9 Aug 2016
Arianna Negrin and Giunio Bruto Cherubini investigate the clinical signs and epidemiology of the most common spinal diseases in cats, with discussion of management using diagnosis acronym “VITAMIN D”.
Figure 2. An 11-year-old female neutered domestic shorthair cat with progressive C6 to T2 hemiparesis and cervical pain. (A) Transverse T2-weighted image. Heterogeneously hyperintense mass lesion extending from the left paraxial muscles into the vertebral canal, with severe compression of the spinal cord. (B) Transverse T1-weighted image post-gadolinium. Heterogeneous contrast enhancement of the neoplasia.
Although gait abnormality is one of the most common neurological presentations in feline neurology, in many cases, a definitive cause of spinal weakness in cats is difficult to reach. In general, the prognosis depends on three main factors – the severity of the clinical signs, their chronicity and the underlined aetiology.
Clinical signs and epidemiology of the most common feline spinal cord diseases – including vascular myelopathy, intervertebral disc diseases, primary spinal cord trauma, spinal cord neoplasia and feline infectious peritonitis – have been extensively reported in the literature; however, data on specific therapies and long-term prognosis have not been generally investigated.
This article aims to describe clinical signs, diagnosis and management of the most common feline spinal diseases.
A neurological examination aims to confirm the presence of a neurological condition and, eventually, localise a lesion within the nervous system. Once the lesion has been localised, a list of potential differential diagnoses are considered in order of probability.
Together with neurological lesion localisation, patient signalment, lateralisation of neurological signs, presence of pain, speed of onset and disease progression, the response to previous therapies needs to be considered to determine the most likely differentials.
However, it is important to underline that spinal pain may help to confirm the clinical localisation once the neurological examination has already localised the specific spinal cord segments affected; however, it should not be used to first localise the lesion site.
Abnormal gait due to a neurological lesion can be characterised by a dysfunction of sensory pathways (ataxia) and/or a lesion in motor pathways (paresis/plegia).
Voluntary motor function – the ability to generate movements – should not be confused with the presence of spinal reflexes. A dysfunction of voluntary motor activity does not imply the spinal reflexes are affected, as plegic limbs can have normal reflexes if the lesion is localised to the C1 to C5 or T3 to L3 spinal cord segments. Detection of voluntary movement is very important to define prognosis; for this reason, confusion between voluntary movements and reflexed activity of a limb should be avoided.
The spinal cord is clinically divided into four segments (C1 to C5, C6 to T2, T3 to L3 and L4 to S2) responsible for specific neurological signs. Asymmetry or lateralisation of neurological signs needs to be carefully evaluated. Lateralised lesions affecting C1 to C5 or C6 to T2 can cause hemiparesis and ipsilateral proprioceptive deficits. Monoparesis is usually observed in markedly lateralised lesions of the spinal cord.
The acronym “VITAMIN D” ensures all possible disease mechanisms responsible for neurological clinical signs are considered (Table 1).
Vascular diseases of the spinal cord usually have peracute or acute onset of non-progressive signs, developing in minutes or hours, causing asymmetrical signs without spinal hyperaesthesia.
Worsening of neurological deficits has been reported in the first 24 to 72 hours and stabilisation and/or improvement of the neurological condition is usually observed later (Wessmann et al, 2008).
However, in some cases, progressive deterioration of clinical signs can be observed after several days due to cytotoxic oedema formation, with free-radical production after cellular necrosis as the final stage (Wessmann et al, 2008).
In severe vascular myelopathy, deterioration of neurological signs over time may also be suggestive of an ascending/descending myelomalacia, associated to poor prognosis.
A major cause of a vascular event in cats is fibrocartilaginous embolism (FCE), particularly in the cervical spinal segments, and feline ischaemic myelopathy due to vascular hyaline degeneration, resulting in vascular aneurysmal dilation and thrombosis (Rylander et al, 2014). Systemic hypertension and vascular malformation have also been reported (Parkes et al, 2009; Schur et al, 2010).
Vascular diseases are one of the most common causes of spinal cord dysfunction in cats (Gonçalves et al, 2009; Marioni-Henry et al, 2004). Spinal cord ischaemic infarction occurs due to obstruction of a spinal cord vessel by fibrocartilaginous material, thought to originate from the intervertebral disc (Neer, 1992).
Mild traumatic events, or migration of the disc material into the spinal arteries due to persistence of a common vascular connection between the intervertebral disc and the spinal cord, have been postulated (Abramson et al, 2002; Mikszewski et al, 2006). Peracute/acute onset of asymmetrical, but not painful, clinical signs are the most typical presentation; in some cases, progression over the first 24 hours has been reported (Abramson et al, 2002, Coradini et al, 2005).
Definitive diagnosis of FCE is only based on histopathological confirmation (Mikszewski et al, 2006); for this reason, antemortem diagnosis is reached by elimination of other causes of myelopathy. CSF analysis may detect neutrophilic pleocytosis and/or increased total protein levels.
MRI is usually characterised by hyperintense signal on T2-weighted images, isointense or mildly hypointense signal on T1-weighted images and mild contrast enhancement after three to seven days (MacKay et al, 2005; Marioni-Henry et al, 2004).
Treatment is supportive and prognosis is guarded. Improvement is frequently recorded within two to six weeks of onset (MacKay et al, 2005).
Ischemic neuropathy more often affects older male cats and is frequently associated with cardiac disease, including hypertrophic cardiomyopathy, which leads to embolisation of the caudal aorta or the bifurcation of the iliac arteries.
Peracute onset of paraparesis or plegia with absent or weak femoral pulses, cold and frequently cyanotic extremities are typically observed. Moreover, muscle pain and cardiac auscultation abnormalities may be detected on physical examination. Abdominal ultrasound of the aortic and iliac arteries may confirm reduced blood flow or the presence of an intraluminal thrombus, while electrocardiography is mandatory in all cats with confirmed aortic/iliac thromboembolism.
Prognosis depends on the primary cause of the thromboembolism, as well as the severity of the neurological deficits. Most cats will die or are euthanised due the underlying cardiomyopathy; initial survival is reported to be around 40% of cases, with a mean survival time of 6 to 12 months (Laste and Harpster, 1995; Schoeman, 1999). Moreover, a high rate of relapses has been reported (Laste and Harpster, 1995; Schoeman, 1999).
Inflammatory spinal cord conditions can have variable onsets – acute, subacute or more insidious, depending on the cause. However, neurological signs usually progress rapidly.
Neurological deficits can be variable in onset and progression, although are often asymmetrical and multifocal (Singh et al, 2005).
A major cause of feline myelitis/meningomyelitis is an infectious disease, which accounts almost 30% of all feline spinal cord diseases and includes bacterial infections, FIP, cryptococcosis, toxoplasmosis, FIV and FeLV (Negrin et al, 2010; Foley et al, 1998, Gerds-Grogan and Dayrell-Hart, 1997).
Moreover, idiopathic granulomatous disease and parasitic migration have been reported; however, the presence of an underlined immune-mediated origin has been suspected in a considerable number of feline myelitis/meningomyelitis.
Spinal trauma is a frequent cause of spinal cord dysfunction in cats. Spinal trauma causes peracute/acute non-progressive neurological signs, which, in some cases, improve over time. In the first 24 to 72 hours, worsening of neurological signs can be noticed due to secondary spinal cord haemorrhage/ischaemia or oedema (Platt and Olby, 2004); however, deterioration of signs after 72 hours may imply spinal instability.
The most common traumatic conditions in cats include thoracolumbar vertebral fracture and luxations, sacrococcygeal subluxation/luxation, traumatic ischemia and disc extrusion (Marioni-Henry, 2004; Platt and Olby, 2004). Neurological signs usually relate to a focal lesion, which might be seen on spinal radiographs in a traumatised cat; however, multiple lesions affecting other spine segments can frequently exist (Platt and Olby, 2004).
Due to the reported radiographic difficulty and limitation in recognised small bone spinal fractures, CT or MRI scans can diagnose suspected spinal injuries (Kinns et al, 2006).
Trauma is an important cause of spinal cord dysfunction in cats. The most common traumatic conditions in cats include thoracolumbar and lumbar vertebral fracture (Bagley, 2000) and luxations (Figure 1), sacrococcygeal subluxation/luxation, traumatic ischemia and disc extrusion (Eminaga et al, 2011; Marioni-Henry, 2004; Papazoglou et al, 2001; Platt and Olby, 2004; Voss and Montavon, 2004). Almost 20% of cats with traumatic spinal injuries also have acute intervertebral disc extrusion (Grasmueck and Steffen, 2004).
Deep pain perception in affected limbs is the most important prognostic indicator following spinal trauma, as a lack of deep pain perception associated with luxated/fractured vertebrae implies a poor prognosis (Platt and Olby, 2004; Voss and Montavon, 2004). In sacrococcygeal subluxation/luxation, attention should be focused to the perineal reflex, deep pain sensation in genital, anal and tail structures, together with the presence of potential urinary and faecal incontinence (Roy et al, 1992; Platt and Olby, 2004; Voss and Montavon, 2004).
About 20% of patients with thoracolumbar fractures have a second spinal column fracture/luxation (Grasmueck and Steffen, 2004); therefore, a CT or MRI image of the whole spine should be performed on any cat with spinal trauma (Platt and Olby, 2004, Grasmueck and Steffen, 2004; Voss and Montavon, 2004).
Management of a cat with spinal trauma should be focused on systemic stabilisation (Eminaga et al, 2011; Platt and Olby, 2004) and evaluation of the airway, breathing and circulation is mandatory before performing a neurological examination. PCV, total protein level, urea and creatinine concentration, and electrolytes should be performed as soon as possible.
Fluid therapy is important to maintain spinal cord perfusion, depending on the severity of hypotension. Isotonic crystalloids, hypertonic saline, colloids or blood products can be used (Platt and Olby, 2004). Steroid use is controversial in acute spinal trauma (Hulbert, 2000; Short et al, 2000) as it may lead to secondary side effects, including infections and gastrointestinal signs (Boag et al, 2001; Rohrer et al, 1999).
Generally, the outcome for cats with spinal trauma is guarded and survival rate in a study was 60% (Grasmueck and Steffen, 2004).
Anomalous conditions include congenital/hereditary malformations of the spinal cord or the surrounding tissues (spinal subarachnoid cyst and vertebral malformations; Lujan et al, 2003; Newitt et al, 2008; Schmidt et al, 2007).
Chronic onset during the early stage of life has been most frequently reported and may progress over time; however, ganglion extradural cysts have been reported in elder cats (de Strobel et al, 2015), suggesting a potential chronic inflammatory or traumatic process of meninges as underlining aetiology.
Metabolic diseases causing neurological deficits compatible with spinal cord localisations are rare.
No idiopathic diseases of the spinal cord are recognised in cats.
Neoplasia is usually associated with chronic progressive clinical signs, although acute/subacute onsets of neurological signs are relatively frequent. Lateralisation of neurological signs is also frequently reported, depending on the lesion site.
The most common neoplasm affecting the spinal cord of cats is lymphoma, followed by sarcoma originated from vertebral column (osteosarcoma) or connective tissue/muscles (fibrosarcoma/myosarcoma; Figure 2) and secondarily compressing the spinal cord (Heldmann et al, 2000; Levy et al, 1997; Marioni-Henry et al, 2008), meningioma (Forterre et al, 2007; Marioni-Henry et al, 2008) and glioma (Marioni-Henry et al, 2008; Stigen et al, 2001).
Lytic lesions can be detected via radiographs of the spine and have been associated more likely with osteosarcoma than lymphoma. Lymphoma has been more frequently reported in the thoracic and lumbosacral spine, while the cervical segment is more frequently affected by gliomas; however, definitive diagnosis of lymphoma may be challenging.
In any case of suspicion of lymphoma, complete work up with blood tests, abdominal ultrasound, chest radiography, bone marrow aspiration and lymph node aspiration should be performed with MRI and CSF analysis.
Degenerative diseases are not common in cats and are typically characterised by chronic, slowly progressing clinical signs. Intervertebral disc disease (IVDD) is the most frequent degenerative condition affecting feline spinal cords (Figure 3).
Clinical signs associated with IVDD may be insidious, starting with reluctance to jump, low tail carriage and constipation, and spinal hyperaesthesia; however, an acute onset may be present in some cats affected by intervertebral disc extrusions (Muñana et al, 2001).
As in dogs, intervertebral disc protrusions (Hansen’s type II) and extrusions (Hansen’s type I) have been reported in the literature, although most of cats with neurological signs due to IVDD are affected by Hansen’s type I (Maritato et al, 2007; Kathmann et al, 2000; King and Smith, 1960; Rayward, 2002).
The cervical region is most commonly affected by chronic bulging of the annulus fibrosus into the spinal canal (King and Smith, 1960). Disc extrusions causing neurological dysfunction are more common in the thoracolumbar junction (T13-L1) and L4-L6 segments (Harris and Dhupa, 2008; Lu et al, 2002; Muñana et al, 2001). The great mobility of lumbar and lumbosacral segments may play an important role in aethiopathogenesis of spontaneous disc extrusion in this region (Muñana et al, 2001).
IVDD occurs more frequently in older cats (Muñana et al, 2001). Neurological signs may be insidious, such as abnormal posture, difficulty in assuming/maintaining the position to defecate (which may cause constipation), reluctance to jump, low tail carriage and spinal pain. Spinal cord compression, secondary oedema/haemorrhage and nerve root compression is well detected by MRI (Lu et al, 2002; Muñana et al, 2001).
Surgery is required once neurological signs are observed and can be associated with a good prognosis (Lu et al, 2002; Muñana et al, 2001), although residual urinary and/or faecal incontinence has been reported (Harris and Dhupa, 2008, Muñana et al, 2001).
Similarly to haematology and serum biochemistry tests, radiographs and ultrasound should be performed in cats before advanced imaging tests, to detect signs of potential metastatic or primary neoplastic conditions and to obtain more information about the general status of the patient before general anaesthesia.
Spinal radiographs are indicated in most vertebral column diseases, but, particularly, to rule out neoplastic diseases causing osteolysis (Marioni-Henry et al, 2008).
CT can provide good tissue detail, especially of the bone, and enables 3D evaluation of the spinal cord and vertebrae following digital reconstruction. It is, therefore, particularly useful in cases of spinal trauma or when a bone tumour is suspected.
MRI is the most sensitive and specific imaging test for the evaluation of the CNS (Negrin et al, 2007; Olby and Thrall, 2004). It has been shown to identify the early stages of vascular lesions and provides good bone detail, distinguishing the primary process (neoplasia/inflammation) from the associated secondary lesions (oedema/haemorrhage).
The severity of clinical signs and the presence of pain are two independent factors predicting whether the MRI would be abnormal in cats with spinal cord diseases (Gonçalves et al, 2009). Cats with plegia and spinal cord pain were more likely to have an abnormal MRI than cats without spinal pain or ambulatory paresis.
CSF analysis is indicated if the differential diagnoses include inflammatory conditions (Hartmann et al, 2003; Rand et al, 1994a and 1994b; Singh et al, 2005); however, some neoplastic conditions, including round cell tumours (lymphoma), can infrequently be diagnosed by CSF analysis (Lane et al, 1994).
Corticosteroid administration decreases the white blood cell count and/or total protein levels (Wamsley and Alleman, 2004); therefore, evaluation of CSF in pretreated cats may give false negative results.
