hydrocephalus in female french bulldog


hydrocephalus in female french bulldog

Hydrocephalus is an active distension of the ventricular san system of the brain resulting from
CSF cannot pass enough production within the ventricles to its point of absorption in the systemic circulation. Loss of brain parenchyma may result in a secondary increase in ventricle size, which has been termed as compensatory hydrocephalus or
hydrocephalus exvacuo.

a congenital predisposition exists in many miniature breed dogs, bulldogs and boston terriers. the condition may be congenital due to obstruction of ventricular drainage (often at the level of the mesencephalic aqueduct) or decreased absorption of CSF due to dysfunction of the arachnoid villi, or it may be the result of secondary obstruction due to acquired disease (e.g. neoplasia, infection or inflammation).

Hydrocephalus may be secondary to CSF overproduction (e.g. choroid plexus tumor [rarely]) or increased viscosity of CSF due to elevated CSF protein content is seen with some tumors and the ‘dry-form’ of FIP in cats.

Hydrocephalus is described here because it involves the accumulation of excessive amounts of CSF in the brain or cranial cavity.

In fact, the correct definition of hydrocephalus is any in the case in the volume of CSF, which means that it is not always related to the cause of any neurologic signs.

A number of expressions or vocabulary have been used on years in reference to hydrocephalus, with varying usefulness (Platt and Garosi, 2012):

- internal hydrocephalus is a ventricular distention with CSF accumulation.
- external hydrocephalus is subarachnoid
space distension with CSF accumulation.
This is also referred to as hydrocephalus ex vacuo.

- non-communicating hydrocephalus is a ventricular dilation due to an intraventricular obstruction of CSF flow preventing the communication between the ventricular system and the subarachnoid space.

- communicating hydrocephalus is a ventricular dilation secondary to an extraventricular obstruction of CSF flow.
- normotensive hydrocephalus is associated with an increase in CSF pressure.
- hypertensive hydrocephalus is associated with an increase in CSF pressure.
- the two major categories of hydrocephalus are compensatory and obstructive.

Hydrocephalus results in diffuse cerebral and/or brainstem signs due to cortical compression and elevated ICP. most commonly, animals have altered mentation, inappropriate behavior, cortical blindness, and seizures.

ventrolateral strabismus is common. Hydrocephalus may be asymptomatic in milder cases.

Congenitally affected animals often have a skull deformity (dome-shaped) and persistent fontanelles (Platt and Garosi, 2012).
Although developmental obstructive hydrocephalus occurs sporadically in all breeds of dogs and there are much higher proportions in toy and brachycephalic breeds, especially in the Chihuahua, Pekingese, Pug, Boston terrier,
Yorkshire terrier, Pomeranian, and English or French Bulldog.

This disorder is uncommon in cats. Despite the presumed fetal genesis of the obstruction, clinical signs may not be evident at birth. It is observed before 3 months of age, some between 3 and 12 months, and rarely beyond 12 months. Some dogs exhibit no clinical signs despite markedly enlarged lateral ventricles with significant cerebral atrophy.

This suggests that the clinical signs may be which are related to CSF compression level, so that be quite variable in these dogs (Lahunta and Glass, 2009).

The most common clinical signs observed are prosencephalic in origin because of the severe expansion of the lateral ventricles, with the compromise of the cerebral tissue and compression of the diencephalon.

materials and methods:

The patient was presented to the doctor at the Veterinary Faculty on April 5th, 2015. The following investigations were performed:
- anamnesis (history);
- clinical and neurological examination;
- cardiologic exam;
- ophthalmological examination;
- biochemical examination;
- NH3 and bile acids;
- hematological examination;
- abdominal ultrasound;
- 4DX Test;
- performed an X-ray on the spinal column T3-L3
- toxoplasmosis test – IgG and IgM
- cerebral MRI.

heavy breathing. the crises were started throughout the day but at night intensified. the crisis worsened and in early September they were continuous. if at first, a crisis was between 5 and 15 minutes, at the beginning of September they sometimes lasted all night. The only days in which the Bulldog did not have any crisis were those in which she had been subjected to anesthesia for MRI and after she began treatment with prednisone and furosemide after seizures came back again with intensity increasingly higher. and it noted that there is almost the same hour when crises occur are 19-20 pm, 2-3 am, 6-7 am. If she is kept the arbitrator in a room one day has no seizures and that if we found in our presence the ”crisis” is stronger.

Method to respond, combine:
shaken powerful head lets her head down on The floor, its neck up sideways, it has uncontrolled movements as if she catches a fly, and especially very violent ”crisis”.

It is clear that they have no reaction to treatment as the crises are continuing in the same characteristics.” when this patient was examined, the result of the neurological exam was:
- moments of nervousness;
- looking in an exact spot (fixed locations);
- catching “flies”;
- Feeling "pinching" and jumping off spot even when calm.
Focal epileptiform crises were suspected. These had taken place only inside the house, outside having normal behavior. It was
established treatment with Gabapentin 10 mg/kg 2 times/day.
During the check-up from August 2016, the owner informed us that for the previous signs, she was supporting herself with her muzzle on the ground.

She continued the treatment with Gabapentin and performed a cerebral MRI in September 2016.
The results were:
- bilateral ventriculomegaly.
- suspicion of a slight enlargement of the mesencephalic aqueduct. No loading with contrast.


hydrocephalus, most probably congenital. Bilateral ventriculomegaly hydrocephalus
The established treatment:
- Furosemide 40 mg 1 mg/kg /day;
- Prednisone 1 mg/kg/day;
- Omeprazole 10 mg/day (1mg/kg/day);
- Aspacardin ¼ CPR/day;
- Diazepam rectally when needed;
- Acetazolamide 10 mg/kg x 2 times/day.
Two weeks later I went back to check.
Administering acetazolamide was stopped because the owner told that Kim was becoming very violent (according to the prospectus) after this medicine. Because the ”crises” had become very frequent and lengthy (approximately 30 minutes) at 10 mg/kg/ 12 h, orally, was added to the treatment.

There have been added to the treatment:
- Phospholipids and ornytine;
- Omega-3 500 mg / day.
The ”crises” have lost in intensity over time,
but in December she was having ”crises”
between 6 and 9 pm, especially before having administered Diazepam rectally.
If Diazepam was not administered rectally, the crises would become more frequent and strong, therefore Diazepam was administered rectally 1-2 mg/day in the afternoon.

Phenobarbital was supplied at 4 mg /kg/day order to remove Diazepam from the treatment. Ever since the outside temperature was low, Kim has felled much better. She still had crises but were light and weak in intensity. She Possible to hit 4 crises a day but it was joyful, present and not aggressive.

For the neurologic examination from January 2017, changes were only noticed on the cranial level: delayed reaction “of attention” (menace) at both eyes, eyelid reflex incomplete in both eyes.

The medical history is very important and the data taken from the owner helped to establish a correct diagnosis.

The neurological examination was performed for each condition separately and was resumed on every control. In the neurological observation, the sheet has noted the results of every done examination.

In this case, Kim had two different neurological diseases: one located in the brain (cerebral hemispheres) and another in the spine. For the differential diagnosis, the acronym "VITAMIN" was used and thus the anomaly as a casual sign of neural signs in this the case was chosen.

To obtain a correct diagnosis, an MRI was performed, which confirmed the presence of hydrocephalus. The treatment for hydrocephalus was established according to the literature, but due to a reaction of the particular patient when taking acetazolamide, the treatment was adopted.

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