Neurology Flashcards
Which spinal lesions would you get normal to hyper-reflexive
C1-C5
What spinal lesions would give normal to hypo-reflexive?
C6-T2
Predisposition for cervical intervertebral disc disease
Large dogs associated with Hansen type II protrusions at disc
Doberman associated with cervical spondylomyelopathy
Signs of cervical intervertebral disc
- radicular pain or nerve root signature often with impingement of C5 and C8
- most common sign = cervical spinal pain, low head, neck carriage, neck guarding, stilted and cautious gait and spasms of muscle
Non surgical treatment for cervical intervertebral disc disease
- conservative indicated with 1st episode of pain only or with milked paresis
- strict cage confinement (4-6 weeks), corticosteroids and muscle relaxants
- harness during limited walking exercises
Surgical treatment for intervertebral disc disease
- persistent pain or moderate to severe neurological deficits
- removal of the disc
- ventral slot decompression - most commonly performed
Predisposition of thoracolumbar intervertebral disc disease
Chondrodystrophic breeds —> hansen type I in thoracolumbar region - progressively decreases from T12-T12 causally
Most common site for Hansen type I in large non-chondrodystrophic breeds - between L1 and L2
Signs of thoracolumbar intervertebral disc
- percute (<1hr), acute (<24hr), gradual (>24hr)
- persecute/acute disc extrusion = “spinal shock” or shiff-Sherrington posture
- (vary) spinal hyperesthesiia/paraplegia with/without pain perception
- dogs with back pain —> reluctant to walk - show kyphosis
Diagnosis of thoracolumbar IVDD
Signalmen’s, history, and neurological examination
CT, MRI, surgery
Differentials for thoracolumbar IVDD
Trauma, fibrocartilaginious emoblism, degenerative myelopathy, discospondilitis, neoplasia etc
Treatment for thoracolumbar IVDD
Non surgical - same as other IVDD
Surgical
- decompression alone is inadequate to restore spinal cord function when an extramural mass is greater than 4mm in diameter (so decompression and remove)
- decompressive procedures = dorsal laminectomy, hemilaminectomy and pediculectomy
Another name for degenerative lumbosacral stenosis
Cauda equina syndrome
Predisposition for cauda equina syndrome
Middle age dogs of medium - large breeds
GSD most commonly affected
7 yrs, 2x more likely in male than female
Working dogs that are heavily trained are prone
Cause of cauda equina syndrome
Degenerative lumbosacral stenosis (DLSS)
Pathogenesis of cauda equina
Soft tissue and bony changes, possibly in conjunction with abnormal motion of the lumbosacral joint, impinge on the nerve roots/vasculature of the cauda equina
Signs of cauda equina
- lumbosacral (caudal) pain
- maintain characteristic posture, keeping their lumbosacral joints flexed (increases the canal —> decreasing nerve root compression)
- pelvic limb lameness, tail paresis or paralysis
- urinary or faecal incontinence
Compression of sciatic nerve (L6-S2)
Abnormal proprioceptive positioning, muscle atrophy, parapetáis, reduced flexor reflex
Compression of pudenal nerve
Reduced/absent perineal reflex, poor anal and urethral sphincter tone and decreased/abnormal perineal skin sensation
Compression of pelvic root
Atomic bladder that’s easily manually expressed
Compression of caudal nerve (CD1-5)
Reduced tail tone, tail paresis/paralysis, decreased tail sensation/paraesthesia of the tail
Diagnosis of cauda equina
Lordosis test = detects pain even in stoic dogs, not specific and doesn’t differentiate lumbosacral pain from hip pain
Extension/traction of tail and palpación of lumbosacral joint per rectum
Survey/stress radiography, myelography, epidurography, discography, CT, MRI
Differentials for cauda equina
Neruologic diseases = degenerative myelopathy, IVDD, myopathies
Orthopaedics: CLR, DJR
Other disease: prostatic, primary disease of urogenitcal, primary dermatological disease
Treatment for cauda equina
Conservative: rest, NSAIDs, weight loss
Surgery: decompression, distraction-fusion
Spinal fracture or luxación
Spinal trauma common cause of spinal cord dysfunction in dogs and cats (trauma either exogenous or endogenous )
Clinical assessment of spinal fracture or luxation
- owner: place animal on rigid movable board (if not available, blanket, like a sling), and multiple people to move and to reduce additional injury
- at hospital: suspected vertebral column injury, should be immobilised ASAP
- need to see if has multiple organ trauma to determine whether life threatening or not
Treatment for spinal fracture or luxation
Corticosteroids
- prior to/during radiographing evaluation - if not severely hypotensive should be given
- methyprednisolone sodium succinate - within 1hr of the trauma is beneficial
Non-surgical
- cage confinement (4-6 weeks), external support bandages/casts
Surgical
- indications: spinal instability and spinal cord compression
Post-operative
- fentanyl patch
- if recumbent, animal needs to be turned at least every 1-4 hr
- extra padding under dog with foam rubber/thick fleece or small soft-sided waterbeds
- measure the urine output, manually expression every 6 hours if not urinating on their own
Head trauma management
Death usually results from progressive increases in intracranial pressure (ICP)
Cause of head trauma management
Vehicle accidents
Gun sohots
Animal bites
Fall
Primary brain injury
- direct parenchymal damage: contusions, lacerations, diffuse axonal injury
- direct vascular damage: intracranial haemorrhage, vasogenic oedema, decreased perfusion
- refers to physical disruption of intracranial structures that occurs immediately at the time of the traumatic event
Secondary brain injury
ATP depletion
Degree of neurological dysfunction
- Pain only
- Ataxia, conscious proprioceptive deficits, paresis
- Paraplegia
- Paraplegia with urinary retention and overflow
- Paraplegia with urinary retention and overflow and loss of deep pain perception
Intracranial pressure definition
ICP = pressure exerted by tissues and fluids within the cranial vault
ICP normal pressure
5-12mmHg
CPP and CBF
Cerebral perfusion pressure is a primary determinant of cerebral blood flow and hence brain oxygenation and nutritional support
What are normal contents of cranial cavity?
Parenchyma, blood and CSF
Pressure auto regulation
Between meal arterial BP (MABP) extremes of 50 and 150mmHg, ICR remains constant
If MABP rises, vasoconstriction occurs in brain, if falls, vasodilation
Chemical auto regulation
Direct responsiveness of brain vasuclature to partial pressure of CO2 in arterial blood, elevated PaCO2 = vasodilation and vice versa
Fluid therapy for brain injury
Aggressive fluid therapy to counteract hypotension but may aggravate brain oedema
Blood pressure must be restored to normal ASAP
Hetastarch, hypertonic saline, dextran-70, crystalloids
Hetastarch
- BEST choice for RESTORING normal BP in head trauma
- 10-20mL/kg for shock
- composed mainly of amylopectin
- can be: rapid bolus in dogs
- cats: 5mL/kg incrementes over 5-10 minutes to avoid vomiting and nausea
- long duration
Hypertonic saline
- shock dose 4-5mL/kg given over 3-5 minutes
- contributes to brain oedema because of Na
- it may disrupt BBB
- short duration can combine hypertonic with dextran 70/hetastarch may prolong
Dextran-70
Composed of linear glucose reditúes
10-20mL/kg to effect for shock in dogs
Cats 5mL/kg a blouses over 5-10minutes, max 20mL/kg
Side effects: renal failure and coagulation disorders possible but v rare
Metabolism of dextran ay lead to increased blood glucose levels, séquela that should be aoivded in severe head trauma
Crystalloids
90mL/kg/h (dogs)
60mL/kg/h (cats) for shock
Specific medical therapy for head trauma victim
Mannitol (osmotic diuretic, reduces brain oedema and ICP in cases of severe brain injury)
Furosemide (loop diuretic)
