Transient Postural Vestibulo-Cerebellar Syndrome Case report

Dr Svetoslvav Penchev

United Veterinary Clinic

Varna, Bulgaria

 

 

Transient Postural Vestibulo-Cerebellar Syndrome is a condition that present as pronounced vestibulo-cerebellar signs. In this  syndrome transient postural symptoms present as  vestibulo-cerebellar signs after altering the position of the head.Vestibular deficits related to head posture have been described, introducing the relationship of nodulus and uvula pathology to various vestibular signs elicited by the postural changes of the head.

 

 

Case report:

 

Signalment: Adopted from a shelter mix breed female dog without previous history.The age of the dog was estimated to be 7-8 months based on general appearance and teeth condition.

 

 

Case presenting sings: Vestibular episodes during sniffing and eating or head position changing(Transient vestibular signs as vertigo and nystagmus  caused by changing the posture of the head). Symptoms are not progressive.

 

Clinical examination: Good overall condition ; Internal body temperature- 38,9; Normal respiratory and heart rate; Color of mucous membranes – pink; CRT – 1,5 sec.

 

Neurological examination:

 

Mentation: Normal

Behavior: Normal

Gait: Normal( no signs of cerebellar ataxia when the dog plays or runs)

Cranial nerves: normal

There was no change in conscious proprioception and bladder function was normal.

Spinal reflexes were normal.

 

Neuroanatomic localisation: Vestibulocerebellum

 

Differential diagnosis: Idiopatic/Anomaly/Metabolic/Degenerative/Neoplastic/Trauma/Vascular

 

Case work-up:

 

CBC and Biochemistry- without any changes

CRP – 8,7 my/L

 

Magnetic resonance of the head was performed with GE MRI 1.5 Tesla.

 

MRI findings:

The T1W and T2W sagittal  and transversal images showed reduced size of the nodulus and uvula of the caudal cerebellum  with CSF filling the space normally occupied by cerebellar parenchyma.This is particularly visible on T2W images due to the hyperintensity of the surrounding CSF.These imaging findings were considered most likely to represent congenital caudal cerebellar hypoplasia.

 

There is no histopathological examination providing a definitive diagnosis, but the most likely diagnosis is Congenital Caudal Cerebellar Hypoplasia.

 

No treatment was recommended. There is no progression of the clinical sings 4 months after the examination.

 

 

 

 

normal dog’s anatomy images-  “vet-Anatomy”

 

 

 

 

 

 

 

 

 

 

Portosystemic shunt

 

Dr Svetoslav Penchev

United Veterinary Clinic

Varna, Bulgaria

 

Portosystemic shunts are anomalies that allow blood returning from the gastrointestinal systems to bypass the liver and pass directly into the systemic circulation. When this occurs, toxins from gastrointestinal tract that are normally cleared by the liver are shunted directly into the systemic circulation. This build-up of these toxins in the bloodstream leads to the clinical signs commonly seen in animals with these shunts. Three categories of clinical signs commonly are associated with the presence of these shunts: neurological, gastrointestinal and urinary. Neurological signs include seizures, head pressing, circling, lethargy and blindness among others- hepatic encephalopathy. Gastrointestinal signs include vomiting, anorexia, weight loss and a reduced rate of growth. Urinary tract signs, including stranguria, pollakiuria and hematuria are generally related to the development of urate cystoliths secondary to the presence of ammonium biurate crystals in the urine.

Case report:

Signalment: Dog, male, 4 months old, Yorkshire terrier

History: The owner noticed hypersalivation and abnormal behaviour of the dog.

Case presenting signs: Seizures, pacing, blindness, depressed mental state, hypersalivation

Clinical examination: Internal body temperature- 37.8; Normal respiratory and heart rate; Color of mucous membranes – pink; CRT – 1,5 sec.

Neurological examination:

Mentation- depressed Behaviour- abnormal Gait- compulsive walking

Cranial nerves – normal

There was no change in conscious proprioception and bladder function was normal. Spinal reflexes were normal.

Neuroanatomic localisation: Forebrain

Differential diagnosis: Idiopatic/Inflammatory/Trauma/ Metabolic/Neoplastic/Anomaly

 

Case work-up:

CBC:

 

 

Biochemistry:

 

 

 

Elevation of liver enzymes

 

 

Elevation of bile acids

 

 

 

 

 

 

 

 

 Abdominal ultrasound:

 

 

 

 

 

 

 

 

Contrast CT study with 64 slice scanner was performed with i.v administration of iopamidol solution 370g/ml (contrast agent) in dosage 1ml/kg.

 

 

 

 

 

 

 

 

 

 

 

 

 

CT findings: There is a abnormal communication between the portal vein and the caudal vena cava using the splenic vein. The portal vein decreases in diameter cranial to the shunt exit and splienic vein is enlarged. The both kidneys are too big and liver is too small.

Diagnosis:

Congenital extrahepatic splienocaval-caval shunt

The treatment consisted of medical and surgical approach. Ten days before the surgery the condition was managed with amoxicillin 12,5 mg/kg p.o q12h for 15, Lactose oral solution 67g/ 100ml in dosage 1ml/kg p.o q12h and hydrolyzed protein food.

The surgery was planned in great teamwork with d-r Kaloyan Voichev in Multidisciplinary Veterinary Clinic Bulgaria. The operation was performed with the kind assistance of the whole team. The operational approach consisted of midline celiotomy and isolation of the shunt from surrounding structures and placement of thin cellophane band surround the vessel.

 

 

 

 

 

 

 

 

Max recovered well from the anesthesia and was discharged after 48 hours with amoxicillin 12,5 mg/kg p.o q12h for 10days, Lactose oral solution 67g/100ml in dosage 1ml/kg p.o q12h for 15 days and hydrolyzed protein food. In postoperative period Max was vomiting sporadic within one week, but with good appetite. The vomiting was stopped with maropitant 1mg/kg s.c q 24h for 3 days.

One month after the surgery Max doesn’t show any clinical signs.

Trigeminal nerve sheath tumor

Dr Svetoslav Penchev

United  Veterinary Clinic

Varna, Bulgaria

 

 

The nerve sheath is a layer of myelin and connective tissue that surrounds and insulates fibers in the peripheral nerves. A nerve sheath tumor is an abnormal growth within the cells of this covering. Nerve sheath tumors include schwannomas, neurilemmomas, and neurofibromas. The trigeminal nerve is the most frequently affected cranial nerve. This results in unilateral atrophy of the temporalis and masseter muscles and facial dysesthesia or anesthesia. Eventually, brain-stem compression can develop.

 

 

Signalmen: 12 years old, female, castrated Labrador retriever

 

History:  The owner noticed that dog`s head has not normal shape.

 

 

Case presenting signs:  Chronic right trigeminal nerve deficit with atrophy of the temporalis and masseter muscles. Reduced facial sensation, absent palpebral reflex with normal menace response reaction and reduced right corneal sensation and enophtalmus.

 

Clinical examination: The overall condition of the dog was normal with normal appetite, good muscle and body condition except the right temporalis and masseter muscles.  Internal body temperature 38,8 ; Normal respiratory and heart rate; Color of mucous membranes – pink; CRT – 1,5 sec.

 

Neurological examination:

Mentation and behavior- Normal

Posture- Normal

Gait – Normal

Cranial nerves – right trigeminal nerve deficit

There was no change in conscious proprioception and bladder function was normal.

Spinal reflexes were normal.

 

Neuroanatomic localization: R Trigeminal nerve

 

Differential diagnosis:

Idiopatic/Inflammatory/Trauma/Metabolic/Neoplastic

 

Case work-up:  CBC – without changes; Biochemistry – Elevation of Liver enzymes (ASAT 69 IU/L; ALAT 90 IU/L)

Contrast MRI study of the head was performed with GE MRI 1.5 Tesla.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

MRI     findings:

There is a large extra-axial T1 hypointense, T2 hyperintense tubular mass that arises at the origin of the right trigeminal nerve and extends rostrally through the trigeminal canal of the temporal bone. The right oval foramen is enlarged because of involving the mandibular branch. Atrophy and denervation of the masticatory muscles (temporalis, masseter and pterygoid muscles) is present with T1-, T2-hyperintesity, reduction of the muscle mass and replacement by fatty tissue. Post contrast images shows marked contrast enhancement of the right trigeminal nerve compared with the left (mild enhancement of the left trigeminal nerve is physiologic).

 

Diagnosis:

Right Trigeminal nerve sheath tumor

 

Intracranial peripheral nerve sheath tumors are relatively uncommon tumors in dogs. Clinically, dogs with intracranial PNST have one or more of the following clinical signs: ipsilateral masticatory muscle atrophy, loss of facial sensation, and Horner’s syndrome. Signs from intracranial brainstem compression can also occur. Radiation therapy is a commonly used modality in the treatment of intracranial PNST. Stereotactic radiation therapy (SRT) is one method used to deliver a curative dose of external beam radiation therapy. This precise and conformal treatment directly targets the radiation at the tumor with rapid dose drop-off, which allows for very high doses of radiation to be administered without increasing toxicity to adjacent normal tissues.

Paradoxical Vestibular Syndrome

Dr Svetoslav Penchev

United Veterinary Clinic

Varna, Bulgaria

 

 

 

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.

Neurological examination:
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

Differential diagnosis:

Neoplastic/Degenerative

Case work-up:
CBC and Biochemistry were normal. Magnetic resonance of the head was performed with GE MRI 1.5 Tesla.

MRI images : Image 1
Image 2
Image 3 –
Image 4-
Image 5

 

 

 

 

 

 

 

 

 

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
Treatment:
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.

Histiocytic Ulcerative Colitis in French Bulldog

Dr Mila Kisyova,

veterinary clinics “Dobro hrumvane!”- Sofia, Bulgaria

1. Introduction

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).

1. 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 :

” Diagnosis:
1: moderate to severe mixed cell colitis with

PAS-positive macrophages and ulceration
2: mild to moderate lymphoplasmocytic enteritis
Critical report:
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
TLI:

Result                  36.8  µg/l             > 5

Inretation:
TLI values < 2.5µg/l are indicative for exocrine pancreas
insufficiency (EPI).
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.

I apply some photos of the dog on the day of euthanasia:

Cerebrovascular accidents in dog

 

Dr Svetoslav Penchev

United Veterinary Clinic

Varna,Bulgaria

 

 

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.

1^st 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.

Image 1

 

 

 

 

 

 

 

 

Image 2

 

 

 

 

Image 3

 

 

 

 

Image 4

 

 

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 2^nd 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.

 

Image 5

 

 

 

 

Image 6

 

 

 

 

Image 7

 

 

 

 

 

 

 

Image 8

 

 

 

 

Image 9

 

 

 

 

 

 

 

Image 10

 

 

 

 

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.

 

Conclusion:

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.

 

Broncholithiasis in cats

Dr Svetoslav Penchev

Unites Veterinary Clinic

Varna, Bulgaria

 

 

 

 

 

 

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  :

 

 

 

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-rays

 

 

 

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.

 

 

 

 

 

 

BRAIN TUMORS- 3 CLINICAL REPORTS

DR SVETOSLAV PENCHEV

United Veterinary Clinic

Varna, Bulgaria

CLINICAL CASE 1

Old Dogs with sudden onset of seizures

 

The 1^st 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.

MRI findings:

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.

 

Thoracic x-ray show :

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.

 

CLINICAL CASE 2

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.

 

 

 

 

 

 

 

 

MRI findings:

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.

 

Meningocele and meningoencephalocele in a dog

Dr Svetoslav Penchev

United Veterinary Clinic

Varna, Bulgaria

 

8 mounts ,female dog with congenital meningocele and hydrocephalus . The dog is with normal behavior and without neurological deficits.

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.

Multilobular Osteochondrosarcoma

12 years mix breed dog, F

 

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

A CT scan was recommended to evaluate local  invasion.

 

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