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Caudal Occipital Malformation Syndrome in Cavalier King Charles Spaniels

C.W. Dewey, DVM, MS, DACVIM (Neurology), DACVS

Introduction

Caudal occipital malformation syndrome (COMS) is the canines analog of Chiari class I malformation of individuals. besides the fact that children only recently described in dogs, COMS is a really general neurologic sickness during this species. This sickness is essentially unique to small breed canines, with the Cavalier King Charles spaniel (CKCS) being essentially the most over-represented. there's convincing proof within the CKCS breed that COMS is a heritable ailment, besides the fact that children the exact mode of inheritance has not been decided. The ailment is a congenital malformation of the caudal occipital area of the cranium, resulting in overcrowding of the caudal fossa and compression of the cervicomedullary junction on the level of the foramen magnum. Most canine with COMS have syringomyelia, an accumulation of fluid inside the spinal wire, resulting from the malformation. In patients with COMS, there tends to be some level of cerebellar compression as well as constriction of the cervicomedullary junction in the region of the foramen magnum. With continual bony compression on the cervicomedullary junction and probable turbulent CSF stream and pressure alterations during this location, it is concept that the underlying meninges turn into hypertrophied with time. In both people with Chiari type I and canines with COMS, there is pathological proof of dural fibrosis in the place of the malformation. In COMS, as in Chiari type I of americans, the caudal element of the cerebellum is commonly projecting into or through (herniation) the foramen magnum, contributing to obstruction of CSF stream between intracranial and spinal compartments.

Pathophysiology

progressive differences in force dynamics between the intracranial and spinal booths are believed to be accountable for the building of clinical signals of COMS. besides the fact that children aberrant force dynamics due to obstruction of CSF pathways at the stage of the foramen magnum are often agreed to trigger syringomyelia in COMS, the real mechanism of this construction is unknown and there are multiple theories proposed to explain it. many of these theories operate on the likely fallacious premise that the syringomyelia fluid is CSF which is forced into the primary canal of the spinal wire. The more moderen theories indicate that the syringomyelia fluid is basically derived from extracellular fluid from the cord itself, both pushed into the valuable canal by way of a pulse force wave from behind the foramen magnum obstruction and/or drawn into the central canal by means of a centrifugally directed hydrostatic pressure force within the spinal twine. In commonplace dogs, there's pulsatile CSF move throughout the foramen magnum from intracranial subarachnoid area to cervical spinal subarachnoid house and again once again throughout systole and diastole, respectively. With an obstruction at the foramen magnum as occurs with COMS, CSF doesn't flow well in both path. during this scenario, the force exerted all the way through systole may additionally pressure both CSF or a force wave from the intracranial compartment into the important canal area of the cranial cervical spinal cord, causing it to steadily extend. This has been spoke of as the "water-hammer" impact. an extra thought proposed is that CSF is "sucked" into the primary canal region of the cervical spinal twine, primarily during maneuvers that cause sudden raises in intrathoracic an intraabdominal drive (e.g., coughing, sneezing, exercising). These Valsalva maneuvers lead secondarily to multiplied intracranial and intraspinal power by way of epidural venous distension. as a result of intracranial force is bigger than in the cervical wire location, CSF fluid is drawn into the cervical cord when there are swift increases in power. force in the spinal compartment tends to raise greater abruptly in the lumbar versus cervical areas, additional merchandising CSF stream into the cervical wire via this "suck" impact. The "slosh" phenomenon may also also be concerned in expansion of a syrinx. With distension of epidural veins right through Valsalva pursuits, CSF flows more freely inside the syrinx than within the compressed subarachnoid area. therefore, unexpected CSF power waves trigger CSF inside the syrinx cavity to "slosh" round, fissuring surrounding parenchyma and enlarging the syrinx. The aggregate of spinal epidural vein distension (and resultant pressurization of the subarachnoid house) and obstruction to CSF circulate from the cervical backbone to the intracranial compartment can also additionally outcomes in forcing subarachnoid CSF down perivascular spaces into the spinal wire parenchyma, regularly enlarging the syrinx. It has additionally been proposed that the displaced caudal cerebellum acts like a "piston". This concept means that the displaced cerebellum moves further caudally all over systole, obstructing the subarachnoid space on the foramen magnum and exaggerating the systolic pulse power wave it is transmitted from intracranial to spinal booths; this additional forces CSF via perivascular areas into the syrinx. besides the fact that children all the above theories may additionally make a contribution to the construction of a syrinx, none of them are sufficient explanations for this phenomenon. It has been shown that the syrinx continually has a far better force than the subarachnoid space, which might argue in opposition t theories that propose CSF is being pressured or sucked right into a low force device kind a higher pressure gadget. moreover, syrinx fluid is not similar to CSF fluid; it has a lower protein attention and is more consistent with extracellular fluid. a couple of linked theories had been proposed that are more likely to properly clarify the pathogenesis of syringomyelia formation with COMS or Chiari type 1 malformation. The "intramedullary pulse power" conception proposes that the spinal wire parenchyma distal to the foramen magnum compression is subjected to distending forces that are likely to pull the tissue in an outward or centrifugal path. The mixture of transmittal of the systolic pulse power wave to the spinal cord parenchyma (as a result of obstruction of the subarachnoid space) and reduced subarachnoid space drive in the spinal wire location (as a result of obstruction of the subarachnoid space rostral to the foramen magnum) cause this mechanical distension. Over time, the distension results in a cavity formation (syrinx), which is stuffed with extracellular fluid. The "Venturi effect" describes an identical mechanical spinal cord distension brought about with the aid of accelerated CSF pace distal to an obstruction. The obstruction (i.e., foramen magnum occlusion in COMS) explanations a narrowing of the subarachnoid house and a resultant multiplied fluid velocity distal to the obstruction. This improved speed lowers the hydrostatic drive, producing a centrifugally directed suction effect, leading to spinal cord distension. This thought additionally assumes that the collected fluid in the syrinx is extracellular fluid and at an improved pressure than the subarachnoid space. eventually, there is a "vascular" thought to clarify the development of syringomyelia in COMS cases. With elevated CSF force in the intracranial compartment vs. the spinal compartment due to foramen magnum obstruction (above all all through Valsalva maneuvers and systole), the venous and capillary beds turn into collapsed in the intracranial region and distended within the cervical spinal wire place (caudal to the obstruction). This happens because CSF and venous power invariably continue to be carefully matched in each cranial and spinal cubicles, and the venous system doesn't turn into obstructed as does the subarachnoid house with foramen magnum obstruction. With foramen magnum compression the transmural pressure (change between intravascular and interstitial drive) of the venous and capillary gadget on both aspect of the obstruction isn't any longer uniform all through the spinal cord. The uneven vascular enlargement and contraction that ensues factors harm to the encompassing spinal cord. This hydrostatic stress-mediated hurt to the spinal twine disrupts the blood-spinal wire barrier, promoting the buildup of extracellular fluid within the spinal wire (i.e., syrinx development). standard to all theories of syrinx development in COMS is the causative element of obstruction of regular CSF move on the foramen magnum.

scientific features of COMS within the CKCS Breed

Most dogs with COMS are presented for evaluation as younger adults, between three and 6 yrs of age. despite the fact, the age range for this ailment is awfully vast, starting from less than 6 mos to greater than 12 yrs of age. dogs which are offered at under 2 yrs of age frequently have more severe medical indications than older dogs. corresponding to Chiari type I of humans, there is a large spectrum of viable neurologic presentations for dogs with COMS, including cervical myelopathy, cerebellovestibular dysfunction, and forebrain dysfunction (e.g., seizure undertaking). by a long way, facts of cervical dysfunction and cerebellovestibular dysfunction are probably the most ordinary and are sometimes each present (e.g., multifocal CNS ailment). most of the COMS cases that the author encounters are presented for signals referable to the cervical place (e.g., neck ache, scratching undertaking) and refined indications of principal vestibular dysfunction are obvious on neurologic examination. sometimes, dogs with COMS and cervical syringomyelia present with a specific variant of cervical myelopathy known as central cord syndrome. in this syndrome, the outwardly increasing syrinx reasons extra LMN hurt to the thoracic limb musculature than white depend harm (to pelvic limbs); the influence is thoracic limb paresis (commonly LMN in nature) it's peculiarly worse than pelvic limb paresis. In some instances, the pelvic limbs may additionally seem usual. Some specific medical findings in canines with COMS consist of cervical and cranial hyperesthesia, diminished risk responses with commonplace vision, positional ventrolateral strabismus, thoracic limb weak point, pelvic limb ataxia, persistent scratching (on the head, neck, and shoulder area-often devoid of making dermis contact), scoliosis, facial nerve paresis/paralysis (unilateral or bilateral), and listening to abnormalities. The persistent scratching endeavor and scoliosis are fairly entertaining scientific signs associated with syringomyelia. within the creator's event, these are extra frequently encountered in the CKCS breed than in different breeds with COMS and syringomyelia. The scratching endeavor is believed to be because of the syrinx interfering with spinothalamic tracts and/or dorsal horn neurons, leading to abnormal sensations (dysesthesia/paresthesia). Scoliosis (torticollis) is obviously due to uneven syrinx harm to sensory proprioceptive neurons innervating cervical musculature; an alternative, less probably hypothesis is syrinx harm to LMNs innervating cervical musculature. Scratching undertaking and neck pain frequently are exacerbated by using abrupt weather changes, stress or exhilaration, and physical contact with the neck/shoulder vicinity (e.g., collar). The presence of both ache and scoliosis has been proven to be vastly correlated with syrinx width in CKCS dogs with syringomyelia secondary to COMS. it's crucial to realize that, primarily within the CKCS breed, different situations may additionally account for one of the vital medical signals. An enigmatic ear problem of the CKCS breed, known as primary secretory otitis media (PSOM) has been described. clinical indications of PSOM encompass apparent ache across the head and neck area, scratching of the top and neck, facial paralysis, and head tilt. Idiopathic epilepsy is additionally a time-honored disorder within the CKCS breed. Seizures were mentioned to ensue in 10% to 12% of humans with Chiari classification I malformation; within the author's experience, seizure endeavor is an rare concurrent prevalence in COMS cases, and it is constantly no longer possible to differentiate even if here is because of COMS or concurrent idiopathic epilepsy. Congenital deafness is also smartly-described within the CKCS breed. The severity and price of progression of COMS in canine is variable, starting from asymptomatic (i.e., discovering evidence of COMS whereas imaging for some other purpose) to intense ache and debilitation with quick worsening. moreover, some canine with COMS produce other concurrent problems (e.g., disk extrusion, inflammatory brain disorder) that may explain observed clinical signals. In such cases, it can be elaborate to discern if the COMS is the leading difficulty, contributory, or an incidental discovering.

analysis of COMS

prognosis of COMS is made by means of MR imaging. Magnetic resonance imaging is also the favourite imaging modality for diagnosing syringomyelia. The malformation is most fulfilling visualized on a midsagittal view (ideally T2-weighted), which includes the caudal fossa and cranial cervical wire. constant findings on MR imaging indicative of COMS are attenuation/obliteration of the dorsal subarachnoid space on the cervicomedullary junction and rostral displacement of the caudal cerebellum with the aid of the occipital bone. different commonplace MRI findings in COMS encompass syringomyelia (usually C2 degree caudally), herniation of the caudal cerebellum during the foramen magnum, and a "kinked" look of the caudal medulla. phase-distinction MRI (cine-MRI) is often used to measure CSF circulation in people with Chiari class I malformation, and has recently been evaluated to be used in canine with COMS. from time to time, dogs with MRI findings per COMS can have proof of different congenital problems equivalent to intracranial arachnoid (quadrigeminal) cyst, malformation of the C1 and or C2 vertebrae, and hydrocephalus. in the writer's opinion, most small breed canine normally have significant lateral ventricles as a breed characteristic (ventriculomegaly) and are not hydrocephalic. within the absence of concurrent disorder techniques, CSF evaluation is usually usual; occasionally, a delicate mononuclear pleocytosis should be obvious, despite the fact.

remedy of COMS

remedy of COMS will also be divided into scientific and surgical remedy. In individuals with symptomatic Chiari classification I malformation, surgical therapy is considered the medicine of choice, with foramen magnum decompression (FMD) being the preferred surgical system. Adjunctive surgical techniques are occasionally performed in people who have had a suboptimal response to FMD; such approaches usually involve placement of a shunt to divert syringomyelia fluid from the spinal wire place to one other place for absorption (e.g., pleural or peritoneal cavity, subarachnoid house). besides the fact that children there is a excessive degree of success in surgical management of Chiari category I malformation in people, there's a re-operative cost various from eight%-30% for FMD; essentially the most normal issue necessitating re-operation is extreme scar tissue formation on the FMD web page inflicting compression on the cervicomedullary junction, simply recreating the original sickness state. scientific remedy for dogs with COMS generally falls into three categories: analgesic medication (implies relief of dysesthesia/paresthesia additionally), medication that reduce CSF construction, and corticosteroid therapy. by means of some distance essentially the most helpful drug purchasable for reduction of scratching activity linked to syringomyelia is gabapentin (10 mg/kg body weight PO, q 8 hrs). It has been shown that neuropathic pain is accentuated over time due to up-law of the α2δ-1 subunit of voltage-gated calcium channels in dorsal root ganglion neurons and dorsal horn nociceptive neurons of the spinal twine. Gabapentin, and the newer gabapentin analog, pregabalin, are believed to exert their antinociceptive effects with the aid of selectively binding to the α2δ-1 subunit and inhibiting calcium inflow in these neurons. facet results of gabapentin are minimal, continually constrained to light sedation, pelvic limb ataxia, and weight benefit. There isn't any counsel available about the use of pregabalin in canines. A dose of two-4 mg/kg body weight PO, q 8hrs has been suggested, in accordance with preliminary pharmacokinetic records in average canines amassed by using the writer and colleagues. It looks that some dogs will hold high plasma pregabalin concentrations with each 12 hr dosing as well. no matter if pregabalin is extra useful or has fewer side consequences compared with gabapentin is unknown. in line with records collected from epileptic canine, pregabalin facet consequences appear to be comparable to these reported for gabapentin. Orally administered opiate drugs are from time to time helpful in alleviating neck and head ache in COMS dogs. The creator has had success the usage of oral tramadol (2-4 mg/kg, q 8-12 hrs). a number of medication aimed at lowering CSF construction were utilized in COMS sufferers, in an effort to lower the CSF pulse force. All information involving efficacy of these medicine is anecdotal. They include omeprazole (a proton pump inhibitor), acetazolamide (a carbonic anhydrase inhibitor), and furosemide (a loop diuretic). extra particular suggestions related to these drugs is covered within the congenital hydrocephalus discussion. Corticosteroids are often utilized in clinical management of COMS. capabilities merits encompass anti-inflammatory effects, diminished CSF construction, and diminished substance P (a nociceptive neurotransmitter) expression in spinal wire dorsal horn neurons. An preliminary antiinflammatory dose of 0.5 mg/kg PO, q 12 hrs is often effective in controlling medical indications. This dose may still be tapered, if in any respect feasible, to an every different day time table in the first month of remedy. In most circumstances of COMS, scientific therapy will curb the severity of medical signs, but resolution is not going. The favorite surgical process for treatment of COMS in canines is FMD. in response to two equivalent reviews, brief term surgical success prices with FMD in canine with COMS are approximately 80%. One record discovered an inverse relationship between the size of time scientific signals had been current just before surgical intervention and the extent of submit-operative improvement. sadly, there looks to be a disease relapse rate starting from 25% to 47% of circumstances; each one of these relapses are suspected to be because of extreme post-operative scar tissue formation at the FMD web site. In most instances, medical signals of pain are robotically relieved with surgical procedure, however scratching pastime tends to persist. currently, the author has tailored a cranioplasty procedure utilized in human FMD surgical procedure to discourage extreme publish-operative scar tissue from recompressing the operative web site. although effects are preliminary, the cranioplasty procedure looks to have substantially decreased the re-operation fee for this disease in canine. there is little guidance regarding the prognosis for COMS in dogs. Most dogs with COMS will respond favorably to clinical therapy, although in many cases this response is brief. in a single group of 10 COMS dogs handled medically, 5 dogs were euthanized inside 2 yrs due to disease development and diminished responsiveness to therapy. In an extra analyze, 36% of COMS dogs handled medically have been euthanized as a result of clinical indications of their disease at imply of 1.7 yrs from the time of analysis. youngsters the surgical success rate is commonly favorable for COMS in dogs, the recurrence expense due to excessive publish-operative scar tissue formation is unacceptably excessive. hopefully, refinements in surgical approach, reminiscent of cranioplasty, will ameliorate this problem. In universal, the universal prognosis for COMS in canine is guarded to respectable for sustained development in scientific indications.

References

1.  Cerda-Gonzalez S, et al. J Vet Intern Med 2006; 20: 736.

2.  Cerda-Gonzalez S, et al. J Vet Intern Med 2006; 20: 737.

three.  Dewey CW, et al. J Am Vet Med Assoc 2005; 227: 1270.

four.  Dewey CW, et al. Vet Surg 2007; 36: 405.

5.  Guay RD. J Geriatr Pharmacother 2005; 3: 274.

6.  Levine DN. J Neurol Sci 2004; 220:three.

7.  Rusbridge C. Vet Surg 2007; 36: 396.

8.  Rusbridge C, et al. J Small Anim Pract 2007; forty eight: 432.

9.  Rusbridge C, et al. J Vet Intern Med 2006; 20:469.

10. Rusbridge C, et al. J Vet Intern Med 2004; 18: 673.


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