CASE STUDY: Prinz

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Prinz is a 9-year-old German Shepherd mix referred to BVNS for an inability to walk in the hind legs and severe back pain of less than 24 hours duration. The prior afternoon, Prinz had been playing ball. He jumped to catch the ball, and upon landing, cried out, and was immediately paralyzed in the back legs. Over the next 15 minutes, he regained movement in the back legs but was unable to walk. He continued to be extremely painful, even biting his owner when they tried to help him, very atypical behavior for him as he’s normally a lover and very playful. He was rushed to an animal emergency hospital and treated supportively with anti-pain medications, NSAIDs, and fluids.

Presenting Complaint:

1. Peracute paraplegia (loss of conscious movement in the pelvic limbs) and severe back pain after a jump while playing ball.

2. Slightly improved neurologic grade, non-ambulatory paraparesis (conscious movement present in the pelvic limbs but unable to walk) and continued intense pain despite analgesics (anti pain medications).

Assessment (Neurolocalization):

Severe non-ambulatory paraparesis, absent postural and placing responses in the pelvic limbs, brisk spinal reflexes with intact superficial pain perception, cutaneous trunci reflex present cranial to T12 on the left and present cranial to L1 on the right, left sided muscle spasms and discomfort extending from T12 to L4/L5.

Prinz's deficits localized to a left lateralizing T3-L3 myelopathy with the primary differentials being a Type I or Type III disc extrusion.

Diagnostics:

Spinal radiographs taken by the emergency hospital revealed predominant finding of a subtle narrowing of the T12-T13 intervertebral disc space.

An MRI of the thoracic to sacral spine was performed. Extra-dural hemorrhagic material was dispersed along the left canal extending from T11 to T13 causing mild cord deviation towards the right of the canal. Nearly 75% of the spinal cord parenchyma, slightly left lateralizing but predominantly central in distribution, demonstrated increased T2W signal consistent with edema, dorsal to the T12-T13 disc space. The left paraspinal muscles extending from T9 to L2 were diffusely swollen and edematous.

These findings were most consistent with a high velocity, low volume disc extrusion at T12-T13 and likely concurrent neurogenic myositis or vasospasm with infarction to the left paraspinal musculature.

Outcome:

A left hemilaminectomy was performed from T11 to T13. Upon fascial incision, the left paraspinal muscles everted out the incision margins and were grossly swollen, edematous, and pale. Biopsies were obtained of the abnormal musculature. Upon entry into the canal, the epidural adipose tissue was discolored and intermixed with hemorrhagic material. Tannish fluid like material was removed from the ventral canal dorsal to the T12-T13 disc space. Samples of each were also submitted for histopathological evaluation. Cultures were also collected and submitted. The venous sinus structures lining the floor of the canal were dilated and pulsating. Histopathology results demonstrated myofiber necrosis with neutrophilic inflammation and mineralized cartilage removed from the spinal canal samples. Cultures were negative for bacterial growth.

Diagnosis

Hansen Type III disc extrusion (high velocity, low volume) at T12-T13 causing internal cord injury and secondary inflammatory muscle necrosis.

Outcome

Prinz recovered to his normal, active, happy self over the following days and was discharged several days later so he could travel with his family to California where they had recently been stationed. We continue to receive updates from the owner’s regarding Prinz and his life as a “beach dog”! We remain humbled by Prinz’s endearing zest for life and for his military family serving our country

Take Home Points:

Review of the three primary classifications of Intervertebral Disc Disease:

1. Hansen Type I: an acute extrusion, under varying velocities, of the nucleus pulposus (inner portion of the disc, normally gelatinous but can become rock like when degeneration occurs) causing moderate to severe cord compression. Often requires surgical intervention to remove compressive elements and continued cord injury. If the disc material ruptures under high velocity forces,internal cord injury occurs. Less than 1% of patients will develop life ending myelomalacia up to 5-7 days following the injury, despite emergent surgical decompression. MRI often helps identify significant intraparenchymal cord injury and can better help predict prognosis following surgical decompression.

2. Hansen Type II: a slow, chronic protrusion or prolapse of the dorsal annulus (ligamentous structure surrounding the nucleus pulposus) into the spinal canal causing slow compression of the spinal cord. One caveat is an “acute on chronic disc” presentation where acute decompensation can occur. If the spinal cord impacts/strikes a mound of protruding dorsal annulus, severe internal cord injury can occur resulting in rapid decompensation.

3. Hansen Type III: a high velocity or "explosive", low volume disc extrusion causing severe internal cord injury. Also referred to as acute non-compressive nucleus pulposus extrusion or ANNPE. If severe enough, myelomalacia, a potentially fatal break down process of the spinal cord, can occur up to 5-7 days from the injury.

To ask a question related to this case or discuss any aspect of it please email Dr. Jarboe.

Case referred to BVNS by Dr. Roque Pereira at the Animal Emergency Clinic of Fredericksburg, Prinz’s primary care veterinarian is Dr. Gary Dunn at White Oak Animal Hospital.

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Archive

CASE STUDY: Tiki

Tiki is a 4 year-old spayed female Maltese referred to Bush Veterinary Neurology Service after one week of 30-60 second episodes of lethargy, shaking and keeping her head down. She became progressively worse, started crying out during the episodes and would intermittently circle to the left.

The owner brought a video of the episode, which showed a two-minute episode of vestibular ataxia, mild left head tilt and holding her head down. Tiki would also hold her right pelvic limb up during the episode and appeared alert and aware (would wag her tail when the owner called her name). Immediately after the episode, Tiki moved normally. Neurologic examination showed evidence of an abnormality in the caudal fossa (caudal cerebrum and cranial brainstem), lateralized to the left. Her intermittent episodes were most likely due to an increase in intracranial pressure, rather than seizure activity.

An MRI of the brain was consistent with diffuse encephalomyelitis and cerebellar herniation. A cerebrospinal fluid analysis was recommended to confirm the diagnosis for inflammatory disease, but considered of increased risk due to the foramen magnum herniation. Despite concerns for her long-term prognosis (due to how severe the changes seen on her MRI and her progressive clinical signs) she has continued to do well on medications.

Presenting Complaint:

Increasing frequency of episodes of keeping her head down and mental dullness, lethargy, decreased appetite, and circling to the left

Assessment (Neurolocalization):

Left lateralized caudal fossa

1. Dull mentation

2. Tendency to hold head and neck down

3. Circling to the left

4. Vestibular ataxia, with intermittent crossing in all four limbs

5. Decreased placing reactions in the left limbs

6. Pain on palpation over the head

Diagnostics:

An MRI of the brain shows moderate enlargement of all ventricles and a non-contrast enhancing hyperintensity within the cervical spinal cord parenchyma. On the post contrast T1W post sagittal image, the caudal aspect of the cerebellum was herniated through the foramen magnum.

Outcome:

Tiki was administered mannitol (1g/kg) intravenously after her MRI to decrease intracranial pressure. Due to her signalment, examination and MR findings, we were most suspicious of an immune-mediated meningioencephalitis, specifically granulomatous meningioencephalitis (GME). Tiki was admitted to the hospital for empirical therapy for her inflammatory disease. She was started on steroid medication (prednisone 0.5mg/kg PO q12h) and immunomodulatory medication with a CRI of intravenous cytarabine (Cytosar) over 48 hours and cyclosporine (5mg/kg PO q12h). She was also placed on famotidine (0.5mg/kg) for gastroprotection while on the steroid. Tiki was discharged from the hospital two days later with an improved neurologic examination (less compulsive circling, mild ataxia and improved postural reactions).

In the few months after her hospitalization, Tiki has shown progressive improvement and is now neurologically normal. She has not required any additional cytarabine therapy and is currently being maintained on daily cyclosporine and a low dose of steroids, which we have been tapering slowly over the past several months. We suspect that due that her prognosis is good, though relapse in patients with immune-mediated inflammatory central nervous system disease is always possible.

Take Home Points:

1. Having clients videotape episodic neurologic abnormalities can be helpful when considered along with the history and neurologic examination in determining a patient’s neurolocalization. This is especially true in cases like Tiki’s, where the neurologic examination is normal between episodes.

2. Cerebellar herniation is a dynamic process and is observed in patients with an increase in intracranial pressure.

3. The prognosis for immune-mediated brain disease like GME was once poor but with the advent of new medications and protocols, the prognosis is much better. A recent retrospective showed that 60% of dogs were normal and the other 40% much improved on azathioprine, the dogs in this study had an average survival of almost 6 years. At BVNS we use prednisone to manage the acute symptoms but try to replace this medication with immune modulators like azathioprine, cyclosporine, leflunomide and/or chemotherapies like cytosar, procarbazine, and lomustine.

To ask a question related to this case or discuss any aspect of it please email Dr. Hague.

A special thank you to Dr. Jennifer Lauer at the Pender Veterinary Center who referred this case. Dr. Lauer is an Ohio State University classmate of Dr. Hague's and is now practicing at Valley Veterinary Emergency and Referral Center.

June 2011: SQUIRREL

The Clinical Management of Status Epilepticus

Squirrel is a 10 year old, male, castrated cat that presented to BVNS for persistent, intermittent 15 second seizures (non-responsive, left side facial twitching progressing to generalized twitching, salivation) despite treatment with multiple doses of valium and 10 mg/kg of phenobarbital. Squirrel’s examination suggested multifocal brain disease because there was a tendency to turn his head to the right, poor postural ability on right side, circling left, and a poor menace and poor palpebral response on the left. Infection, inflammation, or a neoplastic process were considered most likely.

Chemistry, CBC, and later, MRI, spinal tap, and infectious disease titers were all negative and treatment was initiated for infection (likely viral) and seizure. Squirrel was treated with zonisamide, levetiracetam, and phenobarbital as well as low doses of prednisolone and clindamycin. Thirty hours later he had the following story.

Presenting Complaint:

Fever, confusion, dull, non-ambulatory, intermittent eyelid twitching, squinting, and right head turn.

Assessment (Neurolocalization):

Mutlifocal brain disease was noted. Brainstem disease was suggested by weakness, dullness and poor palpebral response; right forebrain disease was suggested based on confusion and head turn. The patient was thought to be having a constant seizure (Status Epilepticus or SE) based on eyelid twitching and fever, however, there are many other causes for fever and eyelid twitching.

Diagnostics:

Dr. Mark Stecker, who is a physician, neurologist and world expert on EEG that has been helping Dr. Bush perform EEG for over 10 years, was asked to assist with Squirrel’s care.

An electroencephalogram (EEG) was recorded in a double banana montage and read real time by Dr. Cuff, Dr. Bush and Dr. Stecker. Dr. Stecker remotely viewed the EEG in order to provide ongoing feedback and consultation. This allowed us to titrate treatment to the dissipation of epileptiform activity with 100 mg/kg of phenobarbital. Phenobarbital was selected because barbiturates are the most useful drugs in this situation in people as opposed to diazepam, propofol or levetiracetam. The patient was intensely monitored (end tidal CO2, blood gas, blood pressure, ECG) but did not require cardiorespiratory support during the 12 hour loading with phenobarbital.

Outcome:

Squirrel developed serious heart disease and azotemia while being treated for SE. A heart murmur had been noted two years ago and current thinking is that this disease may have become clinical due to administration of low doses of fluids and prednisone or possibly related to the cardiovascular effects of the diluent in phenobarbital (a phenomenon reported in the 1940’s in people). After two weeks of intensive care from the Critical Care Service at TLC, CVCA, and BVNS, Squirrel was healthy enough to go home. Above he is pictured with the owners and Dr. Cuff. Squirrel is about two months out from his presumed severe viral brain problem and doing very well.

Take Home Points:

1. Status Epilepticus leads to death of inhibitory neurons, release of excitatory neurotransmitters and generates other pockets of abnormal electrical activity (kindling) leading to more seizure and occasionally death.

2. Patients can have active severe EEG seizure without any autonomic signs (salivation, urination, defecation, pupil dilation or constriction) and without obvious muscle movement.

3. Treatment of SE, ideally guided by the EEG, can require very high doses of phenobarbital.

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December 2010: Cooper

Cooper is a 9 year old Airedale Terrier referred to BVNS for the inability to walk and severe neck pain. The pain had been intermittent for 3 weeks and acutely worsened two days before presentation. Cooper had also been having difficulty rising and was non-ambulatory at the time of presentation.

Presenting Complaint:

• 3 weeks progressive neck pain which became severe

• 2 days progressive weakness in all 4 limbs resulting in an inability to rise upon admission

• Depressed and inappetent

Assessment (Neurolocalization):

• Non-ambulatory with severe tetraparesis; low head and neck carriage; proprioception slow in the thoracic limbs and absent in the pelvic limbs; hopping absent in all limbs; intense pain response with palpation of the cranial cervical region (between the occiput and C2); distended urinary bladder.

• Cranial cervicalmyelopathy with primary differentials being neoplastic, immune mediated or infectious disease process

Diagnostics:

• Bloodwork revealed leukocytosis and thrombocytopenia.

• MRI of the cervical spine showed a paraspinal abscess, primarily right-sided in the C1 region with probable extension of the mass into the epidural space. There was also evidence of meningitis from the posterior fossa through C2-C3.

• Fine-needle aspirate and cytology revealed cocci and neutrophils (both present in quantities too numerous

to count)

Outcome:

Initial treatment with intravenous fluids, antibiotics and analgesics provided subtle improvement; however, Cooper remained non-ambulatory and the thrombocytopenia worsened. The decision was made to proceed with an exploratory surgery of the right paraspinal cranial cervical musculature together with a modified laminectomy of C1. Much of the tissue in the region was found to be necrotic and discolored. The abscess within the muscle was opened and flushed and a small tubular structure was removed from within; histopathology later revealed this to be foreign material resembling plant matter. After laminectomy, fibrin adhesions were detached from the dura and the spinal cord was decompressed. A drain was placed and Cooper was hospitalized for several days after surgery for continued supportive care.

At the time of release, Cooper was able to walk with minimal support and was able to move his head and neck with improved range of motion and comfort. He went on to show continued improvement and made a full recovery over the following weeks.

Take Home Points:

1. Weakness and neck pain can be associated with cervical spinal cord disease.

2. Foreign bodymigration is an uncommon cause of spinal cord disease, but a favorable outcome can often be achieved with advanced diagnostics and surgical intervention.

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October 2010: King

King is a 12 year old mixed breed referred to BVNS for the inability to get up. King’s story started 9 years ago when he was rescued by the current owners after surviving being dragged behind a truck on a highway. When referred King was unable to get up when laying on his side and once assisted to rise he would cross over his back legs, knuckle them and was drunk and weak on the back legs. He was also stiff in his low neck and taking little short steps on the thoracic limbs. King had been examined 1 year ago for back pain and the current problem started 2 months ago. He had not been able to get up for the last 5 days and his symptoms were unresponsive to medication.

Examination supported a neck problem and MRI showed a tumor was severely pressing on the spinal cord. There was a concern that surgery may not remove all of the tumor, the tumor would come back, or that King would never regain the ability to walk, even with surgery.

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