Key Terminology & Definitions - Nervous System Flashcards
Metacestode
Cyst location in intermediate hose
Gravid
Egg-containing
Ovoviviparous
Animals born live
Aberrant host
Accidental/dead-end host
Glioma
Tumour in CNS
Astrocytoma
Astrocyte cell tumour
Oligodendroglioma
Oligodendrocyte cell tumour
Hydrocephalus
Dilation of ventricles, probably congenital
Leuko
White matter
Malacia
Softening and necrosis of the nervous tissue - complete loss of architecture and cells
Polio
Grey matter
Encephalo
Brain
Myelo
Spinal cord
Leukoencephalomalacia
Affecting white matter of the brain
Coup blunt force brain trauma
Lesions immediately below the site of the impact, more severe if the head is stationary but mobile at impact
Contre- coup blunt force brain trauma
Brain moves within solid skull, lesions away from the site of impact , more severe if impact is with a stationary object
Contusion
Bruising, ruptured capillaries, blunt force trauma, brain or SC collide with bone, damage to microvasculature (haemorrhage and oedema)
Haematoma
Focal accumulation of blood
Myelomalacia
Spinal cord necrosis/softening of spinal cord
Vasogenic oedema in brain
Injury to vascular endothelium -> breakdown of BBB -> inc permeability + leakage /permeation of plasma, fluid spreads between cells (intersitium), white matter offers less resistance to passage of fluid in the interstitium -> oedema is more severe (grey matter has dense neuropil)
Cytotoxic oedema
Intracellular = hydrotropic degeneration in other tissues, astrocytes, neurones, endothelial cells -> swelling of the cytoplasm +/- nucleus
Hydrostatic (interstitial) oedema
Accumulation of fluid in interstitial space, commonly around ventricles with hydrocephalus - forces fluid out into surrounding tissues
Hypo-osmotic oedema
Over consumption of water leading to dilution of plasma - over hydration e.g. marathon runner, normal CNS and CSF is slightly higher osmolality than plasma, further reduction of plasma osmolality fluid to move into brain tissue, salt poisoning in pigs
Hypoxia
Reduced O2 supply, cytotoxic oedema (cell swelling) -> necrosis
Anoxia
Complete lack of O2 supply
Vascular obstruction
Ischaemia e.g. thromboembolism -> infarction
Cessation of cerebral circulation
Hypoxia -> anoxia e.g. cardiac arrest
Sustained hypotension
Hypoxia e.g. shock
Hypoxaemia
Reduced arterial oxygenation e.g. sever pneumonia, severe anaemia, CO poisoning, asphyxiation
Impaired cell utilisation of O2
E.g. Cyanide poisoning, fluoroacetate (1080) poisoning
Dorsal nerves =
Sensory
Ventral nerves =
Motor
Encephalitis
Inflammation of the brain (doesn’t always mean infectious agent)
Myelitis
Inflammation of SC
Encephalomyelitis
Inflammation of the brain and SC
Meningitis
Inflammation of the meninges
Leptominenigitis
Inflammation of the leptomeninges (arachnoid and pia mater) = thin meninges over the brain
Pachymeningitis
Inflammation of the pachymeninges (dura mater)
Prions
Proteinaceous and infectious particles, smaller than the smallest known virus, resistant to most disinfectants + treatments
Prion diseases
(Prionoses) chronic progressive fatal NS diseases characterised by spongiform encephalopathy
White matter
Myelin, inside in brain, outside SC
Grey matter
Outside in brain, inside SC
Frontal lobe
Prefrontal association area -coordinates information from other association areas, controls some behaviours
Primary motor cortex + motor association area (premotor cortex)
Skeletal muscle movement
Parietal lobe
Primary somatic sensory cortex, sensory association area - sensory info from skin, MSK, viscera and taste buds, proprioception, conscious perception of pain, touch and temp (body feelings)
Occipital lobe
Visual association area, visual cortex - Vision
Temporal lobe
Auditory function, behaviour and memory
Symmetrical lesion
Affecting whole organ = metabolic, endocrine, toxic
Focal lesion
Often infectious - bacterial, or abscess or tumour
Multifocal lesion
Vascular, embolic (showering of thrombi/septic emboli from other parts of body e.g. heart valve
CNS fibrosis
Fibrogenic cells restricted to meninges and vascular
Derivation of normal anatomy
Malformations
Space-occupying mass
Tumour, abscess, granuloma, cyst
Malacia
With inflammation (abscesses), degeneration and tumours
White matter pallors/softening
Myelin
Haemorrhage
Trauma, vascular lesion, tumour, inflammation
Primary traumatic lesion injury
Mechanical disruption of tissue - penetrating wounds (compressed fracture of skull), haemorrhage and oedema (vasogenic) - brain swelling, confined -> knock-on effects in tissues
Secondary traumatic lesion injury
Occurs within hours to days after injury, cascade of changes, frequently fatal, haemorrhage and oedema (cytotoxic)
Haemorrhage
Space-occupying lesion in CNS - contusion and haematoma, goes out into epidural, subdural, subarachnoid and intracerebral space, eventually stopped by pressure of the calvarium (skull portion including braincase)
Oedema
Causes compression of the CNS within the bony vault of the skull or vertebrae due to 1^y or 2^y injury, can occur as part of congenital disease e.g. hydrocephalus, cytotoxic/vasogenic/hydrostatic/hypo-osmotic (may get combination), localised = less clinical effect
Cervical stenotic myelopathy
“Wobbler syndrome” - large breed horses, dogs, young, rapid growing, static or dynamic types, lead to cord depression (similar to disc herniation), axonal swelling followed by necrosis
Gyri
Folds or bumps in the brain
Sulci
Indentations or grooves of brain
Foramen magnum
Hole in the base of the skull through which the spinal cord passes (site of herniation)
Falx cerebri
Strong crescent-shaped sheet that represents an invagination of the meningeal layer of the dura mater into the longitudinal fissure, found between the medial surfaces of the cerebral hemispheres (site of herniation)
Falx cerebelli
Small sickle-shaped fold of dura mater projecting forwards into the posterior cerebellar notch as well as projecting into the vallecula of the cerebellum between the two cerebellar hemispheres.
Tentorium cerebelli
Second largest dural fold after the falx cerebri, lies in the axial plane attached perpendicularly to the falx cerebri and divides the cranial cavity into supratentorial and infratentorial compartments (site of herniation)
Vermis
Midline of cerebellum
Internal carotid and vertebral arteries
O2 supply to brain, anastomose ventral to the brainstem and at the circle of WIllies, major cerebral arterial vessels have extensive anastomoses in leptomeninges
Leptomeninges
Pia mater and arachnoid (inner meninges)
Infarction
Obstruction of blood supply, because of abundance of lipids (v. soft) and enzymes and relative lack of firbous connective tissue in CNS, infacts undergo liquefactive necrosis and soften (malacia) and swell
Arterial infarcts of grey matter
Red (haemorrhagic) in acute phases
Arterial infarcts of white matter
Pale - grey matter has a denser capillary network than WM
Venous infarcts
In GM + WM appear haemorrhagic (rarer)
Nystagmus
Involuntary movements of the eye
Opisthotonus
Strange ‘star gazing’ posture
Polioencephalomalacia
Thiamine deficiency
Equine leukoencephalomalacia
Fungal toxin - fumonisin B, eating mouldy feed
Focal symmetric encephalomalacia (FSE)
Clostridial toxin
Oedema disease in pigs
E. coli toxin, enterotoxaemic colibacillosis
Enzootic ataxia
Copper deficiency - neurodegenerative disorder in sheep and goats; ‘Swayback’
Nissl bodies
Granules in the cytoplasm of nerve cell bodies that are strongly stained by basic dyes and appear as basophilic clumps on light microscopy. They consist of aggregates of free polyribosomes and rough endoplasmic reticulum.
Chromatolysis
Reactive change that occurs in the cell body of damaged neurones, involving the dispersal and redistribution of Nissl substance (rough endoplasmic reticulum and polyribosomes) in order to meet an increased demand for protein synthesis such as is required to regenerate axons.
Hypomyelinogenesis
Absence or reduction of myelination, congenital, toxic or viral, often associated with tremor in young animals
Leukodystrophy/myelinolytic disease
Loss of myelin that had initially been formed, mainly genetic basis
Spongy myelinopathies
Vacuolation of myelin sheath (no loss of myelin, it is retained), idiopathic/genetic, hepatic and renal encephalopathy more common
Blood-brain-barrier
Capillary level - endothelial cells, pericytes and astrocytic foot processes, endothelial cells - adherent junctions, tight junctions, transport systems that reduce paracellular flux, tighter barrier around endothelium
Microglia
Resident phagocytes of brain, similar to macrophages involved in neuronphagia = removal of individual neurones (viral infections)/neuropil
Astrocytes
React non specifically to many stimuli, fill in tissue spaces (bit like fibroblasts)
Bacterial lesion
Suppurative, fibrinous, fibrinopurulent inflammation
Viral lesion
Lymphoplasmacytic inflammation
Fungal/viral/mycobacteria lesion
Granulomatous and pyogranulomatous inflammation
Parasitic lesion
Eosinophilic inflammation
Gitter
Microglia that phagocytose cellular debris in the brain
Thrombotic meningoencephalitis (TME)
Feedlot cattle, caused by Histophilus somni, acute vasculitis, haemorrhages and thrombosis
Histophilus somni
Gram -ive coccobacillus, normal inhabitant of respiratory flora
Rarefaction
Less dense on histo = spongiosis
Listeriosis
Meningoencephalitis, brain stem (pons, medulla, cerebellum, thalamus), route of infection - Listeria monocytogenes - penetrates damaged oral mucosa, ascends axons of trigeminal nerve into medulla oblongata -> inflammation of leptomeninges +/- extension
Gliosis
Proliferation of larger glial cells (cells that support nerve cells = astrocytes, microglia + oligodendrocytes). These new glial cells can cause scars in your brain (due to viral infection)
Perivascular cuffs
Lymphocytes and plasma cells around blood vessels (inflammation)
Distemper virus
Targets WM
EHV-1 in horses
Tropism for endothelial cells -> vascular lesions
Demyelination histo
Rarefaction (spongiosis - vacuolation) in WM
Protozoan infection
Tachyzoites -> necrosis (+/- inflammation), cysts (containing bradyzoites) -> little host reaction
Coenurosis (Gid)
Taenia multiceps metacestode name (cyst matures into this larval stage)
Granulomatous menigoencephalomyelitis (GME)
Non-infectious encephalitides (auto-immune disease), probably T-cell-mediated delayed-tye hypersensitivity reaction, white matter and leptomeninges, granulomatous inflammation and perivascular cuffs, toy breeds (poodles, terriers)
Necrotising meningoencephalitis (NME)
Non-infectious encephalitides (auto-immune disease) - type unknown, GM of cerebral cortex, necrosis, inflammation and gliosis (pugs, Maltese + chihuahua)
CWD
Chronic masting disease (cervidae = deer) (prion disease/transmissible spongiform encephalopathy)
TME
Transmissible mink encephalopathy (prion disease/transmissible spongiform encephalopathy)
FSE
Feline spongiform encephalopathy (prion disease/transmissible spongiform encephalopathy)
ARR
High resistance (never absolute), scrapies (sheep)
VRQ
High susceptibility to scrapie