.1.1.1.1 Incorporation of neural elements into the virus during assembly resulting in anti-self response
2.2.2 Secondary: Loss of Myelin following axonal damage (i.e. Wallerian degeneration)
2.2.3 Vs. Dysmyelination => Myelin doesn't form properly in first place
2.3 Vascular Disturbances
2.3.1 Reduced blood flow (or complete blockage) leads to ischaemia
2.3.2 Consequences of ischaemia depend on:
2.3.2.1 It's degree & duration
2.3.2.1.1 Size & type of vessel involved
2.3.2.1.1.1 Relative susceptibility of tissue to hypoxia
2.3.3 Consequences of ischaemia:
2.3.3.1 Neuronal necrosis
2.3.3.2 Vasogenic oedema
2.3.3.2.1 The ischaemia is not a direct cause of the oedema, but the two could occur together if the ischaemia was the result of vascular damage
2.3.3.3 Infarct(s)
2.3.3.3.1 Necrosis of a tissue following obstruction of a supplying blood vessel
2.3.3.3.2 Often well demarcated
2.3.3.3.3 Causes:
2.3.3.3.3.1 Thrombosis/thromboembolism (Uncommon in the CNS of animals, can see with DIC or sepsis)
2.3.3.3.3.1.1 Emboli: FCEM (fibrocartilaginous embolic myelopathy), bone marrow embolism following fracture
2.3.3.3.3.1.1.1 Vasculitis: Classical swine fever (hog cholera - pestivirus), MCF (malignant catarrhal fever -herpesvirus), Oedema disease (vasculitis caused by E.coli toxin)
2.3.3.4 Malacia
2.3.3.4.1 Grossly: appreciable softening of brain/spinal cord (usually resulting from necrosis)
2.3.3.4.2 Histologically: Necrosis
2.3.3.4.3 Occurs in infarcts, but there are other causes (toxicosis, hypoxia, nutritional, infectious or metabolic disease)
2.3.3.4.4 The pattern & location of Malacia are often more Dx helpful than the lesion itself
2.3.3.4.4.1 Symmetrical Malacia:
2.3.3.4.4.1.1 Nutritional, Toxic, Metabolic, Genetic
2.3.3.4.4.2 Asymmetrical Malacia:
2.3.3.4.4.2.1 Vascular, Infectious, Traumatic
3 Inflammation of the Nervous System
3.1 Defence (against infection)
3.1.1 Skin
3.1.1.1 Skull/vertebrae
3.1.1.1.1 Meninges & CSF
3.1.1.1.1.1 Barriers (CSF/ECF, CSF/blood, BBB)
3.1.1.1.1.1.1 Microglia (monocyte/ macrophage system)
3.1.1.1.1.1.1.1 Immunologic responses (innate & adaptive)
3.1.1.1.1.1.2 BBB
3.1.1.1.1.1.2.1 Endothelial cell
3.1.1.1.1.1.2.1.1 Not fenestrated
3.1.1.1.1.1.2.1.1.1 Tight junctions
3.1.1.1.1.1.2.1.1.1.1 Fewer transporting vesicles
3.1.1.1.1.1.2.1.1.1.1.1 P glycoprotein
3.1.1.1.1.1.2.2 Astrocytes
3.1.1.1.1.1.2.3 Pericytes
3.2 Inflammation is usually the result of infection
3.2.1 Bacteria, Fungi, Parasites (protozoa)
3.2.2 Main Routes of Entry
3.2.2.1 Haemotogenous (most common)
3.2.2.2 Direct
3.2.2.2.1 Spread from adjacent structure (inner ear, skull sinuses)
3.2.2.2.2 Injection
3.2.2.3 Penetrating trauma
3.2.2.4 Via peripheral nerves
3.2.2.5 Leukocyte trafficking ("Trojan horse")
3.3 Sites of Inflammation
3.3.1 Epidural or subdural space
3.3.1.1 Tends to result in abscess (Uncommon)
3.3.2 Meninges
3.3.2.1 Leptomeninges - Pia & Arachnoid Matter (Leptomeningitis)
3.3.2.1.1 Suppurative:
3.3.2.1.1.1 Most common
3.3.2.1.1.2 Bacterial (E.coli, Streptococcus, Haemophilus)
3.3.2.1.1.3 Swollen brain, meninges opaque, OFTEN NO GROSS LESIONS
3.3.2.1.1.4 Neutrophils predominate initially
3.3.2.1.1.5 Usually fatal
3.3.2.1.1.6 Usually of haemotogenous origin
3.3.2.1.2 Eosinophilic meningoencephalitis:
3.3.2.1.2.1 Porcine salt poisoning/ H2O deprivation
3.3.2.1.2.2 Perivascular eosinophilic cuffing in the cerebrum & meninges
3.3.2.1.3 Lymphocytic:
3.3.2.1.3.1 Usually viral
3.3.2.1.4 Granulomatous:
3.3.2.1.4.1 Fungal disease & mycobacteriosis
3.3.2.1.4.1.1 Idiopathic forms (Mainly Dogs)
3.3.2.2 Pachymeninges - Dura matter (Pachymeningitis)
3.3.3 Parenchyma
3.3.3.1 Encephalitis
3.3.3.1.1 Inflammation of the cerebral parenchyma)
3.3.3.1.2 Classified based on nature of Exudate:
3.3.3.1.2.1 Suppurative
3.3.3.1.2.1.1 Fibrinous
3.3.3.1.2.1.1.1 Granulomatous
3.3.3.1.2.1.1.1.1 Lymphoplasmacytic
3.3.3.1.2.1.1.1.1.1 Eosinophilic
3.3.3.1.2.1.1.1.1.1.1 Haemorrhagic
3.3.3.1.3 Bacterial:
3.3.3.1.3.1 Typically result in Abscesses (Suppurative inflammation - i.e. localized collections of neutrophils)
3.3.3.1.3.2 Single or multiple depending on route
3.3.3.1.3.3 Vary in size with a central, liquefied cavity
3.3.3.1.3.4 Ex. E.coli, Streptococcus, Stapyhlcoccus, Pasteurella & Fusobacterium necrophorum
3.3.3.1.3.4.1 Listeria monocytogenes (Listeriosis)
3.3.3.1.3.4.1.1 Sheep, cattle goats
3.3.3.1.3.4.1.2 3 forms (CNS, abortion, sepsis)
3.3.3.1.3.4.1.3 Compared to other bacteria, pathogenesis in CNS disease is a little different
3.3.3.1.3.4.1.4 Oral mucosa -> Trigeminal nerve -> Trigeminal ganglion in brain
3.3.3.1.3.4.1.5 Source: Silage (pH > 5.4 allows bacterial growth)
3.3.3.1.3.4.1.6 Sxs: Circling, Facial nerve paralysis (unilateral), Drooling, Pharyngeal paralysis, Recumbancy, paddling, death
3.3.3.1.3.4.1.7 Usually NO GROSS lesions
3.3.3.1.3.5 White/grey matter junction predisposed
3.3.3.1.4 Viral:
3.3.3.1.4.1 Lymphoplastic inflammation
3.3.3.1.4.2 Haematogenous & neural routes mainly
3.3.3.1.4.3 Hallmark lesions (regardless of virus type):
3.3.3.1.4.3.1 1) Neuronal necrosis
3.3.3.1.4.3.1.1 2) Gliosis (glial nodules)
3.3.3.1.4.3.1.1.1 3) Vascular changes -lymphoplasmacytic cuffing
3.3.3.1.4.4 Types of Virus:
3.3.3.1.4.4.1 Neurtropic
3.3.3.1.4.4.1.1 Viruses which can overcome innate immunity of brain
3.3.3.1.4.4.1.2 Rabies (rhabdovirus)
3.3.3.1.4.4.1.2.1 Encephalomyelitis & ganglionitis
3.3.3.1.4.4.1.2.1.1 Lesions are macroscopic
3.3.3.1.4.4.1.2.1.1.1 Intracytoplasmic, oval, pink inclusion bodies (Negri bodies)
3.3.3.1.4.4.1.3 Aujesky's disease (Herpesvirus)
3.3.3.1.4.4.1.4 Visna (Ovine lentivirus)
3.3.3.1.4.4.2 Endotheliotropic
3.3.3.1.4.4.2.1 EHV1 (Equine herpesvirus type 1)
3.3.3.1.4.4.2.2 Classical swine fever (pestivirus)
3.3.3.1.4.4.2.3 Infectious canine hepatitis (canine adenovirus)
3.3.3.1.4.4.2.4 Endothelial cell damage leads to vascular injury & secondary parenchymal necrosis & haemorrhage
3.3.3.1.4.4.3 Pantropic
3.3.3.1.4.4.3.1 Canine distemper (morbillivirus)
3.3.3.1.4.4.3.2 Infectious bovine rhinotracheitis (Bovine herpesvirus type 1)
3.3.3.1.4.4.3.3 Respiratory, urogenital & CNS
3.3.3.1.4.4.3.4 Virus can be latent in nerve ganglia
3.3.3.1.5 Prion Diseases:
3.3.3.1.5.1 Transmissable spongiform encephalopathies (TSEs)
3.3.3.1.5.1.1 BSE, scrapie, chronic wasting disease
3.3.3.1.5.1.2 A group of fatal neurodegenerative diseases which occur in a number of species
3.3.3.1.5.2 Proteinaceous infectious particle
3.3.3.1.5.2.1 Abnormal isoform of prion protein (PrP) in the brain -> PrPsc (common to all cases)
3.3.3.1.5.2.1.1
3.3.3.1.5.2.1.2 PrPsc accumulates in nervous tissue as amyloid fibrils
3.3.3.1.5.2.1.2.1 Long incubation period, difficult to Dx (no immune response)
3.3.3.1.5.2.1.2.1.1 Agent is highly resistant
3.3.3.1.5.2.1.3 Alpha helix -> beta pleated sheet
3.3.3.1.5.3 No gross lesions; Characteristic microscopic lesions
3.3.3.1.5.3.1 Spongioform change, Amyloid plaques, Astrogliosis
3.3.3.1.6 Fungal/ Protozoa:
3.3.3.1.6.1 Cryptococcus
3.3.3.1.6.1.1 Opportunistic -Aspergillus
3.3.3.1.6.1.1.1 Neospora
3.3.3.1.6.1.1.1.1 Toxoplasma gondii
3.3.3.2 Myelitis
4 Trauma
4.1 Less common in animals than man
4.1.1 Less risk, Better protection
4.2 Main forms of injury
4.2.1 Concussion
4.2.2 Contusion
4.2.2.1 Pathogenesis:
4.2.2.1.1 Head is moving, but suddenly stopped by solid object
4.2.2.1.1.1 1st point of impact = where object hits the head
4.2.2.1.1.1.1 Head stops, brain doesn't
4.2.2.1.1.1.1.1 Brain strikes inside of skull at first point of impact (Coup)
4.2.2.1.1.1.1.2 Brain moves in cranium, stretching & tearing vessels & nerves on the opposite side to the original impact (Contrecoup)
4.2.3 Laceration
4.2.4 Haemorrhage
4.2.4.1 Locations:
4.2.4.1.1 a) Epidural
4.2.4.1.1.1 b) Subdural
4.2.4.1.1.1.1 c) Leptomeningeal
4.2.4.1.1.1.1.1 d) Subpial
4.2.4.1.1.1.1.1.1 e) Intramedullary
5 Response of Spinal Cord to Injury
5.1 Like the brain, can be affected by infectious, inflammatory, toxic, nutritional & neoplastic disease, & lesions can occur in its parenchyma
5.2 Traumatic injuries:
5.2.1 Concussion, contusion, haemorrhage & Compression
5.2.1.1 Compression
5.2.1.1.1 May arise within (Intra-medullary) or outside (Extra-medullary) the spinal cord
5.2.1.1.2 Causes:
5.2.1.1.2.1 Neoplasia
5.2.1.1.2.2 Abscess
5.2.1.1.2.2.1 Extradural
5.2.1.1.2.2.1.1 Vertebral
5.2.1.1.2.2.1.1.1 Intervertebral
5.2.1.1.2.3 Fracture: Traumatic or pathological
5.2.1.1.2.3.1 Vertebral bodies (e.g. due to abscess, metabolic disease, neoplasia)
5.2.1.1.2.4 Invertebral disk disease (IVDD)
5.2.1.1.2.4.1 Prolapsed disk can cause acute or chronic compression
5.2.1.1.2.4.2 Chrondrodystrophic
5.2.1.1.2.4.2.1 Nucleus pulposus replaced by chondroid tissue
5.2.1.1.2.4.2.1.1 Degeneration of annulus fibrosus is 2ndary
5.2.1.1.2.4.2.1.1.1 Young Dogs
5.2.1.1.2.4.3 Non-chrondrodystrophic
5.2.1.1.2.4.3.1 Degeneration begins in annulus fibrosis
5.2.1.1.2.4.3.2 Nucleus undergoes fibrosis
5.2.1.1.2.4.3.3 Middle aged dogs (TL)
5.2.1.1.2.4.3.4 Age-related & not breed dependent
5.2.1.1.2.5 Malformations (esp. vertebral)
5.2.1.1.2.5.1 Wobbler horses (stenotic myelopathy): Vertebral canal narrows due to malformation & malarticulation of the cervical vertebrae (usually C3-C4)
5.2.1.1.2.5.2 Cervical vertebral malformation-malarticulation (Dogs) - similar pathogenesis to wobbler horses
5.2.1.1.2.5.3 Alantoaxial subluxation of toy Dogs (Hypoplastic dens leads to subluxation)
5.2.1.1.3 Lesions are similar regardless of the cause
5.2.1.1.3.1 Gross: Spinal cord may be indented or flattened
5.2.1.1.3.2 Histologically: Myelin sheath ballooning in all funiculi w/ axonal swelling/loss, Myelin digestion chambers, Neuronal loss, gliosis, malacia (due to vascular damage), oedema
6 Congenital Malformations
6.1 Abnormal development of neural tube
6.2 May involve Spinal cord, Brain, Calvaria, Meninges &/or Vertebral column
6.3 Morphological
6.3.1 Hydrocephalus
6.3.1.1 Increased accumulation of fluid within the cranial cavity
6.3.1.2 Types:
6.3.1.2.1 Internal (fluid w/in ventricles)
6.3.1.2.1.1 Congenital form:
6.3.1.2.1.1.1 Obstruction NOT found
6.3.1.2.1.1.2 Common in brachycephalic dogs (mesenphalic aqueduct may be stenotic)
6.3.1.2.1.1.2.1 Sporadic in cattle
6.3.1.2.1.2 Acquired form:
6.3.1.2.1.2.1 Causes: Obstruction due to inflammation (of meninges &/or ependymal cells) or space occupying lesions compression (neoplasms, abscesses & cholesteatomas)
6.3.1.2.1.3 Common
6.3.1.2.2 External (w/in arachnoid space)
6.3.1.2.2.1 Communicating (w/in both locations)
6.3.1.2.2.1.1 Hydrocephalus ex vacuo (ventricles dilate 2ndary to replace lost tissue)
6.3.2 Others
6.3.2.1 Anencephaly (absence of brain)
6.3.2.2 Lissencephaly (normal in mice, rats, rabbits & birds)
6.3.2.2.1 Meningoencephalocoele
6.3.2.2.1.1 Spinal: spina bifida, hydromyelia & syringomyelia
6.3.3 Cerebellar Defects
6.3.3.1 Cerebellar hypoplasia
6.3.3.1.1 Common
6.3.3.1.2 Inherited: (Arab foals, Jersey cows, Chows, Corriedale sheep)
6.3.3.1.2.1 Acquired: Environmental teratogens attack germinal cells in external granular layer of cerebellum (source of neurons)
6.3.3.1.2.1.1 Ex. Bovine virus diarrhea (BVD), feline parvovirus, CSF (hog cholera), canine parvovirus, schmallenberg virus
6.3.3.2 Cerebellar Abiotrophy
6.3.3.2.1 Premature degeneration of nervous tissue elements after they have formed (form of atrophy) - probably inherited
6.4 Functional (biochemical abnormalites - ex. lysosomal diseases or leukodystrophies)
6.5 Causes:
6.5.1 Inherited
6.5.2 Environmental (most common)
6.5.2.1 Toxic
6.5.2.1.1 Infectious
6.5.2.1.1.1 Nutritional
6.5.2.1.1.1.1 Radiation
7 CNS Neoplasia
7.1 Primary
7.1.1 Meninges
7.1.1.1 Meningioma
7.1.1.1.1 Most frequent in Dogs & Cats
7.1.1.1.2 Compressive, space-occupying lesion (seldom invades)
7.1.2 Glial cells
7.1.2.1 Astrocytoma
7.1.2.1.1 Most common glial tumor
7.1.2.1.1.1 Brachycephalic breeds
7.1.2.1.1.1.1 Solid, firm, grey-white (sometimes mottled red w/ areas of necrosis/haemorrhage)
7.1.2.2 Oligodendroglioma
7.1.2.2.1 Most common in Dogs (brachycephalic breeds)
7.1.2.2.1.1 Soft, grey to pink/red & often gelatinous
7.1.2.3 Ependymoma
7.1.2.3.1 Mainly in ventricles (primarily lateral)
7.1.2.3.2 May spread in the ventricular system via CSF
7.1.2.3.3 Expansile, but can be invasive & destructive
7.1.2.4 Choroid plexus tumors
7.1.2.4.1 Rare, mainly Dogs, 4th ventricle
7.1.3 Neurons (very rare)
7.2 Secondary (Metastatic)
7.2.1 Haemangiosarcoma
7.2.1.1 Mammary or Pulmonary Carcinoma
7.2.1.1.1 Lymphoma
7.2.1.1.1.1 Pituitary tumors
7.2.1.1.1.1.1 Vertebral osteosarcoma
8 Idiopathic Diseases
8.1 Idiopathic Epilepsy
8.1.1 Small group of neurons periodically & spontaneously depolarize
8.1.1.1 Structural : Neoplasma, inflammation, trauma
8.1.1.1.1 Biochemical: Hypocalcemia, Hypoglycemia, Hepatic encephalopathy
8.1.1.1.1.1 Idiopathic: No cause identified (indiviuduals have a low seizure threshold)
9 Diseases of Peripheral Nerves
9.1 Dorsal & Ventral roots, spinal ganglia, spinal & peripheral nerves, cranial nerves & peripheral components of the ANS
9.2 Trauma
9.2.1 Nerves are predisposed to injury because of:
9.2.1.1 Superficial position
9.2.1.1.1 Proximity to bone
9.2.1.1.1.1 Proximity to injection sites
9.2.2 Laceration
9.2.2.1 Avulsion ("pull out" - usually at roots)
9.2.2.1.1 Transection
9.2.2.1.1.1 Compression & stretching (following fracture or dislocation)
9.2.2.1.1.1.1 => Wallerian degeneration
9.3 Infectious
9.3.1 Some infectious agents involve peripheral nerves as well as CNS
9.3.2 Ex. Rabies, Aujesky's disease, Neospora caninum, Toxoplasma gondii
9.3.3 Neospora caninum
9.3.3.1 Dorsal roots (Dog)
9.3.3.2 Equine Guttural Pouch mycosis
9.3.3.2.1 Inflammation in the recurrent laryngeal nerve -> vocal cord hemiplegia
9.3.3.2.2 Macaw Wasting Disease (Proventricular dilation syndrome)
9.3.3.2.2.1 Non suppurative inflammation around myenteric ganglia => gastric dysfunction (wasting, anorexia, depression) => neurological signs (ataxia, seizures)
9.3.3.2.2.2 Borna disease virus ?
9.4 Idiopathic/ Immune mediated
9.4.1 Coonhound paralysis
9.4.1.1 Polyradiculoneuritis (racoon bites) => Quadriplegia
9.4.1.1.1 Lesions in ventral roots of spinal nerves & in peripheral nerves
9.5 Neuropathies
9.5.1 Often breed related -> Inherited pathogenesis
9.6 Degenerative
9.6.1 Equine laryngeal hemiplegia ("roarers")
9.6.1.1 Common
9.6.1.2 Pathogenesis:
9.6.1.2.1 Degeneration of left recurrent pharangeal nerve -> Atrophy of the left dorsal cricoarytenoid muscle -> Inability to abduct arytenoid cartilage & vocal fold => Airways partially obstructed on inspiration
9.6.1.2.2 Cause:
9.6.1.2.2.1 Idiopathic/ inherited, 2ndary to guttural pouch mycosis, Trauma
9.6.1.3 95% cases on Left
9.7 Toxic
9.7.1 Uncommon
9.7.2 Heavy metals (Pb, Hg, Thallium)
9.7.2.1 Pb -> damages Schwann cells -> peripheral degeneration
9.7.2.1.1 Hg -> Targets neuronal cell bodies -> 2ndary axonal degeneration in peripheral nerves
9.8 Neoplastic
9.8.1 Uncommon
9.8.2 Dogs
9.8.3 Peripheral nerve sheath tumors (Benign/ Malignant)
9.9 Nutritional/metabolic
9.9.1 Vitamin A & B, Pantothenic acid & Cu deficiency => Neuropathy
9.9.1.1 Cu deficiency: Swayback (New born lambs) & enzootic ataxia (older lambs)
9.9.2 Metabolic: Diabetes mellitus, Hypothyroidism