- Degenerative diseases
- Anomalous diseases
- Neoplastic diseases
- Nutritional diseases
- Inflammatory diseases
- Bacterial encephalitis
- Canine distemper virus infection
- Feline infectious peritonitis
- Toxoplasmosis and neosporosis
- Granulomatous meningoencephalomyelitis
- Necrotizing meningoencephalomyelitis
- Idiopathic diseases
- Toxic diseases
- Traumatic diseases
- Vascular diseases
- 1 Degenerative diseases
- 2 Anomalous diseases
- 3 Neoplastic diseases
- 4 Nutritional diseases
- 5 Inflammatory diseases
- 6 Idiopathic diseases
- 7 Toxic diseases
- 8 Traumatic diseases
- 9 Vascular diseases
- 10 Related Posts:
Lysosomal storage disorders and neurodegenerative diseases
Lysosomal storage disorders are inborn errors of metabolism in vhich specific deficiencies of degradative enzymes cause substrate accumulation and result in cellular and clinical dysfunction.
Neurodegenerative disorders are diseases associated with an abnormality in the metabolic pathway that leads to early death of the neuron. Several of these conditions can present with ataxia and incoordination suggestive of vestibular disease. ()
Chiari-like malformations are congenital defects characterized by caudal displacement of part of the cerebellum through the foramen magnum. This occurs as a result of occipital bone dysplasia causing the caudal fossa to become abnormal in size or shape. This malformation can cause compression of the brainstem and cerebellum, and result in signs of central vestibular disease.
Of the primary brain tumours seen in dogs, meningiomas and choroid plexus papillomas have a site predilection for the caudal lossa. As such, vestibular signs are commonly encountered in affected animals.
Dermoid and epidermoid cysts are occasionally classified as neoplastic abnormalities. Many of the canine epidermoid cysts reported have been located in the cerebello-pontine angle and can extend into the fourth ventricle (). Although these cysts can be incidental findings on post-mortem examination, dogs with clinical signs consistently have vestibular dysfunction. The cysts have a stratified squamous epithelium lining and expand by progressive exfoliation into the lumen. Definitive treatment is achieved by total surgical removal of the cyst; however, success of surgical resection depends on the location of the lesion.
Intracranial dermoid cysts are rarer than epidermoid cysts in dogs. Dermoid cysts are neoplastic lesions with a complex cyst wall, containing both epidermoid tissue and adnexa. Due to the caudal fossa location of these lesions, they can be associated with vestibulo-cerebellar signs and obstructive hydrocephalus. Both types of cyst have characteristic MRI signs ().
Although now not commonly encountered, a deficiency of thiamine (Vitamin B1) can cause a progressive encephalopathy in both dogs and cats.
Clinical signs. Initial clinical signs include anorexia and lethargy. Neurological deficits develop a few days later, and commonly manifest as vestibular signs, along with pupillary dilation and seizures. As this is a bilaterally symmetrical disease, the vestibular signs often present as wide excursions of the head and neck with poor to absent physiological nystagmus.
Cats can develop marked ventroflexion of the head and neck and will curl up in a tight semicircular posture. Paraparesis can also be seen in dogs.
Pathogenesis. Thiamine plays an essential role as a coenzyme in the metabolism of carbohydrates. Inhibition of carbohydrate metabolism in a thiaminedeficient state leads to energy depletion and results in neuronal necrosis.
Thiamine deficiency in cats most frequently results from feeding a raw fish diet that is rich in thiaminase. Excessive amounts of cereal in the diet has also been shown to predispose cats to thiamine deficiency. Thiamine deficiency can be caused in dogs by feeding them cooked meat or canned food heated to excessive temperatures (>100⁰C). In addition, the use of sulphur dioxide as a preservative can destroy thiamine in food and cause signs of deficiency in both dogs and cats.
Diagnosis. Diagnosis is based on historical findings suggesting a thiamine-deficient diet (although this may not always be evident), along with compatible examination findings and exclusion of other causes. MRI may demonstrate the presence of bilaterally symmetrical areas of haemorrhage and malacia within susceptible nuclei of the brain ().
Gross pathological findings include bilaterally symmetrical petechial haemorrhages in brainstem nuclei, with the caudal colliculi most frequently affected. Microscopic lesions are confined to the grey matter and are characterized byfocal, symmetrical areas of oedema and neuronal necrosis.
Treatment and prognosis. The disease is rapidly progressive and typically fatal if left untreated. However, treatment with thiamine (12.5—50 mg/dog or 12.5—25 mg/cat i.in or s.c q24h until oral supplementation is possible) in the early stages of disease can lead to rapid reversal of clinical signs, although some signs, such as blindness and wide excursions of the head and neck, may be residual.
Meningoencephalitis refers to inflammation of the brain and surrounding meninges.
Clinical signs. As a general rule, inflammatory diseases tend to be acute at onset and progressive, with a multifocal or diffuse, often asymmetrical, distribution within the central nervous system (CNS). Neurological manifestations are quite variable and reflect the location of the inflammatory foci within the nervous system.
Central vestibular signs are commonly encountered, and may be seen alone or combined with other neurological signs. Neck pain may also be present as a manifestation of meningeal inflammation. Animals with CNS infections frequently do not have evidence of systemic involvement. Therefore, the absence of fever, anorexia and depression, and the presence of a normal blood count cannot be used to exclude the possibility of an infectious aetiology in an animal with neurological signs.
Pathogenesis. Infectious causes of CNS inflammation in small animals include viral, protozoal, fungal, parasitic and bacterial organisms. The most commonly recognized CNS infections in dogs include:
• Canine distemper virus
• Rickettsial disease (e.g. ehrlichiosis and Rocky Mountain spotted fever)
• Protozoal infections (e.g. toxoplasmosis and neosporosis)
• Fungal diseases (e.g. cryptococcosis).
Inflammatory, non-infectious causes of CNS dysfunction in dogs include such diseases as granulomatous meningoencephalomyelitis (GME) and necrotizing encephalitis.
CNS infections in cats most commonly involve feline infectious peritonitis (FIP), toxoplasmosis and cryptococcosis.
A detailed list of infectious causes of meningoencephalitis is given in Table:
- Canine distemper
- Canine herpesvirus
- Cahine parainfluenza
- Canine parvovirus
- Infectious canine hepatitis
- Central European tick-borne encephalitis
- Borna disease virus
- Feline infectious peritonitis
- Feline immunodeficiency virus
- Feline leukaemia virus
- Sarcocystis-like organism
- Rocky Mountain spotted fever
- Salmon poisoning disease
- Dirofilaria immitis
- Toxocara canis
- Ancyclostoma caninum
- Angiostrongylus cantonensis
- Granulomatous meningoencephalomyelitis
- Necrotizing meningoencephalomyelitis
- Pyogranulomatous meningoencephalomyelitis
- Eosinophilic meningoencephalitis
- Periventricular encephalitis
Diagnosis. A thorough ophthalmological examination should be performed in every neurological case to look for evidence of fundic changes or uveitis compatible with inflammatory disease. Definitive diagnosis of CNS inflammatory disease is typically based on finding an increase in white blood cell (WBC) numbers or an abnormal cell type distribution, with a concomitant increase in protein concentrations, on CSF analysis (see Chapter 3). In rare instances, normal CSF can be obtained from an animal with confirmed CNS inflammatory disease. This can occur if the inflammation does not involve the meninges or the ependymal lining of the ventricular system or if the animal has been treated with corticosteroids prior to CSF collection. Elevations in protein concentration can result from breakdown of the blood—brain barrier or intrathecal antibody production. It is likely that both of these mechanisms contribute to the elevated protein levels recognized with most”CNS inflammatory disease.
Cytological evaluation of the fluid provides additional information as to possible causes:
• Viral diseases typically result in mild lymphocytic inflammation, an exception to this is FIP, which can cause a neutrophilic pleocytosis
• Bacterial infections usually cause a marked increase in neutrophils in the CSF, with cell counts often >500 cells/II. There is also evidence of toxic changes in cell morphology. However, mixed neutrophilic and mononuclear inflammation may be observed in animals with bacterial diseases that have been previously treated with antibiotics
• Rickettsial infections frequently cause mild mononuclear inflammation, although neutrophilic inflammation can be seen with Rocky Mountain spotted fever, secondary to an associated vasculitis
• Protozoal diseases most often result in mild to moderate inflammation, with a mixed population of neutrophils and mononuclear cells, with occasional eosinophils
• Fungal infections usually cause a mixed or primary neutrophilic inflammation. Eosinophils may also be seen, especially with cryptococcosis.
Additional testing, based on the cytological evaluation, is performed in an attempt to identify an infectious cause for the inflammation. These tests can include: culturing the CSF for bacterial or fungal organisms; measuring serum and CSF antibody or antigen titres; and CSF polymerase chain reaction (PCR) analysis if available. However, despite extensive testing, an underlying cause for the inflammation is not discovered in most cases.
Treatment and prognosis. Treatment is aimed at the primary disease process. Treatment with clindamycin (10 mg/kg orally q12h) and/or trimethoprim/suIphonamide (15 mg/kg orally q12h) for potential protozoal infections may be initiated once a diagnosis of encephalomyelitis has been made based on CSF results, while additional test results are pending. If no infectious cause is discovered upon additional testing, or the animal does not respond to initial antibiotic therapy, treatment with corticosteroids is initiated. Anti-inflammatory doses are often effective in alleviating clinical signs but higher, immunosuppressive doses may be required in some instances to appropriately manage immune-mediated disease.
Prognosis is variable and dependent on both the cause of the inflammation and the extent and severity of associated neurological deficits. Some infections, especially those caused by protozoal and fungal agents, are difficult to eradicate and relapses are common. In addition, residual neurological deficits may persist despite successful treatment of an infection due to irreversible damage caused by the inciting agent.
Bacterial infection is a relatively rare cause of encephalitis in dogs and cats when compared with other species.
Clinical signs. Animals can exhibit a variety of signs of intracranial disease including: vestibular dysfunction; seizures; cerebellar signs; paresis; cervical hyperaesthesia and coma (). Fever is present in approximately 50% of cases at presentation. The signs are usually rapidly progressive and frequently fatal.
Pathogenesis. Bacterial infection of the brain is usually a consequence of direct extension of infection from the middle ear or sinuses () or a penetrating injury to the skull (surgical or traumatic). Haematogenous spread can occur less commonly. Both aerobic and anaerobic infections have been reported. It is possible for the infection to be limited to the extradural or subarachnoid space, especially following bite wounds, in which case the infection may remain localized (intracranial empyema or abscess) and signs may not be so rapidly progressive. Clinical signs are largely the result of the inflammatory reaction that bacteria incite.
Diagnosis. Routine blood work will usually reflect an inflammatory process, but can be normal. A urine sample should be cultured if bacterial encephalitis is suspected, and blood cultures may be indicated in animals in which there is no obvious source of infection. Imaging of the brain (CT or MRI) is helpful to identify defects in the skull and OM/OI and may be suggestive of an inflammatory process. CSF analysis is the most useful test. Typically there is a marked elevation in the protein level and WBC count and the majority of cells are degenerate neutrophils. Bacteria may be visible in the spinal fluid. However, CSF can be unremarkable or may show more non-specific inflammatory changes. CSF should be cultured if it contains degenerate neutrophils, although it is common for cultures to be negative (). Samples for culture should be obtained from the middle ear by myringotomy if OM/OI is present.
Treatment and prognosis. While the results of the culture are pending, treatment with an antibiotic that will penetrate the CNS should be initiated (). The most com mo n bacte rial isof ates are Escherichia coli, Streptococcus and Klebsiella, but anaerobic infections can also occur. Appropriate antibiotics include enrofloxacin and third generation cephalosporins. Many patients are in a critical condition and may need intravenous fluids and anti-inflammatory drugs. Mechanical ventilation may be necessary in comatose patients. Prognosis is poor in animals with rapidly progressing severe signs. Early appropriate treatment is vital to obtain a good outcome.
Canine distemper virus infection
Canine distemper virus (CDV) is a paramyxovirus that commonly infects the CNS of dogs.
• Neurological signs include: seizures; visu,al deficits; vestibular dysfunction; cerebellar signs; paresis; and myoclonus. The presence of myoclonus is most commonly associated with CDV infection but is not pathognomonic as it !nas been described in other inflammatory CNS disorders. Neurological disease associated with CDV infection tends to have a progressive course. Disease can develop in well vaccinated animals, so previous vaccination history does not exclude the possibility of CDV-associated disease.
• Systemic signs of disease, such as respiratory and gastrointestinal involvement, are reported to precede the neurological signs by 2—3 weeks. However, many dogs have no previous history of disease prior to the onset of neurological signs.
• Extraneural signs of disease include: conjunctivitis; rhinitis; fever; respiratory signs; gastrointestinal signs; tonsillitis; cachexia; enamel hypoplasia; and hyperkeratosis of the footpads or nose. These signs are frequently mild ().
• Fundic examination is recommended in all suspected cases, as many dogs have evidence of chorioretinitis.
Pathogenesis. The presence and severity of neurological signs is dependent on such factors as the age and i ininunoco inpetence of th e host and th e neurovirulence of the virus strain. Many dogs probably develop transient CNS infections without concurrent clinical signs. In the CNS, CDV initially replicates in neurons and glial cells, and can cause both grey and white matter lesions, with one usually predominating. These early degenerative lesions are not characteristically inflammatory. A chronic course of CNS infection results from a late or insufficient immune response to CDV, with characteristic inflammatory demyelinating lesions (). Polioencephalomyelopathy (PEM) has been reported most frequently in immature dogs, while leucoencephalomyelopathy (LEM) or a combination of PEM and LEM is more common in mature animals ().
Diagnosis. An indirect fluorescent antibody test for viral antigen in conjunctival smears can be positive in many dogs with CNS distemper, regardless of whether the disease is acute or chronic (). Viral antigen may also be demonstrated in tracheal washings and urine sediment.
CSF analysis is often the most helpful diagnostic test. However, during the acute stage of disease, inflammatory response is lacking and thus cell count and protein level may be normal. In the chronic stage of disease, a mononuclear pleocytosis is more frequently identified. An elevated CSF titre of antibody against CDV relative to the serum titre is supportive of a diagnosis.
PCR analysis of serum and CSF for CDV is available in some laboratories.
MRI may demonstrate multifocal contrast-enhancing white or grey matter lesions ().
Histopathology can confirm the presence of acidophilic intracytoplasmic or intranuclear inclusion bodies within neurons and occasionally astroglia ().
Treatment and prognosis. There is no specific treatment for CDV-associated neurological disease. Overall, prognosis is poor, especially in cases with rapidly progressive signs. Seizures are reported to be an unfavourable prognostic sign as they are often difficult to control with antiepileptic drugs (). However, the disease is not fatal in all instances, and some animals will recover.
Consequently, in cases where the neurological signs are not severe, it is recommended that the animal be administered supportive care and the disease progression monitored over 1—2 weeks before considering euthanasia ().
Feline infectious peritonitis
FIP, a coronavirus-induced disease, is a common cause of meningoencephalitis in cats.
• Neurological signs may include: seizures; cerebellar signs; vestibular dysfunction; and paresis. The disease often has an insidious onset, and may lack distinct clinical signs.
• Affected cats may have concurrent systemic signs, including anorexia and weight loss.
• Ocular lesions may also be identified, including: anterior uveitis; iritis; keratic precipitates; retinitis; and anisocoria.
Pathogenesis. The disease occurs most commonly in cats <3 years old and from multiple cat households (); however, cats as old as 15 years have been diagnosed with the disease ().
Neurological involvement is most common with the non-effusive or ‘dry’ form of the disease. Up to onethird of cats with the non-effusive form of the disease have been reported to have either primary neurological FIP or neurological signs as part of their overall disease presentation (). The FIP virus induces a pyogranulomatous and immune complex-mediated vasculitis involving the meninges, ependymal lining, periventricular brain tissue and choroid plexus of the CNS. Secondary hydrocephalus can be seen due to obstruction of the ventricular system by the inflammation ().
Diagnosis. Haematological findings may include: anaemia; leucocytosis and hyperglobulinaemia; how-ever, no abnormalities are present in some affected cats. Serum tests for anti-coronavirus antibodies are often positive but have low specificity; however, a negative serum titre (i.e. a complete absence of antibody) does not exclude the possibility of FIP-associated neurological disease because soluble antibodies can form immune complexes and escape detection by standard tests.
Advanced imaging of the brain may reveal the presence of ventricular dilation (). Periventricular contrast enhancement may be visible with MRI.
CSF analysis will show variable results. The characteristic finding is of a marked neutrophilic to pyogranulomatous pleocytosis, with cell counts often in the hundreds, and an associated increase in protein concentration to >200 mg/dl (). However, CSF may be normal, show mild mononuclear pleocytosis or have a normal cell count with an elevated protein concentration. Positive CSF titres have been shown to be the most useful ante-mortem indicator of neurological disease. However, positive antibody titres must be interpreted with respect to the integrity of the blood—brain barrier.
PCR assays performed on CSF have not been shown to be a reliable test for confirming disease.
Treatment and prognosis. Prognosis for cats with CNS FIP is poor. Definitive treatment is not available. The use of immunosuppressive drugs may slow the progression of disease. Affected animals should be isolated from other cats to prevent the spread of infection.
Toxoplasmosis and neosporosis
Toxoplasma gondii is an intracellular protozoan parasite of humans and animals that can cause encephalitis in infected dogs and cats. Neospora caninum is a more recently recognized protozoan parasite that is known to cause neurological disease in dogs but not cats.
Clinical signs: Signs of disease are seen most frequently in young or immunocompromised animals, and can occur with concurrent CDV infection or FIP.
• Neurological signs that have been reported with protozoan infections include: seizures; behavioural changes; cranial nerve deficits; cerebellar signs; and diffuse neuromuscular disease.
• A characteristic early sign of the disease is progressive rigidity of one or more limbs as a result of myositis and neuritis.
• Concurrent ocular abnormalities may be identified on fundoscopic examination.
Pathogenesis. Ingestion of tissue from infected intermediate hosts is the most common cause of Toxop/asma gondii infection in dogs and cats. In the case of Neospora, dogs are commonly infected in utero, although they can also be infected by ingestion of intermediate host tissue.
Diagnosis. Imaging may reveal the presence of either solitary or multiple mass lesions in the brain of affected animals ().
CSF analysis typically demonstrates pleocytosis with a inixed population of neutrophils and the presence of small and large mononuclear cells. Eosinophils may also be seen. With toxoplasmosis, a presumptive diagnosis is based on positive antibody titres in the CSF. However, a positive titre can be seen in animals previously exposed to the organism following non-specific immune stimulation and therefore is not definitive evidence of active disease (). Serum and CSF anti/Veospora antibody titres are more reliable than serum titres alone. However, for both infections, evidence of a rising titre should be obtained.
Treatment and prognosis. Clindamycin and/or trimethoprim/sulphonamide (TMS) therapy is recommended in animals with CNS protozoal infections for a duration of 3—4 weeks. TMS can be combined with pyrimethamine (0.5—1 mg/kg q24h for 2 days then 0.25 mg/kg q24h for 2 weeks) and a folic acid supplement (5 mg/day) once the diagnosis has been confirmed. Neurological signs typically improve with treatment but may not resolve because of permanent damage caused by the organism. In addition, relapses are possible.
Cryptococcus neoformans is a saprophytic yeast with a worldwide distribution. The organism can be isolated from several sources, although its main reservoir is pigeon droppings.
Clinical signs. Many affected animals have nonspecific signs: anorexia; weight loss; lethargy; Iymphadenopathy; and pyrexia.
• Respiratory signs such as nasal discharge, sneezing or coughing may also be seen, as well as skin lesions.
• Ocular disease is often seen in association with neurological signs, and includes: anterior uveitis; chorioretinitis; and retinal detachment.
• Neurological signs include forebrain signs (e.g. seizures, behaviour change, altered mentation, circling, head pressing, blindness) in addition to vestibular signs, cranial nerve deficits and paresis ().
Pathogenesis. Dogs and cats most frequently become infected following inhalation of the organism. Neurological involvement results from haematogenous spread or local extension of an infection through the cribriform plate.
Diagnosis. The complete blood count may reveal the presence of monocytosis. In animals with extraneural disease, a definitive diagnosis can often be made based on cytology and/or culture of urine, nasal discharge, lymph node aspirates or cutaneous masses (). In addition, these animals often have positive titres of cryptococcal capsular antigen.
Diagnosis of CNS cryptococcosis can often be made by cytological evaluation of CSF. Neutrophilic, mononuclear or mixed pleocytosis may be seen, and eosinophils are frequently present. The encapsulated organism can be seen in cytological preparations in the majority of cases (). The use of India ink, new methylene blue or Gram’s stain allows the organism to be identified more readily.
In cases in which the organism is not observed on cytology, diagnosis can be made either by detecting cryptococcal capsular antigen in CSF or by culturing CSF samples.
Treatment and prognosis.Treatment with fluconazole or itraconazole is recommended, although overall prognosis is fair to poor. Non-steroidal anti-inflammatory drugs should be administered when antifungal therapy is initiated, to counteract the intense inflammatory reaction that accompanies the killing of Cryptococcus. Long-term treatment is required, ranging from several months to years. It is difficult to rid the body completely of the organism and relapses are common. Treatment should be continued until serum cryptococcal titres are negative, or for 2 months beyond resolution of clinical signs.
Granulomatous meningoencephalomyelitis (GME) is an inflammatory disease, of unknown aetiology, of the CNS of dogs and, less frequently, cats.
Clinical signs and pathogenesis. The disease is most common in middle-aged toy and small-breed dogs, with a possible breed predisposition in poodles and terriers. Three nicopathological forms of the disease exist:
The ocular form of the disease manifests with acute onset of dilated, unresponsive pupils due to optic neuritis
The focal form of the disease presents with nical signs suggestive of a single space occupying mass, with areas of predilection in the pontomedullary region and forebrain
The diffuse form of the disease presents with clinical signs suggestive of a multifocal CNS disorder, with the cerebrum, brainstem, cerebellum and cervical spinal cord most commonly involved. Clinical signs are usually acute in onset and progressive.
Although the cause of GME is unknown, characteristics of the lesion suggest a possible immunological basis for the disease (Vandevelde e/ a/., 1981). Infectious, autoimmune and neoplastic causes have all been proposed.
Diagnosis. CSF analysis typically reveals a mononuclear pleocytosis, with an associated increase in protein concentration (). However, both neutrophilic pleocytosis and normal CSF analysis have been reported ().
A mass lesion may be evident on brain imaging with the focal form of the disease, while the brain parenchyma may have a patchy, heterogenous appearance with the diffuse form (). Definitive diagnosis can only be made histologically on post-mortem examination or by biopsy. Ante-mortem diagnosis is usually presumptive, by exclusion of infectious aetiologies.
Treatment and prognosis. The most commonly prescribed treatment for GME consists of immunosuppressive doses of corticosteroids.
Other immunomodulatory drugs have also been utilized, e.g. cytarabine (cytosine arabinoside) and procarbazine (). Cytarabine is administered at 50 mg/m² s.c. q12h for 2 consecutive days every 3 weeks. Procarbazine has been recommended at a dose of 25—50 mg/m² orally q24h, with an attempt to reduce the dose to every other day after one ino nth of treatment. Both of these drugs are myelosuppressive, and complete blood counts should be monitored regularly during the course of therapy.
In addition, radiation therapy has been recommended as a treatment for dogs with the focal form of the disease ().
Overall, the prognosis is poor, but survival times range from weeks to years. The diffuse form of the disease carries the worst prognosis with a survival time of weeks to months ().
Necrotizing meningoencephalomyelitis is a chronic progressive neurological disorder reported in Pugs (Pug encephalitis), Yorkshire Terriers and Maltese dogs. There are also sporadic reports of similar findings in other small-breed dogs, such as Shih Tzus.
• Pug encephalitis is most commonly seen in juvenile to young adults, and causes seizures and other signs of forebrain dysfunction ().
• The disease described in Maltese dogs also has a predilection for the forebrain ().
• The disease in Yorkshire Terriers causes signs of forebrain and brainstem involvement ().
Pathogenesis. The aetiology of the disease is unknown. Infection with an alpha-type herpesvirus has been suggested, based on histological similarities with this type of infection in humans. However, attempts at viral isolation have been unsuccessful. The disease is associated with necrosis and a non-suppurative meningoencephalitis predominantly in the conex. The subcortical white matter is frequently involved.
Diagnosis. CT may reveal a focal hypodense area within the brain parenchyma relating to the area of necrosis (). Areas of high signal intensity in the brain may be seen on MRI, usually within the white matter ().
A lymphocytic pleocytosis is most frequently recognized on CSF analysis.
Definitive diagnosis is based on histopathology.
Treatment and prognosis. Prognosis is poor; no treatment is available, and the disease is typically fatal.
Intracranial arachnoid cysts are rare but have been described most commonly in small brachycephalic breeds of dog. These cysts have not been reported in cats to date, but probably do occur. Arachnoid cysts are accumulations of CSF that occur between two layers of the arachnoid membrane covering the neural parenChyma. These cysts can occur in any location along the CSF pathway, but in dogs are most commonly reported in the quadrigeminal cistern, a triangular space between the caudal cerebral hemispheres, dorsal to the midbrain and rostral to the cerebellum ().
Clinical signs. Physical examination may reveal evidence of a domed calvarium and a persistent bregmatic fontanelle, as is characteristically seen with hydrocephalus.
Neurological findings in animals with quadrigeininal arachnoid cysts may include vestibular signs such as head tilt, ataxia and circling. Hemiparesis and depression may be apparent due to brainstem involvement.
Many dogs have clinical signs referable to a forebrain lesion including: seizures; visual deficits; and dementia. In these dogs, the cysts may be an incidental finding. Forebrain signs may occur alone, or, in combination with vestibular signs.
Pathogenesis. The cause of these cysts is not known, but in most cases it is believed to be congenital and reflects splitting of the arachnoid mater.
Diagnosis. Diagnosis is based on brain imaging. Both MRI and CT characteristics have been described in dogs (). The cysts are in the typical extra-axial location, have sharply delineated margins and contain a fluid that is either isodense or isointense compared with CSF (). The cyst wall and contents are not enhanced by intravenous administration of contrast media.
Arachnoid cysts of the quadrigeminal cistern can also be identified using ultrasonography, with images obtained through a persistent bregmatic fontanelle, the temporal window in the area of thin bone at the junction of the temporal and parietal bone, or the foramen magnum (). The majority of affected animals have enlarged lateral ventricles in addition to the fluid-filled cyst at the level of the quadrigeminal cistern (). CSF should be collected to rule out the possibility of underlying infectious or inflammatory diseases.
Treatment and prognosis. Reports on treatment for intracranial arachnoid cysts in dogs are limited. Medical management consists of administering antiepileptic drugs to animals with seizures, and prednisolone to decrease CSF production.
Surgical management has been described in a few dogs and consists of either fenestrating or shunting the cyst (). Information on long-term follow-up is not available for dogs treated either medically or surgically, and consequently overall prognosis is unknown.
Clinical signs. Central vestibular signs have been reported in dogs after administration of metronidazole ().
Initial clinical signs are anorexia and vomiting, which can progress rapidly to include bilateral central vestibular signs with either a symmetrical or asymmetrical generalized ataxia and a positiona! vertical nystagmus. Head tilt and seizures are observed less frequently.
Onset of clinical signs can occur as soon as 3 days after initiating treatment but can also be seen after chronic therapy. Dogs reported to have developed toxicity were typically treated with an oral dose of metronidazole >60 mg/kg/day (), although doses as low as 30 mg/kg/day have been incriminated ().
Metronidazole toxicity has also been reported in cats, but affected cats display signs of forebrain and cerebellar involvement rather than vestibular signs (). Toxicity can be seen with lower doses than those reported for dogs.
Pathogenesis. The pathogenesis is poorly understood, but it is hypothesized to be related to interaction of metronidazole with the gamma-aminobutyric acid receptors inthe cerebellum and vestibular nuclei ().
Diagnosis. A history of metronidazole administration and compatible clinical signs should lead to a high suspicion for this disorder.
Treatment and prognosis. Treatment consists of discontinuation of the drug and provision of nursing care. In addition, administration of diazepam has been shown to shorten recovery times in dogs (). An intravenous injection of diazepam (0.43 mg/kg), followed by 0.43 mg/kg orally every 8 hours for 3 days, has been recommended.
Recovery is typically seen within 1—3 days in dogs treated with diazepam, and within 2—3 weeks for dogs in which treatment only consists of drug discontinuation and supportive care.
As is the case with dogs, signs in cats are reversible with discontinuation of the drug.
Head trauma in dogs and cats is most often caused by automobile accidents, and injury to the brainstem can result in vestibular signs along with other signs of brainstem dysfunction. ()
Cerebrovascular disease is being reported more frequently in dogs and cats with the greater availability of MRI as a diagnostic tool. A recent review of cerebellar infarcts in dogs and cats found the majority of animals to have a vestibular component to the neurological signs, either in the form of paradoxical vestibular disease or cerebellovestibular signs.