Final Exam Flashcards
Antebrachiocarpal joint
Lateral coronoid process
A- radial carpal bone
B- 2nd carpal bone
1st metacarpal bone
Blue arrow- supratrochlear foramen
Red arrow- medial epicondyle of the humerus
red and blue arrow
what is the third joint that makes up the elbow?
red- humeroradial joint
blue arrow- humeroulnar joint
third joint- radioulnar joint
medial coronoid process
What is a possible consequence of renal disease in a dog?
Rubber jaw
What is a potential endocrinological cause of osteoporosis?
Cushing’s disease- hyperadrenocorticism
Talk through endochondral ossification
- Degeneration of hypertrophic chondrocytes and mineralization of cartilage matrix
- Vascular invasion of lacunar spaces from metaphyseal vessels
- Osteoprogenitor cells invade with capillaries
- Osteoprogenitor cells differentiate into osteoblasts
- Osteoblasts deposit osteoid spicules on mineralized cartilage
- Osteoid is mineralized to form bone
Nutritional secondary hyperparathyroidism
- Decreased dietary intake of Calcium
- Hypocalcaemia
- Hyperplasia of parathyroid gland (chief cells)
- Increased production of parathyroid hormone (PTH)
- Increased renal retention of Calcium/renal excretion of Phosphorous
- Stimulation of bone resorption and development of rubber jaw (fibrous osteodystrophy)
Causes of osteoporosis in domestic animals
* Gastrointestinal parasitism
* Cushing’s disease
* Starvation
* Inflammatory bowel disease
* Ageing
* Copper deficiency
* Oestrogen deficiency
Predominant lesion in rickets and why?
Persistence of hypertrophic chondrocytes. They do not undergo degeneration and necrosis (because there is not mineralization of the cartilage matrix they produced); when the ossification front approaches, there is no vascular invason from the metaphysis and no bone formation as a consequence.
Lumpy jaw
Common after a traumatic injury to the oral cavity, condition characterized by a suppurative osteomyelitis, affected maxillary bones undergo rapid osteolysis, regional lymph nodes are almost always affected by the same suppurative process
Parathyroid hormone
Stimulates osteoclastic activity in the bones, PTH stimulates the conversion of vitamin D into its active form, PTH stimulates absorpton of Ca from the small intestine and resorption of Calcium from the kidneys (and Phosphorous is excreted), PTH responds to hypocalcaemic stimuli
Rickets (similar to chrondrodysplasia)- the growth plate is thickened, due to the persistence of chondrocytes which do not degenerate and undergo necrosis.
Transverse foramen of the atlas- vertebral artery runs through it on its way to the skull
Costal fovea
Tubercle
The most distal joint
Tarsometarsal joint
Box?
Red x?
Central tarsal bone
Red x- fourth tarsal bone
Site of insertion for the sacrotuberous ligament
Red arrow- 4th tarsal bone
blue arrow- lateral malleolus, also the origin of the Peroneus longus m. and Lateral digital extensor m.
Tibial crest
tentorium cerebelli
Femoropatellar ligament
a. Olfactory bulb
b. Piriform lobe
Where is the lateral ventricle?
Telecephalon
Where is the third ventricle?
Diencephalon
Where is the mesencephalic aqueduct?
Mesencephalon
Where is the fourth ventricle?
Rhombencephalon
What are the muscles of the quadriceps femoris group in the dog?
Rectus femoris, Vastus medialis, Vastus intermedius, Vastus lateralis
What are the cranial thigh muscles?
What are the medial thigh muscles?
Cranial thigh muscles: sartorius, quadriceps femoris, tensor fasciae latae
Medial thigh muscles (adductors): gracilis, adductor, pectineus
What is the innervation of the tensor fasciae latae muscle? The attachments?
Cranial gluteal nerve
Tuber coxae and fascia lata (also covers the vastus lateralis muscle)
What is the innervation of the sartorius muscle?
What are the approximate attachments?
Saphenous nerve (branch of the femoral nerve)
* attachments: iliac crest and medial tibial crest and stifle fascia
What are the shoulder stabilizer muscles?
What are the shoulder flexors?
What is the deltoid innervated by? Approximate attachments?
Innervated by the axillary n.
Attachments: different parts- scapula and acromial head– and then deltoid tuberosity of the humerus
What is the teres major innervated by? Approximate attachments?
Axillary nerve
Caudal angle of the scapula and teres tuberosity of the humerus
What are the elbow flexors? Elbow extensors (generally)?
What is the biceps brachii innervated by? Approximate attachments?
Musculocutaneous nerve
Supraglenoid tubercle of the scapula and the radial and ulnar tuberosity
What are the triceps muscles innervated by? What are the attachments of the lateral head?
Radial nerve
Tricipital line of the humerus and the olecranon process
What are the attachments of the long head of the triceps muscle? Innervation?
Attachments: caudal border of the scapula and the olecranon process
Radial nerve innervation
What is the innervation of the deep digital flexor and the approximate attachments?
Median and ulnar nerves
Attachments: humeral head and distal phalanx II-V
What is the innervation of the superficial digital flexor and the attachments? Forelimb
Median nerve
Medial humeral epicondyle and middle phalanx II-V
What are the “hamstrings” in a dog?
Biceps femoris, semimembranosus, semitendinosus
What is the main innervation of the biceps femoris? Approximate attachments?
Sciatic nerve (tibial n)
Attachments: Ischiatic tuberosity and sacrotuberous ligament AND tibial crest & stifle fascia & tuber calcanei
What is the innervation and approximate attachments of the semitendinosus muscle?
Sciatic nerve
Ischiatic tuberosity and proximal tibia & tuber calcanei
What is the innervation and approximate attachments of the long digital extensor muscle in the hindlimb?
Peroneal nerve
Lateral femoral epicondyle and distal phalanx II-V
What is the innervation and attachments sites in the superficial digital flexor of the hindlimb?
Tibial nerve
Lateral supracondylar tuberosity of the femur and the tuber calcanei & the middle phalanx of digits II- V
What is the innervation and the attachment sites of the deep digital flexor in the hindlimb?
Tibial nerve
Lateral digital flexor: caudal tibia and fibula
medial digital flexor: caudomedial tibia
AND
distal phalanx II-V
What is in the hind brain?
In the hind brain:
Myelencephalon: Medulla
Metaencephalon: Pons and the cerebellum
What do you have in the midbrain?
Midbrain:
Mesencephalon with the tectum and the tegmentum
What do you have in the forebrain?
Forebrain:
Diencephalon: Hypothalamus and the interthalamic adhesion
Telencephalon: Fornix and Corpus callosum
Brain stem with the mesencephalon in red
What is in red? 3 important features?
Mesencephalon
Crus cerebri
Trochlear Nerve (CN IV)
Oculomotor Nerve (CN III)
Metencephalon with the pons and the cerebellum
Thalamus
Myelencephalon
A. interthalamic adhesion
B. Pons
Black arrow- Corpus Callosum
Blue arrow- Lateral ventricle
a. Fourth ventricle
b. Mesencephalic aqueduct
c. Third ventricle
d. interthalamic adhesion
e. Lateral ventricle
f. Septum pellucidum
a. Crus cerebri
b. Trapezoid body
c. Pyramids
d. Transverse fibres of the pons
e. Pons
f. Medulla oblongata
a. Fasciculus cuneatus
b. Fasciculus gracilis
a. Olfactory peduncle
b. Infundibulum
c. Tuber cinereum
d. Mamillary bodies
e. Crus cerebri
f. pons
g. Trapezoid body
h. Medulla oblongata
a. Pituitary gland
b. Optic nerve (CN II)
c. Tentorium ossium
a. Falx cerebri
b. Tentorium cerebelli
a. Corona radiata
b. Hippocampus
a. Cingulate gyrus
b. Corpus callosum
c. Thalamus
d. Hippocampus
a. Frontal
b. Parietal
c. Temporal
d. Occipital
a. Frontal
b. Parietal
c. Occipital
d. Temporal
a. Motor
b. Somatosensory
c. Visual
d. Auditory
e. Olfactory
What are the basal nuclei? What do they do?
a. Caudate Nucleus
b. Hippocampus
Basal nuclei: Slow sustained movement, posture and support (stalking dog) (compared to cerebellar function– fine motor).
What is the limbic system?
Telencephalon and diencephalon.
(archeoneocortex: hippocampus and a lot more, basal nuclei, thalamus, septal nuclei, hypothalamus and more).
It drives affective (emotional) behaviour such as eating, drinking, rage, fear, sexual activity, aggression and anxiety.
What are the prediliction sites for OC in the horse?
* Tarsocrural joint: medial and lateral malleolus, distal intermediate ridge of the tibia, lateral and medial trochlear ridge of the talus
* Stifle: lateral femoral condyle, patella
* Shoulder: glenoid, humeral head
* Fetlock: sagittal ridge, dorsoproximal aspect of the proximal phalanx
** BASICALLY NOT IN THE CARPUS AND NOT IN THE HIP
What the prediliction sites of OC for the dog?
* Shoulder: caudal aspect of the humeral head
* Elbow- medial portion humeral condyle
* stifle: lateral or medial femoral condyle
* tarsus- medial or lateral trochlear ridge
** BASICALLY NOT IN THE CARPUS AND NOT IN THE HIP
What are the functions of astrocytes?
* Star shaped glial cells of the CNS
* fibrous (fibrillary astrocytes) in the white matter; protoplasmic astrocytes in the grey matter)
* regulate the neuronal environment and support and isolate the neurons
* aid in the functioning of the blood brain barrier
* antioxidant functions
* regulate vascular tone
What are the components of a neuron?
* A neuron is the structural and function unit of the nervous system
* soma- cell body
- nucleus (euchromatic- does not stain strongly unless during cell division)
- nissl substance: basophilic substance consisting of RER, free ribosomes, and polysomes in cytoplasm
- axon hillock: conical part of the neuronal soma (body) from which the axon emerges (no Nissl substance– which distinguishes it from the dendrites)
* Cell processes: axons and dendrites
2 large neurons- prominent nucleolus
Neuronal chromatolysis: a histological change in the cell body of a neuron
Ependyma or ependymal cells
* epithelioid cells that line the central canal of the spinal cord
* cuboidal/ columnar cells with cilia, oval hyperchromatic nuclei
* Stars: neuropil (composed of unmyelinated axons, dendrites, and glial cell processes that forms a synaptically dense region containing a relatively low number of cell bodies)
* Small arrows: Oligodendrocytes (small dark nuclei)
* Large arrows- astrocytes
Microglia
a. Epineurium
b. perineurium
c. Endoneurium
d. Schwann cell nucleus
e. axon
Virchow Robin Space
aka perivascular spaces- immunological spaces between arteries and veins (not capillaries) and pia mater that can be expanded by leukocytes. The spaces are fromed when the large vessels take the pia mater with them when they dive deep into the brain.
* Perivascular cuffs are regions of leukocyte aggregation in VRS usually found in patients with viral encephalitis
Ventral root nerve fibre
node of Ranvier
a. capsule
b. ganglion
c. nerve trunks
a. axon hillock
b. Nissl substance
Hyperextension of the metacarpophalangeal joints (fetlock- the metatarsophalangeal joint is also called the fetlock)
Two descriptors
Dorsal flexion and extension
Protraction
Movement of a body part forward
a. Thyrohyoid
b. Basihyoid
c. Ceratohyoid
d. Epihyoid
e. Stylohyoid
f. Tympanohyoid
Cancellous bone (aka Trabecular bone)
1st two arrows: bony trabeculae
Second two arrows: myeloid tissue
Arrows: Ossifying spicule/ trabeculae (the first step in the process of intramembranous ossification– they eventually fuse to become trabeculae– this network is called woven bone which is eventually replaced by lamellar bone)
Intramembranous ossification
Flat bones (skull bones)
* Condensation of embryonic mesenchyme followed by differentiation into osteoblasts and secretion of osteoid to form spicules of woven bone gradually forming a network of trabeculae
Blood supply in long bones
Nutrient artery enters the diaphysis to supply marrow and cortical bone. Metaphyseal arteries and epiphyseal arteries.
** no anatsomosis between epiphyseal and metaphyseal vessuls until skeletal maturity
* Venous drainage accompanies arteries. Except drainage of cortical bone to venules in periosteum
Bone matrix
Type I collagen, glycoproteins, hydroxyapatite (mainly calcium and phosphate)– organized into layers (lamellae) in mature (lamellar) bone…. disorganized in immature (woven) bone
Where is woven bone found?
Immature and healing bone
What is this?
What is the precursor cell?
Osteoblast
Mesenchymal stem cell (just like fibroblasts, myoblasts, etc.)
Osteoid laid down by osteoblasts
a. MC3
b. P1
c. P2
d. P3
e. SDFT
f. DDFT
g. straight sesamoidean ligament
h. digital extensor tendon
i. frog
j. sole
k. hoof wall
l. digital cushion
a. bulb
b. heel
c. bar
d. frog
e. sole
f. white line
Check ligaments in a horse
The superior check ligament connects the superifical flexor tendon to the radius just above the knee. The inferior check ligaments connects the deep flexor tendon with the cannon bone just below the knee. The check ligaments limit the movement of the tendons (for protective purposes).
Cranial cruciate ligaments function and attachments
Function to prevent forward movement of the tibia relative to the femur. (caudal cruciate prevents backward displacement of the tibia relative to the femur)
Cranial cruciate ligament inserts on the cranial intercondylar area of the tibia. And the popliteal surface of the femur.
What does disuse, endocrine, malnutrition, cachexia, and age atrophy of muscle have in common?
They primarily affect type 2 fibres.
What two types of atrophy affect type 1 fibres? Denervation and congenital myopathy
What is hyaline degeneration?
What is floccular degeneration?
Degenerative damage of muscle that you can see histologically. Hyaline (glassy, pale, swollen fibres) comes first and then floccular- disorderly.
Clinical signs of PNS disease
Denervation atrophy of skeletal muscles, paresis (weakness), flacid paralysis of innervated structures, diminished or absent reflexes, diminished pain responses or muscle tone, proprioceptive deficits, paraesthesia (pins and needles for example)
What part of the nervous system are the cranial nerves and their sensory ganglia considered?
PNS
Name the cranial nerves
I. Olfactory
II. Optic
III. Oculomotor
IV. Trochlear
V. Trigeminal
VI. Abducens
VII. Facial
VIII. Vestibulocholear
IX. Glossopharyngeal
X. Vagus
XI. Accessory
XII. Hypoglossal
Wallerian Degeneration
* Acute or focal injury to a myelinated axon or death of its neuronal cell body (if the injury is focal, then degen only to axonal segment distal- if it’s to the cell body- the entire axon degenerates)
- Within 24 hours disruption of axoplasmic flow in the damaged axon–> swelling of the distal segment of the axon to form an axonal spheroid
- Within 48 hours, influx of calcium ions into the damaged axon–> proteolytic destruction of neurofilaments–> collapse, fragmentation of axon
- From 28-96 hours post injury, myelin retracts and fragments to form ellipsoids which surround axonal debris (secondary demyelination)
- Gitter cells (macrophages phagocytosing debris) & schwann cells assist
* Myelin degeneration is usually complete by week 2- some may persist for 3 months
** Regeneration: if the nerve cell body survives, 1-4 mm/day is the rate of regeneration for the axon
What are the factors that allow or inhibit peripheral nerve regeneration?
Slows the rate of regeneration down if the distance between the growing tip and cell body is far.
* integrity of the endoneurial tube distal to the site of axonal injury (endoneurial tube is endoneurium and basal lamina of the Schwann cells)
What role do Schwann cells play in regeneration?
Proliferate and form longitudinal column (Bunger’s bands) along the former course of the axon
** they also can act as phagocytes and are responsible for myelination and maintenance of axons in the PNS
What is different between Wallerian regeneration in the PNS and CNS?
In the PNS, Wallerian regeneration is more rapid than in the CNS– probability of regeneration and remyelination in the PNS is greater.
Equine Laryngeal hemiplegia
* Wallerian degeneration of the distal parts of the left recurrent laryngeal nerve–> unilateral paralysis and denervation atrophy of the intrinsic laryngeal muscles (especially the left cricoarytenoid muscle)–> inability to abduct the left arytenoid cartilage and vocal fold–> partial airway obstruction–> inspiratory stridor (roaring) and decreased athletic performance
Osteochondrosis
failure of endochondral ossification involving the AEC and the metaphyseal growth plate. In immature animals the AEC is dependent on the presence of viable blood vessels.
** focal ischaemic necrosis of growth cartilage initiated by necrosis of cartilage canal blood vessels. Because the necrotic cartilage does not undergo mineralization or vascular penetration, a focal failure of endochondral ossification occurs when the ossification front approaches the lesion.
** THEREFORE, Retention of growth cartilage due to failure to become mineralized and replaced by bone
** in OCD if the lesion is large, it can cause underrunning of the articular cartilage and a flap which then exposes the subchondral bone
Causes of osteoporosis
How does it affect the bone?
* Hyproteinaemia, Vitamin C deficiency, Copper deficiency, Calcium deficiency, Low calcium- high phosphorous diets, Hyperadrenocorticism, and sex hormone deficiency
** quality of bone is normal, quantity is affected however
Rickets and Osteomalacia
Causes
**Rickets- Young, rapidly growing animals– abnormal endochondral ossification and defective bone formation with bone deformities and fractures
** Osteomalacia- pathogenesis similar but in older animals
* failure of mineralization–> failure of hypertrophic chondroctyes to degenerate–> failure of capillary invasion from metaphysis–> lack of osteoprogenitors and osteoblasts–> persistence of hypertrophic chondrocytes at sites of EO causing irregular clumps instead of columns (can be replaced by connective tissue in which metaplastic osteoid forms)
Causes: Vitamin D deficiency, Phosphorous deficiency (vitamin D= goal hypercalcaemia, enhances absorption of P and Ca from SI, stimulates release of P and Ca from bone, enhances P resportion in the kidney)
Fibrous Osteodystrophy
Hyperparathyroidism with increased production of PTH either primary or secondary hyperparathyroidism (primary: parathyroid adenoma or carcinoma– secondary– nutritional low calcium, high phosphorous diets or diets low in Calcium or vit. D OR renal failure)
* Decreased dietary intake of Ca & excess dietary phosphorous and/or vit D–> parathyroid hyperplasia–> increased PTH–> renal retention of calcium–> renal excretion of phosphorous–> bone resorption– rubber jaw
*** Bone resorption and replacement by fibrous tissue
Causes of osteomyelitis
* Haematogenous, direct implantation, local extension
Myasthenia Gravis
Congenital or acquired
* less ACh receptors or antibodies directed against ACh receptors in post synaptic muscle membranes
* weakness– exacerbated by exercise, improved with rest
Equine Stringhalt
Exaggerated hindlimb flexion and delayed extension.
Ordinary- poor prognosis- usually unilateral
Australian- dandelions or mallow– often epidemic– spontaneous recovery
Vulnerable portion of the spinal cord to ischaemic necrosis
Cervical spinal cord supplied by vertebral artery
Thoracic and lumbar spinal cord supplied by radicular arteries
** border zone in the caudal cervical- cranial thoracic area is thought to be particularly vulnerable to ischaemic injury if arterial blood flow slows
Trauma to the spinal cord
* vertebral luxations/ subluxations- developmental or traumatic
* vertebral fractures
* cervical stenotic myelopathy (wobbler syndrome)- horses and dogs
* intervertebral disc disease- dogs
** Consequences of external physical trauma depend on rigidity of bone (influenced by diet, age, hormonal status, etc.), mass velocity and direction of applied force, and ability of the tissues to move in response to the applied force
** Trauma can damage the spinal cord and then become exacerbated by ischaemic necrosis if blood supply is affected
** in the acute phase, the cord may be swollen and softened with dark red discolouration due to haemorrhage and blurring of white and grey matter– later stages: segment may be shrunken and firmer than normal
What will happen cranial to the site of injury of the spinal cord? Caudally?
** Cranial to the site of injury, Wallerian degeneration of white matter is generally limited to ascending (sensory) tracts of the dorsal funiculi and the superifical dorsolateral parts of the lateral funiculi.
** caudal to the site of injury– Wallerian degeneration of white matter is usually limited to the descending (motor) tracts in the ventral funiculi and the more central parts of the lateral funiculus
Most likely location of vertebral fractures
How does vertebral luxation or sub-luxation occur?
Sudden application of external forces on the vertebral column mainly involving the cervical vertebrae because of their longer ligaments and more mobility…. vertebral displacement–> compression of the spinal cord
Intervertebral disc prolapse
* Hansen’s type I Intervertebral disc prolapse (such a large amount of disc displaced)
Vertebral bodies (not C1 and C2) are united by intervertebral discs that together with the synovial articular facets allow some movement between vertebrae.
Discs are attached to the ends of the vertebral bodies in the same way articular cartilage is attached….
** the nucleus pulposes, a remnant of the embryonic notochord– acts as a shock absorber— it is surrounded by the annulus fibrosus (ventral longitudinal ligament fuses with the annulus of each disc as it passed and the dorsal spinal ligament (longitudinal) lies in the vertebral canal and fuses with the dorsal part of each annulus except in the thoracic area where there are conjugal ligaments.
** In chondrodystrophoid breeds of dogs such as dachshunds and toy poodles– degenerate nucleus presses unevenly to the annulus– the annulus is thinner in the dorsal part– the nucleus palposus will normally prolapse dorsally
*** Most disc disease is in the THORACOLUMBAR AREA OR cervical area (beagles)
Discospondylitis: inflammation of an intervertebral disc with osteomyelitis of the adjacent vertebrae- dogs and pigs
** likely due to blood-borne bacterial or sometimes local infection localising in either the outer annulus fibrosis or adjacent epiphysis of the vertebral body…
** Also ankylosing spondylosis bridging between these two vertebral bodies ventral to the affected disc due to INSTABILITY
** not likely a disc prolapse because the disc material should still be present
Spondylosis– common degenerative condition of the vertebral column characterised by the formation of osteophytes… ankylosing spondylosis= bone spurs form complete bridges to unite adjacent vertebral bodies
** Can be caused by any process that causes abnormal mobility of vertebrae and hence abnormal forces being placed on the annulus fibrosis of the IV discs
* if ventral annulus fibrosus abnormally loaded–> collagen fibres degenerate–> fibrocartilaginous metaplasia–> osseous metaplasia–> ventrolateral osteophyte formation
DJD
* imbalance of mechanical stress and catabolic processes acting on a joint (overloading or underloading AC can exacerbate)– overweight or abnormal movement like knock-knees
* sclerosis of subchondral bone
* cartilaginous injury– superficial or deep (pannus– interferes with nutrients into articular cartilage- can cause ankylosing spondylosis)
* Chondromalacia- softening of cartilage from loss of proteoglycans and increase in water content = cartilage fibrillation and wearing
* Eburnation of subchondral bone
* synovial villous hyperplasia
* synovitis– infiltrates of plasma cells, lymphocytes, and macrophages in the subintima
* periarticular osteophytes- conditions with joint instability especially– at or near the transitional zone of synovium EO of foci of metaplasic cartilage (synovial chondromatosis or osteochromatosis- bone and cartilage)
* joint mice (OCD, fibrin, blood clot, synovial villi– further damage to AC and prevent normal movement)
* subchondral bone cysts (often from osteochondrosis or traumatic injury to AC– could be sequestrum haemorrahge or necrotic debris)
* End stage joint– fibrillation, erosion, ulceration of AC, eburnation +/- grooving of exposed subchondral bone, periarticular osteophytes, synovial villous hyperplasia, synovitis, and fibrous thickening or laxity of the joint capsuel +/- joint mice and fibrous or bony ankylosis
** in chronic phase of DJD impossible to tell the original cause
* Primary: no apparent predisposition
* Secondary: predisposing cause such as obesity or joints with restricted movement, larger joints… chronic problems.
Cervical vertebral stenotic myelopathy (WOBBLER SYNDROME)
* Dynamic lesion with compression or stretching of the cord seen when the neck is ventroflexed. Common in young TBs and quarter horses 8-18 months of age.
Clinical signs prior to euthanasia: hindlimb ataxia slowly progressing due to intermittent compression of C3-C5, vague neuro signs may be exacerbated following strenuous activity
** genetic factors that promote rapid growth are believed to be involved in the pathogenesis– high protein and high energy diets that encourages rapid growth. Males more likely to be affected.
Progressive ascending haemorrhagic myelomalacia
* dog spinal cord 24 hours after prolapse of an intervertebral disc
* Any type of traumatic injury to the spinal cord–> affected segment swells and softens due to liquefactive necrosis, oedema, and haemorrhage +/- subdural haemorrhage. May result in seocndary external compression due to the confined space in the intervertebral canal with the risk of COLLAPSE of SMALL BLOOD VESSELS +/- thrombosis if traumatised blood vessels from event and/or compromised venous drainage = secondary ischaemic injury… therefore this may rapidly extend the area of spinal damage both cranial and caudal to the immediate site of trauma.
* Hansen type I disc prolapses likely to result because a large volume of degenerate disc material suddenly enters the vertebral canal and causes severe spinal compression and accompanying epi- and subdural haemorrhage
GRAVE PROGNOSIS– prove fatal once development of respiratory muscles develops.
Where does conscious proprioception travel via the spinal cord to the brain?
Where does unconscious proprioception travel via the spinal cord to the brain?
Conscious Proprioception travels via the Dorsal funiculus of the white matter
Unconscious Proprioception travels via the Lateral funiculus of the white matter
General pathway of Conscious Proprioception
Sensory neuron from hindlimb for example travels via a nerve into the lumbosacral plexus and to the spinal cord–> fasiculus gracilis–> up the dorsal funiculus–> medulla–> crosses over the medial lemniscus and synapses with thalamic nuclei with cell body in the thalamus–> somatosensory grey matter in the cerebral cortex
General pathway of unconscious proprioception
Via sensory nerve in the muscle spindle or golgi tendon organ for example–> sends an impulse via a peripheral nerve via the lumbosacral plexus for example to the fasiculus gracilis–> up the lateral funiculus of the white matter–> medulla–> cerebellum
What are the two major afferent systems which remain largely outside of the realm of conscious perception (UCP)?
Spinocerebellar pathways and ascending reticular formation
What are the two major tracts from the hindlimbs (UCP)?
Dorsal spinocerebellar tract (no decussation therefore direct)
Ventral cerebellar tract (axons decussate twice)
What are the two tracts from the forelimbs (UCP)?
Spinocuneocerebellar pathway (does not decussate)
Cranial spinocerebellar tract (decussates)
What is the pyramidal system (aka corticospinal pathway)?
Pathways that control and initiate skeletal muscle movements. Carries fibers directly from the primary motor cortex of the cerebral hemispheres through to the brainstem where they control LMNs within the ventral horn grey matter or cranial nerve nuclei.
What happens if you damage UMN? What about LMN?
If you damage UMN– release LMN from inhibition– so hindlimbs remain extended.
If you damage LMN– no reflex, loss of motor tone, significant atrophy.
What is the extrapyramidal system?
The other group of pathways that control and initiate skeletal muscle movement… the division between pyramidal and extrapyramidal may be arbitrary.
9 motor centres (forebrain: cerebral cortex, basal nuclei; midbrain: descending reticular formation, red nucleus, tectum; hindbrain: pontine motor reticular centres, lateral medullary motor reticular centres, medial motor reticular centres, vestibular nuclei)
5 motor pathways (pontine reticulospinal pathway, medullary reticulospinal pathway, rubrospinal pathway, vestibulospinal pathway, tectospinal pathway)
How many pairs of spinal nerves in the dog?
23
How are ascending travts of white matter named?
More peripherally located and they are named for their origin and termination… spinocerebellar
How are descending tracts named?
Generally do not cross sides– unilateral spinal cord lesions will cause ipsilateral signs. Most UMN (descending) tracts are named x spinal tract. Fibres originate in x and end in the spinal cord. Coritospinal or Vestibulospinal
Why does loss of deep pain sensation in spinal cord disease signify severe spinal cord damage?
Because DPP (deep pain perception) is carred by non-myelinated fibers of the spinothalamic and spinoreticular tracts deep in the white matter of the lateral and ventral funiculus– indicates severe spinal cord injury– all the way through. Can be caused by Thoracolumbar intervertebral disc disease.
Remembering Cranial Nerves
O
O
O
T
T
A
F
V
G
V
A
H
Cerebellar function vs. basal nuclei
Cerebellar is fine motor control- balance and posture– rapid adjustments to posture
Basal nuclei- Slow sustained movement– inhibitory mainly related to posture and support
Reticular formation- where is it? What is it?
TICKLE! Alert and arousal– reduced activity for sleep or lethargy
Throughout the length of the brainstem. Nuceli that are connected with ascending, descending and transverse white matter tracts. Connections to the telencephalon and the spinal cord. All major integration centres as well.
