Dr Svetoslav Penchev
United Veterinary Clinic
Paradoxical Vestibular Syndrome is a condition that affects flocculonodular lobe or the caudal cerebellar peduncle of the cerebellum and causes vestibular signs. These parts of the cerebellum participate in central components of vestibular apparatus and are responsible for the maintenance of equilibrium and coordination of head and eye movements;
This syndrome is called paradoxical vestibular disease because the head tilt and circling occur contralateral to the lesion. There is usually some evidence of cerebellar disease on neurological examination, such as ipsilateral dysmetria and head tremor.
Signalment: 8 years old, male, not castrated French bulldog
History: The owner noticed that the head of his dog is not in normal position and is tilt to the left. The dog was carried to its personal doctor, and the doctor had doubts that the dog was having problem with the inner ear . The doctor refer the dog to me for computer tomography, and for approval of the diagnosis.
Case presenting signs: Left head tilt, progressive vestibular signs
Clinical examination: Internal body temperature 38,1 ; Respiratory rate: 36 breaths per minute ; Color of mucous membranes – pink; CRT – 1,5 sec.
Puls 110 bpm ; The overall condition of the dog was normal and there was no no signs of pain.
Mentation and behavior-normal; Posture – Left head tilt; Gait – Vestibular ataxia, increase muscle tone and dysmetria of right fore and hind limbs The dog react with cranial and spinal normoreflexia. Menace response reaction of right eye was a little bit reduced. There was no change in conscious proprioception and bladder function was normal. The owners report for intention tremor of the head when the dog is waiting to be fed.
Neuroanatomic localisation: Central Vestibular ; Right Cerebellar Flocculonodular lobe; Paradoxical Vestibular Syndrome
CBC and Biochemistry were normal. Magnetic resonance of the head was performed with GE MRI 1.5 Tesla.
MRI images : Image 1
Image 3 –
MRI findings :
A single oval T1-hypo and T2, T2 FLAIR-hyperintensive intra-axial mass is observed, leading out of the cerebellar vermis and affecting the both cerebellar hemispheres. The mass is well circumscribed by the surrounding tissues, with extracapsular expansion and diffuse infiltration into the the gray matter. There is a significant mass effect that reveals compression of the flocculonodular lobe and reveals obstruction to the flow of cerebrospinal fluid with secondary dilatation of the quarter ventricle and central canal with subsequent syringohydromyelia.
Diagnosis: Cerebellar neoplasia
The clinical condition of the dog did improved after i.v
infusion with Mannitol (0.25g/kg bolus 3 times over 20 minutes) , Harmann`s solution 20ml/kg and Prednisolone p.o 0.5mg/kg – 2 times daily – for 3 days . Next 10 days the dog take Prednisolone 0.5 mg/kg 2 times daily at home.
Control visiting on the 14th day -https://www.youtube.com/watch?v=XRyp9sgqCjE
All of previous clinical signs were more severe present. There was no more improvement with this therapy and the owners chose to euthanize the dog.
With both central and peripheral Vestibular syndorme, the head tilt, circling and nystagmus typically occur ipsilateral to the side of the lesion. Less frequently, lesions affecting the caudal cerebellar peduncle, the fastigial nucleus, or the flocculonodular lobes of the cerebellum can cause central Vestibular disease with a resulting paradoxical head tilt. Bilateral Vestibular disease is characterized by head sway from side to side, loss of balance on both sides and symmetrical ataxia with a wide-based stance. A physiological nystagmus usually cannot be elicited and a head tilt is not observed.
veterinary clinics “Dobro hrumvane!”- Sofia, Bulgaria
Histiocytic ulcerative colitis (HUC) is an inflammatory bowel disease that causes tenesmus, hematochezia, and profound weight loss. The disease is most commonly described in young Boxer Dogs but it has also been reported in other breeds of dogs, including Mastiff, Alaskan Malamute, Doberman Pinscher, French Bulldogs. One cat with HUC also has been described. HUC differs from other forms of inflammatory bowel disease in dogs because it is characterized histologically by periodic acid-Schiff (PAS)-positive macrophages; it is more likely to be associated with mucosal ulcerations; it is less responsive to therapy, and has a poorer long-term prognosis. HUC in Boxer Dogs was 1st described by Van Kruiningen et al in 1965. Since that time, the gross histopathologic and ultrastructural findings have been well characterized. The pathognomonic lesion of HUC is the accumulation of distinctive, PAS-positive macrophages (indicative of glycoprotein within the macrophages) in the lamina propria and submucosa of the colon with loss of the associated epithelial surface. The PAS-positive material may be derived from remnants of bacterial cell wall glycoprotein, and accumulation of PAS-positive material in macrophages may occur because of abnormal lysosomal activity, exhaustion of lysosomal activity, or inhibition of lysosomal activity by toxic substances. The cause of HUC has yet to be determined. Early studies proposed an infectious etiology on the basis of the presence of chlamydia-like organisms in macrophages on electron microscopy and clinical improvement after chloramphenicol therapy. In a subsequent ultrastructural study, organisms were not conclusively demonstrated. Attempts to create the disease experimentally by mycoplasma infection failed. Management of HUC consists of various combinations of the following: dietary modifications; antibiotics such as chloramphenicol, metronidazole, and tylosin and anti-inflammatory or immunosuppressive drugs such as sulfasalazine, prednisone,cyclosporine and azathioprine. Response to treatment is generally poor, frequently resulting in euthanasia of affected animals
Representative histologic images in the dog (HE, bar = 50 μm). A: Lymphocytic-plasmacytic colitis. Note the interstitial diffuse pattern of infiltrate represented by a large amount of lymphocytes mixed with plasma cells and some macrophages; B: Lymphocytic-plasmacytic colitis (follicular variant); C: Histiocytic colitis. Severe mucosal abnormalities with loss of crypts and diffuse infiltration by large macrophages (arrows) that in the insert (PAS stain) are shown as the main cells infiltrating the lamina propria; D: Eosinophilic colitis. Note the presence of a large number of eosinophils (arrows).
- Report and history of the patient
We had a patient dog, named Robin, French Bulldog, male, noncastrated, 2 years old, vaccinated, with chronic diarrhea dating back about a year and a half. Everything started with minor episodes of diarrhea when the dog was about 6-7 months old, the owners also mentioned itching and licking of paws. Аll tests for infectious diseases were negative (CPV/CCV/Giardia) and blood samples were normal. The faecal sample was negative for any parasites. At that time, the patient was treated with probiotics, chemotherapeutics and sulphonamides, gastrointestinal and hypoallergenic diets without any effect. During this time, the owners refused colonoscopy or diagnostic laparotomy combined with a histopathological examination аnd a test for pancreatitis (Idexx cPL).
On April 12, 2019, the dog came to the clinic again with complaints of persistent diarrhea accompanied by blood and tennesms. Robin’s condition had become more serious since the owners had given BARF at their discretion. On the same day we did the CBC and biochemical blood tests and ultrasound of the abdomen. The ultrasound examination showed a high degree of thickening of the layers of the colon and some of the small intestine divisions, as well as enlarged mesenterial limph nodes.
We placed an intravenous catheter and included fluid therapy NaCl 55 ml/h, antiemetics (famotidine and pantoprazole), vitamins (vit C, B- complex, arginine ,ornithine, citrulline), antioxidants (duphalyte, amynoplasmal), probiotics (Fortiflora and Pro-kolin paste), painkillers (buprenorphine), haemostatic drugs (Vit K1 and etamsylate) and tylosinum 25 mg/kg/24h/p.o. Аfter 3 days we took blood tests, which again showed low-grade anemia, leukocytosis and neutrophilia. We also added injectable erythropoietin to therapy.
On April 16, 2019, we performed a diagnostic laparotomy with full thickness biopsy of thr large and small intestine. The material taken was prepared and sent for patho-histological examination in Laboklin Germany. The result was sent by email on May 24, 2019 :
1: moderate to severe mixed cell colitis with
PAS-positive macrophages and ulceration
2: mild to moderate lymphoplasmocytic enteritis
The histological findings (PAS-positive macrophages) in context with the reported breed indicated a histiocytic and ulcerative colitis(HUC).This form of colitis develops especially in
boxer dogs and french bulldogs. Single cases are described forother breeds.A HUC is associated with an infection of certain strains of Escherichia coli. Clinical signs are weight loss, anorexia andpoor condition.A colitis with epithelial lesions and PAS-positive macrophages are typically found in histology.“
On the same day we started methilprednisolon 2 mg/kg/12h/i.v, ampicillin/sulbactam 15 mg/kg/8h/i.v, ceftriaxone 35 mg/kg/12h/i.v in addition to all other therapy.
On April 25, 2019 we only took complete blood count, which established increase of leukocytes and neutrophils, as well as deepening anemia. Clinically, the dog continued to have severe and watery diarrhea with tenesmus, most of which were mixed with blood. Robin began to lose weight progressively and refused to eat at his own will. He was fed by force, following a hypoallergenic diet of “Hill’s z/d cans” and “Royal Canin Hypoallergenic cans”. After a few days Robin felt better and started to eat dry hypoallergenic food.
On April 30, 2019 we took blood for a full blood count where the levels of leukocytes and neutrophils had dropped, but the levels of red blood cells were still low, so an ultrasound examination of the colon was carried out – the wall had begun to decrease in size
Robin’s condition was beginning to improve, the stools were getting better. After a few days, the patient was given home therapy (amoxicillin/clavulanic acid for 5 weeks, marbofloxacin for 6 weeks, prednisolone by scheme with start dose 3 mg/kg/12h/p.o for 7 weeks, b-complex liquit, legaphyton 200 tabl).
On May 09 2019 we took blood for a full blood count – the leukocytosis were even fewer, but still out of norm; the hematocrit, the hemoglobin and the number of red blood cells were still low. We sent another blood sample to Laboklin Germany for TLI (Tripsin-like-immunoreactivity) + Vit B12 + Folic Acid.
“Trypsin-like-Immunoreactivity (TLi) – CLA
Result 36.8 µg/l > 5
TLI values < 2.5µg/l are indicative for exocrine pancreas
With values of > 5.0 µg/l a EPI is most unlikely. 2.5 to 5.0 µg/l
is considered to be a questionable; a control measurement should be considered after 2 3 months time according to the clinical sings.
Reasons for questionable values are:
– acute phase of chronic pancreatitis
– sampling time within 12 hours post feeding
TLI values > 35 µg/l are indicative for pancreatitis. Renal
insufficiency can result in retention of TLI and thus falsely
elevated TLI resp.
Vitamin B12 Concentration – CLA
Vitamin B12 748 pg/ml 300-800
Folic Acid Concentration – CLA
folic acid 5.73 ng/ml 3.0-10.0”
The ultrasound study showed high-grade meteorism and reactive patch plaques. No increased mesenteric lymph nodes were detected. Clinically, diarrhea was accompanied by tenesmus and fresh blood.
Based on TLI levels, we included metronidazole 7,5 mg/kg/12h/p.o for 5 weeks.
On May 23, 2019 We took blood for a full blood count – the leukocytes and neutrophils were at baseline according to the reference values. However, the hematocrit, the hemoglobin and the red blood cells levels were still low. The condition of the patient had worsen after eating food from the rubbish bin. The ultrasound study showed high-grade meteorism and reactive patch plaques; the wall of the colon had begun to decrease in size; corrugation of the colon appeared. We placed an intravenous catheter and included fluid therapy NaCl 55 ml/h, antiemetics (famotidine and pantoprazole), vitamins (vit C, B- complex, arginine ,ornithine, citrulline), antioxidants (duphalyte, amynoplasmal), probiotics (Fortiflora and Pro-kolin paste), haemostatic drugs (Vit K1 and etamsylate), metronidazole, amoxicillin/clavulanic acid, enrofloxacin 5%. We chose to stop the prednisolone and try budesonide sachet in dose 2 mg/kg/24h/p.o. The dog continued to weaken progressively.
On May 30, 2019 we took blood for a biochemical profile, which showed the following results – elevated bilirubin, elevated ALT, AST, ALP, low creatinine. On the same day, we reduced the prednisolone (1 mg/kg/12h) to include ciclosporin. Clinically the dog continued to weaken and lose muscle mass progressive. The owners started adding veterinary ciclosporin liquit in dose 5 mg/kg/24h/p.o. Three hours after the intake of cyclosporine the dog’s condition deteriorated dramatically, began to vomit and defecate only fresh blood. Unfortunately, we hospitalized the dog again.
The condition of the colon was getting worse.
We started intravenous methylprednisolone again in combination with the rest of the therapy to stabilize the patient. He didn’t want to eat alone again.
On June 04 we took blood for a biochemical profile, which showed the following results – improvement in liver enzymes as well as in pancreatic lipase levels and normal creatinine. Two days later, Robin stopped vomiting and received the rest of the therapy. We fed him three times a day with hypoallergenic food (Royal Canin Hypoallegenic cans).
On June 08 the dog felt better; body temperature was in norm; Robin started to eat with appetite again. Diarrhea continued to be abundant and watery, accompanied by blood and tenesmus. We started budesonide, and stopped methylprednisolone.
Despite the applied complex therapy, diarrhea was unaffected. Defecation continued to be extremely frequent with blood and tenesmus. The patient continued to lose weight and muscle mass progressively. On 11 June Robin was discharged from the clinic with home therapy of budesonide and cyclosporine only. The owners had been offered euthanasia.
The wall of the column progressively hyperplasia.
Dr Svetoslav Penchev
United Veterinary Clinic
Stroke or cerebrovascular accident (CVA) is the most common clinical manifestation of cerebrovascular disease, and can be broadly divided into ischemic stroke and hemorrhagic stroke. CVA are characterized clinically by a per acute or acute onset of focal, asymmetrical and non-progressive brain dysfunction. Next cases show the both type of CVA in dogs.
1st case is about 9 years old female boxer. The dog was referring to the clinic with acute onset of seizures. The results of CBC and Biochemistry were normal and MRI was performed.
MRI findings: Intra-axial right piriform lobe and hippocampus lesion with impression of moderate swelling of these portions is present. The cerebral falx is only mildly displaced to the left. There is corresponding low T1 signal intensity in these sections of the brain suggesting edema. There is no enhancement of the lesion after contrast administration. The findings suggest that there is a non-hemorrhagic cerebrovascular accident in right forebrain of the dog.
The 2nd case is about a 8 years old male Cane corso. The dog was present in the clinic with unilateral fore brain deficits and history of epileptic seizures. Biochemistry and CBC were normal and MRI was performed.
MRI findings : There is a well‐delineated T1 iso- to hypointense and T2 hypointense mass lesion with surrounding brain edema in right piriform lobe with a thin peripheral rim of contrast enhancement. There is a mass effect, displacement of the right lateral ventricle and midline shift to the left. This imaging feature is consistent with an acute to subacute intracranial hemorrhage.
MRI features of Hemorrhagic infarction in dogs may not be distinguishable from hematoma caused by vascular disruption. Imaging characteristics will vary depending on the size, location, and chronicity ofthe hematoma.
Hyperacute – 24 hours T1 isointense ; T2 hyperintense
Acute 1-3 days T1 iso- to hypointense ; T2 hyperintense
Early subacute >3 days T1 hyperintense ; T2 hypointense
Late subacute >7 days T1 hyperintense ; T2 hyperintense
Chronic > 14 days T1 hypointense ; T2 hypointense
Secondary features : mass effect, surrounding edema, midline shift , ventricular displacement and compression .
MRI features of Nonhemorrhagic Infarction in dogs include mildly T1 hypointense and T2 hyperintense lesion with minimal mass effect involving both gray and white matter on unenhanced MR images. These changes seen in ischemic parenchyma rely on an increase in tissue water content. Gradually, during the acute stage, the T2-weighted image becomes more hyperintense in the ischemic region, particularly over the first 24 hours. These signal changes seen in the first 24-hours are best appreciated in grey matter and are well visualized in deep grey matter structures such as the thalamus or basal ganglia, in addition to cortical grey matter. Gadolinium enhances infarcts because of vascular rupture but does not enhance ischemia or edema.
Dr Svetoslav Penchev
Unites Veterinary Clinic
3 years old male, not castrated British shorthair cat with history of tetraparesis was referred to the clinic for Computed Tomography. Mineral-attenuating endobronchial lesions were detected in Thorax as accidental finings in spinal CT. The finding is specific for broncholitiasis.
CT features: Multifocal mineral-attenuating endobronchial lesions in cranial and middle right and cranial left lung lobe are present. There is mild generalized thickening of the bronchial walls and consolidation of right middle lung lob with regional bronchiectasis
X-ray features: Multiple mineral opacity nodules with irregular margins are present within left and right cranial and right middle lung lobe. The largest of which lies within the right middle lung lobe and interstitial patter in this region is present.
Broncholithiasis is very rare condition in cats and is defined as the presence of calcified or ossified material within the bronchial lumen. Only four cases of broncholithiasis in cats have been reported in the veterinary literature. Normal this condition is associated with lower airway inflammation, but in this case the owner does not report for respiratory problems. Broncholithiasis is an uncommon condition, which should be considered as a differential diagnosis for cats with chronic respiratory disease. Affected cats may develop broncholithiasis secondary to a diffuse inflammatory lower airway disease with mineralisation of secretions in the airways.
DR SVETOSLAV PENCHEV
United Veterinary Clinic
CLINICAL CASE 1
Old Dogs with sudden onset of seizures
The 1st clinical case is about 13 years old, castrated Belgian shepherd with acute onset of cluster seizures. Before 5 years the dog was operated ( total mastectomy and ovariohysterectomy) , because of mammary gland tumor. Another vet made the blood analysis and there is no change in laboratory results. Contrast MRI study was performed.
There are two, oval shaped, T1 hypo- and T2 hyperintense, intraaxial mass lesion with cystic component. One is in right piriform lobe and another one is in the left olfactory bulb/ frontal lobe. The masses nonuniformly enhances following contrast administration, with more intense enhancement peripherally. Mass effect with mild brain edema surrounding the lesions is present.
Multifocal nodules with soft tissue opacity in lung parenchyma
The reason of seizures are metastatic brain tumors in the right piriform lobe and in the left olfactory bulb and there are multifocal metastatic nodules in the lungs. Although the dog was operated , the primary mammary gland tumor is the reason of this condition
There is no feedback with the owner about dog`s condition.
Next case is about a 9 years, female, not castrated Labrador retriever with acute onset of cluster seizures. The dog present proprioceptive deficit on the right fore and hind limb. There is no history of previous seizures. By abdominal palpation mammary gland mass was find.
There is no change in the blood analysis.
There is oval shaped T1, T2 mixed intensity mass in the parietal part of left cerebral hemisphere with surrounding brain edema. Mass margins are well defined on T2. Peripherally enhancing following contrast administration is present with mass effect and midline shift to the right
Thoracic x-ray show multiple oval shaped masses with soft tissue opacity
In this case we have the same condition. The metastatic lung and brain disease are due the primary mammary gland tumor.
The dog`s owner prefer to euthanized the dog, because the seizures getting longer and stronger.
CLINICAL CASE 3
The last case is about a 9 years, not castrated, female Jack Russell terrier with depressed mental status from a month and acute onset of seizures. The dog reacted with hypersensitivity in right cranial nerves, proprioceptive deficit in left fore and hind limb and proprioceptive ataxia. MRI contrast study was performed. MRI findings:
There is a one, irregularly shaped, T1 hypo and T2- mixed intensity intraaxial mass involving the right midbrain. The mass intensely, but nonuniformly, enhances following contrastadministration. There is a mass effect and surrounding brain edema.
In this case there is no history of neoplastic disease. This midbrain mass has a characteristic of primary tumor and It is the cause of the seizures. Every dog after 5 years of age, who presented with a new onset of seizures should be suspected for a brain tumor. The most common indication for brain tumor in dogs are seizures, especially seizures that began for the first time in a dog older than five years of age. Other signs suggestive for a brain tumor include abnormal behavior, vision problems, circling motions, uncoordinated movements and lethargy.
Dr Svetoslav Penchev
United Veterinary Clinic
Meningocele and meningoencephalocele of the skull are congenital deformities. These deformities, which are observed as cyst-like swellings in the median part of the skull cap, occur very rarely. The intracranial material protrudes through a spontaneous cavity, such as the anterior fontanelle , and they are classified as encephalocele, meningocele, or meningoencephalocele according to the cranial bifida.
History: presented for a large firm mass arising from the right side of the calvarium.
Findings: A dense, mineralized mass with a stippled appearance arising from the right side of the calvarium, with an approximate diameter of 6cm.
Because of the dense appearance of the mass, it’s hard to appreciate the degree of underlying osteolysis just with an Xray
Diagnostic: the radiological appearance it’s of MLTB (multilobular osteochondrosarcoma)
Discussion: MLTB is an uncommon tumour that arises almost exclusively on the flat bones of the skull, mainly on the calvarium, maxilla and mandible and tend to occur in older medium and large breed dogs, although they have been reported in younger and small breed dogs, and have also been reported in cats. It is slow-growing and locally invasive, often recurring after excision. Metastasis may occur
8months old, American bully, Female
History: pain, jaw swelling.
Findings: Periosteal new bone formation, palisading type, affecting the mandible bilateral.
The tympanic bullae and temporomandibular joints are not affected.
Diagnostic: Craniomandibular osteopathy.
Discussion: Craniomandibular osteopathy is a non-neoplastic, proliferative bone disease that affects primarily the mandible, tympanic bullae, frontal bone and occasionally long bones in dogs of about three to eight months.
The proliferation of new bone of the head and jaws decreases as the endochondral ossification of the long bones slows after 7 to 8 months of age.
What is a nasopharyngeal polyp?
Inflammatory polyps that develop at the level of the nasopharynx and the middle ear are non-neoplastic masses which are thought to originate in the epithelial layer of the timpanic bulla or the Eustachian tube. Polyps can also emerge from the epithelium lining the external ear canal in association with otitis.
The etiology of nasopharyngeal polyps is not very clear and congenital pathologies as well as underlining inflammatory diseaseses such as bacterial or viral infections and cronical inflammations are discussed.
Most affected are the cats younger than 3 years of age, but some studies found the average age of the patients to be arround 6-7 years and up to 17,5 years in some cases. The studies citing such advnaced ages implied that polyps developed at a younger age, but remained undiagnosed for a long period.
How to diagnose a nasopharyngeal polyp?
The diagnosis is made based on patient history and clinical examination and confirmed through diagnostic imaging, endoscopy and histopathology.
The clasical clinical signs associated with nasopharyngeal polyps include sneezing andheavy breathing. When a nasopharyngeal polyp reaches a large size (and is located in the nasopharynx) or there are bilateral polyps (extending into the nasal cavities) they cause reduction of the upper airways and are associated with loud breathing noises, nasal discharge, snorring and even vestibular disorders (head tilt, balance disorders). Sometimes nasopharyngeal polyps can be associated with Horner syndrome. Large polyps can lead to difficulties in the act of swallowing and anorexia. Direct or indirect examination (endoscopy and sample retrieval) can be of great help to the clinician in diagnosing this type of pathology (depending on the size and localisation of the polyp). Radiograps (RX), Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) are very good diagnostic tools , providing information about the localisation and size of the polyp and have also a high specificity. Diagnostic imaging can also help differentiate between nasopharyngeal polyps and other pathologies that sometimes similar clinical appearance, such as obstructed or stenotic airways, foreign bodies, neoplasia, thickening or osteolysis of the bullae due to infection. Another advantage when using diagnostic imaging is the ability to assess the regional lymphnodes in order to give a more precise prognosis.
9 years old mix breed dog, F
History: not urinating for 24hours, apathy, lethargy
Findings: Loss of serosal detail especially in the ventral abdomen.
There are multiple radiopaque mineral foreign bodies of varying sizes in the ventral abdomen not included in the digestive tract.
Conclusion: ruptured urinary bladder with radiopaque calculi free in the peritoneal cavity.