module 12 Neurological emergencies Flashcards
Describe assessments that are used in neurological lesion localisation in brain and spinal cord injury
a) BEHAVIOUR; Need to be alert in order for forebrain assessments to be made.
b) CONSCIOUSNESS-assesses Ascending Reticulat Activating system, brainstem and forebrain.
i. Normal – BAR
ii. Obtunded – Dull; will fall asleep when left alone; can be aroused by
non-noxious stimuli
iii. Stuporous – somnolent, can only be aroused by noxious stimuli
iv. Comatose – unconscious; unable to arouse despite noxious stimulus
v. Brain dead – absent cerebrocortical electrical activity, absent brainstem
reflex function
b)Cranial nerves
Assesses specific areas of the brain (origin of the cranial nerves) Not affected by spinal cord lesions E.g. strabismus = rostral brainstem lesion (site of attachment of CN III and IV)(strabismus=eyes not looking at same thing eg crosseyed. Either nerve issue or local muscle issue or some mild congenital)
c) CRANIAL NERVES
1.Olfactory. Check by hiding food. do not use noxious substances.Axons of olfactory n are uniquely capable of regeneration. Anosmia (= loss of smell) rare. have one sided anosmia. Severe rhinitis most usual cause of anosmia but can also be due to shearing injury from head trauma as passes through cribriform plate
2.Optic n. Supplies sensory information for conscious perception of vision as well as for subconscious
reflex pathways. Test by observing hands off initially or obstacle course. Then;
i) Cotton ball drop-assess visual
ii) Menace (from 12 weeks). assesses blindness plus requires intact facial n and coordination by cerebellum.
iii)Plr-if fail to use bright enough light might fail to elicit response esp if very anxious and high sympathetic tone.
iv) Visual Placement response-assess vision and postural control
v)Dazzle reflex-similar to plr but no cortical involvement
COMMON DISORDERS
Based on the assessmncit of the menace response and the PLR. disorders of vision can be subdivided anatomically into;
* DECREASED VISION WITH PLR DEFICITS,
includes lesions of the retina, optic disc, optic nerve,
optic chiasm or optic tract; and
eg Sudden acquired retinal degeneration;
eg Congenital abnormality of Siamese/Birman/Himalayan;
eg Papilloedema;
eg Optic Neuritis;
eg Inflammatory Lesions;
eg Space Occupying Lesions;
* DECREASED VISION WlTH NO PLR DEFICITS, Which
includes lesions of the central Visual pathways from the lateral geniculate nucleus to the visual cortex.
eg. Hydrocephalus;
eg. Space Occupying Lesions;
eg Inflammatory Lesions;
eg Trauma
eg Diffuse Encephalopathy
eg Trauma
eg Vascular Lesion
3. Oculomotor n. functions to constrict pupil and innervates most of the extraocular muscles (dorsal, medial &ventral recti, ventral oblique, and levator palpebrae.) Clinical signs of dysfn include strabismus (usually ventrolateral), absent plr, opthalmoplegia.
Ddx issues i) Inflammatory/neoplastic eg Cavernous sinus syndrome
ii)Increased intracranial pressure (with secondary compression upon cn3)-may initially show pupil small as n just irritated, then pupil dilated as nerve fully compessed)
iii)Dysautonomia-normal vision but no plr. eg Key Gaskell.
4. Trochlear n. innervates dorsal oblique eye muscle. Issue with n results in rotation of eyeball-more easily appreciated in cats as slit pupil as opposed to dogs with round pupil. Rarely affected by itself (usually cn3 also affected, plus or minus other regions)
5. Trigeminal n. Provides sensory function to face (via opthalmic, maxillary and mandibular branches) and motor function to muscles of mastication. Lesions cause partial or complete problems with either sensation or motor fn or both (to ipsilateral side of lesion). Atrophy of masticatory muscles if affected, occurs within 1 week of injury.Lesions affecting cn5 are usually traumatic or neoplastic and are often associated with a poor px and so further imaging often required. There is however also the frequently encountered condition of Idiopathic Mandibular Paralysis or drop jaw. Bilateral or unilateral. Can swallow but v difficult as cannot hold jaw in. Supportive tx often with taping jaw and nasogastric feeding tube. This condition will spontaneously resolve after 2-3 weeks.
6.Abducen n. Innervates lateral rectus and retractor bulbi muscles of eye. Issue results in medial strabismus and lack of eyeball retraction (ddx from congenital medial strabismus are crosseyed but can retract eyeball). Rarely affected in isolation (usually cn3 also affected).
7. Facial n. The facial nerve supplies:
* Motor function to the muscles of facial expression;
* Parasympathetic function to the lacrimal gland, nasal
secretory (less commonly affected) and palantine glands
as well as the mandibular and sublingual salivary glands;
* Some taste sensation and sensation to the rostral two thirds of the tongue and the inner surface of the pinna.
Lesions may result in:
* Ipsilateral facial paresis or paralysis;
* Decrease, or loss, of the blink reflex on the affected side;
* Drooping of the lip on the affected side. This is often
the feature that owners notice due to the dog’s tendency to
dribble saliva and drop food from the affected side, especially during the first few days or weeks of occurrence;
* Drooping of the ear on the affected side; this is more
noticeable in dogs with erect ears.
If parasympathetic function is affected, may have dry eye and dry nose on ipsilateral side.
Two common conditions affeceting facial n are;
i) Idiopathic facial n paralysis. may or may not resolve. supportive care as necessary.
ii) Facial n paralysis secondary to otitis media. May not be able to recognise without mri. May need bulla ostectomy. May need ab’s sulphonomides (check tear production) or cephalexin (25-30mg bid) for 4-6 weeks. Even if otitis clears, signs may not.
iii) Rarer conditions of facial n paralysis may be secondary to hypothyroidism, polyradiculoneuropathies, botulism, myasthaenia gravis etc.
8. Vestibulocochlear n. Allows for vestibular function and hearing. Most often issues are vestibular disease (peripheral or central). Vestibular dz often also has issues with cn v and cn vii (and concomitant signs may be present with central or peripheral vestibular dz). Possible clin signs of vestibular dz include; head tilt, nystagmus, strabismus, ataxia, circling/rolling, truncal deviation, brainstem signs. Sometimes only a few signs, more severe dz has more signs. if have bilateral dz, might see head sway side to side as opposed to tilt.
Peripheral dz far more common. Signs suggestive of central dz include postural deficits (especially conscious proprioceptive deficits or hypermetria), ventral nystagmus, or postural nystagmus( Induced by change in head position). Central dz ddx inflammatory granulomatous meningoencephalopathy (need mri, some may respond to pred or azathioprine, terrier types predisposed), or neoplasia (need mri).
9. Glossopharyngeal. Usually assessed together with Vagus n (10). Together these nerves provide sensation and motor fn to pharynx and larynx, and parasympathetic fn to salivary glands and viscera (not viscera of pelvic canal). Assess for gag reflex and if increased laryngeal noise (if has, may also need to consider whether megaosophagus is possibly also present). Laryngeal paralysis most common issue encountered with these nerves. If have issue with gag reflex, usually indicates central lesion and very poor px.
11.Spinal Accessory n. innervation to shoulder/neck muscles (trapezious, sternocephalicus & brachiocephalicus). V. rarely a clinical issue.
12. Hypoglossal n. Motor fn to tongue. Assess by gently stimulating nose to trigger voluntary licking (also involves cn 5), gently tug on tongue to assess strength of tongue withdrawal response), and observe if tongue to side (will deviate to affected side evident from 5 days post n injury) and may also have visible lesions on tongue. Issues are rare, but usually secondary to neoplasia or central inflammatory dz. ddx masticatory myositis, myasthaenia gravis and botulism.
LOCALISATION OF LESION;
Proprioception
a. Subconscious proprioception
i. Input from limbs and body
ii. Impulses from spinal nerves and spinal cord
iii. Destination: ipsilateral cerebellum
b. Conscious proprioception
i. Input from limbs and body
ii. Destination: contralateral forebrain
c. Head proprioception
i. From vestibular apparatus (inner ear) travelling to the brainstem before
going to:
1. Cerebellum (subconscious)
2. Forebrain (conscious)
Motor function
a. Motor centres arise from both in the brainstem and cerebrum
b. Brainstem
i. Semiautomatic (e.g. walking)
ii. Dysfunction → severe gait abnormalities (e.g. paresis)
c. Contralateral cerebrum
i. Learned, skilled movements (e.g. dog catching a ball in its mouth)
ii. Dysfunction → minimal effect on gait but significant effect on learned
movements
d. Upper motor neurons (UMN or central motor neurons)
i. Arise from both motor centres
ii. Influence lower motor neurons (LMN or peripheral motor neurons) of
1. Brainstem
2. Spinal cord
e. Cerebellum
i. Responsible for coordination
4
ii. Controls activity of extensor and flexor muscles to sustain posture and
smooth movement (mainly by inhibition of excess UMN input)
iii. Requires input of subconscious proprioception to produce movement
with correct rate, range and force of movement (metria) by controlling
the output from UMN centres
iv. Dysfunction:
1. Absence of subconscious proprioception input → ataxia
2. tremor, hypermetria, spasticity (abnormal UMN output
regulation)
3. Nystagmus and head tilt (abnormal cerebellar processing of
vestibular input)
Reflexes
a. Assesses spinal and cranial nerve reflexes
b. Brain lesion:
i. Abnormal CN reflexes but normal spinal reflexes
c. Spinal lesion:
i. Normal CN reflexes, abnormal spinal reflexes.
FOCAL LESION
* Specific neurological deficits
* Identifiable from tracing the coinciding points of multiple neurological deficits
* Can account for all clinical signs by a single lesion
* e.g. Obtunded patient that is non-visual in the right eye with conscious proprioceptive
deficit of the right side. Otherwise normal CN and spinal reflexes.
o Obtundation = diffuse forebrain sign (lesion contralateral to clinical signs)
o Abnormal vision = forebrain sign (contralateral to clinical signs)
o CP deficit – either forebrain or spinal cord
o Absence of other CN abnormality (normal CN III-XII) – NOT brainstem
o No evidence of coordination deficits – NOT cerebellum
o Spinal reflexes intact – NOT spinal cord
▪ Answer: Focal forebrain disease (lesion on the left)
MULTIFOCAL LESIONS
* Unable to be explain all clinical signs by a single lesion
* More commonly associated with inflammatory or metastatic neoplasia
* e.g. Patient with seizures, neck pain, CP deficits of all limbs, spinal reflex
abnormalities, altered respiratory pattern.
o Seizures – only occur with forebrain disease
o Neck pain – intra-cranial vs extra-cranial causes
o CP deficits – Forebrain/ brainstem/ spinal cord
o Spinal reflex abnormalities – spinal cord
o Altered respiratory pattern – brainstem
▪ Answer: Multifocal!
SEE CHARTS FOR FURTHER LOCALISATION
Describe how to perform a neurological examination
Mentation, ambulation, cn nerves assessment, pupils, placements. reflexes,
Discuss primary and secondary traumatic brain injury
Primary brain injury is from blunt or penetrating trauma. Can include acceleration/deacceleration injury.
Secondary brain injury occurs subsequent to hypoxaemia, increased intracranial pressure, increased free radicals, tissue hypoglyaemia etc. Secondary injury is what clinicians aim to minimise.
List the clinical assessments and treatment for traumatic brain injury
Secondary brain injury peaks between 24 and 48 hours post injury.
Glasgow Coma Scores are used to assess patients.
Tx as per a tier system. All head trauma patients require tier 1 tx, and more severe/unresponsives progress to subsequent tiers.
TIER ONE;Consists of fluid therapy, oxygen support and avoiding compromised venous drainage.
Fluid therapy may be crystalloids or colloids. Aim to restore and maintain normal blood pressure (80-100mmHg)and volume. Good start is lactated ringers or normal saline at 10ml/kg boluses and re-assess. 7% hypertonic saline may also be used and causes fluid to shift out of cerebral tissues and reduce intracranial pressure.
If blood pressure remains low, may need to aid vasopressor eg Dopamine 2-10micrograms/kg/min cri.
Position with head slightly raised to facilitate drainage and do not interfere with jugular drainage by doing jugular puncture.
O2 supplement as required. avoid initiating sneezing as will increase intracranial pressure. Maintain PaO2 b/n 80 and 100mmHg and PaCO2 b/n 35 and 40. If patient unconscious and cannot achieve targets, needs intubation and mechanical ventilation.
TIER TWO;
Add in hyperosmolar therapy (mannitol or hypertonic saline) and anti-seizure meds if required.
Mannitol-only use in euhydrated else risk kidney damage.Expands plasma volume but decreases viscosity. Rapidly decreases intracranial pressure and cerebral oedema. Boluses safer than cri as cri increases brain permeability and thus then increases cerebral oedema again. Works within 15-30 minutes and lasts for 2-5 hours. Give 0.5-1gram/kg over a period of 20minutes. Usually only used if Glascow coma score <8. Monitor osmolality-if above 32mOsnol/L considered at risk of renal failure.
Hypertonic saline usually preferred over mannitol as less risk of subsequent hypovolaemia and hypotension. Tx of choice if systemic hypotension and increased intracranial pressure. Hypertonic 7% saline given at 3-5ml/kg over 15min. Repeat as required. Contraindicated if dehydrated and hyponatraemic.
TIER THREE; Desired parameters are not being achieved, patient worsening. Specialist surgery to relieve intracranial pressure as evidence via CT.
Alternatively unsubstantiated theories of promoting
a) hypocapnia to cause cerebral vasoconstriction, thus reduce intracranial pressure. Achieve via intubation and hyperventilation. Aim forPaCO2 of 25-35mmHg but recommended only for 20min periods. Also at risk of reduced cerebral blood flow worsening ischaemic injury.
or
b) hypothermia used to reduce cerebral metabolic rate and thus cerebral oxygen consumption and reduced intracranial pressure. Aim for32-35 degrees celcius. Controversial.
List the diagnostic workup and treatment of seizures and status epilepticus
DIAGNOSTIC WORK UP;
* History: Collection of information about trauma, toxin exposure or previous seizures
and therapies
* Examination of the skull and spine for trauma.
* Blood gas analysis: Obtain an arterial sample if possible. Significant metabolic
acidosis is common post seizure activity.
* Electrolyte assessment: Calcium and sodium in particular. Treat with IV fluids
immediately. If hypocalcaemia is evident administer 10% calcium gluconate at 0.5ml1.5 ml/kg over 10 minutes, monitor cardiovascular signs during administration. This
can induce emesis and rapid bolus can stop the heart.
* Measure blood glucose: If hypoglycaemic administer 50% dextrose at 1 ml/kg
(0.5g/kg) diluted 1 in 5 with an isotonic crystalloid. If using saline as a diluent assess
blood sodium levels first.
* Haematology and biochemistry: Should be performed as soon as practicable. Seizures
may cause elevated liver and muscle enzymes, as well electrolyte changes in
phosphorus and potassium.
* Assess body temperature: Try to maintain a normothermic state.
* Urinalysis: Myoglobinuria may be present. It is advised to place a urinary catheter and
monitor urine output to ensure protection of the renal parenchyma.
* Measure anti-epileptics serum levels: If the patient has known seizure activity and is
on medication blood can be collected to assess if the serum levels are appropriate.
* Toxin screening available.
* Cerebrospinal fluid collection: If you are considering CNS inflammation as a
potential cause and the patient is stable.
** Care in patient with elevated ICP, as it may predispose the patient to herniation.
* Referral for Computed Tomography or Magnetic resonance imaging when the patient
is stable.
* EEG: Perform an electroencephalogram if available to assess if seizure activity has
ceased despite outward clinical signs being controlled. This test can be performed at a
later stage in the diagnostic/treatment plan.
TREATMENT;
i) Diazepam
* Single dose of 0.5mg/kg IV as a bolus. Repeat dosing has been advocated at intervals of 15 – 20 minutes. Doses up to 2mg/kg IV can be given as a bolus
but sedation will be marked at this dose. Contraindicated with concurrent hepatopathy, hypoproteinemia, renal disease or repeated use in cats.
* CRI of diazepam is less preferable to midazolam.
* Substantial adsorption of diazepam into plastic means CRI concentration can be affected when administered through plastic giving sets/ IV lines.
* Large dilution volumes are recommended for CRI administration due to the potential for precipitation to occur, resulting in pain and phlebitis.
* Intranasal administration is effective due to the nasal vascular bed and proximity to the brain. Per rectal administration is effective if IV access cannot be obtained.
ii) Midazolam
* Single dose of 0.1 – 0.5 mg/kg IV may be effective if diazepam is not.
* CRI at 0.1-0.5 mg/kg/hr if a response to bolus dosing was successful.
* Has a superior bioavailability to diazepam and may be used IM.
* Safer to give as CRI than diazepam.
iii) Phenobarbitone
* Loading dose of 6-24 mg/kg IV over 24 hours then a maintenance dose of 2 –5 mg/kg/day PO, IV or IM divided into 2 doses 12 hours apart.
* NB Phenobarbitone is effective at raising the seizure threshold but less effective at stopping a seizure.
* Phenobarbitone with altered mentation needs to be interpreted carefully.
* Side effects include respiratory depression and hypotension and sedation.
iv) Levetiracetam
* Single dose of 20-60 mg/kg IV with varying effectiveness and a duration up to 8 hours.
v) Propofol
* Bolus of 2 – 8 mg/kg IV to effect followed by 4-30 mg/kg/hr (or 0.05-0.6mg/kg/min) CRI
* Recovery from this medication maybe confused with further seizure
activity
vi) Ketamine-dexmedetomidine combination
* Successfully used to treat super-refractory SE in a case series however more studies are required to confirm this
* Ketamine 1mg/kg IV over 5 minutes followed by
* Dexmedetomidine (3ug/kg IV) over 5 minutes followed by
* CRI of ketamine @ 1mg/kg/hr and dexmedetomidine at a variable rate of 3-7ug/kg/hr
Add-on medications
a. Bromide: 20-30 mg/kg/24 hours may be loaded at 600 mg/kg over 4 hours – 4
days, may induce a coma in the patient.
b. Zonisamide: 5-10 mg/kg PO q12h
c. Levetiracetam: 10-20mg/kg PO q8hrs
d. Gabapentin: 10-30mg/kg PO q8hrs
List the diagnostic workup of patients with suspected intracranial disease
neuro exam, bloods, urine, ocular exam,abdo u/s and chest xrays looking for neoplasia elsewhere, csf tap,ct/mri,serology testing
Discuss specific treatments for meningitis and meningoencephalitis
DDX FOR INFECTIOUS MENINGITIS;
bacterial, viral (distemper, fip), fungal, protozoal (toxoplasmosis, neospora).
DDX FOR NON INFECTIOUS MENINGITIS
gme, necrotising vasculitis complex, ne.
OTHER DDX INCLUDE
spinal lesion, intracranial neoplasia, discospondylitis, intervertebral disc disease.
CLIN SIGNS OF MENINGITIS;
are highly variable and may include;
Cervical hyperaesthesia and rigidity,
Reluctance to walk, stiff gait, arched spine, resistance on manipulation of spine or limbs.
Dependent on anatomical location and severity of the inflammation
o Forebrain: seizures, behavioural abnormalities
o Brainstem: various cranial nerve deficits, reduced mentation, and vestibular
signs
* Increased intracranial pressure
o Vomiting/nausea
o Direct irritation of the vomiting centre in the medulla
o Bradycardia with concurrent systemic hypertension (Cushing’s reflex)
o Papilloedema
o Respiratory depression
* Pyrexia Secondary to release of inflammatory cytokines from infectious organisms or WBCs, hypothalamic stimulation (resetting the temperature regulatory
systems) and from heat generated by muscle activity.
Common in SRMA and other causes of inflammatory CNS disease but uncommon in GME.
* Inappetence
* Lethargy
* Reluctance to move
MENINGITIS TX AND TYPES;
1. MENINGITIS OF UNKNOWN ORIGIN (MUO)
treat initially with Prednisolone (0.25-0.5mg/kg by mouth daily) and once infectious causes ruled out, Prednisolone (2-4mg/kg per day, divided) for 2 to 4 weeks
▪ Dose gradually reduced or tapered every 4 weeks when clinical signs
stabilise or improve
▪ Goal: alternate-day therapy at lowest effective dose to maintain
remission of clinical signs or discontinuation of drugs
o ** relapses common
▪ Will need long-term high-dose corticosteroids or,
▪ Alternative immunosuppressive agents eg azathioprine
* Second line immunosuppressive agents:
o Leflunomide, procarbazine, cytosine arabinoside, lomustine, mycophenolate
mofetil, azathioprine; COP (cyclophosphamide, vincristine, prednisolone), and
cyclosporine
o Can be introduced early in diseases with severe neurological signs or rapid
neurologic deterioration
2.GRANULOMETOUS MENINGOENCEPHALITIS(GME)
25% of meningitis are these. cause unknown. may be acute and progressive or chronic. May be focal, multifocal or ocular. Is always progressive. Fatal if untreated. Tx can significantly increase survival time. Best do corticosteroids plus radiation (focal lesion)or cytarabine, procarbazine and cyclosporin combo. Tx;
a. Prednisolone (2-4mg/kg per day, divided)
i. Presumption of immune-mediated disease
b. Cytarabine (cytosine arabinoside) at 50mg/m2 SC q12h for 2 days, every 3
weeks; or
c. Procarbazine 25-50mg/m2 PO q24h
3.NECROTISING ENCEPHALITIS (NE)
no tx,. rapidly progressive. av age 2.5 years, can be 7 months to 7 years old. recommend tx with pred and lomustine.
NME and NLE are subtypes of NE.
4.NECROTISING MENINGOENCEPHALITIS (NME)
Breeds affected: Pug, Maltese, Chihuahua, Pekingese, West Highland White
Terrier, Papillon, Shih Tzu, Coton de Tulear, Brussels Griffion.
no Tx.
5.NECROTISING LEUKOENCEPHALITIS (NLE)
6.STEROID RESPONSIVE MENINGITIS ARTERITIS (SRMA)
excellent px and survival. is self limiting disease (but need pred)
Prednisolone (2-4mg/kg/day, divided) as monotherapy
i. Corticosteroid therapy should be prolonged (4-6 months minimum) and up to 50% cases will relapse if the prednisolone is stopped or weaned too soon.
upper motor neuron vs lower motor neuron signs
UPPER MOTOR NEURON sits entirely with central nervous system. Damage to upper motor neuron with intact lower motor neuron results in signs of increased tone and preserved/increased spinal reflexes. Atrophy in time is mild and general.
Spinal cord lesion cranial to the intumescences (C1-5 or T3-L3) result in upper motor neuron signs. The cell bodies in these areas are within the cns.
DDX for tetraparesis with umn signs:
ivdd, acute non expressive nulclear pulposis extrusion, fce, diskospondylitis, tumour , trauma.
WORK UP for umn tetraparesis includes cbc and biochem, and usually cervical mri.
LOWER MOTOR NEURON has a cell body within the cns yet most of axon is within peripheral nervous system. Damage to lower motor neuron results in loss of spinal reflexes and loss of tone. Atrophy in time is severe and specific.
Damage to Cervical (C6-T2) or lumbosacral (L4-S3) intumescences result in LMN signs.
Both these areas contain peripheral motor neurons where the nerve cell bodies are outside the spinal cord to innervate the muscle groups.
DDX FOR lmn tetraparesis;
tickparalysis, botulism, myasthaenia gravis, polyradiculoneuropathy (coonhound paralysis), coral snake envenomation, polymyositis etc.
WORK UP for lmn tetraparesis might include thorough tick search, cbc, biochem, electrolytes, thoracic xrays (check for aspiration pneumonia and megaoesophagus and mediastinal mass), abdo rads (any evidence having having eaten something which may have led to botulism?), edrophonium challenge, acetylcholine receptor antibody etc.
A reflex involves sensory input (lmn), central connection to brain or spinal cord (umn) and a motor output (lmn). Damage anywhere can lose reflex. Can only preserve eg patella reflex if lmn remains intact.
BLADDER-cranial lumbar spinal cord puts in sympathetic fibres to bladder which relax bladder wall and contracts bladder neck muscle (urine retention). Sacral spinal cord s1-s3 bring in parasympathetic fibres which maintain detrusor tone and stimulates contraction (urination).
Damage cranial to s1-s3 gives rise to umn signs of a toned bladder, difficult to express, perineal reflex intact, anal tone present.
Damage to s1-s3 gives rise to lmn signs, a flaccid bladder easily expressed, loss of anal tone, faecal incontinence, loss of perineal reflex .
SPINAL SHOCK
This occurs only for a few hours, in a patient who would otherwise display umn signs in pelvic limbs, but instead displays lmn in pelvic limbs. Is always symmetrical (if assymmetrical, it is not spinal shock). Areflexia lasts for a few hours, and hypotonia for up to 14 days, before becoming increased as per umn. Onset within few hours of injury. Use cutaneous trunci assessment to localise lesion.
SCHIFF SHERRINGTON
Is a localising syndrome and an indicator of severe dz but does not mean that recovery is impossible. Occurs only within 14 days of injury between T3 and L3. Injury results in damage to long axons of L1-L5. Results in extreme thoracic limb extension and if held, thoracic gait is near normal, paraplegia, analgesia caudal to lesion. Occurs due to acute transverse spinal cord lesion, most commonly spinal cord transection but ddx fce, ivdd.
