Craniomandibular osteopathy in a young dog

421347_10151629937179640_1038846606_nDr Miroslav Todorov

Blue Cross Veterinary Hospital

Sofia, Bulgaria

Case report

40542605_382709382264902_1711454165768601600_nCraniomandibular osteopathy in a young Labrador retriever.

A 4 months old Labrador retriever was presented at the BlueCross Veterinary Hospital in Sofia, Bulgaria, with the owner complaining about painful episodes after touching the head of the animal.

Clinical examination: the dog is in a good clinical stage, no pathological heart or lung sounds.

The temperature was 39,5 C. No abdominal pain or other abnormalities.

The palpation of the skull was painful for the dog, there was slight dome shape of the cranium. The masseter muscles were atrophied. After palpation of the mandibula it was noted that the lower jaw of this dog looked enlarged. Pic 1

Considering the age, breed and the affection of the specific bones, the following list of differential diagnosis was made:

  1. Craniomandibular osteopathy
  2. Osteomyelitis
  3. Calvarial Hyperosthosis
  4. Neoplasia

We took a blood sample for CBC and biochemistry analysis.

On the CBC there was a slight decrease of the RBC – 5,36 (5.5- 8.5 x10/12/L) but this could be normal for younger animals.

On the biochemistry there was a slight decrease of the Total protein – 49 (51- 78) g/L and Albumin – 20(26- 41) g/L. Everything else was WNL.

The patient was sent for CT of the head to search for additional characteristics of the bones of the head and confirm my suspicion about the disease. We put an injection of NSAID for the pain until the test was done.

On the CT we discovered symmetrical bone proliferation of the rami of the mandubule and bone thickening of the calvarium of the animal. No underlying bone lysis was noted. Fortunately, till this moment affection of the temporomandibular joints was not discovered, but it is possible that this could happen during the next months.40574303_322560345178752_5208200230733873152_n 40589358_286835962116167_5128061020073361408_n 40589364_655681474803526_9092529697882898432_n 40623237_513632389060326_2736220804109828096_n 40764141_2203859333191397_5014338687031312384_n

There were not clear signs of neoplastic process or osteomyelitis. As a result, considering the information that we had, a diagnosis of craniomandibular osteopathy was made.

Craniomandibular osteopathy is a non neoplastic proliferative bone disease affecting immature dogs.

Usually the clinical signs start between 3 and 8 months of age. Common clinical presentation is pain episodes, fever, trouble chewing food, drooling and in more advanced cases – inability to open the mouth and eat. The etiology of this disease is unknown.40530022_1906226039680267_8977683290295107584_n

The first written description of CMO appeared in 1958.(9) It was described in five West Highland white terriers affected within a 2-year period. The most common breeds that are affected are West Highland white Terrier, Scottish Terrier, Cairn Terrier. The disease is described in other breeds – in Labradors, Boxers, Great Dane and a few more.

It is believed that this could be an inherited disease (autosomal recessive inheritance pattern) and as such it is advised for such animals to be neutered.

Commonly the affected dogs have bilaterally symmetrical enlarged mandibles and tympanic bulles, and affection of other bones of the calvarium. In severe cases those structures could fuse and this will lead to decreased range of motion of the temporomandibular joint. On examination, the temporal and masseter muscles may be atrophied.

In advanced cases, the diagnosis of craniomandibular osteopathy can be done with good positioned x-rays of the head of the animal. The advance imaging techniques, such as CT or MRI, improve the visualization and confirm the extension of the process.

On x- ray or CT increased irregular bone density is commonly observed –  symmetrical periosteal proliferation, in most of the cases primary affection of the mandibules- 84%; tymplanic bulles – 51% and in some of the cases bones of the calvarium -13%.

The treatment plan is symptomatic with painkillers and anti-inflammatory drugs – commonly used drugs are NSAID and Steoids. Such drugs are needed during pain episodes and fever. Placement of an esophagostomy or gastrostomy feeding tube may be considered in patients that have difficulty eating and their nutritional requirements are not being met. Soft or liquefied food may be easier for some patients to eat. A high protein, high caloric food should be offered in order to meet nutritional needs.

Surgery of the bone proliferated tissues is not helpful in those cases.

The prognosis for these patients depends of the extent of progression of the disease. In those cases where a severe bone proliferation develops, the result is fusion of the temporomandibular joint and the prognosis is poor. Most of those dogs are euthanized because of the extent of the disease. It has been a common observation that when the affected dog is approximately 11 to 13 months of age, the disease may become self-limiting. The growth of abnormal bone slows, often regresses, and sometimes recedes completely. This period of self-limitation coincides with the time of completion of regular endochondral bone growth and ossification.

Our patient felt great after one injection of meloxicam. He is feeling active and has no signs of pain and temperature. Unfortunately, we cannot say whether his condition will progress to the extent to affect the temporomandibular joints and lead to inability to open its mouth.

The owner will return the dog to the breeder. It was advised to watch the dog for any additional signs and painkillers were prescribed.

Porencephaly in a pug dog with seizures – case report

 

 

421347_10151629937179640_1038846606_nDr Miroslav Todorov

Veterinary Clinic Blue Cross

Sofia, Bulgaria

 

Case presentation: a 3 and a half year old female pug dog was presented at the Bluecross Veterinary Clinic in Sofia for additional diagnostics in view of resently started seizure events.

A month ago the dog started having problems with its hind left limb and another vet started him on prednisolone. The limping improved but 20 days later the dog started having seizures.

The patient was examined at the Bluecross Veterinary Clinic in Blagoevgrad within two hours after one of the seizures. At that stage the dog wasn‘t able to see properly and showed a tendency to circle to the left. Blood was taken for Cbc and biochemistry analysis and the results were normal. The patient was started on an antiepileptics drug – Phenobarbital and the steroids were continued (because of the high possibility of an inflammatory process). An examination at the clinic in Sofia and additional advance imaging were scheduled.2 3 4 5 6 7 8 9 10 11 12

Clinical examination:

good general condition, slight difficulties in breathing (because of the brachiocephalic syndrome), normal heart and lung sounds, normal temperature.

Neurological examination: a little overexcited behaviour (but it was impossible to tell if this behaviour was abnormal for the dog or not). Normal cranial nerve reflexes, no nysgmus or circling, normal pupillary light reflexes. There was slight spinal ataxia in all four limbs. The proprioceptive tests were normal on all four. On the hind left limb the dog has pattelar luxation second degree (this explains the limping epizode a month ago). From the video provided by the owner it could be observed that the dog was demonstrating clonic- tonic seizure.

The owner was questioned for possible toxins, drugs and plants that could be the reason for the seizures but he said that the dog couldn’t have eaten anything abnormal.

A forebrain lesion was localised but the possibility of a multifocal process was very high.

The blood results were normal; therefore, possible extracranial reasons for the seizures were excluded. Toxin exposure was excluded by the anamnesis.

The list of differential diagnoses was:

  1. Inflammatory process – Necrotizing Meningoencephalitis (NME or Pug encephalitis)
  2. Idiopathic epilepsy
  3. Brain neoplasia
  4. Congenital lesion- hydrocephalus, cysts

To exclude most of the diagnoses from the list, advance imaging was performed – MRI 1,5tesla was used. The test was done with and without contrast material.

On the MRI we discovered a bilateral enlargement at the cranial part of both lateral ventricles within the frontal lobe of the brain. There was a visible communication between the ventricles and the subarachnoid space at the level of the eyes. They looked like cystic lesions filled with CSF. Bilateral loss of brain tissue was observed in both hemispheres. Around the cavities the cerebral cortex was reduced. These bilateral lesions could explain all the clinical signs that this dog was showing – seizures and the ataxia of all four limbs. There are motor cortex within the frontal lobe of the brain. There was no contrast enchantment after injection of contrast material within the brain tissue.

Therapeutic plan: the dog antiepileptic treatment was continued and regular measurements of the level of phenobarbital were scheduled. I added proton pump inhibitor –Esomeprazole (S enantiomer of omeprazole) because the drug has the effect of reducing the cerebrospinal fluid production. The steroids are slowly taped and they will be discontinued after two weeks.

The dog’s condition will be monitored by the owner and the vets at the BlueCross Veterinary Clinic in Blagoevgrad. In case of progression, especially after we stop the steroids, the necessity to take a CSF sample in order to finally exclude an inflammatory process is being discussed with the owner.

Porencephaly is a rare congenital cerebral defect and it is described in several reports in the field of veterinary medicine. It is more commonly seen in ruminants but there are few reports about dogs and cats.

There are few cystic congenital lesions of the brain, including focal lesions (porencephaly), extensive lesions (hydranencephaly) and very rarely schizencephaly (more commonly seen in humans). In porencephaly the defect creates a communication between the lateral ventricles and the subarachoid space. In schizencephaly the defect may be surrounded by a ring of polymicroglia. The schizencephalic defects are lined by gray matter.

The most frequent classification of these lesions based on their pathogenesis divides these defects into two major categories: developmental and encephaloclastic. Developmental porencephaly is due to a focal neuronal migration disorder, leaving a gap in the developing cerebral hemisphere. Encephaliclastic porencephaly includes cerebral cavities that result from tissue breakdown of various etiologies (cerebral ischemia, infection, trauma). In utero infection is the most common reason, especially in ruminants.

The interesting thing is that this type of lesions are congenital in nature but the clinical signs can start after the birth of the animal (which should be expected from the age) or sometimes later in life (after a few years).

According to the few reports about this type of pathology, the progression of the disease is different in every case. Some of those are completely asymptomatic, other cases are well controlled with drugs (antiepileptic drugs) third – their condition worsened, with poor control on drugs and some of those were euthanized. There was one report on a case of hydranencephaly where a ventriculoperitoneal shunt was placed and the dog’s condition slightly improved. Therefore, this is also a therapeutic option in some of those severe cases.

 

References:

  1. Porencephaly and cortical dysplasia as cause of seizures in a dog: Gisele Fabrino, Maria-Gisela Laranjeira, Augusto Schweigert and Guilherme Dias de Melo BMC Veterinary Research 2012
  2. Porencephaly and hydranencephaly in six dogs: Davies ES1, Volk HA, Behr S, Summers B, de Lahunta A, Syme H, Jull P, Garosi L. Vet Rec. 2012 Feb
  3. Porencephaly in dogs and cats: Magnetic resonance imaging findings and clinical signs: Schmidt MJ1, Klumpp S, Amort K, Jawinski S, Kramer M. Vet Radiol Ultrasound. 2012
  4. Porencephaly in dogs and cats: relationships between magnetic resonance imaging (MRI) features and hippocampal atrophy: Ai HORI, Kiwamu HANAZONO, Kenjirou MIYOSHI and Tetsuya NAKADE, J Vet Med Sci. 2015