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Buddy brown fce final
- 2. Signalment and history 3 year old male entire Boxer Acute onset non ambulatory paraparesis Schiff Sherrington posture No history of trauma
- 3. Physical and neuro Exam Physical Exam: unremarkable Neurological Exam: Hands off: Mental status and behaviour: Normal Posture and body position at rest – Schiff Sherrington Evaluation of gait – non ambulatory paraparesis L>R No Abnormal involuntary movements Hands on: CN assessment: WNL Postural reaction testing: prop. Deficits on both HLs Spinal reflexes: muscle tone and size – decreased withdrawal on Left Hind limb Sensory evaluation: appropriate (expected as presence of voluntary movements) Rem: clinically worse the following day: paraplegia: no voluntary movements
- 4. Paraparesis differentials Spinal Pain No Spinal Pain D: intervertrebral disc, calcinosis cincumscripta, spinal extrasynovial cyst, mucopolysaccharidos D: Degenerate myelopathy, lysosomal storage diseases, spondylosis deformans, dural ossifiation A: intra-arachnoid cysts, spinal dysaphism, syringomyelia, vertrebral malformations, spinal stenosis A: M: hyperchylomicronaemia M: N: Primary: extradural and intradural-extramedullary Secondary: Metastatic N: Primary: Astrocytoma, Ependymoma, Oligodendroglioma I: diffuse idiopathic skeletal hyperostosis, calcinosis circumscripta (idiopathic) I: meningitis, myelitis, discospondylitis, vertebral physitis, GME, SRMA, vascultis I: T: Traumatic disc herniation, verterbral fractures/luxations T: V: epidural haemorrhage V: Fibrocartilagenous Embolism, Thrombosis, Infarction From: BSAVA Neurology Manual
- 5. Clinical Signs of FCE Often yelp once – ass with trauma/exercise Para or Tetra Paretic/Plegic May have schiff sherrington posture Often lateralized signs – hemiparesis May be urinary/faecal incontinent Usually gradual improvement in neuro deficits ACUTE, NON PAINFUL, ASSYMETRICAL AND NON PROGRESSIVE myelopathy
- 6. Schiff Sherrington posture Extensor rigidity in the front legs BUT normal proprioception suggest severe SC injury
- 7. Pathogenesis Disc derived fibrocartilage acts like an emboli and blocks blood vessels supplying the spinal cord Infarction to this area Gets gradually better as neovascularisation occurs in areas of infarction Spinal Shock was also suspected
- 8. Diagnosis Based on History, Clinical signs and signalment Full physical exam and neuro exam – Diagnosis of exclusion often Could do radiography (myelogram)/CSF tap/Bloods to rule out other conditions MRI : expect lateralised lesion within the spinal cord parenchyma ( brightness on the T2 sequence called T2 hyperintensity)
- 9. Buddy’s MRI Extensive T2-hyperintense intramedulary lesion, from T11/12 to L3. T2 weighted image of the thoraco-lumbar portion of the spinal cord
- 10. 1.Abnormal: Brightness within the spinal cord 2.Normal: spinal cord: uniform grey color 1 2
- 11. Treatment Good nursing Rehabilitation: Physiotherapy & hydrotherapy (VIDEO) (+/- lazer) Urinary catheter (if no evident voluntary movements) or expressing of the bladder
- 12. HYDRO VIDEO Buddy’s progress in the under water treadmill
- 13. Prognosis Overall: Generally good with good nursing and physio– get increasingly better of weeks – months Deep pain? If absent poorer prognosis Full recovery may not occur if severe damage caused to the SC Won’t get worse after first 24 hours
- 14. Buddy Today – 8 days later Urinary catheter removed once good movement in the legs was observed Physio every day and getting stronger every time RHL back to almost normal LH still dragging but making some effort to move it, starting at hip as seen in video Still needs sling to support him on short walks but is getting there Gone home!!!
- 15. With thanks to the neurology team for helping me understand Buddy’s case Any questions?
Editor's Notes
- Hello, I’m Rachael Lang and I am going to talk to you about a dog I’ve been looking after this week called Buddy Brown who has a fibrocartilagenous embolism.
- Buddy presented as an emergency case to the neurological service last Wednesday. He is a 3 year old entire male Boxer who had acute onset non ambulatory paraparesis (meaning weakness in his Hindlimbs that prevented him from walking). He also had associated Schiff Sherrington posture in his Forelimbs which is the extension of his forelimbs which I will explain later. He had no known history of trauma.
- Buddy’s physical exam was largely unremarkable but his neurological exam showed up more abnormalities. Firstly we do a hands off assessment of the animal to assess neurological status. We look at mental status and behaviour, posture and body postion , gait and involuntary movements. Buddy had a very obvious abnormal posture known as Schiff Sherrington posture where the forelimbs are extended but the hindlimbs are pareparetic or paraplegic. His left hind limb seemed to be more affected than his right. On his hands on exam he had propreoceptive deficits in both hinglimbs (wasn’t replacing paws) and decreased withdrawal in his Hls
- D = degenerative A = anomaly/autoimmune M = metabolic N = neoplastic/nutritional I = infectious, inflammatory, immune mediated, iatrogenic, idiopathic T= Traumatic/toxic V- Vasculature FCE top as acute and non painful. Next Disc but just not showing pain
- The classic presentation of a dog with FCE is a non chondrodystrophic breed that is out playing/exercising is heard to yelp once and owners go over to find dog pain free but paraparetic or paraplegic. Can be tetraparetic if the lesion occurs more cranially. These dogs also commonly present with Shift Sherrington posture and it is not rare for these signs to be lateralized so worse on one side because the lesion caused by an FCE is usualy asymmetric. They may also be urinary or faecal incontinent. To summarise these dogs present with acute, non painful, asymmetrical and non progressive (after the first 24 hours) paretic or pleglic.
- This is a good example of the shift Sherrington posture I’ve been describing. It occurs when there is an acute severe thoracic or lumbar spinal cord lesion in dogs. Buddy having this helped us to localise the lesion even before the MRI because it tells you there is a problem in this area. The forelimbs are tense and rigid but the reflexes are still present and voluntary movement is possible in addition to paralysis of the pelvic limbs. The shift Sherrington posture usually only lasts hours and upto around 24 hours . No prognostic significance. The reason this occurs is due to a supression of the inhibitory ascending neurones. The inhibitory ascending neurones tell the muscles to stop contracting and these come from the grey matter in the lumbar spinal cord – in buddy his lesion was in the lumbar spinal cord so the inhibitory transmission wasn’t getting to the forelimbs.
- Taking that aside the pathologensis for FCE is not known for definite what causes this. But we do know that disc derived fibrocartilage gets lodged in blood vessels supplying that area of the spinal cord which causes infarction of this area. This only gets better due to neovascularisation which can be a very slow process. FCE often has ass. Spinal shock (which gets better within the first 24 hours or so) – spinal shock is the associated decrease in LMN reflexes due to a big trauma in the spinal cord – explaining his reduced withdrawal. Again the pathogensis for this is not fully known.
- Diagnosis of FCE is based on the presentation and history combined with exclusion of many other diseases through the neuro and physical examination. You could also rule out many other conditions with radiography, csf taps or bloods but FCE will not show up on any other these. MRI is the only real imaging technique to ID an FCE – looking for an intramedullary lesion
- These are Buddy’s MRI’s, I’m not sure if you can see particularly well but in the spinal cord from around here which is T11/T12 there is areas of hyperintensity so they show up paler in comparison to the rest of the spinal cord. This represents odema and reaction to the FCE which is very extensive in Buddy’s case. The report describes an extensive moderately well delinerated and slightly heterogenous intramedullary hyperintensity at the L sided, mainly Ventro-lateral aspect of the spinal cord from T11/12 to Cranial L3. The lesion is involving 2/3 of the spinal cord along 3 vertebrae. It is associated with T11/12 IV space narrowing and reduced nucleous pulposus signal. This is most likly consistent with an extensive infarction process (fce) or traumatic disc which could cause extensive secondary infarction and or spinal cord edema/inflammation also. This is hard to differentiate between a traumatic disc and an FCE but generally only FCE’s present pain free.
- These are the transverse views seen on MRI. Here is the spinal cord right in the middle which should be all over homogenous and fairly dark in colour as the image on the right shows better. However the image on the left is a very obvious area of hyperintensity which is due to the FCE.
- Once you have diagnosed FCE what is it treatment? There is no medical treatment which will fix an FCE but with good nursing and physiotherapy asap the prognosis for an FCE patient is massively improved. Good nursing is essential. These dogs are very difficult to deal with as they can’t walk or move themselves around some are urinary inconintent so will need a urinary catheter placed. The nursing requires regular turning to prevent bed sores, feeding, bringing water to them (buddy wasn’t really able to get to his water himself until you brought it up to his head until the past few days. Early instigation of physio is the best thing you can do for an FCE dog. Hydrotherapy – the water provides bouyance so the dog doesn’t need to bear weight but can still work on the muscles that allow movement ?? Ball exercise and general flexing of the joints and exercises encourages placing and weightbearing to help the muxcles and the joints. Also helps to keep the msucle memory .
- So this is a video of Buddy yesterday in the hydrotherapy treatment, it’s a treadmill underwater as you can see. Clearly his right hind leg is moving as we would like it to now which is great and his left hind is definitely making some effort to move although it is dragging (hence his boot on his foot). Starting at the hip he is definitely making an effort to move his hip. He is really keen on the hydrotherapy and gets super excited with it all.
- When thinking about the prognosis of an FCE dog it is not rare that owners would think it is very poor. However the majority of cases do well and after months do recover the ability to walk on the hind limbs and live a relatively normal life. After the first 24 hours you can be reasonably confident the problem won’t get worse. However in the months of recovery it can be very hard to deal with these dogs and also very expensive so sometimes it is not realistic to treat these animals and unfortunately they are put to sleep.
- Back to Buddy! I’m delighted to say has gone home today and has a physio plan for at home. He will still need a sling around his waist to help support him on small walks as his left hind is still dragging and he will need to wear a boot on this foot when outside to prevent any damage. But as he is doing well he will be happier at home no doubt and there is no real reason to keep him here any longer. He is going to visit a local hydrotherapy place once a week for physio. And we hope he is progressively going to get back to normal buddy after the next few weeks and months weeks/months