---start--- steinberg neuro spinal cord problems are a big part of veterinary neurology practice. yesterday we did vestibular disease; Dr Dayrell Hart will tell us about epilepsy later. Today, cord problems. they are common and can be divided into focal and diffuse types of processes. many focal lesions lend themselves to treatment. The cord is one of those places where already, surgery and medicine converge to treat neuro disease. neurosurgery isn't a big part of veterinary neurology except as it relates to spinal cord disorders. Goals: focus on how much you can learn about your patient from neurologic examination. signs of spinal cord dysfunction: motor signs: paralysis - lack of volitional control of movement. not lack of movement, but inability to move with your will, in some functional way. paraplegia -[? both front or] both hind limbs are paralyzed quadriplegia - all four limbs are paralyzed hemiplegia - the fore and hind limb on one side are paralyzed pentaplegia - four limbs and tail are paralyzed paresis - a kind of disability and weakness that suggests an incomplete paralysis. the same processes which cause paralysis, when incomplete, cause paresis. paraparesis, hemiparesis, etc. sensory signs: anesthesia - loss of capacity to feel proprioception - sensory signals telling us where our parts are, where we are in space it's clear that when you knuckle an animal's feet to see if the animal replaces the feet, that tells you something about proprioception, but presupposes that the animal can move that foot. If the animal is paralyzed, that doesn't mean it lacks proprioceptive sense. it probably does, but it might possibly feel where the foot is, but be unable to move it. CP - conscious proprioception. some people think that for an animal to correct the foot, he must be conscious of the abnormal position. Dr S thinks that is untrue, that the animal probably isn't aware of where his parts are anymore than you are, unless you think about it. your nervous system knows how to hold a pen, proprioception is active when you are writing, but you aren't consciously aware or thinking about it. incontinence - dramatic sign of spinal cord dysfunction. this is the lack of volitional control of bowel and bladder function. not whether urine leaks from the bladder or not, but whether the animal can control in some volitional way bowel and bladder function. human babies are incontinent. rules for localizing spinal cord lesions: few, and terribly important. deficits should exist below the level of the lesion. often bilateral, often asymmetric. more severe signs will be ipsilateral to the lesion. Cervical - C1-C5: cord disease above the brachial intumescence. Cervical syndrome: -spastic hemiparisis to tetraplegia: weak, ataxic, wobbly, longstrided gait on all four limbs; knuckling, dragging feet, scuffing. -increased reflexes and muscle tone in all limbs: stretch reflexes are brisk, excursion is large, very forceful, may show clonus (the rhythmic persistent contraction in response to sustained stretch). may see cross extension when you stimulate flexion on one side - opposite limb will extend. flexion may persist after you stop the stimulus. so stretch and flexor reflexes are present and exaggerated. -cervical pain and/or rigidity -reduced flexion/extension of head and neck -postural reactions depressed in all limbs -bladder incontinence: also sphincter reflex is exaggerated and a tendency exists for retention of feces and urine. -+/- respiratory difficulty, horner's syndrome: because of the requirement for integration of medullary signals with the muscles of respiration for respiratory function, respiration may be impaired. Chris Reeves is tetraplegic, requires respiratory assistance, he has a cervical cord lesion. So these animals have intact, exaggerated segmental reflexes. Cervicothoracic syndrome: C6-T2 this is where nerves to forelimbs go. if mild, animal can walk, but the limbs have different gait movements. the tendency in the functional forelimbs is to be fairly short strided, whereas the hind limbs behind the level of the lesion tend to be long strided and scuffing as with a cervical lesion. if you make the lesion more complete, you again have a tetraplegic animal with no volitional control of fore or hind legs. but character of paralysis is different. why? well, in hind legs, as before, reflexes are present and exaggerated. but in forelegs, the cord damage is disrupting the reflexes. forelegs are hyporeflexic or areflexic. the forelimb muscles tend to be denervated, flaccid, and atrophic. hypesthesia/anesthesia below level of the lesion again - if lesion is at a site that disturbs reflexes, you depress reflexes, make them absent - you have flaccid paralysis, arreflexia. if lesion is above the level of the intumescence - reflexes persist and are exaggerated. Thoracolumbar T3-L3: b/w the plexi hind limbs as before. exaggerated reflexes in hind limbs, sphincters paralysis of hind limbs - paraplegia with extension/spasticity of hind limbs. increased local sensitivity at level of lesion, decreased caudal to lesion. forelimbs are much more normal, however, when the lesion is between the brachial plexus and the lumbosacral plexus you may see the "schiff-sherrington posture" Lumbosacral syndrome: L4-S3...Cy there is the potential to divide this area a bit, but first we'll talk about it as one area. consider it as the lumbar intumescence: lesions there cause paralysis or paresis, decreased to absent segmental reflexes in hind limbs, atrophy in hind limbs dilated anal sphincter, depressed bulbocavernous reflex fecal incontinence, bladder incontinence decreased sphincter tone - instead of retaining, there is dribbling it's important to keep in mind that there is a mismatch b/w the length of the cord and the length of the spine. humans are the best examples - our cord ends at about L1; the rest of the lumbar spine contains the cauda equina. the dog cord is longer, but still ends at about L6-L7. in L3-L5 is the bulk of the innervation to hind limbs. slide: myelogram - DV view - you can clearly see the intumescence, lasting only about 2 lumbar segments - this is where the reflexes are for the multiple nerve roots that are coming off. when the lesion is in the intumescence, reflexes are depressed or absent, and we see flaccidity, denervation, because the ventral horn cells are in that area of the cord. the lower motor neuron cells, that is. people get confused about this and it needs clarification. again - one commonly hears that in the thoracolumbar cord, between the plexi, where there is paralysis and spasticity in hind limbs - people sometimes call that an "upper motor neuron syndrome" the idea being that the descending pathway to those limbs is interrupted, paralysis is not b/c innervation to the limbs being disturbed, but b/c the upper motor neuron pathways aka descending pathways are disturbed. spasticity and hyperreflexia = upper motor neuron syndrome. when lesion is at level of plexus, where paralysis is flaccid and reflexes are depressed it is a lower motor neuron syndrome b/c it involves those lower motor neurons - the ventral horn cells that innervate the hind limb musculature. the spinal cord is the CNS, right? brain and cord = CNS. when you have a segmental lesion of ventral horn cells, you produce peripheral nerve dysfunction, but it is a central nervous system lesion. having assessed the postural ability, reflex ability, sensory ability, you have to try to get an idea of prognosis - how serious is the lesion, what is the outlook? it's not more elegant than saying we judge the severity of the lesion by how much functional integrity exists. paresis with sensation is better than paresis without sensation. our experience tells us the loss of sensation is a significant negative prognostic sign. prognosis, though, requires also a thought about time course. if the animal is paretic and anesthetic acutely, then you are encouraged that some integrity exists, but over two or three weeks if there is no change, the prospect of recovery changes and prognosis is not as hopeful. So, now, we will look at some abnormalities and try to see the relevant clinical signs. But first: recall we talked about the cord lesions causing dysfunction only at or below the level of the lesion - this is the single exception: Schiff-sherrington posture: a lesion below the brachial plexus causes loss of ascending inhibition such that extensor tone is increased in the forelimbs 1. "posture characterized by extensor hypertonicity of the thoracic limbs, and paralysis of the pelvic limbs, usually with intact reflexes" 2. "thoracic limb extensor hypertonicity caused by disinhibition of extensor reflexes, secondary to a cord lesion that interrupts an ascending inhibitory pathway." Slide: Moritz Schiff - a german physician of the last century Sir Charles Sherrington - another physician and Dr S's personal hero Dr vite mentioned cerebral lesions can cause forelimb extension by causing loss of inhibition on the gamma circuit - so forelimbs are extended until you break reflex arc by cutting dorsal root or something; whereas cerebellum acts directly on alpha motor neuron. the schiff-sherrington ascending pathway (Border cells) also acts directly on the lower motor neuron cells. recall the cervical cord lesion causes hyperreflexia and increased tone in fore and hind limbs. can you tell the difference b/w that and the thoracolumbar lesion? yes. the thoracolumbar lesion produces forelimbs that have increased tone and disturbed gait, but not paralysis. he can walk. sensation is not interrupted in front legs and is normal. so the two differences are functional integrity (ability to walk) an the ability to feel. slide: foal in lateral recumbency we saw a doberman with an L4 lesion before who had foreleg extension. this foal also has foreleg extension, caused by thoracic trauma. cats dogs horses frogs etc all show this schiff-sherrington phenomenon. Dr S hasn't seen reference to it in people, though, which is sort of strange. Trauma: some instances are not difficult diagnostic problems, as this obviously displaced thoracic spinal column fracture is not. but this one is more interesting. we see the spine...bodies of the vertebrae are present, the spinal canal is visualized, and the dorsal laminae. at the site of fracture and dislocation, a vertebral body is displaced dorsally, and you'd imagine it would be compressing the cord. so, what is the prognosis? people have all these rules. 50% displacement can be accomodated, 100% is not likely to recover, etc etc. you always have to get two views to check lateral displacement, etc. the dog who owned this spine came in several weeksa fter injury with posterior limb paralysis (this is a thoracic lesion), hyperreflexic hind limbs, and sensation in the hind limbs. that's a surprise, b/c you don't expect to see the sensation. we decided to wait and see what happened despite the obviously severe fracture that couldn't possibly allow recovery since it was 100% displaced. the very first instance of trauma we will see here is of special interest to veterinarians... ---break--- videos: animal that has been traumatized - this is a turtle who was found by a vet student who epoxied a wheel to the shell, so he could move using his front legs - he had a thoracic spinal fracture and hind leg paralysis. flexion of the hind legs produced cross extension - segmental reflexes intact, maybe hyperreflexion. has sensory integrity - moves head away from forelimb pinch. this paraplegic turtle should be an inspiration to you. dog with the severely displaced thoracic spinal fracture. 8 mos post radiograph is running around like a totally normal dog!!!!!!!!!!!! the message here is that the rules we make up are often rules of convenience, rules that owners demand of us, and since there was SOME evidence of functional integrity and a willing owner, this animal profited by our ignoring the rules. the first reference about traumatic events - mainly in small dogs - atlanto-occipital joint abnormalities. either malformation, trauma, or a combination of both can cause instability of this joint, or of C1-C2 atlanto-axial joint. we want to see the dorsal lamina of C2 partly overlapping the dorsal lamina of C1. recently people have asked how much tolerance there is for mobility at this site. slide: myelogram - figuring out what's going on requires flexing and extending the neck under fluoroscopy, and is dangerous. here we see ventral compression of the cord as neck is flexed. dorsal lamina of C2 is no longer superimposed over C1. this is a clearly pathologic situation. but there are times when our rules are inadequate to allow us to make this judgement. we talk about the easy cases that are obvious and reveal how much we know; but this is a real problem we don't know enough about yet. signs: variable - cervical pain and guarding of neck to tetraplegia and death depending on severity of damage. tx: conservative = neck splinting +/- wires/pins used to surgically realign and stabilize the joints. surgery is risky. animals may be apneic immediately post op or, sadly, permanently. slide: spinal cord with a marked depression in it, from having the bone driven into it. one last thing to mention - this is a very happily uncommon but nonetheless terrible event - this is a kitten's vertebral column, dramatically hypomineralized due to nutritional problems. this is very unpleasant. consider a growing puppy - gets diarrhea - the vet puts puppy on rice/meat diet - diarrhea is stopped - no one tells people to change diet back - puppy develops hypomineralized skeleton and pathological fractures. even worse - owner of a kitten, who sought "natural" food, and recognized all the chemicals in prepared catfood. owner knew those were bad and knew cats were carnivores so fed kitten only lean meat - ended up being this kitten in the slide. problem was, didn't feed the kitten any bones, organ meats, stomach contents, etc. just beef, very lean. ugh. disk disease: a kind of traumatic event. a disk prolapses, presses against the cord, either a slow compression or an explosive event. this is often seen in chondrodystrophic breeds but any dog and less commonly cat can get it. slide: mineralized disk visible between two vertebrae. this disk is producing only modest change in the ventral subarachnoid dye column on this myelogram. more caudally, we see a dramatic deviation in dye column, but no mineralized disk is seen. disk degeneration is often marked by mineralization, and myelography is useful to help you identify which disk needs surgical attention - may not be the obviously mineralized one. range of abnormalities seen with disk disease is wide - slide: enormous amount of disk material compressing the cord to threadlike width. sometimes this is so explosive an event that the disk material moves half a vertebra away or to the dorsal side of the cord. slide: another example - narrowed intervertebral space - a sort of radiodensity associated with mineralization in another space - myelogram shows that no problem is associated with the narrow space, but the mineralized area is associated with a complete obstruction of flow of dye. in an old doberman - wobbler syndrome is seen. this is really a collection of abnormalities including disc disease, spondylosis, reshaping of vertebrae as degenerative process, spinal canal abnormalities, and here we see many of those - misshapen C7, spondylosis of C6, distortion of spinal canal, etc. there is an interesting variation - sometimes the disk prolapse is explosive, and sometimes gradual. this cord belonged to an old doberman who was walking up til the moment of death - his cord is not round, but is really flat. but it was a slow degenerative process and he retained a lot of function, I guess is the point. video: beagle with cervical disk disease, commonly a source of pain and only modest neural dysfunction. "root signature" - animal is showing clinical signs referable to irritation of nerve root - he picks up left foreleg, sort of limps on it, etc. conclusion is that the lesion is irritating mainly roots to the left forelimb. another dog with cervical cord disease. slow to correct knuckled positioning - sensory or motor deficit, hard to tell which. probably both. he can hop, but short, choppy way. hind legs maintain completely inappropriate posture; front legs hop.. he wheelbarrows awkwardly but that may be the examiner. the hind limbs are obviously worse than the front. when the dog lies down, he looks normal ;) dog with thoracolumbar lesion - stiff hind legs that won't flex - very hard to flex them, very resistant. lumbosacral lesion dog drags hind legs behind him but uses front legs well. flaccid, areflexic hind legs, urine on fur at hind end. L6 area lesion - hind limb paresis only. dog moving around pretty well. serious complication of cord trauma, seen most often with disk disease - spreading hematomyelia or spreading spinal cord syndrome. dog has hind leg paralysis (dachshund), flaccid paralysis of hind legs but can walk with front legs. 24 hrs later, laterally recumbent, only abdominal respiration, very sensitive forelegs, no tone in hind legs, what has happened is the hemorrhage and edema present at first at the site of the lesion, has spread longitudinally up and down the cord to produce destructive disease. young great dane who has Wobbler disease. note the long stride on all four limbs, ataxia, a bit of paresis, high stepping "floated foreleg" gait. hypermetric, dysmetric foreleg gait. we used to see these in young great danes and older dobermans and various hypothesis exist re: nutritional, body size, etc - result was the kind of vertebral instability and malformation we saw on that slide, with myelographic abnormalities demonstrating compression. we see this much less often now in Great Danes. probably a change in breeding programs. old dane with cervical cord signs - long gait, scuffing of all four limbs, some ataxia. delayed correction of knuckling. also shows "clonus" - continued, rhythmic contraction of the muscle in response to sustained stretch. we cannot wait until we know everything before we act...we must not forget how little we know, as we act. -unattributed. this is a reasonable thought to consider. we are obliged to do as best we can, to help our patients. but as we act we may accidentally start to believe that we know what we're doing. it's best to try to remember that often you do not. IR Griffins...paraphrased: little if any clinical evidence that glucocorticosteroid therapy will convert a previously irrecoverable patient to...[a recoverable one] good clinical studies evaluating the use of these drugs in spinal cord trauma are scarce. NEJM: may 17 1990 study: a randomized, controlled trial of methylpred or naloxone in tx of acute spinal cord injury - there are 17 authors of this paper, using patients from 9 hospitals. 53 people were acknowledged. stats showed that methylpred given under defined circumstances did have value. naloxone did not work. however, realize what significant improvement meant. a quadriplegic with little motor function after injury regained normal upper body strength with gross movement of some fingers. a patient like this might be able to feed himself with the aid of an adapter or brace, and assist with moving himself. another patient with paraplegia gained ability to move about with braces. ....but can he hunt rabbits? no. you aren't getting HUGE gains in function. by our standards, it is important to consider that normal upper body strength with gross paw movement probably isn't enough to prevent euthanasia... slide: hemorrhagic pithing which occured in grey matter of that dachshund's cord. the original lesion sort of spread longitudinally within the cord. slide: another example of that - hemorrhagic areas seen on cross section cranially and caudally from the original lesion. notice it's within the grey matter that this cylindrical pithing seems to occur. signs produced by destroying grey matter along length of cord are not reversible - you get irreversible paralysis. why does that happen? we used to have a simple explanation - the cord is hanging there in subarachnoid space, you traumatize it, it swells, but is constrained by dura, so it goes up and down and if you nick the dura the malacic cord pops out, it's all pressure necrosis. that was the original story. this didn't account for the fact that the lesions occured in grey matter. current story is: autodestruction: a process of spinal cord destruction which begins immediately upon injury but which is not dependent on continuing physical distortion. same story you've heard a million times. injury, petechial hemorrhage and calcium influx, hemoglobin and iron release, thrombin --phospholipase activation, arachadonic acid cascade, prostaglandins, grey matter ischemia, lipid peroxidation destroys myelin, spread to white matter, axonal damage, microvascular damage, ischemia, finally resulting in permanent neurological deficit. the crux may be petechial hemorrhage into grey matter releasing Hb and iron, feeding the whole process. two explanations for the traumatic event - research into oxygen radical scavengers uses the hypothesis we've discussed just now; experimental lesions mimic the spreading syndrome we saw. but we also know that cord lesions can get better, that surgeons can help. so there is clearly more than one thing going on. this model here gets more attention. this is the model which doesn't lend itself to surgical intervention but requires interruption of the chemical cascade. but other injuries get better with cage rest, possibly steroids, possibly surgical intervention. topic change: one feature of disk disease and trauma to the cord in general is acute onset resulting in paresis or paralysis. the cord is acutely injured by prolapsed disk, and consequence is motor/sensory deficits that animal presents to you for. but when youhave an animal with focal cord disease and acute signs, what does the DAMNIT list require you to consider? trauma is one thing that occurs acutely. not degenerative, anomalous, infection, neoplasia ischemia also occurs acutely. this is a second common cause of acute onset focal spinal cord dysfunction - the infarctive process. here we see a cord section in which the right side looks normal but the left side has complete destruction of dorsal, lateral, and most of ventral faniculi, and some of the grey core. this is necrotic. caused most commonly by the fibrocartilaginous embolus coming from (we think) the nucleus propulsus, by mechanisms that we really do not know (how disk material enters vascular tree, that is, is what we do not know). it's a thromboembolic anomaly. outcome for those is a function of how serious the infarct is, how big the vessel is. if modest, animal can recover, if not, can have profound plegia and poor outcome. diagnosis is similar - you know the animal presents with acute onset of discrete cord signs, you localize based on reflexes, neuro exam, myelography in one instance reveals compressive disease (disk disease) or nothing - if you see nothing, you have to infer that focal malacia is the cause. with MRI you can demonstrate an area of necrosis. but we're used to making a dx by exclusion. k video: schnauzer - has evidence of focal cartilaginous emoblization in cord. profound hemiparesis. signs often quite unilateral, quite discrete, suggesting mroe ischemia than trauma, so that is a hint. typical story - dog is running around, yelps, and starts showing signs that evolve over hours. by the time you see it, it's usually completely evolved and animal is painless, though here we see evidence of sensory integrity. he raised his head and looked at foot in response to stimulus. big tetraplegic dog with distinct asymmetric signs - last friday confirmed by MRI right sided cervical infarct encroaching on C5-C7. left side has brisk reflexes but is paralyzed; loss of selective motor response evident as well - tail moves when toe is pinched; these animals often urinate at that time as well. dog also has diaphraagmatic respiration. good cutaneous trunci response on left, also. right side - horner's syndrome. he has right sided cervico/thoracic disease. he can move his head. reflexes on the right are similar to those on the left. segmental reflex abnormalities do not always come as a set. may see exaggerated flexion and not clonus, or whatever. he seems to feel - looks back at what's going on. dramatic tail withdrawal to pain. right front leg - much less tone, depressed reflexes, no flexor reflex, suggesting this is the area of the lesion. in contrast to left side, little cutaneous trunci response. good evidence of cervico/thoracic cord disease. ----end----