The South African Veterinary Association



Pain in the neckDr. A. J. CarterFourways veterinary hospitalSpecialist Veterinary PhysicianIntroductionNeck pain is a common presenting complaint that the veterinary clinician has to deal with on a regular basis. It can often be a very destressing condition for the patient, the owner and the veterinarian. The manifestation of neck pain will vary between individual dogs from something that is very obvious to those patients with more subtle signs. Severe cervical pain is one of the few conditions that will cause “screaming or crying” pain in the dog. Dogs may also display numerous postural abnormalities such as a hunched back, low carriage of the head and torticollis. Sometimes the pain is not obvious to the owners and the dogs present with guarding behaviors where they will not engage with or avoid contact and interaction with other dogs and people or with avoid going up or down stairs. Nerve root signs reflects irritation of the nerve root resulting in unilateral thoracic limb lameness. Deep palpation and manipulation of the neck is sometimes required by the clinician to identify and localize neck pain. It must also be remembered that neck pain can also come from areas outside of the neck such as brain tumors and mid thoracic pathology. When assessing a patient with neck pain the age, breed and size of the dog are extremely important when drawing up a list of the most common differential diagnosis’s. Using the above signalment the following list of the most common diagnosis’s can be made.Young small breed dog: Meningoencephalomyelitis of unknown etiology (MUE).Young large breed dogs: Steroid responsive meningitis/arteritis. Discospondylitis. Beagles: Steroid responsive meningitis and disc disease. Dachshunds: Disc extrusion.Great Danes, Dobermans, Boerboel: Cervical vertebral instability (CVI)., Vertebral canal malformation, Ligamentous hypertrophy, joint capsule proliferation.Chondrodystrophic breeds: Disc disease.Cavalier King Charles Spaniels: Syringomyelia.The above list of diagnosis’s is by no means complete but it will cover the majority of cases of neck pain that the veterinary clinician will see. Meningoencephalomyelitis 0f unknown etiology and steroid responsive meningitis.Granulomatous MeningoencephalomyelitisGME is a devastating inflammatory disease of the CNS that effects young to middle age small and toy breed dogs. Clinical signs may be mild too severe with rapid decompensation and death. GME can be classified into three different forms which include focal, disseminated and ophthalmic forms. The disseminated form is the most common. Diagnosis is based on a combination of MRI imaging and CSF analysis. The CSF analysis typically has a markedly increased protein content and a pleocytosis ranging from 50-900 WBC’s/ul or more. The pleocytosis is typically mononuclear, including mainly lymphocytes (60-90%), monocytes (10-20%) and sometimes a few neutrophils. Common findings on MRI include multiple hyper intensities on T2 weight images and flair images with a predilection for white matter although grey matter may also be involved. T1 images tend to reveal more of a hypo-intensity of the lesions with variable contrast enhancement. On histopathology the lesions are aggregates of eccentric peri-vascular cuffing by macrophages, lymphocytes and plasma cells. These lesions may form granulomas that invade the CNS parenchyma. The focal form of GME is a coalescence of the granulomatous lesions to form a space occupying lesion. In the disseminated form the granulomatous lesions are distributed throughout the CNS while with the ophthalmic form the optic nerve, optic disc and the retina may be involved. The cause of GME is unknown but it is suspected that it is a delayed type hypersensitivity involving major histocompatibility class 2 and a predominance of CD3 antigen-positive T lymphocytes.The prognosis for GME is poor. Life expectance is anything from a few days to months and rarely years. Most dogs require continual therapy to control clinical signs. Treatment revolves around the use of immune suppressive therapy. Corticosteroids have always been the mainstay of therapy for this disease. Immune suppressive dosages of up to 2mg/kg twice daily are used initially to help gain control. Corticosteroids come with many undesirable side effects that can have a major impact on the quality of life. Additional therapies can be added on top of the corticosteroid therapy to get better control and help reduce the corticosteroid dosages. Cytosine arabinoside crosses the blood brain barrier in dogs. It acts on mitotically active cells by inserting into DNA molecules causing premature chain termination. It has been used in dogs and humans to treat CNS neoplasms. The dosage used in dogs with GME is 50mg/m2 given subcutaneously twice daily for two consecutive days. This is initially repeated every three weeks till remission is obtained. Often it is used together with prednisolone and after the second or third treatment cycle the prednisolone dosage can be dropped to the lowest effective dosage. Once control is obtained after 4 cycles of therapy the interval between the cytosine therapies can be increased. Gloves should be worn when using the drug and white cell counts should be obtained at 2 weeks after the first treatment and then periodically though out therapy. Other therapies that can be considered for GME include Procarbazine and Cyclosporine. Necrotizing meningoencephalitis (NME)This condition was first reported in the Pug. Today it is often referred to as Pug dog encephalitis. Small and toy breed dogs are commonly infected including the Maltese terrier, Chihuahuas, Shih Tzu’s, Boston terriers, Pekingese, Papillion’s, Pomeranians and others. The forebrain is primarily involved and it is associated with the infiltration of lymphocytes, plasma cells and macrophages at the grey-white matter junction. The more chronically affected animals develop necrosis of the brain tissue with cavitation’s. The clinical signs are dependent on the area of the brain affected but include forebrain signs such as change in mentation, seizures, circling and behavior changes. Characteristic findings on MRI include asymmetrical, bilateral and multifocal lesions in the forebrain and brain stem. The lesions are hyper intense on T2 and flair weighted images and often hypo intense on T1 weighted images. Necrotic areas in the brain can develop cystic cavitated lesions. CNS evaluation reveals increased protein and a pleocytosis with mainly lymphocytes. The prognosis for this condition is poor and therapy with immune suppressive dosages of corticosteroids and chemotherapy such as cytosine arabinoside can be tried. Necrotizing Leukoencephalitis(NLE)This is a similar syndrome to NME but it predominantly affects the white matter of the fore brain and the brain stem. This is primarily a disease of Yorkshire Terriers although other breeds such as the French Bulldog have been included. Typically, it affects young dogs between 6months to 5 years. Clinical signs are similar to NME. On MRI the lesions are hyper intense on T2 and flair weight images and hypo intense on T1 weight images. Treatment is similar to that of NME. Steroid responsive meningitis-arteritis(SRMA)This is a condition of young large breed dogs usually seen between 7 to 16 months of age. The etiology is unknown and an immune mediated cause is suspected. The clinical signs typically include a painful neck, arched back, reluctance to move, stiff gait, muscle pain and less commonly proprioceptive deficits and paresis. Polyarthritis may also be present. Signs may be acute in onset and progressive or they may be more chronic in nature with a waxing and waning course. The CSF cell counts are usually increased and neutrophils predominate. Bacterial cultures are negative. The protein content in the CSF is usually increased. The diagnosis is based on the history, signalment and CSF findings. Treatment consists of corticosteroids started at immune suppressive dosages until clinical signs have resolves and then slowly reduced to the lowest effective dosage. About 50% of dogs will relapse and they may then require treatment periods of up to 6 months. Prognosis for full recovery is excellent. SyringomyeliaClinical signs are secondary to the fluid filled cavity (syrinx) in the cervical spinal cord and are listed below.Persistent scratching at one side of the shoulder/neck area seen most commonly when walking the dog on a leash. No skin contact is made with the scratching.Excitement, exertion and barking could also elicit the response.Neck pain.Owners report that dogs resent any touching or grooming of the ear, limb or neck of the “scratched” sideLower motor neuron deficits of the thoracic limb ipsilateral to the “scratched “ side.Proprioceptive deficits and ataxia of the pelvic limbs.Facial nerve paralysis.Head twisted to the “scratched” side. Clinical signs are first noted between 6 months and 3 years of age. Signs of pain are not well correlated with the size of the syrinx. Diagnoses of SM can only be made on MRI imaging of the caudal brain and the spinal cord. The goal of imaging is to confirm syrinx formation in the spinal cord and also to demonstrate Chiari type 1 malformation. The caudal baso-occipital bone is short resulting in reduced caudal fossa volume with the caudal cerebellar vermis and medulla extending through the foramen magnum. The ventricles in the brain are also often distended.These dogs often have fluid filled tympanic bulla. As a minimum both T1 and T2 sagittal sequences of the caudal brain and proximal spinal cord should be taken together with T2 transverse sequences through the proximal spinal cord (e-mail Clare Rusbridge).Treatment involves both medical and surgical management. Not all patients require treatment and particularly when the syrinx is small or asymptomatic. Medical treatment revolves around the use of three groups of drugs, analgesics, drugs that reduce CSF production and corticosteroids. Analgesics that can be considered are the NSAIDs and oral opioids. Gabapentin may also be used as it has a damping effect on the hyper-excitable damaged nervous tissue. Furosemide decreases CSF production and is a useful drug in the management of SM. The carbonic anhydrase inhibitor acetazolamide may also help but can have unpleasant abdominal side effects. Corticosteroids are very effective in reducing pain and neurological deficits but the mechanism of action is unknown.It is recommended that furosemide is tried first for 2 weeks and response is evaluated. If response is poor, then a NSAID is added. This is tried for 2 weeks. If poor response, then NSAIDS are dropped and Gabapentin is tried. If clinical signs still not controlled, then furosemide is discontinued and corticosteroids are tried. Surgical treatment is reserved for those dogs with refractory pain or worsening of the neurological signs. The aim of surgery is to restore the CSF dynamics. This is achieved by sub occipital decompression where most of the supraoccipital bone and sometimes the cranial dorsal lamina of the atlas are removed. The largest case series of 16 dogs found that 81.25% of affected dogs had improvement or resolution of clinical signs, but 25% had relapses within the follow up period. The earlier the surgery was performed the better the outcome. Intervertebral disc diseaseCertain breeds are predisposed to IVDD and if one of the predisposed breeds presents with neck pain then this becomes the number one rule out diagnosis before proceeding to further diagnostics. The most common breed presenting with IVDD in South Africa is the Dachshund which is one of the chrondrodystophic breeds. The other chrondrodystophic breeds are also over represented with IVDD and these include the Pug, Bull dog, Bassett, Pekinese, Lhasa Apso, Shih Tzu, Beagle and poodle. The brachycephalic breeds some of which are also chrondrodystophic are noted above and also include the Cavalier King Charles spaniel and Boston Terrier. There are two types of IVDD that have been described:Hansen Type 1. This tends to be more of an acute disease process and is associated with extrusion of disc material (Nucleus Palposa) through a tear in the annulus and into the vertebral canal. The extruded disc material then causes cord compression and /or nerve root compression resulting in neck pain and neurological fall out.Hansen Type 2. This is associated with a more chronic type of process and occurs secondary to tearing of the annulus fibrosis and bulging of the disc dorsally with compression of the spinal cord. When making a diagnosis of IVDD in the neck the first diagnostic procedure following on a clinical examination is a plain cervical radiograph. Following basic radiological principles both lateral and dorsoventral views should be obtain. Radiographs are unable to identify disc prolapses or disc extrusions but can identify disc calcifications and spondylitic changes around the vertebra and also exclude other potential causes of disc pain such as fracture, atlanto-axial instability, vertebral body tumors and articular facet arthritis. Narrowing of disc spaces may be associated with acute disc extrusions but this may often be misleading due to incorrect positioning. Cervical contrast myelography allows evaluation of compressive lesions of the spinal cord and can be used to evaluate and identify disc extrusions and prolapses. Before injecting the contrast CSF should be obtained for evaluation in case the myelogram is negative. Cervical MRI is a more advanced imaging technique that allows better evaluation of areas of disc pathology and is able to evaluate the spinal cord itself. On an MRI study areas of inflammation, spinal cord oedema, cystic changes, syrinx formation, spinal tumors and nerve root compressions can be easily appreciated. Post MRI a CSF tap can be performed if it is indicated on the MRI study. An MRI study also allows evaluation of extra-spinal soft tissue which may be associated with neck pain.Once a disc extrusion or prolapse has been identified treatment may revolve around pain management or surgical decompression of the spinal cord. Conservative management can be considered if there is no neurological fall out and cord compression is mild or if nerve root compression is the primary finding. When considering pain management, it should be combined with cage rest or strict confinement at home to help prevent further disc extrusion. If conservative management fails, then surgery is warranted. A multi drug approach should be used. An effected approach uses a muscle relaxant such a diazepam (Valium), an anti-inflammatory (non–steroidal) and an NADMA receptor antagonist such as Gabapentin. Steroids may initially be used to reduce inflammation but should be limited to the initial 2-4 days before being replaced by non-steroidal. Treatment should be continued for a month after all pain has been controlled. The surgical approach most often used is a ventral slot decompression. This is an extremely effect treatment with resolution of the underlying problem and almost immediate pain control. This should be considered immediately if there is neurological fall out or if pain is non responsive to conservative therapy. Proper diagnostic imaging is required prior to surgical intervention and it should only be attempted by an appropriately trained surgeon. Cervical spondylomyelopathyCervical spondylomyelopathy (Wobbler syndrome) is a condition that is found mainly in large breed dogs and the Great Dane and Doberman pinscher are over represented. In south Africa we can also add the Boerboel to the list of predisposed breeds. It is a multifactor disorder and the following is a list of contributing factors:Vertebral canal malformation, stenosis or both.Vertebral instabilityLigamentous hypertrophyJoint capsule proliferation or cyst formationOsteophyte productionDisc herniationThere is an early onset of clinical signs in the giant breed dogs while other breeds tend to develop clinical signs from middle age onwards most likely from low grade instability resulting froC5/6 and C6/7 but in other breeds the compression may occur more cranially. The most common clinical presentation is a gait disturbance which is most severe in the hind limbs. Usually presents with mild ataxia but can progress to marked paresis. Cervical pain with guarding of the neck may be evident and often there is discomfort and pain on manipulation of the neck. Lameness and muscle atrophy may also be present in the front limbs and sometime a nerve root sign may be evident with traction of the front limbs suggesting nerve root involvement. Neurologically the lesions can be localized to either the C1-C5 region or the C6-T12 region. The gait abnormalities are often suggestive of cervical spondylomyelopathy (CSM) together with the breed involved but careful clinical evaluation is needed to localize the lesion and help rule out the extensive differential diagnosis list. Survey radiographs of the neck are useful in ruling out potential differential diagnoses but are not definitive in diagnosing CSM. Cervical myelography is the standard means to confirm the diagnosis and this helps to identify the area of compression. Myelography also allows manipulation of the neck and lesions can be classified as follows:Traction-responsive lesionsTraction non responsive lesionPositional lesionsThis differentiation will help guide the surgeon with regards to the surgical procedure to be performed. Ideally this should be followed up by CT scans to better define the lesions.In human medicine MR imaging is the modality of choice for classifying diseases of the cervical spine. MRI s are becoming more and more a part of referral veterinary medicine and are often used as the primary modality for identifying and classifying the lesions. MRI has the advantage of good soft tissue resolution, changes in the spinal cord can be evaluated and most of the differential list of diagnoses can be excluded at the same time. Dynamic studies can also be performed with MRI but they do increase the time required to run the study. CSM is a disease that is best treated with surgical intervention but this is beyond the scope of this presentation. References.Sharp NJH, Wheeler SJ, Small animal spinal disorders, diagnosis and surgery. 2nd Edition.Olby NJ, Jeffery ND. Advances in Veterinary Neurology. Veterinary clinics of North America. 2014Rossmeisl JH, Pains in the Neck. Western Veterinary conference 2012Bush W. Evaluation and management of neck pain. International emergency and critical care symposium 2015.Coates J R. An update on Immune –Mediated Brain diseases. British Small Animal Veterinary congress 2011Mariani C L. Inflammatory Brain and Spinal Cord diseases. ACVIM 2010Vernau K M. You Me and GME: Update on Inflammatory CNS disease. Veterinary Neurology Symposium. 2007Platt S R. Inflammatory Nervous system Disease of the dog. WSAVA World Congress 2008.Cuddon P A, Coates J R. New treatments for Granulomatous Meningioencephalomyelitis. ACVIM 2002. ................
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