Download A Day of Neurology Emerency Cases Vascular Events Ischemic

A DAY OF NEUROLOGY EMERENCY CASES
Vascular Events
Ischemic myelopathy or Fibrocartilaginous embolic myelopathy (FCE) is a common disease
caused by obstruction of arterial and or venous supply to the spinal cord by fibrocartilaginous
material. This material is believed to originate from the nucleus pulposus but the mechanism for
getting to the spinal cord is unknown. A typical signalment and presentation is an acute, nonprogressive, non-painful myelopathy of middle aged non-chondrodystrophic dogs. Deficits are
often asymmetric and occur at the level of the intumescences. Diagnostics include MRI, CSF
analysis and negative infectious disease testing. In the literature, prognosis varies from fair to
good but depends on the severity of the neurologic signs. There is no specific therapy aside from
supportive care, rehabilitation and time. Recovery may be incomplete and is often a long road
with weeks to months of physical rehabilitation. A traumatic noncompressive missile disc has a
similar clinical presentation and prognosis to FCE.
Cerebrovascular accidents (CVA) occur when there is either obstruction of a blood vessel
supplying the brain or hemorrhagic via rupture of a vessel. A variety of etiologies may
predispose animals to CVAs including hypertension, endocrine diseases, coagulopathies,
vasculitis, and cardiovascular disease. Clinical signs associated with CVAs are acute, nonprogressive, non-painful and often lateralizing. Diagnostic testing may involve CBC, Chemistry,
UA, TEG, coagulation profile, serial BP, thoracic radiographs, AUS, MRI, CSF analysis and or
infectious disease testing. Therapy primarily involves treating an identifiable underlying
diseases along with supportive care. The clinical signs associated with the nervous system
typically improve with time and or the prognosis is generally fair to good.
Infectious
Canine ehrlichiosis is caused by several different species of Ehrlichia. Those species reported in
the US include E. canis, E. ewingii, E. chafeensis, A. phagocytophilum (E. equi), and A. platys
(E. platys). Ehrlichiosis can either be acute or chronic. The hematological effects of ehrlichiosis
can be variable, but the most common abnormality detected is thrombocytopenia. Despite the
fact that many clinicians suspect ehrlichiosis in dogs with hemolytic anemia, a non-regenerative
anemia is more commonly identified. Ehrlichiosis can also cause pancytopenia,
hyperglobulinemia, hypoalbuminemia, lymphadenopathy, splenomegaly, proteinuria,
polyarthritis and/or uveitis.
Serology is helpful in the diagnosis of Ehrlichiosis. Acute and convalescent (3-4wks) titers
should be performed. A four-fold change is consistent with ehrlichiosis. If the signs are chronic
(> 4wks.), then a single high titer is consistent with infection. In-house tests (SNAP) are not
designed for diagnostic use, but a positive test in conjunction with appropriate clinical findings is
supportive of a diagnosis of ehrlichiosis. A positive PCR test is useful to rule-in the presence of
infection and identify which species is present. A negative PCR test does not rule out the
possibility of ehrlichiosis. Therefore, the resolution of clinical signs in response to therapy
remains an important “test.” Doxycycline (10mg/kg/day for 4 wk.) is considered the treatment
of choice. Other drugs that are reported to be effective include tetracycline, minocycline and
chloramphenicol. I typically add ciprofloxacin (20-25 mg/kg/day for 4 weeks) as well, to cover
for the possible co-existence of other tick-borne diseases (Bartonella).
Rocky Mountain Spotted Fever (RMSF) caused by Rickettsia rickettsii is an acute systemic
disease of dogs. RMSF is generally seasonal (Apr.-Oct.) correlating with the Dermacentor sp.
lifecycle. Thrombocytopenia is the most common hematological abnormality (>85%). The
degree of thrombocytopenia ranges from moderate (75,000 platelets) to severe (< 5,000
platelets). The major mechanism is consumption secondary to vasculitis, but there is some
evidence for immune-mediated destruction. Leukocytosis is the second most common
hematological finding, and may be severe (> 50,000). The anemia associated with RMSF is
often mild (PCV 25-30%). The hematological effects are seen with accompanying clinical signs,
such as fever, lethargy, anorexia, pain, petechia, jaundice and neurologic signs. The most
common neurologic signs are central vestibular dysfunction. Common biochemical abnormalities
identified in dogs with RMSF included hypoalbuminemia, hyponatremia and
hyperbilirubminemia. Serology is very helpful in the diagnosis of RMSF. If the signs are acute,
then paired acute and convalescent (2-4 weeks after the acute) titers must be submitted. A fourfold change is diagnostic for an active infection. If the patient is sick > 10-14 days, then a single
high titer (> 1:1024) is consistent with an active infection. Positive PCR results also indicates
active infection. Response to therapy (doxycycline, tetracycline, enrofloxacin, or
chloramphenicol) is suggestive, but not diagnostic. Doxycycline (5-10mg/kg BID),
chloramphenicol (15-30mg/kg TID), and enrofloxacin (5mg/kg BID) for 4 weeks are effective
treatments.
Malformations
Atlantoaxial Subluxation (AA) is encountered most often in toy or small breed dogs, particularly
Yorkshire terriers, Chihuahuas and Miniature poodles. Clinical signs in congenital atlantoaxial
subluxation are usually seen in immature patients although signs can develop later in life.
Clinical signs may range from mild pain to tetraplegia with hypoventilation. Survey
radiographs, dynamic radiographs or fluoroscopy can provide the diagnosis in most cases,
although cervical ventroflexion should be avoided due to possibility of exacerbation of signs.
Diagnostic MRI and or CT scan are recommended to rule out other etiologies and for surgical
planning. Surgical stabilization is indicated in most dogs with ventral fusion of C1-2,this is my
preferred approach. Stabilization and ultimate fusion of the atlantoaxial joint can be performed
using transarticular fixation, multiple implants and PMMA.
Hydromyelia is fluid dilatation of the central canal and syringomyelia is dilatation within the
spinal cord away from the central canal that may or may not communicate with the central canal.
A vast majority of syringohydromyelia (SHM) cases in dogs appear to be associated with caudal
occipital malformation syndrome (COMS); the most commonly affected breed is the Cavalier
King Charles Spaniel. SHM in the cervical spinal cord may occur concurrently with the
hindbrain anomalies associated with COMS as a consequence of altered CSF flow. Clinical
signs maybe acute or chronic and may or may not be progressive. Diagnostics should include
MRI and CSF analysis. Medical or surgical management may be recommended based on
severity of clinical signs. Medical therapy may include the use of omeprazole, gabapentin, other
analgesics and or steroids. Surgical management may consist of foramen magnum
decompression, cranioplasty and VP shunting.
Neuromuscular Disease
Polyradiculoneuritis, also called coonhound paralysis, is a rapidly ascending LMN paralysis,
with progression from paresis to tetraplegia typically within a few days. It is suggested that
raccoon saliva alters the peripheral nerve antigenicity, resulting in inflammation and
demyelination. It is also seen in dogs with no exposure to raccoons, suggesting that other factors
can stimulate a similar immune-mediated reaction. Ventral roots and motor axons are
preferentially involved. Coonhound paralysis appears to be analogous to a peripheral neuropathy
of humans referred to as Guillain-Barre syndrome.
Patients present with diffuse spinal hypotonia, hyporeflexia and severe neurogenic muscle
atrophy. Generalized hyperesthesia is occasionally observed. Typically, no obvious sensory
deficits are recognized. Cranial nerves appear to be typically spared yet the recurrent laryngeal
nerve may be affected.
Diagnosis is based on clinical signs and exclusion of other causes of LMN tetraparesis: tick
paralysis, fulminant myasthenia gravis, coral snake envenomation, botulism, or cholinesterase
toxicity. Characteristic electrodiagnostic findings distinguish coonhound paralysis from other
acute, progressive LMN diseases. Denervation activity is seen on EMG and motor nerve
conduction velocity is decreased indicating myelin involvement, sensory testing is typically
unremarkable. Serology can be used to rule out infectious etiologies.
Supportive care and rehabilitation are the mainstay of therapy as there is no definitive treatment.
Rarely, assisted ventilation may be indicated if ventilation or respiratory signs are severe.
Prognosis is favorable if clinical signs are not severe and signs of recovery occur within several
days to weeks. Relapse is possible but uncommon.
Myasthenia gravis (MG) is an immune-mediated disorder in which antibodies directed against
the nicotinic acetylcholine (ACh) receptors of skeletal muscle result in impairment of
neuromuscular transmission. Antibodies bind to and destroy the ACh receptors on the postsynaptic membrane decreasing the number of functional ACh receptors increasing the chance of
failure of neuromuscular transmission. With repetitive firing of a motor nerve ending, the few
available ACh receptors are soon bound with ACh molecules and desensitized to further
stimulation resulting in failure of sustained neuromuscular transmission.
The classic presentation of a dog with acquired MG is episodic, generalized muscle weakness
that is worsened by exercise and improves with rest.
The current gold standard for diagnosis of MG involves the use of an immunoprecipitation
radioimmunoassay for the determination of ACh receptor antibody titers in serum. There is a
reported 2% seronegative rate in dogs, although I believe this number is closer to 10-15 % based
on clinical experience. A similar percentage is reported in humans for generalized MG.
Edrophonium chloride is an ultra-short-acting anticholinesterase agent that can be used in a
clinical setting to support the suspicion of MG while titers are pending. The drug temporarily
reduces the breakdown of Ach resulting in more ACh molecules in the synaptic cleft to interact
with the available ACh receptors. This results in recovery of neuromuscular transmission and
improved muscle strength. A presumptive diagnosis of acquired MG may be made if a patient
responds positively to IV injection of 0.1-0.2 mg/kg of edrophonium. A patient that demonstrates
obvious improvement in muscle strength shortly after edrophonium is considered to have a
positive response. I commonly pretreat the patient with atropine (0.02 mg/kg SC) to minimize
muscarinic side effects. In acquired MG, there are two main aspects of therapeutic intervention:
anticholinesterase therapy, immunomodulatory therapy and thymectomy (uncommon). It is
believed that up to 80% of cases may go into spontaneous remission given time (I believe this is
an over estimate clinically).
Anticholinesterase agents, enhance neuromuscular transmission by prolonging the action of
acetylcholine at the neuromuscular junction. Dosage must be adjusted for each patient
depending on individual tolerance of adverse effects and response to treatment. Therapy includes
pyridostigmine bromide (Mestinon 0.5-3 mg/kg PO BID or TID) and dosages are titrated based
on changes in muscle strength. The use of immunosuppressive drugs appears controversial. I
believe long term immunosuppression is often necessary, similar to humans. The mechanisms of
action of immunomodulation includes: inhibition of the cell cycle (azathioprine and
mycophenolate mofetil), immunosuppression of T cells (steroids and cyclosporine) or
plasmapheresis therapy to lower autoantibody levels. I commonly use a combination of
prednisone and azathioprine. One of the most devastating and common side effect of dogs with
MG is megaesophagus and subsequent aspiration pneumonia. Prevention and treatment of
aspiration pneumonia is an essential consideration in animals with acquired MG. Frequent
turning of recumbent animals, antibiotic therapy, nebulization and coupage are examples of
treatment considerations for aspiration pneumonia.
Intracranial Tumors
Brain tumors are common in small animals. Brain tumors may be primary, arising from the
parenchyma or meninges or secondary arising elsewhere and metastasizing to the brain. The
most common primary tumors are meningioma and gliomas. Brain tumors are most frequently
seen in older patients. Clinical signs depend on the specific location of the tumor, and may
include seizures, behavior changes, compulsive pacing or circling, mental dullness, vestibular
and or cerebellar dysfunction. Diagnostic evaluation consists of physical and neurological
examination. Routine blood work is performed to rule out a systemic problem and assess the
anesthetic risk. Thoracic radiographs and AUS are taken to rule out there is no obvious evidence
of metastasis. Imaging of the brain (MR and or CT) and CSF analysis. Therapy may consist of
surgical excision, radiation therapy and or chemotherapy. Steroids are also commonly given to
reduce vasogenic edema associated with the tumor.