Page 556 - ONLINE PROCEEDING BOOK WSAVA 2017
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An Urban Experience
Diagnosis
Diagnosis should ideally be based on a thorough anamnesis with the owner’s description of one or
more of the above symptoms, a clinical examination to rule out dermatological conditions (eg. ectoparasites, dermatitis and allergy) and otitis externa as a cause of the scratching, and a neurological examination to rule out other neurological differential diagnosis; here an
MR scan of the neurocranium and cervical spinal cord
is recommended. The characteristic MRI  ndings are cerebellar indentation or partial herniation and SM. SM has a predilection for the cervical spinal cord segments C2 – C4 (75 % of cases), but dogs with cervical SM also present with thoraco-lumbar (76 %) or lumbar SM (49 %). The clinical manifestations of SM and the degree
of pain are linked to the syrinx diameter relative to that
of the spinal cord and the potential asymmetrical syrinx distribution as directed towards the dorsal horns of the spinal cord. The greater the syrinx to spinal cord ratio and the more asymmetrical distribution on the transverse images, the more severe are the symptoms and signs of pain (7). In addition to CM and SM, the MR images often reveal concomitant kinkingcurvature of the spinal cord in the cranio-cervical junction, ventriculomegaly and otitis media with effusion. The clinical signi cance of these  ndings is subject to continuous debate.
Treatment
The pathophysiology of chronic pain is complex and
the treatment is signi cantly different from the traditional treatment options for acute in ammatory pain in veterinary patients. The mechanisms involved in central neuropathic pain, and thus the core treatment targets, are primarily receptors of the dorsal horn and higher pain centres (eg. the somatosensory cortex, periaqueductal grey and limbic systems). The aim is to identify the pain mechanisms responsible for the clinical signs, to de ne the treatment targets and obtain the best possible analgesia with a minimum of adverse drug reactions. There are no published, evidence-based protocols on the treatment of central neuropathic pain in dogs with CM and SM. The following protocol is based on the author’s personal experience combined with recommendations from published data on central neuropathic pain and treatment protocols in human patients.
Pregabalin (PGN) is a structural gamma-aminobutyric acid (GABA) analogue with anticonvulsant and analgesic properties. The primary target of PGN is the α2-δ- subunit of the voltage-gated calcium channels in the central nervous system. The analgesic effect of PGN is mediated through the inhibition of voltage-gated calcium channel function by a reduction in anterograde α2-δ- subunit traf cking and impairment of upregulation of synaptic expression and inhibition of synaptic excitatory neurotransmitter (glutamate) release in the dorsal root ganglia and dorsal horn. In addition, PGN enhances
the expression of excitatory amino acid transporters (EAAT3) in neuronal plasma membranes. This leads to increased inactivation and reduction of the extracellular concentration of glutamate. A third target site is the spinal cord KATP potassium channel. PGN activates the potassium channel, and the prolonged opening results in neurotransmitter release inhibition (primarily substance P) and modulated neuronal excitability (8). The pharmacokinetics of PGN after PO administration (4 mg/kg) has been investigated in six adult Labrador
/ Greyhound dogs (9). The reported maximal plasma concentration, Cmax was 7.15 (4.6 – 7.9 ) μg/mL and the time for Cmax to occur, Tmax was 1.5 (1.0 – 4.0) hours. Elimination half-life (T1⁄2el) was 6.9 (6.21 – 7.4) hours. No adverse effects were seen. Yet, to date, the available clinical research data on the usage of PGN in canine patients with chronic pain is very sparse. One prospective cohort study on long-term outcome in
48 CKCS has shown improvement or the status quo maintained in 12/48 (25 %) of dogs treated with PGN (2-4 mg/kg PO q8h), gabapentin and/or intermittently carprofen (10). The recommended anticonvulsant PGN dosage for canine patients is 2-4 mg/kg q8-12h. For the treatment of neuropathic pain, we have anecdotal reports and personal experience with a dosage regimen of 2-10 mg/kg (and titrated to effect up to 30 mg/kg) q12h. In human patients with different causes of neuropathic pain, PGN has been found effective in several randomized, double-blind, placebo-controlled clinical trials.
NSAIDs as an add-on to the multimodal protocol will reduce the peripheral micro-in ammation caused by the scratching. In case of an insuf cient analgesic effect, add-on with an opioid (eg. tramadol 1-4 mg/kg PO q4- 8h) or with the tricyclic antidepressants clomipramine
or amitriptyline (1-2 mg/kg PO q24h) may improve the analgesic effect and reduce the scratching in most patients.
Routine follow-up on the effect of the multimodal treatment regimen is imperative. Owners must observe their dogs on a daily basis and report on prede ned parameters, including reduction in scratching events during the day, potential side effects (primarily ataxia
and sedation) and general quality of life. This enables
the veterinary surgeon to evaluate continuously the success of the treatment continuously. The prognosis is guarded and treatment effect varies between individuals, depending on co-morbidities. Twenty percent of CKCS with symptomatic SM will be euthanized due to non- suf cient treatment effects and severe pain manifestation, which results in a markedly reduced quality of life (4, 10).
42ND WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND FECAVA 23RD EUROCONGRESS


































































































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