What to do with a narrowed disc space?

Narrowed Disc Spaces

It's a Tuesday morning and on your schedule is a 2 year old MC Labrador retriever with a 2 week history of back pain. The neurologic examination is normal. Without any neurologic deficits, remember that the pet hasn't been diagnosed with neurologic disease (yet), so spinal pain can be due to bone, joint, nerve, spinal cord, muscle or meningeal in origin. You elect to take sedated spinal radiographs and send them off to the radiologist. A radiologist will report what they see, which often includes "narrowed disc space(s)" on the report. What do you do with this?

Does a narrowed disc space indicate a disc herniation?
No, sorry. A narrowed disc space could be positional (often), beam angling (often), due to disc degeneration, or disc herniation. Disc degeneration occurs when hydration leaves the annulus fibrosis, thus causing the disc to shrink a little. This is a normal aging process and does not indicate a herniation. Herniation occurs when part of the disc (annulus fibrosis (AF) or nucleus pulposus (NP)) leaves it's normal position. When the NP leaves, we call it a Type I disc herniation. Type I disc herniations are common in chondrodystrophic dogs and about 30% of non-chondrodystrophic dogs. Clinical signs often include calcification of the NP which might be visible on radiographs. Remember, in situ calcification is appropriate and normal for chondrodystrophic and some non-chondrodystrophic dogs and does not indicate herniation. Calcification in the canal suggests that the disc has herniated but does not indicate that the current clinical signs are due to THAT disc herniation. This means we cannot diagnose a type I disc herniation strictly on radiographs. An MRI, CT or myelogram is needed to diagnose a type I disc herniation. 

When the AF displaces, it is called a Type II disc herniation. This is more common in non-chondrodystrophic dogs and is often part of disc associated wobblers and lumbosacral disease. No calcification occurs for this form of herniation therefore it cannot be seen radiographically. A narrowed disc space often (but not always) accompanies a type II disc herniation but is not always radiographically visible. An MRI, CT or myelogram is needed to diagnose a type I disc herniation. 

What about FCE or ANNPE?
Acute noncompressive nucleus pulposus extrusion (ANNPE) or fibrocartilaginous embolism (FCE) are two more forms of disc herniation where in a small amount of disc material leaves its normal location, often under great force. A narrowed disc space can be seen with these types of disc herniation as well but would  NOT be diagnostic for either disease. An MRI is needed to diagnose an FCE or ANNPE. 

What causes of back pain CAN you diagnose on radiographs then??
The most common causes of spinal pain are 2 "D"s, 2 "T"s and an "M" (as I teach it to students). Discospondylitis, disc herniation, trauma, tumor, and meningitis. Of these, only discospondylitis, vertebral neoplasia and fracture/subluxation can be diagnosed on plain radiographs.

The patient above could have discospondylitis on their differential diagnoses list therefore radiographs are absolutely indicated. However, please be cautious reading too much into a "narrowed disc space" and instead look for discospondylitis, vertebral neoplasia or signs of trauma. 

I hope you enjoyed this week's TidBit Tuesday! We're almost into March which, if you're a long-time patron, you know means we're approaching St. Patrick's day. My girls are Irish Dancers and, as such, usually perform in over 30 shows in the month of March. That means this proud mamma has a more limited work schedule due to all of the driving so PLEASE reach out if you cannot find a suitable time on the online scheduler. I may (often can) shift things a bit to accommodate your request! Have a great week and stay safe out there. 

Which Reflexes Should I Do?

Have you ever looked down at the patient, laying calmly and quietly in lateral recumbence, and thought “okay, which reflexes do I do?” There are several choices for each limb, but the most commonly assessed reflexes are as follows:

• Thoracic limb (I was trained by Dr. DeLahunta and was taught to never call this the front limb, but you are welcome to do so!): Biceps, triceps, extensor carpi radialis and withdrawal.

• Pelvic limb (same story as above): patellar reflex, cranial tibialis, gastrocnemius and withdrawal.

Some of these reflexes are harder than others to observe and obtain. The purpose of performing the spinal reflexes is to assess the sensory and motor pathways associated with that specific peripheral nerve and the spinal cord segment. For example, the patella reflex evaluates the femoral nerve and the L4-6 spinal cord segment. A present reflex suggests this pathway is intact. An absent reflex suggests that the peripheral nerve (femoral nerve) and/or the L4-6 spinal cord segments are NOT intact. A recent study (Chiang B, Garia G, et al 2024) evaluated each of these reflexes in 101 dogs and asked 1 neurologist and 1 resident to determine if they were obtained, or not (simple binary question).
Several of the reflexes had high intraobserver agreement, which would suggest that these are both easy to detect and possibly easier to obtain. The reflexes which high intraobserver agreement included the extensor carpi radialis, withdrawal reflexes in both thoracic and pelvic limbs, patellar reflex and cranial tibial reflex. Although all reflexes could (might I say should?) be attempted in the neurologic examination, sometimes we don't have this luxury. From this study, I would suggest that the 4 reflexes mentioned above should be reliably present. If you perform these reflex tests and do not observe a response, it is reasonable to consider them absent or delayed. 

Not sure how to perform these reflexes? I run personalized CE events, including live animal neurologic examination practice, in your clinic. Email me to learn more or to schedule. 
Does neurology make you nervous?? Please reach out to schedule your patient for a neurologic examination or reach me via email with any questions. My job is to help you decide if a patient has neurologic disease, or not, and the way we do this is to utilize the neurologic exam.

Thanks for reading. This article can be found here:DOI: 10.1111/jvim.16999

How Effective is Zonisamide in Cats?

Seizures are a common reason for me to evaluate cats and therefore (I assume) something you encounter frequently. Seizures originate from the forebrain (prosencephalon) and can be secondary to idiopathic epilepsy, structural epilepsy (such as congenital disease, neoplasia, meningoencephalitis, cerebrovascular events, head trauma, and on goes the list), or metabolic seizures (hypoglycemia, thiamine deficiency, etc.).

The mainstay treatment for cats has been phenobarbital for many years and not without good reason. Phenobarbital controls seizures in over 90% of cats, regardless of the etiology, and has predictable clinical side effects. When cats cannot tolerate phenobarbital, or have seizures in excess while on phenobarbital, other antiepileptic drugs (AED) are added; one of those is zonisamide. Very little data has been published to date about zonisamide use in cats. A recent study out of UW (go Bucky) was published recently. I thought it was worth a quick summary, TT style.

How many cats were enrolled in this retrospective, multicenter study? 57

The median age of seizure onset was 7 years (range 0.17-22) and the median age of onset for cats diagnosed with idiopathic epilepsy was 8 years. Note the difference between cats and dogs! Dogs have a lower median age at onset! Importantly, note that 30 cats did not have advanced diagnostics (52%) which means a final diagnosis was not reached and therefore their disease may have affected their response to zonisamide (but we don’t know!).
How did the cats on zonisamide respond to treatment?

• There was a significant decrease in seizures/month AND seizures/day after starting zonisamide. Note: we don’t know how long the seizures were monitored before starting zonisamide.

• 70% of cats responded to zonisamide monotherapy (had less than 1 seizure per 3 months)

• 56% of cats responded to zonisamide as add-on therapy

• Almost 70% of cats diagnosed with idiopathic epilepsy responded to zonisamide but it isn’t clear if these cats were on monotherapy or add-on therapy.

• The median dose was 7.5 mg/kg/day with about 1/3 of the cats receiving the drug once daily and 2/3 receiving it twice daily.

• More cats obtained seizure control on twice daily dosing than once daily dosing but the side effects were more profound on twice daily dosing.

• Side effects were noted in 15/57  cats and they included inappetence (10 cats), sedation, ataxia and vomiting for most reports. The duration of the side effects was up to 4 weeks after starting the medication. This is surprising and warrants further investigation. Anorexia has been the side effect I note more commonly but

• No clinically significant CBC or biochemistry changes were noted on the cats in this study

So what’s the take home message? Would I use zonisamide in a cat? A qualified, yes. Phenobarbital still has a better reported seizure control compared to this cohort of cats on zonisamide. BUT it is worth a try if the cat fails treatment with phenobarbital and the don’t have a history of a sulfa drug reaction (zonisamide is a sulfa derivative). Starting dose should be less than 10 mg/kg daily, and side effects appear dose dependent…but last awhile!

Thanks for reading this week’s, TidBit Tuesday! I hope you learned a little something – I know I did! Keep those consults rolling. Have a great week and stay warm and safe out there.
 
 Reference: https://doi.org/10.1111/jvim.16984

Anesthesia for Pets with Seizures

It’s a Tuesday morning, and on your schedule is a 6 year old Maltese dog with a 3 year history of seizures that appear well controlled on phenobarbital monotherapy. She has a history of 1 seizure every 6-8 months and each seizure is less than 3 minutes in length. No interictal signs noted by the owners and she continues to have a normal neurologic exam. Today, they would like to discuss doing a dental for their dear little dog. What should you consider? How does general anesthesia for a patient with neurologic disease differ from those without?

The Risks of Anesthesia

General anesthesia is not necessarily bad. 😊 The biggest two risks of general anesthesia for dogs or cats with seizures are (1) hypotension and (2) negative effect on the seizure threshold. Let’s talk hypotension.
Your goals are to preserve cerebral blood flow, which is largely controlled by the cereal perfusion pressure, which is largely controlled by the mean arterial blood pressure (MABP). MABP is directly related to intracranial pressure (ICP). Thankfully there is a wide range at which MABP will have little negative effect on ICP. MABP between 50-150 mm HG should result in constant ICP, if other parameters are equal. Hypotension can be caused by some of the medications used (I’m looking at you acepromazine) or caused by CO2 levels. If the PaCO2 levels are above 50, a risk of vasodilation occurs which may decrease MABP. Monitoring CO2 can be quite useful to avoid this. If vasodilation occurs, and consequently decreased MABP, perfusion to the brain can be compromised. Hyperventilation will decrease the PaCO2, result in vasoconstriction and maybe lower the ICP. Some references suggest that PaCO2 should be between 30-35 for “appropriate” cerebral perfusion. Big disclaimer today – I am not an anesthesiologist so specific questions about anesthetic protocols should be directed to your local anesthesiologist! Long-standing, serious, hypotension can affect neuronal membranes and in rare situations could cause neuronal cell membrane damage, or a worsening seizure disorder. Thus, try to keep the PaCO2 in a normal range, and monitor blood pressure for pets with seizures undergoing anesthesia. 
With respect to the seizure threshold, isoflurane, diazepam, midazolam, and possibly propofol are neuronal protective. If you have the luxury of choice, consider using one (or all!) of these medications in your anesthetic protocol. If you have a patient with poorly controlled seizures, administration of IV phenobarbital 20 minutes before starting anesthetic recovery may be useful to add seizure protection during the recovery process. ALWAYS go slow! Give the phenobarbital over 20-30 minutes as a slow infusion to avoid severe cardiovascular or respiratory suppression. This drug is closely related to pentobarbital, our common euthanasia solution. Most patients can receive benzodiazepine medication if active seizures are noted during the recovery process. Paradoxycal hyperactivity following benzodiazepine adminsitration occurs rarely but would be a reason to avoid using the drug in the future if a patient exibited these signs. Patients with significant hepatic disfunction such as those with portosystemic shunts should either avoid benzodiazepine drugs due to inadequate metabolism, or be adiminsered a 25% dose. 

Any anesthetic event, even an uneventful one, can put a patient with a known seizure disorder at risk for seizure breakthrough. This risk persists for at least 24 hours following anesthesia but in rare patients it can be longer. Owners should avoid leaving the pet alone for extended periods of time such as traveling by airplane, boarding the pet or other unobserved time in the first 24 hours after anesthesia. Never withhold chronic anticonvulsant medications prior to anesthesia. Bromide can cause vomiting therefore it should be given with a small meal. Patients receiving bromide (liquid) can receive it rectally if they are anesthetized early in the morning and a small snack with their bromide is not possible. Phenobarbital, levetiracetam and zonisamide can be given on an empty stomach without high risk of GI upset.

This topic was suggested by one of your colleagues - thanks for the suggestion! Do you have a topic you wish I’d cover? Please reach out!  Thanks for reading and have a great day!

Limping - Orthopedic or Neurologic?

Limping is often orthopedic in origin however in some situations limping can be of neurologic origin. Nerve root signature (NRS) sign is observed clinically as a non-weightbearing flexion of one limb, during standing, which may also appear like limping when gaiting. The suspected causes for NRS include vascular compression, inflammation or compression of a nerve root. This is most commonly noted in the thoracic limbs but has been reported in the pelvic limbs also.
In a recent study, a group from NCSU evaluated dogs with cervical disc herniations to see what criteria were present when they had signs of a NRS. This study included 47 dogs. Not surprisingly, all 47 had signs of cervical hyperesthesia with signs like ataxia (n=14), intermittent lameness (n=7), tetraparesis (n=2) and tetraplegia (n=1) being observed less frequently. I personally am not sure how you can identify a dog with a root signature sign if they’re plegic…but apparently, they did! Interestingly (to me) the site of disc herniation was C2-C5 in 20 dogs (43%) and C5-T1 in the other 27 dogs (57%). The nerve roots are supposed to arise from the C6-T2 region which is why it would make the most sense that a NRS sign should involve those nerve roots. Why did the C2-C5 region have NRS signs? Perhaps there was tethering of the nerve roots from "tugging" secondary to a cranially located disc. Perhaps anatomically they had a neve root arise more cranial than typical.
Spinal cord compression was mild in the majority of cases but remember it takes a TON of disc material in the cervical spinal cord to result in compression. Mild spinal cord compression is often surgical because the canal is much more voluminous around the smaller spinal cord (which is different from the thoracolumbar spine). Therefore the canal can contain loads of disc material yet the spinal cord has room to scootch over away from the disc, thus resulting in mild compression. Disc material was almost 3x more likely to be located laterally, within the spinal canal, than medially. Additionally, dogs were 2x more likely to have disc material compressing a nerve root compared to dogs without NRS. The last interesting finding is that 75% of the dogs in this study were over 7 years old. Typical chondrodystrophic disc degeneration with resulting herniation occurs in ages 3-7 year old. Is there a relationship between age, site of disc herniation and NRS or was this coincidental? I’m not sure but felt it was worth of comment.
 
Take away message:
Thoracic limb limping is often orthopedic in origin, however NRS should be considered for cases in which orthopedic disease is not identified. Nerve root signature sign secondary to a cervical disc herniation is more likely to be lateralized and therefore referral for surgical correction is strongly recommended to alleviate the compression to the nerve root.
 
Thanks for reading! Are we through deep winter? I’m not sure but I sure hope you’re staying warm! Please reach out with any questions about root signature sign or other neurologic cases. Have a great week!

Heat Tilt, Turn or Neck Turn...so what?

Does a head tilt help with neurolocalization?
 

A recent study by Nagendran et al (The value of a head turn in neurolocalization, JVIM 2023) described 4 distinct areas of neuroanatomic lesion localization for head turn, head tilt and neck turn and looked at head and body position in each of these localizations. If you see a patient with their head deviated to one side yet parallel to the floor, that would be a head turn. If a patient has their head deviated to one side NOT parallel to the floor, we would consider this a head tilt. The head tilt can be anything from 1-90% from the x axis! If the neck is turned to one direction it would be called torticollis and may be (and often is) associated with either head tilt, head turn, or both. This recent article looked at these three signs, in reference to the neuroanatomic lesion localization, with the goal of trying to sort out the underlying neuropathology (totally cool but not "light reading" and therefore saved for another conversation).
Key Points:

• Forebrain disease – The majority or patients had an ipsilateral head turn, with less than ½ of the dogs demonstrating ipsilateral body/neck turn.

• Brainstem disease – All dogs had an ipsilateral head turn, and 5/9 had an ipsilateral head tilt, with a rare dog demonstrating a neck turn.

• Cerebellar disease – All dogs had an ipsilateral head turn and the majority had a contralateral head tilt with a rare neck/body turn noted showing a contralateral neck/body turn.
  

• Cervical spinal cord disease – all dogs had a contralateral head turn along with a majority (6/7) showing a ontralateral head tilt.

Summary:

• Head turn ONLY – consider forebrain disease

• Head turn with neck turn (ipsilateral) – consider forebrain disease, but the neck turn is an inconsistent finding in many dogs with foreain disease.

• Head turn, neck turn AND head tilt – most likely cervical spinal cord disease but cannot rule out cerebellar disease.

• Head tilt only – likely brainstem disease (or peripheral vestibular disease!)

Take Home Points:
A head tilt, head turn, or neck turn is a useful physical examination finding to point you at neurologic disease however they aren’t discretely localizing on their own. Using the information above, you may be able to support a localization noted in concurrence with your other neurologic findings.

Thanks for reading! I made the difficult decision to increase my consultation fees this year so if you didn’t get an announcement please reach out and I can send you the updated fee schedule. Lastly, it’s winter!! That means sometimes travel can be hazardous and cancelations can happen. I don’t charge if we cancel due to inclement weather and will do my best to work your patient into the schedule as quickly as possible afterwards. I appreciate your business very much and do my best to meet your expectations. Have a great week!

Strokes in Dogs

Strokes are an increasingly common cause of seizures and other intracranial signs in dogs (and cats). Why is the diagnosis becoming more common? My theory is that we are simply performing more MRIs, and therefore making the diagnosis more readily, but it is possible that increasing comorbidities or breed related changes may contribute to the increase in diagnosis.

What is a Stroke?
Stroke, or cerebrovascular disease (CVD) occurs when normal brain fuction is disrupted due to hemorrhage or infarction. CVD is typically due to occlusion of an/multiple intracranial vessels however hemorrhagic strokes can occur in rare cases. Around 50% of dogs will have an underlying predisposing facture such as hyperadrenocorticism, hypothyroidism, protein loosing nephropathy, heartworm disease, heart disease (less common as a cause!) or other "hypercoagulable" diseases. The other 50% do not have any identified predisposing factors and are therefore considered to have had an idiopathic vascular event. 

Clinical presentation

• Acute onset, with progression not typically noted after 24 hours (but it can in rare cases)

• Common in older dogs, less common/rare in younger dogs

• Gait changes (hypermetria, ataxia) and seizures are the two most common presenting complaints leading to a diagnosis of CVD

Diagnosis
The best diagnostic tool for CVD is MRI. Indication of vascular occlusion can be seen immediately but tell-tale signs may resolve if imaging is performed too long after the onset of the clinical signs. 

Treatment
Supportive treatment is often the only treatment needed. Supportive treatment may include anticonvulsant drugs, intensive nursing care if non ambulatory, or rehabilitation if gait abnormalities are identified. A neurology consult may help guide treatment for you and the client.

Outcome
The majority of dogs will improve following CVD but time to improvement and degree of improvement is variable, and based on severity of neurologic impairment, and MRI findings. Recurrence can occur, but is less common. We previously though it was rare, but in one study in Japan (see below) 11 of 50 cases available for follow-up had clinical signs of recurrence of disease after a diagnosis of CVD. A persistent seizure disorder is possible following a CVA. Repeated seizures, without the development of other neurologic signs, could suggest a seizure disorder and NOT progression or regression of disease. 

Other Cool Facts
The Japanese study referenced below noted August and December as months with significantly higher stroke diagnoses, compared to all other months, and October as the lowest month. Interesting!

Thanks for reading. Have a great week and keep those consults rolling! With the onset of winter weather, mobile neurology consultations may become challenging at times. Remember a video consult may suit your needs if I cannot be on site due to inclimate weather! Stay safe and warm out there this week, folks!

Reference: Ozawa T, Miura N, Hasegawa H, et al. Characteristics of and outcome of suspected cerebrovascular disease in dogs: 66 cases. JSAP (2022)' 63, 45-51.

Hypokalemia Myopathy and Positioning Head Tilt in Cats?

I read an interesting article recently about positioning head tilts in cats with hypokalemia myopathy (https://doi.org/10.1177/1098612X231175761) This isn't likely to be something you encounter often in practice, but I hope you will also find it an intesting read nontheless. 

Hypokalemic myopathies are common in cats and often result in signs of weakness including cervical ventroflexion and/or tetraparesis. We can see hypokalemia secondary to renal disease, hyperthyroidism, dietary insufficency, chronic vomiting/diarrhea, and other metabolic causes. The subsequent myopathy occurs due to overpolarization of the muscle sarcolemma resting membrane potential making it resistant to depolarisation. Without depolarization, there is no muscle contraction and we see clinical weakness. 

When the head is turned, the cerebellum (specifically the nodulus and uvula) receive input from the vestibular nuclei, who in turn receive sensory information from the stretch receptors in the cervical muscles, on the whereabouts of the head and neck. This allows the cerebellum to modify the head position so that the head remains paralell to the ground as it is turned. With positioning head tilts, the head tilts to the opposite direction that the head is turning. When looking straight, no head tilt is observed. When turning right, the head tilts slightly to the left, for example.  

This article described 14 cats who had a positioning head tilt obseved on neurologic examintation AND had concurrent hypokalemia. One cat had an MRI and no cerebellar lesions were noted. Does that mean the others didn't? No, of course not. However, when the potassium was normalized the positional head tilt resolved. This would suggest cause and effect but isn't definative. The authors supposed that the muscle firing in the spindle fibers (the very small muscles located in the bigger muscles that convert stretch to neuronal impulse for sensory information) weren't able to depolarize appropriately. This lack of depolarization resulted in an absence of information about the whereabouts of the cervcial muscles (and those attached to the head, specifically) and didn't allow the cerebellum to modify head posture when turning. Pretty cool, huh? Although this is just a therory, I personally think it is pretty slick and clever. 

Take home message:
What do you do with a positioning head tilt in a cat? Look for hypokalemia and if identified, address it! 

Do you know that I'm in charge of my own schedule? I'm not corporate or owned by anyone! So if you cannot find a suitable time on the scheduler please email me! I will do my best to find an earlier time to accommodate a more urgent case. Some of you lovely, considerate, folks have told me that you hate to bother me to ask. If you're one of those, please know you're not a bother. We're both trying to work on behalf of your patient! 
Have a great week. I hope you enjoyed this little TidBit as much as I did. I look forward to working with you soon!

How to Localize a Cranial Nerve

As we sit here at the head of the year, I cannot think of a better time to review the cranial nerves. (Yes, I like cheesy jokes. I have kids. Here's another: what's the best present? See the bottom for the answer.)

First important thing to remember about cranial nerves: all cranial nerves except I and II have cell bodies associated with a specific brainstem segment. You might even argue that CN II localizes to the thalamus, which is an embryological part of the brainstem but...well, then we should have a coffee and get to know each other better!  Let's stick to the idea that CN III-XII have cell bodies in specific brainstem segments, thus making it possible (dare I say easy??)  for us to localize a lesion to either a specific brainstem segment OR the peripheral nerve. 

What are the names of the brainstem segments, again? (Mesencephalon, metencephalon, myelencephalon). Okay, whew! Now that that is over, how do you decide if a deficit is coming from the nerve nucleus in the brainstem OR the peripheral nerve?

Take the following steps:

1. Identify the cranial nerve affected (i.e. facial nerve = CN 7).

2. Identify the segment of brainstem associated with the nucleus of this cranial nerve. Don't remember what cranial nerves are associated with which brainstem segment? Midbrain = CN 3,4; Pons = CN 5, Medulla = CN 6-12

3. Are any ipsilateral long tract deficits (postural reaction deficits, hemiparesis) or mentation changes (obtunded, stupor, coma) present?

   1. If yes, the lesion is in the brainstem segment associated with the cranial nerve (i.e. medulla).

   2. If no, the lesion is affecting the peripheral portion of the affected nerve

Guess what? You can apply these steps to any deficit affecting CN III-XII. Yay!
 
Do you need help performing the neurologic exam? I'd love to help! Looking for the answer to the joke? The answer is: a broken drum! You just cannot beat it. Thanks for reading and Happy New Year!

I am Thankful For You

Thank You and Happy New Year


As we near the end of 2023, I'd like to take this moment to thank you. Thank you for welcoming me into your clinic, for subscribing to the TidBit Tuesday emails, for providing great feedback on cases we've seen together AND on the TidBit Tuesdays that spoke to you, for allowing me to help care for your patients and most importantly, for being the kind, caring and thoughtful vets that you are! It is a pleasure to work with you, see patients with you, consult with you, and learn along with you. I hope you had a good 2023 and that 2024 brings joy, health and happiness to you and those you love. 

Happy New Year! I am excited for 2024 and look forward to working with you soon!

When is Lameness not Orthopedic?

Lameness is typically orthopedic, as we know, but there are times when this isn’t true. How do we know when this is true? To answer this question, I’d love to go through a case with you today.

Signalment: 11 year old FS Labrador

History: She has a 4 week history of right thoracic limb lameness. She is a hunting dog, and signs were noted after a busy weekend in the field. On initial evaluation, mild discomfort was appreciated in her elbow therefore carprofen was started. Clinical signs did not improve; they worsened. She became intermittently non-weightbearing lame in the right limb. All other limbs appeared normal. Additionally, she started helping when laying down or rising from laying. At this point, I stepped into the game. What am I looking for to suggest this might be neurologic in origin?

Neurologic Examination:

Mentation: BAR

Cranial nerves: miosis OD, did not dilate in a dark space. Remaining CN normal.

Gait: Ambulatory, moderate right thoracic limb lameness. When toe touching, the limb was touching on tiptoe only.

Reflexes: Reduced withdrawal distal to the elbow on the right (unable to flex the carpus or elbow completely during withdrawal but able to mechanically flex both joints when I flex them), unable to detect triceps reflex on either side, remainder normal. Absent cutaneous trunci reflex on right, normal on left. Normal reflexes both pelvic limbs.

Postural reactions: Normal paw replacement in left thoracic limb and both pelvic limbs. Unable to assess paw replacement in the right thoracic limb due to non-weightbearing status. Reduced hopping on right thoracic limb compared to left thoracic limb.

Palpation: No spinal pain, normal cervical ROM.

What is the neuroanatomic lesion localization?

The first question is always, is the problem neurologic in origin? She has evidence of reduced reflexes so I would suggest, yes, it is. Essentially, our abnormalities are focused on that right thoracic limb with the addition of miosis OD and absent c. trunci right side.

Reduced withdrawal in the thoracic limb suggests a radial nerve injury/damage. Even though signs are distal to the elbow, the lesion could still be proximal, and neurodegeneration has occurred distally. Is the damage inside the spinal canal (central) or in the peripheral nerves (brachial plexus)? To answer this question, look at the right pelvic limb. Do you see any paw replacement deficits or weakness in the right pelvic limb? These are the long tracts going from the limb to the brain and the must pass right through C6-T2 and C1-C5 as they do so. If the lesion is in the canal, we should see paw replacement deficits in the right pelvic limb. We don’t, so the lesion is more likely in the radial nerves after they have exited from the canal.

What do we do with the miosis? The sympathetic pathway to the eye is as follows: thalamus à brainstem à cervical spinal cord à exit T1-T3 à join vagosympathetic trunk and ascend to the head à ganglion  à go through bulla to jump on CN 5 (trigeminal) à end in the iris for dilation. The radial nerve exits from segments C6-T2, which would cross over with T1-T3 and therefore we could make an argument that the miosis is secondary to involvement of this segment of the radial nerve.

What about the c. trunci? This one is pretty simple to understand once we refresh our memory of anatomy. Cutaneous trunci reflex is a simple spinal cord reflex that uses the dorsal sensory spinal nerves as afferent (sensory), and lateral thoracic nerve as efferent (motor). The lateral thoracic nerve arises from C8-T1. This fits with our assumption of a C6-T2 right sided neuropathy because loss of the lateral thoracic nerve on one side would cause an absent cutaneous trunci reflex.

Neuroanatomic lesion localization: Peripheral C6-T2 neuropathy/radiculopathy.

The differential diagnoses for this case were a lateralized intervertebral disc herniation, neoplasia, much less likely neuritis (infectious or inflammatory) and hypothyroidism. As it turns out this dog was diagnosed via MRI with a mass in the right brachial plexus. The owners elected amputation and it was determined to be a nerve sheath tumor. Why did the signs appear acutely? It’s not completely clear but my guess is that the dog was already decompensated slightly, and the heavy work caused inflammation or maybe even hemorrhage around the mass that resulted in an acute exacerbation.

That’s it for now! Reach out if you have any questions about this case, or any other case! I look forward to working with you soon. Have a great week!

Non-Convulsive Seizures in Dogs

Non-Convulsive Seizures in Dogs and Cats With Cluster Seizures

This week we're going to dig into non-convulsive seizures in dogs a bit before we jump off of the seizure bandwagon and back into other topics in neurology next week. (Sorry to the surgeons that read these!) A recent study out of Germany by Tastensen et al (DOI: 10.1111/jvim.16953) evaluated nonconvulsive seizures in dogs and cats with cluster seizures. A few definitions, first....

Cluster seizures: 2 or more seizures within 24 hours in which pets regain consciousness between seizures. 
Status Epilepticus (SE): Seizures lasting for longer than 5 minutes or 2 or more seizures in which consciousness is not regained. 
Nonconvulsive seizures (NCS): no visible somatic or autonomic manifestation of seizures with evidence on EEG. 
Nonconvulsive status epilepticus (NCSE): no visible somatic or autonomic manifestation of seizures, with evidence on EEG and the seizures are lasting longer than 5 minutes. (yikes!)

This study evaluated 26 dogs and 12 cats with EEG monitoring following cluster seizures and found 11 of the animals (9 dogs, 2 cats) had NCS. Of these 11 dogs and cats, 4 dogs and 2 cats (16%) had NCSE. They found repeated doses of benzodiazepine drugs and levetiracetam did not break the seizures. Only inhalant anesthesia with propofol induction resulted in a return to baseline EEG. 

Six of 11 animals had a decreased level of awareness and a few of them had mild twitching of an ear which could have represented the somatic movement of the seizure. Sadly, this group had a much higher mortality rate (73% NCS; 67% NCSE) than the general population of dogs without NCS or NCSE (27%). Overall, cluster seizures have a higher mortality rate than for dogs or cats without cluster seizures (~40%) as well. None of these patients died as a result of NCSE or NCS however several were euthanized. 

The seizure etiology was more often structural epilepsy (neoplasia, encephalitis, malformation, vascular cause or trauma) and accounted for 22/38 (58%) of the animals in the study. About 18% (7/38) had idiopathic epilepsy, 11% (4/38) had unknown epilepsy and about 18% (7/38) had reactive seizures. Does this mean that dogs and cats with structural epilepsy are more likely to have cluster seizures, or does it mean that the prognosis is inherently poorer for animals with structural epilepsy? If the prognosis is poorer, do clients elect humane euthanasia when in a situation of NCSE more readily, driving up the mortality rate, or does the disease make it harder to treat? Non-convulsive epilepsy is more common in humans with cluster seizures as well, and has a higher mortality rate than people without NCE or NCSE. I don't have the answers to these questions but pose them as a way of critically reviewing the data provided.

Take home message:
If you have a dog or cat with a history of cluster seizures and they are persistently, mentally inappropriate (obtunded, stupor or coma) after stopping the physical appearance of the seizure consider nonconvulsive seizures. Inhalant anesthesia would be recommended however without additional diagnostic testing (such as MRI or spinal tap) it would be unknown if there is high intracranial pressure from the underlying disease which could increase the risk of complication with anesthesia. So what do you do in general practice? If the owner wants a referral for 24 care - start there. If not, consider a bolus of diazepam or midazolam. OR you could monitor for 1-2 hours to determine if the change in behavior is secondary to postictal changes. 

Not sure how to manage a seizure case? Feel free to email or call me or schedule a neurology consult! Please always text or call if it is an emergency; I don't check my email very often during the day.  Have a great rest of your day!

Once Daily Phenobarbital for Cats?

A study by Dr. Mojarradi et al, out of Sweden, was recently published in the Journal of Feline Medicine and Surgery reporting on once daily phenobarbital administration for cats with seizures. The reported half-life of phenobarbital in cats is 43-72 hours which could suggest once daily treatment is possible, however based on pharmacokinetic data twice daily dosing has been the standard of care. This retrospective study questioned if this was necessary. 

This study was a retrospective review of 9 cats up to 3 years from enrollment. They tracked the number of seizures before starting phenobarbital (unfortunately for an unknown amount of time) and compared that to the number of seizures after starting phenobarbital. The cats were required to have 2 or more seizures, separated by at least 24 hours, prior to starting phenobarbital however the frequency and duration of the seizure disorder for each cat isn't known. They do comment that 6/9 cats had 1 or more per month prior to starting phenobarbital. Phenobarbital was started at a mean dose of 1.8 mg/kg PO q24h, the mean serum concentration of phenobarbital was 11 ug/ml (range 6-17) at about 1 month (range 19-54 days). All but 1 cat was seizure-free at that first follow-up. The second and third follow-up appointments, roughly 1 year apart, showed a few more seizures in the time range however overall 8/9 cats were considered to be in seizure remission (no seizures for more than 12 months) at the end of the study. Seizure remission, as defined in this study, was less than 1 seizure every 12 months. If they started at 1 seizure/month, and ended at 1 per year that is a pretty remarkable improvement! So remarkable, I wonder if the phenobarbital is responsible for that shift, or not.
My questions:

• Could such a low serum phenobarbital concentration cause such a dramatic response?

• Could this be the natural regression to the mean (shifts that are unrelated to intervention)?

• Did the retrospective nature of the study include only cats that did well on once daily phenobarbital, otherwise they would have taken twice daily phenobarbital and therefore been excluded from the study? Was this group of cats bound to do well, in other words, and it wasn't due to medication?

Another study by Pakozdy (https://doi.org/10.1177/1098612X12464627) noted that over time, most cats have a natural reduction in seizures while on anticonvulsant drugs. They tracked seizures in cats over a 10 year period and noted that most improved, some were seizure-free and some stopped medication. About 16% of the cats that stopped medication needed to have it restarted due to a return of seizures. 

The data reported in the study from Sweden suggests that we could administer phenobarbital once daily but the results are so remarkable (marked seizure improvement in a short period of time, low serum drug concentrations) that I feel compelled to repeat this study with a different, perhaps large, cohort of cats and make sure this is reliable. My advice: don't switch to once daily just yet!

Thanks for reading! I love managing seizures so please schedule a consult if you have a case that you'd like more assistance with seizure management. I'm happy to help!

Status Epilepticus in Cats

Last week we looked at the ACVIM consensus statement for the treatment of status epilepticus and focused on the different stages, and the treatment algorithm outlined by the committee. This week, I thought we should look at this statement through the lens of cat care. Please refer to the article for more details - it's a good one! (DOI 10.111/jvim.16928)
As a reminder, all available literature was reviewed and classified according to it's level of evidence. Studies with a high level of confidence for or against a specific treatment included treatments in which 2 or more clinical studies with a high quality score (more about that in a minute) evaluated this specific intervention. Moderate level of evidence for a treatment needed 2 or more studies with moderate quality score or 1 study with high quality score. A label of low evidence for a specific intervention was used in situations where 2 or more studies with low-quality score were reviewed or 1 with a moderate quality score without any high quality score articles identified. A label of conflicting evidence was used when 2 or more studies, usually with a high quality score, were reviewed and found to have results in conflict. Finally, the label "absence of evidence" is pretty self explanatory. The quality scores were numeric scores assigned each study based on clearly defined criteria such as EEG or clinical confirmation of seizure cessation for each study reviewed. 

Definitions
The definitions are the same for cats as they are for dogs. Any seizure longer than 5 minutes is considered status epilepticus (SE). Similarly, cluster seizures are 2 or more seizures within 24 hours in which consciousness is regained between the seizures. Okay, off to a good start. 

Antiseizure Therapy for Cats
Figure 3, in the aforementioned article, is a pyramid of hierarchy for therapy recommendations for cats in status epilepticus. Sadly, there are no studies with a high level of confidence for any intervention. This means that no high quality studies, evaluating seizure cessation in cats, were identified. We need to fix this! Intravenous bolus or CRI of midazolam, intravenous bolus of diazepam, intravenous levetiracetam, intravenous phenobarbital and inhalant anesthetics were considered to have moderate level of confidence for cats. This suggests that there is at least clinical evidence (if not EEG evidence) that supports these treatments for SE management in cats. Oral levetiracetam, intravenous bolus or CRI of phenobarbital and propofol had low level of evidence suggesting that giving these drugs, via these routes, to cats with seizures is not supported by the literature. Oral midazolam, intravenous CRI, oral or endotracheal diazepam were not supported by the literature. Not surprisingly, there were many drugs that were withheld from analysis due to a lack of evidence for cats. 

As I mentioned last week, the authors made the following statement:
"Although both benzodiazepine drugs are potent and safe for the management of SE in dogs and cats, midazolam may be considered a more potent or safer benzodiazepine drug than diazepam."
Based on this, and my own clinical impression, if you aren't carrying injectable midazolam yet, now is a good time to consider adding this to your cabinet!

The authors also specifically addressed CRI reduction and recommended reducing by 25-50% every 4-6 hours after a cat (or dog) has been seizure free for at least 12 hours, preferred 24 hours. It is always preferred to taper the medication, not stop abruptly, whenever feasible. 


I think that is enough for today. I hope you had a good holiday, didn't go too crazy on Black Friday, and I look forward to working with you soon!

As always, the holidays bring many challenges. If you cannot find a suitable time for a consult using my online scheduler please reach out to me via email. I will always try to accommodate your request if I can. 

Status Epilepticus Consensus Statement 2023

Status Epilepticus and Acute Seizure Management Consensus Statement 2023

The ACVIM Consensus statement about status epilepticus (SE) was published this past summer (2023) and I felt it was applicable to all of us faced with acute seizure management. They dove right in and addressed the need for a definition of a prolonged seizure as one occurring for longer than 5 minutes. The human equivalent of our International Veterinary Epilepsy Task Force (IVETF) is the International League Against Epilepsy (ILAE). The ILAE has recently also revised their definition of SE to any seizure longer than 5 minutes as well. Previously, SE was defined as anything between 5-30 minutes. Thirty minutes was the cut off because at that point, brain damage is common. The reason for adopting the 5 minute rule was to 1) minimize the risk of systemic and brain complications associated with continuous seizure activity reaching up to 30 minutes; 2) prevent worsening of the prognosis and drug resistance associated with increasing duration of uncontrolled seizure activity and 3) limit any potentially unfavorable outcomes and adverse effects associated with the prolonged administration of multiple therapeutic interventions. 

Status Epilepticus is divided into 4 stages:
1) Impending (occurs at 5-10 minutes of seizures) - there is neurotransmitter imbalance and ion channel opening/closing. Animals are likely to be responsive to first line anticonvulsant drugs (ACD) during stage 1. 
2) Established (occurs at 10-30 minutes)- Inhibitory neurotransmitters are reduced, the receptors for the inhibitory neurotransmitters are internalized and there is upregulation of NMDR and AMPAR. Some animals may still be responsive to first line ACD, but most will be responsive to second line ACD.
3) Refractory - (occurs > 30 minutes) - There is a sustained imbalance between inhibitory and excitatory neuropeptides with BBB drug transporter upregulation. Most pets will not be responsive to first or second line ACD, but should be responsive to third line ACD. 
4) (Super)refractory - (occurs > 24 hours) - There are gene expression alterations and animals are expected to be refractory to all ACDs. 

What were considered first line ACDs? IV benzodiazepine drugs were considered the most effective and safest for in-hospital use and intranasal benzodiazepines are the preferred treatment for out-of-hospital treatment. "Although both midazolam and diazepam are potent and safe for the management of SE in dogs and cats, midazolam may be considered a more potent or safer benzodiazepine drug than diazepam." There we go!

They provided a list of the steps to follow, based on the evidence reviewed, when treating SE. I have repeated it here, but encourage you to read the entire article if you treat SE regularly as there are loads of pearls of wisdom peppered throughout the paper.

Steps to follow for SE:

• Give midazolam or diazepam IV. A benzodiazepine bolus is effective if the seizure stops < 5 minutes after administration and no relapse occurs <10 minutes

• If seizure activity is controlled with a benzodiazepine drug but recurs 10-60 minutes later is considered recurrent SE

• Recurrent SE, or those that don't respond to the first bolus of benzodiazepine, should get a second IV dose of benzodiazepine drug

• If seizures persist after two bolus, administer a 3rd dose immediately followed by a CRI. Dogs = midazolam or diazepam CRI is acceptable; Cats = diazepam should be avoided. 

• If seizures still persist, administer a 4th dose of benzodiazepine and administer a second line ACD

• Second line ACD include levetiracetam IV, followed by phenobarbital IV and lastly fosphenytoin IV. Only administer the subsequent drug if the prior failed to stop the seizures. 

Note: Levetiracetam or phenobarbital IV can be started after step 2 above if long-term maintenance is desired for either medication. They do not need to be reserved for second line use only. 

I think that is enough for today. I'll go through some more data from the study in another TidBit Tuesday. I hope you enjoy the rest of this week, have a safe, relaxing holiday and look forward to working with you soon!

What is Cognitive Dysfunction in Cats?

Almost twenty years ago when I left my residency and started out as a newly minted neurologist, feline cognitive dysfunction syndrome (CDS) was not on my radar. That has changed. As we learned more about aging in cats, CDS has become a more recognized disease by yours truly, as well as many others. If you're like me and need a Tidbit-Tuesday style refresher...read on!

What is cognitive dysfunction syndrome?
Cognitive dysfunction syndrome (CDS) is a term used to describe deterioration of mental capabilities associated with age.  Clinical signs of cognitive dysfunction can also be associated with other age-related illnesses (e.g. osteoarthritis, structural intracranial disease such as neoplasia, or cardiovascular disease) which makes it difficult to diagnose. See table 1 for an outline of behavior changes seen in cats with CDS.
The underlying etiology of CDS is yet unknown. Causes such as oxidative stress/damage, neurodegeneration  and vascular changes are among the leading hypothesis for human and canine CDS, and therefore suspected to be similar in feline CDS.  Deposits of extracellular B-amyloid and intracellular accumulation of microtubule-associated protein tau have been seen in human patients with cognitive dysfunction. Similarly,  B-amyloid deposits and increased tau have been detected in aged cats with cognitive decline, however the significance remains unclear. 

What are the clinical signs of cognitive dysfunction in cats?
There is a handy article, published in the Veterinary Clinics of North America in 2020 by Dr. Miele and associates that echoes what others have been reporting in a very concise little table. (See reference at bottom) I have replicated this table, with a few modifications, here. Note: There are other signs such as decreased appetite or thirst, that don't usually drive an owner or veterinarian to seek consultation from a neurologist so I haven't included them here. 

Table 1: Clinical behavioral changes associated with CDS in cats.Increased vocalization, especially at nightAltered social interaction and relationships, either with other or other pet. Altered sleep/wake patterHouse soilingSpatial Disorientation or confusion (i.e. forgetting the location of the litter box)Temporal disorientation (i.e. forgetting if they have been fed)Altered activity (i.e. aimless wandering)AnxietyLearning and memory dysfunction

How is CDS in cats diagnosed?
Oh, this is as tangled of a web as the tau proteins we chase. (A little CDS humor here...the tau proteins can cause the "tangles" seen in human CDS!). Currently, the diagnosis is made by ruling out structural brain disease and systemic causes for diseases that mimic CDS. This may include complete blood count, full biochemistry panel including thyroid screening, urinalysis, chest radiographs, blood pressure assessment, brain MRI and possibly a spinal tap. Imaging changes associated with canine CDS include increased depth of the sulci, dilation of ventricles secondary to neuronal loss (called ex vacuo hydrocephalus) and a measurably small interthalamic adhesion. Exclude everything else, and it's probably CDS.

How can we help these cats age easier?
Currently, there are no proven treatments for feline CDS.  The addition of antioxidants (B vitamins, vitamin C, other) as well as fish oil were evaluated for use in cats in one study and showed promise. The use of S-adenosyl-L-methionine (SAMe) has been recommended for cats based on a study that identified improved performance on cognitive testing. This study only found significant improvement in cognitive function testing in the least affected cats. In addition to medical management, environmental management with ready access to food, water, litter box and areas of comfort (beds, hiding spots) is recommended. Environmental stimulation with low impact toys, or bird feeders in which the cat can choose to ignore any activity if they do not feel inclined to engage, are recommended. Finally, focused veterinary visits can be important for cat owners to feel supported through the aging process. Focus your exam to specifically evaluate body weight, urine production (to assess for signs of dehydration), behavior changes and mobility.This may help detect signs earlier in the course of disease and to identify concurrent morbidity that may contribute to, or be confused with, cognitive dysfunction.

Did I forget anything? Most of you treat and see this more than I do. What have you used (successfully, or not) for treatment? 

Reference:
Miele A, Sordo L, Gunn-Moore DA. Feline Aging: Promoting Physiologic and Emotional Well-Being. Vet Clin North Am - Small Anim Pract. 2020;50(4):719-748. 

Does the Duration of Diazepam and Propofol CRI in Dogs Matter?

Does the Duration of CRI Matter?

If you work in a 24-hour facility, odds are high that you've employed a constant rate infusion (CRI) to control seizures in dogs with cluster seizures or status epilepticus. A recent article evaluated the duration of a CRI of diazepam and propofol to see if there was a superior choice.

Why could duration matter?

On one side, the longer a pet is on a CRI (12 h or 24 h), the longer they must remain in hospital which incurs more charges. However, most dogs will have a recurrence of seizures within 12 hours of hospitalization according to prior studies, so if you run a CRI longer perhaps the less chance they have to have another one and thus return to hospitalization. 

Materials and Methods

Cagnotti et al (Frontiers, 2023) collected 73 dogs and separated them into two experimental groups. The first group received diazepam CRI for 12 hours, the second propofol for 12 hours. No standard dosing was employed for either group, just the duration. These were compared to a prior study of dogs with identical inclusion criterial in which the CRI was continued for 24 hours. 

Results

No difference in outcome, or hospital duration was noted between the 12 hour CRI group (both diazepam and propofol) and the 24 hour group. Surprisingly, the dogs receiving the 12 hour CRI still had a 56 hour hospitalization! I cannot locate any data on breakthrough seizures after stopping CRI in either group but one might suspect this occurred to result in a 56 hour hospitalization for the 12-hour group. Either that, or the CRI dose was much higher and therefore had more step down doses compared to the 24 hour CRI? Those are my suppositions, not verified by data in this study. 

Take Home Message:
It is well established that a CRI should be employed for dogs having cluster seizures or status epilepticus and that 2 step-down doses are typically recommended to avoid withdrawal seizures when stopping. That said, this paper suggests that a 12 hour CRI is comparable to a 24 hour CRI. Personally, I typically start with 0.25 mg/kg/hr diazepam CRI for 12 hours and then step down in 50% increments until the dose is below 0.1 mg/kg/hr. This data would suggest that this is an appropriate approach but I think it is 'loosely' supportive!

Reference: Cagnotti G, Ferrini S. Duration of constant rate infusion with diazepam or propofol for canine cluster seizures and status epilepticus. Frontiers in Vet Sc Aug 2023. 

Thanks for reading! I hope you have a great week and I look forward to working with you next week when we're back stateside again!

Tick Paralysis and Dogs

The ticks are still here but owners may have stopped applying topical treatments. So fall is the time to be on the look out for Tick Paralyses (okay, really anytime but now isn't a BAD time to be aware)!

What causes Tick Paralysis?

Salivary transfer from a Dermacentor (in America) and Ixodes (in Australia, for my Australian readers) will result in neuromuscular blockade. How it actually works is really pretty ingenious. (Skip this next part if you're in a hurry.) At the presynaptic terminal, acetylcholine packets must be released into the neuromuscular junction so they can then bind to the post synaptic (muscle) membrane receptors. The acetylcholine binds to the presynaptic membrane using specific proteins as well as calcium. The saliva from one of the aforementioned types of ticks will interfere with acetylcholine release at the presynaptic terminal by binding calcium. Amazing, really.  

What are the common clinical signs?

If you cannot release acetylcholine from the presynaptic membrane at the neuromuscular junction, what can you do?  Exactly...nothing. 

Therefore clinical signs are an ascending pelvic to thoracic limb flaccid paralysis. No reflexes, no motor, no paw replacement, nada. These signs begin 5-9 days after exposure to the tick saliva. Cranial nerves are RARELY affected. This is important because botulism more commonly affects cranial nerves and this can be one way to try to differentiate between these two diseases. 

How do you make the diagnosis?

1. Find the tick.
2. Remove the tick.
2.5 (Apply Frontline/Bravecto/other)
3. Clinical improvement should begin 24-48 hours after tick removal.
No specific testing is available to confirm the diagnosis. 

I once had to find a tick on an Old English Sheepdog waaaay back in the year 2000. Topical tick treatment wasn't as prevalent then as it is now, so our solution was to shave the dog. We found the tick between the dog's toes. (Insert eye rolling here!!) In 2023, I suggest applying Frontline/Bravecto (your choice of topical flea treatment) first then perform a non-invasive tick hunt and monitoring for clinical improvement. If ineffective after 48 hours you can either commence a thorough tick hunt, or search for other causes of flaccid paralysis. (Or, call me for a neurology consultation!)

How do you manage patients flaccid paralysis?

Flaccid paralysis means that the animal does not have reflexes, or voluntary motor. As such, these animals may be at risk of respiratory failure due to loss of intercostal muscle function. Frequent CO2 monitoring, respiratory watch and ventilatory support if needed can be very important in the early stages of disease. Due to the rapid recovery common with tick paralysis, most patients do not need long-term intensive nursing care or physical therapy. 

Thank you for reading!  I appreciate you, and all that you do for your patients. Please note that I'm currently in Australia and will have delays in email response and NO telephone service. You can message me through FB if you want to but otherwise email is best. Thanks!!

To Seize is to Grab, to Seizure is to Convulse

Seizures and Deficits...What to Do?

Today, we have, back by popular request, another lesion localization practice case! Enjoy!!

Signalment: 7 year old MC Pitbull-X (maybe Boxer dog?)
History: The dog presented with a history of 2 seizures, 1 day apart. Since the seizures, the dog has been walking compulsively to the left, and appears to bump into objects. Although a decreased appetite has been appreciated, the dog is still eating when hand fed. 

Physical Examination: unremarkable

Neurologic Examination:
Mentation: Obtunded
Cranial nerves: Absent menace OD, intact PLR OU, mild head turn left, remainder normal. 
Gait: Ambulatory with intermittent compulsive circling to the left. He is able to walk to the right when asked but will not continue the circles without inspiration. 
Postural reactions: normal all limbs.
Reflexes: Normal all limbs.
Palpation: no spinal pain and normal cervical ROM  and tail jack. 

Neuroanatomic lesion localization (NALL) Practice

Let's look at the examination is sequence as it is listed above. If you wish to use the table format that I prefer, please look at the tables provided in the Small Animal Neuroanatomic Lesion Localization Practice Book (publisher CABI, date 2022 by yours truly). We'll discuss it in conversation format for this TidBit Tuesday. 

Seizures: Seizures ALWAYS localize to the forebrain and are not readily lateralized (left or right side). 

Obtunded: reduced mentation is noted with lesions in the forebrain and brainstem. This is NOT a clinical sign of cerebellar, spinal cord or neuromuscular disease, nor a non-neurologic finding. This narrows our lesion localization to forebrain or brainstem.

Cranial nerves: The menace pathway, in it's most basic sense, involves CN 2, the forebrain and CN 7. PLR involves CN 2, midbrain and CN 3. The blink reflex is not states as being abnormal above (blink reflex: CN 5 and CN 7) therefore by process of elimination, the menace deficit OD is most likely due to a forebrain lesion. The second part of the story is lateralization. Only the right eye is affected. This is a crossing tract (mostly) which means that the lesion should be on the left side of the forebrain.

Gait: The compulsive circling to the left is localized to the forebrain and, rarely, vestibular system. Localization to the vestibular system is most likely when a head tilt is present. Without a head tilt, I would consider a forebrain lesion most likely and they circle TOWARDS their lesion. This would further support a left forebrain lesion. 

NALL: Left forebrain

How'd you do? Did anything surprise you with the NALL? If you enjoyed this case, thank your colleagues for suggesting a seizure NALL case for practice. :)

As a reminder, I will be out of the country starting next week through November 14th. I will be available by email ONLY (no cell phone service) and will be doing my best to keep up on emails. Please expect minor delays in my response because I will be lecturing and we'll be on different time zones but I will do my best to be as responsive as possible. Have a great week!

T3-L3 Myelopathy in a German Shepherd Dog

In July, my colleague Dr. Sam Long and I held a CE seminar on neurology for 2 days here in lovely southwest Wisconsin. During this conference, we discussed a case that I'd love to present to you today. If you were at the conference, you may recall the ensuing debate! Here we go...

Signalment: 9 year old FS German Shepherd Dog
History: 6 month history of slowly progressive paraparesis and proprioceptive ataxia in the pelvic limbs. This dog started with scuffing of one pelvic limb when walking, and progressed to scuffing both pelvic limbs, and then weakness, which had progressed to a moderately poor ambulatory state by her evaluation in clinic. 
Physical examination: mild thickening of both stifles and a history of TPLO in one stifle many years ago. 

Neurologic examination:
Mentation: QAR
Cranial nerves: normal
Gait: Ambulatory with moderate proprioceptive ataxia and mild to moderate paraparesis, worse on the right PL with mild limping on the right pelvic limb. 
Postural reactions: Absent paw replacement test in both pelvic limbs, normal in both thoracic limbs
Reflexes: Normal all limbs, normal c. trunci bilaterally. 
Palpation: Non painful spinal palpation, tail jack or cervical ROM

Neuroanatomic lesion localization: T3-L3 myelopathy. (Not sure how we got here? Please see last week's TidBit Tuesday for a review on neuroanatomic lesion localization practice for the spinal cord.)

Differential diagnoses: Degenerative myelopathy, intervertebral disc herniation (type II), neoplasia. 

Diagnostic plan: We proceeded with a minimum database, which was unremarkable. The MRI showed a mild to moderate disc herniation mid-lumbar, more on the right side. The disc herniation was felt to be a possible cause. Concurrently, the clients had submitted a SOD1 gene test, which is the genetic test available to look for one of the mutations suspected to cause degenerative myelopathy in German Shepherd dogs. The results came back as a homozygous at risk (i.e. she has the genetic mutation). So...now what? We have a dog with evidence of two possible causes for the T3-L3 myelopathy. 

On the one side...
If the clinical signs are due to the disc herniation, surgical correction may provide clinical improvement and stabilize progression. That said, there is a risk of worsening the neurologic status with anesthesia and surgical decompression, especially with chronic compression. Many dogs are worse after decompression for a week or so before then gradually improving. 

On the other side...
If clinical signs are due to degenerative myelopathy (DM), the dog is expected to progressively worsen regardless of the treatment provided. Anesthesia *might* worsen signs, but that isn't clear. Certainly surgery won't help! 

What do we do? We had a lively debate and ultimately it came down to which carries more risk - doing nothing in the face of a possible surgical disease, or doing surgery (and risking making them worse) in the face of a medical disease. What would you do? 

The clients ultimately elected not to proceed with surgery and I supported this decision, however Sam had an opposing viewpoint and would have preferred surgery. It isn't clear cut, and neurologists debate this problem in rounds around the world! I'm grateful that we have many folks working to find solutions to problems like these and will be sure to pass along any new information on diseases like chronic disc herniation or degenerative myelopathy. 

Thanks for reading! Please reach out with thoughts or opinions on the topics, recommended future topics, or questions as they arise.

Please note that I will be out of the country, doing a repeat of this CE but in sunny Australia for 2 weeks, and will not be available by telephone. My email will still work :) but please be patient with expected delays. I leave at the end of October and return mid-November so be sure to book pending consults before I go! Have a great week!